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2015v1.0
Munro Kerr’s
Operative
Obstetrics

THIRTEENTH EDITION

Edited by
Sir Sabaratnam Arulkumaran
KB MB BS (University of Ceylon)
PhD DSc FRCS FRCOG
Professor Emeritus, Department of Obstetrics & Gynaecology
St George’s University Medical School
London, UK

Michael S Robson
MB BS MRCOG FRCS (Eng) FRCPI
Consultant Obstetrician and Gynaecologist
The National Maternity Hospital
Dublin, Ireland

Original illustrations by Ian Ramsden

Edinburgh London New York Oxford Philadelphia St Louis Sydney 2020

© 2020, Elsevier Ltd. All rights reserved.

First published 1908 as Operative Midwifery by J. Munro Kerr

Second edition 1911
Third edition 1916
Fourth edition 1937 as Operative Obstetrics by J. Munro Kerr, D. McIntyre and D. Fyfe Anderson
Fifth edition 1949 by J. Munro Kerr and J. Chassar Moir
Sixth edition 1956 and Seventh edition 1964 as Munro Kerr’s Operative Obstetrics by J. Chassar Moir
Eighth edition 1971 by J. Chassar Moir and P. R. Myerscough
Ninth edition 1977 and Tenth edition 1982 by P. R. Myerscough
Eleventh (Centenary) edition 2007 and Twelfth edition 2014 by T. F. Baskett, A. A. Calder and S. Arulkumaran
Thirteenth edition 2020

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 List of Contributors
The editors would like to acknowledge and offer
grateful thanks for the input of all previous edi-
tions’ contributors, without whom this new edition
would not have been possible.
Sir Sabaratnam Arulkumaran KB, MB, BS
(University of Ceylon), PhD, DSc, FRCS, FRCOG
Professor Emeritus, Department of Obstetrics &
Gynaecology
St George’s University Medical School
London, UK
T. Bergholt, MD, PhD, MSci
Consultant, Department of Obstetrics, Rigshospitalet,
University of Copenhagen, Copenhagen, Denmark
D.J. Brennan, MB, MRCOG, FRCPI, PhD, UCD
Professor of Gynaecological Oncology, National
Maternity Hospital, Dublin, Ireland
D.P. Brophy, FFR-RCSI, FRCR
Specialist in Radiology, Department of Radiology,
St. Vincent’s University Hospital, Dublin, Ireland
Alan Cameron, MD, FRCOG
Professor of Fetal Medicine, Ian Donald Fetal Medicine
Centre, Queen Elizabeth University Hospital,
Glasgow, UK
E. Chandraharan, MBBS, MS (Obs & GYN), DFSRH,
FSLCOG, FRCOG
Lead Consultant Labour Ward, St George’s University
Hospitals NHS Foundation Trust, London, UK
Joanna F. Crofts, MD, MRCOG
Consultant Obstetrician, Women’s and Children’s
Health, North Bristol NHS Trust, Bristol, UK,
NIHR Academic Clinical Lecturer, University of
Bristol, UK
Simon Cunningham, BSc, MRCOG, MSc
Consultant in Feto-Maternal Medicine & Obstetrics,
University Hospitals of North Midlands, Stoke-­on-­
Trent, UK
Timothy J. Draycott, MBBS, BSc, MD, FRCOG
Professor of Obstetrics, North Bristol NHS Trust,
Bristol, UK
Dan Farine, MD, FRCSC
Professor, Maternal Fetal Medicine, Mount Sinai
Hospital, Toronto, Canada
Richard A. Greene, MB, BCh BAO, FRCOG, FRCPI
Consultant Obstetrician and Gynaecologist,
Professor of Clinical Obstetrics, Cork University
Maternity Hospital & University College Cork,
Cork, Ireland
Niamh E. Hayes, MB, FCAI, MSc
Consultant Anaesthesiologist, Honorary Clinical Senior
Lecturer, RCSI Rotunda Hospital, Dublin, Ireland
A. Hedditch, MSc
Senior Midwife, OUH NHS Foundation Trust,
Oxford, UK
Shane P. Higgins, MRCOG, FRANZCOG, MPH
Master, National Maternity Hospital, Dublin,
Republic of Ireland
Kim Hinshaw, MB, BS, FRCOG
Consultant Obstetrician & Gynaecologist, City Hospitals
Sunderland NHS Foundation Trust, Sunderland, UK,
and Visiting Professor, Faculty of Applied Sciences,
Sunderland University, Sunderland, UK
E.J. Hotton, MBChB, BSc
Clinical Research Fellow, North Bristol NHS Trust and
Bristol Univeristy, Bristol, UK
L. Impey, BA, FRCOG
Consultant in Obstetrics and Fetal Medicine, OUH
NHS Foundation Trust, Oxford, UK
Tracey A. Johnston, MBChB, MD, FRCOG
Consultant in Maternal Fetal Medicine, Birmingham
Women’s and Children’s NHS Foundation Trust,
Birmingham, UK
Marie Anne Ledingham, MD, FRCOG
Consultant in Maternal and Fetal Medicine, The Queen
Elizabeth Hospital, Glasgow, Scotland
Siaghal Mac Colgáin, MBBCh, BAO, LRCP SI, FCAI,
DPMCAI
Consultant Anaesthetist, The National Maternity
Hospital and St Vincent’s Healthcare Group, Dublin,
Ireland
vii
viii List of Contributors
Cynthia Maxwell, MD, FRCSC, Diplomate, American
Board of Obesity Medicine (ABOM)
Associate Professor, Maternal Fetal Medicine, Mount
Sinai Hospital, Toronto, Ontario, Canada
Jane E. Norman, MBChB, MD
Professor of Maternal and Fetal Health, MRC Centre
for Reproductive Health, University of Edinburgh,
Edinburgh, UK
Fiona Nugent, BSc, MBChB
Specialty Trainee in Obstetrics & Gynaecology, Royal
Alexandra Hospital, Paisley, NHS Greater Glasgow
& Clyde, Glasgow, UK
Stephen O’Brien, BMBS, PhD
Specialty Registrar in Obstetrics & Gynaecology,
Women’s and Children’s Health, Gloucestershire
Hospitals NHS Foundation Trust, Gloucester, UK
Karl S.J. Olah, MB, BS, MRCOG
Consultant Obstetrician & Gynaecologist, Warwick
Hospital, Warwick, UK
J.M. Palacios ­Jaraquemada, MD, PhD, FRCOG
Obgyn Consultor, CEMIC University Hospital, Buenos
Aires, Argentina
S. Paterson-­Brown, FRCS, FRCOG
Consultant Obstetrician, Queen Charlotte’s Hospital,
Imperial NHS Trust, London, UK
Robert C. Pattinson, MBBCh, MMeD (O&G), FCOG,
MD, FRCOG
Director, MRC Maternal and Infant Health Care
Strategies Research Unit, Department of Obstetrics &
Gynaecology, University of Pretoria, South Africa
Nicole Pilarski, MBBS, MSc
Academic Clinical Fellow in Obstetrics & Gynaecology,
Birmingham Women’s & Children’s NHS
Foundation Trust, Birmingham, UK
S. Renwick, MBChB
Clinical Research Fellow, North Bristol NHS Trust,
Bristol, UK
Heather Richardson, MBChB, MRCOG
Subspecialty Registrar in Fetal and Maternal Medicine,
Queen Elizabeth University Hospital, Glasgow, UK
Michael S. Robson, MBBS, MRCOG, FRCS(Eng), FRCPI
Consultant Obstetrician & Gynaecologist, The National
Maternity Hospital, Dublin, Ireland
Shiri Shinar, MD
Maternal Fetal Medicine Fellow, Mount Sinai Hospital,
Toronto, Canada
Dimitrios Siassakos, MD, MBBS, MRCOG, MSc Dip
Med Ed
Associate Professor in Obstetrics, Institute for Women’s
Health, University College London, London, UK
Priya Soma-­Pillay, MBChB, FCOG, MMed (O&G), Cert
(Maternal and Fetal Medicine), PhD
Professor of Obstetrics & Gynaecology, University of
Pretoria, and Professor of Obstetrics & Gynaecology,
Steve Biko Academic Hospital, Pretoria, South Africa
Abdul H. Sultan, MD, FRCOG
Consultant Obstetrician and Gynaecologist, Croydon
University Hospital, Croydon, UK
Ranee Thakar, MD, FRCOG
Consultant Obstetrician and Gynaecologist, Croydon
University Hospital, Croydon, UK
Andrew J. Thomson, BSc, MBChB, MRCOG, MD
Consultant Obstetrician & Gynaecologist, Royal
Alexandra Hospital, Paisley, NHS Greater Glasgow
& Clyde, Glasgow, UK
Derek J. Tuffnell, MBChB, FRCOG
Consultant Obstetrician, Bradford Teaching Hospitals
NHSFT, Bradford, UK
A. Ugwumadu, PhD, FRCOG
Consultant Obstetrician & Gynaecologist/Clinical
Director, Department of Obstetrics & Gynaecology,
St George’s University Hospitals NHS Foundation
Trust, ­London, UK
Thomas van den Akker, MD, PhD
Gynaecologist-Obstetrician, Department of Obstetrics,
Leiden ­University Medical Centre, Leiden,
Netherlands
Jennifer M. Walsh, MBBCh, BAO, PhD, MRCOG,
FRCPI
Consultant Obstetrician & Gynaecologist, University
College Dublin, The National Maternity Hospital
Dublin, Ireland
Andrew D. Weeks, MBChB, MD, FRCOG
Professor of International Maternal Health/Consultant
Obstetrician; Liverpool Women’s Hospital,
University of Liverpool, Liverpool, UK
 Acknowledgement
Munro Kerr
This book Munro Kerr’s Operative Obstetrics has outlived
a century and is still going strong. It is a much sought-­
after book by practising clinicians, researchers and teach-
ers. This feat would not have been possible if not for the
initiation by Munro Kerr of the book Operative Midwifery
in 1908, which became Munro Kerr’s Operative Obstet-
rics. Until the 12th edition, all the book chapters were
authored by the editors with no contributors. In the 12th
edition the editors recognized the virtue of having indi-
vidual authors who have a clinical interest in the different
topics.
The previous and current edition maintain the old
style of authors’ views (the art) and up-­to-­date scientific
evidence to deliver the best safe and compassionate care.
Emphasis has been placed on evidence-­based guidelines
and Cochrane reviews, but the book retains an element
of pragmatism in best interpreting this evidence. We as
the editors of the current edition want to pay tribute to
the previous editors of the book who have contributed
so much to the art and science of operative obstetrics by
presenting short biographies of our forerunners. We are
also grateful to the authors of chapters in the current and
previous edition.
John Martin Munro Kerr was born in Glasgow
in 1868. He was educated at the Glasgow Academy and
Glasgow University. He occupied three different chairs
of Midwifery in Glasgow; first and briefly in 1910 in
Anderson’s College of Medicine, then from 1911 until
1927 as the first occupant of the Muirhead Chair in
Glasgow University, which was endowed to enhance
the medical education of women, and finally, from 1927
until his retirement in 1934, he was Regius Professor of
Midwifery. He was Foundation Vice President of the
organization that later evolved as the Royal College of
Obstetricians and Gynaecologists in 1927. His major
publications were a classic monograph Maternal Mortal-
ity and Morbidity (1933) and Combined Text Book of Obstet-
rics and Gynaecology (1923).
He introduced and popularized the lower segment
caesarean section in preference to the classical operation
for many years and it became known as the Kerr’s opera-
tion. He developed the principles of trial of labour in the
management of cases of suspect cephalo-­pelvic dispro-
portion – the subject of an almost obsessive focus among
the stunted, malnourished and rachitic gravidae in late
19th and early 20th century. Munro Kerr received many
honours and much international recognition. At the age
of 87 he delivered the first William Hunter Memorial
Lecture to the Glasgow Obstetrical and Gynaecological
Society. He retired to Canterbury and in 1960 he died at
the age of 92.
ix
x Acknowledgement
John Chassar Moir
John Chassar Moir was born in Montrose, Scotland
in 1900. A medical graduate of Edinburgh University,
he was the foundation Nuffield Professor of Obstetrics
and Gynaecology when the chair was established at the
University of Oxford in 1937. Moir is best remembered
for his work with Sir Henry Dale and Harold Dudley on
the isolation and clinical applications of ergometrine in
the prevention and management of postpartum haemor-
rhage. He was a brilliant gynaecological surgeon, notably
in the treatment of vesico-­vaginal fistulae, upon which
subject he wrote a classic monograph. He died in 1977.
Thomas Firth Baskett
Thomas Firth Baskett was born in Belfast, Northern
Ireland, where he attended Belfast Royal Academy and
the Queen’s University of Belfast Medical School. Since
completing his specialist training in the Belfast Teaching
Hospitals he has lived and worked in Canada. He spent
10 years in Winnipeg during which time he acted as a
Consultant in Obstetrics and Gynaecology for the Cen-
tral Canadian Arctic, which he visited regularly. In 1980
he moved to Dalhousie University in Halifax, Nova Sco-
tia where he is currently Emeritus Professor of Obstetrics
and Gynaecology. In the past he has served as the Presi-
dent of the Society of Obstetricians and Gynaecologists
of Canada, the Canadian Gynaecological Society and
Editor-­in-­Chief of the Journal of Obstetrics and Gynaecol-
ogy Canada. He has published widely on clinical obstet-
rics, surgical gynaecology and the history of medicine.
Tom was the senior editor of the last three editions of
Munro Kerr’s Operative Obstetrics, including the centenary
edition.
Philip Roger Myerscough
Philip Roger Myerscough was born in Lancashire in
1924 and studied medicine in Edinburgh, where he spent
his entire clinical career apart from a spell as WHO Vis-
iting Professor at the University of Baroda in India. The
consummate clinician and a highly prized teacher, he was
latterly Senior Obstetrician at the Simpson Memorial
Maternity Pavilion at Edinburgh Royal Infirmary, until
his retirement from the National Health Service in 1988.
Myerscough then spent a further three years in Muscat,
Sultanate of Oman, teaching and directing the develop-
ment of clinical services.
Andrew Alexander Calder
Andrew Alexander Calder was born in Aberdeen,
Scotland – after medical school and specialist training in
obstetrics and gynaecology in Glasgow, Andrew Calder
was a research fellow at Oxford University. His focus was
on prostaglandins and their role in the physiology and
pharmacological control of labour, especially the func-
tion of the uterine cervix. He returned to Glasgow to
pursue a clinical academic career and was subsequently
appointed head of the academic department of obstetrics
and gynaecology in the University of Edinburgh, where
he was founding director of the Jennifer Brown Research
Laboratory. He was Chairman of the Academy of Royal
Colleges and Faculties in Scotland and Vice Dean of the
Edinburgh Medical School. He was also Head of Division
of Reproductive and Developmental Sciences based at the
Queen’s Medical Research Institute and the Royal Infir-
mary of Edinburgh. He retired from clinical practice in
2009. He was co-­editor of the last three editions of Munro
Kerr’s Operative Obstetrics, including the centenary edition.
Sabaratnam Arulkumaran • Michael S. Robson
 Preface for the 13th Edition of
Munro Kerr’s Operative Obstetrics
We are privileged to be the editors responsible for this
13th edition of Munro Kerr’s Operative Obstetrics and we
pay tribute to all the previous editors. In particular we
acknowledge John Martin Munro Kerr himself (1868–
1960) who was responsible for the first edition of this
well-­known and popular text. We would like to acknowl-
edge all the authors and editors who succeeded him. In
particular, we would like to thank Thomas Baskett and
Andrew Calder, who stepped down from the editor team
after the last edition.
The number of chapters has increased in this edition,
and several chapters from the previous edition have been
divided out into smaller chapters. This is to make it easier
to read and to access particular topics quickly.
This book has always primarily covered operative obstet-
rics, caesarean section in particular. Caesarean section has
seen significant changes in practice since first introduced at
the time of Munro Kerr, so its coverage has been signifi-
cantly increased to reflect current clinical thinking.
The authors have used the latest evidence from national
guidelines and the Cochrane Database, and they have been
encouraged to interpret and evaluate evidence in order to
stimulate the reader to think deeper about the subject.
All chapters have been updated and we are most grate-
ful to chapter authors from the previous editions for their
kind contribution.
The book is divided into subsections: Chapters 1 to 7
covers the antepartum period; 8 to 33 cover labour and
delivery; 34 to 42 cover the postpartum period, and 43
and 44 cover the important organizational aspects. The
chapters are well illustrated with figures from the previ-
ous editions and newly commissioned figures. We each
edited every chapter and were pleased with the authors
contributions. Some authors inevitably lean towards a
particular philosophy of management but we expect prac-
tising clinicians to use their knowledge, judgement and
experience in managing a case (taking into account the
views expressed in this textbook). No textbook is perfect,
especially a book that describes management skills and
procedures to an international readership! The editors
and publisher would be happy to receive comments and
criticisms so that we can consider for possible incorpora-
tion in future editions.
Sabaratnam Arulkumaran • Michael S. Robson
xi
This page intentionally left blank
This page intentionally left blank

‘When the child is grown big and the mother cannot continue to provide him with enough nourishment,
he becomes agitated, breaks through the membranes,
and incontinently passes out into the external world free from any bonds’
‘The stimulus for labour may originate in certain states of vital development or physical expansion of the
fundus, corpus or cervix uteri and in altered conditions of the fetus, liquor amnii or placenta and
The safe and effective management of labour and deliv-
ery requires a clear understanding on the part of the birth
attendant of the anatomy, physiology and biochemistry
of human parturition and of its central participants – the
mother and the infant. The 20th century, across most
of which Munro Kerr has stretched, witnessed the most
spectacular growth and advance of medical science and
with it a steady improvement in our understanding of the
birth process. A hundred years ago the obstetrician’s art
depended mainly on the insights brought by the giants of
18th century obstetrics, notably William Smellie (1697–
1763) and William Hunter (1718–1783), both inciden-
tally born within 20 miles of Munro Kerr’s birthplace.
Smellie, who became acknowledged as ‘The Master of
British Midwifery’, was the consummate man-­midwife
and teacher. His monumental Treatise on the Theory and
Practice of Midwifery (1752), based on his extensive clini-
cal experience, described and defined the birth process
as never before and formed the basis for the clinical
conduct of labour. His definition of the mechanisms of
labour shed light on the convoluted journey through the
birth canal which the fetus is required to follow. His Sett
of Anatomical Tables with Explanations and an Abridgement
of the Practice of Midwifery (1754) amplified these funda-
mental principles. This atlas, for which Smellie employed
the Dutch artist Jan van Rymsdyk, was only surpassed
20 years later when Hunter, employing the same artist,
published his spectacular Anatomy of the Human Gravid
Uterus (1774). When Munro Kerr was preparing the
original Operative Midwifery in 1908 there had been little
further progress. The relevant anatomy was fairly well
understood but the physiology of the myometrium and
cervix, and the biochemistry, endocrinology and pharma-
cology of human labour were almost entirely unknown.
At this current time, the young obstetrician may consider
that those mysteries have almost all been solved follow-
ing a century of discoveries which saw the emergence of
oxytocin, oestrogen, progesterone, prostaglandins and
many other hitherto unknown substances. But it would
be surprising indeed if the close of the 21st century does
not reveal an even more complex picture.
CHAPTER 1
Human Birth
R.A. Greene
HIPPOCRATES, ON GENERATION, 4TH CENTURY BC
the loosening or decadence of the membranes….’
JAMES YOUNG SIMPSON, LECTURES ON MIDWIFERY, 1860
CURRENT UNDERSTANDING
As a starting point for the wide range of clinical issues
addressed within this textbook, a brief review follows of
some of the key elements of basic medical science per-
taining to human labour and delivery as currently under-
stood. This, by necessity, will be superficial and selective.
For more detailed and comprehensive accounts the reader
should look to current textbooks of reproductive physiol-
ogy, anatomy, biochemistry and endocrinology.
Labour may be regarded as a release from the inhibi-
tory effects on the myometrium of various chemi-
cals (progesterone, prostacyclin, relaxin, parathyroid
hormone-­related peptide, nitric oxide, calcitonin gene-­
related peptide and others) active during pregnancy,
rather than as an active process secondary to myometrial
stimulation.
Myometrial Function
The myometrium is the engine which drives human
labour, during which it displays a highly sophisticated
and co-­ordinated set of forces. The simple objective of
these is to efface and dilate the cervix and push the fetus
through the birth canal. In contrast to other smooth
muscle systems, the myometrium displays three unique
properties which are crucial for its function:
1. It must remain quiescent for the greater part of human
pregnancy, suppressing its natural instinct to contract
until called upon to do so at the appointed time.
2. 
During labour it must display a pattern which
affords adequate periods of relaxation between con-
tractions without which placental blood flow and
fetal oxygenation would be compromised.
3. It possesses the capacity for retraction, vital to pre-
vent exsanguination after delivery but also essential
during labour. Retraction is a unique property of
uterine muscle whereby a shorter length of the mus-
cle fibre is maintained, without the consumption of
energy, even after the contraction that produced
the decrease in length has passed. As the cervix is
3
4 PART I Antenatal

effaced and pulled around the fetal presenting part,
an inability of the myometrial fibres in the uterine
corpus to retract, in essence to steadily reduce their
relaxed lengths, would mean that the tension on the
cervix could not be maintained.
At its most basic, human labour may be regarded as an
interaction between the corpus and the cervix (Fig. 1.1).
For the maintenance of pregnancy the corpus must be
quiescent and the cervix closed and uneffaced. In labour
the corpus contracts and the cervix yields. A useful anal-
ogy may be to compare this process to the experience of
putting on, for the first time, a roll-­neck pullover. Just
as with the fetus, the head must be flexed to present its
smallest diameters to the cervix, or neck of the pullover,
which is effaced round the presenting part and ultimately
dilated as a result of traction applied by the arms, which
are in this connection analogous to the myometrial fibres.
Although it has been conventional to acknowledge a
‘lower uterine segment’ arising from the uterine isthmus
(between the non-­pregnant corpus and cervix), in prac-
tice it may be more helpful simply to see the boundary
between corpus and cervix as the ‘fibromuscular junction’
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which marks the change from a mostly muscular corpus
to a predominantly fibrous cervix. Obstetric purists may
argue that the concept of a ‘lower segment’ is helpful in
the definition of placenta praevia and in directing the
site of contemporary caesarean sections but, those issues
apart, it is of little relevance and it is a difficult concept
to define either anatomically or physiologically. At its
simplest, contraction of the myometrial cell requires
actin and myosin to combine in the contractile filament
actinomyosin (Fig. 1.2). This reaction is catalysed by the
enzyme myosin light-­chain kinase, which is heavily cal-
cium dependent. Calcium in turn relies for its availability
on oxytocin and prostaglandin F2α, which assist its trans-
port into the cell and also free it from intracellular stores
(sarcoplasmic reticulum).
As term approaches, the uterus becomes activated
in response to stimulants e.g. oestrogen. There is an
increased expression of contraction-­associated proteins
and myometrial receptors for prostaglandins and oxyto-
cin. A particular insight into how the myometrial effort
is co-­ordinated into a concerted function came from the
recognition of the essential requirement for gap junc-
tions (biochemically characterized as connexin-­ 43) to
be formed between individual myometrial cells, allow-
ing cell-­to-­cell transmission of electrical impulses and
ions. Thus, the corpus can display a wave of contractil-
ity propagated across its cell population which becomes a
functional syncytium rather than a disorganized mass of
individual muscle fibres.
Following activation, the uterus can be stimulated to
contract by the action of uterotonic agents such as pros-
taglandin E2, F2α and oxytocin.

The Cervix
FIG. 1.1 n Diagrammatic representation of the relationship of the The recognition, little more than 50 years ago, that the
uterine corpus and cervix in mid pregnancy. cervix possesses a distinct structure based on collagen-­rich

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FIG. 1.2 n Schematic representation of the contractile process of the myometrial cell. Those components shown in dark boxes repre-
sent contraction, those in light boxes represent relaxation.
 1 Human Birth 5

D
FIG. 1.3 n Original dissections prepared by William Hunter in the 18th century. That on the left (a) shows the lower part of the uterus,
cervix, vagina, bladder and urethra in sagittal section in the last few weeks of pregnancy. That on the right (b) shows the cervix from
the intrauterine aspect as it undergoes effacement in the last month of pregnancy (the fibro­muscular junction is now at the periphery
of this specimen).

connective tissue rather than smooth muscle has been

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and delivery to take place (Fig. 1.3). That change is the
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process we now describe as ‘cervical ripening’. YDVFXODU DFWLYDWLRQRI
The requisite loosening and degradation of the col- SHUPHDELOLW\ QHXWURSKLOV
lagen bundles is now recognized as having much in com-
mon with an inflammatory process, which requires the
participation of inflammatory mediators including pros- 'HJUDQXODWLRQ
taglandin E2 and cytokines (especially interleukin (IL)-­8), 5HOHDVLQJFROODJHQDVH
DQGHODVWDVH
the recruitment of neutrophils and the synthesis of matrix
metalloproteinases, including collagenases and elastase FIG. 1.4 n Schematic representation of the control of cervical
ripening. The collagen of the cervical stroma is broken down
(Fig. 1.4). by matrix metalloproteinases, such as collagenase and elastase
derived from neutrophils in an inflammatory-­like process which
requires them to be drawn into the tissue under the influence of
BIOLOGICAL CONTROL OF LABOUR – interleukin-­8 (IL-­8) from capillaries which have been dilated and
TRIGGERING AND MAINTENANCE made more permeable by prostaglandin E2 (PGE2).

The process by which the labour is triggered and main-
tained has been the subject of intensive investigations.
The clinical drive to this area of research has been the
desire:
• to better understand, prevent or suppress preterm
labour with all its complications
• to improve our ability to correct abnormal uterine
action and poor progress in labour
• to enhance our capacity to induce effective labour
when indicated by clinical circumstances.
The following brief review oversimplifies what is a
most complex set of interactions, but it may suffice as a
basis for rational clinical intervention.
It is likely that a biochemical cascade exists (as in many
processes in the body, e.g. thrombus formation) at term
which decreases the factors maintaining uterine quiescence
and/or enhances factors promoting uterine activity (Smith,
2007). Given its importance (the birth of the next gen-
eration), such a cascade as others will likely have multiple
redundant loops to ensure a fail-­safe system. In such sys-
tems, each element is connected to the next in a sequential
6 PART I Antenatal
fashion, and many of the elements demonstrate positive
feed-­forward characteristics. This makes it unlikely a sin-
gle mechanism is responsible for the initiation of labour.
Therefore, it is prudent to describe such a ‘cascade’ as being
responsible for ‘promoting’, rather than ‘initiating’, labour.
Current hypotheses suggest a dynamic biochemical
dialogue between the fetus and mother (paracrine/auto-
crine events) with a probable genetic regulation of the
molecular events that occur before and during labour.
It is now recognized that the trigger for parturition
likely comes from the fetus rather than from the mother.
The maturing fetal brain is thought to provoke the release
of corticotrophin from the fetal pituitary gland (Fig. 1.5)
and oxytocin. This may be considered analogous to the
switching on of pituitary gonadotrophin production at
the time of puberty. The fetal adrenal gland responds by
releasing two main products, cortisol and dehydroepian-
drosterone sulphate:
• Cortisol stimulates fetal pulmonary surfactant pro-
duction to mature the lungs for extrauterine func-
tion and may also influence other organ systems.
This is thought to result in changes in the composi-
tion of the amniotic fluid which provoke the release
of prostaglandin E2 from the amnion. This may
be important for a direct influence on the cervix,
especially focused at the internal os as this is the
portion of the cervix which lies in intimate contact
with the fetal membranes. The internal os needs to
ripen first to initiate cervical effacement. To do this
the activity of the principal prostaglandin degrad-
ing enzyme prostaglandin dehydrogenase within
the chorion must decline, a phenomenon which has
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3*)α *URZWK 3URJHVWHURQH
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FIG. 1.5 n Fetal control of the onset of labour is thought to result
from activation of its hypothalamic–pituitary–adrenal axis, which
leads in turn to modification of placental steroid production and
activation of prostaglandins in the decidua and cervix. ACTH,
Adrenocorticotrophic hormone; CRF, corticotrophin-­releasing
factor; DHEAS, dehydroepiandrosterone sulphate; IL, interleu-
kin; PG, prostaglandin; PGDH, prostaglandin dehydrogenase.
recently been confirmed.
• D ehydroepiandrosterone sulphate is metabolized
in the placenta to enhance oestrogen levels which
stimulates the myometrium as outlined earlier.
Oestrogen may provoke the release of prostaglan-
din F2α from its richest source, the decidua, thereby
exciting myometrial contractions.
• The fetal pituitary secretes oxytocin into the mater-
nal circulation, with calculated oxytocin secretion
rates from the fetus of a baseline of 1 mU/min prior
to labour and approximately 3 mU/min after spon-
taneous labour. Maternal serum oxytocin levels are
not increased prior to the onset of labour or during
the first stage of labour; therefore, oxytocin derived
from the fetus (and local decidua/other uterine
sources) could act on myometrial oxytocin recep-
tors in a paracrine fashion to initiate and maintain
effective uterine contractions.
Inflammation and Labour
Cytokines have long been implicated in the pathophysi-
ology of preterm labour associated with intra-­amniotic
infection. They are also involved in normal term labour.
Proinflammatory mediator levels -­IL-­ 6 and tumour
necrosis factor alpha (TNF-­α) -­increase in the maternal
peripheral circulation before the onset of spontaneous
term labour. The fetus may produce physical (distension)
and hormonal signals that stimulate macrophage migra-
tion to the uterus with the release of cytokines and the
activation of an inflammatory process.
Concentrations of IL-­ 8 in human myometrium,
decidua and fetal membranes are increased during labour.
IL-­8 is a potent chemotactic for neutrophils. It may cause
an increase in collagenase enzyme activity leading to cer-
vical ripening and/or spontaneous rupture of membranes.
Cytokines and prostaglandin production appear to inter-
act and to accelerate each other’s production. It has also
been proposed that the increased inflammatory response
promotes uterine contractility via direct activation of
contractile genes (e.g. COX-­2, oxytocin receptor, con-
nexin) and/or impairment of the capacity of progesterone
to mediate uterine quiescence (Parry et al, 1998).
MEMBRANE RUPTURE
The strength and integrity of fetal membranes derive
from extracellular membrane proteins including colla-
gens, fibronectin and laminins. Matrix metalloproteases
(MMPs) are a family of enzymes with varied substrate
specificities that decrease membrane strength by increas-
ing collagen degradation. Tissue inhibitors of MMPs
(TIMPs) bind to MMPs and shut down proteolysis,
thereby helping to maintain membrane integrity. The
fetal membranes normally remain intact until term due
to low MMP activity and high levels of TIMPs. Peripar-
tum activation of MMPs at term may trigger a cascade of
events that reduce fetal membrane integrity and promote
rupture of membrane. Stretch and shear forces from
uterine contractions during labour probably contribute
to membrane rupture, as well.
 1 Human Birth 7

The precise aetiology of peripartum MMP activation is changes initiated by the fetal brain – hypothalamic–pitu-
not known; several factors may play a role in this process; itary–adrenal axis -­results in the activation of a variety of
such as TNF-­α, IL-­1, prostaglandins E2 and F2α appear endocrine and inflammatory substances which have the
to increase collagenase activity and activate inflammatory effect of co-­ordinating key events:
pathways in fetal membranes at parturition (Maymon • maturing essential fetal organ systems, notably the
et al, 2011). Mechanical stretching of fetal membranes lungs, for the challenges of extra-uterine life
activates MMP-­1 and MMP-­3 and induces IL-­8 expres- • initiating changes in the myometrium to enhance
sion in amnion and chorion cells (Nemeth et al, 2000). its capacity to contract effectively
Progesterone remains an enigma. It is known to inhibit • transforming the rigid cervix into a compliant and
both myometrial contractility and the formation of gap readily dilatable structure
junctions, and is also recognized as supporting the activ- • stimulating the myometrial contractions which will
ity of prostaglandin dehydrogenase, but evidence for its ultimately deliver the fetus through the birth canal
withdrawal prior to parturition remains elusive. It seems • promoting the inflammatory process before and
likely that there is either a process whereby its activity at during labour to allow cervical change, membrane
tissue level declines without a drop in circulating levels, rupture and facilitate myometrial contractions.
or simply that its influence is overcome by other factors. Fig 1.6 summarizes the key biochemical components
We can therefore postulate that a cascade of endocrine which are thought to control the inflammatory-­type pro-
cesses which convert the stroma of the cervix from a rigid
2HVWURJHQV 3URJHVWHURQH 3URJHVWHURQH 2HVWURJHQV structure to a soft and compliant one, and the activation
3*( 3*)α
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  ± 
about its effacement and dilatation.
This brief overview is of necessity simplified. The con-
,QIODPPDWRU\ 0\RPHWULDO trol of the birth process requires the participation of a
UHDFWLRQ DFWLYDWLRQ
myriad of other factors, such as adhesion molecules and
receptors for hormones and prostaglandins, as well as
other hormones such as vasopressin and relaxin. Perhaps
8QULSHFHUYL[ 5LSHFHUYL[
the most important recent change in thinking has been to
7LVVXH 6KDSH see the whole process of parturition as an inflammatory-­
FKDQJH FKDQJH
type event. This has vital consequences for our under-
)LUP 6RIWHU 6RIW standing of those pregnancies which do not follow the
&ORVHG 0RUHFRPSOLDQW 'LODWLQJ normal pattern of labour onset and progress, either
8QHIIDFHG (IIDFHG because it is delayed or activated prematurely. The role
$GYDQFLQJJHVWDWLRQ of infection in the latter is gaining increasing importance
0LGSUHJQDQF\ 7HUP
and it seems likely that some women may be at increased
FIG. 1.6 n A schematic representation of the factors which bring risk of preterm labour on account of an increased sus-
about the softening and dilation of the cervix during the transi- ceptibility to infection from a deficiency of endogenous
tion from pregnancy maintenance to parturition. IL, Interleukin; antimicrobial substances (Fig. 1.7).
PG, prostaglandin.

9HUQL[
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FIG. 1.7 n Some of the natural antimicrobial substances which may be important in resisting infection during pregnancy. A deficiency
of these may predispose to preterm delivery. (By permission of Dr Sarah Stock.) HBD, Human Beta Defensin; HNP, Human Neutrophil
Defensin; SLPI, secretory leukocyte peptidase inhibitor; LL 37, the only cathelicidin-derived antimicrobial peptide found in humans.
8 PART I Antenatal
A better understanding of the pathway to normal birth
should provide the basis for identifying points along the
pathway at which a pathological process may precipi-
tate preterm birth. The effects of stress may be medi-
ated by increased cortisol levels in the maternal or fetal
compartments and consequent increases in placental
corticotrophin-­releasing hormone expression. Infection
activates inflammation and may stimulate prostaglan-
din synthesis in fetal membranes. Abruption appears to
affect the myometrium directly through the release of
thrombin, a potent stimulator of myometrial contraction.
In the case of multiple gestation and polyhydramnios,
increased uterine stretching activates myometrial con-
tractility. Such understanding may also assist improved
intervention outcomes, perhaps through better selection
of appropriate cases for induction of labour.
BIBLIOGRAPHY
Calder AA. Normal labour. In: Edmonds DK, ed. Dewhurst’s Textbook of
Obstetrics and Gynaecology for Postgraduates. Oxford: Blackwell; 1999.
Calder AA. Human birth. In: Basket TF, Calder AA, Arulkumaran S,
eds. Munro Kerr’s Operative Obstetrics. 12th ed. Edinburgh: Saun-
ders; 2014.
Calder AA, Greer IA. Physiology of labour. In: Phillip E, Setchell M,
eds. Scientific Foundations of Obstetrics and Gynaecology. Oxford: But-
terworth; 1991.
Hunter W. Anatomy of the Human Gravid Uterus. Birmingham: Basker-
ville; 1774.
Kerr JM. Operative Midwifery. London: Baillière, Tindall and Cox; 1908.
Maymon E, Romero R, Pacora P, et al. Human neutrophil collagenase
(matrix metalloproteinase 8) in parturition, premature rupture of
the membranes, and intrauterine infection. Am J Obstet Gynecol.
2000;183:94.
Nemeth E, Tashima LS, Yu Z, Bryant-­Greenwood GD. Fetal mem-
brane distention: I. Differentially expressed genes regulated by
acute distention in amniotic epithelial (WISH) cells. Am J Obstet
Gynecol. 2000;182:50.
Olson DM, Mijvoc JE, Sadowsky DW. Control of human parturition.
Sem Perinatol. 1995;19:52–63.
Parry S, Strauss 3rd JF. Premature rupture of the fetal membranes. N
Engl J Med. 1998;338:663.
Smellie W. Treatise on the Theory and Practice of Midwifery. London: D.
Wilson; 1752.
Smellie W. Sett of Anatomical Tables with Explanations and an Abridge-
ment of the Practice of Midwifery. London: D. Wilson; 1754.
Smith R. Parturition. N Engl J Med. 2007;356:271.
 CHAPTER 2

Preterm Labour and Delivery

J.E. Norman

‘The usual period of a woman’s going with child is nine calendar months;
but there is very commonly a difference of one, two or three weeks.
A child may be born alive at any time from three months:
but we see none born with powers of coming to manhood, or of being reared,
before seven calendar months, or near that time. At six months it cannot be.’
WILLIAM HUNTER c. 1760
CITED BY THOMAS DENMAN. IN: INTRODUCTION TO THE PRACTICE OF MIDWIFERY.
NEW YORK: E. BLISS AND E. WHITE, 1825, P. 253

INTRODUCTION the lower limit of preterm birth causes problems in com-

Although preterm deliveries constitute a small proportion
of all births, their contribution to serious complications,
especially those leading to perinatal death and morbidity,
is hugely disproportionate. In 2010 it was estimated that
14.9 million babies worldwide (around 11.1% of all births)
were premature.1 Globally, preterm birth is the single big-
gest cause of neonatal death.2 Babies born at ‘term’ (con-
ventionally considered to be 37−42 weeks of gestation)
have consistently better outcomes than those born ‘pre-
term’, with the risk of neonatal mortality and morbidity
rising exponentially as the gestation of delivery decreases.
Preterm labour is the single biggest cause of preterm
birth, so that effective ‘treatment’ of preterm labour could
have a major impact on global perinatal health. Such treat-
ments include those aimed at preventing or halting pre-
term labour and those that improve outcomes for babies
of women in preterm labour. After decades in which there
were few effective therapies, some promising strategies are
emerging, which improve outcomes in a subset of women
and babies. Despite this, the global toll of the adverse
effects of preterm birth continues to rise, with preterm
labour remaining the single biggest cause of neonatal
mortality and morbidity in resource-­rich countries.
DEFINITION
The definition of preterm birth is not without contro-
versy. The ICD10 (International Statistical Classification
of Diseases and Related Health Problems 10th Revision)
definition of preterm labour is the onset (spontaneous)
of labour before 37 weeks of gestation (http://apps.who.
int/classifications/icd10/browse/2010/en#/O60), thus pre-
term birth under this definition is considered to be birth
before 37 completed weeks of gestation. This definition
remains unchanged in ICD11, due to be published in 2019.
The lower gestational limit is not defined under this sys-
tem, although the WHO recommends that all babies born
with any signs of life should be considered live births (and
hence would be included). The lack of a consensus about
paring data among countries, with many countries (includ-
ing Scotland, the USA and Brazil) not defining their lower
gestational limit, some (such as Switzerland and Denmark)
using a lower limit of 22 weeks and others (including Aus-
tralia and Canada) using 20 weeks as the lower gestational
limit of preterm birth.1 Thus a woman who delivers a baby
at 21 weeks with no signs of life would be likely to be con-
sidered to have had a miscarriage in Switzerland and Den-
mark, and probably in the majority of countries with no
defined lower limit, but would be considered to have had
a stillbirth in Australia and Canada. The birth would be
defined as a preterm birth in the latter two countries but not
the former two. Comparisons are further complicated by
the use in some countries of low birth weight as a surrogate
for preterm birth: this is inappropriate because not all small
babies are preterm, and not all preterm babies are small.3
Lastly, due to the phenomenon of delayed ovulation, where
ultrasound is used to estimate gestational age (as is com-
mon in many resource-­rich countries), the calculated mean
duration of pregnancy is consistently shorter, and the rate
of prematurity is around 20% higher, than when gestation
is calculated from the date of the last menstrual period.4
A recent report by the Global Alliance to Prevent Pre-
maturity and Stillbirth has highlighted that similar aeti-
ologies (albeit in different proportions) are involved in
a pregnancy loss in the second trimester and in the mid
third trimester, and that the risk of adverse outcome for
the neonate decreases progressively as gestation advances,
even beyond 37 weeks’ gestation.5,6 They propose a new
definition and classification system whereby preterm birth
would be ‘any birth (which includes stillbirths and preg-
nancy terminations) that occurs after 16 weeks’ gestation
and before term (i.e. 39 weeks’ gestation). The complete
population of preterm deliveries within the gestational
range as described earlier includes live births, stillbirths,
multiple pregnancies, pregnancy terminations, and new-
born infants with congenital malformations.5 The rec-
ommendation from this group is that ‘gestational age
estimation should, whenever possible, be corroborated
by an early, high quality ultrasound and the best obstetric
estimate be used for all gestational age determinations’.

9
10 PART I Antenatal

PRETERM LABOUR VERSUS PRETERM intrauterine inflammation, utero-­ placental ischaemia,

BIRTH utero-­placental haemorrhage, uterine stretch and mater-
nal stress. It is not possible to determine whether these
The focus of this chapter is preterm labour, although this events ‘cause’ preterm labour, although there is strong
is not the only pathway to preterm birth. A categorization circumstantial evidence of the role of intrauterine infec-
of (spontaneous) preterm labour, preterm prelabour rup- tion and inflammation. This is firstly because, even using
ture of membranes and elective (induced) preterm birth relatively insensitive culture techniques, around 25–40%
has been widely used, with Scottish data suggesting that of women in preterm labour have demonstrable intra-
the proportions of each (amongst all singletons deliver- uterine infection. The proportion rises progressively as
ing preterm) are 62%, 15% and 23% respectively.7 Vil- gestational age of labour onset declines. Secondly, intra-
lar proposes that preterm birth is defined by pathway to uterine infection/inflammation stimulates an inflamma-
delivery (spontaneous or care giver initiated) AND signs tory response, including production of prostaglandins,
of initiation of parturition (evidence of initiation of par- implicated in increasing cervical ripening and myometrial
turition (including preterm prelabour rupture of mem- contractility. Lastly, in animal models, intrauterine injec-
branes) or no evidence of initiation of parturition) AND tion of microorganisms or proinflammatory agents (such
the presence of significant fetal, maternal or placental as lipopolysaccharide) is effective in stimulating preterm
pathological conditions.5 Under this classification, both labour.
preterm labour and preterm prelabour rupture of mem-
branes would be considered to have evidence of initiation
of parturition, whereas elective (induced) preterm birth RISK FACTORS
would not. The pathway to delivery would be spontane-
ous in women presenting in preterm labour and those with The risk factors associated with preterm labour are listed
preterm prelabour membrane rupture (because oxytocin in Table 2.1.
augmentation of contractions is also considered in the
spontaneous category) but would be care-­giver initiated
in women undergoing elective (induced) preterm birth. OUTCOMES
There is a clear inverse dose−response relationship between
INCIDENCE OF PRETERM BIRTH gestation of preterm birth and risk of perinatal death,
with outcomes being worst in babies born at earlier ges-
Despite much effort, there has been little fall in preterm tational ages, and the nadir not being reached until 40
birth rates globally over the last 20 years. In Scotland weeks’ gestation. For example, UK data show 40% of
in 2017, 6.4% of singleton babies were born before 37 babies who are live born at 24 weeks’ gestation survive to
completed weeks’ gestation; these rates have been fairly discharge from hospital, rising through 66% at 25 weeks
constant for the last 20 years (Fig. 2.1). Rates in the USA to 77% at 26 weeks.10 Babies who survive preterm birth
for 2017 were higher, at 9.8%. Globally, preterm birth also have a greater incidence of morbidity, and again this
complications account for an increasing proportion of is inversely proportional to gestational age at delivery.
under-­5 deaths, with a population-­attributable fraction For example, in the EPICure study (a prospective cohort
[95% confidence intervals] of 25.3% ([21.7–28.7], 0.478 of around 300 children who were born before 25 weeks’
million [0.394–0.552]) in 2015.8 gestation in 1995, and who survived to reach the neonatal
unit), 49% had neuromotor or sensory (sight or hearing)
disability (with 23% of the total having severe disability)
when assessed at 30 months of age, and the remainder had
AETIOLOGY AND MECHANISMS no disability according to the study criteria.11 Subsequent

The ‘cause’ of preterm labour is incompletely under-

stood.9 Preterm labour is often accompanied by one or TABLE 2.1 Risk Factors for Preterm Labour.
more of the following pathologies: intrauterine infection,
Risk Factors for Preterm Labour, Adapted From Ref 10
 Black ethnicity

Low socioeconomic group
3URSRUWLRQRIVLQJOHWRQELUWKV

Single marital status

 Extremes of maternal age
WKDWDUHSUHWHUP

 Extremes of maternal BMI

 Short interpregnancy interval
 Previous preterm birth
 Multiple pregnancy
Destructive treatments to cervix for cervical intra-­epithelial

neoplasia

Co-­existent maternal systemic disease (e.g. diabetes

















mellitus)
<HDU Stress
Smoking
FIG. 2.1 n Singleton preterm births in Scotland, expressed as a Drug use
proportion of all singleton births, live and still, 1978 to 2010.53

studies have confirmed a ‘dose dependent’ effect of pre-
maturity on long-­term adverse health outcomes, which is
inversely proportional to gestational age at delivery.12–14
As with death, the nadir of ‘prematurity’ on educational
attainment at school is not reached until birth at 40 weeks
of gestation,15 suggesting that even those who appar-
ently have ‘no disability’ suffer long-­term adverse con-
sequences of prematurity. Although there was no change
in disability rates amongst survivors between 1995 and
2006, babies born extremely preterm were more likely to
survive, suggesting improvements in perinatal care.11
PREDICTION
A major goal of obstetric research is to be able to identify
predictive factors for preterm birth by evaluating asymp-
tomatic women in the first half of pregnancy. Although
clinical risk factors for preterm labour have been identified,
and predictive tests proposed, no strategy is sufficiently
effective to be in widespread use in clinical practice. One of
the most widely used clinical indicators, history of sponta-
neous preterm birth in a previous pregnancy, is associated
with likelihood ratios of 4.62 (95% confidence interval
[CI] 3.28–6.52) and 2.26 (95% CI 1.86–2.74) respectively
for birth before 34 and 37 weeks’ gestation in a subsequent
pregnancy.16 The most widely used and the most effec-
tive tests for preterm labour prediction in asymptomatic
women are detection of fetal fibronectin (fFN) in vaginal
fluid and cervical length measurement.16 The predic-
tive ability of these strategies varies with the gestation of
testing, the definition of a positive test (e.g. the length of
the cervix or the quantitation of the fFN) and the gesta-
tion of delivery being predicted. Typical summary likeli-
hood ratios from meta-­analyses of a range of studies are
shown in Table 2.2. There is some evidence that fFN test-
ing reduces the risk of preterm birth, with odds ratios of
0.54 (95% CI 0.34–0.87), although no benefit in terms of
reduction in adverse outcomes was seen.17 Newer tests are
continually being proposed and evaluated – each of cervi-
covaginal fluid prolactin and proteome profile and matrix
metalloproteinase-­8 in amniotic fluid shows promise, but
they require further studies to define their efficacy.17
TABLE 2.2 Predictive Tests for Preterm Birth
in Asymptomatic Women With Singleton
Pregnancy.
Positive LR 95% CI
Birth Before 34 Weeks’ Gestation:
Cervicovaginal fluid fetal 7.65 3.93–14.68
fibronectin17
Birth Before 35 Weeks’ Gestation:
Cervical length measurement of 4.31 3.08–6.01
< 25 mm (at < 20 weeks’
gestation)20
Birth Before 37 Weeks’ Gestation:
Cervicovaginal fluid fetal 3.40 2.29–5.05
­fibronectin17
CI, Confidence interval; LR, likelihood ratio.
2 Preterm Labour and Delivery 11
DIAGNOSIS
Preterm labour is a diagnosis that can confidently be
made only in established labour. Many women present
with symptoms suggestive of preterm labour (e.g. uter-
ine contractions) but are found to have a closed cervix on
examination. A proportion of such women will labour and
deliver within a short space of time, but it is often very
difficult for both women and their care givers to identify
those who are, and those who are not, in the early stages
of preterm labour. Again, cervicovaginal fluid fibronectin
and cervical length measurements are amongst the best
tests, and both have been endorsed by the National Insti-
tute for Health and Care Excellence for this purpose.18,18a
For women with symptoms of preterm labour, the nega-
tive likelihood ratio (i.e. the effect of a negative test on
the confidence with which preterm labour can be excluded
as a diagnosis) is often the most helpful. For birth within
7−10 days of testing, fFN has a negative likelihood ratio
(i.e. a negative test reduces the risk of preterm birth) of
0.36 (95% CI 0.28–0.47),17 and cervical length measure-
ment of <15mm has a negative likelihood ratio of 0.026
(95% CI 0.0038–0.182)19 in singleton pregnancies.
MANAGEMENT
Treatment with the object of reducing the incidence,
risks and complications of preterm labour falls into three
principal categories:
• Measures aimed at preventing preterm labour, in-
cluding early recognition and treatment of infec-
tion, cervical cerclage, progesterone prophylaxis
and risk modification such as cessation of smoking
and drug abuse.
• Tocolysis to try to abolish or arrest preterm labour.
• Obstetric interventions aimed at minimizing the
complications of preterm delivery.
PREVENTION OF PRETERM LABOUR
Reducing Infection
Given the known link between intrauterine infection and
preterm birth, with ascending infection from the vagina
as the most likely route of entry, it is perhaps disappoint-
ing that antibiotics appear to be ineffective at preventing
preterm birth, even in settings with a high prevalence of
infective morbidity.20,21,21a There is controversy about
treatment of bacterial vaginosis, with some meta-­analyses
suggesting that early treatment, particularly with clindamy-
cin, might reduce the risk of late but not early preterm
birth.22,23 Despite the emerging link between periodontitis
and preterm birth, it is still unclear whether treatment for
periodontal disease reduces the risk of preterm birth.24
Mechanical Methods of Maintaining Cervical
Length
The procedure of cervical cerclage is discussed elsewhere
in this book. For women with a singleton pregnancy, a
12 PART I Antenatal
previous history of preterm birth AND a short cervix on
ultrasound (<25 mm at <24 weeks’ gestation), cerclage
reduces both preterm birth AND perinatal mortality and
morbidity, with a relative risk (95% CI) for this latter
outcome of RR (relative risk) 0.64 (95% CI 0.45–0.91).25
Importantly, in women with a singleton pregnancy and
a previous preterm birth, screening with ultrasound fol-
lowed by selected cerclage in those with a short cervix
appears as effective as routine cerclage insertion based
on history alone.26 Cerclage is ineffective at preventing
preterm birth in women with a twin pregnancy – indeed,
it appears harmful in this scenario.26a An alternative
mechanical method is the Arabin pessary, a device which
covers the cervical os. There has been significant inter-
est in this device, but conflicting evidence from the
published trials. Existing meta-­ analyses highlight this
uncertainty.26a,27 Further studies are required to deter-
mine the place of the Arabin pessary in routine clinical
practice.
Progesterone
Several large studies and a meta-­analysis have suggested
that progesterone reduces the risk of preterm birth
in women with a singleton pregnancy and a history of
preterm birth28,29 and in women with a short cervix on
ultrasound.30–32 Some studies have shown a reduction in
neonatal morbidity.29,31 No study has shown any longer-­
term benefit for the baby. Two other large studies have
failed to show any impact of progesterone either on rates
of preterm birth or neonatal morbidity.32,33 A large indi-
vidual patient data meta-­analysis to address this uncer-
tainty will likely report in early 2019.34b Again, twins
respond differently, with progesterone failing to reduce
rates of preterm birth in twin pregnancy.35
Tocolysis to Abolish or Arrest Preterm Labour
An array of drugs have been used to try to abolish or arrest
preterm labour, including β sympathomimetics (ritodrine),
oxytocin antagonists (atosiban), calcium channel blockers
(nifedipine), prostaglandin synthase inhibitors (indometh-
acin) and nitric oxide donors (nitroglycerine). None has
been shown to improve neonatal mortality or morbidity
in women presenting in preterm labour, leading the Royal
College of Obstetricians and Gynaecologists in the UK to
conclude ‘In the absence of clear evidence that tocolytic
drugs improve outcome following preterm labour, it is
reasonable not to use them’.36 Calcium channel blockers
such as nifedipine have some evidence of benefit in terms
of reducing delivery within 7 days of receiving treatment
(RR 0.76; 95% CI 0.60–0.97) and prior to 34 weeks’
gestation (RR 0.83; 95% CI 0.69–0.99).37 The oxytocin
receptor antagonist atosiban is licensed for the delay of
imminent preterm birth in Europe, but randomised tri-
als have reached varying conclusions on efficacy.38a On
the basis of an updated network meta-­analysis, initially
published by Haas,38b and an economic evaluation, NICE
suggests that clinicians should ‘offer’ either nifedipine
or oxytocin antagonists to women in diagnosed preterm
labour from 30+0 to 33+6 weeks’ gestation, and to women
in suspected preterm labour from 26+0 to 29+6 weeks’
gestation (National Institute of Health and Care Excel-
lence 2015). Importantly, the maternal side effects of
treatment with tocolytic agents are becoming increasingly
clear, with use of multiple agents being particularly prob-
lematic.39 Any decision to give tocolysis should be care-
fully considered by both mother and clinician.
MINIMIZING THE COMPLICATIONS OF
PRETERM DELIVERY
Corticosteroids
In contrast to the unproven effects of tocolytic agents
on improving neonatal outcome, there is overwhelming
evidence that prenatal steroids are of benefit to babies
destined to be born preterm. A single course of antena-
tal corticosteroids (dexamethasone, betamethasone or
hydrocortisone) reduces neonatal death (RR 0.69; 95%
CI 0.59–0.81), intraventricular haemorrhage (RR 0.55;
95% CI 0.40–0.76) and necrotizing enterocolitis (RR
0.50; 95% CI 0.32–0.78) in preterm babies.40 Enthu-
siasm for the beneficial effects of corticosteroids and
difficulties about the diagnosis of preterm labour have
led to many babies being exposed to multiple doses of
corticosteroids before birth. Studies of the effect of such
a strategy have come to differing conclusions, with the
Cochrane review suggesting that multiple doses were
beneficial in the short term, with a significant reduc-
tion in respiratory distress syndrome (RR 0.83; 95% CI
0.75−0.91) and serious neonatal morbidity (RR 0.84;
95% CI 0.75−0.94)41 whereas a single large trial (n>2000
babies) has shown a dose-­dependent reduction in birth
weight in association with antenatal corticosteroids.42
Until the long-­term effects are clearer a single dose of
steroids should be the standard of care for babies likely
to be born preterm.
Magnesium Sulphate
This agent is widely used for seizure prophylaxis in
women with pre-­ eclampsia and for the treatment of
eclampsia. Emerging evidence from a number of studies
suggests that its antenatal administration may also reduce
hypoxic ischaemic cerebral damage in babies destined to
be born preterm. Antenatal magnesium sulphate reduces
both cerebral palsy (RR 0.68; 95% CI 0.54–0.87) and
gross motor dysfunction in premature infants (RR 0.61;
95% CI 0.44–0.88). The optimal regimen is uncertain: a
simple strategy endorsed by an expert consensus group
suggests that women under 30 weeks’ gestation who are
likely to deliver within the next 24 hours should be given
a 4-g loading dose of magnesium sulphate (slowly over
20−30 minutes) followed by a 1 g per hour maintenance
dose via the intravenous route.43 Although the majority
of women studied were at or below 30 weeks’ gestation,
some studies have recruited women up to 34 weeks’ ges-
tation. The NICE guideline group on preterm labour
and birth suggested that magnesium sulphate should be
‘offered’ to all women in established preterm labour from
24+0 to 29+6 weeks’ gestation, and considered in women
from 30+0 weeks to 33+6.18a

Routine Antibiotics
The lack of efficacy of antibiotics to prevent preterm labour
has been described above. An alternative strategy has been
to give antibiotics to women who present in preterm labour,
in the hope that they will delay delivery and improve out-
come for the baby. In women with intact fetal membranes,
such a strategy is singularly unsuccessful, with no short-­term
beneficial effect of either co-­ amoxiclav or erythromycin
for the neonate.44 Additionally, a comprehensive follow-
­up study has suggested that routine antibiotic administra-
tion to women in preterm labour is actually harmful, with
increased rates of cerebral palsy in the offspring exposed
to prenatal antibiotics, with some evidence of a dose-­
dependent effect.45 Thus there is no justification to give
antibiotics routinely to women presenting with preterm
labour and intact fetal membranes. The Royal College of
Obstetricians guideline recommends routine antibiotic pro-
phylaxis against group B streptococcal infection for women
in confirmed preterm labour based on level 4 evidence.46
PRETERM PRELABOUR RUPTURE OF
MEMBRANES
Diagnosis
The diagnosis of preterm prelabour rupture of mem-
branes (pPROM) is made by a combination of history
from the woman, followed by a sterile speculum exami-
nation to visualize amniotic fluid in the vagina. The
false positive rates of the nitrazine test (to identify pH
change) and identification of ‘ferning’ on a slide are such
that these tests are not routinely recommended in clini-
cal practice.47 Ultrasound examination can be helpful if it
confirms a decrease in amniotic fluid volume.
Prognosis and Management
Women with pPROM are at increased risk of spontane-
ous labour, with the average latency period being less
than 3 days.47 In view of the risk of preterm delivery, most
authorities recommend that such women should be given
corticosteroid prophylaxis.47 Women with pPROM are
also at increased risk of ascending infection leading to
chorioamnionitis. In view of this, some clinicians offer
induction of labour to women with pPROM once they
reach 34 weeks’ gestation. Several large randomised trials
have compared such a policy to expectant management.
A meta-­analysis suggests that the benefits of expediting
delivery are minimal, with no effect of early delivery on
neonatal sepsis (RR of 0.96; 95% CI 0.64–1.30) or proven
neonatal infection with positive blood culture. Expedit-
ing delivery did however increase the risk of respiratory
distress syndrome (RR 1.26, 95% CI 1.05–1.53) and cae-
sarean section (RR 1.26, 95% CI 1.11–1.44) but reduced
the risk of chorioamnionitis (RR 0.50, 95% CI 0.26–0.95)
when compared with expectant management.48 Different
women and different care givers may come to different
conclusions about the best policy for them: decision mak-
ing can now be informed by a reasonable body of evi-
dence on the benefits and harms of each strategy.
2 Preterm Labour and Delivery 13
If expectant management is planned, antibiotic prophy-
laxis with erythromycin is recommended18a as it is associated
with an improvement in a composite neonatal outcome in
the short term49 with no evidence of harm in the long term.50
Given the known harmful long-­term effects of antibiotics
to women in preterm labour with intact fetal membranes,45
antibiotics should be withheld if there is any uncertainty
about fetal membrane rupture. Tocolysis is not indicated.
MODE OF DELIVERY FOR PRETERM
INFANTS
The optimal mode of delivery of the preterm infant is
unknown. The greater vulnerability of the preterm infant
might lead some clinicians and pregnant women to wish to
avoid vaginal delivery. Randomized trial evidence on this
issue is extremely limited, with only four studies of 116
women in total being considered of an adequate standard
for a systematic review.51 Not surprisingly, given the small
sample size, there is no evidence from these trials of either
caesarean section or vaginal delivery being superior in
terms of avoiding birth trauma, perinatal death or neona-
tal intensive care admission. A recent observational study
of over 4000 babies has shown that, in babies from 24 to
32 weeks’ gestation, attempted vaginal delivery is safe and
likely to be achieved in babies presenting by the vertex.52
For babies presenting by the breech, there was an increased
risk of death for babies between 24 and 32 weeks, and an
increased risk of the combination of death and asphyxia for
those between 24 and 27 weeks when vaginal delivery was
attempted. Less than 30% of pregnancies presenting by
the breech in which vaginal delivery was allowed between
24 and 32 weeks’ gestation actually managed to deliver
vaginally. Although multivariate analysis was used, the risk
of confounding remains. Nevertheless, in women deliver-
ing preterm, these data support a practice of attempting
vaginal delivery for babies presenting by the vertex. For
babies presenting by the breech, it would appear that the
strategy of planned caesarean section, as recommended for
babies at term with persistent breech presentation, may
have advantages.52 Indeed NICE suggests that caesarean
section be ‘considered’ in this latter scenario.18a
CONCLUSION
Preterm labour remains the biggest contributor to adverse
neonatal outcome in both resource-­rich and resource-­
poor settings. Several interventions, including antenatal
corticosteroid and magnesium sulphate prophylaxis, have
now been shown to improve outcome for the neonate.
Prevention of preterm delivery remains the goal, but it is
essential that any agent used for this indication is shown
to improve long-­term childhood outcomes, and does not
merely change the gestation of delivery. Given intensive
lobbying by many groups, including the Gates Founda-
tion and the March of Dimes in the USA, and Tommy’s
the Baby Charity and Action Medical Research in the
UK, together with support from governmental bodies, it
is to be hoped that novel interventions to prevent pre-
term birth will be identified over the next few decades.
14 PART I Antenatal
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2 Preterm Labour and Delivery 15
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 CHAPTER 3
Cervical Cerclage
S.P. Higgins
INTRODUCTION
Cervical incompetence occurs in approximately 0.1–1% of
all pregnancies. The condition is described where the cer-
vix is unable to retain the contents of the uterus and arises
when the volume or pressure within the uterine cavity
increases beyond that which the competence mechanism
of the cervix is capable of functioning, usually occurring
from the middle of the second trimester onwards.
The insertion of a cervical cerclage (stitch) is an opera-
tive procedure undertaken for the treatment of cervical
incompetence (insufficiency). It was first described by
Shirodkar in 1955, and modified by McDonald in 1957
as a transvaginal approach for the treatment of habitual
abortion, with the first transabdominal cerclage being
described in 1965 by Benson and Durfee.1 Cervical cer-
clage is a much maligned procedure, due in no small part
to the difficulty in diagnosing the condition but also to
the many variations in timing of placement and descrip-
tive terms associated with the procedure.
Traditionally the surgical procedure of placing a cervi-
cal cerclage was undertaken following a history of what
appeared to be a rapid, relatively painless second trimes-
ter miscarriage or early preterm birth. No diagnostic test
was or is available to confirm the condition.
In the final report of the MRC/RCOG2 multicentre
randomized controlled trial, the authors suggested that
only 1 in 25 cerclages were likely to have a beneficial effect
and on balance should only be offered to women with a his-
tory of three or more pregnancies ending before 37 weeks’
gestation. For many years, this trial formed the basis of
guidelines and recommendations (Green Top Guideline
No 60, www.rcog.org.uk/en/guidelines-research-services/
guidelines/gtg60), with the procedure falling out of favour.
With the advent of transvaginal morphological assess-
ment of the cervix in pregnancy, the inverse relationship
between the length of the closed endocervical portion of
the canal and the risk of preterm birth was clearly estab-
lished,3 thereby allowing ultrasound-­indicated cerclages to
be inserted. Ultrasound-­ indicated cerclage is undertaken
between 16 and 24 weeks’ gestational age, and the cervical
length used to determine if a cerclage is required is <2.5 cm
closed endocervical length, representing the shortest 5% for
cervical length at mid gestation. If a patient has an ultrasound-­
indicated cerclage inserted with a successful pregnancy out-
come then an elective cerclage may be inserted in a following
pregnancy at 12–14 weeks’ gestational age, without the need
for ultrasound identification of a short cervix.
Patients may suffer from cervical incompetence which
might only be suspected following a spontaneous pre-
term birth or second trimester loss. Other patients may
be considered at high risk of cervical incompetence and
16
spontaneous preterm birth following surgical procedures
such as large loop excision of the transformation zone
(LLETZ), cone biopsy or trachelectomy.
The insertion of a cerclage based purely on history
without the benefit of serial cervical length measure-
ments is no longer considered best clinical practice.
Patients with a history of spontaneous preterm birth
suggestive of cervical incompetence or with a history of
significant destructive surgical procedures of the cervix
should be enrolled in a surveillance programme involving
serial transvaginal cervical length measurements.4 Con-
sideration should be given to undertaking a prepregnancy
cervical length measurement and visual assessment of the
infravaginal portion of the cervix in patients with a his-
tory of a trachelectomy or several destructive procedures
of the cervix. A short cervix and the absence of sufficient
cervical tissue to place a cerclage during pregnancy is
grounds for considering the prepregnancy laparoscopic
placement of a cerclage. A review5 of 15 studies involving
3490 women identified that cervical cerclage reduced the
risk of preterm birth in women at high risk of preterm
birth and probably reduces the risk of perinatal deaths.
SURGICAL PROCEDURE
McDonald Cerclage
The vaginal approach to inserting a cervical cerclage var-
ies little between an elective or rescue procedure. The
McDonald technique is used, therefore not requiring
reflection of the bladder and further facilitating removal
of the suture when required or at 37 weeks’ gestational age
with an anticipated vaginal delivery. With the patient in
the lithotomy position and under either a general or spinal
anaesthetic, a Sims speculum and two lateral vaginal wall
retractors are used to identify the cervix. Four sponge-­
holding forceps are used to grasp the cervix and are placed
at 12, 3, 6 and 9 o’clock. There is little trauma associated
with their use but by placing four on the cervix the opera-
tor has the capacity to draw the cervix laterally, anteriorly
and posteriorly to maximize access for placement of the
cerclage. If the cerclage is being inserted with membranes
prolapsing through the canal but not beyond the exter-
nal os, a 14-­gauge Foley catheter can be used to displace
the membranes upward by inflating the balloon within the
cervical canal. The material used is a nonabsorbable 5-­mm
Mersilene tape on a curved needle and is prepared by soak-
ing it in normal saline and coating it with sterile lubricat-
ing gel to allow it to pull smoothly through the tissues.
A purse-­string suture is inserted around the infravaginal
portion of the cervix but as high and therefore as close to

the internal os as possible. The starting position is recog-
nized anteriorly by identifying the junction of the rugose
vagina and the smooth cervix. Four non–full-­ thickness
bites of the cervix are taken and the suture is pulled tight
to occlude the internal os and tied anteriorly. If a Foley
catheter is in place, it can be deflated and removed prior to
tightening the cerclage. After the surgical knot is tied, the
ends are cut to approximately 2 cm to facilitate identifica-
tion and removal of the cerclage at a later stage.
The cerclage is removed if rupture of the membranes
occurs, at the onset of significant uterine activity or at 37
weeks’ gestational age to await the spontaneous onset of
labour.
The following complications should be discussed with
the patient prior to placement of the cerclage:
1. Rupture of the membranes at the time of surgery –
this risk is particularly high if the membranes are
prolapsing into the canal but may occur with-
out. Particular care should be taken, as previously
stated, to avoid full thickness bites of the cervix as
this increases the risk of this complication.
2. Bleeding – may occur if the descending cervical
branch of the uterine artery is punctured. These
vessels run at 3 and 9 o’clock and should be avoided
when inserting the cerclage. Significant bleeding is
rarely encountered.
3. Miscarriage – may occur with or without either (1)
or (2) above.
4. Sepsis – chorioamnionitis is a rare but very seri-
ous complication. With the changes that occur to
the cervix associated with shortening of the canal
and loss of the mucus plug, there is a greater risk of
ascending infection to begin with. In the author’s
experience there is not a significantly increased risk
of sepsis associated with insertion of a cerclage.
Laparoscopic Transabdominal Cervical
­Cerclage
Traditionally a transabdominal cerclage was reserved
for patients who had a failed vaginal cerclage and was
inserted early in a subsequent pregnancy at laparotomy.
It was considered a permanent placement with delivery
of the baby undertaken by caesarean section. This proce-
dure was difficult to undertake due to the increased size
and vascularity of the gravid uterus and a desire not to
handle the organ. Historically the preference was not to
insert the cerclage prepregnancy, to facilitate the passage
of the products of conception should a miscarriage occur.
More recently, patients who have had surgical proce-
dures undertaken on the cervix (LLETZ, cone biopsy,
trachelectomy) should also be considered for a transab-
dominal cerclage where it is clearly established that the
cervix is short by way of transvaginal ultrasound and there
is insufficient infravaginal cervix to insert a cerclage.
The author and colleagues describe a prepregnancy
laparoscopic technique for the insertion of a cervical cer-
clage in the following clinical circumstances:
• failed elective cervical cerclage
• surgically shortened cervix, unable to insert vaginal
cerclage
• trachelectomy.
3 Cervical Cerclage 17
Prepregnancy insertion does not hinder the occurrence
of either a spontaneous miscarriage or an evacuation of
retained products of conception in the first trimester or
indeed medical management of an early second trimes-
ter miscarriage, avoiding the need for a hysterotomy.
Delivery of the baby is undertaken by caesarean section.
Posterior colporrhaphy with division of the cerclage has
occasionally been described to avoid the need for caesar-
ean section.
Laparoscopic prepregnancy transabdominal cerclage
has become the preferred procedure of patients with a
success rates of 90–100%6 and cumulative fetal survival
rates of 90%.
The procedure involves placing nonabsorbable 5-­mm
Mersilene tape around the cervix at the level of the inter-
nal os, thereby restoring the competence mechanism of
the damaged cervix. By undertaking this procedure in the
prepregnancy setting the surgeon avoids the risks tradi-
tionally associated with its insertion during pregnancy,
and allows the use of a uterine manipulator to assist in
maximizing the surgical view.
The procedure is undertaken under general anaes-
thetic with the patient in the lithotomy position. A team
of three surgeons is required: two to undertake the lap-
aroscopy and a third to assist with manipulation of the
uterus. A three-­port laparoscopic approach is undertaken
with a 10-­mm primary trocar inserted infraumbilically.
Two accessory ports (5 mm) are inserted in the right and
left iliac fossae, sufficiently lateral to maximize manoeu-
vrability of the instruments. A self-­retaining Foley cath-
eter is inserted prior to commencing the surgery.
The uterovesicular fold of peritoneum is opened with
diathermy and, using the raised intraperitoneal pressure
at laparoscopy and blunt dissection of the pubocervical
fascia, the bladder is advanced inferiorly from the lower
segment and cervix. The peritoneal incision is extended
on both sides to open the anterior leaf of the broad liga-
ment. The uterine vascular pedicle is identified at this
time. Using Maryland forceps a small window is created
in the broad ligament to allow direct observation of the
passage of the needle through the cervical tissue.7
Posteriorly, two small windows are made using dia-
thermy in the visceral peritoneum, approximately 1 cm
superior and lateral to the apex of the uterosacral liga-
ments indicating the entry points of the needle.
A 5-­mm Mersilene tape with straightened needles is
inserted through the 10-­mm port. Using a laparoscopic
needle holder and under direct vision through the win-
dow created in the broad ligament, the needle is passed
from posterior to anterior, medial to the uterine vascular
bundle, and pulled through to a reasonable length. The
procedure is repeated on the opposite side, leaving both
needles anterior and the tape sitting snug to the posterior
aspect of the uterus. Both needles are cut at this stage
and placed in the uterovesical pouch for later removal.
The knot is tied anteriorly at the level of the internal os,
and the tape is cut with ends of approximately 1.5 cm to
minimize the risk of the knot coming undone.
The following specific complications should be dis-
cussed with the patient prior to placement of the cerclage:
• Complications in general of a laparoscopic proce-
dure.
18 PART I Antenatal
• T he need for a hysterotomy in later pregnancy in
the event of a fetal demise.
• The need for a caesarean section to deliver the
baby. The author has not experienced an additional
degree of difficulty at caesarean section with an ab-
dominal cerclage in place.
The straightened needles can be removed through
the 5-­mm port. The abdominal incisions are closed with
monocryl suture material.
DISCUSSION
With the advent of transvaginal ultrasound to measure
cervical length, there are more objective, reproducible
methods of identifying the patient with cervical incompe-
tence and a more timely approach to the insertion of the
cerclage, leading to fewer failed insertions. Where previ-
ously the commonest indication for inserting an abdomi-
nal cerclage was failed vaginal cerclage,8 the author now
finds that patients with previous cervical surgery are con-
stituting an increasing proportion of patients undergoing
this as a primary procedure.
REFERENCES
1. Benson RC, Durfee RB. Transabdominal cervico-­uterine cerclage
during pregnancy for the treatment of cervical incompetency.
Obstet Gynaecol. 1965;25:145–155.
2. Medical
 Research Council/Royal College of Obstetricians and
Gynaecologists Working Party on Cervical Cerclage. Final report
of the Medical Research Council/Royal College of Obstetricians
and Gynaecologists multicentre randomised trial of cervical cer-
clage. Br J Obstet Gynaecol. 1993;100(6):516–523.
3. Iams JD, Goldenberg RL, Meis PJ, et al. The length of the cervix
and the risk of spontaneous premature delivery. National Institute
of Child Health and Human Development Maternal Fetal Medi-
cine Unit Network. N Engl J Med. 1996;334(9):567–572.
4. Higgins SP, Kornman LH, Bell RJ, Brennecke SP. Cervical sur-
veillance as an alternative to elective cervical cerclage for preg-
nancy management of suspected cervical incompetence. Aust N Z J
Obstet Gynaecol. 2004;44(3):228–232.
5. Alfirevic Z, Stampalija T, Medley N. Cervical stitch (cerclage) for
preventing birth in singleton pregnancy. Cochrane Database Syst
Rev. 2017;6:CD008991.
6. Ades A, Parghi S, Aref-Adib M. Laparoscopic transabdominal cer-
clage: outcomes of 121 pregnancies. ANZJOG 2018;58(6):606–611.
7. Ramesh B, Chaithra TM, Prasanna G. Laparoscopic transabdomi-
nal cervical cerclage by broad ligament window technique. Gynaecol
Minim Invasive Ther. 2018;7(3):139–140.
8. Burger NB, Brölmann HA, Einarsson JI, Langebrekke A, Huirne
JA. Effectiveness of abdominal cerclage placed via laparotomy
or laparoscopy. Systematic review. J Minim Invasive Gynaecol.
2011;18:696–704.

Antepartum Haemorrhage – an
Overview
Antepartum haemorrhage (APH) is defined as bleed-
ing from the genital tract after 20 weeks of gestation.
APH complicates 3–5% of all pregnancies, and is a
common emergency presentation to maternity units.
It is therefore essential that clinicians have a thorough
understanding of its causes to be able to identify and
manage scenarios at risk of substantial haemorrhage
(Table 4.1).
Placenta praevia and placental abruption are the
most serious causes of antepartum haemorrhage and
can pose a significant threat to both the life of mother
and fetus.
A new classification of placenta praevia has been
developed by the American Institute of Ultrasound in
Medicine (AIUM).1 They have recommended discon-
tinuing the use of the terms ‘partial’ and ‘marginal’ and
have suggested that the term placenta praevia is used
when the placenta lies directly over the internal os. The
definition is that for pregnancies greater than 16 weeks,
the placenta should be reported as ‘low lying’ when the
placental edge is less than 20 mm from the internal os,
and as normal when the placental edge is 20 mm or
more from the internal os on transabdominal or trans-
vaginal ultrasound. While significant disease occurs in
around 1 in 200 deliveries, the incidence is becoming
more common due to higher caesarean section rates,
assisted reproductive techniques and advancing mater-
nal age.3 The recently published RCOG Green Top
Guideline suggests that adoption of the AIUM clas-
sification could improve the management of placenta
praevia.2
Major placental abruption is now seen less commonly
due to general advances in maternal health, includ-
ing lower maternal smoking rates and improvements in
TABLE 4.1 Causes of Antepartum
Haemorrhage
Site Diagnosis
Uterine Placenta praevia
Placental abruption
Invasive placental disease, e.g. increta
Vasa praevia
Cervix Ectropion
Effacement in labour
Cervical cancer
Cervical ectopic pregnancy
Lower genital Vulvovaginal infections, e.g. candidiasis
tract Vulvovaginal varices
Malignancy
Trauma
CHAPTER 4
H. Richardson • A. Cameron
antenatal care. It is often the case that the cause of ante-
partum haemorrhage can be undetermined. Cases of
repeated unexplained bleeding require increased antena-
tal surveillance.
There are no standard definitions for the severity of
antepartum haemorrhage. Visual estimation of blood
loss may underestimate the true volume of bleeding, for
example in massive concealed abruption. Assessment of
signs of shock and volume of bleeding allows for initial
estimation of blood loss and appropriate location of care.4
Bleeding can be classified as:
• Spotting – staining or streaking on underwear
• Minor APH – blood loss of less than 50 mL which
has settled
• Major APH – blood loss of 50–1000 mL with no
clinical signs of shock
• Massive APH – blood loss of greater than 1000 mL
with signs of shock
CLINICAL ASSESSMENT
Consider a patient presenting acutely to maternity ser-
vices with minor APH. Typically the patient is haemo-
dynamically stable and bleeding will have settled prior to
clinical assessment, allowing for a thorough history to be
obtained.2 Clinical history should cover:
• The identification of risk factors for praevia or ab-
ruptio – for example, previous caesarean section,
smoking.
• Pain associated with bleeding – painless APH may
be associated with placenta praevia; continuous
pain may signal placental abruption.
• Assessment of fetal wellbeing – enquiry about fe-
tal movements and auscultation of the fetal heart
should be carried out.
• Local causes for bleeding – for example, smear his-
tory or postcoital bleeding.
Clinical examination and management should include:
• Documentation of maternal pulse and blood pres-
sure.
• Abdominal palpitation – hard, woody abdomen
should alert staff to suspected placental abruption.
Uterine contractions may indicate labour. An irri-
table uterus on palpation may also suggest placen-
tal separation and predispose to preterm labour.
• Speculum examination – allows for visualization
of the lower genital tract to identify local causes of
bleeding. Any suspicious cervical or vaginal legion
should be referred for colposcopy during pregnancy.
19
20 PART I Antenatal
• A n ultrasound examination, if placental location
is unknown. Ultrasound scan is not helpful in the
diagnosis of placental abruption unless there is a
significant enough separation to show chorioamni-
otic separation. It is likely that this will have clear
clinical signs on examination.
• A check of blood type – rhesus negative women
should have a Kleihauer obtained and anti-­D im-
munoglobulin administered.
• Consideration of a course of antenatal steroids if
between 24 and 36 weeks’ gestation.
• Admission to the antenatal ward for a period of
monitoring, recommended in women who present
with minor or major APH. If bleeding has settled,
then discharge home can be considered.
Digital and speculum vaginal examination should not
be performed until placenta praevia has been excluded.
Patients who present with major haemorrhage and
are clinically unstable should be managed in an acute
area with immediate access to delivery and resuscita-
tion facilities, such as a labour suite. Management should
be multidisciplinary, involving senior obstetricians and
anaesthetists. Immediate resuscitation of the mother
should commence along with assessment of fetal well-
being. Resuscitation should follow a structured ABC
(Airway, Breathing, Circulation) approach.
Consider the following case:
A primigravida with a known posterior placenta
praevia presents at 34 weeks gestation with heavy fresh
per vaginum (PV) bleeding. On arrival to the maternity
unit, she is alert and orientated, but has a tachycardia of
120 bpm and a blood pressure of 90/40 mmHg. There is
active ongoing PV loss and her legs and clothing are
heavily bloodstained. Auscultation of the fetal heart
confirms a fetal heart rate of 160 bpm.
Initial management would include:
• Performing primary survey using an ABCD assess-
ment of the mother.
• Left lateral tilt.
• Commencing facial oxygen at 10–15 L/min.
• Siting two large bore venflons and taking blood for
full blood count; crossmatching 4 units, coagula-
tion screen, urea and electrolytes (U&Es), and C-­
reactive protein (CRP).
• Rapid haemoglobin assessment using bedside
point-of-care testing should be considered if facili-
ties are available.
• E stimation of blood loss, with >1500 mL prompt-
ing initiation of local major obstetric haemorrhage
protocols.
• Starting IV fluid replacement until blood is avail-
able. Up to 3.5 L of warmed crystalloid solution can
be infused as rapidly as required.
• Transfusing blood as soon as available, considering
use of O-­negative blood if haemoglobin is low and
the mother is unstable.
• Transfusing up to 4 units of fresh frozen plasma
(FFP) and 10 units of cryoprecipitate in case of on-
going haemorrhage, until clotting studies are avail-
able. Aim to keep fibrinogen levels >1.0 g/L and
prothrombin time <1.5 × mean control.
• Commencing cardiotocography (CTG) monitoring.
• Delivery by caesarean section if there is ongoing
maternal or fetal compromise.
SUMMARY
Antepartum haemorrhage is a relatively common pre-
sentation to all maternity settings. Clinical staff should
be familiar with the range of possible diagnoses and sub-
sequent management. By undertaking regular in-­house
skills and drills training, clinical staff will maximize the
best outcomes for mother and baby.
REFERENCES
1. Reddy UM, Abuhamad AZ, Levine D, Saade GR. Fetal Imaging
Workshop Invited Participants. Fetal imaging: executive summary
of a joint Eunice Kennedy Shriver National Institute of Child
Health and Human Development, Society for Maternal-­Fetal
Medicine, American Institute of Ultrasound in Medicine, Ameri-
can College of Obstetricians and Gynecologists, American College
of Radiology, Society for Pediatric Radiology, and Society of Radi-
ologists in Ultrasound Fetal Imaging Workshop. J Ultrasound Med.
2014;33:745–757.
2. Jauniaux ERM, Alfirevic Z, Bhide AG, et al. on behalf of the Royal
College of Obstetricians and Gynaecologists. Placenta praevia and
placenta accreta: diagnosis and management. Green-­top Guideline
No. 27a. BJOG. 2019;126(1):e1–e48.
3. Rosenberg T, Pariente G, Sergienko R, Wiznitzer A, Sheiner E.
Critical analysis of risk factors and outcome of placenta previa.
Arch Gynecol Obstet. 2011;284:47–51.
4. Olyese Y, Ananth CV. Placental abruption. Obstet Gynecol.
2006;108:1005–1016.

INTRODUCTION
Vasa praevia is a rare disorder of pregnancy with a devas-
tating outcome when undiagnosed. The condition classi-
cally presents with ruptured membranes, painless vaginal
bleeding and fetal distress (Benckiser’s haemorrhage).1,2
Antenatal ultrasound diagnosis of the condition has been
possible since the late 1980s and planned hospitalization,
targeted steroid administration and scheduled delivery,
usually between 34 and 36 weeks of gestation, results in
improved fetal survival.3–6
DEFINITION
Vasa praevia describes the presence of fetal vessels running
through the fetal membranes close to or over the cervix.
Unsupported by placental tissue or Wharton’s jelly, these
vessels are susceptible to bleeding at the time of membrane
rupture, either spontaneously or at the time of amniot-
omy. Resultant fetal haemorrhage can lead to exsanguina-
tion. There are two types of vasa praevia.7 In type I, there
is a velamentous or marginal cord insertion and the fetal
vessels that lie within the amniotic membranes overlie or
are close to the cervix. Type I vasa praevia is associated
with a low-­lying placenta or placenta praevia.8 In type II
vasa praevia the fetally derived vessels connect to the pla-
centa from a succenturiate or accessory lobe.
INCIDENCE
Vasa praevia is a rare condition with estimates of prev-
alence ranging from 1 in 1200 to 1 in 5000 pregnan-
cies.4,9,10 Risk factors include second trimester placenta
praevia (odds ratio [OR] 19; 95% confidence interval [CI]
5.6–93.8), multiple pregnancies (OR 2.66, 95% CI 0.8–
8.8), assisted reproduction (OR 19; 95% CI 6.6–54.0),
velamentous cord insertion (OR 672; 95% CI 112–4034)
and bilobed placenta or succenturiate lobe (OR 71; 95%
CI 14–349).11 A single risk factor accounts for more than
80% of cases of vasa praevia.11–13 Where a velamentous
cord insertion is associated with a placenta lying within
the lower uterine segment, the incidence of vasa praevia
is estimated as 1 in 50.14 In monochorionic twins with
selective intrauterine growth restriction or twin–twin
transfusion syndrome, velamentous insertion is more
common.12,15,16 Maternal smoking has also been reported
as a risk factor for velamentous insertion and vasa prae-
via.16 Fetal anomalies shown to have an increased associ-
ated risk include renal tract abnormalities, spina bifida,
exomphalos and single umbilical artery.4
CHAPTER 5
Vasa Praevia
M.A. Ledingham
PATHOPHYSIOLOGY
The pathophysiology of velamentous cord insertion
and vasa praevia is uncertain. Both have been linked to
abnormal placental development. Velamentous vessels
lack the normal ‘cushioning’ provided by the placenta
and are more susceptible to compression and other types
of mechanical trauma. Dilatation of the lower uterine
segment results in mechanical stress to the fetal vessels
resulting in haemorrhage. If the vessels are of large cali-
bre, immediate fetal demise is likely.
DIAGNOSIS
Vasa praevia is one of the differential diagnoses of ante-
partum and intrapartum haemorrhage. Bleeding at this
time may be mistaken for placenta praevia, placental
abruption and heavy ‘show’. Signs of fetal distress are
typically acute and out of proportion to the amount of
bleeding. A sinusoidal heart rate pattern may indicate
fetal exsanguination. Rarely, vasa praevia presents less
acutely in labour following ruptured membranes with
minor vaginal bleeding and progressive fetal tachycardia.
Alkali denaturation tests have been described to dif-
ferentiate maternal from fetal blood (as fetal blood
is resistant to denaturation in the presence of 0.1%
NaCl). These are seldom used in modern clinical prac-
tice although a rapid bedside ‘Apt test’ is available. Adult
blood turns brown within 30 seconds but fetal haemoglo-
bin remains pink.17
The condition may occasionally be diagnosed in
labour during digital vaginal examination by palpation of
pulsating fetal chorionic plate vessels inside the cervical
os. Fetal mortality is high in this situation (60%) even if
urgent caesarean delivery is performed.4
INVESTIGATIONS
Ultrasound scan has been shown to have a high diagnos-
tic accuracy and low false positive rate for vasa praevia.10
The diagnosis is made on transvaginal ultrasound by visu-
alization of a linear sonolucent area over or within 2 cm of
the internal os of the cervix. Colour Doppler assessment
demonstrates a typical umbilical artery vascular wave-
form.16,19,20 As a normal loop of cord could be mistaken
for a vasa praevia, it is important that the vessel cannot be
displaced with maternal movement. A combined trans-
vaginal and transabdominal approach allows visualization
of the placental site, cord insertion and placental type
and is therefore the recommended investigation.21 The
21
22 PART I Antenatal
diagnosis is made most accurately in the second trimester
(18–24 weeks) and if made at this time should be con-
firmed in the third trimester (30–32 weeks).4
The antenatal detection rate of vasa praevia var-
ies between 53% and 100%.20 However, antenatal
detection improves chances of survival from 44% to
97%.22 At present there is insufficient evidence to
recommend routine screening at the time of the mid
pregnancy anomaly scan in the general obstetric popu-
lation.4,9,10,13,14 Targeted screening of high-­risk groups
(velamentous or marginal cord insertion, low-­ lying
placenta, bilobed placenta and succenturiate placental
lobes, multiple pregnancy) may reduce perinatal loss
but the benefit of risk verses harm remains to be con-
firmed in further studies.4,5,13,22
MANAGEMENT
When vasa praevia is suspected associated with acute fetal
compromise in labour, a category 1 caesarean section
should be performed under general anaesthesia. The fetal
mortality rate is high under these circumstances, even if
transfusion of the infant is performed.4
If the condition is suspected in labour prior to mem-
brane rupture, immediate transfer to theatre should be
arranged and confirmation of the diagnosis attempted
(amnioscopy or transvaginal ultrasound scan).
If diagnosed antenatally by ultrasound scan, women
should be counselled about the risk of fetal haemorrhage
associated with membrane rupture and offered hospi-
talisation from 30–32 weeks onwards. Steroids should be
administered from 28–32 weeks’ and caesarean section
planned between 34 and 36 weeks’ gestation.4,9 Feto-
scopic laser ablation therapy has been described but the
benefits of this have to be balanced against the risk of
preterm premature rupture of the membranes with this
invasive technique.
REFERENCES
1. Heckel S, Weber P, Dellenbach P. Benckiser’s hemorrhage. 2 case
reports and a review of the literature. J Gynecol Obstet Biol Reprod
(Paris). 1993;22:184–190.
2. Lobstein J. Archives de L’art des Accouchements 1801. Strasbourg;
1801.
3. Derbala Y, Grochal F, Jeanty PJ. Perinat Med. 2007;1(1):2–13.
4. Gagnon R. No. 231. Guidelines for the management of vasa prae-
via. J Obstet Gynaecol Can. 2017;39(10):e415–e421.
5. McQueen V, Speed M, Rutler S, Gray T. Vasa praevia: should we
routinely screen high risk women for this rare but serious condi-
tion? Ultrasound. 2018;26(2):127–131.
6. Melcer Y, Jauniaux E, Maymon S, et al. Impact of targeted scan-
ning protocols on perinatal outcomes in pregnancies at risk of
placenta accreta spectrum or vasa praevia. Am J Obstet Gynecol.
2018;218(4):443.e1–443.e8.
7. Gianopoulos J, Carver T, Tomich PG, Karlman R, Gadwood
K. Diagnosis of vasa previa with ultrasonography. Obstet Gynecol.
1987;69:488–491.
8. Oyelese Y, Smulian JC. Placenta previa, placenta accreta, and vasa
previa. Obstet Gynecol. 2006;107:927–941.
9. RCOG
 Green-­top Guideline No. 27b. Vasa praevia: diagnosis and
management; 2018.
10. Sinkey RG, Odibo AO, Dashe JS. Society for Maternal Fetal Medi-
cine Consult Series. Diagnosis and management of vasa praevia.
Am J Obstet Gynecol. 2015;213(5):615–619.
11. Ruiter L, Kok N, Limpens J, et al. Incidence of and risk indicators
for vasa praevia: a systematic review. BJOG. 2016;123:1278–1287.
12. Sullivan EA, Javid N, Duncombe G, et al. Vasa praevia diagno-
sis, clinical practice and outcomes in Australia. Obstet Gynecol.
2017;130:591–598.
13. 
UK National Screening Committee. Screening for Vasa Prae-
via in the Second Trimester of Pregnancy. External Review Against
Programme Appraisal Criteria for the UK National Screening
Committee (UK NSC). London: UK NSC; 2017. Available at:
https://legacyscreening.phe.org.uk/vasapraevia.
14. Paavonen J, Jouttunpaa K, Kangasluoma P, et al. Velamentous
insertion of the umbilical cord and vasa previa. Int J Gynaecol
Obstet. 1984;22:207–211.
15. R  COG Green-­top Guideline No. 51. Monochorionic twin pregnancy
management; 2017.
16. Jauniaux E, Mercer Y, Ramon R. Prenatal diagnosis and manage-
ment of vasa praevia in twin pregnancies: a case series and system-
atic review. Am J Obstet Gynecol. 2017;(6):568–575.
17. Loendersloot EW. Vasa praevia (letter). Am J Obstet Gynecol.
1979;135:702–703.
18. Silver RM. Abnormal placentation: placenta previa, vasa previa and
placenta accreta. Obstet Gynecol. 2015;126:654–668.
19. Rebarber A, Dolin C, Fox NS, Klauser CK, Saltzman DH, Roman
AS. Natural history of vasa previa across gestation using a screen-
ing protocol. J Ultrasound Med. 2014;33:141–147.
20. Ruiter L, Kok N, Limpens J, et al. Systematic review of accuracy of
ultrasound in the diagnosis of vasa previa. Ultrasound Obstet Gyne-
col. 2015;45:516–522.
21. Baschat AA, Gembruch U. Ante-­and intrapartum diagnosis of vasa
praevia in singleton pregnancies by colour coded Doppler sonog-
raphy. Eur J Obstet Gynecol Reprod Biol. 1998;79:19–25.
22. Oyelese Y, Catanzarite V, Prefumo F, et al. Vasa previa: the
impact of prenatal diagnosis on outcomes. Obstet Gynecol.
2004;103:937–942.

Placental Abruption
Placental abruption is the premature separation of the pla-
centa from the uterine wall after 20 weeks’ gestation and
before birth; the separation can be complete or partial.
It complicates approximately 1% of pregnancies and is a
major cause of maternal morbidity and of perinatal mor-
bidity and mortality. The incidence of abruption is lower
in Nordic countries and higher in south Asian countries.
Traditionally, placental abruptions have been de­­­scri­bed
as ‘revealed’, ‘concealed’ and ‘mixed’ (Table 6.1 and
Fig. 6.1).
RISK FACTORS FOR PLACENTAL
ABRUPTION
Clinical and epidemiological studies have identified a
number of obstetric, medical and social risk factors for
abruption (Table 6.2), though causal pathways remain
largely speculative. A history of abruption in a previous
pregnancy is the most predictive risk factor. A Dutch
study found the risk of recurrent abruption was 5.8%
(compared with 0.06% in women who had an uncompli-
cated first pregnancy).
PATHOPHYSIOLOGY
The aetiology of abruption is, in many cases, unknown. In
trauma or rapid decompression of the uterus, the abrup-
tion is an acute event as shearing forces cause the placenta
to separate from the uterus leading to haemorrhage. In
other cases, the process may start early in pregnancy; low
levels of pregnancy-­associated plasma protein A and raised
levels of maternal serum alpha-­fetoprotein in the first and
second trimesters are associated with subsequent placen-
tal abruption representing abnormal trophoblast invasion.
Placental separation is then the result of haemorrhagic
disruption of decidual arterioles in the basal plate.
TABLE 6.1 Classification of Placental
Abruptions.
Revealed The edge of the placenta separates from the
uterine wall and blood tracks down between
the decidua and the membranes through the
cervix and down the vagina.
Concealed In 5–10% the bleeding is retroplacental and
does not track to the vagina; in this case the
blood accumulates behind the placenta and
there is no vaginal bleeding.
Mixed In a ‘mixed’ abruption there is both retropla-
cental clot and blood tracking down to the
vagina.
CHAPTER 6
F. Nugent • A.J. Thomson
PRESENTATION AND CLINICAL FEATURES
The diagnosis of abruption is clinical, based on symptoms
and signs. The most common presenting symptoms are
abdominal pain, vaginal bleeding and uterine tenderness,
although the presentation can vary widely depending
on the extent of placental separation. In a mild abrup-
tion, there may be minor antepartum haemorrhage in a
woman who is clinically stable and with reassuring fetal
heart rate monitoring. In a severe, concealed abruption
there is acute, severe, constant abdominal pain and asso-
ciated hypovolaemic shock; the uterus is hard and tender
and the fetus may be dead or show evidence of asphyxia.
In some cases of abruption, usually concealed and
mixed, the retroplacental extravasation of blood through
the myometrium may reach the serosal surface and be
seen at caesarean section as bruising and discoloration –
this is known as a Couvelaire uterus.
Ultrasonography has low sensitivity but high specific-
ity in the diagnosis of placental abruption; ultrasonogra-
phy will fail to detect three-­quarters of cases of abruption.
Positive scan findings are associated with poorer perinatal
outcomes and greater maternal morbidity.
MANAGEMENT
Initial Assessment
The initial management of suspected placental abruption
involves prompt assessment of the maternal and fetal con-
dition, as these factors will guide the need for intervention.
This primary evaluation should aim to identify maternal
haemodynamic compromise through routine observa-
tions and accurate measurement of blood loss when pres-
ent, and to identify fetal distress using cardiotocography.
Evidence of Maternal or Fetal Compromise
Immediate delivery is usually required when there is evi-
dence of maternal and/or fetal compromise. If vaginal
birth is imminent then this may be the most appropri-
ate delivery option; however, if significant delay is antici-
pated, then caesarean section under general anaesthetic
with concomitant maternal and fetal resuscitation should
be undertaken (see Chapter 29). Pursuit of the most rapid
mode of delivery, in addition to preserving life, will also
limit the progression of coagulopathy associated with
major haemorrhage. Liaison with other senior members
of the multidisciplinary team is essential in anticipation
of the challenge of anaesthetizing and resuscitating an
unstable patient.
23
24 PART I Antenatal

5HYHDOHG&RQFHDOHG0L[HG
FIGURE 6.1 n Classification of abruptio placentae.

TABLE 6.2 Risk Factors for Placental Abruption. duration of labour, so delay whilst awaiting vaginal deliv-
ery should not automatically be assumed to be associated
Obstetric • P revious pregnancy complicated by an with greater blood loss. Vaginal delivery is preferable
factors abruption
• Pre-­eclampsia when the abruption has been severe enough to result in
• Fetal growth restriction intrauterine fetal death, since disseminated intravascular
• Polyhydramnios coagulation is more frequently encountered and manage-
• High parity ment of intraoperative haemorrhage during caesarean
• Malpresentation
• Preterm, prelabour rupture of the membranes
section can be extremely challenging.
• First trimester vaginal bleeding

Medical
• Short interval between pregnancies
• Low body mass index
Preterm Delivery
factors • Advanced maternal age When the abruption results in preterm labour, con-
• Maternal thrombophilia
• Dietary and nutritional deficiencies sideration should be given to the use of antibiotics for
• Anaemia Group B Streptococcus prophylaxis, corticosteroids
Social • Abdominal trauma (accidental and intentional) to promote lung maturation and magnesium sulphate
factors • Smoking for neuroprotection at appropriate gestations. Admin-
• Drug misuse (cocaine and amphetamines)
istration of tocolysis has been proposed in stable
patients to allow completion of these interventions,
although its use is controversial. More time will be
available to consider the above interventions when
mother and fetus are both stable and when labour has
No Maternal or Fetal Compromise not been established.
If the maternal and fetal conditions are stable, and there
is no contraindication, then vaginal birth may be consid- Conservative Management
ered; this may be associated with less maternal morbid-
ity than birth by caesarean section. Situations where this When a placental abruption is minor, and monitor-
would be a viable option include: ing of the mother and fetus are reassuring, immediate
• When labour has already established delivery may not be required or indicated, especially at
• Where there is notable but less pressing concern preterm gestations. It has been acknowledged that many
regarding the maternal or fetal wellbeing, e.g. sus- of the consequences of abruption on neurodevelopmen-
picious cardiotocography CTG) tal outcomes in the fetus are related to prematurity, so
• In cases of fetal demise where the mother is sta- delay in delivery may be beneficial. However, awareness
ble. that a partial abruption may advance to more signifi-
Continuous fetal heart rate monitoring should be cant abruption without prior warning must be balanced
undertaken and labour should take place in close prox- against the risks of conservative management. Maternal
imity to facilities for operative delivery. Obtaining effec- and fetal surveillance should be undertaken for the dura-
tive uterine activity is often not problematic, as patients tion of the pregnancy, in particular, to observe for signs
are commonly contracting strongly without augmenta- of fetal growth restriction and pre-­eclampsia. Consid-
tion and generally labour progresses rapidly regardless of eration should be given to undertaking delivery when
parity or cervical favourability. However, amniotomy or abruption occurs after 34 weeks’ gestation and certainly
oxytocin can be used if required. The volume of blood by 37 to 38 weeks because of an associated increased risk
loss has been shown to be negatively correlated with of stillbirth.

TABLE 6.3 Postpartum Interventions That May
Be Required Following Placental Abruption.
•  terine packing
U pregnancies.
• Uterine balloon tamponade
• Uterine compression sutures
• Stepwise uterine devascularization
• Internal iliac artery ligation
• Uterine artery embolization
• Hysterectomy
Postpartum Care
Following delivery, steps should be taken to mitigate the
risks of potential complications, including postpartum
haemorrhage. The use of standard uterotonics should be
titrated in response to uterine tone and ongoing haemor-
rhage. In severe cases (Couvelaire uterus), the myome-
trium may respond poorly to uterotonics and surgical and
other interventions may be required to achieve haemo-
stasis (Table 6.3).
Other recognized complications include an increased
risk of acute kidney injury, sepsis, pulmonary oedema and
venous thromboembolism, the pathophysiology of which
are likely mediated by major haemorrhage. Long-­term
maternal renal and cardiovascular morbidity and mortal-
ity have been linked to placental abruption, which may be
a reflection of common causal pathophysiology.
It has been recognized that women with a previous
abruption are at risk of recurrence in a future pregnancy –
6 Placental Abruption 25
a potentially 20-­fold increased risk – with risk of recur-
rence being higher for more severe abruptions. Modi-
fiable risk factors should be addressed prior to future
BIBLIOGRAPHY
Ananth CV, Friedman AM, Lavery JA, et al. Neurodevelopmental
outcomes in children in relation to placental abruption. BJOG.
2016;124:463–472.
Ananth CV, Wapner RJ, Ananth S, et al. First-­trimester and second-­
trimester maternal serum biomarkers as predictors of placental
abruption. Obstet Gynecol. 2017;129(3):465–472.
Downes KL, Grantz KL, Shenassa ED. Maternal, labour, delivery, and
perinatal outcomes associated with placental abruption: a system-
atic review. Am J Perinatol. 2017;34(10):935–957.
Inoue A, Kondoh E, Suginami K, et al. Vaginal delivery after placen-
tal abruption with intrauterine fetal death: a 20-­ year single-­
center experience. J Obstet Gynaecol Res. 2017;43(4):676–681.
Merriam A, D’Alton ME. Placental abruption. In: Copel JA, D’Alton
ME, Feltovich H, Gratacos E, Krakow D, Obido AO, Platt LD,
Tutschek B. Obstetric Imaging: Fetal Disgnosis and Care. 2nd ed.
Elsevier Health Services, Philadelphia, PA; 2017:426–429.
National Institute for Health and Care Excellence (NICE). Preterm
Labour and Birth (NICE Guideline No. 25); 2015. Available at: https://
www.nice.org.uk/guidance/ng25?unlid=9291036072016213201257.
Royal College of Obstetricians and Gynaecologists. Antepartum Haem-
orrhage (Green-­top Guideline No. 63); 2011. Available at: https://
www.rcog.org.uk/en/guidelines-­research-­services/guidelines/gtg63/.
Royal College of Obstetricians and Gynaecologists. Group B Streptococ-
cal Disease, Early-­onset (Green-­top Guideline No. 36); 2017. Available
at: https://www.rcog.org.uk/en/guidelines-­research-­services/guide
lines/gtg36/.
Ruiter L, Ravelli AC, de Graaf IM, et al. Incidence and recurrence rate
of placental abruption: a longitudinal linked national cohort study
in the Netherlands. Am J Obstet Gynecol. 2015;213:573.e1–e8.
 CHAPTER 7
Induction of Labour
T.A. Johnston • N. Pilarski
INTRODUCTION
Induction of labour, which is defined as the process
by which labour is started (or attempted) prior to its
spontaneous onset leading to active labour and birth,
is one of the two options available to women and their
caregivers when the continuation of a pregnancy poses
a greater risk to either the mother or the fetus than
the consequences of interrupting the pregnancy; the
remaining option being caesarean section. As such,
induction of labour is an essential intervention that
is employed on a daily basis throughout the world.
In the UK, there is an abundance of national guid-
ance regarding induction of labour from the National
Institute for Health and Care Excellence (NICE) and
the Royal College of Obstetricians and Gynaecolo-
gists (RCOG), to which the reader is referred via the
respective websites.
HISTORY
Induction of labour dates back to antiquity, and various
methods, many bizarre and some extremely dangerous,
have been employed.1 Some very early methods have
since been shown to have some scientific basis, whereas
others bordered on witchcraft. Literature from the 16th
century contains long lists of ‘medications’ said to be
effective in stimulating labour, including juniper ber-
ries, castor oil, cinnamon, white amber in white wine
and many others. In 1735 Dr Henry Bracken recom-
mended ‘some softening, unctuous application such as
sweet almonds be applied warm with a brush of feathers
to the privities and vagina’ in his text Midwives Compan-
ion – wherein the Whole Art is Explained.1 Massage of the
breasts has been employed for centuries, as the relation-
ship between breast and uterus, via oxytocin, has long
been appreciated, and even now some still employ a
modification of this technique for induction of labour in
the form of breast massage and nipple stimulation with
some degree of success. Insertion of various objects into
the cervix has been utilized for induction as far back as
the 6th century when Aetius inserted cervical sponges to
induce labour following intrauterine death. The 1800s
saw the introduction of other mechanical methods of
induction. Kraus’s bougies were introduced on a wide
scale. These were used to forcibly dilate the cervix, sepa-
rate the membranes from the uterine wall high up into
the uterine cavity, after which the bougie was left in place
until labour ensued – a method used for many years, but
which has now fortunately been laid to rest because of its
relative inefficiency, sepsis rate, and the not insignificant
26
risk of injury to the placenta. Cohen described the injec-
tion of fluid under the fetal membranes in 1846, a method
which was reinvestigated in the 1990s. Laminaria have
also been used since the 1800s and their use has seen
a recent resurgence. Another mechanical method previ-
ously employed which again has seen an increase in pop-
ularity is the use of a balloon catheter inserted through
the cervix into the lower uterine segment and inflated.
It appears that any success related to these mechanical
methods may be secondary to the release of prostaglan-
dins following the mechanical disruption of the tissues,
as is almost certainly the case in sweeping of the mem-
branes. Another ancient method was the use of ecbolics,
which have been used throughout history for abortion as
well as induction of labour. The ingredients and meth-
ods of administration have varied throughout the years,
but the ‘medical induction’ regime used most recently
was standardized by Watson in the 1920s, more recently
referred to as the OBE, and consisted of oral castor Oil
followed by a hot Bath and a soap and water Enema,
which was said to be ‘high, hot and a hell of a lot’. This
practice ceased in the past few decades with the advent
of more successful and less unpleasant methods of induc-
tion. Other forms of medical induction were tried, all
with limited success. Towards the end of the 1800s qui-
nine was used successfully to induce labour but the det-
rimental effects on the fetus were recognized and this
method therefore fell from favour, although its use in
intrauterine death persisted for some time. In the 1900s,
various other substances were tried, with inconsistent
and often unconvincing results. These included oestro-
gens, urea, hyaluronidase, steroids, relaxin and sparte-
ine, to name a few. However, the three major methods
of induction of labour that have stood the test of time
in terms of acceptability, safety and efficacy are amniot-
omy, intravenous oxytocin and prostaglandins, although
mechanical methods in the form of cervical balloons and
laminaria are seeing a resurgence.
MAKING THE DECISION
When considering any intervention, it is important to
be clear about the balance between risks and benefits
(Fig. 7.1). With induction of labour, the objective is safe
vaginal birth, and the intended benefit on the whole is
avoidance of perinatal and/or maternal morbidity and
mortality. The risks and benefits are often different for
the mother and the baby and as such need to be balanced
against each other. If delivery is advocated to reduce
maternal risk, the proposed benefit must be weighed
against any risks associated with the induction process,
 7 Induction of Labour 27

.8
.6

Proportion with SEN (logscale)

.4
5LVNVLI 5LVNVLI
SUHJQDQF\ SUHJQDQF\
FRQWLQXHV LQWHUUXSWHG
.2

FIG. 7.1 n The obstetric balance. .1

including but not limited to potentially increasing the .05

risk of caesarean section, including both immediate
risks and those in subsequent pregnancies.2 For the
fetus/baby, the proposed benefit is often avoidance of
stillbirth or significant morbidity, but the risks include
the consequences of early delivery, both short and long
term.3–7 In the short term, induction of labour prior to
41 weeks’ gestation is associated with an increased risk
of admission to a neonatal facility.6 In addition, fetal
brain development continues throughout pregnancy,
and population data demonstrate that the risk of a child
having special educational needs (SEN) is lowest in
those delivering at 40–41 weeks gestation7 (Fig. 7.2).
After adjusting for maternal and obstetric characteris-
tics and expressed relative to delivery at 40 weeks, when
the subsequent risk of SEN was 4.4%, the risk of SEN
was increased by 36% (95% confidence interval [CI]
27–45%) at 37 weeks, by 19% (95% CI 14–25%) at 38
weeks and by 9% (95% CI 4–14%) at 39 weeks. Because
of these risks, it is important not to offer early delivery
to pregnancies not at increased risk, or where the risks
of early delivery outweigh the benefits.
When trying to balance these risks and benefits for
both the mother and the baby, many factors need to
be taken into consideration. Firstly, the evidence con-
firming benefit of early delivery is not translatable
from one group to another, and evidence of benefit is
often absent or weak. For example, it is common prac-
tice to offer induction of labour to women who pres-
ent with reduced fetal movements (RFM) at term.8 In
the AFFIRM trial,9 which assessed the introduction of
a care package for women with RFM with a reduction in
stillbirth as the primary outcome, the intervention did
not reduce the incidence of stillbirth but did increase
the rates of induction of labour and caesarean section,
and was associated with an increased risk of prolonged
neonatal unit admission: essentially the benefit was not
realized but the risks were increased. From the baby’s
perspective, delivery removes the risk of stillbirth but,
as discussed above, early delivery carries different risks,
and it is important to consider the risk to the baby of
the pregnancy continuing in that particular situation
against the known short-­term and long-­term risks of
early delivery, which change with gestation. It is impor-
tant, therefore, that timing of intervention also needs
to be considered both in terms of risk and successful
induction.
With regards to success (safely achieving a vaginal
birth), the two main factors which influence this are a
24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43
Estimated gestational age (weeks)
FIG. 7.2 n Prevalence of special educational needs by gestation
at delivery. (Reproduced from MacKay DF, Smith GCS, Dobbie R,
Pell JP, PLoS med. 2010, with permission.)
TABLE 7.1 Cervical Scoring System
Cervical Score 0 1 2 3
Dilatation (cm) <1 1–2 2–4 >4
Length of cervix >4 2–4 1–2 <1
(cm)
Station (cm) −3 −2 –1/0 +1/+2
Consistency Firm Average Soft –
Position Posterior Mid; anterior – –
history of a previous vaginal birth and the cervical score
(Table 7.1). If a woman has delivered vaginally in the
past, the chance of vaginal birth following induction
is high, whereas in nulliparous women and those with
a previous caesarean section the incidence of caesar-
ean section is generally increased. The cervical score
reflects how close the woman is to spontaneous labour,
and the chance of successful induction is positively
correlated to the cervical score. These factors should
also, therefore, be taken into account when discussing
the risks and benefits of induction in terms of the likely
outcome, as in some cases the decision to deliver may
be deferred based on the chances of success weighed
against the actual risk of prolonging the pregnancy,
or the decision may be to perform a caesarean section
rather than aim for vaginal birth.
It is accepted that induction of labour has an impact
on the birth experience of women. It may be less efficient
and is usually more painful than spontaneous labour,
and epidural analgesia and assisted delivery are more
common when compared with spontaneous labour.10
A major concern with induction of labour has been the
perceived increase in caesarean section rates following
induction, although there is now evidence that in certain
groups this is not the case, with some trials showing no
increase or a reduction in caesarean section rates.11–13
The recent publication of the ARRIVE trial13 has cre-
ated much discussion regarding timing of induction of
labour, having found that planned induction of labour
at 39 weeks’ gestation in low-­ risk pregnancies was
28 PART I Antenatal

TABLE 7.2 Factors to Consider When Making a Decision Regarding Induction of Labour
Other Factors to
Maternal Benefits Maternal Risks Baby Benefits Baby Risks Consider
Lower morbidity from Hyperstimulation Avoidance of stillbirth Neonatal unit admission Accurate gestational
existing medical age
conditions exacer-
bated by pregnancy
Lower risk of pre-­ ?CS – short- and long-­ Reduced risk of Increased rates of neonatal Parity
eclampsia term risks of CS infection if ruptured jaundice
membranes at term
?Reduced risk of CS – Increased pain Reduced risk of Lower cognitive function Previous CS
short- and long-­ shoulder dystocia with early term delivery
term risks of CS and fractures in big compared with late term
babies delivery
?Less vaginal trauma Uterine rupture Increased frequency of special Cervical score
as baby smaller educational needs with ear-
ly term delivery compared
with late term delivery
Increased operative Higher rates of hospital Organizational
vaginal birth admissions in childhood ability to facilitate
with early term delivery induction
compared with late term
delivery
Increased risk of PPH
Increased epidural use
Failed induction
Poorer birth experience
Delays in care

CS, Caesarean section; PPH, postpartum haemorrhage.

associated with a reduced incidence of caesarean section
(18.6% vs. 22.2%; relative risk [RR] 0.84; 95% CI 0.76–
0.93), although the trial did not demonstrate any dif-
ference in the primary outcome of composite perinatal
morbidity, i.e. the trial showed no evidence of benefit to
the baby. Importantly, long-­term outcomes for the baby
were not assessed and the impact of early delivery on
long-­term outcomes for the baby is therefore unknown.
Based on the outcome of this study, the American Col-
lege of Obstetricians and Gynecologists issued a Prac-
tice Advisory statement14 that
‘it is reasonable for obstetricians and health-­care facilities
to offer elective induction of labor to low-­risk nulliparous
women at 39 weeks gestation. However, consideration for
enactment of this elective induction of labor intervention
should not only take into account the trial findings, but
that this recommendation may be conditional upon the
values and preferences of the pregnant woman, the resources
available (including personnel), and the setting in which
the intervention will be implemented’.
It should be noted that the trial took place in the USA
where practice is different, and the results may not trans-
late to the UK. Before the results of these studies are
applied to all women, further evidence is needed to deter-
mine benefit in all groups of women and, more impor-
tantly, to assess the long-­term outcomes for the baby.
For all these reasons, the most important decision is
not how to induce labour, but whether early delivery is
warranted. In order to ensure that women are aware of
the risks and benefits as they apply to their individual case,
results from one group of women must not be extrapo-
lated to other groups, and we must ensure, where possible,
that we can give accurate individualized information to
women to enable them to make informed choices about
intervention in their particular circumstances, especially
as post-­Montgomery15 there have been cases of litigation
for unnecessary induction of labour. People perceive and
interpret risk differently, and our role as practitioners is
to present the evidence and its limitations to women in an
understandable way to enable them to make an informed
decision regarding their care (Table 7.2).
In 2011 the World Health Organization published rec-
ommendations for induction of labour,16 which included
the following general principles:
• Induction of labour should be performed only when
there is a clear medical indication for it and the ex-
pected benefits outweigh its potential harms.
• In applying the recommendations, consideration
must be given to the actual condition, wishes and
preferences of each woman, with emphasis being
placed on cervical status, the specific method of in-
duction of labour and associated conditions such as
parity and rupture of the membranes.
• Induction should be performed with caution since
the procedure carries the risk of uterine hyperstim-
ulation and rupture and fetal distress.
• Whenever induction of labour is carried out, facili-
ties should be available for assessing maternal and
fetal wellbeing.
• Women receiving oxytocin, misoprostol or other
prostaglandins should never be left unattended.
• Failed induction of labour does not necessarily indi-
cate caesarean section.
• Wherever possible, induction of labour should be
carried out in facilities where caesarean section can
be performed.

INCIDENCE
Figures from the National Maternity Dataset (England)
in 2018 show that over 30% of women now have their
labour induced, compared with around 20% 10 years
ago.10 This is because of changes in national guidance
in a variety of scenarios in which induction of labour is
recommended. In addition, the implementation of the
Saving Babies’ Lives Care Bundle (SBLCB)17 in England
has resulted in a significant increase in both induction
of labour and caesarean section.8 These increases are felt
to be largely due to fetal growth restriction (FGR) and
RFM, and there is concern that some of the intervention
prompted by the introduction of the SBLCB is unwar-
ranted with no evidence of benefit.8 Overall, this substan-
tial increase in the rate of induction of labour has resulted
in significant challenges for service delivery, which in
turn impacts on the birth experience. There are wide-
spread reports of delays in care regarding induction due
to workload, sometimes with disastrous consequences,
and staff are regularly faced with trying to prioritize the
induction workload based on clinical risk in the absence
of a robust tool to individualize actual risk in different
cases. Women are often very unhappy with sometimes
long delays in the induction process that often sees them
in hospital with nothing happening, separated from
their families, or waiting anxiously at home for a bed to
become available after being told that there are increased
risks with continuation of the pregnancy and that induc-
tion was therefore indicated. It is therefore extremely
important that induction is not embarked upon without
a robust indication, as well as taking into account the
impact of increased induction rates on a unit’s ability to
ensure a safe service for all.
INDICATIONS
The indications for induction are many and varied.
Traditionally the most common reason was prolonged
pregnancy, but increasingly growth restriction and dia-
betes, amongst others, prompt induction. The evidence
supporting these clinical indications is of variable qual-
ity and at times there is no evidence to inform our clini-
cal decision-­making. However, in such cases the balance
is between the known risks of induction of labour with
the uncertain and unpredictable risks of complications
in a continuing pregnancy, in particular the risk of still-
birth and its devastating consequences for the individual
families.
Prevention of Prolonged Pregnancy
The evidence regarding prolonged pregnancy is robust.
A Cochrane systematic review was updated in 2018 to
include 33 studies including 12,479 women.12 Induction
of labour before 42 weeks’ gestation was associated with
reduced perinatal morbidity as well as reduced risks of
stillbirth and caesarean section. There was no difference
in length of hospital stay or postpartum haemorrhage.
NICE10 recommends that women with uncomplicated
pregnancies should be offered induction between 41+0
7 Induction of Labour 29
and 42+0 weeks. Those women who decline induction
after 42 weeks should have twice-­weekly cardiotocogra-
phy (CTG) and weekly liquor volume measurement.
Preterm Prelabour Rupture of Membranes
(PPROM)
In approximately 3% of women, rupture of membranes
occurs at less than 37 weeks’ gestation. Routine induc-
tion of labour before 37 weeks is not recommended
unless there are specific indications such as infection or
suspected fetal compromise, as the risks of preterm birth
outweigh the risks of infection.10 After 37 weeks it is
recommended that the risks to mother and baby along
with the availability of local facilities are discussed before
making a decision regarding induction. In this situation,
expectant management is associated with a small increase
in the risk of infection with no significant differences in
caesarean section rates or overall perinatal or neonatal
outcomes. The RCOG Green-­top Guideline on early
onset group B streptococcal (GBS) disease18 is concor-
dant with this NICE guidance. It recommends that at
less than 34 weeks’ gestation, the risks of preterm deliv-
ery outweigh risks of infection even in known carriers of
GBS; however, at more than 34 weeks it may be of ben-
efit to consider delivery in women colonized with GBS,
although evidence is not robust and care should therefore
be individualized. If induction is carried out under 37
weeks, intrapartum antibiotic prophylaxis (IAP) for GBS
should be administered.18
Prelabour Rupture of Membranes at Term
Approximately 8–10% of women experience spontaneous
rupture of the membranes at or beyond 37 weeks, and
60% of these will go into spontaneous labour within 24
hours. NICE guidance19 recommends that these women
are offered either immediate induction or delayed induc-
tion (for 24 hours) to reduce the risk of neonatal infection,
unless there is known GBS, in which case immediate IAP
should be offered with induction as soon as possible.18 A
Cochrane systematic review20 of 12 trials including 6814
women concluded that immediate induction compared
with expectant management up to 96 hours in prelabour
rupture of membranes at 37 weeks and beyond was asso-
ciated with reduced risks of chorioamnionitis (226/3300
vs. 327/3311; RR 0.74; 95% CI 0.56–0.97) and endome-
tritis (5/217 vs. 19/228; RR 0.30; 95% CI 0.12–0.74).
There was no difference in delivery by caesarean section
(333/3401 vs. 360/3413; RR 0.94; 95% CI 0.82–1.08),
instrumental delivery (487/2786 vs. 502/2825; RR 0.94;
95% CI 0.82–1.08), or where assessed women were more
likely to be happy with their care in the immediate deliv-
ery arm. At term, women who are known to be GBS posi-
tive should be offered immediate IAP and induction as
soon as possible.21 This is based on the findings of the
Term PROM trial which randomized women with rup-
ture of membranes at term to either induction or expect-
ant management. Babies of women with known GBS had
three times the odds of neonatal infection compared with
women with negative or unknown GBS status (odds ratio
[OR] 3.08; P<0.0001). GBS status was the second most
30 PART I Antenatal
important predictor of neonatal infection after clinical
chorioamnionitis. In women without confirmed GBS
colonization, national guidance18,19 recommends offering
immediate induction or delaying by 24 hours, based on
increased risks of neonatal infection when delivery was
delayed by 24–48 hours compared with <12 hours (OR
1.97; P=0.02) and a greater risk of infection when delayed
by >48 hours (vs. <12 hours OR 2.25; P=0.01).
Fetal Growth Restriction
It is well established that FGR and small for gestational
age (SGA) are two different entities, and that FGR is
associated with a significantly increased perinatal mor-
tality rate compared with SGA. Thus any ambition to
reduce perinatal mortality must include strategies to
accurately identify those fetuses with FGR, to facilitate
timely delivery to reduce the well-established risk of
intrauterine death.22 The difficulty comes with identi-
fying (1) those fetuses that are small and (2) those that
are at increased risk and would benefit from early deliv-
ery. The introduction of the Saving Babies’ Lives Care
Bundle (SBLCB) in England has significantly improved
SGA detection rates in England, from 33.8% to 53.7%,
and guidance exists to help identify those with FGR and
guide timing of delivery.23,17 The impending revised
SBLCB aims to improve guidance on timing of inter-
vention in SGA/FGR to try and reduce the number of
unwarranted inductions in this group.8 In severe FGR
with confirmed fetal compromise, induction should not
be offered, as delivery by caesarean section is the inter-
vention of choice.10
Reduced Fetal Movements
Fetal movements are a reassuring sign of fetal wellbeing
and women are advised to report any change in their pat-
tern, as in numerous confidential enquiries into stillbirth,
RFM has been associated with poor perinatal outcome.
When a woman presents with RFM, investigation is
aimed at confirming fetal viability and then identification
of the fetus at risk of adverse outcome, particularly those
with FGR, while avoiding unnecessary interventions.24
The risk of adverse outcome is increased in the presence
of recurrent RFM and careful assessment of the fetus is
required.24 The AFFIRM trial9 showed that induction of
labour for recurrent RFM from 37 weeks did not reduce
the stillbirth rate but did lead to increased rates of induc-
tion and caesarean section, and increased rates of pro-
longed neonatal admission with no reduction in perinatal
mortality. In the absence of any concerns regarding fetal
growth and wellbeing, there is no place for induction
prior to 39 weeks.
Multiple Pregnancy
The recommendations regarding timing and mode of
birth are dependent on chorionicity, with monocho-
rionic twins having significantly higher odds of still-
birth compared with dichorionic twins from 32 weeks
onwards. Women with monochorionic twins should have
the timing of birth discussed and be offered induction of
labour from 36+0 weeks with the administration of ante-
natal steroids, unless there is an indication to deliver by
caesarean section or to deliver earlier.25 In pregnancies
with treated twin–twin transfusion syndrome (TTTS)
or type I selective growth restriction (sGR) with normal
growth velocity and Dopplers, delivery is recommended
at 34–36 weeks, with mode of birth being individual-
ized taking other factors such as parity and presentation
of the leading twin into account.25 In uncomplicated
dichorionic twin pregnancies, delivery should be offered
from 37+0 weeks, again with mode of birth being indi-
vidualized, taking other factors such as parity and pre-
sentation of the leading twin into account.26
Suspected Fetal Macrosomia
Suspected fetal macrosomia is defined as a birthweight
above the 95th centile and occurs in approximately 2–10%
of births in the UK. Fetal macrosomia is associated with
an increased risk of birth trauma, particularly shoulder
dystocia, which in turn is associated with hypoxic brain
injury and perinatal death, fractures and brachial plexus
injury (BPI). Induction has been advocated by some to
achieve delivery at a lower birth weight in the hope of
improving outcomes by avoiding shoulder dystocia. Evi-
dence from systematic reviews27,28 comparing induction
with expectant management showed a lower incidence of
shoulder dystocia and fractures in the induction group,
but no difference in maternal or fetal outcomes, such as
caesarean section rates or BPI with suspected fetal mac-
rosomia. Sixty women would need to be induced to avoid
one fracture, and there are implications for the neonate
both short and long term.4 The current recommendation
is that further research is required to identify the opti-
mal gestation for induction and diagnosis of macrosomia,
although current evidence suggests that induction should
not be offered for this indication before 39 weeks.4 There
is currently a multicentre randomized controlled trial
looking at induction versus conservative management in
suspected macrosomia (Big Baby trial) to try and defini-
tively answer this question.
Maternal Diabetes
Maternal diabetes is associated with a significantly
increased risk of stillbirth and fetal macrosomia, which
can lead to shoulder dystocia and its associated risks.
NICE guidance CG329 recommends delivery by 37 to
38+6 weeks in uncomplicated type 1 and type 2 diabetes,
and by 40+6 weeks in women with gestational diabetes,
although evidence supporting this approach is weak. In
cases where there are complications, either fetal or mater-
nal, induction following the administration of steroids for
fetal lung maturity should be considered before 37 weeks.
Hypertension
Hypertension includes pre-­existing or chronic hyperten-
sion, gestational hypertension and pre-­eclampsia (PET),
all of which have different maternal and fetal risks. Pre-­
existing and gestational hypertension are both associated
with increased risks of placental abruption, developing

PET and increased perinatal mortality. In order to
reduce this risk, NICE guidance30 recommends that for
women with chronic or gestational hypertension which is
less than 160/110 mmHg after 37 weeks’ gestation, either
with or without treatment, the timing of birth should be
agreed between the woman and a senior obstetrician. In
PET with mild to moderate hypertension, aim to deliver
between 34+0 to 36+6 weeks, and in PET starting after
37+0 weeks, induction should be offered within 24–48
hours.
Advanced Maternal Age
Epidemiological data show that women over 40 years old
have increased rates of stillbirth compared with younger
women. Their risk of stillbirth at 39 weeks’ gestation is
similar to that of a 25–29-­year-­old at 41 weeks’ gesta-
tion and is higher in nulliparous women.31 Induction is
often offered at 39–40 weeks’ gestation, particularly in
a first pregnancy, after these risks have been discussed
with the women, but there is currently no trial evidence
for this.31
MATERNAL OBESITY
Maternal obesity is associated with increased rates
of maternal and perinatal morbidity and mortality,
including stillbirth and fetal macrosomia.32 There is
some evidence to show that induction of labour in
the obese population is associated with a reduction in
caesarean section rates with no increase in perinatal
morbidity, but longer-­ term follow-­
up is not avail-
able and no reduction in perinatal mortality has been
demonstrated. Current advice is that elective induc-
tion of labour at term in obese women may reduce the
chance of caesarean birth without increasing the risk
of adverse outcomes, and that the option of induction
should be discussed with each woman on an individual
basis.
Obstetric Cholestasis
Obstetric cholestasis is associated with an unpredict-
able increased risk of stillbirth at all gestations, although
the pathophysiology is not fully understood and evi-
dence regarding intervention is weak. As such, the risks
of induction of labour should be balanced and discussed
with the woman after 37 weeks, taking into account the
severity of the biochemical abnormalities.33
Antepartum Haemorrhage
If a woman presents with antepartum haemorrhage
(APH) and signs of fetal compromise, delivery is usually
indicated and the method (induction or caesarean sec-
tion) will depend on the clinical circumstances in each
case. There is no robust evidence regarding APH at term,
with no evidence of maternal or fetal compromise, but
the RCOG Green-­top Guideline No. 6334 recommends
induction to avoid potential complications of abruption,
based on ‘best practice’.
7 Induction of Labour 31
Maternal Request
Women may request induction for a variety of reasons
including being fed up, anxiety that something will go
wrong, geography, partner being away and many others.
In the absence of a robust clinical indication, on the whole
maternal request for induction of labour should not be
encouraged,10 but each case should be assessed individu-
ally by a senior clinician, taking into account the woman’s
wishes and the ability of the service to accommodate such
requests. Having said this, the growing evidence base that
induction of labour from 39 weeks onwards may be asso-
ciated with lower caesarean sections rates may influence
the balance of risk/benefit.
SPECIAL CIRCUMSTANCES
Previous Caesarean Section
A prior history of lower segment caesarean section is
not a contraindication to induction, although induction
in this group of women is associated with an increased
risk of uterine rupture when compared with both elective
repeat caesarean section and spontaneous labour, particu-
larly in women who have not given birth vaginally before.
Uterine rupture in turn is associated with significant peri-
natal mortality and morbidity. The optimal method of
induction is not clear in this scenario, and it is reasonable
to offer induction with low doses of prostaglandins or
mechanical methods such as a balloon catheter or lami-
naria, with close maternal and fetal monitoring in a facil-
ity which allows rapid recourse to caesarean section.10,35
Intrauterine Fetal Death
When intrauterine death is diagnosed, in the absence of
bleeding, signs of infection and ruptured membranes,
women should be offered the choice between immediate
or delayed induction.10,36 The use of mifepristone 36–48
hours prior to the administration of prostaglandins, most
commonly in the form of misoprostol, has been shown
to be effective and associated with a shorter duration of
labour. Where there is a previous history of intrauterine
death, induction of labour at term is commonly offered,
but care must be individualized, taking into account the
timing of the previous death, mode of delivery and other
obstetric/medical factors.36
Failed Induction
In around 15% of cases, attempts to induce labour fail
after one cycle of treatment, consisting of the insertion
of two vaginal prostaglandin E2 (PGE2) tablets (3 mg) or
gel (1–2 mg) at 6-­hour intervals, or one PGE2 controlled-­
release pessary (10 mg) over 24 hours, often at the cervi-
cal ripening stage before rupture of the membranes. In
this situation, management should be individualized, tak-
ing into account the indication for induction, the cervi-
cal score and the woman’s wishes. The options include
deferring induction with appropriate monitoring, con-
tinuing with the induction process or caesarean section.10
32 PART I Antenatal
Previous Failed Induction
In cases where induction of labour has failed, in that the
cervix failed to ripen and dilate despite the use of pros-
taglandins and/or oxytocin, there is an increased risk of
failed induction in future pregnancies and women should
be counselled regarding this. Before a decision is made
to embark on induction again, the cervical score must
be assessed to inform the likelihood of success as if the
cervix is already very favourable, the chance of success
is increased. If the cervix is unfavourable and delivery is
indicated, caesarean section may be more appropriate
than embarking on an induction process with a high rate
of failure.
Previous Hyperstimulation With
Prostaglandins
If a woman has a history of hyperstimulation secondary
to exogenous prostaglandins, caution must be exercised
in any future induction attempt, as the response to pros-
taglandins in this manner appears to be idiosyncratic and
has a high recurrence risk. If the cervix is unfavourable
and amniotomy and oxytocin are not feasible, either
mechanical methods, such as balloon catheters or lami-
nar, or the removable sustained release vaginal insert
(Propess) should be considered.
Outpatient Induction
The very fact that induction is being carried out suggests
that the pregnancy is ‘at risk’, otherwise there would be
no reason to intervene. As already discussed, risk may
mean maternal risk, fetal risk, risk of caesarean section,
or avoidance of a future risk. It makes sense that facili-
ties should be available for continuous electronic fetal
heart rate and contraction monitoring wherever induc-
tion is carried out. However, for many women there is
a lengthy period of cervical ripening before labour itself
becomes established and, as discussed above, induction
impacts significantly on the woman’s birth experience. In
carefully selected cases, outpatient induction is just as safe
and effective as inpatient induction but is associated with
greater maternal satisfaction.37
METHODS OF INDUCTION
Once the decision has been made to induce labour, the
next decision is how labour should be induced (Table
7.3). It would be optimal if the physiological changes
associated with spontaneous labour could be switched on
or mimicked to achieve outcomes similar to those seen
with spontaneous labour. The two main components
of spontaneous labour are cervical ripening followed by
efficient uterine contractility, leading to full dilatation of
the cervix and propulsion of the fetus through the pelvis,
resulting in a successful vaginal birth. Prostaglandins are
key to both cervical ripening and uterine contractility.38
In spontaneous labour, cervical changes occur leading to
softening and shortening of the cervix before myome-
trial contractions begin, which then lead to progressive
dilatation of the cervix and descent of the fetus through
the pelvis. The contractions progressively increase in
strength leading to the expulsive forces required to facili-
tate birth. When it comes to induction of labour, very
often these changes in the cervix need to be achieved
before contractions are initiated and, as such, a period of
cervical ripening precedes myometrial stimulation.
Membrane Sweeping
Prior to induction of labour, membrane sweeping is
advocated10 to reduce the need for formal induction and
to improve the cervical score to make induction itself
easier. Although associated with uncomplicated bleeding
and pain at the time of sweeping, it is not associated with
adverse outcomes for either the mother or the baby and
women find it acceptable. Membrane sweeping should
therefore be offered prior to induction of labour, and
weekly from 40 weeks’ gestation.
Prostaglandins
As described above, prostaglandins are intimately
involved in spontaneous labour, both in terms of cervi-
cal ripening and uterine contractility. Exogenous PGE2
administered vaginally is effective in achieving cervical
ripening and initiating uterine contractions. When the
cervix is unfavourable, it reduces the need for intrave-
nous oxytocin and when the cervix is favourable, its use is
associated with a high rate of birth within 24 hours com-
pared with placebo, and when compared with intravenous
oxytocin, prostaglandins are associated with lower rates
of postpartum haemorrhage and neonatal jaundice, and
higher maternal satisfaction. For these reasons, vaginal
PGE2 is the method of choice for induction of labour.10,39
The main concern with vaginal PGE2 is that it often
stimulates uterine contractility at the same time as cer-
vical ripening is occurring, leading to discomfort before
the cervix is favourable and occasionally to tachysystole
and hyperstimulation. Various preparations are available,
including vaginal tablets, gel and sustained release pes-
saries (Propess). The latter are nonbiodegradable and
release the PGE2 over 24 hours, thus reducing the need
for repeated vaginal examinations and repeat doses if the
cervix is unfavourable. They can be removed should the
administration need to be terminated in cases of tachysys-
tole or hyperstimulation, making this option attractive if
the cervix is unfavourable or where there is a scar on the
uterus. If hyperstimulation occurs with prostaglandins, it
can be treated with a tocolytic such as terbutaline 250 μg
subcutaneously, although if fetal heart rate abnormalities
persist, delivery by emergency caesarean section may be
indicated.
Misoprostol
Misoprostol is a synthetic prostaglandin analogue com-
monly used in the management of postpartum haemor-
rhage and to induce labour in cases of intrauterine death
or termination of pregnancy. It can be administered
orally, sublingually and vaginally and is available in the
UK in two forms – 200 μg tablets which are not licensed
 7 Induction of Labour 33

TABLE 7.3 Different Methods of Induction

Method of Induction
Membrane sweeping
Vaginal PGE2 – either
tablets, gel or controlled-­
release pessary
Amniotomy, alone or com-
bined with intravenous
oxytocin only if vaginal
PGE2 contraindicated
Misoprostol tablets
Mifepristone
Mysodelle
Breast stimulation
Balloon catheters and
laminaria tents
Oral, intravenous, extra-­
amniotic, intracervical
PGE2
Intravenous oxytocin alone
Hyaluronidase
Corticosteroids
Oestrogens
Nitric oxide donors
Herbal supplements
Acupuncture
Homeopathy
Castor oil, hot baths and
enemas
Sexual intercourse
Recommendation
Offer to all
Recommended first line induction
agent
Second line – only if vaginal PGE2
contraindicated
Only in cases of intrauterine death
or in the context of a clinical
trial
Only in cases of intrauterine death
Further research required
Further research required
Further research required
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
No evidence of benefit, do not use
Benefits
Increase in spontaneous la-
bour, reduction in need for
induction
Improved cervical score;
higher rates of birth by 24
hours; less PPH; higher
maternal satisfaction
Comparable to vaginal PGE2
to achieve birth within 24
hours and rates of caesar-
ean birth
Higher success rates at high
dose
Shorter time to delivery
Shorter time to delivery;
lower use of oxytocin
May be effective but research
quality poor
Reduced risk of uterine
rupture
Risks
Increase in uncomplicated
bleeding, pain
Uterine hyperstimulation; in-
creased risk of scar rupture
in previous CS
Increased PPH; more
invasive for women and
requires CEFM; lower
maternal satisfaction
Significantly higher rates of
uterine hyperstimulation;
maternal gastrointestinal
side effects; not licensed
for use in pregnancy in UK
Higher rates of hyperstimula-
tion
Longer time to delivery; in-
creased use of oxytocin

CEFM, Continuous electronic fetal monitoring; CS, caesarean section; PGE2, prostaglandin E2; PPH, postpartum haemorrhage.

for induction of labour, and a 200 μg slow-­release vaginal
insert (Mysodelle). When used for induction of labour
the tablets are comparable to vaginal PGE2 when used at
low doses but there is no commercially available low dose.
At higher, commercially available doses, although a suc-
cessful induction agent with shorter induction to delivery
intervals, it is associated with significantly higher rates of
hyperstimulation, abnormal fetal heart rate patterns and
the risk of uterine rupture.39 In the slow-­release form,
when compared with Propess in a randomized controlled
trial, Mysodelle was associated with shorter induction to
delivery intervals and a lower need for oxytocin, but with
an increased risk of tachysystole and hyperstimulation
(which can be treated as above), although caesarean sec-
tion rates were similar.40,41 Further evaluation is required
as the study was relatively small.
Mechanical Methods
Mechanical methods are seeing a resurgence, particularly
given their ability to ripen the cervix in the absence of
uterine contractility, making them especially attractive in
cases of previous caesarean section. The most commonly
used methods are balloon catheters or laminaria tents. In
randomized trials, balloon catheters seem no better than
vaginal prostaglandins and further evaluation is recom-
mended before they should be offered routinely.10,39 A
large multicentre randomized controlled trial (SOLVE)
comparing Dilapan, a commercially available syn-
thetic osmotic cervical dilator, with Propess is currently
underway.
Amniotomy and Oxytocin
Intravenous oxytocin should not be used while the mem-
branes are intact, and amniotomy alone is inefficient in
inducing labour without the concomitant use of oxytocin.
The combination of amniotomy and intravenous oxyto-
cin, particularly in the presence of a favourable cervix and
in multiparous women, is as effective as vaginal prosta-
glandins but is associated with higher rates of postpartum
haemorrhage and neonatal jaundice, and poorer mater-
nal satisfaction. For these reasons, vaginal prostaglandins
are recommended as the first-­line agents for induction
unless there are specific contraindications such as allergy
or hyperstimulation.10,39 However, amniotomy and oxy-
tocin remain an integral part of the induction process
following vaginal prostaglandins or mechanical meth-
ods, if labour does not establish and progress. The main
concerns with amniotomy are cord prolapse and, in the
Another random document with
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 The British Minister closes his communication to Lord
Pauncefote as follows: "I request that your excellency will
explain to the Secretary of State the reasons, as set forth in
this dispatch, why His Majesty's government feel unable to
accept the convention in the shape presented to them by the
American Ambassador, and why they prefer, as matters stand at
present, to retain unmodified the provisions of the
Clayton-Bulwer Treaty. His Majesty's government have
throughout these negotiations given evidence of their earnest
desire to meet the views of the United States.
{71}
They would on this occasion have been ready to consider in a
friendly spirit any amendments of the convention not
inconsistent with the principles accepted by both governments
which the government of the United States might have desired
to propose, and they would sincerely regret a failure to come
to an amicable understanding in regard to this important
subject."

CANAL, The Kaiser Wilhelm Ship.

See (in this volume)

GERMANY: A. D. 1895 (JUNE).

CANAL, Manchester Ship.

On the 1st of January, 1894, the ship canal from Liverpool to

Manchester, which had been ten years in course of construction
and cost £15,000,000, was formally opened, by a long
procession of steamers, which traversed it in four and a half
hours.

CANAL: The Rhine-Elbe, the Dortmund-Rhine,

and other Prussian projects.

See (in this volume)

GERMANY: A. D. 1890 (AUGUST);
 and 1901 (JANUARY).

CANDIA: A. D. 1898 (September).

Fresh outbreak.

See (in this volume)

TURKEY: A. D. 1897-1899.

CANEA: Christian and Moslem conflicts at.

See (in this volume)

TURKEY: A. D. 1897 (FEBRUARY-MARCH).

CANOVAS DEL CASTILLO, Antonio:

Formation of Spanish Cabinet.

See (in this volume)

SPAIN: A. D. 1895-1896.

CANOVAS DEL CASTILLO, Antonio:

Assassination.

See (in this volume)

SPAIN: A. D. 1897 (AUGUST-OCTOBER).

CANTEEN, The Army.

See (in this volume)

UNITED STATES OF AMERICA:
A. D. 1900 (MAY-NOVEMBER), THE PROHIBITION PARTY;
and 1901 (FEBRUARY).

CANTON: A. D. 1894.
The Bubonic Plague.

See (in this volume)

PLAGUE.
CANTON: A. D. 1899.
Increasing piracy in the river.

See (in this volume)

CHINA: A. D. 1899.

CAPE COLONY.

See (in this volume)

SOUTH AFRICA (CAPE COLONY).

CAPE NOME, Gold discovery at.

See (in this volume)

ALASKA: A. D. 1898-1899.

CAPE SAN JUAN, Engagement at.

See (in this volume)

UNITED STATES OF AMERICA:
A. D. 1898 (JULY-AUGUST: PORTO RICO).

CARNEGIE, Andrew: Gifts and offers to public libraries.

See (in this volume)

LIBRARIES;
and LIBRARY, NEW YORK PUBLIC.

CARNEGIE COMPANY, Sale of the interests of the.

See (in this volume)

TRUSTS: UNITED STATES.

CAROLINE and MARIANNE ISLANDS:

Their sale by Spain to Germany.
 By a treaty concluded in February, 1899, the Caroline Islands,
the Western Carolines or Pelew Islands, and the Marianne or
Ladrone Islands (excepting Guam), were sold by Spain to
Germany for 25,000,000 pesetas—the peseta being equivalent to
a fraction less than twenty cents. Spain reserved the right to
establish and maintain naval and mercantile stations in the
islands, and to retain them in case of war. Spanish trade and
privileges for the Spanish religious orders are guaranteed
against interference.

CARROLL, Henry K.:

Report on Porto Rico.

See (in this volume)

PORTO RICO: A. D. 1898-1899 (AUGUST-JULY).

CASSATION, The Court of.

The French Court of Appeals.

See (in this volume)

FRANCE: A. D. 1897-1899.

CASTILLO, Pedro Lopez de:

Letter to the soldiers of the American army.

See UNITED STATES OF AMERICA: A. D. 1898 (AUGUST 21).

CATALOGUE, International, of Scientific Literature.

See (in this volume)

SCIENCE, RECENT: SCIENTIFIC LITERATURE.

CATALONIA: Independent aspirations in.

See (in this volume)

SPAIN: A. D. 1900 (OCTOBER-NOVEMBER).
CATASTROPHES, Natural: A. D. 1894.

Late in December, the orange groves of Florida were mostly

destroyed or seriously injured by the severest frost known in
more than half a century.

CATASTROPHES, Natural: 1896.

On January 8, a severe earthquake shock was felt at Meshed,

Kelat and other Persian towns, causing over 1,100 deaths.

CATASTROPHES, Natural: 1896.

In March, the Tigris overflowed its banks, causing

incalculable loss of life and property in Mesopotamia.

CATASTROPHES, Natural: 1896.

A succession of earthquake shocks in March, 1896, did great

damage at Santiago, Valparaiso, and other parts of Chile.

CATASTROPHES, Natural: 1896.

On May 15, a cyclone destroyed part of the town of Sherman, in

Texas, killing more than 120 persons, mostly negroes. The same
day a waterspout burst over the town of Howe in the same state,
killing 8 people.

CATASTROPHES, Natural: 1896.

On May 27, a fierce cyclone swept the city of St. Louis,

Missouri, completely devastating a large part of the city, and
causing great loss of life and property.

CATASTROPHES, Natural: 1896.

A destructive wave swept the Japanese coast in June.

 See (in this volume)
JAPAN: A. D. 1896.

CATASTROPHES, Natural: 1896.

On July 26, a tidal wave, 5 miles in width, inundated the

coast of Kiangsu, in China, destroying many villages and more
than 4,000 inhabitants.

CATASTROPHES, Natural: 1896-1897.

A severe famine prevailed in India from the spring of 1896

until the autumn of 1897.

See (in this volume)

INDIA: A. D. 1896-1897.

CATASTROPHES, Natural: 1897.

A severe earthquake occurred at the island of Kishm in the

Persian Gulf, in January, causing great loss of life.

CATASTROPHES, Natural: 1897.

In March and April of this year the floods along the

Mississippi river and its tributaries reached the highest
level ever recorded. In extent of area and loss of property
these floods were the most remarkable in the history of the
continent. The total area under water on April 10 was about
15,800 square miles, containing about 39,500 farms, whose
value was close upon $65,000,000. The loss of life was small.
Congress gave relief to the extent of $200,000, besides
appropriating $2,583,300 for the improvement of the
Mississippi.

CATASTROPHES, Natural: 1897.

 Extensive floods occurred in Galatz, Moldavia, in June,
rendering 20,000 people homeless.

CATASTROPHES, Natural: 1897.

The islands of Leyte and Samar, in the Visayas group, were

swept by an immense wave caused by a cyclone, in October,
thousands of natives being killed, and much property
destroyed.

{72}

CATASTROPHES, Natural: 1897.

On October 6, the Philippine Islands were swept by a typhoon,

which destroyed several towns. The loss of life was estimated
at 6,000, of whom 400 were Europeans. This was followed on
October 12 by a cyclone which destroyed several villages and
caused further loss of life.

CATASTROPHES, Natural: 1897.

By an eruption of the Mayon volcano in the island of Luzon,

Philippine Islands, four hundred persons were buried in the
lava, and the large town of Libog completely destroyed.

CATASTROPHES, Natural: 1898.

A series of earthquake shocks in Asia Minor during the month

of January occasioned considerable loss of life and property.

CATASTROPHES, Natural: 1898.

In January, Amboyna, in the Molucca Islands, was almost

destroyed by an earthquake, in which about 50 persons were
killed and 200 injured.
CATASTROPHES, Natural: 1898.

On January 11, a tornado wrecked many buildings in Fort Smith,

Ark. The loss of life was reported as 50, with hundreds
injured.

CATASTROPHES, Natural: 1898.

A disastrous blizzard occurred in New England, January 31 and

February 1. Fifty lives were reported as lost, and the damage
in Boston alone amounted to $2,000,000. Many vessels were
driven ashore or foundered, with further loss of life.

CATASTROPHES, Natural: 1898.

Floods on the Ohio river in March and April caused much loss
of life and property. Shawneetown, Illinois on the Ohio river,
was almost entirely destroyed by the flood, more than 60 lives
being lost.

CATASTROPHES, Natural: 1898.

On the night of September 10, the island of Barbados was swept

by a tornado which destroyed 10,000 houses and damaged 5,000
more. Three-fourths of the inhabitants were left homeless, and
about 100 were killed. The islands of St. Vincent and St.
Lucia also suffered great losses of life and property.

CATASTROPHES, Natural: 1898.

A typhoon swept the central provinces of Japan in September,

causing heavy floods, and destroying 100 lives.

CATASTROPHES, Natural: 1899.

Severe floods on the Brazos river, in Texas, occasioned the

 death of about 100 people, and property losses to the extent
of $15,000,000.

CATASTROPHES, Natural: 1899.

A destructive tornado in Northern Missouri, in April, did much

damage in the towns of Kirksville and Newtown. Over fifty
persons were killed.

CATASTROPHES, Natural: 1899.

An almost unprecedented failure of crops in eastern Russia

caused famine, disease and awful destruction of life.

CATASTROPHES, Natural: 1899.

A terrific hurricane visited the West Indies August 7 and 8.

Of the several islands affected, Porto Rico suffered most,
three-fourths of the population being left homeless. The total
loss of life in the West Indies was estimated at 5,000.

See (in this volume)

PORTO RICO: A. D. 1899 (AUGUST).

CATASTROPHES, Natural: 1899.

About 1,500 people lost their lives in an earthquake around

Aidin, Asia Minor, September 2.

CATASTROPHES, Natural: 1899.

The island of Ceram, in the Moluccas, was visited by an

earthquake and tidal wave, November 2. Many towns were
destroyed, and 5,000 people killed.

CATASTROPHES, Natural: 1899-1900.

Recurrence of famine in India.
 See (in this volume)
INDIA A. D. 1899-1900.

CATASTROPHES, Natural: 1900.

The city of Galveston, Texas, was overwhelmed and mostly

destroyed, on the 9th of September, by an unprecedented
hurricane, which drove the waters of the Gulf upon the
low-lying town.

See (in this volume)

GALVESTON.

CATASTROPHES, Natural: 1901.

Famine in China.

See (in this volume)

CHINA: A. D. 1901 (JANUARY-FEBRUARY).

CATHOLICS, Roman:
Protest of British peers against the declaration required from
the sovereign.

See (in this volume)

ENGLAND: A. D. 1901 (FEBRUARY).

CATHOLICS, Roman:
Victory in Belgium.

See (in this volume)

BELGIUM: A. D. 1894-1895.

See, also, PAPACY.

CEBU: The American occupation of the island.

 See (in this volume)
PHILIPPINE ISLANDS: A. D. 1899 (JANUARY-NOVEMBER).

CENSUS: Of the United States, A. D. 1900.

See (in this volume)

UNITED STATES OF AMERICA: A. D. 1900 (MAY-OCTOBER).

CENTRAL AFRICA PROTECTORATE, British.

See (in this volume)

BRITISH CENTRAL AFRICA PROTECTORATE.

CENTRAL AMERICA, A. D. 1821-1898.

Unsuccessful attempts to unite the republics.

"In 1821, after numerous revolutions, Central America

succeeded in throwing off the yoke of Spain. A Congress
assembled at Guatemala in March, 1822, and founded the
Republic of Central America, composed of Guatemala, Salvador,
Honduras, Nicaragua, and Costa Rica. The new Republic had but
a short existence; after numerous civil wars the Union was
dissolved, October 26, 1838, and the five States of the
Republic became so many independent countries. Several
attempts toward a reorganization of the Constitution of the
Republic of Central America remained fruitless and had cost
the lives of certain of their authors, when, through the
influence of Dr. P. Bonilla, President of the Republic of
Honduras, a treaty was concluded between Nicaragua and
Salvador, according to which the three Republics constituted a
federation under the name of the Greater Republic of Central
America. The three Republics became States, and the
sovereignty of the federation was exercised by a Diet composed
of three members, one for each State, and which convened every
year in the capital of the Federal States.

"On the invitation of this Diet, the three States appointed a

 delegation which met as a Constituent Assembly at Managua,
Nicaragua, and established a constitution, according to the
terms of which the three States took the name of the United
States of Central America, November 1, 1898. This
Constitution, grand and patriotic, which, in the minds of
those who had elaborated it, meant a complete consolidation of
the three Federal States and a speedy realization of a
reorganization of the Grand Republic of Central America,
dreamed of by Morazan, had a sad ending. The day after the
meeting of the Constituent Assembly a revolutionary movement
hostile to the new federation broke out in Salvador and gave a
new administration to this State. Its first act was to retire
from the Union, and this secession brought about the
dissolution of the United States of Central America; for,
following the example of Salvador, Honduras and Nicaragua took
back their absolute sovereignty."

H. Jalhay,
quoted in Bulletin of American Republics, March, 1899.

{73}

The secession of Salvador was brought about by a revolutionary

movement, which overthrew the constitutional government of
President Gutierrez and placed General Tomas Regolado at the
head of a provisional government, which issued the following
manifesto on the 25th of November, 1898: "Considering—That the
compact of Amapala, celebrated in June, 1895, and all that
proceeds therefrom, has not obtained the legitimate sanction
of the Salvadorean people, and, moreover, has been a violation
of the political constitution of Salvador; That in the
assembled Constituent Assembly of Managua, reunited in June of
the present year, the deputies of Salvador were not directly
elected by the Salvadorean people, and for that reason had no
legal authority to concur to a constituent law that could bind
the Republic; That the union with the Republics of Honduras
and Nicaragua under the contracted terms will seriously injure
 the interests of Salvador: Decrees. ART. 1. The Republic of
Salvador is not obliged by the contract of Amapala to
acknowledge any authority in the constitution of Managua of
the 27th August of the current year, and it is released from
the contract of union with the Republics of Honduras and
Nicaragua. ART. 2. The Republic of Salvador assumes in full
its self-government and independence, and will enter the union
with the sister Republics of Central America when same is
convenient to its positive interests and is the express and
free will of the Salvadorean people."

United States, 55th Congress, 3d Session,

Senate Document Number 50.

CENTRAL AMERICA, A. D. 1884-1900.

Interoceanic Canal measures of later years.

See (in this volume)

CANAL, INTEROCEANIC, with accompanying map.

CENTRAL AMERICA, Nicaragua: A. D. 1894-1895.

Insurrection in the Mosquito Indian Strip.
The Bluefields Incident.

In his Annual Message to Congress, December, 1894, President

Cleveland referred as follows to disturbances which had
occurred during the year at Bluefields, the principal town of
the Mosquito district of Nicaragua, and commonly known as "the
Bluefields Incident:" "By the treaty of 1860 between Great
Britain and Nicaragua, the former Government expressly
recognized the sovereignty of the latter over the strip, and a
limited form of self-government was guaranteed to the Mosquito
Indians, to be exercised according to their customs, for
themselves and other dwellers within its limits. The so-called
native government, which grew to be largely made up of aliens,
for many years disputed the sovereignty of Nicaragua over the
strip and claimed the right to maintain therein a practically
independent municipal government. Early in the past year
efforts of Nicaragua to maintain sovereignty over the Mosquito
territory led to serious disturbances, culminating in the
suppression of the native government and the attempted
substitution of an impracticable composite administration in
which Nicaragua and alien residents were to participate.
Failure was followed by an insurrection, which for a time
subverted Nicaraguan rule, expelling her officers and
restoring the old organization. This in turn gave place to the
existing local government established and upheld by Nicaragua.
Although the alien interests arrayed against Nicaragua in
these transactions have been largely American and the commerce
of that region for some time has been and still is chiefly
controlled by our citizens, we can not for that reason
challenge the rightful sovereignty of Nicaragua over this
important part of her domain."

United States, Message and Documents

(Abridgment, 1894-1895).

In his Message of 1895 the President summarized the later

history of the incident as follows: "In last year's message I
narrated at some length the jurisdictional questions then
freshly arisen in the Mosquito Indian Strip of Nicaragua.
Since that time, by the voluntary act of the Mosquito Nation,
the territory reserved to them has been incorporated with
Nicaragua, the Indians formally subjecting themselves to be
governed by the general laws and regulations of the Republic
instead of by their own customs and regulations, and thus
availing themselves of a privilege secured to them by the
treaty between Nicaragua and Great Britain of January 28,
1860. After this extension of uniform Nicaraguan
administration to the Mosquito Strip, the case of the British
vice-consul, Hatch, and of several of his countrymen who had
been summarily expelled from Nicaragua and treated with
considerable indignity, provoked a claim by Great Britain upon
Nicaragua for pecuniary indemnity, which, upon Nicaragua's
 refusal to admit liability, was enforced by Great Britain.
While the sovereignty and jurisdiction of Nicaragua was in no
way questioned by Great Britain, the former's arbitrary
conduct in regard to British subjects furnished the ground for
this proceeding. A British naval force occupied without
resistance the Pacific seaport of Corinto, but was soon after
withdrawn upon the promise that the sum demanded would be
paid. Throughout this incident the kindly offices of the
United States were invoked and were employed in favor of as
peaceful a settlement and as much consideration and indulgence
toward Nicaragua as were consistent with the nature of the
case."

United States,
Message and Documents (Abridgment, 1895-1896).

CENTRAL AMERICA, Guatemala: A. D. 1895.

Mexican boundary dispute.

See (in this volume)

MEXICO: A. D. 1895.

CENTRAL AMERICA, Nicaragua: A. D. 1896-1898.

Revolutionary conflicts.

Vice President Baca of Nicaragua joined a revolutionary

movement which was set on foot in February, 1896, by the
Clericals, for the overthrow of President Zelaya, and was
declared Provisional President. The rebellion had much support
from exiles and friends in Honduras; but the government of
that State sustained and assisted Zelaya. The insurgents were
defeated in a number of battles, and gave up the contest in
May. During the civil war American and British marines were
landed on occasions at Corinto to protect property there. In
1897, and again in 1898, there were renewed insurrections,
quickly suppressed.
CENTRAL AMERICA, Costa Rica: A. D. 1896-1900.
Boundary dispute with Colombia settled by arbitration.

See (in this volume)

COLOMBIA: A. D. 1893-1900.

{74}

CENTRAL AMERICA, Nicaragua—Costa Rica: A. D. 1897.

A dispute between Nicaragua and Costa Rica, as to the eastern

extremity of their boundary line, was decided by General
Alexander, a referee accepted by the two republics. The
boundary had not been well defined in a treaty negotiated for
its settlement in 1858. According to the terms of the treaty,
the line was to start from the Atlantic at the mouth of the
San Juan river; but changes of current and accumulation of
river drift, etc., gave ground for dispute as to where the
river actually made its exit. President Cleveland in 1888,
acting as arbitrator at the request of the two countries,
decided that the treaty of 1858 was valid, but was not clear
as to which outlet of the delta was the boundary. Finally, in
1896, an agreement was reached for a final survey and marking
of the boundary line, and President Cleveland, on request,
appointed General Alexander as arbitrator in any case of
disagreement between the surveying commissions. The decision
gives to Nicaragua the territory upon which Greytown is
situated, and practical control of the mouth of the canal.

CENTRAL AMERICA, Guatemala: A. D. 1897-1898.

Dictatorship of President Barrios.
His assassination.

In June, 1897, President José M. Reyna Barrios, whose six

years term in the presidency would expire the next March,
fearing defeat in the approaching election, forcibly dissolved
the National Assembly and proclaimed a dictatorship. Three
 months later a revolt was organized by General Prospero
Morales; but Barrios crushed it with merciless energy, and a
veritable reign of terror ensued. In February, 1898, the
career of the Dictator was cut short by an assassin, who shot
him to avenge the death of a wealthy citizen, Don Juan
Aparicio, whom Barrios had executed for expressing sympathy
with the objects of the rebellion of the previous year.
Control of the government was then taken by Dr. Cabrera, who
had been at the head of the party which supported Barrios. A
rising under Morales was again attempted, but failed. Morales,
in a dying condition at the time, was betrayed and captured.
Cabrera, with no more opposition, was elected President for
six years.

CENTRAL AMERICA, Nicaragua—Costa Rica: A. D. 1900.

Agreements with the United States respecting the control of
territory for interoceanic canal.

See (in this volume)

CANAL, INTEROCEANIC, A. D. 1900 (DECEMBER).

CENTURY, The Nineteenth:

Date of its ending.
Its character and trend.
Comparison with preceding ages.
Its failures.

See (in this volume)

NINETEENTH CENTURY.

CERVERA, Rear-Admiral,
and the Spanish Squadron at Santiago de Cuba.

See (in this volume)

UNITED STATES OF AMERICA: A. D. 1898 (APRIL-JUNE);
and (JULY 3).
CHAFFEE, General Adna R.:
At Santiago.

See (in this volume)

UNITED STATES OF AMERICA: A. D. 1898 (JUNE-JULY).

CHAFFEE, General Adna R.:

Commanding American forces in China.

See (in this volume)

CHINA: A. D. 1900 (JUNE-AUGUST);
(JULY); and (AUGUST).

CHAFFEE, General Adna R.:

Report of the allied movement to Peking
and the capture of the city.

See (in this volume)

CHINA: A. D. 1900 (AUGUST 4-16).

CHAKDARRA, Defense of.

See (in this volume)

INDIA: A. D. 1897-1898.

CHALDEA, New light on ancient.

See (in this volume)

ARCHÆOLOGICAL RESEARCH: BABYLONIA.

CHAMBERLAIN, Joseph:
Appointed British Secretary of State for the Colonies.

See (in this volume)

ENGLAND: A. D. 1894-1895; and 1900 (NOVEMBER-DECEMBER).

CHAMBERLAIN, Joseph:
 Conference with Colonial Premiers.

See (in this volume)

ENGLAND: A. D. 1897 (JUNE-JULY).

CHAMBERLAIN, Joseph:
Controversies with the government of
the South African Republic.

See (in this volume)

SOUTH AFRICA (THE TRANSVAAL): A. D. 1896 (JANUARY-
APRIL);
1896-1897 (MAY-APRIL), and after.

CHAMBERLAIN, Joseph:
Testimony before British Parliamentary Committee
on the Jameson Raid.
Remarks in Parliament on Mr. Rhodes.

See (in this volume)

SOUTH AFRICA (THE TRANSVAAL): A. D. 1897 (FEBRUARY-
JULY).

CHAMBERLAIN, Joseph:
Instructions to the Governor of Jamaica.

See (in this volume)

JAMAICA: A. D. 1899.

CHAMBERLAIN, Joseph:
Reassertion of British suzerainty over
the South African Republic.
Refusal to arbitrate questions of disagreement.

See (in this volume)

SOUTH AFRICA (THE TRANSVAAL): A. D. 1897 (MAY-
OCTOBER);
 and 1898-1899.

CHAMBERLAIN, Joseph:
Declaration of South African policy.

See (in this volume)

SOUTH AFRICA (THE FIELD OF WAR): A. D. 1901.

CHANG CHIH-TUNG, Viceroy:

Admirable conduct during the Chinese outbreak.

See (in this volume)

CHINA: A. D. 1900 (JUNE-DECEMBER).

CHEMICAL SCIENCE, Recent advances in.

See (in this volume)

SCIENCE, RECENT: CHEMISTRY AND PHYSICS.

CHEROKEES, United States agreement with the.

See (in this volume)

INDIANS, AMERICAN: A. D. 1893-1899.

CHICAGO: A. D. 1894.
Destruction of the Columbian Exposition buildings.

By a succession of fires, January 9, February 14, most of the

buildings of the Exposition, with valuable exhibits not yet
removed, were destroyed.

CHICAGO: A. D. 1896.
Democratic National Convention.

See (in this volume)

UNITED STATES OF AMERICA: A. D. 1896 (JUNE-NOVEMBER).