Alarm 26thed - Manual - EN

Course Manual
Advances in Labour and Risk Management

26th EDITION, 2019-2020
The ALARM Course Manual is published by the SOGC.
Copyright SOGC 2018–2019. All rights reserved.
Reproduction of this material is not permitted without explicit written consent of the SOGC. Views expressed in the
document
The ALARM do not necessarily
Course Manual reflect
is those of the SOGC
published members.
by the SOGC.
Copyright SOGCCataloguing
Canadian 2018–2019. All rightsData
in Publication reserved.
Reproduction of this material is not permitted without
Main entry under title:explicit written consent of the SOGC.
Views expressed in the documentALARM Manual 26 edition
th
do not necessarily reflect those of the SOGC members.
ISBN
Canadian Cataloguing in Publication Data
1. Health
Main entryCareunder
– Obstetrics
title:
ALARM Manual
2. Labour 25th edition
– Risk Management
ISBN 978-1-897116-53-1
1. Health Care – Obstetrics
2. Labour – Risk Management
26th Edition of the ALARM Course Manual
Purpose
This course arose out of our work in the care of women in labour, their babies, and their families. Our single overriding
objective is to improve the outcome and the process of intrapartum care. One way to achieve that objective is through
our continuing education. The ALARM course is one means of that education. The course is maintained and taught
by family physicians, nurses, midwives and obstetricians. It has the administrative support and backing of the Society
of Obstetricians and Gynaecologists of Canada. It is based on the best current evidence we have about what works to
improve care, and incorporates Canadian practice guidelines.
The information and recommendations in this syllabus reflect the emerging clinical and scientific advances as of
the date of issue and are subject to change without notice. The information should not be construed as dictating
an exclusive course of treatment or procedure to be followed. Correct drug dosages should be verified before
administration.
3
Recognition
This 26th edition of the ALARM Course Manual was revised under the direction of the Obstetrical Content Review (OCR)
committee and the ALARM committee.
Obstetrical Content Review Committee members – 26th Edition
P. James Ruiter (Co-Chair), MD, London, ON
Suzanne Toni Wong (Co-Chair), MD, Toronto, ON
Amanda Ashe, RM, Newcastle, ON
Christine Bloch, MD, Stratford, ON
Sharon Dore, RN, PhD, Burlington, ON
Wesley Edwards, MD, Ottawa, ON (CAS* representative)
William Ehman, MD, Nanaimo, BC
Ronald George, MD, Halifax, NS (CAS* representative)
Robert Gratton, MD, London, ON
Jonathon Hey, MD, Saskatoon, SK
Daniel Kiely, MD, Montreal, QC
Andrew Kotaska, MD, Yellowknife, NT
W. Kim MacDonald, MD, Garibaldi Highlands, BC
Diane Sawchuck, RN, PhD, Vancouver, BC
Karine Vallee-Pouliot, RM, Montreal, QC
Megan Williams, MD, Ottawa, ON
*Canadian Anesthesiologists’ Society
ALARM Committee members – 26th Edition

Catherine Cowal (Co-Chair), MD, Burlington, ON
Marie-Jocelyne Martel (Co-Chair), MD, Saskatoon, SK
Gisela Becker, RM, St. John’s, NL
Fran Berard, MD, Winnipeg, MB
Anne Biringer, MD, Toronto, ON
Hayley Bos, MD, Victoria, BC
Krista Cassell, MD, Charlottetown, PE
Amy Gausvik, MD, Calgary, AB
Narinder Kainth, RN, Markham, ON
Stephanie Morel, MD, Montreal, QC
Suzanne Roberge, MD, Baie-Comeau, QC
Suzanne Roberts, MD, Saint John, NB
4
Disclaimer
SOGC has done its best effort to provide a product that is useful in terms of providing educational information based on
an evaluation of scientific literature and medical experience. The educational content attempts to describe principles of
practice generally applicable in most circumstances.
This document reflects emerging clinical and scientific advances on the date issued and is subject to change. The
information should not be construed as dictating an exclusive course of treatment or procedure to be followed. Local
institutions can dictate amendments to these opinions. They should be well documented if modified at the local level.
None of these contents may be reproduced in any form without prior written permission of the publisher.
All people have the right and responsibility to make informed decisions about their care in partnership with their health
care providers. In order to facilitate informed choice, patients should be provided with information and support that is
evidence-based, culturally appropriate and tailored to their needs.
This document was written using language that places women at the centre of care. That said, the SOGC is committed
to respecting the rights of all people – including transgender, gender non-binary, and intersex people – for whom the
guideline may apply. We encourage healthcare providers to engage in respectful conversation with patients regarding
their gender identity as a critical part of providing safe and appropriate care. The values, beliefs and individual needs of
each patient and their family should be sought and the final decision about the care and treatment options chosen by
the patient should be respected.
5
Suggested Reading
A variety of sources including standard textbooks and articles from the usual journals have been used in the
development of the ALARM manual. These sources include but are not limited to:
1. The Cochrane Pregnancy and Childbirth Database. (Distribution ceased after 1995)
2. The Cochrane Library (http://www.thecochranelibrary.com/).
3. Enkin M, Keirse M, Neilson J, Crowther C, Duley L, Hutton E, et al. A guide to effective care in pregnancy and
childbirth. 3rd ed. Toronto: Oxford University Press; 2000.
4. Basket TF, editor. The essential management of obstetrical emergencies. 4th ed. Bristol (UK): Clinical Press;
2004.
5. Healthy Pregnancy and Infancy sections of the Public Health Agency of Canada website
(http://www.phac-aspc.gc.ca/hp-ps/index-eng.php).
6. Society of Obstetricians and Gynaecologists of Canada clinical practice guidelines
7. Additionally, we have used two video tapes.
a. The Safe and Appropriate Use of Forceps in Modern Obstetrics (available from Janssen-Ortho)
b. Term Breech Patient Selection and Intrapartum Management (available from Wyeth Pharmaceuticals)
6
Table of Contents
Chapter 1 Communication .................................................................................................................................................. 9

Chapter 2 Evidence-Based Obstetrics................................................................................................................................. 34
Chapter 3 Patient Safety..................................................................................................................................................... 45
Chapter 4 Management of Labour..................................................................................................................................... 64
Chapter 5 Support and Pain Management in Labour ........................................................................................................ 96
Chapter 6 Induction of Labour......................................................................................................................................... 110
Chapter 7 Umbilical Cord Prolapse.................................................................................................................................. 145
Chapter 8 Fetal Well-Being During Labour....................................................................................................................... 151
Chapter 9 Vaginal Birth ................................................................................................................................................... 219
Chapter 10 Assisted Vaginal Birth.................................................................................................................................... 228
Chapter 11 Delivery of Twins............................................................................................................................................ 260
Chapter 12 Trial of Labour After Caesarean....................................................................................................................... 276
Chapter 13 Shoulder Dystocia.......................................................................................................................................... 289
Chapter 14 Breech Presentation and Delivery................................................................................................................. 309
Chapter 15 Postpartum Hemorrhage............................................................................................................................... 333
Chapter 16 Hypertensive Disorders of Pregnancy............................................................................................................ 375
Chapter 17 Preterm Labour and Preterm Birth ................................................................................................................ 412
Chapter 18 Prelabour Rupture of Membranes (PROM)................................................................................................... 438
Chapter 19 Antepartum and Intrapartum Hemorrhage................................................................................................... 454
Chapter 20 Prevention of Early-Onset Neonatal Group B Streptococcal Disease............................................................. 481
Chapter 21 Venous Thromboembolism and Amniotic Fluid Embolus............................................................................. 502
7
Table of Contents
Chapter 1 Communication .................................................................................................................................................. 9

Strategies for Effective Communication ....................................................................................................................... 9
Strategies to foster Interprofessional Care and Planning .......................................................................................... 10
Use of Social Media ................................................................................................................................................... 11
Special communication situations ............................................................................................................................. 12
1. Informed Consent ....................................................................................................................................... 12
2. Communication in the Consultation Process.............................................................................................. 13
3. Communicating About Adverse Events....................................................................................................... 14
Effect of Adverse Events on Parents, Families and Caregivers..................................................................................... 15
Response and Coping Mechanisms................................................................................................................ 16
Follow-Up........................................................................................................................................................ 18
Coping Mechanisms: Care Providers.............................................................................................................. 19
Adverse Events and Litigation .................................................................................................................................... 19
Disclosure................................................................................................................................................................... 20
Barriers to Disclosure...................................................................................................................................... 22
What do patients expect?................................................................................................................................ 22
Benefits of Disclosure...................................................................................................................................... 23
How to Disclose............................................................................................................................................... 23
Event Reporting .............................................................................................................................................. 24
Documentation .............................................................................................................................................. 25
Electronic Medical Record (EMR) .................................................................................................................... 26
Communication 8
Chapter 1
Communication
All levels of communication – intra and inter professional, with learners, with support staff, and with women
and families are essential for team work, and effective team work is essential for patient safety.1 A Cochrane review on
interventions to promote collaboration between nurses and doctors showed that increasing collaboration improved
outcomes of importance to patients and health care managers.2 Ineffective communication was cited by The Joint
Commission on Accreditation of Healthcare Organizations as the most common root cause of adverse events leading
to perinatal death and injury between 1995 and 2014.3 An adverse event is defined as an unexpected occurrence that
either causes harm or has the potential to cause harm.4 The 2018 review of HIROC and CMPA data showed breakdown
in team communication occurred in 20% of cases and communication issues with patients and their families occurred in
4% of cases.5
Strategies for Effective Communication

• Mutual respect
• Language that is clear and precise – use defined and agreed upon words and abbreviations.eg:
−− When calling a professional colleague regarding a fetal heart rate tracing don’t say “I have an ugly
tracing with some dippity parts” Say “I have an abnormal tracing with late decelerations occurring with
80% of contractions, a baseline of 160, minimal variability”.
−− Avoid making partial statements and assuming others know what you mean. This is called cognitive
under specification, defined as “a communication style that leads to a gap in knowledge.”14 An example
cited in an ICU was a nurse telling a physician that a patient had low potassium. The response was ‘‘let’s
give him a run of 10 × 4.’’ The nurse entered the order into the computer for potassium chloride 10
meq. IV Q1 hr × 4 doses. This was what the resident intended, despite the lack of a stated drug name,
complete dose, route, or schedule..6 If either the physician or the nurse had been new to the unit,
a serious knowledge gap—and possibly an adverse event—could have occurred. It’s often difficult to
recognize these gaps when they occur in our own domains.
−− When speaking to parents and families use terminology that everyone understands and use plain
language rather than jargon. Patients and their families may not understand the medical terminology
that makes communication with other team members clear and efficient.
• If messages or orders are hand written, they must be neat and legible
• Caution should be taken in individuals who speak a different primary language from the caregiver. In our
multicultural societies, there is a need for capable interpreters. While families can be used for translation,
caregivers need to be aware of potential conflict of interest or values between family members. Use of official
translators or a telephone language line may be considered.
Communication 9
• Timely flow and transfer of relevant information; Use of acronyms to ensure timely, logical and complete
information has been adopted by many health care facilities. Providing a structure for communication
is effective in conveying a clear message. This format can be used in verbal communication as well as
documentation. e.g.: SBAR.
−− Situation Take 5-10 Seconds to Explain
−− Background Provide Context and Data
−− Assessment Describe the Specific Problem/Situation
−− Recommendation Explain What You Want to Do About it and When
• Take the time the time needed to communicate in a clear, patient and respectful manner. This is particularly
important if there has been an adverse event.
• Clear delineation of the roles of the communicators
• Respect for confidentiality
• Conducive environment:
−− Ambiance, emotional tone, privacy, and distractions can enhance or impede the quality of
communication.
• Active listening is an important part of effective communication. It entails using eyes, ears, and brain, and
seeking to understand before being understood.7 Effective listening demonstrates respect.
• Non-verbal messages are generally considered to be five times more influential than verbal messages.
Eye contact is considered part of non-verbal communication. Non-verbal communication is often used
unconsciously and may more accurately indicate a person’s meaning than the words being spoken.8 The tone
of the words and inflections of speech are also major elements of communication. Many people lack insight
into the way they use non-verbal communication, and reviewing videotaped simulations can help them
increase their awareness.
• Include everyone the information affects11
Professionalism in communication requires that caregivers understand and acknowledge the perspective of other
professionals and the perspective of learners within each profession. The hierarchy that has traditionally existed in health
care is not useful in a system that requires professionals from multiple professions to work as a team. No profession can
function in isolation; members of each must call upon the expertise, skills, perspectives, and information of others to
provide comprehensive, coordinated, and safe care.7
Because learning to work within an interprofessional model of care is not part of basic training, many health care
providers find it challenging; however, focussing on the patient and on quality of care makes the transition easier.7
Strategies to foster Interprofessional Care and Planning

• Simulations for emergency situations involving all caregivers
−− Rehearsing responses to emergencies as a team using evidence-based, unit-specific protocols facilitates
efficiency, performance, and effectiveness in real emergencies
−− Drills also provide an opportunity to practise effective communication between caregivers
• Committee structure that involves all professions
• Care planning that incorporates input from a variety of professions
Communication 10
• Debriefing unusual events or normal practices as a team

• Non-punitive interprofessional case reviews
• Development of interprofessional procedures
• Investigating the impact of poor quality relationships as a barrier to improvements in communication and
performance9
Use of Social Media

Social media is increasingly becoming part of communication for health professionals, parents and families.
Engagement with social media, for health-related and educational purposes, can be personal, professional, or both.
However, it can raise questions related to confidentiality, ethics, privacy, and control to which we do not have clear
answers.10 Health care values differ from social media values of sharing, openness and informality.11
Social Media guidelines for health professionals have been created by professional organization. One example from
oncology and vascular specialities suggest:12
Content credibility • Only Share information from credible sources

• Refute inaccurate information
Legalities • Content you write may be used in court
• Comply with privacy laws
• Respect copyright laws
Networking • Do not contact patients with a request to join your network
• Redirect patient who want to join your personal network to your professional site
Patient care • Avoid providing advice to non-patients
• Make appropriate disclosures and disclaimers regarding the accuracy, timeliness, and privacy of electronic
communications.
Patient privacy • Avoid writing about specific patients.
• Make sure you are in compliance privacy laws.
• Obtain patient consent when required.
• Protect patient information through “de-identification.”
• Use a respectful tone when discussing patients.
Personal privacy • Separate personal and professional profiles
• Make sure that your credentials are correctly stated.
• Specify whether or not you are representing an employer.
Social media can be used for public or professional education and support. The Mayo Clinic has a Center for Social Media
devoted offering patients a vast library of podcasts and blog posts written from health professionals (http://socialmedia.
mayoclinic.org/). Facebook groups have been used by universities to provide a stress reduction intervention for medical
students.13 The Canadian Association of Perinatal and Women’s Health Nurses (CAPWHN) has a discussion forum for
Communication 11
members to share information with colleagues across the country. Family Practice has a Family Physician Maternity &
Newborn Care listserv (FPMNC).
When used appropriately, social media sites have the ability to promote health, as well as lay and professional education
and understanding.11 However, when used carelessly, there are potential to pose negative professional and legal
dangers consequences. 8 Guidelines issued by health care and professional organizations and professional provide
sound and useful principles that health care professionals should follow to avoid pitfalls.15
Special communication situations

1. Informed Consent
Informed consent must be obtained to protect the patient’s right to make decisions about treatment. The Canadian
Medical Protective Association states that for consent to be considered valid:
• It must be voluntary: patients must not be coerced and must be free to consent to or refuse the proposed
treatment or investigation
• Patients must have the capacity to consent: they must be able to understand the nature of the proposed
treatment or investigation and its anticipated effect it will have, and the likely consequences of refusing the
treatment or investigation
Patients must be properly informed: they should be informed of the diagnosis, and the proposed investigations and
treatments and their risks and chances of success. They must also be informed about the consequences of refusing the
proposed interventions.14, 15
Consent must be obtained by a caregiver who has knowledge of the procedure, possible side effects, and consequences.
Alternatives to the treatment, if they exist, need to be presented and discussed.
For patients to provide consent, they must have the mental capacity or competency to provide consent, consent must
be given voluntarily, must be informed, and must apply to a specific act or set of acts. The ultimate responsibility for
ensuring informed choice and the mental capacity of the patient to provide consent, and for documenting a valid
consent rests with the caregiver proposing and providing the intervention.16
The patient is the primary decision-maker in the consent process. If she has decreased capacity for comprehension, the
decision for intervention is based on prior informed consent if the patient’s wishes are known.17 If her wishes are not
known, the decision can be based on what is judged to be in her best interests. If time permits, discussion and decision
making should be undertaken collaboratively by the family and health professionals. Care providers should be aware of
the facility’s algorithm for determining the substitute decision-maker if the patient is unable to give consent.
If there is refusal of consent or lack of timely agreement, care providers must ensure complete documentation of the
discussion and woman’s stated rationale for refusal. They must also maintain open communication and show courtesy
and respect while continuing to offer appropriate care alternatives and treatments. The CMPA’s Good Practices Guide
provides further information and a review of key concepts.
Communication 12
2. Communication in the Consultation Process18

Consultation is a crucial element of teamwork, and within the consultative process, all participants share responsibility
for communication.19
PARENT REFERRING CAREGIVER CONSULTANT
Demonstrate courtesy and respect Demonstrate courtesy and respect Demonstrate courtesy and respect
Participate in decision making Assess patient before referral Provide reasonable access to services
Ask questions if unsure of purpose of Communicate reason for consultation and Report hospital admissions and discharges
consultation, investigations, diagnosis, and level of consultation requested (opinion,
Return patient care to referring caregiver
risks and benefits of proposed treatment opinion and shared care, or transfer of care)
when appropriate
options
Read relevant patient education material Provide relevant documentation Provide relevant documentation
Know which caregiver is responsible for care Discuss and confirm with the whole team Discuss and confirm with the whole team
(which includes the patient) who will be the (which includes the patient) who will be the
most responsible provider for current and most responsible provider for current and
ongoing care ongoing care
Ensure the primary care provider is informed

if unrelated problems are discovered so
referral can be made to an appropriate
specialist or sub-specialist.
A consultation can consist of (1) consultation only, (2) consultation with concurrent/shared care, or (3) consultation with
transfer of care.
In a 2012 study, Kessler et al.20 described a standardized approach, using the five Cs of consultation that increased the
effectiveness of communication:
Contact Introduce consulting and consultant physicians. Build relationship.
Communicate Give a concise story and ask focused questions.
Core Question Have a specific question for or request of the consultant. Decide on reasonable timeframe for consultation.
Collaborate Discuss with the referring care provider and the consultant any alteration of management or testing of
patient’s status.
Close the Loop Ensure that both parties have the same understanding of the plan for the patient and that they maintain
proper communication about any changes in the patient’s status.
Communication 13
The need for consultation may be dictated by professional standards or may be established by organizational or
community resources. Consultations may involve social workers, dietitians, nurses, midwives, physicians, lactation
consultants, community nurses, and many others. Professional bodies describe scope of practice for nurses, midwives,
and physicians. The most appropriate course of treatment and referrals should be agreed upon, documented in the
chart, and discussed with and understood by the patient. All parties should know which option has been selected and
should be prepared to fulfill their responsibilities. The patient, her family, and the health care team must all know who
is most responsible for the woman’s care, and this information must be recorded on the patient’s chart. Appropriate
communication and fulfilment of responsibilities will improve patient care and satisfaction, care provider satisfaction,
clarity of care-planning, quality of care, and patient safety.21
3. Communicating About Adverse Events

Care providers often have to break bad news to patients or families, frequently without having had time to prepare. They
must communicate effectively and clearly, but also compassionately. The information they are conveying is life-changing
for patients and families, who often remember for years what is said in such situations.22
Obstetrical health care providers can find it difficult to talk to patients about adverse events such as miscarriage or
termination, fetal anomalies, perinatal death, stillbirth, and the compromised infant. Patients and families are often
dissatisfied with the type and amount of information they receive from their health care providers,23 and many health
care providers do not feel confident in their ability to break bad news, but this skill, like other clinical skills, can be
learned. Although there are no evidence-based guidelines for relaying bad news, qualitative and descriptive research
indicates that appropriate disclosure is an effective risk management strategy.24 Improved communication of bad news
can reduce distress, enhance coping, and reduce the risk of unrealistic expectations, and inappropriate denial for the
patient and her family, and can minimize stress for care providers.
Strategies for the Communication of Bad News

Robert Buckman and Walter Baile have suggested mnemonics for communicating bad news to parents and families :25, 26
SPIKES: CONES:
for breaking bad news for discussing a medical error or sudden deterioration or death
• S setting up the conversation= environment, planning what you • C context = quiet area, patient closest to you, maintain eye
will say, key people present contact
• P perception = assessing the patient’s understanding of the their • O opening shot = alert patient/family of important news
condition • N narrative= explain the chronological sequence of events
• I invitation= get permission to have the discussion; ask before • E emotions= address emotions with empathetic response
you tell • S strategy and summary = summarize discussion and make a
• K knowledge= explain the facts, avoid medical jargon plan; let them know the situation is a priority
• E emotions= be supportive
• S strategy and summary = summarize the conversation and
agree on a plan
Communication 14
Some examples of phrases that could be useful include:
USEFUL TO SAY NOT USEFUL TO SAY
I’m sorry for your loss. This happened for the best.
I wish things could have been different. Time will heal.
I can sit here with you for (specified amount of time) if you’d like Now you have an angel in heaven.
company.
If you’re too overwhelmed to talk now, we can talk again later. Mother Nature knows best.
If you want to talk about this, I can listen. If you have questions, I’ll try It was a blessing. He would never have been normal anyway.
to answer them.
Is there someone I can call for you? You’re young. You can have others.
Would you like to talk to a counsellor? I can arrange that for (this Better for this to have happened now, before you knew the baby.
afternoon/tomorrow/ other specified time).
Are there things we can find for you? (This could be something as He was born dead. You didn’t have a chance to get attached to him.
pragmatic as forgotten reading glasses or as poignant as an item
made for the dead baby.)
Would you like to get out into the fresh air? We have a quiet garden At least you have one already.
nearby.
Is there anything you need? You can have another baby right away.
Just thank God for your healthy children at home.
You have to get on with your life.
Better luck next time.
Practice makes perfect.
It’s God’s will.
Effect of Adverse Events on Parents, Families and

Caregivers 2728
Events occurring in early pregnancy can have a similar effect to those occurring later, although caregivers have
historically considered later pregnancy events more significant.29 Maternal–fetal attachment was originally thought to
begin with maternal perception of fetal movements; however, the literature indicates that attachment for many women
begins as early as pregnancy symptoms appear and increases when the fetus is seen on ultrasound examination.30
Communication 15
Partners also felt significantly enhanced attachment when they watched ultrasound images of the fetus.30 A woman who
has had a negative outcome in a previous pregnancy may delay her attachment until later in the pregnancy.31
Miscarriage is usually considered a distressing experience, regardless of the gestational age at which it occurs.31, 32
The response of the patient and her family may be different when a termination is carried out because of fetal
anomalies, 31, 33 and health care providers must be sensitive to this.
33
A survey of women who had experienced an early loss34 indicated that nearly three quarters experienced it as the death
of their baby, believed they had caused the death of their baby, and felt emotionally and/or physically out of control.
Many had nightmares, and most said they felt that part of them had died.
In a 2004 qualitative study,35 women reported characteristic symptoms of PTSD, such as flashbacks, persistent avoidance
of stimuli associated with the trauma, anxiety, emotional detachment, and fear of future pregnancies.
When a miscarriage occurs or a termination is performed there are no legal requirements with respect to disposal of
the products of conception,36 which are usually dealt with in accordance with institutional guidelines for surgical tissue/
medical waste. For many women, the option of burial may provide some degree of closure. Care providers should also be
sensitive to cultural differences, which may require other approaches to the management of loss.
Although some adverse events are clear (infant is stillborn), others are less so (infant is compromised), and when the
extent of the problem or the long-term effects are not known, it is more difficult for clinicians to explain to the patients
and more difficult for the patients to understand.
Interpretation of the Event

Personal, cultural, and social context influence how patients and families interpret events. For instance, if an adolescent
with significant medical comorbidity delivers a stillborn infant at 24 weeks’ gestation, it’s likely that both the adolescent
and her mother will experience mixed emotions. In addition to feeling loss, the mother, as her daughter’s support
person, may also feel relief because of concerns about coping with a new baby and the potential harm to her daughter’s
health.
Previous personal experience also affects interpretation. A successful outcome with a previous preterm birth will likely
lead to optimism in the event of a second preterm birth, whereas a previous neonatal death may mean ongoing anxiety
with the subsequent pregnancy.
Men and women may not experience grief in the same way and may have discordant coping mechanisms.37Women
generally have higher levels of grief and grieve longer.37 Perceived societal and cultural expectations regarding gender-
specific expressions of grief may influence these differences.
Response and Coping Mechanisms

The individual and family response varies according to the nature of the event, interpretation of the event, and coping
resources available. The way people cope with adverse events is influenced by their cultural traditions and expectations,
their religious affiliations and beliefs, and their family structure.30, 38 Health care providers should be aware that each
Communication 16
patient will have her own definition of “family”, which may include colleagues and friends. They should also be aware of
their own assumptions, and of the variety of responses to perinatal loss and grief they may encounter within the cultural
and religious groups within their geographic area of practice. The ability to cope will also be affected by other events
happening at the same time.
Elisabeth Kubler-Ross proposed 5 stages of grief and loss, denial, anger, bargaining, depression, and acceptance,39
but noted that these stages were not necessarily experienced in the same order or for the same duration. Grief may
present in many ways and time frames. Responses may include mood disorders, social withdrawal, impaired memory
or concentration, appetite changes, and sleep changes. It is also variable based on culture, on the nature of the event,
coping resources, and interpretation of the event.
Up to 20% of parents will suffer psychological symptoms for years following the death of a baby.40, 41 Potential markers
for impaired psychological resolution include not seeing or holding the baby, unsupportive partner or family, and
subsequent pregnancy.
Parents often are very anxious and angry and may blame health care providers. They often experience a loss of
self-esteem and a sense of failure.31 They may have difficulty in coping with the immediate tasks such as funeral
arrangements and death registration.
Siblings may be the forgotten mourners. It is often left to the parturient partner to share information with other children—
their age, awareness of the pregnancy, and personal previous experiences affect their understanding and interpretation.
How Health Care Providers Can Help Patients to Cope

When a baby is sick or dying, it is important for care providers to acknowledge the problem and, in collaboration
with neonatal care providers, explain the immediate care plan. If the baby is to be transported to another centre, care
providers should explain the process to the parents and determine whether the mother can also be moved to be near the
baby. The parents should be involved in important decisions (e.g., withdrawing life support), and care providers should
visit both parents and newborn frequently. Care providers may also:40, 42
• Encourage parents to have as much contact with the baby as possible
• Allow parents to take the dying baby in their arms
• Respect the need for privacy
• Arrange ongoing care for the parents
• Make referrals that will minimize other potential stresses such as the need for accommodation,
transportation, childcare, parental leave
Following a pregnancy loss or the loss of a newborn, parents will often benefit from having tangible mementos such as
the following:
• Footprints and handprints (if no ink is available, iodine-based cleanser will work)
• Name band
• Crib card
• Lock of hair
Communication 17
• Bereavement outfits/receiving
• Written notes or poems to or for the baby
• Certificate of life/baptismal certificate
• Photographs:
−− Photographs of the baby might be important if mother and baby are to be separated
−− If the baby is dead, parents may not be able to view pictures of the baby immediately, but might later
appreciate having been provided with them.
−− Parents’ expectations of the baby’s appearance may be worse than the reality; appropriate bundling
and wrapping of the baby can be helpful to disguise anomalies. (It may be important for health care
providers to demonstrate that they are comfortable with the baby.)
−− Photographers specializing in bereavement photography have developed special water-immersion
techniques to enhance the quality of images provided to families following their loss.43
• Planting trees or flowers
• Ornaments or decorations
• Scrapbooks of cards from friends and family
Health care providers should verify the parents’ cultural or religious preferences before cutting hair, taking photographs,
or making other similar interventions.
There is no one right way to grieve, and while institutional protocols for bereavement can be helpful, loss is a complex
human experience. Support for a family experiencing loss requires the same kind of flexibility and responsiveness on the
part of care providers as other aspects of family-centred maternity care. Listen to the parents’ perceptions and invite their
involvement in exploring what ways of coping will work best for them.
Referrals to hospital services such as social work or pastoral care or to community-based support groups can be helpful
to families. Many hospitals hold group memorial services for families who have suffered a perinatal loss. Both caregivers
and families have found these memorials helpful. Resources for the development of a bereavement program can be
found in the Family Centred Maternity Care guideline.40
Follow-Up
Let the patient and/or family know who will be available to answer their questions in future and whether you will
continue to be available. It is valuable for the primary health care provider to make at least one return visit within
24 hours to allow further discussion and repetition of information. Your hospital’s disclosure policy may be helpful in
determining who should be involved and what to say. Lack of communication is one of the most common complaints by
women and their families.
It is recommended that obstetrical units have a protocol for the investigation and documentation of perinatal losses.
This information gathered in an investigation will be useful in explaining the present event and in planning for future
pregnancies. Documentation should include prenatal records, ultrasound reports, genetic testing (antenatal or post
mortem), and clinical notes of the circumstances of loss, autopsy results, and any follow-up arrangements made.44, 45
When the event is a perinatal loss, families should be informed that autopsy results might take several weeks or
Communication 18
even months to obtain. Counselling for future pregnancies is important but may need to be delayed until complete
information is available.
Coping Mechanisms: Care Providers

The impact of adverse effects on care providers is also highly significant.46
Health care providers who deal with adverse events may experience feelings of sadness or guilt, depletion of emotional
stamina, loss of professional self-esteem or prestige, or fear of litigation. They may not recognize their need for help and
support, or they may be unwilling to request assistance. Care providers should talk to colleagues who have dealt with
adverse events if they appear distressed. After dealing with adverse events, health care providers may psychologically
distance themselves from patients, which can lead to burnout for the care provider and/or ineffective care for patients.
Care providers in this situation should be offered the opportunity to debrief and be offered counselling, support, and
acknowledgment of their feelings.27, 47-55 4849505152535455
The term “second victim,” has been defined as a clinician who “feels personally responsible for the unexpected patient
outcomes and feels as though they have failed their patient, second guessing their clinical skills and knowledge
base.” According to Higgins, “Clinicians can cope by focusing either on the problem or on their emotions. Focusing on
the problem involves learning from a mistake, seeking information, determining what transpired, and dealing with the
problem. It is constructive to accept responsibility and to change personal practice”.56
A 2011 observational study of nine intrapartum nurses who had participated in a traumatic delivery revealed that “the
impact of an unexpected event can be emblazoned on one’s memory for many years, with an immediate response of
secondary traumatic stress disorder symptoms”.46 This observation, while predictable and frequently documented in the
women who experience traumatic birth,35, 43, 57-60 had not been previously documented in care providers. 585960
Caring for ourselves is an essential and normal part of the process. It is acceptable to show emotions in the presence
of death but our emotions should not take precedence over the emotions of the family involved. Feelings of guilt may
result even when the management has been appropriate. When management has been less than ideal, it is important to
participate honestly in a process of self- and peer-evaluation. The most effective form of risk management is caring
for your patient and her family. Seeking out supportive colleagues with whom to acknowledge these feelings can be
an effective way to deal with obstetrical crises.
Adverse Events and Litigation

The Canadian Medical Protective Association (CMPA) and the Healthcare Insurance Reciprocal of Canada (HIROC)
collaborated with Accreditation Canada and Salus Global Corporation to profile the safety and quality of obstetrics
services in Canada and also identifies opportunities for improvement.5 “The goal was to uncover contributing factors
to patient safety incidents and identify additional mitigation strategies for providers and health care organizations. Ten
years of HIROC data showed obstetrics represented 45% of liability costs and 46% of compensation payments.
Communication 19
The Canadian Medical Protective Association (CMPA) provides written resource material and individual confidential
counselling to physicians related to a concerning event even when no litigation has been enacted. Physicians may call
CMPA to report their involvement with a concerning event
The Canadian Nurse Protective Association (CNPA) offers legal advice, risk-management services, legal assistance
and professional liability protection related to nursing practice in Canada. Nurses may be members of CNPA based on
registration in their professional association Alberta, British Columbia1, Manitoba2, New Brunswick, Newfoundland and
Labrador, Nova Scotia, Prince Edward Island, Northwest Territories, Nunavut, Saskatchewan or Yukon. Nurses in Ontario,
Quebec or Manitoba have to join individually.
The Health Insurance Reciprocal of Canada (HIROC) is the insurer for Midwives and not-for-profit healthcare
organizations. HIROC provides risk management services and educational events
In CMPA data, 25% of cases were associated with intrapartum labour and 45% wit intrapartum delivery; HIROC data
showed 33 and 34% respectively. Key factors were
• individual provider decision making and
• individual and team situational awareness and communication
• system issues such as hospital protocols, reduced capacity to respond to obstetrical emergencies
Disclosure 616263646566
According to a patient safety Dictionary, disclosure should be understood as the imparting, by health-care workers to
patients or their significant others, of information pertaining to any health-care event affecting (or liable to affect) the
patient’s interests. The obligation to disclose is proportional to the degree of actual harm to the patient (or the realistic
threat of such) arising from an untoward event.67
Disclosure must be made in accordance with organizational policy and local legislation.
Errors that result in adverse events are inevitable, so it is prudent to have policies, protocols, and an organizational
plan within which the health care providers will be trained to conduct disclosures.68 The plan must be specific to the
circumstances of each individual organization; however, according to the American College of Obstetricians and
Gynecologists, it should address the who, what, when, where, and how:69
• Who: In general, disclosure should be made by the most-responsible care provider. The nature of the
adverse event will likely determine what other members of the health care team should be present.
• What: Only factual information must be communicated to the patient. Patients must be reassured that as
additional, reliable information is obtained, they will be notified promptly.
• When: Even if all details of the incident are not known, disclosure must be timely. Disclosure should occur as
soon as reasonably possible, while emphasizing to patients that it is an ongoing process of communication.
• Where: Disclosure should occur in a quiet and confidential setting that will be most comfortable to the
patient.
• How: Patient dignity must always be respected. A disclosure conversation should include empathy for what
patients and their families have experienced.
Communication 20
Communication of any negative health outcome to a patient or family is difficult for caregivers. Disclosing an adverse
event resulting from error is even more difficult. The normal response of a patient or family to injury (whether or not the
harm was due to a mistake) includes a mix of fear, anxiety, depression, anger, isolation, humiliation, devaluation, and
betrayal.70
Lucien Leape has described serious preventable injury as a medical emergency that has two victims: the patient and the
care provider. The patient suffers a double wound: the actual physical injury and an emotional wound, i.e., a sense of
betrayal and loss of trust. The caregiver can experience profound shame, guilt, and fear resulting in an impaired ability
to practise. The organization must be prepared to treat both emergencies in a timely fashion. The keys to treatment are
honesty, openness, and apology.70
A health care provider’s busy practice and unit may be limited by the inability to keep up and the honest desire for
“things to be all right”. This may be misunderstood by the family as minimizing their concern by the team.
Health care professionals and the organizations within which they work have an ethical, fiduciary, professional,
regulatory, and legal duty to honestly disclose adverse events to their patients and/or families. Most patients want and
expect to be informed of adverse events but care providers are not necessarily in favour of disclosure
• 98% of patients want to be informed of even a minor error; the greater the severity of the outcome, the more
they want information
• 92% of patients believe they should always be told about complications, while 68% of physicians believe
patients should always be told
• 81% of patients believe they should be advised of possible future adverse outcomes of the complications,
while only 33% of physicians believe that patients should be told about possible future outcomes.47, 71-73 7273
A study by Gallagher et al., which explored attitudes and experiences of physicians regarding disclosure, showed wide
variation in how they would disclose error to patients. The study suggested that disclosure standards and training are
necessary to meet public expectations and promote professional responsibility following errors.74, 75
According to the Canadian Medical Protective Association, 8 Canadian provinces and one territory (British Columbia,
Alberta, Saskatchewan, Manitoba, Ontario, Nova Scotia, Prince Edward Island, Newfoundland and Labrador, and
Nunavut) have adopted “apology legislation.” This approach to disclosure is designed to create greater accountability and
transparency in the health care system. Apology legislation:
Allows individuals and organizations, such as hospitals and other public institutions, to apologize for an
accident or wrongdoing, without the apology being used as evidence of liability in a civil legal proceeding
under provincial law;
Promotes accountability, transparency, and patient safety by allowing open and frank discussions between
patients and health care providers;
Reduces the burden on the justice system by encouraging non-litigious resolution of civil disputes.76 76
Communication 21
Barriers to Disclosure
Caregivers may have personal beliefs, or may experience fears, that prevent their disclosing adverse events. They may
believe that:
• Disclosure is unnecessary
• It is in the best interests of patients not to be informed
• The outcome would potentially have occurred without the error or intervention (e.g. the patient was
terminally ill anyway)
• They lack the experience, skill, and training to communicate difficult information
They may fear:
• Retribution from the recipient of the news
• Loss of the trust and respect of patients
• Legal action
• Censure, loss of respect, and prestige among colleagues
• Loss of job and/or income
• Loss of self-esteem and a loss of self-confidence as a care provider27,28
• Dealing with the emotions of the patient and/or family as well as their own
What do patients expect?

When an adverse event occurs, patients and/or their families are often aware that something has gone wrong. If the
event is not disclosed, they may feel devalued and disrespected and may lose trust in the caregivers, the health care
organization, or the system. If they feel that information is being purposely withheld or covered up, they may believe
the only way they can obtain accurate, complete information is by launching a lawsuit. According to a 2004 report from
the Canadian Institute for Health Information, 76% of respondents believed the threat of litigation was important to
ensuring that doctors act in the best interests of their patients.73
Patients or their families are most likely to consider legal action not because of an event but because of their subsequent
interaction with people in the health care system. When the harm becomes apparent despite of the lack of disclosure,
or when the adverse event is finally admitted by the caregiver and/or organization, patients and/or their families often
experience profound anger.50 This compounds the trauma already being experienced and can lead to a desire to punish the
caregivers or to seek revenge against the organization. Conversely, if patients and/or their families have been involved from
the very beginning in all aspects of care and have worked in partnership with the caregivers, disclosure of adverse events,
although still difficult, occurs within an established relationship based on open, honest, and transparent communication.48
Specifically, patients need to know:77
• How do we manage this for my family?
• What you are going to do to help me?
• What specific steps are you taking to ensure this doesn’t happened to another family?
• What can we do to help you achieve those system changes?
Communication 22
Benefits of Disclosure
For patients and/or families:
• Begin to recover from the effect of the unanticipated outcome and deal directly with the pain so that they can
begin to heal
• Regain trust and work out their feelings of distrust with the people inside the institution, rather than look for
help from those outside it
• Understand and obtain the care that may be needed to address the effects of the adverse outcome in the
future
• Receive the information needed to make decisions about the next steps, including the possibility of seeking
appropriate compensation
For caregivers:
• Address the error, and make the changes necessary to prevent future occurrences
• Express regret, assuage guilt, and begin to heal
• Regain self-esteem and continue to practice
For health care organizations:
• Learn from events and improve faulty systems to protect patients, their families, and health care staff in the
future
• Potentially lessen the frequency and severity of litigation through the proper management and control of a
disclosure process
• Share with other organizations to prevent the recurrence of the event elsewhere
How to Disclose
Preparation
• Have an organizational plan that will guide the process and ensure all potential issues are addressed
• Review the facts; be sure you know clearly what happened
• Balance the need to have all the information with the need to disclose the information in a timely manner. It
might be better to say “we do not know yet but we will tell you when we do” rather than wait and potentially
alienate and antagonize the patient and her family
• Determine who needs to be told
• Determine each person’s role
• Assess the readiness (medically stable, awareness level, ability to comprehend, availability of support) of the
patient and/or her family to hear what you have to say
• Choose an appropriate time and setting, keeping in mind the basic principles of effective communication
and timely follow-up
• Ensure that the medical team are not seated on one side of the table and the family on the other, which may
suggest an adversarial relationship.
Communication 23
Meeting with the patient and/or family

• Simply describe what happened in plain, commonly understood language; use a neutral tone
• Describe what is known; give factual, objective information
• Describe the next steps of the process for the patient and/or family; ensure any necessary medical care is
identified and made available; offer to transfer care to another caregiver
• Acknowledge the patient’s suffering and express your sympathy
• Apologize for the harm caused to the patient and for your role in it
• Focus on the needs of the patient and/or family
• Describe the next steps in the investigative process
• Explain what is being done to prevent a recurrence
• Seek and respond honestly to the questions and concerns of the patient and/or family; allow ample time for
questions
• Establish, with the patient and/or family, a plan for follow-up (detailing who, what, where, when)
• Provide a contact person, who will be available indefinitely, and the support of other available resources
(clergy, social services, etc.)
Tasks
• Establish rapport
• Listen actively and empathetically
• Try not to be defensive: this is the time to listen, not to defend your actions
• Recognize and manage your own feelings
• Be open and willing to accept whatever reaction occurs
• Anticipate and be prepared to respond calmly to emotional reactions and behaviours such as crying, yelling,
anger, threats, verbal abuse, walking out
Event Reporting
An adverse event is defined as an unexpected occurrence that either caused harm or had the potential to cause harm.4
Disclosure of an adverse event also involves timely and accurate reporting of the event (whether harm was caused or not)
to the facility in which the care provider works, as well as to their insurers organizations.
Confusion about whether or not a “complication” is an event is one reason for failure to report or delay in doing so, which
can have serious consequences. Waters et al. list situations in which an event may or may not be reported.78 They note
that “Nurses exercise considerable judgment in deciding whether or not to formally report an incident, with estimated
rates ranging from 10% to 55% of incidents.” They also note that culture plays an important role in reporting rates and
that informal reporting occurs where “decisions to report informally or formally were influenced by the knowledge and
experience of nurses; relationships with colleagues, physicians, and managers; types of errors; and workload.” Finally,
they state that “lack of feedback from administrators about an incident reduces reporting. Time-consuming incident
report processes and the inability to report anonymously also reduce incident reporting. Negative relationships amongst
Communication 24
health care providers, within and between disciplines, decrease incident reporting.”79-81 These observations are important
as the majority of incidents are reported by the nursing profession. 8081
Documentation
The principle “if is not documented it is not done” applies to all health care professionals. Thus documentation is
essential for maintaining continuity of care and can form part of legal proceeding. The latter point is particularly
significant as many legal cases occur years after the event when memories have faded.
The health profession needs to assess their own documentation to ensure key principles are adhered to.
To be effective, documentation must be:
• Clear: concise, precise, and legible
−− Legibility is a key factor in medication errors and understanding the plan of care. There is no harm in
printing if cursive writing is not easily interpreted.
• Complete
−− Using a standardized template. One example is SOAP
›› S=subjective information (i.e. what the parent says)
›› O=Objective information (test results, physical exam)
›› A= assessment (analysis of the situation, diagnosis)
›› P=Plan of care (includes what was said to the parent /family, advice, planned actions)
−− Always include a time, date and signature on all documentation
• Contemporaneous
−− Contemporaneous documentation is challenging in emergencies. Having a designated recorder and
a template form for urgent situations promotes quality documentation, Just as there is a flow sheet
for Code Blue documentation, development of flow sheets for other critical situations such as PPH
facilitates complete and timely documentation.
• Consistent
−− With other multi-disciplinary notes and records
• Compliant with institutional and professional standards
Clark et al. reported that in 54% of legal cases involving shoulder dystocia, the failure to clearly document the
management of the dystocia was the primary reason for payment of damages.64 Often the right things were done but
were not documented adequately. A quick, effective system to document procedures and events and excellent verbal
communication would likely minimize litigation.
The MOREOB Case Management Guides20 provide suitable templates. The Vacuum Case Management Guide65 is
appended to this chapter as an example. When this approach is used by an interprofessional team (e.g., physician and
nurse) after a procedure or delivery, it leads to an effective debriefing of the interaction fostering debriefing as a routine
part of practice.
Communication 25
Electronic Medical Record (EMR)

Facilities have increasingly implemented a variety of electronic medical records for either partial or full documentation.
The implementation requires time, money, and consistency in care practice as changes in EMR may be difficult. EMR has
been variously embraced and challenged by different specialities and different generations of health professionals. The
lack of use of a consistent EMR within a region or city poses additional challenges.
STRENGTHS LIMITATIONS
Increased legibility Health professionals require education on system use and potentially
typing skills
A time is always included
Repetitive, less individualized, comments with drop down boxes
Easily retained and printed out
Comments may be in multiple locations- comments may be
Easily accessible at multiple locations if the same EMR is used inconsistently placed
Research date more easily obtained When working more than 1 facility with different EMR systems, it is
Positive environmental impact challenging to remember the different EMR systems and rules
Passwords can expire if not frequently using a given facility EMR
Expensive
Security
Communication 26
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Predictable or haphazard? JAMA. 1989;262:3291-7.
63. Hickson GB, Entman SS. Physician practice behavior and litigation risk: evidence and opportunity. Clin Obstet
Gynecol. 2008;51:688-99.
64. Clark SL, Belfort MA, Byrum SL, Meyers JA, Perlin JB. Improved outcomes, fewer cesarean deliveries, and reduced
litigation: results of a new paradigm in patient safety. Am J Obstet Gynecol. 2008;199:105-7.
65. Vacuum. London (ON): Salus Global Corporation; 2012.
66. Braithwaite J, Wears RL, Hollnagel E. Resilient health care: turning patient safety on its head. Int J Qual Health
Care. 2015;27:418-20. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26294709.
67. Systems Issues Working Group National Steering Committee on Patient Safety. Canadian patient safety dictionary.
Ottawa: Royal College of Physicians and Surgeons of Canada; 2003. Available from: http://www.royalcollege.ca/
portal/page/portal/rc/common/documents/publications/patient_safety_dictionary_e.pdf.
68. When things go wrong: responding to adverse events: a consensus statement of the Harvard hospitals. Burlington
(MA): Massachusetts Coalition for the Prevention of Medical Errors; 2006. Available from: http://www.macoalition.
org/documents/respondingToAdverseEvents.pdf.
69. Committee on Patient S, Quality I. Committee Opinion No. 681: Disclosure and Discussion of Adverse Events.
Obstet Gynecol. 2016;128:e257-e61. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27875473.
70. Leape L. Understanding the power of apology: how saying “I’m sorry” helps heal patients and caregivers. Focus on
Patient Safety. 2005;8:1-3.
71. Hebert PC, Levin AV, Robertson G. Bioethics for clinicians: 23. Disclosure of medical error. CMAJ. 2001;164:509-13.
Available from: http://www.cmaj.ca/cgi/reprint/164/4/509.pdf.
72. Gallagher TH, Waterman AD, Ebers AG, Fraser VJ, Levinson W. Patients’ and physicians’ attitudes regarding the
disclosure of medical errors. JAMA. 2003;289:1001-7.
73. Health care in Canada. Ottawa: Canadian Institute for Health Information; 2004. Available from: https://secure.cihi.
ca/free_products/hcic2004_e.pdf.
74. Gallagher TH, Garbutt JM, Waterman AD, Flum DR, Larson EB, Waterman BM, et al. Choosing your words carefully:
how physicians would disclose harmful medical errors to patients. Arch Intern Med. 2006;166:1585-93.
75. Gallagher TH, Waterman AD, Garbutt JM, Kapp JM, Chan DK, Dunagan WC, et al. US and Canadian physicians’
attitudes and experiences regarding disclosing errors to patients. Arch Intern Med. 2006;166:1605-11.
76. Thompson J. Apology Act passes third reading at Queen’s Park [news release]. Toronto: HIROC; 2009.
77. Sidorchuk R. The patient perspective - what do we really want - do you really want to know? [oral presentation].
Toronto2006.
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78. Waters NF, Hall WA, Brown H, Espezel H, Palmer L. Perceptions of Canadian labour and delivery nurses about
incident reporting: a qualitative descriptive focus group study. Int J Nurs Stud. 2012;49:811-21.
79. Uribe CL, Schweikhart SB, Pathak DS, Dow M, Marsh GB. Perceived barriers to medical-error reporting: an
exploratory investigation. J Healthc Manag. 2002;47:263-79. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/12221747.
80. Wakefield BJ, Blegen MA, Uden-Holman T, Vaughn T, Chrischilles E, Wakefield DS. Organizational culture,
continuous quality improvement, and medication administration error reporting. Am J Med Qual. 2001;16:128-
34. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11477957.
81. Blegen MA, Vaughn T, Pepper G, Vojir C, Stratton K, Boyd M, et al. Patient and staff safety: voluntary reporting. Am J
Med Qual. 2004;19:67-74. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15115277.
Communication 32
Table of Contents
Chapter 2 Evidence-Based Obstetrics................................................................................................................................. 34

Types of Evidence: Qualitative or Quantitative .......................................................................................................... 34
Meta-Analysis ................................................................................................................................................. 35
Caution............................................................................................................................................................ 35
Statistics.......................................................................................................................................................... 35
Definitions....................................................................................................................................................... 36
Statistics in Meta-Analysis .............................................................................................................................. 37
Confidence intervals........................................................................................................................................ 38
Results of Meta-Analysis................................................................................................................................. 39
The Grade Approach.................................................................................................................................................... 41
Strength of Recommendations....................................................................................................................... 42
Evidence-Based Obstetrics 33
Chapter 2
Evidence-Based Obstetrics
In providing maternity care, we endeavour to produce the most desirable results for our patients with minimum risks
and costs. Decision-making is severely hampered when information is non-existent, incomplete, or unavailable. When
information exists but is not used properly or consistently, the care provided may not be appropriate. The goal of the
ALARM course is to promote care based on the best available evidence while also encouraging participants to develop
skills in obtaining and evaluating evidence, and incorporating into daily clinical practice.
Types of Evidence: Qualitative or Quantitative

Qualitative evidence is “the organization and interpretation of non-numerical information for the purpose of discovering
important underlying dimensions and patterns of relationships” (Polit & Hungler, 1995, p. 630). There are various
types of qualitative evidence such as phenomenology, case study, and grounded theory. Qualitative evidence, derived
from empirical research, case studies, and grounded theory, indicates patterns or trends and can influence ways of
thinking about the issues studied. Although qualitative evidence has a role in achieving clinical understanding, evidence
presented in the ALARM course is primarily quantitative.
Quantitative evidence uses numerical data, analyzed through statistical procedures. Quantitative research trials, which
include randomized controlled trials (RCTs), cohort studies, case-control studies and surveys, generally provide stronger
evidence than qualitative studies, although not all are scientifically rigorous.
Evidence collected from prospective research trials is more powerful than evidence collected from retrospective analyses
of outcomes. In a prospective study, a hypothesis is proposed, and then data are collected and analyzed to test it.
Variables can be anticipated, and the study designed to control for them. A retrospective study is not as powerful since it
looks back in time at events that have occurred (e.g., chart review). The researcher cannot control for variables and must
often rely upon charts that are incomplete.
The strongest quantitative evidence comes from randomized controlled trials (RCTs), although even RCTs are variable
in quality. In an RCT, participants investigators do not determine which participants are assigned to an intervention or a
control group. Based on the group results, the average of selected outcomes can be determined by an RCT.
Thus, a prospective RCT, which controls for known and unknown variables between those receiving and those not
receiving a given intervention, is the most powerful way to discover whether the intervention has a significant impact.
Meta-Analysis
A meta-analysis is a statistical evaluation of a collection of studies that are similar in design, study populations, and
outcomes examined. If there are differences between intervention and control groups, they are more likely to be evident
when the numbers studied are large and when the difference in outcome is great.
In obstetrics, most serious outcomes are rare enough that there have been few randomized controlled trials of sufficient
power to demonstrate a difference between an intervention and a control group. Meta-analysis may allow useful
information to be obtained from these studies.
The primary benefit, however, of meta-analysis is that published data are systematically reviewed and the information
synthesized and made more readily available.
Different meta-analyses of the same outcome may make different conclusions. This is due in part to different inclusion
and exclusion criteria. It is therefore important to evaluate the methodology of the meta-analysis to determine its quality.
Caution
The techniques of meta-analysis are such that separate meta-analyses of the same subject may result in different
findings. These generally result from the inclusion of different trials. There are 2 main reasons for this:
• Negative results in a randomized controlled trial are less likely to be published, and therefore cannot
therefore appear in a meta-analysis. This often occurs when several initial small trials show promising results
that are not substantiated in a subsequent well-designed large trial. Failure to include trials in a meta-
analysis may also occur because of an incomplete systematic review of the literature.
• The problem of data “excess”: the inclusion of multiple publications by different authors that are based on
the SAME clinical trial.
Meta-analysis is useful in the absence of a large definitive trial. If a well-designed and well-executed trial exists, the
importance of meta-analysis is lessened.
It must always be remembered that much of what is done is not supported by “good” evidence simply because trials
have not been done.
Whenever possible, information from sound systematic reviews should be used to guide the appropriate and
compassionate practice of medicine
Statistics
Statistical tests are used to ascertain whether research results are valid and reliable. Following are definitions for some
key terms used in the ALARM course.
Definitions
Definitions
y Sensitivity is the likelihood that the diagnostic test will indicate the presence of disease when the disease is
actually present. (True positive rate.) [a/(a+c)]
Sensitivityis isthe
y • Specificity thelikelihood
likelihoodthat
thatthe
thediagnostic
diagnostictest
testwill
willindicate
indicatethe
theabsence
presence of disease
of disease whenwhen
thethe disease
disease is is
actuallyabsent.
actually present. (True
(True positiverate.)
negative rate.)[d/(b+d)]
[a/(a+c)]
• Specificity
y Positive predictive value is the likelihood that atest
is the likelihood that the diagnostic will indicate
positive theactually
test result absencemeans
of disease when
that the the disease
disease is is
actually[a/(a+b)]
present. absent. (True negative rate.) [d/(b+d)]
Positive predictive
y • Negative predictive valuevalue isis the
the likelihood
likelihood that
that aa negative
positive test
testresult
resultactually
actuallymeans
meansthat
thatthe
thedisease
diseaseisis
present. [a/(a+b)]
absent. [d/(c+d)]
• Negative predictive value is the likelihood that a negative test result actually means that the disease is
Bayes’ theorem:
absent.the predictive value of a test will depend on the prevalence of the disease. With high prevalence,
[d/(c+d)]
the positive predictive value will increase and vice versa (a positive test for a low prevalence disease is likely to be a
Bayes’
false theorem: the predictive value of a test will depend on the prevalence of the disease. With high prevalence, the
positive).
positive predictive value will increase and vice versa (a positive test for a low prevalence disease is likely to be a false positive).
DISEASE
Present Absent
+
a b
TEST
c d
For example, a culture screening for group B streptococcus (GBS):

For example,
• a culture screening
Sensitivity of the test for group
(+ve B streptococcus
culture) is the chance(GBS):
that if the woman had GBS it will be detected by the test
Specificityofisthe
y • Sensitivity thetest
chance
(+vethat the test
culture) willchance
is the indicate noifGBS
that the (−ve
womanculture) when
had GBS in fact
it will the woman
be detected by does not
the test
have it is the chance that the test will indicate no GBS (−ve culture) when in fact the woman does not
y Specificity
• Positive
have it predictive value is the chance that a +ve culture represents GBS colonization
Negative
y • Positive predictive
predictive value
value is the
is the chance
chance thatthat a −ve
a +ve culture
culture actually rules
represents out GBS
GBS colonization
y Negative predictive value is the chance that a −ve culture actually rules out GBS
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Statistics in Meta-Analysis
Statistics in Meta-Analysis
Odds Ratio
Odds
Odds
When
Ratio
Ratiostudies together, the odds ratio (OR) compares the likelihood (relative odds) of the outcome being
Oddsgrouping
ratio
studiedgrouping
When
When occurringstudies
grouping in the together,
studies group receiving
together, the
the odds
oddstheratio
intervention
ratio (OR) (the “experimental”
(OR) compares
compares the likelihood or
the likelihood “exposed”
(relative
(relative odds)group)
odds) of thewith
of the the group
outcome
outcome beingnot
being
receivingoccurring
studied
studied the intervention
occurring in
in the (the “control”
the group
group receivingor
receiving the“unexposed”
the interventiongroup).
intervention (the
(the “experimental”
“experimental” oror “exposed”
“exposed” group)
group) with
with the
the group
group not
not
receiving the intervention (the “control” or “unexposed” group).
receiving the intervention (the “control” or “unexposed” group).
Odds of observed outcome in experimental group axd
OR = Odds of = ab xx dc
Odds
Odds of observed
of observed
observed outcome in
in experimental
outcome
outcome in control group
experimental group
group axd
OR =
OR
= Odds =
=
Odds
Odds of
of observed
of observed
observed outcome
outcome in
in control
control group
in experimental
outcome group
group b xx d
a
b cc
OR = = ab xx dc
Relative Risk Odds
Odds
Odds of
of observed
of observed
observed outcome in
in experimental
outcome
experimental group
group axd
OR =
OR
= =
=
Relative
Relative
Relative Risk
Risk
The relative risk
risk
Odds
Odds
(RR, sometimes called
of observed
ofthe
observed
risk ratio)
outcome
outcomethe
compares
in control
in risk
control group b
bx
group of the outcome
or probability x cc
Risk of observed outcome in experimental group a / (a + in d)each group rather
thanrelative
The the odds.
risk RR = of=
The relative risk (RR,
(RR, sometimes
sometimes
Risk called
called
of
RiskRisk
of
the
the risk
observed risk ratio)
of observed
observed ratio)
outcomecompares
compares
in the risk
inthe risk or
in experimental
outcome
outcome control
experimentalor probability
probability
group
group
the outcome
group of the outcome
a
ac // (a
(b +
(a +
in
+ in
each group rather
c)each group rather
d)
d)
than
than the
the odds.
odds. RRRR = = RiskRisk =
= acc // (b
Risk of
of observed
of observed
observed outcome
outcome
outcome in
in control
control group
in experimental group
group (a +
(b + d)
c)
c)
RR = =
Risk of
of observed
RiskRisk of observed
observed outcome in
in experimental
outcome
experimental group
group a
ac // (a
(b +
(a + d)
+ c)
d)
RR
RR = = Risk
=
=
Risk of
of observed
observed outcome
outcome in in control
control group
group cc // (b
(b ++ c)
c)
The odds ratio serves as a surrogate for the relative risk, which is more difficult to manipulate using the statistics
The odds ratio serves as a surrogate for the relative risk, which is more difficult to manipulate using the statistics
performed
The
The odds in meta-analysis.
odds ratio
ratio serves
serves as When the
as aa surrogate
surrogate for outcome
for the studied
the relative
relative risk, is rare,is
risk, which
which the odds
more ratio closely
difficult to approximates
to manipulate using thestatistics
using the relative risk.
performed in meta-analysis. When the outcome studied is rare,isthe
more difficult
odds manipulate
ratio closely approximates the
thestatistics
relative risk.
performed
performed in
in meta-analysis.
meta-analysis. When
When the
the outcome
outcome studied
studied isis rare,
rare, the
the odds
odds ratio
ratio closely
closely approximates
approximates the
the relative
relative risk.
risk.
OUTCOME
OUTCOME
OUTCOME
Present Absent
E Present
Present Absent
Absent
E
X
E +
X
P
X +
+ a b
P
O
P
O
S a
ac bd
b
O
S
U
S cc d
d
—
U
R
U —
—
R
E
R
E
E
Graphically, the odds ratio and relative risk is presented as a point on a horizontal, logarithmic scale. A vertical line drawn
at 1 indicates no difference in the outcome between the 2 groups. Ratios < 1 will be represented to the left of the vertical
Evidence-Based
Obstetrics
Obstetrics 38
37
38

Graphically, the odds ratio and relative risk is presented as a point on a horizontal, logarithmic scale. A vertical line drawn
at 1 indicates no difference in the outcome between the 2 groups. Ratios < 1 will be represented to the left of the vertical
line and those > 1 will be represented on the right side of the vertical line. The data presentation is usually constructed
line and those > 1 will be represented on the right side of the vertical line. The data presentation is usually constructed
so that the results < 1 are an improvement in outcome.
so that the results < 1 are an improvement in outcome.
Confidence Intervals
Confidence intervals
The confidence interval is a measure of statistical significance, generally calculated as the least and greatest results
The confidence interval is a measure of statistical significance, generally calculated as the least and greatest results
within which the reported outcome of the experiment would fall 95% of the time. It is displayed graphically as a
within which the reported outcome of the experiment would fall 95% of the time. It is displayed graphically as a
horizontal line through the outcome point where the left end represents the lowest and the right end represents the
horizontal line through the outcome point where the left end represents the lowest and the right end represents the
highest point. The 95% confidence interval is equivalent to the probability statistic P < 0.05.
highest point. The 95% confidence interval is equivalent to the probability statistic P < 0.05.
Measurements
Measurements of of confidence
confidence do do not
not eliminate
eliminate the the possibility
possibility that
that the
the results
results of
of an
an experiment
experiment are are due
due to
to chance,
chance, they
they
just
just indicate
indicate how
how likely
likely itit isis that
that such
such aa result
result isis due
due to
to chance.
chance. The
The judgement
judgement of of the
the clinician
clinician isis required
required to
to interpret
interpret
whether
whether oror not
not aa result
result isis clinically
clinically significant,
significant, regardless
regardless ofof the
the statistical
statistical expression
expression of
of probability
probability used.
used.
Intervention vs Control
confidence
interval odds ratio or
Outcome A relative risk
treatment significantly
Outcome B better than control
treatment significantly
For a single trial, the
worse than control outcomes of interest
are shown with their
Outcome C individual confidence
results intervals.
Outcome D consistent
with chance
Outcome E
0.01 0.1 1 10 100
Odds Ratio or Relative Risk (95% Confidence interval)
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26th Edition
th
Edition of
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Manual
Results of Meta-Analysis
In aa meta-analysis,
In meta-analysis, the
the result
result isis plotted
plotted below
below the
the individual
individual studies
studies used
used in
in the
the analysis.
analysis. The
The meta-analysis
meta-analysis result
result isis
calculated when
calculated when all
all the
the trial
trial results
results are
are evaluated,
evaluated, weighted
weighted and
and then
then pooled
pooled for
for aa single
single given
given outcome
outcome ofof interest.
interest. TheThe
associated confidence interval will be narrower than the confidence intervals associated with the individual trials
associated confidence interval will be narrower than the confidence intervals associated with the individual trials because because
the number
the number of
of participants
participants represented
represented isis greater.
greater.
Effect
Effect ofofIntervention
Interventionon on Outcome
Outcome of Interest
of Interest
Outcome less likely Outcome more likely
Trial A (n = 220)
Trial B (n = 145)
Trial C (n = 550)
Trial D (n = 205)
Trial E (n = 325)
Meta-analysis result
0.01 0.1 1 10 100
Odds Ratio (95% Confidence Interval)
The confidence intervals displayed for each study will be broader than the confidence interval of the meta-analysis and
The
varyconfidence
according tointervals displayed
study size. for each study
In the example above,will beCbroader
Trial has thethan the confidence
narrowest confidenceinterval
interval of because
the meta-analysis and
of its larger size.
vary according to study size. In the example above, Trial C has the narrowest confidence interval because
The meta-analysis odds ratio is the narrowest of all as it mathematically incorporates all of the trials’ subjects. A trial’s of its larger size.
The
failure meta-analysis
to demonstrate oddsaratio is the narrowest
difference may be due of to
allaaslack
it mathematically
of power (i.e., notincorporates all of the
enough subjects trials’
given thesubjects. A trial’s
effect size), which
failure to demonstrate a difference may be due to a lack of power (i.e., not enough subjects given
is the case in Trial D in the above example. Again, confidence intervals that cross the vertical line at 1 mean that P > 0.05 the effect size), which
isforthe
thecase in TrialinDthat
outcome in the above
trial. example.
Although this Again,
result isconfidence
therefore notintervals that cross
statistically the vertical
significant, if allline
the at 1 mean
studies liethat P >side
to one 0.05
for the outcome in that trial. Although this result is therefore not statistically significant, if all the studies
of the vertical axis, it indicates a trend in the same direction. Trial B is an outlier and requires an explanation (cheating? lie to one side
of the vertical
different axis, it indicates
population? a trend in
misdiagnosis?). Thethe same
trials aredirection.
then saidTrial
to beB homogeneous.
is an outlier andThis
requires
suggests an explanation (cheating?
that a difference may
different population? misdiagnosis?). The trials are then said to be homogeneous. This suggests
truly exist and may become apparent once the typical odds ratio is calculated or more studies are added to the analysis. that a difference may
truly exist and may become apparent once the typical odds ratio is calculated or more studies are added to the analysis.
Evidence-Based
Obstetrics 40
39
The results displayed in a meta-analysis fall into 1 of 3 categories:

1. The result lies to the left of the vertical axis (1) and the confidence interval does not cross 1. This indicates
that the outcome is less likely to occur in the treatment group than in the control group and the result is
statistically significant.
2. The result is at or near 1, and the confidence interval line crosses 1. This indicates that there is no statistically
significant difference in outcomes between the groups.
3. The result lies to the right of the vertical axis, and the confidence interval line is also completely to the right
of 1. This indicates that the outcome is more likely to occur in the treated group than in the control group.
A meta-analysis of studies that failed to achieve statistical significance individually, because of insufficient numbers or
small effect size, may show that most of these studies demonstrate the same trend, indicating that the difference does
exist.
For example, several studies were conducted regarding the use of antepartum glucocorticoids on fetal lung maturity and
the occurrence of neonatal respiratory distress syndrome. Shown are the lead author, year of study publication and
number of subjects in each trial.
The Grade Approach

The Grading of Recommendations, Assessment, Development and Evaluation (GRADE) is a system for rating the
quality of evidence in systematic reviews and other evidence syntheses, such as health technology assessments and
clinical practice guidelines. GRADE offers a transparent and structured process for developing and presenting evidence
summaries and for carrying out the steps involved in developing recommendations.
The GRADE approach uses 4 grades:
QUALITY OF EVIDENCE GRADES
GRADE DEFINITION
High We are very confident that the true effect lies close to the estimated effect.
Moderate We are moderately confident in the effect estimate: the true effect is likely to be close to the estimate of the effect, but there is a
possibility that it is substantially different.
Low Our confidence in the effect estimate is limited: the true effect may be substantially different from the estimated effect.
Very Low We have very little confidence in the effect estimate: the true effect is likely to be substantially different from the estimated effect
The GRADE approach to rating the quality of evidence begins with the study design (trials or observational studies) and
then addresses 5 possible reasons for downgrading the quality of evidence and 3 for upgrading the quality of evidence.
FACTORS THAT CAN REDUCE THE QUALITY OF THE EVIDENCE
FACTOR CONSEQUENCE
Limitations in study design or execution (risk of bias) i 1 or 2 levels
Inconsistency of results i 1 or 2 levels
Indirectness of evidence i 1 or 2 levels
Imprecision i 1 or 2 levels
Publication bias i 1 or 2 levels
FACTORS THAT CAN INCREASE THE QUALITY OF THE EVIDENCE
FACTOR CONSEQUENCE
Large magnitude of effect i 1 or 2 levels
All plausible confounding would reduce the demonstrated effect or increase the effect if no effect was observed i 1 level
Dose-response gradient i 1 level
Strength of Recommendations
The strength of a recommendation reflects the extent to which a guideline panel is confident that desirable
effects of an intervention outweigh undesirable effects, or vice versa, across the range of patients for whom the
recommendation is intended.
GRADE specifies 2 categories of the strength of a recommendation. While GRADE suggests using the terms strong and
weak recommendations, those making recommendations may choose different wording to characterize the 2 categories
of strength.
IMPLICATIONS OF STRONG AND WEAK RECOMMENDATIONS
STRONG RECOMMENDATION WEAK RECOMMENDATION
For patients Most patients in this situation would want the The majority of patients in this situation would want the
recommended course of action, and only a small proportion suggested course of action, but many would not.
would not.
For clinicians Most patients should receive the recommended course Recognize that different choices will be appropriate for
of action. Adherence to this recommendation according different patients, and that you must help each patient
to the guideline could be used as a quality criterion or arrive at a management decision consistent with her or his
performance indicator. Formal decision aids are not likely values and preferences. Decision aids may well be useful
to be needed to help individuals make decisions consistent helping individuals making decisions consistent with their
with their values and preferences. values and preferences. Clinicians should expect to spend
more time with patients when working towards a decision.
For policy The recommendation can be adapted as policy in most Policy-making will require substantial debates and
makers situations including for the use as performance indicators. involvement of many stakeholders. Policies are also more
likely to vary between regions. Performance indicators
The recommendation can be adopted as policy in most would have to focus on the fact that adequate deliberation
situations and can be used as the basis of performance about the management options has taken place.
indicators.
Suggested Reading
1. Higgins JPT, Green S, editors. Cochrane handbook for systematic reviews of interventions. Version 5.1.0 [updated
March 2011]. The Cochrane Collaboration; 2011. Available: http://handbook-5-1.cochrane.org/.
2. Greenhalgh T. How to read a paper: the basics of evidence-based medicine. 4th ed. London: BMJ Books; 2010.
3. Streiner DL, Norman GR. PDQ epidemiology. Shelton (CT): People’s Medical Publishing House; 2009.
4. Norman GR, Streiner DL. Biostatistics: the bare essentials. 3rd ed. Hamilton: BC Decker; 2008.
5. Polit D, Beck CT. Nursing research: principles and methods. 7th ed. Philadelphia: Lippincott Williams and Wilkins;
2004.
6. Norman GR, Streiner, DL. PDQ statistics. 3rd ed. Hamilton: BC Decker; 2003.
7. New grades for recommendations from the Canadian Task Force on Preventive Health Care. CMAJ
2003;(3)169:207-8. Available: http://www.cmaj.ca/content/169/3/207.full.pdf+html.
8. Sackett DL, Richardson WS, Rosenberg W, Haynes RB. Evidence-based medicine: how to practice and teach EBM.
New York: Churchill Livingstone; 1997.
9. Schünemann H, Brozek J, Guyatt G, Oxman A, editors. GRADE handbook for grading quality of evidence and
strength of recommendation. [updated October 2013]. Available from http://gdt.guidelinedevelopment.org/app/
handbook/handbook.html#h.svwngs6pm0f2
10. Thacker MD, Peterson HB, Stroup DF. Metanalysis for the obstetrician-gynecologist. Am J Obstet Gynecol, May
1996;174:1403-7.
Table of Contents
Chapter 3 Patient Safety..................................................................................................................................................... 45

Introduction................................................................................................................................................................ 45
Definitions....................................................................................................................................................... 45
Prevalence ...................................................................................................................................................... 45
Understanding Error in Health Care................................................................................................................ 47
Understanding why we fail............................................................................................................................. 48
Defences against Error.................................................................................................................................... 49
Understanding why we succeed (Safety II Production safety)......................................................................... 52
The Process of Risk Management.................................................................................................................... 53
High Reliability Organizations ....................................................................................................................... 55
Patient Safety 44
Chapter 3
Patient Safety
Introduction
The complexity of healthcare systems exposes patients and care providers to risks that may result in significant adverse
outcomes. The development of quality (which must, but do not always include a sharp focus on patient safety) and risk
management programs in each unit will lead to improved patient care, reduced medico-legal risks, and lower costs.
Systems and processes that balance an understanding of why we fail, as well as why we succeed, increase the likelihood
of success and minimize the likelihood of errors, and are essential to ensuring patient safety.
Definitions
Risk management: The development and implementation of strategies to prevent or limit injury, damage, harm,
discomfort, disability, or distress to the patient.1
Patient safety: Has been defined as: The absence of harm that results from the provision of care and the reduction
and mitigation of unsafe acts, through the use of best practices.2, 3 In this context, safety is hard to quantify as it is a
non-event.
Safety can also be described as the occurrence of successful outcomes. In this way, safety is easier to quantify: it is a
dynamic event.4
Resilience: The ability of a system to sustain required operations in both expected and unexpected conditions.5
Prevalence
A substantial body of evidence points to medical errors as a leading cause of preventable death and injury:6
• Adverse outcome data reported by the Institute of Medicine (IOM) revealed health care provider error
resulted in 44 000 to 98 000 patient deaths per year. This was higher than the number of deaths from
traffic accidents, breast cancer, and HIV infection, making patient death from clinical error the fourth leading
cause of death in the United States.6 Even using the lower number, death due to clinical error ranked
ninth, ahead of motor vehicle accidents, chronic liver disease, alcohol- and drug-induced causes, and various
cancers.6 The overall societal cost of clinical error approached $38 billion annually. Approximately half of this
($17 billion) was associated with preventable errors.6
Patient Safety 45
• In 2004, a report by HealthGrades (Colorado) suggested that the number of deaths due to medical error had
been underreported in the IOM study. Data from their review estimated that approximately 195 000 deaths
per year were due to preventable hospital errors.7
• In 2000, in the United Kingdom, the National Health Services (NHS) reported that adverse events occurred
in association with 10% of all hospital admissions. This resulted in 850 000 reported events at a cost of 2
billion pounds to the NHS annually.8
• The Canadian Adverse Events Study reported a 7.5% incidence of adverse events for all admissions to
Canadian hospitals. This study included data from a random sample of charts for non-obstetric, non-
psychiatric adult patients in acute care hospitals in five provinces (British Columbia, Alberta, Ontario, Quebec,
and Nova Scotia) for the fiscal year 2000. It was estimated that of the nearly 2.5 million admissions to
hospitals, 185,000 were associated with an adverse event. Almost 70 000 of these events were potentially
preventable. The authors also indicated that there were 9250 to 23 750 preventable deaths from adverse
events during this period.9
• An article in 2011 suggested that the “’Global Trigger tool’ shows that adverse events in hospitals may be ten
times greater than previously measured.”10
• In 2013, John James wrote in the Journal of Patient Safety the following conclusion to his study: “Given
limitations in the search capability of the Global Trigger Tool and the incompleteness of medical records on
which the Tool depends, the true number of premature deaths associated with preventable harm to patients
was estimated at more than 400,000 per year. Serious harm seems to be 10- to 20-fold more common than
lethal harm.”11
• His conclusion is particularly poignant: “In a sense, it does not matter whether the deaths of 100,000,
200,000 or 400,000 Americans each year are associated with PAEs (Preventable Adverse Events) in
hospitals.”
• He continues by saying, “Any of the estimates demands assertive action on the part of providers,
legislators, and people who will one day become patients. Yet, the action and progress on patient
safety is frustratingly slow; however, one must hope that the present, evidence-based estimate
of 400,000+ deaths per year will foster an outcry for overdue changes and increased vigilance in
medical care to address the problem of harm to patients who come to a hospital seeking only to be
healed.”
Patient Safety 46
Understanding Error in Health Care

Why does the high rate of clinical error in hospitals persist in the face of a plethora of published clinical practice
guidelines, policies, recommended procedures and standards? The availability of excellent continuing education courses
at the local, regional, and national levels that address evidence-based approaches to patient management has never
been greater.
A few facts:
• Humans are fallible. It is impossible to attain human perfection despite extensive training.
• You cannot eliminate error through education or explanation alone.
We work in a complex world with the support of flawed systems.
“A plethora of Guidelines, policies, recommended procedures….”
Perhaps here may lie some of the problem.
Healthcare has been described as a complex adaptive system. If this is so, then many of our efforts in Safety, which
have revolved around restricting and controlling humans in an effort to mitigate against their fallibility, may have
been misguided. Could these approaches have only considered half of the problem? In so doing, we may have gone
overboard in the production of restrictive tools to “guide” the care we give. We need to ask: Could there be so many tools
in our tool kit, that abiding to them all would make completing our work impossible?
Furthermore, do all these tools really add to safety of our care? “A worker following a safety rule can create a condition to
enable safety to emerge. Too many safety rules can overwhelm, and frustrate a worker, enabling danger to emerge.12
According to Braithwaite et al.2 over 600 guidelines policies, and procedures guide our work in one single day. These
tools constitute what they refer to as work-as-imagined by well-intended managers and policy makers. According to the
authors, work-as-done does not resemble work-as-imagined, because the latter cannot account for “how circumstances
vary, the diversity of patients, how goal-conflicts abound, how expected resources may be missing2” or quite simply
the unpredictable nature of both our patients and environment. In this reality, front-line teams must balance efficiency
against thoroughness every moment of every day. By this we mean that policies, procedures and other tools to guide
the care we give simply cannot be followed the way leaders believe they are. Doing so would lead to the organization
not being able to meet demand. To be successful, organizations favour efficiency in this trade-off principle until, it is
recognized in hindsight, that they should have been more thorough in that particular case.13
How did we come to be here?

A 2015 report from the National Patient Safety Institute examining the slow progress in safety, cited the observation by
Schultz.14 He states that knowledge moves in three phases and notes how those phases apply to risk reduction in health
care.
Patient Safety 47
1. Superficial simplicity: For example, the belief in the early days of safety that simply adopting the structure
and tools of High Reliability Organizations – such as the airline industry (a complicated system, and not a
complex one) – would be sufficient.
2. Confusing complexity: According to the report, this is the current situation in health care, with an
overwhelming number of tools, guidelines, policies, and procedures (work-as-imagined), which are in place
to improve safety but which in practical terms can become a form of barrier to safety.
3. Profound simplicity: According to the report, “Improved culture is not the means to an end but an end
itself. For example, we know that superficial implementation of a surgical checklist changes little.15 However,
a major teamwork and culture intervention that also included checklists (rather than the other way around)
reduced mortality by 50% more than secular trends.16 Thus, according to this checklist example, a core focus
on culture (with checklists as a tool) can improve outcomes. This example helps explain why the panel felt
leadership and culture are crucial to accelerating progress in patient safety.”
The above realization coupled with the principles of resilience may allow us to reach beyond the low-hanging fruit we
have achieved to date. It is important to understand that as complexity and uncertainty rise in our workplace, the usual
restrictive tools no longer work well. In short, Healthcare is a complex adaptive system, but it is run as a complicated
system, as a result, progress in safety has stalled.
Be that as it may for safety to occur, it is not about reinventing the wheel. However, a balance must exist between
reducing the likelihood of things going wrong – the traditional approach: using restrictive tools, or protective safety - and
increasing the likelihood that things go right (see Safety II – below). As such, an understanding of the following sections
is important.
Errors should be recognized as consequences rather than causes.17
Understanding why we fail

Figure 1. The relationship between hazards, defences, and losses
Adapted with permission from: Reason J. Managing the risks of organisational accidents. Aldershot (UK): Ashgate Publishing; 1997.
Patient Safety 48
Defences against Error

Like other organizational structures, the health care system has developed defenses and safeguards. When these
defences are breached by hazards, losses may occur.
Classification of Defences
HUMAN SYSTEM
Training Credentialing
Knowledge Peer review
Judgement Protocols, pathways, and policies
Manual dexterity Special teams
Vigilance Continuing medical education
Risk management and quality management
Classification of Failures
Figure 2. Unsafe acts
Patient Safety 49
In Reason’s view, our current medical system functions like a complex technological system. Professor James Reason
has described how human beings contribute to the breakdown of such systems.18 Unsafe acts can have a direct impact
on the safety of the system with immediate adverse effects. He calls these active failures. These unsafe acts are the
consequences of system failures rather than the causes of the failures.
He also states that “people working in complex systems make errors or violate procedures for reasons that generally
go beyond the scope of individual psychology.”18 He calls these reasons latent failures (conditions). In the healthcare
system, this concept can be visualized as a pyramid (Figure 2). At the sharp end are patients and healthcare providers.
The major factors that determine safety at the sharp end are related to latent conditions located at the blunt end and
at various levels throughout the pyramid. It is at the sharp end of the care system, where we are in a precarious
balance where all of the factors that determine safety come together creating “safe” or “unsafe” conditions for
both patients and caregivers.
Expanding on these two types of failures:18
1. Active failures: These occur at the front-line (individual level). They have an immediate effect, affect the
patient directly, and have traditionally resulted in some form of punishment and/or retraining of the
individual involved. This action discourages reporting, and usually doesn’t prevent similar events from
occurring in the future. It is not educational for the team and/or other colleagues, and allows latent failures
to remain in the system.
Active failures include the following:
−− Mental Slip (often due to fatigue): e.g. administering the wrong drug or the wrong dose. In this case,
care providers know what the right drug or dose is. Retraining would not help prevent this error in the
future.
−− Mental Lapse: e.g. forgetting to catheterize the bladder before a procedure that requires one. In this
case, care providers forget one of a list of items. Retraining would not help. A checklist might mitigate
this risk.
−− Mistake: e.g. misinterpreting an electronic fetal monitor pattern.
−− Procedural violation: e.g. applying obstetrical forceps before full dilatation of the cervix.
2. Latent failures are failures that are distant from direct front-line control, may involve poor design or
maintenance decisions, and have little direct effect but instead have a cumulative effect. Latent failures do
not usually have predictable effects (unlike active failures). They are the greatest threats to patient safety, and
they are indicative of a problem with the system rather than the individual.
Latent failures may be attributable to:
−− Human factors: fatigue from a long shift, stress, multi-tasking , multiple different care providers for one
patient
−− Local workplace factors: inadequate tools/equipment, poor communication and teamwork, unworkable
or ambiguous procedures/protocols, leadership shortcomings, insufficient staff training, staff shortages
Patient Safety 50
−− Organizational factors: strategies and top-level decisions made bythgovernments (e.g., budget cut to
25 Edition of the ALARM Course Manual
hospital), regulatory bodies (e.g., change in scope of practice), manufacturers (e.g., different drugs in
similar appearing containers), or hospital administrators (e.g., staff reductions in face of increasing
patient load).
How BreachesLead
How Breaches Lead to Harm
to Harm
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having many holes—though unlike in the cheese, these holes are continually opening, shutting, and shifting their opening,
shutting, and shifting their location. The presence of holes in any one “slice” does not normally cause
location. They are thus in many ways unpredictable. The presence of holes in any one “slice” does not normally cause a
a bad outcome. Usually, this can only happen when the holes in many layers momentarily line up to
bad outcome. Usually, a bad outcome can only happen when the holes in many layers momentarily line up to permit a
permit a trajectory of accident opportunity — bringing hazards into damaging contact with victims.17
trajectory of accident opportunity—bringing hazards into damaging contact with victims. 19
Figure
Figure 3.
3. Reason’s
Reason’s Swiss
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Theory.
BMJ 2000;320(7237):768-70. Adapted and reproduced with permission from the BMJ Publishing Group.
The above model (Figure 3) assists us in understanding the concept of a sequence of events, whose individual compo-
The above model (Figure 3) assists us in understanding the concept of a sequence of events, whose individual
nents will often
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team who will often not report his or her achievement. Our culture traditionally would not look favorably on an individual not look favor-
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that led us to the point where “we nearly gave the wrong drug”. That sequence, if left in place, will affect our colleagues
(maybe as early as) next week, next month, or next year. Through pure bad luck, one day that arrow will not be stopped
and a patient will be harmed. But the same sequence will have been repeated over and over again (stopped at varying
layers of Swiss cheese) for us to learn through that fateful harm event. This is why it is said that errors lie “dormant” in the
Patient Only by understanding the failures in existing systems can we repair them. A keen understanding of systems, 51
system.Safety
event review, and the ability to create recommendations by the individuals at the front line is key to developing a local
point where “we nearly gave the wrong drug”. That sequence, if left in place, will affect our colleagues (maybe as early as)
next week, next month, or next year. Through pure bad luck, one day that arrow will not be stopped and a patient will be
harmed. But the same sequence will have been repeated over and over again (stopped at varying layers of Swiss cheese)
for us to learn through that fateful harm event. This is why it is said that errors lie “dormant” in the system. Only by
understanding the failures in existing systems can we repair them. A keen understanding of systems, event review, and
the ability to create, and implement, recommendations by the individuals at the front line is key to developing a local
ownership to problems and create a culture of patient safety.20 This ownership creates sustainability in patient safety. This
is the foundation principle of CUSP programs (Comprehensive Unit-based Safety Programs) such as the successful and
effective MOREOB Program.21, 22
A final thought on the Swiss cheese model. Traditional Healthcare will review harm events and develop
recommendations and policies and/or protocols to mitigate new risk - this is a necessary action. These can be seen just as
additional layers of Swiss cheese. These tend to be added to the existing ‘layers of cheese.’ The more of these layers exist,
the harder it can be for a healthcare worker to navigate and the longer before he or she “starts treating” the patient. Thus,
the very presence of all these ‘safety’ layers, over time as they are added to, invite the human to bypass them. The layers –
in place for safety - can in and of themselves become a barrier to safe patient care.
The focus must be on narrowing the holes, not necessarily adding new layers.
We know how to provide a patient with the best care. What we cannot do, it seems, is provide that same level of
care to each and every patient consistently – this can change as we look to High Reliability and Resilience Engineering
approaches and create and embed patient safety into our Teams’ DNA.
Reason’s Swiss cheese model is excellent as a primer, but it needs to be understood that it is a little too simple to explain
all errors in the complex dynamic system of Healthcare.
Understanding why we succeed (Safety II Production safety)

Safety-II offers a complimentary approach to the concept of patient safety.
While understanding the need to improve processes that leave the patient vulnerable to human error (the traditional
approach to safety, also known as Safety I – or protection safety – discussed above), Safety II focuses on the important
realization that it is remarkable that so many patients have positive outcomes despite important challenges to Care
Teams (also known as production safety). These challenges may include an increased patient load, staff calling in sick,
equipment not working, units being on red-alert, etc.
Safety II then, looks at the work as done - which allowed care operations to be maintained despite these challenges – as
a way to improve existing systems (the existing systems are known as: work as prescribed – or the plethora of guidelines
and policies (mentioned above) that we are surrounded by).
The biggest difference between Safety I (the traditional approach to safety) and Safety II is the way in which the human
is viewed: a liability versus a resource. Thereby, an important step to sustainable safety is to understand WHY something
goes right despite so many challenges to its success. Understanding why we succeed allows us to recreate it and improve
the robustness of our processes.
Patient Safety 52
It is important to note that there is no competition between Safety I and Safety II, but a balance between the two. We still
need protection safety, but we also need production safety.
The MORE Programs have identified that for sustainable safety to occur within a unit, the necessary balance between
Safety I and II for that unit needs to be identified and nurtured. The MORE approach seeks to identify that balance -
between Safety I and Safety II - needed for each unit to succeed.
It is clear to many that the traditional approach to safety — Safety I — has managed to fix the proverbial “low hanging fruit.”
But to make real, substantive, and sustainable change in safety will require an understanding and application of Safety II.4
The Process of Risk Management

As inferred above, risk cannot be completely or constantly avoided. The intention in risk management is to anticipate risk
and prevent or limit harm. Risk identification must concern itself with all aspects that may threaten and/or jeopardize the
patient, the care providers, and the facility.
Risk management has five steps23:
1. The Identification of Risk
−− This is an essential first step because risk management is a proactive strategy
−− Patients and providers are best served by informed anticipation of problems
−− Risk is identified with reference to history. Has this event, or something like it, happened before?
−− Risk can also be identified when practitioners are informed about particular risks inherent in their group
or profession
2. Risk Assessment
−− An evaluation exercise
−− Answers the questions of how many or how often (frequency of risk), how much (cost of risk), and under
what circumstances (likelihood of risk)
−− Answers to these questions are essential to designing appropriate preventive programs
Patient Safety 53
3. Action to Manage Risk
AVOIDANCE OF RISK Discontinue procedures associated with high degree or incidence of risk (e.g., high forceps
(RESULTS IN NO LOSS) deliveries).
PREVENTION OF RISK Hospitals and maternity care providers can take steps to prevent or significantly lower the possibility
of mishap. By establishing risk management programs, hospitals and maternity care providers can
take steps to prevent or significantly lower the possibility of mishap and adverse outcomes.
TRANSFER OF RISK A high-risk case (e.g., preterm labour) can be transferred to a higher level of expertise for care.
REDUCTION OF RISK Prevention and reduction may be confused. It is important to note that reduction is the strategy that
(RESULTS IN SOME is called into play after the damaging event has occurred. One of the most important risk reduction
LOSS) strategies is the immediate care of and attention to persons threatened or injured. Losses attended to
immediately can often be mitigated.
Losses can be reduced after an event through early investigation and documentation and the
provision of full and honest disclosure.
SEGREGATION OF RISK Segregation is usually more applicable to facilities (e.g., Level I, II, and III hospitals) than to
individual care providers. At the individual level, segregation of risk would occur when consultations
with other specialists or colleagues are obtained during the management of a difficult situation (e.g.,
consulting a hematologist to assist in the management of a woman with a coagulation disorder
secondary to preeclampsia).
FINANCING OF RISK Premiums are paid by institutions, individuals, and governments to insurance agencies or defence
organizations, which assume the responsibility for the financial compensation awarded by the courts.
4. Implementation of Risk Management Programs

When considering risk management strategies, it is necessary to be aware of current practice and of
alternatives that are both practical and compatible with the objectives of care. It might be attractive from a
risk management perspective to stop some high-risk procedures (risk avoidance). However, the nature of
practice may make such an alternative unacceptable. An example of an unacceptable approach would be to
abandon all forceps deliveries. Another important strategy to manage risk is the development of a process
enabling health care providers to learn from no-harm and harm events (near misses and adverse events).
Reviews of these occurrences must take place in an objective and non-punitive environment. It is imperative
that system-based failure rather than human error is emphasized during reviews of unexpected clinical
processes and/or outcomes.
5. Evaluation of risk management strategies
It is essential to review the effect of a new process or strategy introduced to reduce or eliminate risk to
determine whether it achieved the expected results. Reviews should be as frequent as required to cover all
aspects of risk assessment and management. A committee may be appointed to monitor activities. Reports
on the success of initial attempts at implementation are integrated into the management plan.
Patient Safety 54
Risk management is a continuous process. It starts with identification and analysis of risk, proceeds to the
implementation of strategies to manage risk, and ends with the evaluation of risk-management activities
and their results.
High Reliability Organizations

What is Reliability?
Reliability in Healthcare can be defined as: a process doing what it was intended to do, in the place it was designed to be
performed, with the regular staff complement expected.24-27 252627
Reliability of a process is measured by its success:

• If 90 percent of patients receive their pre-op antibiotics at the appropriate time, the Process is reliable 90% of
the time.
• The failure rate of a process then is the inverse of its success. So in the above example the failure rate is
measured by the 10% of patients who did not get their pre-op antibiotics in time, or 1 in 10, or 10-1.
Research tells us that a failure rate of 10-1 or less is characterized as coming from strategies that include Training,
Reminders and the Reliance on the good will, attentiveness and hard work of Healthcare Staff.24-28 This would suggest
that those ways of doing things hold us to never improving our outcomes.
To improve our system’s reliability, we need to change the Status Quo. Where possible, we must move towards a system
that understands human fallibility and is designed to take it into account. Systems using quality and safety tools,
evidence based procedures, using Human Factors engineering and an understanding of human psychology.24-28
An HRO is defined by its ability to operate technologically complicated systems without error over long periods of
time.24-28
To help distinguish which organizations could be considered high reliability organizations, ask the following question.
“How many times could the organization’s systems have failed with potential catastrophic consequences but did not?” If
the answer to your question is many, many times, then it is a high reliability organization.
Several organizational structures have been studied by behavioral scientists and designated as high reliability
organizations. They are:
• air traffic control
• nuclear-powered aircraft carriers
• nuclear power plants
• the technical side of banking (e.g., ATMs)
These organizations have three defining characteristics:
• They are complicated, internally dynamic and intermittently, intensely interactive.
• They perform exacting tasks under considerable time pressure.
Patient Safety 55
• They carry out these demanding activities with low incident rates and an almost complete absence of
catastrophic failures over long periods of time.
Hierarchy is an interesting facet of an HRO. When an HRO is running in a routine mode, it is governed by the
conventional hierarchical structure. In an emergency situation, that governance shifts and safety takes precedence i.e.
any individual, regardless of position in the organization, takes command of the situation until it is either resolved
or someone else with more expertise takes over the management of the crisis. When the emergency has ended, the
organization returns seamlessly to its routine control mode.19
A strong feature of HROs is front line ownership of operations and their ability to be aware and adaptive. It has not
escaped the attention of most that the front line frequently has the solution to a problem. It is in this way that HRO and
Resilience Engineering are in many ways complementary. However, due to the way hospitals function, it appears that all
too frequently, no one seems to be listening to the front line. This contributes to an unengaged workforce.
A significant risk in an unengaged workforce is that it may be that they are ‘just coming to work’. This is what is meant
by the term ‘it’s just a job’; we might just be content in doing what we are told and finish the day. The only goal we
have is that of: going home. This is a result of ‘buy-in’ (as opposed to Ownership) as described by Zimmerman et al.
and is a warning sign of an organization in trouble. It is a workforce that is content to just follow orders – a disengaged,
complacent workforce that comes to work, completes their shift and goes home.
What we want in our units is the opposite: an engaged workforce that identifies a problem and owns it to its
resolution. Due to the mutual accountability within such a team, the solution has a much likelier chance of success and
sustainability. A unit with such front line ownership has an aware and adaptive culture — a necessary step to an HRO.
HRO’s understand that surprises should never be; they are anticipated. HRO’s are preoccupied with failure.29, 30
“HROs are aware and adaptive enough to intercept or mitigate threatening events and circumstances.”26
The HRO and normalization of deviance

Paradoxically, HROs view successful operations as potentially dangerous. Success leads to system simplification, short
cuts, and “the normalization of deviance.”31, 32 Imperceptibly, as time goes on, technical and professional standards
degrade, i.e., these short cuts, and non-standard activities become “normal” for that individual or unit.
All group cultures become less safe over time. Risky operational systems and clinical practices continue, because
those involved think “they get away with it” most of the time.32 A unit is at its most dangerous when nothing bad has
happened for some time.
HROs “actively and continually question assumptions, promote orderly challenge of operating practices and solicit
outside views of the routine”32 to address normalization of deviance.
Patient Safety 56
Perinatal and obstetrical units and HROs

“Understanding updated and refined concepts of high reliability in the delivery of obstetric care requires an
understanding of what high reliability is not (i.e., a quality improvement method focused on efficiency and productivity.
Rather, high reliability is a creation of a culture and processes that radically reduce system failures and effectively
respond when failures do occur.”33
Perinatal units have many of the characteristics of HROs. They are complex, technical environments with a variety of
professional disciplines that have diverse roles and responsibilities. Patients and their families and friends expect
obstetrical units to function without error over long periods of time.34 Normalization of deviance is a characteristic of
obstetrical/perinatal units as exemplified in the following:
• Application of forceps or vacuum when the cervix is not quite fully dilated
• Chronic under-staffing
• Fundal pushing with shoulder dystocia
• Use of a combination of prostaglandins and oxytocin for induction of labour
• Artificial rupture of membranes when the head is too high
HRO principles in health care:
• Safety is the priority and is everyone’s responsibility
• Operations are a team effort
• Hierarchy disappears in an emergency. Decisions about safety can be made at any level of the organization
• Communication is highly valued
• Emergencies are rehearsed
• There is interprofessional review of routine functions, near misses, and unexpected events34
When obstetrical units successfully adapt HRO principles, they have:34
1. A clearly stated goal and purpose: patient safety.
2. Clear language that defines patient safety.
3. Established clear and agreed-upon markers of well-being.
4. Clearly defined organizational teamwork:
−− Minimized hierarchy: high reliability perinatal units thrive on teamwork
−− Everyone is respected and recognized as competent
−− Everyone knows what everyone else is thinking and seeks opportunities to help other team members
−− Everyone is focused on patient safety
−− Planning, data collection, and quality management are interprofessional exercises.
5. Patient care records that are not divided by profession. The principle is to use one patient care record that is
maintained, completed, and quality managed by the interprofessional team. The record is the narrative of
the patient’s care. Electronic health records have brought a new dimension of challenges in this area.
6. Policies that are unit-wide rather than separate for each profession (nursing, medicine, midwifery, etc.):
Patient Safety 57
−− high reliability units have a minimum number of policies

−− there is an inverse relationship between the number of written policies and existing reliable functions
−− one policy exists in all safe units: a physician, midwife, or nurse will come when requested and no one is
reprimanded, in any way, for a false alarm, since the call was made with only one thought in mind, the
unit’s goal: patient safety.
7. Two clear operating principles:
−− adherence to professional guidelines
−− minimal intervention but with the ability to intervene, when necessary, in a timely manner.
8. An ability to communicate honestly and openly in perceived hierarchical situations. Establishing good
communication in a team environment will break down the barriers of an authority gradient. This enables
optimal patient care in environments dealing with critical events.
9. Ensure patient safety will always override hierarchy.
The Effectiveness of High Reliability Units

The MOREOB program, created in 2001 by the Patient Safety Division of the SOGC, is a patient safety program based on
the HRO and resilience engineering principles and centered on team function and culture change.
Several studies suggest the potential of the HRO approach. One from Alberta, reported that the MOREOB program,
which had been implemented province-wide, had a positive effect on health service delivery as well as newborn and
maternal outcomes.35 Another, designed to address two HRO principles (“operations are a team effort” and “emergencies
are rehearsed”) as they pertain to the management of umbilical cord prolapse found an important improvement in
management, most notably a significant reduction in the diagnosis to delivery time interval.36 And finally, a review of
mandatory reportable harm events in 34 hospitals revealed significant improvement.22
Quality and risk management: health care provider responsibilities37:

• Identify high-risk procedures
• Recognize errors before they result in adverse outcomes
• Ensure that health care providers are aware of their limits and practice within these limits
• Review near misses, accidents, injuries, and adverse events as system failures rather than individual failures
• Establish an environment for clinical error management
• Eliminate the “blame” and “punitive” culture associated with adverse events
• Be aware of local, regional, and national clinical guidelines and policy statements
• Remember the three A’s of quality care and risk management: ability, accessibility, availability
• Promote a culture in which communication and team-building occur.
• Collaborate at a local, regional, and national, level to develop performance indicators and benchmarks for
clinical activities
Patient Safety 58
Care Provider Participation

Interprofessional committees are needed to promote teamwork and patient safety. Without the full participation of all of
its maternity care providers and middle and senior administrators, a facility cannot have an effective risk management
system. Health care providers will accept and support risk management activities if they are aware of the benefits of
these activities for their patients and themselves.
All who work in the unit are orientated to confirming fetal and maternal well-being. Variations are reduced by
standardizing policies and procedures where possible. Teamwork is the hallmark of the unit. Interprofessional review of
adverse outcomes and near misses are practiced in a non-punitive and educational environment.
Patient Safety 59
References
1. Moss F. Risk management and quality of care. Qual Health Care. 1995;4:102-7. Available from: https://www.ncbi.
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3. Davies J, Hebert P, Hoffman C. The Canadian Patient Safety Dictionary2003.
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13. Hollnagel E. The ETTO Principle: Why things that go right sometimes go wrong. Farnham, UK: Ashgate; 2009.
14. Schultz W. Profound Simplicity: Foundations for a Social Philosophy. Hoboken (NJ): John Wiley & Sons; 1982.
15. Urbach DR, Govindarajan A, Saskin R, Wilton AS, Baxter NN. Adoption of surgical safety checklists in Ontario,
Canada: overpromised or underdelivered? Healthc Q. 2014;17:10-2. Available from: https://www.ncbi.nlm.nih.
gov/pubmed/25906458.
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16. Neily J, Mills PD, Young-Xu Y, Carney BT, West P, Berger DH, et al. Association between implementation of a medical
team training program and surgical mortality. JAMA. 2010;304:1693-700. Available from: https://www.ncbi.nlm.
17. McLean P. On the job: legal matters. Liability trends in nursing. Can Nurse. 2002;98:32-4.
18. Reason J. Managing the risk of organisational accidents. Aldershot (UK): Ashgate Publishing; 1997.
19. Reason J. Human error: models and management. West J Med. 2000;172:393-6. Available from: https://www.
20. Boussat B, Seigneurin A, Giai J, Kamalanavin K, Labarere J, Francois P. Involvement in Root Cause Analysis and
Patient Safety Culture Among Hospital Care Providers. J Patient Saf. 2017. Available from: https://www.ncbi.nlm.
21. Pronovost PJ, Holzmueller CG, Ennen CS, Fox HE. Overview of progress in patient safety. Am J Obstet Gynecol.
22. Geary M, Ruiter PJA, Yasseen AS, 3rd. Examining the effects of an obstetrics interprofessional programme on
reductions to reportable events and their related costs. J Interprof Care. 2018:1-9. Available from: https://www.
23. Dickson G. Principles of risk management. Vincent, C, editor. London: BMJ Publishing 1995.
24. Grabowski M, Roberts K. Risk mitigation in large scale systems: lessons from high reliability organizations. Calif
Manage Rev. 1997;39:152-62.
25. Roberts K. Some characterisitics of one type of high reliability organization. Organization Science. 1990;1:160-76.
26. Roberts K. Cultural characteristics of reliability enhancing organizations. J Manag Issues 1993;5:165-81.
27. Rochlin G, LaPort T, Roberts K. The self-designing high-reliability organisation: aircraft carrier flight operations at
sea. Nav War Coll Rev. 1987;40:76-90.
28. Weick K, Roberts K. Collective mind in organizations: heedful Interrelating on flight decks. Adm Sci Q.
1993;38:357-81.
29. Niedner MF, Muething SE, Sutcliffe KM. The high-reliability pediatric intensive care unit. Pediatr Clin North Am.
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cure mindset for patient safety. Healthc Pap. 2013;13:6-22. Available from: https://www.ncbi.nlm.nih.gov/
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36. Siassakos D, Hasafa Z, Sibanda T, Fox R, Donald F, Winter C, et al. Retrospective cohort study of diagnosis-delivery
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Patient Safety 62
Table of Contents
Chapter 4 Management of Labour..................................................................................................................................... 64

Introduction................................................................................................................................................................ 64
Factors that affect Labour................................................................................................................................. 64
Assessing Labour............................................................................................................................................. 65
Care During the First Stage of Labour ........................................................................................................................ 67
Latent Phase of the First Stage of Labour........................................................................................................ 67
Active Phase of the First Stage of Labour......................................................................................................... 68
Care During the Second Stage of Labour.................................................................................................................... 70
Management of The Third Stage of Labour................................................................................................................. 74
Dystocia........................................................................................................................................................... 75
Avoiding a Primary Caesarean Section............................................................................................................ 80
Summary.................................................................................................................................................................... 83
Management of Labour 63
Chapter 4
Management of Labour
Introduction
Labour is a natural physiological process with an expected outcome of vaginal birth. Caregivers should strive to create
a positive family experience while maintaining the maternal and newborn wellbeing, preventing complications and
responding to emergencies.1 As 60% of women enter labour without obstetrical or pre-existing health concerns2,
minimal interventions would be expected to achieve this outcome.
Interventions are considered when the reasons are clearly documented; the benefits outweigh the risks they support a
safer outcome1, the mother is informed of the risks and benefits, and the intervention avoids unintended consequences,
such as, Caesarean section. Avoiding a primary CS provides reduced morbidity and mortality in the index pregnancy and
better outcomes for subsequent pregnancies.
Factors that affect Labour

Personal and environmental factors can affect the course of labour and birth and should be considered by the caregiver.
Some of these include:
• Support for women during active labour and birth may increase a family’s satisfaction with the birth
experience, reduce the use of medications and interventions and enhances the positive attitude women
need to care for their babies.3 Ongoing communication should be clear and timely so that the woman is
engaged in the process.
• Preparation for labour and birth can be obtained from health care providers, prenatal classes, peers/family,
media, internet sites and mobile apps however non English/French speaking and minority population
concerns are not well addressed in the available courses.4
• Ethnocultural diversity in obstetrical families requires caregivers to develop cultural competence and
sensitivity regarding individual practices and the uniqueness of each family.
• Maternal age at birth is increasing across Canada potentially increasing the incidence of medical comorbidity
and assisted reproductive technology.5 In Ontario 4.2% of births occur in individuals >40 years and 18.9%
occurred in individuals between 35-39 years.6 As with all women, the care of the older parturient needs to be
individualized and her care planned based on evidence and her needs.
• Location of birth may include hospitals, birthing centres and home. For out of hospital births care is similar to
births in the hospital setting but consideration must be given availability and timing of transport, emergency
services and attendance of a second caregiver.1
• Maternal BMI (see chapter on Obesity)

• Pain Management (see chapter on Pain Management)
Assessing Labour
1. Verify Expected Date of Delivery
Naegele’s rule, developed in 1812, calculates the expected date of delivery using the last menstrual period (LMP): first
day of LMP – 3 months + 7 days. Limitations include inaccurate reporting of the date of the LMP, bleeding unrelated
to menses, and delayed ovulation. A 1990 retrospective study of uncomplicated pregnancies in Boston compared the
length of pregnancy calculated using Naegele’s rule with the actual date of spontaneous labour. In non-parous women,
labour occurred 8 days later than predicted by Naegele’s rule (411), and in parous women labour was, on average, 3 days
later than predicted by Naegele’s rule (403 weeks).7 A 2015 Cochrane review8 (N = 25 516, 8 studies) of the routine use
of early ultrasound for dating demonstrated a modest reduction in induction of labour for post-term pregnancy from
3.8% to 2.2%. Routine first trimester ultrasound also detects twin gestations at an age when chorionicity can be reliably
determined.
Ultrasound measurement of gestational age at 7 to 23 weeks is more accurate than a “certain” menstrual date. Therefore,
estimated delivery date based on LMP is best confirmed with ultrasound examination.
Sonographic estimation of gestational age is most accurate early in gestation. Between 7 and 16 weeks’ gestation,
ultrasound crown–rump length provides a more accurate estimate of gestational age than certain LMP and should be
used to date pregnancy when available. Between 13 and 16 weeks, biparietal diameter is more accurate.9 Beyond 16
weeks, normal variation in fetal growth and standard error in ultrasound measurement make sonographic estimation of
gestational age increasingly less precise.10
If first trimester ultrasound measurement is not available, gestational age based on certain LMP in a woman with regular
cycles appears to be at least as accurate as ultrasound examination performed between 16 and 23 weeks’ gestation;
however, if the ultrasound estimation differs from the LMP estimation by more than 10 days, then the sonographic
estimate should be used.
When LMP is uncertain, cycles are irregular, or clinical assessment of uterine size differs from gestational age based on
LMP, then first trimester ultrasound examination is indicated, even in settings where routine first trimester ultrasound
is not available. If first trimester ultrasound is not performed in these scenarios, then dating should be based on the
earliest second trimester ultrasound estimation. As the fertilization date is known in pregnancies resulting from assisted
reproductive technologies such as in vitro fertilization, the expected date of delivery should be based on the known
conception date.9, 11
2. Use a Triage Area and Triage Assessment Scale

The use of a triage area to assess women presenting to hospital, versus a labour room, has the potential to reduce the
number of women receiving oxytocin for augmentation, the rate of epidural analgesia for pain relief, and the duration of
the active and second stages of labour, and to improve women’s evaluations of their labour and birth experiences.12
Use of a specific screening tool in obstetrical triage or in the home, similar to what has been used in emergency units,
can facilitate priority setting, responsiveness and flow through the triage unit.13 The Obstetrical Triage Screening Scale
(OTAS) 14, developed in Canada, is a standardized instrument to assess the need for urgency of assessment and for
admission. The percentage of patients admitted to the antenatal or birthing unit decreased from 80% (OTAS 1) to 12%
(OTAS 5). OTAS has demonstrated interrater reliability in both tertiary and community hospitals.
3. Confirm the Woman is in Labour

Labour onset can be difficult to diagnose. Women are anxious for labour to begin and thus frequently assume symptoms
of latent labour indicate a need to go to hospital. Health education for women and families about when they should go
to hospital and what symptoms require urgent action are important components of care during pregnancy.
The diagnosis of active labour requires assessment of uterine activity and cervical status. Description of cervical
status should include dilatation, effacement, station, consistency, and position as summarized in a Bishop score (see
induction of labour chapter for an example). In the USA women are considered in active labour only when they reach 6
cm dilation.15 In contrast, SOGC identifies active labour when the women reaches 4 cm. Using the SOGC definitions of
labour will help guide the diagnosis but it is important to always look at the total clinical picture to determine need for
admission.
Reproduced from SOGC Clinical Practice Guideline no. 336, with permission of The Society of Obstetricians and Gynaecologists Canada.47
4. Determine any Contraindications to Vaginal Delivery

Clinical situations that preclude vaginal delivery or that elevate the risk of labour above the maternal or fetal risk of
Caesarean section include such conditions as placenta previa, vasa previa, cord presentation; abnormal fetal lie; prior
classical CS or significant uterine surgery; active genital herpes, invasive cervical carcinoma.
Care During the First Stage of Labour

Latent Phase of the First Stage of Labour
Studies have shown that “women presenting to the hospital in the latent phase of labour experience increased
obstetrical interventions”, including electronic fetal monitoring, epidural analgesia, oxytocin, and Caesarean section,
than those who are admitted in active labour.16-20 However, it is unclear whether this is because these women spend
longer in the hospital or because women who present earlier have underlying problems. It is important to remember
that dystocia cannot be diagnosed before the onset of labour or during the latent phase of labour. 17181920
Women may be assessed at home to determine if they are in labour. This supports the woman and enables her to await
labour at home.
Women who present to hospital in early labour may be asked to walk around or rest in a prelabour lounge or return
for reassessment. Alternately women may be sent home with a plan to return to hospital if their status changes. These
changes may include increased pain, rupture of membranes, increased frequency or strength of contractions or if the
woman is concerned. It can be beneficial to provide the return to hospital or when to contact care providers instructions
in writing. Observation, rest, and therapeutic analgesia are preferable to a more active approach of amniotomy and
oxytocin induction.
Time Frames for Stages of Labour

The mean and longest acceptable duration of each phase of labour were established by Friedman in the early 1950s
and were based on women who had undergone spontaneous or induced labour and delivery and whose fetuses were
in vertex and in breech presentations. Mounting evidence has suggested that the Friedman curve may no longer be
appropriate for current labour care. The SOGC CPG on MOL stated the active phase is longer and dilation slower than
Friedman’s data. The rate of cervical change ranged from 0.5 to 0.7 cm/hour for nulliparas and 0.5 to 1.3/hour for parous
women.21
Length of spontaneous labour in women with good perinatal outcomes (n >200,000) varied widely. Starting from 4 cm
dilation median length of labour varied from 3.7-5.9h (95th percentiles: 14.5-16.7h).22 The Consortium on Safe Labour
looked at 62,415 women in 19 hospitals in the USA. Data showed labour progress can be slow up to 6 cm and after 6cm
multiparas progressed faster than nulliparas. Second stage length varied with and without epidurals with the 2nd stage in
nulliparas lasting 3.6 and 2.8 hours, respectively.15
Enema
A 2007 Cochrane review showed that enemas did not have a significant effect on women’s satisfaction or on infection
rates (e.g., for perineal wound infection or other neonatal infections) and concludes that routine use of enemas during
labour should be discouraged.23
Active Phase of the First Stage of Labour

Partogram (also called Partograph)
A partogram is a graphic labour curve used to document cervical change and fetal descent over time, some partograms
include 2 and 4 hour action lines. A 2018 Cochrane review of 11 trials (n=9475) found no benefit of partogram use
related to CS rate, oxytocin augmentation or Apgar <7 at 5 minutes.24
Although there is little demonstrated value in clinical outcomes, the partogram is useful as a communication tool, for
handover, for teaching, and to provide a snapshot of labour progress.
Ambulation and Position

Women’s position for labour may be influenced by mother’s choice, caregiver preference, and place of birth, monitoring
or medical interventions. Encouragement of movement, position change and upright positions may reduce the length of
the first stage of labour and reduce pain.
A 2017 Cochrane review of women without epidural anaesthesia compared women labouring in an upright position
(walking or upright non-walking, e.g., sitting, standing, kneeling, squatting, and all fours) versus in recumbent positions
(supine, semi-recumbent, and lateral).25 Authors’ state results should be viewed with caution due low quality of the
research. Researchers found women in an upright position had no difference in CS, serious perinatal tears, had first
stages that were approximately one hour shorter, and were less likely to have epidural analgesia.26 However, there was
no difference in length of the second stage, mode of delivery, or other outcomes related to the well-being of mothers
and babies. For women who had epidural analgesia, there were no differences between those randomized to upright
positions and those in recumbent positions for any of the outcomes examined in the review.27
Several authors proposed hands and knees position for correction of a posterior presentation91. A randomized trial
assessed this approach (n=439) for 10 minutes in first stage demonstrated no benefit in conversion to an anterior
occiput position but a slight increase in comfort.28
Having a comfortable chair in the labour room, not just a bed, encourages flexibility of positions and movement and
removes the assumption that the woman has to be in bed.
Eating and Drinking During the First Stage of Labour

A 2013 Cochrane review on restricting oral fluid and food intake during labour (5 studies, n = 3130) looked at women
in active labour and at low risk of requiring general anaesthesia.29 The studies compared restricting women to nothing
except ice chips / sips of water or providing women with carbohydrate drinks, specific fluids and foods, or the freedom to
eat and drink at will. No significant differences were found in the rate of Caesarean section or assisted vaginal deliveries,
or in Apgar scores. The pooled data were insufficient to assess the incidence of the rare outcome Mendelson’s syndrome
(aspiration associated with general anaesthesia). The authors concluded that there was no evidence of benefits or harms
associated with restricting access to fluid or food for women at low-risk of requiring general anaesthesia.30
Women at low risk of requiring general anaesthesia should have the choice to eat or drink as desired or as tolerated
in labour.21 There have been no studies assessing women with risk factors, so there is no evidence with respect to
restrictions in this group.30-32 3132
Different solutions and volumes of intravenous fluids do not influence the length of labour in nulliparas.33 There was
no significant difference in the time from enrolment to delivery, second stage duration, and cord artery pH and glucose
level.
Amniotomy/Artificial Rupture of Membranes (AROM)

Rupture of membranes appears to affect uterine contractility and cervical dilation through prostaglandin then
endogenous Oxytocin synthesis. However, a 2013 Cochrane review of 15 studies with 5583 women showed no clear
statistically significant difference between women with amniotomy alone versus intention to preserve the membranes re
length of the first stage of labour, caesarean section, maternal satisfaction with birth or Apgar score less than seven at five
minutes.34
A 2012 Cochrane review of 14 RCTs (n = 8033 women) compared early amniotomy and oxytocin for the prevention or
treatment of dystocia. A modest reduction in the duration of labour and CS rate was found, with no difference in other
measures of neonatal and maternal morbidity.35 A smaller RCT (n = 752) comparing early versus late amniotomy without
oxytocin found a higher frequency of severe variable fetal heart rate decelerations and CS for abnormal fetal heart rate,
yet no difference in overall CS rate or neonatal outcome.36
Although the protocols and settings are heterogeneous, routine amniotomy in normally progressing labour is of
questionable benefit and may result in more frequent variable fetal heart rate decelerations, and potentially increased
CS rate.37 Amniotomy does appear indicated to accelerate labour that is not progressing adequately.
If amniotomy is performed, it is necessary to ensure that the fetal head is well-applied to the cervix (not ballot table)
to minimize the risk of cord prolapse. If the head is well applied following amniotomy, a woman may ambulate.
Amniotomy with oxytocin augmentation, and other measures, should be considered if the diagnosis of dystocia has
been made
Active Management of the First Stage of Labour

The active management of labour is a complex process that originally included concrete criteria for the diagnosis
of labour (regular contractions with spontaneous rupture of membranes or complete cervical effacement), routine
amniotomy in labour, close attention to progress in labour, and liberal use of high-dose oxytocin if cervical dilation was
less than 1 cm per hour. The maximum allowable duration of the first stage of labour was 10 hours, and of the second
stage, 2 hours. Observational studies by the initial advocates of active management showed lower CS rates, a lower
incidence of prolonged labour, better neonatal outcomes, and improved maternal satisfaction.38 Follow-up observational
studies supported these results.39, 40 A 2013 Cochrane review (7 trials of 5390 low risk women) showed active
management was associated with small reductions in the CS rate when compared with various regimes of routine care.41
Active management requires more interventions and creates a more medicalized birth process. It is possible that some
components of the active management package are more effective than others.42 Of note, RCTs demonstrating no
increase in CS rate with epidural analgesia compared with parenteral opioids routinely used all components of active
management of labour protocols.43, 44
Care During the Second Stage of Labour

Position
With epidural: A 2018 Cochrane compared women using a recumbent (left, right or semi recumbent – not on their
back or legs raised fin stirrups) position with women in an upright position (8 studies n=4464) showed variations in
findings.25 When only the high quality studies (3 trials n=3609), primarily from a 2017 UK trial BUMPES (n=3236),
were reviewed they reported increased operative and CS births with an upright position. Women with a recumbent (left,
right or semi recumbent) had lower risk of operative birth (CS or AVB), The UK data specifically showed 41.1% SVD in
the recumbent position and 35.2% in the upright position. There was no difference in perineal trauma, or significant
haemorrhage, In Canada, the epidural rate for vaginal births is 49.7%.45 464748
Without epidural: A 2017 Cochrane review (30 studies, n= 9015) compared women using an upright position versus
supine positions. The authors caution that much of the evidence was low quality. The upright position demonstrated:
INCREASED DECREASED NO DIFFERENCE
• Estimated blood loss • Length of second stage however • Rate of CS,

significant variation between studies, • 3rd or 4th degree perineal tears,
mainly decreased in primigravid group • Babies admitted to NICU
• AVD, (moderate)
• Abnormal FHR patterns
A 2015 study of 7832 vaginal deliveries found that squatting or kneeling was associated with an elevated risk of anal
sphincter trauma and that delivering in water was not associated with a greater risk of AST than delivering in bed.49
There is no perfect position for labour for everyone. Enabling the woman to select her position of comfort, assuming it is
clinically safe, often provides the greatest benefit. 505152535455
When to Push
Each labour is unique thus the timing of pushing and woman’s feeling of an urge to push will differ for everyone.
Pushing, generally, may commence when the cervix is fully dilated, the presenting part is engaged and the woman feels
an urge to push. Passive descent from full dilatation to the perception of an urge to push, delayed pushing, may be less
exhausting and more effective, particularly for women with epidural analgesia. Delayed pushing is preferred when the
woman has no urge to push; particularly if the presenting part is above station +2 or in non-occiput anterior position,
the fetal surveillance is normal and the woman’s status is satisfactory.21
However, a 2018 study compared delayed versus immediate pushing in 2414 nulliparous women with epidurals
and term pregnancies.56 There was no significant difference in SVD (85.9% to 86.5%), neonatal morbidity, or perineal
lacerations. The immediate pushing group had mean difference of 9 minutes longer pushing time, lower rate of
chorioamnionitis and PPH.
How to Push
Spontaneous pushing encourages women to follow their body’s urges and generally push 3-5 times during a
contraction. In Valsalva or directed pushing the mother is asked to take a deep breath, hold the breath (closed glottis),
and push downward when uterine contraction starts.
It was suggested that spontaneous pushing allows a slower and controlled descent of the fetus57. Spontaneous pushing
compared to direct pushing showed no difference in overall length of 2nd stage, 3rd or 4th degree laceration/episiotomy,
spontaneous vaginal delivery or neonatal outcomes (cord gases, resuscitations.58 Valsalva pushing negatively affected
urodynamic factors measured at 3 months post partum59.
A 2017 Cochrane review summarized their finding with the comment “for the type of pushing, with or without epidural,
there is no conclusive evidence to support or refute any specific style as part of routine clinical practice, and in the
absence of strong evidence supporting a specific method or timing of pushing, the woman’s preference and comfort and
clinical context should guide decisions”.58
Length of second stage43

Limited evidence and multiple conflicting variables making setting a specific time limit for the second stage difficult.
ACOG and SMFM in United States published an Obstetric Care Consensus extending time frames in labour and second
stage with a view to prevention of Caesarean Section.60 They indicated that a specific absolute maximum length of time
spent in the second stage of labour beyond which all women should undergo operative delivery has not been identified.
It is important to distinguish dystocia from obstructed labour when managing the second stage.
Provided there is ongoing progress and fetal status is normal, arbitrary time limits for the second stage are not well
founded.61 Thus it may be appropriate to avoid early intervention with operative delivery if fetal surveillance is normal.
There is no evidence that a prolonged passive second stage with poor contractions is harmful to the fetus, so time could
be taken to achieve adequate contractions using oxytocin, if necessary. Time limits should be initiated when contractions
are adequate and active pushing begins. However, continued strong contractions without progress in the second stage
indicates obstructed labour and place the fetus and mother at risk.62
Studies report increased asphyxia related complications and low Apgar scores at 5 minutes when women pushed ≥ 4
hours compared to women who pushed ≤ 1hour however the overall risk of concerns was low.63, 64
Table 4. Recommended Practices in Second Stage by Parity and Use of Epidural Analgesia
(after full dilatation and when power is adequate21)
NULLIPAROUS PAROUS
No epidural Epidural No epidural Epidural
Total durationa 3 hours 4 hours 2 hours 3 hours
Passive 2nd stageb May wait up to 2 hours before pushing May wait up to 1 hour May wait up to 2 hours before
particularly when the presenting part is above +2 pushing, provided continued
station or in a non-occiput anterior (OA) position, passive descent
and the urge to push is absent. Encourage waiting to
allow passive descent.
Commence pushing When urge to push present and not able to allow When urge to push present OR after 2 completed hours of
passive descent OR after 2 completed hours of passive second stage
passive second stage
Assessment Hourly for descent and position. Reassess the need for assisted birth after 2 hours of active pushing.
a
Continuing beyond the following time limits should be carefully evaluated and consideration given to expedite delivery. Extending these time limits may be appropriate in the
presence of continued descent of the head, maternal status and fetal surveillance is normal, and spontaneous vaginal birth is imminent.
b
Waiting for up to the time period indicated prior to the onset of pushing is appropriate in the presence of continued descent of the head and fetal and maternal condition are
satisfactory.
Episiotomy and Perineal Management

Routine episiotomy does NOT reduce perineal / vaginal trauma. A 2017 Cochrane examined selective vs routine
episiotomy with 12 studies (n=6177 women) from a variety of countries including Canada.65 In situations when
unassisted vaginal birth was anticipated, selective episiotomy may result in 30% fewer women experiencing severe /
perineal trauma. There may be little or no difference in dyspareunia and urinary incontinence at 6 months with selective
vs routine episiotomy. Further research is suggested for women when instrumental delivery is intended.
Strategies to reduce perineal trauma could include:
• warm compresses: A 2011 Cochrane review (n = 1525) of warm perineal compresses in labour versus
no intervention showed a reduction in third and fourth degree perineal tears from 5% to 2.5%.66 A 2013
Cochrane review (n = 2500) of antenatal perineal massage showed modest reductions in episiotomy rate,
perineal trauma, and pain.67, 68
• Episiotomy angle: The angle at which a mediolateral episiotomy is cut is important. An observational study
showed that the angle of an episiotomy from midline performed when the perineum is distended decreased
by 20 degrees on average after delivery.69 An episiotomy performed at 45 degrees leaves an incision after
delivery at 25 degrees from midline—dangerously close to the anal sphincter. To avoid causing OASI, an
episiotomy should be performed more than 60 degrees from midline when the head is crowning (less than
30 degrees from horizontal). An episiotomy cut at 60 degrees results in a post birth episiotomy angel of
episiotomy should be considered in women considered at increased risk of obstetrical anal sphincter in
(OASI), such as nulliparous women requiring assisted vaginal birth or those with a history of prior OASI.
Randomized evidence is limited116 but corroborates observationalthevidence that more liberal (but not ro
use of mediolateral episiotomy prevents OASI at assisted vaginal births, particularly with forceps.117-119
The angle at which a mediolateral episiotomy is cut is important. An observational study showed that th
angle of an episiotomy from midline performed when the perineum is distended decreased by 20 deg
45 degrees. Midline episiotomy increases the risk of anal sphincter injury, and should not be performed
on average after delivery.
(Figure 3).70-72 An episiotomy performed at 45 degrees leaves an incision after delivery at
120
7172
25 degrees
Perinealfrom midline
infiltration is used –fordangerously close
repair of lacerations and to the anal
episiotomy sphincter.
repair. Generous andTo avoid causing
widespread OASI,
infiltration an episiotom
should
shouldbebe performed
used. Use of an agent morewith than 60 degrees
epinephrine is helpful. from midline
Care should when
be taken not tothe
injecthead is crowning
intravascularly (lessthethan 30 deg
or to exceed
toxic dose.
from horizontal). A episiotomy cut at 60 degrees results in a post birth episiotomy angle of 45 degrees.
There was insufficient evidence to assess the clinical benefits or harms of routine antibiotic prophylaxis
Midline episiotomy
for episiotomy repairdirectly threatens
after normal birth.73 the anal sphincter and should be avoided (see diagram).
121-123
Figure 3. Episiotomy
UsedUsed
withwith
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permission of Salus
SalusGlobal
Global Corporation
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ement of Labour
Risk of obstetrical anal sphincter injury (OASI)

Manual perineal protection was effective in nulliparous women in reducing the risk of OASI by two thirds.72 A
retrospective Australian study found the only statistically significant increase in OASI over time was with non-assisted
vaginal births without episiotomy (linear trend P < 0.001) and forceps with episiotomy (linear trend P = 0.004).74
Authors of a population study of 113 279 Swedish women (singleton pregnancy, SVD without episiotomy) determined
birth position affected rate of OASI. Regardless of parity, the lowest OASI rates were found among women giving birth
in standing position and the highest rates among women birthing in the lithotomy position. Birth seat and squatting
position involved an increased risk of OASI among parous women.75
Although routine episiotomy has been shown to cause more harm than good, selective mediolateral episiotomy should
be considered in women considered at increased risk of obstetrical anal sphincter injury such as nulliparous women
requiring assisted vaginal birth or those with a history of prior OASI. Randomized evidence is limited76 but corroborates
observational evidence that more liberal (but not routine) use of mediolateral episiotomy prevents OASI at assisted
vaginal births, particularly with forceps.77-79
78
Quality improvement efforts in large regions of Norway and Denmark over the past decade have succeeded in reducing
the incidence of OASI from 4% to less than 2%. The key components have been controlled slow delivery of the crowning
fetal head and selective use of mediolateral episiotomy (overall rates between 10% and 20%).79-81 8081
Perineal Repair
• A 2010 Cochrane review involving 10 171 women showed decreased pain and need for resuturing with
synthetic versus catgut suture material for episiotomy and perineal tear repairs.
• Rapidly absorbable synthetic suture needed to be removed less often than regular synthetic suture. There
were no differences in long-term pain or dyspareunia.82
• A 2012 Cochrane review involving 8184 women showed decreased analgesia use, less pain for up to 10
days, and reduced need for suture removal with continuous versus interrupted perineal repair technique.
There was no difference in long-term pain or need for re-suturing.83
• A randomized trial of 147 women with third or fourth degree tears found a single 1 g IV dose of an anti-
anaerobic cephalosporin (cefotetan or cefoxitin) given during repair reduced the incidence of perineal
complications from 24% to 8% (P = 0.037).84
Management of The Third Stage of Labour

Active management of the third stage of labour (AMTSL) involves interventions by the care provider to assist in the
expulsion of the placenta to prevent or decrease blood loss. Personnel with the training and skills to actively manage
the third stage should be in attendance. The most important component of the active management of the third stage of
labour is routine administration of oxytocin.
Further information on third stage management can be found in the Postpartum Hemorrhage chapter.
Dystocia
Dystocia is one of the most common labour problems. Dystocia cannot be diagnosed prior to the onset of the active
phase of the first stage of labour or before the cervix is at least 4 cm dilated
Dystocia is defined as delayed or arrested progress in labour, irrespective of cause. Using the 5th percentile of the
population as a cut off, dystocia is identified when any of the following are seen:
• Dilation of less than 0.5 cm/hour over 4 hours or
• No cervical change over 2 hours in the active first stage of labour or
• Greater than 1 hour of active pushing and no descent of the presenting part in the second stage of labour.
Etiology of Dystocia
Successful labour and vaginal delivery depend upon the dynamic relationship between the fetus, the maternal pelvis,
and uterine and maternal power. Dystocia can be related to difficulty with any of the 4 Ps:
power, passenger, passage, and psyche.
Power Contractions: hypotonic, incoordinate or infrequent
Maternal expulsive efforts: ineffective or contraindicated
During labour, palpation of the uterus is recommended to assess uterine contraction strength. However, palpation and
external tocometry provide only subjective, qualitative estimates of intensity. Indirect clinical evidence of adequate
contraction strength may be obtained by assessing caput and moulding. An intrauterine pressure catheter (IUPC) is the
only accurate way of assessing the intensity (in mm Hg) of contractions. Its use is not indicated routinely but may be
helpful in certain situations such as 85
• augmentation during a trial of labour after previous Caesarean section or in the case of grand multiparity
(> 5).86
• when it is not possible to palpate contractions because of high BMI or body habitus
When using an IUPC, contraction strength is measured with a goal of an increase of at least 50 to 60 mm Hg above
baseline or > 200 Montevideo units (uterine contraction pressure above baseline times number of contractions in 10
minutes). A standard institutional protocol for the augmentation of labour is recommended if the strength of uterine
contractions is inadequate.
Epidural analgesia can interfere with uterine contractions and lead to dystocia requiring oxytocin augmentation.87
Early detection and treatment with active management of labour protocols and oxytocin augmentation can reduce the
likelihood of CS and operative delivery.44, 87
Passenger Fetal-position, attitude, size, abnormalities (e.g., hydrocephalus)
The fetus should be assessed for size and malposition.88 Adequate power in labour will often correct malposition,
whereas inadequate power may result in persistent malposition. A normal-sized fetus may also present an increased
diameter to the pelvis because the head is not flexed or is asynclitic. Adequate uterine power may overcome this
problem. Use of hands-and-knees position for 10 minutes twice daily was not found to correct an occiput posterior fetal
position in late pregnancy.89
The diagnosis of true or absolute cephalopelvic disproportion should be limited to the uncommon instances of real
disproportion, i.e., inability of the well-flexed head (sub-occipito bregmatic presentation) to pass through the bony
pelvis despite evidence of adequate uterine power (caput and moulding present and/ or IUPC demonstrates adequate
contractions). Malposition, on the other hand, may lead to relative disproportion. Accurate assessment and description
will guide management, and if a CS is performed for dystocia, helps determine suitability for a future VBAC.
Passage Pelvic bony structure
Soft tissue factors (tumours, full bladder, full rectum, vaginal septum, high BMI)
Clinical examination of the passage may reveal prominent spines or sacrum, a narrow pubic arch or a space-occupying
mass in the pelvis, such as fibroids. Neither antenatal X-ray pelvimetry nor clinical pelvimetry has been shown to predict
the outcome of labour.90 It is important to ensure the bladder is empty, particularly in the second stage. Soft tissue
obstruction may occur in patients with a high BMI.
Psyche Pain, anxiety
“Hormones released in response to stress can also bring about dystocia. Sources of stress vary for each woman, but the
pain and the absence of a support person are the 2 accepted factors. Confinement to bed and the restriction of maternal
movement can also be a source of psychological stress. Anxiety may inhibit normal cervical dilatation, resulting in
prolonged labour and increased pain perception. Anxiety also causes an increase in the levels of stress-related hormones
(ß-endorphin, adrenocorticotropic hormone, cortisol, and epinephrine). These hormones act on the smooth muscle of the
uterus; increased levels can lead to dystocia by reducing uterine contractions.”91
Prevention of Dystocia
Strategies to prevent dystocia include
• Labour preparation
• Continuous support during labour
• Careful labour assessment (consider a partogram)
• Use of appropriate analgesia
• For women with epidural analgesia, if inadequate labour progress is suspected, early artificial rupture of
membranes and oxytocin for uterine inertia
Management of Dystocia
If a dystocia is suspected in the first stage of labour, management may include
• Formulating, discussing, and documenting a plan
• Amniotomy
• Ensuring adequate maternal hydration92

• Considering therapeutic rest with analgesia, if exhausted
• Oxytocin augmentation
• If clinical assessment of contraction strength inadequate, considering IUPC
• CS (if other interventions have failed)
Dystocia versus obstructed labour

It is important to distinguish dystocia from obstructed labour
• Dystocia is a lack of adequate progress in labour due to any of 4 causes: power, passenger, passage,
and psyche.
• Obstructed labour, a form of dystocia, is lack of cervical dilation or descent of the presenting part
despite adequate power, i.e., evidence of adequate uterine contractions and/or maternal effort.
When dystocia is diagnosed, a common cause is inadequate uterine contractions and oxytocin augmentation is often
indicated. Once strong contractions have been present for 2 to 3 hours without further cervical dilation in the first stage
or for 1 to 2 hours without descent in the second stage, significant caput and moulding are usually present.
• If caput and moulding are absent, consider verifying contraction strength using an intrauterine pressure
catheter (see management of dystocia below).
• If caput and molding are present, labour is obstructed.
A 2016 Canadian study used mathematical modelling of both dilation and descent to better predict the need for CS
intervention.93
Dystocia mandates a search for a cause, then treatment.

Obstructed labour is an indication for Caesarean section or assisted vaginal birth, if safely feasible.
In the event of dystocia due to inadequate power despite appropriate analgesia, hydration, rest, and amniotomy,
oxytocin is indicated to achieve adequate contractions before operative delivery is considered.94 Principal concerns about
the use of oxytocin are fetal compromise and uterine rupture. It must be remembered that it is not oxytocin that causes
the problem but rather excessive contractions. The correct use of oxytocin achieves adequate contractions while avoiding
excess uterine activity that could compromise the fetus or lead to uterine rupture.
Even with close titration of oxytocin, tachysystole / excess uterine activity can occur. All labour and delivery
units must be prepared to manage excess uterine activity whether it is associated with oxytocin use or not.
This is outlined in the chapter on induction of labour and fetal health surveillance.
Complications of oxytocin
POSSIBLE COMPLICATION MECHANISM PREVENTATIVE MANAGEMENT
Fetal compromise Tachysystole Correct dose
Uterine Rupture Tachysystole Correct dose
Water intoxication ADH effect Use crystalloid IV solution with

concentrated oxytocin to limit amount of
water infused
Sensitivity to oxytocin
Each woman’s uterus varies in its sensitivity to oxytocin. Even in the same uterus, the sensitivity may change during
the course of labour. The dose used must be sufficient to achieve adequate contractions. Protocols or guidelines for
the administration of oxytocin vary but many suggest starting with a low dose and small increments at intervals of 30
minutes.95, 96 Starting incremental dosages for augmentation may be less than those for induction. Every obstetrical unit
must have an identified and accessible protocol that will include a starting dose, increment interval, and maximum dose
allowed before reassessment. Electronic fetal monitoring is initiated or continued when oxytocin is started.
Intravenous oxytocin can be administered by low- or high-dose protocol. The choice of protocol should be based on the
relative risks of uterine rupture, sensitivity to oxytocin, and likelihood of placental compromise. The oxytocin protocol
must be based on the uterine response and fetal capacity to tolerate the increase uterine activity generated an early
rapid uterine response is noted with a high-dose protocol or there are concerns about placental function, then a low-dose
protocol should be used. Using a consistent augmentation/induction protocol (whether low or high dose) within a facility
reduced the overall Caesarean section rate in nulliparous women from 35.5% to 24.5% OR −0.58.97
A 2010 meta-analysis of RCTs including 5400 women concluded that high-dose oxytocin protocols were associated with a
lower CS rate than low-dose protocols. Excess uterine activity was more common with high-dose protocols, but there was
no difference in maternal or neonatal morbidity. Low dose was defined as 1 to 2 milliunit (mU)/min increments and high
dose was defined as ≥ 4 mU/min increments, increased every 30 min.96 This meta-analysis was dominated by studies
that included only nulliparous women. Evidence specific to parous women or women with a prior Caesarean section scar
is lacking. Therefore, it is prudent to use a low-dose protocol for labouring women with a prior Caesarean section or other
uterine surgery because of a potential increase in the risk of uterine rupture. It is also prudent to use a low-dose protocol
in women with grand multiparity because of their increased sensitivity to oxytocin. Women with suspected fetal growth
restriction should also receive low-dose oxytocin because of increased risk of placental insufficiency with strong uterine
contractions.
Nulliparous women and women with epidural analgesia in labour are particularly likely to benefit from high- rather than
low-dose oxytocin augmentation.44 A small Canadian pilot RCT of accelerated Oxytocin titration protocol (AOT or high
dose 4mU/min) vs gradual Oxytocin Titration (GOT or low dose 2mu/min) demonstrated a trend to lower CS in the AOT
group.150
In nulliparas with epidural analgesia, to reduce the likelihood Caesarean sections, the clinical goal of augmentation is 4
to 5 contractions in 10 minutes. If IUPC is used, then the goal is 200 to 250 Montevideo units (e.g. 4 contractions of 50
to 60 mmHg in 10 minutes). 44
Example of Low and High Dose Protocol
LOW DOSE PROTOCOL HIGH DOSE PROTOCOL
Initial dose of oxytocin 1 to 2 mU/min 2 to 4 mU/min
Increase interval 30 minutes
Dosage increment 1 to 2 mU 4 mU/min
Usual dose for good labour 8 to 12 mU/minute98
Maximum dose before reassessment 20 to 30 mU/min99, 100
CLINICAL CONSIDERATIONS SUGGESTED OXYTOCIN PROTOCOL
Prior Caesarean section low dose
Fetal growth restriction low dose
Parity > 4 low dose
Parous augmentation, no epidural low dose
Parous induction low or high dose
Parous augmentation with epidural low or high dose
Nullipara augmentation, no epidural low dose
Nullipara induction low or high dose
Nullipara with epidural consider high dose
Most cases of uterine inertia respond to oxytocin doses under 10 mU/min, but individual needs vary greatly. Many
women receiving high-dose oxytocin will never require 10 mU/min and may need finer titration by 1 to 2 mU/min when
they approach adequate uterine activity. Clinical judgement is required. There is no evidence suggesting a maximum
safe dose; however, reassessment is recommended when the dose reaches 20 to 30 mU/min, and very close monitoring
should be employed for doses > 30 mU/min, including IUPC if necessary.99
Second Stage Labour Dystocia
Close attention to contraction strength and progress in the second stage is necessary. Inadequate or
infrequent contractions should prompt oxytocin augmentation, similar to the first stage of labour. It is
uncommon for a parous woman to require oxytocin augmentation and caution is advised. Fetal well-being
must be assured.
It continues to be important to differentiate dystocia and obstructed labour during second stage.
There are 3 common causes: uterine inertia, fetal malposition, and relative or absolute cephalopelvic disproportion.
Differentiating between these causes is essential to assessing fetal risk and determining appropriate management in a
prolonged second stage.
If no urge to push occurs after 1 hour of second stage, assess fetal position, caput and moulding, and uterine contraction
strength. Consider initiating or increasing oxytocin if contractions are felt to be inadequate. There is no evidence that
a prolonged passive second stage with poor contractions is harmful to the fetus.106 Time limits should be initiated
when contractions are adequate and active pushing commences. Oxytocin is often required when epidural analgesia
is present. Recommendations allowing a longer second stage in women with epidural analgesia take into account the
epidural’s inhibitory effect on uterine contraction strength and maternal motor function.
Adequate uterine power will also often correct fetal malposition. Placement of an intrauterine pressure catheter should
be considered if contractions are difficult to assess, although insertion can be challenging at full dilatation.
In the active second stage, if contractions are clearly adequate (with or without oxytocin), significant caput and moulding
are present, and there is no progress over 2 hours for a nullipara or 1 hour for a multiparous woman, then labour is
obstructed. Assisted vaginal delivery or Caesarean section should be considered. A prolonged second stage in obstructed
labour with adequate contractions can be harmful. A population-based, cohort analysis of 120 000 women found an
increase in the risk of maternal obstetric trauma, postpartum hemorrhage, puerperal febrile morbidity, composite
maternal morbidity, low 5-minute Apgar score, birth depression, admission to the neonatal intensive care unit, and
composite perinatal morbidity as the duration of the second stage surpassed 3 hours in nulliparous women and 2 hours
in parous women.101
A 2015 meta-analysis of 12 studies showed that the risks of uterine incision extension, infection, mean blood loss, and
operative time were significantly higher with the push technique than with the reverse breech extraction.102 103
Avoiding a Primary Caesarean Section

The increasing worldwide Caesarean Section (CS) rate is concerning with its associated maternal morbidity and mortality,
health care costs, and potential future pregnancy concerns. Prevention of the primary CS as well as encouragement of
Trial of Labour after Caesarean (TOLAC), in appropriately screened cases, has been the focus for rate reduction. There are
many clinical situations that require a CS for maternal and/or fetal well being however there are many occasions when a
CS is done for less than ideal reasons.
Women with first delivery by CS have an increased risk of severe complications in the second pregnancy. A Nordic study
(N=213,518), comparing women whose first delivery was vaginal or CS, found that abnormally invasive placenta,
uterine rupture and severe postpartum haemorrhage were more common in women with a first CS.104
Thus focus of labour management should be to provide a safe labour and birth and be attentive to avoiding the primary
CS. Optimal support of normal labour processes, appropriate management of dystocia, and consistency of clinical
guidelines and encouragement of TOLAC could lead to a reduction in the CS rate.105 106
Caesarean Section Rates

The overall Canadian CS rate (primary and repeat) 2016/2017 was 28.2% of births with the highest rate in British
Columbia.45 The rate of CS in the USA for the same period was 32% with highest numbers in the southern states i.e.
Mississippi 37.8%, Louisiana 37.5%, Florida 37.2%.106 The global CS rate has moved from 12% in 2000 to 21% in
2015.107 108109
Comparison of CS rates by Province

40
35
30
25
2013
20
2014
2015
15
2016/17
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Causes of Caesarean Sections

Many caregivers rationalize their CS rate based on perceived specific characteristics of their population (e.g.: % of high
risk, higher BMI) and not care practices. The 10-Group Classification System, developed by Robson, can be used to
analyze CS deliveries in a facility or area and compare rates in similar situations110.
This classification system is being used increasingly around the world to focus attempts to control CS rate in Group 1
(nulliparous women in spontaneous labour at term) and Group 5 (women with a prior CS at term).111 Conducting regular
reviews /audits of indicators for CS have provided better understanding of reasons for CS and the potential reduce the
rate of CS.112
The following table outlines the Modified Robson criteria developed by SOGC committee opinion113
DESCRIPTION
1 Nullipara, singleton cephalic, ≥ 37 weeks, spontaneous labour
2 Nullipara, singleton cephalic, ≥ 37 weeks

A: Induced
B: Caesarean section before labour
3 Multipara, singleton cephalic, ≥ 37 weeks, spontaneous labour
4 Multipara, singleton cephalic, ≥ 37 weeks

A: Induced labour
B: Caesarean Section before labour
5 Previous CS , singleton Cephalic, ≥ 37 weeks

A: spontaneous labour
B: Induced labour
C: CS before labour
6 All nulliparous Breeches

B: Induced labour
C: CS before labour
7 All multiparous breeches (including previous CS)

B: Induced labour
C: CS before labour
8 All multiple pregnancies (including previous CS)

B: Induced labour
C: CS before labour
9 All abnormal lies (including previous CS but excluding breech)

B: Induced labour
C: CS before labour
10 All singleton cephalic ≤ 36 weeks (including previous CS)

B: Induced labour
C: CS before labour
Summary
Labour is a physiological process. Normal labour is enhanced by appropriate latent phase management (e.g., maternal
fetal assessment, information and a plan), delayed admission until active labour, continuous support in labour, comfort
measures and appropriate pain management, and intervention only when necessary.
Dystocia can be diagnosed only when active labour is established. Dystocia mandates a search for a cause, then
treatment. Management may include adequate analgesia, hydration and rest, amniotomy, augmentation, and assisted
vaginal birth.
• Obstructed labour is an indication for CS or assisted vaginal birth, if they can be safely preformed.
• For women having epidural analgesia, uterine inertia and inadequate labour progress should be detected
early and augmented with ARM and oxytocin.
• Operative intervention should be undertaken when necessary.
Best care in labour takes into account the wishes of the woman, her individual clinical situation, and evidence informed
practice. Labour management should support the physiological process of birth while identifying potential concerns and
supporting interventions that will increase the likelihood of a vaginal birth.
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Appendix
Appendix
Local infiltration of the pudendal nerve. Transvaginal technique showing the needle extended beyond the
needle guard and passing through the sacrospinous ligament (S) to reach the pudendal nerve (N).
Used with permission from Salus Global
Copyright
Local infiltration © The McGraw-Hill
of the pudendal Companies,
nerve. Transvaginal Inc. Labor
technique showing and delivery.
the needle extended In: Cunningham
beyond et al.and
the needle guard Williams obstetrics.
passing through 22nd ed. ligament
the sacrospinous 2005.135(S) to reach
the pudendal nerve (N).
Copyright © The McGraw-Hill Companies, Inc. Labor and delivery. In: Cunningham et al. Williams obstetrics. 22nd ed. 2005.114

Table of Contents
Chapter 5 Support and Pain Management in Labour ........................................................................................................ 96

Prenatal Education...................................................................................................................................................... 97
Continuous Support................................................................................................................................................... 97
Non-Pharmacological Pain Relief............................................................................................................................... 97
Pharmacological Methods ......................................................................................................................................... 99
Opioids.......................................................................................................................................................... 100
Care and Management in the Second Stage of Labour............................................................................................ 104
Epidural Analgesia, ...................................................................................................................................... 104
Support and Pain Management in Labour 95

Chapter 5
Support and Pain Management in Labour
Women experience a wide range of pain during labour. The severity and tolerance of pain is unique to each labouring
woman and cannot be predicted reliably prior to its occurrence. Two themes emerged from a qualitative meta-analysis of
10 studies regarding women’s ability to cope with pain1 – the importance of individualised, continuous support and an
acceptance of pain during childbirth.
As pain and a woman’s response to it are individual, women need to be aware of a variety of strategies to assist with their
management of pain. Using a pain scale to assess pain in labour helps to determine the need for offering interventions
and the effectiveness of those interventions. It has been suggested that in addition to a pain scale, a coping scale be
used. This differentiates those women able to cope with significant pain from those requiring intervention.2
Some women in labour reach the limit of their pain tolerance. Women experiencing excessive pain or anxiety have high
endogenous catecholamines.3, 4 This produces a direct inhibitory effect on uterine contractility and establishes a vicious circle of
poor uterine progress leading to increased anxiety leading to increased catecholamines leading to further impairment of progress.
The relief of pain by effective support and analgesia may allow release of the uterus from the constraints of the endogenous
catecholamines and allow progress in labour. High endogenous catecholamine levels may also adversely affect uterine blood flow
and therefore fetal oxygenation.5
The management of pain during labour involves more than the simple and timely administration of the best analgesic
agent available. Successful control of pain in labour requires active management of the entire process. This should begin
with prenatal education and counselling. Measures to enhance comfort and reduce apprehension are required for the
care of all women in labour. If appropriate measures are used early in the process of labour, analgesic needs decrease.
Those people who care for women in labour need to be aware of all the available options for the prevention of pain as
well as for its management. When the health care team understands the indications, possible variations, and potential
side effects, the woman and her family are able to make choices in a less stressful environment.
Satisfaction in childbirth is not contingent upon the absence of pain. Many women are willing to experience some pain
in childbirth, but they do not want the pain to overwhelm them. For women whose goals for childbirth include the use
of measures to manage pain with minimal or no drug use, and for those who have little or no access to pharmacological
methods of pain relief, the non-pharmacological methods of analgesia in childbirth, in combination with continuous
support, are integral to labour planning. These measures cannot match epidural analgesia for analgesic effectiveness,
but they do help women and are not likely to have harmful side effects.

Prenatal Education
Women and their partners seek prenatal education to help them understand the process of birth and the potential
options related to labour, pain relief, infant care, and feeding. A 2007 Cochrane review of nine randomized trials
involving 2284 women concluded the effects of prenatal education are unknown and that such education for women
who have previously had a CS has had little effect on rates of VBAC. No data were reported concerning anxiety,
breastfeeding success, or general social support.6
In addition to group and individual classes, many women are now accessing Internet information, reality television
programs on pregnancy and birth, and textbook information. The effect of these sources of information has not been
fully evaluated.
Continuous Support
Continuous labour support (CLS) is associated with lower use of pharmacological analgesia. Supportive care during
labour includes:
• Emotional support - continuous presence, reassurance, and praise
• Information - labour progress and advice regarding coping techniques
• Comfort measures - touch, massage, warm baths/showers, promoting adequate fluid intake
• Advocacy
• Supporting partners in their role as a coach6-8 78
A 2013 Cochrane review of RCTs involving over 15 000 women in both low- and middle-income settings showed that
continuous support in labour increased the likelihood of vaginal delivery, reduced CS rate and the use of epidural
analgesia, and improved APGAR scores and maternal satisfaction. “Subgroup analyses suggested that continuous
support was most effective when the provider was neither part of the hospital staff nor the woman’s social network.”7-9
Doulas, paraprofessionals employed by some women to provide continuous labour support, were the provider in most of
the studies in the review.
Nurses and midwives provide the majority of professional continuous labour support. Nurses identified organizational
barriers to CLS that included increased patient acuity and patient: nurse ratio.10 Studies involving traditional birth
attendants suggest improved birth outcomes but are of poor quality, not randomized, and uncertain with respect to cost-
effectiveness.9, 11
Non-Pharmacological Pain Relief

Smith et al.12 published a 2006 Cochrane review of complementary and alternative therapies for labour pain
management. Evidence of benefit in reducing pain exists for acupuncture (RR 0.70, CI 0.49 to 1.00, 2 trials, n=288), and
self-hypnosis (RR 0.53, CI 0.36 to 0.79, 5 trials, n=749). The efficacy of acupressure, aromatherapy, audio analgesia, and
massage has not been established.12 The requirement for more one-to-one care in these situations may have influenced

outcomes. A 2018 Cochrane Review on relaxation techniques for pain management in the active phase of labour found
that relaxation techniques, yoga, and music have little efficacy in reducing pain and increasing maternal satisfaction, with
low or very low quality of evidence. There was insufficient evidence for mindfulness and audio-analgesia techniques.
Non-Pharmacological Techniques:55
• Techniques that reduce painful stimuli:
−− Maternal movement and position change:
›› For women who do not have epidural analgesia, movement, position change, or upright positions
may reduce the length of the first stage of labour and reduce pain.
›› Women with epidural analgesia who adopt recumbent or supine positions during the second stage
of labour may have little or no difference in operative birth rates.13, 14
−− Counter-pressure
• Techniques that activate peripheral sensory receptors:
−− Superficial heat and cold
−− Immersion in water during labour 15
›› A 2009 Cochrane review identified ten RCTs comparing water immersion during the first stage
of labour versus no immersion. There was a reduction in the use of epidural/spinal/ paracervical
analgesia among women allocated to water immersion compared with controls (OR 0.82, 95% CI
0.70 to 0.98, six trials; n=2499). The authors stated that it was not possible to conclude whether
it was the water immersion itself or the other associated care practices such as support from
caregivers that was responsible for the apparent benefit. There was no difference in assisted vaginal
deliveries, Caesarean sections, perineal trauma, or maternal infection. There were no differences in
Apgar score < 7 at five minutes, neonatal unit admissions, or neonatal infection rates.
›› Regarding water immersion in the second stage of labour, there was inadequate evidence to
support or not to support a woman’s decision to give birth in water.16
−− Hypnosis
›› A 2016 Cochrane analysis (9 studies, n=2954) found only poor quality data related to hypnosis.
Insufficient evidence exists regarding satisfaction with pain relief or sense of coping with labour.17
−− Acupuncture and acupressure
›› There is mixed and limited evidence on the effectiveness of acupuncture or acupressure. An
unblinded RCT (2009) of 607 women compared analgesic use in women treated with acupuncture,
transcutaneous electrical nerve simulations (tens), or usual care (including sterile water papules,
nitrous oxide, warm tub bath, meperidine, and epidural analgesia). Acupuncture was found to
reduce the use of nitrous oxide and sterile water papule injections but did not affect epidural
analgesia use or opioid consumption or pain scores.18
−− Transcutaneous electrical nerve stimulations
›› The analgesic effect of tens was found to be weak.19 A 2009 Cochrane review reported that although
women receiving tens to acupuncture points were less likely to report severe pain (RR 0.41, 95% CI
0.32 to 0.55) and most would use it again (RR 1.54, 95% CI 1.31 to1.80), there was no difference
in pain scores, mode of delivery, duration of labour, use of other analgesia, or augmentation of
labour.19
−− Intradermal injection of sterile water 20

›› A 2009 systematic review (n=828) found that women randomized to intradermal sterile water
injections had significantly reduced visual analogue pain scores for up to two hours and a reduced
caesarean section rate (4.6%) compared to a saline comparison group (9.9%) (RR 0.51, 95%
CI 0.30 to 0.87). The meta-analysis included some small and unblinded studies; therefore the
authors recommended a large RCT to validate their findings.21 a 2012 Cochrane review found the
intradermal sterile water injection was not effective for low back or other labour pain.22
−− Aromatherapy
›› Moderate evidence of some pain relief with inhalation of lavender essence23; this may be restricted
in hospitals with scent restrictions
• Other techniques that enhance descending inhibitory pathways:
−− Attention focusing and distraction
−− Music and audio-analgesia
−− Biofeedback
Pharmacological Methods
Providing effective pain relief in labour is a primary responsibility of the health care team. Having a thorough knowledge
of the pharmacology of the drugs used during labour is necessary in order to promote appropriate and satisfying care
and to limit side effects. It is important to understand that:
• Sedative and hypnotic drugs do not provide pain relief and may increase respiratory depression when given
with opioids.
• No pharmacological method is devoid of maternal or fetal side effects. With almost all pharmaceutical
therapies, some amount of the drug gets access to the fetus. Specifically with intravenous opioids, this may
be important to the success of breastfeeding.
• Each opioid has unique pharmacodynamic characteristics that may result in different therapeutic effects and
side effects.
• Anticholinergic side effects may occur with opioids and care should be directed at recognizing and
addressing these discomforts.
• Women can receive opioids just before birth without significant respiratory depression in the newborn.
• Action should be taken to prevent toxicity with all local anesthetics.
• Epidural analgesia provides the most efficacious pharmacological analgesia, with limited side effects to the
mother and fetus.
When the health care team understands the indications, limitations, and side effects of these drugs, adverse maternal
and fetal outcomes can be minimized. Ideally, the care provider should discuss options regarding medications, possible
variations, and potential side effects during the antenatal period. This allows the woman and her family the opportunity
to make choices in a less stressful environment. When labour occurs, appropriate and individually desired non-
pharmacologic or pharmacologic agents may be used. 24

Opioids
Opioids are used routinely in many centres. A variety of options are available. A number of studies have reported on
the negative effects of opioids with a longer half-life (e.g., meperidine). The negative effects of meperidine are based
on an active metabolite half-life in the newborn that may reach 90 hours and may include respiratory depression and
newborn behaviour effects including lack of responsiveness and impaired suckling reflex.23-25 The use of meperidine is
discouraged and opioids with a shorter half-life (e.g., fentanyl) are preferred.24-26 Opioids may be given intramuscularly
(IM), subcutaneously, or by repetitive intravenous (IV) boluses, either using a patient-controlled pump or administered
by staff. The IV route has the advantage of a rapid effect when needed. Opioids may be usefully combined with an
antiemetic, as opioids increase the risk of nausea and vomiting compared to epidural analgesia.27
Remifentanil patient controlled analgesia (PCA) may offer some benefits over traditional intramuscular (IM) opioids
for labour analgesia. Compared with IM meperidine, labouring women using remifentanil were less likely to choose
epidural analgesia, and had a reduced instrumental delivery rate.28 The narrow therapeutic window, as well as the
increased risk of respiratory complications requiring constant nursing presence and oxygen saturation monitoring, have
limited the wider use of remifentanil for labour analgesia.
When pharmacologic agents are used for pain control in labour, guidelines regarding their safe and effective use should
be available for all staff. These guidelines should include the method of action, average and maximum dose, possible
maternal and fetal side effects, precautions, and resuscitative measures for each drug. When any opioid is used, opioid
antagonists (e.g., naloxone) and resuscitation capabilities should be available. Before a woman is sent home following
opioid administration, she needs to be assessed to determine the effects and side effects of the medication.
Suggested Opioid use in labour:
STAGE OF LABOUR NULLIPAROUS PAROUS
Latent Stage: IM/SC Morphine IM/SC Morphine
Early Active Stage: IM/SC or IV Morphine IV Morphine or Fentanyl
Late Active Stage: IV Morphine or Fentanyl IV Fentanyl
Second Stage: IV Fentanyl IV Fentanyl
Nitrous Oxide
Entonox is a mixture of 50% nitrous oxide, 50% oxygen that provides little analgesia, but high patient satisfaction. It
must be self-administered for safety reasons via a demand-valve; and used with scavenging in a well-ventilated room for
workplace safety.29 Deep inhalation should begin as soon as the woman is aware of the onset of a contraction to allow
for maximal benefit. It is often useful for the woman who has coped well until transition and then requires some form of
analgesia for a short time. Shorter use will decrease environmental exposure, as nitrous oxide is destructive to the ozone
layer and has global warming.30 It may also be used as an adjunct during other procedures such as the placement of a
pudendal block or perineal repair. It has been demonstrated that the majority of women who opt to use nitrous oxide

will convert to neuraxial analgesia, and factors associated with conversion are labour induction (RR 2.0, 95% CI 1.2 to
3.3) and labour augmentation (RR 1.7, 95% CI 1.0 to 2.9).31
Peripheral Nerve Blocks

A pudendal block can be used for analgesia of the perineum in the second stage of labour. This form of analgesia can
be very useful for the sacral nerves and should be considered when other regional analgesia is not available or provides
insufficient sacral spread. A diagram depicting pudendal block administration is included as an appendix. Ten (10) mL
of 1% plain lidocaine or equivalent is injected at two locations through or just inferior to the sacrospinal ligament, just
medial to the ischial spine on each side. The effect is usually felt within three to four minutes.29
Neuraxial Analgesia
The BORN Ontario database indicated that in 2009, 63% of nulliparous women and 39% of multiparous women
received neuraxial analgesia.32 Neuraxial analgesia for labour with a catheter in the epidural space (i.e. labour epidural
analgesia (LEA)) can provide effective pain relief throughout all stages of labour and delivery. The hormonal response to
pain includes a rise in endogenous catecholamines. The effective relief of pain lowers epinephrine concentrations and
may result in improved uterine contractions and possibly improved placental perfusion. A particular benefit of epidural
analgesia exists for women with dystocia who require augmentation. Effective pain relief may increase the acceptance of
augmentation and the likelihood of subsequent vaginal delivery.
Onset of Neuraxial Analgesia

Neuraxial techniques have evolved significantly and modern techniques allow labour neuraxial analgesia to be
administered effectively and safely for both mother and unborn child. Labour epidural analgesia (LEA) can be initiated
with administration of medication (local anesthesia and opioid) into the epidural space or intrathecal space (combined
spinal epidural (CSE)). The advantage of CSE is that it provides faster onset of analgesia compared to LEA initiated
through the epidural catheter. However, CSE may be associated with increased maternal side effects including
hypotension and opioid-induced pruritus.33 The concern that the epidural catheter placed as part of a CSE technique
is “untested” is not evidence based, as CSE is associated with lower failure rates for labour or CS anesthesia compared
to standard epidural34 A dural-puncture epidural (DPE) is a new technique similar to a CSE, however unlike CSE no
intrathecal medications are administered after the dura is punctured. Although the role of DPE has not yet been
sufficiently studied, a RCT published in 2017 has demonstrated that DPE provides better sacral spread and a lower
incidence of asymmetrical block compared to LEA without dural puncture, and less maternal pruritus and hypotension
when compared to CSE35.
Maintenance of Neuraxial Analgesia

Much has changed in the way local anesthetics are administered to give epidural analgesia. Continuous epidural
infusion (CEI) with patient controlled analgesia (PCEA) where a patient can give herself a bolus of local anesthetic with

the push of a button is a standard in most large obstetric centres. PCEA has been shown to produce greater maternal
satisfaction and excellent analgesia despite using low-dose/very low-dose epidural solutions as compared to traditional
CEI. A 2002 meta-analysis of nine studies (n=640) showed lower anesthetic dose and less motor block with PCEA
compared to CEI.36,37
An alternative to CEI is programmed intermittent epidural bolus (PIEB). PIEB allows the pump to give a bolus dose of
local anesthetic at specific intervals (e.g. 8 ml every 45 mins rather than 10 ml/hour). This permits greater spread of local
anesthetics in the epidural space and better analgesia. PIEB can be used in conjunction with PCEA. A 2013 meta-analysis
of RCTs showed PIEB reduces overall local anesthetic dose and improves maternal satisfaction.38 There is a potential that
PIEB may improve instrumental delivery rates and the need for anesthesia interventions. More evidence is required to
investigate its effect on obstetric outcomes. 39
Obstetric Outcomes
A 2018 Cochrane review involving 11,000 women showed that compared with opiate or no analgesia, epidural
analgesia (low and high doses), provides superior pain relief in labour, higher maternal satisfaction with pain relief, a
small decrease in neonatal acidosis, and less need for naloxone.27 Epidural analgesia was associated with:
• Increased risk of assisted vaginal birth (RR 1.44)
−− However a post hoc subgroup analysis of trials conducted after 2005, which include low dose epidural
analgesia, showed that this effect is negated when trials before 2005 are excluded from this analysis (RR
1.19, 95% CI 0.97 to 1.46)
• Maternal hypotension (RR 11.3)
• Motor-blockade (RR 31.7)
• Maternal fever (RR 2.51)
• Urinary retention (RR 14.2)
• Longer second stage of labour (mean difference 15.4 minutes)
• Less nausea and vomiting than opioid analgesia (RR 0.62)
There was no evidence of a significant difference in:
• Overall risk of CS (RR 1.07)
• Risk of CS for abnormal FHR tracing (RR 1.32)
• Dystocia (RR 0.93)
• Long-term backache (RR 1.00)
• Oxytocin administration (RR 1.19, 95% CI 1.00 to 1.26, I2 = 80%)
• Apgar score less than seven at five minutes (RR 0.73)27
Modern epidural techniques use lower concentrations of local anesthetic than previously. In a meta-analysis (n=2000),
low-dose epidurals were as effective as high-dose epidurals at relieving pain, but were less likely to cause motor block,
urinary retention, or to interfere with ambulation.40 A meta-analysis in 2017 evaluated the obstetric outcomes of epidural
analgesia with low concentrations of local anesthetics (e.g. less than 0.1% bupivacaine) compared with no epidural
analgesia. Low concentrations of local anesthetics for epidural analgesia do not prolong labour, and do not increase

the instrumentation rate41. Early detection and treatment with active management of labour protocols and oxytocin
augmentation can reduce the likelihood of CS and operative birth.42, 43
A 2014 meta-analysis of 21 randomized controlled trials (n = 2859 women) compared epidural labour analgesic
solutions of local anesthetics, with or without the addition of opioids, on neonatal outcomes.44 There was no difference
seen in 1 and 5 minute Apgar scores, cord gases or neonatal neurological status at 2 and 24hrs between the two groups.
These results demonstrate that the addition of opioids to the epidural local anesthetic solution is safe for the neonate in
the first 24hrs of life.
As the role of epidural analgesia and maternal fever has become clearer a separate 2012 meta-analysis of RCTs involving
4667 women showed increased neonatal septic workup (RR 2.58) and antibiotic treatment (RR 2.76) in women receiving
epidural analgesia.45 46
Epidural analgesia can be safely used in women choosing vaginal birth after caesarean (VBAC). A large single-centre
retrospective analysis of 7149 women choosing VBAC compared women who received and did not receive epidural
analgesia.47 It was found that maternal and neonatal morbidity did not differ between the two groups. The presence
of epidural analgesia had no impact on the incidence of uterine rupture, PPH, prolonged maternal hospitalization,
neonatal Apgar scores or NICU admission. 48
Timing of epidural analgesia

A 2009 randomized trial of 12,793 nulliparous Chinese women reported that epidural initiation early in the first stage of
spontaneous labour (cervical dilation of at least 1.0 cm) does not seem to prolong labour or increase CS rate compared to
later initiation at a cervical dilation 4.0 cm or greater.49 Similarly a RCT of 750 American nulliparous women comparing
systemic analgesia to early LEA showed no significant difference in CS rate.50 Early LEA compared to systemic analgesia
significantly lowered pain scores and the time between intervention till vaginal delivery.50 A 2014 Cochrane review
of 9 studies (n=15,499 women) comparing early vs late initiation of epidural (< or > 4-5 cm dilatation) showed no
difference in AVB, length of second stage, Apgar score less than 7, or umbilical artery pH.51
Breastfeeding
Neuraxial analgesia with fentanyl doses as high as 2 mcg/ml do not hinder the onset or success at 6 weeks post-partum
of breastfeeding the newborn.52, 53

Care and Management in the Second Stage of Labour

Epidural Analgesia54, 55
Continue epidural analgesia. Discontinuing epidural analgesia in the second stage to allow “effective” pushing,
results in the sudden return of pain that may be worse than if there hadn’t been relief provided at all. The woman may
become so distracted and distressed by the pain that she cannot push effectively. Maintaining epidural analgesia does
not increase the incidence of assisted vaginal birth.56 A secondary analysis of early versus late pushing in a RCT revealed
an increased incidence of Caesarean birth, mid-pelvic procedures, and third- and fourth-degree tears for women who
reported sub-optimal pain control during the second stage of labour.57
• Extend the traditional time limits for second stage as long as progress is being made.
• Avoid early intervention with operative delivery if fetal surveillance is normal.
• Use oxytocin, if needed, for lack of progress.

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based obstetric anesthesia. Malden, MA: Blackwell Publishing; 2005. p. 38-55.
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32. Health Canada H. Prenatal Nutrition Guidelines for Health Professionals. 2010.
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35. Chau A, Bibbo C, Huang CC, Elterman KG, Cappiello EC, Robinson JN, et al. Dural Puncture Epidural Technique
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37. van der Vyver M, Halpern S, Joseph G. Patient-controlled epidural analgesia versus continuous infusion for labour
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38. George RB, Allen TK, Habib AS. Intermittent epidural bolus compared with continuous epidural infusions for labor
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39. Anim-Somuah M, Smyth R, M.D., Jones L. Epidural versus non-epidural or no analgesia in labour [Cochrane
40. Sultan P, Murphy C, Halpern S, Carvalho B. The effect of low concentrations versus high concentrations of
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41. Wang TT, Sun S, Huang SQ. Effects of Epidural Labor Analgesia With Low Concentrations of Local Anesthetics
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42. Torvaldsen S, Roberts CL, Bell JC, Raynes-Greenow CH. Discontinuation of epidural analgesia late in labour for
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Table of Contents
Chapter 6 Induction of Labour......................................................................................................................................... 110

Introduction.............................................................................................................................................................. 110
Definitions .................................................................................................................................................... 110
Morbidity and Mortality............................................................................................................................................ 111
Indications ............................................................................................................................................................... 114
High Priority.................................................................................................................................................. 114
Special Considerations.................................................................................................................................. 115
Contraindications to Induction...................................................................................................................... 117
Pre-Induction Assessment......................................................................................................................................... 118
Predictors of successful induction, ............................................................................................................... 118
Prevention of Induction/Averting Induction............................................................................................................. 119
Prevention Strategies to reduce induction for post-term.............................................................................. 119
Options for Cervical Ripening: Unfavourable Cervix................................................................................................ 121
Mechanical options....................................................................................................................................... 121
Pharmacologic Options................................................................................................................................. 122
Options for IOL with a Favourable Cervix.................................................................................................................. 128
1. Castor Oil................................................................................................................................................... 128
2. Amniotomy................................................................................................................................................ 128
3. Oxytocin .................................................................................................................................................... 128
4. Vaginal PGE2.............................................................................................................................................. 130
Follow-Up.................................................................................................................................................................. 131
Postpartum Considerations........................................................................................................................... 131
Summary.................................................................................................................................................................. 132
Post-Term Pregnancy ................................................................................................................................................ 143
Clinical Management Algorithm................................................................................................................... 143
Induction of Labour 109

Chapter 6
Induction of Labour
Introduction
Definitions1
Induction of Labour (IOL) or induced labour: The initiation of contractions in a pregnant woman who is not in labour to
help her achieve a vaginal birth within 24 to 48 hours.
Successful Induction of Labour: A vaginal delivery within 24 to 48 hours of IOL. (See Management of Labour chapter
for further information on this topic.)
Elective Induction: The IOL in the absence of acceptable fetal or maternal indications.
Cervical Ripening: The use of pharmacologic or other means to soften, efface, or dilate the cervix prior to IOL to increase
the likelihood of a vaginal delivery.
Tachysystole:
• > 5 contractions in 10 minutes, averaged over 30 minutes, and/or
• Inadequate resting tone: uterine resting period between contractions of < 30 seconds OR the uterus does
not return to resting tone between contractions, and/or
• Prolonged contraction: lasting > 90 seconds.
NOTE:
• Tachysystole may occur in presence of a normal, atypical or abnormal fetal heart tracing
• The terms “hyperstimulation” and “hypercontractility” should not be used.
Incidence
The frequency of IOL varies by location and institution, but the overall rate in Canada has remained constant since 1995:
20.7% in 1995–1996; 20.25% in 2004–2005; and 21.2% in 2013–2014 (see Figure 1).1 In British Columbia, the rate of
induction has remained fairly constant at approximately 21% between 2000–2001 and 2014–2015.2 In 2007–2008, the
rate of induction in BC was 27.1% for nulliparous women and 16% for parous women (n = 43,499 total women). 3

Figure 1. Rate of Induction of Labour in Canada, 1995–1996 to 2004–2005
Morbidity and Mortality

When undertaken for appropriate reasons and by appropriate methods, induction benefits both mothers and neonates.1
If done inappropriately, it may expose both mother and neonate to unnecessary risks.
For nulliparous women, IOL is associated with an increased risk of operative delivery and Caesarean section (CS)4, 5 (Figures 2
and 3).6
Figure 2. Caesarean Section Rate in Nulliparous Women by Spontaneous Versus Induced Labour,
Figure 2. Caesarean Section Rate in Nulliparous Women by Spontaneous Versus Induced Labour, British
British Columbia, April 1, 2000 to March 31, 2011
Columbia, April 1, 2000 to March 31, 2011
Figure 3. Caesarean Section Rate in Parous Women by Spontaneous Versus Induced Labour, British Columbia,
April 1, 2000 to March 31, 2011
Figure
Figure 3.
3. Caesarean Section Rate
Caesarean Section Rate in
in Parous
Parous Women
Women by
by Spontaneous
Spontaneous Versus
Versus Induced
Induced Labour,
Labour, British
British Columbia,
Columbia,
Aprilto1,March
April 1, 2000 2000 31,
to March
2011 31, 2011
Source: BC Perinatal Database Registry

Note: Women with late terminations are excluded from the dataset
Source: BC Perinatal Database Registry
Note:
FigureWomen with late terminations
4: Induction are excluded
Rate by LHIN amongfrom theRisk
Low dataset
Women
Source: BORN Ontario Database

The literature examining mode of delivery for induced versus spontaneous labour is controversial. Observational
research suggests a higher risk of operative delivery with IOL. Levine et al. conducted a retrospective cohort study (n =
836) examining term IOL and risk of CS stratified by parity (n = 605); nulliparas undergoing induction had an increased
CS rate compared with those who had spontaneous labour (27% vs. 11%, odds ratio [OR] 3.13, 95% confidence interval
[CI] 1.76 to 5.57) as did multiparas (13% vs. 3%, OR 4.04, 95% CI 1.36 to 11.94).6 However, this was a secondary analysis
that was not powered to evaluate all the indications for induction. Differences in indication may therefore not have been
accounted for. In a 2014 meta-analysis of 31 trials (n = 12,166), Wood et al. showed that in randomly assigned patients,
a policy of indicated IOL was associated with a lower risk of CS compared with expectant management (OR 0.83, 95% CI
0.76 to 0.92).7 However, a 2016 cross-sectional analysis of 42,950 nulliparous women with uncomplicated pregnancies
at term found an increased risk of emergency CS with IOL at 37 to 40 weeks (OR 2.54; 95% CI 2.4, 2.7), with no
difference in perinatal mortality.8 A 2016 cohort study of women > 410 weeks had similar findings.9 A 2017 retrospective
cohort study (n=402,960 singletons) in Austria found IOL was associated with an increased risk for CS (OR 1.53;
95% CI 1.45-1.60) and for operative vaginal delivery (OR 1.21; 95% CI 1.15-1.27). In summary, several randomized
controlled trials have shown no increase in likelihood of CS with IOL; however, epidemiological and cohort data from
many jurisdictions consistently show higher rates of CS in women who undergo IOL, and particularly in nulliparous
women.10 To prevent the risks of IOL, including a possible increase in CS rate, IOL should be performed only with medical
indication, with the exception of logistical considerations.
Risks associated with IOL include:
• Uterine tachysystole with or without fetal heart rate changes
• Failure to achieve labour
• Uterine rupture (scarred or unscarred uterus)
• Chorioamnionitis
• Cord prolapse with artificial rupture of membranes (ARM)
• Inadvertent delivery of preterm infant (with inadequate dating)
• Operative vaginal delivery, especially when epidural analgesia used during labour11
• Caesarean section (CS)
• Postpartum hemorrhage12
• Adverse neonatal outcomes in induction without medical indications at 37 weeks13
• Current evidence does not identify a causal relationship between labour induction generally, or oxytocin
induction specifically, and autism spectrum disorder.14
Every effort should be made to ensure cervical ripening before initiation of induction. If the attempted induction does
not achieve labour, then the need, urgency, and method should be re-evaluated in light of the original indication and
observed fetal response.

Indications
Induction is indicated when the risk of continuing the pregnancy, for the mother or fetus, exceeds the risk associated
with induced labour and delivery. The indication must be convincing, compelling, consented to, and documented. The
most common indication is post-dates.15, 16
Physician or patient convenience are not acceptable indications. However, in rural communities, the need for a woman to
travel to a larger centre for labour and delivery (especially if adverse weather conditions may impede travel) may be an
acceptable indication.
The observed increase in stillbirth in women >40 years of age over 40 weeks justifies offering induction of labour at
390-400 weeks. 17-19,20, 21,22
18
The 2018 ARRIVE trial randomized 3000 low-risk, nulliparous women to induction of labour at 390 to 394 weeks, or
expectant management. No difference was found in the primary outcomes of perinatal death or severe neonatal
complications. The frequency of Cesarean delivery was lower in the induction group (18.6% vs. 22.2%; relative risk,
0.84). Change in practice is not recommended based on this study alone. Research methodology and generalizability of
the study, along with patient preference and resources should be considered.23
For all inductions, the patient, her family, and the primary care provider must have a clear understanding of the potential
risks and benefits involved. Discussion should include reason for induction, method of induction, and risks of induction,
including failure to achieve labour and CS.24
Care providers should determine whether or not labour should be induced according to the urgency of the
clinical situation and the availability of resources. The following are examples of situations in which induction
may be considered:
High Priority
• Severe preeclampsia or eclampsia at any gestational age (GA), or preeclampsia ≥ 37 weeks
• Significant maternal disease
• Significant but stable antepartum hemorrhage
• Term prelabour rupture of membranes with maternal group B streptococcus colonization
• Suspected fetal compromise
Other Indications
• Pregnancies > 410 weeks (see below)
• Uncomplicated twin pregnancy ≥ 38 weeks
• Diabetes mellitus (glucose control may dictate urgency)
• Alloimmune disease at or near term
• Oligohydramnios25

• Gestational hypertension (≥ 38 weeks)

• Intrauterine fetal death
• Prelabour rupture of membranes at or near term, group B streptococcus negative
• Logistical considerations (rapid labour, distance to hospital)
• Intrauterine death in a prior pregnancy (IOL may be performed to alleviate parental anxiety but there is no
known medical or outcome advantage for mother or baby)
• Post-term pregnancy
Special Considerations
Pregnancies ≥ 410 weeks
Prevention of post-term pregnancy is the leading indication for induction and deserves special discussion and
consideration. Post-term is defined as a gestation ≥ 420 weeks (294 days from the first day of the last menstrual period)
and occurs in approximately 6 % of births. Marquette et al. calculated cumulative, day-specific probability for onset
of spontaneous labour (n = 15 253) among pregnancies between 410 and 420 weeks. The likelihood of beginning
spontaneous labour within 24 hours was 14.1%, and the likelihood of beginning labour within 7 days was 67.6%.26
Post-term pregnancies have been shown to have an associated increase in perinatal mortality, morbidity, and operative
delivery.27-29 The most frequent cause of an apparently prolonged gestation is an error in determining accurate dating.
28
Accurate dating based on ultrasonography performed in early pregnancy can reduce the incidence of pregnancies
diagnosed as post-term (relative risk [RR] 0.59; 95% CI 0.42 to 0.83) and subsequently minimize unnecessary
intervention such as IOL.30
Several trials have examined the policy of inducing labour at ≥ 41 weeks’ gestation in an attempt to avert adverse outcomes
associated with post-term pregnancy. The following meta-analysis31 of 19 trials (7,984 women) concluded that a “policy of
labour induction at 41 completed weeks or beyond was associated with fewer (all-cause) perinatal deaths.” (2006)
• The relative risk for perinatal death in the trials where IOL was initiated after 41 weeks was 0.25 with 95% CI
of 0.05 to 1.18 (10 trials, 0/2,835 vs. 6/2,808). For trials where inductions were initiated after 42 weeks, the
RR for perinatal death was 0.41 with CI of 0.06 to 2.73 (2 trials, 1/151 vs. 3/145). When the 41-week and
42-week trials were analyzed together, the RR reached significance at 0.30; CI 0.09 to 0.99.
• In trials where IOL occurred after 41 weeks, there was a reduced risk of meconium aspiration syndrome (RR
0.29; 95% CI 0.12 to 0.68, 4 trials, 1,325 women).
• There was no difference in the risk of Caesarean section (10 trials at 41 weeks, n = 5,755, RR 0.92; 95% CI
0.76 to 1.12; and 5 trials at 42 weeks, n = 810, RR 0.97; 95% CI 0.72 to 1.31).
• There was no difference in the risk of Apgar scores of < 7 at 5 minutes.
A 2018 Cochrane review of 30 trials reporting on 12,479 women found that compared to a policy of expectant
management, a policy of elective IOL for pregnancies at or beyond 41 weeks is associated with:
• fewer (all cause) perinatal deaths (RR 0.33; 95% CI 0.14 to 0.78)
• fewer stillbirths (RR 0.33; 95% CI 0.11 to 0.96)
• fewer CS (RR 0.92; 95% CI 0.85 to 0.99)

• slightly higher operative vaginal births (RR 1.07; 95% CI 0.99 to 1.16)
• lower rates of NICU admission (RR 0.88; 95% CI 0.77 to 1.01)
• fewer infants with Apgar scores < 7 at 5 minutes (RR 0.70; 95% CI 0.50 to 0.98) 3233
There was no difference between the groups for:

• perineal trauma (RR 1.09; 95% CI 0.65 to 1.83)
• postpartum hemorrhage (RR 1.09; 95% CI 0.92 to 1.30)
• neonatal trauma (RR 1.18; 95% CI 0.68 to 2.05)34
Therefore, a policy of induction at ≥ 41 weeks’ gestation is recommended to avert the risks associated with post-term
pregnancy (see Appendix). If, following discussion with the patient, induction is not chosen, then twice-weekly fetal
surveillance is strongly recommended. At a minimum, serial surveillance should consist of daily fetal movement counts
and, for the 41- to 42-week pregnancy, at least twice-weekly non-stress testing and ultrasound assessment of amniotic
fluid volume (AFV).35, 36
Term Prelabour Rupture of Membranes

Intravenous oxytocin is the preferred agent for term prelabour rupture of membranes. However, oral misoprostol is a
promising agent because it has both cervical ripening and uterotonic effect and does not require vaginal examination
with the attendant risk of infection.37, 38 (See Prelabour Rupture of Membranes Chapter.)
Group B Streptococcus + and Rupture of Membranes

Induction should be started as early as possible after rupture of membranes to establish labour within 24 hours.24
(See Prevention of Early-Onset Neonatal Group B Streptococcus Disease Chapter.)
Trial of Labour after Caesarean (TOLAC)

IOL remains an option for women choosing trial of labour after Caesarean (TOLAC). However, the potential increased risk
of uterine rupture associated with any induction, and the potential decreased likelihood of achieving VBAC (especially in
absence of a previous vaginal delivery) should be discussed.39, 40
IOL that requires cervical ripening is associated with a lower rate of success and an increased risk of uterine rupture,
mainly in women who have not experienced a previous vaginal delivery.
IOL in presence of a scarred uterus requires caution:
• Mechanical cervical ripening with a Foley catheter can be safely used
• Prostaglandins have been associated with increased risk of uterine rupture and should not be used.
• Oxytocin using a Low-dose protocol can be used with careful maternal-fetal monitoring and consideration of
the maximum dose to be administered. The timely availability of human and physical resources to respond
to an emergency is required

Suspected Fetal Macrosomia

A 2016 Cochrane review of 4 trials (n = 1190) compared expectant management with IOL for the indication of suspected
fetal macrosomia (birth weight > 4000 g).41
It found:
• Mean birthweight was lower in the induction group (mean difference −178.03 g, 95% CI −315.26 to −40.81)
• No differences in the risk of CS or instrumental delivery
• Increased third and fourth degree tears in the induction group
• Fewer fractures (of any kind) and fewer cases/instances of shoulder dystocia in the induction group
• No differences in risk of brachial plexus injury, measures of neonatal asphyxia, 5-minute Apgar score < 7, or
low arterial cord blood pH
• Increased use of neonatal phototherapy.
The authors conclude that to prevent 1 fracture, it would be necessary to induce labour in 60 women.
The American College of Obstetricians and Gynecologists 2016 Bulletin on fetal macrosomia states induction is NOT
supported because of the inaccuracy of ultrasound estimation of fetal weights and no improvement in maternal or fetal
outcomes. Ultrasound estimation of fetal weight can be used to eliminate macrosomia to reduce intervention. Expert
opinion indicated consideration of CS in the case of estimated fetal weight > 4500 g in women with diabetes mellitus and
> 5000 g in women who did not have diabetes mellitus.42 Women with suspected fetal macrosomia should be informed
about the risks and benefits of vaginal delivery and Caesarean section depending on the severity of macrosomia.35
A meta-analysis of RCTs for induction of labour for suspected macrosomia at term in non-diabetic women vs. expectant
management (4 studies, n=1190) showed no difference in outcomes for those induced vs. those managed expectantly
(CS, operative vaginal delivery, shoulder dystocia, intracranial hemorrhage, brachial plexus palsy, Apgar <7 at 5 min,
cord blood pH<7, and mean birth weight). The induction group had significantly lower time to delivery, lower rate of
birth weight >4000 and >4500 g, and lower incidence of fetal fractures. They conclude that induction of labour > 38
weeks for suspected fetal macrosomia in non-diabetic women can be considered a reasonable option.43
Contraindications to Induction
IOL should not be undertaken if there are any contraindications to labour or vaginal delivery,24 including:
• Placenta or vasa previa or cord presentation
• Abnormal fetal lie or presentation (e.g., transverse lie or footling breech)
• Prior classical or inverted T uterine incision
• Significant prior uterine surgery (e.g., full thickness myomectomy); the operative report information should
be obtained
• Active genital herpes
• Pelvic structural deformities
• Invasive cervical carcinoma
• Previous uterine rupture

Pre-Induction Assessment
Pre-Induction Assessment
Before induction, there are several clinical elements that need to be considered to estimate success and minimize the
risk of CS.
Before induction, there are several clinical elements that need to be considered to estimate success and minimize the
risk of CS.
Predictors of Successful Induction 41
Predictors of successful induction44, 45

y Bishop score > 6
y • prior vaginal
Bishop scoredelivery
>6
• Prior vaginal delivery
The less compelling the indication for induction, the more attention should be paid to adequate cervical ripening.
The less compelling the indication for induction, the more attention should be paid to adequate cervical ripening.
The condition of the cervix at the start of induction is the most important predictor of success. The Bishop score was
The condition
developed of theascervix
in 1964 at the start
a predictor of induction
of success is the most
for an elective important
induction. Thepredictor of success.
most important The Bishop
element score was
of the Bishop score
developed
is dilatationinfollowed
1964 asby a predictor
effacement,of success
station,for
andanposition,
elective with
induction. Theuseful
the least most important element
element being of the
cervical Bishop score
consistency. 42, 43
is dilatation
Xenakis et al.followed by effacement,that
clearly demonstrated station,
women andwho
position,
had awith
Bishopthescore
least at
useful
entryelement being
of ≤ 3 had cervical consistency.
significantly higher rates46,47
of
Xenakis et al. clearly
failed induction (9.4%demonstrated
vs. 0.7%, P <that women
0.01) and ofwho had a Bishop
Caesarean sectionscore
(29%atvs.15.4%,
entry of ≤P3<had significantly
0.01) than thosehigher
with arates
Bishop of
failed
score >induction
3.44 Nova (9.4% vs. 0.7%,
Scotia’s P < 0.01)also
Atlee database andshows
of Caesarean
that thesection
risk of (29% vs.15.4%,
CS in low P < 0.01) than
risk, nulliparous women those with a Bishop
is highest in those
score > 3.48
Nova Scotia’s Atlee database also shows that the risk of
undergoing labour induction when compared with those entering spontaneous labour.CS in low risk, nulliparous
45 women is highest in those
undergoing labour induction when compared with those entering spontaneous labour. 49
4. Likelihood of successful vaginal delivery

Figure 5.
MOST MOST
fabourable multiparous previous vaginal

cervix delivery
unfabourable nulliparous previous C/S

cervix
LEAST LEAST
Reproduced with permission from Salus.

25thth Edition of the ALARM Course Manual
The cervix is considered unfavourable if the Bishop score is ≤ 6 and favourable if it has a Bishop score of > 6.46 Many
The cervix is considered unfavourable if the Bishop score is ≤ 6 and favourable if it has a Bishop score of > 6.50 Many
studies have
studies have used
used other
other Bishop
Bishop score
score values
values to
to separate
separate the
the data.
data.51
47
Table 1. Modified Bishop Scoring System
Score
Factor 0 1 2 3
Dialation 0 1–2 cm 3–4 cm > 5 cm
Effacement (%) 0–30 40–50 60–70 >80
Length (cm) >3 1–3 <1
Consistency Firm Medium Soft
Position Posterior Mid Anterior
Station Sp –3 or above Sp –2 Sp –1 or 0 Sp +1 or lower
Prevention of Induction/Averting Induction

Prevention
Quality of Induction/Averting
improvement programs have been shown to reduce the numberInduction
of elective inductions and unplanned CS.
Several studies have shown a significant reduction in the number of elective inductions after the implementation of an
Quality improvement
induction committee.programs
The role ofhave
the been shownwas
committee to reduce the each
to review number of elective
request inductions
and enforce andofunplanned
the use CS. Severalfor
proper indications
studies have shown a significant reduction in the number of elective inductions after the implementation of an induction
induction. 52-55
535
4
committee. The role of the committee was to review each request and enforce the use of proper indications for induction.48-51
Institutional factors may play a role in the CS rate of induced labours. Brennan et al. compared CS rates in 10 different
Institutional
groups defined factors may
by the play a criteria.
Robson role in the CS rate
In the group of of
induced
low-risklabours.
womenBrennan
inducedetatal. compared
term, the lowCS rates in 10
induction different
centres had a
groups defined
lower overall CSby thethan
rate Robson criteria.induction
the higher In the group
centresof low-risk
(17.7% women induced
vs. 27.8%, at term, the low induction centres had a
P < 0.008). 56, 57
lower overall CS rate than the higher induction centres (17.7% vs. 27.8%, P < 0.008).52, 53
Prevention Strategies to reduce induction for post-term58

Prevention Strategies to Reduce Induction for Post-Term54
Ultrasound
Ultrasound
Every effort should be used to determine dates accurately. Early (8-12 weeks) ultrasound (US) examination provides
Every
the effort
most shouldestimated
accurate be used todate
determine dates
of delivery accurately.
and has beenEarly ultrasoundto(US)
demonstrated examination
decrease (8 to 12ofweeks)
the diagnosis provides
post-term
the most
pregnancy.accurate
59, 60 estimated date of delivery and has been demonstrated to decrease the diagnosis of post-term
pregnancy.55, 56

The 2014 SOGC clinical practice guideline on determination of gestational age by ultrasound states:
“When performed with quality and precision, ultrasound alone is more accurate than a “certain” menstrual date for
determining gestational age in the first and second trimesters (≤ 23 weeks) in spontaneous conceptions, and it is the
best method for estimating the delivery date”.58
If there is more than 1 first-trimester scan with a mean sac diameter or crown-rump length measurement, the earliest
ultrasound with a crown-rump length equivalent to at least 7 weeks (or 10 mm) should be used to determine the
gestational age.58
A 2010 Cochrane review30 by Whitworth et al. reported reduced rates of IOL for post-term pregnancy (RR 0.59; 95% CI
0.42 to 0.83) with routine early pregnancy ultrasound imaging.
Figure 6. Routine/Revealed vs Selective/Concealed Ultrasound in Early Pregnancy. Outcome-Induction for “post-
term” Pregnancy
Sweeping (Stripping) of Membranes at Term

There is evidence that sweeping of membranes (3 circumferential passes within the cervix or cervical massage for 15 to
30 seconds when unable to pass the external cervical os) promotes the onset of labour by increasing local production
of prostaglandins.61, 62 Meta-analyses have found that when sweeping is performed in term women at 38 weeks and
beyond, it is associated with a reduced duration of pregnancy and reduced rate of pregnancy continuing beyond 41
weeks.63-65 A 2014 RCT (n = 134) found pregnancy duration decreased by 3 days (P = 0.001).66 Sweeping of membranes
64

must be performed in 8 women to prevent 1 formal IOL. Discomfort during vaginal examination and other adverse
effects (e.g., bleeding, irregular contractions) were more frequent in women who had the procedure performed. The
reviewers concluded that when membrane sweeping is used, the subsequent reduction in the need for more formal
induction methods needs to be balanced against women’s discomfort and other adverse effects.
Options for Cervical Ripening: Unfavourable Cervix

It is important that cervical ripening be considered before IOL in women with an unfavourable cervix. Many methods for
cervical ripening are effective. Amniotomy and oxytocin are not effective cervical ripening methods.
Mechanical options
The use of balloon catheters and laminaria or synthetic laminaria tents may affect cervical softening, effacement, and
dilatation with fewer or no systemic effects. The probable mechanism of action is local prostaglandin (PG) production.1
Balloon methods have the advantage of cost effectiveness and a lower risk of uterine tachysystole.67, 68
A 2011 systematic review by Fox et al. comparing Foley catheter versus intravaginal misoprostol (9 studies, n = 1603)
found no difference in time to delivery, rate of Caesarean section, or rate of chorioamnionitis. However, the vaginal
misoprostol group had a higher rate of tachysystole.69
Mechanical methods are not likely to be effective in inducing labour on their own. In a 2011 World Health Organization
evidence summary of the comparison of balloon catheter plus oxytocin versus misoprostol alone, the combination
approach was associated with more vaginal deliveries achieved within 24 hours (1 trial, 158 participants).70
However, a 2008 systematic review found there may be an increased risk of both maternal and newborn infection
associated with specific mechanical methods of cervical ripening.71 This review found that for women who underwent
cervical ripening with a Foley catheter alone versus a pharmacological agent, there was an increase in maternal infection
(defined as pyrexia of 38°C, chorioamnionitis, peripartum infection, or chorioamnionitis and/or endomyometritis)
(OR 1.50; 95% CI 1.07 to 2.09) and chorioamnionitis (OR 2.05; 95% CI 1.22 to 3.44). However, with the use of a Foley
catheter, there was no increase in neonatal infection (OR 1.2; 95% CI 0.48 to 2.97). Double balloon catheters have not
been shown to be more beneficial.72-75 737
4
Evidence suggests that for women > 34 weeks with rupture of membranes, use of transcervical Foley catheter in
addition to oxytocin does not shorten the time to delivery compared to oxytocin alone, and may increase the incidence of
intraamniotic infection.76
More recent RCTs and meta-analyses have demonstrated similar safety and effectiveness for Foley catheter as for vaginal
/oral misoprostol66 and vaginal prostaglandin E2 inserts.77-79 Using a Foley catheter is the better option when there are
87
concerns about fetal well-being or placental function, because there is less risk of tachysystole. Use of a Foley catheter is
also cheaper than use of prostaglandin E266, 77 and when used in an outpatient setting, cheaper than ORAL PGE1.80
Reviews of Foley balloon catheter for cervical ripening concluded that its use is relatively safe, even as an option for
outpatient cervical ripening.81-85
82438

• Balloon devices: Foley catheter (for protocol details see the SOGC guideline24 at technique for Foley):
−− no. 14 to 18 Foley with a 30 mL balloon
−− pre-test Foley balloon before insertion
−− sterile technique, insert past internal os
−− inflate with 30 to 60 mL water86, 87
−− Tension is not necessary88 Catheter should be removed within 24 hours if it has not been spontaneously
expelled
−− Insertion may be facilitated by a stylet
−− contraindications: low-lying placenta
−− relative contraindications: rupture of membranes89; genital tract infection
Pharmacologic Options
Prostaglandins
Agents include:
• vaginal PGE2 gel (Prostin)
• posterior fornix slow release PGE2 (Cervidil)
• intra-cervical PGE2 gel (Prepidil)
• oral PGE1 (Oral misoprostol)
Considerations for Prostaglandin Use

When considering prostaglandin use, patient acceptance and preference of the various options are important. Cost
considerations also may play a role in the choice of prostaglandin. Proprietary intravaginal PGE2 formulations cost
between $40 and $80 per dose. Misoprostol is produced generically and costs approximately $0.05 per tablet. In
women with term or late-preterm ruptured membranes, oral misoprostol provides cervical ripening without the need for
vaginal examinations or laminaria (cf. Cervidil). Prostaglandin gels are uterine stimulants whose effects may not easily be
reversed.
Certain precautions must be taken with prostaglandins:
• Electronic fetal surveillance for a minimum of 30 minutes before PGE2 application and for 1 hour post
application. If tracing atypical or abnormal, do not administer prostaglandin.
• Vaginal gel PGE2 (Prostin) should NOT be placed in the cervical canal.
• Prostaglandins should NOT be used as augmentation agents.
• Uterine activity should be carefully assessed before repeating the dose
• Prostaglandins should NOT be used in patients with previous CS because of the increased risk of uterine
rupture.90, 91
• Oral PGE1 (oral misoprostol) 38 or vaginal PGE2 (Prostin)1 may be considered with ruptured membranes at term.

Further research is needed on the use of slow-release PGE2 (Cervidil) in women with ruptured membranes. The
manufacturer suggests that it should be used with caution in these women and that uterine activity and fetal status
should be carefully monitored.92
Adverse reactions may occur:
• Tachysystole with or without fetal heart rate changes (incidence is similar to use of oxytocin)
• Gastrointestinal side effects
• Vaginal irritation
Prostaglandin E2
Also known as dinoprostone, PGE2 is available as an intravaginal or an intracervical gel. Intravaginal gels or preparations
are easier to employ, cause less patient discomfort, and are preferred because they result in more timely vaginal delivery
than mechanical methods.93
CAUTION
It is important to ensure that vaginal agents (Prostin, Cervidil) are not inserted into the cervical canal because
they have a much higher dosage than intracervical preparations (Prepidil).
PGE2 is a bronchodilator and is not contraindicated in women who have asthma.1,94 Adverse cardiovascular events are
rare, idiopathic, and usually occur almost immediately after the gel or preparation has been inserted.
Route and Dose

Vaginal
• PGE2 (Prostin) 1 to 2 mg into posterior fornix
• PGE2 (Cervidil) 10 mg into posterior fornix. Cervidil released at 0.3 mg/hr. Should be removed when the
woman is in active labour or at 12-24 hours post insertion. If a favourable cervix is not achieved a second
dose may be used if there are no contraindications.
Intracervical
• PGE2 (Prepidil) 0.5 mg intracervical
• Intracervical preparations should not be used in women with PROM.
• Any formulation may be used for cervical ripening
• Initial application may be followed by repeat PGE2 or oxytocin, as per the manufacturer’s recommendation
Protocols have been developed to increase the chance of a successful outcome and enhance safety:
• Patients should be seen by experienced staff in a controlled setting where resuscitation and delivery can be
performed
• PGE2 applied by a knowledgeable caregiver

Prostaglandin Advantages
• Patient acceptance
• Lower operative delivery rate than oxytocin
• Less need for oxytocin induction
Prostaglandin Disadvantages
• Increased risk of uterine rupture with previous CS
• Side effects may include: nausea, vomiting and/or diarrhea
• Gel preparations are difficult to remove in instances of tachysystole
Outpatient Management
Outpatient management may be considered with use of vaginal PGE2 gel (Prostin), slow release PGE2 (Cervidil) or
intra-cervical PGE2 gel (Prepidil) when IOL is done for maternal indication, and after post-administration electronic fetal
assessment is complete.95 Outpatient management should not be considered when oral PGE1 (oral misoprostol) is used. 9697
Although some centres use prostaglandins on an outpatient basis, there is limited evidence demonstrating safety,98, 99
so fetal well-being and the absence of significant uterine activity must be assured before discharge. Women should be
carefully instructed to return promptly for assessment if uterine activity increases. Outpatient management is NOT
appropriate when IOL is undertaken because of suspected fetal compromise (e.g., intrauterine growth restriction, poor
biophysical profile).
Prostaglandin E1
Misoprostol is a synthetic prostaglandin E1 analogue manufactured for the prevention and treatment of gastric ulcers
associated with the use of non-steroidal anti-inflammatory drugs.
It is not licensed for use in obstetrics and gynaecology, although it is used off-label worldwide for three main
applications: postpartum hemorrhage (PPH), incomplete miscarriage, and IOL. The American College of Obstetricians
and Gynecologists and FDA have endorsed its off-label use for IOL.100
Like other prostaglandins, misoprostol causes both cervical ripening and uterine contractions in a dose-dependent
fashion. It is available only in oral form (100 mcg and 200 mcg tablets), but is readily absorbed trans-mucosally
(sublingually, buccally, vaginally, or rectally). Following oral or sublingual administration, levels peak at 30 minutes;
however, because of first-pass liver metabolism, the peak maternal serum concentration and the duration and area
under the curve are twice as great for sublingual as for oral dosing. Fifty micrograms orally is approximately equivalent
to 25 mcg sublingual. When it is given vaginally, peak levels are delayed and the area under the curve is lower than with
sublingual administration.101, 102
Route and Dose

Over 200 randomized trials have been published comparing various doses and routes of misoprostol with oxytocin and
other vaginal prostaglandins. The higher the dose, the greater the success with IOL and the greater the risk of uterine

tachysystole. The safety and effectiveness of low-dose misoprostol for IOL is well established. Two Cochrane reviews,
published in 2010 and 2014 and including more than 100 trials and 17 000 women, compared both vaginal and oral
misoprostol with PGE2, oxytocin, and each other. They concluded:
• “Oral misoprostol as an induction agent is effective at achieving vaginal birth. It is more effective
than placebo, as effective as vaginal misoprostol and results in fewer caesarean sections than vaginal
dinoprostone or oxytocin.”103
• “The vaginal route should not be researched further as another Cochrane review has shown that the oral
route of administration is preferable to the vaginal route.”104
The accepted, effective, safe oral dose is 50 mcg every 4 hours as needed. There is not evidence for a safe
maximum number of doses; however, if there is no effect after 4 doses, reassessment and consideration of an
alternate method of cervical ripening are recommended.
The corresponding sublingual dose is 25 mcg; however, this dose is difficult to prepare accurately from commercially
available tablets and may be associated with greater risk of uterine tachysystole with FHR changes than the 50 mcg oral
dose.
Protocols using more frequent, smaller doses of a misoprostol solution prepared from dissolving a 200 mcg tablet in
water have also been studied. Outcomes were similar to those achieved by administration of 50 mcg every 4 hours.103
Preparation and administration of the oral solution are more time consuming, however, and there are concerns
regarding poor tablet solubility.
CAUTION
When inducing labour at term, institutions must take precautions to avoid accidental use of the
200 mcg tablets, commonly used for PPH and for treatment of first and second trimester miscarriage.
Dose Preparation
The risk of accidental overdose can be minimized by having a hospital pharmacy pre-cut 100 mcg tablets into 50 mcg
doses which can be individually foil-packaged. The 50 mcg doses are then kept in a separate location from the larger 200
mcg tablets commonly kept in labour rooms for the treatment of postpartum hemorrhage and miscarriage management.
When misoprostol is given orally, it is important that the tablet or solution be swallowed and not held in the mouth
sublingually or buccally, which would cause higher blood levels and greater risk of uterine tachysystole. Repeat doses
may be given every 4 hours until regular or painful uterine contractions.

Side Effects of Prostaglandins

Potential maternal side effects include nausea, vomiting, diarrhea, abdominal pain, shivering, and chills and fever;
however, these side effects are dose-dependent and are rare with a dose of 50 mcg. Misoprostol does not cause
bronchospasm and is safe for use by patients who have asthma. The most important significant side effect of any
prostaglandin given for induction is uterine tachysystole with or without fetal heart rate changes
The risk of uterine “hyperstimulation” with fetal heart rate changes with a 50 mcg oral dose of misoprostol is the same
as with vaginal PGE2, at approximately 1% to 2%.105 Prostaglandin-related prolonged contractions can rarely cause
placental abruption or uterine rupture. Prostaglandin use is therefore not generally recommended in women with a
history of prior Caesarean section or significant uterine scar; and prostaglandins should be used carefully in grand-
multiparous women. Oxytocin should not be used within 4 hours of the last oral misoprostol dose.92
Eligibility
• Clear indication for IOL
• Greater than 35 weeks’ gestation
Use with Caution

• Grand multipara (>6 prior vaginal deliveries)
• Fetal growth restriction or oligohydramnios
Exclusion criteria
• < 35 weeks’ gestation
• Previous Caesarean section or other significant uterine surgery
• Abnormal fetal heart tracing
• Regular or painful uterine contractions
Initial Patient Evaluation

• Routine initial assessment including vital signs
• History, physical, and admission by physician
• A normal NST should be documented
Monitoring
Continuous electronic fetal monitoring is recommended for 30 minutes after misoprostol administration. It is
recommended for 1 hour whenever there is increased uterine activity within 4 hours of a misoprostol dose. Patients
should remain in hospital but may ambulate after normal fetal assessment with stable uterine activity. If the woman is
not in active labour and contractions are mild 4 hours after the last misoprostol dose, she may return home for sleep as
needed, and return in the morning to continue induction.

Vigilance in identifying uterine tachysystole is critical for the safe use of PGE2 and PGE1.
Management of tachysystole depends on whether FHR changes are present. A treatment protocol for excess
uterine activity is recommended for every labour unit along with a Tachysystole tray.
Tachysystole Tray suggested contents:

• 1 normal saline 1000 ml
• 1 small sterile bowl
• 8 sterile 4 x 4
• 1 nitroglycerine sublingual spray
• 2 sponge forceps
• 2 60 cc syringe Toomey cath tip
• 2 normal saline 100 ml
• # 18 Foley catheter
• Gloves size 6-8, one of each
• Water based lubricant
• IV Nitroglycerine Kit (Nitroglycerine 50 mg/ 10 ml; syringes, needles, alcohol swabs, medication labels)
If there is tachysystole with normal fetal heart tracing:
• Remove prostaglandin if possible (Cervidil or recently applied vaginal gel)
• Decrease the rate of oxytocin infusion rate (if applicable)
• Maintain close continuous EFM
If there is tachysystole with atypical or abnormal fetal heart tracing:
• Undertake immediate assessment (attending physician or midwife)
• Stop oxytocin, if running
• Remove prostaglandin if possible (Cervidil or recently applied vaginal gel)
• Conduct pelvic examination to assess cervical dilatation and rule out prolapsed cord
• Initiate intrauterine resuscitation
• Apply scalp electrode if any question about external FHR pick-up or interpretable tracing
• Consider acute tocolysis with nitroglycerin (50 mcg IV doses every 90 seconds to 3 minutes, to maximum
of 200 mcg over 15 minutes).24, 106-108 To date, the evidence for safety and efficacy remains inconclusive.
701
Necessary monitoring includes maternal BP, maternal SaO2 and continuous EFM. Sublingual nitro does not
work and will give the woman a headache.
• Make immediate preparation for delivery if these measures do not rapidly lead to resolution of the fetal
heart rate abnormality
If tachysystole resolves and the cervix remains unfavourable, indications and fetal well-being should be re-evaluated
before further intervention. Foley catheter cervical ripening may be preferred as it does not carry a risk of tachysystole.

Options for IOL with a Favourable Cervix

1. Castor Oil
Several studies have reported effectiveness of oral ingestion of castor oil for inducing labour within 24 hours of
ingestion, with no maternal or fetal complications, in multiparous women, and reduces need for other medications.109-111 10
It may be tried safely post-dates on an outpatient basis.
2. Amniotomy
Amniotomy creates commitment to delivery, and is effective with a favourable cervix. Trials indicate it should be used in
conjunction with oxytocin in most instances. A 2009 RCT demonstrated that women who receive oxytocin immediately
following amniotomy (compared with those who receive it 4 hours later) are more likely to be in labour within 4 hours,
to have a shorter amniotomy to delivery time and achieve delivery within 12 hours, and to experience greater maternal
satisfaction.112 A 2011 systematic review comparing amniotomy and IV oxytocin to vaginal prostaglandins found that
with IV oxytocin and amniotomy, there were higher rates of PPH and maternal dissatisfaction.113
Care must be taken in cases of high presenting part due to increased risk of cord prolapse. After amniotomy, note the
amount, colour, and consistency of the fluid and assess fetal well-being.
3. Oxytocin
First synthesized in 1955, oxytocin is a hormone produced in the hypothalamus, stored in the posterior pituitary, and
secreted in a pulsatile manner. IV infusion of oxytocin has been the most common method of induction and remains
valuable for properly selected women.
Induction of labour with oxytocin is considered a high-risk area of practice by both the Canadian Medical Protective
Association (CMPA) and the Healthcare Insurance Reciprocal of Canada (HIROC). The two most common issues in
obstetrical incidents involving oxytocin induction (or augmentation) (2004-2013) included failure to reduce or
discontinue oxytocin infusion and delay in notifying or consulting with the physician for unresolved uterine tachysystole,
signs of uterine rupture, or abnormal fetal heart rate patterns.114
All units offering oxytocin induction of labour must have oxytocin induction policies, protocols and safe staffing levels
available when induction of labour with oxytocin is undertaken.
Oxytocin can be used:
• 30 minutes after dinoprostone insert (Cervidil) removal
• 4 hours after oral misoprostol administration
• 6 hours after vaginal prostaglandin E2 gel administration
• Early after amniotomy24
• There is no contraindication to giving oxytocin over several days in the event onset of labour is not achieved
and membranes intact.

Physiology
Oxytocin receptors are found in the myoepithelial cells of the breast, the myometrium, and the deciduas.
• Myometrial smooth muscle
−− rhythmic contraction at low dose
−− increased sensitivity as term approaches (insensitive at < 20 weeks)
−− infusions of 6 milliunits per minute (mU/min) give the same oxytocin levels that are found in
spontaneous labour and most women will have a clinical response at 8 to 10 mU/min at term
• Cervix
−− no direct effect
• Vasoactive
−− very minimal vasopressor response
−− hypotension possible with bolus IV administration
• Antidiuretic activity - water intoxication possible with high-dose oxytocin (> 40 mU/min)
Protocol
• Cervix should ideally be favourable (Bishop Score > 6)
• Experienced care providers and adequate resources should be available to manage dystocia and other
emergencies
• When uterine activity cannot be adequately evaluated by external monitoring and palpation, consider use of
IUPC to monitor uterine activity
• Administration:
−− Given by infusion pump into a mainline IV and titrate to uterine response
−− Describe dosage as milliunits per minute (mU/min)
−− Concentrations vary but avoid large free water load (dextrose 5% in water [D5W] should not be given)
−− Institutional protocols should be used
The goal of oxytocin is to achieve effective uterine contractions and cervical changes with the minimally effective dose.
Once this state is achieved, the oxytocin dose can be maintained.
Oxytocin may be administered using either low- or high-dose protocols.100 (See MOL chapter).
There are no randomized clinical trials comparing different timing of the use of oxytocin after prostaglandin gel. Many
studies have used a 6-hour interval.24

Tachysystole with Oxytocin Administration

Discontinue oxytocin and institute tachysystole protocol.
Restarting oxytocin:
• Remember that the half-life of oxytocin is approximately 6 to 8 minutes. If oxytocin is restarted, consider
beginning at a lower dose.
Discontinuation of oxytocin when active phase of induced labour is established
A 2018 Cochrane Review (10 trials, 1,888 women) compared oxytocin discontinuation after the active phase of induced
labour was established vs. oxytocin continuation.115 The analysis by ‘intention-to-treat’ found that, compared with
oxytocin continuation, discontinuation of oxytocin in the active phase of labour:
• reduced caesarean delivery rate (RR 0.69; 95% CI 0.56 to 0.86) (9 trials, 1784 women, low level certainty*)
• reduced tachysystole combined with abnormal fetal heart rate (RR 0.15; 95% CI 0.05 to 0.46)
• reduced suspicious/pathological fetal heart findings (RR 0.65; 95% CI 0.51 to 0.83).
The authors conclude that discontinuation of oxytocin in active labour had little or no impact on use of epidural
analgesia, Apgar < 7 at 5 minutes and umbical artery pH <7.10.
*Most trials included in the review had “risk of bias” concerns so results should be interpreted with caution.
NOTE: Oxytocin appropriately titrated to the maternal uterine and fetal heart rate response is considered safest clinical
practice.
4. Vaginal PGE2
Comparison of Pharmacologic Methods
A 2009 Cochrane review compared efficacy of oxytocin with vaginal PGE2 and intracervical PGE2 for third trimester
cervical ripening and IOL.116 The odds ratios for a persistently unfavourable cervix after 12 to 24 hours and failure of
vaginal delivery in 24 hours favour the use of vaginal prostaglandins.

Figure 7. Oxytocin Alone vs Vaginal PGE2

Figure 7. Oxytocin Alone vs Vaginal PGE2
OUTCOME OR
Cx unfavourable 2.42 (1.43, 4.09)
No vaginal delivery 24 hrs 1.77 (1.31, 2.38)
Hyperstimulation (NR FHR) 0.35 (0.04, 3.28)
Chorioamnionitis 0.66 (0.47, 0.92)
Caesarean section 1.11 (0.94, 1.30)
5 min. Apgar < 7 0.62 (0.36, 1.05)
Neonatal infection 0.68 (0.42, 1.09)
Serious neonatal morbidity 3.00 (031, 28.82)
0.01 0.1 1 10
Alfirevic Z. Cochrane Database
of Systematic Reviews Odds Ratio
2009 Issue 4 (95% confidence interval)
Follow-Up
Postpartum Considerations
If oxytocin has been used during the labour, anticipate postpartum hemorrhage and take appropriate preventive action.
(For third stage of labour management and prevention of PPH, see the PPH chapter).

Summary
• The reasons for induction must be compelling, convincing, consented, and documented
• The method should match the situation: the degree of urgency of the indication and the status of the cervix
should be considered.
• Ideally, the cervix should be favourable (Bishop score > 6) before amniotomy and before initiation of
oxytocin.
• Oxytocin should always be used with caution and only where policies, protocols and safe staffing levels
are in place at the time of the induction. Oxytocin must be titrated to maternal uterine and fetal heart rate
response.
• Patient preference must be considered.
• Comparison summary113, 117
−− membrane sweeping reduces post-term gestations.
−− mechanical methods (e.g., intracervical balloon) are more likely than PGE2 or misoprostol to reduce the
occurrence of tachysystole.
−− PGE2 and vaginal misoprostol are more effective than oxytocin in bringing about vaginal delivery within
24 hours but are associated with more tachysystole.118
−− oxytocin plus amniotomy is more effective than amniotomy alone in achieving vaginal delivery within
24 hours.119
−− vaginal misoprostol PGE1 is more likely than PGE2 or oxytocin to result in vaginal delivery within 24
hours but is associated with increased tachysystole.
−− vaginal misoprostol may reduce the likelihood of CS compared with intravenous oxytocin in the case of
an unfavourable cervix.
−− oral misoprostol is associated with a greater reduction in the rate/incidence of CS than vaginal PGE2 or
placebo.
−− oral misoprostol is associated with a lower rate of tachysystole but there is more need for oxytocin
augmentation than with vaginal misoprostol.
−− sample sizes in RCTs of induction are too small to exclude differences in rare adverse outcomes such as
uterine rupture, amniotic fluid embolism, or perinatal asphyxia.

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or Misoprostol: A Systematic Review and Meta-analysis. Obstet Gynecol Surv. 2016;71:620-30. Available from:
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80. Ten Eikelder M, van Baaren GJ, Oude Rengerink K, Jozwiak M, de Leeuw JW, Kleiverda G, et al. Comparing
induction of labour with oral misoprostol or Foley catheter at term: cost-effectiveness analysis of a randomised
controlled multi-centre non-inferiority trial. BJOG. 2018;125:375-83. Available from: https://www.ncbi.nlm.nih.
81. Greenberg V KA. Intracervical Foley balloon catheter for cervical ripening and labor induction: A review. Semin
Perinatol. 2015.
82. Ten Eikelder ML, Oude Rengerink K, Jozwiak M, de Leeuw JW, de Graaf IM, van Pampus MG, et al. Induction
of labour at term with oral misoprostol versus a Foley catheter (PROBAAT-II): a multicentre randomised
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83. Kruit H, Heikinheimo O, Ulander VM, Aitokallio-Tallberg A, Nupponen I, Paavonen J, et al. Foley catheter induction
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pubmed/27078202.
84. Policiano C, Pimenta M, Martins D, Clode N. Efficacy and Safety of Foley Catheter Balloon for Cervix Priming in Term
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85. Diederen M, Gommers J, Wilkinson C, Turnbull D, Mol B. Safety of the balloon catheter for cervical ripening in
outpatient care: complications during the period from insertion to expulsion of a balloon catheter in the process of
labour induction: a systematic review. BJOG. 2018;125:1086-95. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/29211328.
86. Sandberg EM, Schepers EM, Sitter RLV, Huisman CMA, Wijngaarden WJV. Foley catheter for induction of labour
filled with 30mL or 60mL: A randomized controlled trial. Eur J Obstet Gynecol Reprod Biol. 2017;211:150-5.
87. Schoen CN, Saccone G, Backley S, Sandberg EM, Gu N, Delaney S, et al. Increased single-balloon Foley catheter
volume for induction of labor and time to delivery: a systematic review and meta-analysis. Acta Obstet Gynecol
Scand. 2018;97:1051-60. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29607491.
88. Fruhman G, Gavard JA, Amon E, Flick KV, Miller C, Gross GA. Tension compared to no tension on a Foley
transcervical catheter for cervical ripening: a randomized controlled trial. Am J Obstet Gynecol. 2017;216:67 e1-
e9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27640940.
89. Mackeen AD, Walker L, Ruhstaller K, Schuster M, Sciscione A. Foley catheter vs prostaglandin as ripening agent
in pregnant women with premature rupture of membranes. J Am Osteopath Assoc. 2014;114:686-92. Available

90. Martel MJ, MacKinnon CJ, Clinical Practice Obstetrics Committee SoO, Gynaecologists of C. Guidelines for vaginal
birth after previous Caesarean birth. J Obstet Gynaecol Can. 2005;27:164-88. Available from: https://www.ncbi.
91. Lydon-Rochelle M, Holt VL, Easterling TR, Martin DP. Risk of uterine rupture during labor among women
with a prior cesarean delivery. N Engl J Med. 2001;345:3-8. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/11439945.
92. Cervidil®: brand of dinoprostone vaginal insert [product monograph]. Rev. St. Louis (MO): Forest Pharmaceuticals,
Inc.; 2006. Available from: https://www.ferring.ca/media/1026/cervidil-approved-pm-english-september-2006.pdf
93. Boulvain M, Kelly A, Irion O. Intracervical prostaglandins for induction of labour. Cochrane Database Syst Rev.
94. Towers CV, Briggs GG, Rojas JA. The use of prostaglandin E2 in pregnant patients with asthma. Am J Obstet
Gynecol. 2004;190:1777-80; discussion 80. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15284797.
95. Barnfield L, Neale E, Reynolds S. Outpatient cervical ripening in a district general hospital: a five-year
retrospective cohort study. J Obstet Gynaecol. 2018;38:301-4. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/28920504.
96. Cundiff GW, Simpson ML, Koenig N, Lee T. Observational Study of Neonatal Safety for Outpatient Labour Induction
Priming with Dinoprostone Vaginal Insert. J Obstet Gynaecol Can. 2017;39:354-60. Available from: https://www.
97. Biem SR, Turnell RW, Olatunbosun O, Tauh M, Biem HJ. A randomized controlled trial of outpatient versus inpatient
labour induction with vaginal controlled-release prostaglandin-E2: effectiveness and satisfaction. J Obstet
98. Wilkinson C, Bryce R, Adelson P, Turnbull D. A randomised controlled trial of outpatient compared with
inpatient cervical ripening with prostaglandin E(2) (OPRA study). BJOG. 2015;122:94-104. Available from:
99. Papoutsis D, Antonakou A, Gornall A, Tzavara C, Mohajer M. The SaTH risk-assessment tool for the prediction of
emergency cesarean section in women having induction of labor for all indications: a large-cohort based study.
Arch Gynecol Obstet. 2017;295:59-66. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27671013.
100. Obstetrics ACoPB--. ACOG Practice Bulletin No. 107: Induction of labor. Obstet Gynecol. 2009;114:386-97.
101. Tang OS, Schweer H, Seyberth HW, Lee SW, Ho PC. Pharmacokinetics of different routes of administration of
misoprostol. Hum Reprod. 2002;17:332-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11821273.
102. Schaff EA, DiCenzo R, Fielding SL. Comparison of misoprostol plasma concentrations following buccal and
sublingual administration. Contraception. 2005;71:22-5. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/15639067.

103. Alfirevic Z, Aflaifel N, Weeks A. Oral misoprostol for induction of labour. Cochrane Database Syst Rev.
104. Hofmeyr GJ, Gulmezoglu AM, Pileggi C. Vaginal misoprostol for cervical ripening and induction of labour.
105. Kundodyiwa TW, Alfirevic Z, Weeks AD. Low-dose oral misoprostol for induction of labor: a systematic review. Obstet
106. Smith GN, Brien JF. Use of nitroglycerin for uterine relaxation. Obstet Gynecol Surv. 1998;53:559-65. Available
107. Mercier FJ, Dounas M, Bouaziz H, Lhuissier C, Benhamou D. Intravenous nitroglycerin to relieve intrapartum fetal
distress related to uterine hyperactivity: a prospective observational study. Anesth Analg. 1997;84:1117-20.
108. Vancouver Island Health Authority V. NRGH - Intervention in the presence of uterine tachysystole (Procedure).
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109. Neri I, Dante G, Pignatti L, Salvioli C, Facchinetti F. Castor oil for induction of labour: a retrospective study. J Matern
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110. DeMaria AL, Sundstrom B, Moxley GE, Banks K, Bishop A, Rathbun L. Castor oil as a natural alternative to labor
induction: A retrospective descriptive study. Women Birth. 2017.
111. Gilad R, Hochner H, Savitsky B, Porat S, Hochner-Celnikier D. Castor oil for induction of labor in post-date
pregnancies: A randomized controlled trial. Women Birth. 2018;31:e26-e31.
112. Selo-Ojeme DO, Pisal P, Lawal O, Rogers C, Shah A, Sinha S. A randomised controlled trial of amniotomy and
immediate oxytocin infusion versus amniotomy and delayed oxytocin infusion for induction of labour at term. Arch
Gynecol Obstet. 2009;279:813-20. Available from: https://www.ncbi.nlm.nih.gov/pubmed/18958483.
113. Mozurkewich EL, Chilimigras JL, Berman DR, Perni UC, Romero VC, King VJ, et al. Methods of induction of labour:
a systematic review. BMC Pregnancy Childbirth. 2011;11:84. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/22032440.
114. Delivery in focus : Strengthening obstetrical care in Canada – A 10 year review of CMPA adn HIROC data. 2018.
115. Boie S, Glavind J, Velu AV, Mol BWJ, Uldbjerg N, de Graaf I, et al. Discontinuation of intravenous oxytocin in the
active phase of induced labour. Cochrane Database Syst Rev. 2018;8:CD012274. Available from: https://www.ncbi.
116. Alfirevic Z, Kelly AJ, Dowswell T. Intravenous oxytocin alone for cervical ripening and induction of labour. Cochrane
117. Burgos J, Arana I, Garitano I, Rodriguez L, Cobos P, Osuna C, et al. Induction of labor in breech presentation
at term: a retrospective cohort study. J Perinat Med. 2016. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/27105484.

118. Alfirevic Z, Keeney E, Dowswell T, Welton NJ, Medley N, Dias S, et al. Methods to induce labour: a systematic
review, network meta-analysis and cost-effectiveness analysis. BJOG. 2016;123:1462-70. Available from:
119. Alfirevic Z, Keeney E, Dowswell T, Welton NJ, Medley N, Dias S, et al. Which method is best for the induction
of labour? A systematic review, network meta-analysis and cost-effectiveness analysis. Health Technol Assess.
120. Program T. British Columbia Reproductive Care Program. Vancouver: 2005.

Appendix
Appendix
Post-Term Pregnancy
Post-Term Pregnancy
Clinical Management Algorithm
Clinical Management Algorithm
(Adapted from BCPHP Guideline: Post-term Pregnancy105 and SOGC: Guidelines for the Management of Pregnancy at 41+0 to
(Adapted
42+0 from
Weeks 33 BCPHP Guideline: Post-term Pregnancy120 and SOGC: Guidelines for the Management of Pregnancy at
)
410 to 420 Weeks36)
GESTATIONAL AGE DETERMINATION
• Use biometry from US done at 7 to 16 weeks, if available

• Use sure LMP if no US < 16 wks and 16- to 23-week US not differ
by ≥ 10 days
• Use 16- to 23-week US biometry if differs from sure LMP by ≥ 10d
• If unsure LPM or irreg. cycles, use earliest 1st or 2nd TM U/S
Healthy Pregnancy
Maternal risk factors
• Offer membrane sweeping
or evidence of fetal compromise
between 38 and 41 weeks
Recommend cervical ripening
• Elective induction, NST and/or To 40+6 weeks
and induction as necessary
AFV assessment are NOT
recommended
At 41 weeks
• Inform woman of risks and

benefits of elective induction
vs. expectant management.
• Offer induction of labour
Elective Induction Expectant Management
• Explain procedure & book

induction
• Establish Bishop score
• Cervical ripening before • Daily fetal movement counts
induction if necessary At 41 weeks • NSTs twice weekly
• US for AFV twice weekly
If AFV assessment not available

Induce OR
If NST or AFV abnormal

Table of Contents
Chapter 7 Umbilical Cord Prolapse.................................................................................................................................. 145

Background.............................................................................................................................................................. 145
Incidence....................................................................................................................................................... 145
Morbidity and Mortality................................................................................................................................ 146
Risk Factors and Risk Reduction.................................................................................................................... 146
Diagnosis.................................................................................................................................................................. 147
Management ........................................................................................................................................................... 147
Recommended actions ................................................................................................................................. 147
Summary.................................................................................................................................................................. 148
Umbilical Cord Prolapse 144

Chapter 7
Umbilical Cord Prolapse
Background
In overt umbilical cord prolapse, the cord lies below the presenting part of the fetus and protrudes through the cervix
after rupture of membranes. In occult umbilical cord prolapse, the cord is alongside the presenting part of the fetus,
and membranes may or may not be ruptured. Cord presentation is the presence of the umbilical cord between the fetal
presenting part and the cervix, with or without membrane rupture.
Incidence
In retrospective reviews of large samples, the incidence of cord prolapse has been reported to be from 0.1% to 0.6%.1-432
The incidence of overt cord prolapse varies with the fetal presentation. The lowest rate occurs in cephalic presentations
and the highest in transverse lie presentations.5


There is significant morbidity associated with umbilical cord prolapse, even with appropriate treatment.6 Markers of
possible morbidity include low Apgar scores and low cord pH.7 These become progressively worse with increasing
decision-to-delivery times.8 Other markers of morbidity are not significantly increased.9 Perinatal mortality ranges from
0.02%4 to 12.6%.10 In Canada the number of deaths due to cord prolapse remains very low, ranging from 1 to 15 deaths
per year during the years 2009 to 2013.11
Risk Factors and Risk Reduction

Factors Associated With Increased Incidence
MATERNAL AND FETAL CHARACTERISTICS3, 5, 12 IATROGENIC FACTORS12
Unstable lie (transverse, oblique) Amniotomy
Malpresentation Scalp electrode application
Polyhydramnios Intrauterine pressure catheter insertion
Preterm labour Attempted external cephalic version
Grand multiparity (i.e., parity of ≥ 5) Expectant management of preterm prelabour rupture of membranes
Male fetal sex Manual rotation of fetal head
Pelvic tumours Amnioreduction
Placenta previa and low-lying placenta
Cephalopelvic disproportion
Multiple gestations
Preterm rupture of membranes
Fetal congenital anomalies
Birth weight < 2500 g
Unengaged presenting part
Risk Reduction
Fifty percent of obstetric interventions are responsible for cord prolapse, therefore, interventions such as amniotomy
should be carefully timed, and thoughtful consideration should be given to the indications and the risks and benefits of

the intervention.1 Care should be taken to ensure good application of the presenting part to the cervix before artificial
rupture of membranes.5
There should be an evaluation of the risks of prolapse and thus the need for fetal surveillance as soon as possible after
membrane rupture.12
Diagnosis
Overt umbilical cord prolapse is most commonly diagnosed by visualizing the cord through the introitus or by palpation
of the cord in the vagina.
A sudden deceleration in fetal heart rate in women with rupture of membranes is often the first indication of cord
prolapse. This should prompt vaginal examination and intrauterine resuscitation.
Occult cord prolapse must be suspected in all patients with persistent or significant decelerations on fetal heart
monitoring. Variable decelerations with contractions associated with a prompt return to baseline is often seen with occult
cord prolapse.5
Cord presentation is diagnosed either by palpation of the cord through the membranes or as an incidental finding on
ultrasound.
Management
Overt prolapse is an emergency situation requiring immediate and life-saving interventions.
Recommended actions
• Call for assistance and ensure the availability of staff capable of resuscitating a potentially depressed infant
• Perform a pelvic examination to determine
−− cervical effacement and dilatation
−− station of the presenting part
−− presence of pulsations within the cord vessels
• Initiate intrauterine resuscitation
• Elevate the presenting part, leaving the examining hand in place, and maintain the elevation until delivery.
This may require insertion of the entire hand into the vagina
• Place the woman in the knee-chest or Trendelenburg position. With beds that restrict the application
of Trendelenburg, it may be acceptable to elevate the woman’s hips instead of placing the bed in
Trendelenburg
• Monitor the fetal heart rate
• Do not attempt to replace the cord. Keep the cord warm (with saline-soaked cloth) if it is outside the vagina,
and manipulate it as little as possible.

• Prepare for immediate Caesarean section. If vaginal delivery is imminent and immediately feasible, then it is
acceptable to proceed with vaginal delivery while a CS is being organized
• If there will be a prolonged time to CS or there is a need to transport the woman to another centre, consider
the following:
−− Place Foley catheter, fill bladder with 500 to 700 mL normal saline, clamp the Foley (this must be
drained before Caesarean section).13 This is to elevate the presenting part and to suppress uterine
contractions
−− Administer tocolytic therapy
−− Expeditiously perform a Caesarean section
Health care providers should communicate with the woman and her partner/support person regarding any management
processes throughout the labour and delivery.
Health care providers should ensure that women at risk are aware of:
• The potential for prolapse
• The need for fetal surveillance as soon as possible after membrane rupture
• Positions that might be helpful to relieve pressure on the cord while awaiting transfer to hospital
• Interventions that will occur in hospital in the event of a cord prolapse
It is suggested that the time from diagnosis to delivery is not the only important predictor of fetal outcomes.13 An
expedited vaginal birth is an acceptable option, if feasible, when CS is not available or cannot be performed in a timely
manner.2, 14
Cord presentation diagnosed in labour is managed by Caesarean section before rupture of membranes when there is a
viable fetus.
Practising emergency drills has demonstrated improved outcomes.15 A 2009 retrospective study shows the impact
of training on cord prolapse outcomes at a maternity unit with 5000–6000 births per annum. In 2000, the hospital
introduced a multi-professional obstetric emergency training course that looked at the key interventions needed to
reduce the decision-delivery interval and improve newborn outcomes. The study reviewed case records for two 7-year
periods (one pre-training and one post-training) and found that decision-to-delivery interval decreased from a pre-
training average of 25 minutes to a post-training average of 14.5 minutes (P < 0.001).
Summary
Umbilical cord prolapse is a true obstetrical emergency with potentially severe consequences. All obstetrical care
providers and units should be intimately familiar with the diagnosis and management of this life-threatening condition.
Protocols should be developed and drills practised routinely to ensure that rapid and accurate care can be provided to
mitigate the effects and improve outcomes.

References
1. Kawakita T, Huang CC, Landy HJ. Risk Factors for Umbilical Cord Prolapse at the Time of Artificial Rupture of
Membranes. AJP Rep. 2018;8:e89-e94. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29755833.
2. Chebsey C, Fox R, Draycott TJ, Siassakos D, Winter C. Umbilical cord prolapse [Green-top guideline no 50]. 2nd
Edition. London: 2014.
3. Kahana B, Sheiner E, Levy A, Lazer S, Mazor M. Umbilical cord prolapse and perinatal outcomes. Int J Gynaecol
Obstet. 2004;84:127-32. Available from: https://www.ncbi.nlm.nih.gov/pubmed/14871514.
4. Woo JS, Ngan YS, Ma HK. Prolapse and presentation of the umbilical cord. Aust N Z J Obstet Gynaecol.
5. Kish K, Collea JV. Malpresentation and cord prolapse. In: DeCherney A, Nathan L, Goodwin TM, editors. Current
Diagnosis and Treatment: Obstetrics & Gynecology 10th ed Toronto, Ontario: McGraw-Hill; 2007. p. 342-58.
6. Murphy DJ, MacKenzie IZ. The mortality and morbidity associated with umbilical cord prolapse. Br J Obstet
Gynaecol. 1995;102:826-30. Available from: https://www.ncbi.nlm.nih.gov/pubmed/7547741.
7. Behbehani S, Patenaude V, Abenhaim HA. Maternal Risk Factors and Outcomes of Umbilical Cord Prolapse: A
Population-Based Study. J Obstet Gynaecol Can. 2016;38:23-8. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/26872752.
8. Alouini S, Mesnard L, Megier P, Lemaire B, Coly S, Desroches A. [Management of umbilical cord prolapse and
neonatal outcomes]. J Gynecol Obstet Biol Reprod (Paris). 2010;39:471-7. Available from: https://www.ncbi.nlm.
9. Bush M, Eddleman K, Belagolovkin V. Umbilical cord prolapse. UpToDate 2017 2017. Available from: www.uptodate.com.
10. Usta IM, Mercer BM, Sibai BM. Current obstetrical practice and umbilical cord prolapse. Am J Perinatol.
11. Deaths, by cause, chapter XVI: Certain conditions originating in the perinatal period (P00 to P96), age group and
sex, Canada. [CANSIM database]. Ottawa, Ontario: 2017.
12. Holbrook BD, Phelan ST. Umbilical cord prolapse. Obstet Gynecol Clin North Am. 2013;40:1-14. Available from:
13. Moses S. Labour and delivery. Obstetrics notebook [monograph online]. Rev. Lino Lakes, MN: Scott Moses; 2006.
14. Huang JP, Chen CP, Chen CP, Wang KG, Wang KL. Term pregnancy with umbilical cord prolapse. Taiwan J Obstet
15. Siassakos D, Hasafa Z, Sibanda T, Fox R, Donald F, Winter C, et al. Retrospective cohort study of diagnosis-delivery
interval with umbilical cord prolapse: the effect of team training. BJOG. 2009;116:1089-96. Available from:

Table of Contents
Chapter 8 Fetal Well-Being During Labour....................................................................................................................... 151

Introduction.............................................................................................................................................................. 151
Part One: The Physiologic Basis of Intrapartum Surveillance................................................................................... 151
Definitions..................................................................................................................................................... 151
Physiology..................................................................................................................................................... 152
Neonatal Encephalopathy............................................................................................................................. 156
Cerebral Palsy................................................................................................................................................ 157
Fetal Acid-Base Balance................................................................................................................................. 160
Acid-Base Assessment in Labour................................................................................................................... 160
Umbilical cord blood analysis....................................................................................................................... 162
Interpretation of results................................................................................................................................ 166
Part Two: Fetal Health Surveillance in Labour........................................................................................................... 167
Normal labour contraction pattern................................................................................................................ 169
Intermittent Auscultation ............................................................................................................................. 171
The Process of Systematic Interpretation....................................................................................................... 182
Scalp stimulation.......................................................................................................................................... 199
Intrauterine resuscitation.............................................................................................................................. 200
General considerations and recommendations............................................................................................ 202
Reducing Unnecessary Interventions as a Result of Fetal Surveillance......................................................... 203
Maintaining Standards in Fetal Surveillance............................................................................................................ 204
Other Technologies....................................................................................................................................... 206
Fetal Well-Being During Labour 150

Chapter 8
Fetal Well-Being During Labour
Introduction
The goal of intrapartum FHS is to detect potential fetal decompensation and to allow timely and effective interventions
to prevent perinatal/neonatal morbidity or mortality. Intermittent Auscultation (IA) and Electronic Fetal Monitoring (EFM)
are screening tests for intrapartum fetal well-being; decisions regarding which method to use are based on maternal/
fetal risk of adverse events and informed decision making by the patient. Caregivers respond to FHS with actions to
maintain/improve fetal oxygenation or expedite delivery. Responses to FHS should correlate with the clinical picture.
Clear communication between members of the interdisciplinary team promotes effective care.1
• It is important to recognize that intrapartum fetal surveillance is only a screening test for fetal
compromise, and that no screening test is perfect. When the IA or EFM tracing is classified this refers
only to the surveillance and does not necessarily reflect the status of the fetus.
Inadequate fetal monitoring is frequently cited as a component of substandard care when compensation is awarded after
litigation for birth asphyxia.2 A collaborative report from Accreditation Canada, Healthcare Insurance Reciprocal of Canada
and the Canadian Medical Protective Association found in the ten years ending in 2015, “ Failure to interpret/respond to
abnormal fetal status” represented, by far, the highest risk as a proportion of maternal/newborn claims (42%)3
Part One: The Physiologic Basis of Intrapartum Surveillance

Definitions
Accurate, non-subjective terms should be used when discussing fetal health.
• Hypoxemia – decreased oxygen content in blood
• Hypoxia – decreased oxygen content in tissues
• Acidemia – increased hydrogen content in blood
• Acidosis – increased hydrogen content in tissues
• Asphyxia (hypoxic acidemia) – hypoxemia, hypercapnia and metabolic acidosis

Incidence
Atypical or abnormal EFM tracing patterns may occur in up to 80% of all labours,4 indicating that in most cases, fetuses
with episodes of EFM tracings classified as atypical or abnormal are not actually experiencing hypoxia or asphyxia.
Physiology
Fetal Oxygenation
All human cells require oxygen and glucose to maintain aerobic metabolism, their main source of energy production.
Glucose can usually be stored and mobilized when needed, but total lack of oxygen supply for just a few minutes is
enough to place the cells at risk. During fetal life, oxygen supply is entirely dependent on maternal respiration and
circulation, placental perfusion, gas exchange across the placenta, and umbilical and fetal circulations. Complications
occurring at any of these levels may result in decreased oxygen concentration in fetal arterial blood (hypoxemia) and
ultimately in the tissues (hypoxia). Some degree of hypoxemia occurs in almost all fetuses during labor, but it is the
intensity, duration, and repetitive nature of the event, together with the individual variation in the capacity of each fetus
to cope with the situation, that will determine the severity of the resulting hypoxia.
Difficulties in carbon dioxide (CO2) elimination across the placenta will result in elevated CO2 concentrations, and this gas
will combine with water to increase carbonic acid (H2CO3) concentration, a phenomenon called respiratory acidemia.
The process is quickly reversible with re-establishment of placental gas exchange, as CO2 diffuses rapidly across the
placenta. There is no evidence of injury from isolated respiratory acidemia.
When hypoxia occurs, cellular energy production can still be maintained for a limited time by anaerobic metabolism, but
this process produces 19 times less energy and results in the accumulation of lactic acid inside the cell, and its dispersion
to the extracellular fluid and fetal circulation. The increased concentration of hydrogen ions of intracellular origin in the
fetal circulation is called metabolic acidemia, but it closely parallels hydrogen ion concentration in the tissues, so the
term metabolic acidosis is frequently used as a synonym. The hydrogen ions of lactic acid are transferred very slowly
across the placenta, but they are buffered by circulating bases, comprised mainly of bicarbonate, hemoglobin, and
plasma proteins. The depletion of these buffering agents (increasing base deficit, or base excess in negative numbers)
indicates the growing inability to neutralize hydrogen ions, and their continued production will ultimately lead to the
disruption of cellular enzyme systems and to tissue injury.5
Although placental permeability to oxygen is high, fetal oxygen concentration (pO2) is markedly low compared with
maternal oxygen concentration (40 mm Hg in umbilical vein vs. 95 mm Hg in maternal artery). However, oxygen
saturation and content in the umbilical vein are almost identical to those in maternal arterial blood. This is because of
a higher hemoglobin concentration in fetal blood and its higher affinity for oxygen. The fetal oxygen dissociation curve
is shifted to the left and is steeper than the maternal curve. This allows the fetus to have a higher oxygen saturation
and content at a low pO2 value and produces a larger fall in oxygen saturation (releases oxygen to the tissues). Another
important compensatory mechanism for the low fetal pO2 is increased tissue oxygen extraction and a high organ blood
flow secondary to high fetal cardiac output.6


important compensatory mechanism for the low fetal pO2 is increased tissue oxygen extraction and a high organ blood
flow secondary to high fetal cardiac output.4
Figure
Figure 1.
1. Oxygen
Oxygen Dissociation
Dissociation Curves
Curves for
for Fetal
Fetal and
and Adult
Adult Blood
Blood
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The fetus depends on the transfer of oxygen from the maternal lungs to the maternal blood, delivery of that oxygen
to the uterus and placenta, diffusion of the oxygen across the placenta to fetal blood, and finally the distribution of
fetal blood to fetal tissues through fetal cardiovascular activity. A problem with any of these processes will reduce the
The fetus depends
availability of oxygen on to
thethe
transfer of oxygen from the maternal lungs to the maternal blood, delivery of that oxygen
fetal tissues.
to the uterus and placenta, diffusion of the oxygen across the placenta to fetal blood, and finally the distribution of
During the contractions
fetal blood of normal
to fetal tissues throughlabour there is a decrease
fetal cardiovascular in uteroplacental
activity. A problem with blood
anyflow. The reduction
of these processesin blood
will flowthe
reduce results
in diminished oxygen delivery to the
availability of oxygen to the fetal tissues. fetus. This causes an increase in pCO 2, a decrease in pO 2, and a decreased pH. These
changes do not fall outside the normal range. The healthy fetus compensates and recovers during the resumption of normal
During theperfusion
placental contractions
that of normal
occurs labourcontractions.
between there is a decrease in uteroplacental
As a result, blood
the healthy fetus flow. The
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not displayin blood flow results
any changes in
in diminished
heart rate. Whenoxygen
theredelivery
has beentochronically
the fetus. This causes an increase
compromised uteroplacental 2, a decrease
in pCOfunction, the in pO2, and
increase a decreased
in pCO 2 and pH.
the These
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in pO2 anddopH,
notmay
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A long of normal
labour or excessive
placental perfusion that occurs between contractions. As a result, the healthy
uterine contractions may challenge even a fetus with normal uteroplacental function. fetus usually does not display any changes in
heart rate. When there has been chronically compromised uteroplacental function, the increase in pCO2 and the decrease
in pO
a) 2 and pH, may
Maternal exceedaffecting
factors critical thresholds,
fetal and there may be1changes in the fetal heart rate. A long labour or excessive
oxygenation
uterine contractions may challenge even a fetus with normal uteroplacental function.
Decreased maternal arterial oxygen tension:
• Respiratory disease
• Hypoventilation, seizure, trauma
Fetal Well-Being
• During
Smoking 7 Labour 8
149

Decreased maternal oxygen carrying capability:

• Significant anemia (e.g., iron deficiency, hemoglobinopathies)
• Carboxyhemoglobin (e.g. smoking: tobacco, cannabis)
Decreased uterine blood flow:
• Hypotension (e.g., blood loss, sepsis)
• Regional anaesthesia
• Maternal positioning
Maternal conditions:
• Vasculopathies (e.g., systemic lupus erythematosus, , chronic hypertension)
• Diabetes mellitus (type 1 and 2) 9
• Antiphospholipid syndrome
• Medical disease (e.g. Cyanotic heart disease, Chronic obstructive pulmonary disease, hyperthyroidism, renal)
• Cholestasis of pregnancy10
• Pre-pregnancy BMI > 3511
b) Uteroplacental factors affecting fetal oxygenation1

Excessive uterine activity:
• Tachysystole secondary to oxytocin, prostaglandins or normal labour
• Placental abruption
Uteroplacental dysfunction:
• Placental infarction-dysfunction marked by intrauterine growth restriction,12 oligohydramnios, or abnormal
Doppler studies
• Uterine rupture
c) Fetal factors affecting fetal oxygenation1

• Preterm (< 370 weeks) or Posterm (>420 weeks) fetus in labour
• Malpresentation (e.g., breech13)
• Polyhydramnios14, 15
• Oligohydramnios16
• Cord compression, prolapse, or entanglement17 18 (e.g., 3 or more nuchal loops19, 20) or umbilical cord knots21
• Velamentous cord insertion22

−− A 2018 study of 53 singletons with velamentous cord insertions (matched with 103 controls) found
associations with pH < 7.20, 5 min. Apgar < 7 and cord avulsion requiring manual placental extraction.
There was also trends for increased surgical delivery for EFM changes, Bwt < 10%, abruption and fetal
and neonatal death
• Single umbilical artery (due to less Wharton’s jelly cushioning and umbilical cord coiling)23.
−− In a 2014 study of 34 196 pregnancies Ashwal et al. reported that the 162 fetuses with single umbilical
artery were associated with:
›› a higher rate of Caesarean section (CS) due to non-reassuring fetal heart rate (5.5% vs. 1%,
P = 0.02)
›› small for gestational age (14.3% vs 4.9%, P = 0.009)
›› lower birth weight
›› higher rate of composite adverse outcome (CS or operative delivery because of non-reassuring
fetal heart rate, prolonged neonatal admission, 5-minute Apgar score < 7 and umbilical artery pH
< 7.2) (20.9% vs. 8.8%, P = 0.005)24)
−− In a 2015 study of 27 752 pregnancies with 127 fetuses with single umbilical artery,25 Naveiro-Fuentes
et al. recommended monitoring fetal growth closely and monitoring intrapartum fetal surveillance
because of its association with a lower weight for gestational age, higher risk of low umbilical cord
blood pH and increased Caesarean section for abnormalities in fetal surveillance
• Decreased fetal oxygen carrying capacity
• Significant anemia (e.g., isoimmunization, fetal-maternal bleed, ruptured vasa previa)
• Carboxyhemoglobin (maternal smoking)
d) Fetal response to hypoxia/asphyxia

Reduction in oxygen delivery to the fetus produces cardiovascular, metabolic, and behavioral responses, including:
• Redistribution of fetal blood flow
−− increased flow to the brain, heart, and adrenal glands
−− decreased flow to the kidneys, lungs, gut, liver, and peripheral tissues
−− increase in blood pressure
• Decreased movement, tone, and breathing action (changes in biophysical profile)
• Fetal tachycardia (this may be preceded by transient bradycardia)
• Anaerobic metabolism (decreased pH)

The central nervous system of the fetus remains vulnerable to damage throughout gestation, but this is particularly
significant between 28 and 32 weeks’ gestation.
Because of the fetal physiologic response to hypoxia (redistribution of blood flow to vital organs including the brain), any
injury to the fetal brain as a result of intrapartum hypoxia must be associated with injury to other organ systems since the
other systems will have been deprived of oxygen first.

1. Neonatal Encephalopathy
Neonatal encephalopathy (NE) is a clinically defined syndrome of disturbed neurologic function in the earliest days of
life in an infant born at or beyond 35 weeks of gestation, manifested by a subnormal level of consciousness or seizures,
and often accompanied by difficulty with initiating and maintaining respiration and depression of tone and reflexes.26
NE and its subset of hypoxic-ischemic encephalopathy are conditions defined for term infants (> 37 completed
weeks of gestation) and near-term infants (> 34 completed weeks of gestation). The incidence of hypoxic-ischemic
encephalopathy is reported as 1.9 per 1000 term births and the incidence of NE is 3.8 per 1000 term births.27
The fetus lives in a relatively hypoxic environment but normally exists with a surplus of oxygen to meet its metabolic
needs. In response to impairments in blood gas exchange, adaptive mechanisms usually maintain fetal oxygenation.
This process is known as compensation.
Hypoxia can occur in degrees. In the simplest form, hypoxia will be brief and the fetus will easily cope with the
physiologic changes that occur (e.g., intermittent cord compression). When hypoxia continues over time, the fetus
begins trying to meet its metabolic needs in a less than optimum oxygen environment. This can lead to metabolic
acidosis. Hypoxia plus metabolic acidosis results in asphyxia. The severity and duration of asphyxia will affect the
outcome. The aim of fetal surveillance in labour is to detect signs of a decompensating fetus before damage.
Sustained hypoxia almost always results in hypotension and ischemia. Regardless of the mechanism, cerebral ischemia
is the final common pathway leading to brain injury. Other mechanisms include diminished systemic perfusion, emboli
(largely cardiac in origin), thrombosis (often from tissue wall damage), or hypercoagulable states. There is no evidence
to suggest that systemic hypoxia alone can produce irreversible brain damage. The severity and duration of asphyxia will
affect the outcome.28-30
92
Neonatal encephalopathy results from many conditions. Seventy percent of cases are secondary to events that occur
before labour. These events include prenatal stroke, infection, cerebral malformation, genetic disorders, and others. Only
19% of cases of NE meet the criteria for intrapartum hypoxia, while another 10% experience a significant intrapartum
event that may be associated with intrapartum hypoxia.31 The pathway from intrapartum asphyxia to subsequent
cerebral palsy must progress through NE. The incidence of NE that can be attributed to intrapartum hypoxia, in the
absence of any other pre-conceptional or antepartum abnormalities, is approximately 1.6 per 10 000.32
Ultimately, sustained hypoxia leading to severe metabolic acidosis and cardiovascular decompensation with systemic
hypotension may lead to cerebral ischemia and brain damage. Asphyxia is the most common pathogenic mechanism
underlying hypoxic-ischemic encephalopathy. Asphyxia may occur at any point in the infant’s antepartum, intrapartum,
or postpartum life. Isolated hypoxia does not cause cerebral damage unless it is prolonged, severe, and associated with a
vulnerable fetus.
The type of cerebral injury caused by hypoxic-ischemia depends on the nature of the insult, the maturation of the brain
and its vascular development
• At term, the injury is predominantly to the subcortical white matter and cerebral cortex. The areas between
the end branches of the major cerebral vessels are the areas of the brain at highest risk. The damage is
usually to the motor cortex that controls the proximal and upper extremities. Spastic quadriplegia is by far
the most common outcome. A severe hypoxic/ hypotensive insult may affect deeper brain tissues.

• Hypoxic-ischemia in the preterm fetus is more likely to cause damage to the periventricular white matter.
The resulting lesion is called periventricular leukomalacia. Moderate injury generally affects the lower limbs
while severe lesions frequently involve both extremities. The long-term manifestations include spastic
diplegia, spastic quadriplegia, and other visual and cognitive deficits.
In humans, no threshold of hypoxia has been determined that reliably predicts biologic injury. Severe metabolic or
mixed metabolic acidosis, indicating decompensation with damage to target organs such as lungs, heart, and kidneys, is
required to diagnose fetal asphyxia.
2. Cerebral Palsy
Cerebral palsy (CP) is considered a neurological disorder caused by a non-progressive brain injury or malformation that
occurs while the child’s brain is under development. CP is characterized by the early onset of abnormal movements
or postures. “Research supports that spastic quadriplegia, especially with associated movement disorders, is the only
type of CP associated with acute interruption of blood supply. Purely dyskinetic or ataxic CP, especially when there is an
associated learning difficulty, commonly has a genetic origin and is not caused by intrapartum or peripartum asphyxia.”32
Incidence
The incidence of CP in term infants is 2 to 3/1000 live births and has remained stable for the past 30 to 40 years.
Advances in neonatal care have increased the survival of extremely premature neonates. The result has been an increase
in the incidence of CP in these very low birth weight babies. However, the small number of these small babies, relative to
the overall population, has had no significant effect on the total incidence of CP.

Factors Associated with CP

• Maternal medical conditions (e.g., hypertension)
• Multiple gestation
• Preterm infants
• Intrauterine growth restriction
• Autoimmune conditions
• Trauma
• Asphyxia (antepartum, intrapartum, or neonatal)
• Neonatal respiratory complications
• Infection (clinical chorioamnionitis and severe—not mild—histological chorioamnionitis)
• Central nervous system anomalies
• Metabolic abnormalities
• Developmental abnormalities
• Substance abuse and/or smoking
• Placental abnormalities
Term and near-term infants make up at least 50% of all cases of CP even though they are at relatively low risk compared
with very preterm infants. Infants weighing < 1500 g at birth make up approximately 25% of all cases of CP.32
Is cerebral palsy the result of intrapartum events?

Many studies reveal that CP is rarely the result of adverse intrapartum events. Even if there has been intrapartum hypoxia
and/or acidosis, CP rarely occurs. Only 10% to 20% of children with CP had demonstrated intrapartum asphyxia.33-3543
Criteria to define an Acute Intrapartum Hypoxic Event as Sufficient to Cause Cerebral Palsy
In 2014, the Report of the American College of Obstetricians and Gynecologists’ Task Force on Neonatal Encephalopathy
emphasized that there are multiple causal pathways that lead to cerebral palsy in term infants and that knowledge
gaps still preclude a definitive test or set of markers that will identify an infant in whom neonatal encephalopathy is
attributable to an acute intrapartum event.26 To determine the likelihood that an acute intrapartum hypoxic–ischemia
event contributed to neonatal encephalopathy, a comprehensive assessment is necessary of neonatal status and all
potential contributing factors, including maternal medical history, obstetric antecedents, intrapartum factors (including
fetal surveillance and issues relating to the delivery itself), and placental pathology.
When more of the following elements are met, it becomes more likely that an acute peripartum or intrapartum hypoxia-
ischemia event played a role in the pathogenesis.26
1. Neonatal signs:
a. Apgar score < 5 at 5 and 10 min.
b. Fetal umbilical artery pH < 7.0, and/or base deficit ≥ 12 mmol/L
c. Neuroimaging evidence of acute brain Injury seen on brain MRI or MR spectroscopy

d. Presence of multisystem organ failure consistent with hypoxic–ischemic encephalopathy (e.g., renal or
hepatic injury, hematologic or metabolic abnormalities, cardiac dysfunction, gastrointestinal injury)
2. Type and timing of contributing factors:
a. A sentinel hypoxic or ischemic event occurring immediately before or during labour and delivery (e.g.,
ruptured uterus, placental abruption, umbilical cord prolapse)
b. Fetal heart rate (FHR) patterns consistent with an acute peripartum or intrapartum event
c. Timing and type of brain injury patterns based on imaging studies consistent with an etiology of an
acute peripartum or intrapartum event
d. No evidence of other proximal or distal factors that could be contributing factors (e.g., abnormal fetal
growth, maternal infection, fetal and/or maternal hemorrhage, neonatal sepsis, and chronic placental
lesions)
3. Developmental outcome is spastic quadriplegia or dyskinetic cerebral palsy (other subtypes of cerebral palsy
are less likely to be associated with acute intrapartum hypoxic–ischemic events).
−− There is a continuum of increasing risk of NE with worsening acidemia, but even in the presence of
significant acidemia, most newborns will be neurologically normal. The presence of metabolic acidemia
does not define the timing of the onset of a hypoxic–ischemic event. MRI is the modality that best
defines the nature and extent of cerebral injury in NE. Distinct patterns of abnormalities are recognized
in hypoxic–ischemic cerebral injury and have prognostic value for predicting later neurodevelopmental
impairments. If no injury is noted on MRI after 24 hours of life then it is unlikely that significant
peripartum or intrapartum hypoxic-ischemic brain injury was a significant factor in NE. The full extent of
injury may not be evident on MRI until after the first week of life.26
A 2012 cohort study of 51 519 neonates who had validated umbilical cord arterial pH values found that the risk of
adverse neurological outcome was significantly increased below 7.10 (0.36%) and more so below 7.00 (2.95%). Seventy-
five percent of the neonates with abnormal neurological outcomes had pH levels above 7.10.36
Precise and effective communication and documentation are essential.
Do not
• Use the term “fetal distress”
• Overstate the significance of meconium
• Use the term “asphyxia” without hard evidence including abnormal umbilical cord blood gas results
• Use qualifiers such as “significant” or “severe”
Instead use
• Normal or abnormal IA or normal, atypical or abnormal EFM tracing
• “Asphyxia” only with biochemical evidence (e.g. scalp pH, cord blood gases)
Summary
• Despite improved technology and neonatal care, rates of CP are still 2 to 3/1000 live births
• Most documented asphyxia does not result in CP
• Most infants diagnosed with CP had uncomplicated term deliveries
• Available tests of fetal well-being are not highly predictive of adverse central nervous system outcomes

Fetal Acid-Base Balance

Normal metabolic processes in the fetus result in a continuous production of hydrogen ions that are buffered by various
mechanisms to maintain a stable pH level.
Definitions of Terms37
pH: pH is a scale used to express the degree of acidity or alkalinity.
Buffer: Substances that interact with acids in the body to minimize changes in pH. The 2 main buffers are hemoglobin
and plasma bicarbonate. Bicarbonate is the buffer result most often reported when a blood gas analysis is performed.
Base deficit/excess: Base deficit (positive number) refers to the number of units of base required to neutralize the
amount of acidosis occurring. Base excess (negative number) refers to the number of units of base that would need to be
reduced to reach neutrality.
3. Acid-Base Assessment in Labour

Fetal scalp blood sampling
Fetal scalp blood sampling can reduce the increased operative intervention rates associated with electronic fetal
monitoring.38
Placental perfusion is reduced with every uterine contraction. Most term fetuses enter labour with normal placental
function and tolerate labour well. However, when placental function is not adequate, as in women with hypertension
in pregnancy or fetuses with intrauterine growth restriction, exposure to uterine contractions may lead to the rapid
development of fetal respiratory and metabolic acidosis. Glucose metabolism in the absence of oxygen results in an
increase in lactic acid. Fetal scalp blood gas or lactate sampling can provide valuable objective clinical information to
help guide decision-making about the preferred timing and method of delivery.
Indications
• Gestational age > 34 weeks’ gestation when delivery is not imminent
• Resources available to perform the analysis and respond to the results in a timely manner
• Membranes ruptured, cervix at least 2 to 3 cm dilated
• Women with atypical and/or abnormal EFM tracings
Contraindications:
• Gestational age ≤ 34 weeks
• Face presentation
• Known or suspected fetal bleeding disorder (hemophilia, thrombocytopenia)
• Family history of a bleeding disorder (hemophilia, von Willebrand)
• Active maternal infection (HIV, genital herpes, hepatitis, known or suspected intrauterine sepsis)

Fetal scalp blood gas testing:

• typically requires a 30 to 50mcL blood sample, and sampling failure rates as high as 21% have been
reported. This may be due to inadequate volume or contamination with air or amniotic fluid. pH alone is
a less accurate predictor of hypoxia than full blood gas assessment, which includes base deficit. BD is helpful
in quantifying metabolic acidosis.
• A 2017 retrospective study of 343 deliveries where the EFM tracing was not normal (would include atypical
and abnormal tracings) and fetal blood gas assessment (FBGA) performed, found the PPV was only 50%
but the NPV was 91% for predicting postpartum acidosis (pH ≤ 7.15). The authors concluded that FBGA can
be used to rule out but not rule in neonatal acidosis. Effectively, they found that it can avoid unnecessary
interventions such as CS or AVB in up to 90% of cases but not reliably detect fetal acidosis 39
• recommended actions related to pH level40:
−− pH ≥ 7.25: Scalp sampling should be repeated within 30 minutes only if the FHR abnormality persists.
−− pH 7.21 to 7.24: Scalp sampling should be repeated within 30 minutes or delivery should be
considered if there has been a rapid fall since the last sample.
−− pH ≤ 7.20: Delivery is indicated.
Fetal scalp blood lactate testing:

• This point of care test requires as little as 0.6 mcL, which reduces sampling failures.
• A 2015 Cochrane review compared intrapartum fetal lactate testing with pH estimation and found that
lactate testing was 99% successful in predicting hypoxia compared with only 79% for pH testing.41 Fewer
incisions were needed to draw blood for lactate testing than for pH testing, and time from sampling to
result was shorter. Despite these potential advantages of lactate testing, there was no difference in mode of
delivery, neonatal outcomes, Apgar scores, encephalopathy, or admission to the neonatal intensive care unit.
However, there was no available evidence comparing the effect of fetal scalp blood lactate estimation with no
sampling on clinical outcomes.
• Although there appears to be an increase in mean umbilical cord blood lactate level from 370 to 420 weeks’
gestation, no studies have addressed whether the gestational age should be considered in determining the
critical level of scalp lactate at which clinical action must be taken.41
• Fetal scalp blood samples taken for lactate measurement within 60 minutes of birth correlate well with
umbilical arterial and venous lactate measurements following delivery.42 Lactate levels correlate well with
both fetal scalp and cord blood pH and BD.43, 44 45
• Predictive lactate values and levels for intervention vary significantly depending on the lactate analyzer used
and the manufacturers’ recommendation; therefore, decision-making criteria should be adjusted according
to the device used.43, 46-48
74
• It may be that the value of scalp lactate testing lies in its strong negative predictive value for fetal acidemia at
birth.
Interpretation of results
The results of fetal scalp sampling should be interpreted with the total clinical picture in mind. This includes the clinical
features of the mother and baby, the existence of any prenatal risk factors, gestational age, the duration of labour,

progress in labour, the presence of meconium, maternal fever, and the severity of the atypical and/or abnormal FHR
characteristics.
The trend of the fetal scalp sampling values should be determined as it will indicate whether the fetal condition is
improving or deteriorating and therefore what, if any, intervention is warranted. Although there is little evidence with
respect to the frequency of fetal scalp sampling. The Society of Obstetricians and Gynaecologists of Canada (SOGC)
had recommends that if the clinical picture does not improve or delivery is not imminent, a repeat sample should be
considered within 30 to 40 minutes.
Limitations of fetal scalp blood sampling
• It provides only instantaneous and not continuous information. Repeat sampling may be necessary.
• There are technical limitations including equipment availability, operator experience and skill level.
• The procedure may be uncomfortable for the woman.
4. Umbilical cord blood analysis

Dr Virginia Apgar developed the Apgar score as a rapid tool to assess the immediate status of the newborn and the need
for resuscitation. It was not developed as a method of assessing the degree of asphyxia. The Apgar score alone cannot
link birth events to neurological sequelae. A low Apgar score can be associated with various maternal-fetal conditions
including fetal malformation, infection, meconium aspiration, vigorous manipulation of the upper airway, and
immaturity.
Umbilical cord blood gas analysis provides an objective method to evaluate the fetal condition at delivery. This facilitates
effective newborn care and quality assurance and/or improvement initiatives.
Recommendations for cord blood analysis from professional organizations:
• The SOGC strongly recommends measuring both umbilical arterial and venous cord gases after all births,
as they may help in providing appropriate care to the newborn and in planning subsequent management.
They also assist quality assurance / improvement initiatives.1
In hospitals where blood gas analysis is not immediately available, alternatives include the following:
• Cord blood samples in pre-heparinized syringes are most accurate and stable at room temperature for 60
minutes.49
• If not analyzed within 60 minutes the sample should be stored at 4-8°C and the time of analysis
documented.
• A clamped, 20 cm segment of cord for delayed analysis. Umbilical artery blood is stable for pH analysis for up
to 60 minutes at room temperature.50
• A 2006 study which sampled umbilical arterial and venous lactate, base excess. pH and PCO2 at 0, 20, 40 and
60 minutes from a doubly clamped segment and a segment still attached to the placenta (unclamped) found
the pH was stable in the clamped vessels over the 60 minutes, however, there was a steady decrease in the
pH of the unclamped vessels. The base excess was significantly lower by 20 min. in the unclamped cord and

by 40 min. in the clamped cord. Lactate levels were significantly higher by 20 min. in both the unclamped
and clamped segments. The study concluded:
−− Delayed sampling from unclamped cords is unreliable for pH, base deficit or lactate by 20 min.
−− For clamped cords, the pH is stable for 60 min. but base excess is unreliable by 40 min and lactate is
unreliable by 20 min.51
Rationale for routine umbilical cord blood gas analysis

The objective of measuring cord pH and acid-base status is to quantify the degree of perinatal asphyxia. Blood gas
measurements reflect fetal and placental oxygenation at birth and assist in the provision of appropriate care to the
newborn and in planning ongoing management. A complete blood gas analysis is necessary (pH, BD, pCO2, HCO3, pO2,
O2 saturation) since the use of pH alone will not differentiate between respiratory and metabolic acidosis.
The availability of cord blood gas analysis may reduce the incidence of successful litigation in the event of a poor
outcome, particularly when the outcome is delayed (i.e., not apparent in the neonate).
A 2016 study of 26 669 term singletons whose 5-minute Apgar scores were all ≥ 7 found that 0.5% of these had an
umbilical cord arterial pH of ≤ 7.0 and 1.4% had a base excess ≤ −12. These infants were found to be at increased risk
of NICU admission because of neonatal complications such as respiratory distress syndrome and sepsis. The authors
concluded that universal rather than selective umbilical cord gas analysis would enable better stratification of neonatal
risk levels and care.52
An observational study of approximately 20 000 births in Australia from 2003 to 2006 during which universal umbilical
(arterial and venous) cord blood gas and (arterial) lactate analysis was performed found a progressive improvement in
these values during the study. The authors concluded that the improvement was independent of obstetric interventions
and suggested that it was due to the provision of fetal acid-base biochemical data at delivery, which progressively
influenced care.53
Normal Umbilical Cord Blood Gas Values

Reference Ranges of 3522 Term* Vaginal Deliveries54
ARTERIAL MEAN SD RANGE
pH 7.27 0.07 7.2 to 7.34
pCO2 (mmHg) 50.3 11.1 39.2 to 61.4
pO2 (mmHg) 18.4 8.2 10.2 to 26.6
HCO3 (mEq/L) 22 3.6 18.4 to 25.6
Base excess (mEq/L) −2.7 2.8 −5.5 to 0.1
O2 saturation (%) 23.3 16.2 7.1 to 39.5

VENOUS
pH 7.34 0.06 7.28 to 7.40
pCO2 (mmHg) 40.7 7.9 32.8 to 48.6
pO2 (mmHg) 28.5 7.7 20.8 to 36.2
HCO3 (mEq/L) 21.4 2.5 18.9 to 23.9
Base excess (mEq/L) −2.4 2.0 −4.4 to 0.4
O2 saturation (%) 49.4 16.9 32.5 to 66.3
*Reference ranges of preterm neonatal umbilical cord gas values are similar to those at term.
Considerations regarding umbilical cord blood gas analysis include:

1. A 2009 Cochrane review suggests that delayed cord clamping may confer some benefit in preterm infants
not requiring resuscitation.55 Evidence suggests that delayed clamping of the cord for 30 to 120 seconds
after birth in preterm infants reduces the rate of intraventricular hemorrhage, anemia, and the need for
transfusions.55, 56 In term infants, delays of up to 180 seconds after birth have not been associated with
adverse outcomes and have resulted in increased iron stores in these infants at 6 months of age although
they may increase the need for phototherapy.57, 58 There is no evidence to support early cord clamping as
part of active third stage management in preventing postpartum hemorrhage.59 A delay in cord clamping
of at least 1 minute provides sufficient placental fetal transfusion.60 The Canadian Paediatric Society, in its
2017 Practice Point, Update for Canadian NRP providers: A case based review stated: For vigorous term and
preterm infants, delayed cord clamping for 30-60 s is recommended.61
There is evidence delayed umbilical cord clamping may have a minor influence arterial blood gas values:
−− Lievaart et al., in 1984, determined that when arterial cord blood samples taken within seconds of birth
were compared with samples taken at 60 seconds, there was a mean decrease in pH of 0.043 (range
0.008 to 0.076) and an increase in the BD of 1.3 (range 0.2 to 3.0). These changes were not observed in
the venous samples.62
−− Wiberg et al., in 2008, sampled cord arterial and venous blood immediately and at 45 and 90 seconds.
Compared with immediate sampling, the mean arterial pH declined from 7.24 to 7.21 and the BD
increased from 4.85 to 6.14. Corresponding venous samples had a much smaller mean pH decrease
from 7.32 to 7.31 and BD increase from 4.93 to 5.19.63
It is therefore important to document when the cord was clamped and when blood was drawn.
2. Sampling both the umbilical artery and umbilical vein is recommended:
−− The umbilical artery values correlate better with fetal status than venous values, which correlate better
with the placenta.
−− The distended umbilical vein stabilizes the arteries making it easier to sample the artery first.

−− In order to ensure enough filling of the umbilical arteries, the cord can be milked from the placenta
to the first clamp before the second is applied; this may be helpful when delayed cord clamping is
performed.
−− If the cord samples are inadequate, samples may be obtained from the fetal (chorionic) side of the
placenta (arteries pass over top of the veins).
−− An umbilical vein sample is required for quality control. Without an umbilical vein sample there is
no way to identify sample error. Up to 25% of samples assumed to be arterial are, in fact, venous.64
Collecting both arterial and venous samples will confirm that the source is arterial or venous. This is
especially valuable in situations where risk factors for fetal compromise are present. The suggested
normal range of difference between vessels is 0.03 in pH and 8 mm Hg in pCO2.
3. To identify the type and severity of fetal acidosis. The following example of 2 cases with similar arterial but
different venous values had dissimilar neonatal outcomes.64 The infant in case A required resuscitation at
birth and assisted ventilation for 48 hours, and developed CP at 1 year of age. The infant in case B had a
5-minute Apgar score of 8 with no neonatal problems.
CASE A CASE B
Artery Vein Artery Vein
pH 7.03 7.10 7.04 7.32
pCO2 (mmHg) 63 50 67 38
pO2 (mmHg) 6.8 20 13.5 34
BE (mmol/L) −12.5 −12.6 −11.2 −5.5
4. Normal blood gas values change during labour: pH, bicarbonate, and pO2 decrease, and pCO2 and BD
increase.65
5. Blood gas analyzers assess pH and pCO2 directly, but BD is calculated and will vary depending on whether
the calculation uses blood or extracellular fluid. Generally BD values calculated using blood are greater than
those using extra cellular fluid.65
6. In the presence of a high pCO2, metabolic acidosis may be erroneously reported when BD is calculated using
blood. In the perinatal period, calculating BD using extracellular fluid will prevent the influence of pCO2 on
reporting of metabolic acidosis. Care providers should be aware that most hospitals do not recognize this fact
and analyze the acid-base status using blood.
7. A low umbilical artery pH by itself does not define asphyxia. All of the criteria, as noted in the CP and fetal
asphyxia sections, should be present to correlate birth hypoxia with adverse neurological outcome.66
8. Arterial-venous pH differences may add information about the cause of the acidemia at birth. Restriction of
umbilical flow increases the difference between umbilical arterial and umbilical venous pH values, while
impairment of maternal perfusion of the placenta may be associated with small differences.66

Neonatal morbidity and mortality according to pH cut-off67
pH NEONATAL DEATHS SEIZURES BOTH
7.15 to 7.19 (n = 2236) 3 (0.1%) 2 (0.1%) 1 (0.05%)
7.10 to 7.14 (n = 798) 3 (0.4%) 1 (0.1%) 0
7.05 to 7.09 (n = 290) 0 0 1 (1.1%)
7.00 to 7.04 (n = 95) 1 (1.1%) 1 (1.1%) 1 (1.1%)
< 7.00 (n = 87) 7 (8%) 8 (9.2%) 2 (2.3%)
Interpretation of results
The pathogenesis and clinical significance of respiratory acidosis are different from those of metabolic acidosis.
Respiratory acidosis is considered a part of normal birth. It develops rapidly and disappears rapidly following the first
neonatal breaths when the newborn is able to eliminate CO2 through respiration. Respiratory acidosis occurs in the blood
vessels and develops when interruption of blood flow occurs, for example with cord compression, causing a decrease
in CO2 transport from the fetus to the placenta. Carbon dioxide accumulates and after reacting with water produces
hydrogen ions and bicarbonate. When the hydrogen ions exceed the buffer capacity of the blood, they accumulate in the
vessel causing a decrease in pH.
Metabolic acidosis, on the other hand, develops as a result of fetal hypoxia that causes the fetus to shift to anaerobic
metabolism (metabolism in a less than optimum oxygen environment) to maintain a positive energy balance. Lactic
acid is produced in the tissue and is dissociated to lactate and hydrogen ions. Some of the latter find their way to blood
vessels, reducing the pH value. Metabolic acidosis is generated in hypoxic tissues, takes longer to develop and to
disappear, and may be associated with significant fetal damage.68
TYPES OF ACIDOSIS (DECREASED pH)
Respiratory Increased pCO2 and normal base excess / deficit
Metabolic Normal pCO2 and high base deficit / base excess
Mixed Increased pCO2 and high base deficit / base excess

Part
PartTwo:
Two:Fetal
FetalHealth
HealthSurveillance
Surveillancein Labour
in Labour
The goal of intrapartum fetal health surveillance is to perform a screening test to detect potential fetal decompensation
and to intervene early enough to prevent fetal injury or death. The fetal brain, which is the primary organ of interest,
cannot currently be evaluated antenatally. Characteristic FHR changes often precede brain injury. The most valuable
non-invasive method of intrapartum evaluation that is currently available is FHR assessment. A consistent and standard
approach to FHR monitoring may provide an opportunity for early intervention.
y • The Thedata
dataobtained
obtainedfrom fromintermittent
intermittentauscultation
auscultationandandthe
theelectronic
electronicfetal
fetalmonitor
monitorshould
shouldalways
alwaysbebeinterpreted
ininterpreted
conjunctioninwith
conjunction
the total with thepicture.
clinical total clinical picture. Interpretation
Interpretation of the
of the fetal heart fetal heart
pattern pattern
and the and the
management
management plan are dependent on the fetal health before labour, the maternal clinical
plan are dependent on the fetal health before labour, the maternal clinical condition, the stage of labour, condition, the stage
and
of uterine
the labour, and the uterine activity.
activity.
y • A Asystematic
systematicmethod
methodforforinterpretation,
interpretation,documentation,
documentation,and andcommunication
communicationwill willhelp
helptotoprevent
preventmissed steps
missed steps in the assessment process and the omission of important elements of
in the assessment process and the omission of important elements of documentation and communication. documentation and
y Allcommunication.
care providers need to have a formal process for communication about the status of the fetus during labour
• thatAll uses
care providers
standardized needterminology.
to have a formal process for communication about the status of the fetus during
labour thatcare
y Supportive usesinstandardized terminology.
labour is an extremely important adjunct to all fetal surveillance techniques and should be
• Supportive care in labour
the basis of intrapartum care. is an extremely important adjunct to all fetal surveillance techniques and should
be the basis of intrapartum care.
Benefits of Continuous Support During Childbirth60
Benefits of Continuous Support During Childbirth69
Outcome RR
Any analgesia 0.90 (0.84–0.97)
Regional analgesia 0.93 (0.88–0.99)
Artificial oxytocin 0.97 (0.90–1.04)
Operative vaginal delivery 0.90 (0.84–0.96)
Caesarean section 0.79 (0.67–0.92)
Low 5-min Apgar score 0.70 (0.50–0.96)
Dissatisfaction 0.69 (0.59–0.79)
Favours support Favours usual care

Principles of Intrapartum Surveillance:
Classify IA or EFM Tracing
å
Interpret clinically (in light of total situation)
å
Respond (communication and teamwork)
Choice
Choice ofofMethod
Methodof of Surveillance
Surveillance in Labour
in Labour
Comparing
Comparing Continuous
Continuous EFM
EFM with
with IA
IA in
in Labour
61
labour 71
Outcome RR (95% CI)

Caesarean section 1.63 (1.29–2.07)
Operative vaginal delivery 1.15 (1.01–1.33)
NICU admission 1.01 (0.93–1.10)
Perinatal death 0.86 (0.59–1.23)
Neonatal seizures 0.50 (0.31–0.80)
Cerebral palsy 1.75 (0.84–3.63)
When comparing continuous EFM with IA during labour, a 2017 Cochrane review (including both low- and high-risk
patients)
When found that:
comparing
70
continuous EFM with IA during labour, a 2013 Cochrane review (including both low- and high-risk
71
patients)61 found that:

• Continuous EFM is associated with a higher rate of CS and instrumental (operative) vaginal deliveries than
IA.
y Continuous EFM is associated with a higher rate of CS and instrumental (operative) vaginal deliveries than IA.
Therewas
y • There wasnonosignificant
significantdifference
differenceininperinatal
perinatalmortality.
mortality.
• There was no difference in the incidence
y There was no difference in the incidence of CP. of CP.
y • The Theonly
onlyclinical
clinicalbenefit
benefitofofEFM
EFMwaswasa a50%
50%reduction
reductionininneonatal
neonatalseizures.
seizures.
Using aa number-needed-to-treat
Using number-needed-to-treat calculation,
calculation, the
the authors
authors estimated
estimated one
that less
667 neonatal
women would
seizurehave
andto11bemore
continuously
Caesarean
sections could be expected in a cohort of 628 women, continuously monitored, than in a control group monitored with
monitored to prevent one neonatal seizure. However, as many as 61 extra caesarean sections would be associated using
preventing one seizure.70
intermittent auscultation. 61
A normal EFM tracing is indicative of fetal well-being. However, an atypical or abnormal tracing has low predictive value
for poor neonatal outcomes.
The woman and her partner must be informed about the various methods of fetal surveillance and be involved in
Fetal Well-Being
decisions During
about their useLabour
in labour and birth. 168
A normal EFM tracing is indicative of fetal well-being. However, an atypical or abnormal tracing has low predictive value
for poor neonatal outcomes.
The woman and her partner must be informed about the various methods of fetal surveillance and be involved in
decisions about their use in labour and birth.
1. Assessment of Uterine Activity
The fetal heart rate is assessed in relation to the uterine activity pattern. Uterine activity is evaluated to:
−− Identify abnormal contraction patterns that might adversely affect oxygen delivery to the fetus.
−− Correctly classify the FHR patterns with EFM.
FHR patterns detected by intermittent auscultation are not classified using the same terminology
used for EFM.
Normal labour contraction pattern

Methods of assessment
• Palpation by hand. The frequency and duration of contractions, and an estimate of their intensity, as well as
the resting tone can be determined by palpation
• External, electronic, fetal tocodynamometer: only the relative frequency and duration of contractions can
be determined using an external tocodynamometer. The external transducer does not measure intensity or
resting tone. Palpation should be used to determine these characteristics
• An internal intrauterine pressure catheter (IUPC) is the most accurate method. It is not used frequently
because of its invasive nature and the restrictions it places on the woman’s mobility
• A combination of the above techniques 72
The woman’s perception of her contractions should always be considered in conjunction with the above methods.
Characteristics of normal contractions and their assessment:

• Frequency: Uterine contractions are quantified as the number of contractions in a 10-minute window,
averaged over 30 minutes.73 Normal is ≤ 5 contractions in 10 minutes. Tachysystole is > 5 contractions in 10
minutes (averaged over 30 min).
• Duration: Measure from the beginning to the end of the contraction and record in seconds. Normal is < 90
seconds.
• Intensity: Assess how strong the contractions feel on palpation and what type of pain the woman states she
is feeling. The intensity of contractions cannot be measured accurately with an external tocodynamometer.
Intensity evaluation may be estimated by palpation (described as mild, moderate, or strong; with a strong
contraction the uterus cannot be indented). Objective, accurate measurement is obtained only when using

an intrauterine pressure catheter. Normal intensity is > 25 mm Hg and < 75 mm Hg above the baseline
(except in the second stage of labour).74
• Resting tone: The uterine tone is described as soft or firm between contractions by palpation. The uterus
y Resting tone: The
is soft between uterine tone
contractions forisadescribed
minimumasofsoft or firm between
30 seconds to allow contractions by palpation.
adequate placental The uterus
perfusion. Normalis
soft between contractions for a minimum of 30 seconds. Normal resting tone with an IUPC is <
resting tone with an IUPC is < 7 to 25 mm Hg.72 Resting tone cannot be accurately measured using an7 to
25external
mm Hg.tocodynamometer.
62
Resting tone cannot be accurately measured using an external tocodynamometer.
Contractions
Contractions are
are rarely
rarely of
of aa fixed
fixed frequency
frequency or
or duration.
duration. Therefore,
Therefore, frequency
frequency and
and duration
duration may
may be
be expressed
expressed in
in aa range.
range.
For
For example,
example, 22 to
to 33 contractions
contractions inin 10
10 minutes,
minutes, each
each lasting
lasting 50
50 to
to 80
80 seconds.
seconds.
Excessive Uterine Activity

Tachysystole:
Excessive uterine activity can be endogenous (spontaneous) or exogenous (overstimulation of the uterus during labour
Excessive uterine activity can be endogenous (spontaneous) or exogenous (overstimulation of the uterus during labour
induction or augmentation). Most commonly, excessive uterine activity is secondary to the use of oxytocin or another
induction or augmentation). Most commonly, excessive uterine activity is secondary to the use of oxytocin or another
uterotonic agent. If a uterotonic medication is not being used, consider the possibility of a placental abruption.
uterotonic agent. If a uterotonic medication is not being used, consider the possibility of a placental abruption.
Tachysystole
Tachysystole is the term used to describe all forms of excessive uterine activity:
Tachysystole
• >is5the
contractions
term usedper 10-minute
to describe periodofaveraged
all forms excessiveover 30 minutes
uterine activity:and/or
• Inadequate resting tone: uterine resting period between contractions of < 30 seconds OR the uterus does
y >not 5 contractions per 10-minute
return to resting tone betweenperiod averaged over
contractions, 30 minutes and/or
and/or
y • Inadequate
Prolonged resting tone: lasting
contraction: uterine>resting period between contractions of < 30 seconds OR the uterus does not
90 seconds
return to resting tone between contractions, and/or
Note: yIf EFM tracing iscontraction:
Prolonged atypical or abnormal
lasting > in90the first 10 minutes of tachysystole a response is required without waiting
seconds
30 minutes
The terms hypercontractility and hyperstimulation (previously used to describe excessive uterine activity with atypical or
The terms FHR
abnormal hypercontractility andbe
tracings) should hyperstimulation
abandoned.63 (previously used to describe excessive uterine activity with atypical or
abnormal FHR tracings) should be abandoned.73
Tachysystole – Normal Tracing
Tachysystole – Normal Tracing

Tachysystole – Abnormal Tracing Tachysystole – Abnormal Tracing
1.
1. Intermittent
Intermittent Auscultation
Auscultation of the Fetal Heart Sounds
Intermittent auscultation is the preferred technique for intrapartum fetal surveillance in low-risk pregnancies if the
(Adapted
following from Fundamentals
criteria are met: of fetal health surveillance: a self-learning manual. 4th ed. Halifax: Canadian Perinatal
Programs Coalition; 2009.62)
• The presence of practitioners experienced in the technique of auscultation, palpation of contractions, and the
Intermittentrecognition
auscultationofisabnormal FHR technique
the preferred patterns onforauscultation
intrapartum fetal surveillance in low-risk pregnancies if the
following The existence
• criteria are met: of a delivery unit protocol / guideline addressing the technique and frequency of assessment
• The presence of a delivery unit guideline outlining the clinical interventions to be used when abnormal FHR
y The presence
findings are of practitioners experienced in the technique of auscultation, palpation of contractions, and the
present
• recognition
The presence of abnormal FHR patterns
of an educational on auscultation.
program to provide fundamental knowledge and to regularly update all staff
y The regarding the delivery unit IA protocol / guidelineaddressing
existence of a delivery unit protocol / guideline the technique
and the steps in clinical and frequencyforofabnormal
intervention assessment
FHR(for
anchanges
exampledetected
go to URL: http://sogc.org/wp-content/uploads/2013/01/gui197CPG0709r.pdf).
on IA
y • The presence of a delivery
The ability to provide skilled unitnursing
guideline outlining
support on athe
1:1clinical interventions
basis once auscultationto be used when
is required abnormal
every 15 minutes
FHR findings
or less are present (for an example go to URL: http://sogc.org/wp-content/uploads/2013/01/
gui197CPG0709r.pdf).
Benefits
y ofTheIntermittent
presence ofAuscultation:
an educational program to provide fundamental knowledge and to regularly update all staff
• regarding
Less costlythethan
delivery unit IAEFM
continuous protocol / guideline and the steps in clinical intervention for abnormal FHR
• changes detectedforonthe
Less restrictive IA.woman (permits increased freedom of movement)
y • The ability totoprovide
Adaptable varied skilled nursing support
labour positions on a 1:1
and practices basis
(e.g., onceimmersion)
water auscultation is required every 15 minutes
• or less.
Lower intervention rates, compared with EFM, without compromising neonatal outcome 1
Limitations of Intermittent Auscultation:
• May be difficult to auscultate fetal heart sounds in obese women
• Some women find it intrusive because of the frequency of auscultation

What is assessed with IA?

• Contraction pattern
• Maternal heart rate (MHR) to differentiate from FHR
• Baseline FHR (the heart rate counted in bpm for 1 minute between contractions)
−− Assessing the FHR is an indirect method for evaluating fetal oxygenation and well-being. Regulation of
the FHR is under the influence of intrinsic (autonomic nervous system) and extrinsic factors.
−− The average fetal heart rate decreases as gestational age increases. It is determined by a pacemaker in
the sino-atrial node in the heart.
−− FHR changes are primarily controlled by a balance between the sympathetic and the parasympathetic
nervous systems. Other factors affecting FHR include
›› Drugs in maternal / fetal circulation
›› Congenital fetal cardiac defects
›› Fetal rest and activity cycles
›› Hypoxemia / hypoxia / acidemia / acidosis
›› Maternal hemodynamics.
• Rhythm (regular or irregular)
• Accelerations and decelerations (abrupt or gradual increases or decreases from the baseline heart rate)
What cannot be assessed with IA?
• Baseline variability
• Classification / type of deceleration heard. There is no research to indicate that a practitioner can distinguish
the type of deceleration on auscultation.75 Therefore, decelerations cannot be classified as they can be when
using EFM
Auscultation technique:
• Palpate the maternal abdomen to identify fetal presentation and position (Leopold’s manoeuvres)
• Assess the uterine contraction pattern by hand; frequency, duration, intensity and resting tone can be
adequately assessed using a hand (or hands) and a watch
• Assess the MHR to differentiate from the FHR
• Place the stethoscope or Doppler monitor over the area of maximum intensity of fetal heart sounds (usually
over the fetal back or shoulder)
• Listen to hear the FHR and place a finger on mother’s radial pulse to differentiate maternal from fetal heart
rate
• Establish a baseline heart rate by listening and counting between uterine contractions for a full minute (60
seconds)
• After the FHR baseline is established, regular assessments immediately after contractions for 30 to 60
seconds will determine whether the FHR is within the same range. In active labour, a 30-second auscultation
period may be more feasible while a 60-second sampling period will improve accuracy.

Table 11 Recommended Frequency Of Intermittent Auscultation During Labour 1

Frequency of assessments, response and documentation should always consider maternal fetal status and will need to
occur more frequently in the presence of abnormal FHS or other changes in the maternal/fetal condition8
1st STAGE: ACTIVE PHASE

1st STAGE: LATENT PHASE 2nd STAGE: ACTIVE PHASE
2nd STAGE: PASSIVE PHASE
• Initial assessment Every 15 to 30 minutes At least every 5 minutes or immediately

• At least every 1 hour if admitted to following each contraction
hospital1
• Individualized based on maternal fetal
status if in triage or midwifery care at
home (not admitted to hospital)
Recommendations for the use of intermittent auscultation

a. IA is preferred for healthy women ≥ 370 weeks’ gestation (up to 413 weeks’ gestation), in spontaneous
labour, and in the absence of risk factors for an adverse perinatal outcome
b. From 413 weeks until 42 weeks’ gestation IA is preferred, provided that a non-stress test and an amniotic
fluid volume assessment are normal. Post-term pregnancy (> 42 weeks’ gestation) is associated with an
increased risk of adverse fetal outcome and EFM is the preferred method of fetal surveillance1
c. Below 370 weeks’ gestation EFM is recommended because the incidence of other pathologies and adverse
outcomes is increased1
d. Intermittent auscultation with epidural analgesia or combined spinal-epidural analgesia
−− Maternal hypotension and fetal heart rate changes are often seen in the first 60 minutes after the
initiation of regional anaesthesia.
›› Combined spinal-epidural analgesia is associated with higher risk of FHR changes than epidural
alone.76
›› The cause of the FHR changes may be related to changes in maternal blood pressure and uterine
and fetal perfusion pressures. The FHR abnormalities are often seen without associated maternal
hypotension and other factors play a role.77
−− In general, epidural and spinal anaesthesia, in the absence of maternal hypotension or uterine
hypertonus, cause minimal changes in the FHR.78
−− The use of IA is appropriate after initiation of regional analgesia.
−− It is recommended that the frequency of auscultation be increased to every 5 minutes for 30 minutes
after the initial dose of an epidural and following any epidural bolus injection (top-up), as long as
maternal vital signs are normal.1
−− Patient-controlled epidural analgesia (PCEA) uses a dilute local anaesthetic and opioid solution rather
than the bolus of concentrated local anesthetic agents used in spinal and traditional continuous
epidurals. It has been proven to be safe for ambulation in labour and hypotension does not occur
after a self-administered bolus.79, 80 Therefore, IA is acceptable when PCEA is used, and the FHR does
not need to be monitored after each PCEA self-administered dose. IA should be done according to the

usual obstetrical protocols. The use of EFM in this circumstance should be based solely on obstetrical
considerations.1
If maternal hypotension is a persistent problem, continuous EFM should be initiated.
e. For women attempting vaginal birth after Caesarean section, continuous EFM is recommended.
f. IA assessment:
Assess FHR before:
• Initiation of labour-enhancing procedures (e.g., amniotomy)
• Administration of medications
• Administration or initiation of analgesia / anaesthesia
• Patient transfer
Assess FHR after:
• Admission of woman
• Artificial or spontaneous rupture of membranes
• Vaginal examinations
• Tachysystole (if persistent convert to EFM)
• Any abnormal event during labour (e.g., maternal hypotension)
IA Interpretation
1. Normal
• Normal contraction pattern
• Normal baseline rate (110 to 160 bpm)
• Presence of accelerations
−− accelerations suggest the presence of fetal well-being. However, since auscultation is done
intermittently, the absence of accelerations on its own is not necessarily concerning and does not make
the auscultation findings “abnormal.” When considering the significance of the absence of accelerations
and whether other actions to determine fetal well-being are indicated, it is important to consider the
auscultation findings in light of the total clinical picture, including the general activity of the fetus, the
stage of labour, and other risk factors.
• Regular rhythm
2. Abnormal
• Tachysystole8182
• Abnormal baseline rate

−− tachycardia (FHR >160 bpm for 10 minutes)
−− bradycardia (FHR < 110 bpm for 10 minutes)
−− Changing FHR baseline (increasing or decreasing over time)1

• Presence of decelerations
• Arrhythmia: An irregular heart rate not associated with uterine activity. An arrhythmia requires further
assessment and EFM
• In the presence of abnormal FHR characteristics detected by intermittent auscultation that

are unresponsive to maternal position change, increased surveillance by continuous EFM and
consideration of fetal scalp sampling or delivery considered.
• If EFM is initiated in response to abnormal IA, EFM does not need to remain in place for the remainder of the
labour. Once a normal EFM pattern has been confirmed, usually for a minimum of 20 minutes, the EFM may
be removed and IA resumed.

3. Electronic Fetal Monitoring

Terminology
Tachysystole Describes all forms of excessive uterine activity
Periodic patterns Those associated with uterine contractions
Episodic patterns Those not associated with uterine contractions.
Repetitive decelerations 3 or more decelerations in a row
Recurrent decelerations Occur with ≥ 50% of contractions in a 20 min. window
Intermittent decelerations Occur with < 50% of contractions in a 20 min. window
Episodic gradual deceleration Gradual deceleration not associated with a contraction
Interpretable EFM tracing EFM tracing that has a continuous display of the UA and FHR with minimal gaps
Admission EFM Tracing (cardiotocography or CTG) Assessment

A 2012 Cochrane review compared the effects of admission CTG with IA on maternal and infant outcomes for women
without risk factors (n = 13000).83
• Main results:
−− although the difference is not statistically significant if the strict P < 0.05 criterion is used, women
allocated to admission EFM had a higher probability of Caesarean section than women assessed with IA
(risk ratio [RR] 1.20, 95% confidence interval [CI] 1.00 to 1.44, 4 trials, 11 338 women)
−− women having admission EFM had significantly increased use of continuous EFM during labour (RR
1.30, 95% CI 1.14 to 1.48, 3 trials, 10 753 women) and fetal blood sampling (RR 1.28, 95% CI 1.13 to
1.45, trials, 10 757 women)
−− no difference was found in the rate of instrumental vaginal birth (RR 1.10, 95% CI 0.95 to 1.27, 4 trials,
11 338 women), fetal and neonatal deaths (RR 1.01, 95% CI 0.30 to 3.47, 4 trials, 11 339 infants) or
other secondary outcomes
• For women at low risk:
−− contrary to its present use, there is no evidence of benefit for the use of admission CTG, and it should
not be used
−− admission EFM probably increases the CS rate by approximately 20%
−− women should be informed that admission CTG is likely associated with an increase in the incidence of
Caesarean section without evidence of benefit83, 84
• These recommendations are supported by a 2018 multicentre randomized trial of 3045 low risk healthy
women presenting with signs and symptoms of possible labour compared admission assessment with IA
vs. EFM. The study found no statistical difference in caesarean section (however, low adherence to the study
protocol made study quality questionable) but did find a statistically significant increased use of continuous

EFM during labour in the EFM group, therefore supporting the use of IA when assessing low risk women with
signs and symptoms of possible labour 85.
Recommendations:
• Admission EFM tracing assessments are not recommended for healthy women at term in labour in the
absence of risk factors for adverse perinatal outcome as they may lead to unnecessary interventions, and
there is no evident benefit1
• Admission EFM tracing assessments are recommended for women with risk factors for adverse perinatal
outcome1, 86, 87
Methods of electronic fetal monitoring:
• External: An ultrasound transducer (heart sound detection) and tocodynamometer (uterine pressure
measurement) are applied to the woman’s abdomen and held in place by external belts or adhesive strips.88
Advantages:
−− Non-invasive
−− Does not require a dilated cervix
−− Does not require ruptured membranes
Disadvantages:
−− Need for re-adjustment with maternal or fetal movement
−− Possibility of false or misleading recording of heart rate
−− Inability to record intensity of contractions
−− The ultrasound transducer may record the maternal pulse and may not obtain a clear tracing in obese
women or women with polyhydramnios. Also, artefact may be recorded, and there may be doubling or
halving of the FHR when it is outside the normal range
−− The tocodynamometer indicates approximately when the uterine contractions start and end but does
not measure the intensity of the contractions
›› Internal: A spiral electrode to record the fetal heart rate is attached to the fetal scalp through the
maternal vagina and cervix. This should be considered any time EFM is indicated when external
monitor is not possible or effective. Eg. Obesity, during epidural placement. . When using a
spiral electrode it is essential to concurrently verify the maternal pulse to differentiate it from the
presumed fetal heart rate.1
›› Membranes must be ruptured. Uterine activity may be assessed concurrently using an external
tocodynamometer or an IUPC.
Contraindications to the use of a spiral electrode:
• Placenta previa
• Face presentation
• Unknown presentation
• HIV seropositivity
• Active genital herpes

• Maternal hepatitis B or C
• Intrauterine infection
An IUPC is placed into the uterine cavity through the open cervix and transmits pressure changes in the uterus. An IUPC
accurately measures the intrauterine resting tone and the intensity, duration, and frequency of contractions.
An IUPC:
• Provides an accurate measure of intrauterine pressure
• Provides a more accurate assessment than external monitoring of the relationship between contractions and
FHR pattern changes
• Is useful in cases of dysfunctional labour
• Is useful in obese women when external monitoring is unsatisfactory
• Allows women greater mobility than external pressure monitoring
• An IUPC may be useful when:
• Contraction strength is difficult to assess clinically (e.g., obesity)
• Oxytocin doses above 30 mU/min are required
• Augmenting labour in women with a prior CS scar
• Amnioinfusion is required to treat variable decelerations due to cord compression.
The relative risks and benefits of the use of IUPC in the case of undiagnosed vaginal bleeding or intrauterine infection
must be considered, as must the contraindications listed above for the spiral electrode.
Studies addressing fetal and maternal risks of internal monitoring report differing conclusions:
• A 2003 Alberta retrospective review of 90 cases of early-onset GBS disease (between 1993 and 1997), at a
time before the recommendation for universal GBS maternal screening, identified intrauterine monitoring
as an independent risk factor for early-onset GBS disease (odds ratio [OR] 2.24; 95% CI 1.22 to 4.13)89
• A case–control study (covering the years 2000 to 2011) of 40 cases of early-onset neonatal sepsis made up of
8 GBS, 11 Escherichia coli, 12 coagulase-negative staphylococci, 4 viridans group streptococci, 1 Enterococcus
faecalis, and 4 other non-specified organisms versus 80 controls, did not demonstrate a significant
relationship between fetal scalp electrode (FSE) use and early-onset neonatal sepsis90
• A 2013 retrospective cohort study by Harper et al. compared women in labour with (n = 3944) and without
(n = 2501) internal monitors (FSE, IUPC, or both)91
−− the use of a fetal scalp electrode alone was not associated with adverse neonatal outcome (a composite
of 5-minute Apgar score < 3, cord pH < 7.1, cord base excess <−2, or admission to level 3 nursery) or
with maternal fever
−− the use of an IUPC alone (adjusted OR, 2.4; 95% CI, 1.8 to 3.2) or the combined FSE and IUPC (adjusted
OR, 2.0; 95% CI, 1.6 to 2.5) was associated with an increased risk of maternal fever but no increase
in adverse fetal outcome. These outcomes were corrected for time from rupture to delivery ≥ 12 hours,
primiparity, group B streptococcus status, and regional anaesthesia. The authors recommended that an
IUPC be used only when external monitoring is inadequate.91
• A 2013 Cochrane review of 3 studies (n = 1945) comparing the ROUTINE USE of internal versus external
tocodynamometry during induced or augmented labour found no differences for any of the outcomes

studied. These included uterine rupture, hyperstimulation, Apgar score < 7 at 5 minutes, umbilical artery
pH, admission to NICU, mode of delivery or instrumental deliveries, maternal infection, neonatal sepsis or
morbidity, and hospital costs.92
Indications for continuous EFM
EFM is recommended for women at risk for adverse perinatal outcome. Pregnancy complications such as hypertension,
placental abruption, fetal growth restriction, multiple pregnancy, prematurity (< 370 weeks), post-term (≥ 420 weeks),
and chorioamnionitis have been associated with an increase in FHR abnormalities and the development of neonatal
encephalopathy, CP, and perinatal death.40, 93 Although there is insufficient evidence to indicate the conditions in which
better outcomes are expected with EFM than IA, it seems reasonable to recommend the use of EFM in the following
situations, as recommended by the Royal College of Obstetricians and Gynaecologists.40
Ambulation remains an important component of care during labour when EFM is being used. When possible, support
maternal upright positions, ambulation and hydrotherapy such as with the patient standing beside the bed, squatting
and kneeling. Where available, use wireless and waterproof technology that allows position changes, hydrotherapy and
movement during labour and pushing.1
Antenatal & intrapartum conditions associated with an increased risk of adverse fetal outcome* where intrapartum electronic fetal
surveillance may be beneficial
• Hypertensive disorders of pregnancy

• Diabetes: Pre-existing and gestational
• Antepartum hemorrhage
• Maternal medical disease (cardiac, anemia, hyperthyroidism, vascular disease, renal disease,
Maternal
smoking7)
• Motor vehicle collision / trauma (EFM recommended for a minimum period of 4–6 hrs)94, 95
• Pre-pregnant BMI >35 kg/m2(see below) 11
• Maternal perception of reduced or absent fetal movement96

• Prematurity (< 370 weeks)
Antenatal • Oligohydramnios
• Polyhydramnios14
• Abnormal umbilical artery Doppler velocimetry
• Abnormal BBP or NST
Fetal • Isoimmunization
• Multiple pregnancy
• Breech presentation13
• Significant congenital anomaly (compatible with life)97
• Single umbilical artery24
• 3 or more nuchal loops19
• Velamentous cord insertion 22, 98

Antenatal & intrapartum conditions associated with an increased risk of adverse fetal outcome* where intrapartum electronic fetal
surveillance may be beneficial
Intrapartum Maternal • Vaginal bleeding in labour

• Intrauterine infection / chorioamnionitis
• Previous CS/Trial of labour after CS99
• Prolonged rupture of membranes (> 24 hours at term)
• Combined spinal-epidural analgesia 76
• Oxytocin induction or augmentation100
• Hypertonic uterus
• Preterm labour (< 370 weeks)
• Post-term pregnancy (> 42 weeks)
• Tachysystole
• Labour dystocia
• Limitations in reliably determining UA and FHR with IA (e.g. maternal position or obese body
habitus)
Fetal • Meconium staining of the amniotic fluid101-103 104

201
• Abnormal FHR on auscultation

• Breech presentation13
• FHR dysrhythmia
* Adverse fetal outcome is defined as cerebral palsy, neonatal encephalopathy, and perinatal death. Adapted from: The use of electronic fetal monitoring: the use
and interpretation of cardiotocography in intrapartum fetal surveillance [Evidence-based clinical guideline no 8]. May 2001.40
BMI
Because of the adverse perinatal outcomes sometimes associated with maternal pre-pregnancy BMI >35, intrapartum
EFM could be considered. Due to the limitations in reliably determining uterine activity and FHR with IA or external EFM
in the presence of obese maternal body habitus, the use of a FSE and/or an IUPC should be considered.
Epidural analgesia and intermittent auscultation

Epidural analgesia may cause maternal hypotension, which will decrease uteroplacental perfusion and result in
intrapartum fetal heart rate abnormalities. These abnormalities usually occur in the first 30 to 60 minutes after initiation
of the epidural. Although some authorities include epidural analgesia as an indication for continuous EFM, there is little
research to suggest best practice. The SOGC Intrapartum Fetal Surveillance guideline states that intermittent auscultation
may be used to monitor the fetus when epidural analgesia is used during labour, provided that a protocol is in place for
frequent IA assessment (e.g., every 5 minutes for 30 minutes after epidural initiation and after bolus top-ups as long as
maternal vital signs are normal).
Following epidural anaesthesia during labour, morbidly obese women (BMI ≥ 40 kg/m2) have more frequent
hypotension and fetal heart rate abnormalities than normal weight women (BMI < 25 kg/m2). This supports the
recommendation that these women receive continuous EFM.105

PCEA is different from an intermittent bolus technique with concentrated local anaesthetic agents. It is used with
dilute local anaesthetic and opioid solution (≤ 0.125% bupivacaine or equivalent). PCEA has been proven to be safe
for ambulation in labour, and there is no evidence supporting the need for maternal vital signs to be taken after a
self-administered bolus, as hypotension does not occur. Since maternal hemodynamics are stable with PCEA, there
is no need to monitor the FHR after each self-administered PCEA top-up, which means that IA is acceptable and
should be carried out according to usual obstetrical protocols, and that use of EFM should be based upon obstetrical
considerations.
Systematic Interpretation of EFM Tracings
Principles:
Classify Tracing
å
Interpret clinically (in light of total situation)
å
Respond (communication and teamwork)
A consistent and systematic analysis and interpretation of EFM tracings must be used by all care providers involved in a
labouring woman’s care. Analysis refers to defining and measuring the characteristics of the tracing, and interpretation
refers to the clinical meaning attributed to these measurements.1 Consistency is the key to achieving effective
communication with other health care providers and patients, to accurate documentation, and to ensuring steps are not
missed in the assessment process.
The definitions and explanations in this section are based in part on the recommendations from the 2008 NICHD
Workshop on Electronic Fetal Monitoring. This NICHD workshop was convened to revisit nomenclature, interpretation,
and research recommendations for EFM.73 An adequate tracing of the FHR and uterine contractions is required. EFM
tracings are dependent on fetal gestational age and fetal and maternal physiologic status, which should therefore be
factors in the assessment and evaluation of EFM. It is essential that the EFM tracing effectively demonstrates both the
uterine activity and the FHR. FHR patterns are categorized as baseline, periodic, or episodic. Periodic patterns are those
associated with uterine contractions, and episodic patterns are those not associated with uterine contractions. A full
description of EFM requires an assessment of maternal risk factors and a qualitative and quantitative description of
• Uterine activity characteristics (frequency, duration, intensity of contractions, and resting tone)
• Maternal heart rate (MHR)
• Baseline FHR
• Baseline FHR variability
• Presence of accelerations
• Presence of decelerations
• Changes or trends in FHR tracings over time
• Classification of the tracing (normal, atypical, or abnormal)

• Overall interpretation of the surveillance

• Response (communication and teamwork)
Electronic fetal surveillance should be reviewed and documented with the same frequency as intermittent auscultation.
The Process of Systematic Interpretation

1. Is the tracing interpretable?
−− Is the uterine activity reliably recorded?
−− Is there FHR artefact interfering with the accurate interpretation? Maternal heart rate (MHR) artefact has
been found to be present in as many as 55% of EFM tracings. The MHR tracing can look quite similar to
a normal FHR tracing, particularly in the active second stage when the mother may be tachycardic and
displaying increases in heart rate with pushing. Consider simultaneous maternal (eg. using the finger
O2 saturation monitor) and fetal heart rate monitoring in labour particularly during the second stage106
It is important to note that in the case of fetal demise a spiral electrode may detect the maternal HR.
−− Some external fetal monitors provide the option of monitoring the MHR and FHR (one or multiple)
simultaneously. When the MHR or FHR(s) are similar, these monitors may emit “Coincidence Alarms”
indicating that that supposed FHR may be maternal or the FHR from one fetus is actually derived from
another. Providers need to be knowledgeable about the monitoring system and how to communicate
and respond to these alarms, including: repositioning the transducers, alternative methods of MHR
assessment (e.g. palpation, SpO2 monitor) and using FECG or direct visualization FHR with US.
−− Is there continuous recording, or are there spaces that make interpretation difficult or impossible?
−− Is the tracing of a sufficient time period to permit an accurate interpretation?
−− Does the quality of the uterine activity and FHR pattern allow for accurate interpretation?
2. What is the paper speed and graph range?

−− Paper speed should be standardized within each region and institution.
−− Appearance of FHR patterns is dramatically different with different paper speeds.
−− The 2019 SOGC guideline on intrapartum fetal surveillance recommends that in Canada institutions
should standardize to a national paper speed of 3 cm/min1. For this reason, only 3 cm/min. tracings are
included.
3. What is the mode of monitoring (external or internal)?
4. What is the uterine activity pattern?
−− Contraction frequency (number present in 10 minutes averaged over 30 minutes)
−− Contraction duration (in seconds)
−− Contraction intensity (mild, moderate, or strong by palpation if using an external tocodynamometer, or
in mmHg with an IUPC)
−− Uterine resting tone (soft or firm by palpation if using an external tocodynamometer, or in mmHg with
an IUPC)

5. What is the baseline FHR?

−− First, assess maternal heart rate to confirm the EFM detected HR is fetal and not maternal.
−− Baseline FHR is the mean FHR rounded to increments of 5 bpm during a 10-minute segment of the
tracing, excluding accelerations and decelerations and periods of marked FHR variability (segments of
the baseline that differ by > 25 bpm). There must be 2 minutes25 Edition of the ALARM(not
Course Manual
th
of identifiable baseline necessarily
25 th
Edition of the ALARM Course
contiguous) in any 10-minute window or the baseline is indeterminate. It may be necessary to assess Manual
a
previous 10-minute period to determine baseline. The normal baseline rate is 110 bpm to 160 bpm. If
the baseline FHR is less than 110 bpm, it is termed bradycardia. If the baseline FHR is greater than 160
— Identify
bpm,deviations
it is termedfrom
tachycardia.
normal: The presence of either of these findings requires further assessment.
— −−Identify
Identify deviations
deviations fromfrom normal:
normal:
Tachycardia
Tachycardia Tachycardia
Bradycardia Bradycardia
Bradycardia
6. What is the baseline variability?

— Variability
is a normal, physiologic characteristic of the FHR. Variability is largely controlled by the effect of
— Variability is a normal,
the vagus nerve on thephysiologic characteristic
heart. Persistent hypoxia of the FHR.
causing Variability
acidosis affectsis the
largely controlled
autonomic by thesystem
nervous effect of
the vagus nerve on the heart. Persistent hypoxia causing acidosis affects the autonomic nervous
early and results in a decrease in FHR variability. Other conditions that can lead to decreased or absentsystem
Fetal Well-Being During
early Labourin a decrease in FHR variability. Other conditions that can lead to decreased or absent 183
and results
variability include:
variability
› Fetal include:
sleep (most common). Decreased variability associated with a fetal sleep state in a healthy term

−− Variability is a normal, physiologic characteristic of the FHR. Variability is largely controlled by the effect
of the vagus nerve on the heart. Persistent hypoxia causing acidosis affects the autonomic nervous
system early and results in a decrease in FHR variability.
−− Variability refers to the fluctuations in the baseline FHR that are irregular in amplitude and frequency.
It is determined in a 10-minute segment of baseline, excluding accelerations or decelerations. The
difference between the lowest and highest rate is the range and/or amplitude of variability. The terms
absent, minimal, moderate, or marked73 rather than “good” or “poor” are used to classify baseline
variability. Because of the subjectivity of the visual evaluation of variability, careful re-evaluation is
recommended in borderline assessments107
−− Other conditions that can lead to decreased or absent variability include
›› Fetal sleep (most common). Decreased variability associated with a fetal sleep state in a healthy
term fetus is usually less than 40 minutes. It may extend to 90 minutes or more in some
cases. Reduced variability longer than 40 minutes requires confirmation of fetal well-being
›› Medications: narcotics, sedatives, ß-blockers
›› magnesium sulphate infusion is associated with a transient decrease in variability during
the bolus and a clinically insignificant decrease in FHR baseline (average 2.4 bpm) without
any other significant change in FHR patterns.82, 108 FHR variability returns to normal during
maintenance infusion
›› betamethasone109 and dexamethasone may affect variability and fetal movements for 3 days
110
after administration and will return to normal110. Studies report a decrease in fetal heart rate
baseline during day 1 and then an increase during days 2 to 3, whereas variability is increased
during day 1 and then decreased during days 2 to 3. All values return to baseline during
day 495
›› Preterm fetus: variability is usually moderate by 32 weeks’ gestation
›› Fetal tachycardia
›› Congenital anomalies
›› While smoking111
−− Moderate variability reliably predicts the absence of fetal metabolic acidemia at the time it is
observed.73 Such variability can be measured only with EFM
−− Marked variability (sometimes referred to as a saltatory pattern) if present for >10 minutes is a
characteristic of an abnormal FHR tracing
CLASSIFICATION RANGE OF AMPLITUDE
Absent Undetectable
Minimal ≤ 5 bpm
Moderate 6 to 25 bpm
Marked >25 bpm

CLASSIFICATION RANGE OF AMPLITUDE
Absent Undetectable
Minimal ≤ 5 bpm
Moderate 6 to 25 bpm
Marked >25 bpm
— −− Absent
Absentvariability
variability(amplitude
(amplituderange
rangeundetectable)
undetectable)
— −− Minimal
Minimalvariability
(amplituderange
range≤≤55bpm)
bpm)
— −− Moderate
Moderatevariability
(amplituderange
range66toto2525bpm)
bpm)

25
Markedvariability
— −− Marked variability(amplitude
(amplituderange
range>>2525bpm)
bpm)
A sinusoidal pattern is a smooth, sine wave-like undulating pattern in the FHR baseline25 th
with Edition of the ALARM
a cycle frequency of 3 toCourse Manual
5 per minute
that persists for ≥ 20 minutes. The amplitude of the oscillations is usually 5 to 15 bpm.
73 107, 112
This differs from and should not be
confused with FHR variability. The sinusoidal pattern is abnormal and is most frequently associated with fetal anemia and/or
hypoxia.
A sinusoidal pattern is a smooth, sine wave-like undulating pattern in the FHR baseline with a cycle
frequency of 3 to 5 per minute that persists for ≥ 20 minutes.63 The amplitude of the oscillations is usually
5 to 15 bpm.97, 98 This differs from and should not be confused with FHR variability. The sinusoidal pattern is
abnormal and is most frequently associated with fetal anemia and/or hypoxia.
7. Are there periodic (with contractions) or non-periodic (not associated with contractions) changes in the
FHR?
Accelerations
An acceleration is an abrupt increase (onset to peak in < 30 seconds) in FHR that is ≥ 15 bpm above the baseline for
≥ 15 seconds (10 bpm for 10 seconds for gestations < 32 weeks) and < 2 minutes from the onset to the return to
baseline. A prolonged acceleration is an increase ≥ 2 minutes. If the acceleration is sustained for ≥ 10 minutes it is
considered
Fetal a change
Well-Being in baseline
During Labour rate. The presence of accelerations is a normal finding but not necessary during labour
Labour 186
185
to define a tracing as being normal.99
7. 7.AreAre there
there periodic
periodic (with(with contractions)
contractions) or non-periodic
or non-periodic (not associated
(not associated with contractions)
with contractions) changes
changes in the in
FHR?the FHR?
Accelerations
Accelerations
≥ 15 seconds (10 bpm for 10 seconds for gestations < 320 weeks) from the onset to the return to baseline. A prolonged
≥ 15 seconds (10 bpm for 10 seconds for gestations < 32 weeks) and < 2 minutes from the onset to the return to
acceleration is an increase ≥ 2 minutes. If the acceleration is sustained for ≥ 10 minutes it is considered a change in
baseline. A prolonged acceleration is an increase ≥ 2 minutes. If the acceleration is sustained for ≥ 10 minutes it is
baseline rate. The presence of accelerations is a normal finding but not necessary during labour to define a tracing as
considered a change in baseline rate. The presence of accelerations is a normal finding but not necessary during labour
being normal.113 Accelerations, in the presence of an abnormal EFM tracing, do not change the classification but may be
to define a tracing as being normal.99
considered as part of the total clinical situation.
Decelerations
A deceleration is a decrease in the FHR.
• Repetitive decelerations are defined as ≥ 3 in a row.1
• Decelerations are defined as “recurrent” if they occur with ≥ 50% of uterine contractions in any 20-minute
segment. Decelerations occurring with < 50% of uterine contractions in any 20-minute segment are defined
as “intermittent”.73
• Decelerations are distinguished on the basis of their waveform, being either “abrupt” or “gradual” onset:
Fetal Well-Being
1. During
AbruptLabour
(onset of the decrease to nadir <30s) = Variable deceleration
186
2. Gradual, usually symmetrical, decrease & return (onset to nadir ≥ 30s)

a. Early deceleration: Onset, nadir & recovery coincident with onset, peak & end of contraction
b. Late deceleration: Onset, nadir & recovery after onset, peak & end of contraction
Note regarding gradual decelerations:
›› Visually apparent without a depth criteria
›› When not associated with an apparent contraction it is termed an episodic gradual deceleration.
These are usually related to undetected contractions which indicates a reassessment of uterine activity.
Early
• A gradual decrease in the FHR (onset to nadir ≥ 30 seconds) and return to baseline associated with a
contraction. Usually symmetrical, the nadir occurs at the same time as the peak of the contraction. In most
cases, the onset, nadir, and recovery of the deceleration are coincident with the beginning, peak, and ending
of the contraction, respectively.

occurring with < 50% of uterine contractions in any 20-minute segment are defined as “intermittent”.
Early
y A gradual decrease in the FHR (onset to nadir ≥ 30 seconds) and return 26thtoEdition
baseline associated
of the ALARM with a Manual
Course
contraction. Usually symmetrical, the nadir occurs at the same time as the peak of the contraction. In most
cases, the onset, nadir, and recovery of the deceleration are coincident with the beginning, peak, and ending
of the contraction, respectively.
y• Secondary
Secondarytotofetal
fetalhead
headcompression
compression
y• Considered to be benign
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y• Not
Notassociated
associatedwith
withfetal
fetalacidemia
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y • a agradual,
gradual,usually
usuallysymmetrical,
symmetrical,decrease
decreaseandandreturn
returntotobaseline
baselineFHR
FHRininassociation
associationwith
witha auterine
uterinecontraction.
The onset, nadir, and recovery of the deceleration occur after the beginning, peak, and
contraction. The onset, nadir, and recovery of the deceleration occur after the beginning, peak, end of theand
contraction.
end of the
The onset to the
contraction. Thenadir
onsetoftothe
thedeceleration
nadir of theisdeceleration
≥ 30 seconds. is ≥The
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seconds. Thedeceleration
nadir of the occurs after the
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occurs
ofafter
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the peak of the contraction.
y • late
latedecelerations
decelerationsareareassociated
associatedwithwithuteroplacental
uteroplacentalinsufficiency
insufficiencyand
andmaymayimply
implya adegree
degreeofofhypoxia.
hypoxia.100114

Variable
• an abrupt decrease in the FHR. The onset of the deceleration to the nadir is < 30ofseconds.
25th Edition The Course
the ALARM FHR decreases
Manual
to at least 15 bpm below the baseline and the deceleration lasts for ≥ 15 seconds but < 2 minutes.
• may be episodic (not associated with contractions) or periodic (associated with uterine contractions) (if
periodic, their onset, depth, and duration commonly vary with successive contractions).
• the most common decelerations seen in labour
Variable
• uncomplicated variable deceleration
y an−−abruptoftendecrease in the FHR.i.e.,
have “shoulders”, Theanonset
initialofacceleration
the deceleration
followedto thebynadir is <deceleration
a rapid 30 seconds.toThe
theFHR decreases
nadir, a rapid
to at least 15 bpm below the baseline and the deceleration
return to the baseline and a secondary acceleration. 115lasts for ≥ 15 seconds but < 2 minutes.
y may be
−− the episodic (not associated
physiology is thought to with
becontractions)
a baroreceptor or response
periodic (associated with uterine
to cord compression contractions)
in labour. During(ifa
periodic, their onset, depth, and duration commonly vary with successive contractions).
contraction there may be a sequential compression of the umbilical vein first (resulting an initial period
y thought of to be a response to cord compression
hypovolemia/hypotension inducing ainbaroreceptor
labour triggered brief increase in FHR: “shoulder”)
y the most common decelerations seen in labour
followed by the compression of the umbilical arteries (resulting in an increase in fetal BP triggering a
y uncomplicated variable
baroreceptor deceleration:
induced rapid decrease in HR) and finally as the contraction fades the artery is released
— often have “shoulders”, i.e.,
but the vein remains compressedan initial(resulting
acceleration followed
in brief by a rapid
hypovolemia anddeceleration
a secondaryto“shoulder”)
the nadir, auntil
rapidthe
return to the baseline
contraction ends andandthe aFHR
secondary
returns acceleration. 101
to the baseline.
— −− notnotconsistently
consistentlyassociated
associatedwithwitha apoor
poorneonatal
neonataloutcome.
outcome. 3140
• Complicated variable deceleration (may be indicative of fetal hypoxia)115, 116

−− failure to return to baseline by end of contraction.
−− deceleration lasting ≥ 60 seconds AND down to ≤ 60 bpm OR decrease by ≥ 60 bpm below baseline 117 118
−− prolonged secondary acceleration (post-deceleration smooth overshoot) of 20 bpm and/or lasting > 20
seconds
−− variable deceleration in the presence of:
›› absent or minimal baseline variability
›› fetal bradycardia or tachycardia
In a 2018 prospective study by Cahill et al, of 8580 women laboring at ≥ 370 weeks gestation with a singleton cephalic
fetus, the total deceleration area, especially in combination with fetal tachycardia was most predictive of acidemia. This
emphasizes the significance of complicated variable decelerations that meet the criteria by their depth and duration. 117

— a deceleration to less than 70 bpm lasting > 60 seconds
eleration to less
— thanloss70ofbpm lastingin>the
variability 60baseline
seconds FHR
of variability in—the baseline
a biphasicFHRpattern
hasic pattern — prolonged secondary acceleration (post-deceleration smooth overshoot) of more than 20 bpm and/or
onged secondary acceleration (post-deceleration 26th Edition of the ALARM Course Manual
smooth overshoot) of more than 20 bpm and/or
lasting > 20 seconds
ng > 20 seconds — the presence of fetal bradycardia or tachycardia
resence of fetal bradycardia or tachycardia
1. Failure to return to baseline by end of contraction
turn to baseline by endtoofreturn
1. Failure contraction
to baseline by end of contraction
Note: Importance of the timing of the periodic variable deceleration’s recovery

Note: Importance of the timing of the periodic variable deceleration’s recovery
rtance of the timing of•
theItperiodic variable deceleration’s
is very important to recognize whenrecovery
the recovery is delayed after the end of contraction. This delayed
It is very important to recognize when the recovery is delayed after the end of contraction. This delayed recovery
portant to recognize whenrecovery
can be abrupt the can be
recovery
or gradual. is abrupt
delayedorafter
Physiologically
gradual. Physiologically
thetype
this endofofcomplicated
thisThis
contraction. type of complicated
delayed
variable recovery variable
is considered
is considered to have the
to have the same
pt or gradual.significance same
Physiologically significance
this decelerationas a late
type of complicated deceleration and
variable isdefine if repetitive
considered to have define the
the same tracing as abnormal.
as a late and if repetitive the tracing as abnormal.
as a late deceleration and if repetitive
2. Deceleration lasting ≥ 60define the tracing
seconds as abnormal.
AND down to ≤ 60 bpm or decrease by ≥ 60 bpm below baseline (“rule of
2. Deceleration < 70 bpm > 60 sec
n < 70 bpm >60’s)
118,119
60 sec

ing Labour 190

3. Overshoot (20 bpm increase for 20 seconds)
4. Absent or minimal baseline variability
5. Baseline tachycardia or bradycardia

25
26th Edition
th
Edition of
of the
the ALARM
ALARM Course
Course Manual
Manual
Fetal
Fetal Well-Being
Well-Being During
During Labour
Labour 193
192
Prolonged Deceleration
A deceleration of ≥ 15 bpm below the baseline and lasting > 2 minutes but < 10 minutes from onset to return to
baseline. (A deceleration lasting > 10 minutes is a change in baseline heart rate.)
In a 2013 retrospective cohort study of 5388 singleton, non-anomalous gestations that had reached full dilation, Cahill
et al. addressed the significance of prolonged decelerations that precede and are unresolved before delivery (termed
“terminal deceleration”). The last portion of EFM before delivery was analyzed (≥10 minutes and up to 30 minutes,
if available). Overall, decelerations greater than 2 minutes (median duration was 3.3 min) occurred in 17.7% of the
women but of these only 1.3% were found to have a pH of ≤ 7.10. For every additional 120 seconds of duration beyond
2 minutes, a decrease in umbilical artery pH of 0.042 was noted. Decelerations of ≥ 10 minutes (termed “terminal
bradycardia”) were associated with a 12.9% overall incidence of pH of ≤ 7.10.119
8. Classification, (Normal, Atypical or Abnormal tracing), Interpretation and Response
−− Normal: Characteristics are within normal parameters.
−− Atypical: Physiological response. Further vigilant assessment is required, especially when combined
features are present. This may involve the correction of a reversible cause for compromise, intrauterine
fetal resuscitation, and/or further fetal evaluation (scalp stimulation and/or scalp blood sampling if
> 34 weeks, ultrasound)
−− Abnormal: Possible fetal compromise. Action is required. The overall clinical situation should be
reviewed, and intrauterine resuscitation and prompt operative delivery (vaginal or Caesarean section) is
indicated unless delivery is imminent or there is evidence of normal oxygenation by scalp pH or lactate
assessment.
SOGC Classification of intrapartum EFM tracings 1
*Note: It requires the presence of only one feature in the table under Atypical and Abnormal to classify the tracing as
atypical or abnormal

NORMAL TRACING ATYPICAL TRACING ABNORMAL TRACING
Uterine activity • Normal contraction pattern • Tachysystole may be present with normal, atypical or abnormal tracings;
monitor closely for concerning FHR characteristics
Baseline • 110–160 bpm • 100–110 bpm • < 100 bpm

• > 160 bpm for 30–80 min • > 160 bpm for > 80 min
• Rising baseline • Erratic baseline
• Arrhythmia (Irregular rhythm)
Variability • 6–25 bpm • ≤ 5 bpm for 40–80 min • ≤ 5 bpm for > 80 min
• ≤5 bpm for < 40 min • ≥ 25 bpm for > 10 min
• Sinusoidal
Accelerations • Spontaneous accelerations • Absence of acceleration with scalp • Usually absent (presence of
present (but not required113) stimulation accelerations does not change the
• Accelerations with fetal scalp tracing classification)
stimulation
Decelerations • None • Repetitive (≥3) uncomplicated • Repetitive (≥3) complicated

• Non-repetitive uncomplicated variable decelerations variable decelerations
variable decelerations • Non-repetitive complicated • Recurrent late decelerations (with
• Early decelerations variable decelerations ≥ 50% of contractions)
• Intermittent late decelerations • Single prolonged deceleration
(occurring with <50% of > 3 min
contractions)
• Single prolonged deceleration >
2 min but < 3 min
Interpret Clinically No evidence of fetal Physiologic response Possible fetal compromise

compromise • Determine the significance/cause (consider clinical situation)
(in light of total of abnormal tracing: • Determine the significance/cause
situation) • Evaluate total clinical picture: of abnormal tracing:
stage of labor, gestational age, • Evaluate total clinical picture:
risk factors stage of labor, gestational
• Determine duration of effect and age, risk factors
reserve tolerance of the fetus • Determine duration of effect and
reserve tolerance of the fetus
Response EFM may be interrupted for VIGILENCE ACTION REQUIRED

periods of up to 30 min. if • Institute intrauterine resuscitation • Institute intrauterine resuscitation
maternal-fetal condition stable • Communicate the tracing and plan for delivery
and/or oxytocin infusion rate classification to the team and • If clinically appropriate, obtain
stable continue with ongoing fetal fetal scalp blood sampling (>34
monitoring weeks, prolonged deceleration
• Perform fetal scalp stimulation < 3 min)
and consider fetal blood • Undertake transfer / operative
sampling (>34 weeks) delivery promptly UNLESS:
• Consider transfer / delivery if • Tracing improves
tracing persists or deteriorates • Fetal scalp sampling is normal
• Spontaneous delivery is imminent

Considerations:
• Does the classified tracing and its interpretation correlate with the clinical picture including the gestational
age, pregnancy history, presence of risk factors, labour pattern, fetal behavioural state, or other extrinsic
factors likely to influence the EFM tracing?
• Is further assessment and/or action necessary?
• The more atypical or abnormal features of EFM tracings that occur concurrently, the greater is the possibility
of fetal compromise
• It is essential that all EFM tracings are considered in relation to previous EFM tracings. As each tracing is
interpreted, an appropriate clinical action can be undertaken to lessen the impact on the fetus or to remove
the effect entirely
NOTE: if an abnormal or atypical tracing improves with resuscitative maneuvers the response will return to that
applied to the improved tracing. Ongoing clear distinction of MHR and FHR is essential.
ELECTRONIC FHR, POTENTIAL CAUSES, ASSOCIATIONS, AND CLINICAL ACTIONS TO BE CONSIDERED
PATTERN DEFINITION ASSOCIATIONS OR POTENTIAL CAUSES ADDITIONAL CLINICAL ACTIONS
Baseline: 110–160 bpm • Normal physiologic response No action necessary. EFM may be interrupted
for periods up to 30 minutes if all other
surveillance elements are normal, maternal-
fetal condition is stable and, if oxytocin is
being administered, the infusion rate is not
increased.
Bradycardia: 100–110 bpm Maternal: 1. Measure maternal pulse and differentiate

• Hypotension fetal from maternal heart rate
• Drug response 2. Vaginal examination (elevate presenting
• Maternal position part if umbilical cord prolapse)
• Connective tissue diseases with 3. Intrauterine resuscitation (see below)
congenital heart block (e.g., systemic 4. Discontinue oxytocin
lupus erythematosus). 5. Decrease uterine activity (tocolysis) if
indicated
Fetal: 6. If cause is not obvious or correctable,
• Umbilical cord occlusion
consider intrapartum U/S to evaluate
Bradycardia: <100 bpm • Fetal hypoxia / acidosis
dysrhythmia
• Vagal stimulation such as with chronic
7. If persistently <100 bpm, and/or
head compression or with vertex associated with other borderline patterns
presentation, occipital posterior or of concern:
transverse position a. obtain scalp sample if clinically
• Fetal cardiac conduction or structural
appropriate
defect b. expedite delivery

Tachycardia: > 160 bpm for 30–80 minutes Maternal: 1. Assess maternal temperature
or rising baseline • Fever 2. Decrease maternal temperature (if
• Infection elevated)
• Dehydration 3. Review maternal medications
• Hyperthyroidism 4. Discontinue oxytocin
• Endogenous adrenaline or anxiety 5. Consider: the duration of rupture of
• Medication or drug response membranes (ROM), positive vaginal
• Anemia culture, especially group B streptococcus
(GBS)
Tachycardia: > 160 bpm for > 80 minutes or Fetal: 6. Intrauterine resuscitation
erratic baseline • Infection
7. If cause is not obvious or correctable,
• Prolonged fetal activity or stimulation
consider intrapartum U/S to evaluate
• Chronic hypoxemia
arrhythmia
• Cardiac abnormalities
8. If persistent (> 80 min):
• Congenital anomalies
a. obtain scalp sample if clinically
• Anemia
appropriate
b. expedite delivery
Irregular FHR • Possible fetal arrhythmia Initiate EFM and further investigations as
indicated
Moderate Variability: • Interaction between the fetal sympathetic No action (normal response)
6–25 bpm and parasympathetic nervous system
≤ 5 bpm for < 40 min. (autonomic nervous system)
Minimal variability: • Fetal sleep 1. Review history for predisposing factors

≤ 5 bpm for 40–80 min • Prematurity (prematurity, medications, etc.)
• Medication (analgesics, sedatives) 2. Attach fetal scalp electrode if possible
• Hypoxic acidemia 3. Obtain fetal scalp sample if clinically
appropriate
4. Prepare for delivery
Absent (undetectable) variability: • Fetal sleep 1. Attach fetal scalp electrode if possible
undetectable or minimal (≤ 5 bpm) for >80 • Prematurity 2. Obtain fetal scalp sample if clinically
min • Medication (analgesics, sedatives) appropriate
• Hypoxic acidemia 3. Prepare for delivery
• Mild hypoxia
Marked variability: ≥ 25 bpm for >10 • Fetal gasping
minutes • Unknown

Sinusoidal pattern • Severe fetal anemia (Hb <70) 1. Consider clinical picture
• Tissue hypoxia in fetal brain stem 2. Attach fetal scalp electrode if possible
• May be transiently present with a healthy 3. Consider fetal scalp stimulation
fetus 4. Consider APT test or Kleihauer Betke;
middle cerebral artery Doppler if
Note: Pseudosinusoidal patterns may be available
similar but are usually transient and retain 5. Prepare for delivery
moderate variability and associated with
good fetal outcomes. May be associated with
medications including narcotic analgesia.120
Accelerations: • Normal FHR response to increased fetal No action (normal response)

activity
Spontaneous May be due to occlusion of umbilical
• Direct sympathetic stimulation of the
vein only, as in association with variable
Periodic fetus
decelerations (see text)
• Occlusion of umbilical vein only
In the presence of atypical or abnormal • Hypoxic acidemia 1. Attach fetal scalp electrode if possible
tracing absent acceleration with fetal scalp • Possible fetal abnormality 2. Obtain fetal scalp sample if clinically
stimulation appropriate
3. Prepare for delivery
Early decelerations: • Associated with head compression No action (normal response)

• Gradual decrease (onset to nadir ≥30 • Not normally associated with fetal
seconds) and return to baseline acidemia.
• Onset, nadir, and recovery of deceleration
coincident with the beginning, peak, and
ending of contraction
Occasional (<3) uncomplicated variable • Not usually associated with poor neonatal 1. No action necessary (normal response)
decelerations: outcome 2. Very common in labour
• Initial acceleration 3. Occurs in more than half of second stages
• Rapid deceleration to the nadir
• Rapid return to baseline
• Secondary acceleration
Repetitive (≥ 3) uncomplicated variable Due to cord compression 1. Observe in early first stage of labour
decelerations 2. Watch for development of combined
patterns or complicated variables

Repetitive (≥ 3) complicated variable May be associated with fetal acidemia 1. Intrauterine resuscitation (see below)
decelerations: 2. Amnioinfusion may ameliorate
• Failure to return to baseline by end of 3. Confirm fetal well-being, directly or
contraction indirectly (fetal scalp stimulation, and
• Deceleration lasting≥ 60 seconds AND fetal scalp blood sampling if clinically
down to ≤ 60 bpm or decrease by ≥ 60 appropriate
bpm below baseline 1 4. Prepare for delivery
• Prolonged acceleration after deceleration
(smooth overshoot) of >20 bpm and/or
lasting > 20 sec
• Loss of baseline variability
• Presence of tachycardia or bradycardia
Occasional late decelerations • May be a response to uteroplacental 1. Mother in left lateral position
Single prolonged deceleration >2 min but function during labour (e.g., reduced 2. Check maternal vital signs
<3 min uterine blood flow associated with 3. Continue to observe
maternal position)
• Fetal chemoreceptor / vagal response
• May be associated with transient fetal
acidemia
Late decelerations: >50% of contractions • Fetal chemoreceptor / vagal response When persistent and repetitive, it is
due to decreased pO2 mandatory to act upon this pattern
A gradual decrease and return to baseline • Altered maternal blood flow to the 1. Intrauterine resuscitation
FHR in association with a uterine contraction. placenta (e.g., maternal hypotension) 2. Obtain fetal scalp sample if clinically
The onset, nadir and recovery of the • Reduced maternal arterial oxygen appropriate.
deceleration occur after the beginning, peak, saturation 3. Prepare for delivery
and end of the contraction. The onset to the • Placental changes altering maternal-
nadir of the deceleration is usually > 30 fetal gas exchange (e.g., placental
seconds and the nadir is beyond the peak of insufficiency, uterine hypertonus or
the contraction. tachysystole)
• May be associated with fetal acidemia
Single prolonged deceleration: >15 bpm • Fetal baroreceptor and chemoreceptor 1. Vaginal examination to rule out cord
for >3 min response to profound changes due to: prolapse
• uterine tachysystole 2. Prepare for delivery
• severe umbilical cord compression
• maternal hypotension
• maternal seizure
• rapid fetal descent

Inadequate tracing for interpretation 1. Ensure that equipment is working

properly
2. If external monitor is in use, reposition to
obtain a clear continuous signal
3. Anticipate need for internal monitoring,
if unable to maintain a technically
adequate tracing despite interventions
4. Confirm uterine activity pattern and
uterine resting tone by abdominal
palpation
5. Assess and document the maternal heart
rate concurrently with the fetal heart rate
to differentiate maternal from fetal heart
rate
6. If using internal EFM, confirm the
presence of fetal heart sounds by
auscultation
EFM monitor HR Coincidence Alarms In singleton gestation, suggest that the 1. Reposition transducers
supposed “fetal” HR signal may be the MHR. 2. Consider alternative methods of
monitoring the MHR including digital
In multiple gestation, may indicate the same palpation, SpO2 monitor
or that the supposed FHR signal from one 3. Consider fetal scalp electrode and/or
fetus is actually derived from another fetus. bedside US to directly visualize FHR
Scalp stimulation1
Digital fetal scalp stimulation provides an indirect assessment of acid-base status.121, 122 It elicits a sympathetic nervous
system response. The fetal scalp is stroked lightly for 15 seconds during a vaginal examination. Gentle digital scalp
stimulation is recommended. Applying substantial pressure may produce a vagal response in the fetus and result
in bradycardia. An FHR acceleration secondary to this stimulus suggests a normoxic fetus.121-123 Digital fetal scalp
stimulation should not be used as a resuscitative intervention.
A 2018 Irish prospective study of 298 fetal scalp stimulations (FSS) followed by fetal blood sampling (FBS) done in
response to abnormal EFM tracings found that FSS resulted in an acceleration or normal variability in over 80% of those
with scalp pH ≥ 7.25, providing reassurance of fetal wellbeing. Reassuringly, all neonates classified as normal by FSS,
but abnormal by FBS (pH ≤ 7.20) had normal Apgar scores and cord pH results. The study suggested that FSS has the
potential to be a reliable and effective alternative to fetal blood sampling in the context of an abnormal EFM tracing.124
• Digital scalp stimulation should not be performed during an FHR deceleration. Decelerations are
secondary to a vagal response that prevents a sympathetic nerve response (acceleration) during scalp
stimulation.125

• An acceleration of 15 bpm amplitude with duration of 15 seconds has a very high negative predictive value
and a very high sensitivity with regard to the absence of fetal acidosis.121, 122
• An acceleratory response is associated with a scalp pH of > 7.20.
• Although an acceleratory response suggests fetal well-being, the absence of an acceleration does not
necessarily predict fetal compromise.
• When acceleration does not occur in response to scalp stimulation, direct assessment with fetal scalp blood
sampling should be considered.
• If fetal scalp blood sampling is not available or possible, consider prompt delivery depending on the overall
clinical situation.
Intrauterine resuscitation1
The goal of intrauterine resuscitation is to improve uterine blood flow, umbilical circulation, and fetal–maternal oxygen
saturation.
NOTE: if an abnormal or atypical tracing improves with resuscitative maneuvers the response should return to
that applied to the improved tracing.
When intrauterine resuscitation is undertaken

• Stop or decrease oxytocin126/remove vaginal PGE2
• Change maternal position (to left or right lateral)
• Check maternal vital signs, including differentiation of MHR from FHR
• Modify or pause pushing efforts if in the second stage of labour
• Improve maternal hydration, with an intravenous fluid bolus, only if indicated eg. maternal hypovolemia
• Evaluate effects of maternal analgesia modality eg. epidural
• Perform a vaginal examination to rule out cord prolapse, relieve pressure from the presenting part on the
cord and assess progress
• Consider tocolysis (e.g., with IV nitroglycerin) in the presence of tachysystole127
• Provide supportive care to reduce maternal anxiety (this reduces catecholamine effects)
• Consider amnioinfusion if variable decelerations are present.
−− A 2012 Cochrane review of amnioinfusion for suspected umbilical cord compression in labour
found that when fetal blood sampling was not used to confirm fetal compromise,128 transcervical
amnioinfusion was associated with the following reductions: Caesarean section overall; FHR
decelerations; Apgar score < 7 at 5 minutes; meconium below the vocal cords; postpartum
endometritis; maternal hospital stay > 3 days; mean cord umbilical artery (Ua) pH was higher with
amnioinfusion group.
−− Perform transcervical amnioinfusion:
›› Instillation of fluid into the amniotic cavity through the cervix via an inserted tube, usually an IUPC
with amnioinfusion capacity (occasionally a 12 to 14 FR pediatric nasogastric feeding tube or Foley
catheter is used).

›› Purpose: used to augment the amniotic fluid volume to decrease the size and frequency of
repetitive and/or complicated variable decelerations associated with low fluid.
›› Prerequisites: ruptured membranes
›› contraindications: chorioamnionitis, low-lying placenta (on ultrasound near term)
›› Complications are rare but include fever and chorioamnionitis
›› Insertion technique: the IUPC is inserted (after membranes ruptured) into the amniotic cavity
beside the fetal presenting part into the uterine cavity. Crystalloid (Ringer’s lactate or normal
saline) is then infused by infusion pump or gravity through the IUPC. There is no benefit in giving
prophylactic antibiotics. There is no evidence that warming the fluid above room temperature is
beneficial129; however, if it is warmed, a blood warmer is recommended.
›› infusion protocol: various options are used: e.g., bolus (50 to 1000 mL) followed by constant
infusion; serial boluses (200 to 1000 mL) given every 20 minutes to 4 hours) or constant infusion.
One documented protocol includes an initial infusion at 10 to 15 mL/minute continued until
decelerations improve when the rate is reduced to 100 to 200 mL/hour.130
›› monitoring: EFM to assess fetal status; intrauterine pressure should be monitored to ensure
satisfactory relaxation between contractions
−− A 2014 Cochrane review assessing amnioinfusion for meconium-stained liquor, in settings with
standard peripartum surveillance, found it to be ineffective in reducing meconium aspiration
syndrome, perinatal death or severe morbidity.131
• Consider administration of oxygen by mask when maternal hypoxia or hypovolemia is suspected or
confirmed.
−− There is little evidence to evaluate its effectiveness when used in the management of suspected fetal
compromise.132 Prophylactic maternal oxygen administration during the second stage of labour has
been associated with abnormal cord blood gas levels at birth, A 2012 Cochrane review found that cord
blood pH values < 7.2 were more frequent when women received prophylactic oxygen (RR 3.51; 95%
CI 1.34 to 9.19).132
−− in 2014, Hamel et al. reviewed the limited evidence available. When supplemental oxygen is given
when suspected fetal hypoxia is not the result of maternal hypoxia:
›› it may correct the fetal hypoxia but will not correct acidosis
›› it can lead to decreased umbilical cord pH, increased need for neonatal resuscitation, and increased
markers of free radical activity
›› it will not reduce the CS rate in the presence of fetal compromise
−− Therefore, maternal O2 supplementation should be reserved for the treatment of maternal hypoxia or
hypovolemia and not used for management of atypical or abnormal fetal heart rate tracings133
Maternal Heart Rate (MHR)1 Assessment with IA or EFM

Assess and document the maternal heart rate concurrently with the fetal heart rate to differentiate maternal from fetal
heart rate1:
a. At initial assessment when confirming fetal life and determining baseline FHR
b. At any time when there is uncertainty between the MHR and FHR.

c. Frequency of assessment and documentation will vary with the stage of labour:
−− In the active first stage and passive second stage of labour every 4 hours with intact membranes;
−− In the active first stage and passive second stage of labour every 2 hours with ruptured membranes;
−− In the active second stage of labour every 15-30 minutes
The incidences of MHR artifact can be a significant and frequent confounder when attempting to interpret the FHR. The
MHR should be verified to differentiate it from the FHR; frequency of assessments will vary with the stage of labour and
FHS. The MHR can be determined using palpation of the radial pulse, oxygen saturation probe or tocodynamometer.
When using the tocodynamometer it is important to initially verify the maternal heart rate on the tracing by concurrent
comparison with the maternal pulse. The use of simultaneous maternal and FHR monitoring for women undergoing
EFM could be considered, especially during the second stage of labour when the work of labour increases the maternal
heart rate. Providers need to be knowledgeable of the monitoring system in their institution, and institutions should
have a clearly communicated process for responding to coincidence alarms and/or cross-channel verifications between
maternal and fetal heart rates.
General considerations and recommendations1

• When a normal tracing is identified, it may be appropriate to interrupt EFM for up to 30 minutes to facilitate
periods of ambulation, bathing, or position change, provided that the maternal and fetal condition is stable,
and, if oxytocin is being administered, the infusion rate is not increased.
• In the case of an atypical intrapartum EFM tracing, any action taken must consider the potential causes, the
duration of the effect, and the reserve (tolerance) of the fetus. Any reversible cause of compromise should
be identified and modified (correction of maternal hypotension, treatment of excessive uterine contractility).
Further fetal evaluation by means of scalp stimulation is recommended, and fetal scalp blood testing (if >
34 weeks) may be considered. Other obstetrical parameters (e.g., gestational age, estimated fetal weight,
presence or absence of meconium,102 and the phase and stage of the labour) will affect decision-making.
Ongoing fetal evaluation is required, and delivery should be considered if the situation persists over time or
if the tracing deteriorates.
• Significance of some EFM Tracing Patterns
−− A 2015 prospective study of 1070 women who had fetal scalp blood lactate analysis performed for EFM
patterns that were not normal found:
›› isolated reduced variability (0 to 4) in most cases was not a sign of lactic acidemia
›› “severe” variable decelerations (defined as abrupt and lasting > 60 seconds) and late decelerations
increased the likelihood of acidemia to the same extent
›› the combination of tachycardia and “severe” variable or late decelerations was associated with the
highest rate of academia
›› fetal scalp lactate was normal in 97.5% of cases with a normal tracing134

Reducing Unnecessary Interventions as a Result of Fetal Surveillance

• The classification system of EFM tracings is intended to be as sensitive as possible to detect fetal acidemia without
a significant false positive rate. A 2012 study reported that the SOGC classification system had an 88% sensitivity
but only 37% specificity for detecting an umbilical arterial pH of ≤ 7.15.135 Although different pH cut-off points
might have yielded different results, it is important to recognize that EFM interpretation is more sensitive than
specific and to consider efforts that may reduce interventions based on false positive EFM interpretation.
Efforts to reduce intervention due to false positive EFM should include:
• Promotion of the use of IA in low-risk pregnancies because of the low incidence of true fetal compromise and
the evidence of increased interventions with EFM for women with low-risk pregnancies.
• Not using “admission tracings” for women without risk factors for fetal compromise
• Assessment of the total clinical picture before making any decision to use EFM
• Fetal scalp blood sampling > 34 weeks’ gestation, if available and possible, to clarify any abnormal FHR
tracing and reduce interventions
• Consideration of intrapartum fetal scalp stimulation. FHR acceleration in response to stimulation suggests
the absence of fetal acidosis, although its absence does not predict fetal acidosis.113
• Consideration of maternal heart rate artefact as the cause106
• Attention to all aspects of the EFM record, including baseline variability. Consideration of the presence of
moderate FHR variability and/or the presence of accelerations to correlate with a high negative predictive
value for severe metabolic acidosis136 and neonatal respiratory morbidity. Intrauterine resuscitation in all
instances of atypical and abnormal tracings (including the reduction or discontinuation of oxytocin and
modifying/pausing pushing in the second stage)
• Regular interprofessional quality assurance and educational fetal health surveillance programs
• Recognition that EFM tracing interpretation is subjective and consequently subject to individual
interpretation82
−− Hindsight bias affects the EFM interpretation and management recommendations when neonatal
outcome is known. Reif et al (2016) reported that 123 health care professionals interpreted 42 tracings
without knowledge of fetal outcome and then again 2 months later with knowledge of the outcome137:
›› When the Ua pH was ≤ 7.0, normal classifications decreased by 76% and “pathologic”
interpretations increased by 51%
›› When the Ua pH was ≥ 7.20 the “pathologic” interpretations decreased by 40%
−− In a 2015 study by Sabiani et al., 22 obstetricians classified the same 30 term intrapartum EFM tracings
twice (3 months apart).34 Their agreement with their own previous interpretations was mediocre and the
agreement with other specialists was low (kappa 0.11 to 0.18).
4. Documentation of Fetal Health Surveillance Assessments (IA and EFM)1

It is essential to document the fetal surveillance throughout both the first and second stages of labour. Documentation
should include the MHR, contraction pattern, FHR patterns, and the classification of IA (normal or abnormal) or the EFM
tracing (normal, atypical or abnormal). Any clinical action taken on the basis of the classification should be documented,
as should the maternal and fetal response to them.

• Accurate and timely documentation of all fetal health assessments and clinical actions taken is essential
• Standardization of documentation tools for both the first and second stages of labour
• Standardization of terminology and acronyms and abbreviations
• Standardization of EFM paper speed
Whatever documentation system is used, the following should be recorded:
Uterine activity characteristics obtained by palpation or electronically:
• Frequency
• Duration
• Intensity
• Relaxation between contractions
MHR
FHR data:
• Indication: if data derived from EFM
• Numerical baseline rate (in bpm)
• Rhythm: if auscultation (regular or irregular)
• Variability: if data derived from EFM
• Nature of changes from the baseline, i.e., acceleration or deceleration (type of deceleration if data derived
from EFM)
The classification, interpretation and response:
• Normal or abnormal IA or normal, atypical, or abnormal EFM tracing
• Specific actions taken when changes in FHR occur
• Maternal and fetal responses to interventions
• Subsequent return to normal findings
• Other maternal observations and assessments
Fetal surveillance should be classified and documented:
• Active first and passive second stages of labour: every 15 to 30 minutes if IA and every 15 min. with EFM.
• Active second stage of labour: every 5 minutes if IA and every 15 min. if tracing and caregiver continuously
present.
Maintaining Standards in Fetal Surveillance

Although there is no best evidence to indicate how often practitioners should update their fetal surveillance knowledge
and skills, periodic review is required. Reviews should be interprofessional to ensure common terminology and shared
understanding and to make it clear that fetal surveillance is a team responsibility. 1
A 2011 systematic review evaluating cardiotocography (CTG or EFM) training programs found that these programs improved
participant reaction, learning, behaviour change, and impact. There was evidence that knowledge was maintained for
6months but clinical skills decreased over that time, suggesting that skills reinforcement training is important. Recognizing

that failure to act and delay in responding to EFM abnormalities are responsible for most cases of suboptimal care, this
review also suggested that training programs include teamwork, communication, and emergency response.138
A 2016 retrospective study evaluated the impact on term neonates of a national multidisciplinary fetal surveillance
education program implemented in Australia and New Zealand in 2004. The outcomes included a significant
improvement in intrapartum hypoxic death, Apgar scores < 5 and rates of hypoxic-ischemic encephalopathy without an
increase in emergency CS in labour.139
The SOGC Board passed the following recommendations in Dec. 2017:
To enhance perinatal safety in Canada, and to improve the quality of intrapartum care provided to labouring mothers:
1. all providers of intrapartum Obstetrical care commit to formal education in fetal surveillance in labour, and
maintain up-to-date status with their education.
2. all providers of intrapartum Obstetrical care participate in regularly scheduled multidisciplinary Obstetrical
skills drills at their hospital.
3. all hospitals that are engaged in Obstetrical care support intrapartum fetal surveillance education for their
physicians, nurses, and midwives, and also assist in the development of regularly scheduled Obstetrical skills
drills for all practitioners.
2018 Canadian Association of Perinatal and Women’s Health Nurses (CAPWHN) Board Position Statement and Recommen-
dations on FHS education:
• All nurses providing pregnancy and intrapartum assessment using fetal health surveillance:
−− Participate in FHS education every 2 years.
−− Maintain documentation of their continuing education.
• FHS education programs should incorporate defined expected outcomes consisting of theory review/update
and face-to-face interdisciplinary case-based education and discussion.
• All health care facilities providing antenatal and intrapartum fetal health surveillance should:
−− Provide opportunities for nurses to attend FHS education.
−− Fund opportunities to enhance FHS knowledge by way of workshops, paid work days, or conference
attendance.
−− Assist in the development and implementation of regularly scheduled ‘obstetrical skills drills’ for all
practitioners (nurses, midwives, physicians and support staff).
Therefore, the following is recommended1:
All providers of intrapartum obstetrical care (Physicians, Nurses, Midwives) should be required to commit to formal
education in fetal health surveillance (FHS) and maintain up to date competence with formal education review every 2 years.
Each facility should provide opportunities for all intrapartum care providers (Physicians, Nurses, Midwives) to regularly
attend an interdisciplinary educational discussion of FHS clinical situations, including both IA and EFM, to ensure
common terminology, shared understanding and to foster the concept of team responsibility.

Other Technologies
Fetal pulse oximetry – Not recommended
This technology is an adjunct to EFM and is intended to continuously monitor intrapartum fetal O2 saturation when an
atypical or abnormal tracing is present. The cervix must be ≥ 2 cm dilated, the fetus must be in a vertex presentation,
and membranes must be ruptured. Sensors may lie against the fetal cheek, temple, or along the fetal back, or attach to
the fetal head by suction or clip.
A 2014 Cochrane review (7 trials, n = 8013)119 compared fetal pulse oximetry and EFM with EFM alone.
• No difference was found in CS (RR 0.99; CI 0.86 to 1.13), CS for dystocia, or in other maternal outcomes
(chorioamnionitis, endometritis, uterine rupture, length of stay or maternal satisfaction) or fetal outcomes
(Apgar scores, Ua pH, NICU admission, skin trauma, death)
• In 2 trials there was a decrease in operative birth (CS, forceps or vacuum) for atypical/abnormal fetal status
but only one small study found any difference in overall operative delivery rates
• The authors concluded that the addition of fetal pulse oximetry does not reduce CS rates. Although there is
limited support for its use when the fetal surveillance is not normal, its use was not recommended.140
This review and others have failed to produce convincing evidence (improved neonatal outcome or reduced operative
delivery rates) for fetal pulse oximetry to be recommended as an adjunct to EFM or as an independent fetal surveillance
technique, and it is not recommended for routine use.1
Fetal electrocardiogram: ST waveform analysis – Not recommended

• This technology is used in combination with standard EFM. Fetal electrocardiogram (ECG) requires a
specialized monitor and proprietary software. It measures the FHR, fetal ECG, and the uterine activity.
• Physiologically, changes occur in the fetal QRS complex and T wave relative to the metabolic state of the
fetal heart. Through analyzing the ST segment and the T/QRS ratio in conjunction with FHR patterns, it is
proposed that decision-making about intervention can be more precise. Care providers need both initial and
continuing training to achieve and maintain expertise in this technique.
• Currently this method uses a fetal scalp clip requiring adequate cervical dilation and ruptured membranes.
A non-invasive abdominal fetal ECG monitor has been developed that uses cutaneous electrodes applied
to the maternal abdomen to detect the fetal ECG. A 2013 study using this method has demonstrated that
the maternal and the fetal heart rate can be simultaneously recorded, which could reduce the chance of
misinterpreting the maternal heart rate as the FHR.141
• A 2015 Cochrane systematic review142 of 6 RCTs, involving 26 446 women, comparing the use of fetal ST
waveform analysis to EFM alone (evidence graded moderate to high), demonstrated
−− No obvious difference in primary outcomes
›› Caesarean section deliveries
›› severe metabolic acidosis (Ua pH < 7.05 and BD > 12 mmol/L)
›› neonatal encephalopathy

−− However, there were

›› fewer fetal scalp samples during labour (RR 0.61; 95% CI 0.41 to 0.91)
›› marginally fewer operative vaginal deliveries (RR 0.92; 95% CI 0.86 to 0.99)
• There was no statistically significant difference in low Apgar scores at 5 minutes, babies requiring neonatal
intubation or admission to special care unit
• The authors concluded that the modest benefit of fewer fetal scalp samplings and instrumental vaginal
births have to be considered against the disadvantages of needing ruptured membranes and the use of
an internal scalp electrode They found little strong evidence that ST waveform analysis had an effect on the
primary outcome measures
Blix et al.143 and Saconne et al.144 published systematic reviews and meta-analyses of the 6 studies included in the 2015
Cochrane review by Neilson.121 Although Blix found a slight reduction in of neonatal metabolic acidosis (OR 0.64; 95%
CI 0.46 to 0.88; NNT 401 to prevent 1 case of metabolic acidosis), this finding was not shared by Saconne et al. (0.5%
vs 0.7%; RR 0.74; 95% CI 0.54 to 1.02). The authors of both studies concluded that the addition of ST analysis does not
significantly improve perinatal outcomes.
The use of ST waveform analysis for the intrapartum assessment of the compromised fetus is not recommended for
routine use.
Intrapartum cardiotocography with computer analysis – Not recommended

• A 2017 trial from the UK and Ireland randomized 47 062 women, with risk factors indicating EFM, to a
computerized interpretation and decision support group or a no computerized-decision-support group. The
authors found no difference in the incidence of poor neonatal outcome between the groups.145
• A 2018 Systematic review with meta-analysis of 3 RCTs (54,492 participants) found that intrapartum fetal
monitoring with computer analysis compared with visual analysis did not decrease the incidence of newborn
metabolic acidosis or obstetric intervention.146

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144. Saccone G, Schuit E, mer-Wahlin I, Xodo S, Berghella V. Electrocardiogram ST Analysis During Labor: A Systematic Review and
Meta-analysis of Randomized Controlled Trials. Obstet Gynecol. 2016;127:127-35.
145. Group IC. Computerised interpretation of fetal heart rate during labour (INFANT): a randomised controlled trial. Lancet.
146. Campanile M, D’Alessandro P, Della Corte L, Saccone G, Tagliaferri S, Arduino B, et al. Intrapartum cardiotocography with and
without computer analysis: a systematic review and meta-analysis of randomized controlled trials. J Matern Fetal Neonatal
Med. 2018:1-7.

Table of Contents
Chapter 9 Vaginal Birth ................................................................................................................................................... 219

Introduction.............................................................................................................................................................. 219
Assessment when birth is imminent........................................................................................................................ 219
Things to ask if possible ............................................................................................................................... 219
Physical Assessment...................................................................................................................................... 219
Consider ....................................................................................................................................................... 220
Signs of imminent birth include .................................................................................................................. 220
Delivery..................................................................................................................................................................... 220
1. Principles................................................................................................................................................... 220
2. Position Mother......................................................................................................................................... 220
3. Equipment................................................................................................................................................ 221
4. Delivery Technique.................................................................................................................................... 221
5. Ongoing Care ........................................................................................................................................... 224
6. Communication and Documentation........................................................................................................ 224
Vaginal Birth 218

Chapter 9
Vaginal Birth
Introduction
The goal of this chapter is to review care of a patient having an imminent birth related to a rapid labour or presenting
late in labour. This information would be useful to any care providers in labour and delivery units. Emergency rooms
as well as paramedics. The care provided will depend on the location, the care providers available, and the status of the
pregnancy and the fetus.
Individual facilities need to adapt the general principles discussed in this chapter according to their location, resources,
and personnel available.
Assessment when birth is imminent

Obstetrical care providers should obtain baseline information by asking clear, concise questions during initial
assessment or when moving to a safe location for birth.
Things to ask if possible

1. Do you have your pregnancy records with you?
2. When is your baby due? / How many weeks are you?
3. Have your membranes ruptured? If so, what colour is the fluid?
4. How many babies have you delivered and were they vaginal or Caesarean section deliveries?
5. Any problems in pregnancy–you or baby?
6. Are you taking any drugs–prescribed by your doctor or recreational or from the health food store?
Physical Assessment
1. Cervical dilatation and fetal position and presentation
2. Fetal Health Surveillance (Contraction pattern and fetal heart assessment by intermittent auscultation or
electronic fetal monitoring)
3. Maternal vital signs
Vaginal Birth 219

Consider
1. Establish IV access and blood work (CBC, X & Type due to PPH risk)
2. Ask additional questions as time permits
a. Results of GBS swab?
b. Has the fetus been moving?
c. Who has been your primary care provider during pregnancy? If it is an obstetrician specializing in high-
risk pregnancies, ensure risk status has been clarified.
3. Obtain antenatal records and ultrasound reports if not available from the patient.
Signs of imminent birth include

• Increased show
• Separation of the labia, bulging perineum and rectum
• Woman says “ baby is coming”1
• Uncontrollable urge to push/bear down
• Sensation of need to have a bowel movement
• Crowning of the presenting part
• Maternal passage of stool
Delivery
1. Principles
The goal is to support a slow and gentle birth in a calm, supportive and safe environment.
• Remain calm—take a deep breath
• Identify yourself to the family
• Use body fluid precautions; use of sterile equipment whenever time and situation allow2
• If delivery is imminent, it is safer to deliver wherever the patient is rather than to attempt transportation to a
birthing unit.
• Transfer site if patient or team at risk
• Try to provide privacy and warmth if in an unplanned location
• Call for equipment and personnel. (e.g.: person skilled in delivery, additional nurses, staff with NRP).
• Remain with the woman; establish rapport and cooperation, provide support and reassurance.
2. Position Mother
Ideally, the parturient’s position should allow good visibility of the perineum and access to permit monitoring of the
fetal heart. It is best to deliver the baby onto a solid surface to increase safety for the baby.
Vaginal Birth 220

3. Equipment
Open equipment for delivery and newborn resuscitation.
An emergency delivery kit should be available for use in non-birthing areas such as the emergency department. A kit
stored in a hospital-grade backpack allows rapid response and staff can carry equipment safely with their hands-free.
If a kit is preset for transport, medications may be stored separately in a medications area near the backpack. Expiry dates
of medications should be regularly reviewed.
Suggestions for a kit
FOR DELIVERY FOR THE INFANT MEDICATIONS
• Gloves, eye protection • Cord clamp • Oxytocin, syringe & needle

• 4 Kelly clamps • Blankets • Misoprostol
• 1 pair scissors • Cord blood syringes and tube or blood
• Towels gas syringes
• Kidney basin
• Sponges
• Documentation forms
4. Delivery Technique
Principles
At the time of delivery, the parturient should be encouraged to adopt whatever positions are comfortable. Encourage a
position that allows visibility and manoeuvres in the event of a concern (e.g., shoulder dystocia).
The obstetrical care provider supporting the birth should
• NEVER take his or her eyes off the perineum once delivery is imminent
• Await restitution of the shoulders and external rotation of the fetal head
• Obtain arterial and venous umbilical cord gases or clamp segment of the cord (pH maintained up to one
hour at room temp)
• Obtain cord blood if the parturient is Rh negative (or if her Rh status is unknown)
Delivery of head
• The woman should be encouraged to push only when she has the urge to do so and to refrain from
prolonged breath-holding (Valsalva) pushing.3
• Use one hand to protect the perineum with gentle pressure using a sponge or cloth. The other hand may
be used to prevent rapid delivery of the head with fingers or hand “lightly placed on the advancing head to
monitor descent and prevent very rapid crowning and extension”.4
Vaginal Birth 221

• Good visualization of the perineum and manual perineal protection has been shown to reduce the risk of
anal sphincter tear.5, 6
• Studies have compared a “hands-on” delivery technique (hands are used to put pressure on the baby’s
head in the belief that flexion will be increased, and to support (“guard”) the perineum, and to use lateral
flexion to facilitate the delivery of the shoulders) with a “hands poised” technique (hands poised, prepared
to put light pressure on the baby’s head in case of rapid expulsion but not to touch the head or perineum
otherwise and to allow spontaneous delivery of the shoulders).7-9 It appears that both hands-on and hands
8
poised techniques are reasonable and that the decision to use one or the other rests with the individual care
provider.3 This recommendation is also supported in the 2014 NICE Guideline on Intrapartum Care.10
• There is evidence that warm, moist packs applied to the perineum in the late second stage may relieve
perineal pain and increase comfort.11 A 2011 Cochrane review (N = 1525) of warm perineal compresses in
labour versus no intervention showed a reduction in third and fourth-degree perineal tears from 5% to 2.5%
(absolute risk reduction 2.5%; number needed to treat = 40 to prevent one anal sphincter injury); however,
no significant difference was found for the outcome of intact perineum.12
• Use a sponge, towel, or bedsheet to cover the anus to prevent contamination of the clean field by maternal feces.
• The parturient should be coached to pant (not push) with crowning,
• The head should, if possible, be delivered between or at the end of a contraction.
Check for nuchal cord

• DO NOT CUT THE CORD until the shoulders are delivered
• If a nuchal cord is found, consider the following:
−− attempting to slide the cord gently over the infant’s head if the cord is very loose
−− pushing the cord back over the shoulder, allowing the shoulder to slip under it as the infant delivers
›› keeping the newborn close to the perineum and having the rest of the body deliver or “somersault”
out.13 This somersault keeps head and torso close to the perineum preventing traction of the cord
Shoulders
• The parturient should be assisted to pant while awaiting restitution, external rotation of the head, and WAIT
until the next contraction to deliver the shoulders.
• In normal birth there is usually a pause between delivery of the head and body. DO NOT RUSH. During this
pause, the uterus relaxes and the fetus restitutes. The drop in the cord pH during this pause is 0.011 per
minute.13 As long as the woman is not pushing and the uterus is relaxed, venous return from the fetal head
to thorax is maintained and therefore so is perfusion of the fetal brain. If fetal heart rate is normal before
delivery, the pause does not alter fetal acidosis and may assist with maternal expulsive efforts.14-16
51
• If the head retracts very close to the perineum after delivery of the head, hyperflex the parturient’s lower
limbs at the hips and lower her head (McRobert’s manoeuvre) while awaiting the next contraction.
• Care providers should NOT PULL ON THE FETAL HEAD or apply downward lateral pressure.
• If the anterior shoulder does not deliver with a contraction, maternal effort, and gentle traction, this indicates
shoulder dystocia. Call for help and begin a planned approach to shoulder dystocia (see Shoulder Dystocia
chapter).
Vaginal Birth 222

Infant
• The infant should be guided in the direction of an upward motion to complete the delivery
• placing the infant skin-to-skin on the mother’s abdomen to reduce temperate loss (or a safe surface if the
mother’s abdomen is not an option).
• Dry and cover with warm blankets.
• Verify that there is no twin.
Cord
• Delay cord clamping by at least 60 seconds (and up to 120 seconds) in newborns not requiring resuscitation.
This delay has been shown to benefit preterm14, 15 and term 16-19 newborns. Apply the first clamp 3 cm to 5 cm
178
from the newborn.

• Apply a second clamp at least 10 cm away from the first clamp to allow newborn venous and arterial samples
to be collected. It may be helpful to milk the cord (from the placenta toward the baby) to fill vessels to allow
easier collection of cord gases.
• Apply a third clamp near the first clamp, and cut the cord.
• Collect cord blood for gases and Rh status.
Placenta
• Signs of placenta separation include gush of blood, cord lengthening, uterine fundus rising up in the
abdomen, and uterus becoming firmer.
• Active management of the third stage, including
−− Administration of prophylactic oxytocin (10 IU IM) after delivery of the anterior shoulder is indicated to
prevent postpartum hemorrhage.18, 20 This may be administered by a nurse when an MD or MW is not
present if a medical directive or standing order is in place. The woman/parturient should be informed of
the medication that is being administered and why.
−− When oxytocin is not available, misoprostol 400 mcg may be given sublingually after the birth of the
baby. The parturient should be informed that fever and shivering are possible side effects.21
−− If medications are not available / declined, encourage breastfeeding.
−− A skilled care provider may use controlled cord traction to assist in delivery of the placenta. Gentle traction
is applied in the axis of the pelvis (45 degrees from the horizontal in a supine parturient) during a uterine
contraction to dislodge the placenta from the uterine cavity to the vagina. Use external counter-traction
(one hand supporting the uterus just above the pubic bone); this reduces the duration of the third stage.
Care must be taken that excessive traction does not cause tearing of the umbilical cord or placenta.
−− In situations where there are no skilled care providers present, controlled cord traction is not
recommended. Wait for signs of placental separation (cord lengthening, uterus firm and globular on
palpation at the umbilicus) after which encourage the woman to bear down with contractions until there
is spontaneous placental delivery.
−− Ensure that all the membranes are delivered using gentle traction and ring forceps, if needed.
Vaginal Birth 223

−− Assess the fundus and ensure that it is well contracted and that there is no significant bleeding; uterine
massage can be performed after delivery of the placenta, as needed.
−− Inspect the placenta for completeness
• Keep the placenta until verified by an experienced provider
Precipitous delivery is associated with an increased risk of postpartum hemorrhage.
• Uterine atony: Prolonged or very rapid labour patterns are associated with less effective clamping down of the
uterine muscle postpartum. If bleeding is excessive, management would include additional uterotonics and uterine
massage. Uncontrollable bleeding is best controlled by bimanual compression of the uterus until help arrives. IM or IV
anesthesia would be nice.
• Cervical, vaginal, or perineal tears: rapid delivery of the baby may contribute to increased risk of such tears. Explore
and identify perineal or other trauma and observe/manage appropriately.
Newborn care
• Place the baby skin-to-skin on the mother
• Perform the initial steps of neonatal resuscitation, if required, and continue as indicated.
• Record Apgar scores at 1 and 5 minutes.
• Perform assessment of the newborn for injuries (e.g., fractures of the clavicle and/or humerus). A rapid
delivery of the baby may also increase likelihood of newborn trauma.
5. Ongoing Care
• Monitor postpartum vital signs, bleeding, fundal height and tone, perineum, and urinary output.
• If the family has no prenatal records and/or there has been no prenatal care, it may be helpful to involve your
facility social worker to determine if support is needed or there are child protection issues.
• Consult with other support services (e.g., chaplain) as needed for the family.
• Explore with women and their support persons factors such as parity, distance to hospital and access to
care that might have contributed to her presenting when birth was imminent or to her having given birth
unexpectedly.
• If the parturient does not have a family physician, determine a strategy for post-hospital newborn care.
6. Communication and Documentation

• Complete the delivery summary.
• A narrative summary may be required for additional details such as place of birth, arrival of health care
personnel, delivery circumstances, newborn resuscitation.
• Determine if any patient safety or learning issues warrant a quality care review.
• Ensure there is notification of the primary care provider.
Vaginal Birth 224

References
1. Schorn MN, Wilbeck J. Unexpected birth in the emergency department: the role of the advanced practice nurse.
Adv Emerg Nurs J. 2009;31:170-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20118867.
2. Snyder SR, Kivlehan SM, Collopy KT. Prehospital childbirth without complications. Part 1: Babies are delivered
everyday--just not by EMS providers. EMS World. 2013;42:34-40. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/24205526.
3. Charles C. Labour and normal birth. In: V. C, C. C, editors. The midwife’s labour and birth handbook, 2nd ed.
Mississauga, ON: Wiley-Blackwell; 2008. p. 1-31.
4. Fraser DM, Cooper MA. The transition and the second stage of labour: physiology and the role of the midwife.
Myle’s textbook for midwives, 15th ed. Toronto: Elsevier Limited; 2009. p. 509-30.
5. Samuelsson E, Ladfors L, Wennerholm UB, Gareberg B, Nyberg K, Hagberg H. Anal sphincter tears: prospective
study of obstetric risk factors. BJOG. 2000;107:926-31. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/10901566.
6. Pirhonen JP, Grenman SE, Haadem K, Gudmundsson S, Lindqvist P, Siihola S, et al. Frequency of anal sphincter
rupture at delivery in Sweden and Finland--result of difference in manual help to the baby’s head. Acta Obstet
Gynecol Scand. 1998;77:974-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9849840.
7. McCandlish R, Bowler U, van Asten H, Berridge G, Winter C, Sames L, et al. A randomised controlled trial of care of
the perineum during second stage of normal labour. Br J Obstet Gynaecol. 1998;105:1262-72. Available from:
8. Mayerhofer K, Bodner-Adler B, Bodner K, Rabl M, Kaider A, Wagenbichler P, et al. Traditional care of the perineum
during birth. A prospective, randomized, multicenter study of 1,076 women. J Reprod Med. 2002;47:477-82.
9. de Souza Caroci da Costa A, Gonzalez Riesco ML. A comparison of “hands off” versus “hands on” techniques for
decreasing perineal lacerations during birth. J Midwifery Womens Health. 2006;51:106-11. Available from:
10. Delgado Nunes V, Gholitabar M, Sims JM, Bewley S, Guideline Development G. Intrapartum care of healthy women
and their babies: summary of updated NICE guidance. BMJ. 2014;349:g6886. Available from: https://www.ncbi.
11. Dahlen HG, Homer CS, Cooke M, Upton AM, Nunn RA, Brodrick BS. ‘Soothing the ring of fire’: Australian women’s
and midwives’ experiences of using perineal warm packs in the second stage of labour. Midwifery. 2009;25:e39-
Vaginal Birth 225

12. Aasheim V, Nilsen AB, Lukasse M, Reinar LM. Perineal techniques during the second stage of labour for reducing
perineal trauma. Cochrane Database Syst Rev. 2011:CD006672. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/22161407.
13. Leung TY, Stuart O, Sahota DS, Suen SS, Lau TK, Lao TT. Head-to-body delivery interval and risk of fetal acidosis and
hypoxic ischaemic encephalopathy in shoulder dystocia: a retrospective review. BJOG. 2011;118:474-9. Available
14. Gurewitsch ED, Allen RH. Reducing the risk of shoulder dystocia and associated brachial plexus injury. Obstet
Gynecol Clin North Am. 2011;38:247-69, x. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21575800.
15. Lerner H, Durlacher K, Smith S, Hamilton E. Relationship between head-to-body delivery interval in shoulder
dystocia and neonatal depression. Obstet Gynecol. 2011;118:318-22. Available from: https://www.ncbi.nlm.nih.
16. Kotaska A, Campbell K. Two-step delivery may avoid shoulder dystocia: head-to-body delivery interval is less
important than we think. J Obstet Gynaecol Can. 2014;36:716-20. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/25222167.
17. Rabe H, Reynolds G, Diaz-Rossello J. Early versus delayed umbilical cord clamping in preterm infants. Cochrane
18. Leduc D, Senikas V, Lalonde AB, Ballerman C, Biringer A, Delaney M, et al. Active management of the third stage of
labour: prevention and treatment of postpartum hemorrhage. J Obstet Gynaecol Can. 2009;31:980-93. Available
19. McDonald SJ, Middleton P, Dowswell T, Morris PS. Effect of timing of umbilical cord clamping of term infants on
maternal and neonatal outcomes. Evid Based Child Health. 2014;9:303-97. Available from: https://www.ncbi.nlm.
20. Mathai M, Gulmezoglu AM, Hill S. WHO recommendations for the prevention of postpartum haemorrhage.
Geneva: 2007.
21. Hofmeyr GJ, Abdel-Aleem H, Abdel-Aleem MA. Uterine massage for preventing postpartum haemorrhage.
Vaginal Birth 226

Table of Contents
Chapter 10 Assisted Vaginal Birth.................................................................................................................................... 228

Introduction.............................................................................................................................................................. 228
Definitions..................................................................................................................................................... 228
Classifications................................................................................................................................................ 228
Incidence ...................................................................................................................................................... 229
Techniques................................................................................................................................................................ 231
Vacuum ........................................................................................................................................................ 233
Forceps.......................................................................................................................................................... 235
Comparison of Vacuum and Forceps for AVB ................................................................................................ 236
Caution: sequential use of vacuum and forceps........................................................................................... 238
Management............................................................................................................................................................ 240
Vacuum Extraction......................................................................................................................................... 240
Forceps Application....................................................................................................................................... 242
Techniques for Use of Vacuum and Forceps.................................................................................................. 243
Follow-Up.................................................................................................................................................................. 249
Documentation............................................................................................................................................. 249
Suggested format for a chart note................................................................................................................. 250
Summary.................................................................................................................................................................. 250
Assisted Vaginal Birth 227

Chapter 10
Assisted Vaginal Birth
Introduction
Assisted vaginal birth (AVB), or operative vaginal birth, refers to the use of vacuum or forceps to achieve a vaginal
delivery in the second stage of labour. Both methods are safe and reliable for assisting childbirth provided that the
operator has adequate training and experience and appropriate appropriate attention is paid to the indications and
contraindications. In every case, consideration must be given to the maternal and fetal risks associated with using either
instrument and to the risks of the alternative choice of Caesarean section (CS). The procedure should be undertaken only
when there is a reasonable chance of success and a backup plan is in place.
The choice of instrument should suit both the clinical circumstances and the preference of the health care provider and
parturient.1 It is essential that the parturient provide informed consent.1
Definitions
Station: The level of the leading edge of the fetal skull is expressed as the number of centimeters around a
reference line of zero drawn at the ischial spines. When the skull is above the spines, it is represented
as a negative number, reaching a value of -5 at the pelvic inlet. When below it is expressed as a positive
number reaching +5 at the perineum. Careful distinction between skull and caput is important.
Engagement: When the biparietal diameter of the head enters the plane of the pelvic inlet. Engagement is usually
complete when the leading edge of the skull is at or below the ischial spines (station 0); however,
extensive moulding and caput can bring the leading edge of the scalp and skull to the level of the
spines before the biparietal diameter is engaged in the pelvic inlet.
Caput: Subcutaneous fetal scalp swelling secondary to pressure of labour.
Chignon: Exaggerated caput secondary to suction force from a vacuum.
Classifications
The classification of operative vaginal deliveries is based on the station of the head within the pelvis and the degree of
rotation from an occiput anterior (OA) position.2
Outlet
• Scalp is visible at a point between the introitus without separating the labia and the perineum
• Fetal skull has reached the pelvic floor
• The sagittal suture is in anterior-posterior diameter, right, or left OA or occiput posterior (OP) position
however rotation does not exceed 45°.

Low
• Leading point of fetal skull is at station ≥ +2 and above the pelvic floor
• Two sub-divisions: rotation is £ 45°; rotation is > 45°
Mid
• Head is engaged and leading point of skull is between station 0 and +2
Incidence
Rates of AVB, particularly forceps use continues to decline nationally and internationally. Reasons postulated for the
decline are the perceptions that Caesarean birth is a safer alternative and that vacuum-assisted delivery is easier. Other
reasons cited are the decline in opportunities for residents to learn to perform forceps-assisted delivery and potential
medical legal implications.
In the United States from 1990 to 2010, the overall AVB rate declined from 11.7% to 5.5%.3 The rate of forceps deliveries
declined steeply from 6.5 % to 1% and the rate of vacuum deliveries has remained roughly the same, around 5%.4
Despite the overall recent trend downward, Portugal recently experienced an increase in both vacuum- and forceps-
assisted births as part of a successful national effort to reduce the overall Caesarean section rate.5
Figure 1. Use of Vacuum and Forceps in Vaginal Deliveries: United States, 1990–2010

Table 1. Assisted
In Canada, Deliveries
the decline in AVB in Canada
rates has been more modest. In 2010–2011, the rates of all AVB, vacuum-assisted
deliveries, and forceps-assisted deliveries in Canada were 13.5%, 9.6%, and 3.2% respectively.6 There is considerable
VACUUM,%
provincial variation within Canada (Table 1) as well FORCEPS,
as variation between % western
selected TOTAL AVB, %
countries (Figure 2). The rate
of AVB is higher inBritish
nulliparous than in parous women.
Columbia 10 4 14
Table 1. AssistedAlberta
Deliveries in Canada 12.5 4 16.5
Saskatchewan 13 3 16
VACUUM,% FORCEPS, % TOTAL AVB, %
Manitoba 6.5 3.2 9.7
British Columbia 10 4 14
Ontario
Alberta 10
12.5 3.84 13.8
16.5
Quebec
Saskatchewan 913 33 1216
Manitoba
New Brunswick 96.5 3.83.2 9.7
12.8
Ontario 10 3.8 13.8
Nova Scotia 8 4.5 12.5
Quebec 9 3 12
Prince Edward Island 4 2.5 6.5
New Brunswick 9 3.8 12.8
Newfoundland
Nova Scotia & Labrador 108 64.5 16
12.5
Prince
YukonEdward Island 74 02.5 76.5
Newfoundland & Labrador
Northwest Territories 5.510 16 6.516
Yukon 7 0 7
Nunavut 1.5 0 1.5
Northwest Territories 5.5 1 6.5
Nunavut
Adapted from Highlights 1.5 the birthing process0 in Canada [Bulletin]. Ottawa:
of 2008–2009 selected indicators describing 1.5 Canadian Institute of
Health Information; 2009 Oct.7
Adapted from Highlights of 2008–2009 selected indicators describing the birthing process in Canada [Bulletin]. Ottawa: Canadian Institute of Health Information; 2009 Oct.7
Figure
Figure 2.
2. Assisted
Assisted Deliveries
Deliveries by
by Country
3, 8-12
Country3, 8 -12 9101
1


Techniques
Careful clinical assessment is a prerequisite to AVB. Pelvic adequacy, fetal station, fetal position, caput and molding
should be assessed. Abnormalities of the position or attitude of the vertex can result in relative cephalopelvic
disproportion (CPD). The fetal station should be assessed abdominally in fifths above the pelvic brim as well as by
pelvic examination (Figure 3). Extensive moulding or caput may confuse the vaginal assessment of descent and may
indicate
The thebenefits
relative possibility of relative
and risks CPD.versus
of vacuum If more thandelivery
forceps one fifthhave
of the
beenfetal
thehead is palpable
subject above
of much study andthe pelvicThe
debate. inlet, AVB is
proper
inadvisable.isAnot
comparison 2013 prospective
of vacuum trial study demonstrated
with spontaneous delivery but of that a strategy
vacuum of manual
with other operativerotation
vaginal for fetuses
delivery in posterior
methods or CS. or
transverse positions at full dilatation is associated with a reduction in the rate of operative delivery. 13
Figure
Figure 3.
3. Abdominal
Abdominal Examination
Examination of
of Fifths
Fifths Above
Above the
the Pelvic
Pelvic Brim
Brim
Used with permission of Salus Global Corporation14 Used with permission of Salus Global Corporation13
Assessment of pelvic adequacy is mandatory. Abnormalities of the position or attitude of the vertex can result in relative
cephalopelvic disproportion (CPD). The fetal station should be assessed abdominally in fifths above the pelvic brim as
well as by pelvic examination (Figure 3). Extensive moulding or caput may confuse the vaginal assessment of descent
and may indicate the possibility of relative CPD. If more than one fifth of the fetal head is palpable above the pelvic inlet,
AVB is inadvisable. A 2013 prospective trial study demonstrated that a strategy of manual rotation for fetuses in posterior
Assisted Vaginal
or transverse Birth at full dilatation is associated with a reduction in the rate of operative delivery.14
positions 231
Manual rotation
Successful rotation after the onset of the second stage of labour is more likely to be successful if it is performed before
arrest occurs. Manual rotation can convert 90% of OP or transverse arrest situations to OA.
Manual rotation is more successful in multiparous women and young women.
Rotation is important if there is a need for a fast delivery and/or if there is minimal or slow descent after a trial of
pushing.
First, empty the bladder.
There are two methods for rotating the fetus.
1. A hand is inserted into the vagina with the palm upward. Digital rotation is performed by placing the tips of the index
and middle fingers in the anterior segment of the lambdoid suture near the posterior fontanelle (see Figure 2.6.E.4).
The fingers are used to flex and slightly dislodge the vertex, rotating the fetal head to the OA position by rotation of
the operator’s hand and forearm. The thumb may also be used with gentle downward pressure more anteriorly on the
parietal bone to aid this rotation. The fetal head should be held in place for a few contractions to prevent rotation back
towards the posterior position.
2. The operator’s four fingers are placed behind the posterior parietal bone with the palm up and the thumb over the
anterior parietal bone. The right hand is used for the left OP position, and the left hand is used for the right OP position.
The head is grasped with the tips of the fingers and thumb. During a contraction, the patient is encouraged to push and
the operator attempts to flex and rotate the fetal head anteriorly. Upward pressure may help to slightly elevate the head
and facilitate rotation (see Figure 2.6.E.5).
As part of informed consent, patients should be informed of the potential risks and benefits of the selected
instrument (vacuum or forceps) before application.
The risk of perineal trauma and the small risk to the with vacuum or forceps must be weighed against the maternal risks
of Caesarean section (at advanced station). If the fetal heart rate is abnormal, the risk to the fetus of any delay required to
deliver by Caesarean section must also be taken into consideration.

FIGURE 2.6.E.5 Manual rotation of occiput posterior to occiput anterior position. Manual rotation of occiput
posterior to occiput anterior position. Reproduced with permission from Argani CH, Satin A. Management of the
fetus in occiput posterior position. In: UpToDate, Post TW (ed.), UpToDate, Waltham, MA (accessed 5/8/14).
© 2014 UpToDate, Inc. For more information visit www.uptodate.com.
Vacuum
Vacuum extractor use in modern obstetrics began with metal mushroom-shaped cups designed by Malmstrom and
Bird. These inspired rigid plastic cups. In an effort to reduce scalp trauma, soft cups of silicone and rubber were later
developed.
Soft cups are less likely to cause cephalohematoma and scalp injury than forceps, but are more likely to lead to an
unsuccessful vaginal delivery. There are no differences in neonatal or maternal outcomes between the two methods.15

Maternal risks can be minimized by ensuring both the non-traumatic insertion of the device and avoiding soft tissue
entrapment as well as controlling the rate of descent and delivery over the perineum.
Application of the vacuum device to the fetal scalp invariably causes exaggeration of subcutaneous caput and formation
of a chignon, which resolves within hours of birth. Bruising is also common and is benign. Large caput and bruising can
easily be confused with a cephalohematoma, which is a deeper collection of blood between a skull bone and periosteum
that occurs in approximately 5% of vacuum deliveries.15 Because the periosteum is tightly adherent to each individual
cranial bone the swelling does not cross suture lines, is self-limiting and forms a tense swelling immediately adjacent
to bone that persists after the caput and chignon have subsided. The swelling does not cross sutures. It is benign and
resolves over weeks to months; however, resorption of hemoglobin can result in modest hyperbilirubinemia. Swelling
that resolves within hours or days is not a cephalhematoma.
A more serious but rare complication of vacuum delivery is subgaleal (subaponeurotic) hemorrhage (SGH) or bleeding
into the potential space between the skull periosteum and the scalp aponeurosis. With SGH, the suture lines of the skull
do not limit hemorrhage into the subgaleal space as they do in cephalohematoma. As a result, subgaleal hemorrhages
25thtoEdition
can extend over the entire calvaria from the brow to the nuchal ridge and from ear ear. Theofvolume
the ALARM Course
of blood thatManual
accumulates can be sufficient to cause severe or fatal hypovolemic shock. However, early detection and prompt
transfusion of blood and plasma will usually be life saving. In modern obstetrical practice, subgaleal hemorrhage is rare,
reported in 1/1000 rigid Kiwi OmniCup deliveries.16
Figure 4. Subgaleal Hemorrhage Versus Cephalhematoma
Figure 4. Subgaleal Hemorrhage Versus Cephalhematoma
Successful vacuum delivery with minimal fetal scalp trauma can best be achieved by minimizing traction forces and
Fetal scalp of
likelihood trauma (hemorrhage
pop-off and laceration)
through correct applicationcan bestcup
of the beover
prevented by avoiding
the flexion point ofexcessive,
the incorrect,
fetal scalp or prolonged
and avoiding
(> 10 minutes) traction, and by not applying any rotational force to the vacuum cup. 18
To minimize
excessive, incorrect, or prolonged (> 10 minutes) traction. Fetal scalp trauma (hemorrhage and laceration) can traction forces
bestand
be
likelihood
prevented ofbypop-off,
avoidingthe vacuum incorrect,
excessive, cup must orbeprolonged
applied to(>the10flexion point.
minutes) Vacuum
traction, andtraction should beany
by not applying coordinated
rotationalto
the
forcematernal expulsive
to the vacuum cup.effort,
17 and the angle
To minimize of traction
traction must
forces and follow the
likelihood ofpelvic curve.
pop-off, The vacuum
the vacuum shouldbenot
cup must be used
applied to the
to apply rotational force, which can cause scalp trauma. Vacuum should be avoided if fetal coagulopathy is known or
suspected.19-23
After every
Assisted successful
Vaginal Birthor attempted vacuum delivery, the condition of the neonate should be monitored closely for 234
SGH. Enlargement of the chignon, increasing head circumference, hypovolemia, or tachycardia should prompt careful
pediatric assessment for SGH.24, 25 Early detection and treatment can be life-saving. A suggested surveillance protocol is
flexion point. Vacuum traction should be coordinated to the maternal expulsive effort, and the angle of traction must
follow the pelvic curve. The vacuum should not be used to apply rotational force, which can cause scalp trauma. Vacuum
should be avoided if fetal coagulopathy is known or suspected.18 -22
19202
1
After every successful or attempted vacuum delivery, the condition of the neonate should be monitored closely for
SGH. Enlargement of the chignon, increasing head circumference, hypovolemia, or tachycardia should prompt careful
pediatric assessment for SGH.23, 24 Early detection and treatment can be lifesaving. A suggested surveillance protocol is
found later in the chapter.
Forceps
Forceps vary by their shank, pelvic curve and cephalic curve, characteristics that may be best suited to the clinical
situation. Simpson forceps are commonly used for delivery of a moulded fetal head, often seen in nulliparous women.
Tucker-McLane forceps have a more rounded cephalic curve, suitable for the unmoulded fetal head seen in multiparous
women. Kjelland forceps are designed for rotation of the fetal head and lack a pelvic curve.
The risk of maternal soft tissue injury is greater with forceps than with vacuum.1 A 2013 study from the United Kingdom
demonstrated an adjusted odds ratio of obstetrical anal sphincter injury (OASI) with forceps delivery of 4.43, P < 0.005.26
Hehir et al. also demonstrated increased risk of OASI with forceps with a rate of 8.6% compared to a spontaneous vaginal
delivery rate of 1.3%.27 An education program in Norway that included good communication with the woman, adequate
perineal support, visualization of the perineum during delivery, and mediolateral episiotomy for most forceps-assisted
deliveries reduced the forceps-associated OASI rate by half. The more liberal but not routine use of episiotomy was felt to
be responsible in part for the reduction in OASI28
The fetal risks with forceps delivery include the risk of facial laceration and cephalohematoma of 1% each. The risk of
symptomatic intracranial hemorrhage is 0.1%.1 External ocular injuries and facial nerve palsies are more common with
forceps than with vacuum.25 A 2009 Canadian-authored study supports the view that facial nerve palsies associated with
operative vaginal delivery have a very good prognosis.26
Neonatal skull fracture has been reported after both spontaneous and forceps deliveries. The incidence is greater after
forceps deliveries.27 Forceps should generally not be used if fetal coagulopathy is known or suspected.
There remains a role for mid-forceps deliveries. The risk of a mid-forceps delivery must be compared with that of its
alternatives: vacuum-assisted birth or intrapartum second stage CS. Mid-cavity and rotational forceps delivery should be
performed only by experienced operators and should be generally conducted as a “double set-up” in an operating room
with immediate ability to perform Caesarean section in case vaginal delivery is not accomplished.
Rotational forceps deliveries have been the subject of several studies in the United Kingdom. Bradley et al. showed there
was no difference in trauma arising as a result of manual or forceps rotation and that there was less trauma if the baby
was delivered in the occiput anterior instead of occiput posterior position.28

Comparison of Vacuum and Forceps for AVB

The choice of vacuum or forceps for AVB should be based on the total clinical picture including the expertise of the
practitioner and the availability of CS.29 A 2010 Cochrane meta-analysis of 32 studies showed forceps and the metal
vacuum cup (versus soft cup) were most successful in completing a vaginal birth; however, use of forceps was associated
with higher rates of maternal complications, including perineal trauma, tears, more use of general and regional
anaesthesia, and more incontinence.25 The metal cup was associated with more neonatal scalp trauma. The urgency
for delivery needs to be balanced against potential risks to the mother and baby. The following graphs from the meta-
analysis of controlled trials compare forceps delivery and vacuum extraction.25
Maternal trauma from AVB is primarily from pelvic floor injury. Arguably, the best long-term data on symptomatic
pelvic floor injury from vacuum delivery is found in a 20-year follow-up of 4000 primiparous Swedish women who
underwent either one spontaneous vaginal birth, one vacuum assisted vaginal birth, or one caesarean section.30 Overall,
the incidence of urinary incontinence, fecal incontinence, and pelvic organ prolapse 25th Edition of the
was almost ALARM20
identical Course
yearsManual
after
spontaneous or vacuum-assisted birth; however, the rate of OASI was almost three times greater after vacuum delivery
(6.3%) than after spontaneous delivery (2.4%). Women who sustained OASI had almost double the incidence of urinary
incontinence (60% vs 40%) and fecal incontinence (30% vs 15%) compared with women without OASI, whether they had
adiffer.
vacuum delivery
It appears or the
that not.risk
Theofincidence of pelvic
urinary and fecal organ prolapse
incontinence is did withIt OASI
not differ.
associated appears that
rather thevacuum
than risk of delivery
urinary and
fecal incontinence
itself. The incidence of is associated with perineal
OASI and severe OASI rather thanis vacuum
trauma delivery
at least twice itself.
as high withThe incidence
forceps of OASI
compared withand severe
vacuum
perineal trauma is at least twice as high with forceps compared with vacuum 25
. A small randomized
(#15 O’Mahoney). A small randomized trial indicated higher risk of fecal incontinence after forceps than after vacuum. trial indicated higher
33
risk of fecal incontinence

If a practitioner afterdelivery
believes that forcepscan
thansuccessfully
after vacuum. 31
If a practitioner
be accomplished withbelieves that deliverychoosing
either instrument, can successfully be
the vacuum
accomplished with either instrument and has
extractor will minimize long-term maternal incontinence.appropriate training and skill using both, choosing a vacuum extractor will
minimize long-term maternal incontinence compared with forceps.
Figure 5. Forceps Delivery Versus Vacuum

Assisted Vaginal
In one study, Birth retinal hemorrhage was found in neonates after both vacuum and forceps delivery, vision at 5 237
although
years of age was normal.32 Clinically significant intracranial hemorrhage is a rare complication of vacuum and forceps
delivery; however, it should be noted that asymptomatic subdural hemorrhage also occurs during spontaneous birth. A
series of 111 asymptomatic neonates screened with postnatal magnetic resonance imaging found subdural hemorrhage
in 6% of spontaneous deliveries, 8% of vacuum assisted deliveries, and 28% of deliveries accomplished with the use
of vacuum and forceps. All infants remained asymptomatic, and all hemorrhages resolved on follow-up magnetic
resonance imaging.33
California surveillance data demonstrated that the lowest risk of fetal intracranial injury occurred with spontaneous
vaginal delivery and CS without labour.34 An intermediate risk occurred in those infants who had vacuum- or forceps-
assisted deliveries or an intrapartum CS. The highest risk was reported in infants delivered with a combination of
vacuum and forceps or who had a CS following unsuccessful assisted vaginal delivery. The relative clinical significance of
these hemorrhages was not reported. Long-term follow-up of children delivered by vacuum or forceps has not revealed
differences in neurological abnormalities or cognitive development when compared with children who delivered
spontaneously.2

Table 2. Effect of Mode of Delivery in Nulliparous Women on Neonatal Intracranial Injury

Singleton Nulliparous Deliveries, California 1992–199434
DELIVERY METHOD NUMBER %
SVD 387 799 66.5
Vacuum 59 354 10.2
Forceps 15 945 2.7
Vacuum & forceps delivery 2817 0.5
Caesarean section 117 425 20.1
Total 583 340 100
INTRACRANIAL
DELIVERY METHOD RATE, %
HEMORRHAGE RATE
CS without labour 1 per 2750 0.04
Spontaneous vaginal delivery 1 per 1900 0.05
Intrapartum CS 1 per 907 0.11
Vacuum assist 1 per 860 0.12
Forceps assist 1 per 664 0.15
CS after attempted AVB 1 per 334 0.33
Vacuum & forceps 1 per 256 0.39
In a Canadian cohort study of 288 women who experienced a failed vacuum delivery, 81.5% had a successful forceps
delivery and 5.9% had a CS following failed vacuum and forceps. There were no subgaleal, intracranial, subdural, or
intraventricular hemorrhages, and no skull fractures.35 Other small studies have concluded that sequential use of
instruments for AVB can increase neonatal injury.36, 37
Caution: sequential use of vacuum and forceps

The Society of Obstetricians and Gynaecologists of Canada, The Royal College of Obstetricians and Gynaecologists, and
the American College of Obstetricians and Gynecologists suggest caution with sequential use of vacuum and forceps
because of the potential for fetal injury.1, 2, 38 If descent is not achieved with traction on a correctly applied vacuum cup,
cephalopelvic disproportion must be suspected, and an attempt at forceps-assisted delivery is not routinely advisable.
However, if a vacuum or forceps cannot be optimally applied, switching instruments before traction may be appropriate.
If an initial vacuum traction effort fails for a technical reason, correcting the problem or switching instruments may also
be appropriate. Occasionally, vacuum traction results in adequate descent, but excessive chignon develops, filling the

cup and removing the surface area required to generate traction. This is a technical failure of the vacuum rather than
CPD, and completion of the delivery with forceps from a low or outlet station is unlikely to compound fetal risk. The
Royal College of Obstetricians and Gynaecologists notes that the risks of forceps versus a Caesarean section at advanced
station should be considered and that judicious use of outlet forceps after failed vacuum may avert a potentially difficult
Caesarean section.38
Table 3. Criteria for Use of Vacuum and Forceps
VACUUM FORCEPS
Indications • Atypical or abnormal fetal heart rate pattern • Atypical or abnormal fetal heart rate pattern
• Medical indications to avoid Valsalva manoeuvre • Medical indications to avoid Valsalva manoeuvre
(e.g., cerebral vascular disease, cardiac conditions) (e.g., cerebral vascular disease, cardiac conditions)
• Inadequate progress of labour • Inadequate progress of labour
• Lack of effective maternal expulsive effort1 • Lack of effective maternal expulsive effort1
• Autorotation of fetal malposition possible • Suboptimal attitude or position of the fetal head
• Assistance at CS if required may be corrected
• Assistance at CS if required
• Assisting with after coming head of a breech
Contraindications • Non-cephalic, face, or brow presentation • Non-cephalic or brow presentation (except Piper
• Lack of knowledge of fetal position forceps for after coming head of a breech)
• Fetal conditions (e.g., bleeding disorder, • Lack of knowledge of fetal position
demineralization disorder) • Fetal conditions (e.g., bleeding disorder,
• Any contraindications to vaginal delivery demineralization disorder)
• Less than 34 weeks’ gestation2 • Any contraindication to vaginal delivery
Prerequisites • Informed consent

• Appropriate anaesthesia
A mnemonic delineating • Maternal bladder empty
these prerequisites is • Vertex engaged
included in this chapter • Cervix fully dilated
and may be copied for • Adequate uterine contractions
use in labour and delivery • Membranes ruptured
suites. • Position of the head must be known
• Experienced operator, adequate facilities, and resources available
• Operator knowledge of the instruments, their use, and the complications that can arise
• Reasonable chance of success (no evidence of CPD)
• Backup plan if the procedure is unsuccessful
• Ongoing fetal and maternal assessment
• Appropriately skilled personnel for neonatal resuscitation

Management
Vacuum Extraction
The vacuum extractor is designed to apply traction upon the fetal scalp to assist maternal expulsive effort and it is
unlikely to succeed in the absence of maternal expulsive effort. It can be used for rotational deliveries; however, it
must not be used to apply rotational forces. The vacuum may be used cautiously to correct attitude (deflexion) if it is
correctly applied and if the direction of traction follows the pelvic curve.
Different types of vacuum extraction devices are available, including hard cups, soft silastic cups, and the Kiwi OmniCup.
Although several comparisons of different cups have been published, the success and complication rates of each device
are difficult to compare because operator training and experience are essential to optimize outcomes. In some reports,
the Kiwi OmniCup is associated with a higher failure rate than the soft cup vacuum, whereas in others (with caregivers
trained and mentored in the use of the Kiwi OmniCup), failure rates are lower.23, 39-42 In a 2010 Cochrane review, the
404
1
anterior soft cup was compared with a metal cup.14 The metal cup had a lower rate of failed delivery (8 studies with 1076
women; RR 1.63, 95% CI 1.17 to 2.28). Scalp injury and cephalohematoma were less likely with the soft cup (RR 0.67
and 0.61 respectively). There was no significant difference in other neonatal or maternal outcomes including Caesarean
section, episiotomy, and perineal and vulvar trauma.
Success with vacuum-assisted birth requires application of the cup to the flexion point on the fetal scalp.43 The flexion
point is just anterior to the posterior fontanelle. In a flexing application, the cup is centered over the flexion point with
the posterior edge over the posterior fontanelle and the anterior edge well back from the anterior fontanelle. This
minimizes the fetal head diameter that must transit the maternal pelvis, reducing the force required, the likelihood of
pop-offs, and the risk of fetal and maternal trauma.
Optimal vacuum success is achieved with a tailored approach that matches an instrument appropriate to the clinical
situation.44 If the fetus is in an anterior position at a low station, any vacuum cup can be successfully applied in a flexing
application, and re-usable or disposable soft cups can be used to minimize minor scalp trauma.45 For mid-pelvic anterior
deliveries, larger cups such as a Kobayashi, Silc, or 6 cm anterior Bird cup can generate more traction and are more
likely to succeed than smaller cups. For deliveries with the fetus in an occiput transverse or posterior position, the Kiwi
OmniCup and the 5 cm Bird posterior cups have pivoting traction handles and side-port suction that allow placement
high enough in the pelvis to achieve a flexing application. This allows autorotation to occur with traction in the axis of the
pelvis. For occiput transverse and posterior deliveries, a vacuum extractor with a handle that is perpendicular to
the plane of the cup should not be used, as the flexion point cannot be reached.46-48 74

Figure 6. Correct Cup Application for Occiput-Posterior and -Transverse Positions
Used with permission of Salus Global Corporation

Figure 7. Cup Positions on the Fetal Head
Used with permission of Salus Global Corporation16
CLINICAL SITUATION SUGGESTED VACUUM DEVICE
Station 0 to +2; occiput anterior Bird 6 cm metal; Kobayashi or Silc silicone cup
Any station > 0; occiput transverse or posterior Kiwi 5 cm OmniCup; Bird 5 cm posterior cup
Station ≥ +3; occiput anterior Kobayashi, Silc, Kiwi OmniCup, Mityvac, or Bird 6 cm anterior cup
The caregiver should have proper training and experience with the specific instrument used, recognizing that skills may
be different for each instrument. Vacuum pop-offs are not normal in a vacuum-assisted delivery.23 Causes include
• Poor seal causing vacuum leak
• Impingement of maternal soft tissue
• Deflexing application
• Cephalopelvic disproportion (CPD)
• Uncontrolled traction technique (no counter-traction)
• Traction that is too rapid
• Improper angle of traction
Forceps Application
Debate about the indications for and safety of forceps operations has continued for over 200 years, and has mostly been
concerned with mid-forceps deliveries. In most countries, rates of CS have risen as operative vaginal delivery rates have
fallen. This trend has not been shown to confer benefit to the mother or baby.

The forceps application is checked in three ways. The following mnemonic assists in this endeavour. Position For
Safety, Posterior fontanelle, Fenestration, Sagittal suture.49
If forceps are applied so that the posterior fontanelle is more than a fingerbreadth above the plane of the shanks, traction
will result in deflexion of the fetal head, increasing the diameter of the presenting part for delivery. If greater than a
fingerbreadth of fenestration is still palpable after application of the blades, then the blades may slip, increasing the
likelihood of fetal injury. When the sagittal suture is not perpendicular to the plane of the shanks throughout its length,
the application of the forceps is asymmetrical, increasing the risk of fetal injury.
Obstetrical forceps are applied to the fetal head to perform the following functions:
• Traction
• Rotation (if required)
• Flexion
• Extension
When one or more of these functions is attempted, there is simultaneous fetal head compression, which is the
primary undesirable effect associated with the use of forceps. Proper technique, including accurate application and
correct traction, can minimize compressive forces.
Forceps should never be applied through a cervix that is not fully dilated or with
an unengaged presenting part.
Techniques for Use of Vacuum and Forceps

In all cases of assisted vaginal delivery, the obstetrical care provider should consider
• Fetal status before and throughout the attempted delivery
• The time required to initiate a Caesarean section if the procedure fails.
• Choice of instrument, based on clinical circumstances and operator experience.
• Location of the delivery, which should be determined in discussion with the team:
−− For delivery from a low or outlet station when the operator is very confident of success, delivery in a
hospital delivery room is appropriate.
−− For delivery from the mid-pelvis (above station +2), when malposition is present (OT or OP), or if the
operator is not confident of success, delivery should be performed in an operating room with immediate
access to Caesarean section.
−− However, if the fetal heart rate is abnormal, it may be appropriate to attempt delivery in a delivery room
while preparations for emergency Caesarean section are underway.50

Figure 8. Assisted Vaginal Birth Decision Tree

Table 4. Assisted Vaginal Birth Mnemonic
VACUUM FORCEPS
A • Address and obtain consent. The indication(s) and plan must be clear, well understood by the birthing woman and
ADDRESS fully documented
ANAESTHESIA • Adequate pain relief is available
ASSISTANCE • Assistance for the neonate is available
ABSENCE • Absence of contraindication to the procedure
B • Bladder catheterized
BLADDER • Backup plan discussed with birthing woman and team, documented; resources available
BACKUP PLAN
C • Cervix fully dilated, membranes ruptured
CERVIX • Adequate contractions and maternal expulsive efforts
CONTRACTIONS
D • Determine fetal position, station, and pelvic adequacy
DETERMINE • Determine location of delivery (in delivery room or trial in OR)
DYSTOCIA • Prepare for possible shoulder dystocia
E • Inspect vacuum cup, pump, tubing, and check pressure • Select forceps according to clinical requirements.
EQUIPMENT • EFM indicated: keep scalp clip applied, re-apply clip • Phantom application
EFM beside vacuum, or ensure adequate transabdominal fetal • EFM indicated: keep scalp clip applied, or ensure
monitoring adequate transabdominal fetal monitoring
F • Introduce the cup into the posterior aspect of the vagina • Forceps are applied between contractions. Traction
while protecting the maternal tissues and making space may be performed with or without a contraction
FONTANELLE with the opposite hand • Left hand, maternal left side, pencil grip and vertical
FLEXION POINT • Soft cups are inserted by compressing the cup in an AP insertion, with right thumb directing blade
FOR VACUUM diameter • Right blade, right hand, maternal right side, pencil
• Hard cups are slid in sideways and flipped onto the fetal skull grip and vertical insertion with left thumb directing
• The cup is centred over the flexion point (the point where blade
traction will facilitate the smallest diameter of the fetal • Fingers should be inserted into the vagina only to
skull passing through the pelvis). The flexion point is over guide the blades and not to apply pressure on or to
the sagittal, suture just anterior to the posterior fontanelle displace the fetal head
on the fetal skull 51-54
525
3
• Lock blade and support; should lock without
• In the correct position the edge of the cup reaches onto the pressure
posterior fontanelle. • Check application PFS:
• When the fetus is OP, the flexion point is usually more −− Posterior fontanelle located midway between
posterior than first appreciated. With correct application, the blades, and 1 fingerbreadth above the
the 11-cm mark on the traction cable of a Kiwi OmniCup plane of the shanks with the lambdoid sutures
should be at the fourchette. equal distance from the forceps blades
• Ensure that no maternal tissue is between the fetal head −− Fenestration of blades barely felt. Equal
and the vacuum cup by sweeping finger around cup to amount of fenestration felt on each side (with
clear maternal tissue. Reconfirm this after any loss of a solid blade, it should be possible to insert no
contact during traction. Note: It is often not possible to more than a fingertip between the blade and
reach to the far edge of a Kiwi OmniCup or 5 cm Bird cup the fetal head)
correctly applied to the flexion point of an OT or OP fetus. −− Sagittal suture perpendicular to plane or
• Initially increase vacuum pressure to resting pressure shanks with occipital sutures 1 cm above
100–200 mm Hg (0.1–0.3 kg/cm2) then, for traction, respective blades
increase to 500–600 mm Hg (0.6–0.8 kg/cm2)

VACUUM FORCEPS
G • The vacuum pressure may be released between • Traction in axis of birth canal
GENTLE contractions to resting pressure or maintained at traction • Handle elevated (do not elevate handle too early)
TRACTION pressure.55
• No rotational force is applied but the fetal head may rotate
on its own with descent.
• Traction is applied in the direction of the pelvic curve—
initially downward and finally upward.
• Non-dominant thumb on cup to provide counter-traction
and finger monitoring edge contact with fetal scalp to
control descent and detect imminent pop-off.
• As contraction begins:
−− ensure adequate vacuum pressure
−− pull in the axis of the birth canal with contraction and
maternal expulsive efforts
H The decision to pause, continue, call for assistance, or move to a backup plan rests with the clinician and is based on
HALT clinical circumstance (e.g., fetal well being, progress, likelihood of success). Guidelines are provided as to when to
reconsider but the decision is made by the clinician performing the procedure based on his/her expertise and assessment
The listed of the clinical situation.
recommendations
should be Caesarean section advised if Caesarean section advised if
considered the • No progress after two pulls with a properly positioned cup • Difficulty or failure of proper application
maximum limits. and good traction • Failure of rotation, if attempted and required
• Delivery is not imminent after four contractions, reassess • No descent with initial traction
the method of delivery • If delivery is not imminent after 3 traction
• 3 pop-offs, without obvious cause attempts57
• 20 minutes elapsed time and delivery is still not
imminent22, 56
The longer the cup is on, the more chance there is of fetal
trauma.15, 17 It is imperative that some descent is observed
with each pull. If these limits are reached and delivery is not
imminent or there is evidence of scalp trauma, the procedure
should be abandoned.55

VACUUM FORCEPS
I • Routine episiotomy is not required for every assisted vaginal birth.2, 58

INCISION • Selective mediolateral episiotomy has been shown to reduce OASI in assisted vaginal birth.59 The number of
episiotomies needed to prevent one OASI appears to be between 8 and 20.60
• An episiotomy should be performed when the perineum is well distended by the fetal head. If performed too early,
the episiotomy is likely to extend and may involve the anal sphincter.
• Midline episiotomies increase the risk of third and fourth degree tears and should be avoided.2, 58, 61
• “Mediolateral” episiotomies are commonly cut too close to the midline.62, 63 To avoid the anal sphincter, the angle
should be 60–70 degrees from midline (20–30 degrees from horizontal) when the perineum is distended. After
delivery, this angle decreases by approximately 20 degrees.64 Initiating the episiotomy 1 cm lateral to the midline on
the fourchette may also be protective63
• Certain factors increase the risk of OASI and should lower the threshold for performing an episiotomy:
−− when forceps are used
−− in nulliparous women
−− when abnormal FHR requires rapid delivery without time for the perineum to stretch
−− in women with a prior history of OASI
J • Remove vacuum when jaw is reachable or delivery • Forceps are removed as the fetal head delivers
JAW assured through the perineum.

Figure 9. Correct Episiotomy Placement

Figure 9. Correct Episiotomy Placement
Used with permission of Salus Global Corporation Used with permission of Salus Global Corporation

Follow-Up
Maternal and neonatal care should include
• Active third stage management
• Umbilical arterial and venous blood gas analysis
• Examination for maternal trauma, including vaginal and/or cervical lacerations and OASI; if OASI occurs,
prophylactic IV antibiotics, stool softeners, and pelvic physiotherapy should be provided
• Examination for neonatal trauma, including scalp trauma, signs of cerebral irritation (poor suckling, listless),
cephalohematoma, or SGH
Many centres have established observation protocols for newborns who have had forceps or vacuum applied during
their delivery.65-68 Evidence for a particular subgaleal surveillance protocol is lacking; however, the following protocol
666
7
is suggested: perform newborn assessments at 1h, 2h, 4h, then q4h x 24 h involving measurement of newborn head
circumference and heart rate. Notify physician of an increase in head circumference of 1 cm or more or heart rate greater
than 170 beats per minute. Further aspects of assessment may include bogginess or ballotable scalp, lethargy, and
colour (modified McMaster protocol).
Neonatal trauma occurs more commonly in primigravidas, but the overall rate after vacuum delivery is low. In a Canadian
study of 1000 deliveries using the Kiwi OmniCup, neonatal trauma rates were abrasions/blister 11.4%, hematoma
14.7%, intracranial hemorrhage 0.4%, and 1 subgaleal hemorrhage (0.1%) that did not require transfusion.35
The delivery should be reviewed with the parturient woman and her partner. Reassurance should be given regarding
chignon, caput, cephalhematoma, or facial marks.
Documentation
The indication and method of operative technique employed must be clearly and completely documented in all
operative deliveries.1 The position and station of the fetal head at the commencement of the intervention must be stated.
A contemporaneous written note and a dictated operative record are recommended.
The need for the intervention must be convincing, compelling, and documented.
Discussion and informed consent are essential before the intervention; however, in cases of abnormal fetal heart rate,
the consent process may necessarily be brief. After assisted vaginal delivery, the parturient women should be given a
clear explanation describing the procedure and its outcome. All questions should be addressed and contemporaneous
documentation can then be completed.

Suggested format for a chart note

• Date/time
• Physician
• Indication
• Record of discussion with the parturient woman of the risks, benefits, and options
• Position and station of the fetal head, (vaginally and abdominally)
• Amount of moulding and caput present
• Assessment of maternal pelvis
• Assessment of fetal heart rate and contractions
• Type of vacuum or forceps used
• Number of attempts and ease of application of vacuum or forceps
• Duration of traction for forceps and duration of application for vacuum (start and stop time noted), and force
used
• Any rotation applied with forceps or autorotation that occurs with vacuum
• For vacuum, number of pop-offs
• Position of chignon on fetal scalp (vacuum): flexing versus deflexing; median versus paramedian (see
Figure 7 above)
• Description of any maternal and neonatal injuries
• Initiation of monitoring for subgaleal hemorrhage (vacuum)
This may also serve as a template to dictate a delivery summary.
Summary
Assisted vaginal birth by vacuum or forceps is an appropriate and effective obstetrical intervention in certain clinical
situations. Clinical indications, contraindications, and expected maternal and fetal/neonatal outcomes should be
carefully assessed before the instrument is applied.

References
1. Cargill YM, MacKinnon CJ, Clinical Practice Obstetrics Committee. Guidelines for operative vaginal birth
[SOGC clinical practice guideline no 148]. J Soc Obstet Gynaecol Can. 2004;26:747-53. Available from:
https://www.jogc.com/article/S1701-2163(17)31107-6/abstract.
2. Operative vaginal delivery. Washington: American College of Obstetricians and Gynecologists; 2000.
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20. Chadwick LM, Pemberton PJ, Kurinczuk JJ. Neonatal subgaleal haematoma: associated risk factors, complications
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23. Vacca A. Vacuum-assisted delivery. Best Pract Res Clin Obstet Gynaecol. 2002;16:17-30.
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J AAPOS. 2013.
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2009;135:634-6.
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and “spontaneous” obstetric depressed skull fractures in a cohort of 68 neonates. Am J Obstet Gynecol.
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28. Bradley MS, Kaminski RJ, Streitman DC, Dunn SL, Krans EE. Effect of rotation on perineal lacerations in forceps-
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30. Nilsson I, Akervall S, Milsom I, Gyhagen M. Long-term effects of vacuum extraction on pelvic floor function: a
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33. Whitby EH, Griffiths PD, Rutter S, Smith MF, Sprigg A, Ohadike P, et al. Frequency and natural history of
subdural haemorrhages in babies and relation to obstetric factors. Lancet. 2004;363:846-51. Available from:
34. Towner D, Castro MA, Eby-Wilkens E, Gilbert WM. Effect of mode of delivery in nulliparous women on neonatal
intracranial injury. N Engl J Med. 1999;341:1709-14.
35. Edgar DC, Baskett TF, Young DC, O’Connell CM, Fanning CA. Neonatal outcome following failed Kiwi OmniCup
vacuum extraction. J Obstet Gynaecol Can. 2012;34:620-5.
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vaginal delivery on neonatal and maternal outcomes. Am J Obstet Gynecol. 2001;185:896-902.
37. Sadan O, Ginath S, Gomel A, Abramov D, Rotmensch S, Boaz M, et al. What to do after a failed attempt of vacuum
delivery? Eur J Obstet Gynecol Reprod Biol. 2003;107:151-5.
38. Operative vaginal delivery. 3rd ed ed. London: Royal College of Obstetricians and Gynaecologists; 2011. Available
from: https://www.rcog.org.uk/en/guidelines-research-services/guidelines/gtg26/.
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extraction device. BJOG. 2005;112:1510-5.
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versus conventional ventouse cups for vacuum-assisted vaginal delivery. BJOG. 2006;113:183-9.
41. Senanayake H. A prospective randomised controlled trial of the Kiwi Omnicup versus conventional ventouse cups
for vacuum-assisted vaginal delivery [letter]. BJOG. 2006;113:978-9.
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44. Johanson RB, Rice C, Doyle M, Arthur J, Anyanwu L, Ibrahim J, et al. A randomised prospective study comparing the
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45. Chenoy R, Johanson R. A randomized prospective study comparing delivery with metal and silicone rubber
vacuum extractor cups. Br J Obstet Gynaecol. 1992;99:360-3. Available from: http://www.ncbi.nlm.nih.gov/
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48. Muise KL, Duchon MA, Brown RH. The effect of artificial caput on performance of vacuum extractors. Obstet
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techniques. Obstet Gynecol. 1997;89:758-62.
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trauma during childbirth: role of forceps delivery routinely combined with mediolateral episiotomy. Am J Obstet
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59. Stedenfeldt M, Oian P, Gissler M, Blix E, Pirhonen J. Risk factors for obstetric anal sphincter injury after a successful
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61. Eason E, Labrecque M, Wells G, Feldman P. Preventing perineal trauma during childbirth: a systematic review.

62. Andrews V, Thakar R, Sultan AH, Jones PW. Are mediolateral episiotomies actually mediolateral? BJOG.
63. Stedenfeldt M, Pirhonen J, Blix E, Wilsgaard T, Vonen B, Oian P. Episiotomy characteristics and risks for obstetric
anal sphincter injuries: a case-control study. BJOG. 2012;119:724-30. Available from: https://www.ncbi.nlm.nih.
64. Kalis V, Karbanova J, Horak M, Lobovsky L, Kralickova M, Rokyta Z. The incision angle of mediolateral episiotomy
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subgaleal bleeding. Eur J Pediatr. 1992;151:532-5.
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70. Bachman JW. Forceps delivery [letter]. J Fam Pract. 1989;29:360.

Appendix A.
Table of Vacuum Conversions69
mm Hg inches Hg lb/in2 KG/CM2
100 3.9 1.9 0.13
200 7.9 3.9 0.27
300 11.8 5.8 0.41
400 15.7 7.7 0.54
500 19.7 9.7 0.68
600 23.6 11.6 0.82

Appendix B: Vacuum Mnemonic
A ADDRESS • consent
ANAESTHESIA • adequate pain relief
ASSISTANCE • neonatal support
ABSENCE • of contraindication
B BLADDER • bladder empty
C CERVIX • fully dilated, membranes ruptured

CONTRACTIONS • adequate
D DETERMINE • position, station and pelvic adequacy

• think possible shoulder dystocia
E EQUIPMENT • - inspect vacuum cup, pump, tubing and check pressure
F FONTANELLE • - position the cup just anterior to or over the posterior fontanelle
• - sweep finger around cup to clear maternal tissue
• 100 mm Hg initially
G GENTLE TRACTION • as contraction begins:

−− increase pressure to APPROX. 600 mm Hg (follow manufacturer’s range)
−− prompt mother for good expulsive effort
−− pull with contractions only
• traction in axis of birth canal

• pressure may be maintained in between contractions, but no traction is to be exerted.
H HALT if:
• no progress after two pulls
• no imminent delivery after 4 contractions
• no progress after 3 pop-offs
• no progress after 20 minutes
I INCISION • consider episiotomy (not routinely required)
J JAW • remove vacuum when jaw is reachable or delivery assured
Adapted from Bachman J. J Fam Pract 1989.70

Appendix C: Forceps Mnemonic
A ADDRESS ANAESTHESIA • consent

ASSISTANCE • adequate pain relief
ABSENCE • neonatal support
• of contraindication
B BLADDER • bladder empty
C CERVIX • fully dilated, membranes ruptured

CONTRACTIONS • adequate
D DETERMINE • position, station and pelvic adequacy

• think possible shoulder dystocia
E EQUIPMENT • check the equipment
F FORCEPS • phantom application

• left blade, left hand, maternal left side, pencil grip and vertical insertion, with right thumb
directing blade
• right blade, right hand, maternal right side, pencil grip and vertical insertion with left thumb
directing blade
• lock blade and support – check application
• posterior fontanelle 1 cm above plane of shanks
• fenestration not > 1 fingerbreadth between it and scalp
• sagittal suture perpendicular to plane or shanks with occipital sutures 1 cm above respective
blades
G GENTLE TRACTION • applied with contraction/expulsive effort
H HANDLE ELEVATED • traction in axis of birth canal

• do not elevate handle too early
I INCISION • consider episiotomy (not routinely required)
J JAW • remove forceps when jaw is reachable or delivery assured
Adapted from Bachman J. J Fam Pract 1989.70

Table of Contents
Chapter 11 Delivery of Twins............................................................................................................................................ 260

Introduction.............................................................................................................................................................. 260
Definitions..................................................................................................................................................... 260
Incidence.................................................................................................................................................................. 262
Morbidity and Mortality ........................................................................................................................................... 262
Reducing Iatrogenic Twin Pregnancies .................................................................................................................... 263
Predisposing Factors................................................................................................................................................. 263
Etiology .................................................................................................................................................................... 263
Diagnosis.................................................................................................................................................................. 263
Chorionicity................................................................................................................................................... 263
Management............................................................................................................................................................ 264
Antenatal Considerations.............................................................................................................................. 264
Delivery Location........................................................................................................................................... 265
Transport Considerations............................................................................................................................... 265
Method of Delivery........................................................................................................................................ 265
Timing of Delivery......................................................................................................................................... 266
Types of Presentations.............................................................................................................................................. 267
Management of Labour............................................................................................................................................ 269
Spontaneous Labour..................................................................................................................................... 269
Preterm Labour ............................................................................................................................................. 269
Induction....................................................................................................................................................... 269
Fetal Surveillance.......................................................................................................................................... 269
Analgesia and/or Anaesthesia for Multiple Gestation................................................................................... 270
Augmentation of Labour............................................................................................................................... 270
Cord Clamping and Blood Sampling............................................................................................................ 270
Third Stage and Postpartum Management................................................................................................... 270
Summary.................................................................................................................................................................. 271
Delivery of Twins 259

Chapter 11
Delivery of Twins
Introduction
Definitions
• Multiple gestation/pregnancy: more than one fetus in the same pregnancy.
• Twin gestation: two fetuses in the same pregnancy.
Twins may be:

• Monozygotic: developed from one ovum (egg).
• Dizygotic: developed from two ova (eggs).
• Monochorionic: developed with a single placenta (always monozygotic).
• Dichorionic: developed with two placenta (always diamniotic).
• Monoamniotic: fetuses in a single amniotic sac (always monozygotic and monochorionic).
• Diamniotic: fetuses in two, separate amniotic sacs.
• Conjoined: bodies of two fetuses are connected (always monozygotic).

Figure 1. Twin Chorionicity and Amnionicity

Figure 1. Twin Chorionicity and Amnionicity

Incidence
Spontaneous twins occur in approximately 1 in 90 pregnancies.1 As the use of ovulation induction and assisted
reproductive technologies (ART) increased, the rate of multiple gestations also increased, reaching 3.1 % in Canada by
2005. The rate has remained relatively stable since: in 2014, it was 3.3%. This is more than 12 000 births annually in
Canada.2 The rate of monozygotic twins (3 to 5 per 1000 birth) is only increased by ART, specifically IVF, whereas the rate
of dizygotic twins fluctuates with heredity, race, maternal age, and parity.3 Twins after ART are mostly dizygotic because
they arise from multi-embryo transfer.
Morbidity and Mortality4

Perinatal mortality rate:
• Monoamniotic twins (50% to 60%)
• Monochorionic diamniotic twins (4.4%)5
• Dichorionic twins (1.2%)5
Antenatal complications:
• Preeclampsia (10% to 20%)
• Prematurity (40% to 50%)
• Discordant growth and intrauterine growth restriction (15% to 25%)
• Twin-to-twin transfusion syndrome (5% to 10%)
• Congenital anomalies
• Death of one fetus (2% to 5%)
• Neurodevelopmental deficit in surviving twin after death of the other twin in a monochorionic twin
pregnancy(25%)6
• Cerebral palsy
• PROM7
Complications related to delivery:
• Cord accidents
• Malpresentation
• Uterine atony
• Placenta Previa
• Vasa previa secondary to a velamentous insertion of the cord
Postpartum complications:
• Hemorrhage
• Postpartum depression

Reducing Iatrogenic Twin Pregnancies

A 2012 cohort study showed that compared with spontaneous twin pregnancies, those conceived using ART had higher
rates of prematurity, Caesarean section, and obstetric morbidity (postpartum hemorrhage (PPH), premature rupture of
membranes, and cervical insufficiency).8 It is therefore incumbent on care providers to be judicious in the application of
ART. Strategies such as single IVF embryo transfer and embryo reduction are recommended,16 and in some jurisdictions
are controlled by legislation.11, 17
Predisposing Factors
The largest influence on the rate of twins is the use of ART, which increases the rate of both monozygotic and dizygotic
twins. The rate of dizigotic twins is also increased with:9
• increasing maternal age and parity
• a history of twins on the maternal side
• women who are Black
• better nutritional status
• elevated pituitary gonadotropins, which is also a possible common link for the other predisposing factors
(above)
Etiology
About two thirds of twins arise from the fertilization of 2 ova. They are called dizygotic or fraternal twins. About one
third of twins arise from the fertilization of a single ovum that subsequently divides into 2 embryos. They are called
monozygotic, or identical twins. Monozygotic embryos that fail to separate completely become conjoined twins.
Either or both processes can also result in more than 2 fetuses. For example, quadruplets may arise from a single ovum
or as many as 4 ova.9
Diagnosis
Twins should be considered in any woman with predisposing factors, and particularly in women who have undergone
assisted reproduction. Routine first trimester dating ultrasound has the advantage of detecting twins early, when the
chorionicity can most reliably be determined.
Chorionicity
• Chorionicity refers to the number of chorionic membranes present. Simply, monochorionic twins share one
placenta and dichorionic twins each have their own placenta

• Chorionicity should not be confused with zygosity. About 25% of monozygotic twins are dichorionic. All
dizygotic twins are dichorionic.
• Monochorionic twins have one placenta with shared vascular circulation
• Dichorionic twins have 2 placenta with separate vascular circulation.
• The incidence of perinatal mortality is higher in monochorionic twins than in dichorionic twins. This
is primarily due to twin-to-twin transfusion syndrome in diamniotic twins and cord entanglement in
monoamniotic twins.
• Determining the chorionicity is important in the management of twin gestation. This is best done by an early
ultrasound examination at 7 to 14 weeks.10
• Establishing chorionicity by ultrasound can also be aided by examining the placenta, seeking the lambda
sign in the dividing membrane, and determining the sex of the fetuses.
When ultrasound has not been obtained, a twin pregnancy should be suspected. Whenever the symphysis–fundal height
is larger than expected. For instance, the late second trimester symphysis–fundal height exceeds the gestational age
by an average of 5 centimetres in a twin gestation. The auscultation of a second fetal heart tone at any gestational age
should also prompt the clinician to consider the diagnosis of twin pregnancy. Abdominal palpation alone is an unreliable
method of detecting twins.9 In rare cases, twins may become apparent only at delivery.10
The differential diagnosis of a large-for-gestational-age-uterus includes9, 11
• Molar pregnancy (hydatidiform mole)
• Inaccurate dates
• Polyhydramnios
• Macrosomia
• Uterine Fibroids
• Adnexal and/or abdominal masses
Management
Antenatal Considerations
Early diagnosis of twins allows for appropriate antenatal, intrapartum and post-partum planning.
Antenatal care focuses on screening for complications specific to twin pregnancies, in addition to care routine in all
pregnancies. Complications specific to twin pregnancies include premature birth, growth discordance, intrauterine
growth restriction, gestational hypertension, and twin-to-twin transfusion syndrome

Prenatal Genetic Testing

• At 11 to 14 weeks, nuchal translucency in combination with maternal age ± serum anylytes can be used to
assess of the risk of aneuploidy.
• Alternatively, non-invasive prenatal genetic testing is now widely available and valid for twins.
Ultrasound Surveillance
• Depending on resources and geography, ultrasound assessments are recommended in monochorionic
diamniotic twins every 2 weeks from 16 weeks gestation to monitor for twin-to-twin transfusion syndrome
(early enough to allow intervention) and selective IUGR.12
• For dichorionic twins, a growth ultrasound is recommended every 4 weeks, starting at20 weeks to assess for
growth restriction. In contrast to growth in singletons, growth in normal dichorionic twins falls off slightly at
approximately 30 to 32 weeks. Normal monochorionic/diamniotic twin growth falls off at 28 weeks.13, 14
There is no evidence that routine hospitalization or bed rest prevents preterm birth for women with twins.15
Delivery Location
Delivery location should be discussed and agreed upon by the woman, her family, and her care providers. The 2000
SOGC consensus statement10 recommends that for a planned twin delivery, anaesthetic, obstetrical, neonatal, and
nursing staff trained in twin delivery be present in hospital. A primary care physician or midwife may provide hands-on
care under the supervision of a consultant physician/obstetrician who has expertise in the delivery of twins. Each of the
twins should have an assigned care provider, skilled in neonatal resuscitation, present at the delivery. Caesarean section
should be available. 1617
Transport Considerations
Antenatal transport of the woman to another centre should be considered when local staffing or resources are
insufficient, particularly when twins are preterm. Careful assessment of the safety of transport and communication
between the sending and the receiving centres are essential, as described in the 2005 SOGC Maternal Transport Policy.18
Local, regional, and provincial guidelines should also be considered.
Method of Delivery
Vaginal delivery should be the goal unless there are contraindications. A 2013 trial that randomized 2804 women to
planned Caesarean section or planned vaginal delivery (with CS if medically indicated) showed no benefit of planned CS.
In this study, twins were ≥ 32 weeks gestation, twin A was vertex, and an obstetrician skilled in vaginal twin delivery was
present.19 Three-month follow-up showed no difference in maternal outcomes including breastfeeding and problematic
incontinence.20 Two-year pediatric follow-up showed no difference in death or neurodevelopmental delay in children

born by planned CS or planned vaginal birth.21 A French case series of 1009 women demonstrated similar safety and
intrapartum CS rate for dichorionic and monochorionic/diamniotic twins with planned vaginal delivery.22 23
Timing of Delivery
The timing of delivery of twins is a controversial topic. The 2011 NICE guidelines recommend a decision tree to help
determine the optimal timing of delivery.24 This includes preparing the woman and her family for the possibility of an
early delivery and its sequelae, even in an uncomplicated pregnancy. According to the NICE guidelines, approximately
“60% of twin pregnancies result in spontaneous birth before 370 weeks. . . . Continuing uncomplicated twin
pregnancies beyond 380 weeks increases the risk of fetal death”24
In determining the optimal timing of delivery, the risk of stillbirth with continuing pregnancy must be weighed
against the risk of adverse outcomes related to prematurity. Elective or spontaneous preterm birth increases the risk
of neonatal admission to the NICU As a result, the NICE guidelines suggest offering elective delivery at 360 weeks for
monochorionic diamniotic twin pregnancies and at 370 weeks for dichorionic twin pregnancies.24 However, further
studies have suggested that elective delivery before 37 weeks is of no benefit and may increase the rate of perinatal
morbidity.25-27 Elective delivery, particularly by CS, at 36 to 37 weeks carries an increased risk of neonatal respiratory
62 28
morbidity. Induction of labour with twins also carries maternal risks including an increased likelihood of CS if the cervix
is unripe.29
30
Further studies are being conducted to determine the optimum time of delivery. Currently, it is reasonable to offer
elective delivery for monochorionic twins at between 36 and 37 weeks’ gestation, and for dichorionic twins at between
37 and 38 weeks’ gestation. If a woman declines elective delivery, weekly appointments with a specialist obstetrician are
recommended with weekly antenatal fetal surveillance and biweekly growth ultrasound assessment.24 Delivery by 39 to
40 weeks is recommended to reduce the risk of stillbirth.
For monoamniotic twins, care in a tertiary centre should be considered from 24 weeks’ gestation due to universal cord
entanglement. Close surveillance and planned CS between 32 and 33 weeks is often recommended, although there is
some evidence that later delivery may be appropriate.10, 23

Types of Presentations
Types of Presentations
Figure 2. Types of Presentation in Twin Gestation

Both Twins Cephalic

• Vaginal delivery should be expected.
• After the delivery of the first twin, the presentation of the second twin should be determined and cord
presentation ruled out. If necessary, presentation should be confirmed using ultrasound.
• When uterine contractions are inadequate, augmentation of labour is recommended to assist in the descent
of the head of the second twin.
• Artificial rupture of the membranes should be attempted when the head of the second twin has descended
to station 0 or −1. Care should be taken to identify cases with cord presentation.
First Twin Cephalic, Second Twin Breech or Transverse

• First twin delivered vaginally.
• Vaginal delivery of the second twin is suggested as long as the estimated fetal weight is between 1500 and
4000 grams and the obstetrician is trained in vaginal breech delivery.31
• Immediately after the delivery of the first twin, the presentation of the second twin must be confirmed. If
there is any doubt about the presentation, ultrasound examination should be used to clarify. The decision
to manage the second twin actively or expectantly is left to the individual obstetrician. If expectant
management is chosen, ongoing fetal surveillance is required.
• If the second twin is in a footling breech presentation or in a transverse lie and fetal monitoring is atypical or
abnormal, there are two options: (1) breech extraction (with internal podalic version if needed), and (2) CS
• If the second twin is in a transverse lie and fetal monitoring is reassuring, there are three options: (1)
external version to vertex, (2) internal podalic version and breech extraction, or (3) CS.
• Breech extraction should not be performed if the second twin is significantly larger than the first. If
breech extraction is performed, it is preferable to leave the amniotic sac intact until one foot or both feet are
identified and secured with the operating hand.
First Twin Breech

When the first twin is in frank or complete breech presentation, the same issues exist as for vaginal delivery of a
singleton breech. The mother must be informed of all pertinent risks, including the possibility of expulsive delay due to
trapped fetal parts resulting in adverse fetal outcome. This risk can be avoided by Caesarean section, which is generally
recommended; however, several case series have shown reasonable safety and potential reduced maternal morbidity
with a trial of labour in women with first twin breech.32-35
3 43
First Twin Non-Longitudinal

If the first twin is not in a longitudinal lie, Caesarean section is indicated.

Spontaneous Labour
Ideally, planned delivery locations should have been previously agreed upon and the woman (re-)located near her
delivery hospital. Should she enter labour in a setting without prerequisite operative and specialist capabilities, the
safety of transport to a larger centre must be weighed against the risks of local delivery with available resources.
Preterm Labour
Preterm labour is a frequent complication of multiple gestations and the primary cause of the increase in perinatal
morbidity and mortality in multiple gestations. Women with multiple gestations should be taught the early warning
signs and symptoms of preterm labour and advised to report promptly for evaluation. When preterm labour is diagnosed
in a smaller hospital, consideration must be given to tocolytic therapy, administration of glucocorticoids, and transport
of the woman to a regional referral centre. A 2012 Cochrane review does not support the routine use of betamimetics to
suppress preterm labour in twin pregnancies.36
Induction
There are no adequate clinical trials to date comparing elective induction of labour versus expectant management for
uncomplicated twin pregnancies. The indications and contraindications for induction of labour with multiple gestations
include all of the factors that would apply to a singleton gestation. Growth restriction of one or both twins, sometimes
manifest as a significant disparity in estimated fetal weights, is a sufficient indication for induction.
The methods used for labour induction should be the same as those used for a singleton pregnancy. The safety of
induction in the presence of a previous CS in a multiple pregnancy is unknown.
Fetal Surveillance
All fetuses must have assessment of their well-being in labour. Twin pregnancy carries higher risk of perinatal morbidity
and mortality than singleton pregnancy. This is related to a number of factors including umbilical cord problems,
placental dysfunction, and/or twin-to-twin transfusion. After delivery of the first twin, the second twin is at additional risk
because of potential cord compression and intrapartum placental abruption.
Continuous, simultaneous electronic fetal monitoring is recommended for twin pregnancies during labour. Some current
electronic monitoring machines have the capacity to use two separate Doppler ultrasound transducers and to externally
monitor each twin successfully. Electronic monitoring may be more successful at producing interpretable tracings if
the leading twin is monitored with a scalp electrode and the second twin with Doppler ultrasound. The scalp electrode
should be applied as soon as labour is well-established.

Following delivery of the first twin, monitoring of the second twin should be continued with an external transducer.
When the second twin is in a longitudinal lie and membranes can be safely ruptured, monitoring with a fetal scalp
electrode can be commenced.
During the second stage of labour with twins, ultrasound is helpful to determine presentation and location of the fetal
heart of twin B if necessary.
Analgesia and/or Anaesthesia for Multiple Gestation

The risks, benefits, and limitations of analgesia and anaesthesia should be discussed with the woman and her family.
Epidural analgesia is used widely during labour with twin gestations. It provides effective labour analgesia and adequate
anaesthesia for intrauterine fetal manipulation or CS, if required.
Augmentation of Labour
If labour is dysfunctional, augmentation is an option. The same indications and methods are used as in a singleton
pregnancy. Augmentation of labour after delivery of the first twin may be appropriate.10
Cord Clamping and Blood Sampling

There is no evidence to guide the practice of delayed cord clamping after delivery of the first twin. Delayed cord clamping
of 60 seconds for each dichorionic twin would seem appropriate. For monochorionic twins, since there may be vascular
communications between the placentas, delayed cord clamping of twin A may result in transfusion from twin B to twin
A. A delay of perhaps 30 seconds might be more appropriate after delivery of a monochorionic twin A. Delayed cord
clamping after delivery of monochorionic twin B is appropriate.
Blood may be obtained for cord gases from an isolated clamped segment of cord at the time of delivery of each twin;
however, since placental vascular connections commonly exist in monochorionic twins, blood sampling or drainage of
the intact cord must be delayed until after the birth of the second twin.
Third Stage and Postpartum Management

After delivery of the second twin, active management of the third stage of labour is indicated. There is an increased
risk of PPH; therefore, an oxytocin infusion should be continued for 2 to 3 hours following delivery of the placenta to
ensure that the uterus stays well-contracted. Sublingual or rectal misoprostol may be used as adjunct prophylaxis against
delayed PPH as its effect lasts for several hours.
Whenever possible, the woman and her babies should be kept together postpartum. Breastfeeding twins can be
challenging. Early initiation and expert assistance may benefit both mother and babies. The increased risk of postpartum
depression following multiple births should be kept in mind, and renewed contact should be made with a multiple
pregnancy support group or other previously identified support providers.

Summary
All complications of pregnancy are more likely to occur in a twin pregnancy, and a high level of vigilance and diligence
is required to minimize the inherent risks and optimize the outcomes. It is important to establish chorionicity early in a
twin pregnancy.
If possible, twins should be delivered in a centre with facilities for continuous electronic fetal surveillance, intrapartum
ultrasound, and emergency CS. Staff skilled in the care of twins should also be available.

References
1. Public Health Agency of Canada. Canadian Perinatal Health Report. Ottawa: 2017.
2. Live births and fetal deaths (stillbirths), by type (single or multiple), Canada, provinces and territories. Table 102-
4515. [CANSIM database]. Ottawa: 2013.
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problem pregnancies, 4th ed. New York: Churchill Livingstone; 2002. p. 775-826.
4. Newman RB, Rittenberg C. Multiple gestation. In: Gibbs RS KB, Haney AF, Nygaard I,, editor. Danforth’s obstetrics
and gynecology, 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 220-45.
5. Glinianaia SV, Obeysekera MA, Sturgiss S, Bell R. Stillbirth and neonatal mortality in monochorionic and dichorionic
twins: a population-based study. Hum Reprod. 2011;26:2549-57. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/21727159.
6. van Klink JM, van Steenis A, Steggerda SJ, Genova L, Sueters M, Oepkes D, et al. Single fetal demise in
monochorionic pregnancies: incidence and patterns of cerebral injury. Ultrasound Obstet Gynecol. 2015;45:294-
7. Pakrashi T, Defranco EA. The relative proportion of preterm births complicated by premature rupture of membranes
in multifetal gestations: a population-based study. Am J Perinatol. 2013;30:69-74. Available from: https://www.
8. Bamberg C, Fotopoulou C, Neissner P, Slowinski T, Dudenhausen JW, Proquitte H, et al. Maternal characteristics and
twin gestation outcomes over 10 years: impact of conception methods. Fertil Steril. 2012;98:95-101. Available
9. Multifetal gestation. In: Cunningham FG, Hauth JC, Leveno KJ, Gilstrap L, Bloom SL, Wenstrom KD, editors.
Williams obstetrics [monograph online]. New York: McGraw-Hill Medical Publishing Division; 2005.
10. Barrett J, Bocking A. Management of twin pregnancies (part I) [SOGC consensus statement no 91]. Journal of
Obstetrics and Gynaecology. 2000;22:519-29.
11. DeCherney AH, Nathan L. Current diagnosis & treatment obstetrics & gynecology [Lange current series], 10th ed. .
New York: McGraw-Hill; 2007.
12. Baud D, Windrim R, Van Mieghem T, Keunen J, Seaward G, Ryan G. Twin-twin transfusion syndrome: a frequently
missed diagnosis with important consequences. Ultrasound Obstet Gynecol. 2014;44:205-9. Available from:
13. Shivkumar S, Himes KP, Hutcheon JA, Platt RW. An ultrasound-based fetal weight reference for twins. Am J Obstet
Gynecol. 2015;213:224 e1-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25899626.

14. Stirrup OT, Khalil A, D’Antonio F, Thilaganathan B, Southwest Thames Obstetric Research C. Fetal growth reference
ranges in twin pregnancy: analysis of the Southwest Thames Obstetric Research Collaborative (STORK) multiple
pregnancy cohort. Ultrasound Obstet Gynecol. 2015;45:301-7. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/25052857.
15. Crowther CA, Han S. Hospitalisation and bed rest for multiple pregnancy. Cochrane Database Syst Rev.
16. McDonald S, Murphy K, Beyene J, Ohlsson A. Perinatal outcomes of in vitro fertilization twins: a systematic review
and meta-analyses. Am J Obstet Gynecol. 2005;193:141-52. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/16021072.
17. Committee on E. ACOG committee opinion. Number 369. June 2007. Multifetal pregnancy reduction. Obstet
18. Wilson AK, Martel MJ, Arsenault MY, Cargill YM, Delaney M, Daniels S, et al. Maternal transport policy. J Obstet
19. Barrett JF, Hannah ME, Hutton EK, Willan AR, Allen AC, Armson BA, et al. A randomized trial of planned cesarean or
vaginal delivery for twin pregnancy. N Engl J Med. 2013;369:1295-305. Available from: https://www.ncbi.nlm.nih.
20. Hutton EK, Hannah ME, Ross S, Joseph KS, Ohlsson A, Asztalos EV, et al. Maternal outcomes at 3 months after
planned caesarean section versus planned vaginal birth for twin pregnancies in the Twin Birth Study: a randomised
controlled trial. BJOG. 2015;122:1653-62. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26328526.
21. Asztalos EV, Hannah ME, Hutton EK, Willan AR, Allen AC, Armson BA, et al. Twin Birth Study: 2-year
neurodevelopmental follow-up of the randomized trial of planned cesarean or planned vaginal delivery for
twin pregnancy. Am J Obstet Gynecol. 2016;214:371 e1- e19. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/26830380.
22. Garabedian C, Poulain C, Duhamel A, Subtil D, Houfflin-Debarge V, Deruelle P. Intrapartum management of twin
pregnancies: are uncomplicated monochorionic pregnancies more at risk of complications than dichorionic
pregnancies? Acta Obstet Gynecol Scand. 2015;94:301-7. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/25494703.
23. Dias T, Mahsud-Dornan S, Bhide A, Papageorghiou AT, Thilaganathan B. Cord entanglement and perinatal outcome
in monoamniotic twin pregnancies. Ultrasound Obstet Gynecol. 2010;35:201-4. Available from: https://www.ncbi.
24. National Collaborating Centre for Women’s and Children’s Health N. Multiple pregnancy: the management of twin
and triplet pregnancies in the antenatal period [NICE clinical guideline 129]. London: 2011.
25. Sullivan AE, Hopkins PN, Weng HY, Henry E, Lo JO, Varner MW, et al. Delivery of monochorionic twins in the
absence of complications: analysis of neonatal outcomes and costs. Am J Obstet Gynecol. 2012;206:257 e1-7.

26. Berezowsky A, Mazkereth R, Ashwal E, Mazaki-Tovi S, Schiff E, Weisz B, et al. Neonatal outcome of late preterm
uncomplicated monochorionic twins: what is the optimal time for delivery? J Matern Fetal Neonatal Med.
27. Breathnach FM, McAuliffe FM, Geary M, Daly S, Higgins JR, Dornan J, et al. Optimum timing for planned delivery
of uncomplicated monochorionic and dichorionic twin pregnancies. Obstet Gynecol. 2012;119:50-9. Available
28. Aiken CE, Fowden AL, Smith GC. Antenatal glucocorticoids prior to cesarean delivery at term. JAMA Pediatr.
29. Stutchfield P, Whitaker R, Russell I, Antenatal Steroids for Term Elective Caesarean Section Research T. Antenatal
betamethasone and incidence of neonatal respiratory distress after elective caesarean section: pragmatic
randomised trial. BMJ. 2005;331:662. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16115831.
30. Jonsson M. Induction of twin pregnancy and the risk of caesarean delivery: a cohort study. BMC Pregnancy
Childbirth. 2015;15:136. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26077416.
31. Houlihan C, Knuppel RA. Intrapartum management of multiple gestations. Clin Perinatol. 1996;23:91-116.
32. Blickstein I, Goldman RD, Kupferminc M. Delivery of breech first twins: a multicenter retrospective study. Obstet
33. Bourtembourg A, Ramanah R, Jolly M, Gannard-Pechin E, Becher P, Cossa S, et al. [Twin delivery with the first
twin in breech position. A study of 137 continuous cases]. J Gynecol Obstet Biol Reprod (Paris). 2012;41:174-81.
34. Sentilhes L, Goffinet F, Talbot A, Diguet A, Verspyck E, Cabrol D, et al. Attempted vaginal versus planned cesarean
delivery in 195 breech first twin pregnancies. Acta Obstet Gynecol Scand. 2007;86:55-60. Available from:
35. Steins Bisschop CN, Vogelvang TE, May AM, Schuitemaker NW. Mode of delivery in non-cephalic presenting twins:
a systematic review. Arch Gynecol Obstet. 2012;286:237-47. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/22465994.
36. Yamasmit W, Chaithongwongwatthana S, Tolosa JE, Limpongsanurak S, Pereira L, Lumbiganon P. Prophylactic
oral betamimetics for reducing preterm birth in women with a twin pregnancy. Cochrane Database Syst Rev.

Table of Contents
Chapter 12 Trial of Labour After Caesarean....................................................................................................................... 276

Introduction.............................................................................................................................................................. 276
Definitions..................................................................................................................................................... 276
Incidence....................................................................................................................................................... 276
Factors to Consider........................................................................................................................................ 277
Benefits and Risks of TOLAC...................................................................................................................................... 278
Maternal Outcomes Associated With TOLAC Versus ERCS............................................................................. 278
Uterine Rupture............................................................................................................................................ 279
Considerations for Future Pregnancies......................................................................................................... 280
Management............................................................................................................................................................ 281
Requirements for a TOLAC............................................................................................................................. 281
Selection of Candidates for a TOLAC.............................................................................................................. 282
Special Considerations.................................................................................................................................. 282
Management of Labour............................................................................................................................................ 283
Fetal Heart Rate Patterns and Uterine Rupture............................................................................................. 283
Induction and Augmentation of Labour........................................................................................................ 284
Signs and Symptoms of Uterine Scar Rupture.............................................................................................. 284
Management of Uterine Rupture.................................................................................................................. 285
Summary.................................................................................................................................................................. 285
Trial of Labour After Caesarean 275

Chapter 12
Trial of Labour After Caesarean
Introduction
The primary indication for Caesarean section (CS) in Canada is a previous CS, accounting for over 30% of the total
number of CS. Every year, over 30 000 women in Canada undergo either trial of labour or repeat CS. Professional
associations, including the Society of Obstetricians and Gynaecologists of Canada, the Royal College of Obstetricians
and Gynaecologists, and the American Congress of Obstetricians and Gynecologists, recommend that eligible women be
offered a trial of labour after CS.1-3
2
If a woman has requested a trial of labour after CS and is a good candidate for a planned trial of labour, she and her
health care providers must understand and accept the risks and benefits. Not all women (or care providers) will find the
same balance of risks and benefits acceptable.2 Discussions about delivery options in future pregnancies may begin as
early as the postpartum period following CS.
Definitions
Vaginal birth after Caesarean (VBAC) Vaginal delivery after a CS in a previous pregnancy.
Trial of labour after Caesarean (TOLAC) A plan to attempt labour and vaginal delivery in a woman who has had a previous CS.
Elective repeat Caesarean section (ERCS) A CS performed before the onset of labour in a woman who has had a CS in a previous
pregnancy.
Uterine rupture The complete separation of the myometrium with or without extrusion of the fetal parts
into the maternal peritoneal cavity.
Uterine dehiscence A clinically occult and incomplete disruption: the fetal membranes are not ruptured and
the fetus is not outside the uterus, and the peritoneum over the defect is usually intact.
Not all studies are consistent in this definition
Incidence
The Canadian Institute for Health Information reported the CS rate in Canada increased to 28.2 % and the repeat CS rate
was 81.2 % in 2016-2017. The primary indication for CS in Canada is a previous CS, accounting for over 30% of the total.
In British Columbia, the proportion of women with a previous cesarean delivery who were deemed eligible for vaginal
birth after cesarean delivery increased from 75% in 2010 to 80% in 20144

In Canada, the TOLAC rate for women with only one previous pregnancy resulting in a CS was 32.8% in 2003–2004,
decreased to 28.2% in 2007–2008 and then increased to 31.4% in 2013– 2014.
A 2011 review found that the overall TOLAC rate among studies in the United States was 58%, with a range of 28% to
70%.5 In studies initiated after 1996, 44% of women had a TOLAC compared with 62% of women in studies initiated
before 1996.5 The success rate among women who underwent TOLAC is approximately 74% in the United States.6, 7
Factors to Consider
In general, VBAC success is approximately 70-75% and is referenced as such in the Canadian, American, British and
Australian/New Zealand guidelines.1-3 A prospective study of 14 529 women who underwent a TOLAC between1999 and
2002 identified factors predictive of outcome.8, 9 The following should be discussed with women considering the choice
of a TOLAC versus repeat CS.
Factors that increase the likelihood of a successful VBAC include:
• Previous successful VBAC
• Previous vaginal delivery
• Favourable cervix
• BMI <30
• birth weight <4000 g
• Spontaneous onset of labour
• Indication for previous CS (e.g., breech presentation) not present in current pregnancy
• Maternal age < 40 years
Factors that decrease the likelihood of a successful VBAC include:
• Previous CS performed for dystocia
• Need for induction of labour requiring cervical ripening
• Need for augmentation of labour
• Gestational age > 40 weeks
• Estimated birth weight > 4000 grams
• Maternal body mass index > 30 kg/m2
• Maternal hypertension
A prediction model for TOLAC success was developed retrospectively from 9616 women who underwent a TOLAC. The
successful VBAC rate was 75%.8 It has been shown to be valid in a Canadian population.10 This model predicts the
probability of VBAC success and may be used in practice as a primary method to refine counselling during antepartum
visits for women who have undergone a prior CS.1-3, 8, 10, 11 https://mfmunetwork.bsc.gwu.edu/PublicBSC/MFMU/
VGBirthCalc/vagbirth.html)
The strongest predictor of a successful VBAC (85-90%) is a previous vaginal delivery. It is also associated with a decreased
risk of uterine rupture. Adolescents are more likely than adult women to attempt VBAC, and they are as likely to be
successful. Adolescents should be encouraged to attempt a trial of labour after prior CS when appropriate to lower the
risks of lifelong maternal morbidity from numerous repeat CS.12

Benefits and Risks of TOLAC

Successful VBAC avoids major abdominal surgery, has a lower risk of hemorrhage, thromboembolism, infection
and a shorter recovery period than ERCS.2 In addition for those anticipating future pregnancies, VBAC reduced the
risks of multiple CS including surgical risks and abnormal placentation. However, TOLAC is associated with maternal
and neonatal risks. Maternal morbidity includes uterine rupture, hemorrhage, thromboembolism, and infection,
hysterectomy and death. Most of the maternal morbidity from TOLAC occurs with failed TOLAC. Successful VBAC has fewer
complications that ERCS but failed TOLAC and consequent repeat CS has a higher risk than ERCS.6, 13, 14. The key point
is that the risk of maternal morbidity is primarily related to the likelihood of a successful VBAC. Stratification of patient
based on prediction models and/or factors associated with success and failure of TOLAC is paramount.2
Maternal Outcomes Associated With TOLAC Versus ERCS

There are currently no randomized controlled trials comparing maternal or neonatal outcomes in women undertaking
TOLAC and those undergoing an elective repeat caesarean section (ERCS). Much of the evidence about the safety of a
TOLAC versus an ERCS is based on observational data. Recommendations and decisions about a TOLAC should therefore
be made cautiously.
A 2011 analysis6 found the following short-term maternal outcomes with TOLAC versus ERCS:
POTENTIAL HARM TOLAC ERCS
Maternal death 3.8 per 100 000 TOLAC 13.4 per 100 000 Significantly higher for ERCS
(95% confidence interval (95% CI 4.3 to 41.6)

[CI] 0.9 to 15.5)
Uterine rupture 4.7/1000 (0.47%) 0.3/1000 (0.026%) Significantly higher for TOLAC
(95% CI 0.28 to 0.77) (95% CI 0.009 to 0.082)
Length of stay 2.55 days 3.92 days Length of stay is higher for ERCS
(95% CI 2.34 to 2.76) (95% CI 3.56 to 4.29)
Hemorrhage 6.6 per 1000 4.6 per 1000 Not statistically significantly different
(95% CI 2.0 to 22.1) (95% CI 1.6 to 13.2)
Hysterectomy 0.17% 0.28% Not statistically significantly different
(95% CI 0.12 to 0.26) (95% CI 0.12 to 0.67)

POTENTIAL HARM TOLAC ERCS
Infection rate 46 per 1000 32 per 1000 Not statistically significantly different
(95% CI 15 to 135) (95% CI 13 to 73) A trend towards increased endometritis was seen
with ERCS compared with TOLAC; in contrast,
chorioam-nionitis was increased in TOLAC
compared with ERCS. Increasing body mass index
was associated with increased fever in patients
undergoing TOLAC
Uterine Rupture
Within the “Evidence Report/Technology Assessment Report Vaginal Birth After Cesarean: New Insights” it was noted
that “While numerous studies have been published relating to uterine rupture and/or dehiscence (393 articles), only 8
cohort studies were good or fair quality, included the population of interest, and used the anatomic definition for uterine
rupture contained in this report.” 6
The risk of uterine rupture for all women with a prior CS regardless of route of delivery is 0.3 percent (95% CI 0.2 to 0.4).
The risk of uterine rupture for women undergoing a TOLAC is significantly elevated at 0.47 percent (95% CI 0.28 to 0.77)
compared with the risk for women undergoing an ERCS (0.026; 95% CI 0.009 to 0.082). There were no maternal deaths
due to uterine rupture in any of the 8 studies reviewed. The risk of hysterectomy due to uterine rupture ranged from 14%
to 33%.6
Risk factors for uterine rupture

Induction of labour increases the risk of uterine rupture. The risk of uterine rupture among women who had induction of
labour was lowest with oxytocin (1.1%), followed by prostaglandin E2 (2%), and highest with misoprostol (6%). However,
these risk estimations may be imprecise given the inconsistency in study design and methodology; the results should be
interpreted with caution.5
Women with a prior classical (vertical) uterine incision are at increased risk of uterine dehiscence or rupture. Compared
with women with prior low transverse CS, women with prior low vertical CS are not at a significantly increased risk of
uterine dehiscence or rupture.6
The following also increase the risk of uterine rupture (and all should be documented):
• Short interval from previous CS (< 18 months)
• More than 2 previous CS
• Previous CS for dystocia in the second stage of labour15
• Locked single-layer closure of the previous uterine incision (single-layer unlocked or 2-layer closure
acceptable)16

Ultrasound assessment of lower uterine segment (LUS) thickness has studied to try to predict an increased risk of uterine
rupture. A meta-analysis of LUS thickness showed a thickness of 2.1-4.0 mm had a strong negative predictive value and
thickness of 0.6-2.0 mm a strong positive predictive value.17 The study could not determine a LUS thickness cut off value
usable in clinical practice.1 This is a research area to watch. Some are advocating for its use.
Neonatal Mortality and Morbidity

A large meta-analysis found the rate of perinatal death to be significantly higher with TOLAC than with ERCS (1.3 per
1000; 95% CI 0.59 to 3.04 versus 0.5 per 1000; 95% CI 0.07 to 3.82).11 The overall risk of perinatal death due to uterine
rupture was found to be 6.2%.11 Overall, the literature relating to response time between premonitory signs of uterine
rupture and perinatal mortality is insufficient. However, there is suggestion that fetal bradycardia is an ominous sign for
fetal extrusion, which is associated with poor perinatal outcomes.11
The same meta-analysis found no differences in Apgar scores or in rates of sepsis or NICU admission between neonates
whose mothers underwent TOLAC and those who underwent ERCS.11 There was insufficient evidence to determine if rates
of respiratory distress, neonatal trauma, or asphyxia/hypoxic-ischemic encephalopathy varied between TOLAC and ERCS.
No studies were found that explored the effect of a TOLAC versus an ERCS on breastfeeding initiation or continuation.11
Considerations for Future Pregnancies
Placenta Previa
A 2010 review of 203 studies found that women who had undergone a prior CS had a statistically significant increased
risk of placenta previa compared with women who had not undergone prior CS at a rate of 12 per 1000 (95% CI 8 to 15
per 1000). The incidence increased with increasing number of prior CS. Prior CS was a significant risk factor for maternal
morbidity in women with placenta previa. Compared with women who had placenta previa but no prior CS, women
with one prior CS and placenta previa had a statistically significant increased risk of blood transfusion (15% vs. 32.2%),
hysterectomy (0.7% to 4% vs. 10%), and composite maternal morbidity (15% vs. 23% to 30%). For women with 3 or more
prior CS and placenta previa, the risk of hysterectomy and composite maternal morbidity rose significantly (0.7% to 4%
vs. 50% to 67%, and 15% vs. 83%, respectively).6
Placenta Accreta
The incidence of placenta accreta rose with increasing number of prior CS. The results were statistically significant for
women with 2 or more prior CS (odds ratio 8.6 to 29.8).6
Women with placenta previa were at increased risk for placenta accreta, and the risk increased with increasing number of
prior CS. Women with more than 3 prior CS and placenta previa had a 50% to 67% incidence of placenta accreta.6

Management
Requirements for a TOLAC
Obstetrical guidelines recommend that a TOLAC should be attempted only in hospitals that can provide emergency
CS, blood products, and neonatal resuscitation.1-3 A TOLAC is always associated with a risk of uterine rupture, however
small, and a good outcome is not guaranteed under any circumstances. There is little evidence to provide guidance
about how quickly a CS would need to be done to prevent serious neonatal morbidity and mortality. The ACOG and
Green-top guidelines indicate the ability to perform an immediate CS. The ACOG guideline states that insettings where
the resources are not immediately available, there should be a clear protocol to perform an emergency CS in a timely
fashion. The SOGC guideline discusses a “timely” response to an emergency CS and recognizes some facilities may take
up to 30 minutes. Timely emergency Cesarean sections (initiated within 30 minutes) although reasonable, may not
prevent serious neonatal morbidity and mortality.18 The 2019 SOGC TOLAC guideline states “that a TOLAC is optimal in
an institution that has in-house obstetric, anesthesia, and surgical staff to reduce the decision-to-delivery interval in cases
of suspected uterine rupture. The SOGC acknowledges that this may not be possible in birthing units across Canada”.19
Hospitals and care providers offering a TOLAC should have emergency protocols that include situations in which the
specialists who are needed to perform CS may not be immediately available.3 Women should be aware of the resources
to effect an urgent CS. Care providers should be able to recognize the signs and symptoms of uterine scar rupture and
have a management plan in place should this occur. Regular emergency drills or other simulation exercises may be
useful for team preparedness in these rare emergencies.
The SOGC recommends that a TOLAC be offered to women with one previous transverse low-segment CS
following appropriate discussion and documentation of maternal and perinatal risks and benefits as part of
obtaining informed consent.3
Access to the previous operative report is desirable, and the opinion of the previous surgeon may be helpful. If the
operative report is not available, TOLAC is permissible if the clinical circumstances of prior CS suggest there was an
uncomplicated lower segment incision. There must be no contraindications to vaginal birth.
The following are contraindications to a TOLAC:
• Any contraindications to labour
• Previous or suspected classical uterine incision for CS
• Previous inverted T uterine incision
• Previous uterine rupture
• Previous major uterine reconstruction (e.g., full thickness repair for myomectomy, repair of müllerian
anomaly, cornual resection)
• Inability to perform an emergency CS
• Patient refusal

Selection of Candidates for a TOLAC

Consent Discussion and Documentation
Informed consent for TOLAC should include a documented discussion of the risks and benefits of elective CS versus
TOLAC. The likelihood of successful VBAC is fundamental to the discussion. Women must understand the evidence if they
are to make informed decisions about planning a TOLAC or a repeat Caesarean section. A consent form specific for TOLAC/
VBAC may be useful for hospitals offering TOLAC to reflect local resources and availability to perform an emergency CS.
Health care providers should be aware of the factors that influence women’s choices. These include:
• Care provider’s recommendation
• Recovery time and the need to return to previous activities, including caring for other children
• Cultural traditions and beliefs
• Safety for parturient and neonate
Patient counselling during the decision-making process (this should be documented):
• Discuss the risks and benefits of TOLAC and ERCS, including possible effects on future pregnancies
• Discuss the likelihood of successful VBAC, prediction models may be helpful.
• Review the risks associated with each of the available induction options if induction of labour is planned
• Offer written information (e.g., published guidelines from professional organizations, decision aids)
• Encourage the woman and her partner to participate in decision-making; respect patient autonomy
• Recommend resources that provide additional information when applicable
• Document the counselling and informed choice process, including the woman’s decision and a plan of care
Special Considerations
Number of previous Caesarean sections
Women with more than one previous CS delivery may still be candidates for TOLAC. A systematic review of 17 studies
reported a rate of uterine rupture after one CS was 0.72 % and after 2 CS was 1.59%. Two large studies provide
conflicting results. One showed no difference in rate of rupture15 while the other showed an increase from 0.9% to
1.8%.20
The selection of candidates for a TOLAC depends on the clinical situation and should be re-evaluated throughout the
pregnancy
Type of previous incision
Guise et al. undertook a comprehensive review of studies comparing the risks and outcomes of VBAC versus Caesarean
section published between 1980 and 2004.21 In their analysis, they combined uterine rupture and dehiscence rates (7
studies from 1983 to 1999). They concluded there was little difference in the incidence of uterine rupture or dehiscence
in women with vertical lower uterine segment incisions and women with transverse low segment incisions.

Type of closure of previous uterine incision

The risk of uterine rupture after an unlocked single-layer closure of the myometrium seems to be comparable with
that after a double-layer closure. However, locked single-layer continuous suturing as opposed to a double-layer
closure of the hysterotomy site may increase the risk of uterine rupture in women undergoing trial of labour in a future
pregnancy.16
Interdelivery interval
A 2010 study by Bujold et al. showed an interdelivery interval shorter than 18 months should be considered a risk factor
for uterine rupture. The population in this study consisted of women with singleton pregnancies and one previous CS
who underwent a TOLAC at term.22
Hypertensive disorders of pregnancy
Data from a retrospective cohort study (n = 25 500) showed that women with gestational hypertension were less
likely than normotensive women to choose a TOLAC and were also less likely to be successful. Women with gestational
hypertension who underwent a TOLAC were no more likely to have uterine rupture than those who were normotensive.10
Twin pregnancy
Outcomes of TOLAC in women with a twin pregnancy are similar to those in women with a singleton pregnancy.2, 5
Studies have reported that women admitted with a more favourable cervical status in spontaneous labour have a 2-fold
increase in the likelihood of VBAC compared with those with an unfavourable cervix. 5, 18
Antepartum consultation with an obstetrician may be advisable, depending on the clinical situation and local practice.
The management of a TOLAC 2, 23 includes careful observation of labour progress—lack of progress with adequate
contractions for 2 to 3 hours warrants reassessment of the mode of delivery—fetal well-being, and maternal well-being.
Epidural or other analgesia may be used for usual indications.
Electronic fetal monitoring (EFM) should be used during active labour, because EFM tracing is the best marker of uterine
rupture. There is no need to restrict activity (telemetry can facilitate mobility while allowing continuous monitoring).
Fetal Heart Rate Patterns and Uterine Rupture

Fetal heart rate (FHR) tracing abnormalities, especially complicated variables or late decelerations are the most
commonly observed signs of uterine rupture.24, 25
Leung et al. analyzed the FHR and uterine contraction pattern immediately prior to 78 cases of uterine rupture.
Prolonged deceleration (alone or preceded by either severe late or variable decelerations) occurred in 71% of the cases of
uterine rupture. In addition, prolonged deceleration occurred in 100% of the FHR tracings in which total fetal extrusion
occurred.26 The appearance of recurrent late decelerations may be an early sign of impending uterine rupture.27

In some cases, it appears that there may be very little warning prior to the bradycardia in terms of fetal heart rate
changes. However, a multicenter case–control study analysed FHR tracings in the two hours preceding uterine rupture
during TOLAC and found that in the hour preceding uterine rupture, there are often significant FHR abnormalities. This
leads us to consider the possibility of an earlier C-section when faced with an atypical or abnormal FHR tracing before the
onset of terminal bradycardia jeopardizing maternal and fetal prognosis.24
Induction and Augmentation of Labour

Induction of labour for maternal or fetal indications remains an option for women undergoing TOLAC. However, the
potential increased risk of uterine rupture associated with any induction and the potential decreased possibility of
achieving VBAC should be made clear to the parturient.2
Induction of labour that requires cervical ripening is associated with a lower rate of successful VBAC and an increased risk
of uterine rupture. This occurs mainly in women who have not had a prior vaginal delivery. Induction and augmentation
of labour in women undergoing a TOLAC remains controversial and requires caution.
Recommendations regarding the induction or augmentation of labour during a TOLAC:
• Mechanical cervical ripening with a Foley catheter has been safely used before induction of labour in this
clinical situation.
• The use of oxytocin is acceptable but careful surveillance is recommended as is consideration of the
maximum dose to be administered. If oxytocin is used, then a low-dose protocol is recommended.
• Prostaglandins have been associated with increased risk of rupture and should not be used
• The timely availability of the human and physical resources to respond to an emergency is required.
All of these issues should be carefully considered and discussed with the woman before a management plan is finalized.
Informed consent is essential before induction commences.
Signs and Symptoms of Uterine Scar Rupture

The signs and symptoms of uterine rupture include fetal heart rate abnormalities, vaginal bleeding, and acute onset of
scar pain or tenderness (seldom masked by an epidural; this sign is neither sensitive nor specific).
The following may also occur:
• Hematuria
• Maternal tachycardia, hypotension, or hypovolemic shock
• Easier abdominal palpation of fetal parts
• Unexpected elevation of the presenting part
• Chest pain, shoulder tip pain, and/or sudden shortness of breath
A change in uterine activity (decrease or increase) is an uncommon and unreliable sign. A 2014 study of 97 028 births
identified 52 uterine ruptures (0.05%): 25 complete and 27 partial. Most (89%) occurred in women with a previous
Caesarean section. In complete ruptures, fetal heart rate abnormalities were the most frequent sign (82%), while the

complete triad of fetal heart rate abnormalities, pain, and vaginal bleeding was present in only 9%. The signs and
symptoms of partial ruptures were very different; these were asymptomatic in 48% of the cases.28
Management of Uterine Rupture

This is an obstetrical emergency. Survival of the mother and fetus depends on:
• Prompt identification
• Rapid volume expansion and the use of blood products
• Timely access to a surgical team for surgical intervention
• Uterine repair or hysterectomy
• Prophylactic antibiotic therapy
• The attendance of a neonatal resuscitation team
Summary
Although some women who attempt a trial of labour will be unsuccessful, the overall maternal morbidity and mortality
is lower than it is with elective repeat Caesarean section. Best evidence suggests that this is a reasonable and safe
choice for the majority of women with previous Caesarean.6 While the incidence of uterine rupture is low, it is a serious
complication with risk to both the parturient woman and the fetus. The increased risk of uterine rupture associated with
a TOLAC underlines the need for careful selection of candidates, counselling, and management in labour. It is essential
to discuss the risks of TOLAC and those of ERCS, including the effect that the mode of delivery will have on subsequent
pregnancies, with women who have had a previous Caesarean section.

References
1. Royal College of Obstetricians & Gynaecologists. Birth after previous caesarean birth, Guideline No. 45. Green-top. 2015.
2. Committee on Practice B-O. Practice Bulletin No. 184: Vaginal Birth After Cesarean Delivery. Obstet Gynecol.
2017;130:e217-e33. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29064970.
3. Martel MJ, MacKinnon CJ. No. 155-Guidelines for Vaginal Birth After Previous Caesarean Birth. J Obstet Gynaecol
Can. 2018;40:e195-e207. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29525045.
4. Perinatal Services BC. Perinatal Health Report: Deliveries in British Columbia 2014/15. 2016. Available from:
http://www.perinatalservicesbc.ca/Documents/Data-Surveillance/Reports/PHR/PHR_BC_2014_15.pdf.
5. Cheng YW, Eden KB, Marshall N, Pereira L, Caughey AB, Guise JM. Delivery after prior cesarean: maternal morbidity
and mortality. Clinics in Perinatology. 2011;38:297-309.
6. Guise JM, Eden K, Denman MA, Marshall N, Fu R, Janik R, et al. Vaginal birth after Cesarean: new insights. Rockville
(MD): Agency for Healthcare Research and Quality; 2010.
7. Davies GA, Hahn PM, McGrath MM. Vaginal birth after cesarean. Physicians’ perceptions and practice. J Reprod
8. Landon MB, Leindecker S, Spong CY, Hauth JC, Bloom S, Varner MW, et al. The MFMU Cesarean Registry: factors
affecting the success of trial of labor after previous cesarean delivery. American Journal of Obstetrics and
Gynecology. 2005;193:1016-23.
9. Brill Y, Windrim R. Vaginal birth after Caesarean section: review of antenatal predictors of success. J Obstet
Gynaecol Can. 2003;25:275-86.
10. Chaillet N, Bujold E, Dube E, Grobman WA. Validation of a prediction model for vaginal birth after caesarean. J
Obstet Gynaecol Can. 2013;35:119-24.
11. Grobman WA, Lai Y, Landon MB, Spong CY, Leveno KJ, Rouse DJ, et al. Does information available at admission
for delivery improve prediction of vaginal birth after cesarean? Am J Perinatol. 2009;26:693-701. Available from:
12. Damle LF, Wilson K, Huang CC, Landy HJ, Gomez-Lobo V. Do They Stand a Chance? Vaginal Birth after Cesarean
Section in Adolescents Compared to Adult Women. J PediatrAdolescGynecol. 2015;28:219-23.
13. Gregory KD, Korst LM, Fridman M, Shihady I, Broussard P, Fink A, et al. Vaginal birth after cesarean: clinical risk
factors associated with adverse outcome. Am J Obstet Gynecol. 2008;198:452 e1-10; discussion e10-2. Available
14. El-Sayed YY, Watkins MM, Fix M, Druzin ML, Pullen KM, Caughey AB. Perinatal outcomes after successful and failed
trials of labor after cesarean delivery. Am J Obstet Gynecol. 2007;196:583 e1-5; discussion e5. Available from:

15. Landon MB, Spong CY, Thom E, Hauth JC, Bloom SL, Varner MW, et al. Risk of uterine rupture with a trial of labor in
women with multiple and single prior cesarean delivery. Obstetrics and Gynecology. 2006;108:12-20.
16. Roberge S, Chaillet N, Boutin A, Moore L, Jastrow N, Brassard N, et al. Single- versus double-layer closure of the
hysterotomy incision during cesarean delivery and risk of uterine rupture. Int J Gynaecol Obstet. 2011;115:5-10.
17. Kok N, Wiersma IC, Opmeer BC, de Graaf IM, Mol BW, Pajkrt E. 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 Obstet Gynecol. 2013;42:132-9. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/23576473.
18. Hehir MP, Mackie A, Robson MS. Simplified and standardized intrapartum management can yield high rates of
successful VBAC in spontaneous labor. Journal of Maternal-Fetal & Neonatal Medicine. 2016:1-5.
19. Dy J, DeMeester S, Lipworth H, Barrett J. Trial of labour after caesarean. Journal of Obstetrics and Gynaecology
Canada. 2019;41.
20. Macones GA, Peipert J, Nelson DB, Odibo A, Stevens EJ, Stamilio DM, et al. Maternal complications with vaginal
birth after cesarean delivery: a multicenter study. Am J Obstet Gynecol. 2005;193:1656-62. Available from:
21. Guise JM, Hashima J, Osterweil P. Evidence-based vaginal birth after Caesarean section. Best Pract ResClin Obstet
Gynaecol. 2005;19:117-30.
22. Bujold E, Gauthier RJ. Risk of uterine rupture associated with an interdelivery interval between 18 and 24 months.
Obstetrics and Gynecology. 2010;115:1003-6.
23. Martel MJ, MacKinnon CJ. Guidelines for vaginal birth after previous Caesarean birth. J Obstet Gynaecol Can.
2005;27:164-88.
24. Desseauve D, Bonifazi-Grenouilleau M, Fritel X, Lathelize J, Sarreau M, Pierre F. Fetal heart rate abnormalities
associated with uterine rupture: a case-control study: A new time-lapse approach using a standardized
classification. Eur J Obstet Gynecol Reprod Biol. 2016;197:16-21. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/26696557.
25. Dore S, Ehman W, Azzam H, Basso M, Bow M, Morin F, et al. Fetal health surveillance: Intrapartum consensus
guideline. Journal of Obstetrics and Gynaecology Canada.
26. Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal consequences.
Am J Obstet Gynecol. 1993;169:945-50. Available from: https://www.ncbi.nlm.nih.gov/pubmed/8238154.
27. Ayres AW, Johnson TR, Hayashi R. Characteristics of fetal heart rate tracings prior to uterine rupture. Int J Gynaecol
Obstet. 2001;74:235-40. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11543746.
28. Guiliano M, Closset E, Therby D, LeGoueff F, Deruelle P, Subtil D. Signs, symptoms and complications of complete
and partial uterine ruptures during pregnancy and delivery. European Journal of Obstetrics, Gynecology, and
Reproductive Biology. 2014;179:130-4.

Table of Contents
Chapter 13 Shoulder Dystocia.......................................................................................................................................... 289

Definition.................................................................................................................................................................. 289
Incidence.................................................................................................................................................................. 289
Risk Factors............................................................................................................................................................... 289
Fetal/Neonatal .............................................................................................................................................. 290
Neonatal brachial plexus palsy (NBPP)......................................................................................................... 290
Fractures of the clavicle and humerus........................................................................................................... 291
Hypoxic ischemic encephalopathy and death............................................................................................... 291
Maternal........................................................................................................................................................ 291
Prediction and Prevention........................................................................................................................................ 291
Diagnosis.................................................................................................................................................................. 292
Management............................................................................................................................................................ 292
After the Baby is Delivered........................................................................................................................................ 295
Clinical.......................................................................................................................................................... 295
Risk Management..................................................................................................................................................... 295
Summary.................................................................................................................................................................. 296
ALARM Mnemonic.................................................................................................................................................... 300
Shoulder Dystocia 288

Chapter 13
Shoulder Dystocia
Definition
Shoulder dystocia is the term used for the situation where one or both shoulders are trapped above the pelvic brim after
the head has delivered. Almost always it is only one shoulder, the anterior one, that is impacted, against the symphysis
pubis. Much rarer, both shoulders are stuck above the pelvic brim, with the posterior shoulder held up by the sacral
promontory.
Clinically, shoulder dystocia is defined by the inability of the fetal shoulders to deliver spontaneously with maternal
effort alone, or with gentle downward traction on the fetal head, after vaginal cephalic delivery.1, 2 Additional obstetric
maneuvers are needed to deliver the shoulders and body.
Incidence
The overall incidence is approximately 1% of all vaginal births.
The reported incidence was 1.4% in the United States and 0.6% in other countries.3 The incidence increases with
increasing birthweight: approximately 5% for birthweight 4,000 – 4,500 grams; 10% for birthweight 4,500 – 5,000
grams; 20% for birthweight >5,000 grams. The incidence is 0.6% with spontaneous delivery and 2% with assisted
vaginal delivery (AVB).3 Whether assisted vaginal delivery is an independent risk factor unrelated to fetal size, or whether
the need for assisted vaginal delivery is a reflection of problems between fetal size and pelvic dimension, is unclear.
The incidence is 2-4 fold higher in women with pre-existing or gestational diabetes. This may reflect the increased
incidence of fetal macrosomia, larger shoulders, and higher body fat compared with nondiabetic infants.
Risk Factors
The main risk factor is fetal macrosomia. However, about half of shoulder dystocia cases occur in women with no obvious
risk factors, who have neither diabetes nor a baby weighing over 4,000 grams. The possibility of shoulder dystocia is
present with every vaginal delivery. Certain factors should raise suspicion for shoulder dystocia.

PRIOR PREGNANCY HISTORY CURRENT PREGNANCY FACTORS INTRAPARTUM FACTORS
Previous shoulder dystocia4 Suspected macrosomia Prolonged second stage
Previous macrosomia Diabetes(pre-existing/gestational) Assisted vaginal delivery5, 6
Obesity
Excessive weight gain
Post dates
Most cases of shoulder dystocia cannot be predicted or prevented. Clinical risk factors are not reliable predictors for
shoulder dystocia or neonatal brachial plexus injury.2, 7 The great majority of deliveries in the presence of risk factors do
not result in shoulder dystocia.

Fetal/Neonatal
Complications of shoulder dystocia include neonatal brachial plexus palsy (NBPP), fractures of the clavicle and humerus,
hypoxic ischemic encephalopathy, and rarely fetal/neonatal death.
Neonatal brachial plexus palsy (NBPP)

About 10-20% of shoulder dystocia cases result in a brachial plexus injury. This can be a consequence of the clinician
exerting downward lateral traction on the fetal head in an attempt to free the impacted anterior shoulder. This causes
stretching of the cervical nerves in the neck; in the worst case the cervical nerves are ruptured or avulsed from the spinal
cord. About 20% of babies with brachial plexus injury will have permanent impairment.
It has been traditionally thought that NBPP was invariably due to physician traction. While lateral downward traction
during shoulder dystocia may be severe enough to injure the brachial plexus, it is clear that not all cases are due
to excess traction by health care professionals.1, 2, 7, 8 There are multiple reports of NBPP in the absence of shoulder
dystocia.7, 8 About half of brachial plexus injuries occur without a diagnosis of shoulder dystocia. The etiology of neonatal
brachial plexus palsy (NBPP) is thought to be multifactorial.1, 2
Other factors such as uterine contractions and maternal expulsive efforts during the labour and delivery process and
individual susceptibility likely also contributed to the development of the NBPP.

Fractures of the clavicle and humerus

Less serious complications are fractures of the clavicle or humerus, which can occur with forced adduction of the fetal
shoulders and removal of the posterior arm respectively. Clavicular and humeral fractures generally heal well.
Hypoxic ischemic encephalopathy and death

The most feared complications for the fetus/baby is death or permanent brain injury1, 2, 7 as a result of asphyxia and/or
hypovolemic shock. The risk increases with an increasing interval of head to body delivery and the number manoeuvres
needed to reduce the shoulder.9 The duration of shoulder dystocia alone is not an accurate predictor of neonatal
asphyxia or death. One study showed that the interval was less than 5 minutes in 47% of cases of death.10 Several factors
may contribute to the risk of morbidity or mortality. In the study cited above, twenty five percent of cases had evidence
of fetal compromise prior to delivery. Occlusion of the umbilical cord may lead to a drop in arterial pH although studies
have shown the rate of decrease in pH may be slower that was traditionally thought.11-13 Occlusion of the umbilical vein
21
or compression of the fetal chest may lead to sequestration of the fetal blood in the placenta and resultant hypovolemic
shock.14, 15 Finally it has been suggested that elevated intrauterine compared with atmospheric pressure impairs venous
return from the fetal brain and can lead to local ischemia.11, 12 These factors are likely responsible for the observation that
hypoxic ischemic encephalopathy cause by shoulder dystocia often occurs with normal or near normal umbilical arterial
cord gases.11, 12, 16
Maternal
Perineal tears may be severe and can occur during appropriate management secondary to the manoeuvres required
to free the impacted shoulder. There is an increased risk of obstetrical anal sphincter injury (OASI).17 Uterine atony and
postpartum haemorrhage are common occurring in 10 – 20 percent of cases. Maternal symphyseal separation and
lateral femoral cutaneous neuropathy have been reported likely secondary to hyperflexion of the hips.
Prediction and Prevention

While there are a number of recognized risk factors (Table 1), studies of these either alone.18 or in combination are poor
predictors of shoulder dystocia.19
There is no clear strategy to predict or prevent shoulder dystocia. In a review of six studies that reported birth rate, 27%
of shoulder dystocia occurred in babies weighting less 4000 gms, 39% of babies weighted 4000-4500 grams and 34%
were over 4500 gms. Ultrasound estimates of fetal weight to identify macrosomia are commonly used. Ultrasound
estimation of fetal weight is imprecise, but it is better than other methods in predicating fetal macrosomia.20
One proposed way to avoid shoulder dystocia is to perform a cesarean section in cases of suspected fetal macrosomia.
Depending on the threshold estimated fetal weight, this approach could result in the performance of up to 1,000
elective cesarean sections to prevent one permanent injury to the fetus.21-23 The ACOG recommendation is to reserve
2

elective cesarean section for nondiabetic women with estimated fetal weight more than 5 kilograms and for diabetic
women more than 4.5 kilograms.1, 24
When there has been previous shoulder dystocia, the recurrence risk if vaginal delivery is allowed is 5 – 10%.4 The
estimated fetal weight, gestational age, maternal diabetes status, and the presence of prior neonatal injury should be
evaluated before deciding the route of delivery
Another approach suggested in the literature is to induce labour at 37-38 weeks in women thought clinically and by
ultrasound to have a macrosomic fetus or in diabetic women. The rationale is if the baby is smaller, presumably there will
be less shoulder dystocia. A randomized trial in nondiabetic women showed that a policy of early induction compared to
expectant management led to less macrosomia (of more than 4 kilograms) and less shoulder dystocia (1% compared to
4%) but no difference in fetal outcomes.25 The cesarean rate was not increased with a policy of induction. A meta-analysis
concluded that induction of labour for suspected macrosomia showed similar findings.26 Conversely, a meta-analysis
of induction of labour in women with macrosomia and gestational diabetes did not show a reduction in shoulder
dystocia.27 The American College of Obstetrics and Gynecology still discourages induction of labour for macrosomia.24
Diagnosis
Shoulder dystocia can be suspected if the fetal chin delivers with difficulty and the head recoils against the perineum
(‘turtle sign’). Spontaneous restitution does not occur. The mother fails to deliver the anterior shoulder with her own
expulsive efforts during the next contraction.
It is recommended by some that an attempt at gentle downward (axial, longitudinal) traction on the head be made
before a diagnosis of shoulder dystocia is made.1, 2 This initial traction attempt is unnecessary and may itself injure
the brachial plexus nerves.28 Without intervention after delivery of the head, the shoulders almost always deliver
spontaneously without downward traction.13 There is no need to deliver the shoulders during the same contraction as
the delivered head and most often, spontaneous delivery of the shoulders occurs with the next contraction. Provided the
antecedent fetal heart rate has been normal, once the head is delivered, it is safe to wait for two or three minutes until
the next contraction occurs and the mother again feels the urge to push.11, 13, 28
Management
Given our inability to predict the occurrence of shoulder dystocia reliably, every delivery should be considered to
have the potential for a shoulder dystocia. Therefore, a management protocol must be in place and well-known to all
caregivers. In pregnancies where shoulder dystocia has a high likelihood, the woman and her support persons need to
be prepared for the manoeuvres that may be used.
Avoid the 4 P’s. DO NOT!
1. Pull, on the head
2. Push, on the fundus
3. Pivot, or rotate, the head
4. Panic

The ALARMER mnemonic has been developed to assist in the appropriate and consistent management of this potential
complication. External manoeuvres (McRoberts Manoeuvre and suprapubic pressure) are often attempted first as they
are simple, rapid, and effective. If unsuccessful, internal manoeuvres (rotation or delivery of the posterior arm) or “all
fours” position should be attempted.
When shoulder dystocia is recognized, it is important to instruct the woman to avoid pushing between
contractions while manoeuvres to relieve the obstruction are carried out. This will facilitate manoeuvers and
maximize fetal cerebral perfusion. Once a manoeuvre is completed, mother may be asked to push to determine
if the manoeuvre resolved the problem.
A Ask for help
L Lift/hyperflex Legs (McRoberts manoeuvre)
A Anterior shoulder disimpaction (suprapubic pressure and/or Rubin manoeuvre)
R Rotation of the posterior shoulder
M Manual removal posterior arm
E Episiotomy
R Roll over onto “all fours”
Ask for help
• Set up unique paging protocols for obstetric emergencies to assure that appropriate equipment and
personnel are available consistent with local circumstances. Get an assistant to help with the McRoberts
manoeuvre. Summon a neonatal resuscitation team. An anaesthesiologist may help with necessary
anaesthesia.
• The initial indication that shoulder dystocia may be present is often a turtle sign. When this occurs, it may
be helpful to elevate the legs in McRoberts position and call for additional help while awaiting the next
contraction. In many instances of a turtle sign, the infant will deliver spontaneously with the next contraction.
If it does not, the team is poised to institute additional measures.
In normal birth there is usually a pause between delivery of the head and body.11, 13. In a healthy baby, who has had
a normal FHR during labour, this pause does not significantly affect fetal acidosis and may facilitate delivery of the
shoulders. The drop in cord pH during this pause is minimal.11, 16 With the following contraction, if the shoulders do not
deliver spontaneously, the diagnosis of shoulder dystocia is made and additional manoeuvres should be instituted.
Maternal positioning
• Flatten the head of the bed, drop or remove the bottom of the bed.
• Bring the woman to the end of the bed
McRoberts manoeuvre
• Hyperflex both legs at the hips (McRoberts manoeuvre). The knees should be close to the mother’s shoulders
to increase the anterior posterior diameter of the pelvis
• With the next contraction, ask the mother to push. Do not pull on the head

Anterior shoulder disimpaction

• Abdominal approach – apply suprapubic pressure with the heel of clasped hands from the posterior aspect
of the anterior shoulder to dislodge it. Apply a steady pressure first and, if unsuccessful, apply a rocking
pressure. It is necessary to know the position of the occiput so as to apply pressure from the correct side for
greater effectiveness. It is also useful to have a stool in all delivery suites in order to facilitate this manoeuvre
in the event of a shorter assistant.
• Vaginal approach – the index or middle finger, or the whole hand is advanced usually laterally and moved
to the anterior shoulder to effect adduction of the anterior shoulder of the baby by applying pressure to the
posterior aspect of the shoulder (i.e., the shoulder is pushed towards the chest, or pressure is applied to
the scapula of the anterior shoulder) (Rubin manoeuvre).29
These manoeuvres attempt to position the shoulders to utilize the smallest possible diameter of the shoulders through
the largest diameter of the pelvis. Rotation is into the oblique diameter. Ask the mother to push. Do not pull on the head.
Rotation of the posterior shoulder
Woods’ manoeuvre is a screw-like manoeuvre. Pressure is applied with the whole hand in the vagina to the anterior
aspect of the posterior shoulder and an attempt is made to rotate the posterior shoulder to an anterior position.
Alternatively, one can rotate the posterior shoulder in the opposite direction with pressure on the posterior aspect of the
posterior shoulder. Success of this manoeuvre allows easy delivery of the anterior shoulder once it is past the symphysis
pubis. In practice, the anterior shoulder disimpaction manoeuvre and Woods’ manoeuvre may be done repetitively to
achieve disimpaction of the anterior shoulder.30
Manual removal of the posterior arm
The arm is usually flexed at the elbow. If it is not, pressure in the antecubital fossa can assist with flexion. The hand
is grasped, swept across the chest and delivered.31 If the posterior hand cannot be reached, delivery of the posterior
shoulder using axillary traction is usually successful.23, 32 With either technique fracture of baby’s humerus is common;
however, fractures heal whereas brachial plexus palsies may be permanent.
Episiotomy
Episiotomy is an option that may facilitate the Woods’ manoeuvre or manual removal of the posterior arm by creating
more room for the accoucheur’s hand. However, shoulder dystocia is not caused by obstructing soft tissue. Therefore,
performing an episiotomy will not, on its own, relieve a shoulder dystocia.
Roll over to “all fours” position
This manoeuvre may be considered early in the management of shoulder dystocia.
Moving the woman onto “all fours” with the back arched appears to increase the effective pelvic dimensions, allowing
the fetal position to shift (Gaskin’s manoeuvre). This may free the impacted shoulder. With gentle downward pressure on
the posterior shoulder, the anterior shoulder may become more impacted (with gravity) but will facilitate the freeing up
of the posterior shoulder. This position may also allow easier access to the posterior shoulder for rotational manoeuvres
or removal of the posterior arm.33 In one series, as a first line manoeuvre, this manoeuvre was successful in 29% of
cases.34

The “all fours” position may be used in the presence of epidural analgesia unless the degree of motor block makes
rolling over and maintaining the position impossible.
Further Considerations
The initial steps of McRoberts manoeuvre and suprapubic pressure will resolve about a quarter of cases. Even if
McRoberts manoeuvre is unsuccessful, the hyperflexed position of the legs will often let the posterior shoulder slide
deeper in the sacral concavity, making rotation manoeuvres and delivery of the posterior arm easier. McRoberts
manoeuvre and suprapubic pressure, even if successful alone, are associated with brachial plexus injury about 10%
of the time, 35, 36 possibly a result of the initial gentle downward traction or subsequent traction after the legs are
hyperflexed. It has been suggested that the first manoeuvre should be delivery of the posterior arm or shoulder.32
If the above steps have not worked, one can repeat the manoeuvres under general anaesthesia. The above manoeuvres
are most likely to fail if neither shoulder is in the pelvic concavity, in other words, the posterior shoulder is also out of the
pelvis. In this situation one may have to resort to cephalic replacement37 or symphysiotomy.38, 39
Brachial plexus palsy can occur regardless of the procedures used to disimpact the shoulders because all maneuvers can
increase the degree of stretch on the brachial plexus.1, 2, 35, 36 There can be significant perinatal morbidity even when
shoulder dystocia is managed appropriately”. The most important principal in the management of shoulder dystocia is
to have a rehearsed, methodical, efficient (not panicked or rushed) approach with a sequence of manoeuvers. These are
supported by the extended care team and practiced in simulation
After the Baby is Delivered

Clinical
Mother
Remember the SIGNIFICANT risk of maternal injury (tears) and postpartum hemorrhage. Actively manage the third stage.
Inspect for and repair lacerations.
Newborn
It is recommended to follow NRP guidelines in appropriate care of the baby. The newborn should be carefully examined
to ensure there is no evidence of injury.
Risk Management
Both HIROC and the CMPA have identified management of shoulder dystocia as one of the 5 top high risk areas for
litigation. (Delivery in focus: Strengthening Obstetrical care in Canada. A 10 year review of CMPA and HIROC data, 2018)

Preparation
Regular training in the management of emergencies (such as shoulder dystocia) results in a sustained improvement
in team performance during the actual events.27 Hands-on training using a mannequin is better than using a video
demonstration. Simulation-based training has been shown to reduce the risks associated with shoulder dystocia.40
The implementation of a shoulder dystocia protocol has been found to decrease the diagnosis of BPI at delivery and at
neonatal discharge.41
Discussion, Documentation and Debriefing

1. Document and describe. Using a preformatted documentation sheet or checklist will aid in proper
documentation.41 Include in your documentation:
b. sequence of all manoeuvres used, including which shoulder was impacted
c. episiotomy, if done
d. individuals present in the room
e. the time of delivery of the head, onset of next contraction and delivery of the body
f. condition of the newborn
g. whether cord gases sent
2. Debrief with the mother and family about what occurred and what management steps were taken.
Document your discussion.
3. Discuss and debrief with the clinical team.
Summary
1. Don’t panic.
2. Be prepared. Develop and practice a standard management protocol (regular and repeated emergency
drills). The ALARMER mnemonic is helpful.
3. Prepare the woman and her partner when the potential for shoulder dystocia appears high.
4. Do not pull on the head, neither to make the diagnosis of shoulder dystocia nor after McRoberts’ manoeuvre
and suprapubic pressure are used. There should be no traction on the baby’s head.
5. If the baby is depressed, do not clamp the cord immediately. Drying, evaluation and stimulation of the baby
for the initial 30 seconds can be done with the cord intact. If ventilation is required at 30 seconds of age
and PPV can be instituted with the cord intact, cord clamping should be delayed another 30 – 60 seconds to
optimize placental auto transfusion.
6. Document events and explain to mother and partner.

References
1. Committee on Practice Bulletins-Obstetrics. Practice Bulletin No 178: Shoulder Dystocia. Obstet Gynecol.
2017;129:e123-e33. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28426618.
2. Shoulder dystocia. 2nd ed. ed. London: Royal College of Obstetricians and Gynaecologists; 2013. Available from:
http://www.rcog.org.uk/womens-health/clinical-guidance/shoulder-dystocia-green-top-42.
3. Hansen A, Chauhan SP. Shoulder dystocia: definitions and incidence. Semin Perinatol. 2014;38:184-8.
4. Kleitman V, Feldman R, Walfisch A, Toledano R, Sheiner E. Recurrent shoulder dystocia: is it predictable? Arch
Gynecol Obstet. 2016;294:1161-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27338567.
5. Dall’Asta A, Ghi T, Pedrazzi G, Frusca T. Does vacuum delivery carry a higher risk of shoulder dystocia? Review and
meta-analysis of the literature. Eur J Obstet Gynecol Reprod Biol. 2016;204:62-8. Available from: https://www.
6. Palatnik A, Grobman WA, Hellendag MG, Janetos TM, Gossett DR, Miller ES. Predictors of shoulder dystocia at the
time of operative vaginal delivery. Am J Obstet Gynecol. 2016;215:624 e1- e5. Available from: https://www.ncbi.
7. Lerner HM, Salamon E. Permanent brachial plexus injury following vaginal delivery without physician traction
or shoulder dystocia. Am J Obstet Gynecol. 2008;198:e7-8. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/18191807.
8. Torki M, Barton L, Miller DA, Ouzounian JG. Severe brachial plexus palsy in women without shoulder dystocia.
9. Nesbitt TS, Gilbert WM, Herrchen B. Shoulder dystocia and associated risk factors with macrosomic infants
born in California. Am J Obstet Gynecol. 1998;179:476-80. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/9731856.
10. Hope P, Breslin S, Lamont L, Lucas A, Martin D, Moore I, et al. Fatal shoulder dystocia: a review of 56 cases reported
to the Confidential Enquiry into Stillbirths and Deaths in Infancy. Br J Obstet Gynaecol. 1998;105:1256-61.
11. Kotaska A, Campbell K. Two-step delivery may avoid shoulder dystocia: head-to-body delivery interval is less
important than we think. J Obstet Gynaecol Can. 2014;36:716-20. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/25222167.
12. Stallings SP, Edwards RK, Johnson JW. Correlation of head-to-body delivery intervals in shoulder dystocia and
umbilical artery acidosis. Am J Obstet Gynecol. 2001;185:268-74. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/11518878.

13. Locatelli A, Incerti M, Ghidini A, Longoni A, Casarico G, Ferrini S, et al. Head-to-body delivery interval using ‘two-
step’ approach in vaginal deliveries: effect on umbilical artery pH. J Matern Fetal Neonatal Med. 2011;24:799-
14. Mercer J, Erickson-Owens D, Skovgaard R. Cardiac asystole at birth: Is hypovolemic shock the cause? Med
Hypotheses. 2009;72:458-63. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19121560.
15. Menticoglou S, Schneider C. Resuscitating the Baby after Shoulder Dystocia. Case Rep Obstet Gynecol.
2016;2016:8674167. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27493815.
16. Leung TY, Stuart O, Sahota DS, Suen SS, Lau TK, Lao TT. Head-to-body delivery interval and risk of fetal acidosis and
hypoxic ischaemic encephalopathy in shoulder dystocia: a retrospective review. BJOG. 2011;118:474-9. Available
17. Gachon B, Desseauve D, Fritel X, Pierre F. Is fetal manipulation during shoulder dystocia management associated
with severe maternal and neonatal morbidities? Arch Gynecol Obstet. 2016;294:505-9. Available from: https://
18. Gherman RB, Chauhan S, Ouzounian JG, Lerner H, Gonik B, Goodwin TM. Shoulder dystocia: the unpreventable
obstetric emergency with empiric management guidelines. Am J Obstet Gynecol. 2006;195:657-72. Available
19. Revicky V, Mukhopadhyay S, Morris EP, Nieto JJ. Can we predict shoulder dystocia? Arch Gynecol Obstet.
20. Campbell S. Fetal macrosomia: a problem in need of a policy. Ultrasound Obstet Gynecol. 2014;43:3-10. Available
21. Menticoglou SM, Manning FA, Morrison I, Harman CR. Must macrosomic fetuses be delivered by a caesarean
section? A review of outcome for 786 babies greater than or equal to 4,500 g. Aust N Z J Obstet Gynaecol.
22. Rouse DJ, Owen J, Goldenberg RL, Cliver SP. The effectiveness and costs of elective cesarean delivery for fetal
macrosomia diagnosed by ultrasound. JAMA. 1996;276:1480-6.
23. Culligan PJ, Myers JA, Goldberg RP, Blackwell L, Gohmann SF, Abell TD. Elective cesarean section to prevent anal
incontinence and brachial plexus injuries associated with macrosomia--a decision analysis. Int Urogynecol J Pelvic
Floor Dysfunct. 2005;16:19-28; discussion Available from: https://www.ncbi.nlm.nih.gov/pubmed/15647962.
24. American College of O, Gynecologists’ Committee on Practice B-O. Practice Bulletin No. 173: Fetal Macrosomia.
Obstet Gynecol. 2016;128:e195-e209. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27776071.
25. Boulvain M, Senat MV, Perrotin F, Winer N, Beucher G, Subtil D, et al. Induction of labour versus expectant
management for large-for-date fetuses: a randomised controlled trial. Lancet. 2015.
26. Boulvain M, Irion O, Dowswell T, Thornton JG. Induction of labour at or near term for suspected fetal macrosomia.

27. Witkop CT, Neale D, Wilson LM, Bass EB, Nicholson WK. Active compared with expectant delivery management in
women with gestational diabetes: a systematic review. Obstet Gynecol. 2009;113:206-17. Available from: https://
28. Menticoglou S. Delivering Shoulders and Dealing With Shoulder Dystocia: Should the Standard of Care Change? J
29. Rubin A. Management of shoulder dystocia. JAMA. 1964;189:835-7.
30. Woods CE. A principle of physics as applicable to shoulder delivery. Am J Obstet Gynecol. 1943;45:796-804.
31. Baskett TF, Calder AA, Arulkumaran S. Shoulder Dystocia. Munro Kerr’s Operative Obstetrics, 11th ed: Saunders
Elsevier; 2007.
32. Menticoglou SM. A modified technique to deliver the posterior arm in severe shoulder dystocia. Obstet Gynecol.
33. Bruner JP, Drummond SB, Meenan AL, Gaskin IM. All-fours maneuver for reducing shoulder dystocia during labor.
J Reprod Med. 1998;43:439-43.
34. Kallianidis AF, Smit M, Van Roosmalen J. Shoulder dystocia in primary midwifery care in the Netherlands. Acta
Obstet Gynecol Scand. 2016;95:203-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26458503.
35. Nocon JJ, McKenzie DK, Thomas LJ, Hansell RS. Shoulder dystocia: an analysis of risks and obstetric maneuvers.
Am J Obstet Gynecol. 1993;168:1732-7.
36. Gherman RB, Ouzounian JG, Goodwin TM. Obstetric maneuvers for shoulder dystocia and associated fetal
morbidity. Am J Obstet Gynecol. 1998;178:1126-30.
37. Gherman RB, Ouzounian JG, Chauhan S. Posterior arm shoulder dystocia alleviated by the Zavanelli maneuver. Am
J Perinatol. 2010;27:749-51. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20414853.
38. Broekman AM, Smit YG, van Dessel T, Dorr PJ. Shoulder dystocia and symphysiotomy: a case report. Eur J Obstet
Gynecol Reprod Biol. 1994;53:142-3. Available from: https://www.ncbi.nlm.nih.gov/pubmed/8194651.
39. Mola GD. Symphysiotomy: technique, problems and pitfalls, and how to avoid them. P N G Med J. 1995;38:231-8.
40. Dahlberg J, Nelson M, Dahlgren MA, Blomberg M. Ten years of simulation-based shoulder dystocia training-
impact on obstetric outcome, clinical management, staff confidence, and the pedagogical practice - a time
series study. BMC Pregnancy Childbirth. 2018;18:361. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/30185169.
41. Crofts JF, Lenguerrand E, Bentham GL, Tawfik S, Claireaux HA, Odd D, et al. Prevention of brachial plexus injury-12
years of shoulder dystocia training: an interrupted time-series study. BJOG. 2016;123:111-8. Available from:

Appendices
Appendix A
Alarm Mnemonic
ALARM
A
Mnemonic
ASK for help
A ASK for help
L LIFT / hyperflex LEGS
L LIFT / hyperflex LEGS
Lift: McRoberts Manoeuvre
Lift: McRoberts Manœuvre
y McRoberts manoeuvre
McRoberts
y • flexion manoeuvre
of thighs on abdomen
y requires assistanceon abdomen
• flexion of thighs
• requires assistance

A ANTERIOR shoulder disimpaction

A ANTERIOR shoulder disimpaction
Anterior disimpaction – Step 1: Suprapubic pressure
Anterior disimpaction – 1) Suprapubic pressure

y Directed from side of fetal back 26th Edition of the ALARM Course Manual
y CPR-type motion
y NO fundal pressure

• directed from side of fetal back

• CPR-type motion
• NO fundal pressure

Anterior disimpaction – Step 2: Rubin manoeuvre

Anterior disimpaction – 2) Rubin manoeuvre

R ROTATION 26th Edition of the ALARM Course Manual
Rotation of posterior shoulder – Step 1

y Pressure on anterior aspect of posterior shoulder
R ROTATION
y May be combined with anterior disimpaction manoeuvres
y ofNOposterior
Rotation fundal pressure
shoulder – Step 1

• pressure on anterior aspect of posterior shoulder
• may be combined with anterior disimpaction manoeuvres
• NO fundal pressure




y May be repeated if delivery not accomplished by Steps 1 & 2
• may be repeated if delivery not accomplished by Steps 1 & 2

M MANUAL removal posterior arm

M MANUAL removal posterior arm
Manual removal of posterior arm
Manual removal of posterior arm
y Splint humerus
splint humerus
y • Pressure in antecubital fossa to flex arm
pressure
y • Sweep arminover
antecubital
chest fossa to flex arm
sweep
y • Grasp arm/ forearm
wrist over chest
y Deliver arm forearm
• grasp wrist /
• deliver arm
E EPISIOTOMY
ER EPISIOTOMY
ROLL over onto ‘all fours’
R ROLL over onto ‘all fours’

Table of Contents
Chapter 14 Breech Presentation and Delivery................................................................................................................. 309

Definitions..................................................................................................................................................... 309
Incidence....................................................................................................................................................... 310
Etiology and Risk Factors............................................................................................................................... 310
Diagnosis of Non-Cephalic Presentation....................................................................................................... 310
Management of Breech............................................................................................................................................ 311
External Cephalic Version.............................................................................................................................. 311
Timing of ECV................................................................................................................................................ 311
Predictors for successful ECV......................................................................................................................... 313
ECV Procedure............................................................................................................................................... 313
Procedures that may Facilitate Turning the Breech....................................................................................... 314
The Limitations Of The Term Breech Trial.................................................................................................................. 316
Vaginal Breech Delivery................................................................................................................................ 317
Setting and Consent...................................................................................................................................... 323
Risks and Complications............................................................................................................................... 323
Preparation and Labour Management.......................................................................................................... 324
Delivery Technique........................................................................................................................................ 324
Follow-Up.................................................................................................................................................................. 326
Care After Breech Delivery Should Include.................................................................................................... 326
Documentation: Breech Delivery.................................................................................................................. 326
Summary.................................................................................................................................................................. 327
GETHIPPOS Mnemonic................................................................................................................................. 331
Breech Presentation and Delivery 308

Chapter 13
Chapter 14
Breech Presentation and Delivery
Breech Presentation and Delivery
Definitions
Definitions
When the buttocks of the fetus enter the maternal pelvis before the head, the presentation is termed a breech.
1
When the buttocks1 of the fetus enter the maternal pelvis before the head, the presentation is termed a breech.
There are three different types of Breech:
There are three different types of Breech:
Complete Breech: Fetal hips flexed, knees flexed (foot may be adjacent to or just below buttocks) (5% to 10% of breech
presentations)
Complete Breech: Fetal hips flexed, knees flexed (foot may be adjacent to or just below buttocks) (5% to 10% of breech
presentations)
Footling or Incomplete: One or both fetal hips extended, foot or knee presenting (10% to 30% of breech presentations)
Footling or Incomplete: One or both fetal hips extended, foot or knee presenting (10% to 30% of breech presentations)
Frank Breech: Fetal hips flexed, knees extended2 (50% to 70% of breech presentations)
Frank Breech: Fetal hips flexed, knees extended2 (50% to 70% of breech presentations)
Figure 1. Types of Breech Presentation
Figure 1. Types of Breech Presentation

Incidence
Breech presentation occurs in 3% to 4% of all pregnancies reaching term.3 The earlier the gestation, the higher the
percentage of breech fetuses. At 28 weeks’ gestation, approximately 24% of fetuses are in the breech presentation.3

Breech presentation is associated with an increased frequency of perinatal mortality and morbidity due to prematurity,
congenital anomalies (which occur in 6.3% of all breech presentations compared with 2.4% of non-breech
presentations4), cord prolapse and birth trauma/asphyxia. A 2009 study by Andersen et al. indicated that breech
presentation alone puts the fetus at higher risk for cerebral palsy than does cephalic presentation. However, vaginal
breech delivery itself was not associated with risk for cerebral palsy.5
Etiology and Risk Factors

As term approaches, the fetus is usually accommodated in the uterine cavity in a longitudinal lie with the vertex
presenting. Any factor that precludes or makes it more difficult for the fetus to be accommodated in the uterus as a vertex
presentation is a risk factor for breech.3 These factors include:
• Prematurity
• Oligohydramnios
• Uterine anomalies (i.e., septate, bicornuate, or didelphic uterus) or tumours (e.g., large fibroids)
• Placenta implanted low in the uterus or placenta previa
• Fetal anomalies (e.g., anencephaly or hydrocephaly)
Other risk factors for breech include previous breech delivery or idiopathic causes. If either the pregnant woman or the
father of her fetus was a breech delivery, then the likelihood that the fetus will be breech is doubled.6
Diagnosis of Non-Cephalic Presentation

Performing Leopold’s manoeuvres during third trimester prenatal examinations will make the diagnosis in the majority of cases. If
there is any doubt, vaginal examination or ultrasound may be performed to confirm the presentation. An abdominal X-ray may be
used to confirm the diagnosis if ultrasound is unavailable.

Management of Breech
Term breech management involves 3 options: external cephalic version, Caesarean section, or vaginal breech delivery.
External Cephalic Version

External cephalic version is a procedure whereby a fetus is turned in utero from a non-cephalic to a cephalic presentation
by manipulation of the maternal abdomen.
A meta-analysis of 5 RCTs comparing ECV at term with no attempt at ECV showed a significant reduction in non-cephalic
births (RR 0.38; 95% CI, 0.18 to 0.80) and CS (RR 0.55; 95% CI 0.33 to 0.91).7 There was no significant effect on perinatal
mortality (RR 0.51; 95% CI 0.05 to 5.54) or other measures of perinatal outcome.7 It is therefore recommended that all
women with breech presentation at or beyond 36 weeks’ gestation, who are appropriate candidates, be offered an ECV.
A recent trial compared obstetrical outcomes for women with a cephalic presentation at birth resulting from successful
ECV to those resulting from spontaneous cephalic version. It showed that women with a cephalic-presenting fetus at
birth as a result of ECV are not at greater risk of obstetrical interventions compared with women whose fetuses turned
spontaneously.8
Timing of ECV
The ideal time to carry out ECV has been the subject of debate. A large multicentre RCT (n = 1543) compared ECV at
between 34 and 36 weeks’ gestation with ECV after 37 weeks’ gestation.9 When ECV was performed at 34 to 36 weeks:
• Fewer fetuses remained breech at delivery (51% vs. 59%)
• There was
−− A 4% absolute reduction in delivery by CS (52% vs. 56%)
−− A 2% absolute increase in preterm birth < 37 weeks: (6.5% vs. 4.5%)
−− No difference in neonatal morbidity
−− No perinatal deaths related to ECV
Waiting to perform ECV allowed spontaneous version to occur more often (25% vs. 14%), whereas earlier ECV allowed
time for repeat attempts if the initial attempt was unsuccessful. Approximately one quarter of repeat attempts in this trial
were successful.9
ECV should not be attempted before 34 weeks’ gestation as most breech fetuses will turn prior to that gestation,
and, if emergency delivery is required for complications, neonatal morbidity is high. After 34 weeks, the timing of ECV
can be decided by a woman and her care provider on the basis of a discussion of the risks and benefits above.
Although the success rate of ECV declines as gestational age advances, ECV may be attempted up until the time of
labour. ECV may even be attempted in early labour if membranes are intact and the uterus remains relaxed long enough
between contractions.

Prerequisites
1. Singleton pregnancy
2. Gestation > 34 weeks
3. No contraindication to labour
4. Fetal well-being established before procedure (i.e., non-stress test or biophysical profile)
5. Amniotic fluid volume adequate
6. Availability of ultrasound
7. Position of fetus known before procedure
8. Facilities and personnel available for immediate Caesarean section
Contraindications
Absolute
1. Any contraindication to labour e.g. placenta previa, or abnormal or atypical fetal heart pattern, compromised
fetus, active genital herpes simplex virus infection, previous classical uterine incision, or other uterine
surgery that would increase the risk of uterine rupture (hysterotomy, myomectomy, full thickness uterine
wall incision, etc.)
2. Antepartum hemorrhage
3. Some major fetal anomalies
4. Multiple gestation (except delivery of second twin)
5. Ruptured membranes
Relative
1. Oligohydramnios
2. Hyperextension of the fetal head
3. Two or more previous Caesarean sections
4. Morbid obesity
5. Active labour
6. Uterine malformation
7. Fetal anomaly
The relative contraindications listed above negatively affect the likelihood of ECV being successful and need to be
considered when deciding whether or not to attempt ECV. It has also been shown that ECV is somewhat less likely to be
successful with an anterior placenta, although this is not statistically significant.10, 11
ECV appears to be safe in women who have had a Caesarean section with a low transverse uterine incision in a previous
pregnancy.12 There are very limited data on the safety of ECV in women who have had 2 or more Caesarean sections.

Risks
1. Placental abruption (0.4% to 1%)9, 13, 14
2. Rupture of the membranes and subsequent possible cord prolapse
3. Initiation of labour
4. FHR abnormalities, the most common being transient bradycardia (1.1% to 47%).13-17 (Note that fetal
51 61
bradycardia necessitating an emergency Caesarean section is uncommon at 0.5%.18)

5. Alloimmunization/maternal-fetal hemorrhage (0% to 5%)1
A 2009 study by Clock et al. did not find an increase in intrapartum risk of delivery by Caesarean section after successful
ECV.19 Intrauterine death is rare, and evidence suggests that the rate is not increased by this procedure.7
Predictors for successful ECV

Clinical Predictors20, 21
• Multiparity
• Lack of engagement
• Relaxed uterus
• Fetal head palpable abdominally
• Low maternal weight
Ultrasound Predictors22
• Posterior placenta
• Complete breech
• Amniotic fluid index >10 cm
ECV Procedure
Obtain informed consent (this should be documented and ideally should include a written signed consent). The patient
should be informed that:
• Successful ECV will reduce the chance of a CS (success varies widely from 30% to 80%)17, 23-26
42 52
• Sedation and tocolysis may be used

• The procedure may be uncomfortable
• There are risks to the procedure (see above)
The procedure must be performed in a facility with the ability to carry out immediate intervention, including a CS, if
needed.
A non-stress test or biophysical profile should be carried out and must be normal before the procedure is started.

An ultrasound examination should be performed to confirm the fetal position. Real-time ultrasound examination should
also be performed intermittently during the procedure to check progress and monitor the fetal heart rate.
The abdomen may be lubricated with ultrasound gel or powder to make the procedure easier.
In the initial ECV attempt, the direction of rotation should be so that the fetus “follows its nose” (i.e., a forward roll).3
Proceed as follows:
• Dislodge the fetal buttocks from the maternal pelvis, pushing upwards and then laterally
• Grasp the fetal head and direct it downwards
• Slowly rotate the fetus by pushing upwards and to the side of the fetal back with the hand holding the
buttocks, at the same time guiding the head downwards and to the opposite side
• When the fetal head reaches a lower level than the maternal buttocks, manoeuvre the head over the pelvic
inlet
• If the forward roll attempt fails, a backward flip (i.e., the opposite direction) may be attempted
An assistant may be helpful to facilitate the ECV.
Stop the procedure if the woman is too uncomfortable or the fetal heart rate is abnormal. Most atypical and abnormal
FHR patterns will resolve. If the FHR doesn’t recover with intrauterine resuscitation, an emergency CS must be done.
Fetal surveillance (i.e., a non-stress test) is continued for a minimum of 20 minutes after an attempted ECV, whether or
not the ECV is successful. If the version was successful, the woman should continue to receive antenatal care and await
labour.
If version is not successful, discuss with the woman appropriate arrangements for her ongoing antenatal care and choice
of delivery method.
Administer Rh immunoglobulin 300 mcg to unsensitized Rh-negative women. Routine assessment with the Kleihauer-
Betke test for the possibility and degree of maternal-fetal bleed is not necessary since it has been shown that only 0.08%
of bleeds with ECV will be greater than 30 mL (300 mcg of Rh immunoglobulin will prevent senitization following a
bleed up to a 30 mL bleed).27
Advise the woman to report any abdominal pain, symptoms of labour, bleeding, fluid leakage, fever, or decreased fetal
movements.
Procedures that may Facilitate Turning the Breech

Tocolytics
Evidence for the use of tocolytics for improving the success of ECV is limited. A 2012 Cochrane review concluded that
beta-mimetic drugs are superior to placebo, nifedipine, or nitroglycerin; however, these are not used in Canada and have
considerable adverse maternal effects.28, 29 The Cochrane authors concluded there was enough evidence on nitroglycerin
to recommend against its use.28

Epidural or spinal analgesia

Several trials have now shown the benefit of spinal or epidural analgesia in improving the success of ECV. A 2011 meta-
analysis of 6 RCTs (n = 508) showed improved success with ECV under regional analgesia (60% vs. 35%), and a trend
toward fewer Caesarean sections (48% vs. 59%).30 More recent trials have confirmed the success of this meta-analysis.31, 32
Moxibustion
Moxibustion is a traditional medicine technique involving the burning of sticks or cones of the herb moxa (Artemisia
vulgaris) close to the pressure point on the fifth toe in order to induce a warming sensation that in turn has been
suggested to promote turning of the baby to cephalic presentation. A Cochrane review concluded that there is
insufficient evidence to support its use and larger trials are needed to evaluate it adequately.33
Postural management
Managing posture (e.g., knee–chest) to promote cephalic version has been assessed in a Cochrane systematic review of
RCTs and has not been shown to be effective. All the trials were small, and no effect on the rate of non-cephalic births
from postural management was detected between the intervention and control groups (5 RCTs, n = 392, RR 0.95; 95%
CI 0.81 to 1.11). Similarly, there were no differences detected for CS (4 RCTs, n = 292, RR 1.07; 95% CI 0.85 to 1.33).33, 34
Controversies in The Management of the Breech Presentation

The management of the breech presentation continues to provoke controversy. A policy of elective CS for all breech
presentations became popular in the 1990s. In a 10-year review of CS trends in Canada, from 1979–1980 to 1988–1989,
Caesarean sections performed because of breech presentation increased by 66%. This policy was instituted without
appropriate supporting evidence.
In 2000, the Term Breech Trial (TBT) was published.35 This trial was a multicentre RCT in which women with breech
singleton pregnancies at term were randomized to either a planned CS or a planned vaginal birth. The trial was stopped
early after the review of an interim analysis showed a large reduction in risk of perinatal or neonatal mortality or serious
neonatal morbidity with planned CS. The final results (developed and developing countries) showed the rate of perinatal
or neonatal mortality or serious neonatal morbidity to be 1.6% in the planned Caesarean group and 5.0% in the planned
vaginal birth group. Perinatal death was also reduced in the planned Caesarean group (0.3% vs. 1.3%; RR 0.23; 95% CI
0.07 to 0.81).
A Cochrane review of planned CS for term breech delivery includes the findings from the Term Breech Trial and 2 prior,
much smaller trials, and confirms these findings. In the total sample (worldwide), perinatal or neonatal death (excluding
fatal anomalies) was reduced overall (RR 0.29; 95% CI 0.10 to 0.86) with a policy of planned CS.36
The reviewed trials indicate that a policy of planned CS compared with planned vaginal delivery was associated with a
decrease in perinatal or neonatal death and/or neonatal morbidity. However, among survivors, there was no significant
difference in outcomes at age 2 and as the long-term outcome following perinatal morbidity appeared good, the most

relevant outcome is the reduction in perinatal and neonatal death. This reduction was found mostly in developing
countries with a baseline perinatal mortality > 20/1000. There was no significant difference in perinatal or neonatal
mortality in developed countries with low baseline perinatal mortality rates.
The Limitations Of The Term Breech Trial

The major limitations of the TBT are critical to estimating the true risk of labour for a breech fetus. They can be grouped as
follows:
1. Inadequate case selection and intrapartum management
Pre- or early labour ultrasound was not required, which may have allowed fetuses with growth restriction
due to placental insufficiency to go undetected. At least 7 of the trial’s 16 perinatal deaths were in growth-
restricted fetuses. Continuous electronic fetal monitoring was also not required, and was used with only one
third of fetuses. The trial protocol allowed cervical dilatation to be as slow as 0.5 cm/hr in the first stage of
labour and allowed the second stage to last for up to 3.5 hours. The findings of the TBT therefore suggest
that the following strategies may increase the safety of term breech deliveries: ultrasound estimation of
fetal weight to detect abnormal fetal growth, fetal head attitude and type of breech presentation, and close
attention to progress of labour.
2. Maternity units with markedly varying levels of skill within the group
Although a practitioner experienced in vaginal birth was expected at every delivery, a licensed obstetrician
was not present at 13% of births in the planned vaginal birth group versus 2% in the planned Caesarean
section group, and there was a high degree of crossover in the trial: 10% of women randomized to planned
CS delivered vaginally.
3. Short-term morbidity used as a surrogate marker for long-term neurological impairment
Despite the large difference in short-term outcome, even with the limitations in the TBT, women had a 97%
chance of having a neurologically normal 2-year old, regardless of planned mode of delivery.
In 2006, Goffinet et al. published the PREMODA study37, a multicentre descriptive study 4 times larger than the TBT.
Prospective data were collected from 8105 women in 174 centres in France and Belgium, using the same short-term
combined outcome of perinatal mortality or serious neonatal morbidity as the TBT. Although not strictly comparable, the
PREMODA outcomes are in contrast to those of the TBT. There was no difference in perinatal mortality (0.08% vs. 0.15%)
or serious neonatal morbidity (1.6% vs. 1.45%) between a trial of labour and planned CS. The only difference in outcome
was a 0.16% incidence of 5-minute Apgar score < 4 in the trial of labour group versus 0.02% in the planned CS group.
The PREMODA study is 8 times larger than the low-perinatal-mortality subset of the TBT, and therefore provides a robust
estimate of the risk of a cautious breech trial of labour in a modern, well-supported obstetrical unit.
In light of these studies, the SOGC published new guidelines for vaginal delivery of breech presentation in June 2009.38
Vaginal breech birth has been associated with a higher risk of perinatal mortality and short-term neonatal morbidity
than elective Caesarean section. However, the short-term neonatal morbidity nearly always resolves, and any increase in
perinatal mortality is small. Although perinatal mortality in developed countries was not significantly different between
the arms of the Term Breech Trial, 2 delivery-related perinatal deaths occurred in 511 labours versus none in the planned

CS group, a point estimate of 1/250. In the PREMODA study, there were no delivery-related perinatal deaths in 2502
labours. Therefore, careful case selection and labour management in a modern obstetrical setting may achieve a level
of safety similar to elective Caesarean section. Planned vaginal delivery is reasonable in selected women with a term
singleton breech fetus. The long-term neurological outcomes of infants do not differ by planned mode of delivery even
in the presence of serious short-term neonatal morbidity.
Vaginal Breech Delivery

The SOGC guideline38 makes the following recommendations for women who choose a trial of labour for a vaginal
breech delivery:
Labour Selection Criteria

For a woman with suspected breech presentation, pre- or early labour ultrasound examination should be performed
to assess type of breech presentation, fetal growth and estimated fetal weight (EFW), and attitude of fetal head. If
ultrasound is not available, Caesarean section is recommended.
Contraindications to planned vaginal breech birth

• Cord presentation
• Footling breech presentation (one or both hip(s) extended)
• Hyperextended fetal head
• Clinically inadequate maternal pelvis
• Fetal anomaly incompatible with vaginal delivery
• Fetal macrosomia ( >4000g)
• Fetal growth restriction (EFW <2500g)
−− Fetal metabolic acidosis in labour due to placental factors puts the fetus at elevated risk of asphyxia if
delay occurs during delivery. It is very important, therefore, to rule out significant fetal growth restriction
before delivery. Significant cord compression (with variable FHR decelerations) leading up to delivery
can also cause metabolic acidosis and predisposes the fetus to compromise if there is delay during
delivery. Any fetus at elevated risk of metabolic acidosis, or with evidence of acidosis in labour, is more
safely delivered by CS.
Vaginal breech delivery can be offered when the EFW is between 2500 g and 4000 g.
Labour Management
• Clinical pelvic examination should be performed to rule out significant pelvic contraction. Radiologic
pelvimetry is not necessary for a safe trial of labour; good progress in labour is the best indicator of adequate
fetal-pelvic proportions

• Continuous electronic fetal heart monitoring is recommended in the first stage and mandatory in the second
stage of labour. Membranes should be kept intact as long as possible. However, when membranes rupture,
immediate vaginal examination is recommended to rule out prolapsed cord.
• In the absence of adequate progress in labour, Caesarean section is advised.
• Induction of labour is not recommended for breech presentation. Oxytocin augmentation is acceptable in
the presence of uterine dystocia during the first and second stage of labour. In the PREMODA study, oxytocin
was routinely administered during the second stage of labour to ensure good uterine activity.37
• A passive second stage without active pushing may last up to 90 minutes, allowing the breech to descend
well into the pelvis. Once active pushing commences, if delivery is not imminent after 60 minutes,
Caesarean section is recommended.
• The active second stage of labour should take place in or near an operating room with equipment and
personnel available to perform a timely Caesarean section if necessary.
• A health care professional skilled in neonatal resuscitation should be in attendance at the time of delivery.
Delivery Technique
• The health care provider for a planned vaginal breech delivery needs to possess the requisite skills and
experience
• The requirements for emergency Caesarean section, including availability of the hospital operating room
team and the approximate 30-minute timeline to commence a laparotomy, must be in accordance with the
recommendations of the SOGC policy statement, “Attendance at Labour and Delivery”.39
• The health care provider should have rehearsed a plan of action and should be prepared to act promptly
in the rare circumstance of a trapped after coming head or irreducible nuchal arms: symphysiotomy or
emergency abdominal rescue can be lifesaving.
• Total breech extraction, where a hand is reached into the uterus and the fetus delivered, should only be used
for the second twin and is inappropriate for term singleton breech delivery.
• Effective maternal pushing efforts are essential to safe delivery and should be encouraged.
• At the time of delivery of the after coming head, an assistant should be present to apply suprapubic pressure
to favour flexion and engagement of the fetal head.
• Spontaneous or assisted breech delivery is acceptable. Fetal traction should not be used, and fetal
manipulation must be applied only after spontaneous delivery to the level of the umbilicus.
• Nuchal arms may be reduced by the Bickenbach or Løvset’s manoeuvres (Figures 2 & 3).
• The fetal head may deliver spontaneously, with the assistance of suprapubic pressure (Bracht manoeuvre), by
Mauriceau-Smellie-Veit manoeuvre (Figure 4), or with the assistance of Piper forceps (Figure 5).

Figure 2. Bickenbach Reduction of Nuchal Arms

Figure 2. Bickenbach reduction of nuchal arms
A B
A. Release of the posterior arm. The legs are grasped at the ankles and raised briskly until the fetal body is near-vertical.
A vaginal hand then reaches into the sacral hollow and sweeps the humerus from posterior to anterior across the fetal
A. Release of the posterior arm. The legs are grasped at the ankles and raised briskly until the fetal body is near-
chest. B. Release of the anterior arm. The fetal body is then lowered briskly toward the floor until the axilla appears at the
vertical. A vaginal hand then reaches into the sacral hollow and sweeps the humerus from posterior to anterior
introitus. A vaginal hand reaches behind the pubic symphysis and sweeps the humerus from posterior to anterior across
across the fetal chest.
the fetal chest.
B. Release of the anterior arm. The fetal body is then lowered briskly toward the floor until the axilla appears at the
introitus. A vaginal hand reaches behind the pubic symphysis and sweeps the humerus from posterior to anterior
across the fetal chest.

Figure 3. Løvset’s Manoeuvre to Reduce Nuchal Arms

Figure 3. Løvset’s manoeuvre to reduce nuchal arms
B
A. Release of the posterior arm. The fetus is grasped by the bony pelvis with 2 hands and initially raised towards the
maternal
A. Releasepubic
of symphysis. Turning
the posterior thefetus
arm. The fetal istorso whilebylowering
grasped the bonyit pelvis
allowswith
the fetal humerus
2 hands to be swept
and initially raisedout under the
towards
the pubic symphysis. B. Release of the first arm brings the other arm posterior. Rotating the fetal trunk back
maternal pubic symphysis. Turning the fetal torso while lowering it allows the fetal humerus to be swept out under through a
sacrum-anterior position to the other side allows the remaining arm to similarly be swept out under the pubic symphysis.
the pubic symphysis.
B. Release of the first arm brings the other arm posterior. Rotating the fetal trunk back through a sacrum-anterior
position to the other side allows the remaining arm to similarly be swept out under the pubic symphysis.

Figure 4. Delivery of the Aftercoming Head Using the Mauriceau Manoeuvre

Figure 4. Delivery of the after coming head using the Mauriceau manoeuvre
Note that as the fetal head is being delivered, flexion of the head is maintained by suprapubic pressure provided by an
assistant,
Note that and simultaneously
as the by pressure
fetal head is being on the
delivered, maxilla
flexion (inset)
of the headbyisthe operator by
maintained as traction is applied.
suprapubic 3
pressure provided by an
assistant, and simultaneously by pressure on the maxilla (inset) by the operator as traction is applied. 3

Figure
Figure 5.
5. Piper
Piper Forceps for delivery
forceps for Deliveryof
ofthe
theafter
Aftercoming Head
coming head
Note the direction of movement shown by the arrows. The fetal body is elevated using a warm towel and the left blade of
the
Noteforceps is applied
the direction to the aftershown
of movement comingbyhead. The right
the arrows. Theblade
fetal is applied
body with the
is elevated bodya still
using warm elevated. Forceps
towel and delivery
the left blade of
after coming
the forceps head.to the aftercoming head. The right blade is applied with the body still elevated. Forceps delivery of
is applied
3
the aftercoming head.3

Setting and Consent

• In the absence of a contraindication to vaginal delivery, a woman with a breech presentation should be
informed of the risks and benefits of a trial of labour and elective Caesarean section, and informed consent
should be obtained. A woman’s choice of delivery mode should be respected.
• The consent discussion and chosen plan should be well documented and communicated to labour-room
staff.
• Hospitals offering a trial of labour should have a written protocol for eligibility and intrapartum
management.
• Women with a contraindication to a trial of labour should be advised to have a Caesarean section. Women
choosing to labour despite this recommendation have a right to do so and should not be abandoned. They
should be provided the best possible in-hospital care.
• Theoretical and hands-on breech birth training simulation should be part of basic obstetrical skills training
programs such as ALARM and MOREOB to prepare health care providers for unexpected vaginal breech births.
Risks and Complications1

• Low 1-minute Apgar scores are commonly due to elevated CO2 that accumulates during cord compression at
delivery. The CO2 is easily excreted through adequate neonatal ventilation.
• Entrapment of the fetal head by an incompletely dilated cervix occurs uncommonly; however, it occurs more
frequently with preterm fetuses (< 32 weeks), since the head is larger than the body. Adequate power from
above (maternal pushing efforts and suprapubic pressure) is usually enough to complete delivery of the
head, but Dührssen incisions of the cervix are sometimes necessary. A Zavanelli-type manoeuvre to push
the fetus back up into the uterus followed by a Caesarean section has been performed successfully in rare
circumstances but must be considered a last resort.
• Nuchal arms, defined as one or both arms stuck between the fetal neck and the maternal pubic bone, occur
in 0% to 5% of vaginal breech deliveries and in 9% of breech extractions. Complications of nuchal arms
include brachial plexus injury and fractured humerus. Most occurrences of nuchal arms can be prevented
by refraining from the use of traction on the fetus during delivery. Nuchal arms can be released using the
Løvset’s or Bickenbach manoeuvres (Figures 2 and 3).
• A case series published in 1976 reported cervical spine injury in fetuses with a hyperextended head
delivered vaginally. Ballas and Toaff reported 20 cases of hyperextended necks, defined as an angle of
extension greater than 90° (“star-gazing”), discovered on antepartum radiographs.40, 41 Of the 11 fetuses
delivered vaginally, 8 (73%) sustained complete cervical spinal cord lesions, defined as either transection or
nonfunction. This forms the basis of recommendations to rule out hyperextension of the fetal head; however,
most of these fetuses were preterm, some may have had existing neurological abnormalities, and the
predominant delivery technique at the time involved traction.
• Cord prolapse occurs in approximately 5% of vaginal breech deliveries. Cord prolapse risk depends on
the type of breech (frank 1%, complete 5%, or footling 10% to 25%). Cord prolapse is also more common
in multiparous women (6%) than in primigravid women (3%). Electronic fetal monitoring in labour and

immediate vaginal examination upon membrane rupture will detect cord prolapse in a timely fashion. In a
monitored setting with ready access to CS, the risks of cord prolapse are almost always mitigated.
Preparation and Labour Management3, 41

A written vaginal breech labour protocol may assist in ensuring all important components are in place.
• If possible, and if time permits, use ultrasound assessment (or recent report) to confirm the lie and
presentation, assess the head position, get an EFW, assess amniotic fluid volume, confirm placental location,
and rule out major congenital anomalies such as hydrocephalus
• Ensure presence of a physician experienced with breech delivery
• Ensure an anaesthesiologist is available or in house
• Call for an anaesthesiologist
• Ensure presence of clinicians experienced in newborn resuscitation
• Ensure presence of experienced nursing staff
• Employ continuous electronic fetal surveillance. A fetal scalp ECG clip applied to the fetal buttocks can
improve FHR detection as the breech descends.
• Monitor labour progress using a partogram. If there is significant delay in the first or second stage, CS is
advised.
• Oxytocin augmentation is acceptable for poor uterine contractions; however, if progress is slow despite
strong contractions (clinically or by intrauterine pressure catheter), oxytocin is inadvisable.
• Empty maternal bladder just before delivery
• Ensure availability of forceps for the after coming head
• Ensure OR staff are in-house during active second stage for possible emergency CS
Delivery Technique
1. Total breech extraction should not be performed to deliver a singleton breech.
2. The necessity of effective pushing in the second stage of labour should be explained to the woman.
3. Analgesia should be adequate; however, dense epidural analgesia will hamper maternal pushing efforts.
4. Spontaneous descent and expulsion to the umbilicus should occur with maternal pushing only: DO NOT
PULL ON THE BREECH!
5. Rotation to the sacrum anterior position usually occurs spontaneously and is desired. If the fetus appears to
be rotating to a sacrum posterior position, grasp the fetal pelvis and gently rotate to sacrum anterior.
6. Episiotomy may be considered once the anterior buttock and anus are “crowning.”
7. Spontaneous delivery of the entire breech fetus is desirable and is common with adequate maternal pushing
efforts and suprapubic pressure, if needed. However, assisted breech delivery is acceptable if there is a delay
in delivery, and the following manoeuvres may be required:
a. Pinard’s manoeuvre to deliver the fetal legs may be considered once the popliteal fossae are visible.

Figure 6. Pinard’s manœuvre

Figure 6. Pinard’s manœuvre
Pinard’s manoeuvre is accomplished by inserting 2 fingers along 1 leg to the knee, which is then pushed away from
the midlinePinard’s
(abducted) at the same
manoeuvre time as flexing
is accomplished the leg at2the
by inserting hip. This
fingers alongcauses
1 legspontaneous flexionisofthen
to the knee, which thepushed
knee and
delivery ofaway
the foot. 42
The knees of a frank breech are hyperextended at this point and it is important
from the midline (abducted) at the same time as flexing the leg at the hip. This causes spontaneous to correctly identify
the popliteal fossae
flexion of to
theavoid
kneefurther hyperextension
and delivery andThe
of the foot.42 damage
kneestoofthe fetalbreech
a frank knee. are hyperextended at this point
and
b. it Løvset’s
is important to correctly
manoeuvre identifyarms.
for nuchal the popliteal
Rotate thefossae
bodytotoavoid further
facilitate hyperextension
delivery of the armsand damage tothe
by sweeping
the fetal knee. humerus across the chest of the fetus (Løvset’s manoeuvre). Rotate the other arm anterior and
anterior
repeat manoeuvre
b. Løvset’s (Figure 3). for nuchal arms. Rotate the body to facilitate delivery of the arms by sweeping the
8. Support the baby to maintain
anterior humerus across thethechest
headofinthe
a flexed position.manoeuvre).
fetus (Løvset’s Suprapubic pressure
Rotate themay help.
other armMaternal
anterior and
expulsive efforts should
repeat (Figure 3). be encouraged.
9. The body should be supported in a horizontal position.
10. The Mauriceau-Smellie-Veit manoeuvre can be used to deliver the head in flexion (Figure 4).
11. Use forceps, if needed. Piper’s forceps were specifically designed for this purpose. (Figure 5).

12. Delivery of the breech with the woman in the upright position, as a means of increasing power from above
seems to reduce the need for intervention, and is commonly used in some countries.43
Follow-Up
Care After Breech Delivery Should Include
• Active third stage management
• Cord blood gas analysis
• Examination for maternal trauma
• Examination for neonatal trauma: examine the hips with care; repeat the examination before discharge
• Review delivery with the family
• Documentation
Documentation: Breech Delivery

A complete review of risks and benefits for vaginal delivery and consent must be clearly and completely documented in
all cases. A contemporaneous written note and a dictated operative record are recommended. It must be documented
whether the vaginal delivery was undertaken as an incidental emergency or was planned and consensual.
Suggested format for a chart note (this may also serve as a template to dictate a delivery summary):
• Date and time
• Health care provider(s) present
• Type of breech
• Record of discussion with the woman of the risks, benefits, and options
• Assessment of maternal pelvis
• Fetal heart rate and contractions
• Progress in labour, including time of commencement of active pushing
• Manoeuvres or manipulations required
• Time between crowning and complete delivery of the fetus
• Number of attempts and ease of application of forceps (if used)
• Duration of traction and force used (if forceps used)
• Description of maternal and neonatal injuries (if any)

Summary
Management of a fetus in breech presentation continues to provoke much discussion and controversy despite many
studies and trials. An informed discussion and consent process involving the woman presenting with a breech is critical.
Currently the recommended management for the singleton term breech is to offer external cephalic version. If ECV is
unsuccessful, declined, or unavailable, and in a setting of appropriate experience, support, and informed consent, a
planned vaginal delivery of a frank or complete breech may then be contemplated. However, all care providers involved
in managing deliveries must be prepared for the unexpected vaginal breech delivery. Therefore, the technique and
manoeuvre for a safe assisted vaginal breech delivery should be practiced and reviewed regularly. GETHIPPOS is a good
example of a mnemonic that can assist in preparedness for vaginal breech birth (see Appendix).

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Appendix
GETHIPPOS Mnemonic
G Growth assessment: rule out IUGR
E EFM recommended
T Type of breech (frank or complete)
H Help needed (from department of anaesthesia, OR staff, pediatrics, second MD)
I IV in place, CBC & group and screen
P Progress in labour adequate? (maximum 60-minute active second stage)
P Power from above after crowning (Bracht manoeuvre & oxytocin) safer than pulling from below
O Oxytocin ready and hanging to ensure strong contractions at delivery
S Smellie-Veit manoeuvre for after coming head if needed

Table of Contents
Chapter 15 Postpartum Hemorrhage............................................................................................................................... 333

Introduction.............................................................................................................................................................. 333
Definitions..................................................................................................................................................... 333
Incidence ...................................................................................................................................................... 333
Identification and Diagnosis..................................................................................................................................... 334
Etiology......................................................................................................................................................... 334
Risk Factors............................................................................................................................................................... 335
Prevention................................................................................................................................................................ 336
Active Management of Third Stage Labour (AMTSL)..................................................................................... 336
Uterotonic Agents.......................................................................................................................................... 337
Non-Pharmcologic Measures Influencing Blood Loss at Delivery................................................................. 343
Management............................................................................................................................................................ 346
Estimating Blood Loss................................................................................................................................... 346
Assess Uterine TONE by palpating the Fundus ............................................................................................. 346
Additional Measures to Stabilize the Patient and Lessen Blood Loss with Uterine Atony............................. 347
Other Causes of Excessive Bleeding at Delivery............................................................................................ 352
Bleeding and Anticoagulants........................................................................................................................ 354
Summary.................................................................................................................................................................. 354
Management of Postpartum Hemorrhage.................................................................................................... 368
Contents of Obstetric Hemorrhage Equipment Tray..................................................................................... 369
Injection of the Umbilical Vein for Retained Placenta: ................................................................................. 371
Uterine Compression Sutures....................................................................................................................... 372
Postpartum Hemorrhage 332

Chapter 15
Postpartum Hemorrhage
Introduction
Definitions
Postpartum hemorrhage (PPH) has been defined as blood loss in excess of 500 mL in a vaginal birth and in excess of
1000 mL in an abdominal delivery.1 Clinical estimates of blood loss are often inaccurate, so for clinical purposes, any
blood loss that has the potential to produce hemodynamic instability should be considered a postpartum hemorrhage.
Primary (immediate/early) postpartum hemorrhage occurs within the first 24 hours after delivery. Approximately
70% of immediate PPH cases are due to uterine atony.
Atony of the uterus is the failure of the uterus to contract adequately after delivery of the infant(s).
Secondary (delayed/late) postpartum hemorrhage occurs between 24 hours after delivery of the infant and 6 weeks
postpartum. Most late PPH is due to retained products of conception, infection, or both.
Incidence
Worldwide, postpartum hemorrhage occurs in about 10% of all deliveries and is a leading cause of maternal mortality.2, 3
A 2012 systematic review on regional prevalence of PPH demonstrated the lowest prevalence in Oceania (7.2%) and the
highest in Africa (25.7%).4 The North American and European rates were similar, at 13.1% and 12.7% respectively. These
authors noted that the reported prevalence of PPH varied not only by region, but also by the methods used to manage
the third stage of labour and to measure blood loss.
The Public Health Agency of Canada reported that between 2010/2011 and 2014/2015, blood transfusion and PPH
were the most common source of major maternal morbidity. PPH was the leading cause of direct maternal mortality
accounting for 49 maternal deaths (1.4/100 000 deliveries).5 6
Studies in high-resource countries have observed an increase in PPH, predominantly due to atonic PPH.7-9 A cohort
8
study analyzed >100,000 deliveries in Montreal between 1978 and 2007 and found that increasing rates of labour
induction, augmentation of labour, previous Caesarean section (CS), placenta previa and abnormal placentation were
associated with the observed rise in PPH.10 A 2014 cohort study reviewing over 2 million deliveries in Canada between
2003 and 2010 identified an increase of PPH by 22% (5.1% to 6.2%), mostly attributable to the increase in atonic PPH.
Increases were also noted in PPH requiring blood transfusion, PPH with hysterectomy, and use of uterine suturing or
embolization/ligation of uterine vessels to control PPH.11

Identification and Diagnosis

The amount of blood loss required to cause hemodynamic instability will depend on the pre-existing condition of the
woman. Hemodynamic compromise is more likely to occur in association with conditions such as anemia (e.g., iron
deficiency, thalassemia) or a volume-contracted state (e.g., dehydration, preeclampsia).
Hypovolemic Shock12
DEGREE OF SHOCK BLOOD LOSS SIGNS AND SYMPTOMS
Mild < 20% • Diaphoresis

• Delayed capillary refill
• Cool extremities
• Anxiety
Moderate 20% to 40% The above plus

• Tachycardia
• Tachypnea
• Postural hypotension
• Oliguria
Severe > 40% The above plus

• Hypotension
• Agitation/confusion
• Hemodynamic instability
Etiology
It may be helpful to think of the causes of PPH in terms of the four T’s:
• Tone – uterine atony, distended bladder
• Trauma – uterine, cervical, or vaginal injury, perineal tears, episiotomy
• Tissue – retained placenta or clots
• Thrombin – pre-existing or acquired coagulopathy
The most common cause of PPH is uterine atony. Myometrial blood vessels pass between the muscle cells of the uterus.
The primary mechanism of immediate hemostasis following delivery is myometrial contraction causing occlusion of
uterine blood vessels, the so-called ‘living ligatures’ of the uterus.
Significant blood loss can occur very quickly. Women can lose up to 500 ml of blood in 1 minute during a PPH. The
average woman has approximately 5 litres of blood in her circulation. At this rate of loss, it is possible for a woman
to exsanguinate within 10 minutes. Rapid, efficient action must be taken to save the woman’s life and to prevent
complications related to significant blood loss.

Risk Factors13-15 14
ETIOLOGIC PROCESS CLINICAL RISK FACTORS
Abnormalities of uterine Over-distended uterus • polyhydramnios

contraction • multiple gestation
(Tone) • macrosomia
Uterine muscle exhaustion • rapid labour

• prolonged labour
• high parity
• oxytocin use
• induction of labour16
Intra-amniotic infection • fever

• prolonged ROM
Functional/anatomic distortion of the uterus • fibroid uterus

• placenta previa
Uterine-relaxing medications • uterine anomalies
Bladder distension, which may prevent uterine contraction
17 • velamentous cord insertion18
• halogenated anaesthetics
• tocolytics including nitroglycerin
Retained Products of Retained placenta or membranes • incomplete placenta at delivery

conception • abnormal placentation • previous uterine surgery
(Tissue) • retained cotyledon or succenturiate lobe • high parity
• abnormal placenta on ultrasound
Retained blood clots • atonic uterus
Genital Tract Trauma Lacerations of the cervix, vagina, or perineum • precipitous delivery
(Trauma) • operative delivery
Extensions, lacerations at CS • malposition

• deep engagement
Uterine rupture • previous uterine surgery
Uterine inversion • high parity

• fundal placenta

ETIOLOGIC PROCESS CLINICAL RISK FACTORS
Abnormalities of Pre-existing states • history of hereditary coagulopathies

Coagulation • Hemophilia A • history of liver disease
(Thrombin) • Von Willebrand disease19 • history of other episodes of
excessive bleeding
Prior invasive treatment of PPH with embolization (39%) and
ligation (26%)20
Acquired in pregnancy • bruising

• idiopathic thrombocytopenic purpura • elevated BP
• thrombocytopenia with preeclampsia • fetal demise
• disseminated intravascular coagulation • fever, neutrophilia or neutropenia
−− dead fetus in utero • antepartum bleed hemorrhage
−− severe infection • sudden collapse
−− abruption
−− amniotic fluid embolus
Therapeutic anti-coagulation • history of thrombotic disease
Other BMI > 3021 22
Selective serotonin reuptake inhibitors23-26

42 52
Serotonin–norepinephrine reuptake inhibitors27
Prevention
Active Management of Third Stage Labour (AMTSL)
Postpartum hemorrhage is the leading cause of direct maternal mortality worldwide. Because of this, the guidelines
of multiple national societies (SOGC,14 RCOG,28 RANZCOG,29 and CNGOF30) and international institutions (FIGO31 and
WHO32) support the use of uterotonics as part of the active management of the third stage of labor. 33
Expectant, or physiologic, management of the third stage allows the placenta to deliver spontaneously and the uterus to
contract spontaneously. By contrast,
ACTIVE MANAGEMENT involves caregiver intervention to assist in the expulsion of the placenta by increasing uterine
contractions, and to avoid PPH by preventing uterine atony. The usual components of AMTSL have included:
• Administration of Uterotonic Agents
• Controlled Cord Traction (CCT)
• Uterine Massage after delivery of the placenta
Of these 3 components, administration of an uterotonic agent (usually oxytocin) has the greatest impact on blood loss.
Controlled cord traction reduces the need for manual removal of the placenta (RR 0.69).34 However, it did not decrease
blood loss of >1000ml in a randomized trial of >23,000 women.35 CCT requires countertraction on the uterine fundus

by a skilled birth attendant to avoid uterine inversion. Evidence is limited regarding the independent benefit of uterine
massage as a preventive measure.36
A joint statement by the International Confederation of Midwives and FIGO33 and a review by WHO32 support the
recommendation that all deliveries should be attended by a caregiver trained to manage the third stage of labour.
A 2015 Cochrane meta-analysis37 of AMTSL determined that compared with expectant management, active management reduced
the risk of PPH ≥1000ml (average Risk Ratio 0.34) and that of hemoglobin concentration less than 9 g/dL (average Risk Ratio 0.50),
regardless of the woman’s bleeding risk profile. Many earlier studies on AMSTL included early cord clamping along with oxytocin
and cord traction. Subsequently, it has been shown that delayed cord clamping does not increase PPH.45
Uterotonic Agents
During the third stage, the muscles of the uterus contract, compressing the blood vessels that pass through the uterine
wall to the placental surface and slowing the flow of blood. The contraction also causes the placenta to separate from the
uterine wall. The absence of uterine contractions is called atony. Uterotonics promote uterine contractions.
The CLASSES OF uterotonic agents include Oxytocics, Ergot Alkaloids, and Prostaglandins.
UTEROTONICS for the prevention and treatment of PPH
MEDICATION CLASS CHARACTERISTICS SIDE EFFECTS/ USE IN PREVENTION USE IN TREATMENT OF

CONTRAINDICATIONS OF PPH PPH
Oxytocics Preferred first line Rare: Nausea, vomiting, 10 unit IM Same as prevention
Oxytocin uterotonic. headache, flushing.
20-40 units/litre of RL or Run infusion wide open
Stimulates muscle of upper Hypotension with rapid IV NS infused quickly
uterine segment causing bolus.
5 units IV over
contraction to compress
Water intoxication with
blood vessels. 1-2 minutes
high doses/prolonged
IV: Acts immediately infusion/hypotonic IV
solution. Use normal saline
IM: 3-5 minutes or Ringers Lactate.
Carbetocin Long-acting oxytocin Nausea, vomiting, flushing, 100 mcg IV over 1 minute, Limited data
analogue headache. or IM, for scheduled
Caesarean Section
Ergot Alkaloids Stimulates myometrium Nausea, vomiting, 0.2 to 0.25mg IM or IV Same as prevention
of the upper AND lower
Hypertension:
uterine segments
CONTRAINDICATED in all Repeat every
IV: Acts< 1 minute
Hypertensive Disorders of
2 hours
IM: 2-5 minutes Pregnancy

Prostaglandins Causes vasoconstriction Fever (most common with 400mcg sublingual Fastest acting:
Misoprostol and enhanced contractility > 600mcg) (achieves highest serum 400 mcg SL
of the myometrium peak level)
Alternate: 800mcg rectally
Prostaglandin E1
Carboprost Causes vasoconstriction Vomiting and diarrhea 250mcg IM or IMM

(Hemabate) and enhanced contractility (intramyometrial) every
Fever
of the myometrium 15 minutes; maximum 8
Bronchospasm doses (2mg)
Prostaglandin F2
Use with EXTREME
CAUTION if asthma or
major cardiovascular/renal/
hepatic dysfunction.
ADDITIONAL MEDICATION 3839
Tranexamic Acid Inhibits fibrinolysis Not proven effective 1 gram IV over 10

minutes, within 3h of PPH
diagnosis
Oxytocin
• Oxytocin is the drug of choice for prevention and treatment of PPH due to efficacy, low incidence of side
effects and low cost.
The Abu Dhabi study40 included in the Cochrane analysis37 demonstrated the benefits of active intervention during the
third stage with controlled cord traction and 10 units of oxytocin administered intramuscularly (IM) compared with
minimal intervention. With active management, there was a lower incidence of PPH (5.8% vs. 11%), reduced incidence
of retained placenta at ≥ 30 minutes (1.6% vs. 4.5%), and less need for additional uterotonic agents (2.3% vs. 5.1%).
A 2011 randomized controlled trial (RCT) in high resource countries compared active (oxytocin 10 U IM, early cord
clamping, and controlled cord traction) versus expectant management in 1802 women. Blood loss was reduced (535 mL
vs. 680 mL) and PPH > 1000 mL was lower (10% vs. 16.8%) in the active versus expectant management groups. Blood
loss increased for increased duration of the third stage (40 mL / 5-min duration) and increased placenta weight (44 mL /
100 gm weight). 414243444546
Higher prophylactic amounts of oxytocin may be required in a woman exposed to oxytocin in labour when delivered by
CS. Lavoie et al. measured that woman who had a CS after labour exposed to exogenous oxytocin needed an infusion
rate of 28 IU/h higher to prevent bleeding as defined by the surgeon compared to women undergoing an elective CS
(44.2 IU/h vs 16.2 IU/h)47 48
Oxytocin may be given IM or by slow IV bolus. The IV route may be more effective: A double-blinded, placebo-controlled
RCT of >1000 women comparing 10u oxytocin given IV push over 1 minute with 10u IM showed less PPH >1000ml

(5% vs 8%) and less need for transfusion (2% vs 4%). The difference in blood loss of 500-999ml did not reach statistical
significance (19% vs 23%; P=0.07).49
IV Oxytocin must be given by slow bolus (≥1 minute) to minimize the impact of hemodynamic changes. Hypotension
and tachycardia have been demonstrated with invasive monitoring during oxytocin bolus.50, 51 ) RCOG NICE 2016
guidelines recommend oxytocin 5U IV infused slowly (to mitigate the hemodynamic and cardiac concerns noted above)
to prevent PPH in all women undergoing CS.52 5354
Additional oxytocin infusion after routine administration of oxytocin bolus in women booked for elective CS reduces
blood loss and the need for additional uterotonics.55, 57
65
Oxytocin has an anti-diuretic effect, and must be given in an isotonic IV solution (Normal Saline or Lactated Ringers) to
avoid hyponatremia/water intoxication.58
Carbetocin
Prevention
• Reduces the need for additional uterotonics but not PPH for elective CS
• Reduces the need for uterine massage but no other measure of bleeding after vaginal delivery in women
with one risk factor for PPH
Treatment
• There is limited data on the use of carbetocin for treatment of PPH.
Carbetocin is a long-acting oxytocic. The recommended dose of carbetocin is 100 micrograms IM or IV given slowly over
one minute. The pharmacokinetics of both administration routes are almost the same: Whether given IV or IM, a firm
uterine contraction occurs within 2 minutes in 90% of women. Durations of action is about 1 hour when given IV and 2
hours when given IM.59
Carbetocin compared with oxytocin infusion has been shown to reduce bleeding secondary to uterine atony in elective
CS and is associated with less need for additional uterotonics but there was no difference in PPH.60
A 2012 Cochrane review61 concluded that, for vaginal deliveries, there is insufficient evidence that 100 mcg IV carbetocin
is as effective as oxytocin in preventing PPH.. The need for uterine massage was decreased with carbetocin (RR 0.54 for
CS and 0.70 for vaginal delivery). Carbetocin should not be used as a first-line agent before other uterotonic agents.
RCTs comparing carbetocin with oxytocin in women with 162 or 2 risk factors63 for PPH in term vaginal deliveries did not
show any significant difference for bleeding, need for other uterotonic medications, and blood transfusion.
Studies of Carbetocin in the treatment, rather than prevention, of PPH are very limited. A randomized trial of 100 women
receiving 100mcg of Carbetocin or 5units of Oxytocin suggested less total blood loss in those suffering a minor PPH
(500-999ml), but no difference in major PPH (≥1000ml).63
There is no efficacy or safety data for repeated doses of Carbetocin.

A new heat-stable form of Carbetocin has been developed. It may be particularly useful in low-resource settings, where
cold storage is not available. A multicentre trial randomized almost 30,000 women to receive 100mcg of heat-stable
Carbetocin IM or 10units of Oxytocin IM immediately after vaginal birth. The Carbetocin was shown to be non-inferior
(as effective) to oxytocin for blood loss of at least 500ml or use of additional uterotonic agents. Non-inferiority was not
shown for blood loss of at least 1000ml; however, the study was not powered for this outcome. There was no significant
difference in adverse effects or other measure of bleeding (blood transfusion, manual removal of placenta, additional
surgical procedures).64
Ergonovine
Prevention
• It is as effective as oxytocin but causes more side effects
• Its use is contraindicated in women with hypertension.
• It stimulates contraction of the lower uterine segment as well as the fundus of the uterus
Treatment
• It can be repeated IM or IV every 2 hours
Ergonovine stimulates the myometrial alpha-adrenergic receptors of the upper and lower segments of the uterus
producing a tetanic contraction. It is an effective agent for the treatment and prevention of PPH, 65, 66, 68 but it has
76
more adverse effects (nausea, vomiting and hypertension) than oxytocin, making it a less preferred agent.69, 70 It is
contraindicated in the presence of hypertension. The dose is 0.2 to 0.25 mg, has a rapid onset of action (< 1 minute for
IV and 2 to 5 minutes for IM) and interval dosing is every 2 hours.71
Compared to placebo, ergonovine reduce the incidence of PPH > 500ml and severe PPH (>1000ml).72 Studies
show inconsistent results regarding retained placenta or need for manual removal. The Dublin trial which used IV
administration had a higher incidence of retained placenta, but used a dose of 0.5mg.39
Compared to oxytocin, ergonovine:
• Is equally effective for the prevention of PPH
• Has a higher incidence of headaches, nausea, and hypertension70 73
Misoprostol
Prevention
• Reduces risk of PPH better than placebo but not as effectively as oxytocin.
• 400 mcg SL is preferred dose and route
Treatment
• Misoprostol dose is 400 mcg SL.
• There is a delay of at least 30 minutes between administration and onset of action.

Misoprostol has been extensively studied in obstetrics as an uterotonic agent. It has not been shown to be superior to
other uterotonics in AMTSL for the prevention and treatment of PPH. Because of its stability at room temperature, ease of
administration, low cost, and uterotonic properties, the World Health Organization includes misoprostol in its essential
medication list, for situations where oxytocin is not available or cannot be safely used.74 75
A 2011 study by Elati and Weeks measured the effect of 3 doses of misoprostol (200 mcg, 400 mcg and 600 mcg) and
10 U IM oxytocin on uterine contractions in the immediate postpartum period using an intrauterine pressure catheter.76
There was no difference between the misoprostol doses. At 10 minutes, the intrauterine pressure (IUP) with oxytocin was
much higher than misoprostol. The pressure was the same at 30 minutes while the IUP was much higher for misoprostol
than for oxytocin from 50 to 120 minutes. The incidence of high fever (temperature > 39 degrees) was the same for
the 200 mcg and 400 mcg doses (8.3%) and much higher for the 600 mcg dose (45.4%).76 A 2013 Cochrane review by
Hofmeyr et al. supported that adverse effects increased at doses greater than 600 mcg.77
Reviews of the pharmacokinetics of misoprostol can be summarized as follows:
ROUTE PEAK ONSET (T-MAX) BIOAVAILABILITY (UAC)
Sublingual 30 minutes 120 minutes
Oral 30 minutes 120 minutes
Vaginal 70 to 80 minutes 6 hours
Rectal 40 to 60 minutes 6 hours
The sublingual route has a much higher serum peak level than the oral route because it avoids the first pass metabolism
by the liver.
There have been many clinical studies involving misoprostol in order to determine its place in the medical prevention
and treatment of PPH. Comparison of studies is challenging because of the variety of doses (400 to 800 mcg) and routes
of administration.
The studies of misoprostol and prevention of PPH can be summarized as follows:
• Misoprostol is more effective than placebo78
• The recommended dose is 400 mcg sublingual78
• Misoprostol is less effective than IM uterotonics in prevention of PPH79-82
08 18
• In low resource countries, misoprostol83 (600 mcg SL) was less effective than oxytocin (10 IU IM) for the
incidence of primary PPH > 500 mL within 24 hours (28.6% vs. 17.4%) for uncomplicated, term vaginal
deliveries84
The misoprostol studies for the treatment of PPH have shown:
• Misoprostol was as effective as IV oxytocin for treatment of PPH in women given prophylactic IM oxytocin85
• Misoprostol was less effective than IV oxytocin for treatment of PPH in women not given prophylactic IM
oxytocin86

• Misoprostol (600 mcg SL) as an adjunct to routine IV oxytocin had a non-significant trend to lower blood loss
in vaginal deliveries87
In women with a retained placenta:
• Injection of misoprostol (800 mcg in normal saline) into the umbilical vein has been associated with a lower
rate of manual removal of placenta than oxytocin infusion or placebo88
• Administration of misoprostol (800 mcg PO) is not associated with a lower rate of manual removal of
placenta compared with placebo89
Carboprost / Hemabate (15-methyl F2 prostaglandin)

Prevention
• Not superior to oxytocin and higher cost
Treatment
• Recommended dose is 250 mcg IM / intramyometrially
• Can be used every 15 minutes, total 8 doses
Carboprost is a synthetic injectable prostaglandin similar to misoprostol. A 2012 Cochrane review did not find it superior to oxytocin
for prevention of PPH.79
For women with severe PPH unresponsive to other oxytocics, studies in the 1980s first showed that PGF2 decreased the need
for hysterectomy.90 In a retrospective study of 236 women with persistent postpartum hemorrhage, bleeding was successfully
controlled with PGF2 in 88%.91 Takagi showed that injection of PGF2 directly into the myometrium produced strong uterine
contractions more quickly than when given IM. Side effects were also less common. Doses above 250mcg were no more effective.92
Tranexamic Acid
Prevention:
1. Reduces blood loss >1000ml in women at risk of bleeding undergoing elective CS but not vaginal birth
2. Used in addition to usual uterotonics in elective CS.
Treatment:
1. Second line medical treatment shown to reduce maternal death but not hysterectomy.
2. Reduces the need for laparotomy to control bleeding
3. Dose is 1g IV (100mg/ml at a rate of 1ml/min = 10ml over 10 minutes)
4. Can be repeated if:
a. Bleeding persists after 30 minutes
b. Bleeding re-starts within 24 hours
Tranexamic acid (TXA) is an inhibitor of fibrinolysis. It acts by preventing the conversion of plasminogens to plasmin,
stabilizing clot formation.

For prevention of PPH, the majority of studies have compared TXA with placebo as adjuncts to usual prophylactic care
with oxytocin. No benefit was shown in the TRAAP study randomizing >4000 women with planned vaginal birth to
receive prophylactic TXA and oxytocin, compared to oxytocin alone.93 In contrast, a review by Novikova 97 showed TXA
9495 96
decreased blood loss > 1000ml in women who underwent CS (RR 0.23, 4 studies 1534 women). Based on the latter
study, RCOG recommends considering IV TXA (0.5 – 1.0 g) in addition to oxytocin for women at increased risk of PPH
undergoing CS.52
In a 2014 RCT, 98 747 women with a high incidence of anaemia were given tranexamic acid (1 g IV slowly 10 minutes
before elective CS). The mean total blood loss was 242 mL in the tranexamic acid group versus 510 mL in the control
group. The mean drop in hematocrit and hemoglobin levels was statistically significantly lower in the tranexamic acid
group than in the control group.
For treatment of PPH, the largest study was the2016 WOMAN trial99 an RCT of 20060 women diagnosed with active PPH
(> 500ml after VD after > 1000ml after CS or sufficient blood loss to cause hemodynamic instability) that compared
the addition of TXA to usual care. Most (96%) women received prophylactic uterotonics and almost all women received
a secondary uterotonic (99.6% in the TXA study group and 99.5% in the control group). The study showed that woman
given TXA less than 3 hours after diagnosis of PPH had a reduction in overall death due to bleeding (1.2% vs 1.7%) and
need for laparotomy to control bleeding (0.8% vs 1.3%). There was no benefit if TXA was given 3 hours after diagnosis
of PPH for death, the need for hysterectomies, or secondary outcomes.99 The majority of centres participating in the
WOMAN trial were in low resource settings. The lack of difference in hysterectomy rate, even with TXA given early, may be
in part due to the move to hysterectomy early in the management of PPH because other medications and intensive care
support are limited.
There was no increase in thromboembolic events with TXA.
NON-PHARMCOLOGIC MEASURES INFLUENCING BLOOD LOSS AT

DELIVERY
Cord Traction
The use of cord traction has been shown to reduce the incidence of retained placenta without significant reduction of
PPH.
The mainstay of AMTSL is the IM injection of oxytocin.35
A 2015 Cochrane review100 as well as a large 2013 randomised controlled trial study (TRACOR)34 both concluded that
controlled cord traction (CCT) resulted in fewer manual removal of placentas but no difference in PPH when compared to
expectant or physiological delivery of the placenta.

Uterine Massage before Placental Delivery

Uterine massage before the delivery of the placenta is of no benefit. It may increase blood loss and should not be
done.101, 102
Two of the trials included in a 2013 Cochrane review found no evidence to show that prophylactic uterine massage to
reduce PPH was effective.103
A multicentre RCT of 2340 vaginal deliveries showed that the addition of uterine massage after routine oxytocin did not
reduce blood loss.104
A secondary analysis of 39 202 births found that uterine massage was associated with increased hemorrhagic risk.48
Timing of Cord Clamping

As with controlled cord traction, the timing of cord clamping has not been independently studied in relation to the
prevention of PPH. However, studies have demonstrated the benefits for the neonate of delayed cord clamping.
Delaying cord clamping by 30 to 120 seconds seems to be associated with less need for transfusion for anaemia and less
intraventricular hemorrhage in non-resuscitated premature infants < 37 weeks compared with early clamping.105, 106
Delayed clamping is supported in term newborns in order to provide an ongoing blood flow from the placenta to the
newborn and facilitates early skin-to-skin contact.107
A 2007 systematic review and meta-analysis by Hutton and Hassan108 comparing early (< 1 minute) with late (>2
minutes) cord clamping suggests that there is a physiological benefit of delayed clamping to the newborn that extends
into infancy. Advantages included prevention of anaemia over the first 3 months of life, and enhanced iron and ferritin
stores for up to 6 months. There was no increase in respiratory distress, defined as tachypnea or grunting. There was no
statistical difference in bilirubin levels or in number of infants receiving phototherapy in the late versus early group. A
2013 Cochrane review45 included 15 RCTs involving a total of 3911 women and infant pairs that compared early (< 60
seconds) to late (> 60 seconds) cord clamping on maternal and neonatal outcomes. The authors concluded that there
was no difference in the rate of postpartum hemorrhage for mothers, and measured the same benefits to the newborns
as did Hutton and Hassan. In contrast to the Hutton and Hassan review, there was an increased risk of neonatal jaundice
requiring phototherapy.
Timing of Placental Delivery

• The incidence of PPH increases when a placenta is retained for > 15 minutes
An important risk factor for PPH is the failure of the placenta to deliver in a timely manner. Fifty percent of placentas
deliver within 5 minutes, and 90% within 15 minutes of the baby’s birth.109 Magann et al. concluded that the risk of PPH
increases 3-fold if the placenta is delivered > 15 minutes after the delivery of the infant rather than < 15 minutes after
(13.3% vs. 4.4%).110 A retrospective study of 25 016 cases correlating outcomes with the timing of placental delivery
determined that the optimal timing for predicting blood transfusion with an undelivered placenta was at 17 minutes

of the third stage and that the risk of transfusion increased 3-fold at ≥ 30 minutes. IV access should be ensured at 15
minutes of an undelivered placenta.111
A 2012 case-control study identified several risk factors for placental retention, including previous retained placenta,
preterm delivery, prolonged oxytocin use, preeclampsia, and ≥ 2 miscarriages or abortions.112
A 2012 RCT by Van Stralen et al.89 studied 99 women with a retained (> 60 minute) placenta after oxytocin prophylaxis
(5 U IM or IV). The study showed no difference in manual removal of the placenta or blood loss for women who received
misoprostol (800 mcg orally) one hour after childbirth compared with those who received placebo.
Placental Cord Drainage

• Reduction in length of third stage and blood loss statistically but not clinically significant
• Studies limited in quality
A 2011 Cochrane review identified 3 studies involving 1257 vaginal deliveries addressing placental cord drainage.
There was a reduction in the length of the third stage of 2.85 minutes and blood loss was reduced by 77 ml. A major
confounding factor was that only 1 of the 3 studies used an uterotonic (methyl-ergomethrine) for prevention. The
definition of a prolonged third stage in the studies varied from 30 minutes to 45 minutes. More research is required to
determine the efficacy of this intervention.113
A prospective study compared cord drainage (cord not clamped after cutting) with routine clamping before cutting in
485 vaginal deliveries. All women received 5 IU oxytocin prophylaxis.114 The mean estimated blood loss was significantly
lower in the cord drainage group than in the control group (207.04 ± 123.3 vs. 277.63 ± 246.9 mL). The third stage of
labour was significantly shorter in the cord drainage group than in the control group (3.5 ± 1.9 vs. 7.7 ± 3.4 minutes).
No adverse events occurred during the cord drainage period.
Injection of the Umbilical Vein for Retained Placenta

• Umbilical cord vein injection of misoprostol but not oxytocin has been shown to avoid manual removal of a
retained placenta, although not PPH
Manual removal of a retained placenta may lead to complications such as infection, uterine perforation, hemorrhage,
and maternal discomfort. Several interventions to prevent these complications have been studied, using various agents
to assist in the detachment of the placenta and avert a manual removal. The timing of the interventions varied between
30 minutes and 45 minutes with a retained placenta.
Intraumbilical injection of misoprostol may be of benefit but data are limited.88, 115-119 Misoprostol can be injected into the
61 1171
81
vein directly using a syringe, or the Pipingas technique can be used. (See Appendix)
Note: If bleeding is heavy, the placenta needs to be removed quickly to allow the uterus to contract. Manual removal
should be done.

Management
Clinicians must keep in mind that the management of PPH requires a team approach including several
simultaneous interventions.120
Estimating Blood Loss

Be prepared with a well-established protocol since this is fundamental to safe patient care. In the case of a severe
PPH, a readily available obstetric hemorrhage equipment tray (see Appendix for contents) will facilitate the prompt
management of hemorrhage.
Estimation of blood loss can be done by weighing blood soaked material or the use of a calibrated under buttock drape in women
suspected of PPH.121
The shock index (heart rate / systolic blood pressure) has been evaluated in the non-obstetrical population as an
objective measurement of hemodynamic instability. In the non-pregnant population, the normal shock index range is
0.5 to 0.7.
A retrospective case-control study of 50 women with massive PPH and 50 women with no PPH was undertaken to
establish an obstetrical shock index (OSI) to enable earlier prediction of significant blood loss and the need for blood
transfusion.122 Mean OSI in the control group (i.e., normal delivery) at 10 minutes and 30 minutes was 0.74 (range, 0.4
to 1.1) and 0.76 (range, 0.5 to 1.1), respectively. In the case group, mean OSI at 10 minutes and 30 minutes was 0.91
(range, 0.4 to 1.5) and 0.90 (range, 0.5 to 1.4), respectively, with 64% requiring blood products. In the case group, 89%
of women with an OSI of 1.1 or more at 10 minutes required transfusion; 75% with an OSI of 1.1 or more at 30 minutes
required transfusion. The study authors recommended that the normal OSI range should be 0.7 to 0.9 for obstetrical
patients. “An OSI of more than 1 seems to be a useful adjunct in estimating blood loss in cases of massive PPH
and in predicting the need for blood and blood products.” 122
A 2015 retrospective cohort study of 233 women with PPH > 1500 mL in low-resource settings found that a shock index
< 0.9 was reassuring whereas an index ≥ 0.9 was predictive of ICU admission, need for blood transfusion, and invasive
surgical procedures.123
Assess Uterine TONE by palpating the Fundus

Uterine atony is the cause of 70% of Postpartum Hemorrhages. Clinicians should address this first. If the
uterine fundus is firm, but bleeding remains excessive, evaluate for retained TISSUE, genital tract TRAUMA, or
coagulopathy (THROMBIN). (See “If the uterus is FIRM” section below.)
If the uterus is boggy/atonic

If the placenta has NOT delivered, it must be removed manually while uterotonics are being given, IV access is
considered and the bladder emptied.

If the placenta has delivered, proceed to external uterine massage and uterotonics. Oxytocin is first-line treatment and
should be given by rapid IV infusion if access is immediately available. Otherwise, IM oxytocin should be given until
IV access can be established. Proceed immediately to bimanual massage if the uterus remains boggy and bleeding
persists. This tamponade will reduce further bleeding until assistance arrives or the uterine tone improves.
Bimanual massage/compression technique: The uterus is compressed between a hand in the vagina against the anterior
part of the cervix and a hand on the fundus.
If analgesia allows, the uterus should be explored at this stage to rule out retained TISSUE (placental fragments,
membranes, and clots), uterine inversion, or uterine rupture.
Remove clots in the upper vaginal area or lower segment of the uterus.
Emptying the bladder may help with assessment and subsequent manoeuvres in the management of PPH. It may also
assist in keeping the uterus contracted. In addition, urine output is a reliable way of monitoring the effectiveness of fluid
resuscitation in a woman with ongoing hemorrhage.
If the uterus is still boggy, proceed with further pharmacologic intervention:
• oxytocin (first line):124, 125 126127128129130
• 5 units of oxytocin by slow IV bolus over 1 minute

• oxytocin 20 to 40 units in 1 litre of normal saline, initially wide open
• 10 units oxytocin IM if cardiovascular collapse or no IV access
If the uterus is still boggy and has not been fully explored, this must be done now.
If bogginess or hemorrhage continues, consider
• Ergonovine
• Carboprost/Hemabate
• Misoprostol
• Tranexamic Acid
ADDITIONAL MEASURES TO STABILIZE THE PATIENT AND LESSEN

BLOOD LOSS with uterine atony
• Uterine balloon tamponade
• External Aortic compression
• Uterine Artery embolization
• Laparotomy for vessel ligation, placement of compression sutures, or hysterectomy
A UK study found that for every 10 000 deliveries there were 2.2 cases of PPH requiring a second-line therapy. (This
did not include those treated with an intrauterine balloon only.) Recognizing that these cases varied in both cause and
complexity, these are the success rates noted for each intervention when it was the initial second-line therapy: Uterine
compression sutures 75%, pelvic vessel ligation 36%, interventional radiology techniques 86% and recombinant Factor
VIIa 31%. 26% had a hysterectomy. 131

Uterine Balloon Tamponade (BT):

• effective method to temporarily stop bleeding
• reduces morbidity (blood loss, transfusion, embolization, hysterectomy, ICU admission)
• safe for transport
• may be used in combination with other interventions (CS + uterine compression sutures)
• more effective when used earlier, particularly in vaginal deliveries; consider early use if bleeding not
controlled after 10 minutes bimanual massage
The use of internal uterine compression has proven to be successful in the management of severe PPH. It involves
intrauterine compression of the endometrial tissue used in conjunction with oxytocin, thereby causing compression of
the uterine surface and decreasing blood flow to the uterine wall. It can be used as a definitive or temporary treatment,
thus making it an excellent tool to control bleeding for cases requiring transfer to higher level treatment centres.
Specific devices have been designed for this purpose, including the Bakri Balloon. The Sengstaken-Blakemore
esophageal catheter and condom catheters (a condom tied over the end of a straight bladder catheter) have also been
shown to be effective.132, 133
The insertion of the balloon device is a relatively simple procedure that requires the operator to ensure that the entire
balloon is positioned past the cervical canal. Once inserted, the balloon is filled with a sterile solution such as normal
saline. Depending on the device, 250ml is infused initially, then further NS more slowly until the bleeding stops, up to
500 mL. The balloon is then left in place.134 Ultrasound can be used to confirm placement. To prevent expulsion of the
balloon, the cervix can be “pinched” with 2 ring forceps on opposite sides to narrow the diameter, or vaginal packing
can be place below the balloon. After successful tamponade, a continued oxytocin infusion may be required to maintain
uterine tone. Prophylactic antibiotics should be considered. The balloon can be left in place from 8 hours to 48 hours and
then gradually deflated and removed, observing for recurrence of bleeding.135 This should be done in a centre prepared
to provide a higher level of care if needed.
Multiple retrospective studies have reported success rates of 80% to 95% using balloon tamponade to treat PPH when
bleeding has not been controlled by massage and uterotonics.136, 137 138139
Clinicians can consider attempting to remove the balloon before 24 hours has elapsed. A 2016 retrospective cohort
study140 of 274 women comparing BT for PPH for 2-12hours vs > 12 hours found no significant differences in blood loss
post-insertion, RBC transfusion, embolization, hysterectomy and ICU admission, but the > 12 hour group had higher
rates of post-partum fever (27% vs 15%) and longer hospital stay (3.7 vs 3.1 days)
Several studies have illuminated the overall success and early use of BT to control PPH after preventative and
secondary uterotonics, avoiding the need for invasive procedures (uterine artery ligation, radiological intervention, and
hysterectomy).141, 142
A retrospective study by Howard and Grobman143 correlating timing of intervention and outcomes, determined that use
of tamponade at an earlier estimated blood loss had higher nadir hemoglobin, reduction of blood transfusion, fewer
intensive care unit admissions, and fewer hysterectomies when compared with arterial embolization.
Use of BT after vaginal delivery (VD) is overall more successful compared to CS.144 A 2016 prospective study141 of 226
women with severe PPH showed BT (after preventative and second line uterotonics) to be successful 83% of the time.

It was more successful after VD than CS (89% vs 66%) and there were more failures (need for invasive procedures and
hysterectomy) in the CS group than in the VD group (50% vs 19%). Blood loss was higher in the failure group (1508ml
vs 1064ml) despite similar estimated blood loss at the time of diagnosis. Coagulopathy was higher in the failure group
(50% vs 17%). Bleeding that stopped or dramatically reduced by 15 minutes was associated with success (98 vs 16%)
External Aortic Compression 145146
In women with active hemorrhage, external aortic compression with the non-pneumatic anti-shock garment (NASG) has
been shown to reduce blood loss and associated maternal morbidity and mortality147 without compromising vascular
flow to the lower limbs.148, 149

The aorta can be compressed manually to slow bleeding while other measures are undertaken. Standing on the woman’s
left, the aorta is compressed with the right fist while using the left hand to determine that femoral artery pulsation is no
longer palpable, indicating successful compression.
Uterine Artery Embolization

Uterine artery embolization has been used as an alternative to surgery for PPH refractory to treatment.150
Success rates vary from 78% to 96 % for emergency and prophylactic embolization.151-153
Factors predictive of failure were disseminated intravascular coagulation, need for massive transfusion, hemodynamic
instability, and hemoglobin level < 95 g/dL. 152, 153
Subsequent pregnancies are possible although may involve higher risk to the mother and/or fetus.
A study by Inoue et al.151 found that following uterine artery embolization, 53% of women who desired fertility became
pregnant. Of the 40 women who became pregnant, 28 gave birth. Four deliveries were preterm, and five were associated
with a hysterectomy due to placenta accreta.
LAPAROTOMY FOR VESSEL LIGATION, COMPRESSION SUTURES AND HYSTERECTOMY

Uterine Artery Ligation (UAL) 154155156
Uterine Artery ligation, in experienced hands, can help control postpartum haemorrhage. A 2012 prospective study
showed a 96% success rate with uterine artery ligation in cases of severe PPH unresponsive to other intervention, thus
avoiding the need for hysterectomy.152 In patients with central placenta previa and a planned caesarean section, a RCT of
100 patients showed lower blood loss when the uterine arteries were ligated prior to the uterine incision.157

Uterine Compression Sutures (see Appendix for diagrams)

Various techniques have been described in which sutures placed around and through the uterus at laparotomy are
then tied to provide sustained compression of the uterus, decreasing bleeding.158-162 The techniques developed by
Christopher B-Lynch and JH Cho are included in the Appendix of this chapter. 159160161162
Numerous studies have demonstrated these techniques to be safe and efficacious for the treatment of severe, atonic
PPH. 124,143,144,152
There were few uterine synechia when the uterine cavity was evaluated 3 to 6 months later.163, 164 165
A 2014 cohort study of 252 women found that having had PPH and a B-Lynch suture was not associated with an
increased risk of future adverse pregnancy outcomes.166
A prolonged delay167 of 2 to 6 hours between delivery and uterine compression suture was associated with a 4-fold
increase in hysterectomy.
Emergency hysterectomy. Although a last resort, this must be considered before the progression of hemorrhage to the
point of cardiovascular collapse. The most common risk factors are multiparity, CS in previous or current pregnancy, and
abnormal placentation.168
If the uterus is FIRM:
• Explore the lower genital tract for TRAUMA (TEARS)
• Ensure adequate analgesia
• Ensure good lighting and exposure
• Undertake surgical repair of vaginal and cervical lacerations
• Temporise with packing
If the bleeding continues and is originating from a firm uterus:
• evaluate for an acquired coagulopathy169 (THROMBIN)
• fibrinogen levels are physiologically elevated in pregnancy. Low normal levels (under 3 g/L) in a setting of
severe postpartum haemorrhage are abnormal and replacement should be considered169, 170
If coagulation is abnormal
• correct with fresh frozen plasma (FFP), cryoprecipitate, platelets, and packed red blood cells
If the coagulation is normal
• prepare for the OR
• rule out uterine rupture or an inadequately repaired incision
• consider vessel ligation or embolization
• Consider using B-Lynch technique or Cho technique, or performing hysterectomy
• if surgical expertise is unavailable, consider tamponade, stabilization, and transport

OTHER CAUSES OF EXCESSIVE BLEEDING AT DELIVERY

Uterine Inversion
• Occurs in 1/25 000 deliveries
• Often is iatrogenic and more common in grand multiparous (parity > 5) women
• The placenta may appear at the introitus with a mass attached
• The woman may experience bradycardia and shock secondary to increased vagal tone
• Replacement of the uterus should be performed promptly without removing the placenta
• Uterine relaxation may facilitate this manoeuvre
• Replacement order is by “last out, first in” Begin by returning the normally most distal part of the uterus to
its original position, followed by the proximal wall, and lastly, the uterine fundus.
• Use exploratory laparotomy for replacement if all else fails
Uterine Rupture
• Most common in women with prior uterine surgery
• Grand multiparous women or those undergoing induction or augmentation are at risk
• Following vaginal delivery, a defect may be palpated on manual exploration
• Vigorous resuscitation and emergency laparotomy are indicated
Placenta Accreta (see also Antepartum Hemorrhage chapter)

• Placenta accreta is the abnormal implantation of the placenta with villus attachment to the myometrium
resulting in loss of the normal cleavage plane
• Occurs in 1/2500 deliveries (10-fold increase in the last 50 years due mainly to increase in CS rate and the
resulting lower uterine scar).
• 13-fold increased risk for PPH171, massive hemorrhage and peripartum hysterectomy172
• Most common in women with prior uterine surgery, especially with an anterior placenta, and increases with
increased number of CS173-175
471
• Women with placenta previa and grand multiparous women are at risk
• Commonly presents as a retained placenta
• Uterine embolization with placenta in situ has been shown to be successful in controlling PPH and avoiding
hysterectomy176, 177
• If the placenta seems adherent at the time of attempted manual removal then consider placenta accreta
• Early recognition, preferably during the antenatal period, and anticipation of this event is preferable in this
high-risk emergency situation
Women in whom placenta accreta is diagnosed antenatally have better outcomes, are less likely to need blood
transfusions, and are less likely to experience attempts to remove the placenta.178

PPH and the need for blood transfusion are less likely when the placenta is left in place to conserve the uterus or before
hysterectomy.178 Appropriate resuscitation and consultation are indicated as the risk for severe hemorrhage is extremely
high. The blood bank should be notified and blood products prepared.
Management of PPH can progress as follows as the volume of blood loss increases:
Blood loss > 500 mL to 1000 mL with normal vital signs (placenta has delivered)
1. Help (nearest members, PPH kit)
2. Bimanual external/internal uterine massage to
a. express intra-uterine blood/clots and
b. stimulate uterine contraction
3. Foley catheter
4. Additional uterotonics
5. IV access with rapid infusion crystalloid fluids (up to 2L)
6. Type and cross 2U RBC
Blood loss continues (up to 1500 mL, or > 2 utertonics) with normal vital signs
1. Help (obstetrics, anaesthesia, ER, ICU, blood lab, OR)
2. Measure vital signs and blood loss
3. O2
4. Second IV access for IV crystalloids
5. Intrauterine balloon catheter
6. Uterotonics + TXA
7. STAT lab (CBC, coagulation factors, fibrinogen)
8. Get 2U RBC, thaw 2U FFP
9. Prepare OR transfer
Blood loss continues (>1500ml OR > 2U RBC OR at risk for bleeding / coagulopathy) OR any patient with hemodynamic
instability
1. Help (obstetrics, anaesthesia, ER, ICU, blood lab, OR)
2. Move to OR for possible hysterectomy
3. Massive transfusion protocol
Don’t forget your ABCs
• Talk to and observe the woman
• Monitor vital signs
• Remember that compensatory responses to blood loss in these women are excellent and may give caregivers
a false sense of security
• Commence at least one large bore IV (preferably 16 gauge or larger)
• Run a crystalloid solution drip wide open (e.g., saline is preferred to Ringer’s lactate)
• Obtain a CBC, cross match, and consider coagulation studies (PT, PTT, LFTs, fibrinogen, calcium, lactate)

Get help
• Consider the need for additional personnel to manage the resuscitation
• Notify the laboratory of the potential need for massive transfusion support
BLEEDING AND ANTICOAGULANTS

Low Molecular Weight Heparin
Low molecular weight heparin (LMWH) is the drug of choice for prevention of thromboembolic disorders, but its impact
on the incidence of PPH is unclear. In a systematic review which included 1320 women receiving prophylactic LMWH,
the RR of PPH was 1.45, just reaching statistical significance, but with a difference in blood loss of just 33ml and no
difference in transfusion.179 Roshani et al.180 performed a retrospective cohort study of 95 women (524 controls) who
received therapeutic doses of LMWH, and who had been advised to stop it at the onset of contractions, rupture of
membranes, or the day before planned induction or CS. The incidence of PPH was not significantly increased, with a rate
of 18% in users and 22% in non-users. There was no increase in PPH or severe PPH, and the median blood loss in normal
vaginal deliveries was actually lower in LMWH users (200 mL) than in non-users (300 mL). These authors note that the
difference may have been due to differing strategies to prevent bleeding.
Summary
1. Active management of the third stage of labour reduces the incidence and severity of PPH.
2. Postpartum hemorrhage is an emergency that requires a clear understanding of the pathophysiology
responsible.
3. A clear management plan that ensures adequate volume replacement and secures hemostasis must be in
place.
4. The importance of the assessment and management of the woman’s Circulation, Airway, Breathing (CABs)
cannot be overstated.
5. The woman should be resuscitated and additional help summoned.
6. Uterine atony is the causes 70% of PPH.

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1985;66:89-92.
174. Miller DA, Chollet JA, Goodwin TM. Clinical risk factors for placenta previa-placenta accreta. Am J Obstet Gynecol.
1997;177:210-4.
175. Gilliam M, Rosenberg D, Davis F. The likelihood of placenta previa with greater number of cesarean deliveries and
higher parity. Obstet Gynecol. 2002;99:976-80.
176. Jung HN, Shin SW, Choi SJ, Cho SK, Park KB, Park HS, et al. Uterine artery embolization for emergent management
of postpartum hemorrhage associated with placenta accreta. Acta Radiol. 2011;52:638-42.
177. Li X, Wang Z, Chen J, Shi H, Zhang X, Pan J, et al. Uterine artery embolization for the management of secondary
postpartum haemorrhage associated with placenta accreta. Clin Radiol. 2012;67:e71-e6.
178. Fitzpatrick KE, Sellers S, Spark P, Kurinczuk JJ, Brocklehurst P, Knight M. The management and outcomes of
placenta accreta, increta, and percreta in the UK: a population-based descriptive study. BJOG. 2014;121:62-70.
Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3906842.
179. Sirico A, Saccone G, Maruotti GM, Grandone E, Sarno L, Berghella V, et al. Low molecular weight heparin use during
pregnancy and risk of postpartum hemorrhage: a systematic review and meta-analysis. J Matern Fetal Neonatal
Med. 2019;32:1893-900.
180. Roshani S, Cohn DM, Stehouwer AC, Wolf H, van der Post JA, Buller HR, et al. Incidence of postpartum
haemorrhage in women receiving therapeutic doses of low-molecular-weight heparin: results of a retrospective
cohort study. BMJ Open. 2011;1:e000257. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/
PMC3221289.
181. Butwick AJ, Goodnough LT. Transfusion and coagulation management in major obstetric hemorrhage. Curr Opin
Anaesthesiol. 2015;28:275-84. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25812005.

25
Appendix A
Management of Postpartum
Management of Postpartum Hemorrhage
Hemorrhage
PPH
Yes
Placenta out Placenta in Active bleeding Manual removal
No
Assess maternal ABC’s Consider draining placental cord blood

Maternal resuscitation or
Umbilical vein injection
(oxytocin / prostaglandin)
Massage uterus Bleeding stopped* Removal under anaesthesia
Oxytocin 20 U/L
Empty bladder
16G / 18G IV access
IV infusion ccrystalloids
Cross match 2 units, CBC, coags, fibrinogen
Get 2U RBC + thaw 2 units FFP
Bimanual compression Bleeding stopped*

(nitronox, fentanyl for pain)
Uterus still atonic Inspect for and repair

Vaginal / cervical trauma
Consider /treat
coagulopathy
Second line uterotonics :
- Carboprost tromethamine 0.25 mg IM/IMM q15 min Bleeding stopped*
- Ergonovine 0.2–0.25 mg IM/IV
- Misoprostol 400 µg SL Bleeding persists
- (800–1000 µg PR if unable to give meds PO/SL)
-TXA (1g IV over 10 minutes)
Yes
Remove retained products Explore uterus for retained products
No
Tamponade, embolization, or surgery

* Continue IV oxytocin infusion
Postpartum
Postpartum Hemorrhage
Hemorrhage 378
368
Appendix B
Contents of Obstetric Hemorrhage Equipment Tray

Access/exposure
• 3 vaginal retractors
• 2 ring forceps
Eye needles
• Straight, 10cm
• Curved 70-80mm, blunt point
Sutures
• No.1 vicryl
• 0 and 2 chromic catgut with curved needle
• ethiguard curved, blunt point monocryl
Uterine/vaginal tamponade
• Vaginal packs
• Kerlix gauze roll
• Uterine balloon (Sengstaken-Blakemore, Rusch urological balloon, Bakri balloon, surgical glove and
catheter)
Diagrams
• Uterine artery and ovarian artery ligation
• Uterine compression techniques; B-Lynch and Cho

Appendix C
MASSIVE TRANSFUSION PROTOCOL

Many institutions will have their own massive transfusion protocols. Once example is:
Stanford University School of Medicine181
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4567035/pdf/nihms691755.pdf

Appendix D
Injection of the Umbilical Vein for Retained Placenta:

Pipingas Technique
1. Explain the procedure and obtain consent.
2. Prepare a syringe with the medication in 30 mL normal saline. Crush and dissolve 4 × 200 mcg tablets misoprostol in 30 mL normal saline
(forms milky solution).
3. Identify the umbilical vein. Recut the cord if necessary.
4. Insert a size 10 nasogastric tube into the umbilical vein. If resistance is felt, retract the catheter by 1 to 2 cm, and then advance further, if
possible.
5. The tube has reached the placenta when the majority of the catheter is inserted and resistance is felt. (The lengths of the umbilical cords
varied between 30 and 47 cm in the Rogers’ study.88)
6. Retract by 3 to 4 cm to ensure that the tip is in the umbilical vein and not in a placental branch.
7. Attach the syringe, and inject the solution, and then clamp off the cord with the catheter.
8. Note the time of the injection.
9. Wait 10 to 30 minutes for the placenta to deliver.

Appendix E 25th Edition of the ALARM Course Manual
Uterine Compression Sutures

Uterine Compression Sutures
B-Lynch Technique
B-Lynch technique
Reproduced
Reproduced from B-Lynch et al. Br J Obstet Gynaecol from B-Lynch
1997;104(3):372-5,158 et al. Br J Obstet Gynaecol 1997;104(3):372-5, 166
with the permission of the Royal College of Obstetricians and Gynaecologists.
with the permission of the Royal College of Obstetricians and Gynaecologists.

Cho Technique
Cho Technique
Reproduced
Reproduced from Cho et al. Obstet Gynecol from Cho et al.Used
2000;96(1):129-31.159 Obstet
with Gynecol
permission.2000;96(1):129-31.
167
Used with permission

Table of Contents
Chapter 16 Hypertensive Disorders of Pregnancy............................................................................................................ 375

Introduction.............................................................................................................................................................. 375
Definitions and Terminology......................................................................................................................... 375
Incidence....................................................................................................................................................... 376
Pathogenesis............................................................................................................................................................ 377
Morbidity and mortality............................................................................................................................................ 378
Morbidity and Mortality with Preeclampsia ................................................................................................. 380
Morbidity and Mortality With Chronic Hypertension.................................................................................... 380
Diagnosis and Evaluation......................................................................................................................................... 380
Clinical Evaluation......................................................................................................................................... 380
Investigations................................................................................................................................................ 382
Risk Factors and Risk Reduction ............................................................................................................................... 385
Predicting Onset of Preeclampsia................................................................................................................. 385
Predicting Maternal and Perinatal Morbidity and Mortality with Established
Gestational Hypertension and Preeclampsia .......................................................................................... 386
Risk Reduction.............................................................................................................................................. 386
Management............................................................................................................................................................ 387
Antihypertensive Therapy.............................................................................................................................. 388
Fluid Management....................................................................................................................................... 390
Symptomatic Support................................................................................................................................... 391
Seizure Prophylaxis....................................................................................................................................... 392
Management of HELLP Syndrome ............................................................................................................... 394
Transport....................................................................................................................................................... 394
Delivery......................................................................................................................................................... 394
Timing of Delivery......................................................................................................................................... 395
Postpartum Management............................................................................................................................. 395
Future Cardiovascular Risk............................................................................................................................ 396
Points to Remember in Management........................................................................................................... 397
Summary.................................................................................................................................................................. 397

Chapter 16
Hypertensive Disorders of Pregnancy
Introduction
Hypertensive disorders are a leading cause of direct maternal death. Women who have had preeclampsia and
gestational hypertension have an increased likelihood of future cardiovascular disease, diabetes mellitus, metabolic
syndrome, and related mortality.1-7 Preeclampsia is a cause of acute renal failure and increases the risk of chronic
23
4 56
kidney disease.8, 9 Women with severe preeclampsia have poorer health-related quality of life, often related to perinatal
death or the admission of their infant to the NICU.10 Women who develop preeclampsia before 37 weeks’ gestation
are at a significant risk in subsequent pregnancies of stillbirth, placental abruption, spontaneous preterm rupture
of membranes, and small for gestational age (SGA) babies, even in the absence of preeclampsia in the subsequent
pregnancy.11 Chronic hypertension is associated with increased risk of congenital malformations in the newborn,
independent of antihypertensive use.12, 13 Evidence suggests that risk of depressive symptoms in adulthood is
increased in offspring of women who developed preeclampsia.14 These offspring may also have increased risk for
impaired cognitive functions in childhood and adulthood.15 They are more likely to be hypertensive by age 21,16 and to
demonstrate an abnormal lipid profile in early adulthood.17
While the incidence of eclampsia has dropped in Canada from 15 per 10 000 deliveries in 2004–2005 to 5 per 10 000
deliveries in 2014-2015,18 the complications resulting from and associated with eclampsia remain significant. Eclampsia
19
is strongly associated with maternal death, need for assisted ventilation, adult respiratory distress syndrome (RDS), acute
renal failure, embolism and neonatal death, neonatal RDS and SGA infants.20
All obstetrical care givers will eventually manage a woman with hypertension in pregnancy or with the complications arising
from this condition. The management options for hypertensive disorders of pregnancy will vary according to resources.
Geography, weather, and access to specialists or Level III hospitals may create conditions in which primary caregivers must
respond to emergency situations such as stabilizing or treating women with hypertensive disorders of pregnancy.
Definitions and Terminology
Classification of the Hypertensive Disorders of Pregnancy21:

1. Chronic hypertension
2. Gestational hypertension
3. Preeclampsia—de novo (in a previously normotensive woman) or superimposed on chronic hypertension
4. White coat hypertension
Hypertensive Disorders of Pregnancy 375

DEFINITIONS
Hypertension sBP ≥ 140 or dBP ≥ 90 mmHg
(see “Diagnosis” section for measurement technique)
Severe hypertension sBP ≥ 160 or dBP ≥ 110 mmHg
Chronic hypertension Predates pregnancy or appears before 20 weeks’ gestation
Gestational hypertension New onset hypertension after 20 weeks’ gestation, with no other
maternal organ dysfunction
Preeclampsia Gestational or chronic hypertension with one or more of the following

new onset conditions:
Early onset = <340 wk; Late onset = ≥340 wk 1. proteinuria
2. other maternal organ dysfunction (renal, liver, neurologic,
hematologic)
3. uteroplacental dysfunction (fetal growth restriction)
White coat hypertension sBP ≥ 140 or dBP ≥ 90mmHg in office/clinic, but lower with home or
ambulatory BP monitoring
Eclampsia The occurrence of seizures in a preeclamptic patient that cannot be

attributed to other causes22
Incidence19, 23-25 22 24
It is estimated that the global incidence of preeclampsia ranges from 1% to 5.6%, while the incidence of eclampsia
ranges from 0.1% to 2.9%. The highest rates are in Africa.26
In Canada, the incidence of chronic hypertension in pregnancy, gestational hypertension and preeclampsia has
remained relatively stable from 2004–2005 to 2010–2011. In the same time period, the incidence of eclampsia dropped
from 1.5 to 0.8 per 1000 deliveries19, 24, and dropped further in 2014-2015 to 0.5 per 1000 deliveries18.
CONDITION INCIDENCE IN PREGNANCY, % RISK OF DEVELOPING PREECLAMPSIA, %
Preeclampsia 1
Chronic hypertension 127 21
Gestational hypertension 5 2527
Gestational hypertension before 34 weeks’ 3528, 29

gestation
Eclampsia 0.05

Pathogenesis
Pathogenesis
The exact etiology of preeclampsia is unknown. A prevalent theory describes a 2-stage process in which Stage 1 is
inadequate placental
The exact etiology perfusion, andis Stage
of preeclampsia 2 is the
unknown. maternaltheory
A prevalent syndrome resulting
describes from the
a 2-stage materials
process generated
in which Stage 1by
is this
insult.29
inadequate placental perfusion, and Stage 2 is the maternal syndrome resulting from the materials generated by this
insult.30
Figure 1. Possible Etiology of Preecampsia
Figure 1. Possible etiology of preeclampsia
Abnormal placentation or
excessive fetal demands
Mismatch between uteroplacental

supply and fetal demands
Maternal endothelial
cell dysfunction
Maternal and fetal manifestations

of preeclampsia
Debate exists as to whether the underlying mechanism of preeclampsia is failure of the maternal cardiovascular system
Debate
to adaptexists as to whether
to pregnancy the underlying
with required mechanism
remodelling of preeclampsia
of arteries, reduction inisarterial
failure stiffness
of the maternal cardiovascular
and enhanced system
endothelial
to adapt to pregnancy
function.31-33
23
This theorywith required
further remodelling
suggests that the of arteries,
nature reduction
of the in arterial
hemodynamic stiffness anddiffers
abnormalities enhanced endothelial
between early onset
function.30-32
preeclampsia (decreased cardiac output and increased systemic vascular resistance) and late onset (increased cardiac
output and relative reduced vascular resistance); these differences would guide the selection of antihypertensive
Preeclampsia34is likely not a single condition, but rather a condition with several subtypes. This would account for the
medications.
varying clinical presentation and lack of highly useful predictive tests or preventive interventions.29
Preeclampsia is likely not a single condition, but rather a condition with several subtypes. This would account for the
varying clinical presentation and lack of highly useful predictive tests or preventive interventions.30

Morbidity and mortality

According to the Canadian Perinatal Surveillance System, the overall maternal mortality rate in Canada was 7.4 per 100
000 deliveries in 2015. It has fluctuated between 5.1 and 11.9 since 1999. Hypertensive disorders of pregnancy are the
second most common cause of direct maternal mortality.18 Eclampsia is associated with need for assisted ventilation,
adult RDS, acute renal failure, and embolism.20
Table 1. Diagnosis Associated With Maternal Deaths
DIAGNOSIS NUMBER OF MATERNAL DEATHS MATERNAL DEATHS PER 100 000 HOS
PITAL DELIVERIES (95% CI)
Diseases of the circulatory system 89 2.5 (2.0-3.1)
Other indirect causes 78 2.2 (1.7-2.7)
Postpartum hemorrhage 49 1.4 (1.0-1.8)
Hypertension complicating pregnancy, childbirth and

42 1.2 (0.8-1.6)
the puerperium
Obstetric embolism 39 1.1 (0.8-1.5)
Major puerperal infection 27 0.8 (0.5-1.1)
Ectopic and molar pregnancy /abortive outcome 26 0.7 (0.5-1.1)
Antepartum hemorrhage, placental abruption, and

21 0.6 (0.3–0.9
placenta previa
Source: Canadian Institute of Health Information (CIHI), Discharge Abstract Database.18 Used with permission.
* Quebec does not contribute to the Discharge Abstract Database. Manitoba data, which were incomplete for earlier years, were included from 2004/2005. CI – Confidence interval

PERINATAL HEALTH INDICATORS FOR CANADA 201715
FIGURE 4.3
RATES OF MOST COMMON SEVERE MATERNAL MORBIDITIES, CANADA (EXCLUDING QUEBEC),
Figure 2. Rate of the most common severe maternal morbidities in Canada
2010/2011 TO 2014/2015
900
800 786.6
Severe maternal morbidity (95% CI) per 100,000 hospital deliveries
700

1 Blood transfusion

2 Blood transfusion with comorbidity
600 565.3

3 Postpartum hemorrhage and blood transfusion

4 Cardiac arrest/failure, myocardial infarction or
pulmonary edema including ICD-10 O75.4
483.9 (other complications of obstetric surgery
500
and procedures)

5 Embolization or ligation of pelvic vessels or
suturing of uterus and postpartum hemorrhage
400
Hysterectomy
6
7 Uterine rupture during labour
300 8 Puerperal sepsis
9 Repair of bladder, urethra, or intestine
Eclampsia
10
200

11 Postpartum hemorrhage and hysterectomy
140.1 147.8
125.0
12 Placenta previa with hemorrhage and
blood transfusion
100 82.9
72.0 68.8
50.7 51.5 46.3
13 Cardiac arrest/failure, myocardial infarction
39.5 or pulmonary edema excluding ICD-10 O75.4
(other complications of obstetric surgery
0 and procedures)

1
2
3
4
5
6
7
8
9
10
11
12
13
Source: Canadian Institute for Health Information-Discharge Abstract Database (CIHI-DAD).

Data for Quebec were excluded because they do not contribute to CIHI-DAD.
CI = confidence interval
Perinatal health indicators for Canada 2017: a report from the Canadian Perinatal Surveillance System.
Ottawa: Public Health Agency of Canada; 2017.18 Used with permission.
LIMITATIONS REFERENCES
The severity of some maternal conditions could not 1. Joseph KS, Liu S, Rouleau J, Kirby RS, Kramer MS,
be distinguished due to limitations of ICD-10 codes. Sauve R, et al. Severe maternal morbidity in Canada,
2003 to 2007: surveillance using routine
Please refer to Appendix B for general data
hospitalization data and ICD-10CA codes. J Obstet
limitations using CIHI-DAD.
Gynaecol Can 2010;32(9):837–846.
2. Liu S, Joseph KS, Bartholomew S, Fahey J, Lee L,

Allen AC, et al. Temporal trends and regional
variations in severe maternal morbidity in Canada,
2003 to 2007. J Obstet Gynaecol Can
2010;32(9):847–855.

Morbidity and Mortality with Preeclampsia 36 35
All caregivers must be able to promptly recognize the signs, symptoms, and laboratory findings of preeclampsia.
Preeclampsia has potential for multi-organ involvement and carries risks for fetal, perinatal, and maternal morbidity and
mortality.
MATERNAL FETAL
Stroke (risk is with sBP ≥ 160 mm Hg) Oligohydramnios
Pulmonary edema Intrauterine growth restriction
Hepatic failure NICU admission
Jaundice Prematurity due to maternal indication for delivery
Seizure (eclampsia) Fetal death (3-fold increase)37
Placental abruption
Acute renal failure
Maternal death
Morbidity and Mortality With Chronic Hypertension

Patients with chronic hypertension will develop superimposed preeclampsia in 21% of cases.27 Those who do NOT
develop preeclampsia are still at increased risk of requiring Caesarean section (rate 41%), perinatal mortality (4 per
1000), and having an SGA baby (< 2500 gm; 17%).38 Neonates are at increased risk of NICU admission (20%), and of
congenital anomalies, particularly cardiac, independent of use of antihypertensive medications.36, 37
Preconception counselling is valuable for optimizing BP control with medications that are safe to use during pregnancy,
and for initiating administration of ASA for risk reduction (see “Management” and “Risk Reduction” sections, below).
Diagnosis and Evaluation

Clinical Evaluation
When blood pressure is measured, ensure that:
• The patient has a minimum rest period of 10 minutes after arrival.
• The patient is in a sitting position with her upper arm at heart level.
• The appropriate size cuff is used (a cuff too small overestimates the BP; a cuff too large underestimates BP).
The length of the cuff should be 1.5 times the arm circumference.
• A blood pressure cuff is never placed over clothing.

• A mercury or aneroid sphygmomanometer is used; automated machines may underestimate systolic and
diastolic BP by 10 to 5 mm Hg, especially in hypertensive patients. If an automated BP monitor is used, it
should be calibrated against a mercury or aneroid sphygmomanometer.39-41 An RCT on follow-up using an
04
automated BP machine (Omron) versus a Hg sphygmomanometer, demonstrated that, once the diagnosis
of hypertension had been made, there were no differences in the outcomes of severe hypertension, nor in
incidence of small for gestational age at delivery, in women who suffer hypertension in pregnancy.42 A blood
pressure device which has been validated specifically for use in pregnancy and preeclampsia is the CRADLE
Vital Signs Alert device.43
44
• Korotkoff sound V (disappearance of pulse sounds) is used to define the diastolic pressure.45
• If the BP is consistently higher in one arm, the arm with the higher values is used for all BP measurements.
Ambulatory blood pressure monitoring using an automated blood pressure machine is useful in ruling out “white coat”
hypertension.4647
Blood pressure criteria for a diagnosis of hypertension in pregnancy36

• A systolic BP of ≥ 140 mmHg or a diastolic BP of ≥ 90 mm Hg based on at least 2 measurements taken in
the same arm ≥ 15 minutes apart after an initial rest period of > 10 minutes.
• Severe hypertension should be defined as a sBP≥ 160 mm Hg or a dBP ≥ 110 mm Hg. A sBP over
160mmHg is associated with increased risk of maternal stroke.47
The following are not criteria for a diagnosis of hypertension in pregnancy
• An incremental and/or relative rise ≥ 30/15 mm Hg in systole or diastole is within the normal variation in BP
seen throughout pregnancy, and is NOT a criterion for a diagnosis of hypertension
• Mean arterial pressure is NOT used as a criterion to define hypertension in pregnancy because it is
cumbersome to calculate.
There is a variation in dBP and sBP by gestational age. Typically, in nulliparous women, dBP drops to a nadir at 19 weeks
while the sBP drops to a nadir at 17 weeks. In parous women, the nadir occurs at 20 weeks for diastole, and at 18 weeks
for systole. In a large prospective study, women with high BMI had BP readings that were 4 mmHg higher than those
with normal BMI.48
Following confirmation of hypertension, assess for symptoms and signs suggesting involvement of other
maternal organ systems (Table 2).

Table 2. Signs and symptoms that suggest involvement of other maternal organ systems
CENTRAL NERVOUS SYSTEM • Presence of a severe headache

• Visual disturbance (e.g., blurring, scotomata)
• Tremulousness, irritability, somnolence
• Hyperreflexia
CARDIORESPIRATORY • Chest pain

• Dyspnea: check maternal 02 saturation
• Distended neck veins
HEMATOLOGIC • Bleeding
• Petechiae
HEPATIC • Right upper quadrant/epigastric pain

• Severe nausea and vomiting
RENAL • Reduced urine output (oliguria) < 15 mL/hr, is non-specific, has many causes, and is not
diagnostic
• Edema (including facial and dependent) and weight gain are NOT diagnostic criteria for
preeclampsia
• Proteinuria indicates glomerular dysfunction (See “Evaluation of Proteinuria” below)
In a woman with preeclampsia, the following symptoms predict eclampsia: right upper quadrant pain, headache, visual
disturbances, and vomiting. Epigastric pain predicts HELLP syndrome.49 In patients with established preeclampsia,
epigastric pain and chest pain have been shown to be moderate predictors of adverse maternal and perinatal
outcomes.50
Investigations
All women with new onset hypertension after 20 weeks’ gestation should have, as a minimum, the following
investigations:
• Platelet count
• AST (Aspartate Transaminase)
• Urinalysis, urine dipstick, or spot urine protein: creatinine ratio to screen for proteinuria
• Ultrasound assessment of fetal growth and amniotic fluid volume, plus umbilical artery Doppler studies if
those are abnormal
If a patient develops thrombocytopenia (<150 x 109/L) or dropping hemoglobin, testing for DIC and hemolysis is
indicated.
Evaluation of Proteinuria
• Urine protein excretion of ≥ 300 mg/day (0.3g/day) on a 24-hour urine collection is the gold standard for a
diagnosis of proteinuria.

• Proteinuria of ≥ 2+ on dipstick is highly suggestive of proteinuria in excess of 300 mg/24 hours and reliably
establishes presence of proteinuria.36 Proteinuria of 1+ on dipstick should be confirmed by a 24-hour urine
collection because of significant false positive and false negative results.51, 52
• A urinary protein to creatinine ratio (UPCR) at a level ≥ 30 mg/mmol urinary creatinine in a spot (random)
urine sample is suggestive of proteinuria. A UPCR level of < 30 mg/mmol rules out proteinuria.
−− measurement of the UPCR offers a less cumbersome alternative to a 24-hour urine collection.
−− samples that are not first void samples were found to have a sensitivity of 90%, specificity of 100%, a
negative LR of 0.1 with an AUC of 1.0.53
NOTE
While the presence of proteinuria has a direct impact on maternal and perinatal outcomes, the degree of
proteinuria (high versus low) has no impact on worsening maternal nor perinatal outcomes.54 Therefore, once
proteinuria >300mg/24 hours has been documented, there is no need to repeat this measurement.
Routine urinalysis should not be used to screen for protein at all prenatal visits in asymptomatic, normotensive, low-risk
women, as there is no evidence that it provides earlier detection of preeclampsia or improves outcome when compared
to blood pressure measurement alone.55, 56
NOTE
Early onset (< 34 weeks) preeclampsia or severe hypertension warrants consideration of further
investigations looking for underlying conditions or alternate diagnoses
(e.g., antiphospholipid antibody syndrome).57
Appendix A provides the differential diagnoses associated with laboratory abnormalities encountered in women with
preeclampsia (Magee et al.36).
Ongoing Evaluation
Some women who develop a hypertensive disorder of pregnancy will require immediate delivery, particularly those with
preeclampsia demonstrating severe features:
• Inability to control maternal blood pressure
• Worsening maternal organ dysfunction (hepatic, renal, neurologic symptoms, HELLP*) (*Hemolysis, Elevated
Liver Enzymes, Low Platelets)
• Fetal indication for delivery
or, those who are close to term. (See “Timing of Delivery” section)
Others, remote from term, might be observed, with ongoing consultation, recognizing that deterioration can occur
quickly. Table 3 provides a guideline for minimum frequency of reassessment.58 Care must be individualized and the

plan of care reassessed at each visit. Women diagnosed with preeclampsia may require hospitalization at the time of
diagnosis.
Table 3. Minimum Frequency of Reassessment
PREECLAMPSIA GESTATIONAL HYPERTENSION CHRONIC HYPERTENSION
Blood pressure Twice daily Minimum 2x/week, or home BP Each visit

monitoring
Proteinuria screen* daily until >300mg/24h, then D/C 1x/week Each visit
CBC, liver enzymes 2x/week, or more frequent if If sharp iBP or proteinuria If sharp iBP or proteinuria
unstable develops develops
NST, amniotic fluid NST daily 1x/week Each visit in 3rd trimester
volume
AFV 2x/week
ultrasound growth/AFV Weekly; more frequent if abnormal Every 2-4 weeks; more frequent if Start of 3rd trimester; repeat if AFV
+/-Doppler abnormal or SF height low
*urine dipstick, urinalysis or UPCR; begin 24h urine collection if ≥ 2+
Inform women with preeclampsia that they should report any decrease in fetal movement, or any new headache, vision
change, right upper quadrant or epigastric pain, or shortness of breath.

Risk Factors and Risk Reduction

Predicting Onset of Preeclampsia
Maternal characteristics and maternal history will identify 30% of women who develop preeclampsia.59, 60 Risk markers of 61
greater importance are highlighted in grey in Table 4. Those in bold within the shaded areas confer the highest risk62
Table 4. Risk markers for preeclampsia
First trimester markers Second or third

trimester markers
Demographics Past history Current pregnancy
• Previous preeclampsia63 • Multiple pregnancy

• Anti-phospholipid
antibodies57, 64
• Pre-existing medical
condition(s)
−− hypertension or first visit
dBP ≥ 90 mm Hg
−− renal disease or first visit
proteinuria65
−− diabetes mellitus
−− Collagen vascular disease
−− Periodontitis66
Maternal age • Obesity (BMI ≥ 35 kg/m2)67 • First ongoing pregnancy

• Family history of preeclampsia • Inter-pregnancy interval ≥
>40 yrs or <18 yrs (mother or sister)68 10 yrs
• First visit sBP ≥ 130 mm Hg
or dBP ≥ 80 mm Hg
• Ethnicity: Nordic, Black, • Non-smoking69 • Inter-pregnancy interval < • Systolic BP > 120 mm Hg
South Asian, or Pacific Island • Increased pre-pregnancy 2 yrs
triglycerides • Reproductive technologies to
conceive (subfertility)
• Lower socioeconomic status • Family history of early-onset • New partner (first pregnancy • Abnormal prenatal genetic
cardiovascular disease or short duration of screen (IPS, FTS or MSS)
• Cocaine and/or exposure) analytes
methamphetamine use • Gestational trophoblastic • Abnormal uterine artery
disease Doppler velocimetry
• Infection during pregnancy • Excessive weight gain in
(e.g., UTI, periodontal pregnancy
disease) • Cardiac output > 7.4 L/min
• Elevated uric acid

Numerous studies continue to examine the usefulness of trophoblast and angiogenic markers, as well as uterine artery
Doppler studies in first or second trimester, to predict the onset of preeclampsia.70 However, these are not currently
recommended as part of regular clinical practice.21, 30, 71
Abnormal levels of some of these markers, such as low PAPP-A (pregnancy associated placental protein A), low PlGF
(placental growth factor) or high total HCG (human chorionic gonadotropin) may be reported as part of an otherwise
normal prenatal genetic screening test. Women with such results, particularly with multiple abnormal biomarkers,
warrant increased surveillance for hypertensive disorders in pregnancy.72
Placental growth factor (PlGF) should not be ordered as an early screening test for preeclampsia.73
Predicting Maternal and Perinatal Morbidity and Mortality with

Established Gestational Hypertension and Preeclampsia
Earlier gestational age, chest pain or dyspnea, low PaO2, low platelets, elevated creatinine, and elevated AST have been
shown to have an excellent predictive value of adverse maternal outcomes occurring within 48 hours and up to 7
days (AUC ROC 0.88).74 In one multicentre study, an oxygen saturation (SpO2) of less than 93% was found to be highly
predictive of poor maternal and neonatal outcome within 48 hours.75 The PIERS (Preeclampsia Integrated Estimate
of Risk) study group created a calculator where the above values can be entered for a given patient (available at:
https://pre-empt.cfri.ca/monitoring/fullpiers), including those with early onset preeclampsia.76
The degree of proteinuria has not been found to be an independent predictor of adverse maternal or perinatal
outcomes.54
Elevated levels of uric acid are not meaningfully associated with adverse maternal or perinatal outcome, so should not
determine timing of delivery.21, 77
Risk Reduction
Calcium Supplementation
Calcium supplementation (≥ 1 g/day) or an increase in dietary calcium intake (3 to 4 dairy servings per day) has been
shown to decrease the rate of preeclampsia only in low- and middle-income country populations with a low dietary
intake of calcium (< 600 mg/day).78-80 A large multicentre study in the United States showed no benefit of calcium
97
supplementation in reducing the rate of preeclampsia.30
Low Dose ASA

Low dose ASA decreases the risk of preeclampsia in high risk populations, particularly those with chronic hypertension,
diabetes mellitus or previous preterm preeclampsia. It should be STARTED after diagnosis of pregnancy, and BEFORE 16
WEEKS whenever possible, to obtain the greatest benefit. 82, 83 It is continued until term. It is taken once daily at bedtime.
81

The OPTIMAL DOSE of ASA has been the subject of much research. 162mg per day appears to decrease the risk of
preterm preeclampsia more than the commonly-used 81mg in those who start it before 16 weeks gestation:
• Meta analyses of studies using 50-150mg daily had shown an overall 10-17% decrease in
preeclampsia,82, 84, 85 with a dosage of <75mg per day providing no significant benefit.83
• 81 mg/day changes platelet function in just 71% of pregnant women, while a dosage of 162mg/day alters
platelet function in 97%.86
• On this basis, the 2017 ASPRE trial used 150mg daily, randomizing high risk women at 11-14 weeks
gestation. In the treated group, the Odds Ratio for delivery with preeclampsia at <37 weeks gestation was
0.38.87
WHO should be offered low dose ASA, based on risk factors that can be identified before 16 weeks gestation, is also an
area of much research. The following table is one example of a tool which can be used: Women with 1 or more Major
Risk Factor, as well as those who have 2 or more Moderate Risk Factors, have a preeclampsia risk of about 3.5%, or a
Relative Risk of about 5, compared to those with no risk factors. Evidence is limited as to which women within these
groups would benefit and to what degree.
MAJOR RISK FACTOR MODERATE RISK FACTOR
Antiphospholipid Antibody syndrome Prior Placental Abruption
Chronic Hypertension Multifetal pregnancy
Prior Preeclampsia Chronic Kidney disease
Pregestational Diabetes Prior Stillbirth
Pre-Pregnancy BMI > 30kg/m2 Maternal age > 40 years
Assisted Reproductive Technology Nulliparity
Systemic Lupus Erythematosus
(Adapted from Bartsch et al62 and Viguiliouk et al88)
In a low risk population, primary prevention of preeclampsia with ASA remains unproven at the present time. It is
currently a topic of research.
There is no evidence of adverse effects of low dose ASA on either the mother or newborn.89, 90
Management
In general, management includes evaluation of the mother and fetus; prevention of severe maternal complications
(organ damage, seizure, cerebral vascular accidents, deep vein thrombosis, and death) and severe fetal complications
(placental abruption, growth restriction, and stillbirth); symptomatic support; and delivery.

Antihypertensive Therapy
Antihypertensive medication reduces the mother’s risk of developing severe hypertension and its potential sequelae
(cerebrovascular accident). It does not necessarily reduce the risk of seizures (eclampsia) or prevent adverse fetal outcomes such
as IUGR. While the acute management of a hypertensive crisis to prevent a maternal cerebrovascular accident is critical, too rapid
a drop in maternal BP may cause a reduction in utero-placental perfusion resulting in fetal compromise. Antihypertensive therapy
should aim to reduce the systolic BP to < 160 mm Hg and the diastolic BP to < 110 mm Hg over a few hours.21
There is insufficient evidence to determine the ideal BP associated with optimal maternal and perinatal outcomes. A reasonable
goal is sBP 130-155mmHg and dBP 80-105mmHg.36
In the presence of some comorbidities, such as pre-existing renal disease, there may be indications for lower target blood pressures
The medications available can be divided into those used for acute (severe hypertension) and those for maintenance therapy.
Acute therapy (severe hypertension)

An obstetric consultation should be obtained to guide therapy when severe hypertension is diagnosed.
Management includes immediate, intensive medical treatment with intravenous access and maternal/fetal
monitoring. It is recommended that all perinatal units have a management protocol for the treatment of severe
hypertension.
Intravenous labetalol, intravenous hydralazine, and oral nifedipine are commonly used to treat acute, severe
hypertension (Table 5). The pharmacokinetics of intravenous labetalol and intravenous hydralazine are very similar. The
first choice is either oral nifedipine or IV labetalol because hydralazine has been associated with more adverse outcomes
including maternal hypotension, placental abruption, abnormal fetal heart rate patterns, maternal oliguria, and need for
Caesarean section.91
Table 5. Treatment for acute hypertension
AGENT DOSE ROUTE ONSET PEAK CAUTION
Labetalol Initial dose 20mg; IV 5 minutes 30 minutes Contraindicated in women with

repeat 20–80 mg every asthma or heart failure; May cause
30 minutes; maximum neonatal bradycardia
300mg
Nifedipine Initial dose 10 mg; Swallowed 30 minutes 45 minutes Immediate release preparation is
repeat 10–20 mg every (not chewed) used here. (PA no longer available in
45 minutes; Canada, and XL not for acute therapy.)
maximum 50 mg
Hydralazine Initial dose 5mg; repeat IV 5 minutes 30 minutes May increase the risk of maternal
5–10mg every 30 hypotension
minutes; maximum 20
mg
References36, 47, 58, 92

When the Maximum dose listed above has been given, consider addition of a second antihypertensive medication. For
refractory cases, IV infusion of labetalol and/or hydralazine may be considered.
NOTE
Nifedipine and magnesium sulphate may be used at the same time.
Although they are both calcium antagonists, concurrent use was NOT shown to cause a potentiation of the
hypotensive effect in a large retrospective review.93
In management of severe hypertension, oral labetalol and oral methyldopa are less effective in lowering BP than
Nifedipine. However, they remain reasonable choices when Nifedipine is not available or intravenous access is not
feasible.94
Maintenance therapy (chronic hypertension)

There is insufficient evidence to determine the ideal ongoing BP levels associated with optimal maternal and perinatal
outcomes for women with chronic hypertension. Blood pressures levels that are too low may compromise placental
perfusion, so suggested targets are sBP 130-155 mmHg and dBP 80-105 mmHg. Women entering pregnancy on
antihypertensive medications may need the dose lowered or medication(s) stopped completely to remain within this
range.95
A 2018 Cochrane review (including 31 studies) showed that treating hypertension below the severe range (<sBP
160 and < dBP110) decreases the risk of progression to severe hypertension by one half, but has little or no impact
on development of preeclampsia, fetal or neonatal death including miscarriage, small for gestational age infants, or
preterm birth below 37 weeks.96
Women with underlying medical conditions, such as renal disease, may have lower target blood pressures, determined
on a case by case basis.
Maintenance therapy (gestational hypertension)

Target blood pressures are the same as for chronic hypertension.
NOTE
About 25% of women with chronic or gestational hypertension will develop preeclampsia. Lowering blood
pressure does not change this, as hypertension is only one (late) manifestation of a complex underlying
process (see “Pathogenesis” section, above). Hence, ongoing close follow-up is critical.

Table 6 shows oral antihypertensive medications commonly used in Canada. No differences in maternal or fetal
outcomes have been demonstrated.96 979899100
Table 6. Maintenance therapy
AGENT DOSE CAUTION
Labetalol Initial dose 100 mg twice a day; Contraindicated in women with asthma.
Maximum 400 mg 3 times a day (1200mg/day)
Nifedipine XL Initial dose 20 mg once daily; Contraindicated in women with aortic stenosis
Maximum 60 mg twice a day Ensure XL Preparation
Methyldopa Initial dose 250 mg twice a day; May cause depression

Maximum 500 mg 4 times a day (2g/day)
References36, 58, 92
NOTE
Angiotensin converting enzyme inhibitors and angiotensin receptor blockers are contraindicated
because of IUGR, prematurity and oligohydramnios. They are not teratogens, but disturb
fetal and neonatal renal function. Women who conceive on them should be switched to
alternate antihypertensive medications as soon in pregnancy as possible.101, 102
Atenolol is not recommended because of increased rates of IUGR among infants
born to women taking Atenolol at conception or during first trimester.103
Beta-blockers taken in late pregnancy increase the risk of neonatal hypoglycemia
and bradycardia (adjusted Odds Ratio for both <2).104
There is an increased risk of congenital anomalies overall (OR 1.3), and congenital heart defects specifically (OR 1.6),
in women with chronic hypertension, independent of their use of antihypertensive medications. This suggests an
underlying association between maternal hypertension and congenital anomalies, independent of the adverse effects of
some medications.105, 106
Fluid Management
Hypertensive women may not tolerate large fluid volume shifts. Iatrogenic pulmonary edema is a concern because of
the large amounts of intravenous fluids that may be inadvertently administered intrapartum. Intravenous and oral fluid
intake should be limited in women with preeclampsia to avoid pulmonary edema. The standard intravenous fluid
bolus routinely administered before regional anaesthesia should not be given. The type of fluid is not as critical as
the volume of fluid. Hypotension and shock may develop with lesser degrees of hemorrhage because of vascular space
contraction.

Urine output is best monitored by an indwelling Foley catheter. A urine output < 15 mL/hour is not unusual in
preeclampsia, particularly postpartum. In the absence of pre-existing renal disease or a rising creatinine level, oliguria
should be tolerated at least for a few hours. The UK Confidential Enquiry into Maternal Deaths found that excess maternal
mortality is associated with aggressive fluid use and not with transient renal compromise.107 In the presence of oliguria,
a careful assessment of volume status and renal function is indicated.24 When a patient is undergoing medical induction
of labour and is receiving MgSO4 with oxytocin, it is prudent to limit IV fluid intake by concentrating the solutions
of oxytocin and MgSO4. Hourly total intake and urine output must be monitored closely in this situation to prevent
pulmonary edema.
Recommendations in the presence of oliguria (< 15 mL/hour):
• Clinically assess volume status
• Measure renal function (creatinine)
• Beware of magnesium toxicity
• Consider a small fluid bolus (500 mL normal saline)
• Monitor O2 saturation (keep > 95%)
• Beware of pulmonary edema
• Consider consultation, if oliguria persists and creatinine is rising
Dopamine or furosemide should not be administered in the presence of persistent oliguria occurring before delivery.
(See “Postpartum Management” section regarding furosemide use after delivery.)
Thromboprophylaxis should be considered for all patients who are immobilized or bedridden for prolonged periods.108
Symptomatic Support
Immediate treatment should include managing symptoms such as nausea and vomiting with an antiemetic to minimize
maternal discomfort. A component of maternal hypertension is adrenergic and may be modified by stress reduction.
There is no evidence to support strict bed rest in the lexicon of therapeutic management of hypertensive disorders of
pregnancy. Such an intervention is harmful.109
Principles of stress reduction:
• Quiet environment
• Presence of a supportive family member or professional
• Clear explanation of management plan to patient / family
• Minimization of negative stimuli
• Consistent, confident team approach (nursing, obstetrics, midwifery, anesthesiology, hematology, pediatrics)

Seizure Prophylaxis
Prevention of seizures is crucial in stabilizing a woman who has preeclampsia. As seizures are rare, there is a high
number needed to treat to prevent a seizure. Neither maternal symptoms nor blood pressure levels reliably predict
seizures; however, because of side effects and cost, selective use of seizure prophylaxis is generally recommended for
women with:21, 36, 58, 110
• Severe hypertension
• Blood pressures below the severe range but with associated
−− significant headache or clonus
−− visual disturbance (blurring, scotomata)
−− right upper quadrant or epigastric pain (severe and persistent), and/or elevated liver enzymes
−− thrombocytopenia (<100 x 109/L)
−− progressive renal insufficiency (doubling of serum creatinine)
• HELLP syndrome
• Secondary prevention after eclamptic seizures
Magnesium sulphate (MgSO4) is the agent of choice when seizure prophylaxis is indicated111 MgSO4 is superior
to phenytoin for the prevention of seizures, and is superior to either diazepam or phenytoin for preventing recurrent
seizures.112-114 MgSO4 reduces the incidence of seizures by 50%.115
31
Magnesium Sulphate Administration

• Intravenous administration of MgSO4 is preferred as therapeutic magnesium levels in the circulation are
achieved rapidly. This is especially important after a seizure has occurred.
−− Dosage: 4 g as an IV bolus given over 20 to 30 minutes followed by 1 g/hour IV
−− A recurrent seizure may require a second 2 to 4 g IV bolus
• Intramuscular: When intravenous access is unavailable, MgSO4 may be given intramuscularly (IM). The
process for IM MgSO4 administration is116
−− Initial dosage: 10 g of 50% MgSO4, one half (5 g) injected deeply in the upper, outer quadrant of both
buttocks through a 3-inch, 20-gauge needle (spinal needle). Maintenance dosage: 5 g of 50% solution
of magnesium sulphate by deep IM injection in the upper, outer quadrant of alternate buttocks every 4
hours after the initial 10 g dose.
−− The Intramuscular regimen may offer a safer alternative than an IV infusion for patients being
transported between health care facilities. The above dosages can be used. Another option shown to be
safe is: 4g IV bolus and 10g IM loading dose (at the same time) followed by 5g IM every 4 hours (called
the Pritchard regimen).116
• Side effects of MgSO4: weakness, paralysis, cardiac toxicity, loss of patellar reflexes, respiratory depression.
The data, however, show that these risks are very low.117
• Monitor reflexes, respiration, level of consciousness, hourly urine output. Magnesium is excreted in the
urine. Clinically, magnesium serum levels can be estimated as follows118:

BLOOD LEVEL MMOL/L
Reflexes present 2 to 3.5
Loss of patellar reflexes 4 to 5
Respiratory depression ≥6
• Routine monitoring of serum magnesium levels is not supported by evidence.116

• Although MgSO4 should be used with caution when combined with calcium channel blockers (i.e.,
nifedipine) and in women in renal failure, the risk of complications is low (< 1%).93 Therefore, calcium
channel blockers may be used simultaneously with MgSO4.
• If toxicity is suspected, discontinue the medication, provide respiratory support, notify the primary health
care provider, consider giving calcium gluconate, and monitor the blood level of magnesium. The antidote
to magnesium is 10 mL of 10% calcium gluconate, IV over 3 minutes.
The incidence of respiratory suppression with the IV regimen above (4gram IV bolus over 20 minutes then 1 gram per
hour) is less than 1%.117 Therefore, if toxicity has developed, it is essential to confirm that the appropriate concentration is
being infused at the correct rate, and that urine output is adequate. Following this, the magnesium sulphate infusion can
be resumed at a lower rate.
Points to remember in management of seizures (eclampsia):
• Call for help
• Turn the woman on her side
• Protect the airway
• Start an IV MgSO4 bolus of 4 g over 20 to 30 minutes and then a maintenance dose at 1 g/hour IV (if
recurrent seizure while on MgSO4, re-bolus with 2 g IV over 20 to 30 minutes)36
• When seizure stops, administer oxygen by face mask, clear airway as required, assess BP, pulse, respiration,
and fetal heart rate frequently until stable
• Assess for evidence of placental abruption
• Be aware that patients with eclampsia are at risk of developing deep vein thrombosis, cerebrovascular
accident, or cardiomyopathy after the seizures119
Protocols for the use of magnesium sulphate should be established, be immediately available in every labour
and delivery unit, and include the following:
• Preparation
• Assessments before administration
• Administration protocol
• Assessment for side effects and drug interactions
• Management of toxicity
• Documentation

Management of HELLP Syndrome

HELLP syndrome consists of Hemolysis, Elevated Liver enzymes (AST, ALT and/or LDH), Low Platelet count.
The management of HELLP syndrome consists of all therapeutic steps for hypertension described above. In addition, the
thrombocytopenia may require specific intervention based on severity:
• Platelet count >50x109/L: If there is no evidence of platelet dysfunction or excessive bleeding, prophylactic
platelet transfusion is not indicated, even before Caesarean section.
• Platelet count <50x109/L: platelet count is falling, or a coagulopathy exists: consider blood product/platelet
transfusion.
• Platelet count <20x109/L: Platelet transfusion before both Caesarean section and vaginal delivery.
Delivery should be undertaken within 48 hours of diagnosis. There are no differences in maternal or perinatal
outcomes when immediate delivery versus expectant management of 48 hours followed by delivery were compared.
However, expectant management of greater than 48 hours was associated with an increased risk for maternal
admission to the ICU.120
Patients with HELLP syndrome are at risk of developing eclampsia, hence MgSO4 should be administered.120
Transport
When local resources are limited and maternal and fetal conditions permit, the outcome may be improved by
transporting the mother to an appropriate referral centre.
A transport protocol should be readily available in every unit. Before transport, the following must be confirmed:
• Maternal blood pressure is stable
• Fetal condition is stable
• Seizure prophylaxis is given if necessary. Consider MgSO4 IM dose (see above) for safety during transport.
• Ventilation equipment and calcium gluconate are available during transport
• The woman is accompanied during transport by a health care provider with the skills and qualifications to
ventilate and to administer any necessary medications
Delivery
Delivery of the placenta is the only cure for preeclampsia. Any of the hypertensive disorders of pregnancy can progress
quickly to endanger mother and infant. Timely delivery minimizes maternal and neonatal morbidity and mortality.
Delivery is based on the following:
• Maternal status must be optimized before intervening with a delivery process
• Delay of delivery, to allow transfer, should occur only when maternal and fetal conditions permit
• Corticosteroid therapy to enhance fetal pulmonary maturity should be considered for all women with
preeclampsia before 346 weeks’ gestation121, 122

• Expectant management is potentially harmful

• Maternal status can worsen, and eclampsia can still occur after delivery
Timing of Delivery
Women with the hypertensive disorders of pregnancy are a heterogeneous group who vary greatly in the severity
and stability of their conditions. The following are broad guidelines regarding timing of delivery. For women who
have chronic hypertension or gestational hypertension and whose BP is stable, ongoing expectant management is
reasonable, provided close surveillance confirms maternal and fetal well-being.
HYPERTENSIVE DISORDER SUGGESTED TIME OF DELIVERY
Chronic hypertension ≥ 38 weeks
Gestational hypertension ≥ 37 weeks
Preeclampsia without severe features (see below) 37 weeks
Preeclampsia with severe features: Deliver regardless of gestational age.

• Inability to control maternal blood pressure
• Increasing maternal organ dysfunction (hepatic, renal, neurologic symptoms, HELLP)
• Fetal indication for delivery
If expectant management is contemplated in a woman with preeclampsia and any of the above severe features,
the pregnancy should be managed in a facility with sufficient resources for maternal intensive care support and for
continuous monitoring. The facility should have the capability to intervene immediately and to manage a premature
infant.
For uncomplicated chronic hypertension, gestational hypertension, and preeclampsia without any of the above severe
features, delivery compared to expectant management between 34 and 366 weeks, showed no reduction in adverse
maternal outcomes but a significant increase in RDS (RR 3, number needed to harm 25) with that risk being higher at 34
weeks than at 366 weeks.123
Postpartum Management
Gestational hypertension and preeclampsia may present initially or worsen following delivery. The peak time for the
appearance of hypertension postpartum is on days 3 to 6 when the mobilization of the extracellular fluid accumulated
during pregnancy occurs.
The timing of seizure occurrence is distributed as follows: 50% first appear before labour, 25% first occur during labour,
25% begin in the early postpartum period. Rarely, a woman will have a seizure 2 days or more after delivery.

Women who have received magnesium sulphate for seizure prophylaxis during labour should have it continued for the
first 24 hours postpartum. All women at risk for hypertensive disorders of pregnancy must be monitored carefully in the
postpartum period with ongoing attention to blood pressure, renal function, seizure risk, and end-organ dysfunction.
Laboratory investigations should be directed towards the particular end-organ that has been affected. Of note, for women
who had severe hypertension in pregnancy, the addition of postpartum furosemide (e.g., 20 mg by mouth every 24
hours for 5 days) to the antihypertensive regimen appears beneficial in lowering BP and in reducing the need for other
antihypertensive medications postpartum.124-127
125 621
Postpartum thromboprophylaxis should be considered, particularly if there has been antenatal bed rest for more than 4
days, if the patient is obese, or if delivery has been by Caesarean section.
Severe postpartum hypertension should be treated with antihypertensive therapy to keep the systolic BP < 160 mm
Hg and the diastolic BP < 110 mm Hg. In addition, antihypertensive therapy should be considered to treat non-severe
postpartum hypertension, particularly in women with comorbidities. Antihypertensive agents acceptable for use in
breastfeeding include nifedipine XL, labetalol, methyldopa, captopril, and enalapril.
Discharge from hospital should occur only when there is a clear trend towards improvement in clinical and laboratory
assessments, when there is an ability to provide adequate outpatient surveillance, and when follow-up can be arranged
within a week for clinical and blood pressure assessment. When there has been end-organ dysfunction, there should be
evidence that it has resolved before the patient is discharged. It is reasonable to discharge women whose BP remains at
< 160/ 110 mm Hg for at least 24 hours.36
NOTE
Although rare, new onset preeclampsia has been documented up to 3 weeks after delivery in an otherwise
normal pregnancy. Advanced maternal age, diabetes mellitus, obesity, and being of Black or Latina heritage
seem to be associated risk factors for these occurrences.128
Future Cardiovascular Risk

Women with a history of a hypertensive disorder of pregnancy have an increased risk of cardiovascular disease later
in life. The risk is higher yet if their pregnancies were also complicated by preterm birth and growth restriction. If
preeclampsia has recurred (as it does for 15% of women in a subsequent pregnancy), the RR for future CVD is about
2.5 compared to women with an unaffected subsequent pregnancy129. Apart from recognition of this risk factor and
encouragement of lifestyle modification, more research is needed to determine what cardiovascular screening or
preventive treatment conveys long term benefit in these women.130-132 With regard to Lifestyle Risk Factors, being
13
overweight or obese is associated with higher risk of chronic hypertension after a hypertensive disorder in pregnancy,
while risk is not influenced by DASH diet, dietary sodium/potassium intake, or physical activity.133
The Canadian Cardiovascular Society recommends that all women with a history of a hypertensive disorder in pregnancy
“be approached for screening with a lipid profile”, but states that there is insufficient evidence to prescribe statins based
solely on the history of a hypertensive disorder in pregnancy.134

International guidelines differ with regard to when, how and whom to screen, hampered by the fact that the
pathophysiology linking preeclampsia and cardiovascular disease is not completely understood.135
Points to Remember in Management

• Do not reduce blood pressure too rapidly or to too low a level: placental perfusion can be compromised.
Keep systolic pressure <160 mmHg to prevent maternal stroke.
• Do not fluid overload: pulmonary edema is more dangerous than transient renal compromise.
• Do remember that MgSO4 decreases seizure risk by 50%
• Do use an interprofessional approach:
−− obstetrical care provider
−− anaesthesiologist
−− pediatrician and/or neonatologist
−− nurses
−− internal medicine specialist and/or hematologist
Summary
1. Severe hypertension is an obstetrical emergency.
2. This clinical presentation requires prompt recognition, stabilization of the mother and fetus, and an
interprofessional approach to management.
3. The primary obstetrical team in rural and remote areas may have to assume the roles of one or several
disciplines until help or transfer is available.
4. The cure is delivery, but the decision to deliver is based on severity, maternal status, fetal maturity, and fetal
well-being.
5. The rationale for antihypertensive treatment is to prevent maternal cerebrovascular accidents, not seizures.
6. Seizure prophylaxis, when indicated, should be with magnesium sulphate.
7. There is no evidence that antihypertensive therapy for hypertension below 160/110 improves perinatal
outcome.
8. There are no investigations, beyond maternal history, that are clinically useful to predict preeclampsia.
9. Women at high risk for preeclampsia should be offered ASA 81-162mg per day, starting after the diagnosis
of pregnancy and before 16 weeks gestation. Significant benefit has not been shown for women at low risk
of preeclampsia.
10. Women with a history of a hypertensive disorder in pregnancy have an increased risk of cardiovascular
disease later in life.

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Appendix A
Laboratory and imaging abnormalities encountered in women with the hypertensive disorders of pregnancy36
INVESTIGATIONS FOR DESCRIPTION IN WOMEN WITH

DESCRIPTION IN WOMEN WITH OTHER CONDITIONS
DIAGNOSIS PREECLAMPSIA
MATERNAL TESTING
Urine testing
Urinalysis (routine and Proteinuria (as discussed under Hemoglobinuria (dipstick “hematuria” without RBCs):
microscopy with/without Proteinuria) without RBCs or casts hemolytic anemia
additional tests for proteinuria)
RBCs alone: renal stones, renal cortical necrosis (also
associated with back pain and oliguria/anuria)
RBCs and/or casts are associated with other glomerular
disease and scleroderma renal crisis and (about half of)
TTP-HUS
Bacteria: UTI or asymptomatic bacteruria
Proteinuria is usually absent in secondary causes
of hypertension such as pheochromocytoma,
hyperaldosteronism, thyrotoxicosis, coarctation of the aorta,
withdrawal syndromes
Oxygen saturation
Pulse oximetry SpO2 <97% associated with a heightened May be decreased in any cardiorespiratory complication (e.g.,
risk of severe complications (including pulmonary embolism)
non-respiratory)
CBC and blood film
Hemoglobin i due to intravascular volume depletion i due to volume depletion from any cause (e.g., vomiting)
s if microangiopathic hemolysis (with s if microangiopathic hemolysis from other cause

HELLP) s with any chronic anemia (nutritional or myelodysplasia)
s with acute bleeding of any cause
WBC and differential fp i due to neutrophilia of normal pregnancy

i with inflammation/infection
i with corticosteroids


Platelet count s - associated with adverse maternal s with gestational, immune (ITP), or thrombotic
outcome thrombocytopenia (TTP), APS, AFLP, myelodysplasia
Blood film RBC fragmentation Microangiopathy due to mechanical causes (e.g., cardiac
valvopathy, cavernous hemangioma), DIC or other disorders
of endothelial function (e.g., APS, TTP-HUS, vasculitis,
malignant hypertension)
Tests of coagulation*
INR and aPTT i with DIC which is usually associated May be i in APS, DIC from other causes including sepsis,
with placental abruption - i is associated amniotic fluid embolism, stillbirth, massive hemorrhage,
with adverse maternal outcome hemangiomas, shock
i is prominent in AFLP
Fibrinogen sfp s with all causes of DIC including massive hemorrhage,

genetic disorders
s more profound with AFLP than with HELLP
Usually normal in TTP-HUS (ADAMTS13 vWF cleaving protein

may be moderately decreased in HELLP but ADAMSTS 13
antibody should be absent)
Serum chemistry
Serum creatinine i due to hemoconcentration and/or i with other acute or chronic kidney disease
renal failure - i associated with adverse
Renal failure prominent in malignant hypertension, TTP-
maternal outcome
HUS (along with thrombocytopenia), AFLP (along with liver
dysfunction)
Serum uric acid i not meaningfully associated with i with dehydration, medication (e.g., HCTZ), genetic causes
adverse maternal or perinatal outcome*
Glucose fp s with AFLP, insulin therapy
AST or ALT i - associated with adverse maternal i with AFLP and other ‘PET imitators’† but to a lesser degree,
outcome and usually normal in TTP-HUS
May be increased in other pregnancy-related conditions

(e.g., intrahepatic cholestasis of pregnancy) or conditions
not associated with pregnancy (e.g., viral hepatitis or
cholecystitis)
LDH i which may be prominent – the i is i with AFLP, intravascular hemolysis

associated with adverse maternal outcome
i LDH/AST ratio (> 22) with TTP-HUS


Bilirubin i - unconjugated from hemolysis or (early) i in AFLP, i with hemolytic anemia, other liver
conjugated from liver dysfunction disease with dysfunction, genetic diseases
Albumin s - associated with adverse maternal and s as negative acute phase reactant with acute severe illness,
perinatal outcomes malnutrition, nephritic syndrome, crystalloid infusion
FETAL TESTING Abnormalities are not specific to the cause of poor placentation and/or placental dysfunction
Uterine artery Doppler Unilateral/bilateral notching, or elevated pulsatility index or resistance index may support a diagnosis of
velocimetry placental insufficiency including preeclampsia
Fetal monitoring Abnormal or atypical FHR tracing (e.g., decreased variability)
Deepest amniotic fluid pocket Oligohydramnios associated with adverse perinatal outcomes
Ultrasonographic assessment of Usually intrauterine fetal growth restriction (typically asymmetrical but can be symmetrical if early and/or
fetal growth severe)
Umbilical artery Doppler Increased resistance, absent or reversed end-diastolic flow
Ductus venosus Doppler Increased resistance, especially absent or reverse “a” wave
Middle cerebral artery Doppler Cerebral redistribution (decreased resistance, or “brain sparing effect”). May be lost in extreme cases prior
to fetal death
*Note: This is a modification from the original table. Adapted with permission.
AFLP: acute fatty liver of pregnancy

APS: antiphopholipid antibody syndrome
CBC: complete blood count
DIC: disseminated intravascular coagulation
FHR: fetal heart rate
HELLP: hemolysis, elevated liver enzyme, low platelet syndrome
TTP-HUS: thrombotic thrombocytopenic purpura - hemolytic uremic syndrome
PET: preeclampsia-eclampsia; SpO2: oxygen saturation
UTI: urinary tract infection
vWF: von Willebrand Factor.
*Tests of coagulation are recommended if there is thrombocytopenia or placental abruption.
† ‘PET imitators’ include AFLP, catastrophic APS, TTP-HUS, malignant hypertension and scleroderma renal crisis.
‡ Abnormal uterine artery Doppler velocimetry is practically defined at 22-24 weeks as bilateral notching with mean resistance index (RI) > 0.55 (i.e., > 50th centile), unilateral
notching with mean RI > 0.65 (> 90th centile), or no notching with mean RI > 0.70 (> 95th centile).

Table of Contents
Chapter 17 Preterm Labour and Preterm Birth ................................................................................................................ 412

Introduction.............................................................................................................................................................. 412
Definition...................................................................................................................................................... 412
Incidence....................................................................................................................................................... 412
Etiology and Risk Factors............................................................................................................................... 412
Predictors of Preterm Birth....................................................................................................................................... 413
Fetal fibronectin............................................................................................................................................ 413
Cervical length measured by transvaginal ultrasonography......................................................................... 413
Diagnosis ................................................................................................................................................................. 414
Risk Reduction and Prevention ................................................................................................................................ 415
Risk Reduction.............................................................................................................................................. 415
Prevention..................................................................................................................................................... 415
Contraindications to Tocolysis ...................................................................................................................... 420
Antenatal Corticosteroid Therapy.................................................................................................................. 421
Magnesium Sulphate Therapy for Fetal Neuroprotection in Imminent
Delivery at ≤ 316 weeks' gestation......................................................................................................... 424
Antibiotic Prophylaxis.................................................................................................................................... 426
Maternal Transport........................................................................................................................................ 426
Summary.................................................................................................................................................................. 427
Preterm Labour and Preterm Birth 411

Chapter 17
Preterm Labour and Preterm Birth
Introduction
Definition
Preterm labour is defined as regular uterine contractions with progressive cervical dilation and/or effacement at > 20
weeks and < 370 weeks’ gestation. Preterm birth is delivery before 370 weeks’ gestation.1 Long-term adverse sequelae of
preterm birth occur mainly in infants born at < 34 weeks’ gestational age.2, 3
Incidence
The incidence of preterm birth in Canada has increased from 6.3% (1981 to 1983) to 7.7% (2009).4-6 Only 1% to 2% of
5
pregnancies deliver before 34 weeks, and neonates born at > 34 weeks’ gestational age in Level III centres have survival
rates of 99% to 100%, although they may require longer hospital stays because of feeding and other difficulties.7, 8
The importance of accurate dating in the management of preterm labour cannot be overstated. A difference of 10 days
can change the chance of survival from 10% (at 22 weeks) to over 40% (at 24 weeks). Accurate dates must therefore be
established and the estimated date of delivery (EDD) must be communicated effectively to the patient. The most accurate
time for dating is within the first trimester, between 7 and 14 weeks’ gestation. If possible, all women should be offered
an ultrasound during this time to confirm dating. Accurate dating will reduce the number of pregnancies prolonged
past 410 weeks.9 By 20 weeks’ gestation, care providers should be able to inform all pregnant women of their EDD from
accurate menstrual data and/or dating from an ultrasound.9

The causes of preterm birth can be divided into two main categories10-13: (1) Induced (iatrogenic) preterm birth
1 21
(accounting for 20% to 30% of preterm births); (2) spontaneous preterm labour (with intact membranes, accounting for
40% to 50% of preterm births, or with preterm pre-labour rupture of membranes, accounting for 30% to 40% of preterm
births).
Clinical maternal or fetal conditions associated with induced preterm birth include:
• Preeclampsia
• Complicated insulin-dependent diabetes mellitus
• Abnormal fetal surveillance results


• Intrauterine death
• Monochorionic, monoamniotic twins
Risk factors for spontaneous preterm labour and birth include1, 14, 15
• Reproductive history: previous spontaneous preterm birth; advanced reproductive technologies16
• Antepartum bleeding
• PPROM
• Cervical/uterine factors: cervical insufficiency, uterine malformation,14 and fibroids17; excisional cervical
treatment for cervical intraepithelial neoplasia18-20
91
• Fetal/intrauterine factors: multifetal gestation; fetal anomaly; polyhydramnios

• Infection: chorioamnionitis; bacteriuria; periodontal disease21-23; current bacterial vaginosis with a prior
2
preterm birth24; malaria (particularly in developing countries)

• Demographic factors: low socioeconomic status; single marital status; low level of education; maternal age
< 18 or > 35 years
• Other maternal factors: problematic substance use, smoking, physical abuse,25 inadequate prenatal care, low
pre-pregnancy weight (BMI < 18.5 kg/m2), poor weight gain in pregnancy,26 stress,27 obesity28
Predictors of Preterm Birth

Fetal fibronectin
Fetal fibronectin (fFN) is a glycoprotein whose presence in cervicovaginal secretions before 34 weeks’ gestation is
associated with preterm labour and birth.29-31 The main benefit of fFN assessment is its negative predictive value. A
03
negative fetal fibronectin test indicates a low probability of delivery within 7 days to 14 days, even in the presence of
contractions. The chance of delivering within 14 days of a negative fFN test (in women with symptoms) is 1% to 5%. The
chance of delivering within 14 days with a positive test in women with symptoms is 17% to 41% (the positive predictive
value).
If fFN assessment is used, it is advisable to obtain the swab before a cervical digital examination is performed. If a digital
examination is performed first or if the patient has had sexual intercourse in the 24 hours, a false-positive fFN test may
result. As lubricants, creams, and disinfectants may also produce a false-positive result, saline, rather than lubricant,
should be used in performing the pelvic examination to obtain the fFN swab.
Cervical length measured by transvaginal ultrasonography

The mean cervical length at 24 weeks’ to 28 weeks’ gestation is 34 mm to 35 mm.32-34 The probability of preterm birth
3
increases in singleton pregnancies when the cervical length is less than 25 mm to 30 mm (20 mm in twins), especially

in women at increased risk of preterm birth (e.g., those with a history of previous preterm birth) or those with threatened
preterm labour. 33-40
3536373
8 93
Funnelling of the internal cervical os may be seen on ultrasound imaging but is significant only when the residual
cervical length is short. Transvaginal ultrasound imaging is preferred because transabdominal scanning requires some
urine in the maternal bladder, which may affect the cervical length.33, 34, 40, 41
One prospective study of 964 women indicated that that routine prenatal cervical length screening of the general
obstetrical population by transvaginal ultrasound has poor positive predictive value.42 However, cervical length
measurement can be used for women identified to be at increased risk of preterm birth,40 as cervical shortening is
associated with an increased preterm birth risk. Transvaginal ultrasound measurement of the cervix has a high negative
predictive value if length is greater than 30 mm after 24 weeks. This information may be used to prevent unnecessary
interventions.
The value of fFN and ultrasound assessment of cervical length is that these tests may make accurate diagnosis of preterm
labour more likely, and they may reduce unnecessary transfer, hospitalization, and intervention, thereby improving
allocation of resources.43 Fetal fibronectin testing and ultrasound assessment of cervical length are currently being used
in some Canadian centres to assist in the identification and management of women at risk of preterm birth, including
those with suspected preterm labour. The effectiveness of these tests needs to be evaluated in large randomized
controlled trials before they can be recommended as universal screening tests.

Preterm birth is a major cause of perinatal morbidity and mortality and is estimated to account for 75% of neonatal
mortality, excluding lethal malformations.2, 3, 44, 45 The short-term complications of preterm birth include respiratory
distress syndrome (RDS), intraventricular hemorrhage (IVH), and necrotizing enterocolitis (NEC).
The long-term sequelae of preterm birth (especially < 28 weeks’ gestation) include CNS complications (e.g., cerebral
palsy), neurodevelopmental delay,46 respiratory complications (e.g., bronchopulmonary dysplasia), blindness, and
deafness.
Diagnosis
Early in their antepartum care, women should be instructed to be vigilant for signs and symptoms of impending preterm
labour—including regular contractions, vaginal fluid loss, vaginal bleeding, change in pelvic pressure, low dull backache,
and vaginal discharge—and to report to the hospital or contact their care provider immediately should any of these occur.
A timely physical assessment is required to confirm preterm labour; a phone consultation is insufficient.
The presence of uterine contractions and a suggestion of early dilatation or effacement on cervical examination should
raise concerns about possible preterm birth. This approach facilitates early institution of therapy but results in an over-
diagnosis of preterm labour. In two studies, approximately 50% of women with these signs remained undelivered 48
hours later, despite having no treatment.47, 48

Risk Reduction and Prevention

Risk Reduction
Screening for risk factors
Screening for and treating bacterial vaginosis in a woman who has had a prior preterm birth has been shown to reduce
the risk of low birth weight (odds ratio [OR] 0.31; 95% confidence interval [CI] 0.13 to 0.75) and PPROM (OR 0.14; 95%
CI 0.05 to 0.38).49
Screening for and treating asymptomatic bacteriuria has been shown to reduce low birth weight (OR 0.60; 95% CI 0.45
to 0.80).50
Encouraging smoking cessation

Cigarette smoking is associated with preterm birth, with a dose–response relationship noted. Smoking cessation should
always be encouraged for its general health benefits. It is likely that decreasing or stopping cigarette consumption
in pregnancy will reduce the overall incidence of preterm birth but this has not been definitively shown.51 Smoking
cessation counselling is encouraged and is shown to be effective in supporting women to quit smoking during
pregnancy. Strategies include simple advice, cognitive behavioural therapy, and support services.52
Addressing problematic substance use

Maternal problematic substance use increases the risk of preterm birth. Health care providers should try to identify
maternal substance use, provide information on the maternal and fetal risks, and support an approach to care for harm
reduction using brief intervention and referral to appropriate community services for counselling and treatment.52
Addressing barriers to prenatal care

The absence of prenatal care has been found to be associated with preterm birth but it unclear whether this association
is causal or is a marker for other factors that contribute to preterm birth. Retrospective studies cannot adequately control
for these confounding factors and prospective randomized trials (no prenatal care versus standard care) would not be
ethical.51, 53
Prevention
Progestogens
Progestogen treatment has been shown to decrease the risk of preterm birth under 34 weeks.54-56 Various
5
routes of administration have been studied, including intramuscular (IM), vaginal suppository, and oral.54, 55
17-hydroxyprogesterone caproate has been shown to decrease the rate of preterm birth < 32 to 34 weeks and birth
weight < 2500 grams in women at high risk who have a history of spontaneous preterm birth.55, 57-59 In a randomized
85
controlled trial comparing intramuscular progesterone with vaginal progesterone, in women with a prior preterm birth,

intravaginal progesterone was associated with greater compliance, fewer reported side-effects, and greater proportion of
deliveries at >34 weeks of gestation than intramuscular progesterone.56
The OPPTIMUM study in women at high risk showed that vaginal progesterone was not associated with reduced risk of
preterm birth or composite neonatal outcomes, and had no effect (beneficial or harmful) on outcomes in children at 2
years of age.60
A randomized controlled trial, PREDICT, and a secondary analysis, both published in 2011, found that progesterone
treatment does not appear to prevent preterm birth in twin pregnancies or in twin pregnancies at high risk.61 In 2017, a
Cochrane review including 17 RCT studies found there was no reduction in risk of improved neonatal outcome in twins if
progesterone was administered.62
In 2015, a meta-analysis by Combs et al.63 found that in women with triplet pregnancies there was no significant
difference on perinatal outcome or pregnancy duration between those who received 17-hydroxyprogesterone
caproate and those who received placebo. The STOPPIT trial found no evidence that in utero exposure to progesterone
had a detrimental or beneficial impact on health and developmental outcomes at 3 to 6 years of age.64
Other important maternal and infant outcomes have not been well-studied to date.65, 66 It is unclear if the prolongation
of gestation results in improved maternal and long-term infant health outcomes. Information regarding the potential
adverse effects of progesterone therapy to prevent preterm birth is limited.
A 2008 SOGC technical update concluded that women at risk for preterm labour should be encouraged to participate in
studies on the role of progestogen treatment in reducing the risks of preterm labour. Women should be informed about
the lack of available data from any neonatal outcome variables and about the lack of comparative data on dosing and
route of administration. Women with a short cervix should be informed of the single large RCT showing the benefit of
progesterone in preventing preterm labour.66 Women and their care providers should be aware that a previous preterm
labour and/or short cervix (< 15 mm at 22 to 26 weeks’ gestation) on transvaginal ultrasound could be used as an
indication for progestogen therapy initiated after 20 weeks’ gestation and continuing until the risk of prematurity is
low.67, 68
A 2012 review by the Society for Maternal-Fetal Medicine recommends the following:
• Singleton pregnancies with prior history of preterm birth: 17-hydroxyprogesterone caproate 250 mg IM
weekly from 16–20 weeks until 36 weeks.
• Singleton pregnancies without prior preterm delivery with short cervix ≤ 20 mm at ≤ 24 weeks: vaginal
progesterone 90 mg gel or 200 mg suppository daily from diagnosis of short cervix until 36 weeks.69
There may be short-term benefits, but there is no evidence of benefit or harm in childhood outcomes. Further studies are
needed to determine the efficacy of these therapies, and optimal combination of dosing and routes of administration of
the various progestogens. Since 17-hydroxyprogesterone is not readily available in Canada, use of progesterone 200 mg
vaginally daily is a reasonable option.

Recommended administration:
1. Women with previous preterm birth < 340 weeks, without a shortened cervix: vaginal micronized
progesterone 200 mg daily, from 16 weeks until 36 weeks. (Some experts recommend treatment for
previous preterm birth <370 weeks though the evidence for benefit between 340 and 370 is not as strong)69
2. Women with a short cervix ≤ 20 mm ≤ 24 weeks: vaginal micronized progestogen 200 mg daily, from
diagnosis until 36 weeks.
Cervical cerclage
A 2013 SOGC technical update recommends that cerclage should be considered in women with a cervix ≤ 25 mm
before 24 weeks’ gestation only if they have a prior history of preterm birth or a prior history of suspected cervical
incompetence. There is no clear benefit to cerclage for an incidental finding of a short cervix, but further surveillance by
ultrasound is recommended in this situation. Additionally, the data do not support the use of progestogen together with
cerclage.70
Cervical pessary
The incidence of preterm birth in both singleton and twin pregnancies has been reduced by use of a cervical pessary
for women who have a short cervix < 25 mm as measured by transvaginal ultrasound71, 72 However, larger multicentre
randomized controlled trials in both singleton and twin pregnancies have not substantiated these early findings.73, 74
Management of Preterm Labour

Successful management of preterm labour requires early diagnosis, identification of the cause, and treatment of the
underlying cause when possible. Labour should be arrested when appropriate, and interventions made to minimize
neonatal morbidity and mortality.
Assessment
• Establish dates: history (EDD, menstrual history, ultrasounds); review the prenatal record for EDD, menstrual
history, pertinent ultrasounds, and clinical growth
• Measure vital signs (temperature, blood pressure, respirations, pulse) and assess fetal well-being
• Evaluate contractions: history (frequency, intensity, duration, changes with time); abdominal examination for
uterine activity; tocodynamometer (frequency of contractions)
• Perform cervical assessment: undertake speculum examination initially to rule out PPROM, obtain swab for
fFN testing, if available, and cultures as required (e.g., gonorrhea culture/Chlamydia culture, GBS swab);
defer digital examination until after confirmation that membranes are intact and there is no placenta previa
• Undertake laboratory evaluation (complete blood count for leukocytosis)
Fetal monitoring is recommended for all preterm labours. Caution should be exercised with fetal scalp electrode if the
fetus is < 34 weeks gestational age and with fetal blood sampling if the fetus is between 34 and 36 weeks gestation
(this is probably best avoided in gestations < 34 weeks).

Tocolysis
Some tocolytics have been shown to prolong pregnancy for 48 hours or more when given before 34 weeks’ gestation.
This provides a window of opportunity for the administration of glucocorticoids. It also allows for the transportation of
the mother to a tertiary centre if necessary. Tocolysis may be contraindicated in a significant percentage of patients in
preterm labour. There is insufficient evidence to support tocolysis for women with PPROM.75
There is evidence that the following have some efficacy
AGENT/
EVIDENCE FINDINGS DOSE SIDE EFFECTS
TREATMENT
Calcium channel • No placebo-controlled • Lower rate of delivery • Ideal dosage regimen • Generally well-
blockers trials; 2003 Cochrane within 7 days and < 34 not yet determined, but tolerated but may
(nifedipine)76 review77: weeks, reduced rates many centres in Canada cause maternal
• 12 trials, n = 1029, of RDS, necrotizing are using this as their dizziness, light
comparing nifedipine enterocolitis, IVH first line tocolytic. headedness, headache,
with another tocolytic and jaundice with • Peak onset of oral flushing, nausea, and
(mainly betamimetics) nifedipine. Findings nifedipine is 30 to 60 transient hypotension
driven mainly by minutes. Half-life is with resulting FHR
Papatsonis et al. study78 90 minutes. Dosing changes.
that found significant of nifedipine 10mg • A 2010 systematic
differences PO should occur at a review and meta-
• Fewer side effects and minimum of 1 hour analysis of 5607
hence less need to intervals. women by Khan
discontinue treatment. • Maintenance therapy suggests caution for
is nifedipine regular total doses of > 60
capsules 10 mg orally mg. A total nifedipine
every 4 to 6 hours dose of > 60 mg is
(maintenance therapy associated with a
should start 6 hours significant increased
following completion risk of adverse events,
of loading dose). particularly those
Maintenance can be associated with
increased up to 20 mg significant morbidity
orally every 4 to 6 hours such as tachycardia and
at physician’s discretion. hypotension.81
• Maximum daily dose is
120 mg. It is stopped 48
hours after first dose of
betamethasone.a
• Close monitoring
of maternal blood
pressure79, 80

AGENT/
EVIDENCE FINDINGS DOSE SIDE EFFECTS
TREATMENT
PG synthetase • 2005 Cochrane review83 • 3 small trials (n = 106) • 100 mg suppository for • Potential fetal
inhibitors compared with placebo: transport and repeat 25 complications of PG
(indomethacin)82 more effective than mg to 50 mg every 6 synthetase inhibitors:
placebo in delaying hours for a maximum of should not be used after
delivery to ≥ 37 weeks 48 hours 32 weeks’ gestation
(this finding based on because of increased
only 1 small study) sensitivity of the ductus
• 5 trials compared with arteriosus to closure
other tocolytics: PG reduced fetal urine
synthetase inhibitors production causing
more effective in oligohydramnios;
delaying delivery neonatal renal
to ≥ 37 weeks and insufficiency has been
decrease in maternal reported. Therefore, PG
drug reaction requiring synthetase inhibitors
cessation of treatment should not be used for
• consult local tertiary more than 48 hours
centre as to local without assessment of
standard of care amniotic fluid volume.
• A systematic review
did not identify
statistically significant
increased risks of
adverse outcomes with
indomethacin use.
However, the limited
power of the review
did not allow exclusion
of the possibility
that indomethacin is
associated with adverse
neonatal outcomes.84
Nitroglycerin There is limited evidence of

the benefit of nitroglycerin
for tocolysis.
a
Modified from Dr Joan Crane, Women’s Health Centre, Eastern Health, St. John’s: personal communication, February 14, 2012.

There is no evidence for the efficacy of the following
AGENT/TREATMENT EVIDENCE CONCLUSION
Magnesium sulphate 2014 Cochrane review (37 trials and No benefit at any dose as a tocolytic
3571 women)85
Progestational agents 2010 Cochrane review (4 trials, 192 No benefit as a tocolytic

women)86
Bed rest 2010 Cochrane review (multiple No reduction of the risk of preterm birth or perinatal mortality
pregnancy)87
Fluid bolus Two small studies (228 women) No evidence of benefit

comparing intravenous hydration
with bed rest alone88, 89
Sedation, narcotics UpToDate review89 No evidence of benefit
Home uterine activity Randomized trials51, 90, 91 Home uterine activity monitoring has not been shown to reduce
monitoring preterm birth rates.
It increases visits to labour and delivery units, obstetric intervention, and

cost of antepartum care.
Contraindications to Tocolysis
Any contraindication to continuing the pregnancy • preeclampsia or other medical indication for delivery
• chorioamnionitis
• mature fetus
• imminent delivery
• intrauterine fetal death or lethal fetal abnormality
• abnormal fetal surveillance
• significant antepartum hemorrhage
Contraindications to specific tocolytic agents

The following tocolytics are not available in Canada: terbutaline, ritodrine, atosiban.
Antenatal Corticosteroid Therapy

RDS is a major concern with preterm delivery. IVH, necrotizing enterocolitis, persistent pulmonary hypertension, and
other respiratory conditions are also associated with preterm birth and are more likely to occur in newborns with RDS.
In the past, RDS accounted for > 20% of all neonatal deaths. The increased use of antenatal steroids and innovations in
neonatal care have reduced its occurrence and consequences.
The benefits of antenatal corticosteroid therapy are now definitively established. Betamethasone and dexamethasone
cross the placenta and induce enzymes that accelerate fetal pulmonary maturity. It takes 48 hours after the first dose for
the full benefit to be achieved. An incomplete course of corticosteroid therapy may still offer benefits. Figure 1 shows the
results of a meta-analysis of corticosteroid administration in women at risk of preterm birth.92 Treatment with antenatal
corticosteroids is associated with an overall reduction in neonatal death,93 RDS, intraventricular hemorrhage, necrotizing
enterocolitis, respiratory support, neonatal intensive care unit admissions, and systemic infections in the first 48 hours of
life.
Debate exists as to the preferred corticosteroid. Two Cochrane reviews, Roberts et al. in 2017 and Brownfoot et al. in 2013
reviewed the effects of these corticosteroids on fetal lung maturity and perinatal outcomes.94, 95 Indirect comparisons
in Roberts et al. showed betamethasone has significant reductions in chorioamnionitis, RDS, and chronic lung disease
compared to dexamethasone. Direct comparisons in Brownfoot et al. demonstrated greater reduction in IVH and lower
length of NICU stay for dexamethasone compared to betamethasone. Both showed similar effects in other perinatal
outcomes. Further studies are may clarify any difference.96, 97 Currently, betamethasone and dexamethasone are
98
acceptable choices.
Repeat corticosteroids
Scheduled repeat courses of corticosteroids are not indicated. It is becoming more evident that there may be some
reduction in the occurrence and severity of neonatal lung disease and serious infant morbidity, but these benefits are
associated with smaller head circumference and low birthweight, and with unknown long-term sequelae 100, 101 A 5-year
99
follow-up study from the preterm birth trial demonstrated that children born at term who were exposed to multiple
courses of antenatal corticosteroid were higher risk for neurosensory disability (adjusted OR 3.70; 95% CI 1.57-8.87)
and severe neurologic102, 103 disability. The 2016 Australasian Collaborative Trial of Repeat Doses of Prenatal Steroids
(ACTORDS) had 6-8 years follow up and found higher frequency of attention deficit and behavioural dysfunction with
multiple-courses of steroid group.96
In light of this evidence, balancing the neonatal benefits and limited evidence of long term effects, planned multiple
courses are not recommended.101, 102 104
Rescue corticosteroids
Rescue corticosteroids refers to the administration of one additional course or dose of antenatal corticosteroids after
already receiving a full course of antenatal corticosteroids during a pregnancy.

A randomized trial of a rescue course of antenatal corticosteroids (women less than 33 weeks of gestation with a
recurring threat of preterm delivery, who had received steroids at least 14 days before) found an improvement in
neonatal outcomes (reduction in composite neonatal morbidity, RDS, ventilatory support, and surfactant use) and no
increase in adverse outcomes. However, there was no significant short term benefits demonstrated with a delay greater
than 7 days between rescue dose and delivery.105 25th Edition of the ALARM Course Manual
The data on rescue corticosteroids is limited and questions remain regarding the long-term effects of multiple courses
of corticosteroids. Rescue corticosteroids can be considered at least 14 days after administration of the first full course,
taking into account the gestational age of the first administration, and after a discussion of the risks and benefits.
Late Preterm Corticosteroids
Late preterm corticosteroids
The 2016 study by Gyamfi-Bannerman et al.99 showed that the administration of betamethasone in women at risk for
The 2016
late ALPS
preterm study by
delivery ( 34+Gyamfi-Bannerman
0 weeks to 36+6etweeks)
al.106 showed that the
significantly administration
reduced the rate ofofneonatal
betamethasone in women
respiratory at risk
complications.
for late preterm delivery (34 0
weeks to 36 6
weeks) significantly reduced the rate of neonatal respiratory complications.
No long-term data are yet available in the cohort. The ASTECS trial indicates a need for caution in relation to long-term
Neonatal hypoglycemia
outcomes of exposure towas more frequent
antenatal after corticosteroid
corticosteroids administration.
late in pregnancy: Noschool
in this trial, long-term data are was
performance yet available in
significantly
the cohort. The ASTECS
poorer in 7-year-olds. trial
100, 101 indicates a need for caution in relation to long-term outcomes of exposure to antenatal
corticosteroids late in pregnancy: in this trial, school performance was significantly poorer in 7-year-olds.107, 108
Figure 1. Antenatal Corticosteroids Versusno
corticosteroids versus notreatment
Treatment
OUTCOME RR (95% CI)

RDS 0.66 (0.59, 0.73)
IVH Dx by US 0.54 (0.43, 0.69)

NEC 0.46 (0.29, 0.74)
Neonatal Infection 0.56 (0.38, 0.85)

Neonatal Death (all) 0.69 (0.58, 0.81)
0.1 1 10
Relative Risk (95% Confidence Interval)

Adapted from Roberts D,
Cochrane Library 2006,
Issue 3
Recommendations for Antenatal Corticosteroids

Women who are at increased risk of preterm delivery (especially within the next 7 days) are candidates for antenatal
steroid therapy.
y Lower gestation limit 24 weeks 102 (< 24 weeks should be assessed on a case-by-case basis)
y Upper gestation limit 34 weeks 6 days 91, 103
Recommendations for antenatal corticosteroids

Women who are at increased risk of preterm delivery (especially within the next 7 days) are candidates for antenatal
steroid therapy.
• Lower gestation limit 24 weeks109 (< 24 weeks should be
• assessed on a case-by-case basis)
• Upper gestation limit 34 weeks 6 days92, 94
• Prophylactic administration depends on diagnosis and risk
−− not recommended for pre-labour CS at term.(37-39 weeks gestation)
Corticosteroid options
• Betamethasone 12 mg IM every 24 hours x 2 doses
• Dexamethasone 6 mg IM every 12 hours x 4 doses
Special considerations with use of corticosteroids

• Contraindications to the use of corticosteroids: active tuberculosis, gastric ulcers, and chorioamnionitis
• If immediate delivery is indicated, it should not be delayed to wait for corticosteroid treatment effect
• Use of corticosteroids will transiently increase maternal blood sugar; it is recommended to delay testing
for gestational diabetes for at least 1 week after administering corticosteroids to avoid elevated glucose
results110
• Use of corticosteroids will also transiently increase the white blood cell count
• Evidence on the long-term academic performance of school-age children calls into question the use of
routine steroids for elective Caesarean section from 37 to 39 weeks107, 108 Due to the benefits and potential
harms, corticosteroid use is not recommended for pre-labour Caesarean section at term.102
• Use of corticosteroids may decrease fetal movements in the first 3 days following initiation of therapy111
• Corticosteroids should be administered in the same gestational age range and dosage in women with
obesity, with twins or higher order multiples, or with a suspected growth restricted fetus.102

Magnesium Sulphate Therapy for Fetal Neuroprotection in

Imminent Delivery at ≤ 336 weeks’ gestation112
1. For women with imminent preterm birth (≤ 336 weeks), antenatal magnesium sulphate administration
should be considered for fetal neuroprotection (Figure 2).
2. Although there is controversy about upper gestational age, antenatal magnesium sulphate for fetal
neuroprotection should be considered from viability to ≤ 336 weeks.
3. If antenatal magnesium sulphate has been started for fetal neuroprotection, tocolysis should be discontinued.
4. Magnesium sulphate should be discontinued if delivery is no longer imminent or a maximum of 24 hours
after therapy has been administered.
5. For women with imminent preterm birth, antenatal magnesium sulphate for fetal neuroprotection should be
administered as a 4g IV loading dose over 30 minutes, followed by a 1g/hr maintenance infusion until birth.
6. For planned preterm birth for fetal or maternal indications, magnesium sulphate should be started, ideally
within 4 hours before birth, as a 4g IV loading dose over 30 minutes, followed by a 1g/hr maintenance
infusion until birth.
7. There is insufficient evidence that a repeat course of antenatal magnesium sulphate for fetal neuroprotection
should be administered.
8. Delivery should not be delayed in order to administer antenatal magnesium sulphate for fetal
neuroprotection if there are maternal and/or fetal indications for emergency delivery.
9. When magnesium sulphate is given for fetal neuroprotection, maternity care providers should use existing
protocols to monitor women who are receiving magnesium sulphate for preeclampsia and/or eclampsia.
10. Indications for fetal heart rate monitoring in women receiving antenatal magnesium sulphate for
neuroprotection should follow the fetal surveillance recommendations of the SOGC 2007 Fetal Health
Surveillance: Antepartum and Intrapartum Consensus Guideline.
11. Since magnesium sulphate has the potential to alter the neonate’s neurological evaluation, causing
hypotonia or apnea, health care providers caring for the neonate should have an increased awareness of this
effect.

Indications for fetal heart rate monitoring in women receiving antenatal magnesium sulphate for neuroprotection
should follow the fetal surveillance recommendations of the SOGC 2007 Fetal Health Surveillance: Antepartum and
Intrapartum Consensus Guideline.
Since magnesium sulphate has the potential to alter the neonate’s neurological evaluation, causing hypotonia or apnea,
health care providers caring for the neonate should have an increased awareness of this effect.
Figure
Figure 2.
2. Magnesium
Magnesium sulphate
sulphate for
for fetal
fetal neuroprotection
neuroprotection in
in imminent
imminent preterm
preterm birth
birth (≤
(≤ 31+6 weeks)
336 weeks)
Woman ≤ 33+6 weeks gestation AND imminent preterm birth

• Active labour with ≥ 4 cm cervical dilatation with either failure
or contraindication to tocolysis
• ≥ 4 cm cervical dilatation with documented progressive
change in dilatation
• PPROM with active labour
• Planned delivery for fetal or maternal indications
YES No
• Administer MgSO4 loading dose, 4g IV Woman currently not eligible for MgSO4 for
over 30 minutes neuroprotection
• Follow with MgSO4 maintenance infusion
of 1g/hour IV until birth or a maximum of
24 hours of therapy
• Administer corticosteroids for fetal lung
maturation (if not already given)
• Monitor maternal vital signs as per existing
MgSO4 protocols
• Provide continuous fetal heart surveillance
CLINICAL TIPS
• MgSO4 may be administered before tocolytic drugs have been cleared from the maternal circulation. If
nifedipine has been used for tocolysis or hypertension, there is NO contraindication to the use of MgSO4
for fetal neuroprotection.
• Delivery should NOT be delayed in order to administer antenatal MgSO4 for fetal neuroprotection if there
are maternal and/or fetal indications for urgent delivery.
• Monitoring of serum Mg levels is NOT required.
“Imminent preterm birth” is defined as a high likelihood of birth, due to one or both of the
following conditions: active labour with ≥ 4 cm of cervical dilation, with or without PPROM;
planned preterm birth for fetal or maternal indications.
Obstetric care providers should consult their regional referral centre for guidance before starting magnesium
sulphate. When inappropriately administered, magnesium sulphate can be cardiotoxic and cause respiratory
Preterm Labour
depression. and Preterm
Magnesium Birth must always be administered via a medication pump to prevent overdose.113 Clinical435
sulphate
hyporeflexia is the first sign of magnesium toxicity and should prompt discontinuation of magnesium drip and
consideration of administration of calcium gluconate and assessment of magnesium levels.

Antibiotic Prophylaxis
Although evidence does not support the routine administration of antibiotics in preterm labour with intact
membranes,114 the antibiotic protocol for group B streptococcus prophylaxis115 should be followed if delivery is
anticipated or imminent.
Maternal Transport
The decision to transport should be made in consultation with the receiving physician.
Considerations
• Availability of neonatal and obstetrical care
• How quickly transport and skilled personnel can be available
• Travel time and travel conditions, e.g., weather
• Stability of the mother and fetus
• Risk of delivery en route
−− parity, length of previous labour
−− contractions: response to tocolytics
−− presentation of fetus
−− cervical status
Contraindications
• Unstable maternal condition
• Abnormal fetal surveillance
• Imminent delivery
• No experienced attendants to accompany mother
• Adverse weather or other hazardous conditions for travel
Transport plan
Every institution should have a transport protocol that includes:
• Availability of antenatal forms, ultrasound reports, and laboratory results
• Communication with patient and family and with receiving health care team (physician and nurses) re:
indication, stabilization, mode of transport, estimated time of arrival
• Appropriate attendant for transport
• IV access, indicated medication, appropriate equipment
• Assessment of patient immediately before transport

Location of preterm birth

It has been clearly shown that preterm infants born in tertiary care (level III) centres experience less mortality and long-
term morbidity than those born in level ll or level 1 centres. Those born during transport fare worst of all.
Summary
• Diagnose promptly and accurately
• Identify and treat underlying cause, if possible; attempt to prolong pregnancy, if indicated
• Consider magnesium sulphate therapy at ≤ 336 weeks for neuroprotection
• Intervene to minimize neonatal morbidity and mortality
• STAT: a mnemonic
−− Steroids: Antenatal corticosteroid therapy
−− Tocolytics: If indicated
−− Antibiotics: GBS prophylaxis
−− Transport

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109. Hayes EJ, Paul DA, Stahl GE, Seibel-Seamon J, Dysart K, Leiby BE, et al. Effect of antenatal corticosteroids on survival
for neonates born at 23 weeks of gestation. Obstet Gynecol. 2008;111:921-6. Available from: https://www.ncbi.
110. Langen ES, Kuperstock JL, Sung JF, Taslimi M, Byrne J, El-Sayed YY. Maternal glucose response to
betamethasone administration. Am J Perinatol. 2015;30:143-8. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/24915559.
111. Koenen SV, Mulder EJ, Wijnberger LD, Visser GH. Transient loss of the diurnal rhythms of fetal movements, heart
rate, and its variation after maternal betamethasone administration. Pediatr Res. 2005;57:662-6.
112. Magee L, Sawchuck D, Synnes A, von Dadelszen P. SOGC Clinical Practice Guideline. Magnesium sulphate for
fetal neuroprotection. J Obstet Gynaecol Can. 2011;33:516-29. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/21639972.
113. Doyle LW, Crowther CA, Middleton P, Marret S, Rouse D. Magnesium sulphate for women at risk of preterm birth
for neuroprotection of the fetus. Cochrane Database Syst Rev. 2009:CD004661. Available from: https://www.ncbi.
114. King J, Flenady V. Prophylactic antibiotics for inhibiting preterm labour with intact membranes. Cochrane Database
Syst Rev. 2002:CD000246. Available from: https://www.ncbi.nlm.nih.gov/pubmed/12519538.
115. Money DM, Dobson S, Canadian Paediatric Society IDC. The prevention of early-onset neonatal group B
streptococcal disease. J Obstet Gynaecol Can. 2004;26:826-40. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/15361281.

Table of Contents
Chapter 18 Prelabour Rupture of Membranes (PROM)................................................................................................... 438

Background.............................................................................................................................................................. 438
Definitions..................................................................................................................................................... 438
Incidence ...................................................................................................................................................... 438
Etiology and Risk Factors.......................................................................................................................................... 438
Risk Factors:.................................................................................................................................................. 439
Diagnosis.................................................................................................................................................................. 440
History .......................................................................................................................................................... 440
Speculum Examination................................................................................................................................. 440
Complications of Term PROM........................................................................................................................ 441
Complications of Preterm PROM.................................................................................................................. 441
Management ........................................................................................................................................................... 441
Management of Term PROM (≥ 37 weeks’ gestation).................................................................................. 442
Expectant Management ............................................................................................................................... 443
Management of PPROM (340 to 366 weeks’ gestation)................................................................................ 443
Management of PPROM (< 34 weeks’ gestation)........................................................................................ 444
Summary.................................................................................................................................................................. 445
Prelabour Rupture of Membranes (PROM) 437

Chapter 18
Prelabour Rupture of Membranes (PROM)
Background
Definitions
Prelabour rupture of membranes (PROM) is rupture of the membranes before the onset of labour when there is at
least an hour between membrane rupture and the onset of contractions.1 PROM may occur at ≥ 37 weeks’ gestation
(term PROM) or at < 37 weeks’ gestation (preterm PROM or PPROM). It is further classified by gestational age: mid-
trimester PPROM (before 24 weeks’ gestation), early PPROM (24 to 34 weeks’ gestation), and near-term PPROM (34 to
37 weeks’ gestation).
The latency period is the interval between the rupture of the membranes and the onset of labour. Later gestational age,
oligohydramnios and multiple gestation are associated with a shortened latency period.2
Almost 90% of women at term will go into spontaneous labour within 24 hours of membrane rupture.3 In women with
preterm rupture of membranes, the latency period tends to be longer. Only 50% of these women establish labour within
24 hours, with 70% to 80% delivering within 1 week of membrane rupture.4
Incidence
Term PROM occurs in approximately 8% of pregnancies.3, 5
Preterm PROM occurs in 2% to 3.5% of pregnancies but accounts for one third of the cases of preterm delivery.6 The
frequency of PROM increases with increasing plurality of gestation (13.3% for singleton, 16.81% for twins, and 20% for
triplets).7

Term PROM results from the normal physiological process of progressive membrane weakening combined with the
shearing forces created by uterine contractions. PPROM can result from a whole array of pathological mechanisms that
act individually or in concert, with evidence pointing to biochemical processes such as disorders in the extracellular
matrix of amnion and chorion, such as those caused by an intrauterine infection.8

Risk Factors:
• Amniocentesis
• Cervical insufficiency
• Cervical cerclage
• Prior cervical conization, laser conization, loop electrosurgical excision procedure
• PPROM in a previous pregnancy
• Prior preterm labour/delivery
• Chronic placental abruption
• Vaginal bleeding in pregnancy
• Polyhydramnios
• Short interpregnancy interval of less than 6 months9 10
• Cigarette smoking
• Sexually transmitted infection
• Low socioeconomic status
• Bacterial vaginosis (BV)
• Periodontal disease11
Bacterial vaginosis is a polymicrobial syndrome resulting in a decreased concentration of lactobacilli and an increase
in pathogenic bacteria. It may or may not be symptomatic. Current evidence does not support screening all pregnant
women for bacterial vaginosis and then treating those with asymptomatic BV to prevent preterm birth and its
consequences. For women with a previous preterm birth, there is little suggestion that screening and treatment of BV will
prevent a further preterm birth. However, it reduces the risk of low birth weight (odds ratio [OR] 0.31; 95% confidence
interval [CI] 0.13 to 0.75) and PPROM (OR 0.14; 95% CI 0.05 to 0.38).12 In the symptomatic woman at low risk for
adverse obstetrical outcome, oral and vaginal antibiotics are equally effective for symptom relief.13 However, women who
have a past history of preterm birth and who are symptomatic for BV should be treated with oral metronidazole 500 mg
or clindamycin 300 mg twice daily for 7 days. Topical (vaginal) therapy is not recommended for this indication because
although cure rates are similar to those observed with oral treatment, they have not been shown to be effective for
preterm birth prevention.14

The risk to both mother and infant is increased after the occurrence of PROM, whether at or before term. Among
women with PPROM, clinically evident intra-amniotic infection occurs in 15% to 25% of these women, with histological
chorioamnionitis in 51%.15 Fetal risks include umbilical cord compression and ascending infection.

Diagnosis
Diagnosis of PROM and PPROM is made by a combination of patient history, clinical suspicion, physical examination,
and testing. As patient history has an accuracy of 90% for the diagnosis of PPROM, it should not be ignored.16
Digital pelvic examination is not recommended because of the increased risk of ascending infection17, 18 and shortening
of the latent period.19 However, sterile speculum examination is appropriate for confirmation of PROM, assessment of
cervical status, and exclusion of cord prolapse. Although ultrasound is not diagnostic, the confirmation of the presence of
a normal amount of amniotic fluid makes the diagnosis of PROM less likely.
History
A careful history should be taken to determine the presence of fluid leaking, including the amount, timing, odour,
persistence, and colour. The vast majority of women with a history of vaginal fluid leakage will have PROM.20
Speculum Examination
A speculum examination should be undertaken to look for
• Fluid pooling in the posterior fornix
• Free flow of fluid from the cervix
• Cord prolapse
• Ferning: assessment for ferning is performed by obtaining a sample of fluid from the posterior fornix,
placing it on a glass slide, and letting it air dry for 10 minutes. When visualized under a microscope, the
presence of characteristic arborization (ferning), caused by the crystallization of sodium chloride, suggests
the presence of amniotic fluid (see Appendix)21
• false positive in a woman in labour: 11.8%; in a woman not in labour: 21.2%22
• false negative in a woman in labour: 2%; in a woman not in labour: 40.6%22
Antiseptic solution, semen, fingerprints, and cervical mucus may cause false-positives, while blood, meconium, and
vaginal secretions will not.23 Therefore the result of ferning should be viewed as supportive rather than conclusive in the
non-labouring woman with non-specific vaginal fluid loss.19
• pH nitrazine testing of fluid. This test is non-specific. Nitrazine paper changes to a dark blue from yellow
with a pH above 6.5. During pregnancy, normal vaginal pH is 4.5 to 6.0. Amniotic fluid pH is 7.1 to 7.3.
False positive results can result from blood, alkaline vaginal infections (e.g., bacterial vaginosis), alkaline
urine, and semen. False negative results may occur with prolonged membrane rupture and minimal residual
fluid.20
Fluid in the vagina may be collected to test for fetal lung maturity indices in preterm cases.
Commercial tests based on biochemical markers for the diagnosis of ruptured membranes such as placental alpha
microglobulin-1 (PAMG-1) (Amnisure™) are available and may be useful in certain clinical settings. Although the

sensitivity of such tests ranges from 94.8 to 98.9% and the specificity from 87.5 to 100%,24 their high cost limits the test
to where the diagnosis remains uncertain.25
Complications of Term PROM

• Fetal/neonatal infection (e.g., RDS, IVH, NEC)
• Maternal infection (e.g., endometritis, chorioamnionitis, bacteremia)
• Umbilical cord compression/prolapse26
Complications of Preterm PROM

• Preterm labour and delivery
• Fetal/neonatal infection
• Maternal infection
• Umbilical cord compression/prolapse
• Increased Caesarean section rate
• With early, severe oligohydramnios
−− pulmonary hypoplasia (< 26 weeks’ gestation)2, 23
−− fetal deformity
The most significant complication of PPROM is preterm birth and its consequences.2, 23
Management
The management of PROM at any gestational age requires
• Confirmation of the diagnosis
• Assessment of maternal and fetal well-being
• Determination of the presence of any associated condition that requires concurrent management or that
may indicate immediate delivery is desirable
• Avoidance of digital examination whenever possible.15,16 If expectant management is planned, the cervix
can be assessed during the speculum examination. If the woman is in labour, digital cervical assessment is
indicated
Determination of fetal presentation using ultrasound if abdominal assessment is inconclusive.
There is scientific evidence that maternal markers (C-reactive protein (CRP) and white blood cell (WBC) counts) are
predictive of early-onset neonatal infection.26, 27 The bedside assessment of amniotic fluid interleukin-6 also seems a
promising measure of microbial invasion of the amniotic cavity (MIAC).28-3092

There is no evidence to support tocolysis for women with PPROM as it is associated with an increase in chorioamnionitis,
increase in Apgar scores < 7 at 5 minutes, and an increase in the need for neonatal ventilation.31, 32
Outpatient management of selective patients with PPROM may be suitable, after a period of observation and provided
specific prerequisites are met. A retrospective cohort trial studying 133 patients with PPROM and a latency of at least
one week showed that the safety of outpatient management of appropriately selected patients is comparable with the
safety of in-hospital management.33 These include assessment of maternal or fetal complications, fetal position, fetal
growth and well-being, signs of labour or chorioamnionitis, and timely access to hospital. In another similar trial of 414
women with PPROM between 24 and 34 weeks, there was no increase in adverse maternal and perinatal outcomes for
women receiving outpatient care compared with hospital care.34 Specific departmental protocols however need to be
followed.1, 35--37
36
Magnesium sulphate is used for neuroprotection in preterm labour before 33 and 6 days’ gestation. In a secondary
analysis of a randomized controlled trial of magnesium sulphate for prevention of cerebral palsy, it was found not to
prolong latency.
Management of Term PROM (≥ 37 weeks’ gestation)

Digital cervical examination should not be undertaken until induction is initiated or labour has begun. The parturient
women should be assessed for infection and cultures obtained, if indicated. Antibiotics should be administered for group
B streptococcus (GBS) prophylaxis, if indicated.
Current evidence supports induction of labour (IOL) within 24 hours rather than expectant management for all
women with term PROM. 38 Induction of labour reduces the risk of maternal infection (e.g., chorioamnionitis and
endometritis) and NICU admission without increasing the rates of Caesarean section or assisted vaginal birth. Expectant
management on the other hand has been shown to increase the likelihood of Caesarean section and prolong maternal
hospitilization.39 Although IOL with vaginal prostaglandin (PGE2) has been shown to be as effective as oxytocin for labour
induction, it is associated with higher rates of chorioamnionitis. Prostaglandins may, however, be considered in women
with unfavourable cervix.40 A Cervical Ripening Balloon should not be used in the presence of PROM due to a possible
increase in the rate of chorioamnionitis.41
Oral misoprostol (50 mcg po q4hrly to a maximum of 4 doses) is an induction agent for PROM. Unlike oxytocin, it
has both uterotonic and cervical ripening effects, which are of particular benefit to women with an unripe cervix. It is
easier to administer than IV oxytocin and after an initial period of monitoring, it does not need continuous EFM until
contractions begin. Compared with vaginal prostaglandins, oral misoprostol does not require vaginal examinations,
lessening concerns about infection. A randomized trial of 758 women showed fewer Caesarean sections for dystocia and
no difference in fetal or maternal complications with a regimen of oral misoprostol than with vaginal PGE2 and oxytocin.
Women receiving misoprostol had a small increase in gastrointestinal side effects.42, 43
For women colonized with GBS, the indication for induction is more compelling because of the additional benefit of this
management in reducing neonatal infection.44
• CS if there are contraindications to IOL and/or vaginal birth.5, 45

• Surveillance for infection if management is expectant. Surveillance includes monitoring the maternal pulse
and temperature, fetal heart rate, presence of uterine tenderness or irritability, and changes in white blood
cell counts and CRP, if indicated.
• Appropriate antibiotics and IOL if chorioamnionitis develops.
• Induction with oxytocin or prostaglandin reduces the risk of chorioamnionitis (relative risk [RR] 0.74, 95% CI
0.56 to 0.97) and endometritis (RR 0.30, 95% CI 0.12 to 0.74) without increasing CS and operative vaginal
deliveries. Although a Cochrane review found there was no difference in neonatal infection (RR 0.83, 95% CI
0.61 to 1.12), fewer infants in the induction groups went to the neonatal intensive care unit compared with
expectant management (RR 0.72, 95% CI 0.57 to 0.92, number needed to treat 20).3 A recent Observational
study showed that outpatient labour induction with dinoprostone for TPROM was both feasible and safe.35
• Chorioamnionitis is reduced and maternal satisfaction is increased if labour is induced with intravenous
oxytocin, compared with inducing labour with prostaglandins (+/- oxytocin) or with expectant
management.46
• Neonatal infection is reduced among women who are GBS positive if labour is induced with intravenous
oxytocin, compared with inducing labour with prostaglandins (+/- oxytocin) or with expectant
management.44, 47 There is insufficient evidence to justify the routine use of prophylactic antibiotics with term
PROM in the absence of an indication for GBS prophylaxis.48-5194 05
Expectant Management
For women who are managed expectantly beyond 24 hours:
• No digital examination should be done in the absence of contractions.
• Women need to be advised to report any sign of infection or decreased fetal movement.
• Fetal movements and fetal heart rate should be evaluated every 24 hours.
• Asymptomatic healthy term babies born after 24 hours of PROM should be observed for the first 12 hours for
signs of infection.52
Management of PPROM (340 to 366 weeks’ gestation)

Optimal timing of delivery between 340 and 366 weeks in pregnancies complicated by PPROM is unclear. There is
evidence supporting expectant management for PPROM at less than 34 weeks, but there is no consensus on the optimal
management of pregnancies with PPROM and no spontaneous labour at 340 to 366 weeks. The 2010 Cochrane review of
planned early birth versus expectant management with PPROM prior to 37 weeks’ gestation did not add any clarity.53
The PPROMEXIL-2 trial and meta-analysis published in 2012 by Van der Ham et al. does not indicate that IOL
substantially improves pregnancy outcomes compared with expectant management.54 The authors concluded that the
risk of neonatal sepsis (suspected or confirmed) after PPROM near term is low and that IOL does not reduce this risk.
Induction does seem to reduce the risk of chorioamnionitis. There were no differences in respiratory distress syndrome
and Caesarean sections between the induction and expectant management group. A large multicentre trial of nearly
2000 women comparing active with expectant management in membrane rupture between 34 and 37 weeks showed

neonatal sepsis occurring in 2% of those induced and in 3% of those treated conservatively. Other neonatal morbidities
did not reach statistical significance. As far as maternal outcomes were concerned, expectant management carried some
risk of antepartum hemorrhage (RR 0.6, 95% CI 0.4-0.9), intrapartum fever and the use of antibiotics, but was associated
with a lower Caesarean section rate. The message from these authors was “in the absence of overt signs of infection or
fetal compromise, a policy of expectant management with appropriate surveillance of maternal and fetal wellbeing
should be followed in pregnant women who present with ruptured membranes close to term.”55
Antibiotics can be used in PPROM > 32 weeks’ gestation if fetal lung maturity cannot be proven and delivery is not
planned.56
The primary motivation for considering IOL earlier than 37 weeks’ gestation in the presence of PPROM is that the risks
associated with preterm birth are outweighed by those associated with maternal, fetal, and neonatal infectious morbidi-
ty.57-60
85 95
Care providers should:

• Not perform digital cervical examination.
• Assess for infection and obtain cultures.
• Undertake ultrasound assessment of fetal position, cervical status, and fluid volume.
• Administer antibiotics for GBS prophylaxis, if indicated.
• Consider transfer to a higher-level centre, if relevant.
• Consider IOL with oxytocin to reduce the risk of chorioamnionitis (at the expense of an increase in mild
neonatal morbidity, respiratory and metabolic).
• Inform women of the benefits and risks of IOL compared with expectant management.
• If management is expectant, assess for infection (monitoring maternal pulse and temperature, fetal heart
rate, presence of uterine tenderness or irritability, and WBC changes if indicated).
• If chorioamnionitis is suspected, administer appropriate antibiotics and deliver the infant.
Management of PPROM (< 34 weeks’ gestation)

For women who have PPROM at less than 34 weeks’ gestation, expectant management is usually preferred, and
attempts should be made to prolong the latent period. A Cochrane meta-analysis of antibiotic treatment with PPROM
(involving over 6000 women in 22 trials) found that the use of an antibiotic following PPROM reduced the risk of
chorioamnionitis, prolonged the latency period, and reduced markers of neonatal morbidity (such as neonatal infection,
use of surfactant, oxygen therapy, and abnormal cranial ultrasound).61 There are several different regimens of antibiotics
that can be used, although two regimes were used in the largest PPROM randomized controlled trials showing a
decrease in both maternal and neonatal morbidity. One recommended approach is “ampicillin (2 g IV every 6 hours)
and erythromycin (250 mg IV every 6 hours) for 48 hours, followed by amoxicillin (250 mg by mouth every 8 hours)
and enteric-coated erythromycin base (333 mg by mouth every 8 hours) for 5 days (Mercer protocol).”4, 57, 62 Another
approach described is erythromycin 250mg orally every 6 hours for 10 days. Azithromycin as well as clarithromycin can
be substituted for erythromycin in the appropriate doses63 without affecting latency or any other measured maternal or
fetal outcomes.56, 64, 65

Amoxicillin with clavulanic acid should not be administered as it appears to increase the risk of necrotizing enterocolitis
in the presence of PROM.61
Assessment of fetal lung maturity may be undertaken at the time of presentation by collecting pooled amniotic fluid
from the vagina with a syringe and angiocatheter. Fluid should be sent for fetal lung maturity indices.
A single course of antenatal corticosteroids is recommended between 240 and 336 weeks of gestation in women with
PPROM, and may be considered for women starting at 230 weeks who are at risk of preterm delivery within 7 days,
irrespective of membrane rupture.66-68 If chorioamnionitis is suspected, delivery is recommended, and expectant
76
management is contraindicated.
In certain circumstances (e.g., transfer), tocolytics may be considered in consultation with a tertiary care centre.66, 69, 70 The
use of progestogen does not prolong pregnancy in singleton gestations with preterm prelabour rupture of
membranes.71
Care providers should:
• Not perform digital cervical examination.
• Assess for infection; obtaining cultures, if indicated.
• Undertake ultrasound assessment of fetal position, cervical status, and fluid volume.
• Administer glucocorticoids between 240 and 336 weeks gestation.
• Administer antepartum antibiotics.
• Administer appropriate antibiotics and IOL if chorioamnionitis develops.
• Administer antibiotics for GBS prophylaxis, if indicated. Restart GBS prophylaxis at the onset of labour, if
indicated.
• Consider transfer to tertiary care centre, if appropriate.
Amniotic fluid may be collected from vagina to assess fetal lung maturity.
In the case of expectant management, maintain surveillance for chorioamnionitis (monitoring maternal pulse and
temperature, fetal heart rate, the development of uterine tenderness or irritability, and differential WBC changes if
indicated).
Summary
1. PROM/PPROM occurs for many different reasons and at any gestational age.
2. Digital cervical examinations should not be performed; sterile speculum examinations are appropriate to
confirm PROM/PPROM.
3. The primary motivation for considering IOL earlier than 37 weeks’ gestation in the presence of PPROM is that
the risks associated with preterm birth are outweighed by those associated with maternal, fetal, and neonatal
infectious morbidity.

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36. Petit C, Deruelle P, Behal H, Rakza T, Balagny S, Subtil D, et al. Preterm premature rupture of membranes: Which
criteria contraindicate home care management? Acta Obstet Gynecol Scand. 2018;97:1499-507. Available from:

37. Dussaux C, Senat MV, Bouchghoul H, Benachi A, Mandelbrot L, Kayem G. Preterm premature rupture of
membranes: is home care acceptable? J Matern Fetal Neonatal Med. 2018;31:2284-92. Available from: https://
38. Leduc D, Biringer A, Lee L, Dy J. Induction of labour. J Obstet Gynaecol Can. 2013;35:840-60. Available from:
39. Sadeh-Mestechkin D, Samara N, Wiser A, Markovitch O, Shechter-Maor G, Biron-Shental T. Premature rupture of the
membranes at term: time to reevaluate the management. Arch Gynecol Obstet. 2016;294:1203-7. Available from:
40. Royal Australian and New Zealand College of Obstetricians and Gynaecologists R. Term prelabour rupture of
membranes (Term PROM). Melbourne: 2014.
41. Mackeen AD, Durie DE, Lin M, Huls CK, Qureshey E, Paglia MJ, et al. Foley Plus Oxytocin Compared With Oxytocin
for Induction After Membrane Rupture: A Randomized Controlled Trial. Obstet Gynecol. 2018;131:4-11. Available
43. Pouralil L, Saghafi N, Eslami Hasan Abadi S, Tara F, Vatanchi AM, Motamedi E. Induction of labour in term
premature rupture of membranes; oxytocin versus sublingual misoprostol; a randomised clinical trial. J Obstet
Gynaecol. 2017:1-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28784054.
44. Money DM, Dobson S, Canadian Paediatric Society IDC. The prevention of early-onset neonatal group B
streptococcal disease. J Obstet Gynaecol Can. 2004;26:826-40. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/15361281.
45. Alfirevic Z, Kelly AJ, Dowswell T. Intravenous oxytocin alone for cervical ripening and induction of labour. Cochrane
46. Mozurkewich EL, Wolf FM. Premature rupture of membranes at term: a meta-analysis of three management
schemes. Obstet Gynecol. 1997;89:1035-43. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9170488.
47. Hannah ME, Ohlsson A, Wang EE, Matlow A, Foster GA, Willan AR, et al. Maternal colonization with group B
Streptococcus and prelabor rupture of membranes at term: the role of induction of labor. TermPROM Study Group.
48. Practice bulletins No. 139: premature rupture of membranes. Obstet Gynecol. 2013;122:918-30. Available from:
49. Nabhan AF, Elhelaly A, Elkadi M. Antibiotic prophylaxis in prelabor spontaneous rupture of fetal membranes at or
beyond 36 weeks of pregnancy. Int J Gynaecol Obstet. 2014;124:59-62. Available from: https://www.ncbi.nlm.nih.
50. Wojcieszek AM, Stock OM, Flenady V. Antibiotics for prelabour rupture of membranes at or near term. Cochrane

51. Saccone G, Berghella V. Antibiotic prophylaxis for term or near-term premature rupture of membranes:
metaanalysis of randomized trials. Am J Obstet Gynecol. 2015;212:627 e1-9. Available from: https://www.ncbi.
52. NICE Pathways N. Prelabour rupture of the membranes at term. London: 2011.
53. Buchanan SL, Crowther CA, Levett KM, Middleton P, Morris J. Planned early birth versus expectant management
for women with preterm prelabour rupture of membranes prior to 37 weeks’ gestation for improving pregnancy
outcome. Cochrane Database Syst Rev. 2010:CD004735. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/20238332.
54. van der Ham DP, van der Heyden JL, Opmeer BC, Mulder AL, Moonen RM, van Beek JH, et al. Management of late-
preterm premature rupture of membranes: the PPROMEXIL-2 trial. Am J Obstet Gynecol. 2012;207:276 e1-10.
55. Morris JM, Roberts CL, Bowen JR, Patterson JA, Bond DM, Algert CS, et al. Immediate delivery compared with
expectant management after preterm pre-labour rupture of the membranes close to term (PPROMT trial):
a randomised controlled trial. Lancet. 2016;387:444-52. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/26564381.
56. Yudin MH, van Schalkwyk J, Van Eyk N. No. 233-Antibiotic Therapy in Preterm Premature Rupture of the
Membranes. J Obstet Gynaecol Can. 2017;39:e207-e12. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/28859768.
57. Naef RW, 3rd, Allbert JR, Ross EL, Weber BM, Martin RW, Morrison JC. Premature rupture of membranes at 34 to 37
weeks’ gestation: aggressive versus conservative management. Am J Obstet Gynecol. 1998;178:126-30. Available
58. Kayem G, Maillard F. [Preterm premature rupture of membranes: active or expectant management?]. Gynecol
Obstet Fertil. 2009;37:334-41. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19356965.
59. Lim JJ, Allen VM, Scott HM, Allen AC. Late preterm delivery in women with preterm prelabour rupture of
membranes. J Obstet Gynaecol Can. 2010;32:555-60. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/20569536.
60. Mateus J, Fox K, Jain S, Jain S, Latta R, Cohen J. Preterm premature rupture of membranes: clinical outcomes
of late-preterm infants. Clin Pediatr (Phila). 2010;49:60-5. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/19643979.
61. Kenyon S, Boulvain M, Neilson JP. Antibiotics for preterm rupture of membranes. Cochrane Database Syst Rev.
62. Kwak HM, Shin MY, Cha HH, Choi SJ, Lee JH, Kim JS, et al. The efficacy of cefazolin plus macrolide (erythromycin or
clarithromycin) versus cefazolin alone in neonatal morbidity and placental inflammation for women with preterm
premature rupture of membranes. Placenta. 2013;34:346-52. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/23465535.

63. Chang KH, Kim HJ, Yu HJ, Lee J, Kim JS, Choi SJ, et al. Comparison of antibiotic regimens in preterm premature
rupture of membranes: neonatal morbidity and 2-year follow-up of neurologic outcome. J Matern Fetal Neonatal
Med. 2016:1-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27687157.
64. Pierson RC, Gordon SS, Haas DM. A retrospective comparison of antibiotic regimens for preterm premature
rupture of membranes. Obstet Gynecol. 2014;124:515-9. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/25162251.
65. Lee J, Romero R, Kim SM, Chaemsaithong P, Park CW, Park JS, et al. A new anti-microbial combination prolongs
the latency period, reduces acute histologic chorioamnionitis as well as funisitis, and improves neonatal outcomes
in preterm PROM. J Matern Fetal Neonatal Med. 2016;29:707-20. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/26373262.
66. Lee MJ, Guinn D. Antenatal use of glucocorticoids in women at risk for preterm delivery. UpToDate. Waltham
(MA)2007.
67. American College of O, Gynecologists Committee on Obstetric P. ACOG Committee Opinion No. 402: Antenatal
corticosteroid therapy for fetal maturation. Obstet Gynecol. 2008;111:805-7. Available from: https://www.ncbi.
68. American College of O, Gynecologists’ Committee on Obstetric P, Society for Maternal- Fetal M. Committee Opinion
No.677: Antenatal Corticosteroid Therapy for Fetal Maturation. Obstet Gynecol. 2016;128:e187-94. Available from:
69. Duff P. Preterm premature rupture of membranes. UpToDate. Waltham (MA): UpToDate, Inc.; 2008.
70. Medina TM, Hill DA. Preterm premature rupture of membranes: diagnosis and management. Am Fam Physician.
71. Quist-Nelson J, Parker P, Mokhtari N, Di Sarno R, Saccone G, Berghella V. Progestogens in singleton gestations with
preterm prelabor rupture of membranes: a systematic review and metaanalysis of randomized controlled trials. Am
J Obstet Gynecol. 2018;219:346-55 e2. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29614278.

Appendix
Appendix A
Reproduced with permission from: WJ Ehman, 2006. Reproduced with permission from: WJ Ehman, 2006.

Table of Contents
Chapter 19 Antepartum and Intrapartum Hemorrhage................................................................................................... 454

Definition...................................................................................................................................................... 454
Incidence....................................................................................................................................................... 454
Physiology..................................................................................................................................................... 454
Placenta Previa......................................................................................................................................................... 455
Definition...................................................................................................................................................... 455
Diagnosis...................................................................................................................................................... 458
Management................................................................................................................................................ 459
Delivery......................................................................................................................................................... 460
Summary....................................................................................................................................................... 461
Abnormal Placentation............................................................................................................................................. 461
Definition...................................................................................................................................................... 461
Diagnosis...................................................................................................................................................... 462
Management................................................................................................................................................ 463
Summary....................................................................................................................................................... 464
Placental abruption.................................................................................................................................................. 464
Definition...................................................................................................................................................... 464
Diagnosis...................................................................................................................................................... 466
Method and Timing of delivery..................................................................................................................... 466
Vasa Previa................................................................................................................................................................ 467
Definition...................................................................................................................................................... 467
Diagnosis...................................................................................................................................................... 468
Management................................................................................................................................................ 469
Diagnosis and Management of Antepartum Hemorrhage (General) ...................................................................... 470
Hemodynamically unstable woman............................................................................................................. 471
Hemodynamically stable woman.................................................................................................................. 471
Summary.................................................................................................................................................................. 472
Appendix A....................................................................................................................................................................... 479
Antepartum and Intrapartum Hemorrhage 453

Chapter 19
Antepartum and Intrapartum Hemorrhage
Definition
Antepartum hemorrhage is vaginal bleeding after 20 weeks’ gestation.
Incidence
Antepartum hemorrhage occurs in 2% to 5% of all pregnancies. The most common identifiable causes of significant
antepartum hemorrhage are:
• Placental abruption (incidence: 1 in 100 births)
• Placenta previa (incidence: approximately 1 in 200 to 300 births)
• Lower genital tract lesion
Physiology
In the non-pregnant state, the uterus receives approximately 1% of cardiac output, whereas in the third trimester it
receives approximately 20%. Uterine bleeding in the third trimester can be massive and can result in hemodynamic
instability.

Placental abruption and placenta previa are leading causes of perinatal morbidity and mortality in the third trimester.
Together, they account for slightly more than one half of the cases of antepartum hemorrhage.
Antepartum hemorrhage is a leading cause of maternal death in Canada.1 Placental abruption and placenta previa
account for 50% of hemorrhage-related deaths, with postpartum hemorrhage accounting for the other 50%.2
Intrauterine growth restriction is reported in 16% of women with placenta previa. Antepartum bleeding is associated
with an increased risk of preterm birth.3

Placenta Previa
Definition
• Placenta previa: The placenta is touching or covering the internal os at term
• Low-lying placenta: The leading edge of the placenta lies within 2 cm of the internal os at term
On second trimester ultrasound from 18 weeks to 23 weeks, placenta previa is diagnosed when the inferior placental
margin reaches or covers the internal cervical os on transvaginal scan. If on endovaginal ultrasound the inferior placental
margin is less than 2 cm from but does not cross the internal os, placentation can be considered normal (Figure 1.)
Incidence
The incidence of placenta previa at term remains approximately one in 200.4, 5
Risk Factors For Placenta Previa4

• Previous placenta previa
• Previous Caesarean section,6 especially when the interpregnancy interval is < 12 months7
• Previous uterine surgery, including myomectomy and dilatation and curettage
• Advanced maternal age (≥ 35 years)
• Multiparity (≥ 3)
• Smoking or cocaine use in pregnancy
• Multiple gestation
• Pregnancy resulting from in vitro fertilization
Classification
Previously, the classification of placenta previa was based on physical examination and transabdominal sonography that
would now be considered imprecise. It described a total (complete) previa as one that entirely covers the internal cervical
os, a partial previa as partially covering the cervical os, and a marginal previa as lying next to the os. The use of the terms
marginal and partial applied to the digital palpation of the placental edge through the cervix, which is has been replaced
in the modern diagnosis of placenta previa by more precise transvaginal ultrasound measurements. The contemporary
classification has been reviewed8 to address areas of controversy in placental location terminology. At term, if the
placenta reaches or crosses the internal cervical os on transvaginal ultrasound, the diagnosis is placenta previa and
the mode of delivery will be by Caesarean section (CS). If in the third trimester the inferior placental margin is low but
does not reach the cervix, “low-lying placenta” is the preferred terminology and vaginal delivery may be considered
depending on the distance between the inferior margin and the cervical os.

Historically, based largely on transabdominal ultrasound, the likelihood of bleeding during labour was found to be
greater when the placenta is within 2 cm of the cervix near term (see Table 1). High-resolution endovaginal ultrasound
has allowed refinement of this threshold. At 35 to 36 weeks’ gestation, the likelihood of safe vaginal delivery can be
predicted using a transvaginal scan measurement from the inferior placental margin to the internal cervical os. Although
based on a small number (approximately 250 women), the risk of bleeding during labour when the inferior placental
margin is less than 11 mm from the internal os is above 70%. A pre-labour CS is recommended. For distances between
11 and 20 mm, the risk of bleeding in labour is substantially lower, and a trial of labour is considered acceptable after
appropriate counseling.9 If a trial of labour is planned, Caesarean section and blood transfusion capability should be
readily available.
A distance greater than 2 cm is considered safe for vaginal delivery; however, significant vaginal bleeding has been
rarely described with a placenta-os distance greater than 2 cm.10, 11
Table 1. Studies of low-lying placenta in which the outcome was Caesarean section performed for bleeding
according to the placenta–os distance at or near term.
N PLACENTA–OS CAESAREAN SECTION PERFORMED FOR

DISTANCE, MM BLEEDING (% OF THOSE IN LABOUR)
Dawson et al.12 1 to 10 90
40
11 to 20 29
Bronsteen et al.13 1 to 9 73
86
10 to 20 27
Vergani et al.14 24 1 to 10 81
Vergani et al.14 29 11 to 20 0
Al Wadi et al.9 17 11 to 20 7.1

Figure 1. Diagnosis & Management of Placenta Previa

Figure 1. Diagnosis & Management of Placenta Previa
Figure 1: Used with permission from Salus Global Used with permission from Salus Global

Diagnosis
In the setting of undiagnosed vaginal bleeding in the late second and throughout the third trimester, pelvic
examination should not be performed until placenta previa has been ruled out. Placenta previa characteristically
presents clinically with painless vaginal bleeding in the second or third trimester. A small percentage of women with
persistent placenta previa at term do not experience bleeding before labour.
Obstetrical Imaging
The advent of ultrasound has dramatically changed the clinician’s approach to placenta previa. Sonography has become
the mainstay in diagnosing placenta previa. The goal is to clearly define the distance of the leading edge of the placenta
from the internal cervical os and to determine whether the placenta partially or completely covers the internal cervical os.
Transabdominal Sonography
Transabdominal sonography (TAS) performed in the second trimester will detect over 85% of placenta previa cases.
TAS evaluation of a placenta previa can be limited for several reasons, including poor visualization of a posterior
placenta,15 myometrial contractions, obesity, and underfilling or overfilling of the bladder.16, 17 For these reasons, TAS is
associated with a false positive rate of up to 25%18 and a false negative rate of 7%19 for the diagnosis of placenta previa.
Transabdominal ultrasound is inaccurate in the diagnosis of placenta previa and should be used only as a screening tool.
Transvaginal Sonography
Transvaginal sonography (TVS) is considered to be safe and is the gold standard for diagnosis,20 with a diagnostic
accuracy rate of 99%.21 Accuracy rates for TVS are high (sensitivity 87.5%, specificity 98.8%, positive predictive value
93.3%, negative predictive value 97.6%).22, 23 With TVS, the internal cervical os is seen as a discrete point, and the
distance from this point to the leading edge of the placenta can be accurately measured. This should be done any time
the placenta is situated low in the uterus and the distance from the os cannot be clearly delineated transabdominally.
The measurement in millimeters by which the inferior margin is clear of the internal os or across the internal os should
be reported. (Figure 1).
In the case of placenta previa with active bleeding, the clinician must proceed with caution, although TVS has been used
safely in women with mild to moderate bleeding from a placenta previa.22, 24

Management
Clinical management
Most diagnoses of placenta previa are now made by routine second trimester ultrasound. If suspected on TAS, TVS can be
used safely to verify the edge of the placenta and to accurately measure the shortest distance from the internal os.23 The
gestational age when placenta previa is diagnosed is critical to management.
“Placental migration” involves the leading edge of the placenta apparently moving away from the cervical os as
pregnancy progresses into the late third trimester.17, 25, 26 This is due to differential growth and development of the lower
uterine segment in the third trimester.17, 25, 26 At 11 weeks to 14 weeks, approximately 40% of placentas will cover the
internal os, yet by 18 weeks to 23 weeks, only 4% to 5% of women will have a low enough placenta on TAS to warrant
TVS.27 On TVS, most of these will be found not to reach or cover the internal os. Only 1% to 2% of women will be found to
have a placenta that reaches or covers the internal os on TVS at 18 weeks to 23 weeks.
In observational studies of 16 000 women, if the inferior margin of the placenta was found not to reach or cover the
internal os on the 18- to 23-week TVS, the incidence of persistent placenta previa at term was zero. Therefore, unless
the placental margin reaches or covers the internal os on the 18- to 23-week TVS, placentation can be considered
normal.17, 19, 23, 28, 29 Follow-up ultrasound is usually not required.23 It is important to evaluate the placental insertion
and the lower uterine segment around the inferior placental margin with Doppler to detect possible vasa previa (see
section on vasa previa below). If there is any suspicion of vasa previa, follow-up ultrasound is indicated.
If the placenta reaches or covers the internal cervical os on second trimester TVS, then follow-up ultrasound is
recommended to determine placental localization nearer term. In many of these women, placenta previa resolves,
leaving only 0.3% to 0.4% with persistent placenta previa at term.19
If placenta previa is diagnosed in the second trimester in an asymptomatic woman, there is no evidence for or against
restriction on maternal activities. Ultrasound examination should be repeated in the third trimester at 30 to 32 weeks’
gestation to re-establish the position of the leading edge of the placenta. The likelihood of persistence of a placenta
previa increases according to the gestational age at which it is first diagnosed.30 If TVS shows that the placenta overlaps
the internal cervical os by ≥ 2.5 cm at 20 weeks to 23 weeks, or by 2 cm after 26 weeks, vaginal delivery is unlikely.19, 20
Expectant management
In a hemodynamically stable woman with bleeding from placenta previa remote from term, a policy of expectant
management, pioneered by MacAfee,31 continues to be the standard. Hospitalization and aggressive transfusion and
delivery as soon as fetal lung maturity is demonstrated have been shown to decrease perinatal mortality.32 However,
46% of women with a diagnosis of placenta previa deliver preterm, usually because of antenatal bleeding.33 Hospital
admission with bed rest is an option, but carefully selected women with readily available access to intervention can be
managed as outpatients. Administration of corticosteroids in selected patients is advised. Almost 75% of all women
with placenta previa experience at least one episode of bleeding at a median gestational age of 29 weeks. The majority
remain stable for a prolonged period and will not require delivery until a median of 36 weeks’ gestation.34

Clinical outcomes of placenta previa are highly variable and cannot be predicted confidently from antenatal events.35
A number of retrospective studies and a randomized controlled trial provide evidence for the safety and cost-efficiency
of the outpatient management of placenta previa.35-38 Women selected for outpatient management are those who are
63 73
highly compliant, have no ongoing bleeding, are hemodynamically stable, live within a short travel distance from the
hospital, and have immediate access to transportation to the hospital.
A Cochrane systematic review did not demonstrate any advantage of home care versus hospital admission in the
following outcomes: episodes of bleeding requiring blood transfusion, Caesarean section, Caesarean hysterectomy,
episodes of bleeding, gestational age at delivery, respiratory distress syndrome, birth weight, intraventricular
hemorrhage, and neonatal sepsis.39
Delivery
The mode of delivery for placenta previa is CS in an institution where blood transfusions and adult intensive care are
available. Consent for possible total abdominal hysterectomy as a life-saving procedure in addition to Caesarean section
should be obtained. It should be clearly documented in the chart if the patient does not want blood transfusions (for
religious or other reasons), and these women should deliver in a tertiary care centre.
Delivery is recommended when the fetus reaches 37 weeks’ gestation, or in the presence of severe maternal hemorrhage
or abnormal fetal surveillance at any gestation.
There is a risk that the placenta may be incised during a low transverse incision at CS. This may cause increased maternal
and/or fetal blood loss. Rapid delivery of the baby will minimize blood loss. The patient should be counselled regarding
the increased risk for blood transfusion and Caesarean hysterectomy due to persistent placental implantation site
bleeding. Placental site uterine bleeding is not usually controlled by uterine muscle contractions and may require direct
suturing of the placental bed. Direct injection of dilute vasopressin (5 to 10 units in 20 mL of saline) into the bleeding
placental site can temporarily slow bleeding while these sutures are placed. The increased risk of placenta accreta
and its associated complications should be considered by clinicians involved in the management of placenta previa
and communicated to the woman.23 Surgeons should consider fertility preservation techniques before considering
hysterectomy.
In a woman with a low-lying placenta who is undergoing a trial of vaginal birth, the following precautions should be
considered:
• Minimize the number of vaginal examinations
• Do not strip membranes
• Do not use mechanical methods for cervical ripening
• Intravenous access throughout labour and delivery
• Group, screen and possibly cross match
• Be prepared for postpartum hemorrhage

Summary
1. Placenta previa is identified primarily by second trimester ultrasound.
2. Transvaginal ultrasound is recommended to confirm or refute the diagnosis whenever it is suspected on the
basis of transabdominal ultrasound. The distance from the inferior placental margin to the internal cervical
os or across the os should be reported.
3. Placenta previa is diagnosed when the inferior margin of the placenta reaches or covers the internal cervical
os on a second trimester ultrasound scan. If the inferior margin does not reach the internal cervical os,
placentation can be considered normal and no follow-up scan is required. Doppler study to preclude vasa
previa is indicated.
4. Placenta previa identified in the second trimester must be reassessed by ultrasound in the third trimester.
5. The majority of placentas that reach or cross the internal cervical os in the second trimester resolve by term.
6. At term, if the placenta lies within 10 mm of or crosses the internal cervical os, Caesarean section is indicated.
If the placenta is between 11 and 20 mm from the internal os, a trial of labour is reasonable with safety
provisions in place for possible hemorrhage.
7. Women with a low-lying placenta are at elevated risk of PPH: pre-delivery preparation and aggressive
management are indicated.
8. Premature birth is the primary fetal complication of placenta previa.
9. Selected women with asymptomatic placenta previa remote from term can be monitored in an outpatient setting.
Abnormal Placentation
Definition
Placenta accreta is the abnormal implantation of the placenta with villus attachment to the myometrium resulting in loss
of the normal cleavage plane.
Placenta increta refers to trophoblast invasion into the myometrium.
Placenta percreta is placental invasion through the entire wall of the uterus and beyond the serosa of the myometrium,
where it could invade the bladder and other pelvic organs.
Incidence
The incidence of placenta accreta has increased dramatically and is linked to the increased rate of Caesarean section. The
American College of Obstetricians and Gynecologists estimates that placenta accreta complicates 1 in 2500 deliveries,
a 10-fold increase over the past 50 years.40 A retrospective study of 64 359 deliveries between 1982 and 2002 reports
an increase in Caesarean section rates from 12.5% (1982) to 23.5% (2002) and an overall incidence of abnormally
invasive placenta (all forms) of between 2 and 90 per 10 000 births.41-43 A 2009 study by Flood et al. showed a decrease
24
in peripartum hysterectomy over the last 4 decades.44 However, placenta accreta as being the indication has increased
10-fold, coinciding with the increase in CS rate.

Placenta accreta is most commonly associated with both placenta previa and previous CS. The incidence of placenta
accreta in association with placenta previa (unscarred uterus) is approximately 3%.45 The incidence related to previous CS
is shown in Table 2.
Table 2. Placenta Previa and Placenta Accreta (Includes Increta and Percreta) by Number of Prior Caesarean
Sections
PROPORTION OF
PRIOR CAESAREAN CAESAREAN PLACENTA PREVIA, PLACENTA ACCRETAA PLACENTA PREVIA
HYSTERECTOMY A (%)
SECTIONS, N SECTIONS, N (%) (%) WITH ACCRETAB
(%)
0 6201 6.4 0.2 13 0.7
1 15 808 1.3 0.3 11 0.4
2 6324 1.1 0.6 40 0.9
3 1452 2.3 2.1 61 2.4
4 258 6 (2.3) 2.3 67 3.5
>5 89 3 (3.4) 6.7 67 9.0
a
Includes increta and percreta. P < 0 .001 from Cochran-Armitage test for trend
b
Increased risk with increasing number of Caesarean sections P < 0.001
Adapted from Silver et al.: Maternal morbidity associated with multiple repeat Caesarean deliveries. Obstet Gynecol 2006;107:1226-32.45
Risk Factors42, 46, 47

• Placenta previa
• Prior CS
• Prior myomectomy
• Asherman’s syndrome
• Endometrial ablation
• Submucous leiomyomata (fibroids)
• Maternal age greater than 35 years
Diagnosis
Placenta accreta should be considered in any woman with a placenta previa. Transabdominal and transvaginal
ultrasound48-50 can detect placenta accreta in up to 85% of cases. Additional investigations using ultrasound
94
Doppler51-54and MRI55-58 may be helpful to increase the detection of a placenta accreta in women at risk. Placenta accreta
25 35 65 75
is suspected on second trimester sonographic examination under the following findings.59

1. The loss of the “clear space” or hypoechogenic space between the placenta and myometrium. It is sensitive
but not specific.
2. Bladder line interruption. The interface between the uterus and bladder is represented on grey scale
sonography as a continuous white line. Its loss is seen best on transvaginal ultrasound with a partially filled
bladder; it is a result of increased vascularity in this space. Its specificity is 96% to 100%.
3. Presence of lacunae, which have high-velocity and low-resistance Doppler flow and are irregular in cross-
section on grey-scale ultrasound.
4. Myometrial thickness of less than 1 mm or loss of myometrial thickness higher in the uterus
The accuracy of diagnosis appears to improve when more than one ultrasound finding is present.
The goal is to diagnose placenta accreta during the antenatal period. Strong clinical suspicion is required in the presence
of risk factors. The clinician should aim to rule out an accreta before performing a Caesarean section. Women with
suspected placenta accreta should deliver in facilities with adequate resources and personnel to manage the potential
complications. In a vaginal delivery, if a lack of a clear cleavage plane is noted during attempted manual removal of
the placenta, clinicians should be aware that further forceful attempts to remove the placenta could result in severe
hemorrhage.60, 61
Management
The management of placenta accreta requires a multidisciplinary team approach involving representatives of
anaesthesiology, blood bank, and other services that may include interventional radiology, urology, and vascular
surgery.62 When the presence of a placenta accreta is known or suspected antenatally, delivery should take place in
a facility with the resources necessary to deal with the potential complications of this condition (preferably a Level III
centre).
Caesarean hysterectomy is required in up to 72% of cases.63 The treatment of placenta accreta requires clinical
judgement and will depend on the clinical situation and whether the diagnosis is made antepartum or intrapartum.
Factors that will influence management include the woman’s wish for future fertility, ease of placental removal, success
of suture hemostasis, amount of bleeding, patient condition, and whether there is a placenta accreta, increta, or percreta.
When bleeding is uncontrollable and the woman is at significant risk of hemodynamic collapse, Caesarean hysterectomy
may be necessary. The use of a temporary intra-abdominal aortic balloon is a promising technique to reduce blood loss
and the need for hysterectomy).64 The use of Cell Saver technology in obstetrics appears to be safe and has been shown
to reduce the need for blood transfusion during difficult surgical management of invasive placenta.65, 66
When the decision to perform a Caesarean hysterectomy is made antenatally, the uterine incision is made away from
the placental insertion, usually at the uterine fundus. Following delivery of the baby, the cord is clamped, the placenta is
left untouched to avoid excessive bleeding, and a hysterectomy is performed. Caesarean hysterectomy can be a complex
surgical procedure and requires a skilled pelvic surgeon.
Reports of successful conservative treatment in women who strongly desire future pregnancy have been published.
A 2007 study reviewed 60 carefully selected cases of conservative treatment in which either uterine preservation was
requested, or risk of damage to surrounding pelvic organs was extremely high because of placenta percreta. Success rate

in this study was 80%.63 However, in general, the number of reported cases has been small and a significant number of
the women in these studies experienced postpartum endometritis and late postpartum hemorrhage. For this reason,
conservative management could be attempted in very specific and select cases after multi-disciplinary approach and
patient informed consent.60, 61
Although there is no consensus with respect to the best time for elective delivery, the period between 34 and 35 weeks
appears optimal.67 Conservative treatments have included40, 68
• The insertion of a balloon catheter through the femoral artery into the internal iliac or the uterine vessels
before the surgery. The balloon is inflated during dissection to prevent excessive bleeding and the placenta
is left in situ. Postoperative embolization of the uterine arteries is carried out.
• Uterine or internal iliac artery ligation
• Curettage and/or over-sewing of the placental site in the case of a localized area of accreta
• Utero-vaginal packing
• Leaving the placenta in place and performing uterine artery embolization
• Leaving the placenta in place and undertaking close postpartum follow-up
Summary
1. The incidence of placenta accreta has increased significantly, mainly because of increased CS rates.
2. Placenta accreta should be suspected in the presence of a placenta previa, especially when there is a history
of prior uterine surgery.
3. The goal is to diagnose placenta accreta during the antenatal period.
4. Diagnosis is generally made by ultrasound; MRI can be used in certain cases.
5. Delivery should take place in a centre with the human resources and facilities to manage the potential
complications.
6. Management requires a multidisciplinary team in a tertiary care centre.62
7. A conservative approach may be attempted in selected patients.
8. Definitive therapy is Caesarean hysterectomy and should not be delayed in the case of severe hemorrhage.
Placental abruption
Definition
Placental abruption is the premature separation of the placenta from the uterine wall.
Physiology
Bleeding into the decidua basalis leads to placental separation. The most probable cause of the bleeding is a process
involving a separation between the decidua and the placenta. Hematoma formation may further separate the placenta

from the uterine wall and decreases the placental villous surface available for gas and metabolic exchange. If the
underlying condition is not self-limiting, bleeding will continue and may extend through the myometrium to the serosa
(a Couvelaire uterus). Bleeding may spread between the decidua and the fetal membrane and pass through the cervix
or may extravasate through the membranes into the amniotic fluid. The amount of blood seen vaginally often does not
correlate with the severity of the abruption.
Incidence
Placental abruption occurs in 0.5% to 1% of all pregnancies in North America.40, 69
Risk Factors
• All hypertensive disorders of pregnancy are important risk factors for placental abruption. A history of a
previous abruption increases the probability of recurrent abruption in subsequent pregnancies to between
5.5% and 16.6%.70
• Ischemic placental disease: there is evidence suggesting a link between preeclampsia, small for gestational
age, and abruption. It is as yet unclear if this triad is causal or simply an association.71
Predisposing Factors and Relative Risk40

• Prior placental abruption 10% to 25%
• Inherited thrombophilia 3% to 7%
• Preterm rupture of membranes 2.4% to 4.9%
• Hypertension 2.1% to 4.0%
• Iron deficiency72 2.4%
• Multiple gestation 2.1%
• Hydramnios 2%
• Chronic hypertension 1.8% to 3.0%
• Maternal age and parity 1.3% to 1.5%
• Smoking 1.4% to 1.9%
• Trauma
• Cocaine abuse
• Previous Caesarean section,6 especially when the interpregnancy interval is < 12 months.7
Most abruptions are idiopathic. 40

Diagnosis
1. Do not undertake a digital pelvic examination until placenta previa has been ruled out by prior or current
ultrasound
2. History and physical examination. Clinical differences will give the first clues to the diagnosis.
3. Placental abruption cannot be reliably diagnosed by ultrasound examination.
4. Once placenta previa has been ruled out, speculum examination should be performed to assess for lower
genital tract bleeding.
5. Electronic fetal monitoring (EFM) and ultrasound will assist in the assessment of fetal well-being.
6. Abdominal pain is usually the presenting symptom of placental abruption. It is generally constant and
greatest at the site of the placental attachment.
7. Uterine contractions, hypertonus, and/or irritability are present in most cases.
8. Vaginal bleeding is usually present and the clinician should be aware that the degree of vaginal bleeding
may not relate to the severity of the abruption.
9. Not all these signs and symptoms must be present to consider a diagnosis. For example, abruption without
vaginal bleeding (concealed abruption) is reported in some cases.
Method and Timing of delivery

Management depends on the hemodynamic condition of the mother, fetal well-being, gestational age, and the degree
of cervical dilatation. A classification of placental abruption that may prove useful in guiding management decision-
making is shown in Table 3. This classification is based on fetal condition. The degree of bleeding and the maternal
hemodynamic status will also influence management.
Table 3. Classification of Placental Abruption
ABRUPTION DEFINITION MANAGEMENT
Mild Evidence of abruption with no fetal compromise • Conservative management if preterm

• Initiate delivery if fetal maturity (induction
with continuous EFM if cervix favourable)
Moderate Evidence of abruption with fetal compromise • Emergency delivery regardless of gestational
age
• Induce if atypical EFM, favourable cervix, and
continuous EFM available
• CS if abnormal EFM or unfavourable cervix
Severe Evidence of abruption with fetal death • Initiate delivery process (non-emergent)
• Be vigilant for disseminated intravascular
coagulopathy

Vasa Previa
Definition
Fetal vessels in the membranes run across the cervical os in front of the presenting part. It can be found with a
velamentous insertion of the umbilical cord or with a succenturiate placental lobe25where
th
Edition
theofumbilical
the ALARMcordCourse
vesselsManual
are unsupported in the membranes. In these circumstances, the blood vessels may tear during spontaneous labour or
during spontaneous or artificial rupture of the membranes. Occasionally the vessels may rupture spontaneously in the
antenatal period.
Figure 2: Velamentous Insertion & Vasa Previa
Figure 2: Velamentous Insertion & Vasa Previa
Incidence
Vasa previa occurs in 1 in 2000 to 5000 pregnancies.72, 73 The incidence is higher in twin pregnancies (due to the
Incidence
Vasa previa occurs in 1 in 2000 to 5000 pregnancies.73, 74 The incidence is higher in twin pregnancies (due to the
increased incidence of velamentous cord insertion) and also in the presence of placenta previa.
Risk Factors
• Velamentous insertion of the cord
• Pregnancy following in vitro fertilization
• Placenta previa
• Presence of succenturiate lobe
• Twin pregnancy

When vasa previa is undiagnosed prior to labour, fetal mortality is estimated to be as high as 60%.75, 76
Antenatal diagnosis is not always possible; however, when antenatal diagnosis is made, up to 97% neonatal survival rate
is possible.77
Diagnosis
In the presence of risk factors, antenatal diagnosis should be considered. Using a standardized ultrasound screening
protocol in pregnancies with risk factors, Rebarber et al. identified 31 cases out of 27 573 pregnancies, for an incidence
of 1.1 per 1000.10
Routine documentation of the placental cord insertion during the second trimester ultrasound should be done to screen
for vasa previa.77 If vasa praevia is suspected, a repeat scan at 30 weeks is recommended since spontaneous resolution
of the vasa previa can occur. Women with a low-lying placenta on second trimester ultrasound should have the lower
uterine segment investigated with Doppler ultrasound to detect any errant fetal vessels near the internal cervical os.
Prenatal diagnosis is now possible using transvaginal ultrasound to observe fetal vessels crossing the internal os or
coursing within 2 cm of the os. A prenatal diagnosis mandates closer observation of the woman and delivery before
term by an elective CS. Some suggest hospital admission at 30 weeks to 32 weeks with CS at 35 weeks to 36 weeks.76
Occasionally, the vessels may be detected on routine ultrasound or felt on digital examination before rupture of the
membranes. A clinical diagnosis should be considered when rupture of the membranes is associated with acute painless
vaginal bleeding and an abrupt change in the fetal heart rate (tachycardia, bradycardia, or sinusoidal pattern). A bedside
Apt test or Wright’s stain on vaginal blood to detect fetal hemoglobin would suggest the diagnosis, although its clinical
utility is questionable and availability may be limited and should not delay management.

Figure 3: EV Ultrasound of Velamentous Insertion & Vasa Previa

Figure 3: EV Ultrasound of Velamentous Insertion & Vasa Previa
Management
Management
If vasa previa is diagnosed and persistent at 30 weeks, glucocorticoids and admission at 30 weeks to 32 weeks to a
centre with a isminimum
If vasa previa diagnosed Level
andIIpersistent
capabilityatcan
30 be considered.
weeks, The pediatric
glucocorticoids team should
and admission at 30beweeks
consulted antenatally.
to 32 weeks A
to a centre
planned Caesarean
with a minimum section
Level at 35 tocan
II capability 36be
weeks’ gestation
considered. Theispediatric
recommended. The patient’s
team should chartantenatally.
be consulted should be clearly labelled
A planned
with the diagnosis to facilitate immediate recognition and CS should rupture of membranes or vaginal bleeding occur.
Caesarean section at 35 to 36 weeks’ gestation is recommended. The patient’s chart should be clearly labelled with the
Delay may result in fetal or neonatal death and must be avoided. With this approach more than 97% neonatal survival is
diagnosis 75to facilitate immediate recognition and CS should rupture of membranes or vaginal bleeding occur. Delay may
expected.
result in fetal or neonatal death and must be avoided. With this approach more than 97% neonatal survival is expected.74
When vasa previa is not known to be present, rupture of the membranes associated with acute painless vaginal bleeding
When vasa previa is not known to be present, rupture of the membranes associated with acute painless vaginal bleeding
and an abrupt change in the fetal heart rate (tachycardia, bradycardia, or sinusoidal) make the clinical diagnosis.
and an abrupt change in the fetal heart rate (tachycardia, bradycardia, or sinusoidal) make the clinical diagnosis.
Immediate Caesarean section is required to prevent fetal exsanguination.
Immediate Caesarean section is required to prevent fetal exsanguination.

Diagnosis and Management of Antepartum

Hemorrhage (General)
1. Obtain history and perform physical examination. Clinical differences will give the first clues to the diagnosis.
Table 4: Comparative clinical presentation and risk factors of placental abruption and placenta previa (these are
NOT exclusive)
PLACENTAL ABRUPTION PLACENTA PREVIA
Age over 35 Multiparity78
In vitro fertilization Previous uterine surgery
Preterm labour Painless (unless in labour)
Smoker78 Uterus not tender
Hypertensive disorders (pre-existing and gestational) Uterus soft
Uterine over distension, abdominal trauma No uterine irritability/contractions
Abdominal pain or backache (often unremitting) Malpresentation or high presenting part
Uterine tenderness Fetal heart usually normal
Increased uterine tone Shock and anemia correspond to apparent blood loss
Uterine irritability/contractions Coagulopathy very uncommon initially
Usually normal presentation Transvaginal ultrasound is the definitive diagnostic test for placenta
previa.
Fetal heart may be absent, atypical or abnormal
Shock and anemia disproportionate with apparent blood loss
May have coagulopathy
Placental abruption may be seen on transabdominal ultrasound but a

negative ultrasound does not rule out abruption.
2. Determine hemodynamic stability and evaluate uterine tone and activity.

3. Evaluate fetal well-being including electronic fetal monitoring and ultrasound. Do not perform a pelvic
examination until placenta previa has been ruled out.
4. Perform an ultrasound examination to rule out placenta previa, if possible, before performing a speculum
examination. Speculum examination is performed to assess the cervix for dilatation or for any lower tract
lesion.
5. A team capable of performing an emergency Caesarean section should be available.

6. Given the inaccuracies in estimating blood loss and the maternal ability to withstand hemorrhage, it is
essential to maintain careful surveillance of the maternal hemodynamic status and fetal well-being.
7. Laboratory assessment should include
a. cross match blood
b. complete blood count (hemoglobin, hematocrit, platelet count)
c. other investigations dictated by the presence of comorbid conditions (e.g., hypertension)
8. Rh immune globulin should be given to all unsensitized Rh negative women with any bleeding or a
suspected concealed abruption.
a. A Kleihauer-Betke test is appropriate in this setting to assist in determining the required dose of Rh
immune globulin.
b. 300 mcg of Rh immune globulin should be given for every 30 mL of fetal blood detected in the
maternal circulation (equivalent to 15 mL of packed red blood cells).
a) Hemodynamically unstable woman

The two immediate objectives for those women actively bleeding and hemodynamically unstable are fluid replacement
and delivery.
While expediting delivery the following management steps occur concurrently:
• Ongoing assessment of maternal (vital signs, urine output) and fetal well-being.
• Active fluid resuscitation and/or blood transfusion through two large bore intravenous lines.
• Maternal oxygen saturation monitoring.
• Oxygen administration for all women who are hypotensive because oxygen consumption is increased 20% in
pregnancy and the fetus is sensitive to hypoxia.
If bleeding is due to a placenta previa or placental abruption and maternal or fetal health is compromised, a Caesarean
section will be necessary (unless vaginal delivery is imminent). Disseminated intravascular coagulation should be
considered. A bedside clot test (no visible clotting in 6 minutes at room temperature) may be helpful. If a coagulopathy
is present, it must be corrected immediately with fresh frozen plasma or cryoprecipitate. Delivery should be performed as
soon as the clotting factors have been corrected and volume replacement is adequate. A protocol for massive transfusion
is helpful. The risk of DIC is increased if the woman presents with an intrauterine fetal death.
If maternal and fetal status is stable and local resources are not available to manage the woman or her baby, consider
transfer to a high-risk centre.
b) Hemodynamically stable woman

• Continue maternal and fetal surveillance for 12 to 24 hours. Appropriate attention should be paid to the
maternal hemodynamic status.
• If the woman has suffered abdominal trauma and is ≥ 20 weeks’ gestation, it is recommended that she be
monitored for a minimum of four hours after the trauma. Placental abruption is seen in about 7% of such

cases. 79 If there is more than one contraction in 15 minutes or there are ominous signs such as bleeding or
78
uterine pain, the duration of surveillance should be longer (at least 24 hours).80-82
18
• If the fetus is preterm, expectant management may be appropriate depending on the maternal
hemodynamic status and fetal well-being. Antepartum corticosteroids are indicated for a gestational age of
24 weeks to 34 weeks. Weigh the risk of significant subsequent bleeding against fetal maturity.
• Transfer to a high-risk centre may be indicated based on the maternal or fetal condition and local resources.
• All women with an antepartum hemorrhage are at risk of recurrent bleeding.
Summary
1. A standard protocol for the management of antepartum hemorrhage is recommended.
2. A “massive transfusions” protocol is recommended in each delivery unit.
3. A medical directive for nursing and midwifery staff to initiate management is recommended.
4. The life-threatening nature of placental abruption and placenta previa for both woman and fetus should be
borne in mind, as should the potential for rapid evolution of these conditions.
5. Vigorous resuscitation should be undertaken when appropriate.
6. Ultrasound determination of placental location should precede pelvic examination when the situation
allows.
7. An antenatal diagnosis of vasa previa warrants the management course previously outlined in this document
to optimize fetal and neonatal outcome.
8. Ongoing surveillance of the maternal, placental, and fetal status and appropriate, active management are
required.

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69. Broers T KW, Arbuckle TE, Liu S. The occurrence of abruptio placentae in Canada: 1990 to 1997. Chronic Dis Can.
2004;25:16-20. Available from: http://www.phac-aspc.gc.ca/publicat/cdic-mcc/25-2/c_e.html.
70. Ananth CV, Getahun D, Peltier MR, Smulian JC. Placental abruption in term and preterm gestations: evidence for
heterogeneity in clinical pathways. Obstet Gynecol. 2006;107:785-92.
71. Ananth CV, Vintzileos AM. Ischemic placental disease: epidemiology and risk factors. Eur J Obstet Gynecol Reprod
Biol. 2011.

72. Arnold DL, Williams MA, Miller RS, Qiu C, Sorensen TK. Iron deficiency anemia, cigarette smoking and risk of
abruptio placentae. J Obstet Gynaecol Res. 2009;35:446-52.
73. Quek SP, Tan KL. Vasa Praevia. Aust N Z J Obstet Gynaecol. 1972;12:206-9. Available from: https://www.ncbi.nlm.
74. Lee W, Lee VL, Kirk JS, Sloan CT, Smith RS, Comstock CH. Vasa previa: prenatal diagnosis, natural evolution,
and clinical outcome. Obstet Gynecol. 2000;95:572-6. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/10725492.
75. Oyelese Y, Smulian JC. Placenta previa, placenta accreta, and vasa previa. Obstet Gynecol. 2006;107:927-41.
76. Oyelese Y, Catanzarite V, Prefumo F, Lashley S, Schachter M, Tovbin Y, et al. Vasa previa: the impact of prenatal
diagnosis on outcomes. Obstet Gynecol. 2004;103:937-42. Available from: https://www.ncbi.nlm.nih.gov/
pubmed/15121568.
77. Gagnon R, Morin L, Bly S, Butt K, Cargill YM, Denis N, et al. Guidelines for the management of vasa previa. J Obstet
Gynaecol Can. 2009;31:748-60.
78. Matsuda Y, Hayashi K, Shiozaki A, Kawamichi Y, Satoh S, Saito S. Comparison of risk factors for placental abruption
and placenta previa: case-cohort study. J Obstet Gynaecol Res. 2011.
79. Creasy RK RR, Lams Jd, Lockwood CJ, Moore TR, editors. Maternal fetal medicine: principles and practice. . 6th ed
ed. Philadelphia: WB Saunders; 2008.
80. Connolly AM, Katz VL, Bash KL, McMahon MJ, Hansen WF. Trauma and pregnancy. Am J Perinatol. 1997;14:331-6.
81. Pearlman MD, Tintinallli JE, Lorenz RP. A prospective controlled study of outcome after trauma during pregnancy.
Am J Obstet Gynecol. 1990;162:1502-7.
82. Dahmus MA, Sibai BM. Blunt abdominal trauma: are there any predictive factors for abruptio
placentae or maternal-fetal distress? Am J Obstet Gynecol. 1993;169:1054-9. Available from:

25
26th Edition
th
Edition of
of the
the ALARM
ALARM Course
Course Manual
Manual
Appendix A
Antepartum Hemorrhage
Antepartum Hemorrhage
Assess maternal hemodynamic

status and fetal well-being
Mother and fetus unstable
Resuscitation Mother and fetus stable
Continuing instability
• Ultrasound examination
• Fetal surveillance
Deliver and watch for DIC

Placental Abruption Previa Not Previa
Dead fetus ± Speculum:

Live fetus coagulopathy • Contact bleeding
• Inflammation / infection
• Labour
Condition Condition • Cervical lesion
abnormal/atypical normal Delivery (e.g., cancer)
(watch for DIC)
Deliver Gestational age Gestational age Follow-up

appropriately
Mature Immature Mature Immature
Vaginal delivery Consider: Caesarean section Consider:

or CS • Steroids (watch for accreta) • Corticosteroids
• Transfusion • Transfusion
• Transfer • Transfer
Antepartum
Appendix A and Intrapartum Hemorrhage 491
479
Table of Contents
Chapter 20 Prevention of Early-Onset Neonatal Group B Streptococcal Disease............................................................. 481

Introduction.............................................................................................................................................................. 481
Incidence....................................................................................................................................................... 481
Physiology................................................................................................................................................................ 482
Risk Factors............................................................................................................................................................... 482
Prevention................................................................................................................................................................ 483
Antepartum Screening.................................................................................................................................. 483
Culture technique..................................................................................................................................................... 484
Management............................................................................................................................................................ 485
Antepartum Management............................................................................................................................ 485
Intrapartum Management............................................................................................................................ 486
Antibiotic prophylaxis................................................................................................................................... 487
Current recommendations............................................................................................................................ 488
Recommended intrapartum antibiotic prophylaxis...................................................................................... 489
Management of Infants............................................................................................................................................ 489
Potential effects of intrapartum antibiotics on neonates and infants........................................................... 490
Current recommendations for infants of mothers who had an indication for GBS prophylaxis.................... 490
Summary.................................................................................................................................................................. 494
Prevention of Early-Onset Neonatal Group B Streptococcal Disease 480

Chapter 20
Prevention of Early-Onset Neonatal Group B
Streptococcal Disease
Introduction
Our understanding of how to prevent early-onset group B streptococcus disease in neonates is evolving, and there is, as
yet, no consensus.
Evidence from several population-based studies and the publication of guidelines from the Society of Obstetricians
and Gynaecologists of Canada,1 the Canadian Paediatric Society (CPS),2 and the US Centers for Disease Control and
Prevention (CDC)3 have led to the current recommendations.
Incidence
GBS is a gram-positive bacterium that causes invasive disease primarily in infants, pregnant or postpartum women,
and older adults (the highest incidence is among young infants).3 It remains the most significant cause of early-onset
sepsis in the term infant.4 Approximately 10% to 30% of pregnant women are colonized in the vagina or rectum. This
colonization may be transient, intermittent, or persistent.3
Without intrapartum antibiotic prophylaxis (IAP), approximately 40% to 70% of neonates born to GBS carriers will
be colonized. Of these infants, 1% to 2% will develop early-onset GBS infections, giving an overall incidence of
approximately 1.8 per 1000 live births.5
GBS disease can be early-onset (< 7 days) or late-onset (7 days to 3 months).
Coinciding with active prevention efforts in the 1990s, the incidence of early-onset GBS disease declined to
approximately 0.5 per 1000 live births in 19993 and to 0.24 cases per 1000 live births by 2014.6 An international 2012
systematic review of 42 studies (published 2000 to 2011; only 81% reported the use of IAP) estimated the global
burden of early-onset disease to be 0.43/1000 live births (95% confidence interval [CI] 0.37 to 0.49). The incidence was
highest in Africa (0.53), followed by the Americas (0.50), Europe (0.45), and Southeast Asia (0.11). The case fatality rate
was 12.1% 7
Widespread use of intrapartum antibiotic prophylaxis for GBS disease has led to concerns about the potential adverse
impact on the incidence of E. coli early onset neonatal disease, Reassuringly however, a 2017 US multistate review
by Schrag et al, covering the years 2005 to 2014 found no evidence of an increasing burden of early-onset E coli.
infections.8


GBS has been associated with stillbirth9 and is responsible for asymptomatic bacteriuria, urinary tract infection, and
chorioamnionitis during pregnancy.
GBS may cause endometritis and wound infection in the early postpartum period.
From 89%10 to 95%11 of neonatal early-onset GBS infection presents in the first 24 hours of life and may be characterized
by bacteremia, pneumonia, or meningitis. A 2003 case-control study found that nearly 40% of neonates with GBS
meningitis will be left with moderate to severe neurologic disability. The overall mortality rate ranges from 5% to
12%.1, 4, 7
Physiology
The maternal lower gastrointestinal tract is the primary reservoir for GBS and is the likely source of vaginal colonization.3
Early-onset neonatal infection may occur when the fetus aspirates GBS in amniotic fluid that has ascended from the
vagina after the onset of labour or rupture of the membranes, although GBS also can invade through intact membranes.3
Infection can also occur as the fetus passes through the birth canal. Most infants exposed to GBS will remain well but
may have their mucous membranes, gastrointestinal, and respiratory tracts colonized with GBS.3
Risk Factors
Significant risk factors for early-onset disease include:
• a previous infant with invasive GBS disease
• GBS bacteriuria (of any level of colony-forming units per mL)12 during current pregnancy
• maternal colonization with GBS (positive screening culture within 5 weeks of labour or membrane rupture)
When maternal GBS culture status is unknown, they also include:
• preterm labour (< 37 weeks’ gestation)
• amniotic membrane rupture ³ ≥18 hours
• intrapartum temperature ³ ≥ 38° C
A 2018 case controlled study from India, where routine antepartum GBS screening is not practiced (a risk-based
intrapartum antibiotic prophylaxis strategy is used) and where the incidence of early onset GBS disease is 0.55/1000
live births, found that >3 vaginal pelvic exams after rupture of membranes was a significant risk factor (OR 8.57 95% CI
3.10-23.6) for early onset GBS disease.13 The authors concluded that where antepartum screening is not available, their
findings should guide caregivers to reduce unnecessary vaginal examinations after ROM.
Note: If GBS status is unknown, knowledge of colonization status in a previous pregnancy may be considered along with
the above risk factors. Four retrospective studies published since 2008 have reported a GBS colonization recurrence rate

in a subsequent pregnancy of 38% to 53%.14-17 The authors of the 2015 review14 suggested that prior GBS colonization be
51 61
considered as an indication for intrapartum antibiotic prophylaxis in women with unknown GBS status.
It is important to note, however, that a 2008 retrospective review found that 38% of the 65 neonates diagnosed with
early-onset GBS had no recognizable antepartum or intrapartum predisposing risk factors (including known maternal
colonization).18 A more recent (2016) retrospective review from Winnipeg found that in the 13 cases of early-onset GBS
disease identified between 2009 and 2013, 9 of the mothers had screened negative for GBS.19 This emphasizes the
importance of the recommendation that any neonate presenting with signs of sepsis should be evaluated appropriately.
Prevention
The findings of a small prospective, double-blind randomized trial conducted in Taiwan suggest that probiotics may
reduce GBS colonization at the time of birth. The study compared oral probiotic (2 strains of lactobacillus) with placebo
given to GBS positive women at 35 to 37 weeks and found that 43% in the probiotic group were negative at delivery
compared with 18% in the placebo group.20 However, because of the trial’s limitations, more study is necessary to
corroborate these findings.
Antepartum Screening
On the basis of a large multicentre retrospective analysis21 and other supporting studies, including a 2015 systematic
review,22 it is recommended that all pregnant women be screened at 35 to 37 weeks’ gestation for GBS colonization and
that all positive women be treated with intrapartum antibiotic prophylaxis at the time of membrane rupture or labour.1, 3
The findings of these and other studies23 suggest that the universal screening approach is over 50% more effective than
the risk-based approach in preventing perinatal GBS disease. In addition, a 2017 meta-analysis of 14 studies provided
reliable evidence that prophylactic antibiotics for GBS-colonized women significantly reduce the vertical transmission
from colonized mothers to their infants and the risk of all cause infections, early onset GBS infection and non-GBS
infections.24
A 2009 systematic review found that the positive predictive value (PPV) of screening for the presence of GBS colonization
at delivery decreased when the interval between screening and delivery increased, especially if it was greater than 5
to 6 weeks. The PPV of cultures done before 35 weeks was 59% to 63% and of those done after 35 weeks, 70% to 93%.
Interestingly, the negative predictive value (NPV) of screening done before 35 weeks (90% to 93%) was only slightly
lower than the NPV (95% to 98%) found after 35 weeks. Because the accuracy of the PPV correlates with shorter duration
between culture and delivery, this review confirmed the recommendation to screen at 35 to 37 weeks. It also noted,
however, that antenatal testing will fail to detect GBS in approximately 6% of colonized women.
If a GBS screening culture is done before 35 to 37 weeks (e.g., threatened preterm labour) and any time that the
interval between the culture and delivery is > 5 weeks, it should be repeated.3, 25, 26
Applying a screening-based strategy will not necessarily increase antibiotic use.3 A 1998 to 1999 multi-state review
of labour and delivery records suggested that the perfect implementation of either the screening or the risk-based
strategies would result in the same proportion of women receiving intrapartum antibiotics (24%).21

There has been research on the applicability of using a rapid test to detect GBS status.27-31 A 2017 study of 902 women in
82 293
0
Denmark (where the GBS prevalence is 12%) concluded that in a population with a low prevalence of GBS, intrapartum
PCR assay performs better than the antepartum culture for identification of GBS vaginal carriers during labour.32 A 2015
study of 200 vaginal/rectal swabs submitted for GBS culture and 3 commercially available nucleic acid amplification
tests (NAATs) following 18- to 24-hour broth enrichment found the culture to be positive in 15%; however, 31.5% were
positive by at least 1 NAAT (sensitivity of the NAATs was 90.9% to 100%, whereas the sensitivity of culture was 53.6%).33
Concerns with intrapartum testing methods include the time the test would take to be reported and the absence of
sensitivity data for women who have anaphylactic allergy to penicillin.29 Although the 2010 CDC guideline states that
current data do not support NAAT, it also states that in settings where NAAT is available, a positive result could be an
indication for intrapartum GBS prophylaxis in the limited circumstance of a woman at term with unknown colonization
status and no other risk factors.3, 34
Culture technique
• A current standardized method should be used for collection, transport, testing, and reporting.
• It is essential that the result of the swab be available at the intended place of delivery and that the woman be
informed of the result and the recommended interventions.
A single swab should be taken from the lower one third of the vagina and then from the anorectum (through the anal
sphincter). Failure to swab the anorectum is associated with a significant false negative rate. A 2018 study form Denmark
reported an overall combined rectovaginal GBS colonization of 17%, however, 9.0% were colonized only in the vagina
and 13% colonized only in the rectum.23
• Cervical cultures are not recommended, and a speculum is not used.
• The swab should be placed in non-nutritive transport medium (e.g., Amies or Stuart). Although this medium
will maintain GBS viability for up to 4 days at room temperature, recovery does decline over this period, but
this can be minimized if the specimen is kept refrigerated. The sensitivity is greatest when the specimen is
stored at 4°C before culture and processed within 24 hours of collection.3
• There is evidence that self-collection of swabs by pregnant women, with appropriate instruction, in the clinic
examination room or washroom, is as effective as collection by care providers.35 However, a 2018 study of
422 Hong Kong women who performed self-screening (after instructions including a video) and also had
screening by a health care worker found the sensitivity of self-screening to be only 61% whereas that by the
health care worker to be 98%.36 The authors recommended that cultural difference needs to be considered if
implementing self-screening.
• If the woman is suspected to be allergic to penicillin
−− Skin testing can be done safely during pregnancy.
−− If she does not have confirmatory testing and has a history of a Penicillin allergy including a Type I IgE
hypersensitivity reaction and no documented allergy to cefazolin, she can safely receive cefazolin for
intrapartum prophylaxis37
›› Type I IgE hypersensitivity reaction includes: anaphylaxis, urticaria, angioedema, hypotension,
bronchospasm, stridor, pruritus

−− Recent literature has demonstrated that allergy cross reaction between penicillin and the
cephalosporins is due to similarities in their chemical side chains.
−− Cefazolin does not share a similar side chain to any penicillin or any other cephalosporin available in
Canada and can be safely administered in the case of suspected penicillin or cephalosporin allergy
other than to cefazolin itself.
−− If the reaction to penicillin or cephalosporins is a severe non-IgE mediated hypersensitivity reaction,
cefazolin should be avoided and sensitivity testing for positive GBS cultures should be requested.
›› Non-IgE mediated hypersensitivity reactions, usually > 72 hours after exposure include: delayed
reactions such as toxic epidermal necrolysis, Stevens-Johnson syndrome, drug reaction with
eosinophilia and systemic symptoms syndrome, severe hepatitis, interstitial nephritis, or hemolytic
anemia.38
›› Sensitivity testing for positive GBS cultures: Penicillin allergy should be stated on the culture
requisition along with a request to perform sensitivity testing for clindamycin. GBS has become
increasingly resistant to clindamycin (13% to 28%).3, 39, 40 A 2012 study of 309 GBS isolates in
Alberta found resistance clindamycin to be 22%.41
The following chart outlines the risk of GBS disease when antibiotics are not used in women with or without risk factors. It
indicates that neonatal GBS disease is most likely to occur when women screen positive and have risk factors.
Table 1: Risk of Early-Onset GBS Disease in the Absence of Antibiotic Prophylaxis
RISK FACTORS* PRESENT RISK FACTORS* ABSENT
Culture positive 1:25 1:200
Culture negative 1:1100 1:3200
Culture unknown (or not done) 1:120 1:800
*In this study, the risk factors (different from those currently recommended by the CDC)3 were defined as preterm labour (< 37 weeks), prolonged membrane rupture (> 12 hours),
or intrapartum fever (> 37.5°); these are slightly different from those used in the current guidelines.42
Management
Antepartum Management
Women with antepartum GBS urinary tract infections (symptomatic or with colony counts >100 000 CFU/mL
[108 CFU/L]) should be treated with appropriate antibiotics for the prevention of adverse pregnancy outcomes such as
pyelonephritis.43 Asymptomatic women with GBS colony counts < 100 000 CFU/mL in pregnancy should not be treated
with antibiotics for the prevention of adverse maternal and perinatal outcomes such as pyelonephritis, chorioamnionitis,
or preterm birth.43 If antibiotics are given to treat GBS bacteriuria, they typically do not eliminate GBS colonization.3 Women
found to have GBS bacteriuria in any concentration should be regarded as colonized at delivery. They do not require
further GBS screening and should receive antibiotic prophylaxis in labour.3

There is no benefit in treating women with positive GBS vaginal cultures before labour or membrane rupture.3
Research continues on development of a vaccine that could be administered to pregnant women and potentially provide
protection for infants during their period of vulnerability to GBS invasive disease (up to 3 months of age).44
Intrapartum Management
No method prevents all GBS disease. Women should be advised that current management approaches will not always
eliminate GBS disease.
A 2014 Cochrane review45 identified only 3 RCTs (n = 500) of intrapartum antibiotics for known maternal GBS
colonization, and noted serious concerns with all 3 regarding bias. The review concluded that intrapartum antibiotic
prophylaxis appears to reduce neonatal early-onset GBS disease but that there was a lack of evidence from well-designed
and conducted trials. Intrapartum antibiotics compared with no treatment for GBS-positive women resulted in the
following:
• A significant reduction in the incidence of early-onset GBS infection (RR 0.17; 95% CI 0.04 to 0.74;
number needed to treat to benefit (NNTB) 25, 95% CI 14 to 100)
• No statistically significant effect on
−− neonatal mortality from all causes, from GBS infection, or neonatal mortality from infections by bacteria
other than GBS
−− the incidence of late-onset (≥ 7 days) GBS infection
−− the incidence of neonatal sepsis, meningitis, urinary tract infection or pneumonia due to bacterial
organisms other than GBS
−− maternal peri- and/or postpartum sepsis, puerperal infection
Similar to the Cochrane review40 a 2018 review of the effectiveness of intrapartum antibiotic prophylaxis (IAP) (including
one systematic review, three clinical trials and five observational studies) concluded that studies have found IAP to be
effective. However the studies did have significant methodological flaws and have not considered the short and long
term risks of IAP.46
The aims of IAP are to:
• decrease maternal colony counts
• prevent ascending maternal infection
• achieve effective concentrations of antibiotic in the fetus during labour
The duration of intravenous antibiotic prophylaxis is important and will guide the management of the neonate.
Current guidelines recommend that prophylaxis with penicillin, ampicillin, or cefazolin given for ≥ 4 is optimal. A 2013
retrospective analysis of 7691 women estimated that the effectiveness of penicillin to prevent early-onset GBS disease
given for ≥ 4 hours was 89%; when given < 4 hours the effectiveness decreased to 38% to 47%.47 A 2014 prospective
study of 60 women who were vaginal-rectal culture GBS positive at 35 to 37 weeks found only 43 (72%) to be positive at
the time of labour. Of the 43 receiving IV penicillin G prophylaxis, 20 (47%) remained positive at 2 hours, and 5 (12%)
were still positive at 4 hours. This study supported the recommendation of a ≥ 4-hour optimal duration for IAP.48

However, when labour is progressing rapidly and is not expected to last ≥ 4hours, it is recommended that prophylaxis
be started as soon as possible because there is evidence that even a short duration of antibiotic therapy (e.g., 1 to 2
hours) will reduce the risk of neonatal colonization49 and early-onset GBS disease of the newborn.50 Furthermore, a study
of fetal penicillin G levels after maternal IV administration demonstrated that the levels peaked at 1 hour and that fetal
serum levels far exceeded the minimal inhibitor concentration at durations of well under 1 hour.51 The effectiveness
of antibiotics other than penicillin and cefazolin (e.g., clindamycin and vancomycin) given for a short duration before
delivery has not been demonstrated. Studies have reported that placental transfer of these antibiotics occurs but at a
slower rate.47, 52
Antibiotic prophylaxis
• IV penicillin G is the drug of choice unless the woman is allergic to penicillin. In North America GBS remains
universally susceptible to the penicillin and cefazolin. For women with for penicillin or cephalosporin allergy
(other than specifically to cefazolin) it is now recognized that it is safe to administer cefazolin.
• For women with documented cefazolin allergy or non-IgE mediated hypersensitivity reactions to penicillin or
cephalosporin, then penicillin and cefazolin should be avoided and sensitivities should be obtained.
−− Clindamycin should be used if the GBS isolate is sensitive to clindamycin. Maternal administration of
clindamycin has been shown to reach therapeutic cord blood levels within 1 to 2 hours.53 If the GBS
5455
isolate is resistant to clindamycin, vancomycin is indicated. GBS remains highly sensitive to vancomycin,
which also has a satisfactory transplacental passage.56 A 2018 prospective study from the USA concluded
that by 2 hours after vancomycin infusion vaginal GBS colony counts declined significantly to 6.7% of
the initial value and were essentially zero within 6 hours57
• A 2003 Alberta retrospective review of 90 cases of early-onset GBS disease (between 1993 and 1997),
before the recommendation for universal GBS maternal screening, identified intrauterine monitoring as an
independent risk factor for early-onset GBS disease (odds ratio [OR] 2.24; 95% CI 1.22 to 4.13).58 However.
a case-control study (covering the years 2000 to 2011) of 40 cases of early-onset neonatal sepsis (EONS)
made up of 8 GBS, 11 Escherichia coli, 12 coagulase negative staphylococci, 4 viridans group streptococci,
one Enterococcus faecalis, and 4 other non-specified organisms versus 80 controls, did not demonstrate a
significant relationship between fetal scalp electrode use and EONS.59
Although there is a theoretical concern about performing procedures such as membrane stripping and mechanical
and/or pharmacologic cervical ripening on GBS-colonized women, the 2010 CDC guideline suggested that “the
available data are not sufficient to determine whether these procedures are associated with an increased risk for early-
onset disease.”3 A 2015 prospective study of 542 women (135 were GBS+) treated with routine membrane stripping
beginning at 40 weeks, found no difference in maternal or neonatal outcomes.60
Topical chlorhexidine as a vaginal disinfectant in labour to prevent early-onset GBS infection was assessed in a 2014
Cochrane review. The authors reported that vaginal chlorhexidine was not associated with reductions in early-onset GBS
sepsis, and although it may reduce GBS neonatal colonization it was associated with increased maternal side effects
(stinging or local irritation). The conclusion did not support its use for the preventing early-onset GBS disease.61

A 2014 review of 309 cases of early-onset disease estimated that the potential reduction in cases with optimal
prevention implementation could have been as much as 26% to 59%. The most common errors were in prenatal
screening (36%) and intrapartum prophylaxis (54%). In 60% of cases, there was more than one error.62
Current recommendations
• Intrapartum antibiotic prophylaxis at the time of membrane rupture or labour should be administered for all
women who have had the following:
−− previous infant with invasive GBS disease
−− GBS bacteriuria during current pregnancy
−− positive screening culture, routinely done at 35 to 37 weeks during current pregnancy
• If GBS status is unknown, intrapartum prophylaxis should be administered for any of the following:
−− preterm labour (< 370 weeks)
−− rupture of membranes for > 18 hours
−− maternal fever ≥ 38ºC (this is best detected by core temperature measurement e.g., rectal).
Note: If GBS status is unknown, knowledge of colonization status in a previous pregnancy may be considered along with
the above risk factors. Retrospective studies published since 2008 have reported a GBS colonization recurrence rate in a
subsequent pregnancy of 38% to 53%.14-17
• Preterm labour with intact membranes
−− If GBS status negative within 5 weeks, antibiotic prophylaxis is not indicated.
−− If GBS status unknown, GBS vaginal/rectal screening should be performed on admission, and intrapartum
prophylaxis is recommended until the results of culture are known. Antibiotics may be stopped if culture
is negative.
• Prelabour rupture of membranes (PROM) and preterm PROM (PPROM) (management is discussed in the
chapter on PROM).
−− For women with term PROM who are colonized with GBS, it is recommended that intrapartum
prophylaxis be initiated and labour induced with oxytocin1, 63 or misoprostol.64 Analysis of data from
the Term PROM study found an overall decreased risk of maternal infection (as indicated by clinical
chorioamnionitis, antibiotics during labour, or postpartum fever) in women who were induced with
oxytocin compared with those in whom labour was induced with prostaglandin or who were managed
expectantly.65 For women colonized with GBS, the Term PROM trial also found that induction of labour
with oxytocin resulted in reduced rates of neonatal infection compared with those in whom labour was
induced with vaginal prostaglandin or who were managed expectantly.66
−− For women with PPROM (< 37 weeks) not in labour with unknown GBS status, IV GBS prophylaxis
should be given for 48 hours (or less if the GBS culture proves negative) along with additional
antibiotics, if indicated (e.g., to prolong latency), while awaiting spontaneous or obstetrically indicated
labour.1
• Situations in which GBS intrapartum prophylaxis is not indicated:
• Previous pregnancy with a positive GBS screening culture (unless a culture was also positive within 5 weeks
in the current pregnancy).

• Planned Caesarean section performed in the absence of labour or membrane rupture (regardless of
maternal GBS culture status). However, routine 35- to 37-week GBS culture is indicated in these women in
case they experience labour or PROM before the planned Caesarean section.3
• Negative vaginal and rectal GBS screening culture, within 5 weeks, regardless of intrapartum risk factors.
• Chorioamnionitis: regardless of GBS status, this diagnosis should be considered in the presence of is
maternal fever > 38°C, fetal tachycardia, and signs of maternal sepsis. Maternal oral temperature may
be inaccurate; consider rectal temperature measurement. If chorioamnionitis is present, treat with broad
spectrum antibiotics (e.g., ampicillin and gentamicin, cefoxitin etc.) and expedite delivery.
Recommended intrapartum antibiotic prophylaxis

• Preferred (narrow spectrum): IV penicillin G 5 million units, followed by 2.5 or 3 million units q4h
−− alternative: IV ampicillin 2 g followed by 1 g q4h
• In the presence of a penicillin or cephalosporin (other than cefazolin) allergy
−− administer cefazolin 2 g IV, followed by 1 g every 8 hours until delivery
• In the presence of documented cefazolin allergy or non-IgE mediated hypersensitivity reaction to penicillin
or cephalosporins
−− if the GBS isolate is sensitive to clindamycin,, administer clindamycin 900 mg IV, every 8 hours, until
delivery
−− if the GBS isolate is not sensitive (or unknown) to clindamycin administer vancomycin 1 g IV, every 12
hours until delivery.
Management of Infants
Management of asymptomatic infants of women who had an indication for GBS prophylaxis is based on clinical
presentation, the adequacy of the maternal intrapartum chemoprophylaxis, gestational age, the duration of membrane
rupture, and the degree of maternal fever if present.2,3 Studies have indicated that 89%10 to 95%11 of infants who
develop early-onset GBS infection have clinical signs within 24 hours (e.g., temperature instability, tachycardia, poor
peripheral perfusion, respiratory distress) or an abnormal CBC (e.g., total WBC count < 5.0x109/L or absolute neutrophil
count (ANC) <1.5 x 109/L). Four percent of infants will develop signs between 24 hours and 48 hours, and only 1% after
48 hours.67 A 2012 retrospective study of 140 000 women at a single centre found 94 neonates with early-onset GBS
sepsis. In 93, this was diagnosed in the first hour of life, and most of these had evidence of sepsis peripartum with an
increase in preterm delivery, Caesarean section, low Apgar scores, and abnormal umbilical cord pH and base deficit.68
• Adequate intrapartum antibiotic prophylaxis is defined as ≥ 4 hours of IV penicillin, ampicillin, or cefazolin
before delivery.3, 67
• Inadequate intrapartum antibiotic prophylaxis is defined as < 4 hours of IV penicillin, ampicillin, or
cefazolin before delivery or when alternative antibiotics (e.g., clindamycin, vancomycin) are used.
There is insufficient evidence regarding these alternative antibiotics to consider them adequate for purposes
of neonatal management.3, 67 This recommendation is supported by a 2013 retrospective analysis, which
found that although penicillin given for ≥ 4 hours was 89% effective in preventing early-onset disease, this

decreased to 38% to 47% when given for < 4 hours.47 This same analysis reported that the effectiveness of
clindamycin was only 22%, even though the mean duration of administration for the women studied was 6.4
hours (whether or not clindamycin sensitivity was determined for these women was not addressed).47
Potential effects of intrapartum antibiotics on neonates and infants

• There is increasing interest in the effect of intrapartum maternal antibiotic administration on the neonate’s
microbiome. A 2015 study of 198 healthy term infants found that intrapartum antibiotics (including those
used for GBS prophylaxis and for prophylaxis at Caesarean section) were associated with changes in the
neonate’s gut microbiota. It appeared that breastfeeding modified some of this effect. The authors concluded
that further research is warranted to explore the healthy consequences of this association.69
• One concern about antenatal and neonatal antibiotic exposure is a potential increase in the child’s later
diagnosis of allergic disease.70 Two retrospective studies published in 2015 offer some reassurance, however.
−− A study from Pennsylvania of 492 women (who delivered vaginally) and their children found no
increase in atopic dermatitis when intrapartum antibiotics were used for < 24 hours.71
−− A study of 80 children with penicillin allergy and 724 without found that intrapartum antibiotics did not
alter the risk of penicillin allergy.72
Current recommendations for infants of mothers who had an

indication for GBS prophylaxis
For full-term infants that appear well
• when the mother received adequate intrapartum antibiotic prophylaxis: there is no need for septic
work-up, additional therapy, or investigations. If these infants are well and other discharge criteria are
met, they may be discharged from hospital after 24 hours if those who will be caring for the infant at
home are knowledgeable about the signs of sepsis and have ready access health care resources.2, 3 This
recommendation is supported by Berger et al. (2012), whose cost-effectiveness analysis suggested that with
adequate IAP, discharging asymptomatic term neonates after 24 hours is preferred over 48 hours inpatient
observation.73
• when the woman received inadequate intrapartum antibiotic prophylaxis:
−− the CPS statement2 recommends careful in hospital assessment(e.g., close observation with vital signs
every 3 to 4 h) for at least 24 hours. A CBC is no longer routinely recommended. If the infant is well and
other discharge criteria are met, the infant may be discharged after 24 hours if those who will be caring
for the infant after discharge are knowledgeable about the signs of sepsis and have ready access to care.
If these conditions not met, infants should be observed in hospital for 48 hours.
−− the CDC guideline3 recommends that the infant should be observed for ≥ 48 hours:
›› for infants delivered at ≥ 37 weeks’ gestational age and when membranes ruptured <18 hours, no
routine diagnostic testing is recommended.
›› for infants delivered at < 37 weeks’ gestational age or when membranes ruptured ≥ 18 hours, a
blood culture and CBC with differential and platelets is recommended.

• For GBS-positive mothers who have additional risk factors (ruptured membranes ≥ 18 hrs or fever ≥ 38ºC),
whether or not they received adequate intrapartum antibiotic prophylaxis, the CPS statement2 recommends
clinicians consider the severity of each factor, the intrapartum antibiotic exposure, and clinical status of the
infant to determine an individualized management plan. Recommendations include close observation for
24 to 48 hours, and a CBC at 4 hours of age if needed for decision-making.
• A 2017 Irish retrospective study by Nielsen et al reported that of the 53 cases of EOGBS disease occurring in
112,361 births, only 3 had no clinical suspicion for sepsis.74 The number of blood cultures taken to detect
one case of GBS bacteraemia in an infant who is well at the time of testing was 3996. This study highlighted
that infected babies generally present early in the postpartum period meaning that an observational
approach in certain GBS-exposed infants could be considered safe
• A 2014 study of 38 infants with early-onset sepsis (including 10 cases of GBS) found that maternal
intrapartum antibiotic treatment did not prolong the incubation time required for blood cultures to become
positive.75
• Preterm infants require individualized evaluation and management. However, the CPS and the CDC
suggest that well-appearing infants delivered at ≥ 35 weeks’ gestation whose mothers receive adequate
intrapartum antibiotic prophylaxis do not need routine diagnostic testing or therapy for prevention of early-
onset GBS disease, but they should be observed for 48 hours before discharge home.2,3
• Infants of mothers with chorioamnionitis require close observation for at least 24 hours and individualized
strategies. These will often include a diagnostic and therapeutic evaluation for sepsis.
• In the case of a planned home birth, it is important that the same principles of care for the mother and
neonate are provided and maintained.
• Symptomatic infants are at very high risk for morbidity, so consultation, investigation, and treatment
should be undertaken early. There is no laboratory test that has sufficient sensitivity to rule out early-onset
sepsis. All infants with signs of sepsis must be treated immediately with IV antibiotics (e.g., amoxicillin
and aminoglycoside) following prompt investigation including CBC, blood culture, LP, and chest X-ray if
respiratory distress is present.2 These infants are best managed in an intensive care facility.
Signs of neonatal sepsis:
• Respiratory distress (apnea, tachypnea)
• Seizures
• Temperature instability, poor peripheral perfusion
• Tachycardia
• Lethargy, hypotonia
• Poor feeding
• Acidosis

Figure 1. Algorithm for the secondary prevention of early-onset group B streptococcal disease among newborns
Figure 1. Algorithm for the secondary prevention of early-onset group B streptococcal disease among newborns
YES Full diagnostic evaluationa

Signs of neonatal sepsis?
Antibiotic therapyb
NO
Close observationd for 24 hrs

YES Individualize management but will
Maternal chorioamnionitisc
oftene include limited evaluationf
and antibiotic therapyb
NO
NO
GBS prophylaxis indicated
Routine clinical careg
for mother
YES
YES Close observationd,g for

Adequate maternal
≥ 37 wks: 24 hrsI,j
intravenous prophylaxish
35–36 wks: 48 hrsj
NO
YES
≥37 weeks, no maternal fever and Close observationd,g for
membrane rupture < 18 hrs 24K –48 hrs
NO
YES
< 37 wks or maternal fever ≥ 38ºC Limited evaluationf
or membrane rupture ≥18 hrs Close observationd,g for ≥ 48 hours
a. CBC, blood culture, LP & CXR (if respiratory symptoms)

b. Antibiotics: ampicillin + coverage for other potential organisms (e.g., aminoglycoside)
a.c. CBC, bloodonculture,
Diagnose LP & CXR
clinical grounds: (iftender
fever, respiratory symptoms)amniotic fluid
uterus, purulent/foul
b.d. Close observation:
Antibiotics: in hospital,
ampicillin including for
+ coverage vitalother
signs every 3 to 4 hours
potential organisms (e.g., aminoglycoside)
e. With multiple risk factors, no intrapartum maternal antibiotics or mother unwell
c. f. Diagnose
CBC± blood onculture
clinical grounds: fever, tender uterus, purulent/foul amniotic fluid
d.g. Close observation:
If signs of sepsis p fullindiagnostic
hospital,evaluation
including vital signs
& antibiotic every 3 to 4 hours
therapy
e.h. Penicillin, ampicillin, or cefazolin for ≥ 4 hrs before delivery
With multiple risk factors, no intrapartum maternal antibiotics or mother unwell
i. May be discharged at 24 hrs if criteria are met and the parents/family have access to care
f. j. CBC± bloodis culture
If the infant well, and if those who will provide care for the infant at home are knowledgeable about signs of sepsis and have ready access to care
g.k. If Ifsigns of sepsis
maternal fever ≥→ 38ºCfull diagnosticrupture
or membrane evaluation
≥ 18 hrs:&observation
antibioticfor
therapy
24 to 48 hrs and consider CBC at 4 h
Modifiedh.from the
Penicillin,
2010 CDCampicillin, orthe
guideline3 and cefazolin
CPS 2017for ≥ 4 hrs2 before delivery
Statement

Figure 2. Management of Term Infants at Risk for Early Onset Bacterial Sepsis
Algorithm from the CPS Fetus and Newborn Committee, Position Statement, January 2017.2

Summary
1. No protocol prevents all GBS morbidity or mortality.
2. Women with GBS bacteriuria in the current pregnancy or who had a prior infant with invasive GBS disease do
not need to be screened and require intrapartum prophylaxis.
3. Screening of all other women at 35 to 37 weeks’ gestation (or within 5 wks of delivery) is recommended,
with intrapartum prophylaxis, if positive.
4. Antepartum treatment of GBS colonization is not justified with the exception of GBS urinary tract infection (≥
105 CFU/mL).
5. Individual centres must adopt strategies for GBS disease prevention.
6. All infants with signs of sepsis must be treated empirically with IV antibiotic once cultures have been taken.

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Table of Contents
Chapter 21 Venous Thromboembolism and Amniotic Fluid Embolus............................................................................. 502

Introduction.............................................................................................................................................................. 502
Definitions..................................................................................................................................................... 502
Incidence....................................................................................................................................................... 503
Pathophysiology....................................................................................................................................................... 503
Risk Factors for Venous Thromboembolism, ................................................................................................. 505
Prevention of VTE...................................................................................................................................................... 506
Thromboprophylaxis .................................................................................................................................... 506
Consent ........................................................................................................................................................ 509
Diagnosis ................................................................................................................................................................. 510
Diagnosis of DVT ........................................................................................................................................... 510
Diagnostic Tests............................................................................................................................................. 510
Pelvic/Ovarian Vein Thrombosis.................................................................................................................... 512
Diagnosis of Pulmonary Embolism .............................................................................................................. 512
Diagnostic Tests............................................................................................................................................. 512
Management of DVT and Pulmonary Embolism in Pregnancy................................................................................. 515
Available Anticoagulants............................................................................................................................... 515
Non-Medical Management........................................................................................................................... 518
Anticoagulation during Pregnancy ............................................................................................................... 518
Caring for Women During the Acute Phase of Anticoagulation ................................................................... 519
Management of Labour and Delivery on PROPHYLACTIC Heparin............................................................... 521
Management of Labour and Delivery on THERAPEUTIC Heparin.................................................................. 521
Postpartum Management............................................................................................................................. 522
Summary.................................................................................................................................................................. 522
Amniotic Fluid Embolism.............................................................................................................................. 523
Venous Thromboembolism and Amniotic Fluid Embolus 501

Chapter 21
Venous Thromboembolism and Amniotic
Fluid Embolus
Introduction
The incidence of thrombophlebitis and deep vein thrombosis in pregnancy has decreased dramatically over the past
six decades. This reduction is very likely the result of reduced prolonged bed rest as an antenatal therapy and early
postpartum ambulation. However, pulmonary embolism remains a leading cause of maternal death.
This chapter reviews venous thromboembolism (VTE) in pregnancy and the puerperium:
• Associated risk factors
• Pathophysiology
• Signs and symptoms
• Diagnostic tools to investigate VTE
• Management of acute thromboembolic events
• Thromboprophylaxis to prevent VTE
• Care of women receiving anticoagulant medications
Definitions
Thrombophlebitis: Inflammation of the wall of a vein leading to clot (thrombus) formation at the site of the
inflammation.
Deep vein thrombosis (DVT): Thrombus formation in the deep veins, usually of the lower extremity but occasionally in
the pelvic veins.
Venous thromboembolism (VTE): A term that includes DVT and embolism of a thrombus that breaks free from venous
thrombosis and travels to another organ, usually the lung.
Post-thrombotic leg syndrome: leg pain, swelling, dermatitis, and ulcers caused by permanent damage to leg vein
valves from prior DVT.
Pulmonary embolism (PE): transport of a thrombus, usually from a DVT, through the venous circulation and heart
to the pulmonary circulation where it becomes trapped. Small emboli lodge in small lung vessels and can dissolve
spontaneously. Larger emboli can lead to cardiopulmonary failure and death.

Low molecular weight heparin (LMWH): a fractionated heparin given subcutaneously for VTE prophylaxis or therapy. It
has a better side effect profile than unfractionated heparin and does not require platelet monitoring; however it cannot
be reversed with protamine.
Incidence
The incidence of VTE is 1-2/1000 pregnancies; however, pulmonary embolism is responsible for 9.2% of maternal deaths
in the US. 4, 5
123 678910
In a large prospective health database in the United Kingdom, the incidence of VTE during the first and second trimester was
not elevated; however the incidence in the third trimester was 6-fold higher than in non-pregnant women.11 Additionally,
12
“The first 6 weeks postpartum was associated with a 22-fold increase in risk, with the peak occurring in the first 3 weeks
(postpartum). The rate then declined rapidly.” Despite this high relative risk, the absolute risk per birth is low.
DVT occurs most often in the left leg during pregnancy and in the puerperium.13-16 This is thought to be due to
41 51
compression of the left iliac vein by the right iliac artery the weight of the pregnant or postpartum uterus. PE occurs more
often postpartum than in pregnancy and is more often associated with Caesarean section. 9,10, 17 181920212223
Pregnant women with mechanical heart valves have a particularly high risk of VTE. Studies published in the 1990s
reported thromboembolic events in 7% to 23%, with valve thrombosis in 50%, leading to a mortality rate of up to 40%.24
More recent studies suggest that modern valves are safer, with associated mortality rates of 1% to 4%.24 Anticoagulation
of patients with mechanical heart valves is problematic because of a preference for warfarin, which is known to have fetal
effects.24 Involvement of a hematologist familiar with pregnancy and cardiology is recommended. Mitral valve stenosis is
also a risk factor for VTE and warrants prophylaxis.
Pathophysiology
Pregnancy and the puerperium predispose to the development of VTE because of increases in each of the factors in
Virchow’s triad:
Figure 1: Virchow’s triad

Coagulation proteins are generally elevated in pregnancy which favors blood clot formation. However, there is also
an enhancement of physiological fibrinolysis. The balance between these two physiological tendencies is not well
understood. Plasminogen activator levels return to normal within 1 hour of birth. 26 25
Table 1. Physiologic tendencies enhancing clot formation in pregnancy
HYPERCOAGULABILITY STASIS VESSEL WALL INJURY
• Increased clotting factors & fibrinogen27 • Decreased venous tone • Vascular damage during birth (Caesarean
• Increased platelet aggregation • Reduced venous flow from the legs section or assisted vaginal birth)29
30
• Decreased protein S, tissue plasminogen (uterine compression of pelvic veins)

activator, factors XI, XIII28
• Increased resistance to activated protein C

When a DVT occurs, prompt treatment must be initiated to reduce:
• Extension of the DVT
• Morbidity and mortality associated with pulmonary embolism (PE)
• Post-thrombotic leg syndrome
Pulmonary embolism is a leading cause of maternal death in North America and Europe. Post-thrombotic syndrome is
a permanent and disabling condition. Sixty-five percent of women who experience DVT during pregnancy will develop
venous insufficiency within 7 years – a higher proportion than in non-pregnant women.31
Table 2. Diagnoses associated with maternal deaths in Canada (excluding Quebec), 2002–2003 to 2009–2010
DIAGNOSIS N MATERNAL MORTALITY RATE PER 100 000 BIRTHS 95% CI

Ante- & intra-partum hemorrhage 15 0.7 0.4–1.1
Puerperal infection 18 0.8 0.5–1.4
Ectopic/abortion/molar pregnancy 19 0.9 0.5–1.4
Pulmonary & amniotic fluid embolism 30 1.4 0.9–2.0
Hypertension 34 1.6 1.1–2.2
Postpartum hemorrhage 34 1.6 1.1–2.2
Cardiovascular disease 67 3.1 2.4–3.9
Other indirect causes 44 2.0 1.5–2.8
Source: Canadian Institute for Health Information, Discharge Abstract Database32

Notes: - Diagnoses do not represent underlying cause of death. Cases could have more than one associated diagnosis hence sum of individual diagnoses exceeds the overall
maternal mortality rate.
- Manitoba data, which were incomplete for earlier years, were included from 2004–05.

Risk Factors for Venous Thromboembolism33, 34

In retrospective case-control studies from large databases, many risk factors have been associated with VTE in pregnant
and postpartum women.35 However, the magnitude of absolute risk with most risk factors is very small. To what extent
risk accumulates in women with more than one risk factor is unknown.36 Pregnant women with a potent thrombophilia
or personal history of VTE are at particularly high risk.
Table 3: Comparative incidence of VTE by risk factors37
RISK FACTOR RISK OF VTE (PER 1000 WOMAN-YEARS)
Use of third generation contraceptive pill 0.3
Pregnancy 1.23
Puerperium 3.2
Pregnancy in thrombophilic woman 40
Pregnancy and previous VTE 110
Table 4. Risk factors associated with VTE
GENETIC BEFORE PREGNANCY38 PREGNANCY RELATED34
Thrombophilias15, 39, 40 41
• Previous VTE44-46 • ICU admission
• Antiphospholipid • Caesarean section15, 48, 50
• Factor V Leiden 42-44 antibody syndrome • Operative vaginal delivery
34
• Protein C & deficiency Protein S 28 • Mechanical heart valve • Preeclampsia39, 48, 51, 52
• Antithrombin deficiency • Mitral valve stenosis • Pelvic surgery postpartum
• Prothrombin gene variant9, 27 • Family history of VTE45
46
• Bed rest 15, 38
• Age > 35 • Infection48
• BMI38, 47, 48 > 30kg/m2 • Multiple pregnancy
• Medical disease (e.g. nephrotic syndrome, • Gestational diabetes
sickle cell disease, inflammatory bowel • Dehydration
disease, cancer) • Postpartum hemorrhage
• Smoking • Preterm birth
• Atrial fibrillation • Stillbirth48
• Current IV drug use49 • Prolonged labour (>24 h)
• Parity ≥ 3
• Gross varicose veins
• Paraplegia49

Prevention of VTE
Women should avoid bed rest during pregnancy and should mobilize early after birth, particularly following Caesarean
section (CS). Compression and/or intermittent pneumatic compression stockings have been recommended during
periods of required bed rest. Intermittent ambulation is advised during prolonged air or automobile travel.
Selective screening for thrombophilia (e.g., factor V Leiden) on the basis of positive personal or family history of VTE is
cost-effective, but universal population screening is not.34, 54-56
53 5 575859
Thromboprophylaxis
Preventing VTE in hospitalized patients is a priority worldwide. The goal is to identify patients at elevated risk of
VTE and provide them with chemoprophylaxis – usually low molecular weight heparin (LMWH). This approach has
been shown to be beneficial for patients at particularly high risk of VTE (major orthopedic surgery, active cancer,
ICU admission, prolonged bed rest, prior history of VTE, and potent thrombophilia). However, for most hospitalized
patients who lack these risk factors, benefit is not well-established.60 Research using asymptomatic DVT as an outcome
is misleading, since more than 90% of asymptomatic DVT resolve without treatment.61, 62 The absolute risk of clinical
6364
VTE in most hospitalized patients is 1% or less, and randomized trials using clinical VTE as an outcome show little or
no benefit in most patients.63-65 Since LMWH therapy carries a risk of bleeding, newer guidelines have scaled back
recommendations and emphasize the importance of carefully weighing any reduction in VTE against bleeding risk. 66 65
In an effort to prevent mortality and morbidity from VTE in birthing women, the obstetrical profession also adopted this
approach. Women with a potent thrombophilia, antiphospholipid antibody syndrome, or personal history of VTE have up
to 10% risk of VTE during pregnancy.67, 68 Unless there is active bleeding or a high risk of bleeding, they should receive
LMWH during pregnancy and for at least four weeks postpartum. Withholding LMWH or switching to unfractionated
heparin at term can be considered to lower the risk of intrapartum and postpartum hemorrhage and to allow regional
anaesthesia. 697071
In an effort to extend this benefit to more birthing women, several professional organizations have published guidelines
that recommend LMWH for women with more common and less potent risk factors.49, 72, 73 Using relative risks from
case-control studies, dozens of risk factors have been incorporated into complex scoring tools that identify up to 50% of
birthing women as high-risk, including up to 85% of those delivering by CS.23, 74 Amid some controversy, the American
College of Obstetricians and Gynecologists has not followed suit.23, 75
These risk scoring tools have not been validated in prospective trials. When applied retrospectively to a birthing
population that did not receive heparin, they did not detect the few women who developed VTE.74 There is not
observational or experimental evidence that LMWH is beneficial for women with common risk factors, who make up
a vast majority of women identified as “high risk.” Cochrane reviewers have noted this lack of evidence and called for
randomized trials.76
The absolute risk of VTE for women with common risk factors is very low and is inadequately reported in guidelines.77, 78
Several factors inflate the implied benefit of LMWH:

• Case control studies have been used to provide relative risks for VTE without attention to the magnitude of
risk.
• Similar ICD 9/10 codes for superficial & deep thrombosis; amniotic fluid and venous pulmonary embolism;
and heparin prophylaxis vs. treatment inflate the incidence of VTE in case control studies by up to 100%.35, 79
• Screening studies of asymptomatic rather than clinical DVT have been used in a risk analysis model that
underpins several guidelines.80
• Data used to estimate VTE risk after CS is taken from non-pregnant general surgical patients who have a risk
that is ten-fold higher.53
• VTE risk for the full postpartum period has not been adjusted for the reality that LMWH is usually only given
for one week.77
The actual magnitude of postpartum VTE risk is very small and difficult to establish. The best prospective data comes
from a large prospective UK database. After CS, the postpartum incidence was 1.5/1000, or 0.35/1000 during the first
postpartum week. The highest risk was after stillbirth: 1.35/1000 during the first postpartum week. Assuming 70%
protection from LMWH approximately 4000 women would need to be treated for one week after CS and 1000 after
stillbirth to prevent one VTE (NNT=4000 and 1000 respectively).77, 81
Even women with multiple common risk factors have a low risk of VTE. In a scoring model based on the UK database
and validated using a Swedish database, a 20 Y/O woman with a BMI of 32 undergoing CS in labour has a VTE risk of
1.1/1000 over 6 postpartum weeks, or approximately 0.27/1000 during the first postpartum week. This gives a NNT of
4300.12 In a separate study, the RCOG risk scoring tool applied retrospectively to a birthing population of 6000 women
from one center yielded a NNT of 4800 for women who qualified as “high-risk”.74
When the NNT is high, the chances are greater that harm outweighs benefit. LMWH is a potent anticoagulant that
increases the risk of bleeding and wound complications compared with placebo. In general surgical patients, compared
with placebo, randomized trials demonstrated an increase in serious hemorrhage of 1.5% (number needed to harm
(NNH) = 67) and need for transfusion of 3.8% (NNH = 26).65
Since there are very few trials comparing LMWH with placebo in pregnant and postpartum women, the excess risk of
bleeding from prophylactic LMWH is unknown. Birthing women have a high physiological risk of hemorrhage, which
might put them at increased risk compared with general surgical patients. However, they are young, healthy, and
generally hypercoagulable, which might lower the risk. In women who received therapeutic doses of LMWH, the increase
in hemorrhage >1000 ml was approximately 4% (NNH = 25).68 If the risk from lower prophylactic doses of LMWH after
CS is only 0.5%, the NNH would be 200. Since the NNT to prevent one VTE is 4000, this means that 20 women would
have serious bleeding for every woman who avoided VTE.
LMWH also increases wound complications. In a large observational study of 1600 women with a BMI >30 and/or age
>35, LMWH increased the risk of significant wound separation after CS by approximately 2% (NNH=50).82 About half
of these women required re-admission. Again the NNH is much lower than the NNT, meaning far more women will
experience wound disruption than will avoid VTE.
It has been suggested that wound complications and harm from bleeding are less important than avoiding a potentially
fatal pulmonary embolus; however, fewer than 1% of all VTE episodes are fatal PE. Assuming 70% protection with LMWH,
the NNT to prevent one PE death is about 400,000.77 If LMWH increases the risk of major hemorrhage by only 0.25%

(1/400), then for every PE death avoided with LMWH, 1000 women will experience a major hemorrhage. Obstetrical
bleeding can be serious, and some of these may be fatal.
It has also been suggested that widespread postpartum LMWH prophylaxis has reduced maternal deaths from
pulmonary embolism in the UK. However recent data does not support this claim. Before the widespread use of heparin,
UK data demonstrated a five-fold decrease in triennial obstetrical pulmonary embolism deaths from 168 (1955–57) to
32 (1985–87), likely caused by the abandonment of postpartum bed rest. Since 1985, the number of triennial deaths
from PE has oscillated – up and down – between 18 and 48 (table 5). This three-fold fluctuation is within normal
statistical variance and similar that for deaths from amniotic fluid embolism, sepsis, and hemorrhage.83 Nonetheless,
improved LMWH prophylaxis for the small number of women with antiphospholipid antibody syndrome, potent
thrombophilias, or a personal history of VTE has very likely improved safety for women with these potent risk factors.
Table 5: Triennial UK Maternal Deaths (MBRACE 2016)
1955-1957 85-87 88-90 91-93 94-96 97-99 00-02 03-05 07-08 09-11 12-15
Sepsis 9 17 15 16 18 13 18 26 16 7
Amniotic Fluid
9 11 10 17 8 5 17 13 7 16
Embolism
Bleeding 10 22 15 12 7 17 14 9 14 13
Venous
168 32 33 35 48 35 30 41 18 30 20
Thrombo-embolism
Pregnant and postpartum women with rare clinical conditions that have a strong association with VTE should be
considered individually for LMWH prophylaxis. This includes:
• Medical comorbidities: (e.g., cancer, heart failure, active systemic lupus, inflammatory bowel disease or
polyarthropathy, nephrotic syndrome, type I diabetes with nephropathy, sickle cell disease.)
• Intensive care admission
• Orthopedic surgery in pregnancy
• Bedrest for three days or longer
Despite a paucity of evidence, clinical judgement is also warranted for women with uncommon combinations of
multiple, marked risk factors such as:
• Class III obesity (BMI > 40) and CS in labour.
• Family history of unprovoked or estrogen-related VTE
• Puerperal sepsis after CS
• Low-risk thrombophilia + family history of VTE
• Stillbirth with pre-eclampsia

Involvement of a hematologist may help guide decisions in complex cases, especially those involving thrombophilias
or a family history of provoked or unprovoked VTE. Potent thrombophilias for which LMWH is currently recommended
include:
• Homozygous Factor V Leiden
• Homozygous Prothrombin Gene mutation
• Heterozygous for both Factor V Leiden & Prothrombin Gene mutation
• Antithrombin III deficiency
• Protein S deficiency
• Protein C deficiency
LMWH is typically given once daily subcutaneously. Table 6 lists recommended prophylactic doses of LMWH based on
bodyweight.
Table 6: Prophylactic daily dose of LMWH49
WEIGHT ENOXAPARIN DALTEPARIN
< 50 kg 20 mg 2500 units
50 to 90 kg 40 mg 5000 units
91 to 130 kg 60 mg 7500 units
131 to 170 kg 80 mg 10,000 units
>170 kg 0.6 mg/kg 75 u/kg
Both LMWH and unfractionated heparin can increase the risk of neuraxial hematoma during epidural or spinal
anaesthesia. Consultation with an anaesthetist is recommended regarding necessary time delays between heparin
dosing and placement or removal of an epidural catheter or dural puncture for spinal anaesthesia.4
Unfractionated heparin is uncommonly used as it has an increased risk of heparin induced thrombocytopenia (HIT) and
osteoporosis compared with LMWH. However, women approaching delivery or at high risk of bleeding may be switched
to unfractionated heparin because it is shorter acting and reversible with protamine. Prophylactic unfractionated Heparin
is given subcutaneously every 12 hours.
Consent
Close scrutiny of the best available evidence shows that the incidence of VTE in women with common risk factors
listed in current obstetrical VTE guidelines is very low. The estimated benefit and harm from LMWH is not quantified
in guidelines. Without access to this information, it is not possible for women to consent to treatment. Giving therapy
without informed consent is not generally considered acceptable in modern medical practice.
The absolute risk of VTE in women with most common risk factors appears to be too low to warrant LMWH. This
includes BMI >30, age >35, smoking, parity > 3, varicose veins, pre-eclampsia, assisted vaginal birth, CS, postpartum

hemorrhage, diabetes, preterm birth, multiple gestation, and prolonged labour. Before LMWH can be recommended for
these women, randomized controlled trials of LMWH versus placebo are needed.77 Benefit and harm must be measured
and stratified by risk factors and this information made available to clinicians and birthing women. Given that the
magnitude of benefit in most women with risk factors is very small, the study sample size will need to be very large, and
the logistics will be daunting. However, when benefit of therapy is small, the chances are higher that harm outweighs
benefit, making it even more important to do the trials before implementing therapy.78 8384858687
Diagnosis
Diagnosis of DVT
The symptoms suggestive of DVT are non-specific and common in pregnancy. Approximately 50% of women thought to
have DVT on clinical examination have a negative ultrasound or venography. However, a high index of suspicion must be
maintained, and investigations and consultation with colleagues used liberally.
A missed diagnosis could be fatal!
DVT in pregnancy occurs in the iliofemoral or calf veins of the left leg 90% of the time.14
Signs and symptoms

• Leg pain and tenderness
• Swelling
• Warmth
• Positive Homan’s sign
• Left leg involvement (83% of DVTs)
• An isolated iliac vein thrombosis may present with vague lower abdominal or pelvic pain with diffuse pain
and swelling of the entire lower limb on the affected side.
Diagnostic Tests
Diagnostic tests may be non-invasive or invasive. If therapy will be altered by the performance of an invasive diagnostic
test, then the benefit outweighs the risk to the mother and fetus.
1. Duplex Doppler ultrasound (compression ultrasonography) 88-92 89909192
This is the initial test for suspected DVT in most centres. It

• is non-invasive
• has 95% correlation with venography in the non-pregnant population for popliteal and femoral veins (90%
sensitive and 99% specific for proximal deep vein thrombosis; 73% sensitivity for distal DVT)93

• is less sensitive for calf veins and pelvic vein thrombosis

• should be performed serially if suspicion of DVT persists despite an initial negative result
A positive result warrants treatment with anticoagulation. A negative result does not rule out a pulmonary embolus.
2. Impedance plethysmography89, 90
• Is no longer commonly used
• Measures changes in electrical impedance as the result of changes in blood volume within the limb
• Can rule out DVT when performed serially (at least 3 tests over 7 to 14 days)
The sensitivity and specificity of this test are compromised in late pregnancy because of physiologic compression of iliac
veins and the resulting decreased venous return.
Both duplex Doppler and impedance plethysmography have poor sensitivity in detecting a DVT in the calf veins. The
tests should be repeated if the first scan has a negative result but there is a high clinical index of suspicion. It is safe to
withhold treatment if serial studies are negative.94
3. Venography88
This is the gold standard for diagnosis of DVT.
• It is invasive and exposes the woman and fetus to radiation. The fetus is exposed to 0.05 rads (50 mrad)
when lead apron shielding is used
• It has a negative predictive value of 98% (if venography is negative, there will be no DVT 98% of the time)
Consider venography if duplex Doppler is unavailable or if the results are equivocal.
4. D-dimer
D-dimer is a fibrin degradation product that is present in the circulation when a thrombus (clot) is present. Measuring
D-dimer levels to exclude the presence of thrombosis is standard practice in non-pregnant patients. However, D-dimer
levels are elevated in normal pregnancy. Pregnancy-specific D-Dimer levels have not yet been established reliably
enough to be clinically useful.9596
5. Radioactive labelled fibrinogen scanning

This is contraindicated in pregnancy.
NOTE: Confirmation of thrombosis by either a non-invasive study or venography justifies treatment with
anticoagulation.33

Pelvic/Ovarian Vein Thrombosis

This rare but serious complication usually occurs within one week after delivery. It can present with fever, chills, nausea,
vomiting, leukocytosis, and adnexal or abdominal pain. The right ovarian vein is most commonly affected. When the
large pelvic veins (e.g., iliac veins) are involved in a thrombophlebitis process, the thrombus may extend into the inferior
vena cava.
Pelvic/ovarian vein thrombosis may be diagnosed with the use of ultrasound or duplex Doppler. Magnetic resonance
imaging or CT should be considered if clinical suspicion is high.
Diagnosis of Pulmonary Embolism

Signs and symptoms
The signs and symptoms of a PE are non-specific and have a poor diagnostic reliability. However, they should raise
clinical suspicion and prompt appropriate diagnostic testing and consultation.96
The most common symptoms of pulmonary embolism and their prevalence in pregnancy-associated PE are:
• Tachypnea 89%
• Dyspnea 81%
• Pleuritic pain 72%
• Apprehension 60%
• Cough 54%
• Tachycardia 43%
• Hemoptysis 34%
• Temperature >37.5° C (99.5° F) 35%
1. Diagnostic Tests
Early diagnostic testing is warranted whenever a diagnosis of PE is suspected. Pulmonary angiography is the gold
standard for the diagnosis of PE but is invasive and carries higher morbidity. Other tests accompanied by thorough
clinical evaluation are, in most cases, used first. These include the following:
a) Chest X-ray and electrocardiogram

• The chest X-ray is rarely, if ever, diagnostic. It is used in conjunction with a ventilation/perfusion (V/Q) scan to
rule out other causes of hypoxemia.
• Results of electrocardiogram are often normal or show non-specific changes.

b) Arterial blood gases

• Measurement of arterial blood gases in women with suspected PE is not diagnostic because arterial blood
gas measurements lack specificity and are only moderately sensitive for PE. Hypoxemia and hypocarbia occur
in conditions that simulate PE, and arterial oxygen tensions can be normal in patients with a minor PE.97
• Significant hypoxemia excludes hyperventilation as the cause of the patient’s symptoms, although this
condition is rare.
c) Ventilation / perfusion scan

This is the least invasive test, and it is therefore often used as the primary investigation.
• Minimal radiation to the fetus
• An inhaled radioactive agent (ventilation) combined with an intravenous injection of a radioactive agent
(perfusion) is administered. The combination of ventilation and perfusion assessments increases the
accuracy of the test over either used alone, especially in cases where other conditions such as pneumonia are
present.
• V/Q scans are reported as high, intermediate, or low-probability scans
• In 1990 the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study in non-pregnant
patients72 reported that:
−− Virtually all patients with a pulmonary embolus had an abnormal (high, intermediate or low-probability)
V/Q scan, BUT
−− Most patients without a pulmonary embolus also had an abnormal (high, intermediate or low-
probability) V/Q scan (sensitivity 98%; specificity 10%)
−− 88% of patients with high-probability V/Q scans had a pulmonary embolism on pulmonary
angiography, BUT
−− Only a minority of patients with a pulmonary embolus have a high-probability V/Q scan (sensitivity
41%; specificity 97%)
• A low-probability V/Q scan together with a low clinical suspicion for a pulmonary embolus essentially rules
out a diagnosis of pulmonary embolism
• A high-probability V/Q scan combined with a high clinical index of suspicion is diagnostic of a pulmonary
embolism
• An intermediate-probability V/Q scan is not helpful in establishing or excluding a diagnosis of pulmonary
embolism. In such circumstances further investigation is necessary. The following should be considered:
−− Duplex Doppler ultrasound (compression ultrasonography) to look for a DVT
−− Serial impedance plethysmography
−− Pulmonary angiography if high clinical suspicion is present and Duplex Doppler ultrasound and
impedance plethysmography are normal
−− The combination of a chest X-ray, a V/Q scan and pulmonary angiography exposes the fetus to less than
0.5 rad radiation (not associated with a significant risk of fetal injury in most studies)94
−− Spiral computerized tomography

In summary, the ventilation-perfusion scan can direct clinical decision-making when the results are normal or indicate
a high-probability of a pulmonary embolus. In other circumstances, spiral CT, pulmonary angiography, or CT pulmonary
angiography is indicated to rule out a PE.72, 98
d) Spiral computerized tomography

This is a non-invasive test that exposes the fetus to minimal radiation. It is accurate to at least the segmental, and
possibly the sub-segmental, branches of the pulmonary artery.
The single detector spiral CT has an 86% sensitivity and 93% specificity for pulmonary embolus in non-pregnant
patients.99 There is a risk in extrapolating the data from studies in men and non-pregnant women.100
It has a negative predictive value of 98%.20
The newer four-channel multi-detector spiral CT is faster and provides higher resolution, allowing for detection of smaller
and more distal emboli.
In some centres, the multi-detector spiral CT has replaced the V/Q scan as the first-line investigation for pregnant
women.20 However, it is important to understand that the hemodynamic changes in pregnancy offer a challenge to the
diagnosis of PE using even the latest CT technology. It has been recommended that in the presence of an abnormal chest
X-ray, CT be offered to diagnose a PE. A V/Q scan should be offered in the presence of a normal chest X-ray.100
e) Magnetic resonance angiography20

This is a fast, high-resolution test that involves no exposure to radiation.
Its sensitivity for isolated subsegmental, segmental, and lobar pulmonary emboli is 40%, 84%, and 100% respectively.
However, it has not been widely used in pregnant women
NOTE:
• Pregnant women with positive non-invasive investigations should be treated for pulmonary embolism
• Symptomatic pregnant women with negative non-invasive studies should undergo pulmonary angiography
since non-invasive tests may be negative in 57% of non-pregnant patients with pulmonary embolism
demonstrated on angiography and V/Q scans of low or intermediate probability
• Non-invasive tests often miss emboli that originate in the pelvic veins during pregnancy101, 102
f) Pulmonary angiography
This highly specific and accurate test is the gold standard for pulmonary embolism. It is, however, invasive and requires
right heart cardiac catheterization and contrast injection. It exposes the fetus to 0.25 rads. Side effects include patient
discomfort, allergic reaction to the injected contrast material, and renal dysfunction or failure.
Serious morbidity (1%) and minor morbidity in 5%103; 1 in 200 (0.5%) mortality.103

NOTE: There are significant implications to a diagnosis of deep vein thrombosis and/or pulmonary embolism. They
include:
• the need for long-term use of anticoagulation with its potential fetal and maternal risks
• the potential need for prophylactic anticoagulation in future pregnancies
• the impact on the woman’s future use of oral contraceptives and estrogen replacement therapy
Because of the seriousness of the diagnosis and the significance of its future implications, any woman suspected of
having venous thromboembolic disease must be aggressively investigated with definitive studies to confirm or rule out
the diagnosis prior to treatment.
Management of DVT and Pulmonary Embolism in

Pregnancy
1. Available Anticoagulants
The anticoagulants currently available for use during pregnancy include unfractionated heparin, heparin-like substances,
warfarin derivatives, and ASA.
a) Unfractionated heparin (UFH)

• Inhibits thrombin by activating antithrombin
• Prevents conversion of fibrinogen to fibrin
• Advantages:
−− Does not cross the placenta and is not teratogenic104
−− Does not cause bleeding in the fetus
−− Not secreted in breast milk
−− Anticoagulation is rapidly reversible with protamine sulfate (1 mg per 100 units of heparin)
• Disadvantages:
−− Usually administered more than once daily
−− Half-life may be shorter in pregnant than in non-pregnant women, so higher dosing may be required
−− Maternal bleeding is the greatest risk, but the risk is very low on prophylactic heparin therapy
−− Heparin-induced thrombocytopenia is a life-threatening complication that may occur in up to 3% of
non-pregnant patients.105
›› Heparin-induced thrombocytopenia usually occurs during the first 2 weeks of treatment
›› Close monitoring of the woman’s platelet count during this interval must take place
›› Once a heparin-induced thrombocytopenia develops, low molecular weight heparin cannot be
substituted for UFH.

›› It is recommended that if a woman is on UFH for more than four days that platelet counts be done
before neuraxial procedures to rule out HIT4.
−− Heparin-induced osteopenia is relatively common in patients given UFH for longer than 1 month. A
reduction in bone density occurs in up to 30% of non-pregnant women, and 2% to 3% will develop
symptomatic vertebral fractures. Heparin-induced osteopenia may not be rapidly reversible because
heparin is sequestered in bone for an extended time.104 Vitamin D and calcium supplements are
recommended for pregnant women who are on thromboprophylactic therapy. Yet research is showing
that at prophylactic dosing during pregnancy, bone loss may not be significant.6
b) Low molecular weight heparin (LMWH) and heparin-like substances67, 106, 107
• Advantages:
−− Usually administered once daily depending on maternal weight
−− Can convert to subcutaneous therapy faster following initial intravenous treatment with unfractionated
heparin
−− Longer half-life, better bioavailability, and a more predictable dose response than UFH108
−− Does not cross the placenta, and is not teratogenic104
−− Does not cause bleeding in the fetus
−− Not secreted in breast milk
−− The risk of heparin-induced thrombocytopenia exists but is much lower (<1%) than for UFH4, 105 It is
recommended that routine monitoring of platelet count is unnecessary.
• The risk of heparin-induced osteopenia is also lower with LMWH than UFH, and research suggests that at
prophylactic dosing during pregnancy, bone loss may not be significant.6
• Maternal weight-based protocols, using weights at 10 to 16 weeks’ gestation, are reliable, at least for women
at intermediate risk for VTE during Caesarean section.109
• Disadvantages:
−− More expensive than UFH
−− Cannot reverse anticoagulation effect with protamine sulfate
−− The longer half-life of LMWH raises issues of timing of an epidural
−− Half-life may be shorter in pregnant than in non-pregnant women, so higher dosing may be required6
−− Maternal bleeding is the greatest risk, but the risk is very low with prophylactic LMWH therapy
compared with therapeutic LMWH
−− Not yet demonstrated to be superior to unfractionated heparin for the treatment of DVT or PE in
pregnancy110
−− Weight-based dosing appears inappropriate in the treatment of acute VTE in pregnancy. While too early
to generalize across the class, weight-based dosing failed to provide therapeutic anticoagulation with
tinzaparin in a small 2013 study by Gibson et al.111
• Contraindications or cautions in use49
−− Known bleeding disorders
−− Active antepartum or postpartum bleeding
−− Women considered at risk for major hemorrhage (e.g., placenta previa)

−− Thrombocytopenia (platelet count < 75x109/L)

−− Acute stroke in previous 4 weeks
−− Severe renal disease
−− Severe liver disease
−− Uncontrolled hypertension (systolic blood pressure > 200 mmHg or diastolic blood pressure > 120
mmHg)
NOTE: Low molecular weight heparins should not be used for anticoagulation in pregnant women with prosthetic heart
valves because of the increased risk of valvular thrombosis (even in the face of apparent adequate anticoagulation).6, 112, 113
NOTE: The multi-dose vials of low molecular weight heparins contain benzyl alcohol as a preservative. Benzyl alcohol has
been associated with the uncommon but potentially fatal “gasping syndrome” in neonates. Because benzyl alcohol may
cross the placenta, LMWH preparations preserved with benzyl alcohol should not be used in pregnant women.114
c) Warfarin
• Inhibits vitamin K
• Blocks synthesis of coagulation factors II, VII, IX, and X
• Contraindicated during pregnancy because of potential fetal effects, BUT may still be considered in
pregnancy for women with mechanical heart valves6: advice should be sought from the appropriate
specialist.
• May be used for postpartum management
• Advantages:
−− Given orally
−− Safe during breastfeeding
−− Low cost
• Disadvantages:
−− Crosses the placenta (fetal anticoagulation)
−− Risk of fetal and neonatal hemorrhage particularly at the time of birth
−− Risk of teratogenesis (the exact level of risk is not known)
−− Congenital warfarin embryopathy (exposure between 6 and 12 weeks’ gestation) including nasal
hypoplasia and/or stippled epiphyses (chondrodysplasia punctata)30
−− May cause intrauterine growth restriction
−− Increase in CNS anomalies if given in the second or third trimester
−− Requires regular monitoring of international normalized ratio (INR) to achieve appropriate therapeutic
levels
For ongoing postpartum therapeutic anticoagulation with warfarin
• Postpartum therapy may be started on the day following delivery
• Administer 7.5 mg/day on postpartum day 1 and 2
• Overlap with intravenous heparin and adjust the dose until the INR is 2 to 3 times the control value for 2
consecutive days
• Monitor the level of anticoagulation by measuring the INR regularly once the woman is on a maintenance dose

d) Acetylsalicylic acid
• Inhibits platelet aggregation
• Advantages:
−− Inexpensive
−− Administered orally
−− Low dose ASA (<150 mg/day) administered in the second and third trimester has been found to be safe
for mother and fetus, but the safety of higher doses has not been determined104
• Disadvantages:
−− Crosses the placenta
−− Safety in the first trimester is unknown
−− Potential for birth defects
−− Maternal and neonatal bleeding
−− Not proven effective in the prevention or management of VTE in pregnancy
2. Non-Medical Management33
The woman should
• Have her legs raised as much as possible to reduce edema
• Not wear compression stockings (no controlled trials using compression stockings during pregnancy or
postpartum are available). Stockings increase the risk of post-thrombotic leg syndrome.
• Avoid prolonged sitting
3. Anticoagulation during Pregnancy

Management is constantly evolving, and there are wide regional differences. There is limited evidence favouring one
treatment over another. It is important to consult with local experts in hematology for guidance. Evidence supports the
following:
a) Initial treatment of a DVT with unfractionated heparin (UFH)
• Obtain baseline CBC, including platelets and activated partial thromboplastin time (aPTT).
• Administer an initial bolus of 5000 units IV
• Measure the aPTT 6 hours following the bolus
• Infuse at a rate of 30 000 units/24 hours
• Repeat the serum aPTT every 6 hours until therapeutic heparin levels are reached.
• Adjust the dosage to keep the aPTT at 1.5 to 2 times the control value for the relevant laboratory
• Repeat the aPTT or serum heparin level daily once stabilized in the therapeutic range. If the serum heparin
levels are being measured, serum heparin should be maintained at 0.2 to 0.4 IU/mL (an aPTT of 60 to 85
seconds)101
• Continue IV anticoagulation for 5 to 7 days

• Switch to subcutaneous unfractionated heparin or low molecular weight heparin

−− Unfractionated heparin:
›› Multiply the total 24-hour dose being administered by 1.5 and divide into 2 doses per day
›› This is usually approximately 12 500 units subcutaneously twice daily
›› Maintain the aPTT at 1.5 to 2.5 times the control
−− Low molecular weight heparin (e.g., a 50 to 70 kg woman):
›› Tinzaparin 175 IU/kg subcutaneously once daily
›› Dalteparin 200 IU/kg subcutaneously once daily
›› The dose is chosen to achieve an anti-Xa heparin level of 0.3 to 0.75 4 hours post-injection
›› No regular monitoring is necessary, but a single anti-Xa level taken in the third trimester
will ensure that the therapeutic range has been achieved, some experts suggest that regular
monitoring in high risk women may be beneficial87
›› Twice per day administration of LMWH during the third trimester appears to result in better
therapeutic levels
b) Longer-term treatment
• Unfractionated heparin or low molecular weight heparin should be used during pregnancy and can also be
given postpartum
• Warfarin can be used postpartum. Treatment is usually initiated with a combination of intravenous UFH and
warfarin. The unfractionated heparin is discontinued after approximately 5 days. If the woman is already
being treated with UFH or LMWH, add the warfarin for four to five days and then discontinue the heparin.
4. Caring for Women During the Acute Phase of Anticoagulation115

The 2017 SOAP guidelines recommend that women on anticoagulants be fully informed and have an advanced plan
for antepartum and intrapartum management. They add that a comprehensive interprofessional approach be followed.
Women on anticoagulants must be readily identified and the date and time of their last dose be known. Furthermore,
the team (which includes the woman and her family) needs to know if dosing can be held during labour and delivery, or
if conversion from LMWH to UFH can occur in advance of labour. Care providers should
• Direct women to rest until swelling is reduced and anticoagulation has reached therapeutic levels Monitor
coagulation laboratory values
• Carefully assess for unusual bleeding. Heavy vaginal bleeding, generalized petechiae, bleeding from
the mucous membranes, hematuria, or oozing from venipuncture sites should alert the care provider to
investigate further
• Ensure the presence of protamine sulfate in close proximity to the point-of-care
• Assess for muscle pain, tenderness, swelling, positive Homan’s sign, and dilated superficial veins
The 2017 SOAP guideline is the only guideline currently available specifically addressing pregnant women.
Their guideline includes excellent decision tools for urgent and emergent neuraxial procedures in the OB patient
receiving both UFH and LMWH. Those recommendations include very clear guidance on when to insert a spinal or
epidural and when to restart anticoagulants upon removal of epidurals.

Summary of recommended doses for prophylactic, therapeutic, and postpartum anticoagulation
POSTPARTUM VAGINAL
MEDICATION PROPHYLACTIC DOSE THERAPEUTIC DOSE POST-CS DOSE
DELIVERY DOSE
Unfractionated • 5000 IU twice daily33 5000 IU bolus and Restart the UFH 4 to 6 hrs post- Restart UFH 4 to 6 hrs after CS
heparin (UFH) OR ~30 000 IU daily delivery or removal of epidural or removal of epidural catheter
• 5000 IU twice daily (aPTT at 1.5 to 2.5 catheter (assuming bleeding is or spinal (assuming bleeding is
(first trimester) control)33 in control and a straightforward in control and straightforward
• 7500 IU twice daily epidural placement procedure- regional anesthesia procedure-
defer to anaesthetist for opinion) defer to anaesthetist for opinion)
(second trimester)
at therapeutic or prophylactic at prophylactic or therapeutic
• 10 000 IU twice daily
dose depending on the situation. dose, depending on the situation.
(third trimester)33 Safe in breast feeding.4, 84 Safe in breast feeding.4, 84
Dalteparin • 2500 IU if < 50 kg 200 IU/kg once Restart LMWH 4 to 6 hrs after Restart LMWH 4 to 6 hrs
• 5000 IU if 50 to 90 kg daily33 delivery or removal of epidural after delivery or removal
• 7500 IU if 91 to 130 kg catheter (assuming bleeding of the epidural catheter or
• 10 000 IU if 131 to 170 kg is in control and epidural spinal anaesthesia (assuming
• 75 U/kg/day if >170 kg procedure was straightforward bleeding is in control and
- defer to anaesthetist opinion) regional anaesthesia procedure
once daily33, 49
at therapeutic or prophylactic was straight forward-defer
dose depending on the to anaesthetist opinion) at
situation. Limited experience therapeutic or prophylactic dose
in lactating women. Safe in depending on the situation. Safe
breast-feeding.4, 84 in breast-feeding.4, 84
Tinzaparin • 3500 units daily if < 50 kg Weight-based dosing As above As above

• 4500 IU daily if 51 to 90 kg is not appropriate
• 7000 IU daily if 91 to 130 kg in achieving
• 9000 IU daily if 131 to therapeutic
170 kg anticoagulation111
• 75 U/kg/day if > 170 kg30, 49
Enoxaparin • 20 mg daily if < 50kg 1.0 mg/kg twice As above As above

• 40 mg daily if 51 to 90 kg daily or 1.5 mg/kg
• 60 mg daily if 91 to 130 kg once daily30
• 80 mg daily if 131 to 170 kg
• 0.6 mg/kg/day if > 170 kg49
Warfarin Contraindicated (except with Contraindicated 7.5 mg daily and adjust to keep No clear guidelines. Keep on
mechanical heart valves) (except with INR at 2 to −330, 33 UFH
mechanical heart
valves)

Management of Labour and Delivery on PROPHYLACTIC Heparin

The woman must be fully informed about the possible complications of anticoagulation. She must be instructed to
discontinue unfractionated heparin
• At the onset of regular uterine contractions
• 6 to 8 hours before the start of induction
• 6 to 8 hours before a planned Caesarean section
Low molecular weight heparin
Change to unfractionated heparin at 36 to 37 weeks’ gestation
• For preterm delivery
−− Discontinue at the onset of regular uterine contractions
−− 24 hours before a planned induction
−− 24 hours before elective Caesarean section.
Management of Labour and Delivery on THERAPEUTIC Heparin

1. Obtain an aPTT on admission.
2. Switch from low molecular weight heparin to intravenous unfractionated heparin and adjust the dose to achieve
a therapeutic level of aPTT, if not already done. It is common make the switch between 36 and 37 weeks.
3. Protamine sulfate, 1mg per 100 units of unfractionated heparin may be used to reverse an aPTT that
is above the therapeutic level. Do not give > 50 mg protamine sulfate over 15 minutes IV. The 2017 SOAP
guideline indicates that its use in pregnancy has not be studied. They are careful to indicate that a single case
study after 25mg IV before delivery was associated with a severe respiratory depression in the infant.4
4. Minimize trauma at the time of delivery:
−− Midline episiotomy, if an episiotomy is required
−− Avoid tears
−− Ensure good hemostasis at Caesarean section
−− There is a slight increase in hematoma formation in vaginal tears or episiotomies but no increase in
postpartum hemorrhage
5. Regional anaesthesia is contraindicated in women on therapeutic heparin.
6. Continue anticoagulation for three to 6 months after the thromboembolic event.
7. Be aware of patient risk factors, aim for early recognition, and practice prompt interdisciplinary management.
The Use of Regional Anaesthesia in Patients Receiving Anticoagulation

Intraoperative or postoperative anticoagulation after regional anaesthesia is thought to be safe. Ideally, LMWH should
not be given until 4 hours after removal of an epidural catheter.

• The Society of Obstetric Anesthesia and Perinatology (SOAP) have produced the only guidelines addressing
the special needs of the obstetric patient. Their guidelines are required reading in this field. (https://www.
ncbi.nlm.nih.gov/pubmed/29099429)
• The safety of using anticoagulants before regional anaesthesia is unclear. The Food and Drug Administration
reported cases of epidural or spinal hematomas with regional anesthesia in non-pregnant patients receiving
LMWH. The American Society of Regional Anesthesia has recommended that patients receiving higher doses
of LMWH should not receive regional anaesthesia for 24 hours from the last dose. In patients receiving low-
dose LMWH, needle placement for regional anesthesia may occur 12 hours after the last dose of prophylactic
LMWH or 24 hours after the last therapeutic dose of LMWH.6
Postpartum Management
• Heparin can be resumed 4 to 12 hours postpartum, if required. The clinical picture, presence of risk factors,
and the mode of delivery will influence management.
• If ongoing anticoagulation is required, oral warfarin or subcutaneous heparin can be prescribed. Both are
safe for breastfeeding.
• It is important to note that the available evidence reassures us that therapeutic doses of LMWH in pregnancy
does NOT increase the likelihood of a PPH or of a severe PPH.116
NOTE: Anticoagulation in women experiencing a VTE in pregnancy should continue throughout pregnancy and for at
least 6 weeks postpartum or for a total of 3 months of anticoagulation.30, 104, 117
Summary
1. Careful screening for risk factors for VTE in the antepartum period is critical.
2. The management of venous thromboembolism in pregnancy is ideally done in conjunction with a
hematology service.
3. Consultation with a perinatal centre is recommended.
4. There are local variations in management regimens, especially with respect to thromboprophylaxis in a
woman with a known thrombophilia or a family history of thrombophilia, with or without a previously
documented DVT or PE.
5. Women experiencing a DVT or PE in pregnancy or the puerperium require investigation for an underlying
thrombophilia once treatment is complete.
6. Functional tests of coagulation will be affected by the pregnant state and in the immediate postpartum
period.
7. Women with a history of VTE, potent thrombophilia or antiphospholipid antibody syndrome should be
recommended thromboprophylaxis with LMWH.
8. Randomized trials are needed to evaluate the magnitudes of risk and benefit from LMWH prophylaxis in
women with most other risk factors for VTE.

Amniotic Fluid Embolism

Amniotic fluid embolism (AFE) is a rare, but often catastrophic, complication of pregnancy. The estimated incidence
is between 1:15 200 and 1:53 800 births.118 The maternal mortality rate is between 11% and 44%.119 The perinatal
mortality rate is between 9% and 44%.118 In addition, increased risks of stillbirth, hysterectomy, and prolonged length of
hospital stay have also been observed.120
• Risk factors associated with AFE
−− Induction of labour120
−− Multiple pregnancy
−− Advanced maternal age
−− Operative delivery (vaginal and Caesarean section)120
−− Eclampsia
−− Polyhydramnios
−− Cervical laceration120
−− Tetanic uterine contractions
−− Tumultuous labour
−− Uterine rupture
• Pathophysiology121, 122
The basic mechanism of the condition is related to the effects of amniotic fluid on the respiratory,
cardiovascular, and coagulation systems. In normal labour, only 1 to 2 mL of amniotic fluid is transferred
to the maternal circulation so that enhanced communication between amniotic fluid sac and the maternal
venous circulation is necessary for AFE.
Amniotic fluid with mucin, fetal debris, vernix, lanugo, fetal hair, and fetal squamous cells coated with white
cells blood cells and granular debris is present in confirmed diagnoses. If meconium is present, the response
is more dramatic.
Once amniotic debris enters the venous system, it travels rapidly to the right heart and enters the
cardiopulmonary circulation.
The exact nature of the response is unknown but is probably immune mediated: direct myocardial
depressant effect, vasospastic mediators (histamines, prostaglandins, serotonin etc.) leading to shock and an
anaphylactoid state.
The hemodynamic response is biphasic: initial pulmonary hypertension and right ventricular failure
(within the first hour), followed by left ventricular failure.
Effects of hypotension and hypoxemia lead to multiple organ failure: cardiovascular collapse, renal
insufficiency, hepatic failure, seizures and coma.
Effects on hematological system: potent thromboplastin and antifibrinolytic activity trigger clotting in the
pulmonary vasculature and result in a consumptive coagulopathy.

• Clinical Features121, 123

General—can occur at any point during labour and delivery. Clinical manifestations are variable, making
diagnosis difficult:
−− Sudden, unexplained peripartum respiratory distress, cardiovascular collapse, and coagulopathy
−− Bleeding secondary to coagulopathy or uterine atony
−− Possible presentations:
›› Respiratory distress, cyanosis
›› Hypotension
›› Seizures or seizure-like activity
›› Fetal bradycardia
• Differential Diagnosis121
−− PE (patients experience more severe chest pain with PE than with AFE)
−− CHF (fluid overload and/or pre-existing heart disease)
−− Other: myocardial infarction, hypotension from sepsis, pulmonary aspiration, anaphylaxis, placental
abruption, reaction to local anaesthetic
• Management123, 124
Early diagnosis and treatment are the most critical factors associated with survival.123(The mortality rate is
very high within the first hour.121) If mother and baby are to survive, rapid delivery of the baby is essential.124
For the mother, aggressive respiratory and circulatory support and interventions must be provided as
required.124
−− Use a multidisciplinary approach122
−− Provide adequate oxygenation, avoid fluid overload
−− Treat PPH from any or all of atony, tear, consumptive coagulopathy
−− Give replacement of depleted hemostatic components as required for the development of consumptive
coagulopathy121
NOTE: A small 2013 study of case reports suggested that caution be used in the treatment of PPH in
the presence of consumptive coagulopathy in patients with AFE. “[T]he use of rVIIa to treat postpartum
hemorrhage in patients with severe consumptive coagulopathy and AFE was associated with worse outcome
compared with cohorts who did not receive rVIIa”. They went on to say “We recommend that the initial
therapy of AFE-associated consumptive coagulopathy should consist of blood component replacement,
including PRBC, FFP, platelets, cryoprecipitate, and possibly fibrinogen concentrate. We recommend that
rVIIa be used in AFE patients only when the hemorrhage cannot be stopped by massive blood component
replacement.”125

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Course Manual

Advances in Labour and Risk Management

ALARM Committee members – 26th Edition

Chapter 1 Communication .................................................................................................................................................. 9

Chapter 1 Communication .................................................................................................................................................. 9

Strategies for Effective Communication

Strategies to foster Interprofessional Care and Planning

• Debriefing unusual events or normal practices as a team

Use of Social Media

Content credibility • Only Share information from credible sources

Special communication situations

2. Communication in the Consultation Process18

PARENT REFERRING CAREGIVER CONSULTANT

Ensure the primary care provider is informed

Contact Introduce consulting and consultant physicians. Build relationship.

Communicate Give a concise story and ask focused questions.

3. Communicating About Adverse Events

Strategies for the Communication of Bad News

Some examples of phrases that could be useful include:

USEFUL TO SAY NOT USEFUL TO SAY

I wish things could have been different. Time will heal.

Just thank God for your healthy children at home.

You have to get on with your life.

Better luck next time.

Practice makes perfect.

It’s God’s will.

Effect of Adverse Events on Parents, Families and

Interpretation of the Event

Response and Coping Mechanisms

How Health Care Providers Can Help Patients to Cope

Coping Mechanisms: Care Providers

Adverse Events and Litigation

What do patients expect?

Meeting with the patient and/or family

Electronic Medical Record (EMR)

Passwords can expire if not frequently using a given facility EMR

Chapter 2 Evidence-Based Obstetrics................................................................................................................................. 34

Types of Evidence: Qualitative or Quantitative

26th Edition of the ALARM Course Manual

For example, a culture screening for group B streptococcus (GBS):

26th Edition of the ALARM Course Manual

0.01 0.1 1 10 100

Odds Ratio or Relative Risk (95% Confidence interval)

Outcome less likely Outcome more likely

0.01 0.1 1 10 100

Odds Ratio (95% Confidence Interval)

The results displayed in a meta-analysis fall into 1 of 3 categories:

The Grade Approach

QUALITY OF EVIDENCE GRADES

FACTORS THAT CAN REDUCE THE QUALITY OF THE EVIDENCE

Limitations in study design or execution (risk of bias) i 1 or 2 levels

Inconsistency of results i 1 or 2 levels

Indirectness of evidence i 1 or 2 levels

Publication bias i 1 or 2 levels

FACTORS THAT CAN INCREASE THE QUALITY OF THE EVIDENCE

Large magnitude of effect i 1 or 2 levels

Dose-response gradient i 1 level

IMPLICATIONS OF STRONG AND WEAK RECOMMENDATIONS

STRONG RECOMMENDATION WEAK RECOMMENDATION

Chapter 3 Patient Safety..................................................................................................................................................... 45

Understanding Error in Health Care

How did we come to be here?

Understanding why we fail