ALARM Manual 2016 Revised PDF

Advances in Labour and Risk Management
23rd Edition — 2016–2017
ALARM
Course Manual
The ALARM Course Manual is published by the SOGC.
Copyright SOGC 2016-2017. All rights reserved.
Reproduction of this material is not permitted without explicit written consent of the SOGC.
Views expressed in the document do not necessarily reflect those of the SOGC members.
Canadian Cataloguing in Publication Data
Main entry under title:
ALARM Manual 23rd edition
ISBN 978-1-897116-53-1
1. Health Care – Obstetrics
2. Labour – Risk Management
23rd 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 and midwives and obstetricians. It has had 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.
We hope that the course helps you as we learn together.
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.
Purpose 1
Recognition
This 23rd edition of the ALARM Course Manual was revised under the direction of the 2016 ALARM Committee members.
2016 ALARM Committee Members: 2016 Obstetrical Content

Review Committee Members:
Kim Butler (Co-Chair), MD, Fredericton, New Brunswick
Sharon Dore (Co-Chair), RN, PhD, Hamilton, Ontario P. James Ruiter, MD, London, Ontario
Heather Baxter, MD, Calgary, Alberta Suzanne Toni Wong (Co-Chair), MD, Toronto, Ontario
Gisela Becker, RM, Calgary, AB Amanda Ashe, RM, Antigonish, Nova Scotia
Virginia Clark, MD, Golden, British Columbia Christine Bloch, MD, Stratford, Ontario
Dean Leduc, MD, Ottawa, Ontario Sheri DeMeester, RN, London, Ontario
Catherine Cowal, MD, Oakville, Ontario Sharon Dore, RN, PhD, Hamilton, Ontario
Caroline Delisle, MD, Greenfield Park, Quebec William Ehman, MD, Nanaimo, British Columbia
Stephen DiTommaso, MD, Montréal, Quebec Robert Gagnon, MD, Montreal, Quebec
Veronique Mareschal, MD, Chicoutimi, Quebec Michael Geary, MD, Toronto, Ontario
Marie-Jocelyne Martel, MD, Saskatoon, Saskatchewan Jonathan Hey, MD, Saskatoon, Saskatchewan
Jonathan Hey, MD, Saskatoon, Saskatchewan Andrew Kotaska, MD, Yellowknife, Northwest Territories
Judy Scrivener (ALARM Coordinator), Ottawa, Ontario Dean Leduc, MD, Orleans, Ontario
Savas Menticoglou, MD, Winnipeg, Manitoba
Diane Sawchuck, RN, PhD, Vancouver, British Columbia
Courtney Green (OCR Coordinator), Ottawa, Ontario
Recognition 1
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 information should not be deemed inclusive or exclusive of all methods of care. The ultimate judgment regarding the care of
a patient must be made by the physician in an informed consultation with the patient, in light of all the circumstances presented
by the patient, the diagnostic and treatment options available, and access to the necessary support resources.
The ALARM program is provided for educational purposes only and is to be used as a tool in assessing the knowledge and skill
of the user. You are advised that it is one of the tools to be used to assess and assist you in upgrading your skills in the subject
matter provided by the program. SOGC makes every effort to provide current information but no representations are made or
implied that the information and materials are completely accurate at all times.
Disclaimer 1
Table of Contents
1. Communication, Consultation, Documentation, and Disclosure
2. Evidence-Based Obstetrics
3. Bad News in the Birthing Room
4. Risk Management and Patient Safety
5. Women’s Sexual and Reproductive Health
6. Management of Labour
7. Induction of Labour
8. Umbilical Cord Prolapse
9. Fetal Well Being During Labour
10. Vaginal Birth
11. Assisted Vaginal Birth
12. Delivery of Twins
13. Vaginal Birth After Caesarean Section (VBAC)
14. Shoulder Dystocia
15. Breech Presentation and Delivery
16. Postpartum Hemorrhage
17. Hypertensive Disorders of Pregnancy
18. Preterm Labour and Preterm Birth
19. Prelabour Rupture of Membranes (PROM)
20. Prevention of Early-Onset Neonatal Group B Streptococcal Disease
21. Antepartum and Intrapartum Hemorrhage
Table of Contents 1
Suggested Readings
The ALARM faculty has used a variety of sources including standard textbooks and articles from the usual journals. In particular,
we have relied on the following:
1. The Cochrane Pregnancy and Childbirth Database. (Distribution ceased after 1995)
2. The Cochrane Library (http://www.thecochranelibrary.com/). Free access (citation and abstracts only) is available
to all users; full-text access is available by subscription (existing provincial licenses currently provide free access to
residents of New Brunswick, Nova Scotia, and Saskatchewan).
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
(http://www.sogc.org/guidelines/index_e.asp) (see also listing on USB).
7. Additionally we have used two video tapes.
• The Safe and Appropriate Use of Forceps in Modern Obstetrics (available from Janssen-Ortho)
• Term Breech Patient Selection and Intrapartum Management (available from Wyeth Pharmaceuticals)
Suggested Readings 1
Chapter 1
Communication, Consultation,
Documentation, and Disclosure
Effective communication is key to inter-professional team work and quality patient care. Guidelines have been developed
by many professional bodies that provide principles to foster optimal care and positive professional communication.
Ineffective communication has been identified as being in top 3 of the leading root causes of sentinel events reported
to the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) between 1995-2014.1
An event is defined as an unexpected occurrence that either caused harm (a harm event), or had the potential to cause
harm (a no-harm event). Both of these are adverse events.2
© Joint Commission Resources: Sentinel event statistics. Oakbrook Terrace (IL):

Joint Commission on Accreditation of Healthcare Organizations; 2006.1 Reprinted with permission.
Communication, Consultation, Documentation, and Disclosure 1

Accreditation of Healthcare Organizations; 2006.3 Reprinted with permission. In addition, several accreditation and professional
organizations have noted that communication issues are the leading reason for complaint investigation. The current emphasis
on patient safety stemming from reports of avoidable harm has revealed intra- and inter-professional communication as a
key focus. The first and essential step toward establishing a clinical world where teamwork is a reality, is in the development
of effective team communication and mutual respect.4 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.5
Principles of Communication
Effective communication occurs when “a message is transmitted, received, understood and acted upon in a timely fashion”.6
The following is a list of enablers of effective communication:
• Mutual respect
• Language that is clear and precise
• Timely flow and transfer of relevant information
• Clear delineation of the roles of the communicators
• Respect for confidentiality
• Conducive environment
• Inclusion of all people to whom the information pertains7
Professionalism in communication requires that caregivers understand and acknowledge the perspective of other professionals
and the perspective of learners within those professions. There has been an historical hierarchy in health care. This hierarchy
is not useful in a health care system that requires members of multiple disciplines to work as a team. No one profession can
function in isolation. All professions must utilize the expertise, skills, perspectives and information of other caregivers to provide
comprehensive, coordinated and safe care.8
Lack of true interprofessional educational programs, as a component of basic training, adds to the challenge in the transition to
an interprofessional model of care. Maintaining the focus, of individuals and teams, on the patient and quality of care will foster
this process.8

Strategies to facilitate interprofessional care and planning might include:

• Simulations for emergency situations involving all caregivers (Rehearsing responses to emergencies as a team
using evidence-based, unit-specific protocols in mock drills—simulations either low, or high fidelity—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 disciplines
• Debriefing unusual events or normal practices as a team
• Non-punitive interprofessional case reviews
• Development of interprofessional procedures
Key Points Related to Communication

1. The topic of your conversation may be your 200th case, but it is likely your patient’s first or second occurrence. Patience,
respect and time are critical—especially when dealing with an event.
2. Non-verbal messages (“body language”) are five times more influential than verbal messages.
Non-verbal communication is unconsciously motivated and more accurately indicates a person’s meaning than the
words being spoken.9 The tone of the words and inflections constitute a major element of communication. Reviewing
video-taped simulations help increase awareness of these important factors. Many of us lack insight into our own
non-verbals.
3. Precision in language is key.
The care team must use language that is clear and with agreed-upon abbreviations understood by all. Written
language must also be accurate—casual use of terms such as “fetal asphyxia” results in inappropriate labelling.
Clearly, it goes without saying that neat and legible must be the standard when handwriting messages in order for
‘precision in language’ to be maintained.
Mutually agreed-upon language is essential for fetal heart rate (FHR) interpretation and documentation. The potential
for miscommunication between team members is decreased when everyone is speaking the same language as with
respect to electronic fetal heart monitoring data for example.10

Cognitive underspecification adds another dimension to precision. Cognitive underspecification was defined by
James Reason as a communication style that leads to a gap in knowledge. The concept was extremely well explained
by Elizabeth Duthie in her work “Recognizing and Managing Cognitive Underspecification.”We quote a paragraph
from her paper:
Cognitive underspecification is ubiquitous whenever verbal communication occurs. It is frequently
unrecognized and may or may not lead to errors. An example of cognitive underspecification is
seen in the following event from critical care. In the ICU, in response to a nurse’s verbal report that
a patient had a low potassium level, the resident said ‘‘let’s give him a run of 10X4.’’The nurse
entered the order into the computer for potassium chloride 10 meq. IV Q1 hr X 4 doses. This
was what the resident intended, despite the lack of a stated drug name, complete dose, route,
or schedule. The intended order and the executed order were identical. The lack of an error can
be attributed to a well-known, familiar communication pattern and a knowledge gap that was
closed with matching, accurate information. If the clinicians were asked if the communication was
complete, accurate, and clear, they very well may have responded ‘‘yes’’ as they had no doubts
about what course of action to follow. Techniques such as repeat/read back will not necessarily
correct cognitive underspecification. If the nurse repeats back ‘‘Give him 10X4’’ and the resident
says ‘‘yes,’’ they have simply confirmed the incomplete communication.11
If we imagine the same conversation between the resident and a co-worker new to the unit, or vice versa, incomplete
communication leading to a serious knowledge gap could occur. We do not recognize the above example as a problem
when it occurs in our domain—as a result, we all do it.
When communicating with patients and families, language and terminology must be standardized, simplified, and
understood by everyone.
Note: Your medical language is likely not be THEIR language! Furthermore, in our multicultural societies, there is also
a genuine need for capable translators.
4. The environment in which a discussion occurs influences communication
Ambiance, emotional tone, privacy, and distractions can facilitate or impede the quality of communication.
5. Effective listening is an important part of effective communication.
Listening with eyes, ears and brain helps us focus on the words being said. Listening actively involves seeking first to
understand, and then to be understood.8 Effective listening also demonstrates respect.

Communication in the Consultation Process

One of the key elements of teamwork is the use of consultation. Within the consultative process, responsibilities for
communication sit with all participants. Responsibilities of all caregivers include:
• Courtesy and respect
• Clear and effective communication, using language understandable by the patient
• Relevant and timely documentation
• Continuity of care, and clear handoffs12
The chart below is a summary of responsibilities of the key participants.
Patient Referring Caregiver Consultant
Courtesy and respect Courtesy and respect Courtesy and respect
Participate in decision making Assess patient prior to referral Provide reasonable access to services
Understand purpose of consultation, Communicate reason for consultation and level Report hospital admissions and discharges
investigations, diagnosis, risks and benefits of of consultation requested (opinion, opinion and Return patient care to referring caregiver when
proposed treatment options shared care, or transfer of care) appropriate
Read relevant patient education material Provide relevant documentation Provide relevant documentation
Understand which caregiver is responsible for Discuss and confirm with the whole team Discuss and confirm with the whole team
their care (which includes the patient) who will be the (which includes the patient) who will be MRP
most responsible provider (MRP) for current and for current and ongoing care
ongoing care
Avoid referrals to another consultant for

unrelated problems
A consultation can involve :

• Consultation only
• Consultation with concurrent/shared care
• Consultation with transfer of care

In a 2012 study, Kessler et al. describe the five Cs of consultation:13

• Contact
Introduction of consulting and consultant physicians. Building of relationship.
• Communicate
Give a concise story and ask focused questions.
• Core Question
Have a specific question or request of the consultant. Decide on reasonable timeframe for consultation.
• Collaboration
A result of the discussion between the emergency physician and the consultant, including any alteration of
management or testing of patient’s status.
• Closing the Loop
Ensure that both parties are on the same page regarding the plan and maintain proper communication about any
changes in the patient’s status.
Kessler et al. describe how this standardization in approach led to an increase in the effectiveness of communication in a consult.13
There must be no confusion on the part of the patient, her family or the health care team as to who is most responsible for the
woman’s care. This information must be recorded on the patient’s chart.
Professional bodies describe scope of practice for nurses, midwives and physicians. The need for consultation may be dictated
by professional standards or may be established by organizational or community resources. Consultations may involve social
workers, dieticians, nurses, midwives, physicians, lactation consultants, community nurses and many others. The most
appropriate option should be agreed upon and 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.
Appropriate communication and fulfilment of responsibilities will improve patient care and her satisfaction, caregiver
satisfaction, clarity of care planning, quality of care and patient safety.14

Communication and Litigation

Only 2% of patients injured by errors ever file a malpractice lawsuit.15 Unfortunately, poor communication between providers
and patients is one of the most often cited reasons for litigation. Lawsuits against physicians and health care teams are not
random. Certain individuals are more likely to be sued then others.16
In a now older study, using data obtained from the Florida Insurance Commissioner, Sloan et al.16 divided obstetricians in Florida
into three groups:
1. No claims
2. Occasional claims
3. High claims
The “High Claims” group represented only 6% of Obstetricians but accounted for 70% of all malpractice expenditures. These
physicians did not have a more litigious patient load and did not manage a greater proportion of high risk cases than the
counterparts in the other groups. They did not appear to be less proficient than other physicians. However, they received three
times more complaints than their “No Claims” colleagues.
A high proportion of their patients expressed concerns that they were ignored, undervalued, and rushed. The “No Claims”
physicians spent only 3 minutes more, on average, with their patients!
In a more recent 2008 article, Hickson and Entman6 refer to a study by Moore et al. which indicates that 60% of a “High
Risk” physician group was able to address the concerns that made them high risk. Whether through mentoring, review or just
the support of their peers, the majority are able to change. However, this change does not come easily and requires the help,
patience, guidance, and goodwill of their colleagues and co-workers.

Consent
Informed consent is a process required to protect the patient’s right to self determination about treatment recommendations.
Consent is informed if:17
• The person received the information about the treatment that a reasonable person in the same circumstances would
require to make a decision; and
• The person received responses to his/her requests for additional information about the treatment.
• The information included the:
• nature of the treatment;
• expected benefits of the treatment;
• material risks and side effects of the treatment;
• alternative courses of action; and
• likely consequences of not having the treatment.
Consent must be obtained by the caregiver with the knowledge of the procedure, side effects, and consequences of the
procedure. Alternatives to the treatment, if they exist, need to be presented and discussed.
For a patient 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, mental capacity of the patient to provide consent, and documenting a valid consent rests with the caregiver
proposing and providing the intervention.18
The woman is the primary decision maker in the consent process. If a woman has decreased capacity for comprehension,
the decision for intervention is based on prior informed consent if the patient’s wishes are known.19 Strategies to consider
may include:
• Early communication when an emergency situation is anticipated or recognized so the patient may make her
wishes known
• Knowledge of the algorithm within your facility to determine the substitute decision maker if the patient is unable
to give consent
• In an emergency situation when the patient is incapable of providing consent, decision can be based on what is
judged to be in her best interest. Discussion and decision making is best if done by family and health professionals
collaboratively, if time permits.

If there is refusal of consent or lack of timely agreement, ensure complete documentation of the discussion and woman’s stated
rationale for refusal. Caregivers must maintain open communication and show courtesy and respect while continuing to
offer appropriate care alternatives and treatments.
Documentation
Effective documentation remains a significant health care problem. Clark reported that in 54% of legal cases involving shoulder
dystocia, a lack of clear documentation of the events that surrounded the management of that dystocia was the primary
reason for payment for damages.20 Often the right things were done but were not documented adequately. More complete
documentation of what did or did not happen, accompanied by excellent verbal communication, would minimize litigation.
A quick, effective system to document procedures and events would address this problem. One option is to use a checklist as a
template from which to create the procedural report. The report should be produced in a timely manner. (See the MOREOB Case
Management Guides21, which fill this need very well and have the supporting infrastructure to be kept up to date. The Vacuum
Management Guides22 is appended to this chapter as an example.) An added benefit of this approach is that, when done as an
interdisciplinary team (e.g., physician and nurse after a procedure or delivery), the tool leads to effectively debrief the interaction.
If done routinely, a culture of debriefing every procedure will grow. The benefits begin with:
• Reducing hierarchy by fostering interprofessional input
• Improved teamwork and communication
• Improved satisfaction for the patient and family
• Charting that is both accurate and match between the disciplines
• The opportunity to identify process issues that were present, even if no harm occurred, and fix them
• The opportunity to identify actions that led to high performance and repeat them them (Productive Safety*)23
• One can save the forms which can then become the basis for a prospective audit on the topic.
The list goes on.
*Productive Safety is a newly defined concept that combines resilience and positive devience to improve quality and safety.
Otherwise known as Safety-II, it is a fundamental part of “debriefing the good,” and an integral part of the MOREOB Program.
The reader is directed to an excellent introduction to the matter by Professor Erik Hollnagel (Hollnagel E. Safety-I and safety-II:
the past and future of safety management. Farnham Surrey, England: Ashgate Publishing, Ltd; 2014.)

The 5 C’s of Effective Documentation

• Clear – concise, precise and legible
• Complete
• Contemporaneous
• Consistent
• Compliant with institutional and professional standards
The best communication is not effective if it is not documented. If events are not documented, they may be interpreted to have
not occurred.
Disclosure
Disclosure is “the imparting by healthcare workers to patients or their significant others, of information pertaining to any
healthcare event affecting (or likely to affect) the patient’s interests. The obligation to disclose is proportional to the degree of
actual harm to the patient (or realistic threat of such) arising from an adverse event”.24 Disclosure must be done in accordance to
organizational policy and local legislation.
Communication of any negative health outcome to a patient or family is a very difficult task for caregivers. Disclosing an adverse
event resulting from error is even more difficult. However, the communication principles and skills required for the conversation
with the patient/family are very similar. A patient’s/family’s normal response to injury includes a mix of fear, anxiety, depression,
anger, isolation, humiliation, devaluation, and betrayal. This response may occur whether or not the harm was due to a mistake.25
Health care organizations and care providers must acknowledge that no matter how excellent the care, there will always be
incidents of error that result in adverse events; it is inevitable in a dynamic complex system. Therefore, it is prudent to anticipate
the need to disclose such events and to be prepared with appropriate policies, protocols and trained personnel to manage
the situation as best as possible when it does occur. The organization’s plan provides the framework within which the health
care providers will be trained and supported to conduct disclosures.26 The plan must be specific to the circumstances of each
individual organization; however, it should, at minimum, address the ‘5 W’s’:27
• What to disclose
• When to disclose
• Who should disclose
• What means of disclosure
• To whom disclosure should be made

In general, disclosure should involve the most-responsible caregiver and be complete, accurate, timely, consistent, thoughtful,
and in surroundings that are non-threatening to the recipient. Questions should be answered as completely as the available
information allows and follow-up meetings arranged. Availability to the individual and family is important to ensure
transparency and therefore avoid the perception of a “cover up”.
Dr. Lucien Leape has described serious preventable injury as a medical emergency that has two victims – the patient and the
caregiver. The patient suffers a double wound – the actual physical injury, and an emotional wound, i.e., the sense of betrayal
and loss of trust. The caregiver sometimes referred to as the ‘second victim’ can experience profound shame, guilt and fear
resulting in an impaired ability to practise. The organization must anticipate, and have processes in place to concurrently treat
both emergencies in a timely fashion. The key to treatment is honesty, openness and apology.25 Additional dimensions are a
health care provider’s very busy practice and unit. Due to these realities, the ability to respond 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 minimalizing 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/families. Research has found that patients overwhelmingly want
and expect to be informed of adverse events. However, such disclosure seldom occurs.
• 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 the physicians believe that patients should be told about possible future outcomes.28-31
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.32,33
In March 2009, the Ontario Apology Act was passed. British Columbia, Saskatchewan, Manitoba, and most U.S. states already
have similar legislation. This legislated approach to disclosure is designed to create greater accountability and transparency in the
health care system. Acts such as the Apology Act will:

• Allow individuals and organizations, such as hospitals and other public institutions, to apologize for an accident or
wrongdoing, without it being used as evidence of liability in a civil legal proceeding under provincial law
• Promote accountability, transparency and patient safety by allowing open and frank discussions between patients and
health care providers
• Enhance the affordability and speed of the justice system by fostering the resolution of civil disputes and shortening or
avoiding litigation34
Barriers to Disclosure
Caregivers may hold personal beliefs, or experience fears that prevent them from choosing to disclose adverse events:
• Belief that disclosure is unnecessary
• Genuine, although misguided, belief that it is in the best interest of patients not to be informed
• Belief that the outcome would potentially have occurred without the error or intervention (e.g., the patient was
terminally ill anyway)
• Lack of experience, training, skill, or comfort in communicating difficult information
• Fear of having to handle the recipients’ as well as their own emotions
• Fear of retribution from the recipient of the news
• Fear of loss of the trust and respect of patients
• Fear of legal action
• Fear of censure, loss of respect, and prestige among colleagues
• Fear of loss of job/income
• Loss of self esteem and self confidence as a caregiver27,28
• The genuine belief that the event was a “complication”
What do Patients Expect?

When adverse events occur, patients/families often sense that something has gone wrong. Failure by caregivers to disclose
the event causes the patient/family to feel devalued and disrespected; this may contribute to a belief that “something is being
hidden”. They lose trust in their caregivers and the health care organization or system; they may feel the only way they can obtain
accurate, complete information is by launching a lawsuit, particularly if they feel that information is being purposely withheld
or covered up. In fact in a Canadian report, 76% of respondents believe that the threat of litigation is important to ensuring that
doctors act in the best interests of their patients.31

The primary driver of considering legal action is not the event itself but rather the patient’s/family’s subsequent interaction
with the people in the health care system. When the harm becomes apparent in spite of the lack of disclosure, or when the
adverse event is finally admitted by the caregiver/organization, patients/families often experience a profound anger.35 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 the patient/family has been involved from the very beginning in all aspects of their care and has
developed a relationship of partnership with the caregivers, disclosure of adverse events is just one more step in an established
pattern of open, honest, and transparent communication. The disclosure is still difficult but it offers the possibility of re-building
trust, forgiveness and the beginning of healing.36
Specifically, patients need to know:37
• 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 again to another family
• What can we do to help you achieve those system changes
Benefits of Disclosure
For Patients/Families:
• To begin to recover from the devastating effect of the unanticipated outcome, to deal directly with the pain so that
they can begin to heal
• To regain trust, to work out their feelings of distrust with the people inside the institution, rather than to look for help
from those outside of it
• To understand and obtain the care that may be needed to address the effects of the adverse outcome in the future
• To receive the information needed to make next-step decisions, including the possibility of seeking appropriate
compensation
For Caregivers:
• To openly and honestly address the error, and engage in ways of preventing future occurrences
• To express regret, to assuage guilt, to begin to heal
• To regain self esteem and continue to practice

For Health Care Organizations:

• To learn from events, and improve faulty systems to protect patients, their families, and health care staff in the future
• To heal psychologically after a mistake by sharing the human face of working in a complex system
• To potentially lessen the frequency and severity of litigation, through the proper management and control of a
disclosure process
• To share with other organizations to prevent the recurrence of the same event elsewhere
How to Disclose
Preparation:
• Ideally you have a pre-developed situation management organizational plan, which can be used to guide the process
and which will serve as a checklist to ensure that all potential issues are appropriately 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
• Identify and involve the appropriate participants for the disclosure
• Determine the roles to be carried out by each person
• Assess the readiness of the patient/family to hear (medically stable, awareness level, ability to comprehend,
availability of support)
• Choose an appropriate time and setting, keeping in mind the basic principles of effective communication and urgency
of timely follow-up
• Be sure to organize the meeting in such a way to not have the medical team on one side of the table, and the family
on the other. This could reinforce an illusion of “us against them.”This adds more stress to an already delicate situation.
A round table goes a long way to avoid this

Meeting with the Patient/Family:

• Simply describe what happened in plain, understandable language; use a neutral tone
• Describe what is known at this point; give factual, objective information
• Describe the next steps of the process for the patient/family; ensure any appropriate medical care is identified and
made available; offer to transfer care to another caregiver
• Acknowledge the patient’s suffering; demonstrate your sincere sympathy and sadness
• Apologize for the harm caused to the patient and for your role in it
• Focus on the needs of the patient/family – at this time it is not about you
• Describe the next steps in the investigative process
• Explain what is being done to prevent a recurrence
• Seek and respond honestly to the patient’s/family’s questions and concerns; allow ample time for questions
• Establish, with the patient/family, a plan for follow-up (who, what, where, when); be specific and be available
• Offer the ongoing availability of a key contact person, and the support of other available resources (clergy, social
services, etc.)
Skills Needed:
• Establishing rapport
• Active, empathetic listening
• Lack of defensiveness – this is the time to listen, not to defend your actions
• Ability to recognize and manage your own feelings
• Openness and willingness to accept whatever reaction occurs
• Ability to anticipate and calmly handle the patient or family’s potential emotional reactions/behaviours such as crying,
yelling, anger, threats, verbal abuse, walking out
• Ability to separate the message from the messenger, so that the messenger can be seen as a support person by the
patient/family
Event Reporting
As stated earlier, “an event is defined as an unexpected occurrence that either caused harm (a harm event), or had the potential
to cause harm (a no-harm event). Both of these are adverse events.”2

Disclosure also involves the timely and accurate reporting of the event (no matter if it is a harm or no – harm event) to the
facility in which the care provider works, as well as their appropriate insurance organizations. Failure to do so or delay in so doing
is never useful.
Confusion as to whether a “complication” is an event or not, is only one of the aspect leading to delay or failure to report. Waters
et al., in their 2012 study and review of the literature, reveal a litany of situations that may or may not lead to a report.38 They
note: “Nurses exercise considerable judgment in deciding whether or not to formally report an incident,39-41 with estimated
rates ranging from 10 to 55% of incidents.”They also note that culture plays an important role in reporting rates. They point out
that informal reporting also 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”.39 And finally,
they state that “lack of feedback from administrators about an incident reduces reporting.42-44 Time-consuming incident report
processes and the inability to report anonymously also reduce incident reporting.41,43,45 Negative relationships amongst health
care providers, within and between disciplines, decrease incident reporting”.45-47
These observations are important as the majority of incidents are reported by the nursing profession.

References
1. Joint Commission. Sentinel Event Data Root Causes by Event Type 2004-2013. 2014. Accessed April 14, 2016. Available
from: http://www.jointcommission.org/assets/1/18/root_causes_by_event_type_2004-2014.pdf.
2. Event review. London: Salus Global Corporation; 2013.
3. Sentinel event statistics. Oakbrook Terrace (IL): Joint Commission on Accreditation of Healthcare Organizations; 2006.
4. Mann S, Pratt SD. Team approach to care in labor and delivery. Clin Obstet Gynecol. 2008;51:666-79.
5. Zwarenstein M, Bryant W. Interventions to promote collaboration between nurses and doctors [Cochrane review].
Cochrane Database of Systematic Reviews 2000 Issue 2. Chichester (UK): John Wiley & Sons, Ltd; 2000.
6. Hickson GB, Entman SS. Physician practice behavior and litigation risk: evidence and opportunity. Clin Obstet Gynecol.
2008;51:688-99.
7. Burglin AG, Tschudin S. [Communication in obstetrics]. Ther Umsch. 2008;65:653-6.
8. Simpson KR, Knox GE. Perinatal teamwork: turning rhetoric into reality. In: Simpson KR, Creehan PA, editors. Perinatal
nursing. 2nd ed. ed. Philadelphia: Lippincott Williams and Wilkins and Association of Women’s Health, Obstetric and
Neonatal Nurses; 2001. p. 53-67.
9. Copeland DB, Douglas D. Communication strategies for the intrapartum nurse. J Obstet Gynecol Neonatal Nurs.
1999;28:579-86.
10. Fetal heart monitoring: principles & practice. 3rd ed. ed. Washington: Association of Women’s Health, Obstetric and
Neonatal Nurses; 2003.
11. Duthie EA. Recognizing and managing errors of cognitive underspecification. J Patient Saf. 2014;10:1-5.
12. Goluboff S, Reynolds L, Klein M, Handfield-Jones R. Privileging and consultation in maternity and newborn care.
Maternity and Newborn Care Committee. Mississauga (ON): College of Family Physicians of Canada; 2004.
13. Kessler CS, Afshar Y, Sardar G, Yudkowsky R, Ankel F, Schwartz A. A prospective, randomized, controlled study
demonstrating a novel, effective model of transfer of care between physicians: the 5 Cs of consultation. Acad Emerg
Med. 2012;19:968-74.
14. Indications for discussion, consultation and transfer of care. Rev. ed. Vancouver: College of Midwives of British Columbia;
2005.

15. Localio AR, Lawthers AG, Brennan TA, Laird NM, Hebert LE, Peterson LM, et al. Relation between malpractice claims and
adverse events due to negligence. Results of the Harvard Medical Practice Study III. N Engl J Med. 1991;325:245-51.
16. Sloan FA, Mergenhagen PM, Burfield WB, Bovbjerg RR, Hassan M. Medical malpractice experience of physicians.
Predictable or haphazard? JAMA. 1989;262:3291-7.
17. Consent. Toronto: Ontario College of Nurses; 2005.
18. Campion JA, Dimmer D. Professional liability in Canada. Scarborough (ON): Carswell Thomson Professional Publishing; 1998.
19. Informed consent. Ethics in obstetrics and gynecology. 2nd ed. ed. Washington: American College of Obstetricians and
Gynecologists; 2004. p. 9-17.
20. 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.
21. MOREOB case audit tools [series]. London (ON): Salus Global Corporation; 2012.
22. Vacuum. London (ON): Salus Global Corporation; 2012.
23. Braithwaite J, Wears RL, Hollnagel E. Resilient health care: turning patient safety on its head. Int J Qual Health Care.
2015;27:418-20.
24. Systems Issues Working Group National Steering Committee on Patient Safety. Canadian patient safety dictionary.
Ottawa: Royal College of Physicians and Surgeons of Canada; 2003.
25. 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.
26. 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.
27. Hawkins PJ. Disclosure of adverse events - risk and legal obligations [oral presentation]. Toronto2006.
28. Hebert PC, Levin AV, Robertson G. Bioethics for clinicians: 23. Disclosure of medical error. CMAJ. 2001;164:509-13.
29. 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.
30. Banja JD. Why, what, and how ought harmed parties be told? The art, mechanics, and ambiguities of error disclosure.
In: Youngberg BJ, Hatlie M, editors. The patient safety handbook. Sudbury (MA): Jones and Bartlett; 2004. p. 531-48.
31. Health care in Canada. Ottawa: Canadian Institute for Health Information; 2004.

32. 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.
33. 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.
34. Thompson J. Apology Act passes third reading at Queen’s Park [news release]. Toronto: HIROC; 2009.
35. Hicock L, Lewis J. Beware the grieving warrior. Toronto: ECW Press; 2004.
36. Disclosure of unanticipated events: the next step in better communication with patients. Part 1 of 3. Chicago: American
Society for Healthcare Risk Management of the American Hospital Association; 2003.
37. Sidorchuk R. The patient perspective - what do we really want - do you really want to know? [oral presentation]. Toronto2006.
38. 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.
39. Covell CL, Ritchie JA. Nurses’ responses to medication errors: suggestions for the development of organizational
strategies to improve reporting. J Nurs Care Qual. 2009;24:287-97.
40. Kingston MJ, Evans SM, Smith BJ, Berry JG. Attitudes of doctors and nurses towards incident reporting: a qualitative
analysis. Med J Aust. 2004;181:36-9.
41. Walker SB, Lowe MJ. Nurses’ views on reporting medication incidents. Int J Nurs Pract. 1998;4:97-102.
42. Elder NC, Brungs SM, Nagy M, Kudel I, Render ML. Nurses’ perceptions of error communication and reporting in the
intensive care unit. J Patient Saf. 2008;4:162-8.
43. Evans SM, Berry JG, Smith BJ, Esterman A, Selim P, O’Shaughnessy J, et al. Attitudes and barriers to incident reporting:
a collaborative hospital study. Qual Saf Health Care. 2006;15:39-43.
44. Jeffe DB, Dunagan WC, Garbutt J, Burroughs TE, Gallagher TH, Hill PR, et al. Using focus groups to understand physicians’
and nurses’ perspectives on error reporting in hospitals. Jt Comm J Qual Saf. 2004;30:471-9.
45. 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.
46. 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.
47. 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.

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.
When information needed to make rational decisions is nonexistent, incomplete or unavailable, our decision-making is severely
hampered. When information exists and is not used properly or consistently, inappropriate care may be provided. The goal of the
ALARM course is to promote care based on the best available evidence while also encouraging participants to develop their
skills in obtaining, evaluating and incorporating evidence 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, Evidence from these types of studies provides
themes or trends from interviews, or focus groups that give direction to ways of thinking. Although qualitative evidence has a
role in achieving clinical understanding, evidence presented in the ALARM course consists primarily of quantitative data.
Quantitative evidence uses numerical data, analyzed through statistical procedures for the purpose of describing phenomena,
relationships and significance of the results (Polit & Hungler, 1995). Quantitative research trials can range from weak to strong
in terms of scientific rigor. Different types of quantitative trials are published such as randomized controlled trials (RCTs), cohort
trials, case control trials and surveys,
Evidence collected from prospective research trials is more powerful than that collected from a retrospective analysis of
outcomes. In a prospective trial, the researcher has an hypothesis or idea and goes forward in time collecting data to observe
the results of an intervention. Variables can be anticipated, and the study can be designed to control for those variables. A
retrospective trial is not as powerful since it looks back in time at events that have occurred (eg 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), keeping in mind the variability of quality
of randomized trials. In a randomized trial, each participant has an equal chance of being in any group in the study. There is no
bias in assigning some participants to one intervention and others to another intervention. Based on the group results, it is the
average of selected outcomes that can be determined by a RCT.
Evidence-Based Obstetrics 1
Thus, a prospective Randomized Controlled Trial (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 if the intervention has a significant impact.
Grades of Evidence and Classification of Recommendations

Since 1976 the Canadian Task Force on the Periodic Health Examination has used explicit analytic criteria to guide its
evaluation of the effectiveness of health care interventions. The criteria are summarized in a classification system that the
SOGC and many other organizations have adopted. Graded strength is placed on published medical evidence based on the
quality of its design. Greatest weight is placed on the features of study design and analysis that eliminate or minimize biased
results. Recommendations are based on the level of evidence. The strongest recommendations (A and E) are reserved for
interventions supported or negated by high quality studies (Type I or RTC’s). Type II evidence is generally associated with B and
D recommendations. In 2003, the Task Force on Preventive Health Care modified the grades to reflect the ongoing evolution of
methodology and reporting. Recommendations after this change include a redefinition of Grade C and the addition of a grade “I”.
C grade recommendations are reserved for cases where evidence of adequate quality and quantity may exist but it is conflicting
in that the effectiveness of the action remains unclear. Grade C signals a situation where other factors, such as values and individual
patient characteristics, may play an even larger role than when evidence is clear-cut. “I” grade implies that the existing body of
evidence is of insufficient quantity or quality (or both) to support a specific recommendation. (CMAJ 2003; (3)169:207-8)
Summary of Grades of Evidence

and Classification of Recommendations
Quality of Evidence
I: Evidence obtained from at least one properly randomized controlled trial.
II-1: Evidence obtained from well-designed controlled trials without randomization.
II-2: Evidence obtained from well-designed cohort or case-control analytic studies, preferably from more than one
centre or research group.
II-3: Evidence obtained from comparisons between times or places with or without the intervention. Dramatic results in
uncontrolled experiments (such as the results of treatment with penicillin in the 1940’s) could also be included in
this category.
III: Opinions of respected authorities, based on clinical experience, descriptive studies or reports of expert committees.
Grades of Recommendations from the Canadian Task Force on

Preventive Health Care (2003)
A: There is good evidence to recommend the clinical preventive action.
B: There is fair evidence to recommend the clinical preventive action.
C: The existing evidence is conflicting and does not allow to make a recommendation for or against use of the clinical
preventive action; however, other factors may influence decision-making.
D: There is fair evidence to recommend against the clinical preventive action.
E: There is good evidence to recommend against the clinical preventive action.
I: There is insufficient evidence (in quantity or quality) to make a recommendation; however, other factors may
influence decision-making.
Meta-Analysis
Instead of looking at just one trial, Meta analysis groups like trials together to determine the cumulative results of all the relevant
evidence. Trials are more likely to show a difference between the intervention and control group, if it truly exists, when the
numbers studied are large and when the difference in outcome is great.
In obstetrics, most serious outcomes are rare. This means it can be very difficult or impossible to carry out randomized controlled
trials that are powerful enough (have enough subjects) to demonstrate a difference between a treatment and control group,
even if it exists. Trials that have been done are often too small alone to provide statistically significant results. Meta-analysis is
one tool that may allow useful information to be obtained from these studies.
A meta-analysis is a statistical evaluation of a collection of several studies which are similar in design, study populations and
outcomes examined. By combining data appropriately, the answer to an important question may be found in the cumulative
information in the medical, nursing and midwifery literature. The primary benefit, however, of meta-analysis is the systematic
review of the medical literature that occurs by the analysts who retrieve and synthesize the information and make it more readily
available for our use.
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.
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
1. 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)]
2. Specificity is the likelihood that the diagnostic test will indicate the absence of disease when the disease is actually
absent. (True negative rate). [d/(b+d)]
3. Positive predictive value is the likelihood that a positive test result actually means that the disease is present. [a/(a+b)]
4. Negative predictive value is the likelihood that a negative test result actually means that the disease is absent.
[d/(c+d)]
Bayes’ Theorem: The predictive value of a test will depend on the prevalence of the disease. With high prevalence, the
positive predictive value will increase and vice versa (a positive test for a low prevalence disease is likely to be a false positive).
For example, in the clinical setting of doing a culture for Group B Strep (GBS):
• Sensitivity of the test (+ve culture) is the chance that if the woman had GBS it would be picked up by the test
• Specificity is the chance that the test will indicate no GBS (-ve culture) when in fact the woman does not have it
• Positive predictive value is the chance that a +ve culture represents GBS colonization
• Negative predictive value is the chance that a – ve culture actually rules out GBS
Statistics in Meta-Analysis
When grouping studies together, the odds ratio (O.R.) compares the likelihood (relative odds) of the outcome being studied
occurring in the group receiving the intervention (the “experimental” or “exposed” group) with the group not receiving the
intervention (the “control” or “unexposed” group).
O.R. (odds ratio) = Odds of observed outcome in experimental group = a x d
Odds of observed outcome in control group: b x c
The relative risk (R.R., sometimes called the risk ratio) compares the risk or probability of the outcome in each group rather
than the odds.
R.R. (relative risk) = Risk of observed outcome in experimental group = a / (a+b)
Risk of observed outcome in control group: c / (c+d)
The odds ratio serves as a surrogate for the relative risk which is more difficult to manipulate using the statistics performed in
meta analysis. When the outcome studied is rare, the odds ratio closely approximates the relative risk.
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 two groups. Ratios less than one will be represented to the left of the
vertical line and those greater than one will be represented on the right side of the vertical line. The data presentation is usually
constructed so that the results that are less than one are an improvement in outcome.
Confidence Intervals
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 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.
Measurements of confidence do not eliminate the possibility that the results of an experiment are due to chance, they just
indicate how likely it is that such a result is due to chance. The judgment of the clinician is required to interpret whether or not a
result is clinically significant regardless of the statistical expression of probability used.
For a single trial, the outcomes of interest are shown with their individual confidence interval.
Results of Meta-Analysis
In a meta-analysis, the result is plotted below the individual studies used in the analysis. The meta-analysis result is calculated
when all the trial results are evaluated, weighted and then pooled for a single given outcome of interest. The associated
confidence interval will be narrower than the individual trials because the number of participants represented is greater.
Effect of Intervention on Outcome of Interest
The confidence intervals displayed for each study will be broader than the confidence interval of the meta-analysis and vary
according to study size. In the example above: Trial C has the narrowest confidence interval given its larger size. The meta-
analysis odds ratio is the narrowest of all as it mathematically incorporates all of the trials’ subjects. At times, a trial may fail to
demonstrate a difference that truly exists due to a lack of power (i.e. not enough subjects given the effect size) – Trial D in the
above example. Again, confidence intervals that cross the vertical line at 1 mean that p > 0.05 for the outcome in that trial.
Although this means that this result is not statistically significant, if all the studies lie to one side of the vertical axis, it indicates
a trend in the same direction. Trial B is an outlier and requires an explanation (cheating? different population? misdiagnosis?).
The trials are then said to be homogeneous. This suggests 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.
The results displayed in a meta-analysis fall into one of three categories:

The result lies to the left of the vertical axis (one) and the confidence interval does not cross one. This indicates that the outcome
for the treated group is less likely to occur than in the control group and the result is statistically significant.
The result is at or near one and the confidence interval line crosses one. This indicates that there is no statistically significant
difference in outcomes between the groups.
The result lies to the right of the vertical axis and the confidence interval line is also completely to the right of one. This indicates
that the outcome is more likely to occur in the treated group than in the control group.
Even though several studies may not all achieve statistical significance individually, perhaps because some have insufficient
numbers or the effect size is small, the meta-analysis display may show most of these studies demonstrate the same trend.
Under this circumstance, when the meta-analysis demonstrates a significant difference, one may be more confident that this
difference truly exists.
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.
Caution
Just because a meta-analysis has been done does not mean that the result is necessarily secure. The techniques of meta-analysis
are such that separate meta-analyses of the same subject may result in differing findings. This is usually based on the inclusion or
exclusion of particular RCT’s into or from the meta-analyses. There are two main reasons for this:
• The danger of publication bias such that negative results in a randomized controlled trial are less likely to be published,
and cannot therefore appear in a meta-analysis. This factor is often suspected to be the culprit when several initial
small trials show promising results that are not substantiated in a subsequent well-designed large trial. Another
possible reason for exclusion of trials from a meta-analysis is an incomplete systematic review of the literature.
• The problem of data “excess”. This relates to the inclusion of multiple publications by different authors based on the
SAME clinical trial.
Meta-analysis is a tool to be used in the absence of a large definitive trial. If a well designed and 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.
We must, whenever possible, use the information from sound systematic reviews to guide us in the appropriate and
compassionate practice of medicine.
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.
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. Thacker MD, Peterson HB, Stroup DF. Metanalysis for the obstetrican-gynecologist. Am J Obstet Gynecol, May
1996;174:1403-7
Chapter 3
Bad News in the Birthing Room
Pregnancy and childbirth are expected to be a happy experience. Perinatal death, stillbirth, or the compromised infant present
challenging situations to all health care providers involved in obstetrics. We will, at times, feel powerless and awkward in
talking about these situations with our patients. There is a growing body of qualitative and descriptive research on attachment
and parental responses in adverse situations. There is insufficient research to be able to present evidence-based guidelines for
communication in these situations. However, there is consensus that appropriate disclosure is a potent risk management strategy.
Patients and families are often dissatisfied with the type and amount of information that they receive from their health
care providers.1 Many health care providers do not feel confident in their ability to break bad news.
This skill, like other clinical skills, can be learned. Improved communication of bad news can reduce distress, enhance coping, and
reduce the risk of unrealistic expectations, inappropriate denial, and overwhelming distress both for the woman, her family, and
for the caregivers.
Bad News Experiences

• Miscarriages
• Abnormal prenatal diagnoses, fetal anomalies
• Terminations
• Stillbirths, neonatal death
• Extreme premature births
• Compromised newborn
• Maternal disease or injury
• Complicated delivery – Different than anticipated outcome
Patient and Family Response to an Adverse Event

The nature of the event itself, its personal interpretation, and available coping mechanisms influence response to an adverse
event. These components contribute to the responses we observe in patients and families.
Bad News in the Birthing Room 1

The Nature of the Event

Events in both early and later pregnancy can have a similar impact although caregivers have historically considered later
pregnancy events more significant. Maternal fetal attachment was thought to begin with maternal perception of fetal
movements. Research indicates that attachment for many women begins as early as pregnancy symptoms appear and increases
with ultrasound visualization of the baby. Partners’ attachment was significantly enhanced when the partners watched the
ultrasounds of their babies. Conversely, a woman who has had a previous negative outcome may delay her attachment until
later in the pregnancy.
Miscarriage has a tremendous impact on women and the loss at an early gestation should not be minimized.2,3 Genetic
termination requires sensitivity to the different reactions women may have when the loss is perceived as “chosen” rather than
unexpected.4
A survey of women who had experienced an early loss indicated:5
• 71% experienced it as death of their baby
• 81% felt that part of them had died
• 63% felt devastated
• 73% felt they had caused the death of their baby
• 42% had nightmares
• 74% felt out of control emotionally and/or physically
When a miscarriage occurs or a D&C is carried out, there is no legal requirement for burial of the remains. Hospitals dispose of
remains as surgical tissue. For many women, the option of burial may provide some degree of closure and offering the option
of burial should be considered. Sensitivity to cultural differences may lead to alternate options in the management of this loss.
Situations are affected by the type of event and uncertainty of the outcome (i.e., intrauterine death versus preterm birth). The
less clear the event, the more difficult it can be for health professionals to communicate and for parents to grasp the potential
adverse outcomes.
Interpretation of the Event

Events are interpreted differently by every person or family. Personal, cultural, and social context influence how we interpret
events. For instance, an adolescent with significant medical comorbidity delivers a stillborn infant at 24 weeks’ gestation. While
the young mother experiences loss, her mother, as her support person, may be greatly relieved because of concerns of coping
with a new baby and potential harm to her daughter’s health. Intrepretation of an event is a personal emotional event.

Previous personal experience with an event alters interpretation. A successful outcome with a previous preterm birth provides
optimism in the event of a second preterm birth, whereas a previous neonatal death may mean ongoing anxiety with the
subsequent pregnancy.
Gender differences in interpretation have been referred to as incongruent grief.6 Fathers and mothers may work through grief
differently and in different time frames. Women generally have higher levels of grief and grieve longer. Perceived societal and
cultural expectations regarding gender-specific expressions of grief may influence these differences.
Post-Traumatic Stress Disorder (PTSD)
A traumatic birth must always be reviewed. A 2011 review of the literature by Goldbort et al. revealed: “Ayers’ (2004) review
found that 10% of women have severe traumatic stress responses to birth, with 1% to 2% of women developing chronic
postnatal PTSD. Beck’s (2004b) qualitative study of 38 mothers’ stories revealed five themes that demonstrated the essences of
the mothers’ PTSD experience. The 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.”7 The impact on caregivers is
also highly significant.7
Siblings may be the forgotten mourners. It is often left to the partner to share information with other children—their age,
awareness of the pregnancy, and personal previous experiences alter their understanding and interpretation.
Coping Mechanisms to an Event

Coping mechanisms are grounded in family structure, culture, and religious beliefs. “Family” is defined by whom the woman calls
family. This may include colleagues and friends. Coping abilities are also influenced by other events happening at the same time.
The Social Resource Scale by Holmes8 attempted to quantify the emotional coping impact of events (higher numbers indicate
greater impact). Some examples include:
• Death of a spouse = 100
• Death of a family member = 63
• Fired at work = 47
• Pregnancy = 40
• Outstanding personal achievement = 28
• Change in residence = 20
• Christmas = 12

Multicultural populations make it essential for obstetrical caregivers to have an understanding of their own assumptions, and
the variety of cultural understandings of perinatal loss and grief they may encounter. What is considered appropriate behaviour
and important as a ritual to mark perinatal loss is culturally based and caregivers should be open and flexible about the family’s
approach. There can be wide variation in the traditions surrounding perinatal loss within defined cultural and religious groups.
If practicing within a specified cultural demographic, the practitioner would benefit from learning as much as possible about the
culture and religions.
Health Professionals’ Actions to Facilitate Coping

When a baby is sick or dying, it is important for caregivers to visit both parents and newborn frequently. If the baby is to be
transported to another centre, caregivers should explain the process to the parents and determine if the mother can also be
moved near to the baby. Additional supportive actions may include:
• Acknowledging the problem and outlining immediate care in collaboration with newborn caregivers
• Involving the parents in important decisions (e.g., ceasing life support)
• Encouraging as much contact with the baby as possible
• Allowing parents to take the dying baby in their arms
• Arranging for photographs of the baby, especially if the mother and baby are to be separated
• Taking footprints of the baby (if no ink is available, iodine based cleanser will work)
• Respecting the need for privacy
• Providing ongoing care for the parents
• Minimizing other potential stresses such as need for accommodation, transportation, childcare, parental leave
Following a pregnancy loss, parents will often derive benefit from tangible remembrances. Verify the parents’ cultural or religious
preferences before cutting hair, taking photographs, or similar interventions. Examples of ways to generate memories for families
include:9,10
• Certificate of life/baptismal certificate
• Photographs—Some parents are not able to view pictures of the baby in the beginning, but might appreciate being
provided with them as time passes. Sometimes parents’ expectations of what the baby looks like are much worse than
the reality. Appropriate bundling and wrapping of the baby can be helpful to make the baby look as normal as
possible. (Demonstrating your own comfort with the baby may also be important.)

• Bereavement outfits/receiving blankets

• Footprints and handprints (if no ink is available, iodine based cleanser will work)
• Name band
• Crib card
• Lock of hair
• Written notes or poems to or for the baby
• Planting of trees or flowers
• Ornaments or decorations
• Scrapbooks of cards from friends and family
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.
Hospital services such as social work or pastoral care and referral 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 and supportive. Resources for the development of a bereavement program can be found in the
Family Centred Maternity Care guideline.11
Response
The individual and family response is variable based on the nature of the event, interpretation of the event, and coping resources
available. Dr. Elisabeth Kubler-Ross described a number of responses to loss:12
• Shock or panic
• Denial
• Grief/anger/guilt
• Bargaining
• Acceptance
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.

After the death of a baby, up to 20 percent of parents will suffer psychological symptoms for years following the death. 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. In their anger, they may ascribe blame to caregivers. They often experience a loss of
self-esteem and a sense of failure. They may have difficulty in coping with the immediate tasks such as funeral arrangements
and death registration. Incongruent parental grief can lead to marital conflict. There may also be behavioural changes in other
children. The children often feel confused or responsible for the death.
When there is a surviving twin or a pregnancy immediately after a loss, the new baby’s identity may be confused with the
idealized lost baby. The new baby may never live up to parents’ expectations and may be a focus of unresolved anger.
Resources for Families and Health Professionals

PAIL (Pregnancy and Infant Loss) Network, formerly Perinatal Bereavement Services Ontario, is a loss resource. The network
offers booklets on perinatal loss for parents, Silent Birth (stillbirth) and Early Loss (miscarriage), both written by nurses and
reviewed annually.
PAIL Network will provide perinatal loss sensitivity training workshop. PAIL Network is also linked with Bereavement Services
(Resolve Through Sharing Bereavement Training in Perinatal Death™) to provide a two-day perinatal death course for health
professionals.
See the appendix for a list of resources available through the PAIL Network. Additional information is available from their web
site at http://www.pailnetwork.ca/resources/.
Strategies for Communication of Bad News

• Consider who should be present
• Position yourself
• Key phrase to open
• Key phrase to close
• Know your resources
• Disclosure
• Document

Caregivers are often placed in unexpected situations requiring them to spontaneously communicate effectively and clearly.
Patients and families often remember statements made at this time for years to come. The strategies below may be helpful in
setting the scene and communicating in difficult circumstances.
Who Should be Present

Relatives, albeit well-meaning, may not realize that the woman requires privacy in speaking with her physician, midwife, or
nurse. Establish privacy by moving to a separate room or by asking, “I need to speak to (patient’s name) privately for a few
minutes, will you please excuse us?”Women often want their significant support person(s) to be present during discussions.
Clarify who the woman wants with her. Although privacy is important, caregivers need to ensure at least one other health
professional remains in the room to verify what has been said and to help the family verify the information they have heard. The
conversation should begin with introductions of all of the people present, including the relationship or role of each participant.
Position Yourself
Eye contact with the patient is important. Position yourself to ensure you have good eye contact and are at eye level. Avoid
standing at the end of the bed; instead, sit beside her next to the bed or on the edge of the bed.
Key Phrase to Open a Conversation

Whenever possible, prepare an opening statement that is compassionate and sets the stage for the discussion that is to follow.
For example:
“I’m sorry for your loss (or identify the event that you are sorry for). It must be difficult for you to talk right
now. However, I know that you must have some questions about what has happened, and I would like to try
to answer your questions. I also have some information that I would like to share with you.”
Explain the situation in clear, simple language without the use of medical terminology. Communicate at a grade four to five
literacy level, particularly in a stressful situation. Start with essential information about the event. Be aware of your choice of
words. Several studies indicated most women, regardless of gestation or certainty of well-being or survival, prefer the use
of “baby” rather than “fetus”, “products of conception”, or “tissue”. Be sensitive to possible differences in the case of genetic
termination. Effective listening to the perspective of the woman and the family is essential and questions and responses should
be documented. Regardless of the clarity of your words, be prepared for repetition of information, occasionaly many times.

It is important to ensure consistency of communication between patient and health professionals and between health
professionals. Any plan of care for mother or baby should be clearly outlined and documented. A plan of care should include:
• The next steps in physical care/testing for mother and baby
• Resources or individuals who will be contacted on behalf of the patient such as chaplain, social worker, community
support nurses, peer support groups, family physician, funeral director, or interpreter.
What Could be Said

I wish things would have been different.
We can talk again later.
Is there anything I can do for you?
I’m sorry for your loss.
I’m here for you.
I want to listen.
Is there someone I can call for you?
What Not to Say

“it’”, “fetus”, or “tissue” when talking about the baby.
This happened for the best.
It’s God’s will.
Time will heal.
Now you have an angel in heaven.
Mother Nature knows best.
It was a blessing. He would never have been normal anyway.
You’re young. You can have others.
Better for this to have happened now, before you knew the baby.
He was born dead. You didn’t have a chance to get attached to him.
At least you have one already.
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.

Follow-Up
Let the woman and family know who is available to answer ongoing questions and whether you will continue to be available.
It is valuable for the primary caregiver to make at least one return visit within 24 hours to allow for further discussion and
repetition of information. Ongoing discussion and full disclosure is important. Your hospital’s disclosure policy may be helpful
in determining who to involve 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 is invaluable for explaining the present event and in planning for future pregnancies. Documentation should include
prenatal records, ultrasound reports, genetic testing (antenatal or post-mortem), clinical notes of the circumstances of loss,
autopsy results, and any follow-up arrangements made.13,14 When the event was a perinatal loss, families should be informed
that autopsy results might take several weeks or MONTHS to obtain. Counseling for future pregnancies is important but may
need to be delayed until complete information is available.
Dr. Robert Buckman has suggested two mnemonics for remembering key features of communicating bad news.15 Adaptations
of his strategies are incorporated in the following mnemonics, which may be helpful as a framework for understanding the
principles of effective communication:
1. SPIKES
S Setting (or context). Use effective listening skills, body language, and good eye contact.
P Perception. What does the patient think? Listen carefully to patient’s comprehension and language. Use the same
layperson’s language and choice of words. Attending to the patient’s understanding will allow you to judge just how
much detail you have to provide.
I Invitation. Ask patients what they understand and find out what further information they would like.
K Knowledge. Give the facts in small bites, not all at once. Check their understanding in a reflective way.
E Explore. Explore their emotions and empathize with them. This does not mean you have to experience the same
feelings as the family. Empathy is a skill, not a feeling.
S Strategy (Summary). Set out a plan and follow through. Check back frequently for further needs and to reassess
their understanding. Those who have experienced grief report that it takes about ten repetitions before reality finally
sinks in.

2. CONES
C Context. A quiet, comfortable, private location is desirable. Adequate uninterrupted time will facilitate the
absorption of the information. Patients also need time to reflect and to be able to ask questions. Dr. Buchman also
suggests that we try to position ourselves at or below patient eye level. If culturally appropriate, some physical
contact such as putting a hand on the patient’s forearm may be comforting. It is probably not appropriate to have this
conversation in the delivery suite and it is certainly not acceptable in the middle of the hospital corridor.
O Opening statement. It helps to have a prepared opening statement. Approaching patients with a prepared initial
statement will facilitate the rest of the disclosure. An example of an opening statement would be something like “I
want to discuss…is this a good time for you? Would you like to have a family member or friend here?”
N Narrative. A running narrative of the events leading to the development of the bad news helps set the stage.
Describing the various events and the responses to these events can help clarify the reasons for some decisions that
were made. Relevant facts about the diagnosis and treatments should be presented. The patient should guide with
regard to the amount of information provided. Avoid medical lingo and jargon. Physicians often provide too much
information, or at least too much in too small a time frame. Allow adequate time at the time of the disclosure, and
again at a later date to facilitate understanding. Information might need to be repeated many times. Patients may
need to ask many questions to understand the events fully. Written material might sometimes be appropriate,
provided that it is directly relevant to the situation, and that it is appropriate to the patient’s level of comprehension.
E Empathetic response. It is important to know what to say and also what not to say. The empathetic response
is something like “This must be awful for you”. It is not saying something like “I know how you feel”. Even those who
have had similar experiences do not know how another person might feel.
S Strategies and summaries. Discuss what sort of follow-up will be provided, as well as any strategies to reduce
the repercussions of the bad outcome and to prevent recurrences of the bad outcome (if possible). Make certain
that the patient has adequate opportunity for questions and clarification. The average physician interrupts a patient
18 seconds into a verbal interaction. In these highly emotional situations, uninterrupted active listening (using
appropriate pauses and repetition of what the parents are saying) will reveal more of what is going on in the family’s
mind. At some time, either at the initial visit or at a follow-up visit, it would be appropriate to ask if counseling can
be arranged. Parents who have experienced the loss of an infant are more likely to experience marital breakdown and
express greater dissatisfaction with their relationship.
Internet usage has been reported as an alternative approach, citing anonymity and difference in the traditional face-
to-face.16 Limitations include the potential for misinterpretation, unsuitability for some, and lack of a reliable and
timely approach to patient crisis management.17

Disclosure
Disclosure is the process by which an adverse event is communicated to the patient. In health care, the use of the term
“disclosure” in communications with patients should not be presented or interpreted in any way to imply/assign blame or
fault with respect to the health care provider(s) involved. The term “error” should be avoided in the context of disclosure since
adverse events are known to result, most often, from a complex interplay of factors that are described by Reason’s model of
causation as systems. This is the basis of a “ systems approach” to improving patient safety.18
Note: Each health care organization should have disclosure policies that support both the patient and the health care provider.
Please refer to your organization’s disclosure policy. The Canadian Medical Protection Association has also produced a helpful
document.19 Other resources are also available.
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/families.20,21,22,23 Research has found that patients overwhelmingly
want and expect to be informed of adverse events. Currently however, that disclosure often does not occur.
• 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 the physicians believe that patients should be told about possible future outcomes.
When adverse events occur, patients and families often sense that something has gone wrong. Failure by caregivers to disclose
the event causes the patient and family to feel devalued and disrespected. They lose trust in their caregivers and the health care
organization or system, particularly if they feel that information is being purposely withheld or “covered up”. Sometimes they feel
that the only way they can obtain accurate, complete information is by launching a lawsuit. In fact, in a Canadian study, 76% of
those surveyed believe that threat of litigation is important to ensuring that doctors act in the best interests of their patients.20
The primary driver of considering legal action is not the event itself but rather the patient’s or family’s subsequent interaction
with the people in the health care system. When the harm becomes apparent in spite of the lack of disclosure, or when the
adverse event is finally admitted by the caregiver or organization, patients and families often experience profound anger. This
compounds the trauma already being experienced, and can lead to a desire to punish the caregivers or to seek revenge against
the organization.

Patients/Families Want to Know:18
• The facts about what happened

• The steps that were and will be taken to minimize the harm that may result
• That the health care provider regrets what happened
• What will be done to prevent similar events from occurring in the future
Barriers to Disclosure
• Lack of training, comfort, or skill in communicating difficult information
• Fear of malpractice lawsuits
• Fear of censure, loss of respect and prestige among colleagues
• Loss of self-esteem and self-confidence as a caregiver
• Fear of loss of job/income
• Fear of loss of the respect of patients
• Genuine belief that it is in the best interest of patients not to be informed.24,25
Benefits of Disclosure
For Patients/Families:
• To begin to recover from the devastating effect of the unanticipated outcome, to deal directly with the pain so that
they can begin to heal
• To regain trust, to work out their feelings of distrust with the people inside the institution, rather than those outside of
it
• To understand and obtain the care that may be needed to address the effects of the adverse outcome in the future
• To receive the information needed to make next-step decisions, including the possibility of seeking appropriate
compensation.
For Caregivers:
• To openly and honestly address the error, and engage in ways of preventing future occurrences
• To express regret, to assuage guilt, to begin to heal
• To regain self-esteem and continue to practice.

For Health Care Organizations:

• To learn from, not repeat, mistakes; to create better systems for prevention of adverse events in the future
• To heal psychologically after a mistake by sharing the human face of working in a complex system
• To potentially lessen the frequency and severity of litigation through the proper management and control
of a disclosure process.
Undertaking Disclosure
Skills Needed:
• Ability to establish rapport
• Active, empathic listening
• Ability to anticipate and calmly handle potential anger and conflict
• Lack of defensiveness
• Ability to recognize and manage your own feelings
• Openness and willingness to accept whatever reaction occurs
• Ability to separate the message from the messenger, so that the messenger can be seen as a support person
by the patient/family
Preparation:
• Learn the facts
• Identify and involve the appropriate participants. Do not forget to involve the primary care provider
• Assess the readiness of the patient/family to hear the news
• Choose an appropriate time and setting, keeping in mind the basic principles of communication (e.g., privacy,
language barriers, patient and family needs
• Be well informed regarding the events that occurred. You may do more harm than good if you have incorrect
information
• Identify in advance who will lead the meeting and plan what will be said
• Be aware of your local legislation

Delivery:26
• Describe what happened in plain clear language
• Acknowledge the harm event and the patient’s suffering
• Focus on the needs of patient and family
• Respond to questions
• Establish a follow-up plan
• Explain what is being done to prevent a recurrence
• Offer ongoing availability of contact and support persons
Documentation:18
• Time, place, and date of the meeting
• Identities of all attendees
• Facts presented
• Offers of assistance and the responses
• Questions raised and the answers given
• Plans for follow-up, including contact information for an appointed contact person
Disclosure most often happens over time. It is helpful to think of disclosure in two broad stages that may require several
conversations with the patient and family.
The first stage, initial disclosure, should occur as soon as possible after the event. In this initial stage, rarely will all of the
contributing factors to the event be known. The facts that are known should be communicated during the initial disclosure.
The second stage of disclosure is called the post-analysis disclosure. These conversations happen when the reasons for the
event are better understood. It is important to share any changes that have been implemented to prevent a similar event in
the future.
As a resource, read the Canadian Patient Safety Institute (CPSI) Canadian Disclosure Guidelines.18

Caring for Caregivers

• Expect feelings of sadness, guilt, erosion of self-esteem as healers, drained emotional stamina, fear of litigation
or loss of prestige
• Anticipate that caregivers may not recognize their need for help and support, or may be unwilling to request
assistance; reach out to them
• Look for later effects such as caregivers psychologically distancing themselves from patients; this unresolved issue
can lead to caregiver burnout and/or ineffective patient care
• Debrief, offer counseling, support and acknowledgment of feelings21,25,27,28,29,30,31,32,33,34
• A 2011 observational study of intrapartum nurses’ experience in a traumatic birth, 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”.7 This observation, while predictable and frequently documented in women
having traumatic birth,35,36,37,38,39,40 had not been previously published. It is only a matter of time before this is
documented for the other members of the health care team.
Caring for Ourselves

• Reflection
• Remember your own losses
• Review your coping style
• Understand your own healing
• Deal with feelings of guilt
• Seek out a supportive colleague
• Many may wish to get professional counseling.
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 emotion 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 birth crises.

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Appendix
http://www.pailnetwork.ca/resources/
The links provided herein are provided for your convenience and are not under the control of Pregnancy and Infant Loss Network,
and are not intended as an endorsement or an affiliation by Pregnancy and Infant Loss Network (PAIL Network) or individual so
linked or named.
1. First Candle: http://www.firstcandle.org/
First Candle is an American nonprofit organization dedicated to safe pregnancies and the survival of babies through
the first years of life. “No matter how deep your grief and how great your pain, remember that you are not alone.
First Candle, along with others who have traveled this road before you, are here to help you through the difficult time
following the death of your baby.”
2. The Canadian Foundation for the Study of Infant Deaths: http://www.sidscanada.org/
Since 1973, volunteers from the Canadian Foundation for the Study of Infant Deaths have provided support to
Canadian families affected by the tragedy of the unexpected loss of an infant or child. This Foundation also raises and
distributes funds to enable ground-breaking research and lifesaving advocacy work. The CFSID delivers infant health
and safety education through an extensive network of volunteers in communities all across Canada. CFSID provides
resources and services for all infant deaths including miscarriage and stillbirth with respect to peer support, public
education, awareness and supports Sudden Infant Death Syndrome (SIDS) related research.
3. Now I Lay Me Down To Sleep: http://www.nowIlaymedowntosleep.org/
NILMDTS aims to introduce remembrance photography to parents suffering the loss of a baby with a free gift of
professional portraiture. NILMDTS educates and mobilizes professional quality photographers to provide beautiful
heirloom portraits to families facing the untimely death of an infant. NILMDTS believes these images serve as an
important step in the family’s healing process by honoring the child’s legacy.
4. Bereaved Families of Ontario: http://www.bereavedfamilies.net/
Dedicated to bereavement support through self-help and mutual aid. BFO programs are facilitated by volunteers
who are themselves bereaved. BFO provides compassionate non-denominational mutual aid support for families
and individuals who have lost a significant person to death. BFO affiliates also support parents, guardians or family
members helping a child grieve. As well, they support the unique circumstances faced by survivors of violent death,
survivors of completed suicide, and families seeking pregnancy after loss.

5. Honored Babies: http://www.HonoredBabies.org/

An American site, on a smaller scale but personal and informative. Honored Babies is a support and resource
organization for women whose babies have died. It also supports family members and informs the community.
6. The Hospital for Sick Children, Toronto: http://www.aboutkidshealth.ca/
This website belongs to the Hospital for Sick Children and is a comprehensive site offering access to information about
various illnesses, diagnoses, and diseases. Parents and family members may find this site helpful if they are seeking
further information and understanding about what conditions may have been associated with their infant’s death. It
includes a link for both Parents, and Health Professionals.
7. Postpartum Support International: http://www.postpartum.net/Get-Help/Loss-Grief-in-Pregnancy-and-
Postpartum.aspx
The purpose of the organization is to increase awareness among public and professional communities about the
emotional changes that women experience during pregnancy and postpartum. When the mental health of the
mother is compromised, it affects the entire family. Its goal is to provide current information, resources, education, and
to advocate for further research and legislation to support perinatal mental health.
8. Compassionate Friends: http://www.compassionatefriends.org/
The Compassionate Friends provides highly personal comfort, hope, and support to every family experiencing the
death of a son or a daughter, a brother or a sister, or a grandchild, and helps others better assist the grieving family.
9. SHARE Pregnancy and Infant Loss Support: http://www.nationalshare.org/
Their mission is to serve those whose lives are touched by the tragic death of a baby through pregnancy loss, stillbirth
or in the first few months of life, to provide support toward positive resolution of grief experienced at the time of, or
following the death of a baby. This support encompasses emotional, physical, spiritual, and social healing, as well as
sustaining the family unit.
10. RESOLVE through Sharing: http://www.bereavementservices.org/
Bereavement Services developed a bereavement care program known as Resolve Through Sharing (RTS), and they
have educated more than 30 000 healthcare professionals over 30 years. Their mission is to provide and promote
dignified, respectful, and compassionate bereavement care for patients and families suffering loss throughout the
continuum of life.
11. Grieve Out Loud: http://www.grieveoutloud.org/
Grieve Out Loud was started in January 2010 by a group of parents who understand the pain of losing a baby and are
passionate about helping others in their own grieving process.
12. March of Dimes: http://www.marchofdimes.com/baby/loss.html

13. MISS Foundation: http://www.misschildren.org/

The MISS Foundation is an international volunteer-based organization providing C.A.R.E. [counseling, advocacy,
research, and education] services to families experiencing the death of a child.
14. Griefwatch (for perinatal loss): http://www.griefwatch.com/
The Grief Watch site was created to provide bereavement resources, memorial products and links that can help
someone through their personal loss. It also serves as an excellent educational tool for all who travel down the road of
grief. Please use this site to learn more about grief and the individual needs of the bereaved.
15. Solace for Mothers (Birth Trauma & Recovery): http://www.solaceformothers.org/
Solace for Mothers is an organization designed for the sole purpose of providing and creating support for women who
have experienced childbirth as traumatic. Birth trauma is real and can result from an even seemingly “normal” birth
experience. The resources available through this site offer immediate, personal support to mothers and others who are
struggling with birth trauma, PTSD after childbirth and anxiety caused by their birthing experiences.
Source: Pregnancy and Infant Loss Network [web site]. Pickering (ON): The Network. Available: http://www.pailnetwork.ca/.

Chapter 4
Risk Management and Patient Safety
Introduction
Human nature is such that everyone makes mistakes. The inevitability of human error exposes patients and all caregivers to
risks. These risks may result in significant adverse outcomes and patient injury. The development of patient safety and risk
management programs in each obstetrical unit offers important benefits including improved patient care, reduced medico-legal
risks, and lower costs. Establishing systems and processes that minimize the likelihood of errors and maximize the likelihood of
intercepting them before they occur is essential to ensuring patient safety.
Definition
Risk management: The development and implementation of strategies to optimize patient well-being and to prevent or
limit patient injury. Its focus is to reduce errors that result in significant costs related to damage, harm, discomfort, disability, or
distress to the patient and to reduce financial loss to individual health care providers and the organizations that they represent.1
Patient safety 2,3
• Absence of harm resulting from the provision of care
• Reduction and mitigation of unsafe acts
• Use of best practices
• Build resilience—adjust to match conditions
• A critical aspect of quality of health care
Risk Management and Patient Safety 1

Clinical Error – The Problem

• 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.4 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.5 The overall social cost of clinical
error approached $38 billion annually. Approximately half of this ($17 billion) was associated with preventable errors.5
• 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.6
• 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.7
• The Canadian Adverse Events Study8 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.8
• An article in 2011 suggested that the “’Global Trigger tool’ shows that adverse events in hospitals may be ten times
greater than previously measured”.9
• In 2013, John James wrote in the Journal of Patient Safety the following conclusion following 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.”10
• 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. 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.”10

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. The
opinion of some health care providers and hospital administrators is that adverse events in obstetrical practice are inevitable.
Is this opinion correct? Realities that influence the relationship between human error, organizational structure, and systems
theory that must be considered include:
• 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 world of flawed systems. However, our systems expect us to be the final protector of the patient from our flawed
systems. Errors should be recognized as consequences rather than causes.11, 12

Defenses Against Error

Like other organizational structures, the health care system has developed defenses and safeguards. When these defenses are
breached by hazards, losses may occur.
Adapted with permission from: Reason J. Managing the risks of organisational accidents. Aldershot (UK): Ashgate Publishing; 1997.
Classification of Defenses
1. Human: e.g.,
• Training
• Knowledge
• Judgment
• Manual dexterity
• Vigilance

2. System: e.g.,
• Credentialing
• Peer review
• Protocols/pathways/policies
• Special teams
• Continuing medical education
• Risk management/quality management
Failures, Errors and Accidents

Our current medical system functions like any complex technological system. Professor James Reason has described how human
beings contribute to the breakdown of such systems.12 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 consequences rather than principal causes.
He states that “people working in complex systems make errors or violate procedures for reasons that generally go beyond the
scope of individual psychology.”12 These reasons he calls latent failures (conditions). In the health care system, this concept
can be described as a pyramid. At the sharp end are patients and health care providers. The major factors that determine safety at
the sharp end are related to latent conditions/systems located at the blunt end and at various levels throughout the pyramid. It is
at the sharp end of the care system that all of the factors that determine safety come together creating
“safe” or “unsafe” health care.

Adapted with permission from: Reason J. Managing the risks of organisational accidents. Aldershot (UK): Ashgate Publishing; 1997.

Classification of Failures:
Two types of failures can occur in the defenses.12
1. Active Failures:
• Occur at the “front-line” level (the individual)
• Have an immediate effect
• Affect the patient directly
• Traditionally have resulted in some form of ‘punishment’ and/or retraining of the individual involved.
Disciplinary action:
• Discourages reporting
• Usually doesn’t prevent recurrence of the same or similar events
• Is not educational for the team and/or other colleagues
• Allows latent failures to remain in the system
Descriptions and examples of active failures include:
• slip (often due to fatigue): Administration of the wrong drug, dosage. Think of dialling a well-known number
(your mom’s) and getting your local pizza dealer! Did you really NOT KNOW the number? Would retraining help you
prevent this error in the future?
• lapse: Forget to catheterize the bladder pre-Caesarean section. Think of going to the store for three items and
forgetting one. As you step in the house you remember what that last item was. Would retraining help? But we can
immediately see how a “checklist” might mitigate this risk.
• mistake: Misinterpretation of an electronic fetal monitor (EFM) pattern.
• procedural violation: Apply vacuum cup before full dilation of the cervix.

2. Latent Failures:
• Are removed or distant from direct “front-line” control
• May involve poor design or maintenance decisions
• Have little direct effect
• Have a cumulative effect
• Do not usually result in predictable effects (active failures)
• Are the greatest threats to patient safety
• Are a problem with the system rather than the individual
• Latent failures may be classified as:
• Human factors. E.g.,
• Fatigue from a long shift
• Stress
• Multi-tasking
• One patient, three different care providers
• Local workplace factors. E.g.,
• Inadequate tools/equipment
• Poor communication and teamwork
• Unworkable or ambiguous procedures/protocols
• Leadership shortcomings
• Insufficient staff training
• Staff shortages
• Organizational factors
Arise from strategies and top-level decisions made by:
• Governments (e.g., budget cut to hospital)
• Regulating bodies (e.g., change in scope of practice)
• Manufacturers (e.g., different drugs in similar appearing containers)
• Hospital administrators (e.g., staff reductions in face of increasing patient load)

How do These Breaches Lead to Harm?

Professor Reason states “In an ideal world, each defensive layer would be intact. In reality, however, they are more like slices of
Swiss cheese, having many holes—though unlike in the cheese, these holes are continually opening, shutting, and shifting their
location. The presence of holes in any one “slice” does not normally cause a bad outcome. Usually, this can only happen when
the holes in many layers momentarily line up to permit a trajectory of accident opportunity—bringing hazards into damaging
contact with victims.”13 Following this theory, one can easily understand that the trajectory of an error is unpredictable.
Current practice cultures make up an environment embedded with potential accidents waiting to
happen.
BMJ 2000;320(7237):768-70. Adapted and reproduced with permission from the BMJ Publishing Group.
The above model assists us in understanding the concept of a sequence of events that when taken individually will often not lead
to harm, but when placed together create the context of an event. We can also understand from this model that the stopping
of an arrow is often the act of a human—usually a wonderful, well-intentioned member of our front-line team who will often

not report his or her achievement. Our culture traditionally would not look favourably on an individual having a ‘near miss’. What
would we say to someone who came up to us and announced: “Look at me! I nearly gave the wrong drug!”Yet, for us to advance
in our efforts in patient safety, we owe it to ourselves and the patients whom we serve, to report these near misses and study
them. We need to understand that a sequence of events exists 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 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 recommendations by the individuals at the front line is key to
developing a local ownership to problems and create a culture of patient safety. 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.14
“We need to grow out of a culture of blame into a just culture…a culture in which individuals are still held
accountable for their actions, but are not held responsible for flawed systems in which they work.”15
Dr. R. Amalberti proposed a further reflection on Reason’s model in 2001. In his reflection he proposed that if an individual is
allowed to ignore a policy (or any other type of defense mechanism—i.e., a slice of Swiss cheese in Reason’s model), then
the arrow simply goes around a slice of cheese. Thus there are fewer layers to navigate before reaching the patient. This clearly
underlies the fact that even though none of our defenses is perfect (all have holes), they are better than nothing. It is essential
for caregivers to follow policies unless there are valid reasons that are understood by the team of caregivers, and documented.
A system should be in place to allow the review of any policy that is of dubious benefit or quality. But until it is replaced, all must
use it consistently. This assists in the standardization of complex care and the promotion of safety.
We know absolutely how to provide a patient with the best care on the planet. We cannot, however, seem to provide it to each
and every patient consistently – this can change as we create and embed patient safety into our team’s 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 errors in
a complex dynamic system such as Healthcare.
Safety II
Safety II is a new concept that looks at safety from a different perspective.
While understanding the need to improving processes that leave the patient vulnerable to human error (the traditional approach
to Safety or Safety I), Safety II focuses on the important realization that it is remarkable that so many patients have positive

outcomes despite important challenges to Care Teams. The 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 to maintain care operations despite these challenges as a way to improve existing
systems (the existing systems are known as: work as imagined).
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.
The important message here is that it is not a competition between Safety I and Safety II, but a balance between the two.
The MOREOB Program has identified that the secret in sustainable safety lies in the balance between the two. MOREOB seeks to
identify that perfect 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.
The Process of Risk Management

Most maternity caregivers in Canada are not actively involved in their own risk management programs. Risk management
programs should be developed in collaboration with provincial regulators, national professional associations, hospital
accreditation bodies (e.g., Accreditation Canada), and other health care organizations. An example of a national initiative is the
SOGC’s Policy Statement on Attendance at Labour and Delivery,16 which has been developed with input from the CMPA and
provides guidelines for physicians attending labour and birth.
Risk identification must concern itself with all aspects that may threaten and/or jeopardize the patient, caregiver, and facility. Risk
cannot be completely or constantly avoided. The intention in risk management is to anticipate risk and prevent or limit harm.
Risk management has five basic steps:17
• Identification of risk
• Risk assessment
• Development of risk management strategies (taking action to manage risks)
• Implementation of risk management programs
• Evaluation of risk management activities

A) 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 it, or something like it, happened before?
• Risk can also be identified when practitioners are informed about particular risks inherent in their group or profession
B) 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
C) Action to Manage Risk:

There are six risk control strategies.
1. AVOIDANCE of risk (results in no loss)
A person can stop carrying out a function that is associated with a high degree or incidence of risk (e.g., high forceps).
2. PREVENTION of risk
Hospitals and maternity caregivers can take steps to prevent or significantly lower the possibility of mishap.
Establishing risk management programs will help prevent events from occurring and thereby reduce adverse
outcomes (e.g., clinical practice guidelines, quality assurance).
3. TRANSFER of risk
A high-risk case can be transferred to a higher level of expertise for care (e.g., preterm labour).
4. REDUCTION of risk (results in some loss)
Prevention and reduction may be confused. It is important to note that reduction is the strategy that is called into play
after the damaging event has occurred. One of the most important risk reduction strategies is the immediate care and
attention to persons threatened or injured. Losses attended to immediately can often be mitigated.
Losses can be reduced after an event, in a number of ways. Losses can be reduced through early investigation and
documentation and the provision of full and honest disclosure.

5. SEGREGATION of risk
Segregation is usually more applicable to facilities (e.g., Level I, II, III hospitals) than to individual caregivers. 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).
6. 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.
D) 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.
E) Evaluation of Risk Management Strategies:

It is essential to review the effect of a new process or strategy that was introduced to reduce or eliminate risk. Did the strategy
achieve the expected results? Reviews should be as frequent as required to cover the entire risk experience. A committee
may be appointed to monitor activities. Reports on the success of initial attempts at implementation are integrated into the
management plan.
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. The process is then repeated.

High Reliability Organizations (HROs)

• An HRO is defined by its ability to operate technologically complex systems without error over long periods of time.18-22
• To help distinguish which organizations could be considered high reliability organizations, ask the following question.
“How many times could the organizations’ systems have failed with potential catastrophic consequences but did not?”
If the answer to your question is many, many times, then it is likely a high reliability organization.
• Several organizational structures have been studied in detail by behavioural 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)
• electric power grids
• These organizations have three defining characteristics:
• they are complex, internally dynamic, and intermittently, intensely interactive
• they perform exacting tasks under considerable time pressure
• 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 structure 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/
crisis has ended, the organization returns seamlessly to its routine control mode.13
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. However, due to the
way hospitals function, it appears that all too frequently, no one seems to be listening. This leads to an unengaged
workforce. A risk of an unengaged workforce is ‘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 ‘buy-in’ as described by Zimmerman et al. and is a warning sign. It is a symptom of 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.23,24
“HROs are aware and adaptive enough to intercept or mitigate threatening events and circumstances”.23
HRO principles as adapted for Healthcare:

1. Safety is the priority and is everyone’s responsibility
2. Operations are a team effort
3. Hierarchy disappears in an emergency. Decisions about safety can be made at any level of the organization
4. Communication is highly valued
5. Emergencies are rehearsed
6. There is interprofessional review of routine functions, near misses and unexpected events25
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”.26,27 Unknowingly, 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.27 A unit is at its most dangerous when nothing bad has
happened for a while.
• HROs “actively and continually question assumptions, promote orderly challenge of operating practices and solicit
outside views of the routine”27 in order to address normalization of deviance.’
Perinatal/obstetrical units and High Reliability Organizations (HROs)

“Understanding updated and refined concepts of high reliability in the delivery of obstetrics care requires and understanding of
what high reliability is not (i.e., a quality improvement method focused on efficiency and productivity like Six Sigma, Total Quality
Management, or LEAN). Rather, high reliability is a creation of a culture and processes that radically reduce system failures and
effectively respond when failures do occur.”28

Perinatal units have many of the characteristics of HROs including:

• They are complex, technical environments with a variety of professional disciplines that have diverse roles and
responsibilities
• Patients, their families, and friends expect obstetrical units to function without error over long periods of time25
• Normalization of deviance is a characteristic of obstetrical/perinatal units. Examples are:
• 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 (ARM) when the head is a little too high
Obstetrical units that have successfully adapted HRO principles have implemented the following:25
1. They have a clearly stated goal and purpose—Patient Safety
2. A clear language that defines patient safety as maternal and fetal well-being
3. They have established clear and agreed-upon markers of maternal and fetal well-being
4. A clearly defined organizational teamwork:
• high reliability perinatal units thrive on teamwork—hierarchies are minimized
• everyone is respected and recognized as competent
• everyone knows what everyone else is thinking and seeks opportunities to help one another
• everyone is focused on patient safety
• planning, data collection, and quality management are interprofessional exercises
5. Patient care records 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 journey in
our care. Electronic Health Records have brought a whole new dimension of challenges in this area.
6. Policies are unit-wide rather than separate for each profession (nursing, medicine, midwifery, etc.)
• 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 does exist 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. There are two clear operating principles:
• Adherence to professional guidelines
• Minimal intervention but with the ability to intervene, when necessary, in a timely manner

8. There is 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. Patient safety will always override hierarchy
A Doctor and an Aviator

I recently had the pleasure of attending an airshow, as a guest of my husband, a military
pilot and astronaut. As an obstetrician and gynecologist and a MOREOB Program trainer,
it was with great curiosity and intrigue that I was able to observe a debriefing for our Air
Demonstration Team, the Canadian Forces Snowbirds.
As a MOREOB Program trainer since 2004, I have been presenting slides and videos that
highlight how medical errors are preventable using principles from High Reliability
Organizations such as the aviation industry but until this weekend, I had no idea just how
applicable, yet difficult to implement, these principles really are.
The Canadian Forces Snowbirds put on a spectacular show. It was precise, sharp, clean and
very, very beautiful. I was awestruck!
And then I attended the debriefing and my delight turned to absolute shock. As a physician
who carries out complex procedures with a healthcare team regularly, I was not prepared
for the discussion that followed.
Utilizing an unforgiving video replay, the Team Lead, Major Wayne Mott asked if there
were any identifiable safety issues during the routine. A few pilots started to describe
some minor issues that could have led to events (i.e., No harm events), and the Team
Lead evaluated this discussion as the team took individual notes. Nothing significant was
identified and they moved along.
The second step was even more remarkable as each member evaluated his own
performance identifying even slight miscalculations for others to watch, consider, and
comment. I sat in amazement as pilots, with rather large egos by nature, openly revealed
the inner workings of their personal show with the goal of indicating to their team
members that they could see the strengths and, more importantly, the weaknesses in their
performance. They debrief after EVERY practice and EVERY show all year long. They don’t

skip the debriefing when they are exhausted, busy, missing their families and trying to get
home. That would be a direct insult to their fellow team members.
To the untrained eye, the show was a miracle in the sky. There were no errors to be seen and
I sat bewildered at the honesty in the room during debriefing. Any one of those pilots could
have easily hidden their tiny mistakes and no one would have known, each busy flying
their own part.
In medicine, if everything goes well, as it usually does, how often do we, as a team, discuss
what COULD have gone wrong? And more interestingly, how often do we identify our own
errors in front of each other, placing them in the open for scrutiny? Consider doing this
after EACH delivery and surgical procedure, even if everything went “perfectly” well.
In talking with a few of the guys after the show, I asked why they were so tough on
themselves, talking about minor movements that had no real impact on their overall
performance. They described to me a culture of professionals that actually LOSE integrity
and the respect of their team if they DON’T see and discuss their own errors. It is seen as a
trust issue.
“If you can’t see your own errors there is a good chance that someone else will and then you
will lose credibility. If you can’t see your inaccuracies then you certainly can’t be trusted to
fix them.” I was told by one tall, handsome man in red.
After teaching the MOREOB Program for eight years, and being married to a pilot for
10 years, I thought I understood the relationship between medicine and aviation. I now
realize that aviation still does HRO principles so much better than we do, that we continue
to have a lot to learn from them, and that even arrogant, seemingly difficult personalities
in medicine can learn to change their culture. That changing the culture of how we view
our own personal errors and our expectations of each other must continue to evolve if we
are to keep patients safe in our hospitals.
One pilot told me he witnessed the vaginal delivery of his baby and, after a delay to cry she
was whipped over to the warmer, assessed, and handed back to his wife. He thought all
seemed well but was uncertain about what had happened and, as a good aviator would,
waited for the debriefing. The doctor walked out leaving him and his wife to wonder
what just happened and how their little girl rated on her entry into life. Was it nominal?
Abnormal? What should they expect? What should they watch for? He was awaiting

communication from the commander in the room. He had just observed a beautiful entry
of life into the world and was left with emptiness and even some fear. As physicians, we
know that if things weren’t okay, the doctor would have stayed longer but my pilot friend
didn’t understand the culture of a profession that walks away from an event so amazing
and doesn’t talk about whether all was as expected.
The airshow events have renewed my motivation and my hope that we can eliminate
preventable errors in our profession too. We are not there yet but, thanks to Salus Global
and the MOREOB Program, we have started down that road of culture change, acceptance,
and recognition of human error and distribution of tools necessary to make the delivery
room as safe as the sky.
(Dr Catherine Hansen, Friendswood (Texas, USA): personal communication, 2013 Feb 18)
Does a High Reliability Unit Work? YES!

The MOREOB program is a patient safety program designed around the HRO principles and centered on team function and culture
change. It was created in 2001 by the Patient Safety Division of the SOGC. Authors from Alberta, a province where the program
was initiated province-wide, revealed that, among the indicators they selected for their 2009 study, the program had a positive
effect on health service delivery as well as on newborn and maternal outcomes.29
Another example of the potential of the HRO approach was published in 2009. Element two of the HRO principles is “Operations
are a team effort”, Element five is “Emergencies are rehearsed”. Using a design intended to address both these elements as they
pertain to the management of cord prolapse, researchers found an important improvement in management, most notably a
significant reduction in the diagnosis-to-delivery time interval.30
In summary, A high reliability obstetrical unit is an organization where a safety oriented culture
prevails
• All who work in the unit are orientated to confirming fetal and maternal well-being. Variations are reduced by
standardizing policies and procedures where they can be
• Teamwork is the hallmark of the unit. Interprofessional review of adverse outcomes and near misses are practiced
in a non-punitive and educational environment

Quality and Risk Management—Health Care Provider

Responsibilities:31
a) Identify high-risk procedures
b) Recognize errors before they become adverse outcomes
c) Ensure that health care providers are aware of their limits and practice within these limits
d) Review near misses, accidents, injuries, and adverse events as system failures rather than individual failures
e) Establish an environment for clinical error management
f) Eliminate the “blame” and “punitive” culture associated with adverse events
g) Be aware of local, regional, and national clinical guidelines and policy statements
h) Remember the three A’s of quality care and risk management:
• ability
• accessibility
• availability
i) Promote a culture where communication and team-building occur. This aids in taking down the hierarchical
professional barriers
j) Collaborate at a local, regional, and national level to develop performance indicators and benchmarks for clinical
activities
Caregiver Participation
Interprofessional committees are needed to promote teamwork and patient safety. A facility cannot pretend that it has a risk
management system if it does not have the full participation of all of its maternity care providers. This includes middle and senior
administrators. It is not enough for a health administrator to handle liability questions that arise in the course of obstetrical care.
Similarly, it is not enough for the Risk Management, Nursing, or Health Information departments to initiate incident recognition
and reporting without the participation of front-line caregivers from all other professions in the unit. Health care providers will only
“buy in” to risk management activities if they are aware of the positive benefits of these activities for their patients and themselves.

Summary
1. The high reliability obstetrical unit is an organization where a safety-oriented culture prevails.
2. HRO principles are incorporated into Birthing Unit activities to successfully promote a culture of safety.
3. Everyone who works in the Birthing Unit is committed to confirming fetal and maternal well-being. Variations in
practice are reduced by standardization of policies and procedures.
4. Teamwork is the hallmark of the unit.
5. Interprofessional review of adverse outcomes (harm events) and near misses (no harm events) are practiced in a non-
punitive and educational environment.
6. Individual practitioners establish risk management strategies in their practice.
7. Everyone participates actively in hospital patient safety and risk management programs.
8. All health care providers are aware of local, state or provincial, and national clinical guidelines and policy statements.
9. The most effective criteria for risk management are:
• ability
• availability
• accessibility

References
1. Moss F. Risk management and quality of care. In: Vincent C, editor. Clinical risk management. London: BMJ Publishing; 1995.
2. Braithwaite J, Wears RL, Hollnagel E. Resilient health care: turning patient safety on its head. Int J Qual Health Care
2015;27(5):418-420.
3. Davies J, Hebert P, Hoffman C. The Canadian Patient Safety Dictionary. 2003. Ref Type: Online Source
4. Kohn LT, Corrigan JM, Donaldson MS. To err is human: building a safer health system. Washington: National Academy
Press; 2000.
5. VanGeest JB, Cummins DS. An education needs assessment for improving patient safety: results of a national study of
physicians and nurses. North Adams (MA): National Patient Safety Foundation; 2003.
6. HealthGrades in the news. Golden (CO): Health Grades, Inc.; 2006.
7. Department of Health. An organisation with a memory: report of an expert group on learning from adverse events in the
NHS. London: The Stationery Office; 2000.
8. Baker GR, Norton PG, Flintoft V et al. The Canadian Adverse Events Study: the incidence of adverse events among hospital
patients in Canada. CMAJ 2004;170(11):1678-1686.
9. Classen DC, Resar R, Griffin F et al. ‘Global trigger tool’ shows that adverse events in hospitals may be ten times greater
than previously measured. Health Aff (Millwood) 2011;30(4):581-589.
10. James JT. A new, evidence-based estimate of patient harms associated with hospital care. J Patient Saf 2013;9(3):122-128.
11. McLean P. On the job: legal matters. Liability trends in nursing. Can Nurse 2002;98(6):32-34.
12. Reason J. Managing the risks of organisational accidents. Aldershot (UK): Ashgate Publishing; 1997.
13. Reason J. Human error: models and management. BMJ 2000;320(7237):768-770.
14. Pronovost PJ, Holzmueller CG, Ennen CS, Fox HE. Overview of progress in patient safety. Am J Obstet Gynecol
2011;204(1):5-10.
15. Saving lives. Saving money. Saving time [brochure]. London (ON): Salus Global Corporation; 2011.

16. Executive Committee of the Society of Obstetricians and Gynaecologists of Canada. Attendance at labour and delivery:
guidelines for obstetrical care [SOGC policy statement no 89]. J Soc Obstet Gynaecol Can 2000;22(5):389-391.
17. Dickson G. Principles of risk management. In: Vincent C, editor. Clinical risk management. London: BMJ Publishing;
1995:18-30.
18. Grabowski M, Roberts KH. Risk mitigation in large scale systems: lessons from high reliability organizations. Calif
Manage Rev 1997;39(4):152-162.
19. Roberts KH. Some characteristics of one type of high reliability organization. Organization Science 1990;1(2):160-176.
20. Roberts KH. Cultural characteristics of reliability enhancing organizations. J Manag Issues 1993;5(2):165-181.
21. Rochlin GI, LaPort TR, Roberts KH. The self-designing high-reliability organisation: aircraft carrier flight operations at sea.
Nav War Coll Rev 1987;40(4):76-90.
22. Weick KE, Roberts KH. Collective mind in organizations: heedful Interrelating on flight decks. Adm Sci Q 1993;38:357-381.
23. Niedner MF, Muething SE, Sutcliffe KM. The high-reliability pediatric intensive care unit. Pediatr Clin North Am
2013;60(3):563-580.
24. Zimmerman B, Reason P, Rykert L, Gitterman L, Christian J, Gardam M. Front-line ownership: generating a cure mindset
for patient safety. Healthc Pap 2013;13(1):6-22.
25. Knox GE, Simpson KR, Garite TJ. High reliability perinatal units: an approach to the prevention of patient injury and
medical malpractice claims. J Healthc Risk Manag 1999;19(2):24-32.
26. Mannarelli T, Roberts KH, Bea R. Learning how organizations mitigate risk. J Contingencies Crisis Manag 1996;4(2):83-92.
27. Vaughan D. The Challenger launch decision: risky technology, culture, and deviance at NASA. Chicago: University of
Chicago Press; 1996.
28. Knox GE, Simpson KR. Perinatal high reliability. Am J Obstet Gynecol 2011;204(5):373-377.
29. Frick C, Nguyen T, Jacobs P, Sauve R, Wanke M, Hense A. Outcomes following province-wide implementation of the
Managing Obstetrical Risk Efficiently (MOREOB) program in Alberta [poster]. 6-17-2009. Halifax. 65th Annual Clinical
Meeting of the Society of Obstetricians and Gynaecologists of Canada. Ref Type: Music Score
30. Siassakos D, Hasafa Z, Sibanda T et al. Retrospective cohort study of diagnosis-delivery interval with umbilical cord
prolapse: the effect of team training. BJOG 2009;116(8):1089-1096.
31. Bodenheimer T. The American health care system--the movement for improved quality in health care. N Engl J Med
1999;340(6):488-492.

Chapter 5
Women’s Sexual and
Reproductive Health
Introduction
Sexual and reproductive health is of concern to both men and women. The Program of Action developed during the 1994
International Conference on Population and Development (Cairo) by the United Nations defines it as:
a state of complete physical, mental and social well-being [which goes beyond the absence
of disease or infirmity], in all matters relating to the reproductive system and its functions
and processes. Reproductive health therefore implies that people are able to have a
satisfying and safe sex life and that they have the capability to reproduce and the freedom
to decide if, when and how often to do so.
Everyone should thus get involved in the search for the optimal state of health and welfare for all with regards to issues of
reproduction, contraception and sexuality. Access to skilled health professionals and information on the subject is a crucial part
of our society. Maternal and perinatal mortality is often a direct consequence of the social and economic inequalities plaguing
women and/or of the violation of their rights.
Fortunately, in our developed society, women benefit from several levels of protection, whether they be legal ones or ones provided
by various governmental and non-governmental organizations. The Canadian Charter of Rights and Freedoms, universal access to
health care for all Canadians, the various family support programs offered by the government, and the policies on access to care
developed by various organizations, including the SOGC, are perfect examples of the reason why maternal mortality rates recorded
in the last few years have never been so low – less than 5 per 100 000 live births (Health Canada, 1995 data).
Women’s Sexual and Reproductive Health 1

However, where some subgroups are concerned, many improvements still need to be made. For example, geographical isolation,
belonging to certain cultural or religious groups, social isolation (due to poverty, violence, sexual orientation, etc.) and the silence
in which the sexuality of adolescents and the handicapped is often shrouded can result in the deterioration of some women’s
sexual and reproductive health. It remains within our purview, as professionals involved in the provision of care to women, to
promote even more equality for all women with regards to choices that may affect their sexual and reproductive health.
An Issue of International Concern

In 2002, the international community reached a global consensus on the reduction of poverty and the major improvement of the
quality of life for people all over the world. The Millennium Development Goals target certain indicators that can influence
global development for all, especially women. Two of these objectives are of particular interest to us:
• Promote gender equality and empower women
• Improve maternal health
In the wake of this consensus, FIGO’s (International Federation of Gynecology and Obstetrics) member societies adopted a code of
ethics that promotes three professional responsibilities aiming to improve women’s sexual and reproductive health.
1. Professional competence: women are entitled to receive care satisfying recognized criteria of excellence, as
well as to a respectful professional attitude from caregivers. This aspect also covers the refusal to promote or perform
interventions that violate human rights.
2. Women’s autonomy and confidentiality: this includes respect of their values and their involvement in the
provision of care.
3. Responsibility to the community: care providers get involved in public education, the improvement of access
to appropriate care and advocacy of women’s rights in terms of their sexual and reproductive health.
Local Involvement
For several years, the SOGC has been involved, through its International Women’s Health Program, in the promotion of women’s
sexual and reproductive rights, in the hopes of improving women’s sexual and reproductive health. The objective is to ensure
adequate management of the care to be provided during pregnancy and childbirth, as well as the presence of skilled personnel
to ensure follow-up, in order to create an environment that is favorable to the provision of quality care with the help of various
professional associations throughout the world. The ALARM International course is one of the tools used for that purpose.

However, it is becoming more and more important to promote those same values locally, and it is essential that all care providers
get involved in the improvement of the quality and accessibility of care. Several factors can explain the rise of maternal and
perinatal morbidity and mortality within certain segments of the population:
• malnutrition (chronic and/or during pregnancy)
• inadequate and inaccessible health care
• poor social and health conditions
• social and economic factors (poverty, lack of decision-making power, etc.)
• teen pregnancy
The ALARM course can therefore contribute to the improvement of the quality of care and to the search for professional skill, as
promoted by FIGO. Other tools are also available to help us reach for excellence in practice and acquire the communication skills
needed to promote and respect women’s autonomy within the process of care.
We must, however, consult in order to pool our resources, so we can globally improve our patients’ sexual and reproductive
health. Indeed:
“It is not enough to be clinically competent. It is not enough to be socially aware and
socially conscious. The obstetrician and gynaecologist must be a champion for ALL
women’s health, welfare and rights… (they) must become the voices of the voiceless, the
champions of the neglected, the militants of the poor. Their leadership and their social
and economic clout are needed to make essential obstetric care available to all women.
Their actions and voices are necessary to shift resources at the national level...to improve
…health systems. It is time…to move beyond the consulting room, beyond the hospital
ward, to play a prominent part in the revitalization of the health system as a whole.”
Dr. T. Türmen, World Health Organization (WHO),
International Federation of Gynecology and Obstetrics (FIGO)
Pre-Congress Workshop, August 2000.

Chapter 6
Management of Labour
Introduction
Labour management should support the physiological process of birth while identifying potential concerns. It should allow
interventions that will increase the likelihood of a vaginal birth. Promotion of normal birth involves a balance between non-
intervention and the judicious use of technologies that support safer outcomes for mother and baby.
Definitions
Labour – first stage Regular uterine contractions plus cervical change (dilatation and effacement). The first
stage of labour includes the latent and active phases.
• Latent phase The presence of uterine activity resulting in progressive effacement and dilatation of the
cervix proceeding to the active phase. It is complete when a nulliparous woman reaches
4 cm dilatation and a parous woman reaches 4–5 cm. Cervical length should be less
than 1 cm.
• Active phase The presence of a pattern of contractions leading to cervical effacement and dilatation
after 4 cm dilatation in a nulliparous woman or 4–5 cm dilatation in a parous woman.
Labour – second stage Full dilatation to delivery of the baby
• Passive second stage Full dilatation but without active pushing
• Active second stage Full dilatation with active pushing
Labour – third stage Immediately after delivery of the baby to delivery of the placenta
Labour – fourth stage Immediately after delivery of the placenta to one hour postpartum
Dystocia – Delayed or arrested progress in labour, irrespective of cause
• In active first stage Greater than 4 hours of < 0.5 cm per hour dilatation, or
No cervical dilatation over 2 hours.1
• In active second stage Greater than 1 hour of active pushing without descent of the presenting part.2
Management of Labour 1
Obstructed Labour: No cervical dilation or descent over 2 hours despite evidence of strong contractions
(caput and molding or measured by intrauterine pressure catheter (IUPC))
Incidence
Data Source: BORN (Better Outcomes Registry & Network) Ontario, fiscal year 2006-2010
Data includes all hospital births (live births and still births)
The above graph illustrates the percentage of women who experienced spontaneous labour, induced labour, and pre-labour
Caesarean section (CS) in Ontario from 2006 to 2010. The proportions have remained stable over the five-year period.
Morbidity and Mortality

Labour is a normal physiological process. Sixty percent of women enter labour without pre-existing or obstetrically-associated
health concerns.3 These women would be expected to experience labour and birth with minimal intervention. Any intervention
should be based on clearly identified problems or risks. Unnecessary interventions may lead to further interventions (including
Caesarean birth).
Over the past few decades there has been a dramatic increase in the number of Caesarean sections.4 Caesarean section is
associated with increased maternal morbidity and mortality, increased neonatal morbidity, and increased health care costs.
Dystocia and elective repeat CS account for the majority of Caesarean sections.5 Optimal support of normal labour processes,
appropriate management of dystocia, and encouragement of vaginal birth after Caesarean could potentially lead to a reduction
in the CS rate.
Factors Affecting Labour and Birth

Maternal Age
Average maternal age is increasing. In a setting of uniform active management, the incidence of oxytocin augmentation,
prolonged labour, instrumental delivery, and intrapartum Caesarean birth in nulliparous women increased progressively with
increasing maternal age.6 Increasing maternal age accounts for some of the increase in CS rate experienced over the past
decades, however, the CS rate in each age category has also increased.7 As average maternal age rises, so does the incidence
of medical co-morbidity.3
Obesity
• Obesity (pre-pregnant BMI > 30 kg/m2) is increasingly prevalent in obstetrical populations. In the United States over
30% of childbearing women are obese.8 Obesity and excessive weight gain in pregnancy are associated with increased
fetal and maternal morbidity, including gestational hypertension, gestational diabetes, fetal macrosomia, stillbirth,
and operative delivery, including caesarean section.9-12
• The duration of the first stage of labour increases with increasing maternal BMI.13,14
• Obese women should ideally be counselled and assisted to achieve a BMI less than 30 pre-conceptually. If this is not
achieved, weight gain during pregnancy of 0-5 kg (less than recommended by the Institute of Medicine) is associated
with lower rates of obstetrical complications. Modest weight loss in women with a BMI > 35 appears safe.15,16
• A 2014 meta-analysis of 16 RCTs involving 3359 women of varying BMIs demonstrated that a dedicated exercise
program can reduce obstetrical weight gain and caesarean section rate.17
Caesarean Birth
In 2008/09, the Caesarean birth rate in Ontario was 29.29% (59.73% primary and 40.27% repeats). Common indications for
CS included previous Caesarean birth, dystocia, atypical or abnormal (non-reassuring) fetal status, and breech position.18
The 2010 British Columbia provincial database reported an overall CS rate of 30.72%.19 Of these, 38.17% were elective. The
indications and percentages for the majority of non-elective Caesarean births include:
Dystocia (failure to progress) 30.6 %
Atypical/abnormal fetal heart rate (FHR) 21.8 %
Malposition & Malpresentation 20.86 %
Induction of labour is associated with an increase in the incidence of dystocia. This leads to an increase in obstetrical
interventions, especially in the nulliparous woman with an unfavourable cervix. In B.C. in 2011, 22% of spontaneously labouring
nulliparous women delivered by Caesarean section compared with 41% of those induced.
In an effort to reduce CS rates, Michael Robson developed an audit-classification system grouping birthing women into ten
mutually exclusive groups based on obstetrical parameters. The number of women in each group is recorded as well as the
CS rate for each group. Groups with high CS rates can be identified as well as the size of their contribution to the overall CS rate.
In a Robson Group analysis of births in British Columbia in 2000 and 2013, the greatest contribution to overall CS rate was in
parous women with a prior Caesarean birth and in nulliparous women in spontaneous and induced labour. The greatest increase
in CS rate and the greatest number of overall number of Caesarean sections was in Group 5: women with a prior CS. Findings
have been similar in Ontario and other high-resource settings. Although CS rates in women with multiple pregnancy and breech
presentation are high, the size of the groups is small, making their contribution to the overall CS rate modest. This classification
system is being used increasingly around the world to focus attempts to control CS rate on Group 1 (nulliparous women in
spontaneous labour at term) and Group 5 (women with a prior CS at term).20
2000 2013
ROBSON GROUP # of CS CS rate (%) Contribn. to # of CS CS rate (%) Contribn. to

Total del. CS rate (%) Total del. CS rate (%)
TOTAL 9613 24.1 100 13 688 31.7 100

39 970 43 157
1 Nulliparous women, single vertex at 37+ 1782 16.2 18.5 2427 21.0 17.7
weeks, spontaneous labour 10 997 11 563
2a Nulliparous women with a single vertex at 1283 32.3 13.4 1954 41.4 14.3
37+ weeks, induced labour 3 969 4718
2b Nulliparous women, single vertex at 37+ 231 100 2.4 569 100 4.2
weeks, no labour 231 569
3 Parous women, no scar, single vertex at 37+ 281 2.3 2.9 330 2.9 2.4
weeks, spontaneous labour 12 161 11 545
4a Parous women, no uterine scar, single vertex 163 5.2 1.7 198 6.8 1.5
at 37+ weeks, induced labour 3124 2922
4b Parous women, no uterine scar, single vertex 120 100 1.3 230 100 1.7
at 37+ weeks, no labour 120 230
5 Parous women with a uterine scar, single 2312 65.8 24.1 4301 79.7 31.4
vertex at 37+ weeks 3513 5397
6 Nulliparous women, single breech 810 92.7 8.4 964 94.4 7.0
874 1021
7 Parous women, single breech, including 539 85.8 5.6 583 88.6 4.3
women with a uterine scar 628 658
8 Women with a multifetal pregnancy, 294 55.6 3.1 525 71.4 3.8
including women with a uterine scar 529 735
9 Women with a single pregnancy with 210 87.1 2.2 229 87.7 1.7
transverse or other abnormal presentation, 241 261
including women with a uterine scar
10 Women with a single vertex at <37 weeks, 447 19.7 4.7 1006 32.2 7.4
including women with a uterine scar 2265 3123
99 Unclassifiable 1141 86.6 11.9 372 89.6 2.7
1318 415
Perinatal Services BC. British Columbia Perinatal Data Registry. Years provided: 2000/01. Resource type: Tabulated data. Data provided on February 12, 2015.
*All inferences, opinions and conclusions drawn in this publication are those of the authors, and do not reflect the opinions or policies of Perinatal Services BC.
Dystocia
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 cause.
• Obstructed labour is lack of cervical dilation or descent of the presenting part despite evidence of adequate
uterine contractions and maternal effort (caput and molding, or IUPC).
When dystocia is diagnosed, a common cause is inadequate uterine contractions and oxytocin augmentation is often indicated.
Once strong contractions have been present for two to three hours without further cervical dilation in the first stage or for one
to two hours without descent in the second stage, significant caput and molding are usually present. If caput and molding are
absent, an IUPC should be considered to verify contraction strength, if available (see management of dystocia below). If power
has been adequate, labour is obstructed.
Dystocia mandates a search for a cause, then treatment.
Obstructed labour is an indication for Caesarean section or assisted vaginal birth, if safely feasible.
Etiology
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 four Ps: Powers, Passenger, Passage, and Psyche.
1. POWERS
• contractions – hypotonic, incoordinate or infrequent
• maternal expulsive efforts – ineffective or contraindicated
During labour, palpation 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 molding. An 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 augmentation during a trial of
labour after previous Caesarean birth (TOLAC), grand multiparity (greater than five deliveries) when uterine tone is in question,
or when maternal obesity interferes with external measurement.21 When using an IUPC, contraction strength is measured with
a goal of an increase of at least 50–60 mm of mercury above baseline or > 200 Montevideo units (sum of 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.22 Early detection
and treatment with active management of labour protocols and oxytocin augmentation can reduce the likelihood of CS and
operative birth.22,23
2. PASSENGER
• fetal
• position
• attitude
• size
• abnormalities (e.g., hydrocephalus)
The baby should be assessed for size and malposition.24 Adequate power in labour will often correct malposition whereas
inadequate power may result in persistent malposition. A normal-sized infant may also present an increased diameter to the
pelvis because the head is not flexed or is asynclytic. Adequate power can also 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.25
The diagnosis of true or absolute cephalopelvic disproportion (CPD) 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 molding or IUPC). Malposition, on the other hand, may lead to relative
disproportion. Accurate assessment and description guides management, and if a CS is performed for dystocia, helps determine
suitability for a future VBAC.
3. PASSAGE
• pelvic structure
• soft tissue factors (tumours, full bladder/full rectum, vaginal septum)
Clinical examination of the passage may reveal prominent spines or sacrum, a narrow pubic arch or a space-occupying
mass in the pelvis. Neither antenatal radiological nor clinical pelvimetry has been shown to predict the outcome of labour.26
It is important to ensure the bladder is empty, particularly in the second stage.
4. 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 two 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 (β-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”.27
Physiology
When does Spontaneous Term Labour Begin?
Naegle’s Rule, developed in 1812, calculates the expected date of delivery (EDD) using the last menstrual period (LMP)
(LMP – 3 months + 7 days). Limitations include uncertainty regarding LMP, bleeding unrelated to menses, and delayed
ovulation. A retrospective study of uncomplicated pregnancies in Boston compared the length of pregnancy calculated using
Naegle’s rule with the actual date of spontaneous labour. Nulliparous’ labour occurred eight days later than predicted by Naegle’s
rule (41 1/7) and labour for parous women was on average three days later than predicted by Naegle’s rule (40 3/7 weeks).28
Estimated delivery date (EDD) based on LMP is now best confirmed with ultrasound (U/S). Sonographic estimation of
gestational age is most accurate early in gestation. Between 7 and 16 weeks’ gestation, U/S biometry provides a more accurate
estimate of gestational age than certain LMP and should be used to date pregnancy when available. A 2015 Cochrane review29
(N=25,516, 8 studies) of the routine use of early U/S 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.
Sonographic measurement of crown rump length (CRL) should be used between 7 and 13 weeks’ gestation. Between 13 and
16 weeks, biparietal diameter (BPD) is more accurate.30 Beyond 16 weeks, normal variation in fetal growth and standard error
in U/S measurement make sonographic estimation of gestational age increasingly less precise.31 If first trimester U/S is not
available, gestational age based on certain LMP in a woman with regular cycles appears to be at least as accurate as ultrasound
between 16 and 23 weeks’ gestation; however, if the U/S estimation differs from that by LMP 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 U/S is indicated, even in settings where routine first trimester U/S is not available. If first trimester ultrasound is not
performed in these scenarios, then dating should be based on the earliest second trimester U/S. In pregnancies resulting from
assisted reproductive technologies such as IVF, EDD based on known conception date is more accurate than U/S.30,32
Labour Time Frames

The mean and longest normal rates of progress were historically established by Friedman in the early 1950s based on a mixed
population of women (spontaneous labour, oxytocin inductions, breech births). Friedman’s data showed:27
Nulliparous Parous
Latent Phase Mean (time) 6.4h 4.8h

Longest normal* 20.1h 13.6h
Active Phase Mean (rate) 3.0cm/h 5.7cm/h

Slowest normal* (rate) 1.2cm/h 1.5cm/h
Second Stage Mean (time) 1.1h 0.4h

Longest normal* 2.9h 1.1h
*5th percentile
At the time of Friedman’s research, the CS rate was less than 5%.34 Also, these time limits were established before the
introduction of epidural analgesia.35 Zhang et al. studied 1329 nulliparous women with a single term vertex presentation
in spontaneous labour and demonstrated a markedly slower curve than Friedman (i.e., dilatation from 4 cm to 10 cm took
5.5 hours).36 Those in the fifth percentile rate of cervical dilatation were all below 1 cm per hour. Based on 2511 women
who did not receive oxytocin or epidurals, Albers determined that the mean length of the active first stage was 7.7 hours for
nulliparous women and 5.6 hours for multiparous women.37
Obesity is also associated with a slower labour curve. An observational study of 120 000 women with term singleton cephalic
gestations demonstrated increasing duration of labour from 4 to 10 cm dilation with increasing body mass index (BMI): in
nulliparas from 5.4 hours for BMI < 25 kg/m2 to 7.7 hours for BMI > 40 kg/m2; in multiparas from 4.6 hours for BMI < 25 kg/m2
to 5.4 hours for BMI > 40 kg/m2. Birthweights, CS rates, and the incidence of diabetes also increased in a linear fashion.13 Given
the rising incidence of obesity, it is increasingly important to consider maternal BMI when assessing length of labour.38 Greater
patience may avoid unnecessary intervention, including Caesarean section with its attendant morbidity.
Diagnosis
The onset of labour is often difficult to define. Women frequently assume symptoms of latent labour indicate a need to go to
hospital. Health education for women and families about when to come to hospital, and what symptoms require urgent action is
an important component 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’s score (see SOGC’s Induction of
labour at term guideline39 for an example).
The diagnosis of dystocia first requires the diagnosis of active labour. A Dublin study demonstrated a decrease in dystocia
when active management of labour principles were followed, including the use of specific criteria to diagnose labour to avoid
inappropriate intervention in the pre-labour period.40 Dystocia cannot be diagnosed prior to the onset of labour or during the
latent phase of labour. Caesarean sections done for this diagnosis at this time are inappropriate.
Contraindications
Clinical situations that preclude vaginal birth or elevate the risk of labour above the maternal or fetal risk of Caesarean birth include:
• Placenta previa, vasa previa, cord presentation
• Abnormal fetal lie
• Prior classical CS or significant uterine surgery
• Active genital herpes, invasive cervical carcinoma
Prevention of Labour Complications

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.41
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.
Management
Assessment and documentation includes fetal health surveillance, uterine activity, maternal comfort, and progress in labour.
Latent Phase of the First Stage of Labour

Management during the latent phase of the first stage of labour is controversial due to the limited number of published studies.
One study by McNiven et al.42 provides the basis of the Cochrane review:
• Assess women in a triage area away from the central delivery suite.
• Avoid admission to the labour and delivery area until active labour is established. A study of 51 104 nulliparious women
in the USA admitted in spontaneous labour determined the admission factors that increased Caesarean Section risk.43 The
highest odds for Caesarean Section was in women with cervical dilation on admission of 1cm (OR 5.1 reference > 5 cm)
A plan must be established to meet the woman’s needs either at home or in a non-labouring hospital unit. The plan
should include information about coping strategies and how and when to access support from caregivers.
• Observation, rest, and therapeutic analgesia are preferable compared to a more active approach of amniotomy and
oxytocin induction.
Active Phase of the First Stage of Labour
Partogram
Documentation of labour progress is essential. One method for documenting cervical change and fetal descent over time is a
graphic labour curve, commonly called a partogram. Evidence assessing the effectiveness of partograms showed no difference
with use or non use of a partogram related to outcomes of CS in women presenting in spontaneous labour at term, instrumental
vaginal delivery or an Apgar score less than seven at five minutes. The partogram is useful as a communication tool, for handover,
for teaching and provides a visual snapshot of labour progress.44
Enema
The evidence from the three RCTs included in 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). The authors conclude:
“This evidence does not support the routine use of enemas during labour; therefore such practice should be discouraged.”45
Active Management 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 the second stage, two 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.40 Subsequent follow-up observational studies also supported these results.46,47
Active management requires more interventions and creates a more medicalized birth process. A 2008 Cochrane review stated:
“Active management is associated with small reductions in the CS rate, but is highly prescriptive and interventional. It is possible
that some components of the active management package are more effective than others. Further work is required to determine
the acceptability of active management to women in labour.”48 Of note, RCTs demonstrating no increase in CS rate with epidural
analgesia compared with parenteral opioids routinely used active management of labour protocols.23,49
Ambulation
For women who do not have epidural analgesia, movement, position change, and upright positions may reduce the length of
the first stage of labour and reduce pain. A 2009 Cochrane review by Lawrence found that compared to recumbent positions
(supine, semi-recumbent and lateral), women randomized to upright positions (walking or upright non-walking, e.g., sitting,
standing, kneeling, squatting, and all fours) had first stages that were approximately one hour shorter (Mean Difference [MD]
– 0.99, 95% Confidence Interval [CI] – 1.60 to – 0.39), and less likely to have epidural analgesia (Relative Risk [RR] 0.83, 95%
CI 0.72 to 0.96). 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. Interestingly, for women who had epidural analgesia, there were no differences between
those randomized to upright positions versus recumbent positions for any of the outcomes examined in the review.50
Eating and Drinking During Labour

A 2010 Cochrane review on restricting oral fluid and food intake during labour (five studies, n=3130) looked at women in active
labour and at low risk of potentially requiring a general anesthesia. The studies compared restricting women to nothing except
ice chips or sips of water or water alone versus providing them with one of the following: carbohydrate drinks, specific fluids
and foods, or the freedom to eat and drink at will. In comparing any restriction versus some nutrition, there were no significant
differences in: Caesarean section assisted vaginal births, or Apgar scores. The pooled data were insufficient to assess the incidence
of the rare outcome Mendelson’s syndrome (aspiration associated with general anesthesia). The author concluded that the
evidence showed no benefits or harms and therefore there is no justification for the restriction of fluids and food in labour for
low-risk women.51
No studies assessed women with risk factors, hence there is no evidence to support or refute restrictions in this group of
women either.51
Amniotomy/Artificial Rupture of Membranes (ARM)

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.52 A smaller RCT (n=752) comparing early versus late amniotomy without oxytocin found a higher frequency
of severe variable FHR decelerations and CS for abnormal FHR, yet no difference in overall CS rate or neonatal outcome.53
Although the protocols and settings are heterogeneous, amniotomy appears indicated to accelerate labour that is not progressing
adequately. However, routine amniotomy is of questionable benefit and may result in more frequent variable FHR decelerations.
If amniotomy is performed, it is necessary to ensure that the fetal head is well-applied to the cervix (not ballottable) to minimize
the risk of cord prolapse. If these conditions have been met, a woman may ambulate after amniotomy. Amniotomy and oxytocin
augmentation should be considered once a diagnosis of dystocia has been made in the active phase.2
Birthing Companion/ Continuous Emotional 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 coach54
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.”55 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.56 Studies involving traditional birth attendants suggest
improved birth outcomes but are of poor quality, not randomized, and uncertain with respect to cost-effectiveness.57
Risk Ratio Outcomes of Continuous Support During Childbirth55
Comfort Measures and Pain Relief

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. 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 these 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.58
Some women in labour reach the limit of their pain tolerance. Women experiencing excessive pain or anxiety have high
endogenous catecholamines.59,60 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.
The management of pain during labour involves more than the simple and timely administration of the best anaesthetic 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.
Non-Pharmacological Pain Relief
Smith et al. 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 0.49–1.00, 2 trials, n=288), and self-hypnosis
(RR 0.53, CI 0.36–0.79, 5 trials, n=749). The efficacy of acupressure, aromatherapy, audio analgesia, and massage has
not been established. The requirement for more one-to-one care in these situations may have influenced outcomes.61
Non-Pharmacological Techniques:62
• 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. However, for women who have epidural
analgesia, there does not appear to be the same benefit in upright positions or ambulation.50
• Counter-pressure
• Techniques that activate peripheral sensory receptors:
• Superficial heat and cold
• Immersion in water during labour
• 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 0.70–0.98, 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.63
• Touch and massage
• Acupuncture and 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
N2O2 and sterile water papule injections, but did not affect epidural analgesia use or narcotic or pain scores.
The analgesic effect of TENS was found to be weak.64,65
• Transcutaneous electrical nerve stimulations
• 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 –0.55) and most would use it again (RR 1.54, 95%
CI 1.31–1.80), there was no difference in pain scores, mode of delivery, duration of labour, use of other
analgesia, or augmentation of labour.66
• Intradermal injection of sterile water
• 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 0.30–0.87). The meta-analysis
included some small and unblinded studies; therefore the authors recommended a large RCT to validate
their findings.67
• Aromatherapy
• Techniques that enhance descending inhibitory pathways:
• Attention focusing and distraction
• Hypnosis and self-hypnosis
• Music and audio-analgesia
• Biofeedback
Pharmacological Methods – Systemic
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 drug is devoid of maternal or fetal side effects. With almost all pharmaceutical therapies, some amount of the drug
gets access to the fetus. This may be important to the success of breastfeeding.
• Not all analgesic agents from the same “family” are the same (e.g., each opioid has unique pharmacodynamic
characteristics that may result in different therapeutic effects and side effects).
• Anticholinergic side effects are common with many of these medications and care should be directed at recognizing
and addressing these discomforts.
• Women can be medicated just before birth without significant respiratory depression in the newborn.
• Action should be taken to prevent toxicity with all local anaesthetics.
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.
Nitrous Oxide
Entonox is a mixture of 50% nitrous oxide, 50% oxygen that provides mild to moderate analgesia. It must be self-administered
for safety reasons via a demand-valve; and used with scavenging in a well-ventilated room for workplace safety.68 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. It may also be used as an adjunct during other procedures such as the placement
of a pudendal block or perineal repair.
Narcotics
Narcotics are used routinely in many centres. A variety of options are available. A number of studies have reported on the
negative effects of narcotics with a longer half-life (e.g., meperidine). The negative effects of meperidine are based on a 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.69,70 The use of meperidine is discouraged and narcotics
with a shorter half-life (e.g., morphine or fentanyl) are preferred.71 Narcotics 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. Narcotics may be usefully combined with an antiemetic.
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 narcotic is used, narcotic antagonists (e.g.,
naloxone) and resuscitation capabilities should be available.
Suggested Opioid Use in Labour:
Stage of Labour Nulliparous Parous
Latent Stage: IM Morphine IM Morphine
Early Active Stage: IM or IV Morphine IV Morphine or Fentanyl
Late Active Stage: IV Morphine or Fentanyl IV Fentanyl
Second Stage: IV Fentanyl IV Fentanyl
Peripheral Nerve Blocks

Pudendal Nerve Blocks
These are used for analgesia of the perineum in the second stage of labour. This form of analgesia can be very useful and should
be considered when other regional analgesia is not available. Local anaesthesia with epinephrine allows the administration of
larger volumes of anesthetic leading to greater effectiveness. This also limits the systemic levels in the mother and transfer to the
fetus. A diagram depicting pudendal block administration is included as an appendix. Ten (10) mL of 1% 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.72
Perineal Infiltration
Perineal infiltration is used for repair of lacerations and episiotomy repair. Generous and widespread infiltration should be used.
Use of an agent with epinephrine is helpful. Care should be taken not to inject intravascularly or to exceed the toxic dose. The
toxic dose of plain lidocaine is 4 mg/kg which, for a 50 kg woman, equals 200 mg or 20 ml of a 1% solution. The toxic dose of
lidocaine with epinephrine is 7 mg/kg.
Regional Analgesia /Anaesthesia

Epidural Block
The BORN Ontario database indicated that in 2009, 63% of nulliparous women and 39% of multiparous women received
epidural analgesia.18 Epidural block 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.
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 continuous epidural infusion. A 2002 meta-analysis of nine studies (N=640)
showed lower anesthetic dose and less motor block with patient-controlled epidural analgesia compared to continuous.73
While providing excellent pain relief, epidural analgesia often slows labour and results in motor blockade that can interfere with
maternal pushing efforts. Modern epidural techniques use lower concentrations of local anaesthetic (0.1 % bupivicaine or less)
than previously (up to 0.25%). In 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. Women with low-
dose epidurals were less likely to require assisted vaginal birth, but there was no difference in CS rate.74 A 2002 meta-analysis of
nine studies (n=640) showed lower anaesthetic dose and less motor block with patient-controlled epidural analgesia compared
to continuous infusion,75 and a 2011 RCT showed lower overall local anaesthetic dose, less motor blockade, and fewer operative
vaginal deliveries with programmed intermittent bolus administration versus continuous epidural infusion of local anaesthetic.76
Overall, minimizing the concentration and total dose of anaesthetic lessens the interference with labour.
A 2009 randomized trial of 12 793 nulliparous 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. 77
A 2011 Cochrane review involving 9658 women showed that compared with opiate or no analgesia, epidural analgesia provides
superior pain relief in labour, a small decrease in neonatal acidosis, and less need for naloxone.49 However, epidural analgesia was
associated with:
• increased risk of assisted vaginal birth (RR 1.42)
• maternal hypotension (RR 18.23)
• motor-blockade (RR 31.67)
• maternal fever (RR 3.34)
• urinary retention (RR 17.05)
• longer second stage of labour (mean difference 13.66 minutes)
• oxytocin administration (RR 1.19)
• increased risk of Caesarean section for fetal distress (RR 1.43).
There was no evidence of a significant difference in:
• overall risk of Caesarean section (RR 1.10)
• long-term backache (RR 0.96)
• Apgar score less than seven at five minutes (RR 0.80)
• maternal satisfaction with pain relief (RR 1.31).49
A 2014 Cochrane review compared epidural /spinal with opioids with local anesthesia. The review of 21 studies (n=2859)
demonstrated no difference in 1 and 5 minute Apgar score, cord gases or neonatal neurological status at 2 and 24 hours.78
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.79,80
Management of Dystocia in the First Stage of Labour
Prevention
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 ARM and oxytocin for uterine inertia
If an arrest disorder is suspected in the first stage of labour, management includes:

• Formulating, discussing, and documenting a plan
• Amniotomy
• Ensuring adequate maternal hydration81
• Considering therapeutic rest with analgesia, if exhausted
• Oxytocin augmentation
• If clinical assessment of contraction strength inadequate, considering IUPC
• CS (if other interventions have failed)
Oxytocin
In the event of dystocia due to inadequate power in spite of appropriate analgesia, hydration, rest, and amniotomy, then oxytocin
is indicated to achieve adequate contractions before operative delivery is considered.82 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
which could compromise the fetus or lead to uterine rupture.
Even with close titration of oxytocin, 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 section on induction of labour.
Complications of Oxytocin
The following are possible complications, their mechanism of occurrence, and the preventive management associated with the
use of oxytocin.
Adverse Effects Mechanism Prevention
Fetal compromise Excessive uterine activity Correct dose
Uterine rupture Excessive uterine activity Correct dose
Water intoxication ADH effect Use crystalloid IV solution
Hypotension Vasodilatation Avoid IV bolus injection
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.83,84 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.
Oxytocin can be administered by low- or high-dose protocol. The choice of which to use should be based on the relative risks of
uterine rupture, sensitivity to oxytocin, and likelihood of placental compromise. Any oxytocin protocol needs to be used based on
the uterine response and the fetus’ capacity to tolerate the increase uterine activity generated.” If 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.
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. 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 1–2 mU/min increments and high-dose was defined as ≥ 4 mU/
min increments, increased every 30 min.84 This meta-analysis was dominated by studies that included only nulliparous women.
Evidence specific to multiparous women or women with a prior Caesarean section scar is lacking. Therefore it is prudent to use
a low-dose protocol in women labouring 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.23 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 200-250 Montevideo units
(e.g. 4 contractions of 50-60 mmHg in 10 minutes).23
Example of low-dose protocol:
Initial dose of oxytocin 1–2 milliunit (mU) per minute
Increase interval 30 minutes
Dosage increment 1–2 mU
Usual dose for good labour 8–12 mU/minute84
Maximum dose before reassessment 20–30 mU/min
Example of high-dose protocol:

Initial dose of oxytocin 2–4 mU/min
Increase interval 30 minutes
Dosage increment 4 mU/min
Usual dose for good labour 8–12 mU/minute84
Maximum dose before reassessment 20–30 mU/min86,87
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 need can vary greatly. Many women
receiving “high-dose” oxytocin will never require 10 mU/min and may need finer titration by 1–2 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 20–30 mU/min, and very close monitoring should be employed for doses
greater than 30 mU/min, including IUPC if necessary.86
Second Stage Labour Management
Position
Two Cochrane reviews (2012 and 2013) compared upright versus recumbent position in the second stage of labour for women
with (n=879) and without (n=7280) epidural analgesia. No difference in outcomes was found for women with epidural
analgesia, although numbers were limited.88,89 For women without epidural, upright posture lowered the likelihood of operative
vaginal birth, abnormal FHR pattern, and episiotomy, but increased the likelihood of second degree perineal laceration and blood
loss > 500ml.88,89
Epidural Analgesia89,91
Continue the epidural. Discontinuing an epidural 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 the epidural does not increase the incidence of assisted
vaginal birth.92 A secondary analysis of early versus late pushing in an 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.93
• 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.
Delayed Pushing. Women should only be encouraged to push when they feel the urge to do so. Passive
descent from full dilation to the perception of an urge to push may be less exhausting and more effective, particularly for women
with epidural analgesia. If no passive descent after 1 hour and no urge to push, consider directed pushing or modifying epidural
analgesia. The 2000 PEOPLE trial randomized 1862 nulliparous women with an epidural at full dilatation to immediate pushing
or delayed pushing for a maximum of two hours. Women who delayed pushing had more spontaneous and fewer difficult births
(22.5–17.8%). This was most marked in women whose baby was above station +2 or in a non-occiput anterior position.94
A 2015 Cochrane review also showed that delayed pushing increased rate of spontaneous vaginal birth (RR 1.07, CI 1.03 -1.11
12 studies n- 3114).95
Spontaneous vs directed pushing

Spontaneous pushing encourages women to follow their body’s urges and generally push 3–5 times during a contraction.
Directed pushing technique encourages women to take a deep breath and bear down throughout the contraction. A Cochrane
review of 7 trials (n=815)compared spontaneous pushing versus directed pushing with or without epidural analgesia.95 The
included studies were of mixed methodological quality. The review did not show any real difference in the duration of the second
stage, perineal laceration and episiotomy, 5 minute Apgar < 7, NICU admission, and mode of birth between the spontaneous
pushing and the directed pushing groups. However women who used valsalva pushing showed a significant decrease in
urodynamic factors in first urge to void and bladder capacity measured at 3 months postpartum.96 Patient preference and the
clinical situation should guide decisions.
Length of second stage

Prolonged 2nd stage is associated with increased fetal and maternal morbidity; however, provided there is ongoing progress and
fetal status is normal, arbitrary time limits for the second stage are not well founded.2 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.
Recommended Practices in Second Stage

Recommended Practices in Second Stage by parity and use of epidural analgesia (after full dilation and power is adequate)83
Nulliparous Parous
No epidural Epidural No epidural Epidural
Total duration* 3 hours 4 hours 2 hours 3 hours
Passive 2nd stage‡ May wait up to 2 hours before pushing particularly when May wait up to 1 hour May wait up to 2 hours
the presenting part is above +2 station or in an non-OA before pushing, provided
position, and the urge to push is absent. Encourage waiting to continued passive descent
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
passive descent OR after 2 completed hours of 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.
* 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.
‡ 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.
Source: 82,97
Management of Dystocia in the Second Stage of Labour

Prolonged second stage
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.
Dystocia in the second stage has three 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 one hour of second stage, assess fetal position, caput and molding, 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. ‘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. Consider placement of an intrauterine pressure catheter 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 molding are present, and there is no progress over two hours
for a nullipara or one hour for a multipara, then labour is obstructed. Operative delivery should be considered, either by assisted
vaginal birth or by Caesarean section. 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 three hours in
nulliparous women and two hours in parous women.98 A small study (n=50) examined the value of the fetal pillow for second stage
CS at term and found inflation of the pillow with 180 ml of saline appeared to elevate the fetal head 4 cm and created a lower rate of
extensions (p<0.03) and shorter operating time (p<0.01) and no difference in newborn outcomes compared to historic controls.
A recent meta analysis of 12 studies comparing techniques used to deliver a deeply impacted fetal head at full dilation showed
that the risks of uterine incision extension, infection, mean blood loss and operative time were significantly higher with the push
technique compared with the reverse breech extraction.99
Episiotomy & Perineal Management

• A 2009 Cochrane review of eight studies related to episiotomy for vaginal birth concluded that restrictive episiotomy
policies appear to have a number of benefits compared to routine episiotomy policies. There was less posterior perineal
trauma, less suturing, and fewer complications, with no difference for most pain measures or severe vaginal and/
or perineal trauma. However, there was an increased risk of anterior perineal trauma with a restrictive episiotomy
policy.100 When the perineum is preventing delivery, particularly if the fetal heart rate is abnormal, an episiotomy may
expedite a vaginal birth, although this has not been examined prospectively.
• 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 (OASI), such as nulliparous
women requiring assisted vaginal birth or those with a history of prior OASI. Randomized evidence is limited101 but
corroborates observational evidence that more liberal (but not routine) use of mediolateral episiotomy prevents OASI
at assisted vaginal births, particularly with forceps.102-104
• 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.105 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 45 degrees. Midline episiotomy directly threatens the anal
sphincter and should be avoided (see diagram).106
Used with permission of Salus Global Corporation
• 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%).97,104,107
• 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 [ARR] 2.5%; number needed to
treat [NNT]=40 to prevent one anal sphincter injury).108
• A 2013 Cochrane review (n=2500) of antenatal perineal massage showed modest reductions in episiotomy rate,
perineal trauma, and pain.109
• Manual perineal protection was effective in nulliparous women in reducing the risk of OASI by two-thirds.110
Perineal Repair
• A 2010 Cochrane review involving 10171 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.111
• A 2012 Cochrane review involving 8184 women showed decreased analgesia use, less pain for up to ten 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.112
• A randomized trial of 147 women with 3rd or 4th 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).113
Third Stage Labour Management

Active management of the third stage of labour involves interventions by the caregiver 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. A multicenter RCT (n=23 000) showed that omission of cord traction did not increase the incidence of post-partum
hemorrhage.114 Further information on third stage management can be found in the Postpartum Hemorrhage chapter.
Summary
• Labour is a normal physiological process
• Normal labour is enhanced by:
• Appropriate latent phase management—eg. maternal fetal assessment, information and a plan
• Delayed admission until active labour
• Continuous support in labour
• Comfort measures & appropriate pain management
• Intervention only when necessary
• There is an increasing trend toward induction of labour and an increase in CS primarily due to dystocia and repeat CS.
Avoid induction for non-medical indications.
• Dystocia can only be diagnosed once active labour is established. Management includes:
• Adequate analgesia, hydration and rest
• Amniotomy
• Augmentation
• Assisted vaginal birth
• For women with epidural analgesia, detect uterine inertia and inadequate labour progress early and augment with
ARM and oxytocin.
• Intervene operatively when necessary
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111. Kettle C, Dowswell T, Ismail Khaled MK. Absorbable suture materials for primary repair of episiotomy and second
degree tears [Cochrane review]. Cochrane Database of Systematic Reviews 2010 Issue 6. Chichester (UK): John Wiley &
Sons, Ltd; 2010.
112. Kettle C, Dowswell T, Ismail KM. Continuous and interrupted suturing techniques for repair of episiotomy or second-
degree tears. Cochrane Database Syst Rev. 2012;11:CD000947.
113. Duggal N, Mercado C, Daniels K, Bujor A, Caughey AB, El-Sayed YY. Antibiotic prophylaxis for prevention of postpartum
perineal wound complications: a randomized controlled trial. Obstet Gynecol. 2008;111:1268-73.
114. Gulmezoglu AM, Lumbiganon P, Landoulsi S, Widmer M, Abdel-Aleem H, Festin M, et al. Active management of the
third stage of labour with and without controlled cord traction: a randomised, controlled, non-inferiority trial. Lancet.
2012;379:1721-7.
115. Labor and delivery. 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.
Appendix
Copyright © The McGraw-Hill Companies, Inc. Labor and delivery. In: Cunningham et al. Williams obstetrics. 22nd ed. 2005.115
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).
Chapter 7
Induction of Labour
Definitions1
Induction of Labour
Induction of labour is the initiation of contractions in a pregnant woman who is not in labour to help her achieve a vaginal birth.
Successful Induction of Labour
Successful induction of labour is a vaginal delivery with optimal maternal and neonatal outcomes. (See Management of Labour
chapter for further information on this topic.)
Elective Induction
Elective induction is the induction of labour in the absence of acceptable fetal or maternal indications.
Cervical Ripening
Cervical ripening is the use of pharmacologic or other means to soften, efface, or dilate the cervix in order to increase the
likelihood of a vaginal delivery after labour induction.
Tachysystole
Tachysystole refers to > 5 contractions per 10-minute period averaged over 30 minutes. This is further subdivided into two
categories, one with and one without fetal heart rate changes.2
The terms “hypertonus”, “hypercontractility”, and “hyperstimulation” are not defined here and should be abandoned.2
Induction of Labour 1
Incidence
The frequency of induction varies by location and institution. The overall rate of induction of labour in Canada has not changed
considerably in recent years: 1995/1996—20.7%; 2004/05—20.25% and 2013/2014—21.2% (see below graph).3 In
British Columbia, the rate of induction has remained fairly constant at approximately 21% between fiscal years 2000/2001 to
2013/2014.4 For 2007/2008, the rate of induction in BC was 27.1% for nulliparous and 16% for parous (n=43 499 women).5

When done for the correct reasons and in the correct way, induction is useful and confers benefit. The goal is to facilitate as
natural a labour and birth experience as possible. If done incorrectly or inappropriately, unnecessary risks may be encountered.
• Increased risk of operative delivery and Caesarean Section (CS) in nulliparous women6 (see graphs) regardless of parity7
CS rate in Nulliparous by Spontaneous vs. Induced Labour

In British Columbia, April 1, 2000 – March 31, 2011
Source: BC Perinatal Database Registry

Note: *Mothers with late terminations are excluded from the dataset
CS rate in Parous by Spontaneous vs. Induced Labour

In British Columbia, April 1, 2000 – March 31, 2011
Source: BC Perinatal Database Registry

Note: *Mothers with late terminations are excluded from the dataset
The literature examining mode of delivery for induced versus spontaneous labour is controversial. Observational research
suggests a higher risk of operative delivery with induction of labour. Levine conducted a retrospective cohort study (n=836)
examining term induction of labour and risk of Caesarean section by parity (n=605). Stratified by parity, nulliparas undergoing
induction had an increased Caesarean rate compared to spontaneous labour (27% versus 11%, odds ratio [OR] 3.13, 95%
confidence interval [CI] 1.76 to 5.57) as did multiparas (13% versus 3%, OR 4.04, 95% CI 1.36 to 11.94).8 However, these
studies were often limited by their incapacity to account for differences in indication, making the two populations incomparable.
The best evidence available is thus from RCTs. In a meta-analysis of 31 trials (n=12 166), Wood et al. showed that in randomly
assigned patients a policy of indicated induction of labour was associated with a lower risk of Caesarean section compared with
expectant management (OR 0.83, 95% CI 0.76 to 0.92).9
Risks associated with induction of labour include:
• Uterine tachysystole with or without fetal heart rate changes
• Failure to achieve labour
• Risk of uterine rupture may be increased in certain situations
• Increased risk of chorioamnionitis
• Cord prolapse with ARM
• Inadvertent delivery of preterm infant (with inadequate dating)
• Uterine rupture in scarred and unscarred uteri
• Operative vaginal delivery
• Postpartum hemorrhage10
Every effort should be made to ensure cervical ripening prior to 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
inducing labour and delivery. The indication must be convincing, compelling, consented, and documented. The most common
indication is post-dates pregnancy. Fetal macrosomia is a debatable indication11,12. Physician or patient convenience are not
acceptable indications. However, rural practice situations where a woman needs to go to a different community for her labour
and birth (especially if adverse weather conditions may impact travel) may be an acceptable indication. There is rationale for
offering induction to women > 40 years of age due to the higher risk for stillbirth at term; women > 40 years of age have a
similar stillbirth risk at 39 weeks’ gestational age (GA) as women in their mid-20’s have at 41 weeks’ GA.13-15 The evidence suggests
induction at 40 weeks’ GA would reduce late antenatal stillbirths but evidence is lacking regarding the effect on perinatal mortality
and surgical deliveries. Further research is required before making this a specific indication for induction of labour.16
For all inductions, the patient, her family, and the caregiver involved must have a clear understanding of the potential risks and
benefits involved. Discussion should include reason for the induction, method of induction, and risks, including failure to achieve
labour and possible risk of Caesarean section.1
Performance of an induction should be prioritized by the health care team according to the urgency of
the clinical situation and the availability of resources. Examples of situations where induction may be considered
include:
High Priority
• Severe pre-eclampsia, eclampsia
• Significant maternal disease not responding to treatment
• Significant but stable antepartum hemorrhage (APH)
• Chorioamnionitis
• Suspected fetal compromise
• Term prelabour rupture of membranes (PROM) with maternal group B streptococcus (GBS) colonization
Other Indications
• ‘Post-dates’ pregnancy (see below)
• Uncomplicated twin pregnancy ≥ 38 weeks
• Diabetes mellitus (glucose control may dictate urgency)
• Pre-eclampsia
• Alloimmune disease at or near term
• Intrauterine growth restriction (IUGR)
• Oligohydramnios
• Gestational hypertension > 38 weeks
• Intrauterine fetal death
• PROM at or near term, GBS negative
• Logistical problems (rapid labour, distance to hospital)
• Intrauterine death in a prior pregnancy (Induction may be performed to alleviate parental anxiety but there is no
known medical or outcome advantage for mother or baby)
Special Considerations
Post-Dates/Post-Term Pregnancy
Since prevention of post-term pregnancy is the leading indication for induction, it deserves special discussion and consideration.
Post-term is defined as a gestation greater than or equal to 42 0/7 weeks (294 days from the first day of the last menstrual
period) and occurs in approximately 6 percent of births. Marquette et al. calculated cumulative, day-specific probability for
onset of spontaneous labour (n=15 253) among pregnancies between 41 0/7 and 42 0/7 weeks. The likelihood of entering
spontaneous labour within 24 hours was 14.1%; within 7 days, it was 67.6%.17 Post-term pregnancies have been shown to
have an associated increase in perinatal mortality, morbidity, and operative delivery.18-20 However, the most frequent cause of an
apparently prolonged gestation is an error in determining accurate dating. 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 induction of labour.21
Several trials have examined the policy of induction at 41 or more weeks’ gestation in an attempt to avert adverse outcomes
associated with post-term pregnancy. The following meta-analysis22 of 19 trials (7984 women) concluded that a “policy of
labour induction at 41 completed weeks or beyond was associated with fewer (all-cause) perinatal deaths.”
• The relative risk for perinatal death in the trials where induction was initiated after 41 weeks was 0.25 with 95% CI
of 0.05 to 1.18 (10 trials, 0/2835 vs. 6/2808). 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 induction occurred after 41 weeks, there was a reduced risk of meconium aspiration syndrome (RR
0.29; 95% CI 0.12 to 0.68, four trials, 1325 women).
• There was no difference in the risk of Caesarean section (10 trials at 41 weeks, n=5755, 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 assisted vaginal birth or Apgar scores of < 7 at 5 minutes.
Hussain conducted a meta-analysis of 14 randomized controlled trials and found that a policy of elective IOL for pregnancies at
or beyond 41 weeks is associated with significantly fewer perinatal deaths (RR 0.31; 95% CI 0.11 to 0.88) compared to expectant
management, but no significant difference in the incidence of stillbirth (RR 0.29; 95% CI 0.06 to 1.38). There was significant
decrease in incidence of neonatal morbidity from meconium aspiration (RR 0.43; 95% CI 0.23 to 0.79) and macrosomia (RR 0.72;
95% CI 0.54 to 0.98).23
The 2012 Gülmezoglu Cochrane review found similar results but did not alter management.24
Therefore, a policy of induction at 41 or more weeks’ gestation is recommended in order to avoid 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. As 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 assessment of amniotic fluid volume (AFV).25,26
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 its attendant risk
of infection.27,28 (see Prelabour Rupture of Membranes chapter)
Group B Streptococcus + and ROM

Induction with oxytocin should be started as early as possible after rupture of membranes in order to establish labour within
24 hours.1 (see Prevention of Early-Onset Neonatal Group B Streptococcal Disease chapter)
VBAC
Prostaglandins E2 (cervical and vaginal) should not be used in the setting of vaginal birth after Caesarean section due to the
increased risk of uterine rupture.29,30 Misoprostol should not be used in the setting of VBAC due to the increased risk of uterine
rupture.1
Oxytocin induction may be considered in the hospital setting of VBAC.1 (see VBAC chapter)
Contraindications to Induction
Any contraindication to labour 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)*
• Active genital herpes
• Pelvic structural deformities
• Invasive cervical carcinoma
• Previous uterine rupture
Medically indicated or elective induction is associated with an increased risk of:1
• Failure to achieve labour
• Caesarean section
• Operative vaginal delivery
• Uterine tachysystole
• Uterine rupture
• Cord prolapse with ARM
• Inadvertent delivery of preterm infant in the case of inadequate dating
• Uterine rupture, scarred and unscarred uteri
Pre-induction Assessment
Before induction, there are several clinical elements that need to be considered in order to estimate success and minimize the
risk of CS. Predictors of successful induction include Bishop score > 6, and parity (prior vaginal delivery); and factors that may
contribute to failure of induction include BMI > 40,6,31,32 maternal age > 35, estimated fetal weight > 4 kg,33,34 and diabetes.33,34
The less compelling the indication for induction, the more attention should be paid to adequate cervical ripening.
* Obtain operative report information
The condition of the cervix at the start of induction is the most important predictor of success. The Bishop Score was developed in
1964 as a predictor of success for an elective induction. The most important element of the Bishop score is dilatation followed by
effacement, station, and position, with the least useful element being cervical consistency.35,36 Xenakis et al. clearly demonstrated
that women who had a Bishop score at entry of three or less had significantly higher rates of failed induction (9.4% vs. 0.7%,
P < .01) and of Caesarean delivery (29% vs.15.4%, P < .01) than those with a Bishop score above three.37 Nova Scotia’s Atlee
database also shows that the risk of CS in low risk, nulliparous women is highest in those undergoing labour induction when
compared to those entering spontaneous labour.38
The cervix is considered unfavourable if the Bishop score is < 6 and favourable if it has a Bishop score of > 6.39 Many studies have
used other Bishop score values to separate the data.40
Avoidance of Induction
Quality improvement programs have been shown to reduce the number of elective inductions and unplanned CS. Several studies
have shown a significant reduction in the number of elective inductions after the implementation of an induction committee.
The role of the committee was to review each request and enforce the use of proper indications for induction.40-44
Institutional factors may play a role in the CS rate of induced labours. Brennan et al. compared CS rates in 10 different groups
defined by the Robson criteria. In the group of low-risk women induced at term, the low induction centres had a lower overall CS
rate than the higher induction centres (17.7% vs. 27.8%, P<0.008).45
Prevention Strategies to Reduce Induction for Post-Dates46

1) Ultrasound (U/S)
Best efforts should be used to determine accurate dating. Early U/S (8 to 12 weeks) provides the most accurate estimated date of
delivery (EDD) and has been demonstrated to decrease the diagnosis of post-date pregnancy.47,48 The SOGC’s 2014 guidelines on
Determination of gestational age by ultrasound state:
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. (II)46
If there is more than one 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. (III-B)46
A 2010 Cochrane review21 by Whitworth reported reduced rates of induction of labour for post-term pregnancy (RR 0.59; 95%
CI 0.42 to 0.83) with routine early pregnancy ultrasound imaging.
2) Sweeping (Stripping) of Membranes
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.49,50 A Cochrane meta-analysis found that when sweeping is performed in at-term women, it is associated with
a reduced duration of pregnancy and reduced frequency of pregnancy continuing beyond 41 weeks (RR 0.59; 95% CI 0.46 to
0.74).51 Ugwu conducted an RCT (n=134) and found pregnancy duration decreased by three days (p = 0.001).52 Sweeping of
membranes must be performed in eight women (i.e., number needed to treat [NNT] equals 8) to avoid one formal induction
of labour. 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/Induction—Unfavourable Cervix

It is important that cervical ripening be considered prior to labour induction in women with an unfavourable cervix. Many
methods for cervical ripening are effective. Amniotomy and oxytocin are not effective cervical ripening methods.
1) Mechanical Options
The use of balloon catheters and laminaria or artificial 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.53,54
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 chorioamnionitits. However the vaginal misoprostol group had
a higher rate of tachysystole.54
Mechanical methods are not likely to be effective in inducing labour on their own and often require oxytocin for induction or
augmentation.53 In WHO’s 2011 evidence summary of the comparison of balloon catheter plus oxytocin, versus misoprostol
alone, the combination approach was associated with more vaginal births achieved within 24 hours (OR 0.30; 95% CI 0.16 to
0.58, one trial, 158 participants).56
A meta-analysis has found that compared with vaginal prostaglandins, the use of a balloon catheter is not as effective in
achieving vaginal delivery within 24 hours.53 However, there may be an increased risk of both maternal and newborn infection
associated with specific mechanical methods of cervical ripening.57 This systematic 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.58
A meta-analysis by Jozwiak compared Foley catheter versus vaginal prostaglandin E2 inserts (3 trials, N=699). Caesarean section
and vaginal instrumental delivery rates did not differ between the groups. Oxytocin was used more often in the Foley catheter
group (RR 1.41; CI 1.17 to 1.68), as was epidural analgesia (RR 1.39; CI 1.23 to 1.58). There was less hyperstimulation during the
ripening phase in the Foley catheter group (RR 0.10; CI 0.02 to 0.52).59
A review of Foley balloon catheter for cervical ripening concluded relative safety, even as an option for outpatient cervical
ripening.60
• Balloon devices—Foley catheter (for protocol details see the SOGC guideline1):
• technique for Foley:
• no. 14–18 Foley with a 30 cc balloon
• pretest Foley balloon before insertion
• sterile technique, insert past internal os
• inflate to 30–60 cc water
• Remove catheter within 24 hours if it hasn’t fallen out spontaneously
• contraindications:
• low-lying placenta
• relative contraindications
• rupture of membranes
• genital tract infection
2) Pharmacologic Options
Prostaglandins (Prostaglandin E2 (PGE2) and Prostaglandin E1 (PGE1))
Considerations for Prostaglandin Use
When considering prostaglandin use, patient acceptance and preference are important. Cost considerations also may play a role
in the choice of prostaglandin. Proprietory intravaginal PGE2 formulations (Prostin and Cervidil) cost between $40 and $80 per
dose. Misoprostol is produced generically and costs approximately five cents per tablet. In women with term or late-preterm
ruptured membranes, oral misoprostol provides cervical ripening without the need for vaginal exams or a foreign body (cf. Cervidil).
Certain precautions must be used with prostaglandins:
• The vaginal gel PGE2 (Prostin) should NOT be placed in the cervical canal.
• Prostaglandins should NOT be used as augmentation agents and should only be used for this purpose in
research protocols.
• Prostaglandins should NOT be used in patients with previous CS due to the increased risk of uterine rupture.29,30
• Oral PGE1 (oral misoprostol)28 or vaginal PGE2 (Prostin)1 may be considered with ruptured membranes at term.
There is limited information on slow-release PGE2 (Cervidil) regarding its use with ruptured membranes and further research is
needed. The manufacturer suggests that it should be used with caution in these women and that uterine activity and fetal status
should be carefully monitored.61
Adverse reactions may occur. These include uterine tachysystole, gastrointestinal side effects, and vaginal irritation.
Prostaglandin gels are uterine stimulants whose effects may not easily be reversed. The incidence of hyperstimulation and risk of
fetal hypoxia are similar to oxytocin.
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.62
CAUTION: Avoid intracervical application of vaginal gels because the dosage is much higher than the
intracervical preparation.
PGE2 is a bronchodilator and may be used in asthmatics.63 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) 1–2 mg into posterior fornix
• PGE2 (Cervidil) 10 mg into posterior fornix
• Intracervical—0.5 mg intracervically
• Any formulation may be used for cervical ripening
• Initial application may be followed by repeat PGE2 or oxytocin, as per the manufacturer’s recommendation
Certain protocols have been developed to increase the chance of a successful outcome and enhance safety:
• Patients seen in controlled setting
• by experienced staff
• where resuscitation and delivery capabilities are available
• Normal electronic fetal surveillance prior to PGE2 application
• PGE2 applied by a knowledgeable caregiver
• Monitor fetal heart rate (FHR) and uterine activity electronically, generally for periods of one to two hours post PGE2
administration
• If labour develops, manage as appropriate
• If no labour, reassess and repeat as necessary or choose an alternative induction method
A Canadian study of 300 women that evaluated outpatient versus inpatient induction with slow-release PGE2 (Cervidil) found
that maternal satisfaction was increased with outpatient management. There was, however, one case of uterine rupture in the
inpatient group in a woman with an unscarred uterus.64
Although some centers use prostaglandins on an outpatient basis, there is limited evidence demonstrating its safety.65 If used,
fetal well-being and the absence of significant uterine activity must be assured prior to discharge. Women should be carefully
instructed to return promptly for assessment if uterine activity increases. When induction is undertaken because of suspected
fetal compromise (e.g., IUGR, poor biophysical profile), outpatient management is inappropriate.
Advantages
• Patient acceptance
• Lower operative delivery rate than oxytocin
• Less need for oxytocin induction
• Intracervical preparations should not be used in PROM
Disadvantages
• Increased risk of uterine rupture with previous CS
• Nausea, vomiting, diarrhea
• Gel preparations are difficult to remove in instances of tachysystole
Prostaglandin E1
Misoprostol is a synthetic prostaglandin E1 analogue manufactured for the prevention of ulcers.
• Available as 100 µg and 200 µg tablets.
• Stable at room temperature.
• Costs approximately five cents per tablet.
• Only available in an oral form but tablet is readily absorbable trans-mucosally (sublingually, buccally, vaginally,
or rectally).
• 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 induction of labour. The American College of Obstetricians
and Gynecologists and FDA have endorsed its off-label use for induction of labour.66
Like other prostaglandins, misoprostol causes both cervical ripening and uterine contractions in a dose-dependent fashion.
Following oral or sublingual administration, levels peak at 30 minutes; however, due to first-pass liver metabolism, the peak
maternal serum concentration and the duration and area under the curve are twice as great for sublingual compared with oral
dosing. Fifty micrograms orally is approximately equivalent to 25 µg trans-mucosally. When given vaginally, peak levels and the
area under the curve are delayed and lower compared with sublingual administration.67,68
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
respectively and involving 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.”69
• “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.”70
The accepted, effective, safe oral dose is 50 µg every four hours as needed.
The corresponding vaginal dose is 25 µg; however, this dose is difficult to prepare accurately from commercially available tablets
and may be associated with greater risk of uterine hyperstimulation with FHR changes than the 50 µg oral dose.
Protocols using more frequent, smaller doses of a misoprostol solution prepared from dissolving a 200 µg tablet in water have
also been studied, with similar outcomes to 50 µg every four hours.69 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 µg tablets, commonly used for PPH and for treatment of first and second trimester miscarriage.
Dose Preparation:
One method of minimizing the risk of accidental overdose is to have a hospital pharmacy pre-cut 100 µg tablets into 50 µg
doses which are individually foil-packaged. The 50 µgdoses are then kept in a separate location from the larger 200 µg tablets
commonly kept close at hand in labour rooms for the treatment of post-partum hemorrhage and miscarriage management.
When given orally, it is important that the tablet or solution be swallowed and not held in the mouth sublingually or buccally
where it would cause higher blood levels and greater risk of uterine tachysystole. Repeat doses may be given every four hours,
also in the presence of contractions if they are painless, or irregular and mildly painful.
Side Effects of Prostaglandins
Potential maternal side effects include nausea, vomiting, diarrhea, abdominal pain, shivering, chills and fever; however, these
side effects are dose-dependent and are rare with a dose of 50 µg. Misoprostol does not cause bronchospasm and is safe for use
in asthmatic patients. The most important significant side effect of any prostaglandin given for induction is excess uterine
activity accompanied by an abnormal fetal heart rate (termed “hyperstimulation with FHR changes” by Cochrane reviewers and
most authors).
The risk of uterine hyperstimulation with fetal heart rate changes with a 50 µg oral dose of misoprostol is the same as with
vaginal PGE2—approximately 1%–2%.71 Prostaglandin-related hypertonic 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 four hours of the last oral misoprostol dose.
Eligibility
• Clear indication for induction of labour

• Greater than 35 weeks’ gestation
• Inpatient induction only
Exclusion criteria
• < 35 weeks’ gestation

• Previous Caesarean section or other significant uterine surgery
• Parity ≥ 4 (i.e., 4 or more prior vaginal births)
• Abnormal fetal heart rate
• Fetal growth restriction or oligohydramnios
• 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
• An IV should be in-situ
• CBC, blood group, and screen
• Continuous electronic fetal monitoring (CEFM) for 30 minutes after each misoprostol dose
• Continuous EFM for 1 hour after any increase in uterine activity
Monitoring
Continuous electronic fetal monitoring is recommended for 30 minutes after misoprostol administration. CEFM is recommended
for one hour anytime there is an increase in uterine activity within four hours of a misoprostol dose. Patients should remain in
hospital but may ambulate after reassuring fetal assessment with stable uterine activity. If the woman is not in active labour and
contractions are mild four hours after the last misoprostol dose, the woman may return home for sleep as needed, to return in
the morning to continue induction.
Vigilance for excess uterine activity is critical for the safe use of PGE2 and PGE1.
Excessive Uterine Activity includes:
• Tachysystole = more than 5 contractions in a 10-minute window averaged over a 30-minute period.
• Inadequate resting tone: Resting period between contractions of less than 30 seconds or the uterus does not
relax between contractions.
• Prolonged contraction lasting more than 90 seconds.
Management:
Management of excessive uterine activity depends on whether FHR changes are present. A treatment protocol for excess uterine
activity is recommended for every labour unit.
Excessive uterine activity without FHR changes:
• Remove prostaglandin if possible (Cervidil or recently applied vaginal gel)
• Decrease the oxytocin infusion rate, if present
• Close continuous monitoring, with scalp electrode if necessary
Excessive uterine activity with FHR changes:
• Immediate assessment by the attending physician or midwife
• Stop oxytocin, if running, or removal of prostaglandins
• Remove prostaglandin if possible (Cervidil or recently applied vaginal gel)
• Pelvic exam to assess cervical dilatation and rule out prolapsed cord
• Intrauterine resuscitation (maternal position changes, oxygen, and IV fluid bolus of 500 cc of normal saline)
• Application of scalp electrode if any question about external FHR pick-up
• Acute tocolysis with nitroglycerin can be considered (50 µg IV doses every 90 seconds to three minutes, to maximum
of 500 µg over 15 minutes). To date, the evidence for safety and efficacy remains inconclusive. Another option is
the use of nitroglycerin spray (0.4 mg, one to two puffs sublingually), which has the advantage of a simple and
rapid administration and uptake, although there have been no clinical trials assessing dosing. Necessary monitoring
includes maternal BP and SaO2 and continuous EFM.
• 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, re-evaluate indications and fetal well-being before further
intervention. Foley catheter cervical ripening may be preferred as it does not carry a risk of excess uterine activity.
Options For Induction with a Favourable Cervix

1) Amniotomy
• Creates commitment to delivery
• Effective with 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 four hours later) are
more likely to:
• Be in labour within four hours (RR 12.8; 95% CI 55.1 to 111.7)
• Have a shorter amniotomy to delivery time and achieve delivery within 12 hours (RR 1.5; 95% CI 1.2 to 12.6)
• Experience greater maternal satisfaction (RR 4.1; 95% CI 1.1 to 16.1)72
• A systematic review by Mozurkewich et al. (2011) comparing amniotomy and IV oxytocin to vaginal prostoglandins
found that with IV oxytocin and amniotomy, there were:
• higher rates of PPH (RR 5.5; 95% CI 1.26 to 24.07, 2 studies, n=160)
• and maternal dissatisfaction73
• 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.
2) 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
• 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
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 8–10 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)
• Current evidence does not identify a causal relationship between labour induction in general, or oxytocin induction
specifically, and autism spectrum disorder.74
Protocol
• Cervix should be favourable (Bishop Score > 6)

• Experienced caregivers and adequate resources available to manage dystocia and other emergencies
• In women where 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
• describe dosage as milliunits per minute (mU/min)
• concentrations vary but avoid large free water load (don’t give dextrose 5% in water (D5W))
• institutional protocols should be utilized
• Emerging evidence suggests that oxytocin may be administered using either low—or high-dose protocols.66 The
benefits of the low-dose regimen include less risk of tachysystole and the use of a smaller overall dose. However, the
high-dose oxytocin regimen has been shown to reduce the length of labour with no appreciable increase in neonatal
morbidity.75
High-dose protocols should consider increased dosage while respecting the pharmocokinetics of oxytocin (oxytocin half-life
6–8 minutes, time to steady state 30–40 minutes (5 half-lives)). An example of a high-dose protocol is 4–6 mU/min, every
30 minutes. RCTs comparing low- and high-dose protocols for induction and augmentation are hampered by moderate to high
risk of bias. A detailed meta-analysis of 10 trials involving 2748 women demonstrated a lower risk of CS and a higher chance of
vaginal delivery,76 whereas a a Cochrane review of 9 trials (N=2391) showed no difference.77 Some of this discrepancy may be
due to differential benefits for sub-populations. In particular, nulliparous women with epidural analgesia appear to have a lower
risk of CS with a high-dose protocol.78,79
High-quality trials in both reviews demonstrated a derease in prolonged labour and an increase in hyperstimulation without
fetal heart rate changes with high-dose protocols. There were no differences in fetal or maternal outcomes.
There are no randomized clinical trials comparing different timing of the use of oxytocin after prostaglandin gel. Many studies
have used a six-hour interval.1
Excessive Uterine Activity with Oxytocin Administration
Discontinue oxytocin and institute tachysystole protocol

Restarting oxytocin:
• Remember that the half-life of oxytocin is approximately 6–8 minutes. If oxytocin is restarted, consider beginning
at a lower dose.
3) Vaginal PGE2
Comparison of Pharmacologic Methods
Alfirevic compares efficacy of oxytocin versus vaginal PGE2 and intracervical PGE2 for the induction of labour.80 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.
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, i.e., consider the degree of urgency of the indication and the status of the cervix.
• Ideally, the cervix should be favourable (Bishop Score > 6) before amniotomy and prior to initiation of oxytocin.
• Patient preference must be considered.
• Comparison summary:73
• Membrane sweeping reduces post-term gestations.
• Mechanical methods (e.g.,intracervical balloon) are more likely to reduce the occurrence of tachysystole
compared with PGE2 or misoprostol.
• PGE2 and vaginal misoprostol are more effective than oxytocin in bringing about vaginal delivery within 24 hours
but are associated with more tachysystole.
• Oxytocin plus amniotomy is more effective than amniotomy alone in achieving vaginal delivery within 24 hours.
• Vaginal misoprostol is more likely to result in vaginal delivery within 24 hours than PGE2 or oxytocin but is
associated with increased tachystole.
• Vaginal misoprostol may reduce the likelihood of Caesarean delivery compared with Intravenous oxytocin in the
case of an unfavourable cervix.
• Oral misoprostol is associated with reduced Caesarean sections compared with vaginal PGE2 and placebo.
• Oral misoprostol is associated with less tachysystole but there is more need for oxytocin augmentation compared
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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Appendix
Post-Term Pregnancy Clinical Management Algorithm
(Adapted from BCPHP Guideline: Post-term Pregnancy81 and

SOGC: Guidelines for the Management of Pregnancy at 41+0 to 42+0 Weeks26)
Chapter 8
Umbilical Cord Prolapse
Definition1
Umbilical cord prolapse is defined as the descent of the umbilical cord through the cervix alongside (occult) or past the
presenting part (overt) in the presence of ruptured membranes. Cord presentation is the presence of the umbilical cord between
the fetal presenting part and the cervix, with or without membrane rupture.
Copyright © 2006 Massachusetts Medical Society.2 Used with permission.
Umbilical Cord Prolapse 1

Incidence
Based on retrospective reviews of large samples, the incidence of cord prolapse has been reported to be from 0.1% to 0.6% of
births.1,3,4 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. Markers of possible
morbidity include low APGARs and low cord pH. These become progressively worse with increasing decision-delivery times.6
Other markers of morbidity are not significantly increased.7 Perinatal mortality ranges from 0.02%3 to 12.6%.7 In Canada the
number of deaths due to cord prolapse remains very low, ranging between three and five deaths in total during the years 2005
to 2008.8
Risk Factors
The following factors are associated with an increased incidence of cord prolapse:4,5,9
• Unstable lie (transverse, oblique)
• Malpresentation
• Hydramnios
• Preterm gestation
• Grand multiparity (i.e., parity of > 5)
• Male gender
• Pelvic tumours
• Placenta previa and low-lying placenta*
• Cephalopelvic disproportion
• Multiple gestations
• Preterm rupture of membranes
• Fetal congenital anomalies
• Birth weight less than 2500 g
Rupture of the membranes (ROM) is a prerequisite for overt umbilical cord prolapse.
* Although placenta previa increases the risk of malpresentation and therefore cord prolapse, a complete previa would prevent overt cord prolapse by obstructing the
uterine outlet to the vagina. Occult cord prolapse could still occur.

Approximately 47% of umbilical core prolapse cases can be associated with iatrogenic factors:9
• Amniotomy
• Scalp electrode application
• Intrauterine pressure catheter insertion
• Attempted external cephalic version
• Expectant management of preterm prelabour rupture of membranes,
• Manual rotation of fetal head
• Amnioreduction
Diagnosis
Overt umbilical cord prolapse is diagnosed most commonly by either visualizing the cord through the introitus or palpation of
the cord in the vagina.
A sudden fetal heart rate deceleration in women with ROM is often the first indication of cord prolapse. This should prompt
vaginal examination along with intrauterine resuscitation.
Cord presentation is diagnosed either by palpation of the cord through the membranes or as an incidental finding on ultrasound.
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
Prevention
Interventions such as amniotomy should be carefully timed and thoughtful consideration given to the indications and the risks/
benefits of the intervention. Care should be taken to ensure good application of the presenting part to the cervix prior to 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.

Management
Women at risk need to be 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
Overt prolapse is an emergency situation requiring immediate and life-saving interventions. The following is a list of
recommended actions. There should be ongoing communication with the woman and her partner regarding any management
processes throughout the event. The management of overt cord prolapse includes:
• 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 your examining hand in place (Maintain the elevation until delivery—this may
require insertion of your entire hand into the vagina)
• Place the woman in the knee-chest or Trendelenburg position (Note: It may be acceptable to elevate the woman’s
hips versus placing the bed in Trendelenburg, especially with some beds that restrict the application of Trendelenburg)
• Monitor the fetal heart rate
• Do not attempt to replace the cord. Keep the cord warm if it is outside of the vagina (e.g., warm, saline-soaked cloth)
and avoid manipulating it
• Prepare for immediate Caesarean section (CS). 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 500–700 cc normal saline, clamp the Foley (this must be drained prior to
Caesarean section).10 This is to mechanically uphold the presenting part and to suppress uterine contractions
• tocolysis
• Expeditiously perform a CS

A recent study has suggested that the time from diagnosis to delivery is not the only important predictor of fetal outcomes.11 An
expedited vaginal birth is an acceptable option, if feasible, when CS is not available or cannot be performed in a timely manner.12
Cord presentation diagnosed in labour is managed by Caesarean section prior to ROM when there is a viable fetus.
A 2009 study13 shows the impact of training on the outcome of cord prolapse. The hospital first performed an audit of cord
prolapse. They then introduced a multi-professional obstetric emergency training course that looked at the key interventions
needed to reduce the decision-delivery interval and improve newborn outcome. The results showed that their local 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).
Post-training more women were likely to receive spinal anaesthesia rather than general anesthesia. Practising emergency drills
have demonstrated improved outcomes.14
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. In this way the effects can be
mitigated and outcomes improved.

References
1. Chebsey C, Fox R, Draycott TJ, Siassakos D, Winter C. Umbilical cord prolapse [Green-top guideline no 50]. 2nd ed.
London: Royal College of Obstetricians and Gynaecologists; 2014 Nov. Available: https://www.rcog.org.uk/globalassets/
documents/guidelines/gtg-50-umbilicalcordprolapse-2014.pdf.
2. Belfort M. Images in clinical medicine. Umbilical-cord prolapse at 29 weeks’ gestation. N Engl J Med 2006;354(16):e15.
Available: http://content.nejm.org/cgi/reprint/354/16/e15.pdf (accessed 2006 Dec 13).
3. Woo JS, Ngan YS, Ma HK. Prolapse and presentation of the umbilical cord. Aust N Z J Obstet Gynaecol 1983;23(3):142-5.
4. Kahana B, Sheiner E, Levy A, Lazer S, Mazor M. Umbilical cord prolapse and perinatal outcomes. Int J Gynaecol Obstet
2004;84(2):127-32.
5. Kish K, Collea JV. Malpresentation and cord prolapse. In: DeCherney AH, Nathan L, Goodwin TM, editors. Current obstetric
& gynecologic diagnosis & treatment. 10th ed. Toronto: McGraw-Hill; 2007. p.342-58.
6. Alouini S, Mesnard L, Megier P, Lemaire B, Coly S, Desroches A. Procidence du cordon : prise en charge obstétricale et
conséquences néonatales [Management of umbilical cord prolapse and neonatal outcomes]. J Gynecol Obstet Biol
Reprod (Paris) 2010;39(6):471-7.
7. Usta IM, Mercer BM, Sibai BM. Current obstetrical practice and umbilical cord prolapse. Am J Perinatol 1999;16(9):479-84.
8. Deaths, by cause, chapter XVI: certain conditions originating in the perinatal period (P00 to P96), age group and sex,
Canada [CANSIM database]. Ottawa: Statistics Canada; 2012. Available: http://www5.statcan.gc.ca/cansim/a26?lang=
eng&retrLang=eng&id=1020536&pattern=&csid=.
9. Holbrook BD, Phelan ST. Umbilical cord prolapse. Obstet Gynecol Clin North Am 2013;40(1):1-14.
10. Moses S. LD [labour and delivery]. In: Obstetrics notebook [monograph online]. Rev. Lino Lakes (MN): Scott Moses;
2006. Available: http://www.fpnotebook.com/OB/LD/UmblclCrdPrlps.htm (accessed 2006 Nov 1).
11. Prabulos AM, Philipson EH. Umbilical cord prolapse. Is the time from diagnosis to delivery critical? J Reprod Med
1998;43(2):129-32.
12. Huang JP, Chen CP, Chen CP, Wang KG, Wang KL. Term pregnancy with umbilical cord prolapse. Taiwan J Obstet Gynecol
2012;51(3):375-80.

13. 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(8):1089-96.
14. Kamoshita E, Amano K, Kanai Y, Mochizuki J, Ikeda Y, Kikuchi S, et al. Effect of the interval between onset of
sustained fetal bradycardia and cesarean delivery on long-term neonatal neurologic prognosis. Int J Gynaecol Obstet
2010;111(1):23-7.

Chapter 9
Fetal Well Being During Labour
Introduction
The term fetal distress, implying hypoxia or asphyxia, has been used inappropriately in the past when fetal heart rate monitoring
was found to be atypical or abnormal. It should be remembered that the predictive value of fetal heart rate monitoring is very
low, especially in the low-risk fetus. The diagnosis of asphyxia can only be made in retrospect or by using fetal blood sampling.
Inappropriate use of the term fetal distress may lead to the false conclusion that there was a significant intrapartum hypoxic
event. This misperception may lead to medical legal action if the child is subsequently compromised in any way.
• The phrase ‘fetal distress’ should not be used.
• The preferred term to describe fetal heart rate monitoring that is not normal by intermittent
auscultation (IA) is ‘abnormal’ and for electronic fetal monitoring, the terms are ‘atypical’ or
‘abnormal’ fetal heart rate tracing’.
• Inadequate fetal monitoring is frequently cited as a component of substandard care when compensation is awarded
after litigation for birth asphyxia. A 2013 Norwegian retrospective study of 161 successful claims between 1994 and
2008 listed fetal monitoring as the main factor in 49% and a contributing factor in 21% of the cases.1
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 H+ content in blood
• Acidosis—increased H+ content in tissues
• Asphyxia (hypoxic acidemia)—hypoxemia, hypercapnia and metabolic acidosis
Fetal Well Being During Labour 1

Incidence
Some studies have shown that up to 80% of all labours are associated with atypical or abnormal electronic fetal monitoring
(EFM) tracing patterns at some point or another.2 In other words, most fetuses that have episodes of EFM tracings classified as
atypical or abnormal are not actually experiencing hypoxia or asphyxia.
Physiology
1) Fetal Oxygenation
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 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 compared with 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.3

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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 availability of oxygen to the fetal tissues.
During the contractions of normal labour there is a decrease in uteroplacental blood flow. The reduction in blood flow results in
diminished oxygen delivery to the fetus. This causes an increase in PCO2, a decrease in PO2 and a decreased pH. These changes
do not fall outside of critical thresholds in the normal situation. The normal, healthy fetus compensates and recovers during
the resumption of normal placental perfusion that occurs between contractions. As a result, the normal 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 PO2 and pH, may exceed these critical thresholds and the fetus may show changes in heart rate. A long
labour or excessive uterine contractions may challenge even a fetus with normal uteroplacental function.
A) Maternal Factors Affecting Fetal Oxygenation4

Decreased maternal arterial oxygen tension:
• Respiratory disease
• Hypoventilation, seizure, trauma
• Smoking 5
• Obesity (BMI >35–40)6
Decreased maternal oxygen carrying capability:
• Significant anemia (e.g., iron deficiency, hemoglobinopathies)
• Carboxyhemoglobin (smokers)
Decreased uterine blood flow:
• Hypotension (e.g., blood loss, sepsis)
• Regional anaesthesia
• Maternal positioning
Chronic maternal conditions:
• Vasculopathies (e.g., systemic lupus erythematosis (SLE), type I diabetes, chronic hypertension)
• Antiphospholipid syndrome
• Cyanotic heart disease
• Chronic obstructive pulmonary disease

B) Uteroplacental Factors Affecting Fetal Oxygenation4

Excessive uterine activity:
• Tachysystole secondary to oxytocin, prostaglandins (PGE2) or normal labour
• Placental abruption
Uteroplacental dysfunction:
• Placental infarction-dysfunction marked by intrauterine growth restriction (IUGR), oligohydramnios, or abnormal
Doppler studies
• Uterine rupture
C) Fetal Factors Affecting Fetal Oxygenation4

Cord compression:
• Oligohydramnios
• Cord compression, prolapse, or entanglement
• 3 or more nuchal loops7
• Single umbilical artery (SUA) (due to less Wharton’s jelly cushioning and umbilical cord coiling)
• In a 2014 study of 34 196 pregnancies Ashwal et al reported that the 162 fetuses with SUA were
associated with:
• a higher rate of Caesarean section (CS) due to non-reassuring fetal heart rate (NRFHR)
(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 due to non-reassuring fetal
heart rate, prolonged neonatal admission, 5 minute Apgar < 7 and umbilical artery pH < 7.2)
(20.9% vs 8.8%, p = 0.005)8)
In a 2015 study of 27 752 pregnancies with 127 fetuses with SUA, Naveiro-Fuentes recommended monitoring fetal growth
closely and monitoring intrapartum fetal surviellance because of its association with a lower weight for gestational age, higher
risk of low umbilical cord blood pH and inceased cesarean delivery for abromalities in fetal surveillance.

Decreased fetal oxygen carrying capability:

• 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 adrenals
• decreased flow to the kidneys, lungs, gut, liver, and peripheral tissues
• increase in blood pressure
• Decreased movement, tone, and breathing activities (changes in biophysical profile)
• Fetal tachycardia (this may be preceded by transient bradycardia)
• Anaerobic metabolism (decreased pH)

2) Neurological Effects
Neurobiology
The central nervous system (CNS) of the fetus remains vulnerable to damage throughout gestation. This vulnerability of the fetal
brain 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.

If brain injury is to be attributed to intrapartum asphyxia, the following would therefore be expected:
• Depressed neonatal vital signs—Apgar ≤ 3 at 5 minutes
• Neonatal neurological sequelae (neonatal encephalopathy)—hypotonia, irritability, seizures
• Neonatal multi-organ dysfunction
• renal—oliguria, anuria, azotemia
• lung—respiratory distress syndrome, pulmonary hypertension
• gut—necrotising enterocolitis
• liver—hypoglycemia, elevated liver enzymes, coagulopathy
• hematologic—thrombocytopenia, leukopenia
• cardiac—cardiomyopathy, patent ductus arteriosus
• biochemical evidence of severe metabolic acidosis
• umbilical artery pH < 7.0
• umbilical artery base deficit (BD) ≥ 12 mmol/L
Accordingly, evidence of damage to several end organs, as well as metabolic acidosis, is required before a diagnosis of fetal
asphyxia can be assumed.

1) Fetal Asphyxia with Hypoxic Ischemic Encephalopathy (HIE)
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 prior to 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.9-11

Neonatal encephalopathy (NE) is “a clinically defined syndrome of disturbed neurological function in the earliest days of life in
the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, sub normal
level of consciousness and often seizures”.12
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 HIE is reported as 1.9 per 1000 term
births and the incidence of NE is 3.8 per 1 000 term births.13
Term and near-term infants make up at least 50% of all cases of cerebral palsy (CP) even though they are at relatively low risk
compared with very preterm infants. Infants weighing < 1500 gm at birth make up approximately 25% of all cases of CP.14
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.15 The pathway from intrapartum asphyxia to subsequent CP must progress through NE.
The incidence of NE that can be attributed to intrapartum hypoxia, in the absence of any other preconceptional or antepartum
abnormalities, is approximately 1.6 per 10 000.14
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
HIE. 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 the most common outcome, by far.
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 (PVL). PVL is visible on cranial ultrasound (U/S). 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 is a chronic motor disorder of cerebral origin. 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.”14
Incidence
The incidence of CP in term infants is 2–3/1000 live births and has remained stable for the past thirty to forty years.4
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)
• CNS anomalies
• Metabolic abnormalities
• Developmental abnormalities
• Substance abuse / smoking
• Placental abnormalities
Is Cerebral Palsy the Result of Intrapartum Events?

The data from the following (and other) studies reveal that CP is rarely the result of adverse intrapartum events. Even if there has been
intrapartum hypoxia / acidosis, CP rarely occurs. Only 10% to 20% of children with CP had demonstrated intrapartum asphyxia.16
Criteria to Define an Acute Intrapartum Hypoxic Event as

Sufficient to Cause Cerebral Palsy
The SOGC, in its Fetal Health Surveillance: Antepartum and Intrapartum Consensus Guideline,4 reiterates the conclusions of
The International Cerebral Palsy Consensus Group. This report required the presence of four essential criteria before an
association between CP and intrapartum asphyxia could be made. All of these conditions must be present. In cases where one
or more of these factors is absent, “one cannot conclude that hypoxic acidemia existed or had the potential to cause neurologic
deficits.”17,18

The four essential criteria are:

• Evidence of metabolic acidosis in umbilical cord arterial blood obtained at delivery (pH < 7 and BD ≥ 12 mmol/L)
• Early onset of severe or moderate neonatal encephalopathy in infants born at or beyond 34 weeks’ gestation
• CP of the spastic quadriplegic or dyskinetic type*
• Exclusion of other identifiable etiologies such as trauma, coagulopathy, infectious conditions, or genetic disorders
*Spastic quadriplegia and, less commonly, dyskinetic CP are the only types of CP associated with acute hypoxic intrapartum
events. Spastic quadriplegia is not specific to intrapartum hypoxia.”17 Hemiparetic CP, hemiplegic CP, spastic diplegia, and ataxia
are unlikely to result from acute intrapartum hypoxia.15,17
In addition to the four essential criteria identified by the International Cerebral Palsy Task Force, the American College of
Obstetricians and Gynecologists and the American Academy of Pediatrics listed five additional criteria that collectively suggest an
intrapartum timing (within close proximity to labour and delivery, e.g., 0 to 48 hours) but are non-specific to asphyxial insults.14
It is not necessary for all five of these to be present and, with the exception of the first criterion, they are only weakly associated
with acute intrapartum hypoxia.
The criteria which suggest an intrapartum insult:
1. A sentinel (signal) hypoxic event occurring immediately before or during labour
2. A sudden and sustained fetal bradycardia or the absence of FHR variability in the presence of persistent late or variable
decelerations, usually after an hypoxic sentinel event when the pattern was previously normal
3. Apgar scores of 0 to 3 beyond 5 minutes
4. Onset of multi-system involvement within 72 hours of birth
5. Early imaging study showing evidence of acute, non-focal, cerebral abnormality
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%). Interestingly, 75% of
the neonates with abnormal neurological outcomes had pH levels above 7.10.19
In order to improve communication and documentation about potential hypoxic events, precise and
effective communication is essential.
Do not:
• Use the term “fetal distress”
• Overstate the significance of meconium
• Use the term “asphyxia” without hard evidence
• Use qualifiers such as “significant”, “severe”, etc.

Instead use:
• Abnormal intermittent auscultation or atypical or abnormal fetal heart rate tracing
• “Asphyxia” only with biochemical evidence (scalp pH, cord blood gases)
Summary
• Despite improved technology and neonatal care, rates of CP are still 2–3/1000 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 Terms:20
pH: pH is a symbol used to express the degree of acidity or alkalinity.
Buffer: Substances that interact with acids in the body to minimize changes in pH. The two main buffers are hemoglobin and
plasma bicarbonate. Usually on a blood gas analysis, bicarbonate is the buffer result reported.
Base deficit/excess: Base deficit / excess refers to the number of units of base required to neutralize the amount of acidosis
occurring. The two terms (deficit / excess) mean the same thing, except that one is reported as a negative number (base excess)
and one is reported as a positive number (base deficit).
During aerobic fetal metabolic activities, (when the fetus carries out its metabolic processes in an optimum oxygen
environment), volatile carbonic acid is produced which rapidly dissociates to carbon dioxide and water. Carbon dioxide diffuses
rapidly across the placenta and is removed by the maternal lungs, presuming cord circulation and placental blood flow are
normal. If this circulation is compromised, carbon dioxide can be retained and carbonic acid is formed.
Anaerobic metabolism, (when the fetus carries out its metabolic processes in a less-than-optimum oxygen environment),
produces non-volatile lactic acid. The process to remove lactic acid from the fetus is slow. It diffuses slowly across the placenta to
the maternal circulation and accumulates in cells and end organs.20

3) Acid-Base Assessment in Labour

Fetal Scalp Blood Sampling (FBS)
Fetal scalp blood sampling can reduce the increased operative intervention rates associated with electronic fetal monitoring.21
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 IUGR, 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 are available to perform the analysis in a timely manner
• Membranes ruptured, cervix at least 2–3 cm dilated
• Women with atypical and/or abnormal EFM tracings
Contraindications
• Gestations ≤ 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 50µL blood sample which may be rejected by the testing equipment due to inadequate
volume or contamination with air or amniotic fluid. pH alone is not as accurate a predictor as full blood gas
assessment, which includes Base Deficit. BD is helpful in quantifying metabolic acidosis.
• Recommended actions related to pH level:22
• pH ≥ 7.25: Repeat fetal scalp sampling within 30 minutes only if the FHR abnormality persists.
• pH 7.21–7.24: Repeat fetal scalp sampling within 30 minutes or consider delivery if rapid fall since last sample.
• pH ≤ 7.20: Delivery is indicated.

Fetal scalp lactate testing

• This point of care test requires as little as 5 µL, which reduces sampling failures.
• A 2015 Cochrane review by East et al., compared intrapartum fetal lactate with pH estimation and found that
lactate testing was 99% successful compared to only 79% for pH testing.23 It also noted that compared to pH
estimation, lactate testing incurred fewer scalp incisions and a shorter time from sampling to result. In spite of
these potential advantages of lactate testing, there was no difference in mode of birth, neonatal outcomes, Apgar
scores, encephalopathy, or admission to the neonatal intensive care unit. However, there was no available evidence
comparing fetal scalp blood lactate estimation with no sampling, on clinical outcomes.
• Although there appears to be an increase in mean umbilical lactate from 37 wks to 42 wks gestation; no studies have
addressed whether the gestational age should be considered in determining the critical action level for scalp lactate.23
• Fetal scalp blood samples of lactate taken within 60 minutes of birth correlate well with umbilical arterial and venous
lactate measured following delivery.24 Lactate levels correlate well with both fetal scalp and cord blood pH and BD.25,26
• A 2015 study from Denmark27 using a hand held lactate testing system to assess scalp samples from 677 monitored
deliveries reported the sensitivity and specificity of lactate ≥ 4.8mmol/l in predicting a pH < 7.20 to be 0.63 and 0.85
respectively. However, importantly, this study also noted that if it had used the ≥ 4.8mmol/l lactate value rather than
pH < 7.20 to indicate delivery, there would have been 155 instead of 56 instrumental deliveries with no decrease in
newborns with severe metabolic acidosis. Therefore, due to the low PPV and NPV of a high lactate to predict a low pH,
in their clinical setting, more instrumental deliveries would be performed using lactate instead of pH in monitoring
fetuses during labor.
• 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.25,28-30
• It may be that the value of scalp lactate testing lies in its strong negative predictive value (NPV) for fetal acidemia at birth.
Interpretation of Results
It is important to interpret the results of fetal scalp sampling 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.
It is important to determine the ‘trend’ of the fetal scalp sampling values in order to identify whether the fetal condition is
improving or deteriorating and therefore what, if any, intervention is warranted. There is no good evidence to guide the frequency
for repeated fetal scalp sampling. If the clinical picture does not improve or delivery is not imminent, a repeat sample should be
considered within 30 to 40 minutes.4

Limitations of fetal scalp blood sampling

• Provides only instantaneous and not continuous information. Repeat sampling may be necessary
• Technical limitations including equipment availability, operator experience and skill level
• The procedure may be uncomfortable for the mother
1) 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 / improvement initiatives.
Recommendations for cord blood analysis from professional organizations
• The Society of Obstetricians and Gynaecologists of Canada (SOGC) recommends measuring 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 intitiatives. If only one sample is possible,
it should be arterial since arterial samples are the best indicator of fetal oxygenation at birth. In situations where risk
factors for adverse perinatal outcome exist, or when intervention for fetal indications has occurred, the SOGC strongly
recommends that both arterial and venous cord gases be measured.4
• The American College of Obstetricians and Gynecologists (ACOG) recommends that physicians obtain arterial and
venous cord blood samples in the circumstances of Cesarean delivery for fetal compromise, low 5-minute Apgar score,
severe growth restriction, abnormal fetal heart rate tracing, maternal thyroid disease, intrapartum fever, or multifetal
gestation.20 ACOG reaffirmed this 2006 recommendation in 2010.
• The Royal College of Obstetricians and Gynaecologists (RCOG) in the UK recommends selective measurement of acid-
base status in the umbilical artery as a minimum.22
In hospitals where blood gas analysis is not immediately available, alternatives include:
• A clamped, 20 cm segment of cord for delayed analysis. Umbilical artery blood is stable for pH and gas analysis for up
to 60 minutes at room temperature.31
• Samples in a pre-heparinized syringe on ice are most accurate within 60 minutes with values changing gradually after
this timeframe.28

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. In the perinatal period, both respiratory and metabolic
acidosis occur in parallel and it is important to identify them separately.
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).
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 attributed to the provision of fetal acid-base biochemical data at delivery, which influenced care in subsequent cases.32
Normal Umbilical Cord Blood Gas Values
• Reference Ranges of 3 522 Term* Vaginal Births33
Arterial Mean SD Range
pH 7.27 0.07 7.2-7.34
pCO2 (mmHg) 50.3 11.1 39.2-61.4
pO2 (mmHg) 18.4 8.2 10.2-26.6
HCO3 (mEq/L) 22 3.6 18.4-25.6
Base Excess (mEq/L) -2.7 2.8 -5.5-0.1
O2 saturation (%) 23.3 16.2 7.1-39.5
Venous
pH 7.34 0.06 7.28-7.40
pCO2 (mmHg) 40.7 7.9 32.8-48.6
pO2 (mmHg) 28.5 7.7 20.8-36.2

HCO3 (mEq/L) 21.4 2.5 18.9-23.9
Base Excess (mEq/L) -2.4 2.0 -4.4-0.4
O2 saturation (%) 49.4 16.9 32.5-66.3
*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 there may be some benefit in delayed cord clamping in preterm infants not
requiring resuscitation.34 Evidence suggests that delayed clamping of the cord for 30–120 seconds after birth in
preterm infants reduces the rate of intraventricular hemorrhage, anemia and the need for transfusions.34,35 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 six months of age but may increase the need for phototherapy.36,37 There
is no evidence to support early cord clamping as part of active third stage management in preventing postpartum
hemorrhage.38 A delay in cord clamping of at least one minute provides sufficient placental fetal transfusion.39 The
Canadian Paediatric Society (CPS), in its 2011 Neonatal Resuscitation Guidelines, states that “cord clamping should
be delayed for at least 1 min in babies not requiring resuscitation”. For babies who require resuscitation, the CPS
document states “there is insufficient evidence to recommend a time for clamping”.40
There is evidence delayed umbilical cord clamping may 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 sampling at 60 seconds, there was a mean decrease in pH of 0.043 (range 0.008–0.076) and an
increase in the BD of 1.3 (range 0.2–3.0). These changes were not observed in the venous samples.41
• Wiberg et al., in 2008, sampled cord arterial and venous blood immediately and at 45 and 90 seconds. Compared
to 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 5.19.42
It is therefore important to document when the cord was clamped and when blood was drawn.

2. Sampling both the umbilical artery (UA) and umbilical vein (UV) is recommended:
• The umbilical artery values are the best assessment of fetal status with the venous values representing 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 is 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 “arterial” samples are, in fact, venous.43 Collecting both arterial and venous samples assures
whether 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 two cases with similar arterial but different
venous values had dissimilar neonatal outcomes. Case A required resuscitation at birth, assisted ventilation for
48 hours, and developed CP at one year of age. Case B had a five-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
Westgate J et al. Br J Obstet Gynaecol 1994;101(12):1054-63.43
4. Normal blood gas values change through labour. pH, bicarbonate and PO2 decrease and PC02 and BD increase.44
5. Blood gas analyzers asses pH and pCO2 directly but BD is calculated and will vary depending on whether the
calculation is in blood or extracellular fluid. Generally BD values calculated in blood are greater than with extra
cellular fluid.44
6. In the presence of a high PCO2, metabolic acidosis may be falsely reported when BD is calculated using blood. In the
perinatal period, calculating BD using extra-cellular fluid will prevent the influence of PCO2 on metabolic acidosis.
Most hospitals do not recognize this fact and proceed to analyze the acid-base status using blood.

7. A low umbilical artery pH by itself does not define asphyxia. All of the criteria, as previously written in the CP and fetal
asphyxia sections, should be present to correlate birth hypoxia with adverse neurological outcome.45
8. Arterial-venous pH differences may add information about the cause of the acidemia at birth. Restriction of umbilical
flow increases the difference between UA and UV pH values, while impairment of maternal perfusion of the placenta
may be associated with small differences.45
Neonatal morbidity and mortality according to pH cutoff 46
pH Neonatal Deaths Seizures Both
7.15 – 7.19 (n=2236) 3 (0.1%) 2 (0.1%) 1 (0.05%)
7.10 – 7.14 (n=798) 3 (0.4%) 1 (0.1%) 0
7.05 – 7.09 (n=290) 0 0 1 (1.1%)
7.00 – 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
Respiratory acidosis and metabolic acidosis have a different pathogenesis and clinical significance. Respiratory acidosis develops
rapidly and disappears rapidly following the first neonatal breaths when the newborn is able to blow off CO2 through respiration.
It is considered a part of normal birth. 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) in order 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 has the potential to to be
associated with significant fetal damage.47

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.
Management
Fetal Health Surveillance (FHS) in Labour
The goal of intrapartum fetal health surveillance is 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, is not currently accessible for evaluation
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.
• The data obtained from intermittent auscultation and the electronic fetal monitor should always be interpreted
in conjunction with the total clinical picture. Interpretation of the fetal heart pattern and the management plan
are dependent on the fetal health prior to labour, the maternal clinical condition, the stage of labour, and the
uterine activity.
• A systematic method for interpretation, documentation, and communication will help to prevent missed steps
in the assessment process and the omission of important parts of documentation and communication.
• All caregivers need to have a formal process for ongoing communication about the status of the fetus during labour
that incorporates standardized terminology.
• Supportive care in labour is an extremely important adjunct to all fetal surveillance techniques and should be the
basis of intrapartum care.

Benefits of Continuous Support During Childbirth48
Choice of Method of Surveillance in Labour
Comparing Continuous EFM with IA in Labour49

When comparing continuous EFM to IA during labour, the Alfirevic Cochrane review (including both low—and high-risk
patients)49 reported:
• Continuous EFM is associated with a higher rate of CS section and instrumental (operative) vaginal births than IA.
• No significant difference in perinatal mortality.
• No difference in the incidence of CP.
• The only clinical benefit of EFM in this review was a 50% reduction in neonatal seizures.
Using a numbers-needed-to-treat calculation, the authors estimated that in a cohort of 628 women, continuously monitored,
a clinician could expect to have one less neonatal seizure and 11 more CS sections compared to a control cohort of women that
were monitored using intermittent auscultation.
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

(Adapted from Fundamentals of fetal health surveillance: a self learning manual. 4th ed. Halifax: Canadian Perinatal Programs
Coalition; 2009.50)
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 as with EFM.
Normal Labour Contraction Pattern
a) Methods of assessment
• The mother’s perception of her contractions should always be considered in conjunction with other methods
• Palpate by hand. The frequency, duration, an estimate of the intensity and 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
b) Characteristics of normal contractions and their assessment:
• Frequency: The 2008 NICHD report recommends that uterine contractions be “quantified as the number of
contractions in a 10-minute window, averaged over 30 minutes”.51 Normal is ≤ 5 contractions in 10 minutes.
Tachysystole is > 5 contractions in 10 minutes.
• 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 (IUPC).
Normal intensity is > 25 mm Hg and < 75 mm Hg above the baseline (except in the 2nd stage of labour).52
• Resting tone: The uterine tone is described as soft or firm between contractions by palpation. The uterus is
soft between contractions for a minimum of 30 seconds. Normal resting tone with an IUPC is <7–25 mm Hg.50
Resting tone cannot be accurately measured using an external tocodynamometer.
Contractions are rarely of a fixed frequency or duration. Therefore frequency and duration may be expressed in a range. For
example, 2–3 contractions in 10 minutes lasting 50–80 seconds.
Excessive Uterine Activity
Excessive uterine activity can be endogenous (spontaneous) or exogenous (over stimulation of the uterus during labour
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.
Characteristics of Excessive Uterine Activity
• Tachysystole: More than 5 contractions in a 10-minute window averaged over a 30-minute period. The term applies
to both spontaneous and stimulated labour. Tachysystole should always be characterized with an interpretation of the
FHR tracing (e.g., normal, atypical, or abnormal). The terms hypercontractility and hyperstimulation (previously used to
describe excessive uterine activity with atypical or abnormal FHR findings) are not defined and should be abandoned.51
• Timing: Doubling or tripling may occur.
• Resting tone: Resting period between contractions of less than 30 seconds or the uterus does not relax between
contractions.
• Duration: Contractions lasting more than 90 seconds

Tachysystole – Normal Tracing
Tachysystole – Abnormal Tracing

2) Intermittent Auscultation Of The Fetal Heart Sounds

(Adapted from Fundamentals of fetal health surveillance: a self-learning manual. 4th ed. Halifax: Canadian Perinatal Programs
Coalition; 2009.50)
Intermittent auscultation is the preferable technique for intrapartum fetal surveillance in low-risk pregnancies if the following
criteria are met:
• The presence of practitioners experienced in the technique of auscultation, palpation of contractions, and the
recognition of abnormal FHR patterns on auscultation
• The existence of a Birthing Unit protocol / guideline addressing the technique and frequency of assessment (for an
example go to URL: http://sogc.org/wp-content/uploads/2013/01/gui197CPG0709r.pdf)
• The presence of a Birthing Unit guideline outlining the clinical interventions to be used when abnormal FHR findings
are present (for an example go to URL: http://www.sogc.org/wp-content/uploads/2013/01/gui197CPG0709r.pdf)
• The presence of an educational program to provide fundamental knowledge and to regularly update all staff regarding
the Birthing Unit IA Protocol / Guideline and the steps in clinical intervention for abnormal FHR changes detected on IA
• The ability to provide skilled nursing support on a 1:1 basis once auscultation is required every 15 minutes or less
Benefits of Intermittent Auscultation:
• Less costly
• Less restrictive for the woman (permits increased freedom of movement)
• Adaptable to varied labour positions and practices (e.g., water immersion)
• Lower intervention rates, compared with EFM, without compromising neonatal outcome4
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 can be assessed with IA?
• Baseline FHR (the heart rate counted in bpm for one minute between contractions)
• 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.53 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 Maneuvers)
• Assess the uterine contraction pattern by hand; frequency, duration, intensity and resting tone can be adequately
assessed using a hand(s) and a watch
• Place the stethoscope or Doppler 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. This recommendation is based on Level III
evidence as there are not sufficient data on which to base a definitive IA timing protocol.
Recommended Frequency of Auscultation

(adapted from Liston R, Sawchuck D, Young D)4
First Stage–Latent Phase First Stage–Active Phase & Second Stage–Active Phase
Before Pushing in the
Second Stage
There are very limited data on

which to base a recommendation
for IA in the latent phase of labour.
Optimally, most women will be in
their own home environment with
family support during this period.
Some may be in hospital due to
geographic, transportation, or
weather considerations.
Society of Obstetricians and Recommended at the time of initial Every 15–30 minutes Every 5 minutes
Gynaecologists of Canada, 2007 assessment and approximately
every 1 hour thereafter.

Recommended Frequency of Auscultation

(adapted from Liston R, Sawchuck D, Young D)4
First Stage–Latent Phase First Stage–Active Phase & Second Stage–Active Phase
Before Pushing in the
Second Stage
American College of Obstetricians Every 15 minutes Every 5 minutes

and Gynecologists, 2005
Association of Women’s Health, Every 15–30 minutes Every 15 minutes (not pushing)
Obstetric and Neonatal Nurses, Every 5 minutes (with pushing)
2000
Royal College of Obstetricians and Every 15 minutes Every 5 minutes

Gynaecologists, 2001
Recommendations for the use of intermittent auscultation4
a) IA is preferred for healthy women after 36 weeks’ gestation (up to 41+3 weeks’ gestation), in spontaneous labour,
and in the absence of risk factors for an adverse perinatal outcome4
b) From 41+3 weeks until 42 weeks’ gestation IA is preferred, provided that a non-stress test (NST) 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 surveillance4
c) Below 36 weeks’ gestation EFM is recommended because the incidence of other pathologies and adverse outcomes
is increased
d) Intermittent auscultation and epidural analgesia:
• Maternal hypotension and fetal heart rate changes are often seen in the first 60 minutes after the initiation of
regional anesthesia.
• 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.54
• In general, epidural and spinal anaesthesia, in the absence of maternal hypotension or uterine hypertonus,
cause minimal changes in the FHR.55
• 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.4
• Patient-controlled epidural analgesia (PCEA) uses a dilute local anesthetic 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.56,57
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.4
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
• Abnormal uterine activity patterns (e.g., increased resting tone or tachysystole)
• 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.

2. Abnormal:
• Tachysystole
• 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)58
• Presence of decelerations
3. Dysrhythmia:
• An irregular heart rate not associated with uterine activity. A dysrhythmia requires further assessment
In the presence of abnormal FHR characteristics detected by intermittent auscultation that are
unresponsive to resuscitative measures, increased surveillance by continuous EFM and consideration
of fetal scalp sampling or delivery.
The Management of an Abnormal FHR Detected by Intermittent Auscultation

(adapted from: Feinstein NF, Sprague A, Trépanier MJ.) 59
TACHYCARDIA • Reposition the woman to increase uteroplacental perfusion or alleviate cord compression.
• Rule out fever, dehydration, drug effect, prematurity.
• Correct maternal hypovolemia, if present, by increasing IV fluids.
• Check maternal pulse and blood pressure.
DECELERATIONS • Reposition the woman

• Examine amniotic fluid for meconium.
• Correct hypotension, if present.
• Consider oxygen by mask at 8 to 10 L/min. in the presence of confirmed or suspected maternal hypoxia or hypovolemia
BRADYCARDIA • Reposition the woman to increase uteroplacental perfusion or alleviate cord compression.
• Perform vaginal exam to assess for umbilical cord prolapse (see below) or relieve cord compression.
• Consider oxygen by mask at 8 to 10 L/min. in the presence of confirmed or suspected maternal hypoxia or hypovolemia
• Correct maternal hypovolemia, if present, by increasing IV fluids.
• Check maternal pulse and blood pressure.
ADDITIONAL MEASURES • If in the second stage, consider modifying or pausing pushing efforts
• Continue to auscultate FHR for clarification and document findings.
• Consider initiation of EFM for clarification and document findings.
• If abnormal findings persist despite corrective measures, and ancillary tests are not available or desirable, expedited
delivery should be considered.
INADEQUATE / • Initiate electronic FHR monitoring (EFM).

UNSUCCESSFUL IA

3) Electronic Fetal Monitoring

Physiologic Basis
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 fetus has an intrinsic heart rate which decreases as gestational age increases. It is determined by a pacemaker in the sino-
atrial node (SA-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.
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.
Other conditions can also lead to decreased or absent variability. These conditions 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, β-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.59,60
• betamethasone and dexamethasone: may affect variability and fetal movements for three days after
administration and will return to normal.61
• Preterm fetus – variability is usually moderate by 32 weeks’ gestation
• Fetal tachycardia
• Congenital anomalies.
Moderate variability reliably predicts the absence of fetal metabolic acidemia at the time it is observed.51 Such variability can only
be measured with EFM.

Admission Cardiotocography (CTG)

A 2012 Cochrane review compared the effects of admission CTG versus IA on maternal and infant outcomes for women
without risk factors (n=13 000).62
• Main results:
• although not statistically significant, using the strict P < 0.05 criteria, 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, four 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, three trials, 10 753 women,) and fetal blood sampling (RR 1.28, 95% CI 1.13 to 1.45, three trials,
10 757 women)
• no difference in the rate of instrumental vaginal birth (RR 1.10, 95% CI 0.95 to 1.27, four trials, 11 338 women),
fetal and neonatal deaths (RR 1.01, 95% CI 0.30 to 3.47, four trials, 11 339 infants) or other secondary outcomes
• For low risk women:
• 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 benefit.62,63
Recommendations:4
• Admission FHR tracings are not recommended for healthy, term women in labour in the absence of risk factors for
adverse perinatal outcome as they may lead to unnecessary interventions and there is no evident benefit.
• Admission FHR tracings are recommended for women with risk factors for adverse perinatal outcome.64,65
Methods of Electronic Fetal Monitoring
a) 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.66
Advantages:
• Non-invasive
• Does not require a dilated cervix
• Does not require ruptured membranes

Disadvantages:
• Need for re-adjustment with maternal or fetal movement
• The ultrasound transducer
• may record the maternal pulse
• may not obtain a clear tracing in obese women or women with polyhydramnios
• artifact may be recorded
• there may be doubling or halving of the FHR when it is outside the normal range
• The tocodynamometer approximates when the uterine contractions start and end but does not measure
the intensity of the contractions
b) Internal: A spiral electrode to record fetal heart impulses is attached to the fetal scalp through the maternal
vagina and cervix. 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
• Mother HIV seropositive
• 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.
Advantages of an IUPC:
• Accurate measure of intrauterine pressure
• More accurate relationship between contractions and FHR pattern changes
• Useful in cases of dysfunctional labour
• Useful in obese women where external monitoring is unsatisfactory
• An IUPC may allow women greater mobility than external pressure monitoring

An IUPC may be useful in the following situations:

• When contraction strength is difficult to assess clinically (e.g., obesity);
• When oxytocin doses above 30 mU/min are required;
• When augmenting women with a prior CS scar; and
• When amnioinfusion is required to treat variable decelerations due to cord compression.
IUPC use should be carefully weighed in terms of relative risks and benefits in the circumstances of undiagnosed vaginal bleeding
or intrauterine infection and considering the same contraindications listed above for the spiral electrode.
Studies addressing fetal and maternal risks:
• A 2003 Alberta retrospective review of 90 cases of early-onset GBS disease (between 1993 and 1997), at a time prior
to 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).67
• A case-control study (covering the years 2000 to 2011) of 40 cases of early-onset neonatal sepsis (EONS) made up of
eight GBS, 11 Escherichia coli, 12 Coagulase negative staphylococci, four Viridans group streptococci, one Enterococcus
faecalis, and four other non-specified organisms versus 80 controls, did not demonstrate a significant relationship
between fetal scalp electrode (FSE) use and EONS.68
• 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).69
• the use of a fetal scalp electrode alone or with an IUPC did not affect neonatal outcome (a composite of five
minute Apgar < 3, cord pH < 7.1, cord base excess < – 12, or admission to level 3 nursery). For maternal
outcomes, the use of a fetal scalp electrode alone was not associated 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. These outcomes were corrected for
time from rupture to delivery ≥ 12 hours, black race, primiparity, group B streptococcus status, and regional
anesthesia. The authors recommended that an IUPC be used only when external monitoring is inadequate.69
• A 2013 Cochrane review of three 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 five minutes, umbilical artery pH, admission to NICU,
mode of delivery or instrumental deliveries, maternal infection, neonatal sepsis or morbidity, and hospital costs. For
the outcomes of infection during labor (RR 0.69, 95% CI 0.44 to 1.08; one study, n=1456) and infection up to three
weeks postpartum in mother or child (RR 0.84, 95% CI 0.61 to 1.16; one study, n=1435), women with an indication
for antibiotic prophylaxis during labour (i.e., GBS positive status, heart disease, or other reasons for prophylaxis) were
excluded from analysis.70

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 (< 36 weeks), post-term (≥ 42 weeks), and
chorioamnionitis have been associated with an increase in FHR abnormalities and the development of neonatal encephalopathy,
CP, and perinatal death.22,71 In spite of insufficient evidence to suggest which, if any, conditions where the use of EFM results in a
better outcome than IA, it seems reasonable to advise the use of EFM in these situations, as recommended by the Royal College of
Obstetricians and Gynaecologists.22
Antenatal & intrapartum Conditions Associated with an Increased Risk of Adverse Fetal Outcome*
Where Intrapartum Electronic Fetal Surveillance may be Beneficial
Antenatal Maternal • Hypertensive disorders of pregnancy
• Pre-existing diabetes mellitus / gestational diabetes
• Antepartum hemorrhage
• Maternal medical disease (cardiac, anemia, hyperthyroidism, vascular disease, renal disease, smoking)5
• Maternal motor vehicle collision / trauma (EFM recommended for a minimum period of 4–6 hrs)72
• Morbid obesity (BMI > 35–40)
• Maternal perception of reduced or absent fetal movement73
Fetal • Intrauterine growth restriction

• Prematurity (< 36 weeks)
• Oligohydramnios
• Abnormal umbilical artery Doppler velocimetry
• Isoimmunization
• Multiple pregnancy
• Breech presentation
• Significant congenital anomaly74
• Single umbilical artery8
• 3 or more nuchal loops7

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
• Prolonged rupture of membranes (> 24 hours at term)
• Induced labour
• Augmented labour
• Hypertonic uterus
• Preterm labour
• Post-term pregnancy (> 42 weeks)
Fetal • Meconium staining of the amniotic fluid75-77

• Abnormal FHR on auscultation
*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 2001.22
Epidural Analgesia and Intermittent Auscultation
Epidural analgesia may cause maternal hypotension decreasing uteroplacental perfusion resulting 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 five minutes
for 30 minutes after epidural initiation and after bolus top-ups as long as maternal vital signs are normal). (III-B)4
Following epidural anesthesia during labor, morbidly obese women (BMI ≥ 40) have more frequent hypotension and fetal
heart rate abnormalities than normal weight women (BMI < 25). This supports the recommendation that these women receive
continuous EFM.78
PCEA is different than an intermittent bolus technique with concentrated local anaesthetic agents. It is used with dilute local
anaesthetic and opioid solution (less than or equal to 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 done according to usual obstetrical
protocols, and that use of EFM should be based upon obstetrical considerations.4

Systematic Interpretation of EFM Tracings
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.4 Consistency is the key to achieving effective communication with other health care
providers and patients, accurate documentation, and preventing missed steps in the assessment process.
The definitions and explanations in this section are based in part on the recommendations from the 2008 National Institute of
Child Health and Human Development (NICHD) Workshop on Electronic Fetal Monitoring. This NICHD workshop was convened
to revisit nomenclature, interpretation, and research recommendations for EFM.51 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. Therefore
EFM should be assessed and evaluated in the context of these factors. FHR patterns are categorized as either baseline, periodic,
or episodic. Periodic patterns are those associated with uterine contractions and episodic patternss 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)
• Baseline FHR
• Baseline FHR variability
• Presence of accelerations
• Presence of decelerations
• Changes or trends in FHR tracings over time
• Classification of the tracing (i.e., normal, atypical, or abnormal)
• Overall assessment of the surveillance
Electronic fetal surveillance should be reviewed and documented with the same frequency as described for intermittent
auscultation.

The Process of Systematic Interpretation

(Adapted from: Canadian Perinatal Programs Coalition. Fundamentals of fetal health surveillance.50)
1) Is the FHR tracing interpretable?
• Is there artifact interfering with the accurate interpretation of variability? Maternal heart rate artificact has been
found to be present in as much 55% of EFM tracings. Consider simultaneous maternal (using the finger O2 saturation
monitor) and fetal heart rate monitoring in labour particularly during the second stage79
• Is there continuous recording, or are there spaces which make interpretation difficult or impossible?
• Is the tracing of a sufficient time period to permit an accurate interpretation?
• Does the quality of the FHR and uterine activity pattern allow for accurate interpretation?
2) What is the paper speed and graph range?
• Paper speed should be standardized within each region and institution.
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?
• 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 two minutes of identifiable baseline (not necessarily contiguous) in any 10-minute
window or the baseline is indeterminate. It may be necessary to assess 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 bpm, it is termed tachycardia. The presence of either of these
findings requires further assessment.
• Identify deviations from normal:
• Tachycardia

• Bradycardia
6) What is the baseline variability?
• Variability refers to the fluctuations in the baseline FHR that are irregular in amplitude and frequency.
• Variability is a normal, physiologic characteristic of the FHR.
• Variability is largely the result of activity of the vagus nerve.
• It is determined in a 10-minute window of baseline that is free from accelerations or decelerations.
• Measure the difference between the lowest and highest rate. The difference is the range / amplitude of variability.
• Baseline variability is classified as absent, minimal, moderate, or marked.51 These terms are preferred, as
opposed to the terms ‘good variability’ or ‘poor variability’.
• Due to the subjectivity of the visual evaluation of variability, careful re-evaluation is recommended in borderline
assessments80
• Moderate FHR variability reliably predicts the absence of fetal metabolic acidosis.51 FHR variability is affected by factors
such as fetal sleep cycles. Variability will therefore be less than moderate for periods, even in the healthy fetus. The
appropriate management in such cases is to extend the observation time. Loss of variability for ≥ 40 minutes requires
further assessment.
• 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 6–25 bpm
Marked >25 bpm
• Absent variability (amplitude range undectable)
• Minimal variability (amplitude range ≤ 5 bpm)

• Moderate variability (amplitude range 6–25 bpm)
• Marked variability (amplitude range > 25 bpm)

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.51 The amplitude of the oscillations is usually 5 to 15 bpm.80,81 This differs from and
should not be confused with FHR variability. The sinusoidal pattern is abnormal and is most frequently associated with fetal
anemia / 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 less than 30 seconds) in FHR that is ≥ 15 bpm above
the baseline for ≥ 15 seconds (10 bpm for 10 seconds for gestations < 32 weeks) and less than 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 a change in baseline rate. The presence of accelerations is a normal finding.

• Spontaneous
• Decelerations
A deceleration is a decrease in the FHR.
• In the SOGC Guideline “repetitive” decelerations are defined as ≥ 34
• In the 2008 (NICHD) Workshop on Electronic Fetal Monitoring document, decelerations are defined as “recurrent” if
they occur with ≥ 50% of uterine contractions in any 20-minute window. Decelerations occurring with < 50% of
uterine contractions in any 20-minute segment are defined as “intermittent”.51
• 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.
• secondary to fetal head compression
• considered to be benign
• not associated with fetal acidemia

• Late
• a gradual, usually symmetrical, decrease and return to baseline FHR in association with a uterine
contraction. The onset, nadir and recovery of the deceleration occur after the beginning, peak, and
end of the contraction. The onset to the nadir of the deceleration is ≥ 30 seconds. The nadir of the
deceleration occurs after the peak of the contraction.
• late decelerations are associated with uteroplacental insufficiency and may imply a degree of hypoxia.82

• Variable
• an abrupt decrease in the FHR. The onset of the deceleration to the nadir is < 30 seconds. The FHR
decreases to at least 15 bpm below the baseline and the deceleration lasts for at least 15 seconds but less
than two minutes.
• may be episodic or periodic (if periodic, their onset, depth, and duration commonly vary with successive
contractions).
• thought to be a response to cord compression in labour
• the most common decelerations seen in labour
• uncomplicated variable deceleration
• often have “shoulders”, i.e., an initial acceleration followed by a rapid deceleration to the nadir, a rapid
return to the baseline and a secondary acceleration.83
• not consistently associated with a poor neonatal outcome.22
• Complicated variable deceleration (may be indicative of fetal hypoxia)83,84

• a deceleration to less than 70 bpm lasting for more than 60 seconds.
• loss of variability in the baseline FHR
• a biphasic pattern
• prolonged secondary acceleration (post deceleration smooth overshoot) of more than 20 bpm and/or lasting
> 20 seconds
• delayed return to baseline
• continuation of the baseline FHR at a lower level than before the deceleration
• the presence of fetal bradycardia or tachycardia.

1. Deceleration < 70 bpm > 60 sec
2. Loss of variability of baseline
3. Biphasic deceleration

4. Overshoot (20 bpm increase for 20 seconds)
5. Delayed return to baseline

6. Baseline rate lower after the deceleration
7. Baseline tachycardia or bradycardia
• Prolonged
A deceleration of ≥ 15 bpm below the baseline and lasting for more than two minutes but less than 10 minutes
from onset to return to baseline. (A deceleration lasting more than 10 minutes is a change in baseline heart rate.)

In a 2013 retrospective cohort study of 5388 singleton, non-anomalous gestations who 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 (at least 10 minutes and up to 30 minutes, if
available). Overall, decelerations greater than two 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 two minutes,
a decrease in UA pH of 0.042 was noted. Decelerations of ≥ 10 min. (termed “terminal bradycardia”) were associated with an
12.9% overall incidence of pH of ≤ 7.10.85
8) Is this a normal, atypical (uncertain significance), or abnormal FHR tracing?

• Normal = Characteristics are within normal parameters
• Atypical = Furthur 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, etc.)
• Abnormal = Action is required: Review the overall clinical situation; intra-uterine resuscitation and prompt operative
delivery (vaginal or Caesarean section) is indicated unless there is evidence of normal oxygenation by scalp pH
assessment.

SOGC Classification of Intrapartum EFM Tracings4

Normal Tracing Atypical Tracing Abnormal Tracing
Baseline • 110–160 bpm • 100–110 bpm • <100 bpm

• >160 bpm for 30–80 min • >160 bpm for >80 min
• Rising baseline • Erratic baseline
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
Decelerations • None • Repetitive (≤3) uncomplicated • Repetitive (≥3) complicated

• Occasional uncomplicated variable variable decelerations variable decelerations
decelerations • Occasional late decelerations • Late decelerations in >50% of
• Early decelerations • Single prolonged deceleration contractions
>2 min but <3 min • Single prolonged deceleration
>3 min but <10 min
Accelerations • Spontaneous accelerations present • No acceleration with fetal scalp Usually absent (presence of accelerations
• Accelerations with fetal stimulation does not change classification of tracing)
scalp stimulation
Action EFM may be interrupted for periods of VIGILENCE ACTION REQUIRED

up to 30 min. if maternal-fetal condition • Institute intrauterine resuscitation • Institute intrauterine resuscitation
stable and/or oxytocin infusion rate • Determine cause of atypical • Determine cause of abnormal
stable tracing tracing
• Determine the duration of effect • If clinically appropriate, obtain
and reserve tolerance of the fetus fetal scalp blood sampling (>34
• Perform fetal scalp stimulation weeks, prolonged deceleration
and consider fetal blood sampling < 3 minutes)
(>34 weeks) • Evaluate total clinical picture:
• Evaluate total clinical picture: gestational age, estimated fetal
gestational age, estimated fetal weight, stage of labour
weight, stage of labour • Undertake transfer / operative
• Continue with close ongoing fetal delivery promptly UNLESS:
surveillance • Fetal scalp sampling is
• Consider transfer / delivery if normall
tracing persists or deteriorates • Spontaneous delivery is
imminent

9) Does this correlate with the total clinical picture?
• Does the tracing, its interpretation, and classification correlate with the clinical picture including the gestational age,
pregnancy history, presence of risk factors, labour pattern, fetal behavioral state, or other extrinsic factors likely to
influence the FHR?
• Is further assessment and/or action necessary?
The more atypical or abnormal features of FHR tracings that occur concurrently, the greater is the possibility of fetal compromise.
It is essential that all FHR tracings are considered in relation to previous FHR tracings. As each tracing is interpreted, an appropriate
clinical action can be undertaken, either to lessen the impact on the fetus or remove the effect entirely (see table below).
Electronic FHR, potential causes, associations, and clinical actions to be considered4

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


Tachycardia: > 160 bpm for 30–80 minutes Maternal: 1. Assess maternal temperature
or rising baseline • Fever
2. Decrease maternal temperature (if elevated)
• Infection
• Dehydration 3. Review maternal medications
• Hyperthyroidism
• Endogenous adrenaline or anxiety 4. Discontinue oxytocin
• Medication or drug response 5. Review for duration of rupture of membranes
• Anemia (ROM), positive vaginal culture, especially group
Tachycardia: > 160 bpm for > 80 minutes or B streptococcus (GBS)
Fetal:
erratic baseline
• Infection 6. Intrauterine resuscitation
• Prolonged fetal activity or stimulation
• Chronic hypoxemia 7. If cause is not obvious or correctable, consider
• Cardiac abnormalities intrapartum U/S to evaluate arrhythmia
• Congenital anomalies 8. If persistent (> 80 min):
• Anemia • Obtain scalp sample if clinically
appropriate
• Expedite delivery
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) • Prematurity
for >80 min • Medication (analgesics, sedatives)
appropriate
• Hypoxic acidemia
Prepare for delivery
Marked variability: ≥ 25 bpm for >10 • Mild hypoxia
minutes • Fetal gasping
• Unknown
Sinusoidal Pattern • Severe fetal anemia (Hb <70) 1. Attach fetal scalp electrode if possible
• Tissue hypoxia in fetal brain stem
2. Consider APT test or Kleihauer Betke
Accelerations: • Normal FHR response to increased fetal No action (normal response) May be due to
activity occlusion of umbilical vein only, as in association
Spontaneous: • Direct sympathetic stimulation of the fetus with variable decelerations (see text)
• Occlusion of umbilical vein only
Periodic:
In the presence of atypical or abnormal • Hypoxic acidemia 1. Attach fetal scalp electrode if possible
tracing absent acceleration with fetal • Possible fetal abnormality
scalp stimulation
approrpriate
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 first stage of labour
• Initial acceleration
• Rapid deceleration to the nadir 3. Occurs in more than half of second stages
• Rapid return to baseline
• Secondary acceleration


Repetitive (≥ 3) uncomplicated Due to cord compression 1. Observe in early first stage of labour
variable 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
• Deceleration to <70 bpm lasting >60 sec.
• Loss of variability in baseline FHR 3. Confirm fetal well-being, directly or indirectly
• Biphasic deceleration (fetal scalp stimulation, and fetal scalp blood
• May demonstrate prolonged acceleration sampling if clinically appropriate
after deceleration (smooth overshoot) of
>20 bpm and/or lasting > 20 sec 4. Prepare for delivery
• Delayed return to baseline
• Continuation at lower baseline FHR than
prior to the deceleration
• 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 function during labour (e.g., reduced
2. Check maternal vital signs
but <3 min uterine blood flow associated with
maternal position) 3. Continue to observe
• Fetal chemoreceptor / vagal response
• May be associated with transient fetal
acidemia
Late decelerations: >50% of contractions • Fetal chemoreceptor / vagal response due When persistent and repetitive, it is mandatory
A gradual decrease and return to baseline FHR to decreased PO2 to act upon this pattern
in association with a uterine contraction. The • Altered maternal blood flow to the
1. Intrauterine resuscitation
onset, nadir and recovery of the deceleration placenta (e.g., maternal hypotension)
occur after the beginning, peak, and end of • Reduced maternal arterial oxygen 2. Obtain fetal scalp sample if clinically
the contraction. The onset to the nadir of the saturation appropriate.
deceleration is usually > 30 seconds and the • Placental changes altering maternal-fetal
nadir is beyond the peak of the contraction. gas exchange (e.g., placental insufficiency, 3. Prepare for delivery
uterine hypertonus or tachysystole)
• May be associated with fetal acidemia


Single prolonged deceleration: >15 bpm Fetal baroreceptor and chemoreceptor response 1. Vaginal examination to rule out cord prolapse
for >3 min but <10 min to profound changes due to:
• Uterine tachysystole
• 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. If using internal EFM, confirm the presence
of fetal heart sounds by auscultation and note
the FHR
5. Confirm uterine activity pattern and uterine
resting tone by abdominal palpation
Scalp Stimulation:4
Digital fetal scalp stimulation provides an indirect assessment of acid-base status.86,87 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. A FHR
acceleration secondary to this stimulus suggests a normoxic fetus.86-88 It should not be used as a resuscitative intervention.
• Digital scalp stimulation should be avoided during a FHR deceleration. Decelerations are secondary to a vagal
response that prevents a sympathetic nerve response (acceleration) during scalp stimulation.89
• An acceleration of 15 bpm amplitude with duration of 15 seconds has a very high NPV and a very high sensitivity
with regard to the absence of fetal acidosis.86,87
• An acceleratory response is associated with a scalp pH of greater than 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 Resuscitation:4
The goal of intrauterine resuscitation is to improve uterine blood flow, umbilical circulation, and fetal-maternal oxygen
saturation. Actions involved in intrauterine resuscitation include:
• Stop or decrease oxytocin90
• Modify or pause pushing efforts if in the second stage of labour
• Change maternal position (to left or right lateral)
• Improve maternal hydration, with an intravenous fluid bolus, if indicated
• Perform a vaginal examination to rule out cord prolapse and to relieve pressure from the presenting part on the cord
• Tocolysis in the presence of tachysystole (e.g. with nitroglycerin)91
• Consider amnioinfusion if variable decelerations are present
• a 2012 Cochrane review of amnioinfusion for suspected umbilical cord compression in labour found that in
settings where fetal blood sampling is not used to confirm fetal compromise:92
• transcervical amnioinfusion was associated with the following reductions:
• caesarean section overall
• FHR decelerations
• Apgar score < 7 at 5 min. meconium below the vocal cords
• postpartum endometritis
• maternal hospital stay > 3 days
• mean cord umbilical artery (Ua) pH was higher with amnioinfusion group
• transcervical amnioinfusion
• instillation of fluid into the amniotic cavity through the cervix via an inserted tube, usually an
Intrauterine Pressure Catheter (IUPC) with amnioinfusion capability (occasionally a 12–14 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 U/S 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 (Ringers 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 beneficial.93 If warmed, a blood
warmer is recommended.
• infusion protocol: various options are used: e.g., bolus (50–1000 ml) followed by constant infusion;
serial boluses (200–1000ml) given every 20 min. to 4 hrs) or constant infusion. One documented
protocol includes an initial infusion at 10–15 ml/min. continued until decelerations improve when the
rate is reduced to 100–200 ml/hour.94
• 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 liquour, in settings with
standard peripartum surveillance, found it to be ineffective in reducing meconium aspiration
syndrome, perinatal death or severe morbidity.95
• Reduce maternal anxiety (this reduces catecholamine effects)
• Coach the woman to modify her breathing or pushing techniques
• 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.96 Prophylactic maternal oxygen administration, during the second stage of labour, has been found
to be 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 mothers received prophylactic oxygen (RR 3.51, 95% CI 1.34 to 9.19).96
• 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 maternal hypoxia or hypovolemia and not used
for management of atypical or abnormal fetal heart rate tracings97

General Considerations / Recommendations:4

• When a normal tracing is identified, it may be appropriate to interrupt EFM for up to 30 minutes to facilitate periods
of ambulation, bath, or position change, provided that the maternal / 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,
if available. Other obstetrical parameters (e.g., gestational age, estimated fetal weight, presence or absence of
meconium,76 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.
• A prospective study of 1070 women who had scalp lactate performed for EFM patterns that were not normal,
reported:
• isolated reduced variability (0–4) in most cases was not a sign of lactic acidemia
• “severe” variable decelerations (defined as abrupt and lasting > 60 sec.) and late decelerations increase 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 acidemia98
• In the presence of an abnormal FHR tracing, delivery should be undertaken promptly unless there is a clear indication
of normal fetal oxygenation by means of scalp pH assessment or spontaneous birth is imminent.
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 ≤ 7.15.99 Although this analysis may have been different
for a different pH cutoff, 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:
• Limited use of EFM in low-risk pregnancies due to the low incidence of true 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
• Consider maternal heart rate artifact as the cause79
• Attention to all aspects of the EFM record, including baseline variability. Consider the presence of moderate FHR
variabliliy and/or the presence of accerations to correlate with a high negative predictive value for severe metabolic
acidosis100 and neonatal respiratory morbidity.
• Intrauterine resuscitation in all instances of atypical and abnormal tracings including the reduction or discontinuation
of oxytocin.
• Recognize that EFM tracing interpretation is subject to individual interpretation59
• Regular interprofessional quality assurance and educational FHS programs
4) Documentation of Fetal Health Surveillance Assessments (IA And EFM)101

It is essential to document the contraction pattern, the baseline FHR, variability, the presence of accelerations, and periodic
(associated with a contraction) or episodic (not associated with a contraction) decelerations when describing FHR tracings. In
addition to this description, it is important to provide an interpretation such as normal or abnormal IA, or normal, atypical, or
abnormal tracing, and any clinical action taken. It is also recommended that the maternal and fetal response to any interventions
be documented.
• Accurate and timely documentation of all fetal health assessments and clinical actions taken is essential
• Standardization of documentation tools
• Standardization of terminology and acronyms
• Standardization of EFM paper speed
• All care-providers document on the same form (e.g., progress notes, partograms)
• Whatever documentation system is used, the following should be recorded:
a) Uterine activity characteristics obtained by palpation or electronically:
• Frequency
• Duration
• Intensity
• Relaxation between contractions

b) FHR data:
• Indication – if EFM
• Numerical baseline rate (in bpm)
• Rhythm – if auscultation (regular or irregular)
• Variability – if EFM
• Nature of changes from the baseline, i.e., acceleration or deceleration (type of deceleration if EFM).
c) The interpretation:
• 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
Electronic fetal monitoring records should be inspected and documented every 15–30 minutes in the active phase of labour and at
least every 5 minutes in the second stage of labour.
Maintaining Standards in Fetal Surveillance

Regular updating of fetal surveillance skills is required. Although there is no best evidence to indicate how often practitioners
should update their knowledge and skills, periodic review is advised. Each facility should ensure that fetal surveillance updates
are interprofessional in order to ensure common terminology and shared understanding, as well as to develop the concept of
team responsibility.4
A 2011 systematic review evaluating cardiotocography (CTG or EFM) training programs with regard to participant reaction,
learning, behaviour change, and impact, found improvement in all levels. There was evidence that knowledge was maintained
for six months 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.102

New Technologies
1) Fetal Pulse Oximetry (FPO)
This technology is an adjunct to EFM and attempts to continuously monitor intrapartum fetal O2 saturation when an atypical or
abnormal tracing is present. The cervix must be ≥ 2 cm dilated, a vertex presentation, and membranes ruptured. Various sensors
are available which 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) compared fetal pulse oximetry and EFM to EFM alone.
• No difference 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 two trials there was a decrease in operative birth (CS, forceps or vacuum) for atypical/abnormal fetal status but
other than for one small study there was no difference in overall operative delivery rates
• The author 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.103
This review and others have failed to produce convincing evidence (improved neonatal outcome or reduced operative delivery
rates) for FPO to be recommended as an adjunct to EFM or as an independent fetal surveillance technique and it is not
recommended for routine use at this time.4
2) Fetal electrocardiogram: ST waveform analysis (STAN)

• This technology is used in combination with standard EFM. FECG 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 with regard to intervention can be more precise. There is a need for both initial training and ongoing education
for caregivers to achieve expertise in this technique.
• Currently this method uses a fetal scalp clip requiring adequate cervical dilation and ruptured membranes. Recently, a
non-invasive abdominal fetal electrocardiogram (ECG) monitor has been developed which uses cutaneous electrodes
applied to the maternal abdomen to detect the FECG. A recent study using this method has demonstrated that
both the maternal and fetal heart rate can be simultaneously recorded which potentially could reduce the chance of
misinterpreting the maternal heart rate as the FHR.104

• A 2015 Cochrane systematic review105 of six 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 births
• severe metabolic acidosis (Ua pH < 7.05 and BD > 12 mmol/L)
• neonatal encephalopathy
• There were, however:
• 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 five 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.
In addition to the recent 2015 Cochrane review by Neilson, Blix et al106 and Saconne et al107 both published systematic reviews
and meta-analysis of the same 6 studies included in that of Neilson. Although Blix found a slight reduction in of neonatal
metabolic acidosis (OR 0.64 95% CI 0.46–0.88; NNT 401 to prevent 1 case of metabolic acidosis), this finding was not shared
by Saconne (0.5% vs 0.7%; RR 0.74, 95% CI 0.54–1.02). Both authors 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 at this time.
Summary
CP
1. Despite improved technology and neonatal care, the rate of CP is still 2–3/1000 live births.
2. Most situations where intrapartum asphyxia is documented do not result in CP.
3. Most cases of CP occur in uncomplicated term births.
4. Currently available tests of fetal well-being are not highly predictive of adverse CNS outcome.

General
5. Women in active labour should receive continuous support from an appropriately trained person.
6. Intensive fetal surveillance by IA or EFM requires the continuous presence of nursing or midwifery staff. One-to-one
care of the woman is recommended, recognizing that the nurse / midwife is really caring for two patients (the woman
and her unborn baby).
7. Hospitals are responsible for ensuring adequate ongoing education programs in all fetal surveillance techniques.
8. A standardized approach to documentation including the use of consistent terminology should be established at each
hospital.
Intermittent Auscultation
9. The preferred method of fetal surveillance in labour for women with no complications is intermittent auscultation.
10. IA should be performed every 15–30 minutes in the first stage and every 5 minutes in the active phase of the second
stage of labour.
11. A protocol / guideline outlining technique, frequency, and potential interventions must be in place.
Electronic Fetal Monitoring

12. EFM must be used according to an acceptable method with well-defined systematic analysis for interpretation,
documentation, and intervention in the case of atypical or abnormal findings.
13. EFM is recommended for pregnancies at risk of adverse perinatal outcome.
Fetal Scalp Blood Sampling

14. Fetal scalp sampling should be used, when available and clinically appropriate, in the presence of atypical / abnormal
FHR findings not responsive to intrauterine resuscitation in gestations >34 weeks and when delivery is not imminent.
Umbilical Cord Blood Gas Analysis

15. Cord blood sampling (arterial and venous) and blood gas analysis is recommended after ALL births.

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95. Hofmeyr GJ, Xu H, Eke AC. Amnioinfusion for meconium-stained liquor in labour. Cochrane Database Syst Rev.
2014;1:CD000014.
96. Fawole B, Hofmeyr GJ. Maternal oxygen administration for fetal distress. Cochrane Database Syst Rev.
2012;12:CD000136.
97. Hamel MS, Anderson BL, Rouse DJ. Oxygen for intrauterine resuscitation: of unproved benefit and potentially harmful.

98. Holzmann M, Wretler S, Cnattingius S, Nordstrom L. Cardiotocography patterns and risk of intrapartum fetal acidemia.
J Perinat Med. 2014.
99. Di Tommaso M, Seravalli V, Cordisco A, Consorti G, Mecacci F, Rizzello F. Comparison of five classification systems
for interpreting electronic fetal monitoring in predicting neonatal status at birth. J Matern Fetal Neonatal Med.
2013;26:487-90.
100. Soncini E, Paganelli S, Vezzani C, Gargano G, Giovanni Battista LS. Intrapartum fetal heart rate monitoring: evaluation
of a standardized system of interpretation for prediction of metabolic acidosis at delivery and neonatal neurological
morbidity. J Matern Fetal Neonatal Med. 2014;27:1465-9.
101. Liston R, Sawchuck D, Young D, Fetal Health Surveillance Consensus Committee. Fetal health surveillance: antepartum
and intrapartum consensus guideline. Chapter 3: maintaining standards in antenatal and intrapartum fetal surveillance:
quality improvement and risk management [SOGC clinical practice guideline no 107]. J Obstet Gynaecol Can.
2007;29:S45-S9.
102. Pehrson C, Sorensen J, Amer-Wahlin I. Evaluation and impact of cardiotocography training programmes: a systematic
review. BJOG. 2011;118:926-35.
103. East CE, Begg L, Colditz PB, Lau R. Fetal pulse oximetry for fetal assessment in labour. Cochrane Database Syst Rev. 2014.
104. Reinhard J, Hayes-Gill BR, Schiermeier S, Hatzmann H, Heinrich TM, Louwen F. Intrapartum heart rate ambiguity:
A comparison of cardiotocogram and abdominal fetal electrocardiogram with maternal electrocardiogram. Gynecologic
and obstetric investigation. 2013;75:101-8.
105. Neilson JP. Fetal electrocardiogram (ECG) for fetal monitoring during labour. Cochrane Database Syst Rev.
2015;12:CD000116.
106. Blix E, Brurberg KG, Reierth E, Reinar LM, Oian P. ST waveform analysis vs. cardiotocography alone for intrapartum
fetal monitoring: A systematic review and meta-analysis of randomized trials. Acta Obstet Gynecol Scand. 2015.
107. 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.

Chapter 10
Vaginal Birth
A woman may require urgent assistance with delivery when she presents late in labour or she progresses so rapidly that the
usual primary care provider (PCP) is not available. This may occur in the labour and delivery unit or in unexpected sites such
as the emergency department (ED) (where she may present with abdominal pain, not aware she is pregnant), ambulance,
automobile, or home. Individual facilities need to adapt the general principles below based on their location, resources and
personnel available.
Assessment when Birth is Imminent

Obtain the following baseline information from antenatal records (if available) and by using clear, concise questions:
While moving woman to safe location
1. When is your baby due or how many weeks are you?
2. Have your membranes ruptured? If so, what colour is the fluid?
3. How many babies have you delivered and were they vaginal or Caesarean deliveries?
4. Any problems in pregnancy—you or baby
5. Ar you taking any drugs—prescribed by your doctor, recreational or from the health food store?
As time allows assess the following
1. Cervical dilation and fetal position, and presentation
2. Contraction pattern and fetal well being (by intermittent auscultation or electronic fetal monitoring
3. Maternal vital signs
Consider
1. Initiate IV. Lab work including blood type
2. Ask additional questions
a) Results of GBS swab?
b) Has baby been moving?
c) Who is your care giver during pregnancy?
Vaginal Birth 1
3. Obtain antenatal records and ultrasound reports

a) Ask mother if she has a copy with her
Signs of Imminent Birth may 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
• Remain calm
• Move woman to as safe an environment as possible; consider privacy, warmth, access to equipment and personnel
for both mother and baby
• Remain with the woman; establish rapport and cooperation, provide support and reassurance
• Summon assistance (e.g., nurse, physician, midwife)
• After assessment determine if the woman can safely be moved to the labour and birth area
• Aim for a slow and gentle birth2
• Use body fluid precautions; use sterile equipment whenever time and situation allow3
2) Position Mother
• The position should allow good visibility of the perineum and access to monitor the fetal heart. There is no need to
break the bed.4 Plan to deliver the baby onto a surface to increase safety for the baby
• Maintain privacy for the women as much as possible.
Vaginal Birth 2
3) Equipment
• Equipment for delivery and newborn resuscitation should be opened and ready to use.
• An emergency delivery kit should be available for use in areas other than the delivery suite such as the ED.
A set of equipment in a backpack allows for rapid response to non-obstetrical areas
The emergency delivery kit:

For delivery For baby
• Gloves,eye protection • Cord clamp
• 4 Kelly clamps • Blankets
• 1 pair scissors • Cord blood syringes and tube
• Towels or blood gas syringes
• Kidney basin
• Oxytocin, syringe & needle
• Sponges
• Documentation forms
Delivery Technique
Principles
• NEVER take your eyes off the perineum once delivery is imminent
• Control the head as needed
• Check for nuchal cord
• Await restitution and external rotation
• Apply a gentle downward traction to facilitate3 delivery of the anterior and then the posterior shoulder
• Obtain arterial and venous umbilical cord gases and cord blood if mother is Rh negative (or unknown)
Vaginal Birth 3
Delivery of Head
• Encourage the woman to push only when she has the urge to do so and avoid prolonged breath—holding (valsalva)
pushing.5 If possible, allow the woman to assume the position that is most comfortable for her.
• One hand can be used 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”.6
• Good visualization of the perineum and manual perineal protection has been shown to reduce the risk of anal
sphinter tear.7,8
• There have been studies comparing 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) to 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).9,10,11 With the lack of compelling evidence it appears that both techniques of “hands on” or
“hands poised” are reasonable and an individual’s decision.5 This recommendation is also supported in the 2014 NICE
Guideline on Intrapartum Care.12
• There is evidence that warm, moist packs applied to the perineum in the late second stage may relieve perineal
pain and increase comfort.13 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
[ARR] 2.5%; number needed to treat [NNT]=40 to prevent one anal sphincter injury); however, no significant
difference was found for the outcome of intact perineum.14
• Use a sponge, towel, or bedsheet to cover the anus to prevent contamination of the clean field by maternal feces.
• Coach mother to pant (not push) with crowning,
• Preferably, deliver the head between or at end of contraction.
Vaginal Birth 4
Check for Nuchal Cord

• Check for nuchal cord by sliding your fingers all around the neck from one shoulder to the other.
If the cord is found consider the following:
• attempt to slide it gently over the infant’s head if it is very loose
• push it back over the shoulder allowing the shoulder to slip under it as the baby delivers
• keep the newborn close to the perineum and have the rest of the body deliver or “somersault” out.15 This
somersault keeps head and torso close to the perineum preventing traction of the cord
• If an extremely tight nuchal loop or multiple loops are found, it may be necessary to cut the cord before delivery
of the shoulder. Clamp the cord twice and cut between the clamps. If there are two or more loops of cord, apply
the two clamps to one loop of cord, cut between the clamps, and unwind cord. In such a case, the baby may be
hypovolemic after birth due to significant blood volume backed up in the placenta.
• It is best to avoid cutting the cord until the shoulders have delivered.
Shoulders
• Assist the mother to pant while awaiting restitution, external rotation of the head, and next contraction before
delivering shoulders.
• in normal birth there is usually a pause between delivery of the head and body. DON’T RUSH. During this pause
the uterus relaxes and the fetus restiitues. The drop in cord pH during this pause is 0.011 per minute.15 As long
as the mother is not pushing and the uterus is relaxed, venous return from the fetal head to thorax is maintained
and thus perfusion of the fetal brain. If a baby has a normal FHR prior to delivery, the pause does not alter fetal
acidosis and may assist with maternal expulsive efforts.16,17,18
• If the head retracts very close to the perineum after delivery of the head, hyperflex both legs at the hips (McRobert’s
manoeuvre) while awaiting the next contraction.
• Once external rotation has occurred, with the next contraction place a hand on either side of head (fingers flat)
and apply GENTLE downward pressure. Encourage the mother to give a small push to assist delivery of the anterior
shoulder. DO NOT PULL ON FETAL HEAD.
• If the anterior shoulder does not deliver with a contraction, maternal effort, and gentle traction, then shoulder dystocia
is present. Call for help and begin a planned approach to shoulder dystocia (see “Shoulder Dystocia” chapter).
Vaginal Birth 5
Baby
• Grasp baby around upper arms and in an upward motion complete the delivery, placing the infant skin to skin on the
mother’s abdomen (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 preterm16,17 and term18,19,20,21 newborns. Apply the first clamp 3–5 cm from the
surface of the newborn.
• Apply a second clamp at least 10 cm away from the first clamp to allow for newborn venous and arterial gases to be
collected.
• 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
• uterus becoming firmer
• Active management of the third stage, including:
• administration of prophylactic oxytocin (10 IU IM) after delivery of the anterior shoulder (may be administered
by a nurse if a medical directive or standing order is in place), is indicated to prevent postpartum hemorrhage
(PPH).25,20 Inform the woman of the medication you are giving and why.
• in situations when oxytocin is not available, you may give misoprostol 600 µg orally or sublingually after the birth
of the baby. Advise mother of risks of fever and shivering.26
• 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 mother) 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.
Vaginal Birth 6
• in situations where there are no skilled caregivers 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.
• assess the fundus and ensure that it is well-contracted and that there is no significant bleeding; uterine massage
after delivery, as needed.
• keep the placenta until verified by the PCP.
Precipitous delivery is associated with an increased risk of PPH.
• 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 bi-manual compression of the uterus until help arrives.
• 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
• Perform the initial steps of neonatal resuscitation, if required, and continue as indicated.
• Apgar scores at 1 and 5 minutes should be documented.
• A rapid delivery of the baby may also increase likelihood of newborn trauma. Assessment of the newborn for injuries
(e.g., fractues of the clavicle and/or humerus) should be performed.
• Child protection issues should be considered. If a woman presents without records or without prenatal care, there is
the possibility that she is avoiding contact with social agencies.
Early Maternal Postpartum Care

• Monitor vital signs, bleeding, fundal height and tone, perineum, and bladder.
Vaginal Birth 7
Communication and Documentation

Document
• Complete the delivery summary
• Identify the delivering caregiver
• Steps taken to notify the PCP
• Time of arrival of additional personnel
• Newborn resuscitation and status
Communicate
• With the woman and her support persons
• With the PCP
• With hospital administration depending on institutional policy
• Consult, as necessary, with social worker, chaplain, or other individuals able to support the woman and family for this
unexpected event
• Explore with women and her support persons possible causes for the imminent birth, such as parity, distance to
hospital, access to care and others.
Vaginal Birth 8
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(2):170-7.
2. Imminent birth. In: Remote area nursing emergency guidelines. 4th ed. Perth (WA): Department of Health Western
Australia; 2005. p.108-13. Available: http://www.ocno.health.wa.gov.au/policy/docs/Remote_Area_Nursing_
Emergency_Guidelines.pdf.
3. 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(10):34-40.
4. British Columbia Perinatal Health Program. Core competencies: management of labour in an institutional setting if
the primary maternal care provider is absent [Guidelines for registered nurses]. 1st ed. Vancouver: The Program; 2009.
Available: http://www.bcphp.ca/sites/bcrcp/files/FHS/Linked_Core_Competencies_with_DST.pdf.
5. Charles C. Labour and normal birth. In: Chapman V, Charles C, editors. The midwife’s labour and birth handbook. 2nd ed.
Mississauga (ON): Wiley-Blackwell; 2008. p.1-31.
6. Fraser DM, Cooper MA. The transition and the second stage of labour: physiology and the role of the midwife. In: Myle’s
textbook for midwives. 15th ed. Toronto: Elsevier Limited; 2009. p.509-30.
7. Samuelsson E, Ladfors L, Wennerholm UB, Gareberg B, Nyberg K, Hagberg H. Anal sphincter tears: prospective study of
obstetric risk factors. BJOG 2000;107(7):926-31.
8. 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(10):974-7.
9. 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(12):1262-72.
10. 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 1076 women. J Reprod Med 2002;47(6):477-82.
11. 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(2):106-11.
Vaginal Birth 9
12. Intrapartum care: care of healthy women and their babies during childbirth [NICE guideline CG190]. London: National
Institute for Health and Care Excellence; 2014. Available: http://www.nice.org.uk/guidance/cg190.
13. 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(2):e39-e48.
14. Aasheim V, Nilsen AB, V, Lukasse M, Reinar LM. Perineal techniques during the second stage of labour for reducing
perineal trauma [Cochrane review]. In: Cochrane Database of Systematic Reviews 2011 Issue 12. Chichester (UK): John
Wiley & Sons, Ltd; 2011. DOI: 10.1002/14651858.CD006672.pub2.
15. 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(4):474-9.
16. Gurewitsch ED, Allen RH. Reducing the risk of shoulder dystocia and associated brachial plexus injury. Obstet Gynecol
Clin North Am 2011;38(2):247-69.
17. 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(2 Pt 1):318-22.
18. 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(8):716-20.
19. Rabe H, Reynolds G, Diaz-Rossello J. Early versus delayed umbilical cord clamping in preterm infants [Cochrane
10.1002/14651858.CD003248.pub2.
20. 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 [SOGC clinical practice guideline no 235]. J Obstet
Gynaecol Can 2009;31(10):980-93. Available: http://www.sogc.org/guidelines/documents/gui235CPG0910.pdf.
21. 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(2):303-97.
22. Mercer JS, Vohr BR, McGrath MM, Padbury JF, Wallach M, Oh W. Delayed cord clamping in very preterm infants
reduces the incidence of intraventricular hemorrhage and late-onset sepsis: a randomized, controlled trial. Pediatrics
2006;117(4):1235-42. Available: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmed
id=16585320.
Vaginal Birth 10
23. Hutton EK, Hassan ES. Late vs early clamping of the umbilical cord in full-term neonates: systematic review
and meta-analysis of controlled trials. JAMA 2007;297(11):1241-52. Available: http://jama.ama-assn.org/cgi/
reprint/297/11/1241.
24. Finan E, Aylward D, Aziz K, Neonatal Resuscitation Program Executive Committee, Canadian Paediatric Society.
Neonatal resuscitation guidelines update: a case-based review. Paediatr Child Health 2011;16(5):289-91.
25. Mathai M, Gülmezoglu AM, Hill S. WHO recommendations for the prevention of postpartum haemorrhage. Geneva:
World Health Organization; 2007. Available: http://whqlibdoc.who.int/hq/2007/WHO_MPS_07.06_eng.pdf.
26. Hofmeyr GJ, Abdel-Aleem H, Abdel-Aleem MA. Uterine massage for preventing postpartum haemorrhage. Cochrane
Database Syst Rev 2013;7:CD006431.
Vaginal Birth 11
Chapter 11
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.1 Both methods are safe and reliable for assisting childbirth provided that appropriate attention is paid
to the indications and contraindications for the procedures. In every case, consideration must be given to the maternal and fetal
risks of using either instrument, and to the risks associated with proceeding with the alternative choice of Caesarean section (CS)
delivery. 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 accoucheur and patient. The
operator should have acquired training, experience, and ability with the instrument chosen.1 Informed consent is essential.
Definitions
Station
• The level of the leading edge of the skull in centimeters above or below the level of the ischial spines. Careful
distinction from the 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 molding 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.
Assisted Vaginal Birth 1

Classification of Assisted Vaginal Birth (AVB)

The classification of operative vaginal deliveries is based on the station of the head within the pelvis.2
Outlet
• Scalp visible at the introitus without separating the labia
• Fetal skull has reached the pelvic floor
• The sagittal suture is in AP diameter or right or left occiput anterior or posterior position (rotation does not exceed 45°)
• Fetal head is at or on the perineum
Low
• Leading point of fetal skull is at station ≥ +2 and not on the pelvic floor
• Two sub-divisions:
• rotation is ≤ 45°
• rotation is > 45°
Mid
• Head is engaged (station 0 or lower)
• Leading position of the skull is above station +2
Incidence
Forceps rates continues to decline nationally and internationally. Reasons postulated for the decline are the perceptions that
Caesarean birth is a safer alternative and that the vacuum is easier. Other reasons cited are the decline in resident learning
opportunities for forceps and potential medical legal implications.
In an analysis of five-year time periods at the National Maternity Hospital, Dublin, the choice of instrument for AVD was primarily
forceps in 1991–1995 at 68.2%. Use of forceps fell to 32.9% of all AVB in 2006–2010 with vacuum becoming the choice of
the majority of caregivers. In the United States from 1990–2012, the overall AVB rate declined from 9.01% to 3.4%. Forceps
deliveries declined from 5.11% to 0.61% whilst vacuum deliveries declined from 3.90% to 2.79%.3 Despite the overall 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.4

Assisted Deliveries by Country5-10
In 2010–2011 the overall rates of AVB, vacuum-assisted deliveries and forceps-assisted deliveries in Canada were 13.5%,
9.6% and 3.2% respectively.11 The rate of forceps deliveries continues to decline from a rate of 4.6% in 2004–2005. There is
considerable provincial variation within Canada as well as variation between selected western countries.
CIHI reported the 2008–2009 percentage of AVD by vaginal births varied by province of residence. The overall Canadian average
rate of vacuum-assisted delivery was 10% and the rate of forceps-assisted delivery was 3.8%.12 (The rates below are rounded to
the approximate percent.)

% Vacuum % Forceps % Total AVB
BC 10 4 14
Alberta 12.5 4 16.5
Saskatchewan 13 3 16
Manitoba 6.5 3.2 9.7
Ontario 10 3.8 13.8
Quebec 9 3 12
New Brunswick 9 3.8 12.8
Nova Scotia 8 4.5 12.5
PEI 4 2.5 6.5
Newfoundland 10 6 16
Yukon 7 0 7
Northwest territories 5.5 1 6.5
Nunavut 1.5 0 1.5
Based on: Highlights of 2008-2009 selected indicators describing the birthing process in Canada [Bulletin].
Ottawa: Canadian Institute of Health Information; 2009 Oct.12
In Ontario, the AVB rate has remained stable at 13.3% of vaginal births in 2011–2012. There was a geographic range of 10.9 %
to 14.4 % across the province. For nulliparous women alone the rate was 23% with a range of 16.8% to 26.7% for women who
had a vaginal birth.

The relative benefits and risks for vacuum extraction versus forceps delivery have been the subject of much study and debate. The
proper comparison is not of vacuum with spontaneous delivery but of vacuum with other operative vaginal delivery methods or CS.
Assessment of pelvic adequacy is mandatory. Abnormalities of the position or attitude of the vertex can result in relative
cephalopelvic disproportion (CPD). The fetus should be assessed abdominally and the station evaluated by pelvic exam.
Extensive molding or caput may confuse the vaginal assessment of descent and may indicate the possibility of relative CPD.

If the fetal head is palpable abdominally above the pelvic inlet, caution is warranted. A 2013 prospective trial study demonstrated
that a strategy of manual rotation for fetuses in posterior or transverse positions at full dilatation is associated with a reduction in
the rate of operative delivery.13
CONSENT
Patients should be informed of the potential risks and benefits of the selected instrument (vacuum or
forceps) prior to application as part of informed consent. The risk of perineal trauma and the small risk to the fetus
of subgaleal or intracranial hemorrhage with vacuum or forceps must be weighed against the maternal risks of cesarean section
(at advanced station). If the FHR is abnormal, the risk to the fetus of any delay required to deliver by cesarean section must also
be taken into consideration.
Vacuum
Types: A meta analysis showed cephalohaematoma and scalp injury were less likely with a soft vs. rigid or metal cup but with
no other significant neonatal outcomes differences. There was no difference in maternal outcome.14
Risks: Maternal soft tissue trauma (hematoma, laceration) can be prevented by:
• avoiding traumatic insertion of the device,
• frequent checking for maternal soft tissue entrapment,
• avoiding vacuum slippage or pop-off,
• controlling the rate of descent, and
• controlling delivery over the perineum.
Application of vacuum to the fetal scalp invariably causes exaggeration of subcutaneous caput and formation of a chignon,
which resolves within hours of birth. Bruising (ecchymosis) is also common and is benign. Large caput and bruising can be
confused with a cephalhematoma, 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, bleeding
in a cephalhematoma is self-limited and forms a tense swelling immediately adjacent to bone that persists after the caput and
chignon have subsided. The swelling is benign and resolves over weeks to months; however, resorption of hemoglobin can result
in hyperbilirubinemia.
A more serious but rare complication of vacuum extractions is subgaleal (subaponeurotic) hemorrhage. The suture lines of the
skull do not limit hemorrhage into the subgaleal space as they do in cephalohaematoma. As a result, subgaleal hemorrhages can
extend over the entire calvarium from the brow ridge to the nuchal ridge and from ear to ear. Several hundred millilitres of blood

can be lost which, if undetected, can produce 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-cup deliveries.16
Cephalhematoma Subgaleal Hemorrhage
Fetal scalp trauma (hemorrhage and laceration) can best be prevented by avoiding excessive, incorrect, or prolonged traction
(> 10 minutes), and by avoiding rotational forces.17 To minimize traction forces and likelihood of pop-off, the vacuum cup must
be applied to the 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 torquing force, which can cause lacerations. Vacuum
should also generally not be used if fetal coagulopathy is known or suspected.18-22
After every succesfull or unsucessfull vacuum delivery, there should be surveillance of the neonate to ensure that the expected
caput and chignon does not thereafter enlarge, signifying a subgaleal hemorrhage. It should also be ensured that there is no
evidence of developing hypovolemia.23,24
Forceps
Types: Forceps vary by shank length, pelvic and cephalic curves. Commonly Simpson forceps are used for a molded fetal head,
often seen in nulliparous women. Tucker-McLane forceps have a more rounded cephalic curve, more suitable for the unmolded
fetal head seen in multiparous women. Kjelland forceps are made for rotation of the fetal head and lack a pelvic curve.

Risks: The risk of maternal soft tissue injury is greater with forceps than with vacuum.1 A 2013 study from England
demonstrated adjusted odds ratio of obstetrical anal sphincter injury (OASIS) with forceps delivery was 4.43, 95% confidence
interval [CI] 2.02 to 9.71, p < .005.25 Hehir (2013) also demonstrated increased risk of OASIS with forceps with a rate of 8.6%
compared to a spontaneous vaginal delivery rate of 1.3%.26 Interestingly, 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 OASIS rate by half. The more liberal but not
routine use of episiotomy is part of the reduction in OASIS.27
The risk is 1% for each of facial lacerations and cephalohematoma and 0.1% symptomatic intracranial hemorrhage.1 External
ocular injuries and facial nerve palsies are more common with forceps than with vacuum.14 A 2009 Canadian-authored study
supports the view that facial nerve palsies associated with operative vaginal delivery have a very good prognosis.28
Neonatal skull fracture has been reported after both spontaneous deliveries and forceps deliveries. The incidence is greater after
forceps deliveries.29 Forceps should also generally not be used if fetal coagulopathy is known or suspected.
There remains a role for mid-forceps operations, especially where a rotation is required. The risk of a mid-forceps delivery must be
compared with that of its alternative, which is an intrapartum second stage CS. Mid- and rotational forceps delivery should only
be planned by experienced operators, and should be conducted as a “double set-up” in an operating room with immediate access
to Caesarean delivery in case vaginal delivery is not accomplished.
Rotational forceps have been the subject of several studies in the United Kingdom. Bradley (2013) showed there was no
difference in trauma between manual or forceps rotation and that there was less trauma if the baby was delivered Occiput
Anterior instead of Occupit Posterior.30
Comparison of Vacuum and Forceps

The choice of a vacuum or forceps for AVD should be based on the total clinical picture, geographic location as well as
practitioner expertise.31 A 2010 Cochrane meta analysis of 32 studies showed forceps and the metal vacuum cup (versus
soft cups) were most successful in achieving a vaginal birth however, forceps were associated with higher rates of maternal
complications, including perineal trauma, tears, more general and regional anesthesia, and incontinence.14 The metal cup was
associated with more neonatal trauma. The urgency for delivery needs to be balanced against potential risks to the mother and
baby. The following two graphs from the meta-analysis of controlled trials compare forceps delivery and vacuum extraction.14

Forceps Delivery versus Vacuum

Although retinal hemorrhage was found after both vacuum and forceps delivery, vision in childhood was normal.32 Clinically
significant intracranial hemorrhage (ICH) is a rare complication of vacuum and forceps. When interpreting data on ICH, it must
be remembered that asymptomatic subdural hemorrhage also occurs during spontaneous birth. A series of 111 asymptomatic
neonates investigated with routine postnatal MRI demonstrated 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 MRI.33
California surveillance data demonstrated that the lowest risk of fetal intracranial injury occurred with spontaneous vaginal
delivery and CS without labour. 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 to children who delivered spontaneously.2
Effect of Mode of Delivery in Nulliparous Women on Neonatal intracranial injury (Towner et al34)
Singleton Nulliparous Deliveries, California 1992-94
Delivery Method Number %
SVD 387 799 66.5
Vacuum 59 354 10.2
Forceps 15 945 2.7
Vacuum & Forceps Delivery 2817 0.5
C-Section 117 245 20.1
Total 583 340 100
Delivery Method Number %
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

Effect of Mode of Delivery in Nulliparous Women on Neonatal intracranial injury (Towner et al34)
Singleton Nulliparous Deliveries, California 1992-94
Forceps Assist 1 per 664 0.15
CS after Assisted Birth 1 per 334 0.33
Vacuum & Forceps 1 per 256 0.39
ICH = Intracranial Haemorrhage
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 intraventrialubar
hemmorrhages and no skull fractures in all 288 births.35 Other small studies have concluded that sequential use of instruments
for AVD can increase neonatal injury.36,37
Caution: Sequential Use of Vacuum and Forceps

The SOGC, RCOG, and ACOG suggest caution with sequential use of vacuum and forceps due to the potential for fetal injury.1,2,38
If descent is not achieved with traction on a correctly applied vacuum cup, cephalopelvic disproportion (CPD) must be suspected,
and an attempt at forceps is generally not advisable. However, if a vacuum or forceps cannot be optimally applied, switching
instruments prior to 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 RCOG, notes that the risks of forceps versus a CS at advanced station should be considered and that judicious use of
outlet forceps after failed vacuum may avoid a potentially difficult Caesarean section.

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 (e.g., cerebral • Medical indications to avoid valsalva (e.g., cerebral
vascular disease, cardiac conditions) 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 • Sub-optimal attitude or position of the fetal head may
• Assistance at CS if required be corrected
• Assistance at CS if required
• Assisting with aftercoming head of a breech
Contraindictions • Non-cephalic, face, or brow presentation • Non-cephalic or brow presentation (except Piper’s for
• Lack of knowledge of fetal position aftercoming head of a breech)
• Fetal conditions (e.g., bleeding disorder, • Lack of knowledge of fetal position
demineralization disorder) • Fetal conditions (e.g., bleeding disorder, demineralization
• Any contraindications to vaginal delivery disorder)
• Less than 34 weeks’ gestation2 • Any contraindication to vaginal delivery
• Rotational force must not be applied. Spontaneous
autorotation of the head may occur with traction and
descent. The Kiwi Omnicup and Bird 5 cm posterior
cups are designed to facilitate this
Previous fetal scalp sampling is not a contraindication to
vacuum-assisted delivery.

Criteria for Use of Vacuum and Forceps

Vacuum Forceps
Prerequisites • Informed consent • Informed consent

• Appropriate anaesthesia • Appropriate anaesthesia
A mnemonic is
• Maternal bladder empty • Maternal bladder empty
included delineating
• Vertex engaged • Vertex engaged
these prerequisites
• Cervix fully dilated • Cervix fully dilated
It is included in this • Adequate uterine contractions • Adequate uterine contractions
syllabus and may • Membranes ruptured • Membranes ruptured
be copied for use in • Position of the head must be known • Position of the head must be known
labour and delivery • Experienced operator, adequate facilities, • Exact position of the head must be determined
suites. and resources available • Experienced operator, adequate facilities, and
• Operator knowledge of the instruments, their use, and resources available
the complications that can arise • Operator knowledge of the instruments, their use,
• Reasonable chance of success (no evidence of CPD) and the complications that can arise
• Backup plan if the procedure is unsuccessful • Reasonable chance of success, no evidence of CPD
• Ongoing fetal and maternal assessment • Backup plan if the procedure is unsuccessful
• Appropriately skilled personnel for neonatal • Ongoing fetal and maternal assessment
resuscitation • Appropriately skilled personnel for neonatal resuscitation
Management
Vacuum Extraction
Vacuum Extractor
The vacuum extractor should not be regarded as an easier alternative to forceps, or for use by less
skilled operators.
The vacuum extractor is designed to apply traction upon the fetal scalp in order to assist the maternal expulsive effort. It can be
used for rotational deliveries; however, it cannot be used to apply rotational forces. Nor is it likely to succeed in
the absence of maternal expulsive effort. The vacuum may be used judiciously 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. Hard cups, soft silastic cups, and the Kiwi Omnicup are some of the
devices from which to choose. Several comparisons of different cups have been published with conflicting results. The success
rate and complication rate of each device is difficult to compare as operator training and experience are essential to optimize
outcomes. For example, in some reports, the Kiwi Omnicup is associated with a higher failure rate than the soft cup vacuum
whereas in other reports (where caregivers are trained and mentored in the use of the Kiwi Omnicup), failure rates are much
lower.23,39-42 In a 2010 Cochrane review, the anterior soft cup was compared to a metal cup. The metal cup had a lower rate
of failed delivery (eight 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, perineal and vulval 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 appropriate instrument to the appropriate
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 are often 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 Omni and 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.

Cup positions on the fetal head16:

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 Omni-cup; Bird 5 cm posterior cup
Station +3 or greater; occiput anterior Kobayashi, Silc, Kiwi Omni or , Mighty-vac, or
The caregiver should ensure that proper training and experience with the specific instrument have been achieved,
46-48
recognizing that skills may not be interchangeable between instruments. Vacuum pop-offs should not be considered a normal
event in a vacuum-assisted delivery.23 Causes include:
• Poor seal causing vacuum leak
• Impingement of maternal soft tissue
• Deflexing or paramedian application
• Cephalopelvic Disproportion (CPD)
• Uncontrolled traction technique (no counter-traction)
• Traction that is too rapid
• Improper angle of traction
Forceps
Debate about the indications for and safety of forceps operations has continued for over two hundred years. Controversies have
mainly focused on mid-forceps deliveries. Delivery trends have been observed showing that, for 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.
Once applied, the forceps application is checked in three ways. The following mnemonic assists in
this endeavor. “Position For Safety”: “P” osterior fontanelle, “F”enestration, “S”agittal suture:49 If the forceps are applied in
such a manner that the posterior fontanelle is more than a fingerbreadth above the plane of the shanks, traction will result in
further deflexion of the fetal head, increasing the diameter of the presenting part for delivery. If greater than a finger width of
fenestration is still palpable after application of the blades, then the application of the blades may be too short, again increasing
the likelihood of fetal injury. When the sagital suture is not perpendicular to the plane of the shanks throughout its length, the
application of the forceps is asymmetrical, thus increasing the risk of fetal injury.

Obstetrical forceps are applied to the fetal head to perform the following functions:
• Traction
• Rotation
• Flexion
• Extension
When one or more of these functions is attempted, there is simultaneous fetal head compression. Head
compression is the undesirable factor 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
Location of Delivery
Prior to any AVB the clinician should consider the following:
• Fetal status prior to and throughout the attempt of assisted vaginal delivery.
• The time to initiate a cesarean section if the procedure fails.
• Choice of instrument based on the clinical circumstances and operator experience.
• Location of the birth including discussion with the team:
• For delivery from a low or outlet station when the operator is very confident of success, delivery in a hospital
birthing 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 cesarean
section. However, if the fetal heart rate is abnormal, it may be appropriate to attempt delivery in a birthing room
while preparations for emergency cesarean section are underway.50

Stanton Algorithm
Assisted Vaginal Birth Decision Tree
Alternatives to AVB have

been considered: Time?,
Oxytocin?,Analgesia?, C-Section?
Yes
AVB indicated
Yes
Prerequisites achieved? No Other Plan

Contraindications absent?
(Including that of a vaginal birth)
Yes
Fetal Status
FHR Abnormal FHR Normal
AVB in labor room Determine best location

and Call for back-up: for AVB: Rotation <45°?
OB, OR,
YesPeds, Spines +2 or more?
Anesthetist as necessary High likelihood of success?
Yes No
Low/Outlet AVB Trial of AVB in OR with

in labor room double set up
Call for back-up as necessary Call for back-up
© 2016 Salus Global Corporation. MOREOB is a registered trademark of Salus Global Corporation. All Rights Reserved moreob.com

Vacuum Forceps
A • Address and obtain consent. The indication(s) and plan must be clear, well understood by the parents, and fully documented.
• Adequate pain relief is available; assistance for the baby is available
ADDRESS • Absence of contraindication to the procedure
ANAETHESIA
ASSISTANCE
ABSENCE
B • Bladder catheterized
• Back-up plan discussed with parents and team, documented; resources available
BLADDER
BACK UP PLAN
C • Fully dilated, membranes ruptured

• Adequate contractions and assessment of maternal expulsive efforts
CERVIX
CONTRACTIONS
D • Determine position, station, and pelvic adequacy

• Determine location of birth (in delivery room or trial in OR)
DETERMINE • Think possible shoulder dystocia
DYSTOCIA
E • Inspect vacuum cup, pump, tubing, and check pressure • Select forceps based on clinical requirements.
• EFM indicated: keep scalp clip applied, re-apply clip • Phantom application
EQUIPMENT beside vacuum, or ensure adequate transabdominal • EFM indicated: keep scalp clip applied, or ensure
EFM fetal monitoring adequate transabdominal fetal monitoring

Vacuum Forceps
F • Introduce the cup into the posterior aspect of the vagina • Forceps are applied between contractions. Traction may
while protecting the maternal tissues and making space be performed with or without a contraction
FONTANELLE with the opposite hand • Left hand, maternal left side, pencil grip and vertical
• Soft cups are inserted by compressing the cup in an insertion, with right thumb directing blade
FLEXION POINT AP diameter • Right blade, right hand, maternal right side, pencil grip
FOR VACUUM • Hard cups are slid in sideways and flipped onto the and vertical insertion with left thumb directing blade
fetal skull • Fingers in the vagina should only guide the blades and
• The cup is centred over the flexion point (the point should not apply pressure on or displace the fetal head
where traction will facilitate the smallest diameter of the • Lock blade and support; should lock without pressure
fetal skull passing through the pelvis). The flexion point • Check application PFS, i.e.,
is over the sagittal, suture just anterior to the posterior • Posterior fontanelle located midway between the
fontanelle on the fetal skull 51-54 blades, and 1 fingerbreadth above the plane of the
• In the correct position the edge of the cup reaches onto shanks with the lambdoid sutures equal distance
the posterior fontanelle from the forceps blades
• When the fetus is OP, the flexion point is usually more • Fenestration of blades barely felt. Equal amount of
posterior than first appreciated. With correct application, fenestration felt on each side (with a solid blade
the 11 cm mark on the traction cable of a Kiwi cup no more than a fingertip should be able to be
should be at the fourchette. inserted between the blade and the fetal head)
• Ensure that no maternal tissue is between the fetal • Sagittal suture perpendicular to plane or shanks
head and the vacuum cup; do this by sweeping finger with occipital sutures 1 cm above respective
around cup to clear maternal tissue. This is reconfirmed blades
prior to each pull on the vacuum and following any
re-application or suggestion of loss of contact during
traction . It is often not possible to reach to the far edge
of a Kiwi or 5 cm Bird cup correctly applied to the flexion
point of an OT or OP fetus.
• Initially increase vacuum pressure to resting pressure
100–200 mm Hg (0.1–0.3 kg/cm2) then, for traction,
increase to 500–600 mm Hg (0.6–0.8 kg/cm2) (follow
the specific manufacturer’s recommendation for your
instrument)

Vacuum Forceps
G • The vacuum pressure may be released between • Traction in axis of birth canal
contractions to resting pressure or maintained at traction • Handle elevated do not elevate handle too early
GENTLE pressure. A randomized trial showed no difference
TRACTION in neonatal outcome if the vacuum was maintained
(without continuous traction) or released between
contractions.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 traction pressure
• pull in the axis of the birth canal with contractions
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 clinical
circumstance (e.g., fetal well being, progress, likelihood of success). Guidelines are provided as to when to reconsider but the
HALT decision is made by the clinician performing the procedure based on his/her expertise and assessment of the clinical situation.
The listed Reassess if: Reassess if:

recommendations • No progress after two pulls with a properly positioned • Difficulty or failure of proper application
should be considered cup and good traction • Failure of rotation, if attemped and required
the maximum limits. • Delivery is not imminent after four contractions, reassess • Inadequate descent with traction
the method of delivery • If no progress is observable in 3 traction attempts,
• 3 pop-offs, without obvious cause abdominal delivery should be considered.57
• 20 minutes elapsed time and delivery is still not
imminent22,56
The longer the cup is on, the more chance there is of scalp
trauma.15,17 It is imperative that some descent is observed
with each pull. If these limits are approached and delivery is
not imminent, progress does not occur, or there is evidence of
scalp trauma, the procedure should be abandoned.55

Vacuum Forceps
I • Routine episiotomy has not been proven to be an essential part of an assisted vaginal birth and may increase maternal
trauma. 2,28
INCISION • In the situation where the perineum is preventing delivery, an episiotomy may expedite a vaginal birth, although this has
not been examined in any prospective studies
• Midline episiotomies have been found to increase the risk of third and fourth degree tears in both spontaneous and operative
deliveries.2,58,59
• An episiotomy should be performed when the perineum is well-distended by the fetal head
• Selective mediolateral episiotomy has been shown to reduce OASIS in assisted vaginal birth.27 Remember to cut at
60-70 degrees from midline (20-30 degrees from horizontal)
• The risk of OASIS is higher and the threshold for performing an episiotomy should be lower:
• when forceps are used
• in nulliparous women
• when abnormal FHR requires rapid delivery without adequate time for the perineum to stretch.
• in women with a prior history of OASIS
J • Remove vacuum when jaw is reachable or delivery • Forceps are removed as the fetal head delivers through
assured. the perineum.
JAW

Follow-Up
Care After Assisted Vaginal Birth
• Active third stage management
• Umbilical arterial and venous blood gas analysis
• Examination for maternal trauma
• OASIS
• Examination for neonatal trauma including:
• scalp trauma
• signs of cerebral irritation (poor suckling, listless)
• signs of scalp swelling, cephalohematoma, or subaponeurotic bleeds
• many centres have established observation protocols for newborns who have had forceps or vacuum applied
during their delivery process. Frequency and duration of the protocols vary with recommendations ranging from
assessment every 1–2 hours with durations of 24–48 hours.60-63 Evidence for a particular subgaleal surveillance
protocol is lacking; however, the following example of newborn assessment is suggested: perform newborn
assessments at 1h, 2h, 4h, then q4h x 24h involving measument of newborn head circumference and heart
rate, Notify physician of head circumference increase 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 was seen more commonly in primigravidas but the overall rate after vacuum delivery is low.
In a Canadian study, neonatal trauma rates using the Omnicup were: abrasions/blister 11.4%, hematoma 14.7%,
and intracranial hemorrhage 0.004%. In the 1000 vacuum deliveries, there was 1 subgaleal hemorrhage.35
• Review birth with the mother +/- father.
• Reassurance regarding chignon, caput, cephalhematoma, or facial marks.
• Stool softeners + pelvic physio if OASIS
• Documentation
Documentation
The indication, definition, 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
• Documented
Discussion and informed consent are essential prior to the intervention followed by a clear explanation to the patient describing
the procedure and its outcome after the delivery is complete. All questions should be addressed and contemporaneous
documentation can then be completed.
Suggested format for a chart note
This may also serve as a template to dictate a delivery summary.
• Date/Time
• Physician
• Indication
• Record of discussion with the woman of the risks, benefits, and options
• Position and station of the fetal head (i.e., vaginally and/or 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 vs. deflexing; median vs. paramedian
• Description of maternal and neonatal injuries
• Initiation of monitoring for subgaleal hemorrhage (vacuum)
Summary
Assisted vaginal birth by vacuum or forceps is an appropriate and effective obstetrical intervention in certain clinical situations.
Careful assessment of the clinical indications, contraindications, and expected maternal and fetal/neonatal outcomes should be
performed before applying the instrument.


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factors and method of delivery - an 8-year analysis across two tertiary referral centers. J Matern Fetal Neonatal Med.
2013;26:1514-6.

27. Stedenfeldt M, Oian P, Gissler M, Blix E, Pirhonen J. Risk factors for obstetric anal sphincter injury after a successful
multicentre interventional programme. BJOG. 2013;121:83-91.
28. Duval M, Daniel SJ. Facial nerve palsy in neonates secondary to forceps use. Arch Otolaryngol Head Neck Surg.
2009;135:634-6.
29. Dupuis O, Silveira R, Dupont C, Mottolese C, Kahn P, Dittmar A, et al. Comparison of “instrument-associated” and
“spontaneous” obstetric depressed skull fractures in a cohort of 68 neonates. Am J Obstet Gynecol. 2005;192:165-70.
30. Bradley MS, Kaminski RJ, Streitman DC, Dunn SL, Krans EE. Effect of rotation on perineal lacerations in forceps-assisted
vaginal deliveries. Obstet Gynecol. 2013;122:132-7.
31. Intrapartum care: care of healthy women and their babies during childbirth. London: National Institute for Health and
Care Excellence; 2014. Available from: http://www.nice.org.uk/guidance/cg190.
32. Johanson RB, Heycock E, Carter J, Sultan AH, Walklate K, Jones PW. Maternal and child health after assisted vaginal
delivery: five-year follow up of a randomised controlled study comparing forceps and ventouse. Br J Obstet Gynaecol.
1999;106:544-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10426611.
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: http://www.ncbi.
nlm.nih.gov/pubmed/15031028.
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.
36. Gardella C, Taylor M, Benedetti T, Hitti J, Critchlow C. The effect of sequential use of vacuum and forceps for assisted
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. London: Royal College of Obstetricians and Gynaecologists; 2011. Available from:
https://www.rcog.org.uk/en/guidelines-research-services/guidelines/gtg26/.
39. Attilakos G, Sibanda T, Winter C, Johnson N, Draycott T. A randomised controlled trial of a new handheld vacuum
extraction device. BJOG. 2005;112:1510-5.

40. Groom KM, Jones BA, Miller N, Paterson-Brown S. A prospective randomised controlled trial of the Kiwi Omnicup 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.
42. Siozos A. A new handheld vacuum extraction device: a randomised control trial [letter]. BJOG. 2006;113:495.
43. Johanson R, Pusey J, Livera N, Jones P. North Staffordshire/Wigan assisted delivery trial. Br J Obstet Gynaecol.
1989;96:537-44. Available from: http://www.ncbi.nlm.nih.gov/pubmed/2667628.
44. Johanson RB, Rice C, Doyle M, Arthur J, Anyanwu L, Ibrahim J, et al. A randomised prospective study comparing
the new vacuum extractor policy with forceps delivery. Br J Obstet Gynaecol. 1993;100:524-30. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/8334086.
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/pubmed/1622904.
46. Hayman R, Gilby J, Arulkumaran S. Clinical evaluation of a “hand pump” vacuum delivery device. Obstet Gynecol.
2002;100:1190-5.
47. Muise KL, Duchon MA, Brown RH. Effect of angular traction on the performance of modern vacuum extractors.
48. Muise KL, Duchon MA, Brown RH. The effect of artificial caput on performance of vacuum extractors. Obstet Gynecol.
1993;81:170-3.
49. Damos JD. Assisted vaginal delivery. Advanced life support in obstetrics (ALSO): course syllabus. Toronto: College of
Family Physicians of Ontario; 2000.
50. Olagundoye V, MacKenzie IZ. The impact of a trial of instrumental delivery in theatre on neonatal outcome. BJOG.
2007;114:603-8.
51. Rydberg E. The mechanism of labour. Springfield (IL): Thomas; 1954.
52. Bird GC. The importance of flexion in vacuum extractor delivery. Br J Obstet Gynaecol. 1976;83:194-200.
53. Vacca A. Handbook of vacuum extraction in obstetric practice. London: Edward Arnold; 1992.
54. McQuivey RW. Vacuum-assisted delivery: a review. J Matern Fetal Neonatal Med. 2004;16:171-80.

55. Bofill JA, Rust OA, Schorr SJ, Brown RC, Roberts WE, Morrison JC. A randomized trial of two vacuum extraction
techniques. Obstet Gynecol. 1997;89:758-62.
56. Vacca A. Operative vaginal delivery: clinical appraisal of a new vacuum extraction device. Aust N Z J Obstet Gynaecol.
2001;41:156-60.
57. Ross MG, Beall MH. Forceps delivery: treatment & management. Medscape. 2013. Available from: http://emedicine.
medscape.com/article/263603-treatment.
58. Hudelist G, Gelle’n J, Singer C, Ruecklinger E, Czerwenka K, Kandolf O, et al. Factors predicting severe perineal trauma
during childbirth: role of forceps delivery routinely combined with mediolateral episiotomy. Am J Obstet Gynecol.
2005;192:875-81.
59. Eason E, Labrecque M, Wells G, Feldman P. Preventing perineal trauma during childbirth: a systematic review. Obstet
Gynecol. 2000;95:464-71.
60. Barrow E. Exsanguinating haemorrhage into the scalp in newborn infants. S Afr Med J. 1968;42:265-7.
61. Govaert P, Vanhaesebrouck P, De Praeter C, Moens K, Leroy J. Vacuum extraction, bone injury and neonatal subgaleal
bleeding. Eur J Pediatr. 1992;151:532-5.
62. Chia CC, Huang SC. Neonatal coagulopathy presents as unusual and severe subgaleal hematomas after vacuum delivery.
Taiwan J Obstet Gynecol. 2008;47:435-7.
63. Symington A, Paes B. Fetal and neonatal alloimmune thrombocytopenia: harvesting the evidence to develop a clinical
approach to management. Am J Perinatol. 2011;28:137-44.
64. Lucas MJ. The role of vacuum extraction in modern obstetrics. Clin Obstet Gynecol. 1994;37:794-805.
65. Bachman JW. Forceps delivery [letter]. J Fam Pract. 1989;29:360.

Appendix
Table of Vacuum Conversions

mm Hg in 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
Lucas MJ. The role of vacuum extraction in modern obstetrics. Clin Obstet Gynecol 1994;37(4);794-805.64

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 1989.65

Forceps 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 • 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 1989.65

Chapter 12
Delivery of Twins
Definition
Twins are a form of multiple birth in which the mother gives birth to “two offspring from the same pregnancy, either of the same
or opposite sex”.1 Multiple pregnancy is the term used to describe more than one offspring from the same pregnancy.1
Twin gestations are broadly classified by zygosity and chorionicity. Zygosity refers to the number of ova fertilized. Dizygotic
or fraternal twins are the result of two ova being fertilized, whereas monozygotic or identical twins are the result of a single
ovum. In addition, monozygotic twins are classified according to chorionicity and amnionicity. Chorionicity and amnionicity
vary according to the age at which embryonic cell division occurs and carry differential levels of risk. A final type of twin is the
conjoint twin, which are twins in which separation was not complete.2
Incidence
Spontaneous twin pregnancy occurs in approximately one in 90 pregnancies.3 With the increased use of ovulation induction
and assisted reproductive technologies, the rate of multiple gestations, mainly dizygotic twins, has increased significantly.
In Canada, the number of multiple births has risen from 10 421 in 2004 to 12 543 in 2011.4 The rate of monozygotic twins
is constant (3–5 per 1000 births) and does not vary among populations. The incidence of dizygotic twins fluctuates with
heredity, race, maternal age, and parity.5
Morbidity and Mortality6

1. Perinatal mortality:
• monoamniotic twins (50–60%)
• diamniotic monochorionic twins (4.4%)7
• dichorionic twins (1.2%)7
Delivery of Twins 1
2. Antenatal complications:
• pre-eclampsia (10–20%)
• prematurity (40–50%)
• discordant growth and intrauterine growth restriction (IUGR) (15–25%)
• twin-to-twin transfusion syndrome (5–10%)
• congenital anomalies—higher than singleton pregnancies matched for maternal age
• death of one fetus (2–5%)
• brain damage in surviving twin after death of one MC/DA twin (25%)8
• cerebral palsy—increased risk
• PROM9
3. Complications related to birth:
• cord accidents
• malpresentations
• uterine atony
• placental abruption
• significant decrease in the second twin’s pH with a birth interval of greater than 30 minutes (A decrease in pH is
not itself a morbidity; it is considered a marker of possible morbidity and therefore a significant consideration.)
• vasa previa secondary to a velamentous insertion of the cord
4. Postpartum complications:
• hemorrhage
• postpartum depression
A 2012 cohort study showed that twin pregnancies conceived with assisted reproductive technologies have higher rates of
prematurity, Caesarean delivery, and obstetric morbidity (postpartum hemorrhage (PPH), premature rupture of membranes, and
cervical insufficiency) compared to those achieved spontaneously.10
Delivery of Twins 2
Risk Factors
The single largest risk factor resulting in a pregnancy complicated by twins is the use of assisted reproduction techniques.
Modern fertility treatments are responsible for an explosion in the incidence of twins such that they now account for 3% of
births in the United States.11 Other risk factors for twin pregnancy include:2
• Maternal age and parity—increasing age and parity increases the incidence of twins
• Heredity—a history of twins on the maternal side is associated with increased risk of twins
• Race—Black race is associated with a higher risk of twinning
• Nutrition—better nutritional status is associated with higher twin rates
• Elevated pituitary gonadotropins—has been proposed as a risk factor and a possible common link for the other risk
factors (above)
Etiology
Twin fetuses commonly result from fertilization of two separate ova and are termed double-ovum, dizygotic, or fraternal twins.
About a third as often, twins arise from a single fertilized ovum that subsequently divides into two similar structures, each with
the potential for developing into a separate individual. These twins are termed single-ovum, monozygotic, or identical twins.
Either or both processes may be involved in the formation of higher numbers of fetuses. Quadruplets, for example, may arise
from as few as one to as many as four ova.2
Early loss of a twin after in-vitro fertilization can leave the surviving twin with increased risks of low birth weight, very low
birthweight, and preterm delivery before 28 weeks.12
Delivery of Twins 3
Delivery of Twins 4
Diagnosis
The diagnosis of twin pregnancy should be considered in any woman with risk factors for twin pregnancy and particularly in
women who have undergone assisted reproduction. Additionally the diagnosis of twins should be suspected in any woman in
whom the symphysis fundal height (SFH) is consistently larger than expected. In the late second trimester the SFH exceeds the
gestational age by an average of five centimeters. The auscultation of a second fetal heart tone at any gestational age should also
prompt the clinician to consider the diagnosis of twins. The abdominal palpation alone is an unreliable method of detection of
twins.2 Some twin pregnancies will not be diagnosed antenatally.13
An ultrasound examination will confirm the diagnosis of twins at any gestational age. One of the advantages of routine first
trimester ultrasound is the early detection of twin gestation and the ability to reliably determine chorionicity.
Delivery of Twins 5
The differential diagnosis of a large-for-gestational-age-uterus includes, but is not limited to:2,14

• Molar pregnancy (hydatidiform mole)
• Inaccurate dates
• Hydramnios
• Macrosomia
• Fibroid uterus
• Adenexal and/or abdominal masses
Chorionicity
• The number of chorionic membranes (one or two).
• Chorionicity should not be confused with zygosity. About 25% of monozygotic twins have a dichorionic placenta,
and approximately 10% of dichorionic twins are monozygotic.
• Perinatal mortality is significantly higher in monochorionic twins compared with dichorionic twins. This is primarily
due to twin-to-twin transfusion syndrome. Dichorionic twins do not share the same circulation. The perinatal risk is
higher for monochorionic twins even when they are diamniotic.
• Determining the chorionicity is important in the management of twin gestation. This is best done by an early
ultrasound (7-14 weeks).13
• Ultrasound examination of the placenta, dividing membrane, and fetal sex usually determines the chorionicity.
The antenatal diagnosis of chorionicity should be confirmed by histological examination of the membranes after birth.
Antenatal Considerations
An early diagnosis of a twin pregnancy is important in establishing chorionicity (i.e., determining whether there is one
versus two chorionic membranes), establishing accurate dating, allowing for psychological preparation, and arrangement of
postnatal support (e.g., financial, social). Early recognition will also allow for appropriate monitoring of the pregnancy for risk of
prematurity and complications such as growth discordance, intrauterine growth restriction, gestational hypertension, and twin-
to-twin transfusion syndrome in monochorinic twins. It also permits the planning for timing and location of delivery. Therefore,
early ultrasound is ideal:, chorionicity is most accurately determined at 7 to 14 weeks. At 11 to 14 weeks, nuchal translucency
can also be measured. Depending on resources and geography, subsequent ultrasound assessments in the late second and
third trimesters are recommended every two weeks for monochorionic diamniotic twins to detect TTTS early enough to allow
intervention15. For dichorionic twins, ultrasound is recommended at 24 weeks and every three to four weeks thereafter to assess
Delivery of Twins 6
growth. Compared with singletons, normal dichorionic twin growth falls off slightly at approximately 30–32 weeks. Normal
monochorionic/diamniotic twin growth falls off at 28 weeks16,17. For monoamniotic twins, care in a tertiary care center should be
considered from 24 weeks gestation.
Some centres are routinely administering prophylactic steroids in multiple gestations. This practice has not been studied and
no recommendations have been developed regarding it. There is no evidence that routine hospitalization or bed rest prevents
preterm birth.18
Prevention
The natural rate of twins is relatively constant. The increasing incidence of twins is due to the increased use of assisted
reproduction. As such, the onus of prevention falls to the medical profession. It is incumbent on those providers to ensure that
they are judicious in the use and application of these technologies. Many experts have identified the increased risks of iatrogenic
twins and strategies such as single IFV embryo transfer and embryo reduction have been advocated.19 Some jurisdictions are
using legislation to manage this.14,20
Management
Delivery Location
The location of delivery should be discussed and agreed upon by the woman, her family, and the caregiver (i.e., attending
primary care physician, midwife, or obstetrician). The 2000 SOGC consensus statement13 recommends for a planned twin
delivery that anaesthetic, obstetrical, neonatal, and nursing staff trained in twin delivery be present in hospital. Antenatal
transport of the woman to another centre should be considered when there are insufficient local resources. If possible, a caregiver
skilled in twin delivery and Caesarean section (CS) should be involved from the onset of labour and should be in attendance at
the births. There should be an attendant present at the birth for each of the twins. One or both of these attendants should be
skilled in neonatal resuscitation.
Delivery of Twins 7
Preparation for Labour and Birth3,13

The following are recommended:
1. A physician in attendance that is competent to manage twin birth. A primary care provider (physician or midwife)
may provide hands-on care under the supervision of this consultant physician.
2. Determination of fetal presentation and estimated weight.
3. Intravenous access.
4. Continuous electronic fetal monitoring of both twins.
5. Anaesthesia available for labour. Epidural anaesthesia is preferred.
6. Availability at the delivery of:
• physician skilled in anaesthesia
• physician(s) skilled in neonatal resuscitation
• intrapartum ultrasound
• blood bank
• adequate human and physical resources to support the newborns
• hospital with the ability to perform an emergency CS
Method of Delivery
Vaginal delivery should be the goal unless there are specific contraindications.
A 2013 trial randomized 2804 women to planned Caesarean section or planned vaginal delivery (with CS if medically indicated).
It 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.21 A French case series of 1009 women demonstrated similar safety and intrapartum
CS rate for dichorionic and monochorionic/diamniotic twins with planned vaginal delivery22.
Monochorionic, monoamniotic twins all have cord entanglement. Close surveillance and planned CS between 32 to 33 weeks for
this type of twin pregnancy is recommended, although there is some evidence that later delivery may be appropriate.13,23
Delivery of Twins 8
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 birth.24 This includes preparing the woman and her family for the possibility of an early birth and its
sequelae, even in an uncomplicated pregnancy. The critical information to transfer was that, despite the fact that preterm birth
of any cause (whether elective or spontaneous) increases the risk of the infant to admission to the NICU:
• Approximately “60% of twin pregnancies result in spontaneous birth before 37 weeks 0 days”24
• “Continuing uncomplicated twin pregnancies beyond 38 weeks 0 days increases the risk of fetal death”24
The decision for optimal timing of delivery is a balance of reducing the risk of stillbirth without increasing the risk of serious
adverse outcomes related to prematurity. As a result, the NICE guidelines recommended that it would be appropriate to offer
elective birth for monochorionic diamniotic twins at 36 weeks 0 days, after a course of corticosteroids has been offered, and
at 37 weeks 0 days for dichorionic twin pregnancies.24 However, since these guidelines have been released, there are been further
studies that have suggested that elective delivery before 37 weeks is of no benefit, and may cause more perinatal morbidity.25-27
Induction of labour with twins also carries maternal risks including an increased likelihood of CS if the cervix is unripe.28
At this time, further studies are being conducted to determine the optimum time of delivery. It would be reasonable to offer
elective delivery for monochorionic twins between 36 to 37 weeks’ gestation, and 37 to 38 weeks for dichorionic twins.
Finally, if the family declines elective birth as detailed, support that choice with the offer of “weekly appointments with the
specialist obstetrician”.24 Offer an ultrasound scan at each appointment (perform biweekly fetal growth scans and weekly
biophysical profile assessments).24 Delivery by 39-40 weeks is recommended to reduce the risk of stillbirth.
Delivery of Twins 9
Types of Presentations
Figure 2: Types of Presentations of Twin Gestation
Delivery of Twins 10
Both Twins Cephalic
• Vaginal delivery should be expected.

• After the birth of the first twin, determine the presentation of the second twin and rule out a cord presentation.
Confirm with ultrasound, if necessary.
• Augmentation of labour is recommended when uterine contractions are inadequate and 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 or the rupture of a vasa previa vessel.
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 accoucheur is trained in vaginal breech delivery.29
• 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 should be used. The decision to actively or expectantly manage the second
twin is left to the individual obstetrician. If expectant management is chosen, ongoing fetal surveillance is required.
• If the second twin is a footling breech or transverse lie and fetal monitoring is atypical or abnormal, two options exist:
1) breech extraction (with internal podalic version if needed) or 2) CS
• If the second twin is a transverse lie and fetal monitoring is normal, three options exist: 1) external version to vertex,
2) internal podalic version and breech extraction, or 3) CS.
• If a breech extraction is being performed, the key points in reducing risk are:
• if possible, the amniotic sac should not be ruptured until one foot or both feet is/are identified and secured in
the pelvis;
• The second twin should not be significantly larger than the first.
First Twin Breech
When the first twin is presenting as a breech, the same issues exist as for the vaginal delivery of the singleton breech. The
mother must be informed of all pertinent risks, including the possibility of “locked” twins, although the incidence of “locked”
twins is very low. Modestly sized case series from experienced centers demonstrate reasonable safety and potential reduced
maternal morbidity with a trial of labour in women with first twin breech.30-33
First Twin Non-Longitudinal
If the first twin is not in a longitudinal lie, Caesarean delivery is indicated.
Cord Blood Sampling
Avoid draining the cord or taking blood samples directly from the cord until after the delivery of the second twin. However, cord
gases may be obtained from an isolated clamped segment of cord at the time of delivery of either twin.
Management of Labour
Spontaneous Labour
Plans regarding the place of delivery should have been previously discussed, tentatively arranged, and be put into effect for the
woman with a known multiple gestation who has entered spontaneous labour at term.
Preterm Labour
Preterm labour is a frequent complication of multiple gestations. Preterm delivery is 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 report promptly for evaluation. When preterm labour is diagnosed, 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.34
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 identified 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 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 constitutes a potential high risk for perinatal
morbidity and mortality. 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, there is an additional risk for the second twin because of cord
compromise and intrapartum placental abruption.
Continuous, simultaneous electronic fetal monitoring is recommended for twin pregnancies in 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 well-being 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
electrode can be commenced.
The use of the ultrasound in the delivery room during the second stage of labour with twins is helpful to determine presentation
and fetal well-being.
Analgesia/Anaesthesia for Multiple Gestation
The usual options regarding analgesia and anaesthesia risks, benefits, and limitations should be discussed with the woman and
her partner. Epidural analgesia is used widely during labour with twin gestations. It provides quality pain relief and also allows
for the provision of urgent anaesthesia for intrauterine fetal manipulation or CS, if required.
Augmentation 0f Labour
If dysfunctional labour is encountered, augmentation of labour 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.13
Third Stage and Postpartum Management
After the second twin has been delivered, there should be active management of the third stage of labour. There is an increased
risk of PPH; therefore, an oxytocin infusion should be continued for two to three 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 it’s effect lasts for several hours. Cord blood sampling (cord blood or cord gases) must be taken after the
birth of the second twin. If necessary, cord gases may be obtained from an isolated clamped segment of cord at the time of
delivery of either twin.
Whenever possible the woman and her babies should be kept together in the early and ongoing postpartum. Assistance by
trained staff with early initiation of breastfeeding will 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.
Transport Considerations
Careful assessment of the suitability of the woman for transport, and communication between the sending and the receiving
centres, should be done as described in the 2005 SOGC Maternal Transport Policy.35 Local, regional, and provincial guidelines
should also be considered.
It is important to consider the available local resources before determining the ideal location for the delivery of preterm twins.
It may be more appropriate to move the woman to a unit with enhanced staffing and facilities.
Summary
Twin pregnancies provide a unique opportunity to establish a rapport with the woman and her family. Given the high-risk nature
of all twin pregnancies, it is imperative that caregivers work diligently at establishing this relationship. A good relationship with
the woman and her family will go a long way to ensuring the ability to deliver quality, effective health care. Elements of this care
should include:
• A thorough and complete explanation to the woman and her partner about all equipment, procedures, and personnel
that they will encounter during the labour and birth is required.
• In the event of a preterm birth or an unexpected occurrence during labor, explanations may need to be repeated due
to high levels of emotional stress. Information should be clear, simple, and directed to each of the family members.
• If the mother and babies need to be separated early in the postpartum period due to the need for specialized neonatal
care, frequent reports of the babies’ conditions and close liaison with the neonatal intensive care unit (NICU) personnel
are essential.
• The increased risk of postpartum depression following a multiple birth should be kept in mind and renewed contact
made with a multiple pregnancy support group or other previously identified support personnel.
• The parents of a multiple birth face many stresses. Antenatal preparation and postnatal support should be made
available to ensure healthy beginnings and the continued well-being of the family unit. Support information
regarding multiple births can be found at http://www.multiplebirthscanada.org/.
• The involvement of someone skilled in breastfeeding support should be considered.
• Virtually all complications of pregnancy are increased in a twin pregnancy.
• It is important to establish chorionicity early in a twin pregnancy.
• If possible, twins should deliver 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.
• Monochorionic, monoamniotic twin pregnancies are associated with significantly increased fetal risks and require
specialized antenatal care. Close surveillance throughout pregnancy and planned CS between 32 to 33 weeks are
recommended.
The delivery of twins is an exciting and rewarding process for all involved. This reality should not cloud the caregivers’ awareness
that twin pregnancies are high risk and that a high level of vigilance and diligence is required to minimize the inherent risks and
optimize the outcomes.
References
1. Twin [monograph online]. San Francisco: Wikipedia; 2008. Available: http://en.wikipedia.org/wiki/Twin (accessed 2008
Jan 8).
2. Multifetal gestation. In: Cunningham FG, Hauth JC, Leveno KJ, Gilstrap L, Bloom SL, Wenstrom KD, editors. Williams
3. Barrett J, Bocking A. Management of twin pregnancies (part II) [SOGC consensus statement no 92]. J Soc Obstet
Gynaecol Can 2000;22(8):607-10.
4. Live births and fetal deaths (stillbirths), by type (single or multiple), Canada, provinces and territories. Table 102-4515.
[CANSIM database]. Ottawa: Statistics Canada; 2013. Available: http://www5.statcan.gc.ca/cansim/a26?lang=eng&ret
rLang=eng&id=1024515&tabMode=dataTable&srchLan=-1&p1=-1&p2=9.
5. Chitkara U, Berkowitz RL. Multiple gestations. In: Gabbe SG, Niebyl JR, Simpson JL, editors. Obstetrics: normal and
problem pregnancies. 4th ed. New York: Churchill Livingstone; 2002. p.775-826.
6. Newman RB, Rittenberg C. Multiple gestation. In: Gibbs RS, Karlan BY, Haney AF, Nygaard I, editors. Danforth’s obstetrics
and gynecology. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2008. p.220-45.
7. 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(9):2549-57. Available: http://humrep.oxfordjournals.org/
content/early/2011/07/04/humrep.der213.full.pdf+html.
8. van Klink JM, van SA, 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(3):294-300.
9. 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(1):69-74.
10. 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(1):95-101.
11. ACOG Practice Bulletin #56: Multiple gestation: complicated twin, triplet, and high-order multifetal pregnancy. Obstet
Gynecol 2004;104(4):869-83.
12. Almog B, Levin I, Wagman I, Kapustiansky R, Lessing JB, Amit A, et al. Adverse obstetric outcome for the vanishing twin
syndrome. Reprod Biomed Online 2010;20(2):256-60.
13. Barrett J, Bocking A. Management of twin pregnancies (part I) [SOGC consensus statement no 91]. J Soc Obstet
Gynaecol Can 2000;22(7):519-29.
14. DeCherney AH, Nathan L. Current diagnosis & treatment obstetrics & gynecology [Lange current series]. 10th ed. New
York: McGraw-Hill; 2007.
15. Baud D, Windrim R, Van MT, Keunen J, Seaward G, Ryan G. Twin-twin transfusion syndrome: a frequently missed
diagnosis with important consequences. Ultrasound Obstet Gynecol 2014;44(2):205-9.
16. Shivkumar S, Himes KP, Hutcheon JA, Platt RW. An ultrasound-based fetal weight reference for twins. Am J Obstet
Gynecol 2015.
17. Stirrup OT, Khalil A, D’Antonio F, Thilaganathan B, Southwest Thames Obstetric Research Collaborative (STORK). Fetal
growth reference ranges in twin pregnancy: analysis of the Southwest Thames Obstetric Research Collaborative (STORK)
multiple pregnancy cohort. Ultrasound Obstet Gynecol 2015;45(3):301-7.
18. Crowther CA, Han S. Hospitalisation and bed rest for multiple pregnancy. Cochrane Database Syst Rev 2010;7:CD000110.
19. 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(1):141-52.
20. Committee on Ethics, American College of Obstetricians and Gynecologists. Mult-fetal pregnancy reduction [ACOG
committee opinion no 369]. Obstet Gynecol 2007;109:1511-5.
21. 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(14):1295-305. Available: http://www.nejm.org/doi/
pdf/10.1056/NEJMoa1214939.
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(3):301-7.
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(2):201-4.
24. National Collaborating Centre for Women’s and Children’s Health. Multiple pregnancy: the management of twin and
triplet pregnancies in the antenatal period [NICE clinical guideline 129]. London: National Institute for Health and
Clinical Excellence; 2011. Available: http://www.nice.org.uk/guidance/CG129.
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(3):257.
26. 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(1):50-9.
27. 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 2015;1-5.
28. Jonsson M. Induction of twin pregnancy and the risk of caesarean delivery: a cohort study. BMC Pregnancy Childbirth
2015;15:136. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4467042.
29. Houlihan C, Knuppel RA. Intrapartum management of multiple gestations. Clin Perinatol 1996;23(1):91-116.
30. Blickstein I, Goldman RD, Kupferminc M. Delivery of breech first twins: a multicenter retrospective study. Obstet Gynecol
2000;95(1):37-42.
31. 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) 2011.
32. 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(1):55-60.
33. Steins Bisschop CN, Vogelvang TE, May AM, Schuitemaker NW. Mode of delivery in non-cephalic presenting twins: a
systematic review. Arch Gynecol Obstet 2012.
34. 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
2012;9:CD004733.
35. Wilson AK, Martel MJ, Clinical Practice Obstetrics Committee. Maternal transport policy [SOGC policy statement no 165].
J Obstet Gynaecol Can 2005;27(10):956-8.
Chapter 13
Vaginal Birth After
Caesarean Section (VBAC)
The primary indication for Caesarean section (CS) in Canada is a previous CS, accounting for over 30% of the total. Every year,
over 30 000 women in Canada are faced with this choice of 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 a trial of labour after Caesarean (TOLAC) be offered to eligible
women.1
Candidates for planned TOLAC are those women in whom the balance of risks and chances of success are acceptable to the
woman and the health care provider. The balance of risks and benefits appropriate for one woman may seem unacceptable for
another.2 Delivery discussions and decisions for future pregnancies following Caesarean section should be considered on an
individual basis as early as the postpartum period.
Definitions
Vaginal birth after Caesarean is vaginal delivery after having a previous Caesarean delivery.3
Trial of labour after Caesaren is the plan to attempt labour when a woman has had a previous Caesarean birth, with the goal of
achieving a successful vaginal birth.
Elective repeat Caesarean section (ERCS) is defined as a Caesarean delivery performed before the onset of labour.
Uterine rupture is the “complete separation of the myometrium with or without extrusion of the fetal parts into the maternal
peritoneal cavity”.3
Uterine dehiscence is where the fetal membranes are not ruptured and the fetus is not outside of the uterus. Usually the
peritoneum over the defect is intact. Morbidity and mortality are NOT increased as they are with uterine rupture.4
Vaginal Birth After Caesarean Section (VBAC) 1

Incidence
The proportion of babies delivered by Caesarean continues to increase in Canada. In 2011–2012, 27.2% of hospital deliveries
were Caesarean deliveries compared to 17.6% in 1995–1996. The repeat Caesarean delivery rate increased from 64.7% in
1995–1996 to 80% in 2004–2005. The VBAC rate thus decreased over the same period.5 In 2012 in the U.S. the percentage
of all deliveries by CS was 32.8%.6
In 2011–2012, the Canadian primary CS rate remained stable at 17.9%. Canadian women age 35 and older continued to have
significantly higher primary CS rates than their younger counterparts (22.3% versus 17.0%).7
The Canadian repeat CS rate—the proportion of women with previous CS who underwent a repeat CS—was 82.5% in
2011–2012.
In British Columbia for 2012–2013, 82.4% of women with previous CS were considered eligible for a VBAC. Of this eligible
group, 32.6% attempted a VBAC and 71.3% were successful.8
In 2006 the VBAC rate in the US was 8.6%. It is estimated that 60% to 80% of appropriate candidates who attempt VBAC will be
successful.2
Success Rate
In a 2008 Canadian study including 3493 women, the TOLAC attempt rate ranged from 50.6% to 81.1%. For women having
TOLAC, the VBAC success rate was between 64.3% and 76.1%.9
The overall TOLAC among American studies was 58%, with a range of 28% to 70%. For studies initiated after 1996, less than half
of women (44%) had a TOLAC, compared with 62% of women in studies initiated before 1996.10 The incidence of VBAC among
women who had a TOLAC is approximately 74% in the United States.11,12
A study conducted by Landon et al. identified factors predictive of VBAC success. This prospective study examined 14 529 women
undergoing a TOLAC from 1999 to 2002. The factors listed below were identified as predictive of outcome and are useful to
consider when discussing the choice of a TOLAC versus repeat CS.13,14
Adolescents are more likely to attempt VBAC and are likely to be as successful as their adult counterparts. Adolescents should
be encouraged to attempt a trial of labor after prior CS when appropriate to lower the risks of lifelong maternal morbidity from
numerous repeat CSs.15

Factors that increase the likelihood of successful VBAC include:

• Previous successful VBAC
• Previous vaginal delivery
• Favourable cervix
• Spontaneous labour
• Non-recurrent indication for previous CS (e.g., breech presentation)
• Maternal age < 40 years
Factors that decrease the likelihood of successful VBAC include:
• Previous CS done 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 (BMI) > 30
• Hypertension16
A prediction model for TOLAC success developed in the United States has been shown to be valid in a Canadian population. This
model allows an accurate estimation of the probability of VBAC success and may be used in practice, without regard to ethnicity,
as a primary method to refine counselling during antepartum visits for women with a prior Caesarean section.1
Calculation tool: https://mfmu.bsc.gwu.edu/PublicBSC/MFMU/VGBirthCalc/vagbirth.html

Major maternal morbidity and mortality includes uterine rupture, hemorrhage, thromboembolism, and infection. Studies
demonstrate that uterine rupture can occur before, during, and even after labour.
Maternal Mortality by Mode of Delivery

Wen et al. retrospectively analyzed 352 215 births between 1998 and 2000 in Canadian women who had a previous Caesarean
delivery (total deliveries during the period were 3 576 980).17 This study examined rates of uterine rupture and maternal death.
The authors concluded that while the rates of uterine rupture, blood transfusion, and hysterectomy were higher in women who
underwent a TOLAC, the rate of maternal death was higher in women who had an elective Caesarean delivery. These findings
have been corroborated in other countries.18

In-Hospital Maternal Death Rates (95% CI) in Canada, 1988 to 2000

Groups # Deliveries # Deaths Death Rate/100 000 Risk Ratio (95% CI)
All deliveries (n=3 576 980)
Women with a CS 685 856 119 17.3 9.11 (6.62–12.53)
Vaginal delivery 2 891 124 55 1.9 1.0 (Reference)
Previous CS (n=352 215)
Elective repeat CS 209 007 23 11.0 5.25 (1.58–17.49)
Trial of labour 143 208 3 2.1 1.0 (Reference)
Eligible* Previous CS (n=308 755)
Eligible* elective repeat CS 179 795 10 5.6 3.59 (0.79–16.37)
Eligible* with TOLAC 128 960 2 1.6 1.0 (Reference)
* Excluding: multifetal pregnancy, pre-eclampsia/eclampsia, breech/transverse/oblique presentation, preterm labour, placenta previa, placental abruption,
herpes simplex, age younger than 14 years.
Adapted from Wen et al.17 Copyright 2004, with permission from Elsevier.
Maternal Outcomes Associated with TOLAC verus ERCS

There are currently no randomized controlled trials determining maternal or neonatal outcomes between women undertaking
TOLAC and those undergoing a repeat Caesarean delivery. Much of the evidence about the safety of a TOLAC versus ERCS is based
on observational data. Recommendations and decisions about a TOLAC should be made cautiously, keeping the limitations of the
literature in mind.
In 2010 the data were summarized in the Evidence Report/Technology Assessment Report Vaginal Birth After Cesarean: New
Insights. The authors of this report identified 3134 citations and reviewed 963 papers for inclusion, of which 203 papers met
inclusion and were quality rated.11

Short Term Maternal Benefits and Harm with TOLAC vs ERCS11

Potential Harm TOLAC ERCS
Maternal Death 3.8 per 100 000 TOLAC 13.4 per 100 000 Significantly higher for ERCS
(95% confidence interval [CI], 0.9 to 15.5) (95% CI, 4.3 to 41.6)
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 1 000 4.6 per 1 000 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)
Infection Rate W46 per 1000 32 per 1000 Not statistically significantly different
(95% CI,15 to 135) (95% CI,13 to 73)
Note: A trend toward increased
endometritis was seen with ERCS compared
with TOLAC; in contrast, chorioam-nionitis
was increased in TOLAC compared with
ERCS. Increasing BMI 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 eight cohort studies
were good or fair quality, included the population of interest, and used the anatomic definition for uterine rupture contained in
this report”.
The risk of uterine rupture for all women with a prior Caesarean delivery 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 women undergoing an ERCS (0.026; 95% CI,0.009 to 0.082).

Maternal Morbidity
There were no maternal deaths due to uterine rupture in any of the eight studies reviewed.The risk of hysterectomy due to uterine
rupture ranged from 14% to 33%.11
Risk Factors for Uterine Rupture
The risk of uterine rupture among those women who had induction was lowest with oxytocin (1.1%), followed by PGE2 (2%),
and highest with misoprostol (6%). However, these risk estimations may be imprecise given the consistency in study design and
methodology; the results should be interpreted with caution.10
Women with a prior classical incision are at increased risk of uterine dehiscence or rupture. Compared with women with prior
low transverse Caesarean delivery, women with prior low vertical Caesarean delivery or with an unknown scar are not at a
significantly increased risk of uterine dehiscence or rupture.11
In a woman with a previous uterine incision, more clinical studies are required to evaluate the relationship between lower uterine
wall thickness and the risk of uterine rupture before recommendations can be made about this practice.11
Women who are postdate may have a higher risk of uterine rupture. Obese and morbidly obese women are more likely to suffer
rupture and/or dehiscence.11
Women who had a previous Caesarean for dystocia in the second stage of labour are at higher risk of second stage uterine
rupture at next delivery, especially in cases of suspected fetal macrosomia or prolonged second stage.19
Considerations for Future Pregnancies

Previa
Women with a prior Caesarean delivery had a statistically significant increased risk of placenta previa compared with women
with no prior Caesarean at a rate of 12 per 1 000 (95% CI: 8 to 15 per 1 000). The incidence increased with increasing number of
prior Caesarean deliveries. Prior Caesarean was a significant risk factor for maternal morbidity in women with previa. Compared
with previa patients without a prior Caesarean delivery, women with one prior Caesarean and 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 three or more prior Caesarean deliveries and previa, the risk of hysterectomy and
composite maternal morbidity rose significantly (0.7% to 4% vs. 50% to 67%, and 15% vs. 83%, respectively).11

Accreta
The incidence of placenta accreta rose with increasing number of prior Caesarean deliveries. The results were statistically
significant for women with two or more prior Caesareans (odds ratio [OR] 8.6 to 29.8).11
Women with placenta previa were at increased risk for placenta accreta, and the risk increased with increasing number of prior
Caesareans. Women with more than three prior Caesareans and previa had a 50% to 67% incidence of accreta.11
Other Considerations
Any previous abdominal surgery, including CS, or other conditions associated with pelvic inflammation are associated with
adhesions. Adhesions were associated with increased perioperative complications, time to delivery, and total operative time.
It is unclear whether adhesions and complications increase with increasing number of prior Caesareans.11
Neonatal Mortality and Morbidity

Neonatal mortality and morbidity are primarily related to uterine rupture. The overall risk of perinatal death due to uterine
rupture is 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
Short-Term Benefits and Harms to the

Baby of Maternal Attempt at TOLAC versus ERCS11
Perinatal Deaths 1.3 per 1 000 0.5 per 1 000 Significantly higher for TOLAC
(95% CI,0.59 to 3.04) (95% CI,0.07 to 3.82)
Sepsis No differences in proven sepsis in infants born after TOLAC versus those delivered by ERCS.
Apgar Scores Four studies found no differences in Apgar scores of less than six and seven at 5 minutes in infants undergoing a TOLAC versus
ERCS.
Neonatal Intensive Six of eight studies found no significant differences in frequency of NICU admissions between TOLAC and ERCS.
Care Unit (NICU)
admission

Breastfeeding No studies were found that explored the effect of a TOLAC versus an ERCS on breastfeeding initiation or continuation.
Additional There was insufficient evidence to determine if rates of respiratory distress, neonatal trauma, or asphyxia/hypoxic-ischemic
Short-term encephalopathy varied between TOLAC and ERCS.
Outcomes
Prerequisites for Offering a TOLAC

Obstetrical guidelines recommend that a TOLAC should only be attempted in hospitals with the capability of providing an
emergency CS.3,20 This includes the availability of blood products and neonatal resuscitation personnel. There is little evidence
to provide guidance about how quickly a CS would need to be done but 30 minutes is considered adequate.3 It is prudent
for hospitals and care providers offering a TOLAC to have protocols about how they will respond in case of an emergency,
including when specialists needed for performing CS may not be “in house”.3 Women attempting a TOLAC should be informed
of the available resources. Caregivers should be able to recognize the signs and symptoms of uterine scar rupture and have a
management plan in place should this occur.
Selection of Candidates for a TOLAC

Informed consent today for any woman who desires a TOLAC should include a documented discussion of the risks and benefits
of elective CS versus TOLAC.
The selection of candidates for a TOLAC depends on the clinical situation and is re-evaluated on an ongoing basis throughout
the pregnancy. Macones and colleagues tried, without success, to develop clinical models using both antepartum and early
intrapartum factors to predict uterine rupture.21 Reviewers of these prediction models suggest that while they may be improving
enough to predict the likelihood of success at a population level, they are not able to predict the likelihood of success for an
individual.22
The following information should be addressed in discussions with women considering a TOLAC or an ERCS to assist them in
making choices appropriate to their individual circumstances. There is growing evidence that the use of formalized decision aids
can be very helpful in providing visual explanations of risks and benefits relating to choice of TOLAC versus ERCS.23 One decision
aid was created by the Ottawa Health Decision Centre23 and may be helpful in assisting women (see Appendix).24

It may also be helpful for practitioners to understand some of the rationales for women’s choices. A review that looked at the
factors that influence women to attempt VBAC versus planning an elective Caesarean birth identified the following issues:
• Physician influence
• Recovery time and the need to return to caring for other children
• Ethnic differences
• Safety for mother and baby.24
Considerations
Type of Previous Incision
Guise et al. did a comprehensive review of the literature from 1980 to 2004 to identify studies comparing the risks and outcomes
of VBAC versus Caesarean birth.25 This review combined uterine rupture and dehiscence rates (seven studies from 1983 to 1999).
They suggested that there may be little difference in uterine rupture or dehiscence in women with vertical lower uterine segment
incisions compared to women with transverse low segment incisions.
Number of Previous Caesarean Deliveries
Retrospective data showed an increase in uterine rupture after two prior CS (3.7% vs. 8%). Better quality prospective evidence
shows no increase in risk in rupture rate compared with one previous CS (0.9% vs. 0.7%).26
Type of Closure of Previous Uterine Incision
The risk of uterine rupture after an unlocked single-layer closure seems to be comparable with that after a double-layer closure.
Single-layer locked, continuous suturing as opposed to a double-layer closure of the hysterotomy site may increase the risk of
uterine rupture in women attempting TOL in a future pregnancy.27
Interbirth Interval
The risk of uterine rupture after an unlocked single-layer closure seems to be comparable with that after a double-layer closure.
Single-layer locked, continuous suturing as opposed to a double-layer closure of the hysterotomy site may increase the risk of
uterine rupture in women attempting TOL in a future pregnancy.28

Hypertensive Disorders of Pregnancy
Data from a retrospective cohort study (n=25 500) showed that women with gestational hypertension were less likely to
choose a TOLAC and were also less likely to be successful in having a VBAC than normotensive women. Women with gestational
hypertension who attempted VBAC were no more likely to have uterine rupture than those who were normotensive.16
Twin Pregnancy
Outcomes are similar to those women with a singleton pregnancy who attempt VBAC.2,10
Summary
Based on the available literature, the SOGC recommends that a TOLAC be offered to women with one previous transverse low-
segment CS following appropriate discussion of maternal and perinatal risks and benefits.3
Women will need to understand the evidence in order to make informed decisions about planning a TOLAC versus a planned
repeat Caesarean. Women with more than one previous CS delivery may be candidates for TOLAC.29
1. Prerequisites for a trial of labour after previous Caesarean birth (these should be documented):
• Cephalic presentation
• Previous operative report (if available, opinion of previous surgeon may be helpful)
• If operative report not available: TOLAC is acceptable if clinical circumstances surrounding prior CS suggest
uncomplicated lower segment incision
• No contraindications to vaginal birth
2. Factors that may increase the risk of uterine rupture (these should be documented):
• Macrosomic fetus
• Short interval from previous CS (< 18 months)
• More than two previous CS
• Previous Caesarean for dystocia in the second stage of labour30
• Locked Single-layer closure of the previous uterine incision (single layer unlocked or two-layer closure
acceptable)27

3. Contraindications to a TOLAC (these should be documented):

• Any contraindications to labour
• Previous or suspected classical 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 of the facility to perform an emergency CS
• Woman requests ERCS rather than a TOLAC
4. Benefits of VBAC:
• Shorter hospitalization
• Shorter recovery time for the woman
• Improved maternal satisfaction
• Reduced health care costs31
5. Patient counselling during the decision-making process (this should be documented):
• Discuss the risks and benefits of both a TOLAC and ERCS, including possible effects on future pregnancies
• If considering induction of labour, carefully review the risks associated with each of the available induction
options
• Offer written information (e.g., published guidelines from professional organizations, decision aids)
• Encourage the woman and her partner to participate in decision-making
• Recommend resources that provide additional information when applicable
• Respect the woman’s autonomy
• Document the counselling and informed choice process, including the woman’s decision and a plan of care
Management
1) Conduct of Labour
Conduct of labour during a TOLAC is similar to the conduct of a normal labour. Studies have reported that women admitted with
a more favourable cervical status in spontaneous labour have a two-fold increase in the likelihood of VBAC compared to those
with an unfavourable cervix.10

Antepartum consultation with an obstetrician may be advisable, depending on the clinical situation and local practice. The
management of a TOLAC includes:3
• Careful observation of:
• labour progress
• fetal well-being
• maternal well-being
• The use of epidural or other analgesia
• Electronic fetal monitoring (EFM). The EFM tracing is an important marker of uterine rupture
• No need to restrict activity (telemetry can facilitate mobility while allowing continuous monitoring)
2) Induction and Augmentation

Induction of labor 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 discussed.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 is mainly in women with no prior vaginal birth. 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 include:1
• Mechanical cervical ripening with a Foley catheter has been safely used prior to induction of labour in this clinical
situation
• The use of oxytocin is not contraindicated 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

Vigilance and early recognition of uterine rupture by the health care team is an essential component of TOLAC.
Classically, the signs and symptoms of uterine rupture include:
• Fetal heart rate (FHR) abnormalities,
• Vaginal bleeding.
• Acute onset of scar pain or tenderness (seldom masked by an epidural; this sign is neither sensitive nor specific)
Other signs and symptoms may include:
• 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 97 028 births identified 52 uterine ruptures (0.05%): 25 complete and 27 partial. Most (89%) occurred in
women with a previous cesarean delivery. In complete ruptures, FHR abnormalities were the most frequent sign (82%), while
the complete triad of FHR abnormalities–pain–vaginal bleeding was present in only 9%. The signs and symptoms of partial
ruptures were very different; these were asymptomatic in half the cases (48%).32
Management of Uterine Rupture

This is a perinatal 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 antibiotics
• The attendance of a neonatal resuscitation team

Summary
The success rate for a TOLAC is quite high. Accepting that some women who attempt TOLAC will be unsuccessful, the overall
maternal morbidity and mortality is less than ERCS. Best evidence suggests that VBAC is a reasonable and safe choice for the
majority of women with previous Caesarean.11
Induction may be attempted, but oxytocin should be used with caution in patients who have a protracted active phase of labour.
While the incidence of uterine rupture is low, it is a serious complication for both the woman and the infant. 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. Chaillet N, Bujold E, Dube E, Grobman WA. Validation of a prediction model for vaginal birth after caesarean. J Obstet
Gynaecol Can 2013;35(2):119-24.
2. American College of Obstetricians and Gynecologists. ACOG Practice bulletin no. 115: Vaginal birth after previous
cesarean delivery. Obstet Gynecol 2010;116(2 Pt 1):450-63.
3. Martel MJ, MacKinnon CJ, Clinical Practice Obstetrics Committee. Guidelines for vaginal birth after previous caesarean
birth [SOGC clinical practice guideline no 155]. J Soc Obstet Gynaecol Can 2005;27(2):164-74. Available:
http://sogc.org/guidelines/public/155E-CPG-February2005.pdf.
4. Miller DA, Diaz FG, Paul RH. Vaginal birth after cesarean: a 10-year experience. Obstet Gynecol 1994;84(2):255-8.
5. Health indicators interactive tool. Ottawa: Canadian Institute for Health Information; 2012. Available: http://www.cihi.
ca/hirpt/search.jspa.
6. Births - method of delivery. [FastStats]. Atlanta (GA): Centers for Disease Control and Prevention; 2015. Available:
http://www.cdc.gov/nchs/fastats/delivery.htm.
7. Highlights of 2011-2012 selected indicators describing the birthing process in Canada. Ottawa: Canadian Institute for
Health Information; 2013. Available: https://secure.cihi.ca/free_products/Childbirth_Highlights_2011-12_EN.pdf.
8. Perinatal health report 2008-09 to 2012-13: residents of Fraser Health. Vancouver: Perinatal Services BC; 2014.
9. Russillo B, Sewitch MJ, Cardinal L, Brassard N. Comparing rates of trial of labour attempts, VBAC success, and fetal and
maternal complications among family physicians and obstetricians. J Obstet Gynaecol Can 2008;30(2):123-8.
10. Cheng YW, Eden KB, Marshall N, Pereira L, Caughey AB, Guise JM. Delivery after prior cesarean: maternal morbidity and
mortality. Clin Perinatol 2011;38(2):297-309.
11. Guise JM, Eden K, Denman MA, Marshall N, Fu R, Janik R, et al. Vaginal birth after Cesarean: new insights [Evidence
report/technology assessment no 191]. Rockville (MD): Agency for Healthcare Research and Quality; 2010. AHRQ publ
no 10-E001. Available: http://www.ahrq.gov/downloads/pub/evidence/pdf/vbacup/vbacup.pdf.
12. Davies GA, Hahn PM, McGrath MM. Vaginal birth after cesarean. Physicians’ perceptions and practice. J Reprod Med
1996;41(7):515-20.

13. 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. Am J Obstet Gynecol 2005;193(3 Pt 2):1016-23.
14. Brill Y, Windrim R. Vaginal birth after Caesarean section: review of antenatal predictors of success. J Obstet Gynaecol Can
2003;25(4):275-86.
15. 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 Pediatr Adolesc Gynecol 2015;28(4):219-23.
16. Srinivas SK, Stamilio DM, Stevens EJ, Peipert JF, Odibo AO, Macones GA. Safety and success of vaginal birth after cesarean
delivery in patients with preeclampsia. Am J Perinatol 2006;23(3):145-52.
17. Wen SW, Rusen ID, Walker M, Liston R, Kramer MS, Baskett T, et al. Comparison of maternal mortality and morbidity
between trial of labor and elective cesarean section among women with previous cesarean delivery. Am J Obstet
Gynecol 2004;191(4):1263-9.
18. Zwart JJ, Richters JM, Ory F, de Vries JI, Bloemenkamp KW, van Roosmalen J. Uterine rupture in The Netherlands: a
nationwide population-based cohort study. BJOG 2009;116(8):1069-78.
19. Jastrow N, Demers S, Gauthier RJ, Chaillet N, Brassard N, Bujold E. Adverse obstetric outcomes in women with previous
Cesarean for dystocia in second stage of labor. Am J Perinatol 2012.
guidelines for obstetrical care [SOGC policy statement no 89]. J Soc Obstet Gynaecol Can 2000;22(5):389-91. Available:
http://www.sogc.org/guidelines/public/89E-PS-May2000.pdf.
21. Macones GA, Cahill AG, Stamilio DM, Odibo A, Peipert J, Stevens EJ. Can uterine rupture in patients attempting vaginal
birth after cesarean delivery be predicted? Am J Obstet Gynecol 2006;195(4):1148-52.
22. Bangdiwala SI, Brown SS, Cunningham FG, Dean TM, Frederiksen M, Hogue CJ, et al. NIH Consensus Development
Conference Draft Statement on Vaginal Birth After Cesarean: New Insights. NIH Consens State Sci Statements 2010;27(3).
Available: http://consensus.nih.gov/2010/vbacstatement.htm.
23. Frost J, Shaw A, Montgomery A, Murphy DJ. Women’s views on the use of decision aids for decision making about the
method of delivery following a previous caesarean section: qualitative interview study. BJOG 2009;116(7):896-905.
24. Eden KB, Hashima JN, Osterweil P, Nygren P, Guise JM. Childbirth preferences after cesarean birth: a review of the
evidence. Birth 2004;31(1):49-60.
25. Guise JM, Hashima J, Osterweil P. Evidence-based vaginal birth after Caesarean section. Best Pract Res Clin Obstet
Gynaecol 2005;19(1):117-30.

26. 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. Obstet Gynecol 2006;108(1):12-20.
27. 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(1):5-10.
28. Bujold E, Gauthier RJ. Risk of uterine rupture associated with an interdelivery interval between 18 and 24 months. Obstet
Gynecol 2010;115(5):1003-6.
29. Tahseen S, Griffiths M. Vaginal birth after two caesarean sections (VBAC-2)-a systematic review with meta-analysis of
success rate and adverse outcomes of VBAC-2 versus VBAC-1 and repeat (third) caesarean sections. BJOG 2010;117(1):5-19.
30. Jastrow N, Demers S, Gauthier RJ, Chaillet N, Brassard N, Bujold E. Adverse obstetric outcomes in women with previous
Cesarean for dystocia in second stage of labor. Am J Perinatol 2013;30(3):173-8.
31. Wymer K, Tina Shih YC, Plunkett B. Cost-effectiveness of a trial of labor after cesarean delivery for successive deliveries.
Obstet Gynecol 2014;123 Suppl 1:84S-5S.
32. 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. Eur J Obstet Gynecol Reprod Biol 2014;179:130-4.

Appendix
Brownlee et al. Should you plan a caesarean birth… Ottawa Health Decision Centre
18
Chapter 14
Shoulder Dystocia
Definition
Shoulder dystocia is the inability of the fetal shoulders to deliver spontaneously or with gentle traction during vaginal cephalic
delivery.1, 2 Additional obstetric manoeuvres are required to deliver the fetal shoulders and body.
Incidence
A U.S. article summarizing a range of studies from the 1970s to the late 1990s reports an overall incidence ranging from 0.2% to
3%.3 This wide range is largely attributable to the variation in diagnostic criteria.4 Approximately 50% of shoulder dystocia occur
in women without risk factors.5,6
The incidence of shoulder dystocia in a population study of non-diabetic women with a spontaneous vaginal delivery of infants
4000 to 4250 grams was 5.1%. The rate increased with birthweight rising to 14.3% for infants at 4500 to 4750 grams and
21.1% for those 4750 to 5000 grams. A 2011 retrospective cohort study from Iceland looked at 343 non-diabetic women who
vaginally delivered infants whose birthweight was ≥ 5000 grams. The study revealed an increased risk of shoulder dystocia
(odds ratio [OR] 26.9; 95% confidence interval [CI] 11.1 to 65.1).7
When considering assisted vaginal delivery, one must anticipate shoulder dystocia, as vacuum and forceps use are independent
risk factors unrelated to fetal size.8 In a 1992 population study, rate of shoulder dystocia increased by 35% in a non-diabetic
population in the presence of assisted vaginal birth.9
Incidence of shoulder dystocia in diabetic women is generally higher than non-diabetics. Although rates vary, for diabetics
delivering infants > 4000 grams, the estimated incidence may be as high as 15% and for infants > 4500 grams as high
as 42%.10-13
Shoulder Dystocia 1

Complications of Shoulder Dystocia Include:
Fetal/Neonatal
• death
• hypoxia/asphyxia and its sequelae
• birth injuries
• fractures – clavicle, humerus
• brachial plexus palsy (rates of 2.3–16% have been reported14-17)
Maternal
• postpartum hemorrhage (11%15)

• uterine atony
• maternal lacerations
• uterine rupture
• 4th degree tears (2–5.1%15)
Fetal asphyxia may result in permanent neurological damage and even death. In the fetal monkey model, the fetal pH drops
by 0.04 per minute when the cord is totally occluded. In shoulder dystocia there may be some preservation of maternal-fetal
circulation and a less rapid drop in pH, unless the cord has been previously clamped and divided. This underscores the reason for
not routinely cutting a nuchal cord in the presence of suspected shoulder dystocia.18 The time you have to deliver the baby before
permanent injury is dependent on fetal-well being and fetal oxygen reserves prior to birth.
A fourth degree tear or fetal trauma can occur during appropriate management. This is preferable to fetal asphyxia.19
Risk Factors
Over 50% of shoulder dystocia cases are not predictable and have no risk factors. Many occur in women who have neither
diabetes nor a child weighing more than 4000 grams.20 Thus, the possibility of a shoulder dystocia must be considered with
every vaginal delivery. However, the following are associated risk factors that may assist the clinician in preparing for shoulder
dystocia:4,5,9,11-13,16,21-34
Shoulder Dystocia 2
• Antepartum factors:
• suspected fetal macrosomia35 (Ultrasound is not an accurate measure or predictor of macrosomia.)
• maternal diabetes
• gestational age > 42 completed weeks
• multiparity
• previous shoulder dystocia (1–25%)21,24,25,30,36-39
• previous delivery of a macrosomic infant
• excessive weight gain (more than 20 kg gain is associated with an increase in shoulder dystocia from
1.4% to 15.2%40)
• extreme maternal obesity (BMI > 50) (7.1%)41
• Intrapartum factors:
• prolonged labour (some of the evidence is contradictory21,42)
• operative vaginal delivery8
• labour induction
• epidural anaesthesia
Although individual population and retrospective studies differ in their emphasis, the most common factors associated with
cases of shoulder dystocia are macrosomia, maternal obesity, post-term pregnancy, and diabetes.43 Newborns of diabetic
mothers were shown to have larger shoulder and extremity circumferences, decreased head-to-shoulder ratio, higher body fat,
and thicker upper-extremity skin folds compared with non-diabetic control infants of similar birth weight and birth length.
These differences may explain the propensity for shoulder dystocia in the diabetic population.44
The existence of predisposing factors is not by itself an indication for Caesarean section (CS) or induction of labour. Women,
especially those who are considered at risk for shoulder dystocia, should be provided with pre-delivery education on the steps
that might be required if the shoulders are difficult to deliver. Preparing the woman, her partner, and the team for McRoberts’
manoeuvre and the potential for rolling over can increase co-operation and understanding during the event (the woman and her
supports are members of that team). Placing a stool on the side of the bed corresponding to the fetal back helps to indicate to
the team the location for application of suprapubic pressure, if required. This action also communicates a clear caring by the team
for the woman and her child.
Due to the risk of recurrence in women with a history of prior shoulder dystocia,37 the estimated fetal weight, gestational
age, maternal glucose intolerance, and the severity of the prior neonatal injury should be evaluated and the route of delivery
discussed with the woman prior to delivery. A number of studies have examined macrosomia as an indication for CS. Most of
these studies are inconclusive.45 Rouse et al. have reported that the number needed to treat, i.e. perform an elective Caesarean
(in a policy of CS at 4 to 4.5 kg estimated fetal weight in non-diabetics), would be 2345 to 3695 to avert one permanent
Shoulder Dystocia 3
brachial plexus injury (BPI).11,46 However, there exists an increased risk of shoulder dystocia in women with diabetes. Using the
same policy of CS at 4 to 4.5 kg estimated fetal weight by ultrasound assessment on women with diabetes, between 443 and
489 sections would need to be performed to prevent one permanent brachial plexus injury. As a result, CS has been proposed
by some as the preferred route of delivery. However, there are significant limitations of the technology for antenatal ultrasonic
fetal weight determination that need to be clearly understood by the woman and her caregivers. Ultrasound has been shown to
have a low sensitivity (60%) for the detection of macrosomia in the third trimester.11 In light of this, clinical judgment remains a
key component in the care of women with diabetes delivering infants with an estimated fetal weight > 4000 grams.47 Inducing
labour for suspected large babies is controversial. Two studies26,45 advise against it; a recent study showed a reduced risk of
shoulder dystocia and no increased risk of caesarean with induction.48
Etiology and Physiology

Shoulder Dystocia
Following the delivery of the head, there is impaction of the anterior shoulder on the symphysis pubis in the anteroposterior
(AP) diameter in such a way that the remainder of the body cannot be delivered by usual methods.46 Less commonly, shoulder
dystocia can result from impact of the posterior shoulder on the sacral promontory. In either case, the head may be tight against
the perineum. This is known as the “turtle sign”. Spontaneous restitution may fail to occur with the next contraction and the baby
fails to delivery by usual maternal effort.
Brachial Plexus Palsy

Although brachial plexus injury (BPI) occurs in 0.06% to 0.26% of all deliveries, it occurs in 16% to 23% of births complicated
by shoulder dystocia.49 Thus, while BPI may be associated with shoulder dystocia, other factors have also been identified. It may
be associated with exogenous, clinician-applied, extreme lateral traction on the fetal head. However, computer simulations using
a model of a fetus whose shoulder is blocked by the maternal pelvis have demonstrated that some of the greatest brachial plexus
stretching occurs with maternal pushing alone.19,50-52 Case reports of BPIs after non-traumatic births (4% occur during Caesarean
delivery) have also led to exploration of pre-labour intrauterine causes. It has been shown that BPIs are not related to shoulder
dystocia in approximately 51% of macrosomic babies.53
In a 2013 study of 1177 deliveries associated with shoulder dystocia, 11% had BPI. An increased number of manoeuvres to
resolve the shoulder dystocia, gestatonal age less than 37 weeks, operative vaginal delivery and concomitant fractures were
associated with BPI when shoulder dystocia occured.20 The risk of brachial plexus injury does seem to increase with the length of
the second stage of labour.54
Shoulder Dystocia 4
Nerve root damage most commonly involves the nerve origins at the C5 and C6 level. These nerve roots supply the forearm
flexors and supinators. Thus the elbow is extended and wrist pronated (waiter’s tip sign), resulting in the classical Erb-Duchenne
palsy. This brachial plexus injury is of varying degree.
Approximately 75% of affected infants will experience a complete recovery within the first month of life. The remaining 25%
of children will demonstrate some degree of permanent residual impairment of function (muscle weakness, bony deformity,
contractures, dislocation, shortening of the arm).55 If complete recovery does not occur by the end of the first month after birth,
the infant should be referred to a specialty facility for assessment.The permanent BP palsy rate is thought to be between 0.1 and
0.2 per 1000 births.56,57
When the damage involves C8 and T1, it is called the Klumpke’s type brachial plexus palsy (claw hand sign). This injury is rare.
Prevention
There is no clear stategy to predict or prevent shoulder dystocia. There are multiple variables affecting shoulder dystocia and in
many situations it is not predictable.58
Diagnosis
• Head recoiling against perineum (‘turtle’ sign) is an alerting sign of potential shoulder dystocia
• Spontaneous restitution does not occur
• Failure to deliver the shoulder with maternal expulsive effort and gentle downward traction with the next contraction
Management
Avoid the 4 P’s. DO NOT!
1. Pull
2. Push
3. Panic
4. Pivot (i.e., severe angulation of the head, using the coccyx as a fulcrum)
Shoulder Dystocia 5
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 potential, the woman and her support persons need to be
prepared for the manoeuvres that may be used.
Regular training in the management of emergencies (such as shoulder dystocia) results in a sustained improvement in team
performance during the actual events.59 A 2013 study demonstrated greater retention of skills if the practice session was hands-
on compared to teaching using a demonstration. Training with the use of simulation models also looks promising.60,61
The implementation of a shoulder dystocia protocol has been found to decrease the diagnosis of BPI at
delivery and at neonatal discharge.1
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) should be 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. There is no association between any individual manoeuvre and neonatal injury or composite morbidity.62
Episotomy should be considered at any point in management when increased access to the fetus would be of benefit; this may
be when any internal manoeuvres are required.
A ASK for help
L LIFT/hyperflex Legs
A ANTERIOR shoulder disimpaction
R ROTATION
M MANUAL removal posterior arm
E EPISIOTOMY
R ROLL over onto “all fours”
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.50-52 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.
Shoulder Dystocia 6
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 the cooperation of the woman, partner,
coach, etc. Notify backup and enlist appropriate personnel.
• 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 McRobert’s manoeuvre 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.
In normal birth there is usually a pause between delivery of the head and body.63 During this pause the uterus relaxes and the
fetus restitutes. During this, as long as the mother is not pushing and the uterus is relaxed, venous return from the fetal head to
thorax is maintained, preserving fetal brain perfusion. 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
0.011 per minute.6,64-66
With the following contraction, if the shoulders do not deliver spontaneously with gentle downward traction in McRobert’s
position, the diagnosis of shoulder dystocia is made and additional maneuvers should be instituted.
Lift the Legs (if not already done with the “turtle sign”)
• Flatten the head of the bed
• Bring the woman to the end of the bed
• Hyperflex both legs at the hips (McRoberts’ manoeuvre)15,44,67
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 (Mazzanti manoeuvre). Apply a steady pressure first and, if unsuccessful, apply a
rocking pressure (the Mazzanti manoeuvre, in association with McRoberts68). 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—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).69
Shoulder Dystocia 7
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.
Rotation of the Posterior Shoulder

Woods’ manoeuvre is a screw-like manoeuvre. Pressure is applied to the anterior aspect of the posterior shoulder and an attempt
is made to rotate the posterior shoulder to an anterior position. Success of this manoeuvre allows easy delivery of that shoulder
once it is past the symphysis pubis. In practice, the anterior shoulder disimpaction manoeuvre and Woods’ manoeuvre may be
done simultaneously and repetitively to achieve disimpaction of the anterior shoulder.70
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.71 If the posterior hand cannot be reached, delivery of the posterior shoulder using axillary
traction is usually successful.72 With either technique fracture of baby’s humerus is common, but fractured humeruses always
heal. Brachial plexus palsies may be permanent.
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.73,74 Prior experience with delivery in this position is an asset.68
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.
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.
Shoulder Dystocia 8
Further Considerations
A recent retrospective study by Leung75 involving 205 cases, compared the perinatal outcomes of shoulder dystocia alleviated by
different types and sequences of manoeuvres. His results indicated that most cases (94.6%) of shoulder dystocia can be resolved
by the application of three manoeuvres in four minutes. The initial step of a McRoberts manoeuvre with or without suprapubic
pressure resolved 25% of cases, of which 7.8% suffered a brachial plexus injury and 3.9% a clavicular fracture. None had a
humeral fracture. Subsequent rotational methods and posterior arm delivery were similarly successful (72.0% versus 63.6%),
whereas the former was associated with less BPI (4.4% versus 21,4%) and humeral fracture (1.1% versus 7.1%), despite similar
risk of clavicular fracture (5.6% versus 7.1%). The cumulative success rates after applying a second and third manoeuvre were
79.0% and 94.6%.
In a retrospective review of electronic records of 2018 cases of shoulder dystocia by Hoffman et al.,76 the authors concluded
that after the McRoberts manoeuvre with suprapubic pressure, delivery of the posterior shoulder should be considered as other
manoeuvres resulted in higher rates of neonatal injuries.
Case studies have reported better outcomes when nuchal cords were not cut prior to delivery in the case of shoulder dystocia.18
If nothing has worked to this point and all of the procedures have been tried again, the following techniques have been
suggested:
1. Deliberate fracture of the clavicle (this may be difficult)
2. Symphysiotomy77 (there must be a clear understanding of this procedure prior to its attempt)
3. Zavenelli manoeuvre (cephalic replacement) – reversing the cardinal movements of labour
• Rotate the head to the occiput anterior position; rotate, flex the head and push it up; rotate the head to the
transverse, disengage the head, and perform a CS
It is clear that despite all of these manoeuvres, brachial plexus palsy may still occur.
Follow Up
Clinical
Mother
• Remember the SIGNIFICANT risk of maternal injury (tears) and postpartum hemorrhage. Actively manage the third
stage. Inspect for and repair lacerations.
Shoulder Dystocia 9
Newborn
• Do cord blood gases (arterial and venous).
• Ensure appropriate neonatal resuscitation and assessment.
• Examine for newborn trauma.
Discussion, Documentation and Debriefing

1. Document and describe. Using a preformatted documentation sheet or checklist will aid in proper documentation.78
Include in your documentation:
• sequence of all manoeuvres used, including which shoulder was impacted
• episiotomy, if done
• indiivudals present in the room
• the time of delivery of the head and time of delivery of the body
• conditionof the newborn
• cord gases sent79
2. Debrief with the mother and family what occurred and what management steps were taken. Document your
discussion.
3. Advise the woman that she is at increased risk for shoulder dystocia in her next pregnancy80
4. 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. Ongoing care of the woman, her partner, and the baby includes a clear explanation of the events as well as
timely and accurate documentation.
Shoulder Dystocia 10
References
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2013. Available: http://www.rcog.org.uk/womens-health/clinical-guidance/shoulder-dystocia-green-top-42.
2. Rodis JF. Shoulder dystocia: intrapartum diagnosis, management, and outcome. In: Lockwood CJ, Barss VA, editors.
UpToDate [database online]. Waltham (MA): UpToDate, Inc.; 2015.
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emergency with empiric management guidelines. Am J Obstet Gynecol 2006;195(3):657-72.
4. Labor and delivery. In: Cunningham FG, Hauth JC, Leveno KJ, Gilstrap L, Bloom SL, Wenstrom KD, editors. Williams
5. Acker DB, Sachs BP, Friedman EA. Risk factors for shoulder dystocia in the average-weight infant. Obstet Gynecol
1986;67(5):614-8.
6. Gurewitsch ED, Allen RH. Reducing the risk of shoulder dystocia and associated brachial plexus injury. Obstet Gynecol
Clin North Am 2011;38(2):247-69.
7. Vidarsdottir H, Geirsson RT, Hardardottir H, Valdimarsdottir U, Dagbjartsson A. Obstetric and neonatal risks among
extremely macrosomic babies and their mothers. Am J Obstet Gynecol 2011;204(5):423.e1-423.e6.
8. Brimacombe M, Iffy L, Apuzzio JJ, Varadi V, Nagy B, Raju V, et al. Shoulder dystocia related fetal neurological injuries: the
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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(2):476-80.
10. Johnstone FD, Myerscough PR. Shoulder dystocia. Br J Obstet Gynaecol 1998;105(8):811-5.
11. Rouse DJ, Owen J. Prophylactic cesarean delivery for fetal macrosomia diagnosed by means of ultrasonography--a
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12. Langer O, Berkus MD, Huff RW, Samueloff A. Shoulder dystocia: should the fetus weighing greater than or equal to
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13. Mehta SH, Blackwell SC, Hendler I, Bujold E, Sorokin Y, Ager J, et al. Accuracy of estimated fetal weight in sholder
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14. Gherman RB, Ouzounian JG, Goodwin TM. Obstetric maneuvers for shoulder dystocia and associated fetal morbidity.
15. Gherman RB, Goodwin TM, Souter I, Neumann K, Ouzounian JG, Paul RH. The McRoberts’ maneuver for the alleviation of
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16. Acker DB, Sachs BP, Friedman EA. Risk factors for shoulder dystocia. Obstet Gynecol 1985;66(6):762-8.
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18. Wood C, Ng KH, Hounslow D, Benning H. Time--an important variable in normal delivery. J Obstet Gynaecol Br
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19. Sandmire HF, DeMott RK. Erb’s Palsy causation: a historical perspective. Birth 2002;29(1):52-4.
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22. Seigworth GR. Shoulder dystocia. Review of 5 years’ experience. Obstet Gynecol 1966;28(6):764-7.
23. Schwartz BC, Dixon DM. Shoulder dystocia. Obstet Gynecol 1958;11(4):468-71.
24. Smith RB, Lane C, Pearson JF. Shoulder dystocia: what happens at the next delivery? Br J Obstet Gynaecol
1994;101(8):713-5.
25. Lewis DF, Raymond RC, Perkins MB, Brooks GG, Heymann AR. Recurrence rate of shoulder dystocia. Am J Obstet Gynecol
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26. Chauhan SP, Grobman WA, Gherman RA, Chauhan VB, Chang G, Magann EF, et al. Suspicion and treatment of the
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27. Kwik M, Seeho SK, Smith C, McElduff A, Morris JM. Outcomes of pregnancies affected by impaired glucose tolerance.
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28. Usha Kiran TS, Hemmadi S, Bethel J, Evans J. Outcome of pregnancy in a woman with an increased body mass index.
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29. Sandmire HF, O’Halloin TJ. Shoulder dystocia: its incidence and associated risk factors. Int J Gynaecol Obstet
1988;26(1):65-73.
30. Bahar AM. Risk factors and fetal outcome in cases of shoulder dystocia compared with normal deliveries of a similar
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31. Gonen R, Spiegel D, Abend M. Is macrosomia predictable, and are shoulder dystocia and birth trauma preventable?
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32. Benedetti TJ, Gabbe SG. Shoulder dystocia. A complication of fetal macrosomia and prolonged second stage of labor
with midpelvic delivery. Obstet Gynecol 1978;52(5):526-9.
33. Overland E, Vatten L, Eskild A. Pregnancy week at delivery and the risk of shoulder dystocia: a population study of 2 014
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34. Temerinac D, Chen X, Sutterlin M, Kehl S. Influence of fetal birth weight on perinatal outcome in planned vaginal births.
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35. Rossi AC, Mullin P, Prefumo F. Prevention, management, and outcomes of macrosomia: a systematic review of literature
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36. Mehta SH, Blackwell SC, Chadha R, Sokol RJ. Shoulder dystocia and the next delivery: outcomes and management. J
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37. Usta IM, Hayek S, Yahya F, Abu-Musa A, Nassar AH. Shoulder dystocia: What is the risk of recurrence? Acta Obstet
Gynecol Scand 2008;87(10):992-7.
38. Ginsberg NA, Moisidis C. How to predict recurrent shoulder dystocia. Am J Obstet Gynecol 2001;184(7):1427-9.
39. Lewis DF, Edwards MS, Asrat T, Adair CD, Brooks G, London S. Can shoulder dystocia be predicted? Preconceptive and
prenatal factors. J Reprod Med 1998;43(8):654-8.
40. Boyd ME, Usher RH, McLean FH. Fetal macrosomia: prediction, risks, proposed management. Obstet Gynecol
1983;61(6):715-22.
41. Crane JM, Murphy P, Burrage L, Hutchens D. Maternal and perinatal outcomes of extreme obesity in pregnancy.
42. Nocon JJ, McKenzie DK, Thomas LJ, Hansell RS. Shoulder dystocia: an analysis of risks and obstetric maneuvers.
Am J Obstet Gynecol 1993;168(6 Pt 1):1732-7.
43. Tsur A, Sergienko R, Wiznitzer A, Zlotnik A, Sheiner E. Critical analysis of risk factors for shoulder dystocia. Arch Gynecol
Obstet 2012;285(5):1225-9.
44. McFarland MB, Langer O, Piper JM, Berkus MD. Perinatal outcome and the type and number of maneuvers in shoulder
dystocia. Int J Gynaecol Obstet 1996;55(3):219-24.
45. Weeks JW, Pitman T, Spinnato JA. Fetal macrosomia: does antenatal prediction affect delivery route and birth outcome?
46. Roberts L. Shoulder dystocia. In: Studd J, editor. Progress in obstetrics and gynaecology. Volume 11. Edinburgh: Churchill
Livingstone; 1995. p.201-16.
47. Alsunnari S, Berger H, Sermer M, Seaward G, Kelly E, Farine D. Obstetric outcome of extreme macrosomia. J Obstet
Gynaecol Can 2005;27(4):323-8.
48. 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.
49. Berger H, Crane J, Farine D, for the Maternal-Fetal Medicine Committee. Screening for gestational diabetes mellitus.
J Obstet Gynaecol Can 2002;24(11):894-903. Available: http://www.sogc.org/guidelines/public/121E-CPG-
November2002.pdf.
50. Gonik B, Walker A, Grimm M. Mathematic modeling of forces associated with shoulder dystocia: a comparison of
endogenous and exogenous sources. Am J Obstet Gynecol 2000;182(3):689-91.
51. Gonik B, Zhang N, Grimm MJ. Defining forces that are associated with shoulder dystocia: the use of a mathematic
dynamic computer model. Am J Obstet Gynecol 2003;188(4):1068-72.
52. Gonik B, Zhang N, Grimm MJ. Prediction of brachial plexus stretching during shoulder dystocia using a computer
simulation model. Am J Obstet Gynecol 2003;189(4):1168-72.
53. Lerner H. Is all brachial plexus injury caused by shoulder dystocia? In: Shoulder dystocia: facts, evidence and
conclusions [monograph online]. Newton (MA): Harry Lerner; 2006. Available: http://www.shoulderdystociainfo.com/
allbrachialcaused.htm (accessed 2006 Oct 26).
54. Moragianni VA, Hacker MR, Craparo FJ. The impact of length of second stage of labor on shoulder dystocia outcomes: a
retrospective cohort study. J Perinat Med 2012;40(4):463-5.
55. Andersen J, Watt J, Olson J, Van Aerde J. Perinatal brachial plexus palsy. Paediatr Child Health 2006;11(2):93-100.
Available: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=19030261.
56. Chauhan SP, Rose CH, Gherman RB, Magann EF, Holland MW, Morrison JC. Brachial plexus injury: a 23-year experience
from a tertiary center. Am J Obstet Gynecol 2005;192(6):1795-800.
57. Gherman RB, Chauhan S, Oh C, Goodwin TM. Brachial plexus palsy. Fetal & Maternal Medicine Review 2003;16(3):221-43.
58. Young BC, Ecker JL. Fetal macrosomia and shoulder dystocia in women with gestational diabetes: risks amenable to
treatment? Curr Diab Rep 2012.
59. Crofts JF, Bartlett C, Ellis D, Hunt LP, Fox R, Draycott TJ. Management of shoulder dystocia: skill retention 6 and 12 months
after training. Obstet Gynecol 2007;110(5):1069-74.
60. Grimm MJ, Costello RE, Gonik B. Effect of clinician-applied maneuvers on brachial plexus stretch during a shoulder
dystocia event: investigation using a computer simulation model. Am J Obstet Gynecol 2010;203(4):339-5.
61. Buerkle B, Pueth J, Hefler LA, Tempfer-Bentz EK, Tempfer CB. Objective structured assessment of technical skills
evaluation of theoretical compared with hands-on training of shoulder dystocia management: a randomized controlled
trial. Obstet Gynecol 2012;120(4):809-14.
62. Spain JE, Frey HA, Tuuli MG, Colvin R, Macones GA, Cahill AG. Neonatal morbidity associated with shoulder dystocia
maneuvers. Am J Obstet Gynecol 2015;212(3):353-5.
63. 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(6):799-803.
64. 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(4):474-9.
65. 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(2 Pt 1):318-22.
66. 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(8):716-20.
67. MacKenzie IZ, Shah M, Lean K, Dutton S, Newdick H, Tucker DE. Management of shoulder dystocia: trends in incidence
and maternal and neonatal morbidity. Obstet Gynecol 2007;110(5):1059-68.
68. Lurie S, Ben-Arie A, Hagay Z. The ABC of shoulder dystocia management. Asia Oceania J Obstet Gynaecol
1994;20(2):195-7.
69. Rubin A. Management of shoulder dystocia. JAMA 1964;189:835-7.
70. Woods CE. A principle of physics as applicable to shoulder delivery. Am J Obstet Gynecol 1943;45:796-804.
71. Cluver CA, Hofmeyr GJ. Posterior axilla sling traction: a technique for intractable shoulder dystocia. Obstet Gynecol
2009;113(2 Pt 2):486-8. Available: PM:19155929.
72. Menticoglou SM. A modified technique to deliver the posterior arm in severe shoulder dystocia. Obstet Gynecol
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74. Bruner JP, Drummond SB, Meenan AL, Gaskin IM. All-fours maneuver for reducing shoulder dystocia during labor.
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75. Leung TY, Stuart O, Suen SS, Sahota DS, Lau TK, Lao TT. Comparison of perinatal outcomes of shoulder dystocia alleviated
by different type and sequence of manoeuvres: a retrospective review. BJOG 2011;118(8):985-90.
76. Hoffman MK, Bailit JL, Branch DW, Burkman RT, Van VP, Lu L, et al. A comparison of obstetric maneuvers for the acute
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Appendix
Lift: McRobert’s Manoeuvre
• McRoberts’ manoeuvre
• flexion of thighs on abdomen
• requires assistance
Anterior Disimpaction – 1) Suprapubic Pressure
• directed from side of fetal back

• CPR type motion
• NO fundal pressure
Anterior Disimpaction – 2) Rubin Manoeuvre
Rotation of Posterior Shoulder – Step 1
• pressure on anterior aspect of posterior shoulder

• may be combined with anterior disimpaction manoeuvres
• NO fundal pressure
• may be repeated if delivery not accomplished by Steps 1 & 2
Manual Removal of Posterior Arm

• splint humerus
• pressure in antecubital fossa to flex arm
• sweep arm over chest
• grasp wrist / forearm
• deliver arm
ALARM Mnemonic
A ASK for help
L LIFT/hyperflex Legs
A ANTERIOR shoulder disimpaction
R ROTATION
M MANUAL removal posterior arm
E EPISIOTOMY
R ROLL over onto “all fours”
Chapter 15
Breech Presentation and Delivery
Definition
When the buttocks of the fetus enter the maternal pelvis before the head, the presentation is termed a breech.
Figure 1. Types of Breech Presentation
• Complete Breech (5%–10%) = hips flexed, knees flexed (foot may be adjacent to or just below buttocks)
• Footling or Incomplete (10%–30%) = one or both hips extended, foot or knee presenting
• Frank Breech (50%–70%) = hips flexed, knees extended1
Breech Presentation and Delivery 1

Incidence
Breech presentation affects three to four per cent of all pregnant women reaching term.2 Based on the latest birth figures for
Canada, there are approximately 10 500 to 14 000 breech deliveries per year.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.2

Breech presentation is associated with an increased frequency of perinatal mortality and morbidity due to prematurity,
congenital anomalies (occur in 6.3% of all breech presentations compared to 2.4% of non-breech presentations4), cord prolapse,
and birth trauma/asphyxia. A 2009 study by Andersen indicated that breech presentation alone is a risk factor for cerebral palsy
when compared with cephalic presentation. The mode of delivery for breech presentation did not significantly influence further
the risk of cerebral palsy.5
Etiology and Risk Factors

As term approaches, the fetus usually is 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.2
E.g.,
• 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 the pregnant woman or the father of her
pregnancy were themselves a breech, there is more than twice the likelihood that their offspring will be breech.6
Diagnosis of Non-Cephalic Presentation
Performing Leopold’s manoeuvres during third trimester prenatal exams will make the diagnosis in the majority of cases. Vaginal
examination or ultrasound may be performed to confirm the presentation if in doubt. An abdominal X-ray may be used to
confirm the diagnosis if ultrasound is unavailable.

Management of Breech
Term breech management involves three options: External Cephalic Version (ECV), Caesarean Section (CS), or Assisted 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 five randomized controlled trials (RCTs) comparing ECV at term to no attempt at ECV showed a significant
reduction in non-cephalic births (relative risk [RR] 0.38; 95% confidence interval [CI], 0.18 to 0.80) and CS (RR 0.55; 95% CI
0.33 to 0.91). 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.
Timing of ECV
The ideal time to carry out ECV has been the subject of debate. A large multicentre RCT (n=1543) compared ECV between
34 weeks’ and 36 weeks’ with ECV after 37 weeks’ gestation.8 When ECV was performed at 34 to 36 weeks:
• Fewer fetuses remained breech at delivery (51% vs. 59%)
• 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.8
ECV should not be attempted before 34 weeks’ gestation for two reasons: first, prior to 34 weeks, ECV is likely
to be unnecessary as most breech fetuses will turn spontaneously by term. Second, if ECV causes preterm birth or emergency
delivery is required for complications, neonatal morbidity increases steeply below 34 weeks’ gestation. After 34 weeks, the
timing of ECV can be decided by a woman and her caregiver based on 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 prior to procedure (i.e., non-stress test or biophysical profile)
5. Amniotic fluid volume adequate
6. Availability of ultrasound
7. Position of fetus known prior to procedure
8. Facilities and personnel available for immediate Caesarean Section
Contraindications*
Absolute
1. Any contraindications to labour, e.g., placenta previa, abnormal or atypical (previously termed non-reassuring) fetal
heart rate (FHR) 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—see Delivery of Twins chapter)
5. Ruptured membranes
* See http://www.medterms.com/script/main/art.asp?articlekey=17824 for a definition of contraindications

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 impact on the likelihood of ECV being successful and need to be considered
when planning 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.9,10
External cephalic version appears to be safe after one CS with a low transverse uterine incision. There are very limited data on the
safety of ECV after two or more CS.
Risks
1. Abruption (0.4%–1%)8,11,12
2. Rupture of the membranes and subsequent possible cord prolapse
3. Labour
4. FHR abnormalities, the most common being transient bradycardia (1.1%–47%).11,12,13,14,15 (Note that fetal bradycardia
necessitating an emergency Caesarean delivery is uncommon 0.5%.16
5. Alloimmunization/fetomaternal hemorrhage (0%–5%)1
A 2009 study by Clock did not find an increase in intrapartum risk of delivery by Caesarean section after successful ECV.17
Intrauterine death is rare and evidence suggests that it is not increased by this procedure.7
Predictors for successful ECV:
Clinical Predictors:18
• Multiparity
• Lack of engagement
• Relaxed uterus
• Fetal head palpable abdominally
• Low maternal weight

Ultrasound Predictors:19
• 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%–80%)13,20,21,22,23
• 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 (reassuring) before the procedure is started.
An ultrasound examination should be performed to confirm the position. Real-time ultrasound is also done 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 baby “follows its nose” (i.e., a forward roll).2 Proceed as
follows:
• Dislodge the buttocks from the pelvis, pushing upwards and then laterally
• Grasp the head and direct it downwards
• Slowly rotate the baby 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 head reaches a lower level than the 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 patient 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 appropriate arrangements with the woman and her partner for her ongoing antenatal care
and choice of delivery method.
Administer Rh immunoglobulin 300 micrograms to unsensitized Rh-negative women. Routine assessment with the Kleihauer-
Betke test for the possibility and degree of fetomaternal bleed is not necessary since it has been shown that only 0.08% of bleeds
with ECV will be greater than 30 ml (300 micrograms of Rh immunoglobulin will cover up to a 30 ml bleed).24
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, the effectiveness of beta-mimetic drugs must be
weighed against their adverse maternal effects.25 A beneficial effect of nifedipine or nitroglycerin versus placebo has not been
demonstrated.25,26 Beta-mimetics for this purpose are not available in Canada. The Cochrane authors concluded there was
enough evidence on nitroglycerin to recommend against its use.25
Epidural or Spinal Analgesia
There are insufficient trials to clearly assess the risks and benefits of epidural or spinal analgesia during ECV. However, a 2011
meta-analysis of six RCTs (n=508) showed improved success with ECV under regional analgesia (60% vs. 35%), and a trend
toward fewer Caesarean sections (48% vs. 59%).27
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. There is level ll evidence from several small trials that moxibustion can help correct
breech presentation.28,29,30,31,32,33 However, a Cochrane review concludes that there is insufficient evidence to support its use.
Larger well-designed trials are needed to adequately evaluate moxibustion.34

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. The size of all the trials was small and no effect on the rate of non-cephalic births
from postural management was detected between the intervention and control groups (five RCTs, n=392, RR 0.95; 95% CI 0.81
to 1.11). Similarly, there were no differences detected for CS (four RCTs, n=292, RR 1.07; 95% CI 0.85 to 1.33).34,35
Caesarean Section
The management of the breech presentation continues to provoke controversy. A policy of elective CS for all breech presentations
became popular in the 1990’s. In a 10-year review of CS trends in Canada, from 1979-1980 to 1988-1989, Caesarean sections
attributable to breech presentation increased by 66%. This policy was instituted without appropriate supporting evidence.
In 2000, the Term Breech Trial (TBT) was published.36 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 which 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 two 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.37
Cochrane Review of Planned CS for Term Breech Delivery—In Developed Countries

Planned CS Planned vaginal birth
Perinatal or neonatal death* 0/641 (0.0%) 4/694 (0.6%)
Serious short-term neonatal morbidity 2/514 (0.4%) 29/511 (5.7%)
* Excludes fetal anomalies

Cochrane Review, 2011
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. Among survivors, there was no significant difference in outcomes at
age two. As the long-term outcome following perinatal morbidity appeared good, the most relevant outcome is the reduction

in perinatal/neonatal death. This reduction was found mostly in developing countries with a baseline perinatal mortality greater
than 20/1000. There was no significant difference in perinatal or neonatal mortality in developed countries with low baseline
perinatal mortality rates.
The TBT’s major limitations 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 seven of the trial’s 16 perinatal deaths were in growth-restricted fetuses. Continuous
electronic fetal monitoring was also not required, and only used in one third of fetuses.The trial protocol allowed labour progress
to be as slow as 0.5 cm/hr in the first stage and up to 3.5 hours for the second stage. Therefore it can be learned from the TBT
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 two-year old, regardless of planned mode of birth.
Goffinet et al. published the PREMODA study: a multicentre descriptive study four times larger than the TBT.38 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 contrast
with 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 (TOL) and planned CS. The only difference in outcome was a 0.16% incidence of five-minute
Apgar score < 4 in the TOL group versus 0.02% in the planned CS group. Eight times larger than the low-perinatal-mortality
subset of the TBT, the PREMODA study provides a robust estimate of the risk of a cautious breech TOL in a modern, well-
supported obstetrical unit.
In light of these studies, new SOGC guidelines for vaginal delivery of breech presentation were published in June 2009.39
Vaginal breech birth can be 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, two 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. Many recent retrospective and
prospective reports of vaginal breech delivery that follow specific protocols have noted excellent neonatal outcomes. Long-term
neurological infant outcomes do not differ by planned mode of delivery even in the presence of serious short-term neonatal
morbidity.
Vaginal Breech Delivery

If a woman chooses a trial of labour for a vaginal breech delivery, the following SOGC recommendations are noted:
Labour Selection Criteria
1. For a woman with suspected breech presentation, pre – or early labour ultrasound should be performed to assess type
of breech presentation, fetal growth and estimated weight, and attitude of fetal head. If ultrasound is not available,
Caesarean section is recommended.
2. Contraindications to labour include:
1. Cord presentation
2. Macrosomia
3. Any presentation other than a frank or complete breech with a flexed or neutral head attitude
4. Clinically inadequate maternal pelvis
5. Fetal anomaly incompatible with vaginal delivery
6. Fetal growth restriction
• 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 prior to 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.
3. Vaginal breech delivery can be offered when the estimated fetal weight is between 2500 g and 4000 g.
4. 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.

Labour Management
1. 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.
2. In the absence of adequate progress in labour, Caesarean section is advised.
3. 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.38
4. 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.
5. 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.
6. A health care professional skilled in neonatal resuscitation should be in attendance at the time of delivery.
Delivery Technique
1. The health care provider for a planned vaginal breech delivery needs to possess the requisite skills and experience
2. An experienced obstetrician comfortable in the performance of vaginal breech delivery should be present at the
delivery to supervise other health care providers, including a trainee.
3. 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” (CPG No. 8940).
4. 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 life saving.
5. Total breech extraction is inappropriate for term singleton breech delivery.
6. Effective maternal pushing efforts are essential to safe delivery and should be encouraged.
7. 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.
8. Spontaneous or assisted breech delivery is acceptable. Fetal traction should be avoided, and fetal manipulation must
be applied only after spontaneous delivery to the level of the umbilicus.
9. Nuchal arms may be reduced by the Bickenbach or Løvset manoeuvres. (Figures 2 & 3)
10. The fetal head may deliver spontaneously, with the assistance of suprapubic pressure (Bracht manoeuver), by
Mauriceau-Smellie-Veit manoeuvre (Figure 4), or with the assistance of Piper forceps. (Figure 5)

Figure 2. Bickenbach reduction of nuchal arms: 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 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: A. Release of the posterior arm. The fetus is grasped by the bony pelvis
with two hands and initially raised towards the maternal pubic symphysis. Turning the fetal torso while lowering it allows the
fetal humerus to be swept out under 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. Note that as the fetal head is being delivered,
flexion of the head is maintained by suprapubic pressure provided by an assistant, and simultaneously by pressure on the maxilla
(inset) by the operator as traction is applied.2

Figure 5. Piper forceps for delivery of the after-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 forceps is applied to the after-coming head. The right blade is
applied with the body still elevated. Forceps delivery of the aftercoming head.2

Setting and Consent
1. 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.
2. The consent discussion and chosen plan should be well documented and communicated to labour-room staff.
3. Hospitals offering a trial of labour should have a written protocol for eligibility and intrapartum management.
4. 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.
5. Theoretical and hands-on breech birth training simulation should be part of basic obstetrical skills training programs
such as ALARM, ALSO (Advanced Life Support Training in Obstetrics), and MOREOB to prepare health care providers for
unexpected vaginal breech births.
Risks/Complications1
• Low one-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 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 delivery has been performed successfully in rare circumstances but must be considered a last resort.
• Nuchal arms, where one or both arms are 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 nuchal arms can be prevented by avoiding traction on the fetus during delivery.
Nuchal arms can be released using the Løvset or Bickenbach manoeuvres (Figures 2 and 3).
• Case series from the early 1970’s 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.41 Of the 11 fetuses delivered vaginally, eight (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%–25%). Cord prolapse is also more common in multiparas (6%) than
in primigravidas (3%). Electronic fetal monitoring in labour and immediate vaginal exam upon membrane rupture
will detect cord prolapse in a timely fashion. In a monitored setting with ready access to CS, cord prolapse is almost
always associated with a favourable outcome.
Preparation and Labour Management2,42

A written vaginal breech labour protocol may assist in ensuring all important components are in place.
• If possible and time permits, obtain an ultrasound (or recent report) to confirm the lie and presentation, assess the
head position, get an estimated fetal weight, assess amniotic fluid volume, confirm placental location, and rule out
major congenital anomalies such as hydrocephalus
• Involve a physician experienced with breech delivery
• Call for an anaesthesiologist
• Ensure presence of individual(s) 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 IUPC), oxytocin is inadvisable.
• Empty maternal bladder just prior to delivery
• Ensure availability of forceps for the aftercoming 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. Explain the necessity of effective pushing in the second stage of labour.
3. Ensure adequate analgesia; 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 fundal pressure, if needed. However, assisted breech delivery is acceptable, and the manoeuvres employed may
be required if there is expulsive delay.
These manoeuvres include:
8. Pinard manoeuvre to deliver the fetal legs may be considered once the popliteal fossae are visible.


Figure 6. Pinard’s manoeuvre is accomplished by inserting two fingers along one leg to the knee, which is then pushed away
from the midline (abducted) at the same time as flexing the leg at the hip. This causes spontaneous flexion of the knee and
delivery of the foot.43 The knees of a frank breech are hyperextended at this point and it is important to correctly identify the
popliteal fossae to avoid further hyperextension and damage to the fetal knee.
1. Løvset manoeuvre for nuchal arms. Rotate the body to facilitate delivery of the arms by sweeping the anterior
humerus across the chest of the fetus (Løvset manoeuvre). Rotate the other arm anterior and repeat. (Figure 3)
2. Support the baby to maintain the head in a flexed position. Suprapubic pressure may help. Maternal expulsive efforts
should be encouraged.
3. The body should be supported in a horizontal position.
4. The Mauriceau-Smellie-Veit manoeuvre can be used to deliver the head in flexion. (Figure 4)
5. Use forceps, if needed. (Piper’s forceps were specifically designed for this purpose.) (Figure 5)
Follow-Up
Care After Breech Delivery
• Active third stage management
• Cord blood gas analysis
• Examination for maternal trauma
• Examination for neonatal trauma
• examine the hips with care; repeat the examination prior to discharge
• Review birth 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 is an incidental emergency vaginal birth or a planned and consensual event.

Suggested format for a chart note (this may also serve as a template to dictate a delivery summary):
• Date/Time
• Healthcare 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
• Duration 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, given 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 individuals involved in managing
deliveries must be prepared for the unexpected vaginal breech delivery. Therefore the technique and manoeuvres for a safe
assisted vaginal 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).

References
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13. Nassar N, Roberts CL, Barratt A, Bell JC, Olive EC, Peat B. Systematic review of adverse outcomes of external cephalic
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14. Brocks V, Philipsen T, Secher NJ. A randomized trial of external cephalic version with tocolysis in late pregnancy.
Br J Obstet Gynaecol 1984;91(7):653-6.
15. Dugoff L, Stamm CA, Jones OW, III, Mohling SI, Hawkins JL. The effect of spinal anesthesia on the success rate of external
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16. Ben-Arie A, Kogan S, Schachter M, Hagay ZJ, Insler V. The impact of external cephalic version on the rate of vaginal and
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17. Clock C, Kurtzman J, White J, Chung JH. Cesarean risk after successful external cephalic version: a matched, retrospective
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18. Kok M, Cnossen J, Gravendeel L, van der Post J, Opmeer B, Mol BW. Clinical factors to predict the outcome of external
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19. Kok M, Cnossen J, Gravendeel L, van der Post JA, Mol BW. Ultrasound factors to predict the outcome of external cephalic
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1999;8(5):203-7.
21. Boucher M, Bujold E, Marquette GP, Vezina Y. The relationship between amniotic fluid index and successful external
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22. Nor Azlin MI, Haliza H, Mahdy ZA, Anson I, Fahya MN, Jamil MA. Tocolysis in term breech external cephalic version.
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23. Lau TK, Lo KW, Wan D, Rogers MS. Predictors of successful external cephalic version at term: a prospective study.
24. Boucher M, Marquette GP, Varin J, Champagne J, Bujold E. Fetomaternal hemorrhage during external cephalic version.
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25. Cluver C, Hofmeyr GJ, Gyte Gillian ML, Sinclair M. Interventions for helping to turn term breech babies to head first
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30. Coyle ME, Smith CA, Peat B. Cephalic version by moxibustion for breech presentation [Cochrane review]. In: Cochrane
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31. Li Q, Wang L. Clinical observation on correcting malposition of fetus by electro-acupuncture. J Tradit Chin Med
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32. Neri I, Airola G, Contu G, Allais G, Facchinetti F, Benedetto C. Acupuncture plus moxibustion to resolve breech
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35. Founds SA. Maternal posture for cephalic version of breech presentation: a review of the evidence. Birth 2005;32(2):137-44.
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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 (Anesthesia, OR staff, Paeds, 2nd MD)
I IV in place, CBC & Group and screen
P Progress in labour adequate? (maximum 60 minute active 2nd 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

Chapter 16
Postpartum Hemorrhage
Definition
Postpartum hemorrhage (PPH) has been defined as blood loss in excess of 500 cc in a vaginal birth and in excess of 1000 cc in an
abdominal delivery.1 For clinical purposes, any blood loss that has the potential to produce hemodynamic instability should be
considered a postpartum hemorrhage. Clinical estimates of blood loss are often inaccurate.
Primary (immediate) 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 defined as the failure of the uterus to contract adequately after the child is born.
Secondary (late) postpartum hemorrhage occurs between 24 hours after delivery of the baby and six weeks
postpartum. Most late PPH is due to retained products of conception, infection, or both.
Incidence
Postpartum hemorrhage occurs in 5% of all deliveries worldwide and is a leading cause of maternal mortality.2,3 A 2012
systematic review by Calvert on regional prevalence of PPH demonstrated a global prevalence of 10.8% with 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.4 The Public Health Agency of Canada reported that between 2006 and 2011, blood transfusion
(750 per 100 000) and PPH (480 per 100 000) were the most common source of maternal morbidity while PPH (1.7 per
100 000 deliveries) accounted for 39 maternal deaths (1.6/100 000 deliveries).5
Studies in high-resource countries have observed an increase in PPH, predominantly due to atonic PPH.6,7,8 A large cohort
study by Kramer et al.9 analyzed 103 726 deliveries in Montreal between 1978 and 2007 and identified that labour induction,
augmentation of labour, and previous Caesarean section (CS) were associated with the observed rise in PPH. A 2014 cohort study
reviewing over 2 miilion deliveries between 2003 and 2010 in Canada identified 122 676 cases of PPH. There was an increase of
PPH by 22% (5.1% to 6.2%), mostly driven by atonic PPH. Increases were also noted in PPH requiring blood transfusion (36.7 to
Postpartum Hemorrhage 1
50.4), PPH with hysterectomy (4.9 to 5.8), and use of uterine/ligation sutures to control PPH (4.1 to 10.7) per 10 000 deliveries.10
The increases applied to most provinces and territories.
Reproduced from Mehrabadi et al. J Obstet Gynaecol Can 2014; Used with Permission.10
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 Shock11
Degree of Shock Blood Loss Signs and Symptoms
MILD < 20% • diaphoresis

• delayed capillary refill
• cool extremities
• anxiety
MODERATE 20–40% Above plus:

• tachycardia
• tachypnea
• postural hypotension
• oliguria
SEVERE > 40% 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 injury12
• Tissue – retained placenta or clots
• Thrombin – pre-existing or acquired coagulopathy
The most common and important 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.
Risk Factors13,14
Etiologic Process Clinical Risk Factors
Abnormalities of Over-distended uterus • polyhydramnios

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

• prolonged labour
• high parity
• oxytocin use
• induction of labour15
Intra-amniotic infection • fever

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

Uterine-relaxing medications • placenta previa
• uterine anomalies
• velamentous cord insertion17
Bladder distension, which may prevent uterine contraction16 • halogenated anaesthetics

• tocolytics including nitroglycerin
Retained Products Retained products • incomplete placenta at delivery

of Conception • abnormal placentation • previous uterine surgery
(Tissue) • retained cotyledon or succenturiate lobe • high parity
• abnormal placenta on ultrasound (U/S)
Retained blood clots • atonic uterus
Genital Tract Lacerations of the cervix, vagina, or perineum • precipitous delivery

Trauma • operative delivery
(Trauma)
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 • hx of hereditary coagulopathies

Coagulation • Hemophilia A • hx of liver disease
(Thrombin) • Von Willebrand’s Disease18
• history of previous PPH
Prior invasive treatment of PPH with embolization (39%)
and ligation (26%)19
Acquired in pregnancy • bruising

• idiopathic thrombocytopenic purpura (ITP) • elevated BP
• thrombocytopenia with pre-eclampsia
• disseminated intravascular coagulation (DIC)
• gestational hypertension with adverse conditions • elevated BP

• dead fetus in utero • fetal demise
• severe infection • fever, neutrophilia or neutropenia
• abruption • antepartum hemorrhage
• amniotic fluid embolus • sudden collapse
Therapeutic anti-coagulation • hx of thrombotic disease
Other BMI > 3019

SSRI 21-24
Prevention
Active Management of 3rd Stage Labour (AMTSL)
Expectant, or physiological, management allows the placenta to deliver spontaneously and the uterus to contract spontaneously.
Multiple national (SOGC13, RCOG,25 RANZCOG,26 CNGOF27) and institutional (FIGO28 and WHO29) guidelines, support the use of
uterotonics as part of the management of the third stage of labor (AMTSL) to assist with delivery of the placenta reducing blood
loss and need for manual removal of the placenta. Oxytocin is preferred to ergotamine (contra-indicated with hypertension and
higher incidence of nausea) and misoprostol (less efficacious and more shivering and maternal fever).
Active management involves caregiver intervention to assist in the expulsion of the placenta with the intention to minimize
blood loss. Active management includes the following:
1. Attendance by providers with the training and skills to actively manage the third stage.
2. Use of uterotonics agents. Oxytocin should be given after delivery of the baby:
a) 10 units (U) intramuscularly (IM), or
b) 20–40 U in 1000 ml normal saline as an intravenous (IV) infusion (100–150 cc/hour)30
c) an IV infusion of 5–10 U given slowly over 1–2 minutes is an acceptable approach following a vaginal birth
in a healthy woman
3. Gentle traction on the umbilical cord with simultaneous suprapubic support of the uterus (see below)
4. Timing of the clamping of the umbilical cord (see discussion, below)
A joint statement by the International Confederation of Midwives and FIGO31 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. Both of these
groups state that the third stage of labour should be managed with the routine use of uterotonics, controlled cord traction, and
uterine massage.
A 2015 Cochrane meta-analysis33 of AMTSL included the routine use of uterotonics, early cord clamping, and controlled cord
traction on the umbilical cord. All of the studies34-37 compared active management with various uterotonic agents versus
expectant management. Meta-analysis determined that compared to expectant management, active management reduced the
risk of PPH and that of hemoglobin concentration less than 9 g/dl, regardless of the woman’s bleeding risk profile. There was no
difference in the incidence of retained placenta or the management of this complication either by manual or surgical removal.
Increases in nausea and hypertension (when ergotamine was used) were statistically significant in the active group.
Cord Traction
The use of cord traction has been shown to reduce the incidence of retained plactenta without significant reduction of PPH.
The mainstay of AMTSL is the IM injection of oxytocin.38
A 2015 Cochrane review comparing controlled cord traction (CCT) versus expected delivery of the placenta included 3 studies
with 27 870 women.39 There was no difference in the risk of blood loss ≥ 1000 mL (three trials, 27 454 women; risk ratio (RR)
0.91, 95% confidence interval (CI) 0.77 to 1.08). Manual removal of the placenta was reduced with CCT (two trials, 27 665
women; RR 0.69, 95% CI 0.57 to 0.83). In the World Health Organization (WHO) trial the reduction in manual removal occurred
mainly in sites where ergometrine was used routinely in the third stage of labour.40 The non-prespecified analysis excluding sites
routinely using ergometrine for management of the third stage of labour found no difference in the risk of manual removal of
the placenta in the WHO trial (one trial, 23 010 women; RR 1.03, 95% CI 0.73 to 1.46). The policy of restricting the third stage
of labour to 30 minutes (4057 women; RR 0.69, 95% CI 0.53 to 0.90) may have had an effect in the French study.41 Among the
secondary outcomes, there were reductions in blood loss ≥ 500 mL (three trials, 27 454 women; RR 0.93, 95% CI 0.88 to 0.99),
mean blood loss (two trials, 27 255 women; mean difference (MD) -10.85 mL, 95% CI -16.73 to -4.98), and duration of the
third stage of labour (two trials, 27 360 women; standardised MD -0.57, -0.59 to -0.54). There were no clear differences in use
of additional uterotonics (three trials, 27 829 women; average RR 0.95, 95% CI 0.88 to 1.02), blood transfusion, maternal death/
severe morbidity, operative procedures nor maternal satisfaction. Maternal pain (non-prespecified) was reduced in one trial
(3760 women; RR 0.78, 95% CI 0.61 to 0.99).
Uterine Massage Prior to Placental Delivery

Uterine massage prior to the delivery of the placenta is of no benefit. It may increase blood loss and should not be done.32,42
A 2013 Cochrane review included two trials that found prophylactic uterine massage inconclusive to reduce PPH.43
A multicenter RCT of 2340 VDs showed that the additional uterine massage after routine oxytocin did not reduce blood loss.44
A secondary analysis of 39 202 births, uterine massage was associated with increased hemorrhagic risk.45
Timing of Cord Clamping

As with controlled traction, cord clamping has not been independently studied in relation to the prevention of PPH. However,
more recent information has been published demonstrating the potential benefits of delayed cord clamping to the newborn.
Delaying cord clamping by 30 to 120 seconds seems to be associated with less need for transfusion for anemia and less
intraventricular hemorrhage in non-resuscitated premature infants <37 weeks compared to early clamping.46,47
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.48
A 2007 systematic review and meta-analysis by Hutton and Hassan49 comparing early (less than one minute) versus late
(two minutes) cord clamping suggests that there is a physiological benefit of delayed clamping to the newborn that extends into
infancy. Advantages included prevention of anemia over the first three months of life and enhanced iron and ferritin stores for up
to six months. There was no increase in respiratory distress defined as tachypnea or grunting. There was no statistical difference
in bilirubin levels and infants receiving phototherapy in the late versus early group. A 2013 Cochrane review50 included 15 RCTs
15 trials 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.
Uterotonic Agents for the Prevention of PPH

During the third stage, the muscles of the uterus contract downward, causing constriction of the blood vessels that pass through
the uterine wall to the placental surface to stop the flow of blood. This action also causes the placenta to separate from the
uterine wall. The absence of uterine contractions is clinically defined as atony, and may cause excessive blood loss. Uterotonics
promote uterine contractions to prevent atony and speed the delivery of the placenta.
The uterotonic agents include oxytocin, ergotamine, syntometrine (combination ergotamine and oxytocin), and misoprostol. All
of the studies in the Cochrane meta-analysis, above,51 used either oxytocin or syntometrine IM, except for the Dublin trial which
used IV ergometrine.35
All of the studies demonstrated a reduced need for manual removal of the placenta except for the Dublin trial. This was the only
trial to administer a uterotonic agent (ergometrine) intravenously.35
Oxytocin
The Abu Dhabi study36 included in Begley’s metanalysis demonstrated the benefits of active intervention during the third
stage with controlled cord traction and 10 units oxytocin intramuscularly (IM) compared to minimal intervention. With active
management, there was a lower incidence of PPH (5.8% vs. 11%, odds ratio [OR] 0.5; 95% CI 0.34 to 0.73), reduced incidence
(1.6% vs. 4.5%) of retained placenta at greater than or equal to 30 minutes, and less need for additional uterotonic agents
(2.3% vs. 5.1%).
A secondary analysis of 11 323 deliveries had less PPH with AMTSL using oxytocin versus nothing for PPH > 500 ml (6.84% vs.
12.82%) and PPH > 1000 ml (1.29% vs. 1.92%). There was no difference between induced/augmented labour and moderate
PPH (P = 0.753), severe PPH (P = 0.273), and blood transfusion (P = 0.603) in the population that received AMTSL.52
A 2010 Cochrane review (n=1671) comparing IV oxytocin before and after delivery of the placenta did not affect the incidence
of PPH greater than 500 ml retained placenta; duration of the third stage; postpartum blood loss; changes in hemoglobin;
blood transfusion; use of additional uterotonics; the incidence of maternal hypotension, or the incidence of severe postpartum
hemorrhage (blood loss ≥ 1000 ml).53
Similar results were found in a 2011 randomized controlled trial (RCT)54 involving 1802 women in a high-resource country
comparing active (oxytocin 10 U IM, early cord clamping, and controlled cord traction) versus expectant management. Blood loss
was reduced (535 ml vs. 680 ml, P < 0.001) and PPH greater than 1000 ml was less (10% vs. 16.8%, P < 0.001) 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).
Two 2013 studies compared IV vs IM routes for oxytocin prophylaxis for AMTSL. A secondary analysis by Sheldon (n=39 202)
found that there was less blood loss for IV compared to IM of > 500ml (12.6% vs 19.6%) and >700 ml (1% vs 3.8%).45
A 2014 prospective RCT study of 600 term, singleton, vaginal deliveries compared the timing (after appearance of anterior shoulder
and after delivery of the fetus) and route (IM versus IV) of oxytocin (10 IU). All the groups had similar outcomes (postpartum blood
loss, additional utertonics, change Hgb and Hct) but the earlier administration of IV oxytocin resulted in a decreased duration of the
third stage. Labor augmentation resulted in significantly increased postpartum blood loss in all groups except in the early IV group.55
There is limited experience in the use of oxytocin given as an IV push (within 10 seconds), although one study involving
99 women given 10 units of oxytocin as an IV push did not have significant hemodynamic effects.56 A 2008 study by Tharakan
demonstrated similar results in safety and a trend towards lesser blood loss.57
Two recent small studies have demonstrated adverse maternal effects with the use of an IV bolus of oxytocin at the time of
elective Caesarean section. One study demonstrated hemodynamic changes in women who were given a 5 unit intravenous
bolus compared with women given 5 units intravenously over five minutes.58 The other study demonstrated transient ECG
changes consistent with myocardial ischemia in women given an intravenous bolus of oxytocin following Caesarean birth.59
These studies suggest a potential maternal effect of the rapid administration (over 30 seconds) of oxytocin. This may be dose-
related. A pilot study comparing a bolus of oxytocin plus an oxtyocin infusion with an oxytocin bolus plus a placebo showed a
reduced need for an additional uterotonic agent in the former group.60
In contrast, a 2011 study61 of 56 women undergoing elective CS did not find any difference in hemodynamic changes after either
oxytocin 5 U IV bolus or carbetocin 100 µg IV bolus.
A 2011 RCT by Sheehan et al. studied the effects of an additional oxytocin infusion after routine administration of oxytocin bolus
in 2069 women booked for elective CS.62 There was a reduced need for additional uterotonics in the intervention group but there
was no reduction in blood loss greater than 1000 ml.62
A Cochrane review63 comparing oxytocin to ergot-oxytocin in active management measured a small benefit in PPH greater than 500 ml
but no difference in PPH greater than 1000 ml. There were more side effects (elevated diastolic blood pressure, nausea, and vomiting) in
the ergotamine-oxytocin group. The authors favoured oxytocin over ergot based on the lower incidence of maternal side effects.
A Cochrane review64 on prophylactic oxytocin use during the third stage demonstrated a significantly reduced need for manual
removal of the placenta compared with ergometrine (RR 0.57; 95% CI 0.41 to 0.79).
Exposure to oxytocin during labor reduces oxytocin’s effectiveness to control bleeding at the time of Cesarean delivery. Lavoie
measured the effective oxytocin infusion dose to control bleeding to be higher in women who had undergone labor (44.2 IU/h
95% CI 33.8-55.6) versus women who had no labor (16.2 IU/h 95% CI 13.1-19.3).65 The net difference in oxytocin infusion rate
was 28 IU/h (95% CI 26-29, p<0.001). Higher doses of oxytocin may be required in a woman exposed to oxytocin in labour.
Carbetocin
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.
A Cochrane review66 concluded that there is insufficient evidence that 100 µg IV carbetocin is as effective as oxytocin in
preventing PPH in vaginal deliveries. Carbetocin should not used as a first-line agent before other uterotonic agents.
RCTs comparing carbetocin to oxytocin in women with one67 or two risk factors68 for PPH in term vaginal deliveries did not show
any significant difference for bleeding, need for other uterotonic medications and blood transfusion.
Misoprostol
Misoprostol has been extensively studied in obstetrics as a uterotonic agent. It has not been shown to be superior to other
uterotonics in AMTSL for the prevention and treatment of PPH. Due to its stability at room temperature, ease of administration,
low cost and uterotonic properties, the World Health Organization added misoprostol to its essential medication list.
A 2011 study by Elati measured the effect of three doses of misoprostol (200 µg, 400 µg and 600 µg) and 10U IM oxytocin on
uterine contractions in the immediate postpartum using an intrauterine pressure catheter.69 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 misprostol than oxytocin from 50 to 120 minutes. The incidence
of high fever (temperature > 39 degrees) was the same for the 200 µg and 400 µg doses (8.3%) and much higher for the 600 µg
dose (45.4%).69 A 2013 Cochrane review by Hofmeyr supported that adverse effects increased at doses greater than 600 µg.70
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 70–80 minutes 6 hours
Rectal 40–60 minutes 6 hours
The sublingual route has a much higher serum peak level than the oral route due to the avoidance of first pass metabolism by
the liver.
Pyrexia was more common in all studies and when the dose exceeded 600 µg.
There have been many clinical studies involving misoprostol in order to determine its place in the medical prevention and
treatment of PPH. Comparing studies is a challenge due to different doses (400–800 µg) and route of administration.
The studies of misoprostol and prevention of PPH can be summarized as follows:
• Misoprostol is more effective than placebo;71
• The recommended dose is 400 µg sublingual;71
• Compared to IM uterotonics, misoprostol is less effective in prevention of PPH;40,72-74
• In developing countries, misoprostol75 (600 µg SL) was less effective then oxytocin (10 IU IM) for the incidence of
primary PPH > 500 ml within 24 hours (28.6% vs 17.4%) for uncomplicated, term vaginal deliveries76
The misoprostol studies for the treatment of PPH have shown:
• Misoprostol was equally effective as IV oxytocin for treatment of PPH in women given prophylactic IM oxytocin;77
• Misoprostol was less effective than IV oxytocin for treatment of PPH in women not given prophylactic IM oxytocin;78
• Adjunct misoprostol (600 µg SL) to routine IV oxytocin had a non-significant trend to lower blood loss in vaginal
deliveries;79
In the situation of a retained placenta:
• Misoprostol (800 µg in normal saline) injected into the umbilical vein had less manual removal of placenta (MROP)
than oxytocin infusion or placebo;80
• Misoprostol (800 µg PO) had no difference in MROP compared to placebo.81
Ergonovine
Ergonovine is an effective agent for the treatment and prevention of PPH but has more adverse effects than oxytocin, making it
a less preferred agent. Ergonovine is contraindicated in the presence of hypertension and there is an increased risk of retained
placenta when it is administered intravenously.
Ergonovine is indicated for the prevention and treatment of primary postpartum hemorrhage secondary to uterine atony.82-84
It stimulates the myometrial alpha-adrenergic receptors of the upper and lower segments of the uterus producing a tetanic
contraction. The dose is 0.2–0.25 mg and there is a rapid onset of action (< 1 minute for IV and 2–5 minutes for IM). The
duration of action of ergonovine is 3 hours for IM and 45 minutes for IV administration.85
Begley’s 2011 meta-analysis51 regarding the active management for the prevention of PPH included the Dublin Trial, which used
IV ergonovine given immediately after delivery of the baby.35 The study group in the Dublin Trial had a reduced incidence of PPH
(clinically estimated blood loss ≥ 500 ml), reduced severe PPH (clinically estimated blood loss ≥ 1000 ml), and less drop in
hemoglobin when compared to physiological management, but a significantly greater incidence of adverse effects including
nausea, vomiting, and hypertension with the use of ergonovine. There was also a greater risk of retained placenta associated with
the intravenous route.
A 2007 Cochrane review86 compared placebo to ergonovine given by various routes during the third stage of labour for
prevention of PPH. Oral ergonovine had no benefit compared to placebo. Ergonovine given IM or IV, resulted in significantly less
blood loss compared to placebo (mean weighted difference 83 ml; 95% CI 99 to 67 ml) and less PPH of at least 500 ml (RR 0.38;
95% CI 0.21 to 0.69). However, as in other studies, ergonovine resulted in more adverse effects including vomiting (RR 11.8;
95% CI 1.78 to 78.28), elevated blood pressure (RR 2.6; 95% CI 1.03 to 6.57) and pain requiring analgesia (RR 2.53; 95% CI
1.34 to 4.78). The IM and IV routes were equally effective but the adverse effects (including retained placentas and manual
removals of placenta) were greater with the IV route.
Cotter’s 2001 Cochrane review,64 involving six studies and 2800 women, compared oxytocin to ergonovine. It revealed no
significant difference for the prevention PPH and the use of additional uterotonics between the two medications. There were
fewer manual removals of the placenta (RR0.57; 95% CI 0.41 to 0.79) and less raised blood pressure (RR 0.53; 95% CI 0.19 to
1.52) with oxytocin.
A prospective study of 600 women87 compared 10 units IV oxytocin to 0.25 mg IV ergonovine given at delivery of the anterior
shoulder. They found that the use of ergonovine resulted in a statistically higher incidence of headaches, nausea, and vomiting.
There was a non-statistically significant trend towards less PPH, need for additional uterotonics, retained placentas and manual
removals of the placenta in the oxytocin group.
A prospective study involving 343 women was performed to compare the efficacy of oxytocin and ergonovine in preventing
PPH.88 Women were given either 5 units IM oxytocin or 0.2 mg IM ergonovine after delivery of the baby, in addition to immediate
clamping and cutting of the cord followed by cord traction to assist delivery of the placenta. Oxytocin had a lower incidence of
PPH greater than 500 ml (RR 0.54; 95% CI 0.32–0.91) and a lower need for additional therapeutic oxytocics (RR 0.42; 95% CI
0.19–0.91).
Tranexamic Acid
Tranexamic acid (TA) is an inhibitor of fibrinolysis used to treat fibrinolytic bleeding. It acts by preventing the conversion of
plasminogens to plasmin stabilizing clot formation in bleeding patients. The World Maternal Antifibrinolytic Trial (WOMAN Trial)
is a large study in progress to determine if TA can reduce PPH mortality.89
The majority of studies have compared TA versus placebo as adjuncts to usual prophylactic care with oxytocin. Several
reviews90-93 show TA to reduce blood loss and blood transfusion where Sentilhes94 felt the current evidence is insufficient to
demonstrate an acceptable benefit to risk ratio.
A 2014 RCT95 of 747 women with a high incidence of anemia were given tranexamic acid (1 g IV slowly 10 minutes before
elective CS). The mean total blood loss was 241.6 (SE 6.77) ml in the tranexamic acid group versus 510 (SE 7.72) 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.
Conflicting results have emerged for the use of TA in the treatment of PPH. A 2011 open-label RCT96 of 144 women compared
high-dose (4 g over 1 hour, then 1 g/hr) tranexamic acid versus placebo in the setting of PPH > 800 ml after vaginal delivery.
Blood loss after enrollment was lower in the TA group (173 ml vs. 221 ml, P = 0.041) with shorter bleeding duration and less
frequent progression to severe PPH P < 0.003). Invasive procedures were done in four of the TA group versus seven in the control
group (P = NS). PPH stopped after uterotonics and packed red blood cell (PRBC) transfusion in 96% of the TA group versus 79%
of the control group (P = 0.016). Bouet97 studied 289 woman in a before-and-after study treated for PPH > 500ml but found no
difference in blood loss and hemoglobin drop.
Low Molecular Weight Heparin
Low molecular weight heparin (LMWH) is the drug of choice for prevention of thromboemblolic disorders but its impact on
the incidence of PPH is unclear. Roshani et al.98 performed a retrospective study on 95 women who received LMWH for DVT
prophylaxis. 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 (RR 0.8; 95% CI 0.5 to 1.4) or severe PPH (RR1.2; 95% CI 0.5 to 2.9), and the median blood loss in normal
vaginal deliveries was actually lower in LMWH users (200 ml) than in non-users (300 ml).
Recombinant Activated Factor VII

Recombinant activated factor VII (rFVIIa) was originally developed for the treatment of bleeding in hemophilia but has also been
applied to treat women with massive postpartum hemorrhage to avoid hysterectomy. Studies are few in number and have been
non-randomized. A review by Francini suggests a potential use for rFVIIa, although further research is required to determine its
role and benefit.99
Timing of Placental Delivery

It is well known that an important risk factor for PPH is the failure of the placenta to deliver in a timely manner. Fifty percent of
placentas deliver within five minutes and 90% within 15 minutes of the baby’s birth.100 Magann et al concluded that the risk of
PPH increases three-fold if the placenta is delivered > 15 minutes compared to < 15 minutes (13.3% vs 4.4%, p=0.012).101
Shinar’s102 retrospective study of 25 016 cases correlating outcomes with the timing of placental delivery measured the optimal
timing for predicting blood transfusion was 17 minutes and the risk of transfusion was three-fold when exceeded 30 minutes. IV
access should be ensured at 15 minutes of an undelivered placenta.
Endler’s 2012 case-control study identified several risk factors for placental retention including previous retained placenta,
preterm delivery, prolonged oxytocin use, preeclampsia, and greater than or equal to two miscarriages or abortions.103
A retained placenta was significantly associated with an increased risk of PPH (PPH > 500 ml, PPH > 1000 ml, blood transfusion).
A 2012 RCT by Van Stralen et al.81 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 (50% vs. 55%) or blood loss (970 ml vs. 1120 ml) for
women who received misoprostol (800 µg orally) one hour after childbirth compared to placebo.
Placental Cord Drainage

A 2011 Cochrane review identified three studies involving 1257 vaginal deliveries addressing placental cord drainage.104 There
was a small reduction in the length of the third stage by 2.85 minutes (95% CI – .04 to – 1.66) and blood loss was reduced by
77 ml (95% CI – 113 to – 40.3). A major confounding factor was that only one of the three 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.104
A prospective study compared cord drainage (cord not clamped after cutting) to routine clamping before cutting in 485 vaginal
deliveries. All women received 5 IU oxytocin prophylaxis.105 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, respectively; p=0.001). The third stage
of labor was significantly shorter in the cord drainage group than in the control group (3.5 +/- 1.9 vs. 7.7 +/- 3.4 minutes,
respectively; p=0.001). No adverse events occurred during the cord drainage period.
Injection of the Umbilical Vein for Retained Placenta3,11,106,107

Manual removal of a retained placenta may lead to complications such as infection, uterine perforation, hemorrhage, and
maternal discomfort. In order to avoid these complications, several interventions have been studied using various agents to
assist in the detachment of the placenta and avoid a manual removal. The timing of the interventions varied between 30 minutes
to 45 minutes with a retained placenta.
Intra-umbilical injection of misoprostol may be of benefit but data are limited.80,108-112
The procedures for injection of the umbilical vein can be either direct injection into the vein using a syringe or by following the
Pipingas technique for the use of misoprostol. The step-by-step technique is described below:
1. Explain the procedure and obtain consent.
2. Prepare a syringe with the medication in 30 cc normal saline. Crush and dissolve 4 x 200 µg 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 1–2 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 30–47 cm in the Rogers’ study.80)
6. Retract by 3–4 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 followed by clamping of the cord with the catheter.
8. Note the time of the injection.
9. Wait 10–30 minutes for the placenta to deliver.
Active Management of the Third Stage:

1. Ensure attendance by individuals skilled in the prevention of PPH and knowledgeable regarding its related
complications.
2. Administer oxytocin after the delivery of the anterior shoulder (oxytocin 10 units IM or 20–40 units in 1000 ml normal
saline given as an IV infusion at 100–150 cc/hour).
3. After delivery of a well-appearing baby, consider waiting 1–2 minutes before clamping and dividing the cord.
4. Take the cord samples, including arterial and venous gases.
5. Immediately palpate the uterine fundus and confirm that the uterus is contracted.
6. Wait for signs of placental separation (vaginal bleeding or laxity of the umbilical cord). Maintain tension on the cord
by pulling gently while at the same time applying suprapubic counter-traction on the uterus with the other hand.
Gentle digital exam along the cord will determine whether the placenta is at the cervix. Pulling hard on the cord may
cause the cord to avulse or cause uterine inversion—an acute obstetrical emergency.
7. If the placenta has not delivered after approximately 15 minutes and oxytocin has not already been administered, give
it at this time. The mean duration of the third stage is 8 minutes to 10 minutes. The longer the third stage the greater
the risk of PPH. After 30 minutes the risk is six times normal. Ensure IV access.106
Following the Third Stage:
• After the placenta is delivered, assess the fundus and ensure that it is well-contracted and that there is no ongoing
significant bleeding. Inspect the placenta for completeness. Note any abnormalities that may indicate retained
products (e.g., vessels crossing the membranes with no attached succenturiate lobe or missing cotyledon).
• Consider the need for an oxytocin infusion after delivery of the placenta.
• Inspect the lower genital tract after all deliveries.
• The cervix and upper vagina should be inspected following all operative vaginal deliveries. Depress the posterior
vaginal wall. The anterior lip of the cervix will come into view. If necessary, grasp this with the ring forceps and pull
upwards to bring the entire cervix into view or ‘walk around’ the cervix with ring forceps. Push the cervix up into the
vaginal vault to inspect the whole vagina for lacerations.
Management
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.
Don’t Forget your CAB’S
• 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 Ringers)
• 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 lab of the potential need for massive transfusion support
Shock index (HR/SBP) 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 0.5–0.7.
A 2013 retrospective study of 50 women with massive PPH was used to establish an obstetrical shock index (OSI) (heart rate /
systolic BP) to identify significant blood loss earlier and need for blood transfusion.113 Mean OSI in the control group (i.e., normal
delivery) at 10 minutes and 30 minutes was 0.74 (range, 0.4–1.1) and 0.76 (range, 0.5–1.1), respectively. In the case group,
mean OSI at 10 minutes and 30 minutes was 0.91 (range, 0.4–1.5) and 0.90 (range, 0.5–1.4), 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. This study suggests that the normal OSI range should be 0.7–0.9 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.
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.114
Assess the Uterine Fundus
Recall that uterine atony is the most common cause of PPH and that the clinician should address this first and have an organized
approach. The management is a team approach that may include several simultaneous interventions.
1) If boggy:
Proceed to external uterine massage and uterotonics. Oxytocin is first line and should be given by rapid IV infusion if access is
immediately available. Otherwise give IM oxytocin 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
bleeding 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. This is an effective way of controlling bleeding until help arrives.
The uterus may be explored at this stage to rule out retained products, uterine inversion, or uterine rupture if analgesia allows.
• 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, monitoring 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):115,116
• 5 units of oxytocin IV bolus
• oxytocin 20–40 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 explored, this must be done now in order to rule out retained clots or
products, uterine rupture, or inversion.
• If bogginess or hemorrhage continues, consider any of the following agents:
• 15-methyl prostaglandin F2α (carboprost/Hemabate)
• 250 µg IM or intramyometrially
• may be repeated every 15 minutes to a maximum cumulative dose of 2 mg (8 doses)
• asthma is a relative contraindication*
• Carbetocin (Duratocin) has been shown to reduce bleeding secondary to uterine atony in CS but there are no
studies that have demonstrated its effectiveness in treating PPH in low-risk vaginal deliveries.117
• 100 µg IM or IV bolus over one minute
• Misoprostol (Cytotec, 400–800 µg SL is the preferred route32) is of considerable interest since it is an inexpensive
medication and requires minimal storage precautions. Review of the pharmacokinetics demonstrated
that misoprostol administered orally or sublingually acts more rapidly as a uterotonic agent than by rectal
administration, although the rectal route acts for a greater period of time. Rectal administration (800–1000 µg) is
preferred if the woman is unable to take medications orally.118,119 There is more pyrexia with the oral route at doses
exceeding 600 µg compared to other routes.120
• one study involving 160 subjects showed misoprostol (200 µg PO and 400 µg SL) to be effective in
decreasing the incidence of blood loss > 500 cc when used in addition to the usual uterotonics.121 There may
be a role for misoprostol if there is a delay anticipated in the management of PPH.
• Ergonovine maleate
• 0.2–0.25 mg IM or IV (every 2–4 hours)
• contraindicated in hypertensive disorders of pregnancy because of the risk of stroke or a hypertensive crisis122
• contraindicated with concomitant use of certain drugs used to treat HIV (e.g., protease inhibitors, non-
nucleoside reverse transcriptase inhibitors)
• If bogginess and hemorrhage continue, consider emergency therapy for uterine atony, which may include:
1. Tamponade with a Sengsten Blakemore oesophageal catheter or the SOS Bakri Tamponade Balloon catheter
(A condom catheter has been shown to be very effective123)
* See http://www.medterms.com/script/main/art.asp?articlekey=17824 for a definition of contraindications
All of the devices have been reported to be successful for the temporary control of active bleeding.124 The insertion technique 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 (250–500 ml normal saline) until bleeding stops and
then left in place.125 Ultrasound can be used to confirm placement. 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.126
2. Emergency embolization.The woman must be stable enough to transport to an embolization suite.
3. Emergency laparotomy with pelvic vessel (internal iliac or uterine artery) ligation
4. Emergency laparotomy with B Lynch or Cho sutures. Techniques where sutures are used to compress the
uterus (see Appendix), A review of case reports from 1996 to 2009 demonstrated the technique to be safe and
efficacious for the treatment of severe, atonic PPH. The complication rate was low when performed correctly
except for a higher rate of uterine ischemia when combined with vessel ligation. There was no negative impact on
fertility after one to three years.127
5. Emergency hysterectomy. Although a last resort, this must be considered prior to 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.128
2) If firm:
• Explore the lower genital tract

• 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 coagulopathy.129
• fibrinogen levels are physiologically elevated in pregnancy. Low normal levels (under 3 g/L) in a setting of severe
postpartum haemorrhage are abnormal and fibrinogen replacement (cryoprecipitate) should be considered.129,130
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
• B-Lynch technique, Cho technique, or hysterectomy
• if surgical expertise is unavailable, consider tamponade, stabilization, and transport
Second-Line Therapies
Uterine tamponade, interventional radiology, rFVII, uterine compression sutures, and pelvic vessel ligation should be considered
before hysterectomy. A prospective population-based study in the U.K. by Kayem et al. found that there were 2.2 cases of PPH
per 10 000 women who underwent a second-line therapy.131
Uterine Balloon Tamponade (BT)

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 conjuction 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 centers. Multiple retrospective studies have reported
success rates of 80-95% when used for PPH refractory to massage and uterotonics to control bleeding and prevent hysterectomy
(thereby preserving future fertility).
Alouini132 reported the mean duration of BT was 7 hours and a mean blood loss of 1600ml. An attempt to remove the balloon
before 24 hours can be considered.
A retrospective study by Howard133 correlating timing of intervention and outcomes, determined that use of tamponade at an
earlier estimated blood loss had higher nadir hemoglobin, reduction blood transfusion, fewer intensive care unit admissions,
and fewer hysterectomies when compared to arterial embolization. In addition, all 19 women who subsequently wanted a
pregnancy were successful.
Tamponade has also been used in conjuction with CS and uterine compression sutures. Success rates measured by Olsen (n=35)
were lower at 67% when used in conjuction with CS.134 In this study, a failure was defined as a need for further intervention
required to control bleeding (interventional radiology, compression sutures, or hysterectomy). Failure was greater in Caesarean
delivery versus vaginal delivery (67% vs. 16%, P = 0.031), use of pre-delivery oxytocin (67% vs. 28%, P = 0.003), need for
ICU admission (58% vs. 4%, P = 0.0003) and need for transfusion (5.4 RBC vs. 1.6, P = 0.007).134
The combination of elective CS + BT + pelvic artery embolization (PAE) in cases of accreta was successful in 97% of women.135
In this study, 41 / 42 uteri were preserved.
External Aortic Compression

In women with active hemorrhage, external aortic compression with non-pneumatic anti-shock garment (NASG) has been
shown to reduce blood loss and associated maternal morbidity and mortality136 without compromising vascular flow to the
lower limbs.137,138
Uterine Artery Ligation (UAL)
Uterine compression sutures are considered safe and effective in treating PPH in 75% (95% CI 67 to 81) of women.127,139,140
A 2012 prospective study showed a 96% success rate with uterine artery ligation in cases of sever PPH unresponsive to
intervention thus avoiding the need for hysterectomy.141
Uterine Artery Embolisation (UAE)
Uterine artery embolization has been used as an alternative to surgery for treatment of PPH refractory to treatment.142
Success rates vary from 78-96 % for emergency and prophylactic embolization.141,143,144
Factors predictive of failure were DIC, need for massive transfusion, hemodynamic instability, and hemoglobin level < 95 g/dL. 141,144
Subsequent pregnancies are possible although involve higher risk.
Inoue’s study143 measured forty women became pregnant after UAE, and the pregnancy rate among those who desired fertility
was 52.6%. Twenty eight gave birth, including four preterm deliveries. Five (16.7%) were associated with a hysterectomy due to
placenta accreta.
Uterine Compression Sutures
Retrospective observational studies by Poujade145, Alouini,146 and Ibrahim147, and Chai148 found that uterine compression sutures
were highly successful in controlling atonic PPH, with few uterine synechia when the uterine cavity was evaluated three to six
months later. One patient had a successful pregnancy 18 months after uterine compression suture.
A cohort study of 252 women who had PPH and a B-Lynch suture was not associated with an increased risk of future adverse
pregnancy outcomes.149
A 2012 retrospective study of 13 patients with severe atonic PPH who failed conventional therapy were treated using a vertical
compression suture technique.150 This suture included another suture added at the fundus to prevent slippage. This technique had
a 92.2% success rate for stopping bleeding.150
A 2011 prospective study by Yoongfound that for all of the 11 women with atonic PPH, uterine tamponade with combined Bakri
balloon and uterine compression sutures was successful in avoiding hysterectomy.151
A prolonged delay152 of two to six hours between delivery and uterine compression suture was associated with a four-fold
increase in hysterectomy.
Uterine Inversion
• Occurs in 1/25 000 deliveries
• Often is iatrogenic and more common in grand multiparous (i.e., parity > 5) women
• The placenta appears 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 APH chapter)

• Placenta accreta is the abnormal implantation of the placenta with villus attachment to the myometrium resulting in
loss of the normal cleavage plane (see Antepartum and Intrapartum Hemorrhage chapter)
• Occurs in 1/2500 deliveries (ten-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 PPH153, massive hemorrhage and peripartum hysterectomy154
• Most common in women with prior uterine surgery, especially with an anterior placenta, and increases with increased
number of CS155-157
• Women with placenta previa and grand multiparas 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
hysterectomy.158,159
• 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 diagnosed antenatally have better outcomes with less need for blood transfusions and less likely to attempt to remove
the placenta.160
There is less PPH and blood transfusion when the placenta is left in to either conserve the uterus or prior to hysterectomy.149
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.
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 CAB’s cannot be overstated.
5. Resuscitate and call for additional help.
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119. Lokugamage AU, Sullivan KR, Niculescu I, Tigere P, Onyangunga F, El RH, et al. A randomized study comparing rectally
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120. Hofmeyr GJ, Walraven G, Gulmezoglu AM, Maholwana B, Alfirevic Z, Villar J. Misoprostol to treat postpartum
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121. Walraven G, Dampha Y, Bittaye B, Sowe M, Hofmeyr J. Misoprostol in the treatment of postpartum haemorrhage in
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124. Tindell K, Garfinkel R, Abu-Haydar E, Ahn R, Burke T, Conn K, et al. Uterine balloon tamponade for the treatment of
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125. Khalil MI, Al-Dohami H, Aldahish MM. A method to improve the effectiveness of the Bakri balloon for management of
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126. Majumdar A, Saleh S, Davis M, Hassan I, Thompson PJ. Use of balloon catheter tamponade for massive postpartum
haemorrhage. J Obstet Gynaecol. 2010;30:586-93.
127. Fotopoulou C, Dudenhausen JW. Uterine compression sutures for preserving fertility in severe postpartum haemorrhage:
an overview 13 years after the first description. J Obstet Gynaecol. 2010;30:339-49.
128. Rossi AC, Lee RH, Chmait RH. Emergency postpartum hysterectomy for uncontrolled postpartum bleeding: a systematic
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129. Cortet M, Deneux-Tharaux C, Dupont C, Colin C, Rudigoz RC, Bouvier-Colle MH, et al. Association between fibrinogen
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Appendix
Management of Postpartum Hemorrhage
HEMOSTASIS Algorithm161
H help
E etiology/ ensure uterotonics and blood
M massage
O oxytocin/prostaglandins
S shift to OR with compression (uterine or antishock garments)
T tamponade test (of effective hemostasis)
A apply compression sutures
S systemic pelvic devascularization
I intervention radiology
S sub/total hysterectomy
Contents of Obstetric Hemorrhage Equipment Tray

Access/exposure
3 vaginal retractors
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
Uterine Compression Sutures

B-Lynch Technique
Reproduced from B-Lynch et al. Br J Obstet Gynaecol 1997;104(3):372-5,162

with the permission of the Royal College of Obstetricians and Gynaecologists.
Cho Technique
Reproduced from Cho et al. Obstet Gynecol 2000;96(1):129-31.163 Used with permission.
Chapter 17
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, arterial disease, cardiac disease, diabetes, metabolic
syndrome, and mortality.1-7 Preclampsia is a contributing cause of acute renal failure in Canada.8 Women with severe preeclampsia
have poor health-related quality of life, including problems with social functioning, emotional well-being, and in mental health,
mostly related to the neonatal problems the mother has to deal with in the postpartum period.9 Women with preeclampsia
occurring prior to 37 weeks are at a significant risk of stillbirth, abruption, spontaneous preterm rupture of membranes, and
small for gestational age (SGA) babies in subsequent pregnancy, even in the absence of preeclampsia in the subsequent
pregnancy.10 There is evidence that hypertensive disorders of pregnancy, particularly in pre-existing (chronic) hypertension, and
independent of antihypertensive use, are associated with increased risk of congenital malformations in the newborn particularly
for esophageal atresia, ventricular septal defects, and hypospadias.11,12 There is also some evidence to suggest that risk of
depressive symptoms in adulthood is increased in offspring of women who suffered preeclampsia.13 Evidence has also shown
that these offspring may have increased risk for impaired cognitive functions in childhood and adulthood,14 are prone to being
hypertensive by age 21,15 and demonstrate an abnormal lipid profile in early adulthood.16
While the incidence of eclampsia has dropped in Canada from 15 per 10 000 deliveries in 2004/2005 to 8 per 10 000 deliveries
in 2010/2011,17 the complications resulting and associated with eclampsia remain significant. Eclampsia is significantly associated
with maternal death, need for assisted ventilation, adult respiratory distress syndrome (RDS), acute renal failure, embolism and
neonatal death, neonatal RDS and SGA babies.18 All obstetrical caregivers will eventually manage a woman with hypertension
in pregnancy or the complications arising from this condition. The management options for hypertensive disorders of pregnancy
(HDP) may vary based on the availability of resources. The roles for rural and remote primary obstetrical caregivers may be quite
different when factors such as geography, weather, and access to specialists or Level III hospitals are considered. Primary caregivers
may be faced with emergent situations such as stabilizing or treating women with hypertensive disorders of pregnancy.
Hypertensive Disorders of Pregnancy 1

Definitions/Terminology
Classification of the Hypertensive Disorders of Pregnancy19
1. Chronic Hypertension
2. Gestational Hypertension
3. Preeclampsia—de novo (in previously normotensive woman) or superimposed on Chronic Hypertension
4. White coat hypertension
Definitions:
Hypertension: Systolic Blood Pressure (sBP) ≥ 140 or Diastolic BP (dBP) ≥ 90 mmHg
(see Diagnosis section for measurement technique)
Severe Hypertension: Systolic BP ≥160 or Diastolic ≥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 along with one or more of the following new onset condtions:
1. Proteinuria
2. Other maternal organ dysfunction (renal, liver, neurologic, hematologic)
3. Uteroplacental dysfunction (fetal growth restriction)
White Coat Hypertension: Systolic BP ≥ 140 or Diastolic BP ≥ 90mmHg in office/clinic, but lower with home or
ambulatory BP monitoring.
Eclampsia: The occurance of seizures in a preeclamptic patient that cannot be attributred to other causes.19

Incidence 17,20-22
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.23
In Canada, the incidence of Chronic Hypertension, Gestational Hypertension and Preeclampsia have remained relatively stable
from 2004/2005 – 2010/2011. The incidence of Eclampsia has dropped (from 1.5 to 0.8 per 1000 deliveries)17
Condition Incidence in pregnancy (%) Risk of developing preeclampsia (%)
Preeclampsia 1
Chronichypertension 0.5 2624-26
Gestational hypertension 5 2527
Gestational hypertension before 34 weeks’ gestation 3528,29
Eclampsia 0.08

According to the Canadian Perinatal Surveillance System report of 2013 the overall maternal mortality in Canada was 6.1 per
100 000 deliveries in 2011. It has fluctuated between 6.1 and 11.9 since 1998. Hypertensive disorders of pregnancy are the
second most common cause of direct maternal mortality, tied with obstetric embolism; postpartum hemorrhage being the most
common cause. Eclampsia remains one of the severe maternal morbidities,associated with need for assisted ventilation, adult
RDS, acute renal failure and embolism.30

DIAGNOSIS ASSOCIATED WITH MATERNAL DEATHS

CANADA (EXCLUDING QUEBEC),* 2002-2003 TO 2010-2011 FISCAL YEARS
Diagnosis Number of maternal deaths Maternal deaths per 100 000 hospital
deliveries (95% CI)
Diseases of the circulatory system 76 3.1 (2.5–3.9)
Other indirect causes 59 2.4 (1.9–3.1)
Postpartum hemorrhage 39 1.6 (1.1–2.2)
Hypertension complicating pregnancy, childbirth 34 1.4 (1.0–1.9)
and the puerperium
Obstetric embolism 34 1.4 (1.0–1.9)
Major puerperal infection 22 0.9 (0.6–1.3)
Ectopic and molar pregnancy /abortive outcome 21 0.9 (0.5–1.3)
Antepartum hemorrhage, abruptio placentae, and 15 0.6 (0.3–1.0)
placenta previa
Source: Canadian Institute of Health Information (CIHI), Discharge Abstract Database
* 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 2013: a report from the Canadian Perinatal Surveillance System.
Ottawa: Public Health Agency of Canada; 2013.30 Used with permission
Morbidity and Mortality with Preeclampsia21,31

All caregivers must be able to promptly recognize the signs, symptoms, and laboratory findings of preeclampsia. Caregivers must
fully appreciate the seriousness of preeclampsia, its potential for multi-organ involvement, and the risks for fetal, perinatal, and
maternal morbidity and mortality.

A) Maternal
• Stroke ( Risk is with a systolic BP ≥ 160 mm Hg)
• Pulmonary edema
• Hepatic failure
• Jaundice
• Seizure (eclampsia)
• Acute renal failure
• Maternal death
B) Fetal
• Oligohydramnios
• NICU admission
• Prematurity due to maternal indication for delivery
• Fetal death (3 fold increase)32
Morbidity and Mortality with chronic Hypertension

Patients with chronic hypertension will develop superimposed preeclampsia in 26% of cases. Those who do NOT develop
preeclampsia still have increased risks including:24
• Caesarean section rate 41%
• Perinatal mortality of 40 per 1000
• SGA baby < 2500 gm
• NICU stay for 20% of neonates
Congenital anomalies, particularly cardiac, independent of use of antihypertensive medications33,34
Preconception couselling is valuable for optimizing BP control with medications safe during pregnancy, and initiation of ASA
(see Management and Prevention sections, below.)

Pathogenesis
Preeclampsia
Despite decades of research, the exact etiology of preeclampsia is unknown. The most popular theory describes a two-stage
process where Stage 1 is inadequate placental perfusion, and Stage 2 is the maternal syndrome resulting from the materials
generated by this insult.35,36
An emerging theory is that preeclampsia is not one disease, but rather has several subtypes. This would account for the varying
clinical presentation and lack of highly useful predictive tests or preventive interventions.36

Diagnosis
1) Maternal Evaluation-Clinical
A) Blood pressure
Blood pressure should be determined under the following conditions:
• A minimum rest period of 10 minutes after arrival.
• Sitting position with upper arm at heart level.
• Appropriate size cuff (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 should NEVER be placed over clothing.
• Use a mercury or aneroid sphygmomanometer since automated machines may underestimate systolic and
diastolic BP by 10–5 mm Hg, especially in hypertensive patients. If an automated BP monitor is used, make sure
that it is calibrated against a mercury or aneroid sphygmomanometer.21,37-39 Once the diagnosis of hypertension
is established, an RCT on follow-up using an automated BP machine (Omron) versus a Hg sphygmomanometer,
demonstrated that 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.40
• Korotkoff sound V (disappearance of pulse sounds) should be used to define diastole.41
• If the BP is consistently higher in one arm, the arm with the higher values should be used for all BP measurements.
Ambulatory blood pressure monitoring using an automated blood pressure machine is useful in ruling out “White Coat”
hypertension.42
Blood pressure criteria for a diagnosis of hypertension in pregnancy 31
• A systolic BP of ≥ 140 mmHg or a diastolic BP of ≥ 90 mm Hg based on at least two measurements taken in the same
arm ≥ 15 minutes apart after an initial rest period of > 10 minutes.
• Severe hypertension should be defined as a systolic BP ≥ 160 mm Hg or a diastolic BP ≥ 110 mm Hg. sBp over
160mmHg is associated with increased risk of maternal stroke.43
NOTE: An incremental/relative rise of greater than or equal to 30/15 mm Hg in systole or diastole is NOT a criterion to define a
patient as hypertensive as it is within the normal variation in BP seen throughout pregnancy.
Mean arterial pressure (MAP) is NOT 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 nullipara, dBP drops to a nadir at 19 weeks while the sBP drops
to a nadir at 17 weeks. In the multipara, the nadir occurs at 20 weeks for diastole, and at 18 weeks for systole. In general, women
with high BMI had BP readings that were 4 mmHg higher than those with normal BMI.44
FOLLOWING CONFIRMATION OF HYPERTENSION, ASSESS FOR SYMPTOMS AND SIGNS SUGGESTING
INVOLVEMENT OF OTHER MATERNAL ORGAN SYSTEMS:
A) Central nervous system
• Presence of a severe headache

• Visual disturbance (e.g., blurring, scotomata)
• Tremulousness, irritability, somnolence
• Hyperreflexia
B) Cardiorespiratory
• Chest pain
• Dyspnea—Check maternal 02 saturation.
• Distended neck veins
C) Hematologic
• Bleeding
• Petechiae
D) Hepatic
• RUQ/epigastric pain
• Severe nausea and vomiting
E) 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.)

Right upper quadrant (RUQ) pain, headache, and visual disturbances are potentially ominous symptoms
requiring immediate assessment.
Headache, visual disturbances, and vomiting had significant sensitivity in predicting eclampsia, while
epigastric pain was significantly sensitive for predicting HELLP syndrome.45
In patients with established preeclampsia, epigastric pain, and chest pain were moderate predictors of
adverse maternal and perinatal outcomes.46
2) Investigations
All women with new onset hypertension after 20 weeks gestation should have the following investigations:
• Complete blood count (cbc)
• Creatinine, electrolytes
• Liver enzymes (AST, ALT)
• 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 thrombocytopenia (<150x109/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.31 Proteinuria of 1+ on dipstick should be confirmed by a 24 hour urine collection
because of significant false positive and false negative results.47-51
• 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 1.0.52

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.53-55 Therefore, once proteinuria >300mg/24 hours
has been documented, there is no need to repeat this measurement.
NOTE: Early onset (< 34 weeks) preeclampsia or severe hypertension warrant consideration of further investigations looking for
underlying conditions or alternate diagnoses.
Appendix A provides the differential diagnoses associated with laboratory abnormalities encountered in women with
preeclampsia, see Table 4 of Reference #21.
Risk Factors
A) Risk Factors For Predicting Onset of Preeclampsia

Adapted from Milne et al.56
There is currently no clinically useful model for the prediction of preeclampsia.57 Maternal characteristics and maternal history
will identify 30% of women who develop preeclampsia.58
Risk markers of greater importance are highlighted in grey in the table below. Those which are in bold font within their shaded
areas confer the highest risk.
First Trimester Markers Second or Third

Trimester Markers
Demographics Past History Current Pregnancy
• Previous preeclampsia59 • Multiple pregnancy

• Anti-phospholipid
antibodies60
• Pre-existing medical
condition(s)
• hypertension or first visit
dBP ≥ 90 mm Hg
• renal disease or first visit
proteinuria
• diabetes mellitus
• Collagen vascular disease
• Periodontitis61

First Trimester Markers Second or Third

Trimester Markers
Demographics Past History Current Pregnancy
• Maternal age • Obesity (BMI ≥ 35)62 • First ongoing pregnancy

≥ 40 yr or • Family history of preeclampsia • Inter-pregnancy interval ≥ 10 yr
<18 yrs (mother or sister)63 • First visit sBP ≥ 130 mm Hg or
dBP ≥ 80 mm Hg
• Ethnicity: • Non-smoking64 • Inter-pregnancy interval < 2 yr • Systolic BP > 120 mm Hg

Nordic, Black, • Heritable thrombophilias • Reproductive technologies to • Abnormal Maternal Serum Screen
South Asian, or • Factor V Leiden conceive (subfertility) (MSS)
Pacific Island • Protein S deficiency • New partner (first pregnancy or • Abnormal uterine artery Doppler
• Lower • Antiphospholipid short duration of exposure) velocimetry
socioeconomic antibodies60 • Gestational trophoblastic disease • Excessive weight gain in
status • Increased pre-pregnancy • Infection during pregnancy (e.g., pregnancy
triglycerides UTI, periodontal disease) • Cardiac output > 7.4 L/min
• Family history of early-onset • Elevated uric acid
cardiovascular disease • Investigational laboratory
• Cocaine and/or metamphetamine markers
use
Numerous studies have examined 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. However, the predictive values are too low to be clinically
useful at this time.36,65
Abnormal levels of some of these markers, such as PAPP-A (pregnancy associated placental protein A) may be reported as part of
an otherwise normal prenatal genetic screening test. Those women do warrant increased surveillance.
B) Risk Factors for Predicting Maternal and Perinatal Morbidity and Mortality in
Patients 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 occuring within 48 hours and up to seven days. (AUC ROC
0.88)66 An oxygen saturation (SpO2) of less than 93% was very predictive of poor maternal and neonatal outcome within
48 hours.67 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)

Proteinuria in preeclampsia, as assessed by dipstick, urinary protein-creatinine ratio or 24-hour urinary collection, was not
strongly associated with maternal nor perinatal adverse outcomes.68
Elevated levels of uric acid are not meaningfully associated with adverse maternal or perinatal outcome. Elevated uric acid level
should not determine timing of delivery.57,69
Prevention
CALCIUM SUPPLEMENTATION
• Calcium supplementation (≥ 1 g/day) or an increase in dietary calcium intake (3–4 dairy servings per day) has only
been shown to decrease the rate of preeclampsia in low and middle income country populations with a low dietary
intake of calcium (< 600 mg/day)70-72. A large multicentre study in the United States showed no benefit of calcium
supplementation in reducing the rate of preeclampsia.36
LOW DOSE ASPIRIN

• In higher risk populations, particularly those with chronic hypertension, diabetes or previous preterm preeclampsia,
low-dose aspirin (e.g. 81mg tablets) results in a small (10-17%) decrease in preeclampsia.73,74 The NNT approaches
50 and initiation of low dose ASA before 16 weeks is suggested.57
• In a low risk population, primary prevention of preeclampsia with aspirin remains unproven at the present time. It is
currently a topic of research.
• There is no evidence of adverse effects of low dose aspirin on either the mother or newborn.
• Aspirin is taken once daily at bedtime, started pre-pregnancy or as early in pregnancy as possible, and continued until
term. Benefits were not observed when ASA was initiated after 16 weeks.75

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, death) and severe fetal complications (placental abruption, growth restriction, stillbirth)
• Symptomatic support
• Delivery
1) Antihypertensive Therapy
The use of antihypertensive medication reduces the risk of developing severe hypertension and its potential sequelae
(cerebrovascular accident) in the mother. 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.57
There is insufficient evidence to determine the ideal BP associated with optimal maternal and perinatal outcomes. A reasonable
goal is to keep sBP 130-155mmHg and dBP 80-105mmHg.31
In the presence of some co-morbidities, 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)

Obstetric consultation is indicated.
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 labetolol, intravenous hydralazine, and oral nifedipine are commonly used to treat acute, severe hypertension. The
pharmacokinetics of intravenous labetalol and intravenous hydralazine, are very similar. The onset of action is five to ten minutes
and peak action occurs in about 30 minutes. Use caution with repeat doses before 30 minutes as maternal hypotension may
result. The first choice is either oral nifedipine or IV labetalol because hydralazine was associated with more adverse outcomes
including maternal hypotension, placental abruption, abnormal (non-reassuring) fetal heart rate patterns, Caesarean section,
and maternal oliguria.76
Agent Dose Route Onset Peak Caution
LABETALOL Initial dose 20mg; IV 5 minutes 30 minutes Women with asthma or
repeat 20-80mg every heart failure; May cause
30 minutes; maximum neonatal bradycardia
300mg
NIFEDIPINE Initial dose 10mg; Swallowed (not 30 minutes 45 minutes Immediate release
Repeat 10 -20mg every chewed) preparation is used here.
45 minutes; Maximum (PA no longer available
50mg in Canada, and XL not
for acute therapy.)
HYDRALAZINE Initial dose 5mg; IV 5 minutes 30 minutes Maternal hypotension
Repeat 5-10mg every
30 minutes; Maximum
20mg
References:31,65,77
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. They are both calcium antagonists. However,
concurrent use was NOT shown to cause a potentiation of the hypotensive effect in a large retrospective review.78
In management of severe hypertension, oral labetalol and oral methyldopa are less effective in lowering BP than Nifidipine.
However, they remain reasonable choices when Nifidipine is not available or intravenous access is not feasible.79

Maintenance Therapy (Chronic Hypertension)

As with the treatment of acute severe 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 which 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.80
Studies and meta-analyses, including the CHIPS (Control of Hypertension in Pregnancy Study)81 have failed to show that blood
pressure targets lower than 155 mmHg systolic or 105 mmHg diastolic lead to a reduction in onset of preeclampsia, HELLP, DIC,
eclampsia, liver failure, perinatal deaths, prematurity, SGA, NICU admissions and NICU length of stay.82
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.
Oral antihypertensive medications commonly used in Canada are listed below. No differences in maternal or fetal outcomes have
been demonstrated.83,84
Agent Dose Caution
LABETALOL Initial dose 100mg bid; Maximum 400mg tid Asthma
(1200mg/day)
NIFEDIPINE XL Initial dose 20mg OD; Maximum 60mg bid Aortic stenosis ENSURE XL PREPARATION
METHYLDOPA Initial dose 250mg bid; Maxium 500mg qid Depression
(2g/day)
References31,77,85
NOTE: Angiotensin converting enzyme (ACE) Inhibitors and angiotensin receptor blockers (ARB's) are contraindicated because of
IUGR, prematurity, oligohydramnios, and anomalies in pregnancy. Atenolol is not recommended due to increased rates of IUGR,
hypotension and bradycardia.86,87

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 adverse effects of some medications. 33,34
2) 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 that is often routinely
administered prior to regional anesthesia should be avoided. The type of fluid is not as critical as the volume of fluid. Hypotension
and shock may develop at lesser degrees of hemorrhage in the third stage of labour 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.88 In the presence of oliguria, a careful assessment of volume
status and renal function is indicated.23 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
Do not administer dopamine or furosemide in the presence of persistent oliguria occurring prior to delivery. (See Postpartum
Management section regarding furosemide use after delivery.)
Consider thromboprophylaxis for all patients that are immobilized or bedridden for prolonged periods.21
Oliguria at this point should not precipitate any (other) specific intervention except to lower the threshold for considering
early delivery.

3) 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.89
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, anesthesiology, hematology, pediatrics)
4) 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 seizures Neither maternal symptoms nor blood pressure levels reliably predict who
will seize. However, because of side effects and cost, selective use of seizure prophylaxis is generally recommended for
women with: 31,57,77,90
• 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 persistant), and/or elevated liver enzymes
• Thrombocytopenia (<100x109/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 indicated91 MgSO4 is
superior to phenytoin (Dilantin) for the prevention of seizures, and is superior to either diazepam (Valium) or phenytoin for
preventing recurrent seizures.92-94 MgSO4 reduces the incidence of seizures by 50%.95

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 20–30 minutes followed by 1 g/hour IV 23 163
• a recurrent seizure may require a second 2–4 g IV bolus
• Intramuscular: When intravenous access is unavailable, MgS04 may be given intramuscularly (IM). The process for
IM MgSO4 administration is:97
• 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
• Side effects of MgSO4—weakness, paralysis, cardiac toxicity, loss of patellar reflexes, respiratory depression. The
data, however, show that these risks are very low.98
• Monitor—reflexes, respiration, level of consciousness, hourly urine output. Magnesium is excreted in the urine.
Clinically, magnesium serum levels can be estimated as follows:97
Blood level mmol/L
Reflexes present 2 – 3.5
Loss of patellar reflexes 4–5
Respiratory Depression ≥6
• 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%).78 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.
• Routine monitoring of serum magnesium levels is not supported by evidence.21
The antidote to magnesium is: 10 cc of 10% calcium gluconate, IV over 3 minutes.

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 20–30 minutes and then a maintenance dose at 1 g/hour IV (if recurrent seizure
while on MgSO4, re-bolus with 2 g IV over 20–30 minutes)21
• 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
• Watch patient for development of DVT, CVA, or cardiomyopathy as these patients are at risk to develop these
complications after the seizures99
Protocols for the use of magnesium sulphate should be established, immediately available in every
Birthing Unit, and include the following:
• Preparation
• Assessments prior to administration
• Administration protocol
• Assessment for side effects / drug interactions
• Management of toxicity
• Documentation
5) 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 prior to CS
• Platelet count <50x109/L, platelet count is falling, or a coagulopathy exists: Consider blood product/platelet
transfusion
• Platelet count <50x109/L: Consider the administration of corticosteroids to improve maternal hematological and
biochemical indices
• Platelet count <20x109/L: Platelet transfusion prior to both CS and vaginal birth
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.100
Patients with HELLP syndrome are at risk to develop eclampsia, hence MgSO4 should be administered.100
6) 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.
Principles to be addressed prior to transport include:
• Maternal blood pressure is stable

• Fetal condition is stable
• Seizure prophylaxis if necessary. Consider MgSO4 IM dose (see above) for safety during transport
• Intubation/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 intubate,
ventilate, and administer any necessary medications
• A transport protocol should be readily available in every unit

7) Delivery
DELIVERY OF THE PLACENTA IS THE ONLY CURE FOR PREECLAMPSIA. DELIVERY IS BASED ON THE FOLLOWING
PRINCIPLES:
• Any of the Hypertensive Disorders of pregnancy can progress quickly to endanger mother and baby
• Timely delivery minimizes maternal and neonatal morbidity and mortality
• 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 34 weeks’ gestation101
• 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 represent a very heterogeneous group who vary enormously in the
severity and stability of their conditions.The following are broad guidelines regarding timing of delivery. For women with
Chronic Hypertension or Gestational Hypertension 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 dysfuntion (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 34–36 6/7 weeks, showed no reduction in adverse maternal
outcomes but a significant increase in RDS (RR 3, 95% CI 1.3 to 6.99, NNH 25) with that risk being higher at 34 weeks than
36 6/7 weeks.102
8) 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 3–6 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 two days or more after delivery
Women requiring seizure prophylaxis (preeclampsia) should be treated with magnesium sulphate during labour and 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 any end-organ dysfunction. Laboratory
investigations should be directed toward the particular end-organ that has been affected. Of note, for women who had severe
hypertension in pregnancy, the addition of postpartum furesomide (40 mg by mouth every 24 hours) to the antihypertensive
regimen in the postpartum period appears beneficial in lowering BP, in reducing the need for other antihypertensive
medications, and in shortening length of stay.103,104
Postpartum thromboprophylaxis should be considered, particularly if there has been antenatal bed rest for more than four days,
patient obesity, or a CS.
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 co-morbidities. Antihypertensive agents acceptable for use in breastfeeding include:
nifedipine XL, labetalol, methyldopa, captopril, and enalapril.

Discharge from the 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 prior to discharging the woman. It is reasonable to discharge women whose BP remains at < 160/ 110 mm Hg for
at least 24 hours.31
NOTE: Although rare, new onset preeclampsia has been documented up to three weeks after delivery in an otherwise normal
pregnancy. Advanced maternal age, being black or hispanic, diabetic, or obese seem to be associated risk factors for these
occurrences.105
Points to Remember in Management:

• Do not reduce blood pressure too rapidly or too low: Placental perfusion can be compromised. Keep systolic
pressure <160mmHg to prevent maternal stroke.
• Do not fluid overload: Pulmonary edema is more dangerous than transient renal compromise
• Do not fluid overload
• MgSO4 decreases seizure risk by 50%
• Use an interprofessional approach:
• Obstetrical care provider
• Anesthesiology
• Pediatrics / neonatology
• Nursing
• Internal medicine / hematology

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. Currently there are no therapies that effectively prevent preeclampsia. There are no investigations, beyond maternal
history, that are clinically useful to predict preeclampsia.

References
1. McDonald SD, Malinowski A, Zhou Q, Yusuf S, Devereaux PJ. Cardiovascular sequelae of preeclampsia/eclampsia: a
systematic review and meta-analyses. Am Heart J. 2008;156:918-30.
2. Magnussen EB, Vatten LJ, Smith GD, Romundstad PR. Hypertensive disorders in pregnancy and subsequently measured
cardiovascular risk factors. Obstet Gynecol. 2009;114:961-70.
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Appendix
Laboratory and Imaging Abnormalities encountered in women with the Hypertensive Disorders of Pregnancy 31
Investigations for Diagnosis Description in women with preeclampsia Description in women with other conditions
MATERNAL TESTING
Urine testing
Urinalysis (routine and microscopy Proteinuria (as discussed under Proteinuria) without Hemoglobinuria (dipstick ‘hematuria’ without RBCs):
with/without additional tests for RBCs or casts hemolytic anemia
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 risk of severe May be decreased in any cardiorespiratory complication
complications (including non-respiratory) (e.g., pulmonary embolism)
CBC and blood film
Hemoglobin ↑ due to intravascular volume depletion ↑ due to volume depletion from any cause (e.g.,
vomiting)
↓ if microangiopathic hemolysis (with HELLP)
↓ if microangiopathic hemolysis from other cause
↓ with any chronic anemia (nutritional or
myelodysplasia)
↓ with acute bleeding of any cause

WBC and differential ↔ ↑ due to neutrophilia of normal pregnancy

↑ with inflammation/infection
↑ with corticosteroids
Platelet count ↓ associated with adverse maternal outcome ↓ with gestational, immune (ITP), or thrombotic
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 ↑ with DIC which is usually associated with placental May be ↑ in APS, DIC from other causes including
abruption sepsis, amniotic fluid embolism, stillbirth, massive
hemorrhage, hemangiomas, shock
↑ is associated with adverse maternal outcome
↑ is prominent in AFLP
Fibrinogen ↓↔ ↓ with all causes of DIC including massive hemorrhage,

genetic disorders
↓ more profound with AFLP than with HELLP
Usually normal in TTP-HUS (ADAMTS13 vWF cleaving
protein may be moderately decreased in HELLP106 but
ADAMSTS 13 antibody should be absent)
Serum chemistry
Serum creatinine ↑ due to hemoconcentration and/or renal failure ↑ with other acute or chronic kidney disease
↑ associated with adverse maternal outcome Renal failure prominent in malignant hypertension,
TTP-HUS (along with thrombocytopenia), AFLP (along
with liver dysfunction)
Serum uric acid ↑ associated with adverse maternal outcome ↑ with dehydration, medication (e.g., HCTZ), genetic
causes
Glucose ↔ ↓ with AFLP, insulin therapy

AST or ALT ↑ associated with adverse maternal outcome ↑ with AFLP and other ‘PET imitators’† but to a lesser
degree, 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 ↑ which may be prominent – the ↑ is associated with ↑ with AFLP, intravascular hemolysis
adverse maternal outcome
↑ LDH/AST ratio (>22) with TTP-HUS107
Bilirubin ↑ unconjugated from hemolysis or conjugated from (early) ↑ in AFLP, ↑ with hemolytic anemia, other liver
liver dysfunction disease with dysfunction, genetic diseases
Albumin ↓ associated with adverse maternal and perinatal ↓ as negative acute phase reactant with acute severe
outcomes illness, malnutrition, nephritic syndrome, crystalloid
infusion
FETAL TESTING Abnormalities are not specific to the cause of poor placentation and/or placental dysfunction
Uterine artery Doppler velocimetry Unilateral/bilateral notching, or elevated pulsatility index or resistance index may support a diagnosis of placental
insufficiency including preeclampsia
Fetal monitoring Abnormal or atypical FHR tracing (e.g., decreased variability)
Deepest amniotic fluid pocket Oligohydramnios associated with adverse perinatal outcomes90
Ultrasonographic assessment of Usually intrauterine fetal growth restriction (typically asymmetrical but can be symmetrical if early and/or severe)
fetal growth
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

Chapter 18
Preterm Labour and Preterm Birth
Definition
Preterm labour (PTL) is defined as regular uterine contractions with progressive cervical dilation and/or effacement at greater
than 20 weeks and less than 37 weeks 0 days gestation. Preterm birth (PTB) is delivery before 37 weeks 0 days gestation.1
Long-term adverse sequelae of preterm birth occur mainly in those infants born at less than 34 weeks’ gestational age (GA).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
pregnancies deliver before 34 weeks. Neonates born at greater than 34 weeks’ GA in Level III centres have survival rates
of 99% to 100%, although they may require longer hospital stays due to feeding and other difficulties.7,8
The importance of accurate dating cannot be overstated in the management of preterm labour. A difference of 10 days can
change the chance of survival from 10% (at 22+ weeks) to over 40% (at 24 weeks).7 For this reason, accurate dates must 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 41 +0 weeks.(I-A)9
By 20 weeks’ gestation, all pregnant women should know their EDD from accurate menstrual data and/
or dating from an ultrasound.9
Preterm Labour and Preterm Birth 1


Preterm birth is a major cause of perinatal morbidity and mortality and is estimated to account for 75% of neonatal mortality,
excluding lethal malformations.2,3,10,11 The short-term complications of preterm birth include:
• Respiratory distress syndrome (RDS)
• Intraventricular hemorrhage (IVH)
• Necrotizing enterocolitis (NEC)
The long-term sequelae of preterm birth (especially less than 28 weeks’ gestation) include:
• CNS complications (e.g., cerebral palsy)
• Neurodevelopmental delay12
• Respiratory complications (e.g., bronchopulmonary dysplasia)
• Blindness and deafness
Etiology and Risk Factors

The causes of preterm birth can be divided into three main categories:13-16
1. Preterm pre-labour rupture of membranes (PPROM) (30–40% of preterm births)
2. Spontaneous preterm labour with intact membranes (40–50% of preterm births)
3. Indicated (20–30% of preterm births)
Clinical maternal or fetal conditions associated with indicated preterm birth include:
• Preeclampsia
• Complicated insulin-dependent diabetes mellitus
• Abnormal fetal surveillance
• Abruption
• Intrauterine death
• Monochorionic, monoamniotic twins
Risk factors for spontaneous preterm labour and birth include:1,17,18

• Reproductive history:
• previous spontaneous preterm birth
• advanced reproductive technologies19
• Antepartum bleeding
• PPROM
• Cervical/uterine factors
• cervical insufficiency, uterine malformation,17 and fibroids20
• excisional cervical treatment for cervical intraepithelial neoplasia21-23
• Fetal/intrauterine factors
• multifetal gestation
• fetal anomaly
• polyhydramnios
• Infection
• chorioamnionitis
• bacteriuria
• periodontal disease24-26
• current bacterial vaginosis with a prior preterm birth27
• malaria (particularly in developing countries)
• Demographic factors
• low socioeconomic status
• single women
• low level of education
• maternal age < 18 and > 35 years

• Lifestyle issues
• illicit drugs
• smoking (e.g., smoking > 10 cigarettes/day)
• physical abuse28
• inadequate prenatal care
• low pre-pregnancy weight (weight < 55 kilograms)
• poor weight gain in pregnancy29
• stress30
• obesity31
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.32-34 The main benefit of assessing fFN has been shown to be its negative predictive value. A negative
fetal fibronectin 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 fetal fibronectin (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).
A number of Canadian centres currently use fFN in the assessment of women presenting with threatened preterm labour. If fFN is
being used, it is advised to obtain the swab before a cervical digital examination is performed. Doing a digital examination first
may give false/positive fFN results.
Cervical Length Measured by Transvaginal Ultrasonography
Cervical length has a normal distribution throughout gestation. The mean length at 24 weeks’ to 28 weeks’ gestation is 34 mm
to 35 mm.35-37
The probability of preterm birth 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.36-43 Cervical length may be useful in either a research trial or after discussion with your
tertiary care centre.

Funneling of the internal cervical os may be seen on ultrasound imaging but is only significant 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.36,37,43,44
Routine prenatal cervical length screening of all women by transvaginal ultrasound is not supported by available evidence.45
However, cervical length measurement can be used for women identified to be at increased risk of preterm birth,43 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 avoid unnecessary interventions.
The value of fetal fibronectin and ultrasound assessment of cervical length is that these tests may improve the diagnostic
accuracy of preterm labour, reduce unnecessary transfer, hospitalization, and intervention, and, as a result, improve allocation
of resources.46 Fetal fibronectin testing and ultrasound assessment of cervical length are currently being used in some Canadian
centres in order to assist in the diagnosis 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.
Diagnosis
1. Women should be educated early in their antepartum care to be vigilant for signs and symptoms of impending
preterm labour and to contact her caregiver. These include:
• regular contractions
• vaginal fluid loss
• vaginal bleeding
• change in pelvic pressure, low dull backache, or vaginal discharge
2. In the presence of worrisome signs and symptoms, women should report to the hospital immediately.
3. Timely assessment (a physical assessment is required to confirm preterm labour; a phone consultation is insufficient).
Clinical suspicion should be raised by the presence of uterine contractions combined with a cervical exam suggestive of early
dilation or effacement. This approach facilitates early institution of therapy but results in an over-diagnosis of preterm labour.
Studies have reported that approximately 50% of these women would remain undelivered in 48 hours if not treated.47,48

Prevention
Primary Prevention
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.49
Stopping Maternal Substance Abuse
• Maternal substance abuse increases the risk of preterm birth. Health care providers should try to identify maternal
substance abuse, provide information on the maternal and fetal risks, and help patients stop using these substances.49
Addressing Barriers to Prenatal Care
• The absence of prenatal care has been found to be a risk factor for preterm birth but it is less clear whether this
association is causal or 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.49,50
Secondary Prevention
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).51
• Screening for and treating asymptomatic bacteriuria has been shown to reduce low birth weight (OR 0.60;
95% CI 0.45 to 0.80).52

Progesterone
Progesterone has been shown to decrease the risk of preterm birth under 34 weeks in various trials. Various routes of
administration have been studied, including intramuscular (IM), vaginal suppository, and oral.53,54 17 OH hydroxy-progesterone
caproate has been shown to decrease the rate of preterm birth < 32–34 weeks and birth weight < 2500 grams in “high risk”
women with a history of spontaneous preterm birth.54-57 In a randomized controlled trial comparing intramuscular progesterone
to vaginal progesterone, in women with a prior preterm birth, intravaginal progesterone was found to be associated with
greater compliance, less reported side-effects and greater proportion of deliveries at >34 weeks of gestation as compared to
intramuscular progesterone.58
A randomized controlled trial, “PREDICT”, published in 2011, and a secondary analysis in the same year, found that progesterone
treatment does not appear to prevent preterm birth in twins or in twins at high risk.59,60 In 2015, a meta-analysis by Coombs
et al.61 found no difference in perinatal outcome or pregnancy duration in triplets.
Other important maternal and infant outcomes have not been well studied to date.62,63 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.
An SOGC Technical Update in 2008 has concluded that women at risk for PTL should be encouraged to participate in studies on
the role of progesterone 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 PTL. Women
and their caregivers should be aware that a previous preterm labour and/or short cervix (< 15 mm at 22–26 weeks’ gestation)
on transvaginal ultrasound could be used as an indication for progesterone therapy initiated after 20 weeks’ gestation and
continuing until the risk of prematurity is low.64,65
A more recent review in 2012 by the Society for Maternal Fetal Medicine recommends the following:
1. Singeton pregnancies with prior history of preterm birth: 17 hydroxy-progesterone caproate 250 mg IM weekly from
16–20 weeks until 36 weeks.
2. Singleton 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.66
These recommendations provide some clinical guidance for using progesterone for prevention preterm birth. Further studies
are needed to determine the efficacy of these therapies, and optimal combination of dosing and routes of administration of the
various progestins. Since 17 hydroxy-progesterone is not readily available in Canada, use of progesterone 200 mg vaginally daily
is a reasonable option.

In summary, regarding progesterone therapy the following should be considered:

1. Women with previous preterm birth < 34 weeks, without a shortened Cx: vaginal micronized progesterone
200 mg daily, from 16 weeks until 36 weeks.
2. Women with a short Cx ≤ 20 mm ≤ 24 weeks: vaginal micronized progesterone 200 mg daily, from diagnosis
until 36 weeks.
Cervical Cerclage
With respect the role of cervical cerclage, a 2013 SOGC Technical Update recommends that cerclage should only be considered
in women with a cervix ≤ 25 mm before 24 weeks’ gestation 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 does not support the use of progesterone
together with cerclage.67
Cervical Pessary
Recently there has been encouraging results on reducing the incidence of preterm birth in both singleton and twin pregnancies
by using a cervical pessary for women diagnosed with a short cervix < 25 mm as measured by transvaginal ultrasound.68,69
Management of Preterm Labour

Objectives
1. Early diagnosis of preterm labour
2. Identify the cause of preterm labour
• treat the underlying cause when possible
3. Attempt to arrest labour when appropriate
4. Intervene to minimize neonatal morbidity and mortality.

Assessment
The healthcare team provides both medical and emotional support of the patient while evaluation of the following occurs:
• Establish dates
• history (EDD, menstrual history, ultrasounds)
• review the prenatal record for EDD, menstrual history, pertinent ultrasounds, and clinical growth
• Vital signs (temperature, BP, respirations, pulse) and assessment of fetal well-being
• Evaluate contractions
• history (frequency, intensity, duration, changes with time)
• abdominal examination for uterine activity
• tocodynamometer (frequency of contractions)
• Cervical Assessment
• speculum exam initially to rule out PPROM, obtain swab for fetal fibronectin testing, if available, and cultures as
required (e.g., GC/Chlamydia, GBS swab)
• defer digital examination until after confirmation that there is no:
• PPROM
• Placenta previa
• Laboratory evaluation (CBC for leukocytosis)
• Fetal monitoring recommended for all preterm labours.
• Caution with fetal scalp electrode if the fetus is < 34 weeks gestational age.
• Caution with fetal blood sampling if the fetus is between 34 and 36 weeks gestation and probably best avoided in
gestations < 34 weeks.
I) 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.70

Evidence for some efficacy
• Calcium channel blockers (nifedipine):71

• no placebo-controlled trials
• Cochrane Database of Systematic Reviews 2003, Issue 172
• 12 trials (n=1029) comparing nifedipine with another tocolytic (mainly betamimetics)
• lower rate of delivery within seven days and < 34 weeks, reduced rates of RDS, NEC, IVH and jaundice
with nifedipine (These significant findings are driven mainly by one study finding significant differences
– Papatsonis et al 1997.73)
• fewer side effects and hence less need to discontinue treatment
• dose: ideal dosage regimen not yet determined, but many centres in Canada are using this as their first line
tocolytic. The Women’s Health Centre, Eastern Health (Newfoundland) follows a regimen with a loading dose
of nifedipine regular capsule 10 mg po (i.e., orally) every 15 to 20 minutes until contractions stop, to a maximum
of four doses (or 40 mg in the first hour). Maintenance therapy is nifedipine regular capsules 10 mg po
every four to six hours (maintenance therapy should start six hours following completion of loading dose).
Maintenance can be increased up to 20 mg po every four to six hours at physician’s discretion. Maximum daily
dose is 120 mg. It is stopped 48 hours after first dose of betamethasone (Dr. Joan Crane, Women’s Health Centre,
Eastern Health, St. John’s: personal communication, 2012 Feb 14).
• side effects: generally well tolerated but may cause maternal dizziness, lightheadedness, headache, flushing,
nausea, and transient hypotension with resulting FHR changes.
• a 2010 systematic review and meta-analysis of 5607 women by Khan suggests caution for total doses of
> 60 mg. A total nifedipine dose of > 60 mg is associated with a significant increased risk of adverse events,
particularly those associated with significant morbidity such as tachycardia and hypotension.74
• PG synthetase inhibitors (indomethacin):75
• 3 small trials (n=106) compared with placebo:
• more effective than placebo in delaying delivery to > 37 weeks (this finding based on only
one small study)
• 5 trials compared with other tocolytics:
• PG synthetase inhibitors more effective in delaying delivery to > 37 weeks and decrease in maternal
drug reaction requiring cessation of treatment
• consult local tertiary centre as to local standard of care
• dose: 100 mg suppository for transport and repeat 25 mg to 50 mg every 6 hours for a maximum of 48 hours

• potential fetal complications of PG synthetase inhibitors:

• should not be used after 32 weeks’ gestation because of increased sensitivity of the ductus
arteriosis to closure
• reduced fetal urine production causing oligohydramnios; neonatal renal insufficiency has been reported.
Therefore, PG synthetase inhibitors should not be used for more than 48 hours without assessment of
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.77
• Nitroglycerin:
• there is limited evidence of the benefit of nitroglycerin for tocolysis.
Tocolytics not available in Canada
• Terbutaline, ritodrine, atosiban
No evidence for efficacy
• Magnesium sulphate
• 37 trials and 3571 women – no benefit at any dose as a tocolytic
• Progestational agents
• 4 trials, 192 women showed no benefit as a tocolytic
• Bed rest – A 2010 Cochrane review showed that routine bed rest in hospital for multiple pregnancy did not reduce the
risk of preterm birth or perinatal mortality.80
• Fluid bolus – Two small studies (228 women) comparing intravenous hydration with bed rest alone found no
evidence of benefit.81,82
• Sedation, narcotics – No evidence of benefit.82
• Home uterine activity monitoring – Randomized trials have not shown that home uterine activity monitoring reduces
preterm birth rates. However, it does increase visits to Labour and Delivery units, obstetric intervention, and cost of
antepartum care.49,83,84

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
II) Antenatal Glucocorticoid Therapy

RDS is a major concern with preterm delivery. IVH, NEC, 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 more
than one-fifth 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 glucocorticoid 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 steroid therapy may still offer worthwhile benefits. The graph below shows the results of a
meta-analysis of steroid administration in women at risk of preterm birth.85 Treatment with antenatal corticosteroids is associated
with an overall reduction in neonatal death,86 RDS, intraventricular haemorrhage, necrotising enterocolitis, respiratory support,
neonatal intensive care unit admissions, and systemic infections in the first 48 hours of life.
Debate exists as to the preferred glucocorticoid. A recent meta-analysis comparing randomised clinical trials of betamethasone
and dexamethasone noted a reduction in IVH with dexamethasone as compared with betamethasone, but a higher rate of
NICU admission with dexamethasone.87 The authors concluded that the suggestion of increased benefit (by IVH reduction) of
dexamethasone over betamethasone from the review is not sufficient evidence to support dexamethasone over betamethasone.
A recent observational study found fewer adverse neurological outcomes at 18 to 22 months of age after betamethasone use,
but not dexamethasone, highlighting this uncertainty.87,88
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 unknown long-term sequelae89,90 A two-year follow-up study from the preterm

birth trial demonstrated that planned multiple courses of prenatal corticosteroid therapy did not alter the likelihood of death
or neurologic impairment to age two, when compared to those receiving only a single course of corticosteroid.89 In light of this
current evidence, planned multiple courses are not recommended.90
A randomized trial of a “rescue course” of antenatal steroids in 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.91
Recommendations for Antenatal Steroids
Women who are at increased risk of preterm delivery (especially within the next 7 days) are candidates for antenatal steroid therapy.

When Should Steroid Therapy be Given When Time Permits?85
Lower gestation limit 24 weeks92 (anything below 24 weeks should be

approached on a case-by-case basis)
Upper gestation limit 34 weeks
Prophylactic administration depends on diagnosis and risk
Steroid Options
• Betamethasone 12 mg IM every 24 hours x 2 doses

• Dexamethasone 6 mg IM every 12 hours x 4 doses
Caution with use of steroids
• Contraindications to the use of corticosteroids are active tuberculosis, gastric ulcers, and chorioamnionitis
• If immediate delivery is indicated, do not delay to wait for steroid effect
• Will transiently increase the maternal blood sugar (one may wish to delay testing for gestational diabetes
for at least 72 hours after last dose of corticosteroid given to avoid elevated glucose results)
• Will transiently increase the white blood cell count
• New evidence on the long term academic performance of school-age children calls into question the use
of routine steroids for elective CS from 36 to 39 weeks93.
III) Antibiotic Prophylaxis
Although evidence does not support the routine administration of antibiotics in preterm labour with intact membranes,94
the antibiotic protocol for group B streptococcus (GBS) prophylaxis95 should be followed if delivery is anticipated or imminent.

IV) Magnesium Sulphate Therapy for Fetal Neuroprotection in Imminent

Delivery at ≤ 31 weeks 6 days’ gestation96
1. For women with imminent preterm birth (≤ 31+6 weeks), antenatal magnesium sulphate administration should
be considered for fetal neuroprotection.
2. Although there is controversy about upper gestational age, antenatal magnesium sulphate for fetal neuroprotection
should be considered from viability to ≤ 31+6 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 of 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/ 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.

Magnesium sulphate for fetal neuroprotection in imminent preterm birth (≤ 31+6 weeks)
“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 givers should consult their regional referral centre before starting magnesium sulphate
for guidance. When inappropriately administered, magnesium sulphate can be cardiac toxic and cause respiratory depression.
Magnesium sulphate must always be administered via a medication pump to avoid overdose.97 Clinical hyporeflexia is the
first sign on magnesium toxicity and should prompt discontinuation of magnesium drip and consider calcium gluconate and
assessment of magnesium levels.

V) Maternal Transport
The decision to transport should be made in consultation with the receiving physician.
Consider
• Availability of neonatal and obstetrical care

• Availability of transport and skilled personnel
• 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 to Transport
• Unstable mother
• Abnormal fetal surveillance
• Imminent delivery
• No experienced attendants to accompany mother
• 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 lab results
• Communication
• with patient and family
• with receiving healthcare team (physician and nursing) re: indication, stabilization, mode of transport, estimated
time of arrival
• Appropriate attendant for transport
• IV access, indicated medication, appropriate equipment
• Assessment of patient immediately prior to transport

These issues are detailed in the SOGC Maternal Fetal Transport Guidelines98 and in other provincial guidelines.
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 other settings.
Best: Level III Hospital
Level II Hospital
Level I Hospital
Worst: During Transport
Summary
• Diagnose promptly and accurately
• Identify and treat underlying cause, if possible (Attempt to prolong pregnancy, if indicated
• Consider magnesium sulphate therapy at ≤ 31 weeks 6 days for neuroprotection
• Intervene to minimize neonatal morbidity and mortality
• STAT: A mnemonic
• Steroids: Antenatal steroid therapy
• Tocolytics: If indicated
• Antibiotics: GBS Prophylaxis
• Transport

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39. Vendittelli F, Volumenie J. Transvaginal ultrasonography examination of the uterine cervix in hospitalised women
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40. Honest H, Bachmann LM, Coomarasamy A, Gupta JK, Kleijnen J, Khan KS. Accuracy of cervical transvaginal sonography
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41. Crane JM, Hutchens D. Transvaginal sonographic measurement of cervical length to predict preterm birth in
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43. Lim K, Butt K, Crane JM. Ultrasonographic cervical length assessment in predicting preterm birth in singleton
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44. Iams JD. Prediction and early detection of preterm labor. Obstet Gynecol 2003;101(2):402-12.
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47. Iams JD, Casal D, McGregor JA, Goodwin TM, Kreaden US, Lowensohn R, et al. Fetal fibronectin improves the accuracy
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48. King JF, Grant A, Keirse MJ, Chalmers I. Beta-mimetics in preterm labour: an overview of the randomized controlled
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49. Norwitz ER. Prevention of spontaneous preterm birth. In: UpToDate [database online]. Waltham (MA): UpToDate, Inc.;
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50. Multicenter randomized, controlled trial of a preterm birth prevention program. Collaborative Group on Preterm Birth
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52. Smaill F. Antibiotics for asymptomatic bacteriuria in pregnancy [Cochrane review]. In: Cochrane Database of Systematic
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53. Likis FE, Edwards DR, Andrews JC, Woodworth AL, Jerome RN, Fonnesbeck CJ, et al. Progestogens for preterm birth
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54. Romero R, Nicolaides K, Conde-Agudelo A, Tabor A, O’Brien JM, Cetingoz E, et al. Vaginal progesterone in women with
an asymptomatic sonographic short cervix in the midtrimester decreases preterm delivery and neonatal morbidity: a
systematic review and metaanalysis of individual patient data. Am J Obstet Gynecol 2012;206(2):124-19.
55. Dodd JM, Flenady V, Cincotta R, Crowther CA. Prenatal administration of progesterone for preventing preterm birth
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56. Rode L, Langhoff-Roos J, Andersson C, Dinesen J, Hammerum MS, Mohapeloa H, et al. Systematic review
of progesterone for the prevention of preterm birth in singleton pregnancies. Acta Obstet Gynecol Scand
2009;88(11):1180-9.
57. Dodd JM, Crowther CA. The role of progesterone in prevention of preterm birth. Int J Women Health 2009;1:73-84.
58. Maher MA, Abdelaziz A, Ellaithy M, Bazeed MF. Prevention of preterm birth: a randomized trial of vaginal compared with
intramuscular progesterone. Acta Obstet Gynecol Scand 2013;92(2):215-22.
59. Klein K, Rode L, Nicolaides KH, Krampl-Bettelheim E, Tabor A, PREDICT Group. Vaginal micronized progesterone and
risk of preterm delivery in high-risk twin pregnancies: secondary analysis of a placebo-controlled randomized trial and
meta-analysis. Ultrasound Obstet Gynecol 2011;38(3):281-7.
60. Rode L, Klein K, Nicolaides KH, Krampl-Bettelheim E, Tabor A, PREDICT Group. Prevention of preterm delivery in
twin gestations (PREDICT): a multicenter, randomized, placebo-controlled trial on the effect of vaginal micronized
progesterone. Ultrasound Obstet Gynecol 2011;38(3):272-80.
61. Combs CA, Schuit E, Caritis SN, Lim AC, Garite TJ, Maurel K, et al. 17-Hydroxyprogesterone caproate in triplet pregnancy:
an individual patient data meta-analysis. BJOG 2015.
62. Meis PJ, Klebanoff M, Thom E, Dombrowski MP, Sibai B, Moawad AH, et al. Prevention of recurrent preterm delivery by 17
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63. Dodd JM, Flenady VJ, Cincotta R, Crowther CA. Progesterone for the prevention of preterm birth: a systematic review.
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64. Farine D, Mundle WR, Dodd J. The use of progesterone for prevention of preterm birth [SOGC technical update no 202].
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no. 130: prediction and prevention of preterm birth. Obstet Gynecol 2012;120(4):964-73.
66. Society for Maternal-Fetal Medicine Publications Committee, with assistance of Vincenzo Berghella. Progesterone and
preterm birth prevention: translating clinical trials data into clinical practice. Am J Obstet Gynecol 2012;206(5):376-86.
67. Brown R, Gagnon R, Delisle MF, Maternal Fetal Medicine Committee, Gagnon R, Bujold E, et al. Cervical insufficiency
and cervical cerclage. J Obstet Gynaecol Can 2013;35(12):1115-27. Available: http://sogc.org/guidelines/cervical-
insufficiency-cervical-cerclage/.
68. Goya M, De La Calle M, Pratcorona L, Merced C, Rodo C, Munoz B, et al. Cervical pessary to prevent preterm birth in
women with twin gestation and sonographic short cervix: a multicenter randomized controlled trial (PECEP-Twins).
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69. Goya M, Pratcorona L, Merced C, Rodo C, Valle L, Romero A, et al. Cervical pessary in pregnant women with a short
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70. Mackeen AD, Seibel-Seamon J, Grimes-Dennis J, Baxter JK, Berghella V. Tocolytics for preterm premature rupture of
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71. Haas DM. Preterm birth. Clin Evid 2006;(15):1966-85.
72. King JF, Flenady VJ, Papatsonis DNM, Dekker GA, Carbonne B. Calcium channel blockers for inhibiting preterm labour
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73. Papatsonis DN, Van Geijn HP, Ader HJ, Lange FM, Bleker OP, Dekker GA. Nifedipine and ritodrine in the management of
preterm labor: a randomized multicenter trial. Obstet Gynecol 1997;90(2):230-4.
74. Khan K, Zamora J, Lamont RF, Van Geijn HH, Svare J, Santos-Jorge C, et al. Safety concerns for the use of calcium channel
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76. King J, Flenady V, Cole S, Thornton S. Cyclo-oxygenase (COX) inhibitors for treating preterm labour [Cochrane review].
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77. Loe SM, Sanchez-Ramos L, Kaunitz AM. Assessing the neonatal safety of indomethacin tocolysis: a systematic review
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78. Crowther CA, Brown J, McKinlay CJ, Middleton P. Magnesium sulphate for preventing preterm birth in threatened
preterm labour. Cochrane Database Syst Rev 2014;8:CD001060.
79. Su L, Samuel M, Chong Y. Progestational agents for treating threatened or established preterm labour [Cochrane
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81. Stan C, Boulvain M, Hirsbrunner-Amagbaly P, Pfister R. Hydration for treatment of preterm labour [Cochrane review].
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84. Reichmann JP. Home uterine activity monitoring: the role of medical evidence. Obstet Gynecol 2008;112(2 Pt 1):325-7.
85. Roberts D, Dalziel S. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth
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86. Mwansa-Kambafwile J, Cousens S, Hansen T, Lawn JE. Antenatal steroids in preterm labour for the prevention of
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88. Lee BH, Stoll BJ, McDonald SA, Higgins RD. Neurodevelopmental outcomes of extremely low birth weight
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89. Asztalos EV, Murphy KE, Hannah ME, Willan AR, Matthews SG, Ohlsson A, et al. Multiple courses of antenatal
corticosteroids for preterm birth study: 2-year outcomes. Pediatrics 2010;126(5):e1045-e1055.
90. Murphy K. Multiple courses of antenatal corticosteroids for preterm birth study. Am J Obstet Gynecol
2007;197(6 Suppl):S2.
91. Garite TJ, Kurtzman J, Maurel K, Clark R. Impact of a “rescue course” of antenatal corticosteroids: a multicenter
randomized placebo-controlled trial. Am J Obstet Gynecol 2009;200(3):248-9.
92. 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(4):921-6.
93. Aiken CE, Fowden AL, Smith GC. Antenatal glucocorticoids prior to cesarean delivery at term. JAMA Pediatr
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10.1002/14651858.CD000246.
95. Money DM, Dobson S, Infectious Diseases Committee. The prevention of early-onset neonatal Group B streptococcal
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97. Doyle LW, Crowther CA, Middleton P, Marret S, Rouse D. Magnesium sulphate for women at risk of preterm birth for
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J Obstet Gynaecol Can 2005;27(10):956-8. Available: http://sogc.org/guidelines/public/165E-PS-October2005.pdf.

Chapter 19
Prelabour Rupture of
Membranes (PROM)
Definition
The definition of prelabour rupture of membranes is rupture of the membranes before the onset of labour and where there is
at least an hour between membrane rupture and the onset of contractions.1 PROM may occur when the fetus is ≥ 37 weeks’
gestation (term PROM) or before 37 weeks’ gestation (preterm PROM or PPROM). It is further classified by gestational age:
mid-trimester PPROM ( before 24 weeks), early PPROM (24 to 34 weeks) and near-term PPROM (34-37 weeks).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. The
mechanical strength of the fetal membranes is due to the extracellular matrix.2 The risk to both mother and baby are increased
after the occurrence of PROM, whether at or before term. Among women with preterm PROM, clinically evident intra-amniotic
infection occurs in 15% to 25% of these women, with histiological chorioamnionitis in 51%.3 Fetal risks include umbilical cord
compression and ascending infection.
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.4
Almost 90% of women at term will go into spontaneous labour within 24 hours of membrane rupture.5 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 one week of membrane rupture.6
Incidence
Term PROM occurs in approximately 8% of pregnancies.5,7
Prelabour Rupture of Membranes (PROM) 1

Preterm PROM occurs in 2% to 3.5% of pregnancies but accounts for one-third of the cases of preterm delivery.8 The frequency of
PROM increases with increasing plurality of gestation (13.3% for singleton, 16.81% for twins, and 20% for triplets).9
Risk Factors of PROM10

• Amniocentesis
• Cervical insufficiency
• Cervical cerclage
• Prior cervical conization, laser conization, loop electrosurgical excision procedure
• PPROM in a previous pregnancy
• Prior preterm labour/delivery
• Chronic abruptio placentae
• Vaginal bleeding in pregnancy
• Polyhydramnios
• Cigarette smoking
• Sexually transmitted infection
• Low socioeconomic status
• Bacterial vaginosis (BV)
Bacterial vaginosis is a condition where the vaginal flora is altered. It may or may not be symptomatic. It has been associated
with preterm birth. Current evidence does not support screening and treating all pregnant women 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).11 In the symptomatic woman at low risk
for adverse obstetrical outcome, oral and vaginal antibiotics are equally effective for symptom relief.12 Women with a past history
of preterm birth should be treated with oral metronidazole 500 mg or clindamycin 300 mg twice daily for seven 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.9
Diagnosis of PROM
Diagnosis of PROM and PPROM is made by a combination of patient history, clinical suspicion, physical exam, and some testing.
Patient history has an accuracy of 90% for the diagnosis of PPROM and should not be ignored.13

Digital pelvic exam is not recommended because of the increased risk of ascending infection14,15 and shortening of the latent
period.16 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
• Take a careful history 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 PROM17
Speculum Exam
• 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).18
• False positive in a woman in labour: 11.8%; in a woman not in labour: 21.2%19
• False negative in a woman in labour: 2%; in a woman not in labour: 40.6%19
Antiseptic solution, semen, fingerprints, and cervical mucus may cause false-positives, while blood, meconium, and
vaginal secretions will not.20 Therefore the result of ferning should be viewed as supportive rather than conclusive in
the non-labouring woman with non-specific vaginal fluid loss.16
• pH testing of fluid (nitrazine paper)—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.17 Immunoassay for
placental alpha microglobulin-1, a protein marker of the amniotic fluid, seems promising for confirming the diagnosis
in problematic cases. Cousins et al. demonstrated that the test had a sensitivity of 98.9%, specificity of 100%, positive

predictive value of 100%, and a negative predictive value of 99.1%.21 Controlled clinical trials are needed to determine
the clinical effectiveness over standard diagnostic methods.
• Fluid in the vagina may be collected for lung maturity indices in preterm cases
Note: Commercial immunological bedside tests for the diagnosis of ruptured membranes such as lactate determination are
currently being evaluated and may be useful in certain clinical settings.22
Complications of Term PROM

• Fetal/neonatal infection (e.g., RDS, IVH, NEC)
• Maternal infection (e.g., endometritis, chorioamnionitis, bacteremia)
• Umbilical cord compression/prolapse5
Complications of Preterm PROM

• Preterm labour and delivery
• Fetal/neonatal infection
• Maternal infection
• Umbilical cord compression/prolapse
• Increased Caesarean section (CS) rate
• Abruptio placentae
• With early, severe oligohydramnios
• pulmonary hypoplasia (< 26 weeks’)2,23
• fetal deformity
The most significant complication of PPROM is preterm birth and its consequences.2,23

Management of PROM
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 which requires concurrent management or may indicate
that 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 exam. If the woman is in labour, digital cervical assessment is indicated.
• Determination of fetal presentation using ultrasound if abdominal assessment is inconclusive
There is emerging scientific evidence that maternal markers (C-reactive protein (CRP) and white blood cell (WBC) counts) are
predictive of early-onset neonatal infection.24 The bedside assessment of amniotic fluid interleukin-6 also seems a promising
measure of microbial invasion of the amniotic cavity (MIAC).25
There is no evidence to support tocolysis for women with PPROM as it is associated with an increase in chorioamnionitis, increase
in Apgars at 5 minutes of less than 7, and an increase in the need for neonatal ventilation.26
Outpatient management of selective patients with PPROM may be suitable, after a period of observation (such as 48 hours) and
provided specific prerequisites are met. 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 a 2014 Cochrane Review, the authors found that
there was insufficient statistical power in the studies reviewed to detect meaningful differences between the two groups.Therefore,
specific departmental protocols need to be followed.27
Magnesium Sulphate is used for neuroprotection in Preterm labour before 31 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.28

Management of Term PROM (37 or More Weeks’)

• Avoid digital cervical exam until induction is initiated or labour has begun
• Assess for infection: Obtain cultures, if indicated
• Antibiotics for Group B streptococcus (GBS) prophylaxis, if indicated
• Current evidence supports induction of labour (IOL) for all women with Term PROM within 24 hours rather than
expectant management29
• This management reduces the risk of maternal infection (e.g., chorioamnionitis and endometritis) and NICU admission
without increasing the rates of Caesarean infection or assisted vaginal birth. Although IOL with vaginal prostaglandin
PGE2 has been shown to be equally effective for labour induction compared to oxytocin, it is associated with higher
rates of chorioamnionitis. Prostaglandins may, however, be considered in those women with an unfavourable cervix.30
• Oral misoprostol (50 mcg po q4 hourly to a maximum of 4 doses) is a promising induction agent for PROM. Compared
with oxytocin, it has both uterotonic and cervical ripening effects – of particular benefit to women with an unripe
cervix. It is easier to administer than IV oxytocin and does not require fetal monitoring until a woman is contracting.
Compared with vaginal prostaglandins, oral misoprostol does not require vaginal examinations, lessening concerns
about infection. A randomized trial of 758 women showed fewer CS for dystocia and no difference in fetal or maternal
complications with a regimen of oral misoprostol compared with vaginal PGE2 and oxytocin. Women receiving
misoprostol had a small increase in gastrointestinal side effects.31
• For women colonized with GBS, the indication for induction is more compelling because of the additional benefit of
this management in reducing neonatal infection32
• CS if there are contraindications to IOL and/or vaginal birth7,33
• 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,
if indicated.
• Appropriate antibiotics and IOL if chorioamnionitis develops

The management of PROM at term is based on the Term PROM Study 7 and the Cochrane review.5,33
• 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 births. Although
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).5
• Chorioamnionitis is reduced and maternal satisfaction is increased if labour is induced with intravenous oxytocin,
compared with either inducing labour with prostaglandins (+/ – oxytocin) or expectant management).34
• Neonatal infection is reduced among women who are GBS positive if labour is induced with intravenous oxytocin,
compared with either inducing labour with prostaglandins (+/ – oxytocin) or expectant management.32,35 There is
insufficient evidence to justify the routine use of prophylactic antibiotics with Term PROM in the absence of an indication
for GBS prophylaxis.2,36-38
Expectant Management
For women who choose expectant management beyond 24 hours:
• No digital exam 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.39
Management of PPROM (34 to 36+6 Weeks’)

Optimal timing of delivery between 34 and 36.6 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 34 to 36+6 weeks. The 2010 Cochrane Review of planned early birth
versus expectant management with PPROM prior to 37 weeks’ gestation did not add any clarity.40
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.41 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 versus expectant

management in membrane rupture between 34 and 37 weeks showed neonatal sepsis occurring in 2% of those induced and
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 term42”.
• Antibiotics can be used in PPROM > 32 weeks if fetal lung maturity cannot be proven and delivery is not planned.43
The primary motivation for considering IOL earlier than 37 weeks’ gestation in the presence of PPROM is based on balancing the
risks associated with preterm birth with the risks of maternal, fetal, and neonatal infectious morbidity.44-47
• Avoid digital cervical exam
• Assess for infection: Obtain cultures
• Ultrasound assessment of fetal position, cervical status, and fluid volume
• Antibiotics for GBS prophylaxis, if indicated
• Consider transfer to a higher level centre, if relevant
• Consider IOL with oxytocin to reduce the risk of chorioamnioitis (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.
Management of PPROM (< 34 Weeks’)

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).48 There are several different regimens of antibiotics that can be used. 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).”6,44,49 Azithromycin can be substituted for erythromycin in the appropriate doses without affecting latency or any other
measured maternal or fetal outcomes.50

Amoxicillin with clavulinic acid should be avoided as it appears to increase the risk of necrotizing enterocolitis.48
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 is sent for fetal lung maturity indices.
One course of steroids, to accelerate fetal lung maturity, is indicated if gestational age is less than or equal to 32 weeks’
gestation.51,52 If chorioamnionitis is suspected, delivery is recommended and expectant management is contraindicated.
For women between 32 and 34 weeks’ gestation, glucocorticoids may be considered,52 although the evidence to support this
practice is lacking.
In certain circumstances (e.g., transfer), tocolytics may be considered in consultation with a tertiary care centre.22,51,53
• Avoid digital cervical exam
• Assess for infection: Obtain cultures, if indicated
• Amniotic fluid may be collected from vagina to assess fetal lung maturity
• Ultrasound assessment of fetal position, cervical status, and fluid volume
• Glucocorticoids should be given < 32 weeks’ and considered from 32 weeks’ to 34 weeks’
• Antepartum antibiotics: Consider the administration of erythromycin
• Antibiotics for GBS prophylaxis, if indicated. Restart GBS prophylaxis at the onset of labour, if indicated
• Consider transfer to tertiary care centre, if appropriate
• Expectant management
• Surveillance for chorioamnionitis (monitoring maternal pulse and temperature, fetal heart rate, the development of
uterine tenderness or irritability, and differential WBC changes if indicated)
• Appropriate antibiotics and IOL if chorioamnionitis develops
Summary
1. PROM/PPROM occurs for many different reasons and at any gestational age.
2. Digital cervical exams should be avoided and sterile speculum exams are appropriate to confirm PROM/PPROM.
3. The primary motivation for considering IOL earlier than 37 weeks’ gestation in the presence of PPROM is based on
balancing the risks associated with preterm birth with the risks of maternal, fetal, and neonatal infectious morbidity.

References
1. Abou El Senoun G, Dowswell T, Mousa HA. Planned home versus hospital care for preterm prelabour rupture of the
membranes (PPROM) prior to 37 weeks’ gestation. Cochrane Database Syst Rev 2014;(4).
2. Practice bulletins No. 139: premature rupture of membranes. Obstet Gynecol 2013;122(4):918-30.
3. Magee B, Smith G. Histological chorioamnionitis associated with preterm prelabour rupture of membranes at Kingston
General Hospital: a practice audit. J Obstet Gynaecol Can 2013;35(12):1083-9.
4. Ekin A, Gezer C, Taner CE, Ozeren M, Uyar I, Gulhan I. Risk factors and perinatal outcomes associated with latency
in preterm premature rupture of membranes between 24 and 34 weeks of gestation. Arch Gynecol Obstet
2014;290(3):449-55.
5. Dare MR, Middleton P, Crowther CA, Flenady VJ, Varatharaju B. Planned early birth versus expectant management (waiting)
for prelabour rupture of membranes at term (37 weeks or more) [Cochrane review]. In: Cochrane Database of Systematic
Reviews 2006 Issue 1. Chichester (UK): John Wiley & Sons, Ltd; 2006. DOI: 10.1002/14651858.CD005302.pub2.
6. Mercer BM, Miodovnik M, Thurnau GR, Goldenberg RL, Das AF, Ramsey RD, et al. Antibiotic therapy for reduction of
infant morbidity after preterm premature rupture of the membranes. A randomized controlled trial. National Institute of
Child Health and Human Development Maternal-Fetal Medicine Units Network. JAMA 1997;278(12):989-95.
7. Hannah ME, Ohlsson A, Farine D, Hewson SA, Hodnett ED, Myhr TL, et al. Induction of labor compared with
expectant management for prelabor rupture of the membranes at term. TERMPROM Study Group. N Engl J Med
1996;334(16):1005-10.
8. Kenyon S, Boulvain M, Neilson J. Antibiotics for preterm rupture of the membranes: a systematic review. Obstet Gynecol
2004;104(5 Pt 1):1051-7.
9. 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(1):69-74.
10. Smith G, Rafuse C, Anand N, Brennan B, Connors G, Crane J, et al. Prevalence, management, and outcomes of preterm
prelabour rupture of the membranes of women in Canada. J Obstet Gynaecol Can 2005;27(6):547-53.
11. McDonald HM, Brocklehurst P, Gordon A. Antibiotics for treating bacterial vaginosis in pregnancy [Cochrane review].
10.1002/14651858.CD000262.pub3.

12. Yudin MH, Money DM. Screening and management of bacterial vaginosis in pregnancy [SOGC clinical practice guideline
no 211]. J Obstet Gynaecol Can 2008;30(8):702-16.
13. Canavan TP, Simhan HN, Caritis S. An evidence-based approach to the evaluation and treatment of premature rupture of
membranes: part I. Obstet Gynecol Surv 2004;59(9):669-77.
14. Schutte MF, Treffers PE, Kloosterman GJ, Soepatmi S. Management of premature rupture of membranes: the risk of
vaginal examination to the infant. Am J Obstet Gynecol 1983;146(4):395-400.
15. Seaward PG, Hannah ME, Myhr TL, Farine D, Ohlsson A, Wang EE, et al. International Multicentre Term Prelabor Rupture
of Membranes Study: evaluation of predictors of clinical chorioamnionitis and postpartum fever in patients with prelabor
rupture of membranes at term. Am J Obstet Gynecol 1997;177(5):1024-9.
16. Lewis DF, Major CA, Towers CV, Asrat T, Harding JA, Garite TJ. Effects of digital vaginal examinations on latency period in
preterm premature rupture of membranes. Obstet Gynecol 1992;80(4):630-4.
17. Parsons M, Spellacy W. Premature rupture of membranes. In: Danforth DM, Scott JR, editors. Danforth’s obstetrics and
gynecology. 8th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p.269-77.
18. Bennett SL, Cullen JB, Sherer DM, Woods JR. The ferning and nitrazine tests of amniotic fluid between 12 and 41 weeks
gestation. Am J Perinatol 1993;10(2):101-4.
19. El-Messidi A, Cameron A. Diagnosis of premature rupture of membranes: inspiration from the past and insights for the future.
20. Gaddey H, Bailey J, Smith RF. Clinical inquiry: ferning in amniotic fluid: is it a useful indicator of ruptured membranes?
J Fam Pract 2011;60(12):769-71.
21. Cousins LM, Smok DP, Lovett SM, Poeltler DM. AmniSure placental alpha microglobulin-1 rapid immunoassay versus
standard diagnostic methods for detection of rupture of membranes. Am J Perinatol 2005;22(6):317-20.
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(accessed 2008 Apr).
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24. Popowski T, Goffinet F, Maillard F, Schmitz T, Leroy S, Kayem G. Maternal markers for detecting early-onset neonatal
infection and chorioamnionitis in cases of premature rupture of membranes at or after 34 weeks of gestation: a two-
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2393/11/26.

25. Kacerovsky M, Musilova I, Hornychova H, Kutova R, Pliskova L, Kostal M, et al. Bedside assessment of amniotic fluid
interleukin-6 in preterm prelabor rupture of membranes. Am J Obstet Gynecol 2014;211(4):385-9.
26. Mackeen AD, Seibel-Seamon J, Muhammad J, Baxter JK, Berghella V. Tocolytics for preterm premature rupture of
membranes. Cochrane Database Syst Rev 2014;2:CD007062.
27. Abou El Senoun G, Dowswell T, Mousa HA. Planned home versus hospital care for preterm prelabour rupture of the
membranes (PPROM) prior to 37 weeks’ gestation. Cochrane Database Syst Rev 2014;4:CD008053.
28. Horton AL, Lai Y, Rouse DJ, Spong CY, Leveno KJ, Varner MW, et al. Effect of magnesium sulfate administration for
neuroprotection on latency in women with preterm premature rupture of membranes. Am J Perinatol 2015;32(4):387-
92. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369158.
Gynaecol Can 2013;35(9):840-57.
30. Term prelabour rupture of membranes (Term PROM). [C-Obs 36]. Melbourne: Royal Australian and New Zealand College
of Obstetricians and Gynaecologists; 2014 Mar. Available: https://www.ranzcog.edu.au/doc/term-prom.html.
31. Bricker L, Peden H, Tomlinson A, Al-Hussaini T, Idama T, Candelier C, et al. Titrated low-dose vaginal and/or oral
misoprostol to induce labour for prelabour membrane rupture: a randomised trial. BJOG 2008;115(12):1503-11.
32. Money DM, Dobson S, Infectious Diseases Committee. The prevention of early-onset neonatal Group B streptococcal
disease [SOGC clinical practice guideline no 149]. J Soc Obstet Gynaecol Can 2004;26(9):826-32. Available: http://sogc.
org/guidelines/public/149E-CPG-September2004.pdf.
33. Alfirevic Z, Kelly AJ, Dowswell T. Intravenous oxytocin alone for cervical ripening and induction of labour [Cochrane
10.1002/14651858.CD003246.pub2.
34. Mozurkewich EL, Wolf FM. Premature rupture of membranes at term: a meta-analysis of three management schemes.
Obstet Gynecol 1997;89(6):1035-43.
35. 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. Am J
Obstet Gynecol 1997;177(4):780-5.
36. 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(1):59-62. Available: http://www.ijgo.org/article/S0020-
7292%2813%2900505-5/fulltext.

37. Wojcieszek AM, Stock OM, Flenady V. Antibiotics for prelabour rupture of membranes at or near term. Cochrane Database
Syst Rev 2014;10:CD001807.
38. 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(5):627-9.
39. Prelabour rupture of the membranes at term. [NICE pathways]. London: National Institute for Health and Clinical
Excellence; 2011. Available: http://pathways.nice.org.uk/pathways/intrapartum-care#path=view%3A/pathways/
intrapartum-care/prelabour-rupture-of-the-membranes-at-term.xml&content=close.
40. Buchanan SL, Crowther CA, Levett KM, Middleton P, Morris J. Planned early birth versus expectant management for
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41. van der Ham DP, van der Heyden JL, Opmeer BC, Mulder AL, Moonen RM, van Beek JH, et al. Management of late-
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42. 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 2015.
43. Yudin MH, van Schalkwyk J, Van Eyk N, Boucher M, Castillo E, Cormier B, et al. Antibiotic therapy in preterm premature
rupture of the membranes. J Obstet Gynaecol Can 2009;31(9):863-7, 868-74.
44. Naef RW, 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(1 Pt 1):126-30.
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Gynecol Obstet Fertil 2009;37(4):334-41.
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Obstet Gynaecol Can 2010;32(6):555-60.
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preterm infants. Clin Pediatr (Phila) 2010;49(1):60-5.
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CD001058.pub2.

49. 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(4):346-52.
50. Pierson RC, Gordon SS, Haas DM. A retrospective comparison of antibiotic regimens for preterm premature rupture of
membranes. Obstet Gynecol 2014;124(3):515-9. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4147675.
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53. Medina TM, Hill DA. Preterm premature rupture of membranes: diagnosis and management. Am Fam Physician
2006;73(4):659-64. Available: http://www.aafp.org/afp/20060215/659.html.

Appendix
Reproduced with permission from: WJ Ehman, 2006.

Chapter 20
Prevention of Early-Onset Neonatal
Group B Streptococcal Disease
Introduction
The prevention of early-onset group B streptococcus (GBS) disease in neonates is an evolving issue and under constant
review. Evidence from several population-based studies and the publication of guidelines from the Society of Obtetricians and
Gynaecologists of Canada (SOGC),1 Canadian Paediatric Society (CPS),2 and the U.S. 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 will be colonized in the vagina or rectum
(this 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. One to two percent of these infants will develop early-onset GBS infections, giving an overall incidence of
approximately 1.8/1000 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 1990’s, the incidence of early-onset GBS disease declined to
approximately 0.5/1000 live births in 19993 and 0.26/10006 to 0.41/10004 by 2009. 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, 95% CI 0.15– to 0.92), followed by the Americas (0.50, 95% CI 0.43 to –0.57), Europe
(0.45, 95% CI 0.34 to – 0.56) and southeast Asia (0.11 95% CI 0.012 to – 0.22). The case fatality rate was 12.1%
(95% CI 6.2– to 18.3).7
Prevention of Early-Onset Neonatal Group B Streptococcal Disease 1

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 which has ascended from
the vagina after the onset of labor or rupture of the membranes. Infection can also occur as the fetus passes through
the birth canal. However, most infants exposed to GBS will remain well but may have their mucous membranes,
gastrointestinal and respiratory tracts colonized with GBS.3

• GBS has been associated with stillbirth8 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.
• 89%9 to 95%10 of neonatal early-onset GBS infection presents in the first 24 hours of life and may be characterized
by bacteremia, pneumonia, or meningitis. Nearly 40% of neonates with GBS meningitis will be left with moderate to
severe neurologic disability.11
• The overall mortality rate ranges from 5% to 12%. 1 ,4,7
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) during current pregnancy
• maternal colonization with GBS (positive screening culture within five weeks of labour or membrane rupture)
• for women whose GBS culture status is unknown:
• preterm labour (< 37 weeks’ gestation)
• amniotic membrane rupture ≥ 18 hours
• intrapartum temperature ≥ 38° C
• Note: If GBS status is unknown, knowledge of colonization status in a previous pregnancy may be considered
along with the above risk factors. Recent retrospective studies have reported a GBS colonization recurrence rate in a
subsequent pregnancy of 38% to 53%. 12-15 The authors of the 2015 review12 suggested that prior GBS colonization be
considered as an indiction for intrapartum antibiotic prophylaxis in women with unknown GBS status.

• Importantly, however, a 2008 retrospective review noted that 38% of the 65 neonates diagnosed with early-onset
Group B streptococcus had no recognizable antepartum or intrapartum predisposing risk factors (including known
maternal colonization).16 This emphasizes the recommendation that any neonate presenting with signs of sepsis
should be evaluated appropriately.
Antepartum Screening
• Based on a large multicentre retrospective analysis17 and other supporting studies, it is recommended to screen all
pregnant women at 35 to 37 weeks’ gestation for GBS colonization and to treat all positive women with intrapartum
antibiotic prophylaxis at the time of membrane rupture or labour.1,3 This evidence suggests that the universal screening
approach is over 50% more effective than the risk-based approach at preventing perinatal GBS disease.
• 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 greater
than five to six weeks. The PPV of cultures done before 35 weeks was 59% to 63% and if done after 35 weeks was
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 approximately 6% of GBS carriers will be undetected with antenatal cultures.18
• If a GBS screening culture is done before 35 to 37 weeks (e.g., threatened preterm labor) and anytime that the interval
between the culture and delivery is > 5 weeks, it should be repeated.3,18,19
• 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%).17
• Research continues on the applicability of using a rapid test to detect GBS status.20-23 In 2011, Young et al prospectively
evaluated a rapid, real-time intrapartum nucleic acid amplification test (NAAT) for GBS. This polymerase chain
reaction (PCR) test demonstrated sensitivity of 90.8% (84.6% to 95.2%), specificity of 97.6% (95.6% to 98.8%), and
predictive values > 92%. The authors noted that the characteristics of the NAAT were superior to those of intrapartum
culture and suggested that it could be used to guide intrapartum treatment.23 A 2014 prospective study of 600 women
with term PROM compared intrapartum PCR testing with vaginal/rectal cultures at the time of presentation and found
PCR sensitivity and specificity were 89.0% (95% CI 82.8 to 93.6%) and 97.9% (95% CI 96.0 to 99.0%), respectively,
compared with culture. Seventy-two percent of the PCR results were available within 3 hours.24 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.22 AAlthough 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.25,26
Culture Technique:
• Use a current standardized method 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 is informed
of the result and the recommended interventions.
• A single swab is taken from the lower third of the vagina and then the anorectum (through the anal sphincter). Failure
to swab the anorectum is associated with a significant false negative rate. Cervical cultures are not recommended and
a speculum is not used.
• Place the swab in non-nutritive transport medium (e.g., Amies or Stuart’s). Although this medium will maintain GBS
viability for up to four days at room temperature, recovery does decline over this period and 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.33
• 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 caregivers.27
• If the woman is penicillin allergic and at high risk for anaphylaxis, then this should be stated on the culture
requisition along with a request to perform sensitivity testing for clindamycin and erythromycin. There has been
increasing resistance of GBS to clindamycin (13% to 28%) and erythromycin (25% to 38%).3,28,29 A 2012 study of
309 GBS isolates in Alberta found resistance to erythromycin to be 25% and clindamycin to be 22%.30 Resistance
to erythromycin is frequently associated with clindamycin resistance and may develop into either.3 High risk for
anaphylaxis is defined as a history of immediate hypersensitivity reaction (anaphylaxis, urticaria, angioedema, or
respiratory distress following administration of a penicillin or a cephalosporin).3
The following chart outlines the risk of GBS disease when antibiotics are not used in women with or without risk factors. It
indicates that newborn GBS disease is greatest with mothers that screen positive and have risk factors.

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” were defined by 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.31
Management
Antepartum Management
• Treat women with antepartum (symptomatic or with colony counts > 100 000 CFU/mL) GBS urinary tract infections
with appropriate antibiotics for the prevention of adverse pregnancy outcomes such as pyelonephritis.32 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.32
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 prior to labour or membrane rupture.3

Intrapartum Management
• No method prevents all GBS disease. Women should be advised that current management
approaches will not always eliminate GBS disease.
• The 2014 Cochrane Review, Intrapartum antibiotics for known maternal Group B streptococcal colonization,33
identified three RCTs (n=500), each with concerns regarding bias. The author concluded that intrapartum antibiotic
prophylaxis appears to reduce neonatal early-onset GBS disease but there was a lack of evidence from well designed
and conducted trials. Intrapartum antibiotics compared to 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/postpartum sepsis, puerperal infection
• The aims of IAP are
• to decrease maternal colony counts,
• to prevent ascending maternal infection,
• to achieve effective concentrations of antibiotic in the fetus during labour.
• The duration of intrapartum antibiotic prophylaxis (IAP) is important and will guide the management of the neonate.
Current guidelines recommend that at least four hours prophylaxis with penicillin, ampicillin, or cefazolin 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%.34 A 2014
prospective study of 60 women who were rectovaginal culture GBS positive at 35-37 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 hrs and
5 (12%) were still positive at 4 hours. This study supported the recommendation of a 4hr optimal duration for IAP.35
• However, in situations where labour is progressing rapidly and the four-hour duration is not anticipated, it is
recommended that prophylaxis be commenced as soon as possible because of evidence that even a short duration of
antibiotic therapy (e.g., one to two hours) will reduce the risk of neonatal colonization36 and early-onset GBS disease
of the newborn.37 Furthermore, a study of fetal penicillin G levels after maternal IV administration demonstrated that
the levels peaked at one hour and that fetal serum levels far exceeded the minimal inhibitor concentration at durations

of well under one hour.38 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.34,39
• Antibiotic Prophylaxis
1. penicillin is the drug of choice unless the woman is allergic to penicillin. For women at low risk of anaphylaxis,
cefazolin is indicated.
2. for women at high risk for penicillin anaphylaxis:
• Clindamycin should be used if the GBS isolate is sensitive to both clindamycin and erythromycin;
erythromycin is no longer recommended because of erthromycin’s poor transplacental transfer (3% of
maternal concentration).40,41
• if the GBS isolate is resistent to clindamycin or erythromycin by antimicrobial susceptibility testing (or the
sensitivities are unknown), vancomycin is indicated. GBS remains universally sensitive to vancomycin, which
also has a satisfactory transplacental passage.42
• however, in the case where the GBS is resistent to erythromycin but susceptible to clindamycin by standard
susceptibility tests, clindamycin may be used if testing for inducible resistance to clindamycin is
negative. Inducible resistance is determined with a double-disk diffusion method (D-zone test) or other
validated tests.3
A 2003 Alberta retrospective review of 90 cases of early-onset GBS disease (between 1993 and 1997), at a time prior to 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].43 A case-control study (covering the years 2000 to 2011) of
40 cases of early-onset neonatal sepsis (EONS) made up of eight GBS, 11 Escherichia coli, 12 Coagulase negative staphylococci,
four Viridans group streptococci, one Enterococcus faecalis, and four other non-specified organisms versus 80 controls, did not
demonstrate a significant relationship between fetal scalp electrode use and EONS.44
• Although there is a theoretical concern about procedures such as membrane stripping and mechanical and/or
pharmacologic cervical ripening on GBS-colonized women, the 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.45
• 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 EO 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 EO GBS disease.46

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.26
Current Recommendations:
1. Intrapartum antibiotic prophylaxis at the time of membrane rupture or labour for all women who have had:
• previous infant with invasive GBS disease
• GBS bacteriuria during current pregnancy
• positive screening culture, routinely done at 35–37 weeks during current pregnancy.
• if GBS status is unknown, use intrapartum prophylaxis for any of the following:
1. preterm labour (< 37 weeks)
2. rupture of membranes for > 18 hours
3. maternal fever ≥ 38ºC.
Note: If GBS status is unknown, knowledge of colonization status in a previous pregnancy may be
considered along with the above risk factors. Recent retrospective studies have reported a GBS colonization
recurrence rate in a subsequent pregnancy of 38% to 53%.12-15
2. Preterm labour with intact membranes:
• if GBS status negative within five weeks, antibiotic prophylaxis need not be initiated.
• if GBS status unknown, GBS vaginal/rectal screening should be performed on admission and intrapartum
prophylaxis is recommended pending results of culture. Antibiotics may be stopped if culture is negative.
3. Management of prelabour rupture of membranes (PROM) and preterm PROM (PPROM) is discussed in the chapter
on PROM.
• for women with term PROM who are colonized with GBS, it is recommended that labour be induced with
oxytocin.1,47 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 those women who
were induced with oxytocin compared to those who were induced with prostaglandin or who received expectant
management.48 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 induced with prostaglandin or who
received expectant management.49
• 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

4. Situations where GBS intrapartum prophylaxis is not indicated:

• previous pregnancy with a positive GBS screening culture (unless a culture was also positive within five weeks in
the current pregnancy).
• planned Caesarean delivery 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 prior to the planned Caesarean section.3
• negative vaginal and rectal GBS screening culture, within five weeks, regardless of intrapartum risk factors.
5. Chorioamnionitis:
• regardless of GBS status, consider this diagnosis with maternal fever > 38°, fetal tachycardia, and signs of
maternal sepsis. Maternal oral temperature may be inaccurate; consider rectal temperature.
• 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 allergy
• if woman is at low risk for anaphylaxis, administer: cefazolin 2 g IV, followed by 1 g every 8 hours until delivery
• if woman is at high risk for anaphylaxis:
• if the GBS isolate is sensitive to both clindamycin and erythromycin, administer:
• clindamycin 900 mg IV, every 8 hours, until delivery
• if the GBS isolate is not sensitive (or unknown) to clindamycin or erythromycin, administer:
• vancomycin 1 g IV, every 12 hours until delivery. However, if GBS isolate was sensitive to clindamycin
but resistant to erythromycin by antimicrobial susceptibility testing, clindamycin may be used if testing
for inducible resistance to clindamycin is available and negative.3
Management of Infants
Management of asymptomatic infants of mothers who had an indication for GBS prophylaxis is based on clinical presentation,
the adequacy of the maternal intrapartum chemoprophylaxis, gestational age, and the duration of membrane rupture.2 89%9
to 95%10 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). Four
percent of infants will develop signs between 24 hours and 48 hours, and only 1% after 48 hours.2 A 2012 retrospective study of
140 000 women at the Parkland Hospital in Dallas, Texas found 94 neonates with early-onset GBS sepsis. Ninety-three of these

were diagnosed in the first hour of life. Most of these had evidence of sepsis peripartum with an increase in preterm delivery,
Caesarean section, low Apgars, and abnormal umbilical cord pH and base deficit.50
• Adequate intrapartum antibiotic prophylaxis is defined as ≥ 4 hours of IV penicillin, ampicillin or cefazolin before
delivery.2,3
• 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.2,3 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.34 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).34
Potential neonatal and infant effects of intrapartum antibiotics
• There is increasing interest in the effect of intrapartum maternal antibiotic administration on the neontates 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 health consequences of this association.51
• One concern about antenatal and neonatal antibiotic exposure is a potential increase in the child’s later diagnosis of
allergic disease.52 Reassuringly, a 2015 retrospective study from Pennsylvania of 492 women(who delivered vaginally)
and their child(ren) found no increase in atopic dermatitis when intrapartum antibiotics were used for <24 hours.53
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 workup,
additional therapy, or investigations. These infants should be observed for 48 hours for signs of infection.
However, the infants may be discharged from hospital after 24 hours if other discharge criteria are met, provided
the caregiver is able to access health care resources if clinical signs of sepsis develop.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.54

• when the mother received inadequate intrapartum antibiotic prophylaxis:

• the CDC guideline3 recommends that the infant should be observed for ≥ 48 hours:
• for infants ≥ 37 weeks’ gestational age and when membranes ruptured <18 hours, no routine
diagnostic testing is recommended.
• for infants < 37 weeks’ gestational age or when membranes ruptured ≥ 18 hours, a blood culture and
CBC with differential and platelets is recommended.
• the CPS Statement2 recommends that a CBC be performed and that the infant not be discharged before
24 hours. If the white blood cell (WBC) count is < 5.0x109/L, then the risk of sepsis is substantially increased
and a full diagnostic evaluation and empirical antibiotics should be considered. If the infant is well, discharge
at 24 hours to 48 hours is conditional on the parents’ ability to immediately access health care if clinical signs
of sepsis develop.
• For infants being investigated with blood cultures, a 2014 study of 38 infants with early onset sepsis
(including 10 cases of GBS) found that maternal intrapartum antibiotic treatment did not delay the time to
blood culture positivity. The authors concluded that the duration used to determine a positive blood culture
result is not afftected by maternal receipt of intrapartum antibiotics.55
• in the situation of a planned home birth it is important that the same principles of care for the mother and
neonate are provided and maintained.
• Preterm infants require individualized evaluation and management. However, the CPS and CDC guidelines suggest that
well appearing infants 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.2,3
• Infants of mothers with chorioamnionitis require a diagnostic and therapeutic evaluation for sepsis.
• Symptomatic infants are at a very high risk for morbidity and require early consultation,
investigation, and treatment. These infants are ideally managed in an intensive care facility.
A septic workup includes a complete blood-cell count and differential, blood culture, chest X-ray, and a lumbar
puncture, if possible.
Early signs of neonatal sepsis:
• Apnea
• Tachypnea
• Temperature instability
• Tachycardia
• Lethargy
• Poor feeding

The following is an algorithm for the secondary prevention of early-onset group B streptococcal (GBS)
disease among newborns (modified from the 2010 CDC guideline6)

a) CBC (WBC, diff., plat.), blood culture, CXR (if resp. Sx), +/ – LP
b) Antibiotics: ampicillin + coverage for other potential organisms
c) Diagnose clinically: fever, tender uterus, purulent/foul amn. fluid, etc.
d) CBC (WBC, diff., plat.) & blood culture
e) If signs of sepsis → full diagnostic evaluation & antibiotic therapy
f) Penicillin, ampicillin, or cefazolin for ≥ 4 hrs before delivery
g) May be discharged @ 24 hrs if criteria met & access to care
h) Canadian Paediatric Society recommends: CBC (WBC, diff., plat.). Well infants may be discharged @ 24 hrs if criteria
met and immediate access to care5
Conclusions
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’ is recommended with intrapartum prophylaxis, if positive.
4. Antepartum treatment of GBS colonization is not justified with the exception of urinary tract infection.
5. Individual centers must adopt strategies for GBS disease prevention.

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15. Page-Ramsey SM, Johnstone SK, Kim D, Ramsey PS. Prevalence of group B Streptococcus colonization in subsequent
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time polymerase chain reaction assay. Obstet Gynecol. 2008;111:1335-41.
21. El Helali N, Nguyen JC, Ly A, Giovangrandi Y, Trinquart L. Diagnostic accuracy of a rapid real-time polymerase chain
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23. Young BC, Dodge LE, Gupta M, Rhee JS, Hacker MR. Evaluation of a rapid, real-time intrapartum group B streptococcus
assay. Am J Obstet Gynecol. 2011;205:372-6.
24. Chan WS, Chua SC, Gidding HF, Ramjan D, Wong MY, Olma T, et al. Rapid identification of group B streptococcus
carriage by PCR to assist in the management of women with prelabour rupture of membranes in term pregnancy.
Aust N Z J Obstet Gynaecol. 2014;54:138-45.
25. Couturier BA, Weight T, Elmer H, Schlaberg R. Antepartum screening for group B Streptococcus by three FDA-cleared
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26. Verani JR, Spina NL, Lynfield R, Schaffner W, Harrison LH, Holst A, et al. Early-onset group B streptococcal disease in the
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27. Price D, Shaw E, Howard M, Zazulak J, Waters H, Kaczorowski J. Self-sampling for group B streptococcus in women 35 to
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28. Gygax SE, Schuyler JA, Kimmel LE, Trama JP, Mordechai E, Adelson ME. Erythromycin and clindamycin resistance in
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29. Capanna F, Emonet SP, Cherkaoui A, Irion O, Schrenzel J, Martinez de Tejada B. Antibiotic resistance patterns among
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30. Church D, Carson J, Gregson D. Point prevalence study of antibiotic susceptibility of genital group B streptococcus isolated
from near-term pregnant women in Calgary, Alberta. Can J Infect Dis Med Microbiol. 2012;23:121-4.
31. Boyer KM, Gotoff SP. Strategies for chemoprophylaxis of GBS early-onset infections. Antibiot Chemother. 1985;35:267-80.
32. Allen VM, Yudin MH, Gouchard C, Goucher M, Caddy S, Castillo E, et al. Managment of group B streptococcal bacteriuria
in pregnancy [SOGC clinical practice guideline no 276]. J Obstet Gynaecol Can. 2012;34:482-6.
33. Ohlsson A, Shah VS. Intrapartum antibiotics for known maternal Group B streptococcal colonization. Cochrane Database
Syst Rev. 2014;6:CD007467.
34. Fairlie T, Zell ER, Schrag S. Effectiveness of intrapartum antibiotic prophylaxis for prevention of early-onset group B
streptococcal disease. Obstet Gynecol. 2013;121:570-7.
35. Scasso S, Laufer J, Rodriguez G, Alonso JG, Sosa CG. Vaginal group B streptococcus status during intrapartum antibiotic
prophylaxis. Int J Gynaecol Obstet. 2014.
36. Berardi A, Rossi C, Guidotti I, Vellani G, Lugli L, Reggiani ML, et al. Factors Associated with Intrapartum Transmission of
Group B Streptococcus. Pediatr Infect Dis J. 2014;33:1211-5.
37. Illuzzi JL, Bracken MB. Duration of intrapartum prophylaxis for neonatal group B streptococcal disease: a systematic
review. Obstet Gynecol. 2006;108:1254-65.
38. Barber EL, Zhao G, Buhimschi IA, Illuzzi JL. Duration of intrapartum prophylaxis and concentration of penicillin G in fetal
serum at delivery. Obstet Gynecol. 2008;112:265-70.
39. Onwuchuruba CN, Towers CV, Howard BC, Hennessy MD, Wolfe L, Brown MS. Transplacental passage of vancomycin from
mother to neonate. Am J Obstet Gynecol. 2014;210:352-4.

40. Heikkinen T, Laine K, Neuvonen PJ, Ekblad U. The transplacental transfer of the macrolide antibiotics erythromycin,
roxithromycin and azithromycin. BJOG. 2000;107:770-5.
41. Bulska M, Szczesniak P, Pieta-Dolinska A, Oszukowski P, Orszulak-Michalak D. The placental transfer of erythromycin in
human pregnancies with group B streptococcal infection. Ginekol Pol. 2015;86:33-9.
42. Laiprasert J, Klein K, Mueller BA, Pearlman MD. Transplacental passage of vancomycin in noninfected term pregnant
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43. Adair CE, Kowalsky L, Quon H, Ma D, Stoffman J, McGeer A, et al. Risk factors for early-onset group B streptococcal
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44. Nakatsuka N, Jain V, Aziz K, Verity R, Kumar M. Is there an association between fetal scalp electrode application and
early-onset neonatal sepsis in term and late preterm pregnancies? A case-control study. J Obstet Gynaecol Can.
2012;34:29-33.
45. Kabiri D, Hants Y, Yarkoni TR, Shaulof E, Friedman SE, Paltiel O, et al. Antepartum Membrane Stripping in GBS Carriers,
Is It Safe? (The STRIP-G Study). PLoS One. 2015;10:e0145905.
46. Ohlsson A, Shah VS, Stade BC. Vaginal chlorhexidine during labour to prevent early-onset neonatal group B streptococcal
infection. Cochrane Database Syst Rev. 2014;12:CD003520.
Gynaecol Can. 2013;35:840-57.
48. Hannah ME, Ohlsson A, Farine D, Hewson SA, Hodnett ED, Myhr TL, et al. Induction of labor compared with expectant
management for prelabor rupture of the membranes at term. TERMPROM Study Group. N Engl J Med. 1996;334:1005-10.
49. 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.
50. Tudela CM, Stewart RD, Roberts SW, Wendel GD, Stafford IA, McIntire DD, et al. Intrapartum evidence of early-onset
group B streptococcus. Obstet Gynecol. 2012;119:626-9.
51. Azad MB, Konya T, Persaud RR, Guttman DS, Chari RS, Field CJ, et al. Impact of maternal intrapartum antibiotics, method
of birth and breastfeeding on gut microbiota during the first year of life: a prospective cohort study. BJOG. 2015.
52. McKeever TM, Lewis SA, Smith C, Hubbard R. The importance of prenatal exposures on the development of allergic
disease: a birth cohort study using the West Midlands General Practice Database. Am J Respir Crit Care Med.
2002;166:827-32.

53. Wohl DL, Curry WJ, Mauger D, Miller J, Tyrie K. Intrapartum antibiotics and childhood atopic dermatitis. J Am Board Fam
Med. 2015;28:82-9.
54. Berger MB, Xu X, Williams JA, Van de Ven CJ, Mozurkewich EL. Early hospital discharge of infants born to group B
streptococci-positive mothers: a decision analysis. BJOG. 2012;119:439-48.
55. Sarkar SS, Bhagat I, Bhatt-Mehta V, Sarkar S. Does maternal intrapartum antibiotic treatment prolong the incubation
time required for blood cultures to become positive for infants with early-onset sepsis? Am J Perinatol. 2015;32:357-62.

Chapter 21
Antepartum and
Intrapartum Hemorrhage
Definition
Antepartum hemorrhage (APH) 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 (formerly referred to as abruptio placentae) (incidence: 1 in 100 births)
• Placenta previa (incidence: approximately 1 in 200–300 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 account for slightly more than half of the cases of antepartum hemorrhage and are two
of the leading causes of perinatal morbidity and mortality in the third trimester. Antepartum hemorrhage is listed as 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 (IUGR) is reported in 16% of
women with placenta previa. Antepartum bleeding is associated with an increased risk of preterm birth.3
Antepartum and Intrapartum Hemorrhage 1

Placenta Previa
Definition
• Placenta previa: The placenta is touching or covering the internal os at term
• Low-lying: The leading edge of the placenta lies within 2 cm of the internal os at term
• On second trimester ultrasound (U/S) 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.
Incidence
The incidence of placenta previa at term remains at approximately one in 200.4, 5
Risk Factors For Placenta Previa5

• Previous placenta previa
• Previous Caesarean delivery,6 especially when the interpregnancy interval is < 12 months7
• Previous uterine surgery, including myomectomy and dilation and curettage (D&C)
• Advanced maternal age (≥ 35 years)
• Multiparity (≥ 3)
• Smoking and cocaine use in pregnancy
• Multiple gestation
• In vitro fertilization
Classification
Previously, the classification of placenta previa was based on physical exam and imprecise sonography. It described a total
(complete) previa as one which 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. This practice is no longer applicable in the modern diagnosis of placenta previa and has been replaced
by more precise transvaginal ultrasound measurements. The contemporary classification has been recently reviewed8 to address
areas of controversy in placental location terminology. Currently suggested classification depends on whether the cervix is closed
or open. Partial placenta previa should be restricted to the situation of an open cervix. If the cervix is closed, the distinction
between a placental edge at the margin of the internal os or covering it is not clinically important and should be grouped as

placenta previa. The mode of delivery will be by Caesarean section (CS) for viable pregnancy. If the placenta is implanted in the
lower part of the uterus 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 lowest part of the placental edge and the cervical os.
The likelihood of bleeding during labour has been consistently greater when the placenta is within two cm of the cervix (see
Table). At 35 weeks’ 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 in total), the overall risk of bleeding during labour with a low-lying placenta (1–20 mm from the os) is
approximately 30%.8 For distances less than 11 mm, the estimated risk of bleeding in labour 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. If a trial of labour is planned, the capability of performing a Caesarean
delivery urgently and to provide immediate blood transfusions in case of severe vaginal bleeding is recommended.
A distance greater than 2 cm is considered safe for vaginal delivery. However, there is a continuum and significant vaginal
bleeding has been rarely described with a placenta-os distance greater than 2 cm.9, 10
Studies of low-lying placenta in which the outcome was Caesarean delivery performed for bleeding
according to the placenta-os distance at or near term.
N Placenta-os Distance Caesarean Delivery for Bleeding
Dawson et al.11 40 1–10 mm 90% of those in labour
11–20 mm 29% of those in labour
Bronsteen et al.12 86 1–9 mm 73% of those in labour
10–20 mm 27% of those in labour
Vergani et al.13 24 1–10 mm 81% of those in labour
Vergani et al.13 29 11–20 mm 0% of those in labour
Diagnosis
Avoid a pelvic exam 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 prior to 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 whether the placenta partially or completely covers the internal cervical os.
Transabdominal Sonography (TAS)
Transabdominal sonography 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 placenta14 caused by the fetal head interfering
with visualization of the lower uterine segment,15 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 (TVS)
Transvaginal sonography 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 in situations when the placenta is situated low in the
uterus and the distance from the os cannot be clearly delineated transabdominally. TVS is particularly useful for a posterior
placenta previa near or at term.
In the case of 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 a placenta previa is diagnosed is critical to management.
Placental “migration”, involves the leading edge of the placenta “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 be previa, 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 cross the internal os. Only 1% to 2% of women will have a placenta that reaches or crosses 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 did not reach or cross 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 crosses 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
If the placenta reaches or crosses 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 a placenta previa is diagnosed in the second trimester in an asymptomatic woman, there is no evidence to support or refute
restriction on maternal activities. An ultrasound should be repeated in the third trimester at 28 weeks’ to 30 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 the previa 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.35,36,37,38 Women selected for outpatient management are those who are highly compliant, have
no ongoing bleeding, are hemodynamically stable, live within a short travel distance from the hospital, and have an immediate
transportation capability to the hospital. The evidence suggests that for these selected women, outpatient management appears
to be an acceptable alternative.23

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
CS is the mode of delivery for placenta previa 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 (e.g., Jehovah’s Witness).
Delivery is recommended when the fetus reaches 37 weeks’ gestation; the fetal lungs are mature as confirmed by amniocentesis
before 37 weeks’, or in the presence of severe maternal hemorrhage or abnormal (non-reassuring) 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 cc 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 need to
be aware of all the fertility preservation techniques before considering hysterectomy. For example, fertility preservation using
utero-vaginal packing at the time of Caesarean section can be achieved with a success rate of up to 94%.40
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 exams
• Avoid membrane stripping
• Avoid mechanical methods for cervical ripening
• Intravenous access throughout labour and delivery
• Group, screen +/- cross match
• Be prepared for possible PPH

Summary
1. Placenta previa is diagnosed primarily by a second trimester ultrasound (preferably TVUS).
2. Placenta previa is diagnosed when:
a) the inferior margin of the placenta reaches or crosses the internal cervical os on a second trimester ultrasound
scan
b) if the inferior margin is less than 2 cm from the internal os on ultrasound and does not reach the internal os, the
preferred terminology is low-lying placenta
3. Placenta previa identified in the second trimester is reassessed by U/S in the third trimester.
4. The vast majority of low-lying placentas diagnosed early in pregnancy resolve by term
5. Premature birth is the primary fetal complication of placenta previa.
6. Selected women with symptomatic 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 Caesarean birth rate. 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.41 A retrospective study of 64 359 deliveries between 1982 and 2002 reports an increase in Caesarean rates
from 12.5% (1982) to 23.5% (2002) and an overall incidence of placenta accreta (all forms) of 1 in 533.42,43 A 2009 study by
Flood et al. showed a decrease in peripartum hysterectomy over the last four 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 seen in the
table below.
Placenta Previa and Placenta Accreta (Includes Increta and Percreta)

by Number of Prior Caesarean Deliveries
No. prior Number Number of Number (%) Number (%) Number (%) No
Caesarean Caesarean Placenta previa Placenta accreta* Placenta previa Placenta previa
Deliveries Deliveries with accreta** with accreta
0 (Primary CS) 6201 398 (6.42) 15 (0.24) 13 (3) 2 (0.03)
1 15 808 211 (1.33) 49 (0.31) 23 (11) 26 (0.2)
2 6324 72 (1.14) 36 (0.57) 29 (40) 7 (0.1)
3 1452 33 (2.27) 31 (2.13) 20 (61) 11 (0.8)
4 258 6 (2.33) 6 (2.33) 4 (67) 2 (0.8)
≥5 89 3 (3.37) 6 (6.74) 2 (67) 4 (4.7)
* Includes increta and percreta. P< .001 from Cochran-Armitage test for trend
** Increased risk with increasing number of Caesarean deliveries P< .001
Adapted from Silver et al.: Maternal morbidity associated with multiple repeat cesarean deliveries. Obstet Gynecol 2006;107:1226-32.45
Risk Factors43,46,47
• Placenta previa with or without previous uterine surgery
• Prior CS
• Prior myomectomy
• Asherman’s syndrome
• 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 ultrasound48,49,50
can detect up to 85% of placenta accretas. Additional investigations using ultrasound Doppler51,52,53,54 and MRI55,56,57,58 may
be helpful to increase the detection of a placenta accreta in women at risk. Placenta accreta 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. Lacunae. They have high-velocity and low-resistance flow and are irregular in cross-section on grey-scale ultrasound.
4. Myometrial thickness of less than 1 mm or its loss higher in the uterus can be ominous.
5. Combination of grey-scale and colour Doppler ultrasound. The accuracy of diagnosis appears to improve using more
than one ultrasound finding. Vessels can be seen bridging the placenta to myometrium, improving the performance of
grey-scale ultrasound in the diagnosis.
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 delivery. Women with suspected placenta
accreta should be delivered 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 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 in a Level III care 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.

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 where either uterine preservation was requested, or risk
of damage to surrounding pelvic organs was extremely high due to placenta percreta. Success rate in this study was 80%.64
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 postpartum hemorrhage bleeding. For this reason, conservative management could
be attempted in very specific and select cases after multi-disciplinary approach and patient informed consent.60, 61
The decision as to WHEN to best deliver is still not clear from randomized controlled or more rigorous observational studies.
However, the best available evidence to date seems to indicate that in most cases, in the absence of clinical indications, the
period between 34 weeks and 35 weeks is optimal.65
Conservative treatments have included:41,66
• 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. Post-
operative 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 uterine artery embolization
• Leaving the placenta in place and close postpartum follow-up

Summary
1. The incidence of placenta accreta has increased significantly, mainly due to 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. Ultrasound is highly diagnostic and 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.62
7. A conservative approach may be attempted in selected patients.
8. Definitive therapy is Caesarean hysterectomy and should not be delayed.
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 condition is not self-limited, bleeding
will continue and may extend through the myometrium to the serosa, causing 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.41, 67

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 5.5% to 16.6%.68 Ischemic
Placental Disease: evidence is emerging that seems to indicate a link between pre-eclampsia, small for gestational
age, and abruption. It is as yet unclear if this triad is causal or simply an association.69
Predisposing Factors and Relative Risk41

• Prior placental abruption 10–25
• Inherited thrombophilia 3–7
• Preterm rupture of membranes 2.4–4.9
• Hypertension 2.1–4.0
• Iron deficiency70 2.4
• Multiple gestation 2.1
• Hydramnios 2
• Chronic hypertension 1.8–3.0
• Maternal age and parity 1.3–1.5
• Smoking 1.4–1.9
• Trauma N/A
• Cocaine abuse N/A
• Previous Caesarean delivery, especially when the interpregnancy interval is < 12 months.7
6
Remember ……Most abruptions are idiopathic.41

Diagnosis
1. Avoid a pelvic exam until placenta previa has been ruled out.
2. History and physical examination. Clinical differences will give the first clues to the diagnosis.
3. Ultrasound does not reliably diagnose a placental abruption.
4. Controversy exists about performing a speculum exam in the absence of a prior ultrasound. If available, an ultrasound
should be done prior to a speculum exam to first rule out placenta previa. Speculum exam is performed to assess the
cervix for dilatation or any lower genital tract lesion.
5. Electronic fetal monitoring (EFM) and ultrasound will assist in the assessment of fetal well-being.
6. Abdominal pain is usually the presenting symptom. 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
follows. This classification is based on fetal condition. The degree of bleeding and the maternal hemodynamic status will also
influence management.
Abruption Definition Management
Mild Evidence of abruption with no fetal compromise • Conservative management if pre-term

• 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 (non-reassuring) EFM or unfavourable cervix
Severe Evidence of abruption with fetal death • Initiate delivery process (non-emergent)
• Be vigilant for disseminated intravascular coagulopathy (DIC)

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 lobe where the umbilical cord vessels 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.
Incidence
Vasa previa occurs in 1 in 2000–5000 pregnancies.71,72 The incidence is higher in twin pregnancies (due to the increased
incidence of velamentous cord insertion) and also in the presence of a placenta previa.
Risk Factors
• Velamentous insertion of the cord
• In vitro fertilization
• Placenta previa
• Presence of succenturiate lobe
• Twin pregnancy

When undiagnosed, fetal mortality is estimated to be as high as 60%.73, 74
Older studies referenced in Gabbe’s Obstetrics: normal and problem pregnancies suggest an overall perinatal mortality rate for
vasa previa of between 58% and 73%.66 Antenatal diagnosis is not always possible. However, when antenatal diagnosis is made,
up to 97% neonatal survival rate is possible.75
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 1000.9 If

the placenta is low-lying, the placental cord insertion is marginal, or there is multiple pregnancy or pregnancy following in vitro
fertilization, a careful assessment of the placental cord insertion during the second trimester ultrasound should be done.75 A
repeat scan at 28 weeks is recommended since spontaneous resolution of the vasa previa can occur.
Prenatal diagnosis is now possible using transvaginal ultrasound to observe fetal vessels crossing the internal os or within 2
cm of the os. A prenatal diagnosis mandates closer observation of the woman and delivery prior to term by an elective CS.
Some suggest hospital admission at 30 weeks to 32 weeks with CS at 35 weeks to 36 weeks.74 Occasionally, the vessels may
be detected on routine ultrasound or felt on digital exam prior to 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 or bradycardia). 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.
Management
If vasa previa is diagnosed and persistent at 28 weeks, antenatal glucocorticoids should be administered at 28 weeks’ to 30
weeks’ gestation. Admission at 30 weeks to 32 weeks to a centre with a minimum Level II capability is recommended. Antenatal
consultation with paediatrics should be obtained as well. A planned Caesarean section at 35 weeks’ to 36 weeks’ gestation
with the paediatric team present is recommended. A clearly labelled patient’s chart with the diagnosis is necessary in order to
facilitate immediate recognition and intervention should vaginal bleeding occur. Thus any unnecessary delay resulting in fetal
and/or neonatal death may be avoided. Using this approach, more than 97% neonatal survival is expected.73
In the setting of rupture of the membranes associated with acute painless vaginal bleeding and an abrupt change in the fetal
heart rate (tachycardia or bradycardia), STAT Caesarean section is required to avoid fetal exsanguination.
Diagnosis and Management of Antepartum Hemorrhage (General)

1. History and physical exam. Clinical differences will give the first clues to the diagnosis.
Comparative clinical presentation and risk factors of placental abruption and placenta previa
(these are NOT exclusive)
Placental Abruption Placenta Previa
Age over 35 Multiparity76

Comparative clinical presentation and risk factors of placental abruption and placenta previa
(these are NOT exclusive)
Placental Abruption Placenta Previa
In Vitro Fertilization-Embryonic Transfer Associated with previous uterine surgery
Preterm Labor
Smoker76
Associated with hypertensive disorders (pre-existing and gestational) ,
Uterine over distension, abdominal trauma
Abdominal pain or backache (often unremitting) Painless (unless in labour)
Uterine tenderness Uterus not tender
Increased uterine tone Uterus soft
Uterine irritability/contractions No uterine irritability/contractions
Usually normal presentation Malpresentation or high presenting part
Fetal heart may be absent, atypical or abnormal Fetal heart usually normal
Shock and anemia disproportionate with apparent blood loss Shock and anemia correspond to apparent blood loss
May have coagulopathy Coagulopathy very uncommon initially
Placental abruption may be seen on transabdominal ultrasound but a Transvaginal ultrasound is the definitive diagnostic test for placenta previa.
negative ultrasound does not rule out abruption.
2. Determine hemodynamic stability and evaluate uterine tone and activity.

3. Evaluate fetal well-being. Electronic fetal monitoring and ultrasound will assist in the assessment of fetal status.
4. Avoid a pelvic exam until placenta previa has been ruled out.
5. Controversy exists regarding performing a speculum exam in the absence of a prior ultrasound. Perform an ultrasound
to rule out placenta previa, if possible, prior to speculum exam. Speculum examination is performed to assess the

cervix for dilatation or for any lower tract lesion. 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
b) Complete blood count (hemoglobin, hematocrit, platelet count)
c) Other investigations dictated by the presence of co-morbid 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 µg of Rh immune globulin should be given for every 30 cc of fetal blood detected in the maternal circulation
(equivalent to 15 cc 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.
A CS will be required if bleeding is due to a placenta previa or placental abruption when maternal or fetal health is compromised
(unless vaginal delivery is imminent). A DIC should be considered. A bedside clot test (no visible clotting in six 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 massive transfusion protocol is useful. The risk of DIC is increased if the woman presents with an intrauterine fetal
death.

Once maternal and fetal status is stable, and if 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. All women with an APH are at risk for recurrent bleeding.
• 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.77 If there is
greater than one contraction in 15 minutes or there are ominous signs such as bleeding or uterine pain, the duration of
surveillance should be longer (at least 24 hours).78,79,80
• If the fetus is preterm, expectant management may be appropriate depending on the maternal hemodynamic status
and fetal well-being. Antepartum steroids 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.
• There is insufficient information to recommend the use of tocolytics.
• All patients with an antepartum hemorrhage are at risk of recurrent bleeding.
Summary
1. A standard protocol for the management of antepartum hemorrhage is helpful.
2. A “massive transfusions” protocol should be implemented in each birthing 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 mother 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, placenta, and fetal status and appropriate, active management are required.

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Advances in Labour and Risk Management

23rd Edition — 2016–2017

2016 ALARM Committee Members: 2016 Obstetrical Content

© Joint Commission Resources: Sentinel event statistics. Oakbrook Terrace (IL):

Communication, Consultation, Documentation, and Disclosure 1

Communication, Consultation, Documentation, and Disclosure 2

Strategies to facilitate interprofessional care and planning might include:

Key Points Related to Communication

Communication, Consultation, Documentation, and Disclosure 3

Communication, Consultation, Documentation, and Disclosure 4

Communication in the Consultation Process

Patient Referring Caregiver Consultant

Courtesy and respect Courtesy and respect Courtesy and respect

Avoid referrals to another consultant for

A consultation can involve :

Communication, Consultation, Documentation, and Disclosure 5

In a 2012 study, Kessler et al. describe the five Cs of consultation:13

Communication, Consultation, Documentation, and Disclosure 6

Communication and Litigation

Communication, Consultation, Documentation, and Disclosure 7

Communication, Consultation, Documentation, and Disclosure 8

Communication, Consultation, Documentation, and Disclosure 9

The 5 C’s of Effective Documentation

Communication, Consultation, Documentation, and Disclosure 10

Communication, Consultation, Documentation, and Disclosure 11

What do Patients Expect?

Communication, Consultation, Documentation, and Disclosure 12

Specifically, patients need to know:37

• How do we manage this for my family

Communication, Consultation, Documentation, and Disclosure 13

For Health Care Organizations:

Communication, Consultation, Documentation, and Disclosure 14

Meeting with the Patient/Family:

Communication, Consultation, Documentation, and Disclosure 15

Communication, Consultation, Documentation, and Disclosure 16

Communication, Consultation, Documentation, and Disclosure 17

Communication, Consultation, Documentation, and Disclosure 18

Communication, Consultation, Documentation, and Disclosure 19

Types of Evidence – Qualitative or Quantitative

Grades of Evidence and Classification of Recommendations

Summary of Grades of Evidence

Grades of Recommendations from the Canadian Task Force on

Effect of Intervention on Outcome of Interest

The results displayed in a meta-analysis fall into one of three categories:

Bad News Experiences

Patient and Family Response to an Adverse Event

Bad News in the Birthing Room 1

The Nature of the Event

Interpretation of the Event

Bad News in the Birthing Room 2

Post-Traumatic Stress Disorder (PTSD)

Coping Mechanisms to an Event

Bad News in the Birthing Room 3

Health Professionals’ Actions to Facilitate Coping

Bad News in the Birthing Room 4

• Bereavement outfits/receiving blankets

Bad News in the Birthing Room 5

Resources for Families and Health Professionals

Strategies for Communication of Bad News

Bad News in the Birthing Room 6

Who Should be Present

Key Phrase to Open a Conversation

Bad News in the Birthing Room 7