4 6019193414606653039

Essentials of Obstetrics
Front Matter.indd 1 19-07-2015 13:00:44

Essentials of
Obstetrics
Dr Lakshmi Seshadri, md
Senior Consultant in Obstetrics and
Gynecology
Thirumalai Mission Hospital, Vellore
Formerly, Professor and Head of the
Department
Christian Medical College Hospital
Vellore, Tamil Nadu
Dr Gita Arjun, facog

Director
E. V. Kalyani Medical Foundation Pvt. Ltd.
Chennai
Formerly, Director, and Obstetrician and
Gynecologist
E.V. Kalyani Medical Centre
Chennai, Tamil Nadu

Manager Commissioning: P. Sangeetha
Consultant Editor: Dr Vallika Devi Katragadda
Production Editor: Pooja Chauhan
Asstt Manager Manufacturing: Sumit Johry
Copyright © 2015 by Wolters Kluwer Health (India)
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Preface
A medical student is on a journey of discovery. Every day of his or her progress through medical educa-
tion is crowded with, overwhelming amount of information. The young student struggles hard to not
only acquire and assimilate knowledge but also reproduce that knowledge in examinations. An ideal
textbook, therefore, should help him or her on both counts; it should make knowledge easy to acquire
and exciting, and also help the student replicate it in an examination.
In the course of our medical education, some textbooks will always stand out in our minds. A book
that introduces us to a completely new subject and fans the embers of curiosity to explore and learn
more, is priceless. The authors have clearly poured their passion into the book and succeeded in bring-
ing alive all the intricacies of the subject.
For students of Medicine, learning never stops. It is a lifelong process that involves years of dedica-
tion to the gathering of knowledge from textbooks, journals, and from clinical experiences. Both the
novice student and the practicing clinician can be overwhelmed by the vast amount of information
that is currently available. Information is easily assimilated only when it is put together in a concise,
simple, and easy-to-read format.
Authoring a textbook with an undivided focus on the student and his or her needs is daunting. As
authors, the onus is upon us to make sure that the facts presented to the student are evidence based
and clinically applicable. To this end, we have researched every piece of information before including
it in the text. On the other hand, it is imperative that the book spurs the student to learn more without
being intimidated by the subject matter.
A student cannot grow to become a good practitioner without a thorough understanding of the
pathophysiology of diseases. Skills in diagnostic evaluation and management must follow. We have
ensured this pattern in the book so that the subject is presented in a cogent fashion. Clinical guidelines
which are tailored to the needs of the population we deal with have been emphasized and included at
appropriate places.
Each chapter begins with a commonly seen clinical case scenario pertaining to the topic of the
chapter and goes on to introduce the topic, explain and illustrate the relevant concepts, and closes with
self-assessment. The questions based on the case scenarios are answered at the end of the chapter.
Keeping in mind that examinations are a major challenge in a student’s life, the details are pre-
sented in Boxes, Tables, Flowcharts, and Figures (line illustrations and clinical images). Figures have
simple explanations placed along with the captions. These visuals are of immense help during revi-
sion. Besides, the Key Points section at the end of the chapter presents the entire chapter in a nut-
shell—this feature too is useful in quick recapitulation of essentials.
The Boxes and Tables introduced in the sister volume, Essentials of Gynecology (authored by Prof
Lakshmi Seshadri), have been a huge success with students. Naturally, we have retained these features
in this book as well.
The book is a joint effort by the two of us but with unstinting and generous help and support from
our family, colleagues, former and current students, and friends. We are indebted to the editorial team
at Wolters Kluwer for their professional inputs.
Lakshmi Seshadri
Gita Arjun

Acknowledgements
Essentials of Obstetrics has been a collaborative effort between the two of us. Our greatest inspira-
tion and motivation for writing this book has come from the widespread appreciation of Essentials of
Gynecology by undergraduate and postgraduate students, teachers, and colleagues and, of course, a
request for the companion volume.
We would like to place on record our sincere thanks to those who have supported, encouraged,
and helped us in several ways. We would like to thank Dr S Suresh and his team at Mediscan Systems,
Chennai, for their generous contribution of ultrasonographic images. The colorful clinical photographs
are from our former student, Dr Rajnish Samal, Bangalore, and also from the team at Seethapathy
Clinic and Hospital, Chennai. Some of the laparoscopic images were provided by Dr Sandip Datta Roy.
The cardiotocography traces, partographs, and images were provided by Dr Santosh Benjamin and
the postgraduate students of Christian Medical College, Vellore. We gratefully acknowledge their help.
Dr Padmini Jasper, Dr Alice George, and other faculty members from the Department of Obstetrics
and Gynecology, Christian Medical College Hospital, Vellore, have gone through the chapters and have
given their constructive comments for which we are thankful.
Our respective husbands, Dr M.S. Seshadri and Dr Arjun Rajagopalan, have been patient and tol-
erant of our late working hours, our labile moods, and have managed to survive our ignoring them
for long periods of time. They have been our most supportive critics, have read through many of our
chapters, and given their expert inputs (at the risk of marital disharmony).
The team at Wolters Kluwer: Mrs P Sangeetha, Manager, Commissioning; Dr Vallika Devi Katragadda,
Consultant; and Mrs Pooja Chauhan, Manager, Prepress; has worked tirelessly to make this book a
possibility and a dream come true. We are indebted to them for their support and contribution. We are
thankful to Mr P Saravanan and his team at Digiprezz Media Solutions, for excellent composition and
to Mr S Kartikeyan, for beautiful illustrations. Their co-operation and hard work are truly appreciated.
Lakshmi Seshadri
Gita Arjun

Table of Contents
Preface v
Acknowledgements vii
Section 1: Basic Science in Obstetrics 1

1 Anatomy of the Female Reproductive Tract 2
2 Anatomy of the Bony Pelvis and Fetal Skull 24
3 Maternal Physiology in Pregnancy 35
4 Fertilization, Implantation, and Fetal Development 48
5 Placenta, Fetal Membranes, and Amniotic Fluid 61
6 Physiology of Labor 79
7 Clinical Manifestations and Diagnosis of Pregnancy 88
Section 2: Antenatal Management 98

8 History Taking and Examination of the Obstetric Patient 99
9 Preconceptional and Antenatal Care 119
10 Obstetric Ultrasound and Other Imaging 133
11 Antepartum Fetal Surveillance 148
12 Prenatal Screening, Prenatal Diagnosis, and Fetal Therapy 163
13 Medical Termination of Pregnancy 179
Section 3: Intrapartum Management 190

14 Normal Labor: Mechanics, Mechanism, and Stages 191
15 Management of Normal Labor and Delivery 208
16 Induction of Labor 226
17 Intrapartum Fetal Surveillance 238
18 Obstetric Analgesia and Anesthesia 253
19 Operative Vaginal Delivery and Destructive Operations 266
20 Cesarean Section and Management of Pregnancy with Previous Cesarean 282
Section 4: Postpartum Management 300

21 The Normal Puerperium 301
22 The Abnormal Puerperium 308
23 The Newborn 320
24 Common Problems of the Newborn 332
25 Lactation and Breastfeeding 346
26 Contraception: Temporary Methods 355
27 Emergency Contraception and Sterilization 378

Section 5: Obstetric Complications: Antepartum 397
28 Hyperemesis Gravidarum 398
29 Miscarriage and Recurrent Pregnancy Loss 405
30 Ectopic Pregnancy 428
31 Intrauterine Fetal Death 447
32 Multifetal Pregnancy 455
33 Fetal Growth Disorders: Growth Restriction and Macrosomia 474
34 Disorders of Amniotic Fluid 495
35 Preterm Labor and Birth 508
36 Prelabor Rupture of the Membranes 522
37 Postterm Pregnancy 534
38 Red Cell Alloimmunization 542
39 Antepartum Hemorrhage 560
Section 6: Obstetric Complications: Intrapartum 582

40 Abnormal Labor: Abnormalities in Passage and Powers 583
41 Abnormal Labor: Malpositions and Malpresentations 599
42 Abnormal Labor: Breech Presentation and Shoulder Dystocia 621
43 Complications of the Third Stage of Labor 641
44 Obstructed Labor and Uterine Rupture 662
45 Nonhemorrhagic Shock in Pregnancy 670
46 Abnormalities of the Placenta, Umbilical Cord, and Fetal Membranes 683
Section 7: Maternal Diseases Complicating Pregnancy 693

47 Hypertensive Disorders 694
48 Pregestational and Gestational Diabetes 724
49 Hematological Disorders 740
50 Cardiovascular Diseases 758
51 Hepatobiliary and Gastrointestinal Disorders 774
52 Endocrine Disorders and Obesity 790
53 Respiratory, Dermatological, and Connective Tissue Disorders 807
54 Thromboembolic Disorders 815
55 Urinary Tract and Renal Disorders 827
56 Infections 842
57 Benign and Malignant Tumors of the Reproductive Tract 863
Section 8: Social Obstetrics 876

58 Maternal Mortality 877
59 Perinatal Mortality 887
60 National Health Programs in Obstetrics 895
Index 904

Section 1
Basic Science
in Obstetrics
CH 01_p001-023_v3.indd 1 17-07-2015 10:41:03

Anatomy of
1 the Female
Reproductive Tract
Case scenario
Mrs. AV, 24, primigravida was admitted to labor room at term. Labor was
augmented with oxytocin for dysfunctional labor. Second stage of labor
was prolonged; therefore, baby was delivered by forceps after pudendal
block. There was a fourth degree perineal laceration. Consultant obste-
trician was called in to perform an accurate anatomical perineal repair.
Introduction • Muscles
• Peritoneum
A comprehensive knowledge of the anatomy of
the reproductive tract, changes in the anatomy
in pregnancy, the anatomy of the bony pelvis, Skin
different pelvic configurations, and the anatomy
Skin of the anterior abdominal wall stretches
of the fetal skull is essential for understanding
in pregnancy. There is pigmentation along the
the mechanism of labor and managing problems
midline forming linea nigra. Stretch marks that
that arise during pregnancy and labor.
develop in pregnancy are known as striae grav-
idarum. The Langer’s lines or dermal fibers are
arranged transversely.
Anterior abdominal wall
Consists of the following layers: Subcutaneous tissue
• Skin Consists of superficial fatty layer or Camper’s
• Subcutaneous fascia fascia and deep membranous layer or Scarpa’s
• Rectus sheath fascia.
CH 01_p001-023_v3.indd 2 17-07-2015 10:41:03

Anatomy of the Female Reproductive Tract 3
Rectus sheath abdominis muscles lie on either side of midline.

Transverse incisions for cesarean section are
Rectus sheath is formed by the aponeurosis of usually extended up to the lateral border of these
external and internal oblique and transverse muscles. Pyramidalis is visualized when the
abdominis muscles. This sheath covers the rec- anterior rectus sheath is dissected from the mus-
tus abdominis muscle. Midway between umbili- cle near the pubic symphysis. These small mus-
cus and pubic symphysis is the arcuate line. The cles may be left attached to the rectus sheath.
formation of the rectus sheath is different above
and below the arcuate line. Above the arcuate
line, the internal oblique aponeurosis splits Peritoneum
into two layers: the anterior layer fuses with the This is part of the parietal peritoneum that cov-
external oblique aponeurosis and the posterior ers the abdominal cavity.
layer fuses with transverse abdominis aponeu-
rosis to form the anterior and posterior rectus
sheath, respectively. Below the arcuate line, the Blood supply
aponeuroses of the internal oblique and trans- Blood supply is from branches of femoral and
verse abdominis fuse with the external oblique external iliac arteries (Box 1.1).
aponeurosis anteriorly to form anterior rectus The superficial epigastric vessels are encoun-
sheath (Fig. 1.1). tered during transverse (Pfannenstiel) incision in
the subcutaneous tissue. The inferior epigastric
Muscles vessels are larger and lie posterior to the rectus
muscle. These have to be identified and ligated
The muscles of the anterior abdominal wall are: or cauterized.
• External oblique
• Internal oblique Box 1.1 Blood supply of the anterior abdominal
• Transverse abdominis wall
• Rectus abdominis
• Branches from femoral artery
• Pyramidalis Ŧ 5WRGTſEKCNGRKICUVTKE
The fibers of the internal oblique and trans- Ŧ 5WRGTſEKCNEKTEWOƀGZKNKCE
verse abdominis become aponeurotic more Ŧ External pudendal
• Branches from the external iliac artery
medially than external oblique. Therefore,
Ŧ &GGR
KPHGTKQTGRKICUVTKE
these muscle fibers may have to be cut laterally
Ŧ &GGREKTEWOƀGZKNKCE
while making a transverse incision. The rectus
Skin Anterior rectus

Subcutaneous tissue sheath
External oblique Rectus muscle
Internal oblique
Transverse abdominus Posterior rectus
Transversalis facia sheath
a.
Rectus sheath
b.
Figure 1.1 The rectus sheath. a. Above the arcuate line. The internal oblique aponeurosis splits into two layers. b. Below
the arcuate line. The aponeuroses of internal oblique and transverse abdominis fuse with external oblique aponeurosis.
CH 01_p001-023_v3.indd 3 17-07-2015 10:41:04

4 Essentials of Obstetrics
muscle and may be entrapped or divided if the

Clinical implications
transverse incision extends too far laterally.
Incisions on the abdominal wall for cesarean section
may be vertical midline or Pfannenstiel. Vertical incisions
CTGCUUQEKCVGFYKVJOQTGRQUVQRGTCVKXGRCKPCPFJKIJGT
risk of incisional hernia; hence, transverse incisions are
RTGHGTTGF 1VJGT ENKPKECN KORNKECVKQPU
CFXCPVCIGU CPF External genitalia (vulva)
UWTIKECNCPCVQO[QHtransverse incisionCTGIKXGPDGNQY
• #FXCPVCIGU
Vulva or the external genitalia consists of ana-
Ŧ 2GTHQTOGFCNQPI.CPIGTŏUNKPGU tomical structures listed in Box 1.2 (Fig. 1.2).
Ŧ Cosmetically better
Ŧ Less pain Mons pubis
Ŧ Less risk of hernia
• 5WTIKECNCPCVQO[ This is the triangular area anterior to the pubic
Ŧ Lateral extent of transverse incision bones; it is continuous with the abdominal wall
Up to lateral border of rectus abdominis above and with the labia below. It is filled with
Ŧ +PHGTKQTGRKICUVTKEXGUUGNU adipose tissue and covered by hairy skin.
Lie under rectus muscles
Must be clamped/cauterized
Ŧ +NKQKPIWKPCN+NKQJ[RQICUVTKEPGTXGſDGTU
May be entrapped/divided in transverse incision Box 1.2 External genitalia (vulva)
• Mons pubis
• Labia majora
• Labia minora
• Clitoris
Nerve supply • Vestibule
Innervation is by T7–T12 and L1. Abdominal • 7TGVJTCNQTKſEG
wall at the level of the umbilicus is supplied by • 8CIKPCNQTKſEG
T10. Ilioinguinal and iliohypogastric nerves (L1) • Hymen
• $CTVJQNKPŏUINCPFU
supply the suprapubic area, lower abdomen,
• 5MGPGŏUINCPFU
and mons pubis. These nerve fibers run between
• Vestibular bulbs
the layers of rectus sheath lateral to the rectus
Mons pubis
Prepuce
of clitoris
Clitoris
Urethral orifice
Vestibule
Labia majora
Labia minora
Vaginal orifice
Hymen
Figure 1.2 Structures in the vulva.
CH 01_p001-023_v3.indd 4 17-07-2015 10:41:04

Labia majora Hymen

These are folds of fatty tissue covered by skin Hymen is the thin membrane that covers the
that extend from mons pubis to perineum to vaginal orifice. This ruptures during the first
meet in front of the anus, forming the poste- intercourse and remains as small rounded tags.
rior fourchette. The skin on the lateral aspect of
labia majora is pigmented and covered by hair.
Inner aspect is smooth and shiny and contains Bartholin’s glands
apocrine, sweat, and sebaceous glands. These are small glands located on the postero-
lateral aspect of vaginal orifice, beneath the
bulbospongiosus muscle, at 4 o’clock and 8
Labia minora
o’clock positions. The glands are about 1 cm in
Labia minora are folds of skin that lie medial size and not palpable normally. The ducts are
to the labia majora, encircling the urethral and 2 cm long and open into the vaginal orifice,
vaginal orifices. Posteriorly they fuse with the superficial to the hymen. The glands are com-
posterior fourchette but anteriorly they divide pound racemose and lined by cuboidal epithe-
to form a hood or prepuce and a frenulum for lium. Ducts are lined by cuboidal epithelium
the clitoris. proximally and transitional epithelium distally.
The secretions provide lubrication during sex-
ual intercourse.
Clitoris
Clitoris is the homologue of the penis in men
Skene’s glands
and is formed by two corpora cavernosa and
erectile tissue. It is about 1.5–2 cm in length and These are paraurethral glands that are homol-
is located anterior to the urethral orifice between ogous of the prostate and are located on either
the anterior folds of labia minora. side of the distal urethra. The ducts open into the
urethra, close to the external meatus.
Vestibule
The area between the labia minora is referred to
Vestibular bulbs
as the vestibule. This is perforated by the urethral These are elongated masses of erectile tissue
and vaginal orifices. located beneath the bulbospongiosus muscle on
The urethral orifice (meatus) is a vertical either side of the vaginal orifice. They meet ante-
opening above the vaginal orifice. The ducts of riorly as a narrow strip.
Skene’s (paraurethral) glands open just inside or
outside the meatus.
Changes in pregnancy
Vulva becomes soft in pregnancy and varicosi-
7TGVJTCNQTKſEG
ties may develop. Vulval edema may develop in
This is otherwise known as external urethral severe preeclampsia.
meatus and is located in the anterior part of the
vestibule.
Clinical implications of changes in vulva during preg-
8CIKPCNQTKſEG nancyCTGIKXGPDGNQY
This lies between the labia minora and is par- • Varicose veins of the vulva
tially covered by a thin membrane called hymen. Ŧ $NGGFKPIFWTKPIFGNKXGT[
• Vulval edema
The ducts of the Bartholin’s glands open into the
Ŧ &KHſEWNV[KPGRKUKQVQO[
vaginal orifice laterally between the hymen and
Ŧ +ORCKTGFJGCNKPI
labia minora.
CH 01_p001-023_v3.indd 5 17-07-2015 10:41:04

Pubic symphysis
Pubic symphysis ubpubic angle
schiopubic rami
Ischial Urogenital triangle
tuberosity uperficial trans erse
perinei muscle
schial tuberosity
Coccyx acrotuberous
ligament
Coccy
Figure 1.3 The anatomical perineum. This is a diamond- Figure 1.4 6JGWTQIGPKVCNVTKCPING6JGDQWPFCTKGUCTG
shaped area that extends from the pubis anteriorly to UWDRWDKECPINGCPVGTKQTN[UWRGTſEKCNVTCPUXGTUGRGTKPGK
the coccyx posteriorly and the ischial tuberosities muscle posteriorly; ischiopubic rami and the ischial
laterally. tuberosities laterally.
The perineum Box 1.4 Muscles of the perineum

• 5WRGTſEKCNRGTKPGCNOWUENGU
The anatomical or true perineum is a diamond- Ŧ Ischiocavernosus
shaped area that extends from pubis anteriorly Ŧ $WNDQURQPIKQUWU
to coccyx posteriorly and the ischial tuberosities Ŧ 5WRGTſEKCNVTCPUXGTUGRGTKPGK
laterally (Fig. 1.3). This is divided by an imagi- • Deep perineal muscles
nary line between the two ischial tuberosities into Ŧ Deep transverse perinei
anterior or urogenital triangle and posterior or Ŧ Urethral sphincter
anal triangle.
The urogenital triangle Muscles of the perineum

The urogenital triangle forms the anterior trian- They fall into two groups—superficial and
gle of the perineum. deep—as demarcated by the perineal membrane
(Box 1.4; Fig. 1.5).
Boundaries
5WRGTſEKCNRGTKPGCNOWUENGU
• Anterior: Subpubic angle
• Posterior: Superficial transverse perinei muscles The ischiocavernosus muscles run along the
• Lateral: Ischiopubic rami and ischial tuberosi- ischiopubicrami, originate at the ischial tuber-
ties (Fig. 1.4) osity and are inserted into the ischiopubis. The
bulbospongiosus muscles are medial and lie
over the vestibular bulbs. They originate at the
Contents perineal body and are inserted into the clitoris.
The contents of the urogenital triangle are listed The superficial transverse perinei muscles are
in Box 1.3. attached to the ischial tuberosities laterally and
perineal body medially (Box 1.5).
Box 1.3 Contents of the urogenital triangle Deep perineal muscles

• Vulva and its contents The urethral sphincter consists of a sheet of mus-
• 7TQIGPKVCNFKCRJTCIO cle that arises from the ischiopubis and is inserted
• 5WRGTſEKCNRGTKPGCNOWUENGU
into the urethra and vagina. This muscle functions
• Deep perineal muscles
along with deep transverse perinei, pubourethra-
• Blood vessels, nerves, and lymphatics
lis fibers of the levator ani, and bulbospongiosus
CH 01_p001-023_v3.indd 6 17-07-2015 10:41:04

Ischiocavernosus
Bulbospongiosus
Perineal body
Pubovaginalis
Urogenital
diaphragm
Transversus perinei
superficialis
Iliococcygeus
Sphincter
ani externus
Coccygeus
Coccyx
Figure 1.5 /WUENGUQHRGTKPGWO5WRGTſEKCNOWUENGUQHVJGRGTKPGWOCTGUGGP
Box 1.5 5WRGTſEKCNCPFFGGRRGTKPGCNOWUENGU The anal triangle

Muscle Origin Insertion Boundaries
Ischiocavernosus Ischial Ischiopubis
tuberosity • Anterior: Superficial transverse perineal muscles
• Posterior: Coccyx
$WNDQURQPIKQUWU 2GTKPGCNDQF[ %NKVQTKU
• Lateral: Ischial tuberosities and sacrotuberous
5WRGTſEKCN +UEJKCN 2GTKPGCN
ligaments (Fig. 1.6)
transverse perinei tuberosity body
Urethral sphincter Ischiopubis Urethra and
XCIKPC
Contents
Deep transverse Ischium Lateral Contents of anal triangle are listed in Box 1.6.
RGTKPGK XCIKPCNYCNN
Anal canal
Anal canal extends from the anorectal junction
muscles to aid the bladder muscles in closing the to the anal verge and is approximately 4 cm in
urethra. The deep transverse perinei muscles are length. The dentate line is located 2 cm from the
located above the perineal membrane, arise from anal verge. The canal is lined by columnar epi-
the ischial bone, and are inserted into the lateral thelium above the dentate line and squamous
vaginal wall. epithelium below the dentate line.
The anal sphincters

Perineal membrane
There are two anal sphincters—external and inter-
Perineal membrane is a dense triangular conden- nal. The external anal sphincter is made of skeletal
sation of fascia that stretches between the two
ischiopubic rami and is pierced by the urethra and
Box 1.6 Contents of anal triangle
vagina. This membrane separates the superficial
from the deep compartment of the perineum. The • Lower end of anal canal
perineal membrane and the deep transverse per- • Anal sphincters
• #PQEQEE[IGCNDQF[
TCRJG
inei muscles attach the lower vagina and urethra
• Ischiorectal fossae
to pubic rami and provide support to these
• Blood vessels, lymphatics, and nerves
structures.
CH 01_p001-023_v3.indd 7 17-07-2015 10:41:04

uper icial tra s erse

peri ei muscles
al tria le Ischial tuberosity
al sphi cters
acrotuberous li ame t
al ca al ococcy eal raphe
Coccyx
Figure 1.6 6JGCPCNVTKCPING6JGDQWPFCTKGUCTGUWRGTſEKCNVTCPUXGTUGRGTPGKOWUENGUCPVGTKQTN[EQEE[ZRQUVGTKQTN[

KUEJKCNVWDGTQUKVKGUCPFUCETQVWDGTQWUNKICOGPVUNCVGTCNN[
muscle and has three parts—subcutaneous,

Box 1.7 Boundaries and contents of
superficial, and deep. The fibers of external anal ischiorectal fossa
sphincters merge with each other and are attached
to perineal body anteriorly and to puborectalis • Boundaries
Ŧ Base: Perineal skin
and anococcygeal body posteriorly.
Ŧ Apex: Point where obturator and anal fascia meet
Anococcygeal body is a fibromuscular struc-
Ŧ Lateral: Ischial tuberosity, obturator internus muscle,
ture located between the anus and coccyx. The obturator fascia
fibers of the levator ani and anal sphincters are Ŧ Medial: Sphincter ani internus, levator ani
attached to it. Ŧ 2QUVGTKQT)NWVGWUOCZKOWUUCETQVWDGTQWUNKICOGPV
• Contents
Ischiorectal fossae Ŧ Ischiorectal pad of fat
Ŧ Inferior rectal nerve and vessels
These lie on either side of the anal canal. They Ŧ Pudendal canal and its contents
are wedge-shaped, fat-filled spaces. Boundaries Ŧ Posterior labial nerve, perineal branch of fourth
and contents of the fossae are given in Box 1.7 sacral nerve, cutaneous branch of S2, S3
and Fig. 1.7.
Perineal body 2GNXKEƀQQT

Perineal body is a fibromuscular structure that The pelvic organs are supported in the upright
forms the center point of the perineum and is sit- position by a fibromuscular floor that includes
uated between the anus and lower vagina. Several the pelvic diaphragm, muscles of the deep peri-
muscles are inserted into it (Box 1.8; Fig. 1.8). neal compartment, and the perineal membrane.
ectum an Le ator ani

anal canal
bturator muscle
schium
Pu en al
bturator fascia
essels an ner e
at nal sphincter
Figure 1.7 %QTQPCNUGEVKQPQHVJGKUEJKQTGEVCNHQUUCG6JGUGCTGYGFIGUJCRGFURCEGUQPGKVJGTUKFGQHVJGCPCNECPCN
CH 01_p001-023_v3.indd 8 17-07-2015 10:41:05

ulbospongiosus
Pubo aginalis
eep trans erse
perinei
Perineal bo y
uperficial trans erse
perinei
phincter ani
e ternus
Puborectalis
Coccygeus
Figure 1.8 Muscles that form perineal body.
Box 1.8 Muscles inserted into perineal body Box 1.9 Components of levator ani
• Sphincter aniexternus • 2WDQEQEE[IGWU
• $WNDQURQPIKQUWU Ŧ Puborectalis
• 5WRGTſEKCNVTCPUXGTUGRGTKPGK Ŧ 2WDQXCIKPCNKU
• Deep transverse perinei • +NKQEQEE[IGWU
• Levator ani
Ŧ 2WDQXCIKPCNKU
Ŧ Puborectalis
The muscle fibers of the levator ani mus-
cles arise from the arcus tendineus or white line
which is a thickening of the fascial covering of
the obturator internus muscle and extends from
2GTKPGCN DQF[ UVTGVEJGU FWTKPI FGNKXGT[ CPF VJG OWU- the pubic bone to ischial spine (Fig. 1.10). The
ENGUCTGKPXQNXGFKPRGTKPGCNVGCTU&COCIGVQRGTKPGCN
fibers of levator ani pass backwards and medi-
DQF[ECWUGUCFGſEKGPVRGTKPGWOICRKPIQHVJGKPVTQK-
tus with resultant sexual problems, and loss of support ally to be inserted into perineal body, rectal wall,
HQT NQYGT QPGVJKTF QH XCIKPC 6JKTF CPF HQWTVJ FGITGG anococcygeal raphe, and coccyx. In addition, the
VGCTUNGCFVQCPCNKPEQPVKPGPEG5WTIKECNKPEKUKQPQPVJG medial and anterior fibers that arise from the
RGTKPGWOVQGPNCTIGVJGKPVTQKVWUVQHCEKNKVCVGFGNKXGT[KU pubis (pubovaginalis) cross the lateral vaginal
known as episiotomy (see Chapter 15, Management of
wall between the middle and lower third and
normal labor and delivery).
are inserted into the vaginal wall and perineal
body. Some fibers decussate behind the urethra
as well. They form a sling around the urethra,
Pelvic diaphragm vagina, and rectum, pulling these structures
Pelvic diaphragm consists of levator ani mus- anteriorly toward the pubis. When the muscle
cle covered by pelvic fascia. The muscle covers contracts, the urethra, vagina, and rectum are
the space from the pubic bone to coccyx and kinked and narrowed. The uterus and vagina
from one pelvic side wall to another forming lie horizontally on the pelvic floor. The contrac-
a funnel-shaped support. The muscle has two tion of the levator ani also maintains the vagina
components (Box 1.9; Fig. 1.9). The coccygeus, in its horizontal position at rest.
formerly called ischiococcygeus, extends from The coccygeus, also called ischiococcygeus,
the ischial spine to coccyx but is not a part of though not part of the levator ani, also forms
levator ani. the posterior part of the pelvic floor and pelvic
CH 01_p001-023_v3.indd 9 17-07-2015 10:41:05

Urethra Pubic bone
Pubo aginalis
Vagina
rcus ten ineus

fascia pel is
nal canal
schial tuberosity
Puborectalis
leococcygeus
Coccygeus Coccy
Figure 1.9 %QORQPGPVUQHNGXCVQTCPKOWUENGōRWDQTGEVCNKURWDQXCIKPCNKUCPFKNKQEQEE[IGWU
Box 1.10 Internal genital organs

• 8CIKPC
• Uterus
• Fallopian tubes
• Ovary
bturator ascia
a obturator
i ter us muscle
Pubis Internal genital organs

rcus te i eus The internal genital organs are listed in Box 1.10
e ator a i and elaborated in the following text.
a i a
Vagina
Figure 1.10 Arcus tendineus fascia pelvis. It extends from
the pubic bone to the ischial spine. Vagina is the fibromuscular tube that extends
from vestibule to uterine cervix (Box 1.11).
The attachment of vagina to the cervix is at its
Clinical implications middle (Fig. 1.11). Therefore, a gutter is formed
The location, attachments, and functions of the levator all around the cervix, between it and the vagina,
ani muscle have several clinical implications.
• 6JGNGXCVQTCPKOWUENGJCUCTGUVKPIVQPGVJCVMGGRUVJG
RGNXKEƀQQTENQUGFCPFRTGXGPVUJGTPKCVKQPQHVJGWVGTWU Box 1.11 Vagina
and cervix.
• Fibromuscular tube from vestibule to cervix
• The shape of the levator ani muscle and the direction
• Axis horizontal
QHVJGſDGTURNC[COCLQTTQNGKPKPVGTPCNTQVCVKQPQHVJG
• Closely applied
RTGUGPVKPIRCTVKPNCDQT
Ŧ Anteriorly
• Puborectalis contributes to anal continence.
Bladder
• +PLWT[VQNGXCVQTCPKOWUENGFGVGEVGFD[WNVTCUQPQITC-
RJ[ CPF OCIPGVKE TGUQPCPEG KOCIKPI QEEWTU FWTKPI Urethra
XCIKPCNFGNKXGT[CPFECWUGURGNXKEQTICPRTQNCRUG Ŧ Posteriorly
Posterior cul-de-sac
Rectum
Anal canal
support. It originates from the ischial spine and
Perineal body
sacrospinous ligament and is inserted into the
• Anterior and posterior walls in apposition
lateral part of the lower sacrum and coccyx.
CH 01_p001-023_v3.indd 10 17-07-2015 10:41:06

Uterus
Box 1.12 Structure of vagina
la er • Mucosa
Ŧ 5VTCVKſGFUSWCOQWUGRKVJGNKWO
• Subepithelial connective tissue
Pouch of • Muscle layer
nterior forni
ouglas Ŧ 1WVGTNQPIKVWFKPCN
Pubic bone
Ŧ Inner circular
ectum
Urethra • Condensed endopelvic fascia
Posterior forni
Vagina
a. Perineal bo y Clinical implications
Clinical implications of changes in vagina during preg-
nancyCTGIKXGPDGNQY
• Bluish discoloration of vulva
Ŧ &KCIPQUKUQHRTGIPCPE[
• .QYGTKPIQHXCIKPCNR*
Ŧ 2TQVGEVKQPCICKPUVXCIKPCNKPHGEVKQPU
Uterine
artery
Lateral Ureter
forni Uterus
Vagina Uterus is a pear-shaped hollow viscus located
b. between the bladder and rectum. It is divided
into cervix and uterine corpus, the dividing line
Figure 1.11 a.5CIKVVCNUGEVKQPQHVJGXCIKPCUJQYKPIVJG
being the internal os.
CZKUQHVJGXCIKPCVJGCPVGTKQTCPFRQUVGTKQTHQTPKEGUCPF
its relationship to bladder and urethra. b. Coronal section of
VJGXCIKPCUJQYKPIVJGNCVGTCNHQTPKEGUCPFVJGKTRTQZKOKV[ Cervix
to ureters.
The attachment of the vagina divides the cervix
into upper supravaginal cervix and lower por-
tio vaginalis (Fig. 1.12). It has an external os and
called fornices. Ureter and uterine artery are in
internal os, and a cervical canal in between. Total
close proximity to lateral fornices. The posterior
length of cervix is 2.5–3 cm. The external os is cir-
attachment is at a higher level making the poste-
cular in the nullipara but becomes a transverse
rior fornix deep. The anterior wall of the vagina
slit after childbirth. Anatomical features of cervix
is, therefore, shorter than the posterior wall.
are given in Box 1.13.
The opening at the vestibule is partially covered
by hymen. The vaginal walls have rugae which
allow stretching during parturition. The axis of
the vagina is horizontal. Box 1.13 Anatomical features of the cervix
• Cervix divided into
UWRTCXCIKPCNEGTXKZ
Structure of vagina
RQTVKQXCIKPCNKU
Vaginal wall is composed of three layers (Box 1.12). • Consists of
Ŧ external os
Ŧ internal os
Changes in vagina during pregnancy Ŧ endocervical canal between the two
There is increased vascularity and bluish discol- • Structure includes
oration of the vagina, described as Chadwick’s Ŧ ſDTQOWUEWNCTYCNN
Ŧ endocervical canal—columnar epithelium
sign. Increase in glycogen-containing cells results
Ŧ GEVQEGTXKZōUVTCVKſGFUSWCOQWUGRKVJGNKWO
in lowering of pH due to increase in lactic acid.
Ŧ INCPFUōUGETGVGOWEWU
This offers protection from infection.
CH 01_p001-023_v3.indd 11 17-07-2015 10:41:06

un us
cm
Corpus
upra aginal cer i

Cer i cm
Portio aginalis cer i
Vagina
Figure 1.12 Uterus and cervix. Uterine fundus is the part above the line of attachment of the fallopian tubes. The part of
VJGEGTXKZCDQXGVJGCVVCEJOGPVQHVJGXCIKPCKUUWRTCXCIKPCNEGTXKZCPFDGNQYVJKUKURQTVKQXCIKPCNKUEGTXKZ
Changes in cervix during pregnancy mechanism, and stages). During labor, cervix
Cervix undergoes changes in pregnancy. In the undergoes effacement and dilatation to allow
first trimester of pregnancy, the lower part of the passage of fetus.
the uterus softens, while the fundus and cervix Early effacement and dilatation occurs in
are firmer. This softening of the lower segment is some women, leading to recurrent pregnancy
described as Hegar’s sign (see Chapter 7, Clinical loss or preterm labor.
manifestations and diagnosis of pregnancy). The
cervix remains closed in pregnancy till onset of Uterine corpus
labor. Endocervical epithelium proliferates and The size and shape of the uterus changes with
gives rise to ectropion. There is also plenty of changes in hormone levels associated with
mucus production and a mucous plug forms in puberty and pregnancy. The dimensions of nul-
the cervical canal, which is expelled at the onset liparous uterus are given in Box 1.14. The uterus
of labor along with bloody discharge known as is normally anteverted and anteflexed. Flexion is
show (see Chapter 14, Normal labor: Mechanics, the angle between the uterus and cervix and ver-
sion is the angle between the uterus and vagina.
Clinical implications of changes in cervix during preg-
nancyCTGIKXGPDGNQY Box 1.14 Uterus
• *GICTŏUUKIP • Pear shaped
Ŧ &KCIPQUKUQHRTGIPCPE[ • .GPIVJEO
• /WEQWURNWI • Anteroposterior thickness: 2.5 cm
Ŧ 2TQVGEVUCICKPUVCUEGPFKPIKPHGEVKQP • .GPIVJQHECXKV[EO
• Show • Body: Cervix ratio
Ŧ 5KIPQHſTUVUVCIGQHNCDQT Ŧ At birth: 1:1
• Effacement and dilatation Ŧ Adult: 2:1
Ŧ Normal labor • Corpus is divided into
• Dilatation before term Ŧ Isthmus: Just above the internal os
Ŧ Preterm labor Ŧ Cornu: At insertion of fallopian tube
Ŧ 2TGIPCPE[NQUU Ŧ Fundus: Above the level of cornu
CH 01_p001-023_v3.indd 12 17-07-2015 10:41:06

Structure of uterus Box 1.15 Histology of uterus

The uterine wall consists of three layers—inner • Endometrium
endometrium, outer serosa, and a middle layer Ŧ Columnar epithelium
composed of smooth muscles called myome- Ŧ Cellular stroma
trium. The endometrial cavity is continuous with Ŧ Glands
that of the tubes, cervix, and vagina. The endome- Ŧ Specialized stroma
trium, including glands and stroma, is very sensi- • Myometrium
tive to estrogen and progesterone and undergoes Ŧ Inner circular
Ŧ /KFFNGKPVGTNCEKPI
changes during menstrual cycle and pregnancy.
Ŧ 1WVGTNQPIKVWFKPCN
The myometrium consists of three layers.
• Serosa (peritoneum)
These layers are more distinct during pregnancy. Ŧ Incomplete anteriorly
• Outer longitudinal Ŧ Complete posteriorly
• Middle interlacing, crisscross
• Inner circular
Changes in uterus during pregnancy
The outer longitudinal fibers of myometrium
are continuous with those of the tubes. The mid- Major anatomical changes take place in the
dle layer of interlacing fibers is important for uterus during pregnancy.
uterine contraction and retraction. The blood
vessels pass through this layer and the contrac- a. Changes in size and shape
tion of the fibers in this layer occludes the ves- In the prepregnant state, uterus is a pear-shaped
sels, forming living ligatures and stopping the organ, which weighs about 100 g, measures 10 ×
bleeding after parturition. The inner circular 5 × 2.5 cm, and has a cavity of about 10 mL. Rapid
layer is thin and insignificant (Fig. 1.13). growth in pregnancy is due to hyperplasia and
The serosa or peritoneum covering the uterus hypertrophy. By term, uterus weighs 1000 g and
stops at the uterovesical junction anteriorly but has a capacity to hold 5 L or more. Shape of the
extends down to form the cul-de-sac or pouch of uterus changes with advancing pregnancy from
Douglas posteriorly (Box 1.15). The cul-de-sac is pear shaped to spherical at 20 weeks and elon-
the most dependent part of the pelvis, and there- gates toward term, becoming longitudinally oval
fore, fluids, pus, and blood collect here to form (Box 1.16).
abscess or hematocele. This can be easily accessed
through the posterior fornix. b. Formation of lower segment
The lower segment develops from the isthmus
and is about 10 cm in length by term. The differ-
ence between the two segments becomes more
obvious as pregnancy advances. The junction
between the two segments is at the level of the
pubic symphysis and is marked by the level at
uter longitu enal
Mi le crisscross
Box 1.16 Changes in the uterus during
loo essels
pregnancy
nner circular
• Size
• Increase in uterine size
Ŧ More at the fundus
Ŧ Due to hypertrophy and hyperplasia
• Shape
Figure 1.13 &KCITCOOCVKETGRTGUGPVCVKQPQHVJGOWUENG
Ŧ Spherical by 12 weeks
layers of the uterine myometrium. The myometrium
Ŧ .QPIKVWFKPCNN[QXCND[VGTO
EQPUKUVUQHQWVGTNQPIKVWFKPCNKPPGTEKTEWNCTCPFOKFFNG
• Volume
KPVGTNCEKPIETKUUETQUUſDGTU6JGDNQQFXGUUGNURCUU
Ŧ Increases to 5 L or more
VJTQWIJVJGOKFFNGNC[GT
CH 01_p001-023_v3.indd 13 17-07-2015 10:41:06

which the peritoneum becomes loosely adher-

Box 1.17 Fallopian tubes
ent to the anterior uterine wall.
• .GPIVJ#DQWVEO
E%JCPIGUKPDNQQFƀQY • (QWTTGIKQPU
Ŧ Interstitial: Narrowest, within the uterine cornu
Blood flow to the uterus and cervix increases Ŧ Isthmus: Narrow, close to uterine cornu
steadily to 500 mL/min, which is five times more Ŧ Ampullary: Broader, thin walled, lateral to isthmus
than the nonpregnant state. Uterine vessels Ŧ +PHWPFKDWNWO(WPPGNUJCRGFGPFUKPſODTKCG
enlarge gradually and become tortuous. • Functions
Ŧ Ovum pickup
d. Changes in myometrium Ŧ Site of fertilization
The three layers become distinct and the middle Ŧ Transport of fertilized ovum
layer becomes prominent.
nfun ibular
e. Uterine activity nterstitial sthmus
Spontaneous contractions called Braxton Hick’s
contractions begin at about 20 weeks and con-
mpullary
tinue till term. This uterine activity facilitates the
development of lower segment and softens the
cervix. imbriae
Fallopian tubes Figure 1.14 The fallopian tube. The tube is narrow at the
isthmus and broad at the ampullary part.
The tubes are about 10 cm in length and
extend laterally from the cornual ends of the
uterus into the peritoneal cavity. Each tube is Box 1.18 Structure of the fallopian tube
divided into four regions (Box 1.17; Fig. 1.14). • Mucosa
The infundibulum has fimbriae with cilia to Ŧ Ciliated columnar epithelium
aid in ovum pickup. Fertilization takes place • Muscularis
in the tube, and the blastocyst is transported Ŧ 1WVGTNQPIKVWFKPCN
to the uterine cavity where implantation takes Ŧ Inner circular
place. • Outer
Ŧ Serosa
The structure of the tube is given in Box 1.18.
The tube has three layers—inner mucosa, outer
serosa, and muscularis layer between the two.
When implantation of fertilized ovum takes place in the
HCNNQRKCPVWDGGEVQRKERTGIPCPE[TGUWNVU+VECPTWRVWTG
Clinical implications NGCFKPI VQ JGOQRGTKVQPGWO UJQEM CPF RGNXKE JGOC-
Clinical implications of changes in uterine anatomy tocele.
during pregnancyCTGIKXGPDGNQY
• %JCPIGUKPUK\GUJCRGRQUKVKQP
Ŧ #EEQOOQFCVGUITQYKPIHGVWU Ovaries
• %JCPIGUKPO[QOGVTKWO
Ŧ Uterine contraction in labor The tube and ovary together are referred to as
Ŧ 4GVTCEVKQPCPFJGOQUVCUKUKPVJKTFUVCIG adnexa. The ovaries are the female gonads. The
• (QTOCVKQPQHNQYGTUGIOGPV size of the ovaries varies with age, sex, steroid
Ŧ Facilitates labor hormone levels, and certain medications. The
• 6JKPPKPIQHNQYGTUGIOGPV ovaries are located on either side of the uterus,
Ŧ Predisposes to rupture uterus close to the infundibulum of the tubes. They are
• (QTOCVKQPQHTGVTCEVKQPTKPI
connected to the uterine cornu by the ovarian lig-
Ŧ Indicates obstructed labor
aments and to the broad ligament by mesovarium
CH 01_p001-023_v3.indd 14 17-07-2015 10:41:07

arian
Hilum Meso arium Box 1.20 Structure of the ovary
ligament
Mesosalpin • Cortex
Ŧ Cuboidal surface epithelium
Ŧ Specialized stroma
Ŧ Follicles
• Medulla
Ŧ Fibromuscular tissue
Ŧ Blood vessels
Ligaments of the uterus

and cervix
The endopelvic fascia condenses in some areas
nfun ibulopel ic to form ligaments that support the uterus and
ligament
other pelvic structures (Box 1.21; Fig. 1.16).
Figure 1.15 Attachments of the ovary. Infundibulopelvic
NKICOGPVCVVCEJGUVJGQXCT[VQVJGNCVGTCNRGNXKEYCNNCPF
Cardinal or Mackenrodt’s ligaments
QXCTKCPNKICOGPVVQVJGQXCT[/GUQXCTKWONKGUDGVYGGP
VJGQXCT[CPFVJGDTQCFNKICOGPV These extend from the lower part of the uterus,
supravaginal cervix and lateral vaginal fornix to
the lateral pelvic wall. The loose cellular tissue
Box 1.19 Ovaries in this area is referred to as parametrium. The
• Size
Ŧ 3 x 2 cm
• Connected by Box 1.21 Ligaments of the uterus and cervix
Ŧ mesovarium (mesentery) to posterior surface of
DTQCFNKICOGPV • %CTFKPCNNKICOGPVU
Ŧ QXCTKCPNKICOGPVVQWVGTKPGEQTPW • 2WDQEGTXKECNNKICOGPVU
Ŧ KPHWPFKDWNQRGNXKENKICOGPVVQNCVGTCNRGNXKEYCNN • 7VGTQUCETCNNKICOGPVU
• 4QWPFNKICOGPVU
• $TQCFNKICOGPVU
(Fig. 1.15). The ovarian vessels are carried in a • 1XCTKCPNKICOGPVU
• +PHWPFKDWNQRGNXKENKICOGPVU
fold of peritoneum, called the infundibulopelvic
ligaments, from the lateral pelvic wall to the ovary
(Box 1.19).
Pubocer ical
li ame t
Structure la er
urethra
The ovary is divided into an outer cortex and
inner medulla (Box 1.20). The cortex contains a i a
the specialized stroma and the follicles and is
responsible for the important functions of ovu-
lation and steroid hormone production. Car i al li ame t
ectum
Changes in ovaries during pregnancy terosacral

li ame t
Ovaries enlarge and become vascular. The cor-
acrum
pus luteum continues to grow and secrete hor-
mones till 7–8 weeks and begins to degenerate at Figure 1.16 .KICOGPVUCVVCEJGFVQVJGNQYGTWVGTWUCPF
12 weeks when placenta takes over. EGTXKZōECTFKPCNWVGTQUCETCNCPFRWDQEGTXKECNNKICOGPVU
CH 01_p001-023_v3.indd 15 17-07-2015 10:41:07

ureter, before entering the bladder, traverses this Infundibulopelvic ligaments

ligament and is encased in a fascial sheath called
ureteric tunnel which lies 2 cm lateral to the cer- These are lateral extensions of the broad liga-
vix. The uterine artery crosses to the uterus above ments between the ovary and pelvic wall. They
the ureter at this point. The descending cervical contain the ovarian vessels.
branch of the uterine artery courses through this
ligament.
Pelvic ureters
Pubocervical ligaments The ureters are located retroperitoneally and
run from the renal pelvis to urinary bladder. The
This condensation of the pubovesicocervical fascia abdominal segments lie on the psoas muscle
passes from the anterolateral aspect of the cervix and run downwards and medially. They enter the
to the posterior surface of pubic bone. Some fibers pelvis by crossing the common iliac vessels from
extend from the bladder and the pubis and form lateral to medial aspect at their bifurcation just
the bladder pillars. Pubocervical ligaments merge medial to the ovarian vessels (Fig. 1.17a and b).
posterolaterally with the cardinal ligaments. They can be found attached to the medial leaf
of the posterior peritoneum during dissection.
Uterosacral ligaments At the level of the ischial spines, they turn for-
ward and medially toward the base of the broad
These ligaments extend from the posterior ligament. They then enter the ureteric canal in
part of the supravaginal cervix to the sacrum. the cardinal ligament, crossing under the uterine
They lie on either side of the rectosigmoid. vessels. Here they are 2 cm lateral to the cervix.
Anterolaterally they merge with cardinal lig- The ureters run medially and enter the bladder
aments. Frankenhauser’s plexus of nerves are close to the anterior vaginal wall (Box 1. 22).
located mainly along these ligaments.
Round ligaments Box 1.22 The course of the pelvic ureters

These are vestiges of the gubernaculums and are • Cross the common iliac at bifurcation
made of fibromuscular tissue. They extend lat- • Lie attached to the posterior peritoneum
erally from the uterine cornu extraperitoneally, • 4GCEJVJGNGXGNQHWVGTQUCETCNNKICOGPVU
enter the inguinal canal, and finally merge with • Turn forward at ischial spine
the skin and connective tissue of the mons pubis • 'PVGTVJGDCUGQHDTQCFNKICOGPVU
and labia majora. • Cross under the uterine vessels
• 'PVGTWTGVGTKEECPCNKPECTFKPCNNKICOGPVU
• Run forward to enter the bladder
Broad ligaments • .KGENQUGVQCPVGTKQTXCIKPCNYCNN
The peritoneum on the anterior and poste-
rior surface of the uterus spreads out laterally
toward the pelvic wall to form the broad liga- Clinical implications
ments. Between the two layers of peritoneum is
Due to the close proximity to other structures in the pel-
the pelvic cellular tissue containing ureter and XKUVJGWTGVGTKURTQPGVQKPLWT[FWTKPIXCTKQWUUWTIKECN
the plexus formed by the anastomosis of uterine procedures. Points at which ureter is prone to injury are
and ovarian vessels. The round ligaments, tubes, listed below.
and ovarian ligaments are covered by the perito- Site Procedure
neum of the broad ligament and are contained 2GNXKEDTKO %NCORKPIQHKPHWPFKDWNQRGNXKE
in its upper part. NKICOGPVU
$KHWTECVKQPQH +PVGTPCNKNKCECTVGT[NKICVKQP
common iliac
Ovarian ligaments $TQCFNKICOGPV 7VGTKPGCTVGT[NKICVKQP
They pass from the medial pole of the ovaries to %CTFKPCNNKICOGPV &KUUGEVKQPQHWTGVGTKEVWPPGN
%NCORKPIQHECTFKPCNNKICOGPV
the uterine cornu posterior to the attachment of
7RRGTXCIKPC %NCORKPIQHXCIKPCNCPING
the tubes.
CH 01_p001-023_v3.indd 16 17-07-2015 10:41:07

la er
bturator
artery
teri e
artery
reter
uperior esical
artery a i a
reter aria artery

i u ibulopel ic li ame t
ectum
a.
arian Ureter Common iliac artery

artery
acrum
ifurcation
ternal
iliac Uterus
nternal
iliac ary
Urinary
bla er
Uterine artery
b. Pubic bone
Figure 1.17 The pelvic ureters. a. The course of the ureters. b. The relationship of the pelvic ureters. The Ureters enter
VJGRGNXKUD[ETQUUKPIVJGEQOOQPKNKCECTVGT[CVKVUDKHWTECVKQPVWTPHQTYCTFVQGPVGTVJGWTGVGTKEECPCNETQUUKPIWPFGTVJG
uterine vessels.
The ureters receive rich blood supply from Urinary bladder and urethra
all the blood vessels in the pelvis. These vessels
anastomose to form a plexus on the adventitia of The urinary bladder and urethra are in close
the ureters before entering it. Therefore, the ure- proximity to the anterior surface of uterus and
ter is protected from devascularization unless it vagina. The proximity and susceptibility to injury
is skeletonized. varies with the amount of urine in the bladder.
CH 01_p001-023_v3.indd 17 17-07-2015 10:41:08

into external and internal iliacs at the sacroiliac

joints. The ureters cross the common iliacs at
Since the urinary bladder lies just anterior to lower uter- their bifurcation.
KPGUGIOGPVKPLWTKGUVQVJGDNCFFGTCTGEQOOQPFWTKPI
UWTIGT[ 6JG DNCFFGT QT WTGVJTC OC[ DG EQORTGUUGF
The internal iliac (hypogastric) artery lies pos-
between the fetal head and pubic bone in obstructed teromedial to the external iliac vessels. The ureter
NCDQTNGCFKPIVQRTGUUWTGPGETQUKUCPFWTKPCT[ſUVWNCG is anterior and the internal iliac vein is posterior
Obstetric injuries of the urinary bladder to the artery. The artery on each side divides into
• Rupture uterus
anterior and posterior divisions. The posterior
• Cesarean section division exits the pelvis and does not give off any
Ŧ 9JKNGGPVGTKPIRGTKVQPGWO visceral branches. The anterior division gives rise
Ŧ 9JKNGKPEKUKPIWVGTQXGUKECNRGTKVQPGWO to several branches which supply the internal
Ŧ 9JKNGRWUJKPIDNCFFGTFQYP and external genitalia (Box 1.23; Fig. 1.18).
Ŧ Downward extension of uterine incision The obturator and superior vesical are the
• 8CIKPCNFGNKXGT[ first two branches of the anterior division, fol-
Ŧ Rotational forceps lowed by the uterine artery. The vaginal artery
Ŧ Destructive operations may arise from the uterine artery. After giving
• Obstructed labor off these branches in the pelvis, the internal iliac
Ŧ 2TGUUWTGPGETQUKUCPFſUVWNC
artery continues as internal pudendal artery
which hooks behind the ischial spines to enter
The superior surface of bladder is adjacent to the pudendal canal in the ischiorectal fossa. Here
the anterior uterine surface. Base of the bladder it gives off two more branches—the inferior rec-
is located adjacent to the anterior vaginal wall. tal and perineal arteries. The vessel then ends as
Bladder neck and urethra lie anterior to the ante- dorsal artery of the clitoris. The parietal branches
rior vaginal wall. The space between the bladder supply the respective muscles and tissues.
and pubic symphysis is called space of Retzius.
Uterine arteries
Blood supply The uterine arteries run medially and cross over
the ureter about 2 cm lateral to the internal os in
The internal and external genitalia have a rich the broad ligament. At the lateral border of the
blood supply in order to allow for the needs of uterus, they turn sharply upward and run along
pregnancy and labor. the side of the uterus as arcuate artery (Fig. 1.19).
Before turning upward, they give off the descend-
The ovarian vessels ing cervical branches. The descending branch
The ovaries are supplied by ovarian vessels. The

ovarian arteries arise from the aorta just below
Box 1.23 Branches of the anterior division of
the renal vessels. They descend retroperitoneally, internal iliac artery
cross the ureter anteriorly, and enter the infun-
dibulopelvic ligaments. After supplying the ovary, • Parietal branches
Ŧ Obturator
they give off branches to supply the fallopian
Ŧ +PHGTKQTINWVGCN
tube and finally anastomose with the ascending
Ŧ Internal pudendal
branch of uterine artery near the uterine cornu in Inferior rectal
the broad ligament. The right ovarian vein drains Perineal
into the inferior vena cava but the left ovarian Dorsal artery of the clitoris
vein joins the left renal vein. • Visceral branches
Ŧ Superior vesical (umbilical)
Internal iliac (hypogastric) Ŧ Uterine
Ŧ 8CIKPCN
vessels Ŧ Middle vesical
Ŧ Middle rectal
The aorta bifurcates into common iliac arteries
Ŧ Inferior vesical
at the level of L4 vertebra. Common iliacs divide
CH 01_p001-023_v3.indd 18 17-07-2015 10:41:08

orta Changes in the blood

supply to pelvic organs
Common
iliac artery in pregnancy
The blood supply to the uterus increases man-
nternal ifold in pregnancy. The internal iliac, uterine,
iliac artery descending cervical, and arcuate arteries are
Posterior enlarged and dilated. In addition there is rich
ternal i ision collateral circulation.
iliac artery
nterior
i ision
Clinical implications of changes in the blood supply to
uperior esical
artery pelvic organs during pregnancyCTGIKXGPDGNQY
• The increase in blood supply is essential for placental
bturator artery DNQQF ƀQY CPF UWRRN[ QH QZ[IGP CPF PWVTKGPVU VQ VJG
Uterine artery fetus.
• .KICVKQPQHVJGXGUUGNUUWRRN[KPIVJGWVGTWUTGFWEGUVJG
Vaginal artery
RWNUG RTGUUWTG YKVJQWV ECWUKPI C XCUEWNCT EJCPIGU KP
Mi le rectal nferior gluteal VJGWVGTWU6JKUKUWUGFVQCTTGUVDNGGFKPIKPRQUVRCTVWO
artery artery JGOQTTJCIG
nferior esical
artery nternal Ŧ .KICVKQPQHKPVGTPCNKNKCECTVGT[
pu en al Ŧ .KICVKQPQHWVGTKPGCTVGT[CVVJGDCUGQHVJGDTQCF
artery
NKICOGPV
Figure 1.18 Internal iliac artery and its branches. Ŧ 5VGRYKUGFGXCUEWNCTK\CVKQP.KICVKQPQHVJGTCFKCNCT-
VGTKGUKPVJGDTQCFNKICOGPVCUVJG[GPVGTVJGWVGTWU
Ŧ .KICVKQPQHVJGCPCUVQOQUKPIXGUUGNUQHVJGWVGTKPG
and ovarian arteries at the uterine cornu
aria Blood supply to the vulva

artery
The vessels that supply the structures of the vulva
ccurate
artery
are as listed in Box 1.24. The internal pudendal
artery hooks around the ischial spine to enter
the pudendal (Alcock’s) canal in the lateral wall of
the ischiorectal fossa and reaches the perineum
(Fig. 1.20). Here it lies close to the pudendal nerve.
teri e artery Once the vessel enters the perineum, it gives rise
esce i
to several branches to supply the muscles of the
cer ical artery perineum, vestibular bulb, lower urethra, and
Figure 1.19 The uterine artery and its branches. The
uterine artery runs upwards lateral to the uterus as
CTEWCVGCTVGTKGUIKXGQHHDTCPEJGUECNNGFTCFKCNCTVGTKGU Box 1.24 Blood supply to the vulva
and anastomose with branches of the ovarian artery.
• Branches of the internal pudendal artery
Ŧ Inferior rectal artery
runs in the cardinal ligament to supply the cervix Ŧ Perineal arteries
and vagina. The arcuate arteries give off several Ŧ Urethral artery
branches to the uterus that run transversely, Ŧ Artery of the bulb
called radial arteries. The terminal part of the Ŧ Deep artery of the clitoris
Ŧ Dorsal artery of the clitoris
uterine artery ultimately anastomoses with the
• Branches of the femoral artery
ovarian vessels and gives off branches to supply
Ŧ External pudendal artery
the fallopian tube.
CH 01_p001-023_v3.indd 19 17-07-2015 10:41:08

Para aortic o es
o e at bi urcatio o aorta
Commo iliac o es
I ter al iliac o es
Pu en al
essels
xter al iliac o es
lcoc s
canal
acrospinous ligament
an coccygeus bturator o es
Figure 1.20 The course of pudendal artery. acral o es Parametrial o e
Figure 1.22 Lymph nodes of the pelvis that drain the
IGPKVCNQTICPU
orsal artery
o clitoris Nerve supply
The pelvis is supplied by somatic nerves and the
Peri eal autonomic nervous system (Fig. 1.23).
artery
I erior Somatic innervation

rectal artery
Somatic innervation of genital tract and perineum
is from T12 to S4 through the following nerves:
Figure 1.21 The course of perineal artery. • Lumbosacral trunk

• Obturator
• Pudendal
Clinical implications • Iliohypogastric
The pudendal vessels are in close proximity to the • Ilioinguinal
pudendal nerve as they hook round the ischial spine • Genitofemoral
VQGPVGTVJGRWFGPFCNECPCN6JGXGUUGNUECPIGVRWPE- • Posterior femoral cutaneous
VWTGFFWTKPIKPLGEVKQPQHNQECNCPGUVJGVKEKPVQVJGPGTXG
(pudendal block). The lumbosacral trunk, obturator, and puden-
dal nerves supply the muscles of the pelvis, glu-
teal region, thigh, obturator muscle, pelvic and
clitoris (Box 1.24; Fig. 1.21). In addition, external urogenital diaphragm, and perineal muscles.
pudendal artery arising from the femoral artery The sensory nerve supply to the mons pubis and
supplies the pubic area and labia majora. labia majora are from the ilioinguinal and geni-
tofemoral nerves. Perianal area, perineum, ves-
tibule of the vagina, and clitoris are supplied by
Lymphatic drainage the pudendal nerve.
Lymphatic drainage is usually along the veins

that drain the organs. There are groups of lymph
Autonomic innervation
nodes along all the major vessels—inguinal, exter- The autonomic nervous system controls the
nal, internal and common iliac, and para-aortic contraction and relaxation of the smooth mus-
(Fig. 1.22). cles of the uterus, bladder, rectum, and the
CH 01_p001-023_v3.indd 20 17-07-2015 10:41:09

pinal cor
Lumbar ple us
uperior
Parasympathetic fibers
hypogastric ple us
nferior
hypogastric ple us
Pel ic ple us
Figure 1.23 Autonomic innervations of the reproductive tract. The sympathetic nerves arise from T10–L2, form the superior
CPFKPHGTKQTJ[RQICUVTKERNGZWUGUVJG[CTGLQKPGFD[RCTCU[ORCVJGVKEſDGTUHTQO555VQHQTORGNXKERNGZWUGU
blood vessels. Sympathetic system stimulates the base of the broad ligament. Nerves from the
contraction and parasympathetic system causes pelvic plexus form the Frankenhauser’s plexus
relaxation. along the uterosacral and cardinal ligaments.
Sensory nerve fibers from the uterus, blad- These two plexuses together supply the uterus,
der, and rectum travel via the sympathetic and cervix, vagina, anus, rectum, and urinary blad-
parasympathetic fibers to reach the spinal cord der. Ovary is supplied by ovarian plexus which is
and cranial ganglia. They transmit visceral sen- derived from nerves from the renal plexus.
sations such as bladder and rectal distension, The afferent sensory fibers from uterus, cervix,
and pain of cervical stretching and uterine con- and vagina traverse through the Frankenhauser’s
tractions. Pain from the perineum, labia, clitoris, plexus, pelvic plexus, inferior and superior hypo-
and anus are transmitted through the pudendal gastric plexus, and finally the lumbar and tho-
nerve to spinal segments S2–S4. racic plexus to enter the spinal cord at T10–L2.
Sympathetic system Parasympathetic system

The sympathetic nerve supply arises from T10 The efferent parasympathetic nerve supply to
to L2. The sympathetic ganglia are located in the pelvis emerges along with the ventral rami
the lumbar and sacral regions. The lumbar sym- of S2–S4 as myelinated, preganglionic nerves
pathetic plexus lies along the aorta. This contin- and joins the sympathetic fibers from the
ues downward to form the superior hypogastric hypogastric plexus to form the pelvic plexuses
plexus. Nerves from this plexus descend to form (Box 1.25). As already mentioned, these pelvic
the inferior hypogastric plexus at the bifurcation plexuses have an inhibitory effect on rectum,
of the common iliac. As they continue downward, bladder, and erectile tissue of the clitoris and
they are joined by the parasympathetic fibers cause vasodilatation of the ovarian and uterine
from S2, S3, and S4 to form the pelvic plexuses at vessels.
CH 01_p001-023_v3.indd 21 17-07-2015 10:41:09

Box 1.25 Sensory pathway of the genital tract Clinical implications

• 7VGTWUEGTXKZCPFWRRGTXCIKPC Clinical implications of nerve supply to pelvisCTGIKXGP
Ŧ Frankenhauser’s plexus below.
Ŧ Pelvic plexus • Pain of uterine contractions felt at T12–L2 level.
Ŧ +PHGTKQTJ[RQICUVTKERNGZWU • 'RKFWTCNURKPCNCPCNIGUKCTGNKGXGURCKPQHEGTXKECNFKNCVC-
Ŧ 5WRGTKQTJ[RQICUVTKERNGZWU tion and uterine contraction.
Ŧ Lumbar plexus • 2WFGPFCNDNQEMRTQXKFGUCPCNIGUKCVQRGTKPGWONCDKC
Ŧ Spinal cord, T11–L2 CPFNQYGTXCIKPC
• .QYGTXCIKPCRGTKPGWONCDKCCPFENKVQTKU
Ŧ Pudendal nerve
Ŧ Spinal cord S2–S4
Key points
• The anterior abdominal wall consists of skin, subcuta- KTGEVKQPQHKVUſDGTURNC[COCLQTTQNGKPTQVCVKQPQHVJG
F
neous tissue, rectus sheath, muscles, and peritoneum. RTGUGPVKPIRCTVKPNCDQT
• The rectus sheath has no posterior layer below the • +PVGTPCNIGPKVCNQTICPUEQPUKUVQHVJGXCIKPCWVGTWU
arcuate line. fallopian tubes, and ovaries.
• Transverse incisions for cesarean section should be • There is increase in vascularity, bluish discoloration,
extended up to the lateral border of rectus muscles. CPFNQYGTKPIQHR*QHVJGXCIKPCKPRTGIPCPE[
• Blood supply to the abdominal wall is from branches • 6JGTGKUUQHVGPKPIQHEGTXKZKPRTGIPCPE[6JGOWEQWU
QHHGOQTCNCPFGZVGTPCNKNKCECTVGTKGU+PHGTKQTGRKICUVTKE RNWIVJCVKUHQTOGFFWTKPIRTGIPCPE[KUGZRGNNGFKPſTUV
vessels lie under the rectus muscles and must be iden- UVCIGQHNCDQT%GTXKZGHHCEGUCPFFKNCVGUKPNCDQTVQ
VKſGFENCORGFCPFNKICVGFFWTKPIVTCPUXGTUGKPEKUKQPU facilitate delivery of the fetus.
• The reproductive tract consists of external and internal • 6JGUK\GCPFUJCRGQHVJGWVGTWUEJCPIGOCTMGFN[
TGRTQFWEVKXGQTICPU KPRTGIPCPE[6JGO[QOGVTKWORNC[UCOCLQTTQNG
• 6JGGZVGTPCNTGRTQFWEVKXGQTICPUKPENWFGVJG KPEQPVTCEVKQPFWTKPIRCTVWTKVKQPCPFEQPVTCEVKQPCPF
structures of the vulva and perineum. TGVTCEVKQPCHVGTFGNKXGT[6JGNQYGTUGIOGPVQHVJG
uterus is formed in labor.
• 6JGXWNXCDGEQOGUUQHVKPRTGIPCPE[CPFXCTKEQUKVKGU
may develop. • Fertilization of the ovum takes place in the fallopian
tube and the fertilized ovum is then transported to the
• The anatomical perineum is a diamond-shaped area uterine cavity.
which extends from pubis to coccyx. This is divided
KPVQCPVGTKQTCPFRQUVGTKQTVTKCPINGUD[CPKOCIKPCT[ • 6JGQXCTKGUDGEQOGOQTGXCUEWNCTKPRTGIPCPE[
line between the two ischial tuberosities. They house the corpus luteum which provides the
JQTOQPCNUWRRQTVHQTVJGFGXGNQRKPIHGVWUVKNNYGGMU
• 6JGEQPVGPVUQHVJGCPVGTKQTVTKCPINGKPENWFGXWNXC QHIGUVCVKQPCNCIG
WTQIGPKVCNFKCRJTCIORGTKPGCNOWUENGUDNQQF
vessels, nerves, and lymphatics. • The pelvic ureter is closely related to the ovarian and
WVGTKPGXGUUGNUFWTKPIKVUEQWTUGKPVJGRGNXKU6JGTG
• Muscles of the perineum are separated by the perineal are several points where it is prone to injury. Care
OGODTCPGKPVQUWRGTſEKCNCPFFGGROWUENGU UJQWNFDGVCMGPVQCXQKFKPLWT[VQVJGWTGVGTFWTKPI
• Deep perineal muscles are the sphincter urethrae and RGNXKEUWTIGTKGU
deep transverse perinei muscles. They compress the • The lymphatics that drain the various parts of the
WTGVJTCCPFUWRRQTVVJGNQYGTXCIKPCTGURGEVKXGN[ IGPKVCNVTCEVNKGCNQPIVJGTGURGEVKXGDNQQFXGUUGNU
• 6JGEQPVGPVUQHVJGRQUVGTKQTVTKCPINGKPENWFGCPCN • The pelvic structures are supplied by somatic nerves and
ECPCNCPCNURJKPEVGTUCPQEQEE[IGCNDQF[KUEJKQTGE- autonomic nervous system. The sensory motor nerve
tal fossae, lymphatics, blood vessels, and nerves. UWRRN[KUVJTQWIJVJGNWODQUCETCNVTWPMRWFGPFCN
• 6JGRGTKPGCNDQF[KUCſDTQOWUEWNCTUVTWEVWTGVJCV KNKQKPIWKPCNCPFIGPKVQHGOQTCNPGTXGUHTQO6VQ5
forms the center point of the perineum. It stretches • 5GPUQT[RCKPſDGTUHTQOVJGWVGTWUCPFEGTXKZ
FWTKPIFGNKXGT[CPFOC[DGFCOCIGFKPRGTKPGCNVGCTU VTCXGTUGCNQPIVJGU[ORCVJGVKEPGTXGſDGTUVJTQWIJ
5WTIKECNKPEKUKQPQHVJGRGTKPGWOVQGPNCTIGVJGKPVTQK- VJGRGNXKEJ[RQICUVTKECPFNWODCTICPINKCVQLQKP
tus is known as episiotomy. the spinal cord at T11–L2 levels. Pain from lower
• 6JGRGNXKEFKCRJTCIOKUOCFGQHVJGVYQEQORQPGPVU IGPKVCNVTCEVKUVTCPUOKVVGFVQ5Ō5NGXGNUQHVJG
of levator ani. The shape of this muscle and the spinal cord.
CH 01_p001-023_v3.indd 22 17-07-2015 10:41:09

Self-Assessment
3. 6JGXCIKPCNOWEQUCOWUENGUQHVJGRGTKPGWOō
Case-based questions UWRGTſEKCNVTCPUXGTUGRGTKPGKDWNDQURQPIKQUWUFGGR
transverse perinei, and external anal sphincter—and
Case 1 anal mucosa.
/TU #- RTKOKITCXKFC YCU CFOKVVGF VQ NCDQT TQQO CV 4. This is from the perineal artery, a branch of internal
VGTO5GEQPFUVCIGYCURTQNQPIGFVJGTGHQTGDCD[YCUFG- pudendal artery.
livered by forceps under pudendal block. There was a fourth
FGITGG RGTKPGCN NCEGTCVKQP %QPUWNVCPV QDUVGVTKEKCP YCU
called in to perform an accurate anatomical perineal repair. Case 2
1. 9JCVKURWFGPFCNDNQEM!9JGTGKUKVIKXGP! 1. 6JGDNGGFKPIKUHTQOVJGWVGTKPGCTVGT[YJKEJ
2. 9JGTGFQVJGUGPUQT[ſDGTUCNQPIVJGRWFGPFCN turns medially at the level of the internal os and
nerve enter the spinal cord? CUEGPFUDGVYGGPVJGNC[GTUQHVJGDTQCFNKICOGPV
CPFNKGUENQUGVQVJGNCVGTCNCPINGQHVJGWVGTKPG
3. 9JCVCTGVJGUVTWEVWTGUKPXQNXGFKPHQWTVJFGITGG
incision.
perineal tear?
2. $[NKICVKPIVJGWVGTKPGCTVGT[VCMKPIECTGPQVVQKPLWTG
4. What is the blood supply to the perineum?
the ureter which lies close to the vessel.
3. .KICVKQPQHVJGKPVGTPCNKNKCECTVGT[HTQOYJGTGVJG
Case 2 uterine artery arises.
4. Parietal branches are obturator and internal pudendal
/TU#0OWNVKITCXKFCYCUFGNKXGTGFD[EGUCTGCPUGEVKQP arteries. Visceral branches are superior vesical,
(QNNQYKPI VJG FGNKXGT[ VJGTG YCU RTQHWUG DNGGFKPI HTQO WVGTKPGXCIKPCNOKFFNGTGEVCNCPFOKFFNGCPFKPHGTKQT
VJGCPINGUQHVJGWVGTKPGKPEKUKQP vesical arteries.
1. 9JCVECWUGURTQHWUGDNGGFKPIHTQOVJGCPINGUQHVJG
uterine incision?
2. *QYYKNN[QWOCPCIGVJKU! Sample questions
3. +HVJGDNGGFKPIXGUUGNECPPQVDGENCORGFFWGVQRQQT
visibility, what is the next step? Long-answer questions
4. What are the branches of the internal iliac artery? 1. Describe the course of the pelvic ureter. What is its
UKIPKſECPEGKPQDUVGVTKEU!
2. &KUEWUUVJGCPCVQO[QHKPVGTPCNTGRTQFWEVKXGQTICPU
Answers CPFVJGEJCPIGUKPRTGIPCPE[
Case 1
Short-answer questions
1. Pudendal block is the injection of local anesthetic
CIGPVKPVQCPFCTQWPFVJGRWFGPFCNPGTXG6JKUKU 1. Perineal body
IKXGPCVVJGRQKPVYJGTGVJGRWFGPFCNPGTXGEWTXGU 2. Levator ani
round the ischial spine before it enters the pudendal 3. Anatomy of the internal iliac artery
canal in the ischiorectal fossa. 4. +PVGTPCNKNKCECTVGT[NKICVKQP
2. At S2–S4 level. 5. Innervation of the reproductive tract
CH 01_p001-023_v3.indd 23 17-07-2015 10:41:09

Anatomy of the
2 Bony Pelvis and
Fetal Skull
Case scenario
Mrs BN, a second gravida at 39 weeks of pregnancy, was admitted to

labor room with pains. She had gone to a local hospital for delivery but
was told that the passage was inadequate for the baby and was referred
to a tertiary care center. On abdominal examination, contractions were
every 5 minutes lasting for 40 seconds. On vaginal examination, cervix
was 5-cm dilated and the pelvic shape was abnormal. The husband
was informed that delivery had to be by cesarean section.
Introduction pelvis and negotiate its diameters at various lev-

els before it is born. The pelvis is made of sacrum,
The anatomy of female pelvis is of special impor- coccyx, ilium, ischium, and pubis. The latter
tance in obstetrics since the fetus has to pass three are fused together to form the innominate
through this before being born. Its shape, size, bone. The ischium is joined to sacrum at the two
and configuration can affect the course of labor. sacroiliac joints and the pubic bones are joined
The fetal skull and its diameters are equally to each other at the pubic symphysis (Fig. 2.1).
important. The obstetrician must be aware of the The bony pelvis is divided into true and false
normal anatomy and its variations for appropri- pelvis by an oblique plane passing through the
ate management of normal labor and diagnosis sacral promontory, arcuate line, pectineal line,
and management of abnormal labor. pubic crest, and pubic symphysis. This plane is
called the linea terminalis or pelvic brim (Fig. 2.1).
The bony pelvis False (greater) pelvis

The bony pelvis is of great importance in obstet- This lies above the linea terminalis and is
rics since the fetus has to pass through the bounded by the lumbar vertebrae posteriorly,
CH 02_p024-034_v5.indd 24 16-07-2015 15:05:13

Anatomy of the Bony Pelvis and Fetal Skull 25
acroiliac oint
lium
acrum
cm
Linea terminalis cm
cm
cm
Pubis
schium
Pubic symphysis
Figure 2.1 Bones and joints of the bony pelvis and the
linea terminalis. Anterior view of the pelvis showing bones
of the pelvis and the two joints—sacroiliac joint and pubic Figure 2.2 Diameters of the pelvic inlet. The three
symphysis. Linea terminalis or pelvic brim is marked important diameters of the inlet are anteroposterior,
in green. transverse, and oblique diameters.
Box 2.1 Plane of the pelvic inlet

iliac fossae laterally, and abdominal wall ante-
riorly. This part of the pelvis is not of obstetric Boundaries
importance. • Posterior: Sacral promontory, sacral alae
• Lateral: Pectineal and arcuate lines
• Anterior: Pubic ramus and pubic symphysis
The true (lesser) pelvis Shape
This part of the bony pelvis is of great impor- • Round

tance in obstetrics. This is bounded posteriorly Diameters
by sacrum, laterally by ischium and sacrosciatic • Anteroposterior
notches, and anteriorly by pubic bones, obtura- Ŧ True conjugate: 11 cm
tor foramen, and ischiopubic rami. True pelvis is Ŧ Obstetrical conjugate: 10 cm
divided into four planes. Ŧ Diagonal conjugate: 12 cm
• Transverse: 13.5 cm
• Plane of the pelvic inlet • Oblique: 12.5 cm
• Plane of the pelvic outlet
• Pelvic cavity—between the inlet and the out-
let. It has two planes:
– Plane of least pelvic dimensions acral promo try
– Plane of greatest pelvic dimensions rue
co
u
ate
Plane of the pelvic inlet ia

o bs
al tet
co ric
Essential features of the plane of the pelvic inlet co
u u
at ate
are given in Box 2.1 and Figure 2.2. e
Pubic
The transverse and oblique diameters are symphysis
larger than the anteroposterior diameter. The
transverse diameter lies 4 cm anterior to the
sacral promontory. The oblique diameter is mea-
sured from the sacroiliac joint to the iliopectin-
eal eminence. The right and left oblique diam- Figure 2.3 Anteroposterior diameters of the plane of
eters extend from the right and left sacroiliac pelvic inlet. The three anteroposterior diameters extend
joints respectively. There are three anteroposte- from sacral promontory to three different points on
rior diameters (Fig. 2.3). the pubis.
CH 02_p024-034_v5.indd 25 16-07-2015 15:05:14

Anatomical (true) conjugate Box 2.2 Features of the plane of the pelvic
This is the distance from the sacral promon- outlet
tory to the upper border of pubic symphysis. It Boundaries
is referred to as the anteroposterior diameter of
• Posterior: Tip of sacrum
the pelvic inlet and is usually 11 cm.
• Lateral: Sacrosciatic ligaments, ischial tuberosities
• Anterior: Subpubic arch, ischiopubic rami
Obstetric conjugate
Shape
This is the distance between the sacral promon-
• Diamond shaped
tory and the most prominent point on the poste-
• Two triangles with common base
rior surface of the pubic bone. It is the diameter
• Separated by a line joining ischial tuberosities
that the fetal head has to negotiate and is the
shortest diameter at the inlet (10 cm). This diam- Diameters
eter is obtained by subtracting 1.5–2 cm from the • Anteroposterior: 12 cm
diagonal conjugate. • Transverse: 10.5 cm
• Posterior sagittal: 7.5 cm
Diagonal conjugate
This is the anteroposterior diameter that can be the sacrum (Fig. 2.5). This is the largest diameter
clinically measured. It is the distance between of the outlet. Transverse diameter runs between
the sacral promontory and the inferior border of the ischial tuberosities. Posterior sagittal diam-
the pubic symphysis (12 cm). This is measured eter is the part of the anteroposterior diameter
by inserting the index and middle fingers into that lies posterior to the line joining the ischial
the vagina, tipping the sacral promontory with tuberosities. This diameter compensates for a
the middle finger, and marking off the point of narrow subpubic angle which pushes the fetal
contact on the radial border of the hand with the head posteriorly. All diameters of the outlet can
inferior border of pubic symphysis (Fig. 2.4). be measured clinically.
Pelvic cavity
This is the part of the pelvis between the inlet
Subpubic and outlet. It is shaped like a truncated cylinder
angle (Box 2.3; Fig. 2.6). The anterior wall is shallow
and is formed by the pubic bone; the posterior
wall is deep and concave and is formed by the
sacrum.
ubpubic angle
Sacral
promontry nteroposterior
iameter cm
schial tuberosity
Figure 2.4 Measurement of diagonal conjugate. The rans erse
diagonal conjugate is the distance between the tip of the iameter cm
OKFFNGſPIGTYJKEJVQWEJGUVJGUCETCNRTQOQPVQT[CPFVJG Posterior sagittal
iameter cm
point of contact with the undersurface of pubic symphysis,
on the radial border of hand.
ip of sacrum
Plane of the pelvic outlet
Figure 2.5 Diameters of the pelvic outlet. The important
The features of pelvic outlet are given in Box 2.2 diameters of the pelvic outlet are anteroposterior,
and Fig. 2.5. transverse, and posterior sagittal diameters. The posterior
The anteroposterior diameter of the plane of sagittal diameter is that part of the anteroposterior
pelvic outlet is from subpubic angle to the tip of diameter that lies posterior to the transverse diameter.
CH 02_p024-034_v5.indd 26 16-07-2015 15:05:14

Box 2.3 Features of the pelvic cavity

• Shape: Truncated cylinder
• Plane of greatest pelvic dimensions Pla e o
Ŧ At the level of second and third piece of sacrum least pel ic
Ŧ 0QVQHQDUVGVTKEUKIPKſECPEG ime sio s
• Plane of least pelvic dimensions
Ŧ At the level of
ischial spines u ctio o
fourth and fifth piece of sacrum th th
Ŧ Interischial diameter sacral
Measures 10 cm ertebrae
Smallest diameter of the pelvis Ischial spi e
Of great obstetric significance
Figure 2.7 Plane of least pelvic dimensions. The plane of
least pelvic dimensions is at the level of ischial spines and
the 4th and 5th sacral vertebrae.
alse pel is
engaging diameter in the transverse or oblique

Pel ic inlet
diameter of the inlet and has to rotate through 90
degrees or more to bring the engaging diameter
to the anteroposterior diameter at the outlet for
normal delivery to occur. This is achieved through
the cardinal movements of labor (see Chapter 14,
Normal labor: Mechanics, mechanism, and stages).
Pel ic outlet
The diameters of the pelvis are summarized
in Box 2.4.
Figure 2.6 Pelvic cavity: Lateral view.
The axis of the pelvis
Plane of greatest pelvic dimensions The axis of the pelvis is downward and backward
This part of the cavity is roomy and has the larg- in the upper half and downward and forward
est dimensions. It is at the level of the second in the lower half. The anatomical axis is repre-
and third sacral vertebrae posteriorly and poste- sented by the curve of Carus, which is a line join-
rior surface of the pubis anteriorly. The antero- ing the midpoints of the anteroposterior diame-
posterior diameter is 12.5 cm and transverse ters at the inlet, outlet, and cavity. The shape of
diameter is 13 cm. This plane has no obstetric
significance.
Box 2. 4 Diameters of the pelvis
• Inlet
Plane of least pelvic dimensions Ŧ Anteroposterior
Anatomical conjugate: 11 cm
As the name implies, this is the plane of smallest
Obstetric conjugate: 10 cm
diameters. It is at the level of ischial spines and Diagonal conjugate: 12 cm
the fourth and fifth sacral vertebrae. The interi- Ŧ Transverse: 13.5 cm
schial spinous diameter (transverse diameter) is Ŧ Oblique: 13 cm
the smallest diameter that the fetal head has to • Outlet
pass through (10 cm) (Fig. 2.7). The anteropos- Ŧ Anteroposterior: 12 cm
terior diameter is 11.5 cm and posterior sagittal Ŧ Transverse: 10.5 cm
diameter is 5 cm. Ŧ Posterior sagittal: 7.5 cm
It should be noted that the transverse diam- • Plane of least pelvic dimensions
eter is the widest at the inlet and the anteropos- Ŧ Anteroposterior: 11.5 cm
terior diameter is the widest at the outlet. Hence, Ŧ Transverse: 10 cm
Ŧ Posterior sagittal: 5 cm
the fetal head normally enters the pelvis with the
CH 02_p024-034_v5.indd 27 16-07-2015 15:05:15

the curve corresponds to the sacral curvature. Changes in pelvis during

The obstetric axis is, however, slightly differ-
ent. The presenting part moves downward and pregnancy
backward initially and turns abruptly forward at Pelvic joints relax due to the hormones of preg-
ischial spines (Fig. 2.8). nancy. There is an increase in the width of the
pubic symphysis. The mobility of the sacroil-
Waste space of Morris iac joints also increases, especially in lithot-
omy position. This results in an increase in the
While the head is being delivered, it passes
anteroposterior diameter at the brim.
through the pelvic outlet between the ischiopu-
bic rami, behind the subpubic angle. The space
between the subpubic angle and the circumfer- Clinical implications
ence of the fetal head is normally <1 cm. When The clinical implications of anatomy of pelvis and
the subpubic angle is narrow as in an android changes in pelvis during pregnancy are given below.
pelvis, the head emerges more posteriorly, • The transverse diameter is more at the pelvic inlet;
increasing the space to >1 cm. This is the waste therefore, the fetal head engages in the transverse
space of Morris (Fig. 2.9). This has to be compen- diameter.
sated by an adequate posterior sagittal diameter • The anteroposterior diameter is more at the outlet;
for the head to deliver. A liberal episiotomy is therefore, the fetal head has to rotate through 90° to
achieve delivery.
necessary in this situation to avoid deep perineal
• The interspinous diameter is the smallest. Malrota-
lacerations. tion, nonrotation, and arrest of descent occur at this
level.
• The direction of descent of the fetal head is along the
axis of the pelvis. This must be followed in instrumen-
tal deliveries.
• Relaxation of the pelvic joints increases the diameter
of the pelvis and helps in descent of the fetal head
Po Cur e of Carus
f in
let anatomical a is and delivery.
• Relaxation of pubic symphysis causes pain in the
P of
mi
bstetric a is pubic region.
pel
is cm • Backache is common in pregnancy and is partly due
cm
to the relaxation of sacroiliac joints
P of outlet cm
Pelvic shapes
Figure 2.8 The anatomical and obstetric axis of the Pelvic shape can influence fetal presentation,
pelvis. position and course of labor. Maternal body struc-
ture, nutritional status, and deformities of the
Pubic symphysis spine and hip can affect pelvic shape. However,
aste space
four parent types of pelvis have been described.
o orris
%CNFYGNNŌ/QNQ[ENCUUKſECVKQP
etal hea
Caldwell and Moloy have classified pelves into
Ischial tuberosity four types, based on the shape, transverse diam-
eter of the inlet, and character of the anterior and
posterior segments of the pelvis. The four types
of pelvis and their percentage of occurrence in
acrum women are as follows (Fig. 2.10):
Figure 2.9 Waste space of Morris. This is the space • Gynecoid (typical female): 50%
between the fetal head and subpubic angle. • Android (typical male): 20%
CH 02_p024-034_v5.indd 28 16-07-2015 15:05:15

a. .
b. .
Figure 2.10 Types of pelvis. a. Gynecoid. b. Android. c. Anthropoid. d. Platypelloid. The four types of pelvis according to
EQPſIWTCVKQP
%CNFYGNNŌ/QNQ[ENCUUKſECVKQPCTGFKCITCOOCVKECNN[TGRTGUGPVGF
• Anthropoid (oval): 25% transverse diameter of the outlet is less than nor-
• Platypelloid (flat): 5% mal. The fetal head engages in occipitoposterior
position and does not rotate beyond the ischial
The gynecoid pelvis spines, leading to deep transverse arrest and
obstructed labor.
Gynecoid pelvis is the typical female pelvis and
is most favorable for normal labor and delivery.
The anthropoid pelvis
The inlet is round, the sacral promontory is not
prominent, sacrum is concave and well curved, The anthropoid pelvis is anteroposteriorly oval;
the sacrosciatic notch is wide and admits two therefore, anteroposterior diameters are more
fingers, pelvic sidewalls are straight and parallel, than the transverse diameters at all levels. The
the forepelvis is wide and rounded, ischial spines sacral promontory is not prominent, sacrum is
are not prominent, subpubic angle is wide and curved, sacrosciatic notch is wide and deep, side
>90 degrees, and interischial tuberous diameter walls are straight, forepelvis is wide, ischial spines
is adequate and admits four knuckles. Fetal head are not prominent, subpubic arch is medium
engages in transverse diameter, cardinal move- (about 90 degrees), and transverse diameter of
ments take place, vertex rotates anteriorly and is the outlet is average. The fetal head engages as
delivered by extension. occipitoposterior, short posterior rotation takes
place (since anterior rotation is difficult with
The android pelvis a slightly reduced interspinous diameter), and
head delivers as face to pubis.
Android pelvis is the typical male pelvis. The
inlet is heart shaped due to the prominent sacral
The platypelloid pelvis
promontory, the sacrum is flat, the sacrosciatic
notch is narrow and does not admit two fingers, The platypelloid or flat pelvis is the least common
pelvic sidewalls converge downward, forepelvis type of pelvis and is transversely oval. The trans-
is narrow and beaked, ischial spines are prom- verse diameters are more than the anteroposte-
inent making the transverse diameter smaller, rior diameter at all levels. The sacral promon-
subpubic angle is narrow and <80 degrees, and tory is prominent, reducing the anteroposterior
CH 02_p024-034_v5.indd 29 16-07-2015 15:05:15

Table 2.1 Distinctive features of the four types of pelves
Gynecoid Android Anthropoid Platypelloid

Shape Rounded Heart shaped Anteroposteriorly oval Transversely oval
Inlet
6TCPUXGTUG&
EO 13.5 <12 <12 13.5
#PVGTQRQUVGTKQT&
EO 11 11 >12 10
Forepelvis Wide 0CTTQY
DGCMGF Straight Divergent
Cavity
Sidewalls Straight and parallel %QPXGTIGPV Straight Straight and wide
Sacrosciatic notch Wide Narrow Wide Short
Ischial spines Not prominent Prominent Not prominent Not prominent
Outlet
Subpubic arch Wide Narrow Medium Wide
6TCPUXGTUG&
EO 10.5 <10 10.5 >10.5
diameter at the brim. Sacrum is flat, sacrosciatic Fetal skull

notch is wide and shallow, sidewalls are straight,
forepelvis is wide and rounded, ischial spines are The fetal skull consists of several bones joined
not prominent, subpubic angle is wide and >90 at the sutures. The bones of the face are joined
degrees, and transverse diameter of the outlet is together firmly while those of the vault of the
also wide. The narrow anteroposterior diameter skull are joined at sutures that are soft and mem-
at the brim acts as the fulcrum at the fetal bipa- branous. The bones of the vault are as follows:
rietal diameter and the head undergoes exten-
sion and face presentation results. Alternatively, • Two frontal bones
asynclitic engagement takes place so that the • Two parietal bones
biparietal diameter can negotiate the anteropos- • Two temporal bones
terior diameter. • One occipital bone
Pelves may have mixed characteristics as well The two frontal bones are joined to each other
and classification into a distinct type may be at the frontal suture and attached to the parietal
difficult. bones at the coronal suture. The parietal bones
The distinctive features of the four types of meet at the sagittal suture (parietoparietal suture)
pelves are listed in Table 2.1. and they are attached to the occipital bone at the
lambdoid suture (occipitoparietal) (Fig. 2.11).
%NKPKECNKORNKECVKQPUQHthe shape and type of pelvis on
labor are given below.
• The gynecoid pelvis is the most favorable—the ver- rontal agittal
tex engages in the transverse or oblique diameter suture suture
and labor progresses normally. nterior Posterior
• The android pelvis is the least favorable. Occipi- fontanel fontanel
toposterior positions and deep transverse arrest are
Coronal Lamb oi
common with this type. suture suture
• The anthropoid pelvis favors occipitoposterior posi-
tion and face-to-pubis delivery.
• Asynclitic engagement and face presentations are Figure 2.11 5WVWTGUQHHGVCNUMWNNCPFHQPVCPGNU%QTQPCN
VJGRTQDNGOUGPEQWPVGTGFKPRNCV[RGNNQKFRGNXKU
see sagittal, lambdoid and frontal sutures and anterior and
%JCRVGT Abnormal labor: Abnormalities in pas-
posterior fontanels are seen in the superior view of the
sage and powers
fetal skull.
CH 02_p024-034_v5.indd 30 16-07-2015 15:05:16

This allows sliding of bones under each other,

Box 2. 5 Features of the two fontanels
thus reducing the diameters of the skull. This is
Anterior fontanel or bregma known as molding (see Chapter 14, Normal labor:
• Diamond shaped Mechanics, mechanism, and stages). The two fon-
• Junction of tanels are described in Box 2.5.
Ŧ coronal suture
Ŧ sagittal suture
Ŧ frontal suture
• Four sutures radiate from the fontanel Landmarks of the fetal skull
• (GNVGCUKN[KHVJGJGCFKUFGƀGZGFQTGZVGPFGF
Practice of obstetrics and management of labor
Posterior fontanel or lambda
is not possible without a thorough understand-
• Triangular ing of the landmarks of the fetal skull (Fig. 2.12).
• Junction of These are listed in Box 2.6.
Ŧ sagittal suture
Ŧ lambdoid suture
• Three sutures radiate from the fontanel
• (GNVGCUKN[YJGPVJGJGCFKUƀGZGF Diameters of the fetal skull
• Used to identify position of the vertex
The diameters of the fetal skull are listed in
Two fontanels are formed at the junction of Box 2.7 and shown in Figure 2.13. There are four
the various sutures. These are areas covered by anteroposterior or engaging diameters and three
membranes, as the sutures are not firmly united. transverse diameters.
Parietal eminence
Verte
nterior fontanel Posterior fontanel
iparietal iameter
a. Parietal eminence
Ve
rte
ro
inciput
labella
cciput
ace
b. Mentum
Figure 2.12 Landmarks of the fetal skull. a. Vertex and biparietal diameter. Vertex is the diamond-shaped area bounded
by anterior and posterior fontanels and two parietal eminences. b.1VJGTNCPFOCTMUKPENWFGVJTGGDQP[RQKPVU
QEEKRWV
UKPEKRWVCPFOGPVWOCPFVJTGGCTGCU
HCEGDTQYCPFXGTVGZ
CH 02_p024-034_v5.indd 31 16-07-2015 15:05:16

ubmentobregmatic face
Box 2.6 Landmarks of the fetal skull
• Vertex: Diamond-shaped area Verticomental bro
Ŧ Boundaries
cm
cm
Anterior: Anterior fontanel
Posterior: Posterior fontanel
Lateral: Parietal eminences cm ccipitofrontal
• (CEG%JKPVQINCDGNNC erte military
• Brow: From anterior fontanel to orbital ridges
cm
• Glabella: Between the orbital ridges
• Occiput: Prominent area behind and below the uboccipitobregmatic
posterior fontanel erte fle e
• Sinciput: Prominent part of the frontal bone above
glabella
• /GPVWO%JKP Figure 2.13 The anteroposterior diameters of fetal skull.
Box 2.8 Terminology in obstetrics

Box 2.7 Diameters of the fetal skull
• 2TGUGPVKPI RCTV 2CTV VJCV KU ſTUV HGNV QP XCIKPCN
• 5WDQEEKRKVQDTGIOCVKE
EO (TQO C RQKPV DGNQY examination.
occiput where it meets the neck to the center of ante- Ŧ Vertex
TKQTHQPVCPGN
DTGIOC Ŧ Brow
• 1EEKRKVQHTQPVCN
EO(TQOQEEKRKVCNRTQVWDGTCPEG Ŧ Face
to glabella • #VVKVWFG &GITGG QH ƀGZKQP QT GZVGPUKQP QH VJG HGVCN
• 8GTVKEQOGPVCN
EO(TQOOKFRQKPVQHXGTVGZVQ neck
EJKP
OGPVWO Ŧ %QORNGVGƀGZKQP8GTVGZ
• 5WDOGPVQDTGIOCVKE
EO (TQO C RQKPV YJGTG Ŧ &GƀGZKQP1EEKRKVQRQUVGTKQT
neck meets lower jaw to the center of anterior fonta-
Ŧ Partial extension: Brow
PGN
DTGIOC
Ŧ %QORNGVGGZVGPUKQP(CEG
• $KRCTKGVCN
EO (TQO QPG RCTKGVCN GOKPGPEG VQ
the other • Denominator: Bony point on the presenting part for
the particular presentation
• $KVGORQTCN
EO (TQO QPG VGORQTCN DQPG VQ VJG
other Ŧ Used as reference point
• 5WDRCTKGVQŌUWRTCRCTKGVCN
EO (TQO C RQKPV Occiput
above one parietal eminence to a point below the Mentum
other parietal eminence. Frontum
• Position: Relationship of the denominator to the pel-
vic quadrants
Ŧ Left anterior /posterior
Ŧ Right anterior/posterior
Terminology used in
obstetrics Clinical implications
The clinical implications of landmarks and diameters of
These are summarized in Box 2.8. fetal skull are given below.
The cephalic presentations, fetal attitudes,
• 6JGUWVWTGUCPFHQPVCPGNUCTGWUGFHQTVJGKFGPVKſEC-
engaging diameters, and denominators are sum- tion of presentation and position of the fetus.
marized in Table 2.2. • The engaging diameter is an important factor that
determines the progress of labor.
Table 2.2 Cephalic presentations, engaging diameters, attitudes, and denominators
Presentation Attitude Engaging diameter (cm) Denominator

Vertex %QORNGVGƀGZKQP 5WDQEEKRKVQDTGIOCVKE
Occiput
Face %QORNGVGGZVGPUKQP 5WDOGPVQDTGIOCVKE
Mentum
Brow Partial extension 8GTVKEQOGPVCN
Frontum
1EEKRKVQRQUVGTKQT
RQUKVKQP &GƀGZKQP 1EEKRKVQHTQPVCN
Occiput
CH 02_p024-034_v5.indd 32 16-07-2015 15:05:16

Key points
• The bony pelvis is made of sacrum, coccyx, ilium, • #EEQTFKPIVQ%CNFYGNNŌ/QNQ[ENCUUKſECVKQPVJGTGCTG
ischium, and pubis joined together by two sacroiliac four types of pelves: gynecoid, android, anthropoid,
joints and pubic symphysis. and platypelloid.
• The bony pelvis is divided into a false pelvis above • The gynecoid pelvis is the typical female pelvis and
and true pelvis below. The false pelvis is not of any is most favorable for the cardinal movements of labor
QDUVGVTKEUKIPKſECPEG and normal delivery.
• The true pelvis has an inlet, cavity, and outlet. The • Android pelvis is the typical male pelvis and has nar-
cavity has two planes: the plane of greatest pelvic row interischial spinous diameter and forepelvis. Deep
dimensions and the plane of least pelvic dimensions. transverse arrest is common in this type of pelvis.
• The transverse diameter of the inlet is greater than • The anthropoid pelvis is longitudinally oval and favors
the anteroposterior diameter; therefore, the fetal head occipitoposterior position and face-to-pubis delivery.
engages in the transverse diameter of the inlet.
• The platypelloid pelvis is transversely oval and favors
• There are three anteroposterior diameters at the inlet: face presentation and asynclitic engagement.
the anatomical, obstetric, and diagonal conjugates.
• The fetal head is made of face and vault. The bones
The diagonal conjugate can be measured clinically
of the vault of skull are frontal, parietal, temporal, and
and obstetric conjugate can be deduced from this.
occipital.
• The pelvic outlet is diamond shaped and divided into
• The sutures of the skull are coronal, sagittal, and
anterior and posterior triangles by a line joining the
lambdoid.
ischial tuberosities.
• There are two fontanels: anterior and posterior. They
• The anteroposterior diameter is greater than the trans-
CTGWUGFHQTVJGKFGPVKſECVKQPQHVJGRQUKVKQPQHXGTVGZ
verse diameter; therefore, the fetal head has to rotate
in labor.
by 90 degrees for delivery to occur.
• Vertex is the diamond-shaped area bounded by anteri-
• The plane of the greatest pelvic dimensions is of no
or and posterior fontanels and two parietal eminences.
QDUVGVTKEUKIPKſECPEG
• Bony points of the skull used as landmarks are
• The interischial spinous diameter at the plane of the least
occiput, sinciput, face, brow, mentum and glabella.
pelvic dimensions is the smallest diameter of the pelvis.
• #VVKVWFGQHVJGHGVCNJGCFKUVJGFGITGGQHƀGZKQPCVVJG
• The axis of the pelvis is the line joining the midpoint of
HGVCNPGEM6JGRTGUGPVCVKQPFGRGPFUQPƀGZKQPCPF
the anteroposterior diameters at all levels. It is curved
extension of the head.
with its concavity facing anteriorly and is called the
curve of Carus. • The diameters of engagement also vary with the
FGITGGQHƀGZKQPQTGZVGPUKQP
Self-Assessment
Case-based questions Case 2
A multigravida, at term, was admitted in labor. She had
Case 1 TGIWNCTWVGTKPGEQPVTCEVKQPUGXGT[ŌOKPWVGU6JGJGCF
A second gravida at 39 weeks of pregnancy was admit- YCUHQWTſHVJRCNRCDNGUKPEKRWVYCUCVCNQYGTNGXGNVJCP
ted to labor room with pains. On abdominal examination, occiput. On pelvic examination, the anterior fontanel was
contractions were every 5 minutes lasting for 40 seconds. easily felt.
On vaginal examination, cervix was 5-cm dilated and the 1. What is the presentation likely to be? What other
pelvic shape was abnormal. RCTVUQHVJGJGCFUJQWNFDGKFGPVKſGF!
1. What are the four major types of pelves? 2. What is the attitude of the head and engaging
2. What problems do you expect with android pelvis and diameter?
why? 3. If the head was fully extended what would the
3. What is ‘waste space of Morris’? In which type of presentation be? What is the engaging diameter?
pelvis is this seen and why? 4. What is “denominator”? What are the denominators in
4. Why is asynclitic engagement common in platypelloid vertex and face presentations?
pelvis?
CH 02_p024-034_v5.indd 33 16-07-2015 15:05:16

2. Attitude is incomplete extension. Engaging diameter

Answers is verticomental.
3. When the head is completely extended, the presen-
Case 1 tation is face. The engaging diameter is submento-
1. Gynecoid, android, anthropoid and platypelloid. bregmatic.
2. The following problems can be expected: 4. The denominator is a reference point on the present-
a. Occiput posterior position:The bulky occiput occu- ing part used to identify position. It is occiput in vertex
pies the broader posterior part of the pelvis since and mentum in face presentations.
the forepelvis is narrow.
b. &GGRVTCPUXGTUGCTTGUV+PVGTPCNTQVCVKQPKUFKHſEWNV
since the interischial spinous diameter is narrow. Sample questions
c. Obstructed labor:Due to cephalopelvic dispropor-
tion and deep transverse arrest. Long-answer questions
3. The space between subpubic angle and the circum- 1. &KUEWUUVJGENCUUKſECVKQPQHRGNXGUVJGKTUCNKGPV
ference of the fetal head is the waste space of Morris. HGCVWTGUCPFVJGKTKPƀWGPEGQPNCDQT
This space is more in android pelvis because the
head emerges more posteriorly due to the narrow
subpubic angle. Short-answer questions
4. The anteroposterior diameter at the inlet is less in
platypelloid pelvis and the biparietal diameter cannot 1. Sagittal suture
negotiate this. The head tilts to one side bringing the 2. Diagonal conjugate
UWDRCTKGVQŌUWRTCRCTKGVCNFKCOGVGTVQPGIQVKCVGVJG 3. Diameters of the fetal skull
anteroposterior diameter of the pelvis. 4. The fontanelles of the fetal skull
5. Anthropoid pelvis
6. Waste space of Morris
Case 2
1. When the sinciput is lower than the occiput, the head
is extended. When anterior fontanel is easily felt with
an extended head, the presentation is brow. The
frontal bones and orbital ridges should also be felt to
EQPſTODTQYRTGUGPVCVKQP
CH 02_p024-034_v5.indd 34 16-07-2015 15:05:16

Maternal Physiology
3 in Pregnancy
Case scenario
Mrs. KT, 20, a primigravida at 32 weeks of pregnancy, came to the clinic

for routine antenatal checkup. She was quite troubled by minor but
multiple problems such as pedal edema, which was obvious by evening,
constipation, backache, and breathlessness on walking. She wanted
to know if these would affect her pregnancy and labor. Her husband,
a 25-year-old software engineer, was equally concerned and needed
reassurance.
Introduction of maternal physiology in pregnancy. A knowl-

edge and understanding of the changes during
Extensive anatomic, physiological, and bio- pregnancy is, therefore, absolutely essential for
chemical changes occur in the mother during management of normal pregnancy and recog-
pregnancy. These are intended to prepare the nition of abnormality.
mother to meet the demands of pregnancy,
labor, and puerperium and to protect the
fetus. Some of these changes give rise to symp-
toms which can be troublesome. Many of the
Changes in body water
changes are brought about by the physiological and electrolytes
hormonal changes of pregnancy. All the organ
systems return to prepregnancy state after Retention of sodium and water due to the
delivery and lactation. The process takes about increased levels of progesterone during pregnancy
6 weeks. Some of these changes would be con- leads to an increase in total body water (volume
sidered abnormal in the nonpregnant state and overload). Total body water increases by 6–8 L
may be interpreted as disease if one is not aware which is distributed as shown in Box 3.1.
CH 03_p035-047_v3.indd 35 17-07-2015 10:42:54

blood volume, through stimulation of barore-

Box 3.1 Distribution of additional body water in
pregnancy ceptors and volume receptors, leads to increased
secretion of arginine-vasopressin by posterior
• Maternal blood volume: 1500–1600 mL pituitary and this contributes to the fall in osmo-
Ŧ Plasma volume: 1200–1300 mL
lality. Further, thirst is experienced at a lower
Ŧ Red cell volume: 300–400 mL
osmolality than in the nonpregnant state, lead-
• Uterus and breasts:
• 'ZVTCXCUEWNCTƀWKF
ing to increased water consumption.
1500–2500 mL Sodium is an important determinant of body
• +PVTCXCUEWNCTƀWKF
• Adipose tissue: water. During pregnancy, sodium balance is
• (GVWURNCEGPVCCPFCOPKQVKEƀWKFO. maintained by factors that increase sodium lev-
els and those that decrease the levels. Despite
additional retention of sodium, water reten-
Box 3.2 Factors contributing to increase
tion exceeds sodium retention, resulting in fall
in body water in pregnancy in serum sodium levels by 3–4 mmol/L. Factors
that alter renal tubular absorption of sodium are
• Increased levels of progesterone
listed in Box 3.3.
• Increased sodium retention by kidneys
• Increase in renin-angiotensin-aldosterone
• Sodium retention and changes in osmolality enin angiotensin
• Altered secretion of arginine-vasopressin
• Increase in atrial natriuretic peptide (ANP) aldosterone system
A four-to-five fold increase in renin, renin sub-
strate (angiotensinogen), and angiotensin lev-
Increase in total body water is due to sodium
els occurs in pregnancy which, in turn, increase
retention, changes in osmoregulation, and
vascular tone and play a role in maintaining
changes in vascular tone brought about by fac-
normal blood pressure. Aldosterone levels rise
tors listed in Box 3.2.
in response to increase in angiotensin levels and
Increase in total body water affects all organ
this leads to increased sodium and water reten-
systems and contributes to other changes in
tion. As pregnancy advances, there is refracto-
pregnancy.
riness to the pressor effects of angiotensin II.
Women who are not refractory to the pressor
Clinical implications effect develop gestational hypertension.
The clinical implications of increase in body water are
given below.
Atrial and brain natriuretic
• Maternal weight gain
• Hemodilution peptides
• Physiological anemia of pregnancy These are secreted by the cardiomyocytes in the
• Increase in cardiac output, stroke volume
left atrium and ventricles in response to a stretch
• Pedal edema
induced by the increased blood volume. Atrial
• Laxity of joints
Ŧ Intervertebral joints
natriuretic peptide (ANP) is secreted by atria
Ŧ Pubic symphysis
• Gingival edema
• Tracheal edema Box 3.3 Factors that alter sodium balance
• Sodium retention
Ŧ Renin-angiotensin-aldosterone system
Sodium metabolism and Ŧ Deoxycorticosterone
Ŧ Estrogen
osmoregulation Ŧ Progesterone
Increase in total body water results in a fall in • Sodium excretion
plasma osmolality by 8–10 mOsm/kg in preg- Ŧ Atrial and brain natriuretic peptides
nancy. This occurs by 10 weeks and continues Ŧ PGE2
till postpartum period. The increased circulating P prostaglandin E2.
CH 03_p035-047_v3.indd 36 17-07-2015 10:42:54

Maternal Physiology in Pregnancy 37
and B-type or brain natriuretic peptide (BNP) by Maternal weight gain

the ventricles and brain. They cause natriuresis
or sodium loss in the urine. The increased body Weight gain is usually 11–16 kg. Maternal body
water coupled with natriuresis accounts for the water, fat, fetus, amniotic fluid, placenta, breast
fall in osmolality and mild decrease in serum changes, blood volume, and extracellular fluid
sodium observed in pregnancy. contribute to this. The average weight gain is
about 0.5 kg per week in the second and third tri-
ther electrolytes mesters. In the first trimester, women may lose
about 2–3 kg due to distaste for food and vomiting.
and minerals
There is very little change in metabolism of
most minerals. Small amounts required for the
growth of the fetus may be retained. Changes
Metabolic changes
in iron metabolism are discussed in Chapter Several metabolic changes occur in pregnancy
49, Hematological disorders pregnancy. Dietary due to increase in caloric requirements and
requirements of other minerals are discussed endocrine changes.
in Chapter 9, Preconceptional and antenatal
care.
Changes in potassium, calcium, and magne- Energy requirement
sium metabolism during pregnancy are given in
The mother and growing fetus require extra
Box 3.4.
energy in pregnancy. The total requirement varies
between individuals. The requirement increases
Box 3.4 Changes in potassium, calcium, gradually from the end of the first trimester
and magnesium metabolism during (Box 3.5). The additional caloric requirement aver-
pregnancy ages to 300 kcal/day through the entire pregnancy.
• Potassium
Ŧ Increased retention Carbohydrate metabolism
Ŧ Increase in tubular reabsorption
Increase in total body potassium Several changes take place in carbohydrate
Ŧ Increased plasma volume metabolism in pregnancy. Glucose is the primary
Mild decrease in serum potassium energy source for the fetus. There is a continuous
• Calcium and increasing transport of glucose to the fetus
Ŧ Required for fetal skeleton as pregnancy progresses. The mother’s fasting
Ŧ Increased demand in pregnancy
glucose levels are lower due to continuous fetal
Ŧ Increased intestinal absorption
utilization of maternal glucose. The mother,
Ŧ Increased intake and supplementation required
• Magnesium
on the other hand, tends to use fatty acids and
Ŧ Mild decrease in serum magnesium levels amino acids as energy source. The mother there-
fore has a tendency for fasting hypoglycemia and
ketosis (accelerated starvation).
The increase in levels of some hormones and
Clinical implications other diabetogenic substances listed in Box 3.6
Clinical implications of changes in rennin-angiotensin- leads to increased insulin resistance.
aldosterone system and electrolyte metabolism are
given below.
• Increased sensitivity to angiotensin II
Box 3.5 Energy requirement during pregnancy
Ŧ Predictor of hypertension
• %CNEKWOFGſEKGPE[ • Total energy requirement: 80,000 kcal
Ŧ Implicated in • Average additional requirement: 300 kcal/day
gestational hypertension Ŧ First trimester: No increase
preeclampsia Ŧ Second trimester: 350 kcal/day
preterm labor Ŧ Third trimester: 450 kcal/day
CH 03_p035-047_v3.indd 37 17-07-2015 10:42:55

Box 3.6 Substances causing increase in insulin Box 3.8 Protein and fat metabolism during
resistance in pregnancy pregnancy
• Human placental lactogen • Protein metabolism
• Cortisol, prolactin Ŧ Increase in dietary requirement
• Estrogen and progesterone Ŧ Proteins utilized by
• Tumor necrosis factor-D fetus
• C-reactive protein placenta
• Interleukin-6 breasts
uterus
hemoglobin
plasma proteins
Box 3.7 Changes in glucose metabolism
Ŧ Fall in maternal amino acid levels due to
in pregnancy
placental transfer to fetus
• Fasting hypoglycemia maternal gluconeogenesis
• Mother prone to ketosis • Fat metabolism
• Increase in insulin resistance Ŧ Increase in
• Increase in postprandial glucose levels triglycerides
• Increase in insulin response to glucose fatty acids
• Increase in hepatic glucose output low- and high-density lipoproteins
Increase in peripheral resistance to insulin,

caused by these factors, leads to a diabetogenic
state. The predominant changes in glucose Clinical implications of metabolic changes during preg-
nancy are given below.
metabolism are listed in Box 3.7.
Levels of diabetogenic hormones are signifi- • Screening for gestational diabetes to be done at
24–28 weeks.
cantly elevated by 24–28 weeks. Screening for
• Ketosis occurs readily in pregestational diabetes.
gestational diabetes is therefore performed at
• Insulin requirements increase in pregnancy.
this period of gestation.
Changes in glucose metabolism are discussed
in Chapter 48, Diabetes.
Changes in the
Protein and fat metabolism
cardiovascular system
Dietary requirement of proteins increases in
pregnancy from 0.8 g/kg/day to 1 g/kg/day. This Important anatomical and physiological changes
is due to an increase in demand due to the fetus, take place in the cardiovascular system as dis-
placenta, uterus, breasts, and increase in mater- cussed below.
nal production of hemoglobin and plasma pro-
teins. Amino acids are required by the mother
as an energy source and by the fetus for growth.
Anatomical changes
Circulating level of amino acids in the pregnant Elevation of the diaphragm due to the upward
mother falls due to placental transfer and utili- enlargement of the uterus and changes in the
zation of amino acids by the mother’s liver for shape of the rib cage lead to the anatomical
gluconeogenesis. changes described in Box 3.9. The heart is dis-
Fat is also used as a source of energy between placed upward and to the left and apex beat
meals by the mother. Therefore, circulating is felt in the fourth intercostal space, lateral to
levels of fatty acids increase. Serum levels of the midclavicular line. Due to the hemody-
triglycerides and low-density (LDL) and high- namic changes in pregnancy, functional sys-
density (HDL) lipoproteins increase in preg- tolic murmurs in the aortic and tricuspid areas,
nancy. Elevated levels of estrogen, progesterone, functional ejection systolic murmur in pulmo-
and human placental lactogen are probably nary area can be heard. Increased blood flow
causative (Box 3.8). through the mammary vessels may give rise
CH 03_p035-047_v3.indd 38 17-07-2015 10:42:55

Box 3.9 Anatomical changes in the heart Box 3.12 Symptoms and signs of cardiac
during pregnancy disease in pregnancy
• Examination • Dyspnea on mild activity
Ŧ Heart displaced upward and to the left • Dyspnea at rest/orthopnea
Ŧ Apex beat shifted upward and laterally • Paroxysmal nocturnal dyspnea
Fourth intercostal space lateral to midclavicular • Hemoptysis
line • Pedal edema up to the knees
• Auscultation • Edema not subsiding with overnight rest
Ŧ 5RNKVſTUVJGCTVUQWPF • Grade III or IV systolic murmurs
Ŧ Appearance of physiological third heart sound • Murmurs associated with thrill
Ŧ Functional murmurs • Diastolic murmurs
Ejection systolic murmur in pulmonary area
Continuous murmur
- Venous hum if patient is anemic
- Mammary vessels Physiological changes
The physiological changes in cardiovascular
system during pregnancy are multiple and pro-
to continuous murmurs along the sternal bor- found. These are meant to maximize oxygen
der. A third heart sound may be heard and first delivery to the fetus.
sound may be split. Unless one is aware of these
physiological changes, they may be mistaken for
organic cardiac disease.
Cardiac output
Symptoms and signs that mimic cardiac dis- Cardiac output increases by 30%–50% in preg-
ease are listed in Box 3.10. nancy, due to an increase in stroke volume and
There are changes in ECG and chest radiogra- heart rate. It begins to increase by 5 weeks, and
phy, as listed in Box 3.11. reaches a peak at 25–30 weeks. Changes in heart
Therefore, a diagnosis of cardiac disease rate, stroke volume, and cardiac output are given
should be made only if symptoms and signs in Box 3.13.
given in Box 3.12 are present. In labor, with pain and associated catechol-
amine release, the heart rate increases further.
The increased venous return as a result of pump-
Box 3.10 Symptoms and signs that mimic ing of blood from uterus during contractions
cardiac disease in pregnancy increases the cardiac output further. Vigorous
pushing efforts in second stage increase the car-
• Breathlessness
• Palpitation
diac output even further.
• Lightheadedness and syncope
• Easy fatigability
• Pedal edema Box 3.13 Changes in heart rate, stroke volume,
• Increase in pulse volume and cardiac output in pregnancy
• Heart rate
Ŧ Starts increasing by 5 weeks
Ŧ Peaks at 32 weeks
Box 3.11 '
%)CPFEJGUVTCFKQITCRJKEſPFKPIU
Ŧ Increases by 15–20 beats
in pregnancy
• Stroke volume
• ECG Ŧ Starts increasing by 8 weeks
Ŧ Left axis deviation Ŧ Peaks by 20 weeks
Ŧ 0QPURGEKſE566EJCPIGU Ŧ Increases by 20%–30%
Ŧ ST depression • Cardiac output
• Chest X-ray Ŧ Product of heart rate and stroke volume
Ŧ Apparent cardiomegaly (inadequate inspiration) Ŧ Starts increasing by 5 weeks
Ŧ Apparent straightening of left heart border Ŧ Reaches a peak by 25–30 weeks
Ŧ Prominent pulmonary conus Ŧ Increases by 30%–50%
CH 03_p035-047_v3.indd 39 17-07-2015 10:42:55

Cardiac output in pregnancy depends on position causes marked fall in blood pressure,
maternal position; it is more in the lateral and leading to supine hypotension manifested as diz-
knee chest positions. In the supine position, ziness, nausea, and sometimes syncope. These
pressure exerted by the gravid uterus on inferior changes are more pronounced after 24 weeks.
vena cava reduces venous return and hence car-
diac output. Renal and placental blood flow are
also decreased in the supine position.
enous pressure
Pressure on the inferior vena cava by the gravid
Systemic vascular resistance uterus causes an increase in venous pressure in
the lower half of the body. This leads to pedal
Systemic vascular resistance (SVR) falls in preg- edema, varicose veins, and less commonly hem-
nancy and remains low till term. This is largely orrhoids can also predispose to venous throm-
responsible for the fall in blood pressure during bosis in the lower limbs.
pregnancy. Reduction in SVR is caused by the
following:
Cardiovascular changes
• Progesterone-mediated relaxation of smooth
muscles in labor
• Increase in nitric oxide (NO), which decreases Labor has several effects on cardiovascular sys-
vascular responsiveness to pressors like angio- tem (Box 3.15).
tensin II.
Box 3.15 Effects of labor on cardiovascular
Blood pressure system
Blood pressure should be measured in the sit- • Effects of pain
ting position and disappearance of Korotkoff Ŧ Increase in heart rate and stroke volume
sounds should be used to determine diastolic Ŧ Increase in mean arterial pressure
pressure. Blood pressure falls during pregnancy Ŧ Further increase in cardiac output
• Immediate postpartum (10–30 minutes after delivery)
and is position dependent, being lower in lat-
Ŧ Fall in heart rate
eral recumbent position. Diastolic pressure falls
Ŧ Further increase in cardiac output
more than the systolic pressure. Overall, the Ŧ Increase in stroke volume
decrease in mean arterial pressure and diastolic • Postpartum 1 hour
pressure is between 5–10 mm Hg (Box 3.14). Fall Ŧ Fall in cardiac output
in blood pressure starts by 8 weeks, reaches a
nadir by 24–26 weeks and returns to prepreg-
nancy levels by term. Clinical implications
In about 10% of pregnant women, compres- Cardiovascular changes in pregnancy have important
sion of vena cava by gravid uterus in supine clinical implications as listed below.
• Anatomical and physiological changes: Misinterpreted
as cardiac disease
Box 3.14 Changes in S and blood pressure • ncrease in heart rate especially in labor : Risk of pul-
monary edema in valvular disease
• SVR
• ncrease in cardiac output: Congestive cardiac failure
Ŧ Decreases (CCF) in valvular disease
Due to smooth muscle relaxation • idtrimester fall and later rise in blood pressure: Mis-
Caused by diagnosed as pregnancy induced hypertension (PIH)
- progesterone • ascular smooth muscle rela ation and increase in
- nitric oxide venous pressure: Varicose veins, pedal edema and
• Blood pressure hemorrhoids
Ŧ falls by 8 weeks • Pressure of gravid uterus on vena cava in supine
Ŧ nadir at 24–26 weeks position: Supine hypotension, fetal heart decelerations,
Ŧ returns to normal by term hypotension during epidural/spinal anesthesia
Ŧ is lower in lateral recumbent position • Changes in labor: Increased risk of pulmonary edema,
CCF in labor and immediate postpartum
S systemic vascular resistance.
CH 03_p035-047_v3.indd 40 17-07-2015 10:42:55

ematological changes Box 3.17 Changes in coagulation system

during pregnancy
The physiological changes in pregnancy, involv-
• Increase in all clotting factors except XI and XIII
ing the hematological system, are important for
• Decrease in plasminogen activator
the mother and fetus.
• Increase in plasminogen-activator inhibitor
• Decrease in protein S
Blood volume
Blood volume increases by 40%–50%. This starts in Clinical implications
first trimester (6 weeks), reaches a peak by 32–34
Clinical implications of hematological changes in preg-
weeks, and plateaus thereafter. Plasma volume nancy are given below.
increases by 50% but red cell volume increases by
• Increase in blood volume
30%. This gives rise to ‘physiological hemodilu- Ŧ Coping mechanism against blood loss
tion’ or ‘physiological anemia’ of pregnancy. The Ŧ Diagnosis of hemorrhagic shock may be delayed
increase in red cells is due to increase in erythro- Ŧ Increases risk of congestive cardiac failure (CCF) in
poietin levels, begins at 10 weeks and continues valvular disease
till term. • Hemodilution
The increase in blood volume is meant for Ŧ Anemia in women with low iron reserve
• Leukocytosis
• extra blood flow to uterus and placenta; Ŧ Cannot be used for diagnosing infection
• filling the expanded vascular system; • Thrombocytopenia
• protection against blood loss at delivery. Ŧ Mistaken diagnosis of idiopathic thrombocytopenic
purpura (ITP)
In addition to changes in blood volume, there • Elevated erythrocyte sedimentation rate (ESR) and
are other hematological changes which are given C-reactive protein (CRP)
in Box 3.16. Ŧ Cannot be used for diagnosing infection
• Increase in clotting factors
• &GETGCUGKPſDTKPQN[UKU Risk of venous thrombosis
Box 3.16 Changes in blood cells and

KPƀCOOCVQT[OCTMGTU
• Blood cells Changes in respiratory
Ŧ Decrease in hemoglobin
Ŧ Increase in white cell count system
To 12,000–14,000 in pregnancy
To 20,000–30,000 in labor Significant changes occur in anatomy of the
Ŧ Decrease in platelets (gestational thrombocytopenia) respiratory system and pulmonary functions
• +PƀCOOCVQT[OCTMGTU during pregnancy.
Ŧ Increase in
CRP
complement factors C3 and C4
Anatomical changes
ESR Anatomical changes in the respiratory tract are
C P C-reactive protein; S erythrocyte sedimentation rate. given in Box 3.18.
Box 3.18 Anatomical changes in respiratory

Coagulation system tract
Pregnancy is a hypercoagulable state caused by • Hyperemia and edema of mucosa of respiratory tract
an increase in coagulation factors and a decrease • Increased secretion of mucus
in inhibitors of coagulation and fibrinolytic activ- • Expansion of chest
ity (Box 3.17). The commonly used coagulation Ŧ Relaxation of ligaments attaching ribs to sternum
Ŧ Upward displacement of diaphragm: 4 cm
tests (bleeding time, clotting time, prothrombin
Ŧ Increase in chest circumference: 5–7 cm
time, and activated partial thromboplastin time)
Ŧ Increase in transverse diameter of chest: 2 cm
are unaffected.
CH 03_p035-047_v3.indd 41 17-07-2015 10:42:55

Clinical implications Anatomical changes

Clinical implications of changes in respiratory system Anatomical changes take place in the kidneys, ure-
during pregnancy are given below. ters, and urinary bladder during pregnancy. These
• Congestion and edema of mucosa are listed in Box 3.20. The dilatation of the renal
Ŧ 0CUCNUVWHſPGUU pelves and ureters is due to the following reasons:
Ŧ Epistaxis
Ŧ &KHſEWNV[KPKPVWDCVKQPCPFFKHſEWNV[KPRNCEKPIPCUQ- • Mechanical pressure by gravid uterus
gastric tube • Progesterone-induced relaxation of smooth
• Low maternal PaCO2 muscles
Ŧ Chronic respiratory alkalosis
• Increase in oxygen consumption These changes begin by the second month of
Ŧ Increased susceptibility to effects of respiratory infec- pregnancy and are maximal at midpregnancy.
tion and hypoxia during intubation
They revert to normal after delivery. The dilata-
tion is more on the right and this is attributed to
the following:
Pulmonary function
There are changes in pulmonary function as • Dextrorotation of uterus
well (Box 3.19). Increase in progesterone levels • Cushioning and protection of left ureter by sig-
and elevation of diaphragm contribute to these moid colon
changes. Chronic hyperventilation and the resul- • Pressure on the right ureter by engorged right
tant drop in PaCO2 help in creating a gradient and ovarian vein complex
facilitating carbon dioxide transfer from fetus to
Changes in bladder and urethral pressure also
mother. Maternal oxygen consumption increases
occur. These cause stress incontinence.
in pregnancy by 20%–40%, and there is a further
increase in labor. This increased demand for oxy-
gen is met by increase in minute ventilation.
Changes in renal function
Changes in renal hemodynamics and renal func-
Changes in urinary system tion begin by 5–7 weeks of pregnancy and con-
tinue till term (Box 3.21). They revert to normal
Being close to the enlarging uterus, several sig- postpartum.
nificant changes occur in the urinary system in
pregnancy.
Box 3.20 Anatomical changes in the urinary

Box 3.19 Changes in pulmonary function tract during pregnancy
during pregnancy
• Kidneys
• Respiratory rate unchanged Ŧ Increase in size and weight
• Decrease in lung volumes at resting state Increase in renal vasculature
Ŧ Functional residual capacity Increase in interstitial volume
Ŧ Residual volume Pelvicalyceal dilatation
Ŧ Total lung capacity • Ureter
• $TQPEJKCNƀQYWPCNVGTGF Ŧ Dilatation: More on right than left
Ŧ Forced expiratory volume • Bladder
Ŧ 2GCMGZRKTCVQT[ƀQYTCVG Ŧ First trimester
Ŧ Maximum breathing capacity Compression by gravid uterus
• Chronic hyperventilation leads to Ŧ Second trimester
Ŧ increase in Elevation of trigone
tidal volume Hyperemia of bladder wall
minute ventilation Ŧ Labor
PaO2 Pressure by presenting part
Ŧ decrease in - Edema
PaCO2 - Congestion
CH 03_p035-047_v3.indd 42 17-07-2015 10:42:55

Box 3.21 Changes in renal function Changes in

during pregnancy
• Renal hemodynamics
gastrointestinal system
Ŧ +PETGCUGKPTGPCNRNCUOCƀQYD[ Changes occur in all parts of the gastrointestinal
Ŧ +PETGCUGKPINQOGTWNCTſNVTCVKQPTCVG
)(4D[ system including oral cavity, stomach, intestines,
Causes reduction in
liver, and gall bladder.
- serum creatinine
- blood urea nitrogen
- uric acid
Ŧ Increase in creatinine clearance to 150–200 mL/min Anatomical changes
Ŧ Increase in urine volume
Ŧ Nocturia Anatomical changes in the gastrointestinal
• Renal tubular function tract are mainly due to upward displacement
Ŧ Glycosuria by enlarging uterus. The appendix is displaced
Ŧ Conservation of potassium superiorly and reaches the right flank.
Ŧ Increase in Gums become hypertrophic and hyperemic
protein and albumin excretion and may bleed, commonly known as gingival
amino acid excretion hypertrophy of pregnancy.
calcium excretion
bicarbonate excretion
Physiological changes
Creatinine clearance is used as a measure Appetite increases in pregnancy except in first
of glomerular filtration rate (GFR). Increase in trimester. Craving for unusual foods (pica)
renal plasma flow and GFR are thought to be may be present in some. Secretion of saliva
due to the effect of nitric oxide (NO). Serum and other gastrointestinal secretions increases.
creatinine and blood urea nitrogen decrease Progesterone causes relaxation of the smooth
gradually throughout pregnancy. However, muscles of the entire gastrointestinal tract. This
serum uric acid, which shows a decrease up to leads to decrease in gastric and intestinal motil-
24 weeks, increases thereafter due to increased ity, constipation, and stasis of contents in gall
renal tubular function. Glycosuria occurs due bladder (Box 3.22).
to increase in GFR and reduced tubular reab-
sorption of glucose.
Glycosuria is not related to plasma glucose
levels and can be intermittent. It is extremely
common and should not be misdiagnosed as Box 3.22 Changes in gastrointestinal system
gestational diabetes. When glycosuria is per- during pregnancy
sistent, screening for diabetes is indicated. • Anatomical changes
Ŧ Upward displacement of stomach and intestines
Ŧ Gum hypertrophy
Clinical implications Ŧ Change in the position of appendix
• Physiological changes
The changes in urinary system have several clinical Ŧ Due to smooth muscle relaxation by
implications as given below.
progesterone
• Pelvicalyceal dilatation estrogen-mediated release of NO
Ŧ Increase in risk of pyelonephritis mistaken for obstruc- Ŧ Decrease in gastric tone and motility
tive uropathy Ŧ +PETGCUGKPICUVTQGUQRJCIGCNTGƀWZ
• Increased vascularity of bladder Gastric compression by gravid uterus
Ŧ Hematuria Relaxation of gastroesophageal sphincter
• Glycosuria Ŧ Decreased intestinal motility
Ŧ Mistaken diagnosis of diabetes Ŧ Stasis of contents of gall bladder
• Increased bicarbonate excretion Ŧ Increase in biliary cholesterol content
Ŧ Compensates for respiratory alkalosis
nitric oxide.
CH 03_p035-047_v3.indd 43 17-07-2015 10:42:55

Clinical implications Pituitary gland

Clinical implications of changes in gastrointestinal sys- Pituitary gland enlarges in pregnancy. Prolactin-
tem are given below. secreting tumors also increase in size. Due to the
• Change in position of appendix increase in size, pituitary gland is more suscep-
Ŧ &KHſEWNV[KPFKCIPQUKUQHCRRGPFKEKVKU tible to ischemia when SVR falls in postpartum
• )CUVTQGUQRJCIGCNTGƀWZ hemorrhage (Sheehan’s syndrome).
Ŧ Heart burn and dyspepsia Changes in pituitary hormones are given in
• Delayed intestinal emptying
Box 3.24. Prolactin-secreting cells in the pituitary
Ŧ Constipation
increase in number and secrete large amounts of
• Gall bladder stasis and increase in cholesterol content
in bile the hormone. Suppression of follicle-stimulat-
Ŧ Formation of biliary sludge, gall stones ing hormone and luteinizing hormone is due to
• Increase in hormone-binding proteins feedback inhibition by estrogen, progesterone,
Ŧ Increase in total hormone levels and inhibin. Placental production of growth hor-
Ŧ Decrease in free hormone levels mone suppresses the pituitary growth hormone
• Increase in portal venous pressure but the serum growth hormone level increases.
Ŧ Formation of hemorrhoids
Thyroid gland
Changes in liver functions Moderate increase in size of the thyroid gland
No anatomical or histological changes are seen occurs in pregnancy to meet the need for increased
in the liver. Spider naevi and palmar erythema thyroid hormone production. There is glandular
appear due to increased estrogen levels and hyperplasia and increase in vascularity. The gland
disappear after delivery. Total serum protein enlarges more in iodine-deficient women. Iodine
and serum albumin show a modest progressive requirement increases in pregnancy.
decrease due to hemodilution. However, levels of Changes in thyroid function are listed in
fibrinogen, hormone-binding proteins, transfer- Box 3.25.
rin, and ceruloplasmin increase. Serum alkaline The increased estrogen levels in pregnancy
phosphatase increases but the main source is cause stimulation of thyroid-binding globulin
placenta and not the liver. Changes in liver func- production by the liver. This leads to a transient
tion are listed in Box 3.23. fall in free T3 and T4, which, in turn, leads to
increased production of T3 and T4 by the thy-
roid, such that the serum total T3 and T4 increase
Box 3.23 Changes in liver function during
pregnancy and free T3 and T4 are restored to values near the
• Fall in
Ŧ serum total protein
Box 3.24 Changes in pituitary hormones during
Ŧ serum albumin pregnancy
• Increase in
Ŧ binding proteins • Anterior pituitary hormones
Ŧ ſDTKPQIGP Ŧ Prolactin
Ŧ transferrin Begins to increase by 5–8 weeks
Ŧ ceruloplasmin Marked increase prior to labor
Ŧ alkaline phosphatase Prepares breast for lactation
• Increase in portal venous pressure Ŧ FSH/LH
Markedly decreased
Ŧ Growth hormone
Decreased
Changes in endocrine • Posterior pituitary hormones
system Ŧ Oxytocin
Increases markedly in third trimester
The endocrine changes play a major role during Peak levels in labor
pregnancy, labor, and puerperium. S follicle-stimulating hormone; luteinizing hormone.
CH 03_p035-047_v3.indd 44 17-07-2015 10:42:55

levels. Elevated cortisol levels cause weight gain,

Box 3.25 Changes in thyroid function
during pregnancy increase in plasma glucose, and striae. This is
termed physiological hypercortisolism.
• Increase in thyroid-binding globulin
• Increase in total T3 and total T4 ineralocorticoi s
• Slight increase in free T3 and free T4
• 6TCPUKGPVFGETGCUGKP65*KPſTUVVTKOGUVGT The increased aldosterone levels along with the
high cortisol levels tend to cause sodium and
S thyroid-stimulating hormone.
water retention and oppose the natriuretic effects
of ANPs.
upper limit of the normal range. Placental hCG
is the principal thyroid stimulator in the first tri- Adrenal androgens
mester. The serum thyroid-stimulating hormone Most of the circulating maternal dehydroepi-
is therefore transiently suppressed in the first tri- androsterone is derived from the fetal adrenals
mester. In hyperemesis gravidarum, twin preg- and serves as the precursor for maternal adrenal
nancy, and molar pregnancy, where the serum hormone production.
hCG levels are very high, there may be transient Changes in adrenal function are summarized
thyrotoxicosis. in Box 3.26.
Fetal thyroid begins to function from the
12th week of gestation. The fetus is depen-
Box 3.26 Changes in adrenal function during
dent on placental transmission of maternal pregnancy
T4 for early development (up to 12 weeks). In
women with autoimmune thyroid disease such ncrease in
as Grave’s disease and Hashimoto’s thyroiditis, • Placental CRH
maternal thyroid-stimulating and inhibiting • Maternal ACTH
immunoglobulins may cross the placenta and • Corticosteroid-binding globulin
• Total cortisol
cause fetal hyper- or hypothyroidism. Iodine in
• Free cortisol
maternal circulation crosses the placenta with
• Aldosterone
ease and the fetal thyroid avidly takes up iodine. • Deoxycorticosterone
Therefore, excessive iodine intake or radioactive
AC adrenocorticotropic hormone; C corticotrophin-releasing
iodine should be avoided in pregnancy since hormone.
they can cause fetal hypothyroidism.
Parathyroid glands
Adrenal glands
Parathyroid hormone is secreted in response
Even though there is no net increase in the size to low calcium levels. Calcium utilization, and
of the adrenals in pregnancy, there is selective therefore, requirement increases since it is
increase in the size of the zona fasciculata which required for formation of fetal bones. Maternal
secretes glucocorticoids. levels of ionized calcium are unchanged in preg-
nancy. Most of the calcium required for fetal
Changes in adrenal function skeleton formation is obtained from increase
in maternal intestinal calcium absorption, but
lucocorticoi s some calcium resorption from maternal bones
The placenta produces large amounts of a occurs. In countries like India, where dietary
placental corticotrophin-releasing hormone calcium intake may be insufficient, calcium
(pCRH) which in turn stimulates adrenocorti- reserves decrease. Supplementation with 1000–
cotropic hormone (ACTH) production by the 1300 mg of calcium/day is, therefore, recom-
maternal pituitary. This leads to an increase in mended for all pregnant women. Parathormone
maternal serum cortisol levels. The increase in levels remain unchanged throughout pregnancy
cortisol-binding protein (CBP) from maternal according to recent studies (Box 3.27). Similarly,
liver also contributes to the increase in cortisol serum vitamin D levels are also unchanged
CH 03_p035-047_v3.indd 45 17-07-2015 10:42:55

except when the maternal intake of vitamin D

Box 3.27 Changes in parathyroid function and
levels of calcium and vitamin D during is poor and exposure to sunlight is inadequate.
pregnancy Routine screening for vitamin D deficiency and
supplementation in pregnancy are not required
• No change in levels of
except in populations with deficiency.
Ŧ parathyroid hormone
Ŧ serum calcium
Ŧ vitamin D
• Mild increase in bone resorption
Skeletal system
Lumbar lordosis helps to shift the center of
Clinical implications gravity backward and relaxation of pubic and
Clinical implications of changes in endocrine system sacroiliac joints may increase pelvic diame-
during pregnancy are given below. ters during labor. These changes are associated
• Enlargement of pituitary with backache and pain in the sacroiliac and
Ŧ Susceptibility to infarction after postpartum hemor- pubic joints (Box 3.28).
rhage
• Increase in prolactin
Ŧ Preparation for lactation
• Increase in oxytocin in labor
Ŧ Uterine contraction
Box 3.28 Changes in skeletal system
• Elevated total T3 and T4 during pregnancy
Ŧ Over diagnosis of hyperthyroidism
• Stimulation of thyroid by human chorionic gonadotropin • Lumbar lordosis
(hCG) Ŧ Shifts center of gravity
Ŧ Gestational thyrotoxicosis, thyrotoxicosis of hydatid- Ŧ Causes backache
iform mole • Relaxation of sacroiliac joint
• Increased cortisol secretion Ŧ Causes backache
Ŧ Hyperglycemia, weight gain, striae gravidarum • Relaxation of pubic symphysis
• Increase in calcium demand Ŧ Increases pelvic diameter
Ŧ Calcium supplementation required Ŧ Causes pubic pain
Key points
• Extensive anatomic, physiological, and biochemical • There is increased insulin resistance caused by diabe-
changes occur in the mother during pregnancy to pre- togenic hormones. Fasting plasma glucose levels are
pare the mother to meet the demands of pregnancy. lower but postprandial levels are higher. The pregnant
• Total body water increases by 6-8 L due to increase in woman is more prone to development of glucose
progesterone, renin-angiotensin-aldosterone, sodium intolerance and diabetes.
retention, and increase in atrial natriuretic peptide. • Dietary requirements of proteins also increases. Fat is
Increase in body water contributes to hemodilution, broken down and is used as a source of energy.
increase in cardiac output, pedal edema, and maternal
• Anatomical and physiological changes in cardiovas-
weight gain.
cular system can mimic clinical features of cardiac
• Water retention exceeds sodium retention leading to disease. There is increase in cardiac output, stroke
fall in serum sodium levels. volume, and heart rate along with fall in systemic
• There is increase in renin, angiotensin and aldoster- vascular resistance. Due to these changes, preg-
one levels which increase vascular tone. nant women with cardiac disease can deteriorate in
pregnancy.
• There is increased demand for calcium in pregnancy
• Blood volume increases. The increase in plasma
necessitating calcium supplementation.
volume is more than the increase in red cell volume,
• Additional caloric requirement averages to 300 kcl/day resulting in physiological anemia.
through the entire pregnancy.
(Continued)
CH 03_p035-047_v3.indd 46 17-07-2015 10:42:55

Key points Continued

• Changes in coagulation system results in the hyperco- • Increase in binding proteins results in increase in
agulable state of pregnancy. levels of total hormones but decrease in levels of free
• Anatomical and physiological changes in respiratory hormones.
system leads to chronic respiratory alkalosis. • Pituitary gland enlarges and level of oxytocin increas-
• Pelvicalyceal and ureteric dilatation occur. Renal es in third trimester. Thyroid gland enlarges and there
DNQQFƀQYCPFINQOGTWNCTſNVGTCVKQPTCVGKPETGCUG is transient increase in thyroid-stimulating hormone in
There is increase in susceptibility for urinary tract ſTUVVTKOGUVGT
infection and pyelonephritis. • Zona fasciculate of adrenal gland increases in size
• Relaxation of smooth muscles of the gastrointestinal and there is increase in cortisol and deoxycorticos-
U[UVGONGCFUVQICUVTQGUQRJCIGCNTGƀWZEQPUVKRCVKQP terone leading to physiological hypercorticolism.
and stasis of contents in the gall bladder.
Self-Assessment
3. Symptoms like dyspnea on mild activity, orthopnea,
Case-based questions paroxysmal nocturnal dyspnea, and hemoptysis
CPFENKPKECNſPFKPIUUWEJCURGFCNGFGOCWRVQVJG
Case 1 knees, grade III or IV systolic murmurs, murmurs
Mrs. KT, a 20-year-old primigravida, at 32 weeks of preg- associated with thrill, and diastolic murmurs.
nancy came to the clinic for routine antenatal checkup.
She was quite troubled by minor but multiple problems
such as pedal edema, which was obvious by evening,
Case 2
palpitation, feeling tired, and breathlessness on walking 1. Urine microscopy, urine culture, and sensitivity.
2. Pyelonephritis.
1. Are the symptoms suggestive of valvular heart
3. Due to dilatation of the collecting system of the
disease?
kidneys and stasis of urine in bladder due to incom-
2. 9JCVſPFKPIUOC[DGRJ[UKQNQIKECNDWVOKOKEECTFKCE plete bladder evacuation.
disease?
4. Pelvicalyceal and ureteric dilatation, compression
3. What symptoms and signs would be suggestive of QHDNCFFGTD[WVGTWUKPſTUVVTKOGUVGTGNGXCVKQPQH
valvular disease? trigone in second trimester, hyperemia of bladder
wall, and compression by fetal head in labor.
Case 2 These changes are due to progesterone effect on smooth
A 30-year-old second gravida, presented with loin pain muscles and pressure by enlarging uterus.
and fever.
1. How will you evaluate? Sample questions
2. What is your diagnosis?
3. Why is this condition common in pregnancy? Long-answer question
4. What are the changes in urinary tract in pregnancy?
1. Describe the changes in respiratory and cardio-
vascular systems, and hematological changes in
Answers pregnancy. What are the clinical implications of these
changes?
Case 1
1. No, symptoms such as palpitation, breathlessness, and Short-answer questions
easy fatigability can occur in normal women in preg-
nancy due to the changes in cardiovascular system. 1. Urinary tract changes during pregnancy
2. Findings on examination include pedal edema, shift- 2. Hematological changes in pregnancy
KPIQHCRGZDGCVVQNGHVURNKVVKPIQHſTUVJGCTVUQWPF 3. Carbohydrate metabolism in pregnancy
appearance of third heart sound, and functional systolic 4. Glycosuria in pregnancy
murmurs in tricuspid and aortic areas and continuous 5. Cardiovascular changes in pregnancy
OWTOWTKPFKECVKPIDNQQFƀQYKPOCOOCT[XGUUGNU
CH 03_p035-047_v3.indd 47 17-07-2015 10:42:55

Fertilization,
4 Implantation, and
Fetal Development
Case scenario
Mrs. LN, 28, married for 4 years, came to the hospital with a history of
three previous children with congenital anomalies and early neonatal
death. She was advised preimplantation genetic diagnosis.
Introduction the timing of intrauterine insemination (IUI) or

sexual intercourse (Box 4.1).
An understanding of the biology of ovulation, fer- Immediately after the LH peak, the primary
tilization, implantation, and development of the oocyte undergoes the first meiotic division.
fetus is important when one deals with condi- A space forms between the zona and vitel-
tions like infertility, recurrent pregnancy loss and line membrane covering the oocyte, known as
fetal anomalies. This is not only helpful in appro- the perivitelline space. The first polar body is
priate evaluation and treatment but is invaluable extruded into the perivitelline space. The sec-
while counseling and discussing prognosis. For ondary oocyte, which is haploid, is surrounded
a discussion on physiology of menstruation and by the corona radiata and zona pellucida and
ovulation, the reader may refer to Essentials of moves toward the periphery of the follicle. The
Gynecology by Dr. Lakshmi Seshadri. second meiotic division in the oocyte is arrested
in metaphase. When the follicle ruptures and the
oocyte is released with the surrounding cumu-
lus, it is picked up by the fimbriae of the fallopian
vulation tube and directed into the tubal lumen (Fig. 4.1).
Ovulation occurs on Day 14 of a 28-day menstru-
ation cycle and 14 days prior to the onset of men-
struation in longer cycles. Luteinizing hormone Fertili ation
(LH) surge begins 36 hours prior to ovulation
and peaks 12 hours before ovulation. The LH Fertilization is the fusion of the nucleus of the
surge can be detected by simple tests and is used oocyte with that of the sperm. This takes place
as an indicator of ovulation and for determining in the fallopian tube. For fertilization to occur,
CH 04_p048-060_v3.indd 48 17-07-2015 10:44:12

Fertilization, Implantation, and Fetal Development 49
Box 4.1 The process of ovulation Box 4.2 Fertili ation

he process he process
• LH surge begins 36 hours prior to ovulation • Occurs in fallopian tube
• LH surge peaks 12 hours prior to ovulation • Fertile period
• First polar body released soon after LH surge Ŧ Begins 48 hours prior to ovulation
• Second meiotic division arrested in metaphase Ŧ Ends 24 hours after ovulation
• Oocyte with surrounding cumulus released Clinical implications
Clinical application • Couples with infertility
• Tests for ovulation help in determination of Ŧ Planned intercourse during fertile period recom-
Ŧ fertile period mended
Ŧ timing of IUI • Couples desirous of contraception
Ŧ Avoidance of intercourse during fertile period
intrauterine insemination; luteinizing hormone.
recommended
imbrial e opportunity or the fertile period is from 48 hours

o tube
prior to ovulation to 24 hours after ovulation. This
ary ith ollicles
has implications in planning or avoiding preg-
nancy (Box 4.2).
Several sperms penetrate the corona radi-
ate and zona pellucida but only one pierces the
irst vitelline membrane. Enzymes secreted by the
polar bo y oocyte immobilize the other sperms. Fusion of
Coro a
ra iata Peri itelli e the nucleus of the oocyte and that of the sperm
space takes place, followed by completion of the
o a second meiotic division. The second polar body
pelluci a
is released into the perivitelline space (Fig. 4.2).
Figure 4.1 1XWNCVKQP6JGUGEQPFCT[QQE[VGYKVJVJGſTUV
polar body in the perivitelline space surrounded by corona
radiata, is released from the ovary and picked up by the
ſODTKCGQHVJGHCNNQRKCPVWDG
Preimplantation events
the sperm must enter the vagina <48 hours prior The fertilized ovum is now known as a zygote and
to ovulation. The oocyte can be fertilized up to is diploid. It divides by cleavage into 2 cells, then
24 hours after ovulation. Thus, the window of into 4 cells and so on. A ball of 16 cells, known
permato oa Male pronucleus
irst polar bo y
econ polar bo y
a. emale pronucleus b.
Figure 4.2 Fertilization. a. Penetration of zona pellucida by sperm. Though several sperms enter the zona, only one
pierces the vitelline membrane. b. Fusion of the nucleus of the oocyte and sperm, completion of second meiotic division,
and extrusion of second polar body.
CH 04_p048-060_v3.indd 49 17-07-2015 10:44:12

Polar
bo ies
a a a
Figure 4.3 (QTOCVKQPQHOQTWNC6JG\[IQVGKUFKXKFGFKPVQEGNNUſTUVVJGPKPVQEGNNUCPFDGEQOGUCDCNNQHEGNNUMPQYP
as the morula.
as a morula, is formed by Day 3 postfertilization

(Fig. 4.3). The morula enters the uterine cavity and o a pelluci a
is covered by mucus and endometrial fluid at this
stage. The endometrial fluid is absorbed by the
morula and enters between the cells. The solid
morula transforms into the blastocyst which con-
tains a cavity (Fig. 4.4). By Day 4 or Day 5, the cells
rophoblast
differentiate into an inner cell mass, known as the
embryoblast, and cells arranged in the periphery, I er cell mass
known as the trophectoderm or trophoblast. Lytic
lastocyst ca ity
enzymes from the blastocyst cause dissolution of
the zona pellucida and the blastocyst is released, a
process known as zona hatching (Fig. 4.5).
Figure 4.5 Release of blastocyst (zona hatching). The
blastocyst is extruded from the zona pellucida.
Preimplantation genetic
diagnosis
Box 4.3 Preimplantation biopsy procedures and
In order to arrive at the diagnosis of a suspected their timing
heritable disease, one will need to remove cells
• Polar body biopsy
Ŧ First polar body biopsy
Conducted on unfertilized oocyte
Ŧ Second polar body biopsy
rophoblast Shortly postfertilization
• Blastomere biopsy
o a pelluci a Ŧ Day 3 postfertilization
• Blastocyst biopsy
I er cell mass
Ŧ Day 5 postfertilization
embryoblast
lastocyst ca ity
from the oocyte, blastomere or blastocyst and
subject them to genetic testing. These proce-
dures are usually performed on Day 3 or Day 5
from fertilization, in assisted reproductive cycles
Figure 4.4 Blastocyst. The morula becomes a blastocyst (see Chapter 12, Prenatal screening, prenatal
YJGPƀWKFGPVGTUDGVYGGPVJGEGNNUCPFHQTOUCECXKV[ diagnosis, and fetal therapy). Different preim-
The cells arrange themselves as an inner cell mass or plantation biopsy procedures and their timing
embryoblast and an outer cell mass or trophoblast. are given in Box 4.3.
CH 04_p048-060_v3.indd 50 17-07-2015 10:44:13

Implantation Box 4.4 Implantation

• Stage of apposition
Successful implantation requires the appropri-
Ŧ Trophoblast covers the embryoblast pole
ately timed arrival of a viable blastocyst into a
Ŧ First contact between trophoblast and decidua
receptive endometrium. The most receptive time Ŧ At the upper posterior wall of uterus
period of the endometrium is from Day 20 to Day • Stage of adhesion
24 of the menstrual cycle and this is known as Ŧ Stronger attachment of trophoblasts
the implantation window. Implantation of the Ŧ Trophoblastic penetration of endometrium mediat-
blastocyst into the uterine decidua takes place ed by progesterone, proteoglycans, integrins, and
6–7 days postfertilization. ſDTQPGEVKP
The process of implantation has three phases, • Stage of invasion
as given in Box 4.4. Initially, the trophoblast lying Ŧ Further invasion of trophoblasts into endometrium
Ŧ Firmer attachment
over the embryoblast pole gets attached to the
decidua. Following that, it gradually burrows
into the stratum compactum and invades it fur-
ther. By Day 10 postfertilization, the blastocyst The trophoblasts work their way into the uterine
is totally enclosed within endometrium. The decidua and later become part of the placenta.
process of implantation is a complex interac- Complete penetration of the blastocyst into the
tion between the trophoblast and decidua. This endometrium takes place by Day 8 or 9 following
process is facilitated by progesterone, proteogly- fertilization. The maternal vessels are eroded by
cans, integrins, and fibronectin. the trophoblast between Day 11 and Day 13. The
trophoblasts further differentiate into villous and
Differentiation of trophoblast extravillous trophoblast. These are discussed in
detail in Chapter 5, Placenta, fetal membranes, and
By Day 6 following fertilization, the trophoblast amniotic fluid.
cell layer multiplies rapidly and differentiates into
(a) an outer layer of multinucleated syncytium
without distinct cell walls, called syncytiotropho- Abnormal implantation
blast, and (b) an inner layer of cells with distinct
cell walls and nuclei, called cytotrophoblasts The blastocyst may also get implanted in the fal-
(Fig. 4.6). This differentiation is complete by Day 8. lopian tube, ovary, peritoneum, or cervix, result-
ing in an ectopic pregnancy. A tubal pregnancy
is the most common type of ectopic pregnancy.
The fallopian tube cannot distend to accommo-
date the pregnancy; therefore, it ruptures, result-
ing in intraperitoneal hemorrhage and shock.
The pregnancy may also miscarry through the
yncytiotrophoblast
fimbrial end into the peritoneal cavity (see
Chapter 30, Ectopic pregnancy).
Cytotrophoblast Implantation in the lower uterine segment
results in placenta previa. This causes antepartum
hemorrhage, as discussed in detail in Chapter
mbryoblast 39, Antepartum hemorrhage. Abnormalities of
implantation are listed in Box 4.5.
Figure 4.6 Differentiation of trophoblast. The trophoblast Box 4.5 Abnormalities of implantation
cell layer multiplies and differentiates into an outer
• Ectopic implantation
layer of multinucleated syncytium without distinct cell
Ŧ Fallopian tube, ovary, cervix, or peritoneum
walls, known as syncytiotrophoblast and an inner layer
• Implantation in lower segment
of cells with distinct cell walls and nuclei, known as
Ŧ Placenta previa
cytotrophoblasts.
CH 04_p048-060_v3.indd 51 17-07-2015 10:44:13

The decidua (endometrium

of pregnancy) eci ua parietalis
The decidua is the specialized and modified

endometrium of pregnancy. The process of eci ua capsularis
decidualization of the secretory endometrium
takes place under the influence of progesterone eci ua basalis
secreted by both the corpus luteum and the blas-
tocyst. The process of decidualization is unique
to hemochorial placentae in which maternal
blood comes in direct contact with the chorionic Figure 4.7 Decidua. The decidua covering the blastocyst
villi (described later in this chapter). The decidua is decidua capsularis; decidua lining the rest of the
is termed decidua basalis, decidua capsularis, uterus is decidua parietalis; and the decidua invaded by
or decidua parietalis depending on its location trophoblast is decidua basalis.
relative to the site of implantation (Fig. 4.7).
Decidua basalis and decidua parietalis consist
of three layers each. By 12–14 weeks’ gestation, Box 4.6 The decidua
as the embryo enlarges to fill the uterine cavity,
• /QFKſGFURGEKCNK\GFGPFQOGVTKWOQHRTGIPCPE[
decidua capsularis and parietalis oppose and
• Unique to hemochorial placenta
fuse. The uterine cavity is completely obliterated
• &GXGNQRUWPFGTRTQIGUVGTQPGKPƀWGPEG
at this point. • Consists of three parts:
Important features of decidua are summa- Ŧ Decidua basalis: Site of implantation
rized in Box 4.6. Ŧ Decidua capsularis: Covers the embryo
Ovulation, fertilization, and implantation are Ŧ Decidua parietalis (vera): Lines the rest of the uter-
shown in Figure 4.8. ine cavity
• Decidua basalis and decidua parietalis each have
three layers:
istology of decidua Ŧ Stratum compactum near the surface
Histologically, the stratum compactum con- Ŧ Stratum spongiosum, the intermediate layer
sists of large polygonal cells (epithelioid cells) Ŧ Stratum basalis near the myometrium
Morula cell ygote

cell ygote
ertili ation
lastocyst
econ ary
Cytotrophoblast oocyte
nner cell
mass
ary
yncytiotrophoblast
Figure 4.8 1XWNCVKQPHGTVKNK\CVKQPCPFKORNCPVCVKQP6JGRTQEGUUQHQXWNCVKQPRKEMKPIWRQHVJGQXWOD[VJGſODTKCG

transfer to the tubal lumen, fertilization in the tube, development of zygote into morula and later into blastocyst, and
implantation into the uterine decidua are diagrammatically represented.
CH 04_p048-060_v3.indd 52 17-07-2015 10:44:14

Box 4.7 istology of decidua Development of the embryo

• Stratum compactum
The conceptus is known as an embryo from the
Ŧ Large polygonal cells with long processes
first mitotic division (fertilization) for a period of
Ŧ Natural killer lymphocytes
Ŧ .GWMQE[VKEKPſNVTCVKQP
8 weeks, that is, from the 3rd to 10th week of gesta-
• Stratum spongiosum tion. However, the critical period of organogenesis
Ŧ Large glands in early pregnancy begins 2 weeks postfertilization; therefore, others
Ŧ Glands disappear in late pregnancy consider this as the beginning of the embryonic
• Stratum basalis period. Organogenesis continues through the
Ŧ Arteries and large veins embryonic period, till the end of the 8th week post-
Ŧ Invaded by trophoblasts fertilization. Cytotrophoblast secretes human cho-
rionic gonadotropin (hCG) by Day 14 postfertiliza-
tion and this is used for the diagnosis of pregnancy.
The inner cell mass of the blastocyst develops
with long processes, lymphocytes called natural into the embryo. By Day 8 postfertilization, the
killer (NK) cells, and stroma. There is leukocytic cells arrange themselves in two layers adjacent
infiltration as well. The stratum spongiosum to each other known as epiblast and hypoblast.
contains large glands in early pregnancy that The hypoblast layer is adjacent to the blastocyst
disappear by late pregnancy. The stratum basa- cavity. The amniotic cavity develops as a fluid-
lis forms part of the basal plate of the placenta. filled space in the epiblast (Fig. 4.9). A layer of
It consists of arteries and dilated veins and is flattened cells originating from and continuous
invaded by trophoblasts. Histology of decidua is with the hypoblast forms a thin membrane on
summarized in Box 4.7. the inner surface of the cytotrophoblasts of the
The decidua produces large amounts of pro- blastocyst. This is the exocoelomic membrane.
lactin, under the influence of progesterone. The cavity lined by the membrane and hypoblast
Decidual prolactin plays a role in maintaining is now called the primitive yolk sac.
amniotic fluid volume, regulating immunological By Day 11 or 12, extraembryonic mesoder-
functions, and enhancing angiogenesis during mal cells, derived from the yolk sac cells, appear
implantation. between the cytotrophoblasts and the exocoelomic
yncytiotrophoblast
Cytotrophoblast
mniotic ca ity
piblast
ocoelomic membrane
Hypoblast
Primiti e yol sac
Figure 4.9 Development of epiblast, hypoblast, amniotic cavity, and yolk sac. The cells of the inner cell mass are
arranged in two layers—epiblast and hypoblast. Amniotic cavity appears in the epiblast and the cells of the hypoblast line
the blastocyst to form the primitive yolk sac.
CH 04_p048-060_v3.indd 53 17-07-2015 10:44:14

y cytiotrophoblast
m iotic ca ity
ilami ar embryo
Primiti e yol sac
xtraembryo ic meso erm

Cytotrophoblast
Figure 4.10 Formation of extraembryonic mesoderm. Extraembryonic mesodermal cells, derived from the cells of the
primitive yolk sac, appear between the exocoelomic membrane and the cytotrophoblasts.
membrane (Fig. 4.10). These cells are loosely The embryonic disc is now known as the bilami-
arranged with cavities in between. The cavities nar disc and has two layers, namely, epiblast and
coalesce to form the chorionic cavity. Another layer hypoblast, and two cavities on either side-amniotic
of cells originates from the hypoblast to line the cavity dorsally and definitive yolk sac ventrally.
inner surface of the exocoelomic cavity and forms The chorionic cavity surrounds the bilaminar disc,
the definitive yolk sac, which is smaller than the the amniotic sac, and the definitive yolk sac.
primitive yolk sac (Fig. 4.11). The chorionic cav-
ity expands and covers the definitive yolk sac and
amniotic cavity. Extraembryonic mesodermal cells
Gastrulation
running between the yolk sac and chorion con- Gastrulation is the process of formation of the
dense into the body stalk that later becomes the three germ cell layers, namely, ectoderm, endo-
umbilical cord. derm, and mesoderm. By the beginning of the
Venous sinuses
mniotic ca ity
ilaminar embryo
econ ary efiniti e yol sac
Chorionic ca ity
traembryonic meso erm
o y stal
Figure 4.11 (QTOCVKQPQHFGſPKVKXG[QNMUCE%GNNUQTKIKPCVGHTQOVJGJ[RQDNCUVCPFNKPGVJGKPPGTUWTHCEGQHVJGRTKOKVKXG

[QNMUCECPFHQTOVJGFGſPKVKXG[QNMUCE6JGECXKVKGUDGVYGGPVJGGZVTCGODT[QPKEOGUQFGTOCNEGNNUJCXGEQCNGUEGFVQ
become the chorionic cavity.
CH 04_p048-060_v3.indd 54 17-07-2015 10:44:14

Box 4.8 rganogenesis

piblast • Occurs during embryonic period
• Extends for 8 weeks from fertilization
Primiti e o e • Formation of all organ systems
• Period most vulnerable to the effects of
Ŧ drugs
Primiti e strea Ŧ radiation
Ŧ infections
Ŧ metabolic/endocrine abnormalities
of the three germ cell layers. It is almost com-

Figure 4.12 Primitive streak and node. Primitive streak pleted by the end of the embryonic period
appears as a thickening on the dorsal surface of epiblast. (Fig. 4.14). The embryo measures about 40 mm
Primitive node is at the cephalic end of the primitive streak. in length; external genitalia are not developed
at this time. A summary of organogenesis is pre-
3rd week postfertilization, a thickening is noted sented in Box 4.8.
on the dorsal aspect of the epiblast and this is The three layers of the trilaminar embryo
called the primitive streak. The cephalic end contribute to the development of organ systems
of this streak is the primitive node (Fig. 4.12). with different functions (Box 4.9).
The cells of the epiblast invaginate in the area
of the primitive node and streak. Some cells dis-
place the hypoblast and form a layer called the
endoderm, and other cells that extend between Fetal period
the endoderm and epiblast become the meso-
derm. The dorsal layer of epiblast forms the ecto- The fetal period begins 8 weeks after fertilization,
derm. The embryo is now trilaminar with three or after 10 completed weeks’ gestation, and con-
layers—ventral endoderm, dorsal ectoderm, and tinues until delivery. During this period, growth
a third layer between the two, the mesoderm of various organs takes place (Box 4.10). The
(Fig. 4.13). embryo grows laterally and longitudinally. The
ends curve inward to assume the typical fetal
shape. Further growth and development of the
rganogenesis fetus to complete maturity depends on uteropla-
Organogenesis or differentiation of cells into dif- cental blood flow, fetal oxygenation, and genetic
ferent organ systems begins after the formation and environmental factors.
Primiti e strea
an no e
piblast ecto erm
n o erm Meso erm

Figure 4.13 Trilaminar disc. The embryo has three layers. The cells of epiblast differentiate into dorsal ectoderm, ventral
endoderm, and a layer of cells between the two, the mesoderm.
CH 04_p048-060_v3.indd 55 17-07-2015 10:44:15

LMP ertili ation
ee s after LMP
ee s after fertili ation
ertili ation
Preimplantation
mplantation
rganogenesis
mbryonic perio etal perio

Figure 4.14 The embryonic and fetal period. Graph shows the embryonic and fetal period in weeks from the last
menstrual period and from the day of fertilization.
Box 4.9 rgan systems developing from layers of embryo

Ectoderm Endoderm Mesoderm
• Epidermis, nails, hair • Lining of gastrointestinal tract • All connective tissue
• Central nervous system • Liver, pancreas • Spleen
• Peripheral nervous system • Lining of respiratory tract • Entire body musculature
• Sensory epithelium of • Thyroid/parathyroid • Blood/lymphatics
ear, nose, and eye • Lining of lower urinary tract • Urogenital system and
• Subcutaneous glands • Lining of tympanic cavity and suprarenal cortex
(pituitary, mammary, and auditory tube • Skeletal system
sweat glands)
Clinical implications Development of fetal organ

Clinical implications of events during fertili ation are systems
given below.
The organ systems that are of relevance to the
• Prior to organogenesis (from fertilization to Day 14)
Ŧ Teratogens have no effect on the embryo
obstetrician are discussed in the following text.
Ŧ Severe insults cause miscarriage
• Secretion of human chorionic gonadotropin (hCG) by Fetal cardiovascular system
trophoblast by Day 14
Ŧ Used for diagnosis of pregnancy
In the cardiogenic plate, the heart develops initially
• Organogenesis (Day 14–Day 56) as two tubular structures which fuse to form a single
Ŧ Susceptible to teratogenic effects from contractile tube and later into a four-chambered
exposure to radiation/drugs and infections structure. The beating heart can be seen as cardiac
poor glycemic control in diabetics activity on ultrasound scan by the 4th week after
fertilization (6th week of gestation).
Box 4.10 Fetal period

etal circulation
Fetal circulation differs from adult circulation for
• From the end of embryonic period till delivery
the following reasons:
• Growth of organ systems affected by
Ŧ WVGTQRNCEGPVCNDNQQFƀQY • Oxygen and nutrients are supplied by the
Ŧ oxygenation umbilical vein.
Ŧ genetic factors • Lungs are not functional and pulmonary cir-
Ŧ Environmental factors such as
culation does not oxygenate the blood.
smoking/tobacco
• Pulmonary vascular resistance is high.
infections
Ŧ Metabolic/endocrine milieu
• Deoxygenated blood is carried to the placenta
by the umbilical arteries.
CH 04_p048-060_v3.indd 56 17-07-2015 10:44:15

Fetal circulation is shown in Figure 4.15 and but fibrosis and complete occlusion occur few
schematically represented in Figure 4.16. days later. The fibrosed ductus venosus becomes
The oxygenated blood from the placenta the ligamentum venosum. The lungs expand;
enters the fetus through the umbilical vein, which the blood flows through the pulmonary circula-
divides into the ductus venosus and portal sinus tion and gets oxygenated. The distal hypogastric
in the liver (hepatic circulation). Most of the blood arteries get obliterated and are called the umbil-
flows through the ductus venosus to the inferior ical ligaments (Box 4.11). The transition from
vena cava and reaches the right atrium. The por- intrauterine to extrauterine life is explained in
tal sinus drains into the liver and the blood also more detail in Chapter 23, The newborn.
reaches the right atrium through the hepatic vein.
Deoxygenated blood from the lower half of the etal bloo
body (below the diaphragm) is also brought to the
Erythrocytes are produced initially by the yolk
right atrium by the inferior vena cava.
sac and later by the liver. By 18 weeks, bone
Part of the blood from the right atrium is
marrow is formed. Fetal erythrocytes are nucle-
shunted into the left atrium through the foramen
ated and larger in size than adult erythrocytes.
ovale and the rest flows into the right ventricle.
Erythropoiesis is controlled by fetal erythropoie-
Blood from the left atrium is pumped into the left
tin. Fetal hemoglobin or hemoglobin F has higher
ventricle and through the aorta supplies blood
affinity for oxygen, making it easier for the fetus
to the head and neck region. The deoxygenated
to extract oxygen from maternal circulation. The
blood from these regions returns through the
level of hemoglobin F decreases toward term, and
superior vena cava to the right atrium. The blood
it is gradually replaced by adult hemoglobin.
that enters the right ventricle is pumped into the
Platelets are produced in the yolk sac, and
pulmonary artery. Almost 90% of this blood is
leukocytes are produced by the spleen and thy-
shunted through the ductus arteriosus into the
mus. Immunoglobulin M (IgM) is produced by the
descending aorta and supplies the entire body
fetus in response to infection. Maternal immuno-
distal to the left subclavian. Deoxygenated blood
globulin G (IgG) crosses the placenta and can be
returns through the hypogastric artery (umbili-
detected in fetal circulation.
cal artery) to the placenta.
Changes in circulation at birth Fetal respiratory systems

Shortly after birth, the umbilical vein and ductus The anatomical development of lungs begins
venosus collapse and close. Functional closure by 25 weeks. Fetal breathing movements can
of foramen ovale and ductus arteriosus occurs be seen, but the lungs do not serve the function
o heart an brain
rch of aorta
uctus arteriosus
uperior ena ca a Pulmonary artery
Hepatic ein
oramen o ale
uctus enosus
Portal sinus escen ing aorta
Umbilical
ein nferior ena ca a
Hypogastric
umbilical arteries
Figure 4.15 The fetal circulation, a diagrammatic representation.
CH 04_p048-060_v3.indd 57 17-07-2015 10:44:15

Pulmonary artery
Pulmonary
circulation
ight entricle Pulmonary uctus arteriosus

eins
ight atrium oramen o ale Left atrium Left entricle orta
nferior ena ca a rain an heart hole bo y istal to

subcla ian
Hepatic circulation
Portal sinus
uctus enosus uperior ena ca a Umbilical arteries
Hepatic ein
Umbilical ein
Placenta
Figure 4.16 The fetal circulation, a schematic representation.
Box 4.11 Changes in circulation at birth Box 4.12 Fetal respiratory system
• Closure of • Development of lungs begins at 25 weeks
Ŧ umbilical vein • Breathing movements seen at 12 weeks
Ŧ ductus venosus • Oxygenation of blood begins at birth
Ŧ foramen ovale • Type II pneumocytes produce surfactants
Ŧ ductus arteriosus • Surfactants
• Expansion of lungs Ŧ Consist of glycerophospholipids such as
• Establishment of pulmonary circulation dipalmitoylphosphatidylcholine
• Obliteration of hypogastric arteries phosphatidylglycerol
phosphatidylinositol
of oxygenation until after birth. Type II pneu- Ŧ Prevent alveolar collapse
Ŧ Are required to prevent RDS
mocytes produce surfactants which prevent
Ŧ Can be induced by corticosteroids
alveolar collapse. Surfactants are made of glyc-
erophospholipids, mainly lecithin. Lecithin DS respiratory distress syndrome.
may be dipalmitoylphosphatidylcholine, phos-
Fetal thyroid gland
phatidylglycerol, or phosphatidylinositol. Lack
of surfactant (in a premature neonate) results Thyroid hormones are secreted by 12 weeks’
in respiratory distress syndrome (RDS). Levels gestational age. They play a major role in fetal
of surfactants increase with gestational age growth and the development of organ systems,
and lung maturity. Corticosteroids induce pro- including the brain. Congenital hypothyroidism
duction of surfactant and are used in preterm does not manifest as cretinism at birth because
deliveries to accelerate pulmonary maturity and small amounts of maternal T4 cross the pla-
prevent RDS. Box 4.12 summarizes important centa. However, early neonatal screening using
features of the fetal respiratory system. thyroid-stimulating hormone (TSH) levels must
CH 04_p048-060_v3.indd 58 17-07-2015 10:44:16

be performed so that congenital hypothyroidism

Box 4.13 Fetal thyroid gland
is diagnosed and treatment initiated immedi-
ately after birth to avoid mental retardation. • Fetal thyroid hormone
Thyroid-stimulating/-inhibiting immunoglob- Ŧ Secreted by 12 weeks
Ŧ Plays major role in fetal growth and development
ulins cross the placenta and can cause neonatal
Ŧ Affects development of brain
hyperthyroidism or hypothyroidism. Antithyroid
• Thyroid-stimulating/-inhibiting immunoglobulins
drugs cross the placenta, and therefore, overtreat- Ŧ Cross the placenta
ment of maternal hyperthyroidism can lead to Ŧ Can cause neonatal hyper-/hypothyroidism
fetal hypothyroidism, interfering with fetal growth • (GVCNVJ[TQKFJCUJKIJCHſPKV[HQTKQFKPG
and development.
The fetal thyroid has a greater affinity for
iodine; therefore, administration of excess of 12 weeks’ pregnancy. The contents of the fetal
iodide to the mother must be avoided. The use bowel, known as meconium, consist of undi-
of radioactive iodine for treatment of the mother gested debris, lanugo hair, desquamated cells,
is contraindicated in pregnancy. Important fea- secretions of glands, and swallowed vernix. The
tures of fetal thyroid gland are listed in Box 4.13. green color is due to biliverdin. Meconium pas-
sage occurs due to passage of bowel peristal-
sis which is normal at term. It can also occur
Fetal gastrointestinal system
in response to vagal stimulation and hypoxia.
Gastrointestinal peristaltic movements, fetal When aspirated, meconium causes chemical
swallowing, and gastric emptying are seen by pneumonitis.
Key points
• Ovulation occurs on Day 14 of a 28-day cycle and • The decidua has three layers—stratum compactum,
14 days prior to onset of menstruation in longer cycles, spongiosum, and basalis. Stratum compactum con-
36 hours after the beginning of the luteinizing hormone sists of epithelioid cells and natural killer (NK) cells.

.*UWTIGCPFJQWTUCHVGTVJGRGCM6JGſTUVOGK- • The conceptus is known as embryo for a period of 8
QVKEFKXKUKQPQHVJGQQE[VGVCMGURNCEGCPFVJGſTUVRQNCT weeks from fertilization and as fetus thereafter till birth.
body is released immediately after the LH surge.
• The inner cell mass, which develops into the embryo,
• Fertilization is the fusion of the nucleus of the oocyte
arranges itself into two layers—the epiblast and hypo-
with that of the sperm. This takes place in the fallopian
blast—by the 2nd week. The amniotic cavity and the yolk
tube. The window of opportunity for fertilization, or the
sac develop in the epiblast and hypoblast respectively.
fertile period, extends from 48 hours prior to ovulation
to 24 hours after. • Extraembryonic mesoderm and chorionic cavity ap-
pear in the space between trophoblasts and yolk sac.
• The fertilized ovum, known as the ygote, divides and be-
comes a morula in 3 days. This enters the uterine cavity. • The primitive streak and node appear in the epiblast.
Cells from the epiblast invaginate at the streak and
• 9KVJCEEWOWNCVKQPQHƀWKFVJGUQNKFOQTWNCDGEQOGU
node to form mesoderm and endoderm. The dorsal
a blastocyst. The cells differentiate into the inner cell
layer of epiblast forms the ectoderm. The embryo now
mass and peripheral trophoblasts.
has three layers.
• Zona hatching occurs and implantation of the blasto- • The critical period of organogenesis begins 2 weeks
cyst into the uterine wall takes place. after fertilization and extends till the end of the embry-
• The trophoblasts differentiate into inner cytotropho- onic period. During the fetal period, only growth and
blasts and outer syncytiotrophoblasts. They burrow development take place.
into the decidua and later form the fetal component of • From ectoderm, endoderm, and mesoderm various
the placenta. organ systems develop.
• Implantation has three stages—apposition, adhesion, • Fetal circulation is different from the adult one in that
and invasion. the placenta supplies oxygen and nutrients, lungs are
• The specialized endometrium of pregnancy is called not functional, the umbilical vein carries oxygenated
decidua. Depending on its location in the uterus, the blood, a large amount of blood from the right atrium is
decidua is termed decidua capsularis, basalis and shunted to the left atrium through the foramen ovale,
parietalis. and blood from the pulmonary artery is redirected to
the descending aorta through the ductus arteriosus.
(Continued)
CH 04_p048-060_v3.indd 59 17-07-2015 10:44:16


• Surfactant is essential to prevent alveolar collapse cross the placenta. The fetal thyroid has a great
and is secreted by type II pneumocytes. The produc- CHſPKV[HQTKQFKPG
tion of surfactant increases with gestational age and • Meconium is formed in the lumen of the intestines
pulmonary maturity. from debris, lanugo hair, vernix, and glandular secre-
• Fetal thyroid hormone is essential for fetal growth tions. Biliverdin gives the green color. Meconium
and development including development of the brain. passage occurs when the fetus is mature or due to
Thyroid-stimulating and -inhibiting immunoglobulins hypoxia/vagal stimulation.
Self-Assessment
2. First polar body is released immediately after luteinizing
Case-based questions hormone surge, just before ovulation, while the second
polar body is released immediately after fertilization.
Case 1 3. Diagnosis of chromosomal or genetic disorders by
Mrs. LN, 28, married for 4 years, came to the hospital sampling polar body, blastomere, or blastocyst, to
with a history of three previous children with congenital select embryos which are not affected by abnormality.
anomalies and early neonatal death. She was advised
preimplantation genetic diagnosis.
Case 2
1. Describe the preimplantation phase of embryonic 1. Fetus can be affected by the following:
period. a. Transplacental passage of thyroid-stimulating
2. 9JGPCTGVJGſTUVCPFUGEQPFRQNCTDQFKGUTGNGCUGF! immunoglobulin, causing neonatal hyperthyroidism.
3. 9JCVKURTGKORNCPVCVKQPIGPGVKEFKCIPQUKU! b. Transplacental passage of antithyroid medica-
tions, causing fetal hypothyroidism.
2. The patient can be managed by close monitoring
Case 2 of thyroid function tests and adjustment of dose of
Mrs. NC, primigravida, presented at 14 weeks with hyper- medications to avoid overtreatment.
thyroidism under treatment with antithyroid medication. 3. 6JGHGVCNVJ[TQKFJCUJKIJCHſPKV[HQTKQFKPG4CFKQ
active iodine treatment should not be given in
1. Can the fetusDGCHHGEVGF!*QY! pregnancy.
2. *QYYKNN[QWOCPCIGVJKURCVKGPV!
3. She was advised treatment with radioactive iodine
LWUVDGHQTGUJGEQPEGKXGF9KNN[QWRTQEGGFYKVJKV! Sample questions
Long-answer question
Answers
1. Discuss the process of fertilization and implantation.
Case 1
1. Embryonic period begins with fertilization. The fer- Short-answer questions
tilized embryo or zygote becomes morula by mitotic
division by Day 3. Fluid accumulates between the 1. Implantation
cells and this becomes a blastocyst. The cells in the 2. Fetal circulation
blastocyst arrange themselves into inner cell mass 3. Organogenesis
and peripheral trophoblasts. Trophoblasts burrow 4. Surfactant
into the decidua and implantation takes place.
CH 04_p048-060_v3.indd 60 17-07-2015 10:44:16

Placenta, Fetal
5 Membranes, and
Amniotic Fluid
Case scenario
Mrs. DK, 23, primigravida at 30 weeks of pregnancy, was referred to the

outpatient clinic for evaluation of reduced amniotic fluid. Mr. and Mrs.
DK were software engineers and the couple had been surfing the net for
information regarding amniotic fluid. They wanted to know why the
fluid was less, how the fluid is produced, and what were the clinical
implications of reduced fluid.
Introduction blastocyst have differentiated into the inner cell

mass or embryoblast and the outer cell mass or
The human placenta is the anatomical and trophoblast (see Chapter 4, Fertilization, implan-
physiological connection between the fetus and tation, and fetal development). The trophoblast
mother. The fetal membranes are an integral differentiates further, invades the decidua and
component of the placenta and gestational sac. develops into the placenta.
Amniotic fluid fills the amniotic cavity and sur-
rounds the fetus. The placenta, membranes, and
amniotic fluid play a key role in fetal nutrition, Differentiation of trophoblast
oxygenation, and maintenance of pregnancy The trophoblast further differentiates into an
through their many functions. outer multinucleated layer with no distinct
cell walls, known as syncytiotrophoblast, and
an inner layer of mononucleated cells, known
as cytotrophoblast. The syncytiotrophoblast
Development of the is formed by mitotic division and migration of
placenta cytotrophoblast cells. The cytotrophoblast fur-
ther differentiates as shown in Figure 5.1. The
Placental development starts with implanta- differentiated trophoblast has specific functions
tion. At the time of implantation, the cells of the which will be discussed later.
CH 05_p061-078_v3.indd 61 17-07-2015 10:45:36

rophoblast
yncytiotrophoblast Cytotrophoblast
tra illous
Villous trophoblast
trophoblast
nterstitial n o ascular
trophoblast trophoblast
Figure 5.1 Differentiation of trophoblast.
Implantation of the blastocyst takes place at cells invade the villi and the villi are now known
the embryonic pole; the trophoblast in this area as secondary villi. Angiogenesis takes place in the
develops into the fetal portion of placenta. By mesoderm, giving rise to tertiary villi (Fig. 5.4a
Day 9–10, vacuoles appear in the syncytiotro- and b). Characteristic features of chorionic villi
phoblast at the embryonic pole and coalesce to are presented in Box 5.1.
form large lacunae. The maternal capillaries are The tertiary villi protrude into the sinusoids
dilated to form sinusoids (Fig. 5.2). The lacunae and the fetal blood is separated from the mater-
and sinusoids merge to form intervillous spaces nal blood by the following four layers:
(Fig. 5.3). Blood from the maternal spiral arteries
• Syncytiotrophoblast
later enters the intervillous spaces.
• Cytotrophoblast
• Connective tissue of the villi
Development of chorionic villi • Vascular endothelium
By Day 11–12, solid columns arising from the The human placenta is hemochorial, that is,
cytotrophoblast project into the decidua. These the maternal blood (hemo-) comes in contact
have an inner core of cytotrophoblasts covered with chorionic villi (-chorial). The villous capil-
by a layer of syncytiotrophoblasts and form the laries connect with vessels in the connecting stalk
primary villi. The extraembryonic mesodermal (umbilical cord) and later with intraembryonic
ometrial
stroma
ater al si usoi s
ometrial la s
mbryo
rophoblastic lacu ae
Cytotrophoblast
y cytiotrophoblast
Figure 5.2 Formation of trophoblastic lacunae and maternal sinusoids. Vacuoles appear in the syncytiotrophoblast and
coalesce to form lacunae. The maternal capillaries dilate to from maternal sinusoids.
CH 05_p061-078_v3.indd 62 17-07-2015 10:45:36

2NCEGPVCHGVCNOGODTCPGUCPFCOPKQVKEƀWKF 63
Materal sinusoi s
rophoblastic lacunae
nter illous spaces

fille ith bloo
mbryo
Cytotrophoblast
yncytiotrophoblast
Figure 5.3 Formation of intervillous spaces. The lacunae and maternal sinusoids merge to form intervillous spaces.
y cytiotrophoblast eso erm

I ter illous spaces
ille ith bloo
Cytotrophoblast
i ii
eso erm
loo essels
a. iii
y cytiotrophoblast eso erm loo essels
Cytotrophoblast
b. i ii iii
Figure 5.4 Structure of villi. a. Longitudinal section i. Primary villi lined by syncytiotrophoblast and cytotrophoblasts
ii. Extraembryonic mesoderm extends into the secondary villi iii. Blood vessels are formed in the mesoderm in tertiary villi. b. Cross-
section showing the trophoblast, mesoderm, and inner core of blood vessels i. Primary villi ii. Secondary villi iii. Tertiary villi.
CH 05_p061-078_v3.indd 63 17-07-2015 10:45:37

spiral arteries and exchange of nutrients and

Box 5.1 Chorionic villi
gases takes place between capillaries in the villi
• Primary villi and maternal blood (Fig. 5.5).
Ŧ Syncytiotrophoblast The chorionic villi surround the entire blas-
Ŧ Cytotrophoblast
tocyst to begin with. The villi at the embryonic
• Secondary villi
pole of the blastocyst proliferate further and are
Ŧ Inner core of mesoderm
• Tertiary villi
known as chorion frondosum. These later develop
Ŧ Blood vessels in the mesoderm into the fetal side of the placenta. The villi cov-
ering the rest of the blastocyst (facing the uter-
ine cavity) degenerate and are known as chorion
blood vessels, thus establishing the fetoplacen- laeve (Fig. 5.6). As the blastocyst expands to fill
tal circulation by the end of the 3rd week. The the uterine cavity, the amnion, chorion laeve and
heart begins to beat by early 4th week and the decidua capsularis fuse to form the amniocho-
circulation begins to function. Maternal blood rion, which in turn fuses with the decidua pari-
enters the intervillous space in spurts from the etalis and obliterates the uterine cavity (Fig. 5.7).
Maternal bloo essel

yncytiotrophoblast
loo entering
in spurts into
inter illous
space
ertiary illi
nter illous
space
Figure 5.5 Hemochorial placenta. Maternal blood enters the intervillous spaces in spurts, bathing the chorionic villi to
exchange nutrients and gases.
eci ua
eci ua basalis
parietalis
m iotic ca ity Chorio
eci ua ro osum
capsularis Chorio
ro osum
Chorio
lae e
m iotic ca ity
m iochorio
Figure 5.6 Chorion frondosum and chorion leave. The

chorionic villi at the embryonic pole of the blastocyst Figure 5.7 Formation of amniochorion. Amniotic sac,
proliferate to form chorion frondosum and the chorionic chorion leave, decidua capsularis, and decidua parietalis
villi covering the rest of the blastocyst degenerate to form fuse to form the amniochorion and obliterate the uterine
chorion leave. cavity.
CH 05_p061-078_v3.indd 64 17-07-2015 10:45:38

From the tip of some of the villi, cytotrophoblas- In the myometrium, they fuse and form mult-
tic cells proliferate and attach themselves to the inucleated giant cells known as placental bed
decidua basalis, forming the stem villi or anchor- giant cells. The interstitial trophoblast cells in
ing villi. Smaller villi branch off from the side of the the myometrium interact with cells of maternal
stem villi and float freely in the intervillous space. immune system. The endovascular trophoblast
These are the terminal villi. Meanwhile, placental cells penetrate the lumen of the spiral arteries
septae develop from the decidua and extend into and cause remodeling of the vessel wall. They
the intervillous space between the main stem villi. initially form cellular plugs that are later dis-
Each main stem villus with its branches supplies placed, allowing blood to flow through the spiral
one cotyledon (Fig. 5.8). arteries. Eventually the musculature of the ves-
By 12–14 weeks, the cytotrophoblast cells and sel wall is destroyed and replaced by fibrinoid
connective tissue of the villi disintegrate and the material. This leads to the spiral arteries being
maternal blood is separated from the fetal blood converted into low-resistance vessels to facilitate
by only two layers: blood flow (Fig. 5.9).
Trophoblastic invasion of spiral arteries
• Thinned out syncytiotrophoblastic layer
occurs in two phases. The first phase occurs by
• Vascular endothelium
12 weeks after fertilization and extends into the
This further facilitates exchange of nutrients decidua basalis. The second phase of invasion
and oxygen. extends to the myometrium and is completed
by 16 weeks postfertilization (Box 5.2). Failure of
trophoblastic invasion of spiral arteries results
in reduction in placental blood flow and is
Extravillous trophoblastic implicated in the causation of preeclampsia, fetal
growth restriction, placental abruption, prelabor
invasion rupture of membranes, and preterm labor.
Meanwhile, the interstitial trophoblastic cells The syncytiotrophoblast, villous and extravil-
first invade the decidua basalis, inner third of the lous trophoblasts serve different functions as
myometrium, and surround the spiral arteries. listed in Box 5.3.
Cotyle on
Uterine eci ua
nchoring illi
eptum
erminal illi
Umbilical cor
Figure 5.8 Formation of cotyledon. Placental septae extend between main stem villi. Each main stem villus with its
branches separated by septae forms a cotyledon.
CH 05_p061-078_v3.indd 65 17-07-2015 10:45:38

teri e eci ua Maternal bloo essel

arteriole
nterstitial piral eci ua

trophoblast
n o ascular
trophoblasts
Cytotrophoblast
Materal bloo
Figure 5.9 Extravillous trophoblastic invasion. The interstitial trophoblast invades the decidua and myometrium. The
endovascular trophoblast penetrates the lumen of the spiral arterioles.
egulation of trophoblastic Box 5.4 Substances regulating trophoblastic

invasion
invasion
• Matrix metalloproteinases
Early trophoblastic invasion and later limita- • Vascular endothelial growth factor (VEGF)
tion of the same process are regulated by several • Insulin-like growth factor 2 (IGF-2)
substances produced by the placenta as listed in • Tissue inhibitors of metalloproteinases
Box 5.4. • Oxygen
• Decidual natural killer cells (lymphocytes)
- insulin-like growth factor 2; vascular endothelial

growth factor.
Box 5.2 Extravillous trophoblastic invasion
• Interstitial trophoblast
Ŧ Invades decidua basalis and myometrium The placenta
Ŧ Forms placental bed giant cells
• Endovascular trophoblast The placenta is well formed by 12 weeks and
Ŧ Invades spiral arteries consists of fetal portion (chorion frondosum)
First phase (by 12 weeks): Invades arteries in and maternal portion (decidua basalis), with
decidua intervillous spaces between the two. The fetal
Second phase (by 16 weeks): Invades arteries
surface is covered by chorion and amnion. The
in myometrium
umbilical cord is attached to the fetal surface
usually at a central location. Decidual septae
extend from the decidua basalis toward the cho-
Box 5.3 Functions of the trophoblasts rion and from grooves on the maternal surface
• Syncytiotrophoblast of the placenta that separate the cotyledons. The
Ŧ Transports nutrients and gases septae do not reach the chorionic plate but stop
Ŧ Secretes peptide and steroid hormones short at the intervillous space so that blood flow
• Villous trophoblast between the cotyledons is uninterrupted. Fetal
Ŧ Formation of villi macrophages known as Hofbauer cells infiltrate
Ŧ Transports of nutrients and gases the placental stroma. They have immunosup-
• Interstitial trophoblast pressive function and secrete cytokines. The
Ŧ Interacts with cells of maternal immune system
placenta enlarges as gestation progresses and
• Endovascular trophoblast
covers 15%–30% of the uterine surface. At term,
Ŧ (CEKNKVCVGURNCEGPVCNDNQQFƀQY
the placenta is 15–25 cm in diameter and weighs
CH 05_p061-078_v3.indd 66 17-07-2015 10:45:38

about 500–600 g (one-sixth the weight of the

Box 5.5 The placenta
fetus) (Fig. 5.10). Some important features of the
placenta are given in Box 5.5. • Well formed by 12 weeks
• Term placenta
Ŧ 15–25 cm in diameter
Ŧ 500–600 g in weight
Development of the Ŧ 3 cm in thickness
umbilical cord Ŧ Covers 15%–30% of inner uterine surface
• Has two parts:
At 5–6 weeks after fertilization, the embryo lies Ŧ Fetal: Chorion frondosum
between the amniotic cavity and yolk sac. The Ŧ Maternal: Decidua basalis
• Maternal surface
dorsal surface of embryo grows faster and the
Ŧ Cotyledons
embryo curves ventrally as the dorsal surface
• Fetal surface
bulges into the amniotic cavity. The yolk sac is Ŧ Covered by amnion and chorion
incorporated into the body of the embryo; the Ŧ Blood vessels
Ŧ Umbilical cord attachment (usually central)
amniotic cavity enlarges and fuses with the cho-

rion laeve. The body stalk is also covered later-
ally by the amnion and this is now known as the
umbilical cord (Fig. 5.11).
The primitive umbilical cord contains part
of the yolk sac, the allantois, vitelline duct, and
loops of bowel. Later, the loops of bowel are
gradually withdrawn, the allantois and vitell-
ine duct are obliterated, the two umbilical
arteries and one vein are covered by Wharton’s
jelly, which is in turn covered by the amnion
(Fig. 5.12). Occasionally, obliterated vitelline
duct and allantois may be present. The con-
tents of the umbilical cord at term are listed
a.
in Box 5.6.
Box 5.6 Contents of the umbilical cord at term

• Covering epithelium
• Wharton’s jelly
• Blood vessels
Ŧ Two arteries
Ŧ One vein
• Occasionally
Ŧ Obliterated vitelline duct
Ŧ Obliterated allantois
Fetal membranes
The two fetal membranes are amnion and chorion.
b.
The chorion
Figure 5.10 Gross appearance of the placenta. a. Fetal
surface with umbilical cord attached. b. Maternal surface The chorionic membrane is derived from chorion
showing cotyledons. laeve. It is separated from the amnion initially
CH 05_p061-078_v3.indd 67 17-07-2015 10:45:38

llantois hartons jelly
a. b.
Figure 5.11 Formation of umbilical cord. a. At 10 weeks’ gestation, the yolk sac, allantois, umbilical arteries, and vein
are included in the umbilical cord. b. At 20 weeks’ gestation, only the umbilical arteries and vein are present, covered by
Wharton’s jelly.
oops o ut
mbilical artery
mbilical ei
a. b.
Figure 5.12 Cross-section of the cord. a. At 10 weeks’ gestation, containing loops of gut, allantois, and umbilical vessels.
b. At term, containing two arteries and a vein, covered in Wharton’s jelly.
by the chorionic cavity but later, as the chori- Functions of amnion

onic cavity disappears, fuses with the amnion
(Fig. 5.7). There may be loose connective tissue Amnion is not just a membrane forming a cavity
between the amnion and chorion. to house the fetus. The epithelial cells synthesize
fibronectin, prostaglandin, interleukin, vasoac-
tive peptides such as endothelin and parathyroid
hormone–related peptide (PTH-RP), and cortico-
tropin-releasing hormone (CRH). The mesenchy-
The amnion mal cells of the amniotic fibroblasts synthesize
The amnion is derived from fetal ectoderm and collagen, interleukin, and prostaglandins. The
is a tough membrane that surrounds the fetus. It collagen provides remarkable tensile strength
lines the fetal surface of the placenta and umbil- and does not break or rupture easily. It is elas-
ical cord. The amnion has no blood vessels, tic and expands to accommodate the growing
nerves, or lymphatics. It has five layers: fetus. Solute and water transport also takes place
through the amnion (Box 5.7).
• Inner layer of cuboidal epithelium
• Basement membrane
• Acellular compact layer made of collagen #OPKQVKEƀWKF
• Fibroblast-like mesenchymal layer
• Outer layer of acellular, loose connective tis- Amniotic fluid fills the amniotic cavity and sur-
sue between amnion and chorion rounds the fetus from early pregnancy.
CH 05_p061-078_v3.indd 68 17-07-2015 10:45:39

and the chorionic cavity disappears, leaving only

Box 5.7 Functions of amnion
the amniotic cavity filled with amniotic fluid.
• Synthesis of substances
Ŧ Epithelial cells synthesize
Fibronectin Sources
Prostaglandin
Amniotic fluid is produced and cleared contin-
Interleukin
Vasoactive peptides
uously. It has been estimated that the entire vol-
- Endothelin ume of amniotic fluid is replaced several times a
- Parathyroid hormone–related peptide day. The sources of amniotic fluid and routes of
Corticotropin-releasing hormone clearance are listed in Box 5.8 and also shown in
Ŧ Mesenchymal cells synthesize Figure 5.13.
Collagen
Prostaglandin
Ma or sources of production
Interleukin
• Mechanical functions Fetal urine production increases gradually from
Ŧ Collagen provides midtrimester and is about 1000–1200 mL/day
tensile strength at term. Maternal position and gestational age
elasticity influence rate of urine production. Hourly urine
• Metabolic functions
production reduces 2 weeks prior to onset of
Ŧ Transport of water and solutes
Box 5.8 2TQFWEVKQPCPFENGCTCPEGQHCOPKQVKEƀWKF

Formation
• Major sources of production
Early in pregnancy, there are two cavities sur- Ŧ Fetal urine
rounding the embryo—the amniotic cavity sur- Ŧ (GVCNNWPIƀWKF
rounded by amnion, and the exocoelomic cav- • Major routes of clearance
ity (or chorionic cavity) surrounded by chorion Ŧ Fetal swallowing
and containing coelomic fluid, (see Chapter 4. Ŧ Intramembranous transfer to fetal blood
Fertilization, implantation, and fetal develop- • Minor sources of production
Ŧ Secretions from fetal oral–nasal cavities
ment). The amniotic cavity gradually enlarges and
• Minor routes of clearance
the chorionic cavity decreases in size. By the 14th
Ŧ Transmembranous transfer to maternal blood
week of gestation, the amnion and chorion fuse
mL
Urine
mL
Lung flui
mL
ral nasal secretions
mL
allo ing
mL
ntramembranous transfer
mL
ransmembranous transfer
Figure 5.13 &KCITCOOCVKETGRTGUGPVCVKQPQHUQWTEGUCPFTQWVGUQHENGCTCPEGQHVJGCOPKQVKEƀWKF
CH 05_p061-078_v3.indd 69 17-07-2015 10:45:39

labor. Placental insufficiency, fetal cardiac fail- (TGF) D and E, insulin-like growth factor-1 (IGF-
ure, and outflow obstruction in the urinary tract 1), erythropoietin, and granulocyte colony-stim-
cause marked reduction in urine production. ulating factor (G-CSF) are also found in amniotic
This can result in oligohydramnios. fluid. These factors are involved in the growth of
Fetal lung secretions fill the respiratory tract. various tissues and organs in the fetus.
The total volume secreted is about 400 mL/day. Cells suspended in amniotic fluid are fetal
Fifty percent of the fluid exits through the mouth epithelial cells, fibroblasts, amniocytes, pluripo-
into the amniotic fluid and the other 50% is swal- tent stem cells, and cells from the respiratory
lowed by the fetus. Lung secretions are reduced and urinary tract of the fetus. Fetal lanugo hair is
in fetal asphyxia and during labor. also present. The fibroblasts obtained by amnio-
centesis are used for karyotyping and diag-
Ma or routes of clearance nosis of genetic and chromosomal disorders.
Composition of amniotic fluid is given in Box 5.9.
Fetal swallowing increases with gestational age
and is about 500–1000 mL/day at term. Swallowing
is much less in fetuses with esophageal or duode- Box 5.9 %QORQUKVKQPQHCOPKQVKEƀWKF
nal atresia and in neurologic abnormality such as
• Carbohydrates, proteins, lipids
anencephaly. This may result in polyhydramnios.
• Urea, creatinine, uric acid, lactate, and pyruvate
Intramembranous transfer occurs across the
• Electrolytes, enzymes, hormones
blood vessels on the fetal surface of the placenta. • Glycerophospholipids
Water and solutes are transported to the fetus Ŧ Lecithin
due to osmotic gradient between the amniotic Ŧ Sphingomyelin
fluid and fetal blood. About 400 mL of fluid is Ŧ Phosphatidylglycerol
absorbed by this route. Ŧ Phosphatidylinositol
• Growth factors
Ŧ Epidermal growth factor
Minor sources of production and
Ŧ Transforming growth factors D and E
routes of clearance Ŧ Insulin-like growth factor-1
Ŧ Erythropoietin
These are secretions from the nasal/oral cav-
Ŧ Granulocyte colony-stimulating factor
ities that account for about 25–30 mL of fluid.
• Cells
Transmembranous absorption of about 10 mL of Ŧ (GVCNGRKVJGNKCNEGNNUſDTQDNCUVU
amniotic fluid occurs through the decidua into Ŧ Amniocytes, stem cells
the maternal circulation.
Composition Characteristics
The amniotic fluid contains carbohydrates, pro- The pH of amniotic fluid is 7–7.5, which is much
teins, peptides, lipids, urea, creatinine, uric acid, higher than the pH of the vagina (4–4.5). This
lactate, pyruvate, electrolytes, enzymes, and hor- change in pH is used as a test for rupture of
mones. Glycerophospholipids in the amniotic membranes. The osmolality is 260–280 mOsm/L
fluid include lecithin, sphingomyelin, phosphat- (Box 5.10). The fluid is clear in early gestation but
idylglycerol, and phosphatidylinositol. The pres- becomes straw colored in the third trimester and
ence of these components is used for diagnosis bits of vernix appear by term.
of fetal pulmonary maturity.
The hormones in amniotic fluid include estro-
Box 5.10 %JCTCEVGTKUVKEUQHCOPKQVKEƀWKF
gens, progesterone, cortisol, human chorionic
gonadotropin (hCG), and insulin. Inhibin A and • pH: 7–7.5
B are also present in the fluid. Levels of inhibin A, Ŧ &KHHGTGPVKCVGUKVHTQOXCIKPCNƀWKF
hCG, estriol, and alpha fetoprotein are used for • Color
prenatal screening for birth defects. Ŧ Early gestation: Clear
Ŧ Third trimester: Straw colored, contains vernix
Several growth factors such as epidermal
• Osmolality: 260–280 mOsm/L
growth factor (EGF), transforming growth factors
CH 05_p061-078_v3.indd 70 17-07-2015 10:45:39

olume • Provides space for the growth and develop-

ment of
The volume of amniotic fluid varies with ges- – Fetal skeleton
tational age. It has been estimated at different – Lungs
gestational ages using dye dilution technique. It – Gastrointestinal systems
increases progressively and rapidly from 8 weeks’ • Provides growth factors
gestation till 28 weeks’ gestation, increases rela- • Has antibacterial properties
tively slowly till 34 weeks, and remains more or • Maintains even temperature
less constant till 38 weeks. Thereafter, it reduces • Forms a hydrostatic wedge in labor
by 100 mL per week and is about 500 mL at 40 – Helps in cervical dilatation
weeks (Box 5.11).
Box 5.11 8QNWOGQHCOPKQVKEƀWKF

Placental circulation
• 12 weeks: 50 mL
• 16 weeks: 200 mL Oxygenated maternal blood enters the intervil-
• 28 weeks: 800 mL lous space in spurts, under pressure, through the
• 34 weeks: 1000 mL spiral arteries. It bathes the villi which are free
• 40 weeks: 500 mL
floating, and exchange of gases and nutrients
takes place. The pressure gradually decreases as
the blood enters the maternal veins and returns
Clinical applications to the maternal circulation (Fig. 5.14).
Amniotic fluid analysis is performed for prena- The oxygenated blood from the villi enters
tal screening and diagnosis, and evaluation and the umbilical vein and reaches the fetal heart.
management of certain clinical situations. The Less oxygenated blood is brought by the umbil-
clinical applications are given in the Box 5.12. ical arteries to the villi as described in Chapter
4, Fertilization, implantation, and fetal devel-
Functions opment. About 750 mL of blood flows through
the placenta every minute and the blood in the
Amniotic fluid surrounds the fetus and has sev- intervillous space is replaced 3–4 times/min.
eral functions. During uterine contractions, there is no arterial
• Protects the fetus from trauma or venous blood flow (Box 5.13).
• Prevents umbilical cord compression
• Supplies nutrients Box 5.13 Placental circulation
• 4CVGQHDNQQFƀQYO.OKP
Box 5.12 %
NKPKECNCRRNKECVKQPUQHCOPKQVKEƀWKF • Replaced 3–4 times/min
CPCN[UKUCPFR*QHXCIKPCNƀWKF • 0QDNQQFƀQYFWTKPIWVGTKPGEQPVTCEVKQPU
• Second trimester
Ŧ Karyotyping of fetal cells
Fetal gender for X-linked disorders Functions of placenta
Chromosomal defects
Ŧ Diagnosis of intrauterine infections The placenta is a unique organ that has a short life
Rubella span but performs multiple key functions. It trans-
Toxoplasma fers nutrients and oxygen to the fetus, secretes
Cytomegalovirus hormones and has immunological functions.
Parvovirus
• Third trimester
Ŧ Bilirubin: Rh alloimmunization Placental transfer
Ŧ Lecithin/sphingomyelin
Ŧ Phosphatidylglycerol
• R*QHXCIKPCNƀWKF
} Fetal pulmonary
maturity
Transfer of nutrients, gases, and other sub-
stances is an important function of the placenta.
Placental transfer is influenced by several factors
Ŧ Rupture of membranes
as given below:
CH 05_p061-078_v3.indd 71 17-07-2015 10:45:39

Umbilical essels
Chorionic illi
nter illous space
piral artery
Vein
Figure 5.14 Placental circulation. Oxygenated blood from maternal blood enters the intervillous spaces through the spiral
arteries. The blood returns to the maternal circulation through the veins.
• The concentration of the substance in mater- Substances transferred across placenta by

nal and fetal blood and the gradient between various mechanisms are listed in Table 5.1.
the two
• Proportion of bound and free forms of the
substance
Metabolic functions
• Blood flow through placenta and villous The placenta, in addition to transporting nutrients
capillaries from the mother to fetus, also synthesizes glyco-
• Mechanism of transfer gen to supply energy to the developing fetus, cho-
• Area available for exchange of substance lesterol as a precursor for steroid hormones and
• Amount of substance metabolized by placenta proteins for fetal nutrition. Lactate is produced as
a waste product of metabolism (Box 5.15).
Mechanism of transfer
The mechanism of placental transfer of gases, Endocrine functions
nutrients and other substances is summarized Placental hormones play a major role in main-
in Box 5.14. tenance of pregnancy, fetal and maternal
Box 5.14 Mechanism of placental transfer Table 5.1 Substances and their mechanisms of
• Simple diffusion transport
Ŧ Passive transfer along concentration gradient
Substances Mechanism of
Ŧ Transfers molecules of molecular weight <500 Da
transport
• Facilitated diffusion
Ŧ Active transfer against concentration gradient Oxygen
• Endocytosis and exocytosis Carbon dioxide
Ŧ 'PIWNſPIQHUWDUVCPEGKPCXGUKENGCPFTGNGCUGQH Water Simple diffusion
contents at the other end Electrolytes
• Carrier-mediated active transport
Anesthetic gases
Ŧ Uses ATP
Ascorbic acid
Ŧ Involves a carrier substance Facilitated diffu-
• $WNMƀQYUQNXGPVFTCI Iron
sion
Ŧ Along hydrostatic/osmotic pressure gradient Lactate
Ŧ Transfers water and dissolved substances Glucose
Carrier-mediated
• Transfer through channels Amino acids
active transport
Ŧ Involves micropores in plasma membrane Calcium
Ŧ Transfers small molecules Fatty acids and triglycerides Endocytosis and
Proteins exocytosis
A P, adenosine triphosphate.
CH 05_p061-078_v3.indd 72 17-07-2015 10:45:39

After 5 weeks, it is produced by only the syncy-

Box 5.15 /GVCDQNKEſPEVKQPUQHRNCEGPVC
tiotrophoblast. It has two subunits: D and E. The
Synthesis of the following: D subunit is shared by LH, follicle-stimulating
• Glycogen hormone (FSH) and thyroid-stimulating hor-
• Cholesterol mone (TSH), but the E subunit is characteristic
• Proteins and specific to hCG. Therefore, the E subunit is
• Lactate used in all measurements of hCG in pregnancy.
Characteristics of hCG are given in Box 5.17.
metabolism, and parturition. The corpus luteum
secretes hormones, mainly estrogen and pro- Box 5.17 uman chorionic gonadotropin
gesterone, in early pregnancy, but the placenta
• Glycoprotein
takes over as the major source of hormones by
• Has D and Esubunits
7–9 weeks. Hormones secreted by the placenta
x E5WDWPKVKUURGEKſEVQJ%)
are peptide hormones and steroid hormones. x DSubunit shared by LH, FSH, and TSH
Placental hormones also serve autocrine or • Secreted by syncytiotrophoblast
paracrine functions, that is, they act on the cells • Regulated by placental GnRH, inhibin, and activin
producing the hormone or on adjacent cells.
The peptide and steroid hormones secreted S follicle-stimulating hormone; n gonadotropin-releasing
hormone; luteinizing hormone; S thyroid-stimulating
by the placenta are listed in Box 5.16. hormone.
hCG levels in maternal serum and urine

Peptide and glycopeptides
hormones Human chorionic gonadotropin can be detected
in maternal blood and urine 8–10 days after fertil-
A number of peptide and glycopeptides hor- ization. The serum level is 100 mIU/mL at 2 weeks
mones are produced by the placenta that play after fertilization, peaks to 100,000 mIU/mL at 10
a crucial role in maintenance of pregnancy, glu- weeks, and declines as shown in Fig. 5.15. By 16
cose, fat and protein metabolism, and initiation weeks, a nadir is reached (20,000 mIU/mL) and
of parturition. maintained for the rest of the pregnancy (Box 5.18).
uman chorionic gona otropin Box 5.18 Maternal serum human chorionic gon-
In the blastocyst stage, hCG, a glycoprotein, is adotropin levels in pregnancy
produced by both cyto- and syncytiotrophoblast. • Detected by 7–10 days after fertilization
• Levels double every 48 hours
Box 5.16 ormones secreted by the placenta • Peaks by 8–10 weeks to 100,000 mIU/mL
• Begins to decline by 10–12 weeks
• Peptide hormones • Reaches a nadir by 16 weeks
Ŧ Human chorionic gonadotropin
Ŧ Human placental lactogen
Ŧ Chorionic adrenocorticotropin
Ŧ Relaxin
Ŧ Parathyroid hormone–related peptide
U mL
Ŧ Growth hormone variant

Ŧ Releasing hormones similar to hypothalamic hor-
mones
Gonadotropin-releasing hormone
hC
Corticotropin-releasing hormone
Growth hormone–releasing hormone
Ŧ Other peptide hormones
Leptin
Neuropeptide Y ee s of pregnancy
Inhibin and activin
Figure 5.15 Serum human chorionic gonadotropin (hCG)
• Steroid hormones
levels in pregnancy. Level of hCG begins to rise by 7–10
Ŧ Estrogens
days after fertilization, peaks by 8–10 weeks, and declines
Ŧ Progesterone
by 16 weeks.
CH 05_p061-078_v3.indd 73 17-07-2015 10:45:40

Maternal urine contains the degradation uman placental lactogen levels

product, namely, beta-core fragment. Levels in in maternal serum
urine follow the serum levels. Human placental lactogen can be detected 5–10
Functions days after fertilization. Levels start rising by 10
weeks, continue rising till 34–36 weeks, and pla-
Refer to Box 5.19. teau thereafter (Fig. 5.16).
Box 5.19 Functions of human chorionic
gonadotropin
• Maintenance of corpus luteum
g mL serum
• Stimulation of
Ŧ testicular testosterone in male fetus
Ŧ maternal thyroid hormone production
Ŧ relaxin secretion by corpus luteum
hPL
Clinical applications
Clinical applications of hCG are listed in the
Box 5.20. The most important application is in
the diagnosis of pregnancy. High levels (>100,000
mIU/mL) are found in multifetal pregnancy, ges-
tational trophoblastic disease (GTD), Down syn- ee s of pregnancy
drome, and erythroblastosis fetalis. Low levels Figure 5.16 Serum human placental lactogen (hPL)
are found in ectopic pregnancy and early preg- levels in pregnancy. Human placental lactogen is
nancy loss. detected 5–10 days after fertilization, continues to rise till
34–36 weeks, and plateaus thereafter.
Box 5.20 Clinical applications of human
chorionic gonadotropin (hCG) Functions
Testing levels of hCG helps in the diagnosis of the fol- Human placental lactogen is secreted mainly
lowing: into maternal blood. It plays a major role in
• Pregnancy maternal carbohydrate and lipid metabolism
• Gestational trophoblastic disease (Box 5.22).
• Down syndrome
• Ectopic pregnancy
• Early pregnancy loss Box 5.22 Functions of human placental lactogen
• Lipolysis
uman placental lactogen • Acts as insulin antagonist
• Growth and differentiation of glandular tissue of breast
Also known as chorionic somatomammotropin, • Fetal angiogenesis
human placental lactogen (hPL) is secreted by
syncytiotrophoblasts. The characteristics of this
hormone are given in Box 5.21.
Other pepti e hormones
Box 5.21 Characteristics of human placental Though hPL and hCG are the two most import-
lactogen ant peptide hormones, there are several others
which also play a significant role in pregnancy.
• Polypeptide hormone
• Secreted by syncytiotrophoblasts
These are listed in Table 5.2.
• Has a structure similar to prolactin
• Has plasma half-life of 20–30 s Steroi hormones
• Levels depend on placental mass Steroid hormones produced by the placenta are
• Stimulated by insulin and IGF-1 essential for the key events of pregnancy, includ-
• Inhibited by PGE2 and PGF2D ing maintenance of uterine quiescence, prepara-
- , insulin-like growth factor 1; P prostaglandin E2; P tion of the breasts for lactation, and initiation of
prostaglandin F2. parturition.
CH 05_p061-078_v3.indd 74 17-07-2015 10:45:40

its sulfate (DHEAS) are used as precursors by the

Table 5.2 ther peptide hormones of placenta
placenta (Fig. 5.18).
ormone Function In pregnancy, the main source of the estro-
Chorionic Exact function not known gen precursor DHEAS is the fetal adrenal gland,
adrenocorticotropin though the maternal adrenal gland also pro-
Relaxin Uterine relaxation in duces it in small amounts. Fetal liver and adrenal
pregnancy glands synthesize cholesterol from lipoproteins.
PTH-RP Calcium transport for fetal This cholesterol is used as substrate for synthesis
growth of DHEAS by fetal adrenal glands. The fetal adre-
hGH-V Insulin resistance nal glands have a prominent fetal cortical zone
GnRH Regulation of hCG production that secretes DHEAS; this is transported from the
CRH Placental ACTH secretion; adrenal glands to the placenta, where it is con-
initiation of parturition verted to estrogens (Fig. 5.19).
Growth hormone– Regulation of hGH-V Most of the estrogens produced by the pla-
releasing hormone production
centa enter the maternal circulation. Three forms
Leptin Fetal growth and development
of estrogen are usually seen—estrone, estradiol,
Neuropeptide Y Release of CRH and estriol. Estriol is produced in small amounts
Inhibin Inhibition of FSH and ovulation; in nonpregnant women but is the predominant
inhibition of GnRH
form of estrogen in pregnancy. Hydroxylation of
Activin Exact function not known
DHEA to 16 (OH) DHEA, which is essential for
AC adrenocorticotropic hormone; C corticotropin-releasing
hormone; S follicle-stimulating hormone; n gonadotropin-
estriol synthesis, occurs in fetal adrenal gland and
releasing hormone; hC human chorionic gonadotropin; h - final conversion to estriol occurs in the placenta.
growth hormone variant; P - P parathyroid hormone–related Additional 15-hydroxylation of DHEA in fetal
protein.
adrenal gland/liver leads to synthesis of estetrol,
which is unique to the pregnant state (Box 5.23).
Placental estrogen production is reduced in
some conditions (Box 5.24).
Functions
stra iol ng mL
Estrogen has many important functions in preg-

nancy and parturition (Box 5.25).
Sulfatase
ee s of pregnancy
3 beta-hydroxysteroid
Figure 5.17 Serum estrogen level in pregnancy. Estrogen dehydrogenase
level begins to rise by 8 weeks, and remains elevated till
the onset of labor. roste e io e
Aromatase
strogens
stro e
Large amounts of estrogens are produced by
the placenta throughout pregnancy (Fig. 5.17).
During the first 6 weeks, the corpus luteum
secretes estrogens, but this is taken over by the stra iol
placenta by the 7th week. The ovary synthesizes
estrogen from cholesterol or progesterone but Figure 5.18 Placental estrogen synthesis. D A
the placenta lacks the enzymes required for this; dehydroepiandrosterone; D AS dehydroepiandrosterone
therefore, dehydroepiandrosterone (DHEA) or sulfate.
CH 05_p061-078_v3.indd 75 17-07-2015 10:45:40

a a
H H stetrol stetrol
Li er
ary
stra iol
H H
striol striol
H H H
renal
renal glan
glan stra iol stra iol
strone strone
Figure 5.19 Synthesis of estriol and estetrol in the placenta.
Box 5.23 Placental estrogens Box 5.24 Conditions which reduce placental
estrogen production
• Precursor of estrogens (DHEAS) is produced by
Ŧ fetal adrenal gland • Fetal conditions
Ŧ maternal adrenal gland Ŧ Anencephaly
• Estrogens Ŧ Fetal death
Ŧ Estrone Ŧ Adrenal hypoplasia
Synthesized from DHEAS Ŧ &GſEKGPE[KPEJQNGUVGTQNU[PVJGUKU
Ŧ Estradiol Ŧ Down syndrome
Synthesized from DHEAS • Placental
Ŧ Estriol Ŧ 5WNHCVCUGFGſEKGPE[
Synthesized from 16(OH) DHEAS Ŧ #TQOCVCUGFGſEKGPE[
16-hydroxylation occurs in fetal adrenal • Maternal
Is the predominant estrogen in pregnancy Ŧ Adrenal dysfunction
Ŧ Estetrol Ŧ Gestational trophoblastic disease
Synthesized from 15, 16(OH) DHEAS Ŧ Glucocorticoid therapy
15 hydroxylation occurs in fetal liver
Produced only in pregnancy
Box 5.25 Functions of estrogen
D AS dehydroepiandrosterone sulfate.
• +PETGCUGUWVGTKPGDNQQFƀQY
• Prepares breast for lactation
rogesterone • Stimulates hormone-binding globulin production in liver
As mentioned earlier, the corpus luteum is the main • Increases fetal surfactant production
source of progesterone till 8–10 weeks. In pregnan- • Initiates parturition
cies where exogenous progesterone support is con- Ŧ By increasing prostaglandin production
sidered necessary, it should be administered only
up to 10 weeks. Beyond this period of gestation, the Box 5.26 Placental progesterone
placenta takes over and produces large quantities
• Production begins by 8–10 weeks
of progesterone (Box 5.26; Fig. 5.20).
• Precursor: LDL cholesterol from mother
Functions • Rate of production: 250 mg/day
• Metabolized to pregnanediol
Functions of progesterone are listed in Box
5.27. Maintenance of pregnancy and uterine D low-density lipoprotein.
CH 05_p061-078_v3.indd 76 17-07-2015 10:45:40

relaxation are important functions of progester-

one. Deficiency of progesterone in early preg-
nancy can lead to miscarriage.
Progesterone ng mL
ther substances produced by the

placenta
Vascular endothelial growth factor (VEGF), pla-
cental growth factor, epidermal growth factors
(EGF), insulin-like growth factor 1 and 2 (IGF-1
and IGF-2), and fibroblast growth factor (FGF) are
substances produced by syncytiotrophoblasts.
ee s of pregnancy
They play a role in regulation of cell proliferation,
Figure 5.20 Serum progesterone level in pregnancy. The cell differentiation, and angiogenesis in the villi.
progesterone levels rise gradually from early pregnancy
but fall toward term.
Immunologic functions
Pregnancy can be considered an allograft.
Several protective mechanisms are in place to
Box 5.27 Functions of progesterone
prevent rejection of this allograft by the mother.
• Preparation of endometrium for implantation It was believed that the placenta serves as an
• Maintenance of pregnancy anatomic barrier between the mother and fetus,
• Uterine relaxation but now there is evidence that maternal cells
• Suppression of uterine contraction come in contact with fetal cells. The placental
• By inhibition of prostaglandin production
immunological function is complex but crucial
Ŧ Stimulation of glandular proliferation in breast
for normal fetal development and the continua-
P prostaglandin. tion of pregnancy.
Key points
• Development of the placenta starts with implantation. • The term placenta weighs about 500–600 g and is
The blastocyst differentiates into inner cell mass or 15–25 cm is diameter.
embryoblast and trophoblasts.
• The amniotic sac expands and fuses with the chorion
• Trophoblasts differentiate into syncytiotrophoblasts laeve and lines the sides of the body stalk. This later
and cytotrophoblasts. develops into the umbilical cord.
• Implantation of the blastocyst takes place at the • Placental circulation consists of oxygenated blood
embryonic pole. Trophoblasts in this area develop brought to the placenta by spiral arterioles and trans-
into placenta. The decidua at the site of implantation port of nutrients and gases through the intervillous
develops into the maternal portion of the placenta. space into fetal vessels in chorionic villi; these nutrients
• By Day 11 or 12, chorionic villi begin to develop. and gases are then transported through the umbilical
Primary, secondary, and tertiary villi are formed by vein to the fetus. The less oxygenated blood from fetus
trophoblasts, inner core of mesoderm, and angio- is brought to the placental villi by umbilical arteries.
genesis. • Functions of the placenta include placental transfer and
metabolic, endocrine, and immunological functions.
• Further trophoblastic invasion into the decidua is by
interstitial trophoblasts and into the spiral arteries by en- • Placental transfer of nutrients and gases takes
dovascular trophoblasts. This takes place in two phases. place by simple diffusion, facilitated diffusion, active
• The fully developed placenta has fetal and maternal VTCPURQTVDWNMƀQYGPFQE[VQUKUCPFVTCPUHGTVJTQWIJ
surfaces. The fetal surface is covered by chorion and channels.
amnion, with umbilical cord attached centrally. The • Placenta also synthesizes glycogen, cholesterol, and
maternal surface is divided into cotyledons. some proteins.
CH 05_p061-078_v3.indd 77 17-07-2015 10:45:41


• Placenta produces peptide and steroid hormones. • Human placental lactogen plays a major role in carbo-
This is one of the major functions of placenta. hydrate and lipid metabolism.
• The important peptide hormones are human chorionic • Placenta produces estrone, estradiol, estriol, and
gonadotropin (hCG) and human placental lactogen estetrol from fetal and maternal precursors. Estrogen
(hPL). The important steroid hormones are estrogen is essential for initiation of labor.
and progesterone.
• Progesterone is the hormone that causes uterine
• Human chorionic gonadotropin is required for main- relaxation and maintains pregnancy. This is produced
tenance of corpus luteum and for stimulation of fetal by the corpus luteum in early pregnancy and by the
testosterone. Serum hCG is used for diagnosis of placenta from 8 to 10 weeks.
pregnancy, gestational trophoblastic disease, Down
• Placenta also has immunological functions which are
syndrome, and ectopic pregnancy.
complex but essential for continuation of pregnancy.
Self-Assessment
Case-based questions 3. Volume is about 800 mL at 28 weeks, 1000 mL at 34
weeks and reduces to 500 mL at term.
Case 1 4. (KTUVVTKOGUVGT(QTMCT[QV[RKPIHQTKFGPVKſECVKQPQH
fetal gender and chromosomal anomalies
Mrs. DK, 23, primigravida, at 30 weeks of pregnancy, was Second trimester: Diagnosis of intrauterine infections
referred to the outpatient clinic for evaluation of reduced Third trimester: Measurement of bilirubin levels,
COPKQVKEƀWKF lecithin/sphingomyelin ratio and phosphatidylglycerol
1. What are the major sources and routes of clearance levels.
QHCOPKQVKEƀWKF!
2. 9JCVCTGVJGHWPEVKQPUQHCOPKQVKEƀWKF!
3. 9JCVKUVJGXQNWOGQHCOPKQVKEƀWKFCVXCTKQWUIGUVC- Case 2
VKQPCNCIGUKPVJGVJKTFVTKOGUVGT! 1. hCG is produced by the cytotrophoblast and syncy-
4. 9JCVCTGVJGENKPKECNCRRNKECVKQPUQHCOPKQVKEƀWKF tiotrophoblast of the placenta initially and only by the
CPCN[UKU! syncytiotrophoblast later. EhCG is a subunit which is
RTQFWEGFQPN[D[VJGRNCEGPVCCPFVJGTGHQTGURGEKſE
to pregnancy.
Case 2 2. It maintains the corpus luteum, stimulates relaxin
Mrs. AB, 32, multigravida, presented with vaginal bleed- production by corpus luteum, stimulates produc-
ing at 8 weeks of pregnancy. She was asked to perform a tion of relaxin, thyroid hormone, and testosterone in
blood test to estimate serum E hCG levels. the mother by the corpus luteum, thyroid gland, and
1. Where is EJ%)RTQFWEGFKPRTGIPCPE[!9JCVKUE testes respectively.
J%)CPFYJCVKUKVUKORQTVCPEG! 3. High levels indicate hydatidiform mole, low levels in-
2. What are the functions of EJ%)KPRTGIPCPE[! dicate failing pregnancy or ectopic pregnancy, normal
3. How does measurement of E hCG levels help in man- levels indicate normal ongoing pregnancy.
CIGOGPVQHDNGGFKPICVYGGMUŏRTGIPCPE[!
Sample questions
Answers Long-answer question
Case 1 1. Discuss the development, structure, and functions of
placenta.
1. 6JGOCLQTUQWTEGUQHCOPKQVKEƀWKFCTGHGVCNWTKPG
CPFHGVCNNWPIƀWKF6JGOCLQTTQWVGUQHENGCTCPEG
are fetal swallowing and intramembranous transfer Short-answer questions
across the blood vessels on the fetal surface of
1. Implantation
placenta.
2. Human chorionic gonadotropin
2. #OPKQVKEƀWKFRTQVGEVUVJGHGVWURTGXGPVUEQTFEQO-
pression, provides nutrients and growth factors, has 3. Placental estrogens
antibacterial properties, and maintains even tempera- 4. Human placental lactogen
ture. It also helps in cervical dilatation in labor. 5. Placental circulation
6. Chorionic villi
CH 05_p061-078_v3.indd 78 17-07-2015 10:45:41

6 Physiology of Labor
Case scenario
Mrs. KT, 25, primigravida, was brought to the labor room with history
of watery vaginal discharge for 4 hours. Examination revealed a term-
size uterus with the fetus in vertex presentation. There were no uterine
contractions. On speculum examination, there was clear fluid draining
and the cervix was long and closed. After discussion with the consult-
ant, it was decided to induce labor.
Introduction Box 6.1 Phases of labor

• Phase 1: Quiescent phase
Labor is a complex process that ultimately
• Phase 2: Activation phase
results in the expulsion of the fetus and placenta
• Phase 3: Stimulation phase
through the birth canal. The physiology of labor • Phase 4: Involution phase
has not been fully understood yet and varies
with each species. Preparations for labor begin
several weeks before the actual onset. Onset of
labor is controlled by endocrine and paracrine
signals from both mother and fetus. Phase 1 uiescent phase
The quiescent phase starts even prior to implan-
tation and continues till the onset of the acti-
Phases of labor vation phase, which begins 6–8 weeks before
labor. The quiescence of the myometrium is
Four phases have been described, beginning essential to retaining the pregnancy inside the
with the quiescent phase (Box 6.1). uterus. In this phase, which comprises 95% of
CH 06_p079-087_v3.indd 79 17-07-2015 10:50:39

Box 6.2 Features and mediators of Phase 1 Box 6.3 Features and mediators of Phase 2
of labor of labor
eatures e iators eatures e iators
• Unresponsive myometrium • Progesterone • Changes in the myometrium • Estrogen
• Cervical softening • Relaxin Ŧ Increase in contractility • Progesterone
• Changes in the matrix • Prostaglandin I2 Ŧ Increase in uterine • CAPs
• Changes in collagen • Nitric oxide responsiveness • Glycosaminogly-
• PTH-RP Ŧ Increase in gap junctions cans
• Changes in the cervix • Proteoglycans
P - P, parathyroid hormone-related peptide.
Ŧ Cervical ripening • pCRH
Changes in collagen • Prostaglandins
structure • Cortisol
pregnancy, the uterine smooth muscle is unre- Increase in collagen • Interleukin-8
sponsive to natural stimuli. The cervix softens solubility • MMP
due to changes in matrix components and Infiltration by
inflammatory cells
changes in collagen. The uterine unrespon-
siveness is mediated by several hormonal and CAPs contraction-associated proteins; P matrix metallopro-
tease; pC placental corticotropin-releasing hormone.
nonhormonal inhibitors. The features of Phase
1 and its mediators are given in Box 6.2.
Changes in the cervix

Phase 2 Activation phase Changes in the cervix in Phase 2 include alter-
The activation phase begins about 6–8 weeks ation in collagen structure and alteration in rel-
before term and ends with the onset of regular ative concentrations of matrix metalloproteases
uterine contractions. Changes in the myome- (MMP), glycosaminoglycans (GAGs), and pro-
trium and cervix that are essential to this phase teoglycans. In addition, there is inflammatory
are regulated by the fetal hypothalamo–pituitary– cell infiltration, leading to an increase in inflam-
adrenal axis, maternal hypothalamo–pituitary matory cytokines, especially interleukin-8.
axis, and placental endocrine/paracrine factors. These changes result in extensive remodeling of
the cervix known as cervical ripening. Cervical
ripening takes place from 2 weeks to few days
Changes in the myometrium before labor, in preparation for effacement and
and cervix dilatation with uterine contractions in labor.
The features of Phase 2 of labor and the medi-
The changes in the myometrium and cervix are
ators of this phase are given in Box 6.3.
preparatory to uterine contractions and cervical
dilatation.
Parturition cascade
Changes in myometrium The series of events at term, beginning with the
Increase in uterine responsiveness and contrac- removal of factors ensuring uterine quiescence and
tility is characteristic of this phase. The primary activation of factors promoting uterine contrac-
change responsible for the uterine respon- tions that take place in Phase 2 of labor, is known
siveness is an increase in the expression of as the parturition cascade. It is a complex phenom-
contraction-associated proteins (CAPs), namely, enon involving the fetus, mother, and placenta.
oxytocin receptors, prostaglandin (PG) receptors,
and connexin 43. Connexin 43 is a gap junction ole of the fetus in the parturition
protein and its level increases due to an increase
cascade
in the area of gap junctions in the myometrium.
The increase in gap junctions between the myo- In Phase 2, activation of the fetal hypothalamic–
metrial cells permits electrical synchrony and pituitary–adrenal axis takes place. This plays a
allows effective coordination of contractions. major role in the initiation of uterine contractions.
CH 06_p079-087_v3.indd 80 17-07-2015 10:50:39

Physiology of Labor 81
The increase in secretion of fetal hypothalamic cor- lacks the enzyme 17D-hydroxylase unlike other
ticotropin-releasing hormone (CRH) stimulates mammalian placentae. Therefore, conversion of
fetal pituitary secretion of adrenocorticotropic progesterone to estrogen does not take place in
hormone (ACTH), which increases and stimulates the placenta. However, placenta produces estro-
the fetal adrenal gland. This leads to the produc- gens from DHEAS and 16(OH) DHEAS. These
tion of dehydroepiandrosterone sulfate (DHEAS), estrogens play an important role in Phase 2 of
which is converted into estradiol by the placenta. labor as mentioned earlier in the text.
Some of the DHEAS undergoes 16-hydroxylation
in the fetal liver to 16(OH) DHEAS. This is in turn strogens
converted to estriol by the placenta. Estrogens in maternal blood are primarily from
Placental estrogens act on the uterus and the placenta. DHEAS from the fetus is converted
stimulate the production of prostaglandin to estradiol and 16(OH) DHEAS to estriol. They
F2D(PGF2D) and an increase in oxytocin receptors, stimulate uterine contraction by binding with
PG receptors, and gap junctions. Fetal adrenals estrogen receptors and thereby stimulating pro-
also secrete cortisol which, in addition to stim- duction of CAPs. The estrogen receptors in the
ulating prostaglandin and oxytocin secretion by uterus are suppressed by progesterone through-
the placenta, causes the synthesis and release of out pregnancy. At term, functional withdrawal
large amounts of placental CRH (Fig. 6.1). of progesterone removes this suppression and
uterine contractility increases.
ole of placenta in the parturition
cascade rogesterone
Progesterone plays an important role through-
The placenta actively participates in the process out pregnancy. It is secreted by the corpus luteum
of labor through the production of estrogens, initially and after 7–9 weeks, by the placenta. It is
progesterone, placental corticotropin releasing responsible for maintaining uterine quiescence.
hormone and other substances. Human placenta The levels were thought to drop markedly before
onset of labor. Current research, however, has
shown that there is no actual fall in the level of
Hypothalamus progesterone, but there are changes in the relative
expression of progesterone receptors leading to a
C H ‘functional withdrawal’ or decrease in progester-
one effect. The role of estrogens and progesterone
Pituitary in Phase 2 of labor is summarized in Box 6.4.
C H lacental corticotropin releasing

hormone
renal Placental corticotropin-releasing hormone
(pCRH) is an important placental hormone pro-
duced in response to stimulation by fetal cortisol.
H Cortisol Placenta Box 6.4 ole of estrogens and progesterone

in Phase 2 of labor
• Estrogens
Ŧ Alter estrogen: Progesterone receptor ratio
Li er H H Ŧ Stimulate production of CAPs by placenta
Ŧ Cause uterine contraction
Figure 6.1 Fetal hypothalamic–pituitary–adrenal axis. • Progesterone
AC , adrenocorticotropic hormone; C , corticotropin- Ŧ Causes uterine quiescence
releasing hormone; D AS, dehydroepiandrosterone Ŧ *CUCPVKKPƀCOOCVQT[GHHGEVQPVJGO[QOGVTKWO
sulfate; D AS, 16-hydroxy Ŧ Undergoes functional withdrawal at term
dehydroepiandrosterone sulfate. CAPs, contraction-associated proteins.
CH 06_p079-087_v3.indd 81 17-07-2015 10:50:40

It acts on fetal pituitary and adrenals and increases

Box 6.6 xytocin
the production of ACTH and DHEAS, respec-
tively; it also acts on the decidua and increases the • Secreted by
production of prostaglandins that cause uterine Ŧ maternal posterior pituitary
Ŧ fetal posterior pituitary
contractions.
Ŧ placenta
• Inactivated by
Other placental pro ucts
Ŧ liver, kidney (nonpregnant state)
Contraction-associated proteins (CAPs) are Ŧ placental oxytocinase (in pregnancy)
released by the placenta in response to estro- • Best known uterotonic
gen. Other substances produced by the pla- • Binds to oxytocin receptors
centa that are important in labor initiation are • Contractile effect related to gestational age
given in Box 6.5. • Plays a major role in
Ŧ active phase of labor
Ŧ third stage of labor
Box 6.5 Substances produced by placenta for
Ŧ uterine involution
labor initiation
• Estradiol: From fetal DHEAS sensitivity to oxytocin is due to the marked
• Estriol: From fetal 16(OH) DHEAS increase in oxytocin receptors. Oxytocin receptors
• CRH: In response to fetal cortisol
increase 100–200 fold toward term, in response to
• CAPs
estrogens produced by the placenta.In addition,
Ŧ Oxytocin receptors
Ŧ PG receptors
oxytocin also induces prostaglandin production
Ŧ Gap junctions (connexin 43) in the decidua and fetal membranes. Uterine sen-
• Prostaglandins sitivity is gestational age related, i.e., later the ges-
• Oxytocin tation, less the dose of oxytocin required to induce
CAPs contraction-associated proteins; C corticotropin-
uterine contractions. Though oxytocin may not
releasing hormone; D AS, dehydroepiandrosterone sulfate; P , play a major role in the initiation of labor, it is an
prostaglandin. integral and essential uterine stimulant in active
labor and the third stage of labor. It also contrib-
ole of the mother in the parturition utes to uterine involution in the puerperium.
cascade rostaglan ins
Maternal oxytocin secreted by the pituitary, Prostaglandins are fatty acid derivatives that act
along with prostaglandins produced in the locally (paracrine) unlike hormones which are
decidua and fetal membranes, plays a pivotal secreted into the bloodstream to act at distant
role in labor initiation. sites. They are produced in several organs in the
body including the uterus. Most prostaglandins
O ytocin are uterotonins but some cause uterine relaxation.
In the nonpregnant state, oxytocin is secreted by Prostaglandin F2D (PGF2D) causes uterine contrac-
the posterior pituitary gland in a pulsatile fash- tions. Prostaglandin E2 (PGE2) plays a major role
ion. It has a short half-life of 3–4 minutes and is in cervical ripening. Prostaglandins also increase
inactivated in the liver and kidney. Levels of oxy- oxytocin receptors in myometrium (Box 6.7).
tocin do not increase throughout pregnancy and
in early labor but increase significantly in active Box 6.7 Prostaglandins
labor (Phase 3) and the third stage of labor, puer-
• Fatty acid derivatives
perium, and during lactation. In active labor, • Produced by several tissues
secretion by the fetal pituitary gland, and to a • High levels in decidua and fetal membranes
lesser extent by the placenta, accounts for the rise • Increase in oxytocin receptors
in oxytocin levels. Oxytocin degradation during Ŧ Uterotonins (PGF2D, PGE1, thromboxane)
pregnancy is by placental oxytocinase (Box 6.6). Ŧ Mediator of cervical ripening (PGE2)
Oxytocin is the best known uterotonic. Though Ŧ Uterine relaxant (PGI2)
there is no rise in the level of oxytocin during preg- P prostaglandin E; P prostaglandin F; P
nancy, the progressive increase in myometrial prostaglandin I.
CH 06_p079-087_v3.indd 82 17-07-2015 10:50:40

Phospholipi s
Phospholipase A2
ree arachi onic

aci
Prostaglandin synthetase
(Cyclooxygenase)
P α P P hrombo ane
Figure 6.2 Prostaglandin synthesis. P prostaglandin E2; P D

prostaglandin F2D; P prostaglandin I2.
Prostaglandins are synthesized from free Mechanical factors

(unesterified) arachidonic acid as shown in Figure
6.2. Fetal membranes and decidua contain phos- Mechanical factors such as uterine disten-
pholipase and cyclooxygenase enzymes. They are sion due to the growing fetus and the resultant
activated by local inflammatory reaction, trauma, stretching of myometrial fibers also play a role in
stretch, estrogens, and progesterone. Arachidonic the initiation of labor.
acid released from the phospholipids of the cell
membranes is converted into prostaglandins.
In turn, prostaglandins bind to myometrial PG
Myometrial contraction
receptors and exert their effects.
The roles of the fetus, placenta, and mother The ultimate goal of the parturition cascade is to
in Phase 2 of labor are pictorially represented in stimulate myometrial contractions. The uterine
Figure 6.3. myometrium is poorly innervated. Contraction
a a
Pituitary Cholesterol
C C
Pre e olo e Pituitary
C
P
Pro estero e
xytoci
I
C
striol xytoci
i er
stra iol
C
P
P eceptors
xytoci receptors
re al la terus
ap u ctio s
Figure 6.3 Role of fetus, placenta, and mother in Phase 2 of labor. AC , adrenocorticotropic hormone; C ,
corticotropin-releasing hormone; D A, dehydroepiandrosterone sulfate; P , prostaglandin.
CH 06_p079-087_v3.indd 83 17-07-2015 10:50:40

and relaxation are, therefore, mediated by hor-

mones and other locally produced paracrine
factors (such as prostaglandin) in the myome- Myosin Myosin
trium. There are myometrial surface recep- light chain inase phosphorylation
tors located on the cell surface. Hormones and Ca calmo ulin comple ctin myosin comple
prostaglandins exert their effect by binding to
the receptors. The receptors are upregulated Calmo ulin P
or downregulated by hormones, mainly estro-
gen and progesterone. At term, the receptors ntracellular Ca Contraction
for uterotonics such as oxytocin and PGF2D are
upregulated by estrogen.
At the cellular level, myometrial contraction tracellular Ca
involves (a) interaction between the muscle
Figure 6.4 Cellular biology of myometrial contraction.
proteins, actin, and myosin and (b) interaction Figure depicts the series of events beginning with the
between myometrial cells (Box 6.8). movement of calcium to intracellular compartment to
Actin–myosin interaction is calcium depen- activation of ATP and myometrial contraction.
dent. Calcium moves from the extracellular
compartment to the intracellular compartment
and combines with calmodulin, a carrier pro-
tein, to form calcium–calmodulin complex. This
activates the enzyme myosin light chain kinase
yocyte yocyte yocyte
which, in turn, catalyzes the phosphorylation of
myosin. This ultimately leads to myosin–actin
interaction and activation of ATP, resulting in
myometrial contraction (Fig. 6.4). Entry of cal-
cium into the cells to increase intracellular cal- ap u ctio s Passa e o io s
cium is, therefore, an essential first step in the impulses a metabolites
initiation of myometrial contraction.
Figure 6.5 Passage of signals through gap junctions.
The passage of signals, causing contraction or
Gap junctions are channels between myometrial cells
relaxation, between myometrial cells is through
through which ions, metabolites, and electrical impulses
gap junctions (Fig. 6.5). These are channels are transmitted.
formed by proteins, the most important one in
labor being connexin 43. Ions, electric impulses,
and metabolites pass through these gap junc-
tions to cause synchronized contraction of the
myometrium. Phase 3 Stimulation phase
This is the phase during which active uterine
contractions, cervical dilatation, descent of the
Box 6.8 Biology of myometrial contraction
presenting part, and expulsion of the fetus and
placenta take place. Conventionally, this phase is
• Actin–myosin interaction divided into three stages.
Ŧ Brought about by
calcium influx
calcium–calmodulin complex
myosin light chain kinase
First stage of labor
myosin phosphorylation The first stage of labor begins with the onset of
activation of ATP labor pains and extends till full dilatation of the
• Intermyocyte interaction cervix. This stage is characterized by progressive
Ŧ Gap junction proteins
uterine contractions associated with effacement
• Myometrial receptors
and dilatation of the cervix. Engagement and
Ŧ Upregulation of oxytocin/PGF2D receptors
descent of the presenting part also occur in the
A P adenosine triphosphate; P D
prostaglandin F2D.
first stage of labor.
CH 06_p079-087_v3.indd 84 17-07-2015 10:50:40

Second stage of labor Box 6.10 Features and mediators of Phase 4

of labor
The second stage extends from the time of full
dilatation of the cervix to delivery of the fetus. eatures e iators
• Involution of uterus and cervix • Oxytocin
Third stage of labor • Responsiveness of endometrium • Local factors
to ovarian hormones
The third stage begins with delivery of the fetus
and ends with expulsion of the placenta. Following
endometrium slowly becomes responsive to
placental separation and expulsion, the uterus
cyclical hormonal production by the ovary. The
contracts and retracts to achieve hemostasis.
maternal hypothalamic–pituitary–ovarian axis
The three stages of labor are discussed in detail
starts functioning again in the normal cyclical
in Chapter 14, Normal labor: Mechanics, mecha-
fashion when lactation ceases. Features of Phase
nism, and stages. Continued uterine stimulation
4 and its mediators are listed in Box 6.10.
is maintained by the action of oxytocin and PGF2D.
The phases of parturition and the factors
Features of Phase 3 of labor and the factors
involved are shown in Figure 6.6.
that mediate this phase are listed in Box 6.9. In
addition to the increasing levels of oxytocin and
prostaglandins in active labor, locally produced Clinical applications
endothelin-1, epidermal growth factor, and
platelet-activating factors also stimulate uterine A comprehensive understanding of the physiol-
contractions in this phase. ogy of labor and the factors involved in the var-
ious phases has helped in the management of
Box 6.9 Features and mediators of Phase 3 labor, induction of labor, and medical manage-
of labor ment of preterm labor. The clinical applications
eatures e iators are given in Table 6.1.
• First stage
Ŧ Uterine contraction – Prostaglandins
Ŧ Cervical effacement – Oxytocin
Ŧ Cervical dilatation – Endothelin-1
Table 6.1 Clinical applications of physiology
Ŧ Fetal descent – Epidermal growth factor
of labor
• Second stage – Platelet-activating factor
Ŧ Delivery of the fetus Physiological Application
• Third stage function
Ŧ Separation of placenta
Progesterone causes Used to prevent preterm
Ŧ Expulsion of placenta uterine quiescence labor
Ŧ Uterine contraction and retraction
PGF2D causes uterine • Used to stimulate uterine
contractions contractions
• First and second trimester
Phase 4 Involution phase pregnancy termination
• Prevent and control PPH
The involution phase is described as the puerpe- • Antagonists used as
rium. The uterus and cervix shrink and return to tocolytics
their normal state and integrity during this phase. PGF2D is released by Sweeping of the cervix for
These changes take place over a period of 4–6 fetal membranes labor induction
weeks. Multiple factors are responsible for uterine PGE2 causes cervical Used for cervical ripening
softening
involution and return of the tissues to the prepreg-
Oxytocin causes uterine Used for induction and
nant state. Local inflammatory processes resolve, contractions acceleration of labor
production of glycosaminoglycans (GAGs) and
Calcium is essential for Calcium channel blockers
proteoglycans ceases, and changes in the colla- myometrial contraction used as tocolytic
gen and other tissues of the cervix regress. Magnesium competes Magnesium sulphate used
Uterine involution is aided by oxytocin with calcium as tocolytic
that is released in response to suckling. The P prostaglandin; PP postpartum hemorrhage.
CH 06_p079-087_v3.indd 85 17-07-2015 10:50:41

PH PH PH PH
uiescence cti ation timulation n olution
Uterine contractility
Progesterone strogen P ytocin

ela in Progesterone ytocin Local factors
P C Ps n othelin
itric i e pC H
P H P lycosaminoglycans P
Proteoglycans
P
Cortisol
MMP
nterleu in
Figure 6.6 The four phases of parturition and their mediators. CAP, contraction-associated protein; , epidermal
growth factor; P, matrix metalloproteases; PA , platelet-activating factor; PC , placental corticotropin-releasing
hormone; P , prostaglandin; P , prostaglandin I2; P - P, parathyroid hormone–related peptide.
Key points
• Labor is a complex process controlled by endocrine, • Oxytocin and PGF2D are the most potent uterotonics.
paracrine, and other factors.
• Prostaglandins are synthesized in the fetal mem-
• Four phases of labor have been described: quies- branes and decidua and act on the uterus.
cent phase, activation phase, stimulation phase, and • The increase in oxytocin and PG receptors in the
involution phase. myometrium plays a key role in uterine contractions.
• Phase 1 or quiescent phase begins even prior to %CNEKWOKPƀWZKPVQVJGO[QOGVTKCNEGNNUKPTGURQPUG
implantation and continues till the onset of labor. In to hormonal stimuli is the most important event in the
this phase, the uterine myometrium is unresponsive initiation of contractions. Myometrial contraction during
and the cervix is softened. the parturition cascade is through actin and myosin
interaction and interaction between myometrial cells
• Phase 1 is mediated by progesterone, relaxin, prosta-
via gap junctions.
glandin I2 (PGI2), and other substances.
• Phase 2 or activation phase begins 6–8 weeks before • Phase 3 or stimulation phase includes the three
term. The uterus becomes responsive to contractile stages of labor, begins with the onset of labor, and
stimuli and changes take place in cervical collagen. ends with the expulsion of the placenta and control of
bleeding.
• Phase 2 is mediated by several hormones and non-
• Phase 4 or involution phase is known as the puerper-
hormonal substances produced by the fetus, placenta,
ium. The uterus and cervix return to the prepregnant
and mother.
state during this phase.
• The fetal hypothalamic-pituitary-adrenal axis, placen-
ta, and maternal hypothalamic-pituitary-uterine axis • The physiological processes involved in labor have
play major roles in phase 2. These events together are important clinical applications.
known as the parturition cascade.
CH 06_p079-087_v3.indd 86 17-07-2015 10:50:41

Self-Assessment
2. In the activation phase.
Case-based questions 3. Prostaglandin and oxytocin are the main mediators.
Endothelin-1, platelet-activating factor, and epidermal
Case 1 growth factor also play a role.
Mrs. KT, 25, primigravida, was brought to the labor room 4. Prostaglandin E2 is used to soften the cervix.
with history of watery discharge per vaginum for 4 hours.
Examination revealed a term-size uterus with fetus in ver-
tex presentation. There were mild uterine contractions, Case 2
once in 20–30 minutes, lasting for 10–15 seconds.
1. Atonic postpartum hemorrhage.
1. What further examination would you like to do to ar- 2. Oxytocin and prostaglandin F2D.
rive at a diagnosis? 3. Oxytocin binds to receptors and stimulates uterine
2. What phase of labor is she in? contraction. It also induces prostaglandin production
3. What are the mediators of this phase? by the decidua and fetal membranes. Prostaglandin
4. Which prostaglandin will you use to soften the cervix? binds to its receptor and stimulates uterine contrac-
tions. Prostaglandin and oxytocin are the most effec-
tive uterotonics.
Case 2
Mrs. MA, 23, multigravida, came to the emergency room Sample questions
with profuse vaginal bleeding following vaginal delivery.
On examination, the patient was hemodynamically stable Long-answer question
but the uterus seemed relaxed and vaginal bleeding was
persistent. 1. What are phases of labor? Explain the parturition
cascade.
1. What is the diagnosis?
2. What can you use to make the uterus contract?
3. How do these agents act? Short-answer questions
1. Prostaglandins
Answers 2. Oxytocin
3. Myometrial contraction
Case 1 4. Role of placenta in labor initiation
1. Speculum examination to visualize draining of

COPKQVKEƀWKFVJTQWIJVJGEGTXKZCPFCUUGUUOGPVQH
cervical effacement and dilatation.
CH 06_p079-087_v3.indd 87 17-07-2015 10:50:41

Clinical
Manifestations
7 and Diagnosis
of Pregnancy
Case scenario
Mrs. AT, 24, had missed her period and wanted to confirm pregnancy.
She came to the hospital at 45 days, amenorrhea and wanted to know
if she was pregnant. She was fatigued. She had breast tenderness and
nausea for 5 days.
Introduction Duration of pregnancy

The normal duration of pregnancy is 280 days
Knowing how to diagnose pregnancy, and famil-
(40 weeks), calculated from the first day of the last
iarity with the early signs and symptoms of preg-
menstrual period (corresponds to conceptional
nancy, are essential for the practice of obstetrics.
age of 266 days). This can also be expressed as 9
Pregnancy is usually suspected from the history
calendar months and 7 days. Pregnancy is divided
and is confirmed by physical examination along
into three trimesters:
with laboratory testing. In some cases sono-
graphic confirmation may be required. • First trimester: 0–13 weeks
• Second trimester: 14–27 weeks
Gestational age versus • Third trimester: 28–40 weeks
conceptional age The trimesters are based usually on a preg-
In a woman with regular periods, conception nancy duration of 40 weeks. Sometimes, tri-
usually occurs 14 days prior to the next expected mesters are based on a pregnancy duration
period. However, in clinical practice, gestational of 42 weeks. Then the first trimester is consid-
age is calculated from the first day of the last ered to be 0–14 weeks, the second trimester
menstrual period and not from the day of con- is 15–28 weeks, and the third trimester is 29–
ception (conceptional age). 42 weeks.
CH 07_p088-097_v3.indd 88 17-07-2015 10:59:42

Clinical Manifestations and Diagnosis of Pregnancy 89
Symptoms and signs blastocyst burrows into the decidua. Bleeding

is usually light but can be mistaken for normal
of pregnancy in the menses and the woman may not realize that she
is pregnant.
ſTUVVTKOGUVGT
Pregnancy is associated with characteristic ausea with or without vomiting
symptoms and signs, which vary with each
Nausea with or without vomiting is perhaps the
trimester.
commonest symptom of pregnancy, found to
affect about 50%–90% of pregnant women. It is
Symptoms also the most common reason for hospitalization
in the first half of pregnancy. It tends to begin at
Amenorrhea is the universal symptom which
4–6 weeks, peaks at 8–12 weeks, and resolves by
leads to the suspicion of pregnancy. Nausea and
20 weeks in 90% of women. The term morning
vomiting are more marked in the first trimester.
sickness is a misnomer because the symptoms
may occur at any time of the day. There is evi-
Amenorrhea dence that women with nausea and vomiting in
Amenorrhea is the fundamental symptom of early pregnancy have a lower rate of miscarriage
early pregnancy. Whenever a woman in the than women without these symptoms.
reproductive age group misses a period, preg- The exact etiology of nausea and vomiting is
nancy should be suspected. The chances of poorly understood and is most probably multi-
pregnancy increase as the days past the missed factorial. The most likely etiology is the change
period increase. If the woman has been sexually in hormonal milieu during pregnancy. Rising lev-
active without the use of contraception or has els of E human chorionic gonadotropin (E hCG)
not consistently used contraception, the suspi- may have a role, as also estradiol. Vomiting can
cion of pregnancy increases. sometimes be excessive, leading to electrolyte
Amenorrhea is not always indicative of preg- disturbance and dehydration, and is referred
nancy; it can be a misleading symptom. In to as hyperemesis gravidarum (see Chapter 28,
women with irregular periods, pregnancy may Hyperemesis gravidarum).
be difficult to diagnose just on the basis of a pro- Nausea and vomiting may be exacerbated by
longed cycle. Even women with regular cycles • multiple gestation,
may occasionally have prolongation of a cycle • hydatidiform mole,
in spite of not being pregnant. In these situa- • heartburn and acid reflux.
tions, biochemical tests for pregnancy or the
sonographic imaging of the pregnancy may be
necessary. Fatigue and generali ed malaise
One of the commonest symptoms reported by
lee ing in normal pregnancy pregnant women is a sense of overwhelming
Many women present with one or two episodes tiredness, fatigue, and intense sleepiness. This
of bleeding during pregnancy (Box 7.1). Bleeding usually occurs in the first trimester and gener-
may occur 7–8 days after fertilization when the ally resolves by the 4th month of pregnancy. It is
thought to be due to the sleep-inducing property
of the high level of circulating progesterone.
Box 7.1 Bleeding in normal pregnancy
• In 10% of normal pregnancies
• +PVJGſTUVYGGMU Breast enlargement and tenderness
• Around the time of expected periods Under the influence of hCG, the breast ducts
Ŧ Implantation bleeding
undergo proliferation and enlargement. This
Ŧ Usually light
may lead to an increase in size of the breasts and
Ŧ 5VQRUQPKVUQYP
may also cause breast tenderness.
CH 07_p088-097_v3.indd 89 17-07-2015 10:59:42

Increased frequency of urination Box 7.3 Changes in the uterus and cervix in the
without dysuria ſTUVVTKOGUVGT
The enlarging uterus presses on the bladder, • Changes in the uterine shape and size
especially over the trigone, and may lead to an Ŧ Becomes globular
Ŧ Enlarges in size
increased urge to urinate. This is not associated
• egar s sign
with dysuria and may resolve after the 4th month
Ŧ 5QHVGPKPIQHNQYGTWVGTKPGUGIOGPV
KUVJOWU
of pregnancy. Ŧ #DFQOKPCNCPFXCIKPCNſPIGTUECPDGCRRTQZKOCVGF
Symptoms of pregnancy in the first trimester • Chadwick s sign
are summarized in Box 7.2. Ŧ Bluish appearance of the cervix
Ŧ Due to increased vascularity
Box 7.2 5
[ORVQOUQHRTGIPCPE[KPVJGſTUV • oodell s sign
trimester Ŧ /CTMGFUQHVGPKPIQHEGTXKZ
• Amenorrhea
• Nausea and vomiting between uterine size and gestational age is
Ŧ $GIKPUCVŌYGGMU learned by experience. The uterus and cervix feel
Ŧ 2GCMUCVŌYGGMU softer than the nongravid uterus (Box 7.3).
Ŧ 4GUQNXGUD[YGGMU
Hegar’s sign: At approximately 6 weeks gesta-
Ŧ Etiology multifactorial
Ŧ Exacerbated by tional age, softening of the lower uterine segment
multiple gestation occurs, just above the cervix. During bimanual
hydatidiform mole (abdominal and vaginal) examination, when
heartburn and acid reflux the uterus is compressed between the examin-
• Fatigue and generalized malaise ing fingers, the uterine wall feels thin and the
Ŧ Due to high levels of progesterone abdominal and vaginal fingers can be approxi-
• Breast enlargement and tenderness mated (Fig. 7.1).
Ŧ Due to increase in hCG and other hormones
• Increased urinary frequency Chadwick’s sign: Though not used routinely to
Ŧ Due to pressure of uterus on trigone confirm pregnancy, on a speculum examina-
hC human chorionic gonadotropin.
tion the cervix will appear bluish-red due to the
increased cervical vascularity in early pregnancy.
Signs
Enlargement of the uterus is the most important
sign of pregnancy.
terine examination
The uterus begins to enlarge after the implanta-
tion of the blastocyst. Uterine examination may
confirm the presence of an intrauterine preg-
nancy after the 6th week of pregnancy, that is,
after 6 weeks’ amenorrhea (see Chapter 8, History
taking and examination of the obstetric woman).
Prior to that, the uterine enlargement is difficult
to ascertain. It is also easier to confirm the preg-
nancy by pelvic examination in a thin woman as
compared to a woman with excess abdominal
fat. It is important to have the woman empty her
bladder before performing a pelvic examination
to assess uterine size.
On physical examination, the pregnant uterus
is soft, globular, and enlarged. The correlation Figure 7.1 Hegar’s sign.
CH 07_p088-097_v3.indd 90 17-07-2015 10:59:42

Goodell’s sign: The cervix is normally firm like

the cartilage at the end of the nose. Goodell’s
sign is when there is marked softening of the cer-
vix. This is present from 6 weeks’ pregnancy.
The uterus remains a pelvic organ until
approximately 12 weeks’ gestation, when it
enlarges enough to be palpable abdominally just
above the symphysis pubis.
Problems in assessing uterine si e
Uterine fibroids, obesity, a full bladder, a ret-
roverted uterus, and multiple gestation may
interfere with accurate assessment of the ges-
tational age. The uterus might appear larger
than is normal for the period of amenorrhea
if the menstrual history is not accurate (wrong
dates), and also in the presence of multi-
ple pregnancy, molar pregnancy, and uterine
fibroids (Box 7.4). Figure 7.2 Handheld Doppler device.
Box 7.4 easons for uterine si e larger than

period of amenorrhea
Box 7.5 Symptoms in the second trimester
• Wrong dates
• Multiple pregnancy • 3WKEMGPKPIQTſTUVHGVCNOQXGOGPVU
• Molar pregnancy Ŧ #VYGGMUKPOWNVKRCTCU
• 7VGTKPGſDTQKFU Ŧ #VYGGMUKPPWNNKRCTCU
• $TCZVQP*KEMUEQPVTCEVKQPU
Ŧ Irregular, painless
Fetal heart tones Ŧ No associated cervical changes
Handheld Doppler devices (Fig. 7.2) can usually

detect fetal heart tones at 10–12 weeks’ gesta-
tion. They are easier to detect in women who are Fetal movements
thin. It might require persistence to detect the
The first fetal movements or quickening is per-
fetal heart tones before 11 weeks’ gestation.
ceived by 16–18 weeks by multiparas and by
18–20 weeks by nulliparas. Initial movements are
like a flutter, but they become more definite and
Symptoms and signs clear in 2–3 weeks. Active movements are per-
ceived through the rest of pregnancy.
of pregnancy
ra ton ic s contractions
Second trimester
Irregular contractions of the uterus known as
The symptoms of the first trimester decrease or Braxton Hicks contractions, appear in the late
disappear and the mother is more comfortable second trimester. They are painless and do not
in this trimester. cause any cervical changes. They become more
prominent toward term.
Symptoms
Nausea and vomiting subside and there is a
Signs
sense of well-being. Symptoms of the second tri- In addition to uterine enlargement, other signs
mester of pregnancy are listed in Box 7.5. make their appearance in the second trimester.
CH 07_p088-097_v3.indd 91 17-07-2015 10:59:43

terine enlargement Melasma: Facial darkening, also called chloasma,

is a diffuse macular facial hyperpigmentation.
The uterus remains a pelvic organ until approx- As far as women are concerned, it is the most
imately 12 weeks’ gestation, when it enlarges disturbing of all skin pigmentations occurring
enough to be palpable abdominally just above in pregnancy. The distribution is usually malar
the symphysis pubis. At 16 weeks the fundus (over the cheeks) but can be central or mandibu-
is palpable at one-third the distance between lar. Because it is related to the hormones of preg-
the pubic symphysis and the umbilicus, and at nancy, it lessens after delivery.
20 weeks it is palpable at two-thirds the distance
between the pubic symphysis and umbilicus. Striae gravidarum: Stretch marks (striae grav-
idarum) appear on the abdomen and thighs
Changes in the breast (Fig 7.3).
The breasts enlarge further and the secondary
areola is formed. Small protuberances called
Spi er angioma or nevi
Montgomery’s tubercles appear. Milk (colostrum) A spider angioma or nevus consists of a cen-
secretion may be noticed in some women. These tral arteriole with radiating thin-walled vessels.
changes occur due to high levels of estrogen and Compression of the central vessel produces
progesterone. blanching and temporarily obliterates the lesion.
When released, the thread-like vessels quickly
Skin changes refill with blood from the central arteriole. Spider
nevi are caused by the increased circulating lev-
Increase s in pigmentation els of estrogen.
Linea nigra: Most pregnant women develop
some degree of skin pigmentation. Though the almar erythema
etiology is not clearly understood, one possibility Reddening of the palms occurs on both the
is that estrogens and progesterone cause mela- thenar and hypothenar eminences and may be
nocytic stimulation. This is typically evident in associated with itching.
the nipples and areola, umbilicus, axillae, and
perineum. The linea alba, stretching from the
umbilicus to the pubic symphysis, darkens and Fetal parts and fetal movements
is termed the line nigra (Fig. 7.3). By 18–20 weeks, fetal parts can be appreciated
within the uterus on palpation. Active fetal move-
ments can also be felt by the examining physician.
External ballottement: With the the woman lying
in the dorsal position, the examining physician
places both hands on either side of the uterus.
When the uterus is tapped on one side, the fetal
parts move and bounce back. This is called
external ballottement. At this period of gesta-
tion, amniotic fluid volume is much more than
the fetal size and the fetus can be moved freely
within the fluid.
Fetal heart sounds

Fetal heart sounds are audible on auscultation
from 20 weeks. In addition, soft murmurs or
blowing sounds known as uterine souffle and
fetal souffle can also be heard. These are due to
Figure 7.3 .KPGCPKITC
[GNNQYCTTQYCPFUVTKCG increased blood flow through the uterine vessels
ITCXKFCTWO
YJKVGCTTQYU and umbilical vessels, respectively.
CH 07_p088-097_v3.indd 92 17-07-2015 10:59:44

Signs of the second trimester of pregnancy are

Box 7.7 Symptoms and signs in third trimester
summarized in Box 7.6.
• Symptoms
Ŧ Uterine enlargement
Box 7.6 Signs of second trimester
Ŧ Breathlessness
of pregnancy
Ŧ Palpitation
• Changes in the breast Ŧ Pedal edema
Ŧ Enlargement Ŧ $CEMCEJG
Ŧ Formation of secondary areola Ŧ Lightening near term
Ŧ Formation of Montgomery’s tubercles • Signs
Ŧ Secretion of colostrum Ŧ Further uterine enlargement
• %JCPIGUKPVJGUMKP Ŧ (WNNPGUUQHƀCPMU
Ŧ Pigmentation Ŧ Shelving
Breast, abdomen
Linea nigra
Striae gravidarum
Chloasma Laboratory evaluation
Ŧ Spider nevi
Ŧ Palmar erythema for the diagnosis
• On abdominal palpation
Ŧ Fetal parts of pregnancy
Ŧ Fetal movements
External ballotment Pregnancy is often diagnosed by the characteristic
• Fetal heart sounds symptoms and signs, but early in pregnancy, labo-
• 7VGTKPGCPFHWPKEUQWHƀG ratory tests are required to confirm the diagnosis.
Several peptide and steroid hormones are
secreted by the placenta (see Chapter 5, Placenta,
Symptoms and signs fetal membranes, and amniotic fluid). Of these, the
most commonly assayed hormone for the confir-
of pregnancy Third mation of pregnancy is the E subunit of hCG.
trimester
The majority of the symptoms in the third tri-
uman chorionic gonadotropin
mester are due to the enlargement of the uterus. • Human chorionic gonadotropin is a
glycoprotein similar in structure to follicle-
Symptoms stimulating hormone (FSH), luteinizing hor-
mone (LH), and thyroid-stimulating hormone
The enlarging uterus causes obvious abdominal (TSH). Human chorionic gonadotropin is
distension. Cardiovascular changes and splint- composed of D and E subunits.
ing of the diaphragm can lead to palpitation and • Modern immunoassays for hCG, whether in
breathlessness. Pressure of the gravid uterus urine or serum, specifically identify the E sub-
can cause pedal edema and backache. Toward unit of hCG.
term, when the fetal head enters the pelvis, the • Human chorionic gonadotropin is detectable
mother appreciates a decrease in the pressure 8 days after conception in the serum of approx-
on the diaphragm and lower ribs. This is called imately 5% of womans.
lightening. • More than 98% of womans will have detectable
levels in the serum by Day 11 after conception,
that is, before the next period.
Signs • At 4 weeks’ gestation, the level of hCG in serum
Uterine enlargement in the second and third doubles approximately every 2 days.
trimester is described in Chapter 8, History tak- • The level of hCG peaks at 10–12 weeks’ gesta-
ing and examination of the obstetric woman. The tion and then begins to decline rapidly. A more
flanks appear full, the uterus falls forward by gradual rise begins again at 22 weeks’ gesta-
40 weeks and shelving occurs (Box 7.7). tion, which continues until term.
CH 07_p088-097_v3.indd 93 17-07-2015 10:59:44

Pregnancy tests result if done too early. The home pregnancy

kits claim to be very accurate but they are most
Pregnancy tests can be performed on the wom- sensitive after 45 days’ amenorrhea. If it is done
an’s urine or serum (Box 7.8). earlier and shows a negative result, it should be
repeated after 1 week.
Box 7.8 Laboratory testing for hCG The results of a urine pregnancy test should
(pregnancy tests) be confirmed with a physical examination and,
• Urine
when still in doubt, with sonographic visualiza-
Ŧ Qualitative tion of the intrauterine pregnancy (Box 7.9).
hCG highest in first morning urine specimen
False negative may occur due to high concentra- Box 7.9 rine pregnancy test
tions of hCG-EEH
EQTGHTCIOGPV
• Serum • /QUV EQOOQPN[ WUGF KP VJG YGGM CHVGT VJG OKUUGF
Ŧ Quantitative menstrual period
Important to use same assay for serial tests • Most sensitive after 45 days’ amenorrhea
In a viable pregnancy, hCG usually doubles over • 5JQWNFDGEQPſTOGFD[QPGQHVJGHQNNQYKPI
48 hours Ŧ Physical examination
Ŧ Qualitative Ŧ Sonographic visualization of pregnancy
Rapid but not as sensitive as quantitative
Should use quantitative if detection of pregnancy
is critical Serum pregnancy test
hC human chorionic gonadotropin. The most sensitive method for detecting hCG
in early pregnancy is a serum pregnancy test.
Though both the qualitative (checking just for
rine pregnancy test the presence of hCG) and quantitative (checking
for the total amount of hCG present) methods
Urine pregnancy testing is the most common
can be used, serum hCG is almost always mea-
method for diagnosing pregnancy in the clinic
sured using the quantitative method (Box 7.8).
or hospital and is the preferred method for
The sensitivity of methods used for serum
home pregnancy tests. On an average, the result
hCG assay is high. Some methods can detect hCG
can be obtained in 5 minutes because it is a
levels as low as 2–20 mIU/mL. Serum pregnancy
qualitative test.
tests, therefore, are more sensitive than urine
Urine pregnancy tests are most commonly
tests but are not routinely used for diagnosis
used in the week after the missed menstrual
or confirmation of pregnancy. They are used in
period (4th completed gestational week). The
women who undergo assisted reproductive tech-
woman passes urine on the strip or dips it into
nologies (ART), when ectopic pregnancy is sus-
urine and waits for 5 minutes. The strip has a
pected, or in the follow-up of hydatidiform mole.
plasma membrane containing three types of
It is important to remember that early in preg-
antibodies and dyes in three distinct test zones:
nancy a serum pregnancy test may be positive
the reaction, test, and control zones. The result is
while the urine pregnancy test is still negative.
considered positive by the appearance of a line
This is due to the fact that in the first trimester,
or dot in a designated color in the test zone.
hCG is present in higher levels in serum than
Standard urine pregnancy tests used in clin-
in urine.
ical practice use the sandwich enzyme-linked
In normal intrauterine pregnancy, the serum
immunosorbent assay (see page 95). These have
level of hCG doubles approximately every 48
a urine hCG threshold of 20–50 mIU/mL. A first
hours. Failure to achieve this on serial moni-
morning specimen is recommended since hCG
toring is suggestive of ectopic pregnancy or an
concentration in the urine will be the highest at
abnormal intrauterine pregnancy.
that time. However, a random urine sample can
also be used for testing. Since urine hCG values
Methods of hCG assay
can be variable very early in pregnancy (values
can range from 12 mIU/mL to >2500 mIU/mL), Several methods exist to assay for the presence
the home pregnancy test may show a negative of hCG Box (7.10).
CH 07_p088-097_v3.indd 94 17-07-2015 10:59:44

The woman's urine/serum is allowed to react

Box 7.10 Methods of hCG assay
with the monoclonal antibody directed against
adioimmunoassay hCG. A second antibody is then added to ‘sand-
• Sensitivity: 5 mIU/mL wich’ the bound hCG. In some assays, the second
• )GUVCVKQPCNCIGYJGPſTUVRQUKVKXGŌYGGMU antibody is linked to an enzyme, such as alkaline
• Time to complete: 4 hours phosphatase.
mmunoradiometric assay If hCG is present in the urine/serum specimen,
• Sensitivity: 150 mIU/mL an antibody-hCG-antibody enzyme complex
• )GUVCVKQPCNCIGYJGPſTUVRQUKVKXGYGGMU will be formed. When substrate to the enzyme is
• Time to complete: 2–30 minutes added, a color develops. The intensity of the color
n yme-linked immunosorbent assay SA is proportional to the concentration of hCG pres-
• Sensitivity: 25 mIU/mL
ent in the urine/serum specimen. Visual compari-
• )GUVCVKQPCNCIGYJGPſTUVRQUKVKXGYGGMU son of the intensity of the color with test specimen
• Time to complete: 5–15 minutes indicates the concentration of hCG t 25 mIU/mL
of hCG in the test specimen.
luoroimmunoassay A
• Sensitivity: 1 mIU/mL
• )GUVCVKQPCNCIGYJGPſTUVRQUKVKXGYGGMU luoroimmunoassay
• Time to complete: 2–3 hours The fluoroimmunoassay (FIA) technique uses
hC , human chorionic gonadotropin. an antibody tagged with a fluorescent label to
detect serum hCG.
a ioimmunoassay
This method uses a radioactive plasma membrane
False-negative pregnancy test
receptor site containing anti-hCG antibodies to
bind hCG, and in some cases, to react specifically The reasons for a false-negative test may be the
with the E subunit of hCG. Radioimmunoassays following:
are accurate and can detect pregnancy as lit-
• Testing done too early (especially home preg-
tle as 8 days after ovulation. However, they are
nancy tests). The chance of a false negative test
expensive to conduct, rely on highly specialized
reduces if the test is done 1–2 weeks after the
equipment and medical personnel, and result in
missed period.
radioactive medical waste.
• Wrong dates due to irregular periods.
Immunora iometric assay
Both intact hCG and the free E subunit can be False-positive pregnancy test
measured with this method. Samples, stan-
dards, and controls are incubated for 60 min- The reasons for a false-positive test may be the
utes at 370C with two monoclonal antibodies, following:
one labeled with I125 and the other covalently • ‘Biochemical’ pregnancy, where there has
linked to magnetizable particles. After incuba- been a pregnancy loss soon after implantation
tion, the unbound labeled antibody is removed but the hCG levels are still detectable.
by decanting after magnetic sedimentation or by • hCG administered as part of infertility treatment
centrifugation. The radioactivity in the washed may be detected. Exogenous hCG will still be
precipitate is counted and the hCG concentra- present for 2 weeks after being given as an injec-
tion is calculated from the standard curve. The tion and this must be taken into consideration.
sensitivity of the assay is 150 mIU/mL. • hCG secretion from a tumor.
n yme lin e immunosorbent assay
Abnormal rise of hCG level
Commonly, the sandwich enzyme-linked immu-
nosorbent assay (ELISA) is utilized for testing In certain conditions, the level of hCG may not
urine/serum for the presence of the E subunit rise in the usual manner. The conditions result-
of hCG. A unique monoclonal antibody combi- ing in either a slow rise or an accelerated rise are
nation which is specific against E hCG is used. listed in Box 7.11.
CH 07_p088-097_v3.indd 95 17-07-2015 10:59:44

Box 7.11 Abnormal rise of hCG levels Box 7.12 Transabdominal versus transvaginal
sonography
• 5NQYTKUG
Ŧ Ectopic pregnancy • Transabdominal sonography
Ŧ Failed pregnancy Ŧ )GUVCVKQPCNUCEXKUKDNGYGGMNCVGTVJCPD[685
• High or accelerated rise Ŧ &KHſEWNVKPQDGUGYQOGP
Ŧ Molar pregnancy Ŧ Full bladder required
Ŧ Multiple gestation • Transvaginal sonography
Ŧ Chromosomal abnormalities Ŧ +FGPVKſGUIGUVCVKQPCNUCEYGGMGCTNKGTVJCP6#5
Ŧ 7UGHWNKPQDGUGYQOGP
Ŧ Full bladder not required
7NVTCUQWPFEQPſTOCVKQP Ŧ More accurate in early pregnancy

AS, transabdominal sonography; S transvaginal sonography.
of pregnancy
Sonographic examination of the uterus can be Box 7.13 Transvaginal sonography in early
pregnancy
used to confirm the presence of a pregnancy and
determine whether it is intrauterine or extra- • Gestational sac
uterine (ectopic). It is also useful when the via- Ŧ +UVJGſTUVUKIPQHKPVTCWVGTKPGRTGIPCPE[
bility of the pregnancy has to be assessed. Ŧ 8KUWCNK\GF
#VŌYGGMU
First trimester sonograms can be performed via
When serum hCG is 1000–1500 mIU/mL
the transvaginal (TVS) and/or the transabdomi-
Ŧ Eccentric in location
nal (TAS) route (Box 7.12). The accuracy of TVS is &QWDNGFGEKFWCNUKIPD[ŌYGGMU
greater for early first trimester evaluation of the • ;QNMUCE
gestational sac, yolk sac, and developing embryo, Ŧ #RRGCTUD[ŌYGGMU
while TAS may be unable to detect an intrauterine Ŧ 2TGUGPVWPVKNYGGMU
gestation, especially in an obese woman. • Embryonic pole
Using TVS, the gestational sac, yolk sac, and Ŧ 8KUKDNGD[ŌYGGMU
embryo can be identified and measurements Ŧ )TQYUCVVJGTCVGQHOOFC[
taken for diagnosis of pregnancy and assessment Ŧ CRL accurate measure of gestational age
of gestational age (Box 7.13). Ŧ Cardiac activity visible
The ultrasonographic diagnosis of pregnancy #VYGGMU
At CRL of 5 mm
is discussed in greater detail in Chapter 10,
Obstetric ultrasound and other imaging. C ETQYPŌTWORNGPIVJhC , human chorionic gonadotropin.
Key points
• Pregnancy is usually suspected from the history and is • #NOQUVCNNRTGIPCPVYQOGPYKNNJCXGCRQUKVKXGWTKPG
EQPſTOGFD[RJ[UKECNGZCOKPCVKQPCNQPIYKVJNCDQTC- RTGIPCPE[VGUVYGGMCHVGTVJGOKUUGFOGPUVTWCN
tory testing. period.
• Amenorrhea is the fundamental sign of early pregnancy. • The most sensitive method of detecting hCG is a
serum pregnancy test.
• #WVGTKPGGZCOKPCVKQPOC[EQPſTOVJGRTGUGPEGQHCP
KPVTCWVGTKPGRTGIPCPE[CHVGTVJGVJYGGMQHRTGIPCPE[ • 6JGU[ORVQOUQHRTGIPCPE[KPVJGſTUVVTKOGUVGT
6JGEQTTGNCVKQPDGVYGGPWVGTKPGUK\GCPFIGUVCVKQPCN include nausea and vomiting, breast enlargement and
age is learned by experience. tenderness, fatigue and generalized malaise, and
• The diagnosis of early pregnancy is based primarily urinary frequency.
upon laboratory estimation of human chorionic gon- • 6JGUKIPUQHRTGIPCPE[KPVJGſTUVVTKOGUVGTKPENWFG
CFQVTQRKP
J%) globular enlargement of the uterus, Hegar’s sign
• Urine pregnancy testing is the most common method
UQHVGPKPIQHVJGWVGTKPGKUVJOWU%JCFYKEMŏUUKIP

DNWKUJCRRGCTCPEGQHVJGEGTXKZCPF)QQFGNNŏUUKIP
for diagnosing pregnancy in the clinic or hospital and is

UQHVGPKPIQHVJGEGTXKZ
also the preferred method for home pregnancy tests.
(Continued)
CH 07_p088-097_v3.indd 96 17-07-2015 10:59:44


• In the second trimester, nausea and vomiting usually • Sonographic examination of the uterus can be used to
UWDUKFG6JGOQVJGTHGGNUVJGſTUVHGVCNOQXGOGPVU EQPſTOVJGRTGUGPEGQHCRTGIPCPE[CPFFGVGTOKPG

SWKEMGPKPI$TCZVQP*KEMUEQPVTCEVKQPUUVCTVKPVJG YJGVJGTKVKUKPVTCWVGTKPGQTGZVTCWVGTKPG
GEVQRKE+VKU
late second trimester. CNUQWUGHWNYJGPVJGXKCDKNKV[QHVJGRTGIPCPE[JCUVQ
• In the second trimester, the uterus can be felt ab- be assessed.
FQOKPCNN[CPFEQPVKPWGUVQITQY(GVCNRCTVUCTGHGNV • 6JGIGUVCVKQPCNUCEKUVJGſTUVWNVTCUQWPFUKIPQHCP
5MKPOCPKHGUVCVKQPUUVCTVVQCRRGCTKPETGCUGFUMKP intrauterine pregnancy. It is usually visualized trans-
RKIOGPVCVKQP
KPENWFKPINKPGCPKITCCPFEJNQCUOC XCIKPCNN[YJGPVJGUGTWOJ%)NGXGNJCUTKUGPVQ
UVTGVEJOCTMUURKFGTPGXKCPFRCNOCTGT[VJGOC(GVCN 1500 mIU/mL.
heart tones can be auscultated. • +PGCTN[RTGIPCPE[VJGKFGPVKſECVKQPQHECTFKCECEVKX-
• +PVJGVJKTFVTKOGUVGTU[ORVQOUTGƀGEVVJGRTQITGUUKXG KV[YKVJVTCPUXCIKPCNUECPKUCIQQFUKIPQHCXKCDNG
enlargement of the uterus: breathlessness, palpita- pregnancy.
VKQPURGFCNGFGOCCPFDCEMCEJG
Self-Assessment
3. *GICTŏUUKIPKUVJGUQHVGPKPIQHVJGNQYGTWVGTKPG
Case-based questions UGIOGPVLWUVCDQXGVJGEGTXKZ
WVGTKPGKUVJOWU+V
QEEWTUCHVGTYGGMUŏRTGIPCPE[
Case 1 4. A gestational sac should be visualized by transvaginal
/TU #6 RTGUGPVGF YKVJ YGGMUŏ COGPQTTJGC CPF WNVTCUQPQITCRJ[YJGPVJGUGTWOJ%)KUO+7O.
C RQUKVKXG JQOG RTGIPCPE[ VGUV 5JG YCPVGF JGT RTGI-
PCPE[EQPſTOGF
Case 2
1. 9JCVKUVJGWTKPGVJTGUJQNFQHJ%)CVYJKEJCJQOG
RTGIPCPE[VGUVYKNNDGRQUKVKXG! 1. The etiology of nausea and vomiting in pregnancy is
probably multifactorial. Rising levels of E hCG and
2. Which is the most sensitive laboratory test for
estradiol play a role.
RTGIPCPE[!
2. Excessive vomiting leading to electrolyte disturbance
3. 9JCVKU*GICTŏUUKIP!
and dehydration is referred to as hyperemesis
4. #VYJCVUGTWONGXGNQHJ%)UJQWNFCIGUVCVKQPCNUCE
gravidarum.
DGXKUWCNK\GFD[VTCPUXCIKPCNWNVTCUQWPFGZCOKPCVKQP!
3. The uterus may be larger than the period of amenor-
TJGCDGECWUGQHYTQPIFCVGUOWNVKRNGIGUVCVKQP
Case 2 OQNCTRTGIPCPE[QTWVGTKPGſDTQKFU
4. #VYGGMUŏIGUVCVKQPCIGUVCVKQPCNUCEC[QNMUCE
/TU -6 UGEQPF ITCXKFC RTGUGPVGF YKVJ YGGMUŏ CPFCPGODT[QPKERQNGYKNNDGKFGPVKſGFQP685
amenorrhea, nausea, and vomiting. %CTFKCECEVKXKV[YKNNDGUGGPKPCXKCDNGHGVWU
1. 9JCVECWUGUPCWUGCCPFXQOKVKPIKPRTGIPCPE[!
2. 9JCVKUJ[RGTGOGUKUITCXKFCTWO!
3. What can be suspected if the uterus is larger than the
Sample questions
RGTKQFQHCOGPQTTJGC!
4. 9JCVUVTWEVWTGUYKNNDGXKUWCNK\GFKPVJGWVGTKPGECXKV[
Long-answer questions
on transvaginal ultrasonography at this period of 1. *QYKURTGIPCPE[FKCIPQUGF!9JCVCTGVJG
IGUVCVKQP! NCDQTCVQT[OGVJQFUQHCUUGUUKPIJ%)NGXGNU!
2. 9JCVCTGVJGUKIPUCPFU[ORVQOUQHRTGIPCPE[!
Answers
Case 1 1. Hegar’s sign
1. Urine hCG threshold of 20–50 IU/L. 2. %JCFYKEMŏUUKIP
2. The estimation of the serum level of hCG is the most 3. hCG
accurate laboratory test for pregnancy and can detect 4. Urine pregnancy test
J%)NGXGNUCUNQYCUŌO+7O. 5. Quantitative hCG assessment
CH 07_p088-097_v3.indd 97 17-07-2015 10:59:44

Section 2
Antenatal
Management
CH 08_p098-118_v3.indd 98 17-07-2015 10:30:52

History Taking and
8 Examination of the
Obstetric Patient
Case scenarios
Mrs. TM, 24, was married 1 year ago and was 5 months pregnant. She
was not sure if she could feel fetal movements and wanted to know if
her pregnancy was normal.
Mrs. SS, 26, had come for a routine antenatal examination close to
term. She wanted to know how the pregnancy was progressing and was
anxious to know if the head was engaged.
Introduction istory taking in the

A detailed history and properly performed obstetric patient
obstetric examination can give significant infor-
mation regarding diagnosis of pregnancy, identi- History of an obstetric patient begins with the
fication of risk factors, appropriate management name of the woman, age, occupation, educational
and follow-up. Gestational age, fetal growth, pre- status, and income. An outline of the details to be
sentation, and position of the fetus can be deter- obtained in history is given in Box 8.1.
mined at different stages of gestation. Findings
at physical examination can prompt appropriate
investigations.
At the first and subsequent visits, the preg- Demographic data
nant woman should be greeted and made to feel
comfortable. All details of history and findings Making the pregnant woman feel at ease is an
at each visit should be documented. A printed important part of history taking. Starting off
antenatal case record with a template is useful with personal information such as her name
for this purpose. and age, her husband’s name and age, and how
CH 08_p098-118_v3.indd 99 17-07-2015 10:30:52

Box 8.1 istory taking of the obstetric patient Table 8.1 bstetric complications in the young
gravida ( 19 years) and the elderly
• Demographic data—from both partners
gravida ( 35 years)
Ŧ Name
Ŧ Age oung gravida ( 19 years) Elderly gravida ( 35 years)
Ŧ Occupation/income
Ŧ Educational status Anemia Chromosomal anomalies
• Menstrual history Miscarriage Miscarriage
Ŧ &WTCVKQPQHƀQY Chronic hypertension/
Gestational hypertension/
Ŧ +PVGTXCNDGVYGGPRGTKQFU gestational hypertension/
preeclampsia
Ŧ Regular/irregular preeclampsia
• Marital history (GVCNITQYVJTGUVTKEVKQP Diabetes
• Obstetric history Abnormal labor Abnormal labor
Ŧ Obstetric score • Dysfunctional labor • Malpresentation
Ŧ LMP, EDD, and gestational age • Obstructed labor • Obstructed labor
Ŧ History of present pregnancy
Cesarean section Cesarean section
• Presenting complaints
Ŧ History of presenting complaints Perinatal mortality Preterm labor
• Contraception used prior to pregnancy Psychological stress Fetal macrosomia
• Past medical history
Perinatal mortality
Ŧ Medical disorders
Ŧ Medications
Ŧ Past surgeries
diabetes are usually seen in women in socioeco-
• Family history
nomic class 1 or 2.
Ŧ Diabetes
Ŧ Hypertension
Ŧ Multiple pregnancy
• Personal history Menstrual history
Ŧ Smoking/alcohol/drugs
Ŧ Diet The menstrual history is very important in a
pregnant woman. Box 8.2 lists the questions
DD estimated date of delivery; P last menstrual period.
to be asked regarding the woman’s menstrual
cycles. It is important to know the pattern of
long they have been married helps to make her cycles prior to conception.
less nervous, and more comfortable with the Women with irregular periods may con-
obstetrician. ceive later in the cycle, usually 14 days prior
to the expected date of menses. Corrected esti-
Age mated date of delivery (EDD) has to be calcu-
lated by adding the number of days beyond 28
There is an increased risk of obstetric complica- to EDD (e.g., if cycle length is 35 days [7 days
tions at both ends of the age spectrum. Because beyond 28 days], corrected EDD = calculated
of this, both a young gravida (<19 years) and an EDD + 7 days). The gestational age in these
elderly gravida (>35 years) should be monitored
carefully in pregnancy. Age-related obstetric
risks are listed in Table 8.1.
Box 8.2 Menstrual history
• Pattern of cycles prior to pregnancy
Education, occupation, and income
• 0WODGTQHFC[UQHƀQY
History concerning education, occupation, and • +PVGTXCNDGVYGGPRGTKQFU
income helps to determine the woman’s socio- • Last menstrual period (LMP)
economic status, level of comprehension, and Ŧ First day of last period
risk factors associated with a particular occupa- Ŧ Delayed or scanty period
Possibility of
tion. A low socioeconomic status (class 3 or 4)
- implantation bleeding
is associated with anemia, preterm labor, and
- ectopic pregnancy
gestational hypertension, whereas obesity and
CH 08_p098-118_v3.indd 100 17-07-2015 10:30:52

History Taking and Examination of the Obstetric Patient 101
women must be confirmed by an ultrasound pregnancy ended in a miscarriage/termination

examination. or resulted in a live birth. A gravida refers to a
In women who do not know the exact LMP, pregnant woman.
EDD may be calculated based on ‘quickening’
• Gravida: A woman who is pregnant
(first perception of fetal movement).
• Nulligravida or gravida 0: A woman who has
• Primigravidas usually feel quickening at 18–20 never been pregnant
weeks. • Primigravida or gravida 1: A woman who is
• Multigravidas can feel quickening as early as pregnant for the first time
16 weeks. • Multigravida: A woman who has been preg-
nant more than once and is currently pregnant
Ultrasonographic confirmation of gestational
• Elderly primigravida: A woman in her first
age is essential in these women as well.
pregnancy, who is 35 years or older
It is also important to know whether the LMP
was delayed, normal, or scanty. Some women
may have a scanty period even after they have
conceived (implantation bleeding), so there arity
might be a discrepancy in the gestational age. A Parity is defined as the number of pregnancies
scanty period after conception may also occur carried to viable gestational age. Viable ges-
with an ectopic pregnancy, so this history may tational age varies in different countries. This
be significant. depends on the neonatal facilities available to
help the preterm baby survive. In the United
States it is defined as 20 weeks. In the United
Marital history Kingdom and Europe it is considered to be
24 weeks. In developing countries viability could
It is important to know how long the couple has be considered to be 24 or 28 weeks. In this book
been married. If the duration of marriage is >2 24 weeks will be considered as a viable gesta-
years, check for a history of infertility. History tional age.
must be obtained to find out if it was a spon- • Para: Number of >24-week births (including
taneous conception or assisted reproductive stillbirths); pregnancies consisting of mul-
techniques (ART) were used. Assisted repro- tiples, such as twins or triplets, count as one
ductive techniques for infertility is associated birth
with a higher risk of multifetal pregnancy, mis- • Nullipara or para 0: A woman who has never
carriage, and other complications. carried a pregnancy beyond 24 weeks
Obtaining a history of consanguinity is • Primipara: A woman who has given birth after
important since consanguineous marriages are 24 weeks once before
still prevalent in India. The risk of congenital and • Multipara: A woman who has given birth to a
chromosomal abnormalities is higher in consan- viable fetus two or more times
guineous marriages. • Grand multipara: A woman who has given
birth to a viable fetus five or more times.
Examples
bstetric history
• Gravida 2, para 1, living 1 (G2 P1 L1): Pregnant
bstetric score for the second time, one delivery after 24
weeks, and child alive
Certain terms used in obstetrics are defined in • Gravida 3, para 0, abortion 2 (G3 P0 A2):
the next subsections. Pregnant for the third time, two pregnancies
ended in miscarriage (before 24 weeks)
ravi ity • Multiple pregnancy
Gravidity is defined as the number of times – Para 1, living 2 (P1 L2): One pregnancy and
the woman has been pregnant, including the delivered twins after 24 weeks, currently not
present pregnancy, regardless of whether the pregnant
CH 08_p098-118_v3.indd 101 17-07-2015 10:30:52

LMP, EDD, and gestational age antenatal care), whether the pregnancy has pro-
ceeded normally so far, or whether there has been
The date of the first day of the LMP is very any maternal/fetal complications identified.
important information and should be obtained
in all pregnant women. A provisional EDD can be istory of past pregnancies
calculated from the menstrual history in women
with 28- to 30-day cycles by adding 7 days to A detailed obstetric history of past pregnancies is
the first day of the LMP and then subtracting 3 important (Box 8.6). Was the previous pregnancy
months (Naegele’s rule). This is based on the full term or preterm? Did it end in a miscarriage
fact that a normal pregnancy has a duration of or was there an induced abortion? The number
roughly 280 days (40 weeks). Only 5% of women of live children must be noted. Details of each
deliver on the calculated EDD. delivery must be obtained with emphasis on
Naegele’s rule for calculating the EDD applies any complication that occurred during the preg-
only to women who have regular 28- to 30-day nancy or at delivery.
cycles (Box 8.3). Gestational age is calculated The past obstetric history has a bearing on
from the LMP to the current date. This should be the management of the current pregnancy
documented in completed weeks and days (e.g., since many obstetric complications (gestational
30+6 weeks). hypertension, preterm labor, placental abrup-
It is important to determine the EDD because tion) can recur in subsequent pregnancies.
it helps in many aspects of diagnosis and deci-
sion making in pregnancy (Box 8.4).
Presenting complaint(s)
istory of present pregnancy
Most pregnant women who come for antena-
Details of the pregnancy from confirmation to the tal care may not have any specific complaints.
present must be obtained (Box 8.5). It is import- However, they may have minor problems that
ant to know whether she had received preconcep- are common in pregnancy such as backache,
tional advice (see Chapter 9, Preconceptional and constipation, vomiting, or mild swelling of the
legs. Physiological changes in the various organ
systems in pregnancy and symptoms arising
Box 8.3 aegele s rule for calculating EDD
from these changes are discussed in Chapter 3,
(in women with 28- to 30-day cycles)
#FF FC[U VQ VJG ſTUV FC[ QH ./2 CPF UWDVTCEV
3 months.
Box 8.5 istory of present pregnancy
Example:
First day of LMP: February 21, 2014 • Preconceptional care received or not
Add 7 days: February 28, 2014 • First trimester
Subtract 3 months: November 28 Ŧ &CVGQHEQPſTOCVKQPQHRTGIPCPE[
EDD: November 28, 2014 Ŧ Any bleeding/excessive vomiting
Gestational age on August 10: 24+3YGGMU Ŧ Fever/medications/exposure to radiation
Ŧ Folic acid supplementation
DD estimated date of delivery; P last menstrual period. Ŧ Ultrasonography
Ŧ Date of quickening
Box 8.4 Importance of estimated date of delivery
Ŧ Ultrasonography
• Timing of investigations Ŧ Iron and calcium supplementation
Ŧ (KTUVVTKOGUVGTUETGGPKPIHQT&QYPU[PFTQOG
CP- Ŧ Hypertension/diabetes
euploidy screen) • Third trimester
Ŧ 5GEQPF VTKOGUVGT UETGGPKPI HQT &QYP U[PFTQOG Ŧ History of bleeding
(aneuploidy screen) Ŧ Hypertension
Ŧ Screening for gestational diabetes Ŧ Preterm labor
• Calculating preterm or postdates Ŧ Fetal movements
• Timing of interventions Ŧ (GVCNITQYVJTGUVTKEVKQP
• /QPKVQTKPIHGVCNITQYVJ Ŧ Any other complications
CH 08_p098-118_v3.indd 102 17-07-2015 10:30:52

Box 8.6 Past obstetric history Box 8.8 istory of presenting complaint(s)
umber of pregnancies • Duration
• Full term • Severity
• Preterm • Frequency
• Miscarriage • Other associated symptoms
• Abortion (induced)
• Ectopic pregnancy
• Living children ectopic pregnancy, whereas mild cramping can
• Multiple gestation be associated with a threatened miscarriage.
or each delivery note the following:
Intermittent abdominal pain associated with
• Date and place of delivery watery discharge in the third trimester may indi-
• Gestational age at delivery cate preterm labor with rupture of membranes.
• Mode of delivery (vaginal/instrumental/cesarean) Specific questions must be asked regarding the
• Indication for instrumental delivery/cesarean section presenting complaints (Box 8.8).
• Sex of child/children
• $KTVJYGKIJV
• Length of labor
• Analgesia or anesthesia used Contraception prior to
• Outcome (miscarriage, ectopic, live birth, stillbirth)
• %QORNKECVKQPU QH FGNKXGT[
FKHſEWNV HQTEGRU VGCTU pregnancy
excessive bleeding)
• Complications of pregnancy (maternal/fetal) It is important to enquire whether the couple
had been using contraception prior to the cur-
rent pregnancy. This will indicate whether the
Box 8.7 Symptoms that are not physiological in pregnancy is due to failure of contraception or
pregnancy
whether the couple had planned this pregnancy.
• 'ZEGUUKXGXQOKVKPI
YKVJYGKIJVNQUU Women who were on oral contraceptive pills
• Bleeding in any trimester may have a few irregular cycles after stopping
• Abdominal pain the oral contraceptives and so their EDD should
• Pedal edema present in the morning
be calculated accurately.
• Dyspnea/orthopnea/hemoptysis
• Headache/visual disturbances/epigastric pain
• Decreased/absent fetal movements
• Watery vaginal discharge
• &[UWTKCƀCPMRCKPHGXGT
Past medical surgical
history
Maternal physiology in pregnancy. Women may Past medical history may have obstetric impli-
also present with bleeding, watery discharge cations (Box 8.9). A history of maternal diabetes,
per vaginum, abdominal pain, or reduced fetal rheumatic valvular heart disease, hypertension,
movements. Symptoms that are not physiologi- thyroid dysfunction, and epilepsy is important.
cal and may jeopardize the pregnancy are listed A history of present and past medications should
in Box 8.7.
Box 8.9 Past medical history
istory of presenting complaint(s)
• Medical illnesses
Details regarding the nature, duration, fre- Ŧ Diabetes
quency, and severity of the complaints must be Ŧ Hypertension
noted. Profuse bleeding in the first trimester Ŧ Epilepsy
indicates incomplete or inevitable abortion and Ŧ Thyroid dysfunction
Ŧ Hereditary diseases
requires admission, whereas mild spotting can
• Medications and allergies
be managed at home. Acute abdominal pain
• Past surgeries
in the first trimester can be due to ruptured
CH 08_p098-118_v3.indd 103 17-07-2015 10:30:52

be obtained since many drugs are contraindi- • Jaundice

cated in pregnancy and may have to be stopped • Lymphadenopathy
or changed. Allergies must be asked for and • Thyromegaly
noted prominently on the antenatal card. Past • Gait
surgical history should also be elicited.
eight, weight, and BMI

Family history The patient’s height and weight are taken. The
body mass index (BMI) is calculated (Box 8.10).
Family history of medical disorders such as dia-
The patient must be counseled on the optimal
betes, hypertension, epilepsy, thyroid dysfunc-
weight gain based on her prepregnancy BMI
tion, and hereditary diseases must be asked for.
(Table 8.2).
A history of multifetal pregnancies and chro-
A high BMI (>30 kg/m2) is associated with
mosomal anomalies such as Down syndrome
complications such as miscarriage, preterm labor,
should also be noted.
gestational diabetes, hypertensive disorders, and
macrosomia. A low BMI of <18 kg/m2 along with
inadequate weight gain is associated with low
Personal history birth weight and preterm delivery (Box 8.11).
Smoking, addiction to alcohol, and drug abuse
can affect the growing fetus and lead to com- Pulse, blood pressure, cardiovascu-
plications. Women should be asked about these lar and respiratory systems
details and counseled accordingly.
The basal blood pressure is recorded with the
Detailed information regarding the wom-
patient in the seated position (Box 8.12). The
an’s diet is mandatory. This helps in identifying
respiratory and the cardiovascular systems are
dietary deficiencies and excesses. Information
examined and the findings noted.
regarding the woman's bowel and micturition
habits should also be obtained.
Examination of the breast
Breast examination is an integral part of exam-
Examination of the ination of the pregnant woman (Box 8.13).
obstetric patient
Box 8.10 Calculating BMI
6JG$/+KUECNEWNCVGFCUHQNNQYU
General physical Weight (kg)
BMI =
examination Height (m2)
ample: kg m B of kg m
Obstetricians are primary care physicians, and a
first obstetric consultation is a good opportunity
to perform a complete physical examination. B body mass index.
It is customary clinical practice to have a nurse
or trained birth attendant by the physician’s Table 8.2 ptimal weight gain based on BMI
side while doing the examination. A chaperone
Prepregnancy BMI Weight gain recommended
is essential if a male physician is examining a
(kg)
female patient.
On general examination, one should look for <18.5 13–18
the following: 18.5–24.9 11–16
25–29.9 7–11
• Pallor >30 5–9
• Pedal edema
B body mass index.
CH 08_p098-118_v3.indd 104 17-07-2015 10:30:52

Box 8.11 BMI and pregnancy outcome Box 8.13 Breast examination in pregnancy
igh B kg m associated with • Asymmetry common
• Miscarriage • Areola
• Preterm labor Ŧ Montgomery nodules (prominent sebaceous glands)
• Gestational diabetes • Nipples
• Hypertensive disorders of pregnancy Ŧ Normal
• Macrosomia Ŧ Flat
• Shoulder dystocia Ŧ Inverted
• Dysfunctional labor %QWPUGNKPITGICTFKPIFTCYKPIPKRRNGQWV
• Cesarean section • Masses
ow B kg m associated with Ŧ Fibroadenoma
• .QYDKTVJYGKIJV Ŧ Fibrocystic disease
• Preterm delivery
B body mass index. The mother might be sensitive about an

obstetric examination and extra care and kind-
Box 8.12 Method of recording blood pressure in ness are required to make it as comfortable as
pregnancy possible for her.
• Mercury sphygmomanometer recommended
• Aneroid or automated blood pressure recorders First trimester
replacing mercury sphygmomanometers due to ban
on mercury Since the uterus is not felt abdominally in the
• Seated position first trimester, both an abdominal and a vaginal
• Left lateral recumbent position can be used, particu- examination are required.
larly during labor
• Large blood pressure cuff if upper arm circumference
>33 cm Abdominal examination
• (KHVJ
- -QTQVMQHH UQWPF WUGF VQ FGſPG FKCUVQNKE Abdominal examination is an integral part of the
blood pressure
obstetric examination. The uterus is not palpa-
ble abdominally until 12 weeks. However, the
uterus may be larger than the period of amenor-
Inverted nipples should be looked for, and if rhea and may be felt abdominally in the follow-
present, the woman is counseled to draw the ing conditions:
nipple out regularly during the antenatal period
(see Chapter 25, Lactation and breastfeeding). • Wrong dates
Advice regarding breastfeeding and care of the • Uterine fibroids
breasts can also be given at this time. • Multiple gestation
• Molar pregnancy
Examination of spine
Presence of kyphosis, scoliosis, or pelvic defor-
aginal (bimanual) examination
mity should be looked for. Spinal deformities A vaginal examination is the most personal
may affect the shape of the pelvis. This may, in examination a woman will undergo and must be
turn, have an impact on labor and delivery. handled with sensitivity to her feelings. It should
never be performed without
• a short explanation about the procedure she
bstetric examination will be undergoing,
• asking permission to perform the examination,
The obstetric examination is distinct from other • a clear indication for the examination
examinations since the physician has to assess (Box 8.14), and
the health and well-being of two individuals— • measures taken to maintain the modesty of
the mother and the fetus. the woman.
CH 08_p098-118_v3.indd 105 17-07-2015 10:30:52

Box 8.14 Indications for a vaginal examination

KPVJGſTUVVTKOGUVGT
• Diagnosis of pregnancy
• Assessment of the gestational age
• Detection of anatomical or pathological abnormalities
QHVJGNQYGTIGPKVCNVTCEV
• Investigation of leucorrhea or bleeding per vaginum
• Examination of the cervix
A vaginal examination must always be pre-

ceded by an abdominal examination.
roce ure or a vaginal e amination

Preparing the patient
Figure 8.1 Bimanual pelvic examination.
In preparation for a vaginal examination, the fol-
lowing steps are followed: The middle finger of the gloved right hand, after
• The patient is asked to empty her bladder lubrication, is introduced into the introitus.
because a full bladder may interfere with the When the patient relaxes a little more, the index
assessment of the uterine size. finger is also introduced. The left hand is placed
• The patient must be made aware of the subse- on the abdomen, on the suprapubic area.
quent procedure with a short explanation. The intravaginal fingers palpate the cervix
• The patient is placed in a dorsal position with and lift up the uterus. The size, shape, consis-
her knees bent. tency, and contour of the uterus are noted. The
• The knees may be kept partially covered with a fingers are first introduced into the right fornix
sheet or even part of her own clothing. and subsequently the left fornix, to palpate for
• If the examination is done gently, there is less any adnexal masses or tenderness. The abdomi-
chance of the patient tensing up her adductors nal hand feels the uterus and any other palpable
and her abdominal muscles. pelvic mass (Box 8.15).
• Asking the patient to take deep breaths relaxes
the abdominal muscles and also distracts the
patient from the procedure.
Examination of the vulva

The vulva must be carefully inspected for any Box 8.15 Information obtained from a vaginal
external abnormality. (bimanual) examination
• Congenital anomalies • Cervix

• Genital warts (condylomata acuminata) Ŧ Length
Ŧ Firm or soft
• Varicosities
Ŧ External os closed or open
• Ulcers
Ŧ If external os open
• Discharge YJGVJGTKPVGTPCNQUENQUGFQTQRGP
Ŧ Presence of discharge or bleeding
Bimanual pelvic examination • Uterus
Ŧ Size
A bimanual pelvic examination is so named
Ŧ Firm or soft
because both hands are required for the exam-
Ŧ Anteverted or retroverted
ination (Fig. 8.1). Ŧ Regular or irregular contour
Procedure • Fornices and adnexa
Ŧ Presence of unilateral or bilateral adnexal masses
CH 08_p098-118_v3.indd 106 17-07-2015 10:30:52

Figure 8.2 Position of the patient for abdominal palpation.
Box 8.16 Examination of the abdomen in the

second trimester inspection
• #DFQOKPCNFKUVGPUKQPEQPUKUVGPVYKVJRTGIPCPE[
• Position of the umbilicus
• Flanks—usually not full
• Skin changes
Ŧ Striae gravidarum
Ŧ Linea nigra Figure 8.3 2CNRCVKPIVJGWVGTKPGHWPFWUYKVJVJGWNPCT
• Presence of scars aspect of the hand.
Ŧ Previous cesarean section
Ŧ Any other surgery Box 8.17 terine si e by abdominal palpation
• Presence of umbilical/incisional hernia
YGGMU 7VGTWU LWUV RCNRCDNG CDQXG VJG RWDKE
symphysis
YGGMU 1PGVJKTFVJGFKUVCPEGDGVYGGPRWDKE
Second trimester symphysis and umbilicus
Abdominal examination YGGMU 6YQVJKTFUVJGFKUVCPEGDGVYGGPRWDKE

symphysis and umbilicus
After having emptied her bladder, the pregnant YGGMU #VVJGNGXGNQHWODKNKEWU
woman is asked to lie comfortably on her back. YGGMU 1PGVJKTFVJGFKUVCPEGDGVYGGPWODK-
Keeping her knees partly flexed helps relax the licus and xiphisternum
abdominal wall muscles (Fig. 8.2). YGGMU 6YQVJKTFU VJG FKUVCPEG DGVYGGP WO-
The pregnant woman should ideally be bilicus and xiphisternum
exposed from the pubic bone to just below her YGGMU #VZKRJKUVGTPWO
breasts. The obstetrician should stand on the
YGGMU #VYGGMUDWVƀCPMUHWNN
woman’s right side.
It is best to put the pregnant woman at ease by
asking her a general question: How are you feel-
ing today? Are you feeling any movements? uterus and then the hand is moved down till the
top of the uterus is felt. Some obstetricians pre-
Inspection fer feeling the top of the uterus with the palms of
Details to be noted on inspection of the abdo- both hands.
men are listed in Box 8.16. After the 12th week of pregnancy, the uterus is just
palpable above the pubic symphysis (Box 8.17).
alpation The distance between the pubic symphysis and
the umbilicus is divided into three equal parts,
Palpation begins with measurement of fundal
corresponding to 16, 20, and 24 weeks. At 24
height. This is done with the patient’s legs in the
weeks, the uterus is at the level of the umbili-
extended position.
cus. Again, the distance between the umbilicus
Assessing fundal height and the xiphisternum is divided into three equal
The fundus of the uterus is palpated by hold- parts, corresponding to 28, 32, and 36 weeks. At
ing the hand in a ‘chopping’ position, with the 36 weeks, the fundus is at the level of the xiphis-
medial (ulnar) aspect of the hand along the top ternum. After 36 weeks, the fundal height is
of the uterus (Fig. 8.3). Usually the palpation lower, as the head may have descended into the
is started slightly above the visible curve of the pelvis and the uterus falls forward. At 40 weeks,
CH 08_p098-118_v3.indd 107 17-07-2015 10:30:53

op o uterus
s
s Pubic
symphysis
s
s
s
s
Figure 8.4 (WPFCNJGKIJVCVFKHHGTGPVYGGMUQHRTGIPCPE[ Figure 8.6 Landmarks for measuring the symphysio-
fundal height.
ymphysio fun al height
M
un al height cm
estation ee s
Figure 8.5 Metrogram or gravidogram for plotting

symphysio-fundal height. SD standard deviation.
Figure 8.7 Measuring the symphysio-fundal height.
the fundus is at the same level as 32 weeks but or gravidogram; Fig. 8.5). Persistent deviation
the flanks are full (Fig. 8.4). above the 90th centile or below the 10th centile
Measuring symphysio-fundal height
(or ±2 SD) from the normal for the population
needs further evaluation to exclude fetal mac-
Measurement of fundal height can be used rosomia or growth restriction. This is a simple
to estimate the gestation of the pregnancy. and inexpensive screening method for fetal
Between 20 and 32 weeks gestation, the fun- growth restriction in low-resource countries
dal height (in cm) roughly corresponds to the and is recommended as a routine practice by
weeks of gestation. For example, if the sym- the World Health Organization (WHO).
physio-fundal height (SFH) is 26 cm, it corre-
sponds to 26 weeks’ gestation. A difference of ±2 Procedure
cm is considered normal. A difference of ±3 cm The upper border of the pubic symphysis is pal-
on a single measurement alerts one to the pos- pated, and the distance between this and the top
sibility of abnormality. Serial measurement of of the fundus is measured with a measuring tape
SFH should be plotted on a graph (metrogram (Figs 8.6 and 8.7).
CH 08_p098-118_v3.indd 108 17-07-2015 10:30:54

Box 8.18 easons for discrepancy in the SF Box 8.19 b ectives of abdominal and vaginal
measurements examination in the third trimester
Causes for higher-than-e pected S measurement • Abdominal examination
• Wrong dates Ŧ (GVCNITQYVJ
• Macrosomia Ŧ Lie
• Multiple pregnancy Ŧ Presentation
• Polyhydramnios Ŧ Attitude
Ŧ Position
Causes for lower-than-e pected S measurement • Vaginal examination
• Wrong dates Ŧ Cervix
• Transverse lie Effacement
• (GVCNITQYVJTGUVTKEVKQP Dilatation
• Oligohydramnios Ŧ Station of presenting part
Ŧ Bony architecture of the pelvis
S symphysio-fundal height.
The reasons for a discrepancy in the SFH Third trimester

measurements are given in Box 8.18.
The objectives of the abdominal examination in
Auscultation o the etal heart the third trimester are to monitor fetal growth and,
In the second trimester, the uterus is felt above after 32–34 weeks, to determine the lie, presenta-
the pubic symphysis. Between 12 and 20 weeks, tion, and position of the fetus. The objectives of
fetal heart tones will be difficult to identify with the vaginal examination in the late third trimester
anything other than a handheld Doppler device. are to assess the cervix and the pelvis (Box 8.19).
After 20 weeks, fetal heart tones may be picked
up with a specialized obstetric stethoscope Fetal lie, presentation, attitude, and
(fetoscope) or, with practice, with a regular
stethoscope.
position
In the early months, fetal heart tones will usu- ie o the etus
ally be heard around the midline in the lower
The lie of the fetus refers to the position of the
pole. As pregnancy progresses, they will be heard
long axis of the fetus in relation to the mother.
better on the side of the abdomen where the fetal
spine is palpable. • Longitudinal lie: The long axis of the fetus and
mother are parallel (Fig. 8.8a).
a. b. .
Figure 8.8 Fetal lie. a. Longitudinal lie. b. Transverse lie. c. Oblique lie.
CH 08_p098-118_v3.indd 109 17-07-2015 10:30:54

• Transverse lie: The long axis of the fetus is per- Attitude of the fetal head is determined by
pendicular to the mother’s long axis (Fig. 8.8b). abdominal examination (described later).
• Oblique lie: The long axis of the fetus lies at
an oblique angle to the mother’s long axis osition o the etus
(Fig. 8.8c). The position of the fetus refers to the relationship
of a specific point of the fetal presenting part to
resentation o the etus the front, back, or sides of the maternal pelvis.
The point referred to is called the reference point
Presentation of the fetus is determined by the
or denominator (Table 8.3).
fetal lie and the presenting part:
Although the fetal position can be assessed
• Vertex or cephalic: Longitudinal lie with the by feeling for the position of the spine on
head in the lower pole abdominal examination, it is best determined
• Breech: Longitudinal lie with the breech in the by a vaginal examination, through a dilated
lower pole cervix.
• Other presentations
– Shoulder presentation (common in trans-
verse lie) Fetal positions using vertex presentation as
– Face presentation an example
– Brow presentation Fetal positions using vertex presentation as an
example are as follows (Fig. 8.10):
etal attitu e
• Left occipitoanterior (LOA): The fetal occiput
Attitude refers to the degree of flexion, deflexion, is in the left anterior quadrant of the maternal
or extension of the fetal head. The fetal diame- pelvis.
ters presented to the birth canal increase with • Right occipitoanterior (ROA): The fetal occiput
progressive deflection. A completely extended is in the right anterior quadrant of the mater-
head is a face presentation which has the same nal pelvis.
presenting diameter as a flexed vertex presen- • Occipitoanterior (OA): The fetal occiput is
tation. The various attitudes described are as directly behind the symphysis pubis.
follows: • Left occipitotransverse (LOT): The fetal occiput
• Flexion: Vertex presentation (Fig. 8.9a) is on the mother’s left.
• Deflexion: Vertex in occipitoposterior position • Right occipitotransverse (ROT): The fetal
(Fig. 8.9b) occiput is on the mother’s right.
• Extension • Left occipitoposterior (LOP): The fetal
– Partial: Brow presentation (Fig. 8.9c) occiput is on the mother’s left and pointing
– Complete: Face presentation (Fig. 8.9d) posterior.
a. cm b. cm . cm . cm
Figure 8.9 (GVCNCVVKVWFG0QVGVJGKPETGCUGFFKCOGVGTU

TGFNKPGURTGUGPVGFVQVJGDKTVJECPCNYKVJRTQITGUUKXGFGƀGZKQP
a. Flexed (vertex). b.&GƀGZGFXGTVGZ
ŎOKNKVCT[ŏRQUKVKQPc.2CTVKCNN[GZVGPFGF
DTQYd. Fully extended (face).
CH 08_p098-118_v3.indd 110 17-07-2015 10:30:54

Table 8.3 eference point for determining fetal position in different presentations
Presentation Attitude Presenting part eference point

ongitu inal lie
Cephalic Flexion Vertex Occiput
&GƀGZKQP Vertex Occiput
Partial extension $TQY Frontum (forehead)
Complete extension Face Mentum (chin)
reech
Complete Flexed hips and knees Buttocks Sacrum
Flexed hips, extended
Frank Buttocks Sacrum
knees
Footling (single, double) Extended hips and knees • Feet • Sacrum
• Knees • Sacrum
ransverse or obli ue lie
Shoulder Variable Shoulder, arm, trunk Scapula
P L P
Posterior
ight et
terior
L
Figure 8.10 Fetal vertex (occiput) positions in relation to the maternal pelvis. A left occipitoanterior; P left
occipitoposterior; left occipitotransverse; A right occipitoanterior; P right occipitoposterior; right
occipitotransverse.
CH 08_p098-118_v3.indd 111 17-07-2015 10:30:55

• Right occipitoposterior (ROP): The fetal Determining lie, presentation, and engagement
occiput is on the mother’s right and pointing Lie, presentation, and engagement are deter-
posterior. mined by the Leopold’s maneuvers, which are
• Occipitoposterior (OP): The fetal occiput is four specific steps in abdominal palpation of the
directly in front of the sacrum. uterus. These steps help determine the lie and
presentation of the fetus. They also help identify
whether engagement of the presenting part has
Abdominal examination in the third occurred.
trimester
Leopold s maneuver 1 (fundal grip)
Inspection Leopold’s maneuver 1 helps answer the following
The details to be noted on inspection are as question:
listed in Box 8.16. However, in the third trimester, What is in the fundus?
special attention must be paid to the following
additional details: The examiner stands on the patient’s right
side, facing her head. The hands are placed at
• Flanks—full after 38 weeks the fundus and an attempt is made to identify
• Uterine ovoid the fetal part at the fundus (Fig. 8.12). In most
– Longitudinal—in cephalic and breech cases, the breech is palpated. The breech is less
presentations hard than the head and is not defined as easily.
– Transverse—in transverse and oblique lie It is soft, broad, more irregular, and not inde-
Shelving pendently ballotable. The breech is also in con-
tinuity with the fetal back with no intervening
Shelving occurs when the uterus falls forward at groove as is found with the head (Box 8.20).
or after 38 weeks. The patient should be placed
in a semirecumbent position at 45 degrees and
shelving at the fundus should be noted (Fig. 8.11).
alpation
Measuring fetal growth
After palpating the fundus of the uterus and
identifying the top border of the symphysis
pubis, the SFH is assessed or measured.
Figure 8.12 Leopold's maneuver 1.
Box 8.20 Identifying the breech

• Less hard than head
• Irregular
• Soft and broad
• Not independently ballotable
Figure 8.11 5JGNXKPI+VUJQWNFDGPQVGFYKVJVJGRCVKGPV
• +PEQPVKPWKV[YKVJHGVCNDCEMYKVJPQKPVGTXGPKPIITQQXG
in a semirecumbent position.
CH 08_p098-118_v3.indd 112 17-07-2015 10:30:55

Leopold s maneuver 2 (umbilical grip) Leopold s maneuver 3 (pelvic grip 1)

Leopold’s maneuver 2 helps answer the following Leopold’s maneuver 3 helps answer the following
question: question:
Where is the fetal spine? What is the presenting part?
The examiner continues to stand in the same
This maneuver is also called the Pawlik’s grip. It
position. The hands are placed on the sides of the
is performed with the examiner still by the side of
abdomen, at the level of the umbilicus (Fig. 8.13).
the patient, facing her head. The lower uterine seg-
The location of the back and small parts is iden-
ment is grasped between the thumb and fingers of
tified (Box 8.21). The back is identified by feeling
one hand (Fig. 8.14), while the other hand steadies
the uniform resistance of the smoothly curving
the uterus at the fundus. In most cases, the head
firm arch of the spine. On the other side, there
will be in the lower pole of the uterus. It can be
will be small, irregular parts that represent the
identified as a hard, globular smooth structure,
limbs. Movements of the limbs may be felt, con-
which is in contrast to the less defined breech.
firming the diagnosis. Once the spine is identi-
The head is then grasped and moved from
fied, it is obvious that the occiput will be on the
side to side. If it moves freely, it is considered to
same side as the spine.
be floating, that is, it has not yet descended into
The fetal spine is felt easily and more ante-
the bony pelvis. In contrast, if most of the head
riorly in occiput anterior positions. The spine
seems to have entered the bony pelvis, it may be
is felt more posteriorly (toward the flank) and
engaged or fixed (see below). This is confirmed
limbs felt easily and anteriorly in occiput poste-
by the second pelvic grip. In late pregnancy, the
rior positions.
lower uterine segment can be tender, so the first
pelvic grip should be performed as gently and as
quickly as possible.
This step also establishes the fetal lie and pre-
sentation. If the head is felt in the lower pole, it is
then known that the fetus is in a longitudinal lie
with a cephalic presentation.
Figure 8.13 Leopolds' maneuver 2.
Box 8.21 Identifying fetal spine and limbs

• Fetal spine
Ŧ Uniform resistance
Ŧ Smoothly curving
Ŧ Firm arch
• Fetal limbs
Ŧ Small, hard, irregular parts
Ŧ On the opposite side of spine
Ŧ Movements might be felt
Figure 8.14 Leopolds' maneuver 3.
CH 08_p098-118_v3.indd 113 17-07-2015 10:30:55

Leopold s maneuver 4 (pelvic grip 2) prominence therefore will be on the same side
Leopold’s maneuver 4 helps answer the following as the small parts. When the head is extended
questions: and the fetus is in an extended attitude (face
or brow presentation), the occiput will be felt
• What is the presenting part? first. In this case, the cephalic prominence will
• Where is the cephalic prominence? be on the same side as the fetal back. When the
• What is the attitude of the fetal head? head is deflexed, the occiput and sinciput are
• Is the head engaged? felt at the same level (Box 8.22).
The examiner still stands on the right side of • Engagement of the presenting part is deter-
the patient but now faces her feet. mined. When the widest diameter of the pre-
The two hands are placed on either side of senting part has passed through the pelvic
the uterus just below the level of the umbilicus inlet, engagement is said to have taken place
(Fig. 8.15), and the tips of the fingers of each (Fig. 8.17). If engagement has taken place, the
hand glide along the sides of the uterus toward leading bony presenting part is at or nearly at
the pubis (‘walk down’ with the fingertips). the level of the ischial spines.
• The presenting part is reconfirmed. Since the suboccipitobregmatic diameter and

• The cephalic prominence is identified. It is the the biparietal diameter are at the same level, this
most prominent part of the fetal head that is felt diameter also enters the pelvic brim at the same
on palpation. It may refer to the sinciput (fore-
head) or the occiput, depending on the attitude
of the fetus. Feeling the cephalic prominence
helps determine whether the head is flexed or
extended. The cephalic prominence is identi-
fied by the resistance felt by one of the examin-
ing hands.
• The attitude of the fetus is determined. When
the head is flexed, the sinciput is felt first and
the occiput is lower (Fig. 8.16). The cephalic
inciput
cciput
Figure 8.16 6JGUKPEKRWVKUHGNVCVCJKIJGTNGXGNKPCYGNN

ƀGZGFXGTVGZRTGUGPVCVKQP
Box 8.22 +PVGTRTGVCVKQPQHſPFKPIUQP.GQRQNFŏU

maneuver 4
• (GVCNXGTVGZƀGZGF
Ŧ 5KPEKRWV
HQTGJGCFHGNVſTUV
Ŧ 1EEKRWVNQYGT
Ŧ Cephalic prominence same side as small parts
• 8GTVGZFGƀGZGF
12RQUKVKQP
Ŧ Occiput and sinciput at the same level
Ŧ Cephalic prominence on the same side as the back
• (GVCNXGTVGZGZVGPFGF
HCEGQTDTQYRTGUGPVCVKQP
Ŧ 1EEKRWVHGNVſTUV
Ŧ 5KPEKRWV
HQTGJGCFNQYGT
Ŧ Cephalic prominence same side as fetal back
Figure 8.15 Leopolds' maneuver 4. P occipitoposterior.
CH 08_p098-118_v3.indd 114 17-07-2015 10:30:56

Box 8.24 Guidelines for locating the fetal heart

• Heard on the same side as fetal spine
• Vertex presentation
Ŧ $GNQYVJGWODKNKEWU
1#ōLWUVNCVGTCNVQOKFNKPG
12ōVQYCTFVJGHNCPM
• Breech presentation
Ŧ Above the umbilicus
inciput cciput
A occipitoanterior; P, occipitoposterior.
schial spines aginal examination in the late

Figure 8.17 Engagement. Widest diameter of the fetal
third trimester
head has passed the pelvic inlet. A vaginal examination may be performed at or
after 38 weeks’ gestation. It provides information
time. Therefore, on the second pelvic grip, in about the cervix, presenting part, membranes,
vertex presentation, when the head is engaged, and pelvis (Box 8.25).
only the sinciput is felt and the head is 1/5th pal-
pable (Fig. 8.17; see Chapter 14, Normal labor: Box 8.25 Indications for performing a vaginal
Mechanics, mechanism, and stages). The fingers of examination at term
the examining hands diverge beyond this point.
• Cervical effacement and dilatation
Leopold's maneuvers are summarized in
• Presenting part
Box 8.23.
Ŧ Presentation
Ŧ Position
Box 8.23 Leopold s maneuvers Ŧ Station
• Maneuver 1 (fundal grip) • Status of membranes
Ŧ +FGPVKſGUHGVCNRCTVKPHWPFWU • Clinical pelvimetry to assess pelvic capacity
Ŧ Fetal lie
• Maneuver 2 (umbilical grip)
Ŧ Side of fetal spine Procedure for vaginal examination
Ŧ Fetal lie and presentation
• Maneuver 3 (pelvic grip 1)
at term
Ŧ Presenting part The procedure for vaginal examination at term
• Maneuver 4 (pelvic grip 2) consists of the following steps:
Ŧ 4GEQPſTOURTGUGPVCVKQP
Ŧ +FGPVKſGUEGRJCNKERTQOKPGPEG • A vaginal examination at term should be done
Ŧ Fetal attitude with a sterile glove.
Ŧ Engagement of head • Since the cervical os may be open or there may be
a very small possibility of rupture of membranes
at the time of examination, it is important to use
Auscultation sterile techniques to avoid ascending infection.
In the third trimester, in a vertex presentation, • The procedure is briefly explained to the
the fetal heart is usually heard below the level mother so that she is at ease.
of the umbilicus, on the same side as the fetal • She is placed in the dorsal position with her
spine, along the line connecting the umbilicus knees bent. She is asked to breathe deeply
and anterior superior iliac spine (spinoumbili- through her mouth, which helps her relax and
cal line). It is heard just lateral to the midline in makes the vaginal examination easier.
occipitoanterior positions and toward the flank • Adequate lubrication should be used.
in occipitoposterior positions. In a breech pre- • The middle finger of the examining (right)
sentation it may be heard at or above the level of hand is first inserted and then the index finger.
the umbilicus (Box 8.24). The normal fetal heart • The examination should be done gently because,
rate ranges between 120 and 160 bpm. at term, the vagina is very hyperemic and tender.
CH 08_p098-118_v3.indd 115 17-07-2015 10:30:56

Contraindications to vaginal mother’s right and left and not that of the exam-
examination at term ining physician (Box 8.27).
Contraindications to vaginal examination at Box 8.27 Determining fetal position in vertex

term are as follows: presentation
• Suspected placenta previa • 5CIKVVCNUWVWTGKFGPVKſGF
• Suspected ruptured membranes (in which • Anterior or posterior fontanelle located
case, a speculum examination must be done • Occiput behind posterior fontanelle
to confirm or rule out rupture of membranes) • Relationship of occiput to maternal pelvis
Assessment of effacement and Station o the presenting part

dilatation of the cervix The station of the presenting part is described using
Assessment of effacement and dilatation of the the ischial spines as the reference point. When the
cervix is discussed in Chapter 14, Normal labor: presenting part is at the level of the spines, the
Mechanics, mechanism, and stages. station is ‘0.’ Assessment of the station of the pre-
senting part is discussed further in Chapter 15,
Evaluation of the presenting part Management of normal labor and delivery.
etal presentation Assessment of the capacity of the

ertex (occiput) presentation
bony pelvis (clinical pelvimetry)
The fetal skull feels hard and rounded (Box 8.26).
If the cervix is open, the coronal and sagittal It is good clinical practice to make a rapid assess-
sutures will be felt by gliding the examining fin- ment of the bony architecture of the pelvis. This
gers over the skull. The fontanelles can be iden- may alert the obstetrician to the possibility of
tified as shallow spaces, which have a little give dystocia in labor. This is discussed further in
on gentle pressure. If the head is well flexed, only Chapter 40, Abnormal labor: Abnormalities in
the triangular posterior fontanelle will be felt. passage and powers.
roce ure
Box 8.26 Identifying the vertex on vaginal
Assessment of the pelvis or internal pelvimetry
examination
begins with palpation of the sacral promontory.
• Skull feels hard and round The examination proceeds in the order described
• Coronal and sagittal sutures felt in Box 8.28.
• (QPVCPGNNGUKFGPVKſGFCUUJCNNQYURCEGUDGVYGGPUWVWTG At the end of the obstetric examination, the
lines
patient must be clearly informed about the findings,
the progress of her pregnancy, and the fetal status.
Identification of the breech, brow, and face
presentations is given in the respective chapters
(see Chapter 41, Abnormal labor 2: Malposition Box 8.28 Assessment of the bony pelvis
and malpresentations and Chapter 42, Abnormal • Sacral promontory
labor 3: Breech presentation and shoulder • &KCIQPCNEQPLWICVG
dystocia). • Curvature of the sacrum
Ŧ #DQXGFQYPYCTFU
etal position Ŧ Side to side
• Sacrosciatic notch
ertex or cephalic presentation • 2GNXKEUKFGYCNNU
The sagittal suture is identified. Once either the • Ischial spines
anterior or the posterior fontanelle is identified, • Forepelvis
the position of the fetus is recorded depending • Subpubic angle
• Transverse diameter of the outlet (intertuberous
on the relation of the occiput to the maternal
diameter)
pelvis. The terms ‘right’ and ‘left’ refer to the
CH 08_p098-118_v3.indd 116 17-07-2015 10:30:56

Key points
History determine the lie and presentation of the fetus. They
CNUQJGNRKFGPVKH[YJGVJGTGPICIGOGPVQHVJGRTGUGPV-
• A detailed history from an obstetric patient can ing part has occurred.
IKXGUKIPKſECPVKPHQTOCVKQPTGICTFKPIFKCIPQUKUQH
• The lie of the fetus refers to the position of the long
RTGIPCPE[KFGPVKſECVKQPQHTKUMHCEVQTUCRRTQRTKCVG
axis of the fetus in relation to the mother. The fetus
OCPCIGOGPVCPFHQNNQYWR
can be in longitudinal lie (cephalic or breech), trans-
• 6JGFCVGQHVJGſTUVFC[QHVJGNCUVOGPUVTWCNRGTKQF verse lie, or oblique lie.
(LMP) is a very important information and should be
• Presentation of the fetus is determined by the fetal lie
QDVCKPGFKPCNNRTGIPCPVYQOGP
and the presenting part. It could be cephalic, breech,
• 0CGIGNGŏUTWNG#RTQXKUKQPCNGZRGEVGFFCVGQHFGNKXGT[ UJQWNFGTHCEGQTDTQY
ECPDGECNEWNCVGFHTQOVJGOGPUVTWCNJKUVQT[KPYQOGP
• The position of the fetus refers to the relationship of a
YKVJVQFC[E[ENGUD[CFFKPIFC[UVQVJGſTUV
URGEKſERQKPVQHVJGHGVCNRTGUGPVKPIRCTVVQVJGCPVG-
day of the LMP and then subtracting 3 months.
rior, posterior, or lateral sides of the maternal pelvis.
• &GVCKNUQHVJGRTGUGPVRTGIPCPE[HTQOEQPſTOCVKQPQH The point referred to is called the reference point or
pregnancy to date must be obtained. denominator.
• A detailed obstetric history of the past pregnancies is • 9JGPVJGYKFGUVFKCOGVGTQHVJGRTGUGPVKPIRCTVJCU
important. passed through the inlet, engagement is said to have
• Past medical and surgical history, family history, and taken place.
personal history should be elicited. • In a vertex presentation, engagement of the fetal head
is determined by evaluating the extent of the head
Examination RCNRCDNGRGTCDFQOGPFGUETKDGFKPVGTOUQHſHVJUQH
the fetal head.
• A properly performed obstetric examination can give
UKIPKſECPVKPHQTOCVKQPHQTVJGFKCIPQUKUCPFHQNNQYWR • #XCIKPCNGZCOKPCVKQPCVVGTOUJQWNFDGFQPGYKVJC
of pregnancy. sterile glove.
• #XCIKPCNGZCOKPCVKQPOWUVCNYC[UDGRTGEGFGFD[CP • Vaginal examination at term is contraindicated in
abdominal examination. suspected placenta previa and suspected ruptured
membranes. In the case of suspected rupture of
• A vaginal examination is the most personal examina- membranes, a speculum examination should be done
VKQPCYQOCPYKNNWPFGTIQCPFOWUVDGJCPFNGFYKVJ VQEQPſTOQTTWNGQWVTWRVWTGQHOGODTCPGU
sensitivity to her feelings.
• Reasons for performing a vaginal examination at term
• Gestational age can be assessed by recording the KPENWFGEQPſTOCVKQPQHVJGRTGUGPVKPIRCTVCUUGUUOGPV
U[ORJ[UKQHWPFCNJGKIJV$GVYGGPCPFYGGMU of station of the presenting part, assessment of the cervix
GCEJEGPVKOGVGTEQTTGURQPFUVQYGGM for ripening (effacement and dilatation), and assessment
• .GQRQNFŏUOCPGWXGTUCTGHQWTURGEKſEUVGRUKP of the capacity of the bony pelvis (clinical pelvimetry).
abdominal palpation of the uterus. These steps help
Self-Assessment
Mrs. SS, 26, had come for a routine antenatal examina-
Case 1 VKQP ENQUG VQ VGTO 5JG YCPVGF VQ MPQY JQY VJG RTGI-
/TU6/YCUOCTTKGF[GCTCIQCPFYCUOQPVJU PCPE[ YCU RTQITGUUKPI CPF YCU CPZKQWU VQ MPQY KH VJG
RTGIPCPV5JGYCUPQVUWTGKHUJGEQWNFHGGNHGVCNOQXG- JGCFYCUGPICIGF
OGPVUCPFYCPVGFVQMPQYKHJGTRTGIPCPE[YCUPQTOCN 1. 9JCVFQGU.GQRQNFŏUHQWTVJOCPGWXGTCEJKGXG!
1. *QYKU'&&ECNEWNCVGF! 2. 9JCVKUHGVCNNKG!
2. 9JGPFQGUCRTKOKITCXKFCHGGNSWKEMGPKPI! 3. 9JGTGYKNNVJGHGVCNJGCTVDGDGUVJGCTFKPCXGTVGZ
3. 9JGTGYKNNVJGWVGTKPGHWPFWUDGHGNVCVYGGMUŏ RTGUGPVCVKQP!
IGUVCVKQP! 4. 9JCVKUGPICIGOGPV!
4. 9J[KUU[ORJ[UKQHWPFCNJGKIJVKORQTVCPV!
CH 08_p098-118_v3.indd 117 17-07-2015 10:30:56

3. In a vertex presentation, the fetal heart is usually

Answers JGCTFDGNQYVJGNGXGNQHVJGWODKNKEWUQPVJGUCOG
side as the fetal spine.
Case 1 4. 9JGPVJGYKFGUVFKCOGVGTQHVJGRTGUGPVKPIRCTVJCU
1. 6JG'&&KUECNEWNCVGFWUKPI0CGIGNGŏUTWNGAdd 7 passed through the inlet, engagement is said to have
FC[UVQVJGſTUVFC[QHVJG./2CPFVJGPUWDVTCEV taken place.
OQPVJU6JKUKUCRRNKECDNGVQYQOGPYKVJVQ
day cycles.
2. A primigravida usually feels quickening at 18–20 Sample questions
YGGMU
3. 6JGWVGTKPGHWPFWUYKNNDGHGNVVYQVJKTFUQHVJGFKU- Long-answer question
VCPEGDGVYGGPVJGRWDKEU[ORJ[UKUCPFWODKNKEWUCV 1. &GUETKDG.GQRQNFŏUOCPGWXGTU
YGGMUŏIGUVCVKQP
4. The symphysio-fundal height is used to measure the
WVGTKPGUK\G$GVYGGPCPFYGGMUŏIGUVCVKQP Short-answer questions
the fundal height (in cm) roughly corresponds to the 1. Gravidity
YGGMUQHIGUVCVKQP 2. Parity
3. Fetal lie
Case 2 4. Fetal attitude
5. Fetal presentation
1. .GQRQNFŏUHQWTVJOCPGWXGTTGEQPſTOURTGUGPVCVKQP
KFGPVKſGUEGRJCNKERTQOKPGPEGCPFFGVGTOKPGUHGVCN 6. Fetal position
attitude and engagement of the head. 7. &GUETKDGJQYGPICIGOGPVQHVJGRTGUGPVKPIRCTVKU
2. The lie of the fetus refers to the position of the long determined
axis of the fetus in relation to the mother. The fetus
can be in longitudinal lie (cephalic or breech), trans-
verse lie, or oblique lie.
CH 08_p098-118_v3.indd 118 17-07-2015 10:30:56

Preconceptional
9 and Antenatal Care
Case scenarios
Mrs. YL, 25, had been married for a year. The couple was planning a
pregnancy. She had a strong family history of diabetes mellitus. Before
marriage she was diagnosed to have polycystic ovarian syndrome with
mildly elevated blood sugars. The couple wanted to know what com-
plications could occur during pregnancy and what precautions were
necessary.
Mrs. HM, 23, was pregnant for the first time. At 32 weeks’ gestation she
was found to have hypertension. She wanted advice on managing her
hypertension and what effect it would have on her baby.
Introduction maternal, perinatal and neonatal outcomes,

especially in developing countries such as India.
Childbearing is one of the commonest experi-
ences that a woman in the reproductive age group
will undergo. Improving the mother’s preconcep-
tional health can result in improved reproductive Preconceptional care
health outcomes, with the potential for reducing
the economic burden on society. Preconceptional Preconceptional care is the process of identify-
counseling and care has been shown to improve ing social, behavioral, environmental, and bio-
pregnancy outcomes, including low birth weight, medical risks to a woman’s future pregnancy
premature birth, and infant mortality. outcome and then reducing these risks through
The antenatal period is an extremely import- appropriate intervention.
ant time during pregnancy and the care received
during this time will have short- and long-term oals o preconceptional care
effects on both the mother and the fetus. It is well Goals of preconceptional care include screen-
recognized that good antenatal care improves ing for risk factors, initiating preventive health
CH 09_p119-132_v3.indd 119 17-07-2015 10:31:49

Box 9.1 5RGEKſEIQCNUQHRTGEQPEGRVKQPCNECTG Box 9.2 pportunities to initiate

preconceptional care
• Screening for risk
Ŧ Personal and family history • Any visit to a doctor during reproductive years
Ŧ Physical examination • Annual health checkup
Ŧ Laboratory screening • Postpartum checkup
• Preventive health • A visit for a pregnancy test (especially if negative)
Ŧ Nutrition and supplements • Emergency visit
Ŧ Weight and exercise • Visit for infertility treatment
Ŧ Vaccination • Premarital counseling
• 5RGEKſEKPFKXKFWCNKUUWGU
Ŧ Chronic diseases
Ŧ Medications
Stop teratogenic drugs Interventions in the preconceptional
Substitute safer drugs perio
Specific preconceptional interventions are rec-
ommended to all women in the reproductive age
measures, and identifying and addressing indi- group (Table 9.1). These interventions improve
vidual health issues (Box 9.1). the outcome of pregnancy.
Several medical disorders may affect women
Opportunities to initiate before or during their pregnancy. These
preconceptional care women need counseling regarding the effects
Most women do not consult the obstetrician on pregnancy, complications they are prone
for preconceptional advice prior to pregnancy. to, and the special precautions to be initiated.
Therefore, all available opportunities should be Therefore, women with specific risk factors
utilized by the obstetrician/physician to initiate require individualized, specific recommenda-
preconceptional care (Box 9.2). tions (Table 9.2).
Table 9.1 4GEQOOGPFGFRTGEQPEGRVKQPCNKPVGTXGPVKQPUHQTCNNYQOGP
Intervention 2TQXGPJGCNVJDGPGſV
Folic acid supplementation (400 μg); consider higher Reduces occurrence of neural tube defects by two-thirds
dose for women (a) taking antiseizure medications and
other drugs that might interfere with folic acid metabo-
lism, (b) who are obese, or (c) with a previous neural
tube defect (NTD)
Hepatitis B vaccination for at-risk women Prevents transmission of infection to the infant
HIV/AIDS screening and treatment Allows for appropriate treatment and provides women

QTEQWRNGUYKVJCFFKVKQPCNKPHQTOCVKQPVJCVECPKPƀWGPEG
the timing of pregnancy and treatment
Screening and treatment of sexually transmitted diseases (a) Reduces the risk of ectopic pregnancy, infertility, and
chronic pelvic pain associated with Chlamydia trachomatis
and eisseria gonorrhoeae (b) Reduces the possible risk
of fetal death, physical and developmental disabilities,
including mental retardation and blindness
Rubella vaccination Protects against congenital rubella syndrome
Optimizing weight in overweight and obese women Reduces the risks of neural tube defects, preterm delivery,
diabetes, cesarean section, and hypertensive disease
Smoking cessation Prevents smoking-associated preterm birth, low birth
weight
Eliminating alcohol use before and during pregnancy Prevents fetal alcohol syndrome; other alcohol-related birth
defects
A DS CESWKTGFKOOWPGFGſEKGPE[U[PFTQOG JWOCPKOOWPQFGſEKGPE[XKTWU
CH 09_p119-132_v3.indd 120 17-07-2015 10:31:49

Preconceptional and Antenatal Care 121
Table 9.2 4GEQOOGPFGFRTGEQPEGRVKQPCNKPVGTXGPVKQPUHQTYQOGPYKVJURGEKſETKUMHCEVQTU
4KUMHCEVQT Intervention 2TQXGPJGCNVJDGPGſV

Antiepileptic drug use Changing to a less teratogenic Decreases risk of fetal malformations
treatment regimen
Diabetes mellitus Achieving and maintaining Decreases congenital anomalies, length of neonatal
hemoglobin- A1C <7% intensive care unit admission, perinatal mortality, and
long-term health consequences in infant; decreases
miscarriage risk
Hypertension (HTN) Avoid ACE inhibitors and ARBs. Decreases congenital anomalies, HTN complications,
If long-standing HTN, then cesarean, FGR, placental abruption, preterm birth,
assess for renal disease, ven- perinatal death
tricular hypertrophy,
and retinopathy
Hypothyroidism Thyroxine supplementation to Decreases infertility, preterm birth, low birth weight, fetal
maintain TSH level at death, and possibly neurological problems in infant
<3.0 mL U/L
Hyperthyroidism Propyl thiouracil supplementation Decreases spontaneous pregnancy loss, preterm birth,
to maintain FT4 in high normal preeclampsia, fetal death, FGR, maternal conges-
range, and TSH in low normal tive heart failure and thyroid storm; neonatal Graves’
range disease
Asthma Management with inhalation Decreases infertility, preterm birth, low birth weight,
therapy (bronchodilators/ preeclampsia, perinatal mortality
glucocorticoids)
Systemic lupus ŮOQPVJUQHSWKGUEGPEGQP Decreases risk of HTN, preeclampsia, preterm birth,
erythematosus stable therapy fetal death, FGR, neonatal lupus erythematosus
AC angiotensin converting enzyme; A Bs angiotensin receptor blockers; fetal growth restriction; S thyroid-stimulating hormone.
2TKPEKRNGUQHVGTCVQIGPKEKV[ • No damage at all because the pleuripotent

embryonic cells can replace the cells destroyed
A prenatal visit is a good opportunity to screen or damaged by the teratogen
for and educate the woman about exposure This is referred to as the ‘all or none’ period of
to teratogens. Any factor that alters normal embryogenesis.
intrauterine development can be considered Fetal susceptibility to teratogens is largely
a teratogen. This includes exposure to the dependent on the period of development. A
following: particularly susceptible period is between gesta-
• Drugs tional days 15 and 60. Different organs have dif-
• Chemicals ferent critical periods (Box 9.3).
• Radiation The effect on the embryo/fetus also depends
• Maternal medical conditions on the dose and duration of exposure to a
• Infectious agents
• Genetic factors
Box 9.3 %
TKVKECNRGTKQFU
YGGMUQHIGUVCVKQP
QHUWUEGRVKDKNKV[HQTFKHHGTGPVHGVCN
All or none period QTICPU
QHGODT[QIGPGUKU • Heart: 3–4
• Limbs: 4.5–7.5
The first 2 weeks after conception is a remark- • Eyes: 4.5–8.5
able period for the embryo. At this stage, expo- • Ears: 4.5–9.5
sure to teratogens can result in • External genitalia: 8–9
• Complete loss of pregnancy (spontaneous • Brain and skeletal system: Beginning of week 3 to end
of pregnancy
miscarriage) due to severe cellular insult, or,
CH 09_p119-132_v3.indd 121 17-07-2015 10:31:49

teratogen. Some teratogens may have a more del-

Box 9.4 5CHGV[TCVKPIU[UVGOHQTFTWIU
eterious effect in a single large dose than the same
dose spread over several days, whereas another Category A: Safety established
teratogen may be more harmful when exposure • %QPVTQNNGFUVWFKGUKPYQOGPUJQYPQTKUMVQHGVWUKPſTUV
is prolonged instead of a single exposure. trimester
Drug–drug interactions can also be important. • No evidence of a risk in later trimesters
Two drugs administered together may compound • Possibility of fetal harm appears remote
the effects, or one drug may protect against the Category B: Safety likely
teratogenic effects of the other. For example, folic • Animal studies show no fetal risk but no controlled stud-
acid is prescribed to prevent the increased risk of ies in pregnant women or
open neural tube defects in women who are pre- • Animal studies have shown adverse effect but not con-
scribed antiepileptic drugs. ſTOGFKPYQOGPKPſTUVQTNCVGTVTKOGUVGTU
To minimize the potential risk of teratogenic- Category C: eratogenicity possible
ity when prescribing drugs, it is important to • Studies in animals have revealed adverse effects on the
fetus (teratogenic, embryocidal, or other) but no con-
• Use drugs or drug classes known to be of low trolled studies in women or
teratogenic potential • Studies in women and animals not available.
• Avoid prescribing drugs during critical periods • 6JGUGFTWIUUJQWNFDGIKXGPQPN[KHVJGRQVGPVKCNDGPGſV
of toxicity (e.g., during organogenesis for all LWUVKſGUVJGRQVGPVKCNTKUMVQVJGHGVWU
drugs and near delivery for some drugs) Category D: eratogenicity probable
• 2QUKVKXG GXKFGPEG QH JWOCP HGVCN TKUM DWV VJG DGPGſVU
DTWIUCPFVGTCVQIGPKEKV[ from use in pregnant women may be acceptable despite
the risk, if the drug is needed in
KPRTGIPCPE[ Ŧ a life-threatening situation or
Ŧ a serious disease for which safer drugs cannot be
A preconceptional visit is an excellent opportu- used or are ineffective
nity to have an in-depth discussion regarding
Category : eratogenicity likely
prescribed and over-the-counter medications
that the patient may be on. Ingesting teratogenic • Studies in animals and humans have demonstrated fetal
abnormalities and or
drugs may result in congenital malformations or
• There is evidence of fetal risk based on human experi-
other negative fetal outcomes. ence and
The most widely used tool for evaluating drug • The risk of the use of the drug in pregnant women clearly
safety during pregnancy is the US Food and Drug QWVYGKIJUCP[RQUUKDNGDGPGſV
Administration (FDA) safety rating system. The • Contraindicated in women who are or may become
FDA system rates medication risk using catego- pregnant.
ries A, B, C, D, and X, based on the available data
in human and animal studies (Box 9.4).
in addition, the patient should be placed on
%QWPUGNKPIHQTYQOGPQPMPQYP folic acid (Box 9.5).
In cases where the woman has conceived
VGTCVQIGPKEFTWIU while on a teratogenic drug, a decision must be
If a woman plans to become pregnant while made to either continue the drug or change it
taking a teratogenic medication for a known for another one. The mother’s anxiety must be
medical disorder, it is important to change understood and addressed. Since most drugs
the medication to a drug that is either not only marginally increase the risk of congenital
teratogenic or teratogenic to a lesser degree. malformations, termination of the pregnancy is
However, it is important to not stop an essen- usually not required. However, this decision must
tial drug. For example, although all antiepilep- be based on the type, dose, and duration of medi-
tic drugs are known to be teratogenic to some cation ingested. Special monitoring or treatment
degree, the patient should still receive medica- may be warranted during pregnancy depending
tion to avoid seizures. Since valproic acid is the on the drug exposure. For example, fetal echo-
most teratogenic among antiepileptic drugs, it cardiography may be indicated if a medication is
should definitely be avoided in pregnancy and, known to cause fetal cardiac defects.
CH 09_p119-132_v3.indd 122 17-07-2015 10:31:49

The following imaging studies have no effect

Box 9.5 5
QOGVGTCVQIGPKERTGUETKRVKQPFTWIU

%CVGIQT[: on the fetus:
• Androgens and testosterone derivatives (e.g., danazol) • Diagnostic X-rays of the head, neck, chest, and
• Angiotensin-converting enzyme (ACE) inhibitors limbs
(e.g., enalapril, captopril) and angiotensin II receptor • Ultrasound and magnetic resonance imaging
blockers (MRI)
• Coumadin derivatives (e.g., warfarin) • Dental X-rays
• Carbamazepine
• CT scans not involving the abdomen or pelvis
• Diethylstilbestrol
• Folic acid antagonists (methotrexate and aminopterin)
• Lithium 5CHGV[RTGECWVKQPU
• Phenytoin
• Primidone
The pregnant woman should wear a lead apron to
• Statins minimize fetal exposure whenever non-abdomi-
• Streptomycin and kanamycin nopelvic radiological imaging is being carried out.
• Tetracycline Women who work professionally with radi-
• 6JCNKFQOKFGCPFNGƀWPQOKFG ation should always wear a dosimeter to make
• Trimethadione and paramethadione sure that they are not exposed unnecessarily to
• Valproic acid high doses of radiation.
• Vitamin A above recommended daily allowance (RDA),
and its derivatives (e.g., isotretinoin, etretinate, and
retinoids)
Antenatal care
The majority of women will have an uncompli-
Exposure to radiation cated pregnancy and deliver a healthy infant
In women who are planning pregnancy, diag- with minimal medical intervention. However, a
nostic X-rays must preferably be done in the first significant number will develop medical or fetal
14 days of the menstrual cycle, to avoid inadver- complications. Antenatal care helps in recogni-
tent exposure to radiation. tion and appropriate intervention for the com-
plications that may arise. The goals of optimal
'HHGEVQHTCFKCVKQPQPVJGHGVWU antenatal care are summarized in Box 9.7.
The human embryo and fetus are particularly sen-

sitive to ionizing radiation. High radiation doses TJGſTUVQTDQQMKPIXKUKV
may lead to growth restriction, malformations, Ideally, the first or booking visit should be before
impaired brain function, and cancer. Fortunately, 10 weeks’ gestation. Regardless of when the
most common diagnostic radiological proce- woman presents for her first visit, a thorough his-
dures will not expose the fetus to significant levels tory and physical examination must be carried
of radiation. out. Investigations specific to the first visit must be
The effect on the fetus depends on the ges- performed. Advice must be offered with emphasis
tational age and the dose of ionizing radiation
(Box 9.6).
Box 9.7 )QCNUQHCPVGPCVCNECTG
• Early, accurate estimation of gestational age
Box 9.6 'HHGEVQHKQPK\KPITCFKCVKQPUQPHGVWU • +FGPVKſECVKQPQHTKUMHCEVQTU
Ŧ Existing risks (e.g., diabetes)
• First 14 days after conception, >0.1 Gy or 10 rad Ŧ Risks that develop during pregnancy (e.g., hyper-
Ŧ Death of embryo or no effect (all or none principle) tension, fetal growth restriction)
• At all gestational ages, <0.05 Gy or 5 rad • Regular evaluation of mother and fetus
Ŧ No adverse effect • Anticipation of problems and intervention, if possible, to
• #HVGTYGGMU)[QTTCF prevent or minimize morbidity
Ŧ No effect • Patient education and communication
CH 09_p119-132_v3.indd 123 17-07-2015 10:31:49

on diet and nutrition, hematinics, exercise, travel, both maternal and perinatal complications, and
intercourse, and management of common signs adverse events. Risk categorization also helps in
and symptoms of pregnancy (Box 9.8). planning appropriate level of care.
History, physical examination, and gesta- The assessment of risk factors starts during
tional age assessment are discussed in detail in antenatal care. Simple determinants (e.g.,
Chapter 8, History taking and examination of the maternal age, height, and parity) and obstetric
obstetric patient. history of complications (e.g., previous stillbirth
or cesarean section) will help place the woman
4KUMGXCNWCVKQPCPFTKUM in a low- or high-risk category. Subsequent visits
might reveal abnormalities in the present preg-
ECVGIQTK\CVKQP nancy, such as hypertension, severe anemia,
During the initial antenatal examination, it is multiple pregnancy, antepartum hemorrhage, or
important to try and categorize the pregnant abnormal lie.
woman into a low- or high-risk group. Initial The four combinations of risk categoriza-
and ongoing evaluation of a woman’s chance tion are listed in Box 9.9. The difficulty with risk
of giving birth normally is crucial in preventing assessment lies in group II where the baby is
unexpectedly compromised. The likelihood of
predicting all adverse outcomes is limited, and
Box 9.8 (KTUVQTDQQMKPIXKUKV several scoring systems have been used but have
failed to consistently identify this group.
• History
A pregnant woman can be placed in the high-
Ŧ Personal information
Ŧ Menstrual and gynecological history
risk category based on maternal or perinatal fac-
Ŧ Obstetric history tors (Table 9.3).
Ŧ Personal and family medical history
Ŧ Psychosocial information
Box 9.9 4KUMECVGIQTKGU
Ŧ Past medical and surgical history
Ŧ Genetic history I. Low-risk mother with a low-risk fetus, for example,
Ŧ Current pregnancy history normal pregnancy, mother and baby well
Ŧ Current medications and allergies II. Low-risk mother with a high-risk fetus, for example,
• Physical examination normal pregnancy, mother well but baby unexpectedly
compromised
Ŧ Baseline blood pressure, weight, and height, body
mass index (BMI) III. High-risk mother with a low-risk fetus, for example,
maternal asthma
Ŧ Complete physical examination (including breasts)
IV. High-risk mother with a high-risk infant, for example,
Ŧ Pelvic examination
severe hypertension with fetal growth restriction
Uterine size
Uterine shape
Evaluation of adnexae
• Gestational age assessment Table 9.3 *KIJTKUMITQWRU
Ŧ Ultrasonography if discrepancy exists between
uterine size by physical examination and that by /CVGTPCNHCEVQTU 2GTKPCVCNHCEVQTU
dates Hypertension Previous adverse events
Ŧ Assignment of expected date of delivery Renal disease Recurrent pregnancy loss
• Risk evaluation for subsequent management
Respiratory disease Prematurity (including
• Tests rupture of membranes and
Ŧ Blood investigations labor)
Ŧ Aneuploidy screening Cardiac disease Rhesus disease
Ŧ Screening for gestational diabetes/gestational
Hemoglobinopathy Diabetes
hypertension
• Advice Psychiatric conditions Monozygotic multiple
pregnancy
Ŧ Nutrition, including hematinics
Ŧ Exercise Infections (e.g., aricella) Fetal anomaly
Ŧ Travel Drug misuse Assisted conception
Ŧ Work Extremes of age
Ŧ Common symptoms and management Obesity
CH 09_p119-132_v3.indd 124 17-07-2015 10:31:49

6GUVUCPFKPXGUVKICVKQPUCVſTUV 6GUVHQTJGRCVKVKU$UWTHCEGCPVKIGP
DQQMKPI Hepatitis B antigen screening is recommended
for all pregnant women to prevent perinatal
A standard panel of laboratory tests should be transmission to the newborn (see Chapter 51,
obtained on every pregnant woman at the first Hepatic and gastrointestinal disorders). Women
prenatal visit. Additional testing may be required who have been vaccinated should also undergo
in women at risk for specific conditions. testing because no screening is done prior to
vaccination to rule out carrier status.
Stan ar panel o investigations
*GOQINQDKPJGOCVQETKVDNQQFRKEVWTGCPFOGCP 6GUVHQTJWOCPKOOWPQFGſEKGPE[XKTWU
corpuscular volume Universal screening for human immunodefi-
Tests for hemoglobin, hematocrit, blood pic- ciency virus (HIV) is recommended for all preg-
ture, and mean corpuscular volume (MCV) are nant women (see Chapter 56, Infections) (Box 9.11).
done to identify anemia. The MCV differentiates Screening is usually done with an enzyme-linked
between iron-deficiency anemia (MCV < 80 fL) immunosorbent assay (ELISA) test for the pres-
and B12-deficiency anemia (MCV > 115 fL). Blood ence of HIV antibodies. If this test is reported
picture reveals microcytic hypochromic red cells as positive, HIV infection is confirmed with the
in iron deficiency, and macrocytes in B12 and folic Western blot test. Confirmation can also be done
acid deficiencies (see Chapter 49, Hematological with an indirect fluorescent antibody (IFA) test,
disorders). which detects HIV antibodies using a special flu-
orescent dye and a microscope.
$NQQFITQWRCPF4JV[RKPI
Polymerase chain reaction (PCR) test finds
All pregnant women should have their blood either the RNA of the HIV virus or the HIV DNA
group and Rh typing done and these should be in white blood cells infected with the virus. PCR
documented. If a woman is identified as Rh(D) testing is done when a very recent infection is
negative, her husband’s/partner’s Rh typing suspected. It is not done for routine screening in
must be done to determine if he is Rh(D) posi- pregnancy.
tive. If he is Rh(D) positive, she could be at risk for
4WDGNNCUWUEGRVKDKNKV[UETGGPKPI
Rh alloimmunization in pregnancy and her baby
could have hemolytic disease of the newborn The pregnant woman is tested for the presence
(see Chapter 38, Red cell alloimmunization). All of IgG antibody to rubella. If the test is positive,
Rh(D)-negative women should be tested for the she is immune to rubella. If it is negative, she is
presence of alloantibodies (Box 9.10). susceptible to rubella. She will require vaccina-
tion in the postnatal period for the protection of
6GUVHQTU[RJKNKU
future pregnancies.
Either the rapid plasma reagin (RPR) test or the
5ETGGPKPIHQT614%*KPHGEVKQPU
Venereal Disease Research Laboratory (VDRL)
test is done to rule out syphilis. Although syphilis Routine screening for TORCH infections in preg-
is rare, the consequences of congenital syphilis nancy is not advised. The TORCH panel consists
are severe and so this test should be done for all of serum tests for Toxoplasmosis, Other, Rubella,
women. Cytomegalovirus and Herpes simplex. It is not
Box 9.10 4JVGUVKPI Box 9.11 7

PKXGTUCNVGUVKPIHQT*+8GCTN[
KPRTGIPCPE[
• All women to be tested
• If Rh negative Advantages
Ŧ Rh typing of husband/partner • Informed decision to continue or terminate pregnancy
• If husband/partner Rh positive • Initiation of early treatment for mother
Ŧ Test for alloantibodies • 2TGXGPVKQPQHVTCPUOKUUKQPVQRCTVPGTQTKFGPVKſECVKQPQH
Ŧ If positive infected partner
Risk of alloimmunization • Measures to prevent vertical transmission to the
Hemolytic disease of the newborn newborn
CH 09_p119-132_v3.indd 125 17-07-2015 10:31:50

indicated even with a history of recurrent preg- is reserved for those women who book later in
nancy loss. pregnancy.
5ETGGPKPIHQTIGUVCVKQPCNFKCDGVGU
Screening for diabetes is performed at the book-
&KGVCT[CPFPWVTKVKQPCNCFXKEG
ing visit for all Indian women since they are con- CVVJGDQQMKPIXKUKV
sidered to be at an intermediate/high risk. If the Obtaining a good dietary history and giving
first trimester screening test is negative, the test proper dietary advice are essential at the booking
should be repeated at 24–28 weeks. Both fast- visit (Box 9.13). It is an opportunity to set right
ing plasma glucose, and 75 g glucose followed the woman’s misconceptions of food require-
by plasma glucose 2 hours later, are acceptable ments in pregnancy. It also allows recommenda-
as screening tests. Screening for diabetes in tion of weight gain goals that are appropriate for
pregnancy is discussed in detail in Chapter 48, the individual.
Diabetes. Undernourished mothers (body mass index-
5ETGGPKPIHQTCU[ORVQOCVKEDCEVGTKWTKC (BMI) <18 kg/m2), particularly low-income
women, need special attention and dietary
Asymptomatic bacteriuria is an established risk
advice for meeting their dietary needs. Unless
factor for preterm delivery, low birth weight, and
they gain adequate weight during pregnancy,
acute pyelonephritis. Identification and treat-
they are at risk for preterm labor and delivering
ment of asymptomatic bacteriuria reduces the
low birth weight infants (Box 9.14).
risk of such complications. It is usually offered at
Women who gain excessive weight are at an
the booking visit.
increased risk for preeclampsia, failed induction,
The screening is done with a culture of a
cesarean delivery, and a macrosomic infant.
clean-catch urine specimen. In underresourced
Women who gain more weight than the recom-
areas, this may not be possible. Nitrite dipsticks
mended amount during pregnancy are three
may be used and if positive, a urine culture may
times more likely to retain 5 kg or more at 1 year
be done to confirm bacteriuria.
postpartum.
If the culture shows bacteriuria, appropriate
For those women whose BMI is >30 kg/m2 at
antibiotics are prescribed (see Chapter 55, Renal
the initial visit, information on the complica-
and urinary tract disorders).
tions of obesity on fetal and maternal well-be-
5ETGGPKPIHQTCPGWRNQKF[ ing should be given (see Chapter 52, Endocrine
Screening for Down syndrome should be offered disorders).
to all women at booking, and the choice whether
to have the screening test done or not, is left to
Box 9.13 +PETGCUGFFKGVCT[TGSWKTGOGPVU
the couple. The test that should ideally be offered KPRTGIPCPE[
is a first trimester screening (Box 9.12) done at
11 to 13+ 6 weeks (i.e., from the first day of the 11th • Calories: The recommended intake is an increase in
daily caloric intake by
week of gestation to the last day of the 13th week).
Ŧ 300 kcal/day in the second trimester
The second trimester triple test or quadruple test Ŧ 400 kcal/day in the third trimester
• Carbohydrate: The recommended daily allowance for
carbohydrates
Ŧ Pregnant women: 175 g/day
Box 9.12 (
KTUVVTKOGUVGTUETGGPKPIHQT Ŧ Nonpregnant women: 130 g/day
CPGWRNQKF[
&QYPU[PFTQOG
• Protein
=VTKUQO[?VTKUQO[VTKUQO[
Ŧ Fetal/placental unit
• 11–13 weeks Consumes approximately 1 kg of protein
• Nuchal thickness /QUVN[KPVJGNCUVOQPVJU
• Serum biochemistry Protein requirement in pregnancy
Ŧ Pregnancy-associated plasma protein-A (PAPP-A) 1.1 g/kg/day
Level reduced in Down syndrome • Vitamins and minerals: These are provided by
Ŧ Ehuman chorionic gonadotropin (EhCG) Ŧ ingestion of fresh fruits and vegetables
Level raised in Down syndrome Ŧ oral supplements essential
%*ARAXKPFF 17-07-2015 10:31:50

Box 9.14 '

HHGEVQHYGKIJVICKPQPRTGIPCPE[ Box 9.16 4GEQOOGPFGFFQUCIGQHHQNKECEKF
outcomes
• 400 μg of folic acid daily to be started preconceptionally
• Low weight gain • 4 mg of folic acid daily in women with a previous history of
Ŧ Associated with Ŧ neural tube defect
preterm labor Ŧ anticonvulsant therapy
low-birth-weight infants Ŧ pregestational diabetes
• Excessive weight gain
Ŧ Associated with
preeclampsia Folic acid
failed induction
cesarean delivery Pregnant women should be informed that
macrosomia dietary supplementation with folic acid before
postpartum obesity conception and throughout the first 12 weeks’
pregnancy reduces the risk of having a baby with
a neural tube defect. The recommended dose is
400 μg/day (Box 9.16).
#FXKEGQPFKGVCT[ Patients who are at risk (previously have a baby
affected by neural tube defect, on anticonvulsants,
supplements pregestational diabetes) should have 4 mg daily.
+TQPCPFHQNKECEKF Calcium
Iron and folate supplements must be given to all
Fetal skeletal development requires approxi-
pregnant women since total iron loss associated
mately 25–30 g of calcium during pregnancy,
with pregnancy and lactation is approximately
primarily in the last trimester. Most of this cal-
1000 mg.
cium can be mobilized from the maternal stores.
In countries such as India where the prevalence
Calcium absorption increases during pregnancy
of anemia is nearly 70%–80% among pregnant
and allows progressive retention throughout
women, iron supplementation is routinely given
gestation. The recommended dietary intake in
(Box 9.15). Iron-deficiency anemia may be related
pregnancy and lactation is 1000–1300 mg/day.
to preterm birth and low birth weight. For further
Routine calcium supplementation is not rec-
details about iron supplementation in pregnancy,
ommended in pregnancy except for women
see Chapter 49, Hematological disorders.
with low dietary calcium intake (Box 9.17).
Indian women with poor dietary calcium intake
are advised calcium supplementation with cal-
Box 9.15 4GEQOOGPFGFFQUCIGQHKTQP cium carbonate or calcium citrate.
• 6CDNGVEQPVCKPKPICVNGCUVOIQHGNGOGPVCNKTQPCPF
500 μg of folic acid should be given 1–2 times daily 8KVCOKP&
• The Government of India (Ministry of Health) recom-
mends for all pregnant women Severe maternal vitamin D deficiency causes
Ŧ 100 mg of elemental iron (335 mg of ferrous neonatal hypocalcemia and seizures. There
sulfate) and 500 μg of folic acid is also an association between milder forms
Ŧ for 100 days of deficiency and preeclampsia, gestational
Ŧ from 14 weeks’ gestation diabetes, and impaired growth and skele-
Ŧ tablets of ferrous sulfate and folic acid are supplied
tal problems in infancy (Box 9.18). Vitamin D
free of cost by the Government of India
• If the Hb is <7.0 g/dL, the dose should be doubled
• The dose should be taken
Box 9.17 %
CNEKWOUWRRNGOGPVCVKQP
KPYQOGP
Ŧ on an empty stomach
YKVJNQYFKGVCT[ECNEKWOKPVCMG
Ŧ with citrus juice
• The dose should not be taken with • 500 mg of elemental calcium twice daily
Ŧ calcium tablet • Not to be taken with iron
Ŧ milk, tea, or coffee • Taken after food
CH 09_p119-132_v3.indd 127 17-07-2015 10:31:50

Women with complicated pregnancies are

Box 9.18 'HHGEVUQHXKVCOKP&FGſEKGPE[
discouraged from excessive physical activity for
aternal effects fear of adverse impact on the underlying disor-
• Preeclampsia der or on maternal and fetal outcomes.
• Gestational diabetes
etal and infant effects
• Low birth weight
• Impaired growth and skeletal problems in infancy
+OOWPK\CVKQPCICKPUV
• Neonatal hypocalcemia and seizures tetanus
Tetanus kills an estimated 50,000 neonates/year,
Box 9.19 %CWUGUHQTXKVCOKP&FGſEKGPE[ worldwide. A total of 5% of all maternal deaths
are due to tetanus. If at least two doses of teta-
• South Asian origin (includes Indians)
nus toxoid (TT) vaccination are given during
• Limited exposure to sunlight
pregnancy, neonatal deaths due to tetanus can
Ŧ Mostly housebound
Ŧ Completely covered when outdoors
be prevented (Box 9.20). Immunizing the mother
• Diet low in vitamin D allows tetanus antitoxin to be actively trans-
Ŧ 9QOGPYJQEQPUWOGPQQKN[ſUJGIIUOGCV ported by the placenta to her fetus, providing
• Prepregnancy body mass index above 30 kg/m2 passive protection against tetanus during the
neonatal period and the following 1 or 2 months
of life. TT schedule for women of childbearing
deficiency has a high prevalence in Indian age and pregnant women is given in Table 9.4.
pregnant women (Box 9.19) and coexists with
other nutritional deficiencies, particularly cal-
cium deficiency. There is no necessity for rou-
tine testing of vitamin D levels in pregnancy, 1VJGTCFXKEGCVDQQMKPI
but in women at high risk for vitamin D defi-
ciency, 1000–2000 IU/day of vitamin D can be
visit
given as a supplement.
9QTM
Fish oil capsules or docosahexae Women with uncomplicated pregnancies may
noic acid supplements be allowed to carry on their normal activities.
Women can continue their employment till they
The use of docosahexaenoic acid (DHA)–rich fish go into labor.
oil capsules during pregnancy does not improve
cognitive and language development in the off-
spring during early childhood. Supplementation Travel
with DHA is not recommended. Travel by a two- or three-wheeler vehicle, car,
or train is safe in pregnancy. Most women are
‘low risk’ and can expect no problems with air
'ZGTEKUGKPRTGIPCPE[ travel during pregnancy, although long air travel
is associated with an increased risk of venous
thrombosis.
Exercise is safe for both mother and fetus during
pregnancy, and women should therefore be
encouraged to initiate or continue exercise to
Box 9.20 4
GEQOOGPFGFFQUCIGQHVGVCPWU
derive the health benefits associated with such toxoid
activities. Women should be advised to walk
briskly for 30–45 minutes in a day. Women who • First dose of tetanus toxoid (TT) at the booking visit
• Second dose after 4–8 weeks
are involved in physical labor (light or heavy)
• 6JKTFFQUGOQPVJUCHVGTVJGUGEQPFKPLGEVKQP
should be reassured that it will have no ill effect
Ŧ Provides protection for at least 5 years
on the fetus.
CH 09_p119-132_v3.indd 128 17-07-2015 10:31:50

Table 9.4 6
GVCPWUVQZQKF
66VGVCPWUFKRJVJGTKC
6FXCEEKPCVKQPUEJGFWNGHQTYQOGPQHEJKNFDGCTKPICIG
CPFRTGIPCPVYQOGPYKVJQWVRTGXKQWUGZRQUWTGVQ666F
9*1TGEQOOGPFCVKQP
0WODGTQHGCTNKGT 9JGPVQIKXG Expected protection period

66D[JKUVQT[
1 #VſTUVEQPVCEV None
2 At least 4 weeks after TT 1 1–3 years
3 #VNGCUVOQPVJUCHVGT66UWDUGSWGPVRTGIPCPE[ At least 5 years
4 At least 1 year after TT 3 or subsequent pregnancy At least 10 years
5 At least 1 year after TT 4 or subsequent pregnancy Through childbearing age
and possibly longer
Sexual intercourse • Assessment of the uterine size or fundal height

to assess fetal growth
Sexual intercourse in pregnancy is not known – Symphysio-fundal height (see Chapter 8,
to be associated with any adverse outcomes. History taking and examination of the
Sexual activity between 29 and 36 weeks does obstetric patient)
not increase the risk of preterm delivery. • Documentation of fetal cardiac activity by
auscultation
5OQMKPICPFCNEQJQNKPVCMG – Fetoscope
– Stethoscope
Smoking should be discouraged. Pregnant – Handheld Doppler device
women should be advised to avoid drinking • Maternal blood pressure and weight
alcohol in any part of pregnancy. Alcohol con- • Urine for protein and glucose
sumption may be associated with an increased • Fetal presentation (in the third trimester)
risk of miscarriage, fetal alcohol syndrome and • Follow-up of modifiable risk factors
other congenital anomalies. There is no known
safe amount of alcohol to drink while pregnant.
There is also no safe time during pregnancy to
%QOOQPU[ORVQOUCPFVJGKT
drink and no safe kind of alcohol. OCPCIGOGPVKPRTGIPCPE[
The physiological changes in the various organ
systems, along with the hormonal changes of
Further antenatal visits pregnancy, result in some common symptoms.
Other problems are caused by the the growing
Standard antenatal visits are usually scheduled gravid uterus causing pressure symptoms on
• Every month till 28 weeks maternal organs, especially the vena cava. The
• Every 2 weeks from 28 to 36 weeks physiological basis for these symptoms has been
• Every week from 36 weeks till delivery discussed in Chapter 3, Maternal physiology in
pregnancy. Some common symptoms and their
In under-resourced areas, the World Health management are summarized in Table 9.5.
Organization recommends at least four visits
during the pregnancy for low-risk women (first
trimester, 26, 32, and 38 weeks). This improves 8KUKVUDGVYGGPCPF
compliance without increasing complications. YGGMU
The mother feels more comfortable at this stage
+PVGTXGPVKQPUCVUWDUGSWGPV of pregnancy. She is offered the following tests
antenatal visits and advice:
At subsequent visits, the uterine height, fetal • Triple test or quadruple test for second trimes-
heart sounds are documented and other required ter screening for Down syndrome should be
investigations are done. offered if first trimester screening has not been
CH 09_p119-132_v3.indd 129 17-07-2015 10:31:50

already been found to have diabetes by earlier

Table 9.5 %
QOOQPU[ORVQOUCPFVJGKTOCPCIG
screening (see Chapter 48, Diabetes).
OGPVKPRTGIPCPE[
• Antibody screening for Rh-negative women is
5[ORVQO /CPCIGOGPV done at 28 weeks and if antibodies are absent,
Nausea and vomiting • Small frequent meals it is recommended that antenatal anti-D
• Low fat, bland food immunoglobulin be administered to nonsen-
• Avoidance of triggers sitized Rh-negative women (see Chapter 38,
• Supportive therapy Red cell alloimmunization).
• Medications
Heart burn • Avoidance of large meals
• Avoiding lying down for 8KUKVUDGVYGGPCPF
2 hours after a meal
• Semi recumbent position YGGMU
when lying down
• Antacids The following need to be done in visits between
Pica (craving for %QTTGEVKTQPFGſEKGPE[ 32 and 36 weeks:
unusual foods) • The woman must be educated about signs of
Ptyalism (excessive Reassurance preterm labor and labor.
salivation)
• A third trimester ultrasound is not required
Constipation • *KIJſDTGFKGV
• Mild laxatives
routinely. It may be indicated in the follow-
Hemorrhoids • Stool softeners
ing situations (see Chapter 10, Obstetric ultra-
• Sitz bath sound and other imaging):
Varicosities • Rest, elevation of foot
– Confirmation of abnormal fetal presentation
• Elastic stockings – Suspected placenta previa or follow-up of
Backache • Proper posture placenta previa
• Exercises – Suspected small-for-gestational-age fetus
• Symptomatic therapy or growth-restricted fetus
Vaginal discharge • Reassurance – Suspected macrosomia
(without itching) • Personal hygiene – Suspected abnormalities of amniotic fluid
(oligohydramnios or polyhydramnios)
– Follow-up of multiple pregnancy
• Fetal presentation is confirmed at 36 weeks.
done (see Chapter 12, Prenatal screening, pre-
• External cephalic version (ECV) is offered to
natal diagnosis, and fetal therapy).
women with breech presentation at 36 weeks.
• Detailed ultrasound examination for screen-
ECV reduces the chance of breech births and
ing of fetal anomalies is offered between 18
cesarean section.
and 22 weeks (see Chapter 10, Obstetric ultra-
• Women must be taught to do a daily fetal move-
sound and other imaging).
ment count. The significance of decreased
• The pregnant woman should be advised to
movements must be emphasized and explained
start her antenatal exercises if she has not
to the pregnant woman.
already done so. She should also be advised to
walk briskly for 30–45 minutes each day.
8KUKVUDGVYGGPCPFYGGMU
8KUKVUDGVYGGPCPFYGGMU The following need to be done in visits between
The following tests are recommended in visits 37 and 41 weeks:
between 24 and 28 weeks:
• The woman must be educated on signs of
• Hemoglobin and hematocrit are retested to labor and when to seek help for labor.
assess anemia and to modify iron supplemen- • When a woman goes postterm, the plan for
tation if needed. induction and the process of induction are
• Screening for gestational diabetes is offered discussed.
for all women between 24 and 28 weeks unless • Motivation for breastfeeding and a discussion
they are pregestational diabetics or have of contraceptive options are also initiated.
CH 09_p119-132_v3.indd 130 17-07-2015 10:31:50

-G[RQKPVU
• Preconceptional counseling and care has been shown is either not teratogenic or teratogenic to a lesser
to improve pregnancy outcomes, including low birth degree.
weight, premature birth, and infant mortality. • The human embryo and fetus are particularly sensitive
• Preconceptional care is the process of identifying to ionizing radiation. High radiation doses may lead to
social, behavioral, environmental, and biomedi- growth restriction, malformations, impaired brain
cal risks to a woman’s future pregnancy outcome function, and cancer.
and then reducing these risks through appropriate • Most common diagnostic radiological procedures will
intervention. PQVGZRQUGVJGHGVWUVQUKIPKſECPVNGXGNUQHTCFKCVKQP
• Most women do not consult the obstetrician for pre- • Advice must be offered with emphasis on diet and
conceptional advice prior to pregnancy. All available nutrition, hematinics, exercise, travel, intercourse,
opportunities should be utilized by the obstetrician/ and management of common signs and symptoms of
physician to initiate preconceptional care. pregnancy.
• Antenatal care helps in recognition and appropriate • The standard panel of investigations includes blood
intervention for the complications that may arise. group and Rh typing, hemoglobin and hematocrit,
• +FGCNN[VJGſTUVQTDQQMKPIXKUKVUJQWNFDGbefore testing for syphilis, hepatitis B surface antigen,
10 weeks’ gestation. Regardless of when the woman JWOCPKOOWPQFGſEKGPE[XKTWUUETGGPKPIHQTTWDGNNC
RTGUGPVUHQTJGTſTUVXKUKVCVJQTQWIJJKUVQT[CPF susceptibility, gestational diabetes, and asymptomatic
physical examination must be carried out. bacteriuria.
• Several medical disorders may affect women before or • Screening of aneuploidy should be offered when
FWTKPIVJGKTRTGIPCPE[9QOGPYKVJURGEKſETKUMHCEVQTU available and includes ultrasound examination along
TGSWKTGKPFKXKFWCNK\GFURGEKſETGEQOOGPFCVKQPU with serum markers.
• 'ZRQUWTGVQVGTCVQIGPUKPVJGſTUVYGGMUCHVGT • Iron and folic acid supplements must be prescribed.
conception can result in complete loss of pregnancy or • Calcium supplements must be prescribed in women
no damage at all. This is referred to as the ‘all or none’ with low dietary calcium intake.
period of embryogenesis.
• Immunization for tetanus must be carried out to
• The most widely used tool for evaluating drug safety prevent neonatal tetanus.
during pregnancy is the US Food and Drug Adminis-
tration (FDA) safety rating system. The FDA system • Subsequent antenatal visits are used to assess fetal
rates medication risk using categories A, B, C, D, and growth.
X, based on the available data in human and animal • Maternal screening for anemia, gestational diabetes,
studies. and antibody screening in Rh-negative women is also
• If a woman plans to become pregnant while taking a carried out in the follow-up antenatal visits.
teratogenic medication for a known medical disorder, • The woman must be educated about signs of preterm
it is important to change the medication to a drug that labor and labor.
5GNH#UUGUUOGPV
%CUGDCUGFSWGUVKQPU Case 2
Mrs. KT, 32, primigravida, presents at 10 weeks for con-
Case 1 ſTOCVKQPQHRTGIPCPE[*GT$/+KUMIO2.
Mrs. YL, 25, married for 1 year, is planning a pregnancy. 1. What are the routine blood tests done in the booking
She has a strong family history of diabetes mellitus and visit?
has been under treatment for polycystic ovarian disease.
2. What are the complications associated with a high
1. What preconceptional advice would you give her? BMI?
2. When will she need to be screened for diabetes in 3. How much iron and folic acid supplementation does
pregnancy? she require?
3. If she was found to be a pregestational diabetic, 4. What is the recommendation for tetanus toxoid vac-
what risks does her fetus face and how can they be cination?
avoided?
CH 09_p119-132_v3.indd 131 17-07-2015 10:31:50

#PUYGTU 2. Women with a high BMI are at increased risk for

preeclampsia, failed induction, cesarean delivery, and
a macrosomic infant.
Case 1 3. VCDNGVEQPVCKPKPICVNGCUVOIQHGNGOGPVCNKTQP
1. She should be tested for impaired glucose tolerance and 500 μg of folic acid should be given 1–2 times
or diabetes before she plans a pregnancy. She must daily.
be advised about diet and exercise since she is at the 4. 6JGſTUVFQUGQHVGVCPWUVQZQKF
66KUIKXGPCVVJG
risk for developing diabetes in pregnancy. booking visit, the second dose after 4–8 weeks,
2. She must be screened at the booking visit and if CPFVJGVJKTFFQUGECPDGIKXGPOQPVJUCHVGTVJG
negative, then at 24–28 weeks. second injection.
3. If she is not euglycemic (normal blood sugars) at the
time of conception, she is at risk for fetal anomalies
particularly of the CVS and CNS. She is also at risk 5CORNGSWGUVKQPU
for fetal macrosomia and cesarean section. Strict
control of blood sugar levels prior to pregnancy and .QPICPUYGTSWGUVKQP
during pregnancy can avoid these complications.
1. Describe in detail the aims of antenatal care.
Case 2 5JQTVCPUYGTSWGUVKQPU
1. The routine blood tests at the booking visit are
hemoglobin, hematocrit, blood picture, and mean 1. Preconceptional counseling
corpuscular volume, blood group and typing, tests 2. Importance of antenatal care
for syphilis, hepatitis B, and HIV. Urine is tested for 3. ‘All or none’ period of embryogenesis
asymptomatic bacteriuria. Aneuploidy screening 4. Dietary supplements in pregnancy
should be discussed. 5. Immunization during pregnancy
CH 09_p119-132_v3.indd 132 17-07-2015 10:31:50

Obstetric
10 Ultrasound and
Other Imaging
Case scenario
Mrs MP, 11-weeks pregnant, was a gravida 2, para 1, live 1. She had
vaginal bleeding and was concerned about the pregnancy. She wanted
assurance that the baby was doing fine. She was referred for an ultra-
sound examination.
Introduction Basics of diagnostic

Ultrasonographic examination is the most com- ultrasound
mon imaging technique used in pregnancy.
Since its introduction in the 1970s, sonography The term ‘ultrasound’ denotes that the sound
has revolutionized the management of preg- waves used for imaging have a frequency higher
nancy. The capacity to image both the struc- than the upper human auditory limit of 20 kHz.
ture and the function of the fetus has improved Obstetric imaging uses waves with a frequency
the clinician’s ability to bring about a decrease ranging between 2 and 12 MHz.
in perinatal morbidity and mortality. The intro- Ultrasound transducers contain piezoelectric
duction of sonography has also facilitated the crystals. These crystals produce high-frequency
ability to investigate the fetus with prenatal ultrasound waves when electrically stimulated.
diagnostic techniques and treat the fetus with Each transducer crystal transmits as well as
prenatal therapeutic procedures (see Chapter 12, receives mechanical energy. When the sound
Prenatal screening, prenatal diagnosis, and fetal waves hit tissue, they bounce back depending
therapy). on the density of the tissue encountered. The
CH 10_p133-147_v3.indd 133 17-07-2015 10:32:49

An orientation marker is located on the ultra-

Box 10.1 Physics of ultrasound imaging
sound transducer. It helps to orient the image on
• Frequency of sound waves the screen with respect to the right and the left of
Ŧ Higher than human auditory limit the mother.
Ŧ 2–12 MHz
Gel is placed on the patient’s skin for trans-
• Piezoelectric crystals
abdominal scans and on the covered probe for
Ŧ Are electrically stimulated
Ŧ Produce ultrasound waves
transvaginal scans. This prevents air from com-
Ŧ Transmit and receive mechanical energy ing between the transducer and the tissue. The
Ŧ Convert returning echoes into electrical energy gel also acts as a lubricant so that the ultrasound
Ŧ Display returning echoes as images probe glides easily over the abdomen or along
the vagina.
crystal converts the returning echoes into elec-
trical energy. These returning electrical signals or
echoes are displayed as images on the monitor of
B-mode imaging
the sonography equipment (Box 10.1). B-mode imaging, or brightness modulation,
is used for imaging in obstetrics and gynecol-
ogy. Different tissues will reflect sound waves
Transducers with different intensities. Echoes with greater
Abdominal transducers are commonly used for intensity are displayed with greater degrees of
obstetric ultrasound imaging. They have frequen- brightness. Fluid (e.g., urine in the bladder) will
cies ranging from 3 to 5 MHz, which provide suf- appear dark, whereas bone will appear white.
ficient penetration and resolution. Curvilinear The images are two-dimensional (2D).
probes are preferred for obstetric scans (Fig. 10.1).
Transvaginal transducers (with a frequency
of 5–10 MHz or higher) may be used in early eal-time imaging
pregnancy to better visualize the fetus (Fig. 10.2).
Obstetric ultrasound uses real-time imaging,
Transvaginal probes are not useful in obstetrics
which is the rapid acquisition of images with the
beyond 12 weeks except to evaluate the cervix or
ability to evaluate movement as it is happening.
localize a low-lying placenta. A condom is always
These images are rapidly displayed in succes-
used on a transvaginal probe to prevent trans-
sion, thereby creating a video of the area being
mission of infection from one woman to another.
targeted. This allows evaluation not only of the
structure but also of the function of an organ.
That is why real-time ultrasound is especially
useful in obstetrics where it enables the obser-
vation of the moving fetus and fetal cardiac
activity.
M-mode imaging
Figure 10.1 Curvilinear transabdominal transducer.(Photo M-mode imaging represents movement of struc-
courtesy: Mediscan Systems, Chennai.) tures over time. In obstetrics it helps in docu-
menting fetal heart rate and movement of the
valves.
3D sonography
Three-dimensional (3D) sonography provides 3D
images of the fetus (Fig. 10.3). Special probes and
Figure 10.2 Transvaginal transducer. (Photo courtesy: software are needed to acquire and render the
Mediscan Systems, Chennai.) images. 3D sonography is especially useful for
CH 10_p133-147_v3.indd 134 17-07-2015 10:32:50

Obstetric Ultrasound and Other Imaging 135
First trimester
ultrasonography
Timing
First trimester ultrasonography is an ultrasound
examination performed before 13+6 weeks’ ges-
tation. Ideally, to assess the anatomy, including
nuchal translucency (NT), the examination is
performed between 11 and 13+6 weeks’ gestation.
Transabdominal versus
transvaginal examination
Both transabdominal and transvaginal exam-
inations can be performed in the first trimes-
Figure 10.3 3D sonography of fetal face. (Photo courtesy:
ter.Transvaginal ultrasound is more useful in
Mediscan Systems, Chennai.)
very early pregnancy (before 8 weeks), in obese
women, for identifying anomalies and in mea-
delineating facial abnormalities and neural tube suring the NT.
defects in the fetus.
Procedure
4D sonography The woman is in the supine position for a trans-
4D sonography refers to 3D images that can abdominal ultrasound and in the dorsolithot-
be viewed in realtime. It is also called dynamic omy position for a transvaginal examination.
3D sonography. It is useful in studying the fetal The maternal bladder should be full when a
heart, fetal movement, and fetal behavioral transabdominal probe is used, to allow visual-
states such as breathing. ization of the early pregnancy. If a transvaginal
probe is being used, the bladder should be emp-
tied. First trimester ultrasonography is summa-
Doppler ultrasound rized in Box 10.2.
Doppler ultrasound is used to study blood flow
in the fetus and the placenta. It is discussed in
detail later in this chapter.
+PFKECVKQPUHQTſTUVVTKOGUVGT
ultrasound
The indications for first trimester ultrasound
ecommended ultrasound examination are listed in Box 10.3.
examinations in pregnancy Box 10.2 First trimester ultrasonography
All pregnant women should be offered ultra- • Done before 13 weeks +6 days
sound examination and assessment of the fetus. • Transabdominal examination
The ideal time to undergo this examination is at Ŧ Performed with a full bladder
• Transvaginal examination
• 11–13+6 weeks (first trimester). Ŧ Performed with an empty bladder
• 18–22 weeks (second trimester). Ŧ More useful
Third trimester ultrasound is done mainly to in early pregnancy (before 8 weeks)
in obese women
assess growth, placental localization and fetal
for identifying anomalies
well-being and in some cases to look for evolving
for measuring nuchal translucency
abnormalities.
CH 10_p133-147_v3.indd 135 17-07-2015 10:32:50

Box 10.3 +PFKECVKQPUHQTſTUVVTKOGUVGT valuation o gestational sac

ultrasound The gestational sac is a small anechoic fluid col-
• Location and documentation of pregnancy lection surrounded by an echogenic ring that
• Assignment of gestational age by measuring represents trophoblasts and decidual reaction.
Ŧ gestational sac The earliest the gestational sac can be identi-
Ŧ crown–rump length fied by transvaginal ultrasound is 4 weeks and
• Documenting cardiac activity 3 days of gestation, when the mean sac diame-
• Number of viable fetuses ter is 2–3 mm (Box 10.4). Before the appearance
Ŧ Amnionicity, chorionicity of the embryo, the mean sac diameter can be
• +FGPVKſECVKQPQHHGVCNCPQOCNKGU used to calculate the gestational age. The mean
Ŧ Acrania/anencephaly sac diameter (in mm) +30 will give the gesta-
Ŧ Alobar holoprosencephaly
tional age in days. For example, using a sac size
Ŧ Major abdominal wall defects
of 10 mm, the calculated age would be 40 days
Ŧ Gross limb reduction defects
• Uterine anatomy and adnexae
(10 + 30) or 6 weeks. An intrauterine gesta-
Ŧ Uterine anomalies tional sac, being embedded in the endome-
Ŧ 2TGUGPEGQHſDTQKFU trium is eccentrically located (Fig. 10.4) and, is
Ŧ Ectopic pregnancy surrounded by two concentric rings of decidua
Ŧ Adnexal masses (double decidual sac sign).
• Screening for aneuploidy (chromosomal abnormality) The gestational sac is evaluated for the pres-
Ŧ Nuchal translucency ence or absence of a yolk sac and embryo. In
Ŧ Combined with biochemical screening early pregnancy (before 5 weeks’ gestation), the
embryo may not be identified. In that case the
mean sac diameter may be recorded to calculate
the gestational age. The embryo is identified as
Location and documentation a 1- to 2-mm structure by 5.5 weeks’ gestation.
of pregnancy
A transabdominal or transvaginal probe is used Box 10.4 Gestational sac
to look for a gestational sac in the uterus (intra-
• Seen by transvaginal ultrasound at 2–3 mm size
uterine pregnancy), cervix, or adnexae (ectopic
• Clearly visible at 4.5–5 weeks
pregnancy). The location of the gestational sac is
• Gestational age (days) = mean sac diameter (in mm) + 30
documented using ultrasonography. • Eccentric in location
• Surrounded by two rings of decidua
Assignment of gestational age
The gestational age is assigned by measuring
the crown–rump length (CRL). Measuring the
CRL at 8–14 weeks is the most accurate method
of dating pregnancy. It predicts the expected
date of delivery (EDD) to within 3–5 days.
Accurate assessment of gestational age in the
first trimester is especially important in high-
risk pregnancies (e.g., with hypertensive dis-
orders or diabetes), where delivery before term
may be required.
Once assigned, the gestational age is not
changed in subsequent scans. The assigned ges-
tational age forms the basis for the following:
• EDD Figure 10.4 Gestational sac. The sac (arrow) is seen
• Assessment of fetal growth lying eccentrically in the cavity and demonstrates the
• Timing of invasive procedures double decidual sac sign (double arrows). (Photo
• Labor induction at or before term as indicated courtesy: Mediscan Systems, Chennai.)
CH 10_p133-147_v3.indd 136 17-07-2015 10:32:50

In the presence of an ectopic pregnancy, intra-

uterine fluid collection could also mimic a ges-
tational sac (pseudogestational sac). A pseudo-
gestational sac is centrally located in the
endometrial cavity and is not surrounded by a
double decidual ring.
ol sac
The yolk sac is the first structure that appears
within the gestational sac. It should be visible
when the mean sac diameter is 20 mm by trans-
abdominal scan or 8–10 mm by transvaginal
scan (5 weeks). The presence of the yolk sac is
indicative of an intrauterine pregnancy. The nor-
mal yolk sac size is <6 mm (Fig. 10.5) and a larger
yolk sac may be indicative of an abnormal preg-
nancy. As pregnancy advances, the yolk sac dis- Figure 10.6 Crown–rump length at 10 weeks’ gestation.
appears and cannot be identified on ultrasound (Photo courtesy: Mediscan Systems, Chennai.)
by 14 weeks.
Box 10.5 Crown rump length
• Most accurate for pregnancy dating
• Best measured between 7 and 10 weeks
Ŧ Accuracy ±3 days
• Can be measured between 11 and 14 weeks
Ŧ Accuracy ±5 days
motion should be present at 6 weeks’ gestation

when the embryo is 5 mm or greater in length.
Absence of cardiac motion beyond that fetal
length raises the suspicion of a miscarriage.
Figure 10.5 Gestational sac, yolk sac, and fetus at 7 weeks.
(Photo courtesy: Mediscan Systems, Chennai.) umber of fetuses
The number of fetuses is documented. In case
Cro n rump length of multiple gestation, zygosity, amnionicity and
The crown rump length (CRL) is the longest chorionicity should be reported if possible in
straight-line measurement of the length of the the first trimester. The presence of 2 placentas
embryo or fetus (excluding the limbs and yolk sac). clearly indicates dizygotic twins. The ultrasound
It is the measurement from the top of the head signs for defining amnionicity and chorionicity
(crown) to the bottom of the buttocks (rump). in monozygotic twins are given in Box 10.6.
The CRL of the embryo (Fig. 10.6) provides the The twin peak sign and T sign are accurately
most accurate estimate of gestational age and assessed between 11 and 14 weeks and are
should be used to determine EDD. The CRL at described in Chapter 32, Multifetal pregnancy.
7–10 weeks predicts the due date with an accuracy
of ±3 days. Between 11 and 14 weeks, the accuracy Fetal anatomy
of the CRL falls slightly to ±5 days (Box 10.5).
Embryonic or fetal anatomy should be assessed
according to gestational age. Some fetal anom-
Cardiac activity
alies (acrania/anencephaly, alobar holoprosen-
Presence or absence of cardiac activity should be cephaly, gross limb reduction defects) may be
documented. With transvaginal scans, cardiac identified in the first trimester.
CH 10_p133-147_v3.indd 137 17-07-2015 10:32:50

Box 10.6 ltrasound imaging in twin pregnancy Box 10.7 Measurement of nuchal translucency
( T)
• 2 placentas
Ŧ Dizygotic twins • Between 11 and 13+6 weeks
Dichorionic, diamniotic • Fetus in midsagittal plane
• Single placenta • Fetal neck in neutral position
Ŧ Monozygotic twins • +OCIGOCIPKſGFVQſNNUETGGPYKVJ
Dichorionic twins Ŧ fetal neck
- 2 sacs visible Ŧ head
- Dividing membrane >2 mm thick Ŧ upper thorax
Monochorionic diamniotic twins
- Thin membrane
- Difficult to see in first trimester
Monochorionic monoamniotic twins abnormalities (see Chapter 12, Prenatal screening,
- Single amniotic cavity prenatal diagnosis, and fetal therapy).
terine anatomy and adnexae ltrasonographic evaluation of

The uterus should be evaluated for obvious ſTUVVTKOGUVGTEQORNKECVKQPU
anomalies (e.g., bicornuate uterus). The pres-
ence of any fibroids should be documented, Vaginal bleeding in early pregnancy should raise
including their size and location. The presence, suspicion of one of the following first trimester
location, and size of adnexal masses should be complications:
documented. • Miscarriage
• Hematoma
Screening for aneuploidy • Ectopic pregnancy
(chromosomal abnormality) • Molar pregnancy
Nuchal translucency is the anechoic strip at the Miscarriage
posterior fetal neck (Fig.10.7). It is measured
according to the established guidelines (Box 10.7). Miscarriage can be threatened, inevitable, incom-
Increased NT is associated with trisomy 21, plete, or complete (see Chapter 29, Miscarriage
Turner syndrome, and other chromosomal and recurrent pregnancy loss). Ultrasound plays
defects as well as fetal cardiac anomalies. an important role in identifying the type of
Nuchal translucency is combined with mater- miscarriage.
nal biochemical testing to screen for chromosomal
• Threatened miscarriage: Fetal cardiac activity
is identified on ultrasound.
• Inevitable miscarriage: Ultrasound shows an
open cervix with the pregnancy lying low in
the uterine cavity or in the cervical canal.
• Incomplete miscarriage: Only some products
of conception are seen in the uterine cavity
with a previous ultrasound having shown a
pregnancy.
• Complete miscarriage: The uterine cavity is
empty, with a previous ultrasound having
shown a pregnancy.
• Missed miscarriage: This may be an anembry-
onic pregnancy or early fetal demise.
In addition
Figure 10.7 Nuchal translucency. The translucent nuchal
space (anechoic strip) is seen over the posterior fetal neck. • The diagnosis of blighted ovum or anem-
(Photo courtesy: Mediscan Systems, Chennai.) bryonic pregnancy (early pregnancy loss
CH 10_p133-147_v3.indd 138 17-07-2015 10:32:50

without the formation of an embryo) is Molar pregnancy

made when
– mean sac diameter is >8 mm without a yolk When molar pregnancy is suspected due to vag-
sac or inal bleeding associated with abnormally raised
– mean sac diameter is >16 mm without an hCG values, ultrasonography can help with the
embryo diagnosis. Transvaginal sonography will show
• When there is no cardiac activity in an embryo multiple fluid-filled vesicles in the uterine cav-
>5 mm by transvaginal ultrasonography, a ity without detecting an embryo/fetus/its parts.
diagnosis of embryonic demise is made.
ematoma Second trimester

Intrauterine hematomas are blood accumula-
tions that are subchorionic, retroplacental, or ultrasonography
both. Intrauterine hematomas do not have a
deleterious effect on pregnancy outcome even in Timing
women with recurrent miscarriage. Second trimester ultrasonography is an ultra-
sound examination performed between 18 and
Ectopic pregnancy 22 weeks’ gestation. An ultrasound done at this
Implantation of the fertilized ovum outside the time has become part of routine obstetric care.
uterine cavity is called ectopic pregnancy. It is • This gestational age is an optimum time where
estimated that 95% of ectopic pregnancies occur a fetus can be labeled as ‘normal’ with a good
in the fallopian tube. A combination of a serum degree of accuracy. Approximately 70% of
test for human chorionic gonadotropin (hCG) major anomalies and 45% of minor anomalies
and transvaginal ultrasound is used for diagnos- can be detected at this time.
ing ectopic pregnancy (see Chapter 30, Ectopic • It is the time when dating of the pregnancy can
pregnancy). Failure to detect an intrauterine be done with accuracy to within ±7 days.
gestational sac by transvaginal ultrasound when
the hCG value exceeds 1000–2000 mIU/mL indi-
cates an increased risk for the presence of ecto- Procedure
pic pregnancy.
The criteria for ultrasound diagnosis of ecto- The woman is in the supine position for a trans-
pic pregnancy are given in Box 10.8. abdominal ultrasound. At 18–22 weeks, a full
bladder is not needed to visualize the fetus. At
this stage of pregnancy, a transvaginal scan is
Box 10.8 Criteria for ultrasound diagnosis of
indicated only for the evaluation of the cervix
ectopic pregnancy for cervical insufficiency (incompetence) or for
localization of the placenta.
7VGTKPGſPFKPIU
• Diagnostic signs
Ŧ Absence of gestational sac in uterine cavity Indications for second
Ŧ Absence of embryo/its parts in uterine cavity
• Suggestive signs trimester ultrasound
Ŧ Enlarged uterus
The various indications for second trimester
Ŧ Thick endometrium
Ŧ Pseudodecidual sac
ultrasound are listed in Box 10.9.
#FPGZCNſPFKPIU
• Diagnostic signs Estimation of gestational age
Ŧ Ectopic gestational sac with/without living embryo If a gestational age has not been assigned in the
Ŧ Mixed solid and cystic mass first trimester, it is calculated in the second tri-
• Suggestive sign
mester. Gestational age calculated in the second
Ŧ (TGGƀWKFKPVJGEWNFGUCE
trimester is accurate up to ±7 days.
CH 10_p133-147_v3.indd 139 17-07-2015 10:32:51

Box 10.9 Indications for second trimester

ultrasound
6TCPUCDFQOKPCNGZCOKPCVKQP
• Fetus
Ŧ Estimation of gestational age
Ŧ Fetal biometry
Ŧ Number
Evaluation of multiple gestation
Ŧ Screening for fetal anomalies
Ŧ Evaluation of fetal growth
• #OPKQVKEƀWKF
• Placenta
• Adjunct to prenatal diagnostic procedures
Ŧ Amniocentesis
Ŧ Chorionic villus sampling
Ŧ Fetal blood sampling Figure 10.8 Measurement of the biparietal diameter
6TCPUXCIKPCNWNVTCUQWPF (BPD) and the head circumference. (Photo courtesy:
• 'XCNWCVKQPQHEGTXKECNKPUWHſEKGPE[ Mediscan Systems, Chennai.)
• Placental localization
than BPD when the shape of the head is round
(brachycephaly) or elongated (dolichocephaly).
etal biometry
Fetal biometry (imaged transabdominally) mea- Abdominal circumference
sures four fetal parameters. Gestational age is A transverse section of the abdomen is obtained
calculated based on the following parameters: to measure the AC (Fig. 10.9). It is measured at
• Biparietal diameter (BPD) a level where the transverse section includes the
• Head circumference (HC) portal vein (intrahepatic portion of the umbili-
• Abdominal circumference (AC) cal vein), the stomach, and a true cross-section
• Femur length (FL) of the spine with three ossification centers. The
image should be circular in shape.
Once these measurements are obtained, the ges-
tational age is assigned according to standardized
charts.
Biparietal diameter
The BPD is the widest transverse diameter of the
fetal head. When measured between 14 and 20
weeks’ gestation, it can predict gestational age
within ±7 days.
The correct plane for the measurement of the
BPD and the HC must include the cavum sep-
tum pellucidum, thalami, and the falx cerebri
(Fig. 10.8). Once the measurement is obtained,
the gestational age is assigned according to stan-
dardized charts.
ead circumference
The HC is measured at the same level as the BPD,
around the outer perimeter of the fetal skull. It is Figure 10.9 Measurement of abdominal circumference. It
the most accurate measurement for the predic- is done at the level where the spine, stomach, and portal
tion of fetal age. This measurement is not affected vein are visualized. (Photo courtesy: Mediscan Systems,
by head shape and is therefore more accurate Chennai.)
CH 10_p133-147_v3.indd 140 17-07-2015 10:32:51

The measurement of the AC is crucial in ther biometric measurements

detecting growth disorders in the fetus. In a In addition to the four biometric measurements
growth-restricted fetus, the AC will be less than mentioned above, there are other less commonly
the other three biometric values. This happens used ones. They include the following:
because of (a) depletion of abdominal adi-
pose tissue and (b) decreased hepatic size as a • Length of long bones of the extremities
result of reduced glycogen storage in the liver • Intraorbital and interorbital diameters
(see Chapter 33, Fetal growth disorders: Growth • Transverse cerebellar diameter
restriction and macrosomia). • Clavicle length
• Foot length
Femur length
These additional measurements are used
Measurement of the FL is an important part of
while evaluating specific system anomalies
fetal biometry. The femoral shaft is seen as a
especially skeletal defects.
slightly curved, brightly echogenic structure that
produces an acoustic shadow (Fig. 10.10). The
Calculating gestational age using fetal biometry
FL is measured by aligning the long axis of the
femur to the transducer. Only the osseous por- The four biometric values (BPD, HC, AC, and FL)
tion of the diaphysis and the metaphysis of the are the standard parameters used for estimat-
proximal femur are measured. The gestational ing gestational age in the second and third tri-
age is assigned according to standardized charts. mesters. Standardized charts are available that
predict gestational age using these four values.
The charts may need to be modified according
to ethnic background; for example, the value for
an Indian fetus will be different from that for a
Western fetus. Therefore, appropriate charts
should be used for calculating the gestational
age in different populations.
The range of error in predicting delivery dates
by ultrasound examination increases as preg-
nancy progresses. While the range is ±5–7 days in
the first and second trimesters (before 20 weeks),
it can be up to ±21–28 days in the third trimester.
Sonographic assignment of fetal age is therefore
best done before 20 weeks. Table 10.1 shows the
range (in days) with which accuracy of dating
Figure 10.10 Measurement of femur length. (Photo decreases as pregnancy progresses.
courtesy: Mediscan Systems, Chennai.)
Table 10.1 Correlation of accuracy of fetal age estimation with

weeks of pregnancy
Parameter used Gestational age (weeks) Accuracy of fetal age

at which the fetal age estimation
estimation is done (range in days)
Mean sac diameter 4.5–6 ± 5–7
Crown-rump length 7–10 ± 3
Crown-rump length 11–14 ± 5
BPD, HC, FL, AC 14–20 ± 7
21–30 ± 14
>30 ± 21–28
AC abdominal circumference; BPD biparietal diameter; femur length; C head
circumference.
CH 10_p133-147_v3.indd 141 17-07-2015 10:32:51

Discrepancy between LMP-derived Spine

and ultrasound-derived fetal age The spine and sacrum are examined for ossi-
fication centers, cervical widening, and sacral
In a woman who has irregular periods or is
tapering. Spines should be evaluated in the sag-
uncertain of her last menstrual period (LMP),
ittal, coronal, and transverse planes.
ultrasound assignment of fetal age is done and
the expected date of delivery (EDD) is assigned hora
according to that. In some women, there might
be a discrepancy in the fetal age obtained by A four-chamber view of the heart is obtained,
ultrasound and the one calculated by the LMP. and the heart’s position in the chest cavity is doc-
In such a situation, a decision has to be made umented. The outflow tracts are imaged to rule
to reassign a new EDD. The sonographically out anomalies such as tetralogy of Fallot. The
derived gestational age is used to calculate lungs are homogenously echogenic. Intrathoracic
EDD only if it differs from that calculated using masses or cysts should be ruled out. The dia-
LMP by phragm should be imaged to rule out diaphrag-
matic hernia.
• >7 days before 16 weeks
• >10 days between 16 and 22 weeks Ab omen
• >14 days between 22 and 28 weeks In the upper abdomen, the stomach is identi-
• >21 days after 28 weeks fied and its position with reference to the heart
is noted (situs). The liver and the portal vein are
Screening for fetal anomalies imaged. In the mid-abdomen, the kidneys and
small bowel are evaluated. Dilated, fluid-filled
Apart from fetal biometry, an ultrasound exam- bowel loops could indicate obstruction or atresia.
ination done between 18 and 22 weeks is essen- In the lower abdomen, the bladder, two umbili-
tial for identifying fetal anomalies. cal arteries, and the genitalia are identified.
The genitalia will define the gender of the
Targeted or detailed scan fetus. In certain anomalies such as bladder out-
let obstruction, identifying the fetus as male will
An ultrasound done for fetal anatomical survey confirm posterior urethral valves that occur only
is called a targeted or detailed scan. At this ges- in males. Ambiguous genitalia is commonly seen
tational age (18–22 weeks), fetal organ develop- in congenital adrenal hyperplasia. Sex determi-
ment is optimal to identify approximately 70% of nation, for a non-medical reason, is prohibited
major anomalies and 45% of minor anomalies. by law in India.
The following anatomical landmarks are eval-
uated in detail during the targeted scan. tremities
All four limbs must be evaluated. The extremities
ea are evaluated for abnormalities in size, morphol-
The midline falx and the cavum septum pel- ogy, and number.
lucidum are imaged. The lateral ventricles are Box 10.10 lists the essential components of a
measured at the level of the atria. Dilatation of targeted or detailed fetal anatomical scan.
the lateral ventricles signifies ventriculomegaly.
The cerebellar hemispheres, vermis, and cis-
terna magna are identified. Nuchal fold thick- Fetal environment
ness is important for the diagnosis of chromo- The placenta, amniotic fluid, and umbilical cord
somal and other anomalies. The posterior fossa comprise the fetal environment.
should be evaluated for cysts (Dandy–Walker
malformation) and abnormal anterior curvature
of the cerebellum (‘banana sign’). Placenta
The placenta is assessed in terms of location,
ace with specific reference to its lower edge and its
The orbits, nose and nasal bone, and the mouth distance from the internal os (to rule out pla-
including the lips are imaged. centa previa). If placenta previa is diagnosed in
CH 10_p133-147_v3.indd 142 17-07-2015 10:32:51

documented. If only two vessels are seen (instead

Box 10.10 Components of a targeted or detailed
fetal scan of three), a thorough search for fetal structural
and chromosomal anomalies must be made.
• Head and neck
Ŧ Midline falx and cavum septi pellucidum
Ŧ Lateral cerebral ventricles and choroid plexus 'XCNWCVKQPQHEGTXKECNKPUWHſEKGPE[
Ventriculomegaly
Routine cervical length measurement is not
Ŧ Cerebellar hemispheres, vermis, and cisterna
magna
recommended in low-risk pregnancies. When
‘Banana sign’ cervical insufficiency is suspected, serial evalu-
Dandy-Walker malformation ation of the cervical length may identify those at
Ŧ Nuchal fold thickness increased risk of primary or recurrent preterm
• Face birth. The length of the cervix is measured by a
Ŧ Orbits transvaginal or transperineal scan. A high-risk
Ŧ Nose and nasal bone woman with a cervical length of 2.5 cm or less
Ŧ Mouth including lips is considered to be at risk for preterm labor. The
• Spine internal os is examined for funneling which is a
Ŧ 1UUKſECVKQPEGPVTGU sign of cervical insufficiency.
Ŧ Cervical widening
Ŧ Sacral tapering
• Thorax Ad unct to prenatal diagnostic
Ŧ Heart
Four-chamber view procedures
Outflow tracts Ultrasound may also be done to guide prenatal
Ŧ Lungs diagnostic procedures such as amniocentesis,
Intrathoracic masses or cysts
chorionic villus sampling, or fetal blood sampling
Ŧ Diaphragm
(see Chapter 12, Prenatal screening, prenatal diag-
Diaphragmatic hernia
• Abdomen nosis, and fetal therapy).
Ŧ Stomach (presence, size, and situs)
Ŧ Liver
Ŧ Kidneys and bladder
Ŧ Bowel
Third trimester
Ŧ Umbilical cord insertion site into the fetal abdomen ultrasonography
Ŧ Umbilical cord vessel number
Ŧ Genitalia Third trimester ultrasonography is not done
• Extremities routinely. The indications for a third trimester
Ŧ Size, morphology, and number ultrasound examination are enumerated in
Box 10.11.
the second trimester, a repeat scan must be done
in the third trimester to confirm whether the pla-
centa has migrated away from the os or not. Doppler in pregnancy
#OPKQVKEƀWKF Doppler ultrasound is an indispensable tool in
evaluating pregnancies at risk for conditions
The amniotic fluid can be assessed by the subjec- such as preeclampsia, fetal growth restriction,
tive method, single deepest pocket, or amniotic fetal anemia, and umbilical cord abnormalities.
fluid index (AFI). Subjective assessment of liquor Pulsed wave Doppler and color Doppler are used
is done in the 18–22 week scan (see Chapter 11, in obstetric practice.
Antepartum fetal surveillance). Assessment is done using Doppler of the
following:
mbilical cord
• Umbilical artery
Examination of the umbilical cord should be an • Middle cerebral artery (MCA)
integral part of the second trimester ultrasound • Uterine artery
scan. The number of vessels in the cord should be • Ductus venosus
CH 10_p133-147_v3.indd 143 17-07-2015 10:32:51

Box 10.11 Indications for a third trimester Principle

ultrasound examination
Ultrasound images of flow in fetal and maternal ves-
• 5KIPKſECPVFKUETGRCPE[DGVYGGPWVGTKPGUK\GCPFENKPKECN sels are obtained from measurements of movement
dates of blood flow. The transducer transmits a series of
Ŧ Evaluation of fetal growth
pulses to detect movement of blood. Echoes from
• Assessment of fetal well-being
moving objects (red blood cells) exhibit slight dif-
Ŧ #OPKQVKEƀWKF
ferences in the frequencies of the echoes received.
Ŧ $KQRJ[UKECNRTQſNG
Ŧ Doppler evaluation These differences are termed as the ‘Doppler shift’
• Vaginal bleeding and can be heard as audio signals. These frequen-
Ŧ Suspected placental abruption cies are then processed to produce either a Doppler
Ŧ Suspected placenta previa waveform or a color flow display (Fig. 10.11). Color
• Multiple gestation Doppler depicts blood flow in red and blue. Red
• Suspected fetal death color signifies flow toward the probe, and blue
• Preterm rupture of membranes color signifies flow away from the probe.
• Fetal well-being in an obese parturient
• Estimation of fetal weight Doppler waveform
• Fetal presentation
• Guidance for external cephalic version A Doppler waveform is a graphic representation
• Follow-up evaluation of fetal anomaly of flow velocities throughout the cardiac cycle
• Women registering late for antenatal care (Fig. 10.12).
• Systolic waveform represents the cardiac pump
– In uterine artery waveform: Maternal heart
Doppler studies are invaluable in the manage- – In umbilical artery waveform: Fetal heart
ment of complications arising from preeclamp- • Diastolic waveform represents the status of
sia and fetal growth restriction. the placental vascular bed
Doppler ultrasonography is a noninvasive
technique used to assess
• Presence or absence of blood flow in a vessel
• Direction of flow
• Flow characteristics such as
– velocity of flow during phases of the cardiac
cycle
– impedance to flow during diastole Figure 10.12 Umbilical artery velocity waveforms. (Photo
oppler elocimetry
oppler a eform Color flo isplay
lue color e color

flo from flo
probe probe
Figure 10.11 Doppler velocimetry in obstetrics.
CH 10_p133-147_v3.indd 144 17-07-2015 10:32:51

Box 10.12 Indications for Doppler studies in

obstetrics
(KTUVVTKOGUVGT
• Screening for aneuploidy
• As a marker for congenital heart disease
• Screening for preeclampsia
5GEQPFVTKOGUVGT
• Screening for preeclampsia
• +FGPVKſECVKQPQHHGVCNCPGOKC
• Evaluation of vascular malformations in the fetus and
placenta
• +FGPVKſECVKQP QH ECTFKCE CPF TGPCN CPQOCNKGU CPF
Figure 10.13 Sample waveform marked for systolic diaphragmatic hernia
(S) and diastolic (D) measurements. (Photo courtesy:
6JKTFVTKOGUVGT
• Evaluation of a growth-restricted fetus
• Assessment of fetal hypoxia
Doppler indices
The peak systolic velocity (S), the end-diastolic -rays and CT scans
velocity (D), and the mean velocities are mea-
sured in the Doppler waveform (Fig. 10.13). From A single diagnostic X-ray does not result in
these measurements three Doppler indices are radiation exposure adequate enough to cause
calculated that give a measure of the resistance damage to the embryo or fetus and is not an indi-
of the vascular bed which are as follows: cation for therapeutic abortion (see Chapter 9,
Preconceptional and antenatal care). It is best to
• Systolic/diastolic ratio (S/D ratio) avoid imaging where multiple doses of ionizing
• Resistance index (RI; also called resistive index radiation will be delivered to the fetus. CT scans
or Pourcelot’s index) are preferably avoided in pregnancy. In such
– RI = (peak systolic velocity – end diastolic situations, magnetic resonance imaging (MRI)
velocity)/peak systolic velocity or (S − D)/S may be useful.
• Pulsatility index (PI)
– PI = (peak systolic velocity – end diastolic veloc-
ity)/peak systolic velocity or (S − D/mean) Magnetic resonance
imaging
Indications for Doppler With MRI, instead of ionizing radiation, mag-
nets that alter the energy state of hydrogen pro-
in obstetrics tons are used. This technique is useful for diag-
The indications for Doppler in obstetrics are nosis and evaluation of fetal central nervous
enumerated in Box 10.12. system anomalies and placental abnormalities
The use of Doppler in evaluating fetal such as placenta previa and accreta. MRI is not
well-being is described in detail in Chapter 11, associated with adverse fetal effects. However,
Antepartum fetal surveillance. cost restricts its routine use in pregnancy.
uclear medicine
ther imaging modalities Rarely, nuclear studies such as pulmonary venti-
in obstetrics lation–perfusion, thyroid, bone, and renal scans
may be required in pregnancy. When pulmo-
In certain circumstances, pregnant women may nary embolism is suspected during pregnancy,
be required to undergo imaging with modalities a ventilation–perfusion scan may be performed.
other than ultrasonography. The amount of radiation to which the fetus
CH 10_p133-147_v3.indd 145 17-07-2015 10:32:52

is exposed is extremely small (approximately Safety guidelines for imaging

50 mrad).
Radioactive iodine readily crosses the pla- modalities in pregnancy
centa and has an adverse effect on the fetal thy-
roid, especially if used after 10–12 weeks’ ges- The safety guidelines for imaging modalities in
tation. Radioactive isotopes of iodine used for pregnancy are summarized in Box 10.13.
treatment of hyperthyroidism are contraindi-
cated during pregnancy. Box 10.13 Safety guidelines for imaging
modalities in pregnancy
• X-ray exposure not harmful to fetus in case of
Contrast agents Ŧ single diagnostic procedure
Ŧ exposure <5 rads
Oral and intravascular contrast agents are used • Diagnostic X-ray procedures may be performed
for better imaging with X-rays, CT scans, and Ŧ when medically indicated
MRIs. Most radiopaque agents used with CT and • Multiple diagnostic X-rays
conventional radiography contain derivatives Ŧ Dosimetry should be calculated
of iodine and have been associated with neo- • Ultrasonography or MRI safer than X-rays
natal hypothyroidism. These are therefore best • CT scans to be avoided
avoided unless absolutely essential. • Radiopaque and paramagnetic contrast agents to be
avoided
• Radioactive isotopes of iodine contraindicated
Key points
• Ultrasonographic examination is the most common • The ideal time to undergo ultrasonographic examina-
imaging technique used in pregnancy. tion is between 11 and 13+6 weeks
ſTUVVTKOGUVGTCPF
between 18 and 22 weeks (second trimester). Third
• The sound waves used for imaging have a frequency
trimester ultrasound is done for evaluation of growth,
higher than the upper human auditory limit of 20 kHz.
placenta, liquor, and fetal well-being.
Obstetric imaging uses waves with a frequency
ranging between 2 and 12 MHz. • +PVJGſTUVVTKOGUVGTIGUVCVKQPCNCIGKUCUUKIPGFD[
• Abdominal transducers are commonly used for obstet- measuring the gestational sac or the crown–rump
ric ultrasound imaging. They have frequencies ranging length (CRL).
from 3 to 5 MHz. • Measuring the CRL at 7–14 weeks is the most
• Transvaginal transducers (with a frequency of accurate method to date pregnancy and predicts the
5–10 MHz or higher) may be used in early pregnancy expected date of delivery (EDD) to within 3–5 days.
to better visualize the fetus. • Presence or absence of cardiac activity should be
documented.
• B-mode imaging, or brightness modulation, is used
for imaging in obstetrics and gynecology. Different • Some fetal anomalies (acrania/anencephaly, alobar-
VKUUWGUYKNNTGƀGEVUQWPFYCXGUYKVJFKHHGTGPVKPVGPUK- holoprosencephaly, gross limb reduction defects) may
ties. Echoes with greater intensity are displayed with DGKFGPVKſGFKPVJGſTUVVTKOGUVGT
greater degrees of brightness. • Nuchal translucency (NT) is measured according to
• Obstetric ultrasound uses real-time imaging, which established guidelines. Increased NT is associated
is the rapid acquisition of images with the ability to with trisomy 21, Turner syndrome, and other chromo-
evaluate movement as it is happening. somal defects as well as fetal cardiac anomalies.
• M-mode imaging helps in documenting fetal heart rate • 8CIKPCNDNGGFKPIKPVJGſTUVVTKOGUVGTKUKPXGUVKICVGF
and movement of the valves. with ultrasonography, which helps in the diagnosis of
miscarriage, hematoma, ectopic pregnancy, or molar
• 3D sonography is useful for delineating facial
pregnancy.
abnormalities and neural tube defects in the fetus.
• The fetus is evaluated for number, viability, and age,
• 4D sonography refers to 3D images that can be
and a targeted scan is done to rule out fetal anomalies.
viewed in realtime. It is useful in studying the fetal
heart, fetal movement, and fetal behavioral states • Fetal biometry measures four fetal parameters:
such as breathing. biparietal diameter, head circumference, abdominal
(Continued)
CH 10_p133-147_v3.indd 146 17-07-2015 10:32:52

Key points
%QPVKPWGF
circumference, and femur length. Gestational age is • Doppler ultrasound is an indispensable tool in
calculated based on these parameters. evaluating pregnancies at risk for conditions such as
• In the second trimester, the estimated date of delivery preeclampsia, fetal growth restriction, fetal anemia,
can be calculated with an accuracy of ±7 days. and umbilical cord abnormalities.
• An ultrasound done for fetal anatomical survey is • Assessment is done using Doppler of the umbilical
called a targeted or detailed scan. At 18–22 weeks, artery, middle cerebral artery, uterine artery, and
70% of major anomalies and 45% of minor anomalies ductus venosus.
ECPDGKFGPVKſGF • Pulsed wave Doppler and color Doppler are used in
• 6JGRNCEGPVCCOPKQVKEƀWKFCPFVJGWODKNKECNEQTF obstetric practice.
comprise the fetal environment and are evaluated • Of the other imaging modalities available, magnetic
during a second trimester scan. resonance imaging is useful and has no deleterious
effect on the fetus. However, cost restricts its use.
Self-Assessment
3. In the presence of molar pregnancy, transvaginal
Case-based questions UQPQITCRJ[YKNNUJQYOWNVKRNGƀWKFſNNGFXGUKENGUKP
the uterine cavity without detecting an embryo/fetus/
Case 1 its parts.
Mrs. MP, 27 years old, is a gravida 2, para 1, live 1. She is 4. An anembryonic pregnancy is early pregnancy loss
11 weeks pregnant. She presented with vaginal bleeding without the formation of an embryo. The ultrasound
and mild lower abdominal pain. The ultrasound showed scan will show a gestational sac >8 mm with no yolk
a fetus corresponding to 11 weeks’ gestation. Cardiac sac or >16 mm with no embryo. Early fetal demise
activity was seen. is diagnosed when an embryo with CRL of 5 mm
reveals no cardiac activity.
1. How accurate is fetal age determination at 11 weeks?
2. 9JCVCTGVJGWNVTCUQWPFſPFKPIUKPCPKPGXKVCDNG
miscarriage? Case 2
3. What are the ultrasound signs of molar pregnancy?
1. Fetal biometry measures four fetal parameters:
4. What are anembryonic pregnancy and early fetal
biparietal diameter, head circumference, abdominal
demise?
circumference, and femur length. Gestational age is
calculated based on these parameters.
Case 2 2. Abdominal circumference measurement is most use-
ful for determining fetal growth restriction.
A 31-year-old primigravida presented at 33 weeks’ gesta- 3. The diastolic portion of the waveform represents
tion with hypertension. The uterine size appeared smaller the status of the placental vascular bed. Placental
than the gestational age. KPUWHſEKGPE[NGCFKPIVQHGVCNITQYVJTGUVTKEVKQPYKNNDG
FKCIPQUGFD[TGFWEGFCDUGPVQTTGXGTUGFƀQYKPVJG
1. Which are the biometric parameters used for deter-
umbilical artery.
mining fetal age?
2. Which is the parameter most useful for predicting
fetal growth restriction?
3. Why is Doppler of the fetal umbilical artery indicated
Sample questions
in fetal growth restriction?
1. Discuss the usefulness of ultrasound imaging in
Answers pregnancy.
Case 1
1. The accuracy of the CRL between 10 and 14 weeks
is ±5 days. 1. 7NVTCUQPQITCRJ[KPVJGſTUVVTKOGUVGT
2. Ultrasound will show an open cervix with the pregnancy 2. Estimation of gestational age using ultrasound
lying low in the uterine cavity or in the cervical canal. 3. Nuchal translucency
CH 10_p133-147_v3.indd 147 17-07-2015 10:32:52

11 Antepartum Fetal
Surveillance
Case scenario
Mrs. BG, 34, was pregnant for the first time after 8 years of marriage. She
was found to have high blood pressure in the 28th week of pregnancy.
At 32 weeks, the fetus was found to be smaller than expected (fetal growth
restriction). She was referred by the local doctor to a tertiary center for
evaluation of the mother and fetus, and further obstetric management.
Introduction Tests of fetal well-being

The aim of antepartum fetal surveillance is to Several tests are in use to assess fetal well-
prevent fetal demise. In the presence of risk fac- being in utero. Biochemical tests (e.g., estima-
tors that may affect fetal well-being, antepar- tion of urinary estriol) were used in the past
tum fetal surveillance gives information about but have now been replaced by biophysical
the intrauterine status of the fetus. Fetal heart tests. The tests for fetal well-being include the
rate assessment, real-time ultrasonography, following:
and Doppler velocimetry are commonly used to
evaluate fetal well-being. Antepartum fetal sur- • Fetal movement count
veillance techniques are useful in assessing the • Cardiotocography (CTG) or electronic fetal
risk of fetal death in pregnancies complicated monitoring (EFM)
by preexisting maternal conditions (e.g., hyper- – Nonstress test (NST)
tension) as well as those in which complications – Vibroacoustic stimulation
have developed (e.g., fetal growth restriction). – Contraction stress test (CST)
When an antepartum fetal test is abnormal, it is • Ultrasonography
called a nonreassuring test. – Amniotic fluid assessment
CH 11_p148-162_v3.indd 148 17-07-2015 10:33:22

Antepartum Fetal Surveillance 149
• Biophysical profile (BPP), which combines pregnancy. There is no gestational age cutoff at
ultrasonography and CTG which it should be initiated.
– Fetal breathing Initiating testing at 32–34 weeks’ gestation
– Fetal movement is appropriate for most high-risk pregnancies.
– Fetal tone If the mother reports decreased or absent fetal
– Amniotic fluid index (AFI) movements in the third trimester, then ante-
– NST partum surveillance is immediately initiated. If
• Doppler studies there has been an adverse event in the previous
– Fetal umbilical artery pregnancy (e.g., stillbirth), then the testing is
– Fetal middle cerebral artery (MCA) initiated 2 weeks before the gestational age at
– Fetal ductus venosus which the adverse event occurred in the previ-
ous pregnancy. In a postdated pregnancy, non-
The indications for antepartum fetal surveil-
stress test (NST) and amniotic fluid assessment
lance are listed in Box 11.1.
are started at 40 weeks’ gestation. Antepartum
testing in insulin-dependent or insulin-
Box 11.1 Indications for antepartum fetal requiring pregnancies that are well controlled
surveillance and otherwise uncomplicated should begin at
34–36 weeks’ gestation. Fetal surveillance in a
Previous obstetric history
hypertensive pregnancy is started at 34 weeks’
aternal gestation or even earlier if it was early onset
• Hypertensive disorder of pregnancy hypertension of pregnancy or if the woman had
• Placental abruption been hypertensive prior to pregnancy (chronic
etal hypertension). When fetal growth restriction is
• Fetal growth restriction diagnosed, a baseline surveillance is done and
• Stillbirth then it is repeated for follow-up. The initiation
Current pregnancy and suggested frequency for fetal testing are
given in Box 11.2.
aternal
• Postterm pregnancy
• Hypertensive disorders of pregnancy
• Diabetes
Ŧ Pregestational diabetes Box 11.2 Initiation and frequency of antepartum
Ŧ Gestational diabetes requiring insulin
fetal surveillance
• Antiphospholipid antibody syndrome nitiation
• Advanced maternal age (elderly gravida) • Decreased or absent fetal movement
• Vaginal bleeding Ŧ Immediate
• Prelabor rupture of membranes • Previous adverse event
• Pregnancy after assisted reproductive technologies Ŧ 2 weeks before gestational age at which adverse
etal event occurred
• Decreased fetal movement • Insulin-dependent diabetes in pregnancy
• Fetal growth restriction Ŧ 34–36 weeks
• Oligohydramnios/polyhydramnios • Postdated pregnancy
• /WNVKRNGRTGIPCPE[
YKVJUKIPKſECPVITQYVJFKUETGRCPE[ Ŧ 40 weeks
• Preterm labor • Hypertension in pregnancy
Ŧ 32 weeks
• Fetal growth restriction
Ŧ At the time of diagnosis
Initiation of antepartum Ŧ For follow-up
re uency
fetal surveillance • Usually 1–2 times per week
Antepartum fetal surveillance is individual- • Twice weekly in high-risk pregnancies
• Every 24–48 hours in preterm cases where every day
ized and initiated depending on the severity
gained increases the chance of neonatal survival
of the risk factor or factors associated with the
CH 11_p148-162_v3.indd 149 17-07-2015 10:33:23

Fetal movement counting Evaluation of decreased fetal

movements
ationale
If the pregnant woman reports decreased fetal
A pregnant woman usually starts perceiving movements, the following evaluations are car-
fetal movements at approximately 20 weeks’ ried out:
gestation, although a multigravida may per-
ceive movements at an earlier gestational age • CTG
(Box 11.3). In the presence of fetal hypoxia – To record the fetal heart rate
and placental dysfunction, the fetus decreases – To perform an NST
gross body movements to conserve oxygen. The presence of accelerations (see below).
Decreased fetal movements may precede • Ultrasound evaluation
intrauterine fetal death. Early recognition of – To demonstrate fetal movements to the
decreased fetal movement makes it possible to mother
initiate interventions at a stage when the fetus – To assess amniotic fluid volume
is still compensated, and thus prevent progres- – To perform a BPP, if needed (see below)
sion to fetal death. The advantages and disadvantages of fetal
Fetal movement counting is an easy method movement count are listed in Box 11.5.
of fetal surveillance because most women
can be taught to recognize and note their
baby’s movements. Even healthy pregnant Box 11.5 Advantages and disadvantages of
women without risk factors for adverse peri- fetal movement count
natal outcomes should be educated about the
• Simple and inexpensive
significance of fetal movements in the third
• Approximately 20% of patients unable to comply
trimester and asked to perform a fetal move-
Ŧ Do not perceive movements reliably
ment count. Women should be instructed on • Only gross movements appreciated by mother
any one method of counting fetal movements • +PUWHſEKGPV GXKFGPEG VQ TGEQOOGPF HGVCN MKEM EQWPV
(Box 11.4) and advised to report decreased routinely to prevent fetal death
movements.
Box 11.3 Fetal movements

Cardiotocography
• (GNVſTUVCVCRRTQZKOCVGN[YGGMU Continuous recording of the fetal heart rate is
• Felt earlier by parous women called cardiotocography (CTG) or electronic fetal
• Decreased movements monitoring (EFM).
Ŧ Fetal hypoxia may be present The use of CTG (Fig. 11.1) involves the place-
Ŧ May precede intrauterine death ment of two transducers on the abdomen of the
woman. One transducer records the fetal heart
rate using ultrasound. The other transducer
(tocodynamometer) monitors the contractions
Box 11.4 Methods of counting fetal movements of the uterus. It does this by measuring the ten-
• Cardiff kick chart: Movements counted over 12 hours sion of the maternal abdominal wall during a
and noted on a chart contraction. This provides an indirect indication
Ŧ 10 movements or more in 12 hours: eassuring of intrauterine pressure (Box 11.6).
• Counting distinct movements while lying on the side
for 2 hours
Ŧ 10 movements or more in 2 hours: eassuring
External cardiotocography
• Counting movements for 1 hour every day External CTG is used for antepartum fetal sur-
Ŧ At least 4 movements within an hour: eassuring veillance and also during labor (intrapartum) to
• Counting movements for 1 hour 3 times/week monitor the fetal heart rate. An ultrasound trans-
Ŧ Equals or exceeds the woman’s previously estab-
ducer placed on the mother’s abdomen detects
lished baseline count: eassuring
the fetal heart rate. Jelly is applied between the
CH 11_p148-162_v3.indd 150 17-07-2015 10:33:23

rate than external monitoring because factors

such as movement do not affect it. Internal mon-
itoring may be used when external monitoring of
the fetal heart rate is inadequate, or closer sur-
veillance is needed. This will be further discussed
in Chapter 17, Intrapartum fetal surveillance.
&GſPKVKQPUCPFVGTOKPQNQI[WUGFKP
cardiotocography
Identification of normality versus abnormality of
a CTG trace is based on the following features:
• Baseline heart rate
• Baseline variability
Figure 11.1 A cardiotocograph. • Periodic changes
– Accelerations
– Decelerations
Box 11.6 Cardiotocograph (CTG) for continuous
monitoring of fetal heart rate (F ) aseline etal heart rate
• 2 Transducers Normal baseline fetal heart rate after 30 weeks’
Ŧ Ultrasound for FHR gestation is 110–160 bpm. A heart rate above
Ŧ Tocodynamometer for contractions
160 bpm is referred to as tachycardia, and a
• External CTG
heart rate below 110 bpm is referred to as bra-
Ŧ Jelly applied
Ŧ Transducer placed on maternal abdomen
dycardia. Baseline heart rate should be deter-
Ŧ FHR recorded on paper strip mined over a minimum period of 10 minutes.
• Internal CTG
Ŧ Used in labor aseline variability
Ŧ Scalp electrode Baseline variability is a function of the autonomic
Ŧ After cervical dilatation nervous system. The interval between consec-
Ŧ Membranes should be absent utive heartbeats is termed short-term variabil-
Ŧ Better recording obtained ity. This cannot be visualized on the usual CTG.
• Tocodynamometer Long-term variability refers to the oscillations
Ŧ Indirect recording of intrauterine pressure
above and below the baseline and can be seen
Ŧ Graphic recording on paper strip
on the trace. Normal long-term variability is
5–25 bpm. Variability of <5 bpm indicates fetal
transducer and the maternal skin to facilitate hypoxia, but it can also occur with certain drugs.
better apposition and conduction of the signal.
Acceleration
The transducer is placed at the point where the
fetal heart is best heard. This is done by moving Acceleration is defined as a rise in the fetal heart
the transducer over the abdomen till the best sig- rate above the baseline of 15 bpm that lasts for
nal is obtained. The fetal heart rate is recorded 15 seconds or more (after 32 weeks’ gestation).
on a strip of paper. This occurs in response to fetal movements,
scalp stimulation, and uterine contractions.
Accelerations are a sign of fetal well-being.
Internal cardiotocography
Internal CTG is used only during labor, after the Deceleration
membranes have ruptured. An electronic trans- Deceleration is a visually apparent gradual or
ducer is connected directly to the fetal scalp abrupt decrease in the fetal heart rate by >15
using an electrode called a spiral or scalp elec- bpm, lasting for t15 seconds but <2 minutes in
trode. Internal monitoring provides a more accu- duration. Decelerations may be early, late or
rate and consistent transmission of the fetal heart variable in relation to a contraction. They are
CH 11_p148-162_v3.indd 151 17-07-2015 10:33:23

indicative of fetal hypoxia, cord compression, or

vagal stimulation.
Baseline fetal heart rate, variability, and peri-
odic changes are discussed in detail in Chapter 17,
Intrapartum fetal surveillance.
onstress test
The NST is performed using an external CTG.
The fetal heart rate is recorded in the absence of
contractions. Accelerations of the fetal heart rate
are looked for.
ationale
Figure 11.2 Nonstress test. The mother is in a reclining
The heart rate of the healthy fetus will tempo- position. She is recording perceived movements with a
rarily accelerate with fetal movement. A fetus marker button. The graph is recording the fetal heart rate.
that is acidotic or neurologically depressed will
not show accelerations on CTG. The presence
Interpretation
of accelerations with movements is called reac-
tivity. Heart rate reactivity is considered a good An NST is interpreted as follows:
indicator of normal fetal autonomic function.
• Reactive (Fig. 11.3): Two or more fetal heart
Loss of reactivity is associated most commonly
rate accelerations reaching a peak of at least
with a fetal sleep cycle but may result from any
15 bpm above the baseline rate and lasting for
cause of central nervous system depression,
at least 15 seconds from onset to return in a
including fetal acidosis (Box 11.7).
20-minute period (Box 11.8). The duration of
Performing an ST
With the patient in the lateral recumbent or reclin-
ing position, the fetal heart rate is monitored with
the external transducer of a cardiotocograph. The
fetal movements are perceived by the mother and
recorded by the press of a button (Fig.11.2). The
fetal heart rate is recorded on a graph. The trace
should be recorded for at least 20 minutes.
Box 11.7 Fetal heart rate accelerations in the

nonstress test
• Rationale Figure 11.3 Reactive nonstress test showing
Ŧ Accelerations present with fetal movements accelerations. The waveform represents the fetal heart
(reactivity)
rate. The arrows point to the accelerations.
• Presence
Ŧ Well-oxygenated fetus
Ŧ 15 bpm above baseline
Box 11.8 eactive nonstress test
Ŧ Lasting for at least 15 seconds
• Absence • 2 or more acceleration
Ŧ Fetal sleep Ŧ Recorded over 20 minutes
Ŧ Narcotic medications to the mother Ŧ Up to 40 minutes if no accelerations
Ŧ Fetal hypoxemia • Peak at least 15 bpm above baseline
Ŧ Fetal acidosis • Lasting at least 15 seconds
CH 11_p148-162_v3.indd 152 17-07-2015 10:33:23

Box 11.10 Causes for nonreactive nonstress

test
• Associated with
Ŧ fetal immaturity
Ŧ quiet fetal sleep
Ŧ fetal hypoxemia or acidosis
Ŧ fetal neurological or cardiac anomalies
Ŧ fetal sepsis
Ŧ maternal ingestion of drugs with cardiac effects
1–2 seconds. Acceleration of the fetal heart rate

is looked for (Box 11.11). This can also be used to
reduce the duration of a nonreactive NST.
Figure 11.4 Nonreactive nonstress test showing no 1VJGTſPFKPIUQPCP056

accelerations. The upper waveform represents the fetal
heart rate. ra ycar ia
Significant bradycardia is associated with
the test should be extended to 40 minutes if
increased perinatal mortality and morbidity and
there are no accelerations.
has a higher positive predictive value than a non-
• Nonreactive (Fig. 11.4): A nonreactive NST is
reactive NST. In the presence of bradycardia, fur-
defined as one that does not show accelera-
ther evaluation by a BPP may be indicated.
tions over a 40-minute period. A nonreactive
test may indicate fetal hypoxemia or acidosis. achycar ia
Additional tests such as vibroacoustic stimula-
tion or a BPP may be needed to confirm that Preterm fetuses have a higher baseline fetal heart
the fetal condition is nonreassuring (Box 11.9). rate. In a term fetus, tachycardia may be due to
• Decelerations during an NST: Fetal heart rate maternal fever, fetal hypoxemia, or acidosis.
decelerations during an NST that persist for 1
minute or longer are significant and are asso-
oss o variability
ciated with an increased risk of both cesarean Loss of variability may occur with maternal
delivery and fetal demise. sedation. When loss of variability occurs along
with baseline tachycardia, it is indicative of fetal
A nonreactive NST may be due to fetal sleep acidosis and requires further evaluation.
or prematurity but may be indicative of fetal
hypoxia or sepsis (Box 11.10). Hence, a nonreac-
tive NST needs further evaluation.
Predictive value of an ST
The following points should be noted regarding
ibroacoustic stimulation test the predictive value of an NST:
Auditory stimulus to the fetus can alert a sleep- • An NST predicts the fetal status for the next
ing or inactive fetus. An acoustic stimulator is 72 hours; therefore, in high-risk pregnancies
applied on or just above the maternal abdomen. such as postmaturity, diabetes mellitus, or
A short burst of sound is delivered to the fetus for
Box 11.11 ibroacoustic stimulation test
• Auditory source placed on maternal abdomen
Box 11.9 onreactive nonstress test
• Short burst of sound delivered (1–2 seconds)
• No accelerations in 40 minutes • Rules out quiet fetal sleep
• May be repeated after feeding the mother • Accelerations
• 8KDTQCEQWUVKEQT$22TGSWKTGFVQEQPſTO Ŧ Healthy fetus
• Decelerations lasting tOKPWVGUKIPKſECPV • Absence of accelerations
Ŧ Fetal hypoxemia or acidosis
BPP DKQRJ[UKECNRTQſNG
CH 11_p148-162_v3.indd 153 17-07-2015 10:33:23

severe hypertension, the test should be per- decreased amniotic fluid (oligohydramnios) in a
formed twice a week. high-risk pregnancy. This can result in variable
• A reactive NST has a higher predictive value. decelerations (Fig. 11.5).
The false-negative rate is approximately
0.2%–0.8%. Performing a CST
• A nonreactive NST has a false-positive rate of
50%. This means that half the fetuses show- The patient lies in the lateral recumbent posi-
ing a nonreactive pattern may actually be well tion, and the fetal heart rate and uterine con-
oxygenated. Hence, fetuses with a nonreactive tractions are simultaneously recorded with an
NST should be evaluated further and manage- external fetal monitor. Contractions are induced
ment decisions should not be based on the with either nipple stimulation or intravenous
NST alone. administration of dilute oxytocin till there are at
• An NST cannot predict sudden events such as least three contractions of 40 seconds' duration
placental abruption or cord accidents. within 10 minutes (Box 11.12).
The criteria for interpretation of a CST are
given in Box 11.13.
Contraction stress test
Contraction stress test is performed using a car- Contraindications to CST
diotocograph. The fetal heart rate is recorded
in the presence of induced contractions. The CST-induced contractions can lead to compli-
response of the fetal heart rate is noted in rela- cations such as stimulation of regular uterine
tion to the contractions. contraction and rupture of membranes. Hence,
it is not commonly performed and is contraindi-
cated in the following situations:
ationale
During a uterine contraction, there is a tran-
Box 11.12 Contraction stress test
sient decrease in fetal oxygenation. If a fetus is
already hypoxemic, the intermittent worsen- • Lateral recumbent position
ing in oxygenation during a uterine contraction • Contractions induced
will result in late decelerations of the fetal heart Ŧ Nipple stimulation
rate (see Chapter 17, Intrapartum fetal surveil- Ŧ Intravenous oxytocin
• 3 contractions in 10 minutes
lance). Uterine contractions may also cause fetal
• Contractions recorded
umbilical cord compression in the presence of
• Decelerations recorded
ransient hypo emia Box 11.13 Interpretation of contraction stress

ith contraction test
• Positive (nonreassuring)
Ŧ Late decelerations following 50% or more contractions
• egative (reassuring)
Healthy compensate Ŧ 0QNCVGQTUKIPKſECPVXCTKCDNGFGEGNGTCVKQPU
Hypo emic fetus
fetus • Equivocal-suspicious
Ŧ Intermittent late decelerations or
Ŧ 5KIPKſECPVXCTKCDNGFGEGNGTCVKQPU
orsening in • Equivocal-hyperstimulatory
o ecelerations
o ygenation Ŧ Decelerations that occur in the presence of
hyperstimulation
Contractions >6 in 10 minutes
Contractions lasting >90 seconds
ecelerations • nsatisfactory
Ŧ Tracing is uninterpretable or
Ŧ Contractions <3 in 10 minutes
Figure 11.5 Rationale for contraction stress test.
CH 11_p148-162_v3.indd 154 17-07-2015 10:33:24

• Preterm labor or high risk of preterm labor easily applied, accurate means for predicting the
• Preterm rupture of membranes presence of significant fetal hypoxemia/acidosis.
• History of extensive uterine surgery or classical However, it may take 30–60 minutes to perform
cesarean delivery because the fetus might be in its normal sleep
• Known placenta previa cycle and time has to be given for it to be in a
wake cycle.
$KQRJ[UKECNRTQſNG
ationale
The BPP combines an NST with four biophysical
variables measured by ultrasonography — fetal Fetal biophysical activities such as body move-
movements, breathing, tone and amniotic fluid ments, breathing, fetal heart rate, and tone are
volume (Box 11.14). The BPP is a noninvasive, regulated and controlled by discrete centers
within the brain. The presence of these biophys-
ical variables implies normal oxygenation of the
Box 11.14 %QORQPGPVUQHCDKQRJ[UKECNRTQſNG fetal central nervous system. On the other hand,
fetal hypoxemia/acidosis causes loss of accelera-
• Nonstress test tions of the fetal heart rate, decreased body and
• Fetal breathing movements
breathing movements, and hypotonia. These
• Gross body movements
four variables reflect acute hypoxia. Decreased
• Fetal tone
• #OPKQVKEƀWKFXQNWOG amniotic fluid volume reflects chronic hypoxia
(Fig. 11.6).
iophysical acti ities

controlle by fetal brain centers
etal brain centers affecte by

egrees of hypo ia
cti ities absent or

cti ities present
iminishe
rain centers
Hypo ia
ell o ygenate
cute hypo ia Chronic hypo ia
etal heart rate

bo y mo ements mniotic flui olume
breathing an tone ecrease
affecte
Figure 11.6 RCVKQPCNGHQTHGVCNDKQRJ[UKECNRTQſNG
CH 11_p148-162_v3.indd 155 17-07-2015 10:33:24

Table 11.1 5EQTKPIQHDKQRJ[UKECNRTQſNG
ormal (Score 2) Abnormal (Score 0)
Nonstress test Reactive Nonreactive

Fetal breathing movements • ŮGRKUQFGUQHTJ[VJOKEHGVCN No fetal breathing movements in
breathing movements 30 minutes
• .CUVKPIŮUGEQPFU
• Within 30 minutes
Gross body movements • ŮFKUETGVGDQF[QTNKODOQXGOGPVU <3 movements in 30 minutes
• Within 30 minutes
Fetal tone • ŮGRKUQFGUQHGZVGPUKQPQHHGVCN No movements or slow movements
GZVTGOKV[YKVJTGVWTPVQƀGZKQP
or
• Opening or closing of a hand
#OPKQVKEƀWKFXQNWOG • Single vertical pocket of amniotic Largest single vertical pocket <2 cm
ƀWKF EO
Performing a BPP abnormal and immediate delivery should be

considered (Table 11.2).
An ultrasonographic examination is done, and
gross body movements, fetal breathing move- Measuring the amniotic
ments, and fetal tone are noted. The amniotic
fluid volume is also measured. An NST is per- ƀWKFXQNWOG
formed using a fetal monitor. Each variable The amniotic fluid volume is measured during
is given a score of 2 (normal) or 0 (abnormal, an ultrasound examination. The transducer
absent, or insufficient) using the criteria in must be kept perpendicular (at right angle) to the
Table 11.1. uterine contour. Two methods–single deepest
pocket and amniotic fluid index–are described
Interpretation of BPP to measure the volume.
A score of 8 or 10 is considered normal provided Single eepest poc et

the amniotic fluid is normal. If the score is 8
The vertical dimension of the largest pocket of
and amniotic fluid volume is abnormal, chronic
amniotic fluid not containing umbilical cord
hypoxia is likely and a repeat evaluation or deliv-
or fetal extremities is measured in centimeters
ery is indicated. A score of 4 or less is definitely
(Fig. 11.7). This is referred to as the single deep-
est pocket measurement (Box 11.15). This mea-
Table 11.2 Interpretation and management of surement is usually utilized as part of the BPP.
BPP score
BPP score Management

10/10 Low risk of developing fetal asphyxia
8/10, normal AFV Low risk of developing fetal asphyxia
8/10, low AFV • Consider chronic hypoxia
• Repeat test or deliver
6/10 • 5KIPKſECPVRQUUKDKNKV[QHFGXGNQR-
ing fetal asphyxia
• If AFV abnormal – deliver
• If AFV normal – repeat test and
consider delivery
4/10 High risk of fetal asphyxia within one
week – deliver
0 – 2/10 Certain fetal asphyxia – deliver
Figure 11.7 Measurement of single deep pocket. (Photo
A COPKQVKEƀWKFXQNWOG$22DKQRJ[UKECNRTQſNG courtesy: Mediscan Systems, Chennai.)
CH 11_p148-162_v3.indd 156 17-07-2015 10:33:24

Box 11.15 Single deepest pocket measurement

QHCOPKQVKEƀWKFXQNWOG
• Largest pocket
• Vertical measurement
• No cord or extremities
• 2CTVQHDKQRJ[UKECNRTQſNG
Box 11.16 Interpretation of single deepest

pocket measurements
• Oligohydramnios: Depth <2 cm
• 0QTOCN&GRVJŮCPFEO
• 2QN[J[FTCOPKQU&GRVJŮEO
Figure 11.9 Ultrasonographic measurement of the

COPKQVKEƀWKFKPFGZ6JGUKPINGFGGRGUVRQEMGVKPGCEJ
The interpretation of the single deepest pocket
quadrant is measured and added up. (Photo courtesy:
measurements is given in Box 11.16.
#OPKQVKEƀWKFKPFGZ
are added, and this gives the AFI expressed in
To measure the AFI, the uterus is divided into centimeters (Box 11.17).
four imaginary quadrants. The linea nigra is used This measurement is usually utilized as part
to divide the uterus into right and left halves. The of the modified BPP (mBPP; see below). The
umbilicus serves as the dividing point for the interpretation of the AFI measurements is given
upper and lower halves (Fig. 11.8). in Box 11.18.
The maximum vertical amniotic fluid pocket
diameter in each quadrant is measured in cen-
timeters (Fig. 11.9). Care is taken to see that the Predictive value and usefulness
pocket does not contain cord or fetal extremities. of BPP
The four measurements from all the quadrants The following points should be noted regarding
the predictive value and usefulness of a BPP:
• The false-negative rate of a BPP is low, and a
normal BPP correlates well with good outcome.
Box 11.17 #OPKQVKEƀWKFKPFGZ

• Abdomen divided into four quadrants
Ŧ Linea nigra to divide right and left quadrants
Ŧ Umbilicus to divide upper and lower quadrants
• /CZKOWOXGTVKECNFKCOGVGTQHCOPKQVKEƀWKF
Ŧ All four quadrants measured
Ŧ Cord and extremities avoided
Ŧ Measured in centimeters
Ŧ All four measurements added up
Box 11.18 +PVGTRTGVCVKQPQHCOPKQVKEƀWKFKPFGZ

Figure 11.8 /GCUWTGOGPVQHCOPKQVKEƀWKFKPFGZ6JG
• 1NKIQJ[FTCOPKQU#(+ŭEO
uterus is divided into four imaginary quadrants. The linea
• Normal: AFI >5 and <24 cm
nigra is used to divide the uterus into right and left halves.
• 2QN[J[FTCOPKQU#(+ŮEO
The umbilicus serves as the dividing point for the upper
and lower halves. A COPKQVKEƀWKFKPFGZ
CH 11_p148-162_v3.indd 157 17-07-2015 10:33:24

• The earliest manifestations of hypoxia are an

Box 11.20 +PVGTRTGVCVKQPQHVJGOQFKſGF
abnormal NST and loss of breathing movements. DKQRJ[UKECNRTQſNG
• A low BPP score has a high positive predictive
value, and an abnormal BPP of <4 correlates • Normal
Ŧ NST reactive
with fetal asphyxia.
Ŧ AFI, 5 or >5 cm
However, • Abnormal
Ŧ NST nonreactive
• Evidence shows no difference in outcome when Ŧ AFI <5 cm
a BPP is compared with doing an NST alone.
• The BPP is a time-consuming test. A COPKQVKEƀWKFKPFGZ S , nonstress test.
Therefore, the BPP is not a first-line fetal sur-

veillance test. Predictive value and usefulness
of mBPP
/QFKſGFDKQRJ[UKECNRTQſNG The following points should be noted regarding
the predictive value and usefulness of the mBPP:
A properly performed BPP may take 30–60 min-
utes to perform. To make it less time consum- • The false-negative rate of the mBPP is low.
ing, the modified biophysical profile (mBPP) was • The predictive value is as good as that of other
introduced. In the mBPP, just two variables are biophysical tests.
measured: AFI and NST. • The mBPP has been found to be an excellent
fetal surveillance tool.
ationale
Amniotic fluid volume will decrease in the pres- mbilical artery Doppler
ence of placental dysfunction. With decreased velocimetry
placental perfusion, there is reduced perfusion
of ‘nonessential’ organs such as the kidneys. Doppler ultrasonography is a noninvasive tech-
This results in decreased urine production and nique used to measure blood flow in the pla-
is reflected as oligohydramnios. Amniotic fluid centa and fetal umbilical artery. In the presence
volume assessment can therefore be used to of fetal growth restriction and/or preeclampsia,
evaluate long-standing or chronic hypoxia it helps differentiate the compensated healthy
(Box 11.19). Amniotic fluid volume is measured fetus from the hypoxemic/acidotic fetus. In
by the AFI. growth-restricted fetuses, antepartum assess-
The NST, on the other hand, is a short-term ment with this modality has been clearly shown
indicator of fetal hypoxemia/acidosis. It there- to decrease perinatal mortality.
fore assesses the presence of acute hypoxia.
The interpretation of the mBPP is given in ationale
Box 11.20.
A healthy, normally growing fetus will have a
high-velocity diastolic flow in the umbilical
artery. Under normal conditions, the placenta
Box 11.19 4
CVKQPCNGHQTOQFKſGFDKQRJ[UKECN offers little resistance to fetal and maternal blood
RTQſNG flow, even during maternal diastole. In certain
• Less time consuming than BPP conditions of abnormal placentation, blood flow
• Measures 2 components to the placenta may be reduced and accompa-
Ŧ #(+YJKEJTGƀGEVU nied by increased resistance to perfusion. This
Chronic hypoxia will be reflected in the umbilical artery diastolic
Ŧ NST, which indicates flow. Abnormal placentation may result in a
Acute hypoxia growth-restricted fetus. In this situation, there is
a decrease in the umbilical artery diastolic flow.
A COPKQVKE ƀWKF KPFGZ BPP DKQRJ[UKECN RTQſNG S
nonstress test. With severe growth restriction, as the placental
CH 11_p148-162_v3.indd 158 17-07-2015 10:33:24

Umbilical artery iastolic flo
bnormal placentation
ormal placentation
eg
o resistance to ncrease resistance to

bloo flo in placenta bloo flo in placenta
o resistance to bloo High resistance to bloo

flo in umbilical artery flo in umbilical artery
High elocity iastolic

ecrease iastolic flo
flo
bsent re erse
iastolic flo
Figure 11.10 %JCPIGUKPWODKNKECNCTVGT[FKCUVQNKEDNQQFƀQYYKVJPQTOCNCPFCDPQTOCNRNCEGPVCVKQP

, fetal growth restriction.
resistance increases, the diastolic flow can be • Reversed end-diastolic flow: Preterminal
absent or even reversed. This indicates severe event associated with poor perinatal outcome
hypoxia and acidosis (Fig. 11.10). (Fig. 11.12). Immediate delivery is warranted.
7ODKNKECNCTVGT[ƀQYKPFKEGU Doppler velocimetry of other

Peak systolic and end-diastolic blood flow in the fetal vessels
fetal umbilical artery is measured and various In addition to the umbilical artery, Doppler veloci-
indices are calculated (see Chapter 10, Obstetric metry can be performed on other vessels and this
ultrasound and other imaging). As the diastolic contributes to the information on fetal status.
flow decreases, the indices rise. Therefore, high
indices indicate increased resistance to blood flow.
he application o Doppler in obstetric

ecision ma ing
Umbilical artery Doppler velocimetry helps in
deciding the time of delivery in the presence of
fetal growth restriction.
• Normal indices: Continue to observe with
weekly Doppler studies, NST, and AFI.
• Absent end-diastolic flow: Ominous find- Figure 11.11 #DUGPVGPFFKCUVQNKEƀQYKPVJGHGVCN
ing with increased risk of perinatal mortality umbilical artery. The arrows point to the absence of
(Fig. 11.11). Immediate delivery should be FKCUVQNKEƀQYHQNNQYKPIVJGU[UVQNKERGCM
Photo courtesy:
considered if beyond 34 weeks’ gestation. Mediscan Systems, Chennai.)
CH 11_p148-162_v3.indd 159 17-07-2015 10:33:25

Predictive value and usefulness of

Doppler velocimetry
The usefulness of different Doppler studies in
fetal surveillance is summarized in Box 11.22.
Sequential changes in the

presence of hypoxia
Figure 11.12 4GXGTUGFGPFFKCUVQNKEƀQYKPVJGHGVCN Changes in fetal heart rate (nonreactive NST)
WODKNKECNCTVGT[6JGCTTQYURQKPVVQFKCUVQNKEƀQYUGGP
are often the earliest signs of fetal compromise
below the baseline (reversal). (Photo courtesy: Mediscan
(Fig. 11.13). Sequential changes in the fetal MCA
Systems, Chennai.)
and umbilical artery are detectable next. This is
followed by abnormalities in biophysical param-
i le cerebral artery eters such as fetal breathing movements, fetal
When there is fetal hypoxia, there is preferential body movements, and fetal tone. These changes,
blood flow to preserve ‘essential’ organs such as however, do not always follow this sequence.
the brain. Increased diastolic flow in the fetal Some fetuses who exhibit the full range of these
MCA indicates that the blood is being shunted findings may still not exhibit significant meta-
preferentially to the brain. This is termed the bolic acidosis at birth.
brain-sparing effect (Box 11.21). This is an early
sign of fetal hypoxia.
onreacti e nonstress test
Box 11.21 Middle cerebral artery Doppler

• In the presence of fetal hypoxia
Ŧ +PETGCUGFƀQYVQDTCKP a
Ŧ 4GƀGEVUCUKPETGCUGFFKCUVQNKEƀQY MC rain sparing effect
Ŧ ‘Brain-sparing’ effect U ecrease absent
Ŧ Early sign of hypoxia re erse en iastolic flo
V bnormal flo
&WEVWUXGPQUWU
Changes in the waveform pattern of the fetal a
ductus venosus occur late in hypoxia and indi- ecrease fetal breathing
cate cardiac decompensation. This indicates a mo ement gross bo y
poor prognosis. mo ements fetal tone
Box 11.22 Predictive value of Doppler velocimetry Figure 11.13 5GSWGPVKCNEJCPIGUKPHGVCNDNQQFƀQYCPF

in antepartum fetal surveillance biophysical parameters in the presence of worsening hypoxia.
$22DKQRJ[UKECNRTQſNG&8FWEVWUXGPQUWU/%#OKFFNG
• Umbilical artery Doppler
EGTGDTCNCTVGT[7#WODNKECNCTVGT[
Ŧ Useful for fetal surveillance
Ŧ Reduces the perinatal mortality in growth restricted
fetuses
Ŧ 0QDGPGſVKPFKCDGVGUQTRQUVFCVGFRTGIPCPE[ Management of pregnan-
Ŧ Used to decide on timing of delivery when
BPP is abnormal or, cies with nonreassuring
AFV is low
• Middle cerebral artery Doppler
antepartum testing
Ŧ Useful as an adjunct to umbilical artery Doppler Management of the fetus with nonreassuring
• Ductus venosus Doppler
antepartum surveillance results depends on
Ŧ Good but late predictor of poor perinatal outcome
the clinical condition and the availability of
A COPKQVKEƀWKFXQNWOGBPP DKQRJ[UKECNRTQſNG clinical services. After 36–37 weeks’ gestational
CH 11_p148-162_v3.indd 160 17-07-2015 10:33:25

age, immediate delivery might be indicated or reversed end-diastolic flow in the umbilical
to prevent further morbidity from worsening artery is an indication of perinatal morbidity
hypoxemia/acidosis. and mortality. In pregnancies complicated by
Repetitive late decelerations or severe vari- fetal growth restriction, absent or reversed end-
able decelerations on an NST or CST generally diastolic flow mandate immediate delivery if >34
mandate immediate delivery. Doppler velocim- weeks’ gestation. Management in the presence
etry indices must be used in conjunction with of prematurity has to be tailored to the individ-
other tests such as NST, AFI, and BPP. Absent ual pregnancy, to optimize fetal outcome.
Key points
• The aim of antepartum fetal surveillance is to prevent • A nonreactive NST does not show accelerations over
fetal demise. a 40-minute period.
• Antepartum fetal surveillance techniques are useful • In a contraction stress test (CST), the fetal heart rate
in assessing the risk of fetal death in pregnancies is recorded in the presence of induced contractions.
complicated by preexisting maternal conditions as well
• In a CST, late or variable decelerations indicate fetal
as those in which complications have developed.
hypoxia.
• Indications may include conditions that occurred in the • #DKQRJ[UKECNRTQſNG
$22KPENWFGUCP056CPF
previous pregnancy or maternal or fetal conditions that assessment of gross body movements, fetal breathing
have developed in the current pregnancy. OQXGOGPVHGVCNVQPGCPFCOPKQVKEƀWKFXQNWOG
• Decreased fetal movements may precede intrauter-
• 6JGOQFKſGF$22KPENWFGUQPN[056CPFCOPKQVKE
ine fetal death. Fetal movement counting is an easy
ƀWKFKPFGZ
method of fetal surveillance but has not been shown to
decrease stillbirth rates. • Fetal umbilical artery Doppler velocimetry is very
useful in assessing the growth-restricted fetus and
• The nonstress test (NST) looks for the presence of determining the timing of delivery.
accelerations of the fetal heart wrate.
• Middle cerebral artery Doppler is useful in assess-
• A reactive NST shows two or more fetal heart rate
ing the brain-sparing effect in the presence of fetal
accelerations reaching a peak of at least 15 bpm above
hypoxia.
the baseline rate and lasting for at least 15 seconds
from onset to return in a 20-minute period.
Self-Assessment
Case-based questions 1. 9JCVKUVJGſTUVVGUVVJCVUJQWNFDGRGTHQTOGFHQTHGVCN
well-being?
Case 1 2. What should be done in the presence of a nonreactive
NST?
#[GCTQNFYQOCPYCURTGIPCPVHQTVJGſTUVVKOGCHVGT 3. What is vibroacoustic testing?
8 years of marriage. She was found to have high blood 4. 9JCVCTGVJGEQORQPGPVUQHCDKQRJ[UKECNRTQſNG!
pressure in the 28th week of pregnancy. At 32 weeks the
fetus was found to be smaller than expected (fetal growth
restriction). Answers
1. When should fetal surveillance be started?
2. What is a reactive nonstress test? Case 1
3. What are the two methods of measuring the amniotic 1. Fetal surveillance should be started immediately on
ƀWKFXQNWOG! the diagnosis of fetal growth restriction.
4. Will Doppler studies be useful in a case of fetal 2. A reactive NST shows two or more fetal heart rate
growth restriction? accelerations reaching a peak of at least 15 bpm
above the baseline rate and lasting for at least 15 sec-
Case 2 onds from onset to return in a 20-minute period.
3. Single deepest pocket and measurement of
A 26-year-old gravida 2, para 1 developed hypertension VJGCOPKQVKEƀWKFKPFGZCTGVJGVYQOGVJQFUQH
at 34 weeks. She was admitted at 37 weeks with the com- OGCUWTKPICOPKQVKEƀWKFXQNWOG
plaint of decreased fetal movements.
CH 11_p148-162_v3.indd 161 17-07-2015 10:33:25

4. Fetal umbilical artery Doppler velocimetry is very 4. #DKQRJ[UKECNRTQſNGKPENWFGUCP056CPFCUUGUU-

useful in assessing the growth-restricted fetus, ment of gross body movements, fetal breathing
determining the timing of delivery, and improving OQXGOGPVHGVCNVQPGCPFCOPKQVKEƀWKFXQNWOG
perinatal outcome.
Sample questions
Case 2
1. In the presence of decreased fetal movements, an Long-answer question
056KUVJGſTUVVGUVVQDGRGTHQTOGF What is antepartum fetal surveillance? What are the
2. A nonreactive NST has a false-positive rate of 50%. indications and tests performed?
Therefore, a fetus with a nonreactive NST should be
evaluated further with a BPP or mBPP.
3. Vibroacoustic testing uses a short burst of sound for
1–2 seconds. It results in accelerations in a healthy Short-answer questions
fetus and rules out a nonreactive test due to quiet 1. Nonreactive nonstress test
fetal sleep. 2. Contraction stress test
3. /QFKſGFDKQRJ[UKECNVGUVKPI
4. #DUGPVCPFTGXGTUGFGPFFKCUVQNKEWODKNKECNCTVGT[ƀQY
CH 11_p148-162_v3.indd 162 17-07-2015 10:33:25

Prenatal Screening,
12 Prenatal Diagnosis,
and Fetal Therapy
Case scenario
Mrs. AM, 36, married for 6 months, was 10 weeks pregnant. She was con-
cerned that her baby might be abnormal because of her age. She had
heard of Down syndrome affecting children of older mothers. She wanted
screening for chromosomal abnormalities.
Introduction Prenatal screening

In the past few decades, there has been bet-
ter understanding of the genetic basis of a large Prenatal testing may be broadly divided into
number of fetal diseases. Screening and diagnos- screening tests and diagnostic tests.
tic techniques have been developed that make it Screening is the process of testing a population
possible to diagnose abnormalities early. Early that is apparently healthy, using a specific marker
diagnosis enables obstetricians and perinatolo- or markers, to detect a particular condition.
gists to offer counseling regarding continuation of Screening tests do not specify whether an indi-
pregnancy or termination, and decide on timing vidual is affected. They help divide the screened
and place of delivery. It also allows for a discus- population into high- and low-risk groups for the
sion of postnatal intervention, including surgery. condition in question, using a predefined cutoff.
Fetal imaging may reveal abnormalities that The high-risk group is then offered a diagnostic
could not have been treated even a decade or two procedure.
ago. Advances in technology have provided the Prenatal screening tests are used most com-
ability to offer fetal therapy. Instead of resorting monly to screen for chromosomal abnormalities,
to termination of pregnancy, active intervention especially aneuploidy. Aneuploidy refers to chro-
is instituted to improve the long-term outcome mosomal mutations where the chromosomal
of the fetus. number is abnormal. The number could be less
CH 12_p163-178_v3.indd 163 17-07-2015 10:38:39

than or more than the normal chromosomal means that if 100 women have this test result, the
number. In humans, each cell normally con- chances are that 1 of these women would have
tains 23 pairs of chromosomes, for a total of 46. a baby with Down syndrome and that 99 would
Twenty-two of these pairs are called autosomes. not. In other words, the baby has a 1% chance of
The 23rd pair comprises the sex chromosomes. having Down syndrome and a 99% chance of not
Aneuploidy can present as a trisomy, trip- having the syndrome.
loidy, or monosomy (Box 12.1). Approximately The results of the screening tests are expressed
90% of these involve chromosome 21, 18, 13, as high risk, intermediate risk, and low risk
X, or Y. One of the major objectives of prenatal depending on whether the risk result is above or
screening programs is the antepartum detection below an arbitrary cutoff point of 1 in 250. This
of fetal aneuploidy. helps in deciding whether further invasive tests
Of the aneuploidies, Down syndrome (trisomy are required to confirm or rule out trisomy.
21) is the most common chromosome abnormal- Screening is applied to a population, whereas
ity and the most frequent cause of mental disabil- diagnosis is applied at the individual patient
ity in humans. The syndrome is characterized by level. For example, screening for Down syn-
moderate-to-severe learning disability and low drome can be offered to all pregnant women.
IQ, in combination with short stature, charac- When a woman’s screening test places her in a
teristic facial features, heart defects, intestinal high-risk group, a diagnostic test is done to con-
malformations, and problems with vision and firm or rule out fetal Down syndrome. Terms
hearing. Prenatal screening programs were first commonly used in screening programs are listed
introduced to detect Down syndrome. in Table 12.1.
Down syndrome is caused by the presence
of an extra copy of chromosome 21, as a free
chromosome, a Robertsonian translocation, or a
Who should be screened
reciprocal translocation involving chromosome All women should be offered screening for aneu-
21. Approximately 95% of cases result from spo- ploidy, regardless of age. In developing coun-
radic nondisjunction during parental meiosis. tries, screening tests may not be accessible to
Chromosomal abnormalities result in a high
rate of fetal loss. Due to this, chromosomal abnor-
malities are more commonly detected in the first Table 12.1 Common terms used in screening for
aneuploidies
and second trimesters than in live-born infants.
Term in aneuploidy
screening Explanation
Calculation of risk
Screen-positive The group that has been identi-
A risk is the chance of an event occurring. For ſGFCUDGKPICVhigh risk for
example, the risk of Down syndrome of 1 in 100 aneuploidy
Screen-negative The group that has been identi-
ſGFCUDGKPICVlow risk for
aneuploidy
Box 12.1 Aneuploidies
Sensitivity/detection The effectiveness of screening is
• Aneuploidy rate measured by the sensitivity of
Ŧ More chromosomes (trisomy, triploidy) the test used. The proportion
Trisomies 21,18, and 13 of affected cases that are
XXY (Klinefelter syndrome) KFGPVKſGFCUUETGGPRQUKVKXG
Triploidy (69 chromosomes) by the test determines its
sensitivity
Ŧ Less chromosomes (monosomy)
XO (Turner syndrome) False-positive rate The group that has been identi-
ſGFCUDGKPICVJKIJTKUM
• Most common aneuploidy
but does not actually have
Ŧ Down syndrome (trisomy 21)
aneuploidy
Extra copy of chromosome 21
Positive predictive The proportion of people with
- Robertsonian translocation
value screen-positive results in
- Reciprocal translocation whom fetal aneuploidy is
Due to nondisjunction EQPſTOGF
CH 12_p163-178_v3.indd 164 17-07-2015 10:38:39

Prenatal Screening, Prenatal Diagnosis, and Fetal Therapy 165
everyone. However, screening should be offered

Box 12.2 Maternal age alone as screening test
where facilities are available. Many centers in
India are now offering screening for aneuploidy. • *KIJTKUMYKVJCIG [GCTU
Ŧ +PETGCUGKPTKUMEQPVKPWQWUYKVJKPETGCUGKPCIG
• Aged oocytes
Counseling before screening Ŧ +PETGCUGFTKUMQHPQPFKULWPEVKQP
• Reason for not using maternal age alone
All couples who are being offered screening for Ŧ 70% of Down babies born to women <age 35
aneuploidy should be counseled about why
the test is being done, and should be helped to
understand the interpretation of the results. Table 12.2. As seen in the Table, the risk of Down
They should also be aware about the follow-up syndrome is continuous with increasing age,
of a positive result. with no significant change at age 35.
However, maternal age is taken into consider-
Maternal age as a screening ation while calculating the background risk and
likelihood ratios for the final risk of aneuploidy.
test These likelihood ratios are derived based on
The risk of chromosomal problems, such as triso- population-based statistics and may differ from
mies, varies with the age of the mother. In an older one population to another.
mother, the oocyte has aged along with her and
is prone to nondisjunction errors in the meiotic
division, thereby increasing her chances of hav-
ing a baby with aneuploidy. Therefore, the risk of
Screening tests for fetal
trisomies 21, 18, and 13 increases with maternal aneuploidy
age. However, the risk of triploidy and Turner syn-
drome (XO) does not vary with maternal age. Maternal age, maternal serum markers, and
Because the risk of Down syndrome is higher sonographic findings are all considered in
in older women, initially maternal age over 35 screening for aneuploidy.
years was used as a cutoff for offering testing. Screening tests for aneuploidy (specifically
However, nearly 70% of Down syndrome babies for Down syndrome, trisomy 18 and trisomy 13)
are born to mothers who are younger than 35 are listed in Box 12.3.
years. Therefore, maternal age is not recom-
mended in isolation as an indication for further
invasive testing (Box 12.2).
Maternal serum screening
The risk of having a baby with Down syn- In the 1980s, serum screening for neural tube
drome with increasing maternal age is given in defects was introduced. At that time it was
Table 12.2 isk of Down syndrome (DS) in the fetus in relation to maternal age (MA) at estimated date of
delivery (EDD)
MA at EDD isk of DS MA at EDD isk of DS MA at EDD isk of DS

20 1:1450 30 1:940 40 1:85
21 1:1450 31 1:820 41 1:70
22 1:1450 32 1:700 42 1:55
23 1:1400 33 1:570 43 1:45
24 1:1400 34 1:460 44 1:40
25 1:1350 35 1:350 45 1:35
26 1:1350 36 1:270 46 1:30
27 1:1200 37 1:200 47 1:30
28 1:1150 38 1:150 48 1:30
29 1:1050 39 1:110 49 1:25
CH 12_p163-178_v3.indd 165 17-07-2015 10:38:39

Box 12.3 Screening tests for fetal aneuploidy Table 12.3 Changes in levels of serum markers in
the common trisomies
• First trimester combined test
• Second trimester testing Trisomy 21 Trisomy 18 Trisomy 13
Ŧ Triple test
irst trimester
Ŧ Quadruple test
• Integrated test PAPP-A Decreased Decreased Decreased
• Sequential testing EhCG Increased Decreased Decreased
• Contingent testing Secon trimester
• Genetic sonogram AFP Decreased Decreased Decreased
• Noninvasive prenatal screening (cell-free DNA) in mater- hCG Increased Decreased Decreased
nal blood uE3 Decreased Decreased Decreased
Inhibin A Increased Decreased Increased
noticed that serum levels of a few analytes were at A P alpha fetoprotein; hC human chorionic gonadotropin;
different levels in mothers carrying fetuses with PAPP-A pregnancy-associated plasma protein A; u unconju-
gated estriol.
Down syndrome when compared with those in
the rest of the population. These differences are
now used to screen for Down syndrome, trisomy
as seen on ultrasound in the first trimester (see
18 and trisomy 13.
Chapter 10, Obstetric ultrasound and other imag-
The analytes used for screening for Down syn-
ing). The term, increased nuchal translucency
drome, trisomy 18, and trisomy 13 include the
(NT) was introduced in 1992. This has become
following:
an integral and essential component of screen-
• First trimester ing for Down syndrome in the first trimester
– E human chorionic gonadotropin (E hCG) (Fig. 12.1). NT is also expressed in MoMs and
– Pregnancy-associated plasma protein A uses maternal age–related risk as the back-
(PAPP-A) ground risk for calculation.
• Second trimester Other ultrasound markers for Down syn-
– Unconjugated estriol (uE3) drome in the first trimester include the following:
– Alpha fetoprotein (AFP)
• Absent nasal bone
– E hCG
• Increased impedance to flow in the ductus
– Inhibin A
venosus
The concentration of each serum marker is • Tricuspid regurgitation
expressed as a multiple of the median (MoM) for
unaffected pregnancies of the same gestational
age. The serum marker is plotted on a graph, and
whether it is higher or lower than the MoM of an
unaffected pregnancy is calculated.
In the first trimester, the level of EhCG is ele-
vated and that of PAPP-A is decreased in Down
syndrome, but both are decreased in trisomy 18
and trisomy 13. In the second trimester, while
AFP, uE3, and PAPP-A are lower, levels of EhCG
and inhibin A are higher in women whose fetuses
have Down syndrome (Table 12.3).
Maternal serum screening may be carried out
in isolation but usually is combined with ultra-
sound estimation of nuchal translucency.
ltrasound markers
Figure 12.1 Ultrasound image of nuchal translucency. The
Fetuses affected by Down syndrome and other CTTQYRQKPVUVQVJGCPGEJQKECTGCDGJKPFVJGHGVCNPGEM
trisomies have increased fluid behind the neck (Photo courtesy: Mediscan Systems, Chennai.)
CH 12_p163-178_v3.indd 166 17-07-2015 10:38:39

These require higher expertise to image and

Box 12.5 #FXCPVCIGUQHſTUVVTKOGUVGTUETGGPKPI
so NT continues to be the most important ultra-
sound marker for Down syndrome. • 'CTN[TKUMRTGFKEVKQP
Using the serum and ultrasound markers, the • 1RRQTVWPKV[HQTGCTN[FGEKUKQPOCMKPI
• +PETGCUGF06KUCOCTMGTHQT
detection rate of Down syndrome in the first tri-
Ŧ Trisomies
mester is 90%–95% (Box 12.4).
Ŧ Major cardiac defects
Ŧ Diaphragmatic hernia
First trimester combined test Ŧ Renal anomalies
Ŧ $QF[UVCNMFKUTWRVKQP
The first trimester combined test includes serum Ŧ Abdominal wall defects
testing for free E hCG and PAPP-A and ultra- • Decreased PAPP-A/increased EhCG predicts
sound measurement of the NT. It is done at Ŧ 7VGTQRNCEGPVCNKPUWHſEKGPE[
11–13+6 weeks. This test should be offered to all Ŧ Preeclampsia
women to screen for Down syndrome. The risk
E C , human chorionic gonadotropin; , nuchal translucency;
for trisomy 18 and trisomy 13 can also be pre- PAPP-A, pregnancy-associated plasma protein A.
dicted with this test.
Serum markers invasive testing, the pregnancy needs to be care-

As mentioned earlier, several factors influence fully monitored with serial ultrasound scans.
the serum levels and once these are factored in, Decreased PAPP-A or increased EhCG is also a
the built-in software generates a screening risk predictor of uteroplacental dysfunction and can
based on the serum levels of the analytes and NT. be used for screening for preeclampsia.
In twin pregnancies, a first trimester com-
bined screening test is the best screen for Down
#FXCPVCIGUQHſTUVVTKOGUVGT syndrome and trisomy18.
combined screening
First trimester combined screening enables early Second trimester testing
risk prediction in pregnancy, so decisions can be
taken earlier (Box 12.5). Invasive diagnostic tests Serum markers
can be offered early and the couple can make
Second trimester maternal serum screening is
decisions about further management.
best offered between 15 and 20 weeks’ gestation
Increased NT is not only a marker for triso-
and involves the analysis of three analytes (triple
mies but also a marker for major cardiac defects,
test)or four analytes (quadruple test) (Box 12.6).
diaphragmatic hernia, renal anomalies, body
stalk disruption, and abdominal wall defects.
Box 12.6 Second trimester screening for aneu-
Therefore, when the NT is increased and the
ploidy (Down syndrome, trisomy 18,
fetus is proved to have normal chromosomes by trisomy 13)
• &QPGDGVYGGPCPFYGGMU
• Serum biochemistry
Box 12.4 First trimester screening for aneuploidy
Ŧ Triple test
• 11–13+6YGGMU AFP
• 5GTWOOCTMGTU uE3
Ŧ E human chorionic gonadotropin (EhCG) hCG
Ŧ Pregnancy-associated plasma protein A (PAPP-A) Ŧ Quadruple test
• Ultrasound Above 3 + inhibin A
Ŧ Nuchal translucency (most important) Ŧ AFP and uE3
Ŧ Nasal bone Both decreased in Down syndrome
Ŧ &WEVWUXGPQUWUƀQY Ŧ hCG and inhibin A
Ŧ Tricuspid regurgitation Both doubled in Down syndrome
• 90%–95% detection rate
• Can be used in twin pregnancy A P alpha fetoprotein; hC human chorionic gonadotropin;
u unconjugated estriol.
CH 12_p163-178_v3.indd 167 17-07-2015 10:38:39

The serum markers used for the second tri- abnormality, whereas if two or more minor mark-
mester triple test are as follows: ers are identified, the risk of trisomy increases.
Markers associated with certain chromo-
• Triple test
somal abnormalities are listed in Table 12.4.
– AFP
– uE3
– EhCG Integrated test
• Quadruple test
Integrated screening test is a two-step screen-
– The above 3 + inhibin A
ing process and requires measurement of serum
The levels of the analytes are interpreted as markers in both the first and second trimes-
MoMs from the unaffected population and a risk ters. Ultrasound may or may not be included.
algorithm is created. Although the detection rate is high, the woman
The levels in vitro of these serum markers are has to wait till the second trimester to know her
affected by various factors that need to be taken risk estimate.
into consideration before allocating the preg- The full integrated test consists of ultrasound
nancy into a high-risk or a low-risk category. measurement of NT at 11–13+6 weeks, PAPP-A
These factors are as follows: obtained at 10–13 weeks, and AFP, uE3, E hCG,
and inhibin A obtained at 15–18 weeks. The inte-
• Maternal weight
grated test has detection rates of 85% or 95% and
• Maternal diabetes
the lowest false-positive rate among Down syn-
• Number of fetuses
drome screening tests.
• In vitro fertilization
• Smoking
Sequential screening
ltrasound markers The stepwise sequential screening process
involves performing the first trimester portion
There are both major and minor markers for
aneuploidy in the second trimester scan.
Major markers for aneuploidies include the Table 12.4 Markers associated with aneuploidies
following:
Chromosome Markers
• Increased nuchal fold thickening abnormality
• Exomphalos (aneuploidy)
• Duodenal atresia Trisomy 21 (Down Increased nuchal translucency,
• Atrioventricular septal defects syndrome) absent nasal bone, cardiac
defects (especially atrioventric-
When major markers for aneuploidy are iden- ular canal defects), echogenic
tified, they should prompt further workup and/ bowel, short femur/humerus,
or correlation with laboratory data and risk fac- renal pelviectasis, and sandal
tors. They are an indication for a diagnostic test gap deformity of the feet
for karyotyping. Turner syndrome Cystic hygromas and coarctation
(45, XO) of the aorta; pleural effusion,
Minor markers for aneuploidies include the ascites, and cardiac defects (in
following: lethal type)
• Choroid plexus cysts Trisomy 18 Choroid plexus cyst, overlapping
(Edwards ſPIGTUCDPQTOCNEQTRWUECNNQ-
• Echogenic foci in the fetal heart syndrome) sum, strawberry-shaped head,
• Mild hydronephrosis micrognathia, omphalocele,
• Echogenic bowel diaphragmatic hernia, clenched
• Short femur hands, radial ray anomalies,
ENWDHGGVCPFTQEMGTDQVVQOHGGV
Minor markers (or soft markers) do not carry Trisomy 13 (Patau Polydactyly, microcephaly, holo-
the implications that a major marker does. In syndrome) prosencephaly, cleft lip/palate,
general, an isolated minor marker does not ocular anomalies, neural tube
appear to carry a significant risk for chromosomal defects, and cardiac defects
CH 12_p163-178_v3.indd 168 17-07-2015 10:38:40

of the integrated screen and then offering coun- and expensive. Recently, massively parallel
seling and chorionic villus sampling (CVS) to genomic sequencing or chromosome selective
women who are reported as being very high sequencing allows accurate detection of trisomy
risk (e.g., t1 in 50) of having an affected fetus. 13, trisomy 18 and trisomy 21. The test can be
Those women who are at low or moderate risk done as early as the 10th week of pregnancy and
do not have their results disclosed to them and the result may be available in 1 week. Detection
undergo a subsequent second trimester serum rates for fetal trisomy 13, trisomy 18, and trisomy
screening. An integrated risk of screen-positive 21 are greater than 98% with false-positive rates
or screen-negative is given. <0.5%. Cell-free fetal DNA appears to be the most
effective screening test for aneuploidy in high
risk women.
Contingent sequential Noninvasive prenatal testing should be
screening offered to only patients at high risk of aneu-
ploidy. Factors that make the pregnancy high
In contingent sequential screening, three groups
risk are listed in Box 12.7.
are identified based on risk: (a) women identified
It is recommended that these assays only be
as being at very high risk (e.g., >1 in 50) of having
used as screening tests. A positive result requires
a fetus with Down syndrome after first trimester
confirmation with invasive prenatal diagnosis.
testing are offered immediate invasive prena-
tal diagnosis, (b) women at low risk (e.g., <1 in
2000) after first trimester testing are provided
with their risk estimate and will not undergo any
additional testing, and (c) women at intermedi-
Management of
ate risk (between 1 in 50 and 1 in 2000) will have the screen-positive
a second trimester blood screening to complete
the integrated test. pregnancy
A screen-positive result provokes anxiety in the
Genetic sonogram couple. Detailed counseling and explanation of
the results are important (Fig. 12.2).
Ultrasound markers, both minor and major A screen-positive result does not mean that
(Table 12.4), are assessed at 18–20 weeks’ ges- the fetus is affected. However, a screen-positive
tation to modify the age-related risk for Down test requires follow-up with an invasive test for
syndrome. karyotyping to confirm or rule out aneuploidy.
Based on the gestational age, CVS or amniocen-
oninvasive prenatal testing in tesis should be offered (see below).
Even with a normal karyotype, fetuses with
maternal blood significantly increased NT are at risk for congen-
Noninvasive prenatal testing (NIPT) for aneu- ital anomalies. However, fetuses with increased
ploidy using cell-free DNA(cf DNA) in the mater- NT and normal karyotype that have a normal
nal blood has been available for clinical use since scan at 18–20 weeks have <5% chance of an
2011. It is an expensive test and is not available adverse outcome in the postnatal or late antena-
freely in developing countries. tal period.
Fetal cell-free nucleic acids (cfDNA and
cfRNA) not contained within cell membranes are
abundant in the maternal circulation. Screening Box 12.7 isk factors for which noninvasive
using cfDNA can identify common autosomal prenatal testing should be offered
trisomies (chromosomes 21, 18, and 13), as well • /CVGTPCNCIGŮ[GCTUCVFGNKXGT[
as select sex chromosome aneuploidies (45X, • (GVCNUQPQITCRJ[KPFKECVKPICPKPETGCUGFTKUMQHCPGW-
47XXY, 47XYY, 47XXX). ploidy
Initially, detecting trisomies using fetal cfDNA • A previous pregnancy with fetal trisomy
• Parental balanced Robertsonian translocation with
required the use of multiple placental DNA or
KPETGCUGFTKUMQHHGVCNVTKUQO[QTVTKUQO[
RNA markers, making the test time-consuming
CH 12_p163-178_v3.indd 169 17-07-2015 10:38:40

creening for aneuploi y
creen negati e creen positi e
enetic counseling
outine prenatal care CV or amniocentesis
aryotyping
bnormal ormal
ollo up ith serial

scans for
enetic counseling
congenital anomalies
fetal gro th restriction
Figure 12.2 Counseling and management of the screen-positive pregnancy. C S, chorionic villus sampling.
Pregnancies with a low PAPP-A value are

Box 12.8 Indications for prenatal diagnostic tests
at increased risk for small-for-gestational-age
(SGA) fetuses and therefore should be monitored • Positive screening test for chromosomal anomaly
for fetal growth. • Past/family history of previous child with
Ŧ congenital malformation
Ŧ chromosomal anomaly
Ŧ inherited disorder
• %QWRNGMPQYPECTTKGTQHEJTQOQUQOCNVTCPUNQECVKQP
Prenatal diagnosis • 5WURGEVGFQTEQPſTOGFXKTCNKPHGEVKQPUFWTKPI
pregnancy
Prenatal diagnosis focuses on detection of • Maternal exposure to teratogenic drugs
abnormalities in the fetus in pregnancies sus- • Maternal diabetes
pected to be at high risk for congenital or chro- • Polyhydramnios
mosomal abnormalities. • Early onset fetal growth restriction
Indications
Indications for performing prenatal diagnostic
tests are listed in Box 12.8.
oninvasive tests
Ultrasonography is the most commonly used
test for prenatal diagnosis. Noninvasive prenatal
Tests for prenatal diagnosis diagnostic tests are listed in Box 12.9.
Both noninvasive and invasive techniques are These tests are described in Chapter 10,
used for prenatal diagnosis. Obstetric ultrasound and other imaging.
CH 12_p163-178_v3.indd 170 17-07-2015 10:38:40

amniocentesis are performed to obtain samples

Box 12.9 oninvasive prenatal diagnostic tests
for karyotyping.
• Ultrasonography
Ŧ Three-dimensional (3D) ultrasonography Single gene e ects
Ŧ Fetal echocardiography
• MRI Hemoglobinopathies, sickle cell disease, thal-
• Plain radiography assemias, and cystic fibrosis are the common
inherited genetic disorders. When these are sus-
pected due to a positive family history or carrier
Invasive techniques status in the parents, genetic analysis is per-
formed on the sample obtained by CVS or fetal
Invasive tests are used to obtain samples of blood sampling (FBS).
amniotic fluid, fetal blood, or fetal tissue for fur-
ther testing. The tests are listed in Box 12.10. ects o intrauterine in ections
Intrauterine infections with viruses such as par-
vovirus, rubella, cytomegalovirus, and herpes
Box 12.10 Invasive prenatal diagnostic tests
simplex virus or a parasite such as Toxoplasma
• Amniocentesis gondii can give rise to congenital anomalies.
• Chorionic villus sampling (CVS) When the mother has an acute infection during
• Fetal blood sampling (FBS) or percutaneous umbilical pregnancy suggestive of one of the infections
blood sampling (PUBS)
mentioned, fetal infection is confirmed or ruled
• Percutaneous biopsy of organs
• Preimplantation biopsy of blastocyst
out by amniocentesis or FBS. Decision regarding
• Fetoscopy termination of pregnancy may be made based
on the results.
Prenatal diagnostic tests are used for the Prenatal invasive diagnostic
investigation of the following conditions:
procedures
• Congenital malformations
The commonly used invasive tests for prenatal
• Chromosomal anomalies
diagnosis are amniocentesis, CVS, and FBS.
• Single gene defects
Fetal blood sampling (cordocentesis) car-
• Effects of intrauterine infections
ries a greater risk of pregnancy loss and there-
Congenital mal ormations fore is reserved only for clinical situations in
which amniocentesis, CVS, or maternal blood
Structural malformations affecting one or more sampling does not provide adequate diagnostic
organs of the fetus may occur in women with pre- information.
gestational diabetes or who have been exposed
to infections, teratogenic drugs, or radiation.
First trimester ultrasonography may identify Karyotyping following invasive
some anomalies, but second trimester sonog- diagnostic procedure
raphy at 18–20 weeks is used for the identifica-
tion of most malformations. The malformation Karyotyping is done to count the number of
may involve the central nervous, cardiovascular, chromosomes (Fig. 12.3) and look for structural
renal, gastrointestinal, skeletal, or respiratory changes in chromosomes. It is done using one or
system. Fetal echocardiography is used when more of the following methods:
cardiovascular anomalies are suspected. MRI • Metaphase analysis of cultured amniocytes
may be required in certain situations. or chorionic villus cells is highly accurate, and
takes between 1 and 3 weeks to obtain results.
Chromosomal anomalies • Fluorescence in situ hybridization (FISH) anal-
Screening for aneuploidy has been discussed ysis provides a result in 48–72 hours (Fig. 12.4).
earlier in this chapter. When screening is pos- It is specific for chromosomes 21, 13, 18, X,
itive, further diagnostic tests such as CVS or and Y.
CH 12_p163-178_v3.indd 171 17-07-2015 10:38:40

Figure 12.3 Karyotype showing three sets of chromosome 21 in Down syndrome. The red arrow points to chromosome
21. (Photo courtesy: Mediscan Systems, Chennai.)
• A newer technique has been introduced

recently for the rapid detection of aneuploi-
dies involving chromosomes 21, 18, and 13
and is called quantitative fluorescent polymer-
ase chain reaction (QF-PCR).
Chorionic villus sampling

Chorionic villus sampling is a procedure in which
placental villi are obtained through a transcervi-
cal or transabdominal route for prenatal genetic
diagnosis. The fact that the results are available
earlier in pregnancy as compared with amniocen-
tesis is the primary advantage of CVS. The advan-
tages of the procedure are given in Box 12.11.
Procedure
The transabdominal route has come to be the Figure 12.4 2KEVWTGQHCƀWQTGUEGPEGKPUKVWJ[DTKFK\CVKQP
preferred route in most centers performing inva- (FISH) test showing three signals for chromosome 21
sive prenatal diagnosis. (arrows) in a sample from a fetus with trisomy 21. There
The transcervical route can also be used but is are two blue signals for chromosome 13 and two green
technically more challenging and may be associ- signals for chromosome 18. (Photo courtesy: Mediscan
ated with vaginal bleeding. Systems, Chennai.)
CH 12_p163-178_v3.indd 172 17-07-2015 10:38:40

Box 12.11 Advantages of chorionic villus

sampling
• 2GTHQTOGFKPVJGſTUVVTKOGUVGTCHVGTYGGMU
• Results available early
• /CMGUVGTOKPCVKQPQHRTGIPCPE[
KHPGGFGFGCUKGTCPF
safer
• Miscarriage rate low: 0.5%–1%
The following steps are followed:

• The procedure is done under aseptic condi-
tions and under ultrasound guidance.
• A long 20-gauge needle with stylet is inserted
transabdominally under continuous visualiza-
tion, into the thickest portion of the placenta
(Fig. 12.5a). If the transcervical route is used, Figure 12.6 Ultrasound image of chorionic villus
a flexible catheter is introduced (Fig. 12.5b). sampling. The needle (arrow) is seen in the placenta.
Figure 12.6 demonstrates the ultrasound (Photo courtesy: Mediscan Systems, Chennai.)
image of transabdominal CVS.
• The stylet is removed and the culture medium– Box 12.12 Amniocentesis
containing syringe is then attached to the hub • #URKTCVKQPQHCOPKQVKEƀWKF
of the needle. • 2GTHQTOGFCHVGTYGGMUŏIGUVCVKQP
• An adequate sample of placental villi is aspirated • Performed under ultrasound guidance
by negative pressure created in the syringe. • Miscarriage rate: 0.5%–1%
• Advantages
• High-resolution banding of cells possible
Amniocentesis • Useful for diagnosis of structural chromosomal rear-
rangements
Amniocentesis is an invasive procedure done
under ultrasound guidance to obtain a sample of
amniotic fluid from the uterine cavity (Box 12.12). with cells obtained from amniocentesis, so this
The amniotic fluid contains exfoliated fetal cells is the preferred procedure when structural chro-
that are cultured and used for karyotyping. High- mosomal rearrangements need to be identified.
resolution banding of chromosomes is possible
Procedure
The procedure of performing amniocentesis
consists of the following steps:
• Using ultrasonography, a pocket of amniotic
fluid is identified.
• A fine needle is passed transabdominally into
a.
the amniotic cavity (Figs 12.7 and 12.8) and 20
mL of amniotic fluid is aspirated.
Fetal blood sampling

b. The indications for FBS are as follows:
• Rapid karyotype
• Fetal hemolytic disease (see Chapter 38, Redcell
alloimmunization)
Figure 12.5 Chorionic villus sampling a. Transabdominal. • Severe early onset fetal growth deficiency
b. Transvaginal. • Suspected congenital infection
CH 12_p163-178_v3.indd 173 17-07-2015 10:38:40

Figure 12.7 Amniocentesis under ultrasound guidance.

Figure 12.8 Ultrasound image of amniocentesis. The
echogenic tip of the needle (yellow arrow) is seen in
Fetal blood sampling is not routinely used VJGCOPKQVKEƀWKF
Photo courtesy: Mediscan Systems,
for karyotyping, although karyotyping can be Chennai.)
accomplished in 24–48 hours on fetal blood cells.
It is performed only if neither CVS nor amnio-
centesis is possible. The procedure-related preg- • A 20- to 22-gauge spinal needle is passed
nancy loss rate is <2%. transabdominally.
• The fetal umbilical vein is punctured and
blood is obtained from the fetal umbilical cord
Procedure (Figs 12.9 and 12.10).
The procedure of performing FBS consists of the • Usually 2–5 mL of blood is collected.
following steps:
• It is done under aseptic precautions, using
ultrasound guidance.
Placenta
Umbilical
Cor Figure 12.10 Ultrasound image of fetal blood sampling.
The needle (yellow arrow) is seen entering the insertion
of the umbilical cord (two white arrows) into the placenta.
Figure 12.9 Fetal blood sampling from the umbilical cord. (Photo courtesy: Mediscan Systems, Chennai.)
CH 12_p163-178_v3.indd 174 17-07-2015 10:38:41

Table 12.5 Prenatal invasive diagnostic procedures
Chorionic villus sampling Amniocentesis Fetal blood sampling

Gestational age (KTUVVTKOGUVGT
CHVGTYGGMU #HVGTYGGMU #HVGTYGGMU
Route Transabdominal/transcervical Transabdominal Transabdominal
Site of sampling 6JKEMGUVRCTVQHRNCEGPVC /QUVCEEGUUKDNGRQEMGVQH Umbilical cord/intrahepatic
ƀWKF portal vein/fetal heart
Tissue obtained Placental villi #OPKQVKEƀWKF
COPKQE[VGU Fetal blood (RBCs, serum)
6KOGVCMGPVQQDVCKP • /GVCRJCUGEWNVWTGŌYGGMU • Metaphase culture: 1–3 48–72 hours
MCT[QV[RKPI • FISH: 48–72 hours YGGMU
• FISH: 48–72 hours
4KUMQHRTGIPCPE[NQUU 0.5–1% 0.5–1% <2%
S ƀWQTGUEGPEGKPUKVWJ[DTKFK\CVKQP BCs red blood cells.
• Fetal blood can also be obtained from the intra- Indications for PGS
hepatic portal vein or rarely, the fetal heart.
• If the fetal blood sample is obtained from The various indications for PGS are as follows:
the cord at its insertion into the placenta, the • Women at high risk for aneuploid embryos
blood must be tested to confirm that it is fetal – Women over age 35
blood and not maternal contamination. – Multiple IVF failures
– Recurrent pregnancy loss
Table 12.5 lists the different invasive diagnos-
tic procedures available.
Indications for PGD
The various indications for PGD are as follows:
Preimplantation screening • Inherited familial disorder
• One or both partners with balanced
and diagnosis translocation
• High risk of recurrent pregnancy loss
Technology is now available to perform tests for
• Sex selection to avoid sex-linked disorders
genetic disorders on the DNA extracted from an
oocyte or an embryo.
A couple that has no known chromosomal D A for analysis
abnormality may undergo preimplantation The DNA for preimplantation genetic testing is
screening (PGS) to rule out a genetic defect. obtained from different cells (Box 12.13).
Preimplantation screening may help avoid
transfer of aneuploid embryos, reduce the risk of
pregnancy failure, and improve the probability
of conceiving a viable pregnancy with assisted Box 12.13 Source of D A for preimplantation
reproductive technology (ART). testing
In certain couples, one or both partners may • Polar body biopsy
have an inheritable genetic disorder or a bal- Ŧ First or second polar body of oocyte
anced translocation. In these couples, preim- Ŧ Indicated for maternally inherited mutations
plantation diagnosis (PGD) for chromosomal • Blastomere biopsy
abnormality or genetic defect may be offered. Ŧ &C[CHVGTHGTVKNK\CVKQP
Any couple that chooses to have PGS or PGD Ŧ 6- to 9-cell stage
will necessarily have to use ART even if they have Ŧ 1 or 2 blastomeres removed
no problem conceiving. The testing is done on • Blastocyst biopsy
Ŧ &C[QTCHVGTHGTVKNK\CVKQP
the embryo obtained by using ART or the polar
Ŧ Hundreds of cells available
body of the oocyte. Patients should be aware of
Ŧ Provides maximum DNA for analysis
this because ART is expensive and invasive.
CH 12_p163-178_v3.indd 175 17-07-2015 10:38:41

Fetal therapy are more commonly unilateral. They can arise in

association with many problems including con-
genital malformations, chromosomal abnormal-
The exponential advances in fetal imaging and
ities, chylothorax, anemia, heart defects, cardiac
increased understanding of fetal physiology
arrhythmias, and viral infections.
have changed the way many fetal problems,
Once the mother and fetus are investigated
both structural and physiological, are managed.
to identify any treatable underlying causes of
Instead of resorting to termination of pregnancy,
the pleural effusion such as anemia or cardiac
active intervention is instituted to improve the
arrhythmias, an attempt is made to aspirate
long-term outcome of the fetus.
the fluid under ultrasound guidance. If the fluid
recollects, thoracoamniotic shunt placement is
Fetal interventions used to drain the pleural effusion.
Most fetal therapy involves the use of ultra-

sound-guided interventions, fetoscopy, or open Fetoscopic interventions
fetal surgery. Using a fetoscope through a small abdominal
incision, the procedure is performed inside the
ltrasound-guided interventions uterus. Ultrasound guidance is required along
with the view obtained through the fetoscope.
Intrauterine etal trans usion Indications for fetoscopy-guided interven-
The commonest indication for intrauterine tions include the following:
transfusion is Rh alloimmunization in preg-
• Ligation of umbilical cord in acardiac twin
nancy. This is discussed in detail in Chapter 38,
• Selective laser photocoagulation of communi-
Red cell alloimmunization.
cating vessels in twin-to-twin transfusion
• Ablation of posterior urethral valve
esicoamniotic shunt
Fetal lower urinary tract outflow obstruction
prevents the fetus from passing urine. This can
pen fetal surgery
result in a reduction in the volume of amniotic Open fetal surgery is an extremely expensive
fluid. Severe oligohydramnios may interfere with option and is performed only at very few centers
the development of the fetal lungs and kidneys. in the West. Complications such as chorioamnio-
A vesicoamniotic shunt is a tube that is nitis, preterm labor, bleeding, and direct trauma
inserted into the fetal bladder to drain the excess to the fetus are risks in most of these procedures.
urine into the amniotic cavity. The amniotic Open fetal surgery has been attempted success-
fluid is maintained at normal levels till delivery fully in the following fetal problems:
is decided upon. Fetal chromosomal analysis
• Neural tube defects such as myelomenin-
is advised before the procedure to diagnose or
gocele and spina bifida
exclude associated chromosomal abnormalities.
• Congenital diaphragmatic hernia
horacoamniotic shunt • Congenital cystic adenomatoid malformation
• Congenital heart disease
Isolated fetal pleural effusions are uncommon • Pulmonary sequestration
but can result in pulmonary hypoplasia (nonde- • Sacrococcygeal teratoma
velopment of the lung). They may be bilateral but
Key points
• Aneuploidy refers to chromosomal mutations where • Of the aneuploidies, Down syndrome (trisomy 21) is
the chromosomal number is abnormal. It can present the most common chromosome abnormality and the
as a trisomy, triploidy, or monosomy. most frequent cause of mental disability in humans.
(Continued)
CH 12_p163-178_v3.indd 176 17-07-2015 10:38:41


• Screening is the process of testing a population that • Noninvasive prenatal testing (NIPT) for aneuploidy
KUCRRCTGPVN[JGCNVJ[WUKPICURGEKſEOCTMGTQTOCTM- uses cell-free DNA in the maternal blood and can be
ers, to detect a particular condition. QHHGTGFVQYQOGPCVJKIJTKUMHQTCPGWRNQKF[
• The results of the screening tests for aneuploidy are • A screen-positive result requires follow-up with an
GZRTGUUGFCUŎJKIJTKUMŏŎKPVGTOGFKCVGTKUMŏCPFŎNQY KPXCUKXGVGUVHQTMCT[QV[RKPIVQEQPſTOQTTWNGQWV
TKUMŏFGRGPFKPIQPYJGVJGTVJGTKUMTGUWNVKUCDQXGQT aneuploidy.
below an arbitrary cutoff point of 1 in 250.
• Chorionic villus sampling (CVS) is a procedure in
• /CVGTPCNCIGOCVGTPCNUGTWOOCTMGTUCPFUQPQ- which placental villi are obtained through a transab-
ITCRJKEſPFKPIUCTGCNNEQPUKFGTGFKPUETGGPKPIHQT dominal or transcervical route for prenatal genetic
aneuploidy. FKCIPQUKU+VKUWUWCNN[RGTHQTOGFKPVJGſTUVVTKOGUVGT
• Maternal age is not recommended in isolation as a CHVGTYGGMUŏIGUVCVKQP
screening parameter. • Amniocentesis is an invasive procedure done under
ultrasound guidance to obtain a sample of amniotic
• 6JGſTUVVTKOGUVGTEQODKPGFVGUVKUFQPGCV
ƀWKFHTQOVJGWVGTKPGECXKV[+VKUWUWCNN[RGTHQTOGF
11–13+6YGGMU+VKPENWFGUUGTWOVGUVKPIHQTHTGG
EhCG and pregnancy-associated plasma protein CHVGTYGGMUŏIGUVCVKQP
A (PAPP-A), and ultrasound measurement of the • (GVCNDNQQFUCORNKPIKUPQVTQWVKPGN[WUGFHQTMCT[Q-
nuchal translucency. V[RKPICNVJQWIJMCT[QV[RKPIECPDGCEEQORNKUJGFKP
• Second trimester maternal serum screening is best 24–48 hours on fetal blood cells.
QHHGTGFDGVYGGPCPFYGGMUŏIGUVCVKQP • #EQWRNGVJCVJCUPQMPQYPEJTQOQUQOCNCDPQTOCNKV[
• 6JGUGTWOOCTMGTUWUGFHQTVJGUGEQPFVTKOGUVGT may undergo preimplantation screening (PGS) to rule
triple test are alphafetoprotein (AFP), unconjugated out a genetic defect. This supposedly avoids transfer of
estriol (uE3), and human chorionic gonadotropin CPGWRNQKFGODT[QUTGFWEGUVJGTKUMQHRTGIPCPE[HCKN-

J%)6JGCFFKVKQPCNUGTWOOCTMGTHQTVJG uadruple ure, and improves the probability of conceiving a viable
test is inhibin A. pregnancy with assisted reproductive technology (ART).
• /CLQTWNVTCUQWPFOCTMGTUHQTCPGWRNQKFKGUKPENWFGKP- • In certain couples, one or both partners may have an

ETGCUGFPWEJCNHQNFVJKEMGPKPIGZQORJCNQUFWQFGPCN inheritable genetic disorder or a balanced transloca-
atresia, and atrioventricular septal defects. tion. In these couples, preimplantation diagnosis
P D for chromosomal abnormality or genetic defect
• /KPQTWNVTCUQWPFOCTMGTUHQTCPGWRNQKFKGUKPENWFG may be offered.
choroid plexus cysts, echogenic foci in the fetal heart,
mild hydronephrosis, echogenic bowel, and short • Most fetal therapy involves the use of ultrasound-guid-
femur. ed interventions, fetoscopy, or open fetal surgery.
Self-Assessment
Mrs. JK, 31, gravida 2, para 1, live 1, underwent routine
Case 1 UETGGPKPIHQTCPGWRNQKF[CVYGGMU6JGTGUWNVUJQYGF
Mrs. AM, 36, was married 6 months ago. She was 10 VJCVJGTTKUMQHJCXKPICDCD[YKVJ&QYPU[PFTQOGYCU
YGGMURTGIPCPV5JGYCUEQPEGTPGFVJCVJGTDCD[OKIJV in 100 (normal cutoff 1 in 250).
be abnormal because of her age. She had heard of Down 1. What invasive diagnostic procedure can be offered
syndrome affecting children of older mothers. She wanted to her?
screening for chromosomal abnormalities. 2. 9JCVCTGVJGOGVJQFUHQTQDVCKPKPICMCT[QV[RG!
1. *QYFQGUOCVGTPCNCIGKPETGCUGVJGTKUMHQTCPG- 3. 9JCVCTGVJGWNVTCUQWPFOCTMGTUHQT&QYPU[PFTQOG
uploidy? KPVJGſTUVVTKOGUVGT!
2. Which screening test for aneuploidy can be offered in 4. 9JCVKUVJGTKUMQHOKUECTTKCIGHQNNQYKPIEJQTKQPKE
VJGſTUVVTKOGUVGT! villus sampling and amniocentesis?
3. What is nuchal translucency?
4. 9JKEJUGTWOOCTMGTUCTGWUGFKPVJGUGEQPF
trimester?
CH 12_p163-178_v3.indd 177 17-07-2015 10:38:41

3. Increased NT, absent nasal bone, increased imped-

Answers CPEGVQƀQYKPVJGFWEVWUXGPQUWUCPFVTKEWURKFTG-
IWTIKVCVKQPCTGVJGWNVTCUQWPFOCTMGTUHQTCPGWRNQKF[
Case 1 KPVJGſTUVVTKOGUVGT
1. In an older mother, the oocyte has aged along with 4. 6JGTKUMQHOKUECTTKCIGHQNNQYKPIEJQTKQPKEXKNNWUUCO-
her and is prone to nondisjunction errors in the pling or amniocentesis is 0.5%–1%.
meiotic division, thereby increasing her chances of
having a baby with aneuploidy.
2. 6JGſTUVVTKOGUVGTEQODKPGFVGUVECPDGQHHGTGFCV Sample questions
11–13+6YGGMU+VKPENWFGUUGTWOVGUVKPIHQTHTGG
EhCG and pregnancy-associated plasma protein Long-answer questions
A (PAPP-A), and ultrasound measurement of the
nuchal translucency. 1. Discuss prenatal screening for aneuploidy.
3. Fetuses affected by Down syndrome and other triso- 2. Discuss prenatal diagnostic tests and the common
OKGUJCXGKPETGCUGFƀWKFDGJKPFVJGPGEMCUUGGPQP KPFKECVKQPU$TKGƀ[FGUETKDGVJGRTQEGFWTGU
WNVTCUQWPFKPVJGſTUVVTKOGUVGT6JKUKUECNNGFPWEJCN
translucency (NT) on ultrasound examination.
4. 6JGUGTWOOCTMGTUWUGFHQTVJGUGEQPFVTKOGUVGT
triple test are alpha fetoprotein (AFP), unconjugated 1. First trimester screening for Down syndrome
estriol (uE3), and human chorionic gonadotropin 2. Nuchal translucency

J%)6JGCFFKVKQPCNUGTWOOCTMGTHQTVJGSWCFTW- 3. Integrated test for Down screening
ple test is inhibin A. 4. Noninvasive screening (cell-free DNA) in maternal
blood
Case 2 5. Chorionic villus sampling
6. Amniocentesis
1. She can be offered chorionic villus sampling. 7. Fetal blood sampling (percutaneous umbilical blood
2. Metaphase analysis of cultured amniocytes or sampling)
EJQTKQPKEXKNNWUEGNNUƀWQTGUEGPEGKPUKVWJ[DTKFK\C-
VKQP
(+5*CPCN[UKUCPFSWCPVKVCVKXGƀWQTGUEGPV
polymerase chain reaction (QF-PCR) can be used for
MCT[QV[RKPI
CH 12_p163-178_v3.indd 178 17-07-2015 10:38:41

Medical Termination
13 of Pregnancy
Case scenario
Mrs. AD, 34, mother of two children, came to the clinic with history
of having missed her periods. Her last child was 2 years old and she
had an intrauterine contraceptive inserted 2 months after delivery. Her
menstrual periods had always been regular. The pregnancy test done
at home was positive. She wanted termination of pregnancy since her
financial situation was not good enough to take care of a third child. She
was also upset that she had conceived in spite of using contraception.
Introduction Gynecologists of India (FOGSI), and the Indian

College of Obstetrics and Gynecology (ICOG),
Termination of pregnancy is required in many governing all aspects of termination of preg-
situations; pregnancy in spite of using con- nancy. Thorough knowledge of the guidelines,
traception, pregnancy where the fetus has a the methods available for termination of preg-
chromosomal anomaly, an unintended pregnancy, and the evidence-based guidelines for
nancy, and pregnancy in a woman with a med- the choice of method is essential for the prac-
ical problem. Annual estimates of abortion in ticing obstetrician.
India vary from 4 to 6 million but the majority
of abortions are not reported. The majority of
terminations are performed in the first trimes-
ter but about 10% are performed in the second &GſPKVKQPCPFVGTOKPQNQI[
trimester. Unsafe abortion is one of the major
causes of maternal mortality. To make abortion Abortion is the termination of pregnancy
safe and accessible to Indian women, guide- before the period of viability. The cut off as
lines have been developed by the Government defined by WHO is gestational age before 20
of India, the Federation of Obstetricians and weeks and fetal weight <500 g.
CH 13_p179-189_v2.indd 179 17-07-2015 10:40:13

The terms used for abortion or termination of • If 12–20 weeks, opinion of two medical practi-
pregnancy are as follows: tioners is required before proceeding.
• Miscarriage: Spontaneous abortion
• Induced abortion: Termination of pregnancy Consent
by medical or surgical methods.
– Therapeutic abortion: Induced abortion for • Consent of the pregnant woman is essential.
medical indications • If the girl is a minor (<18 years) or mentally ill,
– Elective abortion: Induced abortion at the consent of the guardian is essential.
request of woman, not for medical reasons
– Medical termination of pregnancy (MTP):
Induced abortion for indications described 2NCEGYJGTGKVECPDG
under the MTP Act RGTHQTOGF
• Hospital established or maintained by the
government.
6JG/GFKECN6GTOKPCVKQP • A place that has been approved for this pur-
pose by the District Level Committee con-
QH2TGIPCPE[#EV stituted by the government, with the Chief
Medical Officer or the District Health Officer
The Medical Termination of Pregnancy (MTP) as chairperson.
Act, formulated in 1971 by the Government of
India, was aimed at improving maternal health
by preventing unsafe abortions, legalizing abor- 2GTUQPUSWCNKſGFVQRGTHQTO
tion services, and promoting access to safe
abortion services for women. An amended act
MTP
with some changes was passed in 2002. The act • Registered medical practitioner
clearly defines • Person whose name is with recognized medical
qualification
• indications for MTP,
• Person whose name is entered in State Medical
• persons who are qualified to perform the pro-
Register
cedure, and
• Person with experience in gynecology and
• place of implementation of MTP.
obstetrics
Indications
• Continuation of pregnancy constitutes risk to Preprocedure preparations
the life or grave injury to the physical or men-
Before embarking on an MTP, a through history,
tal health of the woman.
examination, evaluation, and counseling are
• Substantial risk of physical or mental abnor-
essential (Box 13.1).
malities in the fetus as to render it seriously
handicapped.
• Pregnancy caused by rape (presumed grave 7NVTCUQPQITCRJ[
injury to mental health).
Ultrasonography is not mandatory before per-
• Contraceptive failure in married couple (pre-
forming the procedure. If the woman has regular
sumed grave injury to mental health).
menstrual cycles, she is sure of dates and if the
uterine size corresponds to the period of gesta-
)GUVCVKQPCNCIG tion, menstrual date is acceptable.
When in doubt about the presence of preg-
• Can be performed up to 20 weeks’ gestation. nancy or the gestational age, ultrasonography
• If <12 weeks, opinion of one medical practi- is useful for the confirmation and assessment of
tioner is required before proceeding. the pregnancy.
CH 13_p179-189_v2.indd 180 17-07-2015 10:40:14

Medical Termination of Pregnancy 181
unintended pregnancy. Contraceptive choices

$QZ Preprocedure preparations for
OGFKECNVGTOKPCVKQPQHRTGIPCPE[ should be discussed prior to the procedure with
all women.The type of contraception offered
• History depends on the woman’s preference.
Ŧ LMP
Ŧ Medical illnesses • Tubectomy can be performed along with sur-
• Clinical examination gical termination or following medical termi-
• Assessment of gestational age nation, for women who have completed their
Ŧ LMP family.
Ŧ Clinical examination • Immediate postabortal insertion of intrau-
Ŧ Ultrasonography if required or in doubt
terine devices is safe and practical and is
• Counseling
recommended by the WHO and the American
Ŧ Procedures available
Ŧ Complications
College of Obstetricians and Gynecologists
Ŧ Subsequent contraception/sterilization (ACOG). Expulsion rate is slightly higher and
• Investigations women should be counseled regarding this.
Ŧ Hemoglobin and hematocrit • Prescription for oral contraceptives should be
Ŧ Blood group and Rh type given at the time of discharge from hospital.
Ŧ HIV/Hepatitis B surface antigen screening
Ŧ Urine sugar/protein
• Informed consent Methods of MTP
JWOCPKOOWPQFGſEKGPE[XKTWU P last menstrual period. Methods of termination of pregnancy used in
the first trimester are different from those used
#PVKDKQVKERTQRJ[NCZKU in the second trimester. In the first trimester, the
fetal bony structures are not formed; therefore,
Antibiotic prophylaxis is recommended for sur- removing the products of conception vaginally is
gical abortions since randomized trials have not difficult.
shown that it significantly reduces the frequency
of postabortal endometritis. The antibiotics are
given on the day of the procedure. /GVJQFUQH/62KPVJGſTUV
Options include the following: VTKOGUVGT
• Doxycycline 100 μg orally twice a day Methods used for MTP in the first trimester
or include medical and surgical methods.
• Ofloxacin oral 400 μg orally twice a day
/GFKECNOGVJQFU
or
• Ceftriaxone 1 g intravenously 30 minutes Termination of pregnancy by medical meth-
prior to the procedure ods is very safe and effective and is the method
of choice in the first trimester. It has a success
rate of 95%–99%. Three drugs are used for this
4JKOOWPQINQDWNKP purpose (Box 13.2). Prophylactic antibiotics are
Rh typing should be done for all women under- not required for termination of pregnancy using
going MTP. If the mother is Rh negative, Rh medical methods.
immunoglobulin should be administered at the The recommended dosage of mifepristone and
following dosage: misoprostol is given in Box 13.3. It may be admin-
istered by the clinician or self-administered at
• 50 μg, if gestational age <12 weeks home by the patient.
• 300 μg, if gestational age >12 weeks Misoprostol is associated with diarrhea, nau-
sea and vomiting, and occasionally fever (lasting
less than 24 hours). The vaginal route is more
Contraceptive advice effective and is usually preferred. The dose of
Women who are undergoing an MTP should 800 μg may be administered as a single dose or
be given contraceptive advice to avoid another as two divided doses 4 to 6 hours apart.
CH 13_p179-189_v2.indd 181 17-07-2015 10:40:14

• Repeat visit 2 weeks after first visit to ensure

$QZ &TWIUWUGFHQTVGTOKPCVKQPKPVJGſTUV
VTKOGUVGT complete abortion by history, pelvic examina-
tion, and ultrasonography, if necessary.
• Mifepristone • If the pregnancy is ongoing, surgical evacua-
Ŧ Antiprogestin
tion is indicated; if the abortion is incomplete,
Ŧ Acts by
repeat misoprostol or proceed with surgical
decidual degeneration
release of prostaglandins
evacuation.
Induces uterine contractions
Softens the cervix Other me ications
• Misoprostol Misoprostol with or without methotrexate can
Ŧ Prostaglandin E1
also be used.
Ŧ Induces uterine contractions
• Methotrexate
Ŧ Folic acid antagonist /KUQRTQUVQNCNQPG
Ŧ Causes trophoblastic degeneration This is less effective than when used with
mifepristone. It may be used alone where mife-
pristone is not available.
$QZ &QUCIGTGIKOGPHQTOKHGRTKUVQPGCPF /GVJQVTGZCVGCPFOKUQRTQUVQN
OKUQRTQUVQN
Methotrexate (75 μg oral or 50 μg/m2 IM) fol-
• Mifepristone 200 μg oral lowed by 800 μg of misoprostol 5–7 days later is
• Followed 36–48 hours later by
also used. This regimen is less efficacious and
Ŧ Misoprostol 800 μg vaginal or 400 μg oral
termination may take longer.
Complications
roce ure
Medical methods of termination of pregnancy
The procedure of medical termination includes
are associated with very few complications.
the following steps:
Complications and their management are listed
• Preprocedure assessment and counseling in Table 13.1. Rarely, if pregnancy continues, ter-
• Administration of oral mifepristone mination by surgical methods is recommended
• Instructions regarding misoprostol adminis- because of the risk of teratogenic effects of the
tration at home/clinic drugs. Occasionally, an ectopic pregnancy is
• Oral or parenteral nonsteroidal anti-inflammatory diagnosed after medical methods have been
agents (NSAIDs) for pain/cramping tried with the assumption of an intrauterine
• Prophylactic antibiotics not indicated pregnancy. This should be managed surgically.
6CDNG %QORNKECVKQPUCPFOCPCIGOGPVQH/62
%QORNKECVKQPU /CPCIGOGPV
Side effects of drugs
Nausea, vomiting, diarrhea, Symptomatic treatment
headache, dizziness
Abdominal pain, cramps NSAIDs
Excessive bleeding Exclude incomplete abortion
Incomplete abortion Repeat misoprostol/MVA
Ongoing pregnancy Surgical methods of termination
Fever and infection Antibiotics
Ectopic pregnancy Surgical intervention
POGFKECNVGTOKPCVKQPQHRTGIPCPE[ AOCPWCNXCEWWOCURKTCVKQP SA Ds, nonsteroi-
FCNCPVKKPƀCOOCVQT[FTWIU
CH 13_p179-189_v2.indd 182 17-07-2015 10:40:14

Outcome • The procedure is performed under paracervi-

Success of medical methods in the first trical block.
mester is 95%–98%. About 5% of women expel • The cannula is inserted into the uterine cav-
with mifepristone alone, before misoprostol ity and moved in and out and rotated through
administration. 360 degrees simultaneously till the products
are completely aspirated.
• The aspirated products are placed in a bowl of
5WTIKECNOGVJQFU saline and the blood clots washed away. If fetal
Surgical methods used for first trimester preg- membranes or fronds of villi are seen, histo-
nancy termination are listed in Box 13.4. pathological examination is not required.
• If products of conception are not visualized, the
anual vacuum aspiration procedure should be repeated. In the absence
In very early pregnancy, manual vacuum aspi- of intrauterine products of conception, an
ration (MVA) may be used. It is also used to ectopic pregnancy should be excluded.
evacuate the uterus in an incomplete abortion
following medical termination.
lectric vacuum aspiration
Electric vacuum aspiration (EVA) is usually
• Manual vacuum aspiration is an outpatient referred to as suction evacuation. This can be
procedure. performed anytime in the first trimester and is
• It is performed up to 10 weeks’ gestation. also used to evacuate vesicular mole, incomplete
• Prophylactic antibiotics are not recom- abortion, and missed abortion. If the pregnancy
mended. is beyond 7 weeks, dilatation of the cervix is
• The equipment consists of a handheld 50–60 required.
mL plastic syringe in which a vacuum is cre-
ated by withdrawing the plunger. The syringe %GTXKECNFKNCVCVKQP
is connected to a Karman cannula (6–8 mm Dilatation of the cervix is required in order to
size) (Fig. 13.1). insert the suction cannula. This may be achieved
by the following:
$QZ 5WTIKECNOGVJQFUQH/62WUGFKPVJG • Manual dilatation with metal dilators
ſTUVVTKOGUVGT
• Osmotic dilators—laminaria tent
• Manual vacuum aspiration • Vaginal misoprostol
• Electric vacuum aspiration or suction evacuation Manual dilatation is done just before the pro-
• Dilatation and evacuation cedure, using Hegar’s dilators (Fig. 13.2). The
P medical termination of pregnancy. diameter of the dilator in millimeters should be
a. b.
(KIWTG Manual vacuum aspirator and Karman cannula. CThe syringe is used to create a vacuum to aspirate the
products of conception and the cannula is introduced into the uterine cavity. D The plunger of the aspiration syringe is
withdrawn to create vacuum and cannula is connected to the syringe.
CH 13_p179-189_v2.indd 183 17-07-2015 10:40:16

• The procedure is performed under general or

spinal anesthesia.
• After pelvic examination to assess the size of the
uterus, a uterine sound is passed into the uter-
ine cavity to measure the uterocervical length.
• The cannula is introduced just beyond the
internal os and connected to suction.
• The cannula is rotated in both directions but
not moved in and out. This minimizes the risk
of perforation.
• Intravenous ergometrine is given to promote
uterine contraction and reduce bleeding.
• After completion of aspiration, a gentle check
curettage is performed with a metal curette
(KIWTG Hegar’s dilators. Blunt-tipped Hegar’s dilators (Fig. 13.4). When the uterus is empty, a gritty
of different sizes are used to dilate the cervix prior to sensation is felt while curetting.
curettage. Photo courtesy: Dr Rajnish Samal
equal to the gestational age in weeks (i.e., 8 mm

dilator for 8 weeks’ gestational age).
Osmotic dilators should be inserted 10–12
hours before the procedure. They absorb water and
increase in diameter, dilating the cervix gradually.
Misoprostol at a dose of 400 μg can be used
vaginally 12 and 6 hours before the procedure.
Procedure
• Manual vacuum aspiration is an inpatient
procedure.
• A rigid plastic or metal cannula of size in mil-
limeters equal to that of the gestational age in
(KIWTG Uterine curette. Blunt and sharp curettes
weeks is used. The cannula is connected to the
used for curetting the uterine cavity. Photo courtesy:
electric suction device through polythene tub- Dr. Rajnish Samal
ing (Fig. 13.3).
a. b.
(KIWTG Metal cannula for suction evacuation and electric suction. C Metal cannula used for aspiration of products of
conception for dilatation and evacuation. Photo courtesy: Dr Rajnish Samal D Electric suction apparatus used for creating
suction.
CH 13_p179-189_v2.indd 184 17-07-2015 10:40:20

Dilatation an evacuation is then gently curetted with the largest metal

In this procedure, dilatation of the cervix is curette that can be passed through the dilated
followed by evacuation of the products using cervix. This procedure has a higher risk of per-
ovum forceps and finally curettage using a foration and therefore has been replaced by suc-
metal curette. Dilatation of the cervix may be tion evacuation.
achieved using one of the methods described
earlier. Ovum forceps can be used to remove Complications
large chunks of products (Fig. 13. 5). The cavity Complications with surgical methods are
uncommon. These are listed in Table 13.2.
Outcome
MVA and EVA are successful in 98%–100% of
cases.
#FXCPVCIGUCPFFKUCFXCPVCIGUQH
OGFKECNXGTUWUUWTIKECNOGVJQFU
QHCDQTVKQP
These are listed in Table 13.3. In the first trimes-
ter, both methods have equal success rate and
acceptability. Since medical abortion does not
(KIWTG Ovum forceps. The tip of the ovum forceps necessitate admission to hospital, anesthesia,
is shaped like a spoon to grasp and remove products of and antibiotics, and the cost is low, it is recom-
conception. Photo courtesy: Dr. Rajnish Samal mended as the first choice.
6CDNG %QORNKECVKQPUQHUWTIKECNOGVJQFU
%QORNKECVKQPU Prevention /CPCIGOGPV

Hemorrhage Ergometrine IM/IV Ergometrine/PGF2D
Cervical laceration Dilatation with laminaria/misoprostol Observation/suture
Uterine perforation Meticulous surgical technique Observation/laparoscopy
Incomplete abortion Thorough curettage Repeat evacuation
Endometritis, sepsis Prophylactic antibiotics Antibiotics
Ectopic pregnancy %QPſTOKPVTCWVGTKPGRTGIPCPE[DGHQTGRTQEGFWTG Surgical intervention
KPVTCOWUEWNCT KPVTCXGPQWUP , prostaglandin F2D.
D
6CDNG /GFKECNXGTUWUUWTIKECNOGVJQFUQHVGTOKPCVKQPQHRTGIPCPE[
2CTCOGVGT /GFKECNOGVJQFU 5WTIKECNOGVJQFU

Hospitalization Not required Required except for MVA
Anesthesia Not required Required
Number of visits Two or more Single
Duration Days to weeks At single visit
Success rate 95%–98% 98%–100%
Bleeding Perceived as moderate Perceived as light
Follow-up Required to ensure completion Not routinely required
A manual vacuum aspiration.
CH 13_p179-189_v2.indd 185 17-07-2015 10:40:21

/GVJQFUQHVGTOKPCVKQPQH $QZ &QUCIGTGIKOGPHQTOKHGRTKUVQPGCPF

RTGIPCPE[KPVJGUGEQPF OKUQRTQUVQNKPUGEQPFVTKOGUVGT/62
• Mifepristone 200 μg oral
VTKOGUVGT • Followed 36–48 hours later by misoprostol 800 μg
Termination of pregnancy in the second trimes- vaginal
Ŧ Followed 3 hours later by misoprostol 400 μg oral/
ter is technically more difficult and has a higher
vaginal
rate of complications. The usual indications are Ŧ Repeated every 3 hours
as follows: Ŧ Maximum of 5 doses
• Diagnosis of pregnancy has been delayed P medical termination of pregnancy.

• Maternal illness (e.g., malignancy)
• Fetal anomalies—congenital, chromosomal
• Intrauterine death of the fetus Complications
These are listed in Table 13.4.
Medical methods using mifepristone and
misoprostol or dilatation and evacuation (D&E)
are the preferred methods. The patient must O ytocin
be hospitalized for both medical and surgical Oxytocin infusion with progressively and
procedures. gradually increasing concentrations (from 50
The methods used are as follows: units to 300 units in 500 mL of normal saline)
has been used. This is preceded by cervical
• Medical methods dilatation using misoprostol or osmotic dila-
• Intra-amniotic/extra-amniotic instillation of tors for better efficacy. Oxytocin infusion is
substances not a routine method of choice. This is used
• Surgical methods only when mifepristone or misoprostol are
not available.
/GFKECNOGVJQFU
Termination of pregnancy using medications is 'ZVTCCOPKQVKEKPLGEVKQP
the method of choice. The medications used are of ethacridine
listed in Box 13.5. Prostaglandin F2D, which was
Extra-amniotic injection of ethacridine stimu-
popular earlier, is associated with nausea, vom-
lates uterine contractions directly and by releas-
iting, and other systemic side effects. Hence, it is
ing prostaglandins from the decidua.
no longer recommended for MTP.
i epristone an misoprostol thacri ine lactate

Ethacridine lactate is an aromatic organic com-
The combination of mifepristone and misopros-
pound. Extra-amniotic instillation of ethacridine
tol is the recommended medical method of ter-
mination. The dosage is given in Box 13.6.
Outcome 6CDNG %QORNKECVKQPUQHOGFKECNOGVJQFUQH

The success rate with mifepristone and miso- VGTOKPCVKQPKPVJGUGEQPFVTKOGUVGT
prostol is 95%. %QORNKECVKQP /CPCIGOGPV
Incomplete abortion
Dilatation and curettage
Retained placenta
$QZ &TWIUWUGFHQTUGEQPFVTKOGUVGT/62 Uterine rupture Surgical intervention
• Mifepristone Cervical laceration Surgical intervention
• Misoprostol Infection Antibiotics
• Oxytocin Hemorrhage • Oxytocics/ blood transfusion
P medical termination of pregnancy. • Exclude incomplete abortion
CH 13_p179-189_v2.indd 186 17-07-2015 10:40:22

• Ethacridine lactate is injected through the

$QZ 'VJCETKFKPGNCEVCVGKPUGEQPF
VTKOGUVGT/62 catheter.
• The Foley’s catheter is clamped, left in situ,
• Aromatic organic compound and is removed after 8 hours.
• Instilled into extra-amniotic space for midtrimester
abortion The induction-abortion interval is usually
• Dosage 24–36 hours. This interval can be shortened by
Ŧ 0.1% solution the additional use of vaginal misoprostol.
Ŧ 10 mL/week of gestation, maximum 150 mL
• Action
Ŧ Local release of prostaglandin
Ŧ Stimulates uterine contractions
+PVTCCOPKQVKEKPUVKNNCVKQP
P medical termination of pregnancy. QHUWDUVCPEGU
Hypertonic saline and hyperosmolar urea
for midtrimester abortion has been well studied are used for this purpose (Box 13.8). A needle
and its safety has been established (Box 13.7). is inserted into the uterine (amniotic) cavity
transabdominally (Fig. 13.7). A small quantity of
roce ure amniotic fluid is initially aspirated. Hypertonic
saline or urea is then instilled slowly at the
• A Foley’s catheter (14–16 F size) is introduced
rate of 10 mL/min. The induction-abortion
through the cervix into the extra-amniotic
interval with saline is 28–36 hours. Using urea
space (Fig. 13.6).
along with PGF2D, reduces the interval to 15–
• The bulb is inflated with 10 mL of saline and
20 hours.
pulled down to occlude the cervix.
Instillation methods are not frequently used
at present, largely because alternative meth-
ods, including prostaglandins and surgical
options, have fewer side effects, lower risk of
complications, and shorter induction-abortion
intervals.
$QZ +PVTCCOPKQVKEKPUVKNNCVKQPQHUWDUVCPE
GUHQTUGEQPFVTKOGUVGT/62
• Hypertonic (200%) saline
Ŧ Dosage
tra amniotic space 10 mL/week of gestation
Slow instillation at the rate of 10 mL/min
Ŧ Contraindications
Cardiac disease
oley s catheter Renal disease
Ŧ Complications
Hypernatremia
Pulmonary edema
Infection
Disseminated intravascular coagulation
• Hyperosmolar (40%) urea
Ŧ Dosage
80 g in 200 mL of distilled water
Used along with low-dose PGF2D (intra-amniotic)
Ŧ Complications minimal
(KIWTG Extra-amniotic instillation. A Foley’s catheter Ŧ Superior to saline
is introduced into the extra-amniotic space and the bulb is P OGFKECNVGTOKPCVKQPQHRTGIPCPE[P 2D
KPƀCVGF'VJCETKFKPGNCEVCVGKUKPUVKNNGFVJTQWIJVJGECVJGVGT prostaglandin F2D.
CH 13_p179-189_v2.indd 187 17-07-2015 10:40:22

• Fetus and placenta are removed.

• Intravenous ergometrine or oxytocin infusion
may be used to promote uterine contraction,
reduce bleeding, and reduce the risk of perfo-
ration during curettage.
• Cavity is curetted to complete the procedure.
Dilatation an e traction (D )
The fetus is removed intact through a dilated
cervix using fetal extraction forceps. This proce-
dure has been replaced by medical methods.
ysterotomy
Delivering the previable fetus through an inci-
sion on the uterus is known as hysterotomy. A
transverse incision is made on the lower part of
the uterus. If the woman has opted for a con-
comitant tubectomy, a vertical incision on the
upper segment may be used. A hysterotomy may
have to be resorted to in cases where medical
(KIWTG Transabdominal instillation. Needle is
methods fail.
introduced into the amniotic cavity transabdominally and
saline or urea is instilled.
Complications o surgical metho s
5WTIKECNOGVJQFU The complications of surgical methods used in
the second trimester are listed in Box 13.9.
Surgical methods include the following:
• Dilatation and evacuation
• Dilatation and extraction
• Hysterotomy
$QZ %QORNKECVKQPUQHUWTIKECNOGVJQFU
QHUGEQPFVTKOGUVGT/62
Dilatation an evacuation (D ) • Cervical laceration
• This procedure is usually performed up to 16 • Uterine perforation
weeks’ gestation though this was used up to 20 • Hemorrhage
weeks earlier. • Infection
• Incomplete abortion
• It is not often used now since prostaglandins
• Late sequelae
are very effective.
Ŧ Due to cervical lacerations
• Spinal or general anesthesia is required. Recurrent abortions
• Prophylactic antibiotic should be given. Preterm labor
• Cervix should be dilated prior to the procedure Ŧ Due to infection
with osmotic dilators. Misoprostol may also be Infertility due to tubal block
used but osmotic dilators are preferred. Ectopic pregnancy
• Further dilatation to 16–18 mm with metal Chronic pelvic pain
dilators may be required. Ŧ Psychological
• Fetus is removed by large bore suction cannula Depression
(size 16–18 mm). Anxiety
Feeling of guilt
• Fetal extraction forceps may be used to crush
and disarticulate fetal parts. P medical termination of pregnancy.
CH 13_p179-189_v2.indd 188 17-07-2015 10:40:22

Medical Termination of Pregnancy
-G[RQKPVU
• Abortion is the termination of pregnancy before the • /GVJQFUWUGFKPVJGſTUVVTKOGUVGTCTGOGFKECNCPF
period of viability (<20 weeks’ gestation, <500 g fetal surgical. A combination of mifepristone and misopros-
weight). Termination of pregnancy by medical or surgi- tol is the medical method of choice.
ECNOGCPUHQTURGEKſECPFUQEKCNKPFKECVKQPUKUMPQYP
• Manual vacuum aspiration, suction evacuation, and
as medical termination of pregnancy
dilatation and curettage are the surgical methods used
• The Medical Termination of Pregnancy (MTP) Act, KPVJGſTUVVTKOGUVGT
FGſPGUVJGKPFKECVKQPURNCEGUQHKORNGOGPVC-
• Medical termination of pregnancy in the second
VKQPCPFRGTUQPUSWCNKſGFVQRGTHQTOVJGRTQEGFWTG
VTKOGUVGTKUVGEJPKECNN[OQTGFKHſEWNVCPFJCUOQTG
• #P/62OC[DGRGTHQTOGFKPVJGſTUVQTUGEQPF complications.
trimester. First trimester termination is technically
• Mifepristone and misoprostol have a high success rate
simpler and associated with fewer complications.
in the second trimester as well.
• Preprocedure preparations consist of history,
• Extra-amniotic instillation of ethacridine lactate is a
especially last menstrual period, assessment of
safe and effective procedure.
gestational age clinically, ultrasonography when
required, counseling, and a few investigations. • %QORNKECVKQPUQH/62KPVJGſTUVCPFVJGUGEQPF
trimester include hemorrhage, incomplete abortion,
• Antibiotic prophylaxis is recommended for all surgical
and infection. Late sequelae are due to cervical injury
procedures.
and pelvic infection.
5GNH#UUGUUOGPV
%CUGDCUGFSWGUVKQPU for MTP, persons who can perform it, and places
where it can be performed. It is meant for making
abortions safer.
Case 1 Counseling regarding (a) procedure, (b) complica-
Mrs. AD, 34, mother of two children, came to the clinic with tions, and (c) permanent method of contraception.
history of having missed her periods. Her last child was 2 Mifepristone 200 μg orally followed 36–48 hours later
years old and she had an intrauterine contraceptive inserted by misoprostol 800 μg vaginally.
2 months after delivery. Her menstrual periods had always
been regular. A pregnancy test done at home was positive.
She wanted termination of pregnancy. Case 2
What is the indication for MTP in this woman? Mifepristone 200 μg orally followed by misoprostol
What is the MTP Act? 800 μg vaginally, followed by 400 μg of misoprostol
What counseling would you give this woman? orally every 3 hours up to a maximum of 5 doses.
If the gestational age was 9 weeks, what method of Excessive bleeding, retained placenta, incomplete
termination would you recommend? abortion, infection, and cervical laceration.
Prophylactic antibiotics followed by suction evacua-
tion or D&E.
Case 2
Mrs. SN, 30, second gravida, was diagnosed as having
an anencephalic fetus at 16 weeks’ gestation.
5CORNGSWGUVKQPU
How will you terminate this pregnancy? .QPICPUYGTSWGUVKQP
What complications do you anticipate? What is medical termination of pregnancy (abortion)?
If she presented with retained placenta and bleeding, What are the indications and procedures used in the
what is the management? ſTUVCPFUGEQPFVTKOGUVGTU!
#PUYGTU 5JQTVCPUYGTSWGUVKQPU
/GVJQFUWUGFHQTſTUVVTKOGUVGT/62
Case 1
The MTP Act
The indication is failure of contraception. Complications of MTP
The MTP Act was formulated by the Government of Methods used in second trimester MTP
India to provide guidelines regarding the indications
CH 13_p179-189_v2.indd 189 17-07-2015 10:40:22

Section 3
Intrapartum
Management
CH 14_p190-207_v3.indd 190 17-07-2015 12:01:22

Normal Labor:
Mechanics,
14 Mechanism,
and Stages
Case scenario
Mrs. PS, 27, primigravida, was admitted to the labor room at 40 weeks’
and 3 days’ gestation with blood-stained discharge and uterine contrac-
tions. Her husband was very anxious since this was the first delivery.
He wanted to know why she had the vaginal discharge, how long she
would be in labor, when the delivery was expected, and if all was well.
Introduction throughout labor and delivery. The infant is born

spontaneously in the vertex position between 37
Normal labor is considered to be a retrospective and 42 completed weeks of pregnancy. After
diagnosis since no one can predict the course birth, the mother and infant are in good condi-
and complications of labor in a particular indi- tion’ (Box 14.1). There is no absolute time cutoff,
vidual. While the fetus passes through the birth though an arbitrary duration of 24 hours is con-
canal and is born, it has to go through a compli- sidered normal. Preterm labor is the onset of
cated but well-orchestrated sequence of move- labor before 37 weeks’ gestation.
ments, the uterus has to contract and the cervix
has to dilate. There are several factors that facili-
tate the process of labor.
Box 14.1 &GſPKVKQPQHPQTOCNNCDQT
The following criteria should be met to classify labor as
&GſPKVKQP being normal.
• Spontaneous in onset
Labor is the process by which the fetus, after the • Term gestation: 37–42 weeks
period of viability, is expelled from the genital • Vertex presentation
tract. The World Health Organization (WHO) • Uncomplicated
defines normal labor as ‘spontaneous in onset, • Natural expulsive forces
low-risk at the start of labor and remaining so • Vaginal delivery
CH 14_p190-207_v3.indd 191 17-07-2015 12:01:22

/GEJCPKEUQHNCDQT 6CDNG (GVCNHCEVQTUKPƀWGPEKPINCDQT
Uterine contractions act during labor to achieve (CXQTCDNG 7PHCXQTCDNG

both cervical dilatation as well as the expulsion Lie Longitudinal • Transverse
of the fetus through the birth canal. To achieve • Oblique
this, normal progress of labor depends on the Presentation Vertex • Face
complex interaction of three factors known as • Brow
the ‘three Ps’: passage, passenger, and powers. • Breech
Abnormality in any of these can lead to abnor- Position LOA ROP
mal labor. Attitude Flexion • &GƀGZKQP
• Extension
Station 0 and below Above 0
Passage Fetal size 2–3.5 kg >4 kg
A, left occipitoanterior; P, right occipitoposterior.
The fetal passage consists of the bony pelvis and
soft tissues. These are listed in Box 14.2. The
gynecoid pelvis and its dimensions are described
in Chapter 2, Anatomy of the bony pelvis and fetal Fetal factors indicating the best prognosis
skull. Shape and diameters of the true pelvis are for successful vaginal delivery include the
usually assessed by clinical pelvimetry. X-ray, following:
computerized tomography (CT), and magnetic
resonance imaging (MRI) are rarely used to per- • Average weight
form pelvimetry. • Longitudinal lie
The soft tissues (i.e., cervix and pelvic mus- • Vertex presentation
cles) undergo changes over several weeks before • Well-flexed attitude
the onset of labor. With uterine contractions, the • Left occipitoanterior position
lower uterine segment is formed, the cervix Fetal factors indicating poor prognosis for
effaces and dilates, and the vagina distends and successful vaginal delivery are as follows:
stretches, as described later. The fetus is gradu-
ally pushed down into the lower segment, • Fetal weight >4 kg
through the dilated cervix into the vagina, and • Deflexed head
delivered. Pelvic muscles offer resistance that aid • Occipitoposterior positions
inflexion and rotation of the presenting part in • Malpresentations such as breech, brow, and face
the first and second stages of labor.
Powers
2CUUGPIGT
HGVWU
The fetus contributes several factors that play a
2QYGTU
WVGTKPGEQPVTCEVKQP
crucial role in the mechanics of labor and lead to Uterine contraction is the most important force
successful delivery (Table 14.1). that contributes to the progress of labor.
Hydrostatic pressure exerted by the amniotic
fluid also helps in cervical dilatation. Uterine
Box 14.2 (GVCNRCUUCIG contractions are intermittent, with periods of
• Bony pelvis relaxation in between, which permit uteropla-
Ŧ Inlet cental perfusion. The interval between contrac-
Ŧ Midpelvis tions (measured in minutes) gradually decreases
Ŧ Outlet and the intensity of contractions (measured in
• Soft tissues Montevideo units) gradually increases. Three to
Ŧ Lower uterine segment five contractions in 10 minutes is considered
Ŧ Cervix
normal and adequate during active labor (Table
Ŧ Vagina
14.2). More than five contractions in 10 minutes
Ŧ Pelvic muscles
is called tachysystole.
CH 14_p190-207_v3.indd 192 17-07-2015 12:01:22

Normal Labor: Mechanics, Mechanism, and Stages 193
6CDNG terine contractions Box 14.3 7VGTKPGEJCPIGUKPNCDQT
2JCUGQHNCDQT Contraction Intensity • Formation of upper uterine segment

Ŧ 5JQTVGPKPIQHOWUENGſDGTU
Duration +PVGTXCN Ŧ Thickening of uterine segment

UGEQPFU
OKPWVGU • Formation of lower uterine segment
Latent phase 20–30 5–10 Ŧ 5VTGVEJKPIQHOWUENGſDGTU
Ŧ Thinning of uterine segment
Active phase 30–60 2–3 200–250 MVU
• Physiological retraction ring
Second stage 60–90 1–2
Ŧ Junction between upper and lower uterine segments
montevideo units.
• Elongation of uterine ovoid
Ŧ Increases fetal axis pressure
Ŧ Helps in cervical effacement
Assessment of uterine contractions is discussed
in Chapter 40, Abnormal labor: abnormalities in
passage and powers. Uterine contractions are usu- the upper and lower segments of the uterus is
ally assessed by simple palpation of the abdomen. the physiological retraction ring. In obstructed
During the peak of contraction, fingers cannot labor, this becomes the pathological retraction
‘indent’ the uterus. External tocography is a non- ring or Bandl’s ring (see Chapter 44, Obstructed
invasive method of assessing uterine contractions labor and uterine rupture).
and often used along with external fetal heart As labor progresses, the uterus becomes more
monitoring. Intra-amniotic pressure during con- elongated. This increases the downward fetal
tractions, as measured by intrauterine pressure axis pressure and also pulls the cervical fibers
catheter, is 20–60 mm Hg (mean—40 mm Hg). The upward, resulting in cervical effacement.
strength of uterine contractions is expressed in
Montevideo units (MVU). MVU is calculated by
the average strength of contraction in mm Hg × *[FTQUVCVKERTGUUWTG
number of contractions in 10 minutes. It is 200– QHVJGCOPKQVKEƀWKF
250 MVU in active phase of labor.
With uterine contractions, there is an increase in
the hydrostatic pressure of the amniotic fluid
(QTOCVKQPQHVJGWRRGTCPF (Fig. 14.2). This in turn dilates the cervical canal
and forms the bag of membranes that lies below
NQYGTWVGTKPGUGIOGPVU the presenting part.
As pregnancy advances, the isthmus of the

uterus stretches and becomes the lower uterine /GEJCPKUOQHPQTOCNNCDQT
segment. As labor progresses, an active upper
segment and passive lower segment become Due to the irregular shape of the pelvis and the
evident. The myometrium of the upper segment relatively large dimensions of a term fetal
contracts but the muscle fibers do not return to head, not all the diameters of the head will fit
their original length after contraction; instead through all the diameters of the pelvis. The
they remain slightly shorter. Similarly, the mus- mechanisms of labor allow for changes in fetal
cle fibers of the lower segment stretch during position to be made throughout labor which
contraction and do not return to their original allow the fetal head to be accommodated
length after contraction. They remain slightly within the pelvic canal and ultimately facili-
longer or stretched (receptive relaxation). tate delivery.
Gradually, a thick upper segment and a thinner Towards term, the fetus assumes an attitude
lower segment are formed (Box 14.3; Fig. 14.1). of universal flexion with the head well flexed and
The lower segment is identified by the loose the chin almost touching the chest. Therefore,
attachment of the peritoneum on its anterior the normal presentation is vertex. The occiput
surface. The contents of the uterus are thus may be on the left or right side of the pelvis,
slowly pushed down into the lower segment and pointing anteriorly, posteriorly, or laterally, giv-
the cervix also dilates. The boundary between ing rise to left occipitoanterior (LOA), left
CH 14_p190-207_v3.indd 193 17-07-2015 12:01:23

Uterine bo y Upper segment
sthmus
Lo er segment
Cer i
Cer i
a. b.
Upper segment Upper segment
Lo er segment Lo er segment
. .
Figure 14.1 Formation of upper and lower segment.The isthmus of the uterus stretches as pregnancy advances and
becomes the lower segment. a. Nonpregnant uterus. The isthmus is marked. D Term pregnancy. c and d. Early and late
labor. Lower segment is well differentiated as labor progresses.
terus
m iotic lui
ore aters
a o membra es
Cer ix
a. b.
Figure 14.2 Increase in hydrostatic pressure and formation of bag of membranes. The hydrostatic pressure increases with
uterine contractions. a. The pressure is directed downward. D Bag of membranes is formed below the presenting part.
occipitoposterior (LOP), or left occipitotrans- fetal skull). Therefore, the fetus has to enter the
verse (LOT) positions and right occipitoanterior pelvis with the engaging diameter in the oblique
(ROA), right occipitoposterior (ROP), or right or transverse diameter of the pelvis and rotate,
occipitotransverse (ROT) positions (Fig. 14.3). so as to bring the largest diameter to lie in the
The transverse and oblique diameters are anteroposterior diameter at the pelvic outlet.
greater than the anteroposterior diameter at the This is achieved by the cardinal movements, dis-
pelvic inlet; the anteroposterior diameter is more cussed below. The engaging diameter in the ver-
than the transverse diameter at the pelvic outlet tex presentation with a well-flexed head is the
(see Chapter 2, Anatomy of the bony pelvis and suboccipitobregmatic diameter (Fig. 14.4).
CH 14_p190-207_v3.indd 194 17-07-2015 12:01:23

a. L . L . L P
b. . . P
Figure 14.3 Positions of the fetal head in vertex presentation. The occiput may be on the left or right side of the pelvis,
pointing anteriorly, laterally, or posteriorly, giving rise to a. left occipitoanterior (LOA), D right occipitoanterior (ROA), c. left
occipitotransverse (LOT), d. right occipitotransverse (ROT), e. left occipitoposterior (LOP), and H right occipitoposterior (ROP)
positions.
Box 14.4 4
GCUQPUHQTNGHVQEEKRKVQCPVGTKQT
RTGUGPVCVKQP
Longitudinal lie Uterine ovoid longitudinal
Cephalic Bulky breech occupies
presentation broad upper pole of uterus
Vertex presentation Attitude of universal
ƀGZKQP
uboccipitobre matic Occipitoanterior Maternal abdominal wall
iameter position accommodates fetal
vertebral column
Left occipitoanterior Left oblique diameter of
position pelvis occupied by
sigmoid colon
Figure 14.4 Suboccipitobregmatic diameter. This is the
GPICIKPIFKCOGVGTKPXGTVGZRTGUGPVCVKQPYKVJYGNNƀGZGF
head.
Vertex presentation with LOA or LOT position

%CTFKPCNOQXGOGPVU
is the most common. When the fetus enters in the QHNCDQT
LOT position, rotation to LOA takes place soon
after labor begins. LOA is the most common posi- The cardinal movements of labor help the fetus
tion, for the reasons given below (Box 14.4). to successfully negotiate the birth canal.
CH 14_p190-207_v3.indd 195 17-07-2015 12:01:23

The position of the fetal head rotates during On abdominal examination, the back of the
its passage through the birth canal because of an fetus and the occiput are to the left and the sin-
asymmetry in both the shape of the fetal head ciput is to the right of the midline. Vaginal exam-
and the maternal bony pelvis. ination reveals the sagittal suture in the right
Seven distinct cardinal movements of the oblique or transverse diameter, posterior fonta-
fetus occur over the course of labor and delivery nel in the left anterior quadrant of the pelvis, and
(Box 14.5). the anterior fontanel in the right posterior quad-
The following terms are important for under- rant of the pelvis (see Fig. 14.3).
standing the cardinal movements:
• Engaging diameter is the anteroposterior 'PICIGOGPV
diameter of the fetal skull that enters the pelvis. When the greatest transverse diameter (bipari-
• Diameter of engagement is the diameter of the etal diameter) of the fetal head passes through
pelvic inlet in which the engaging diameter the pelvic inlet, the head is said to be engaged.
lies. The widest transverse diameter is the biparietal
• Denominator is the reference point on the fetal diameter (9.4 cm) in cephalic presentations (Fig.
skull. It is the occiput in vertex presentation. 14.5). The suboccipitobregmatic diameter is at
At the onset of labor, the following are the the same level as the biparietal diameter; there-
findings in an example of vertex presentation fore, when the head is engaged, the occiput enters
with LOA or LOT: the pelvis and only the sinciput is felt per abdo-
men (head is one-fifth palpable). When the head
• Presentation: Vertex is engaged, the leading bony point of the vertex is
• Attitude: Flexion at or below the ischial spines. Engagement of
• Position: LOA/LOT the head implies that there is no disproportion
• Engaging diameter: Suboccipitobregmatic (9.4 cm) at the level of the pelvic inlet (Box 14.6).
• Denominator: Occiput
• Diameter of engagement: Right oblique/trans-
verse diameter of pelvis Box 14.6 'PICIGOGPV
• Biparietal diameter enters pelvic inlet
• Implies no disproportion at inlet
Box 14.5 %CTFKPCNOQXGOGPVUQHNCDQT
• Occurs at
• Engagement Ŧ 38 weeks or later in primigravidae
• Descent Ŧ Onset of labor in multigravidae
• Flexion • Diagnosis
• Internal rotation Ŧ Abdominal examination
• Extension Head one-fifth palpable
• Restitution Occiput not felt
• External rotation Ŧ Vaginal examination
• Expulsion Leading bony part of vertex at level of ischial spines
a. b.
Figure 14.5 Engagement of the fetal head in vertex presentation. a. The biparietal diameter lies above the pelvic brim
when the head is not engaged. D The biparietal diameter is below the pelvic brim when the head is engaged.
CH 14_p190-207_v3.indd 196 17-07-2015 12:01:24

In primigravidae, engagement may occur 2

weeks prior to the onset of labor (38 weeks) but
often occurs at the onset of labor. In multigravi-
dae, it usually occurs after the onset of labor.
#U[PENKVKUO
When the head enters the pelvis in the occipitotrans-
verse position, the sagittal suture should lie in a. b.
the transverse diameter of the pelvis, midway
between the pubic symphysis and sacral prom- Figure 14.6 Asynclitism. a. Anterior asynclitism. When
VJGUCIKVVCNUWVWTGQHVJGHGVCNJGCFFGƀGEVURQUVGTKQTN[
ontory. But in order to negotiate the anteropos-
the anterior parietal bone enters the pelvis. D Posterior
terior diameter of the inlet, the head tilts later-
CU[PENKVKUO9JGPVJGUCIKVVCNUWVWTGFGƀGEVUCPVGTKQTN[
ally and the subparieto-supraparietal diameter
the posterior parietal bone enters the pelvis.
enters the pelvis. The sagittal suture is deflected
anteriorly or posteriorly. When the suture is
deflected toward the sacral promontory, the
with the pubic symphysis (Fig. 14.7). The number
anterior parietal bone enters the pelvis: this is
of fingers required to cover the part of the head
known as anterior asynclitism. When the suture
above the symphysis is equal to the number of
is deflected toward the symphysis pubis, the
fifths of head palpable. When the whole head is
posterior parietal bone enters the pelvis and is
above the inlet, it is five-fifth palpable; as the head
known as posterior asynclitism (Box 14.7; Fig.
descends, it may be four-fifth, three-fifth, two-fifth,
14.6). In moderate degrees of asynclitism, labor
or one-fifth palpable. When it is one-fifth palpa-
progresses normally. When asynclitism is
ble, only the sinciput is felt, the occiput has
severe, dystocia can occur. Anterior parietal
entered the pelvic brim, and the lowermost bony
presentation (anterior asynclitism) has a better
point of the head is at the level of the ischial
prognosis for successful vaginal delivery.
spines; the head is engaged.
Descent (NGZKQP
Descent of the fetus occurs with uterine contrac-
At the beginning of labor, when flexion is not
tions. In the second stage, bearing down efforts
complete, the engaging diameter (Fig. 14.8) is
also contribute to fetal descent. Descent is assessed
the occipitofrontal diameter (12 cm). Flexion of
by abdominal examination and expressed in terms
the fetal head is essential to enable the smallest
of ‘fifths’ of the fetal head palpable above the pubic
diameter, which is the suboccipitobregmatic
symphysis (Crichton’s maneuver). Five fingers of
(9.5 cm), to present. With increasing flexion, the
the examining hand are placed on the abdomen
fetal chin touches the chest. Flexion is brought
with the ulnar or radial border of the hand in line
about by the resistance offered by (a) the cervix,
(b) pelvic walls, and (c) the pelvic floor.
Box 14.7 #U[PENKVKUO
• Head tilted to one side +PVGTPCNTQVCVKQP
• 5CIKVVCNUWVWTGFGƀGEVGFCPVGTKQTN[QTRQUVGTKQTN[
• Subparieto-supraparietal diameter enters anterioposterior Internal rotation brings the occiput toward the
diameter of pelvis pubic symphysis and aligns the suboccipitobreg-
• Normal delivery occurs with moderate asynclitism matic diameter to the anteroposterior diameter of
• Anterior asynclitism the pelvic cavity. This is essential for normal
Ŧ Sagittal suture toward sacral promontory delivery to occur. Rotation is through 45 degrees
Ŧ Anterior parietal presentation (one-eighth of a circle) in occipitoanterior posi-
Ŧ Better prognosis tions. This movement is brought about by (a) the
• Posterior asynclitism
shape of the pelvis, (b) impetus given by the
Ŧ Sagittal suture toward pubic symphysis
ischial spines, and (c) the shape and elastic recoil
Ŧ Posterior parietal presentation
of the levatorani muscle. Internal rotation
CH 14_p190-207_v3.indd 197 17-07-2015 12:01:24

a.
i Hea is mobile ia Hea accommo ates full ii Hea is abo e iia Hea accommo ates
abo e the i th of fi e fingers abo e symphysis pubis t o fingers abo e the
symphysis pubis the symphysis pubis symphysis pubis
b omen
Pel ic brim
Pel ic ca ity
Completely inciput inciput inciput inciput one of hea

abo e high easily felt felt felt palpable
occiput occiput occiput occiput
b. easily felt felt just felt not felt
Figure 14.7 Descent of the presenting part. a. (KXGſPIGTUQHVJGGZCOKPKPIJCPFCTGRNCEGFQPVJGCDFQOGPVQEQXGT
VJGRCTVQHVJGHGVCNJGCFVJCVKUCDQXGVJGRWDKEU[ORJ[UKUCPFVJGFGUEGPVKUGZRTGUUGFKPſHVJU9JGPVJGYJQNGJGCF
KUCDQXGVJGDTKOCNNſXGſPIGTUCTGTGSWKTGFVQEQXGTVJGJGCFKVKUſXGſHVJRCNRCDNGD Diagrammatic representation of
FGUEGPVKPſHVJU
usually occurs at the level of the ischial spines

but can occur at a lower level.
Extension
When the head reaches the outlet, the occiput
hitches under the inferior margin of the sym-
physis pubis. The biparietal diameter stretches
the vulval outlet. Since the pelvic canal curves
anteriorly at this point, the head extends gradu-
ally and sequentially, the occiput, bregma, nose,
mouth, and chin are born. Uterine contractions,
maternal bearing down efforts, and force exerted
by the levatorani are responsible for extension
and delivery of the fetal head.
a. b.
Figure 14.8 Flexion of the fetal head. a. When head is estitution
EQORNGVGN[ƀGZGFVJGGPICIKPIFKCOGVGTEJCPIGUVQ
suboccipitobregmatic. D9JGPJGCFKUPQVHWNN[ƀGZGFVJG The fetal head rotates back to the original posi-
occipitofrontal diameter engages. tion in a quick untwisting movement, in a
CH 14_p190-207_v3.indd 198 17-07-2015 12:01:24

direction opposite to that of internal rotation. The

occiput is directed toward the maternal thigh.
5VCIGUQHNCDQT
Labor is a continuous process. However, it is
'ZVGTPCNTQVCVKQP divided into three stages to assist in clinical man-
agement. The stages of labor are described from
The shoulders engage in the opposite (left) the onset of regular contractions. However, pre-
oblique diameter of the pelvis. The anterior paratory changes take place for a few weeks prior
shoulder rotates toward the pubic symphysis by to the onset of labor, described as ‘prelabor’ or
45 degrees. This causes external rotation of the ‘preparatory stage of labor.’
head in the same direction in which restitution Labor has three stages:
occurred.
• First stage: Stage of dilatation
• Second stage: Stage of expulsion of the fetus
&GNKXGT[QHVJGUJQWNFGTU • Third stage: Stage of expulsion of placenta
When the anterior shoulder rotates, the bisacro- The contraction and retraction of the uterus
mial diameter lies in the anteroposterior diame- and the arrest of bleeding that follow delivery are
ter of the pelvis. The anterior shoulder hitches also described as the fourth stage of labor. These
under the pubic symphysis and the posterior extendfor 1–2 hours after delivery. Postpartum
shoulder distends the perineum and is born by hemorrhage due to uterine atony can occur
lateroflexion of the spine. This is followed by during this phase; therefore, close monitoring is
delivery of the anterior shoulder. essential.
'ZRWNUKQP 2TGRCTCVQT[UVCIGQTRTGNCDQT
With uterine contractions, delivery of the shoul- This stage extends over a few days (see Chapter 6,
ders is followed by the delivery of the rest of the Physiology of labor). This phase is mediated by
fetus. estrogen, progesterone, prostaglandin, and
Cardinal movements in mechanism of labor, other substances. During this period, changes
how they occur, and what they achieve are sum- occur in the genital tract in preparation for the
marized in Table 14.3 and Figure 14.9. onset of labor (Box 14.8).
6CDNG %CTFKPCNOQXGOGPVUQHNCDQT
/QXGOGPV What it achieves *QYKVKUDTQWIJVCDQWV
Engagement Engaging diameter enters pelvic inlet Uterine contractions
Descent Downward movement of fetus Uterine contractions
Flexion Suboccipitobregmatic diameter presents • Uterine contractions
• 4GUKUVCPEGD[EGTXKZRGNXKEYCNNRGNXKEƀQQT
Internal rotation Suboccipitobregmatic diameter comes • Uterine contractions
to lie in AP diameter of pelvis
• Shape of pelvis, shape of levatorani muscle, elastic
recoil
Extension Delivery of fetal head • Shape of birth canal, uterine contractions, force of
levatorani
• Maternal expulsive efforts
Restitution Untwisting of fetal neck Spontaneous
External rotation Brings shoulders in AP diameter Uterine contractions, shape of pelvis, shape of
levator ani
Expulsion Delivery of shoulders and whole fetus Uterine contractions, maternal expulsive efforts
AP anteroposterior.
CH 14_p190-207_v3.indd 199 17-07-2015 12:01:24

a. b.
. .
. .
. .
Figure 14.9 Cardinal movements of labor. The cardinal movements of a. engagement, DƀGZKQPCPFFGUEGPVc. internal
rotation, d. beginning of extension, e. complete extension and delivery of head, H external rotation g. delivery of anterior
shoulder, and h. delivery of posterior shoulder.
CH 14_p190-207_v3.indd 200 17-07-2015 12:01:25

Box 14.8 2TGRCTCVQT[UVCIGQHNCDQT Box 14.9 'XGPVUKPVJGſTUVUVCIGQHNCDQT

• Corresponds to activation phase of labor • Uterine contractions
• Changes Ŧ Regular
Ŧ Falling forward of the uterus Ŧ Painful
Shelving Ŧ Progressive increase in
Lightening intensity
Ŧ Ripening (softening) of cervix duration
Ŧ Increase in uterine contractility frequency
• Mediated by • Show
Ŧ estrogen • Cervical changes
Ŧ progesterone Ŧ Effacement
Ŧ contraction-associated proteins Ŧ Dilatation
Ŧ prostaglandins • Formation of lower uterine segment
Ŧ MMP, GAGs • Descent of presenting part
Ŧ interleukin-8 • Formation of bag of membranes
A s, glycosaminoglycans; P, matrix metalloproteinases. Ŧ Rupture of membranes
Falling forward of the uterus is due to the forma- %GTXKECNGHHCEGOGPV

tion of the lower uterine segment and the head
entering the pelvis. This is described as shelving. The cervix is soft and ‘ripens’ as term approaches,
The uterine height comes down from the level of in preparation for effacement and dilatation (see
the xiphisternum by 2 cm or so and the flanks Chapter 6, Physiology of Labor). Cervical efface-
appear distended. The woman perceives a feeling ment and dilatation are fundamental to the first
of relief since the upward pressure on the dia- stage of labor.
phragm is reduced. This is described as lightening. Effacement or ‘taking up’ refers to the short-
Ripening or softening of the cervix is due to ening of the cervix in labor. The fibers of the cer-
alteration in collagen structure and relative con- vix are thinned out, pulled upward into the lower
centration of matrix metalloproteinases (MMP) segment of the uterus, and the cervix that is 4 cm
and glycosaminoglycans (GAGs). Increase in long before the onset of labor, becomes progres-
uterine contractility is mediated by oxytocin and sively shorter (Box 14.10; Fig. 14.10). Effacement
prostaglandins. may begin before the onset of labor but is com-
pleted in labor. At the onset of labor, in a nulli-
para, the cervix is about 4 cm long and the inter-
(KTUVUVCIGQHNCDQT nal os is closed. Effacement takes place first and
The first stage begins with the onset of regular dilatation begins after the cervix is fully effaced.
uterine contractions and ends with full cervical In a multipara, the cervical canal and internal os
dilatation. The exact time of onset of labor is dif- are partially open, admitting one or two fingers
ficult to establish. The time at which regular, at the onset of labor. Effacement and dilatation
painful uterine contractions begin, leading to progress simultaneously in labor. Effacement is
cervical effacement and dilatation, is the time of expressed either as a percentage of the length of
true onset of labor. It is not possible to determine cervix that is taken up (e.g., 25%, 50%) or in terms
this accurately. of the actual length of the cervix below the pre-
Events that take place in the first stage of labor senting part (e.g., 3 cm, 2 cm).
are listed in Box 14.9.
Show Box 14.10 %GTXKECNGHHCEGOGPV
Mucosanguineous discharge that is normally seen • May begin prior to onset of labor
in the first stage of labor is known as show. This is • Completed before active phase of labor
• Cervix thinned out and pulled upward
the expulsion of the mucous plug of the cervix
• Merges with lower uterine segment
mixed with a small quantity of blood. It occurs as a
• Expressed in percentage or centimeters of length
result of cervical effacement and dilatation.
CH 14_p190-207_v3.indd 201 17-07-2015 12:01:25

Box 14.11 %GTXKECNFKNCVCVKQP

• Occurs due to
Ŧ uterine contractions
Ŧ J[FTQUVCVKERTGUUWTGQHVJGCOPKQVKEƀWKF
Ŧ pressure of the presenting part
• &KNCVGUVQEOD[VJGGPFQHVJGſTUVUVCIG
• Mediated by
Ŧ prostaglandins
Ŧ oxytocin
cm long
ot ilate
a. b.
cm long
Figure 14.10 Cervical effacement. a. Cervical effacement
KPPWNNKRCTC6JGEGTXKZſTUVGHHCEGUDGEQOGUUJQTVGT cm ilate
and thinner, and dilates later. D Cervical effacement
in multipara where the internal os is partially open.
Effacement and dilatation proceed simultaneously.
ully efface
%GTXKECNFKNCVCVKQP
cm
Cervical dilatation is an essential prerequisite to ilate
delivery. The internal os is closed prior to labor
in primigravidae but may be patulous in multi-
gravidae. With increasing uterine contractions ully efface
and pressure exerted by the amniotic fluid and
the presenting part, the cervix dilates to 10 cm ully
ilate
(full dilatation) at the end of the first stage of
labor (Box 14.11; Fig. 14.11).
Figure 14.11 Cervical dilatation. The cervix dilates
2JCUGUQHſTUVUVCIGQHNCDQT ITCFWCNN[VQEOD[VJGGPFQHſTUVUVCIG
Cervical dilatation is divided into two phases:

phase, which in turn is divided into accelera-
• Latent phase tion phase, phase of maximum slope, and
• Active phase deceleration phase (Fig. 14.12). Both latent and
– Acceleration phase active phases together constitute the first stage
– Phase of maximum slope of labor.
– Deceleration phase
This is based on the graph of cervical dilata-
atent phase
tion and phases of labor (Friedman labor The latent phase is the period between onset of
curve). It is a sigmoid curve that begins with labor and beginning of the active phase. It is the
the latent phase and goes on to the active early phase of labor during which cervical
CH 14_p190-207_v3.indd 202 17-07-2015 12:01:25

The rate of cervical dilatation begins to increase

in the acceleration phase, proceeds faster during
the phase of maximum slope, and slows down
Phase of ma imum slope

cceleration phase
toward the end (after 8 cm), during the decelera-
Cer ical ilation cm
eceleration phase
econ stage
tion phase. The rate of dilatation in the active
phase is 1.5 cm/hour in a multipara and 1.2 cm/
hour in a nullipara (two standard deviations
below the mean). A minimum dilatation of 1 cm/
hour should occur, below which progress of labor
is considered abnormal. The mean duration of
the active phase is 3–4 hours in a multipara and
Latent phase cti e phase 5–6 hours in a nullipara. The duration is affected
by several factors (Box 14.13).
ime hr Friedman’s curve was introduced in the
Figure 14.12 Friedman’s curve showing the phases of 1950s. More recent studies have refuted some of
labor. The active phase begins at 3 cm in this curve and is his findings. The following facts are considered
divided into acceleration phase, phase of maximum slope, to better reflect actual labor patterns:
and deceleration phase.
• The increase in rate of dilatation in active
phase is gradual.
effacement occurs (thinning from 4 cm to 0.5 • Latent phase ends and active phase begins at
cm) and the cervix dilates to 4 cm. Time of onset 4 cm dilatation.
of labor is difficult to determine, as already dis- • More rapid dilatation occurs after 6 cm.
cussed. Initiation of regular uterine contrac- • There is no deceleration phase.
tions as perceived by the woman is usually • Due to these differences, the shape of the
taken as the time of onset. Cervical dilatation of curve is not sigmoid.
4 cm marks the end of the latent phase and • Total duration of labor is longer.
beginning of the active phase. (In the original
Friedman curve, active phase began at 3 cm dil- (QTOCVKQPQHNQYGTWVGTKPGUGIOGPV
atation.) Duration of latent phase is variable but
This has been described earlier in this chapter.
the average duration in a nullipara is 6–8 hours
The active upper segment contracts and pushes
and in a multipara is 4–6 hours (Box 14.12).
the fetus down into the passive lower segment,
which stretches to accommodate it.
Active phase
The active phase begins at 4 cm dilatation and
ends with full dilatation of cervix. This phase is Box 14.13 #EVKXGRJCUGQHNCDQT
divided into the following phases:
• Divided into
• Acceleration phase Ŧ acceleration phase
• Stage of maximum slope Ŧ stage of maximum slope
• Deceleration phase Ŧ deceleration phase
• Duration
Ŧ Multipara: 3–4 hours
Ŧ Nullipara: 5–6 hours
Box 14.12 .CVGPVRJCUGQHNCDQT
• Rate of dilatation
• Begins with onset of labor Ŧ Multipara: 1.5 cm/hour
• Ends with onset of active labor (4 cm dilatation) Ŧ Nullipara: 1.2 cm/hour
• Duration variable Ŧ Minimum: 1cm/hour
Ŧ Nullipara: 6–8 hours • Duration increased by
Ŧ Multipara: 4–6 hours Ŧ fetal malposition
• Increase in duration Ŧ FGƀGZKQP
Ŧ Inadequate ripening of cervix Ŧ inadequate uterine contractions
Ŧ Early sedation Ŧ large baby
CH 14_p190-207_v3.indd 203 17-07-2015 12:01:26

&GUEGPVQHVJGRTGUGPVKPIRCTV Most of the descent of fetal head occurs during

late first stage and early second stage, when uter-
During the latent phase, engagement of the ver- ine contractions are more frequent and last lon-
tex may take place. Some descent occurs in the ger. In addition, the mother feels the urge to
active phase, especially in the latter part. ‘push’ or ‘bear down’ when the head enters the
vagina and presses on the rectum. The resistance
(QTOCVKQPQHDCIQHOGODTCPGU offered by the soft tissues is overcome by
As the cervix effaces and dilates, a portion of the • voluntary bearing down by the mother and
amniotic sac with amniotic fluid bulges into the • uterine contractions.
cervical canal and serves as a dilating fluid wedge.
The occiput rotates and hitches under the
This lies below the presenting part and is known
symphysis pubis and does not recede between
as bag of membranes or forewaters (Fig. 14.13).
contractions. This is known as crowning. With
This fluid wedge further dilates the cervix when
further contractions and maternal efforts, expul-
the uterus contracts and increases the hydro-
sion of the fetus occurs (Box 14.14). Duration of
static pressure of the amniotic fluid.
the second stage is 30 minutes in a multipara
and 1 hour in a nullipara but, in the absence of
4WRVWTGQHOGODTCPGU
The bag of membranes ruptures due to further
increase in intra-amniotic pressure. This usually Box 14.14 5GEQPFUVCIGQHNCDQT
occurs toward the end of the first stage when the • Has two phases
cervix is nearly fully dilated but may occur earlier. Ŧ Phase I: Pelvic phase or phase of descent
Ŧ Phase II: Perineal phase or phase of expulsion
• Uterine contractions
5GEQPFUVCIGQHNCDQT Ŧ Increase in frequency
The second stage of labor begins with full cervi- Ŧ Increase in duration
cal dilatation and ends with the delivery of the • Bearing down pains
Ŧ Maternal expulsive efforts
fetus. This is the stage in which descent of the
• Crowning
presenting part leads to expulsion of the fetus.
Ŧ Occiput hitches under symphysis pubis
Events in the second stage are as follows: Ŧ Does not recede between contractions
• Descent of the fetus • Expulsion of fetus
• Bearing down pains • Duration
Ŧ Multipara: 30 minutes
• Crowning of the head
Ŧ Nullipara: 1 hour
• Delivery of the fetus
a. b. .
Figure 14.13 Formation of the bag of waters. With uterine contractions and increasing hydrostatic pressure, the portion
of amniotic sac above the cervix, below the presenting part, bulges into the cervical canal. This is known as bag of
membranes or forewaters. a. Early in labor D Formation of bag of waters begins c. Bag of waters formed below the head.
CH 14_p190-207_v3.indd 204 17-07-2015 12:01:26

fetal heart rate abnormalities, up to 1 hour in a • Contraction phase: Uterine wall at the placen-
multipara and 2 hours in a nullipara are consid- tal site contracts.
ered normal. • Detachment phase: Placenta separates from
the uterine wall.
2JCUGUQHUGEQPFUVCIGQHNCDQT • Expulsion phase: Placenta is expelled from the
uterine cavity.
The second stage of labor has been divided into
two phases: Two methods of placental separation, namely
Schultz method and Duncan method, are shown
• Pelvic phase
in Figure 14.14.
• Perineal phase
hase I elvic phase or phase Central separation (Schult )

o escent The central cotyledons separate first and the
blood collects retroplacentally. The separation
The pelvic phase extends from full dilatation of
continues peripherally and the entire placenta
cervix to the time when the head reaches the pel-
separates. The placenta is expelled, with the fetal
vic floor. The beginning of this phase is difficult to
define precisely since pelvic examination is usu-
ally performed 4 hourly. The rapid descent of the
fetal head occurs during this phase. The end of
this phase is marked by ‘bearing down’ pains that
loo
begin when the head reaches the pelvic floor.
hase II erineal phase or phase

Placenta
o e pulsion Umbilical
The perineal phase extends from the beginning Cor
of ‘bearing down’ pains to delivery of the fetus.
The duration of this phase is important. When
this phase of second stage is prolonged, fetal
hypoxia and damage to pelvic floor muscles and
fascia can occur.
6JKTFUVCIGQHNCDQT
This extends from the time of expulsion of the
fetus to the expulsion of the placenta. The dura-
tion of the third stage is usually 5 minutes but up
to 30 minutes is considered normal.
2NCEGPVCNUGRCTCVKQP
Contraction of the uterus causes thickening of the
uterine wall and reduction in surface area of the
placental site. The disparity in the surface areas of
the placenta and placental site causes a shearing
force, and the placenta separates from the uterine
wall along the spongy layer. The fetal membranes
peel off the uterine wall, aided by uterine contrac- a. b.
tions. Expulsion of the placenta follows.
Figure 14.14 Methods of placental separation. a. Central
The process of placental separation is divided
separation or Schultz method in which the centre of the
into four phases:
RNCEGPVCUGRCTCVGUſTUVD Marginal separation or Duncan
• Latent phase: Placenta-free wall of the uterus OGVJQFKPYJKEJVJGOCTIKPQHVJGRNCEGPVCUGRCTCVGUſTUV
contracts. and extends to the center.
CH 14_p190-207_v3.indd 205 17-07-2015 12:01:26

surface presenting at the introitus, with the cord middle layer of myometrium act as ‘living liga-
attached, like an inverted umbrella. During the tures’ and compress the blood vessels (Fig. 14.15).
separation, external bleeding is minimal. Clots form in the vessels, completing the occlu-
sion and controlling hemorrhage (Box 14.16).
arginal separation (Duncan) This phase, which extends over 1–2 hours after
This is the mechanism of separation of a fundal placental expulsion, is referred to as the fourth
placenta. The separation begins in the periph- stage of labor.
ery and extends to the center. Bleeding is evi-
dent. The placenta folds upon itself and is loo essels
expelled. This method of separation is more
common (Box 14.15).
#TTGUVQHDNGGFKPI

HQWTVJUVCIGQHNCDQT
After the separation and expulsion of placenta, Myometrial fibers
a. b.
there is bleeding from the torn ends of the pla-
cental vessels. The uterine myometrium con- Figure 14.15 Living ligatures. The arrest of bleeding
tracts and retracts. The crisscross fibers of the after the third stage occurs by compression of the blood
vessels in the middle layer of myometrium. a. Before
FGNKXGT[QHRNCEGPVCVJGOWUENGſDGTUCTGCTTCPIGF
Box 14.15 2NCEGPVCNUGRCTCVKQP around the blood vessels in a criss-cross manner. D After
FGNKXGT[QHRNCEGPVCVJGOWUENGſDGTUEQOGVQIGVJGTCPF
• Central separation (Schultz)
compress the blood vessels to occlude them.
Ŧ Starts in the central cotyledons
Ŧ Formsretroplacental hematoma
Ŧ Expelled as inverted umbrella
Box 14.16 #TTGUVQHDNGGFKPI
Ŧ External bleeding less
• Marginal separation (Duncan) • Uterine contraction and retraction
Ŧ Starts in the periphery • Occlusion of arterioles by myometrium—‘living ligatures’
Ŧ Associated with bleeding • Formation of clots and thrombosis of vessels
Ŧ More common
-G[RQKPVU
• Labor is the process by which the fetus, after the • Vertex presentation with left occipitoanterior or left
period of viability, is expelled from the genital tract. occipitotransverse position is the most commonly seen
• Three factors (3 Ps) are involved in the mechanics presentation.
of labor—passage, passenger, and powers. • The head is said to be engaged when the bipari-
• The fetal passage consists of the bony pelvis and etal diameter crosses the pelvic inlet. Asynclitism
soft tissues. is common during labor but, if severe, can lead to
dystocia.
• 2CUUGPIGTQTVJGHGVCNHCEVQTUKPƀWGPEKPINCDQTCTGHGVCN
lie, presentation, position, attitude, size, and station. • Descent of the fetal head is assessed by abdominal
GZCOKPCVKQPCPFGZRTGUUGFKPŎſHVJUŏQHJGCFRCNRCDNG
• Uterine contraction is the most important power. above pubic symphysis.
Frequency and duration of contractions increase as
labor progresses. • Flexion, internal rotation extension, and delivery are
brought about by uterine contractions, resistance
• The uterus differentiates into an active upper offered by bony pelvis, and levatorani muscle.
segment and passive lower segment during labor.
• External rotation of head indicates internal rotation of
• Mechanism of labor consists of seven distinct cardinal the shoulder.
OQXGOGPVUGPICIGOGPVFGUEGPVƀGZKQPKPVGTPCN
rotation, extension, restitution, and external rotation.
(Continued)
CH 14_p190-207_v3.indd 206 17-07-2015 12:01:26

-G[RQKPVU Continued
• Preparatory stage of labor extends over few days to • Cervical dilatation is divided into two phases. Latent
few weeks prior to labor. Lightening, shelving, soften- phase extends upto dilatation of 3–4 cm.
ing of the cervix, and increase in uterine contractility • Active phase extends from 3–4 cm to full dilatation.
occur during this phase. This is divided into acceleration phase, phase of
• Labor is divided into three stages. First stage is further maximum slope, and deceleration phase.
divided into two phases. • Second stage of labor is the stage of expulsion of
• 6JGſTUVUVCIGQHNCDQTGZVGPFUHTQOQPUGVQHNCDQTVQ fetus and extends from full cervical dilatation to
full dilatation of cervix. delivery of the fetus.
• +ORQTVCPVGXGPVUKPVJGſTUVUVCIGCTGEGTXKECNGHHCEG- • Third stage is the stage of placental expulsion.
ment and dilatation, formation of the lower uterine Separation and expulsion of placenta and membranes
segment, and rupture of membranes when cervix is takes place during this stage.
nearly fully dilated. • After delivery of the placenta, bleeding is arrested by
• Cervical effacement is expressed as percentage of myometrial contraction and retraction and formation
cervix effaced or length of cervix in centimeters below of thrombi in the vessels. This is described as the
the presenting part. fourth stage of labor.
5GNH#UUGUUOGPV
%CUGDCUGFSWGUVKQPU 3. Latent phase.
4. When the cervix is 4 cm dilated.
Case 1
Mrs. PS, a primigravida at 40 weeks’ and 3 days’ ges-
Case 2
tation, was presented with mucosanguineous discharge 1. By placing the hand on the lower abdomen with the
and pains. ulnar border of the hand along the pubic symphysis.
+VKUGZRTGUUGFCUVJGPWODGTQHŎſHVJUŏQHHGVCNJGCF
1. What is the mucosanguineous discharge known as
palpable above the symphysis.
and why does it occur?
2. 9JGPVJGJGCFKUQPGſHVJRCNRCDNGVJGQEEKRWVKU
2. What changes do you expect in the cervix if she is in
not felt, only the sinciput is felt abdominally. A vaginal
labor?
examination will show the leading bony point of the
3. If the cervix is 3 cm long and 2 cm dilated, which
head at or below the level of the ischial spines.
phase of labor is she in?
3. 1.5 cm/hour since she is a multipara in the active
4. When will she be considered to be in active phase of
phase of labor.
labor?
Case 2 5CORNGSWGUVKQPU
Mrs. TD, wsecond gravida, at 39 weeks’ gestation, was .QPICPUYGTSWGUVKQPU
admitted to the labor room with pains.
1. &GſPGPQTOCNNCDQT&GUETKDGVJGOGEJCPKUOQH
1. How will you assess descent of the fetal head by labor in occiput anterior position.
abdominal palpation? 2. What are the stages of labor? Discuss the events
2. How will you identify engagement of the head? in each stage.
3. If she is 5 cm dilated at admission, what is the
expected rate of dilatation from this point?
5JQTVCPUYGTSWGUVKQPU
1. Monitoring uterine activity during labor
Answers 2. Engagement
3. First stage of labor
Case 1 4. Restitution
1. The mucosanguineous discharge is known as show. 5. Cervical effacement
It is the mucus plug of the cervix mixed with blood 6. Friedman’s curve
that is expelled in early labor. 7. Placental separation
2. Progressive effacement and dilatation. 8. Formation of lower segment of uterus
CH 14_p190-207_v3.indd 207 17-07-2015 12:01:26

Management
15 of Normal Labor
and Delivery
Case scenario
Mrs. BN, 22, a primigravida at 40 weeks’ gestation, was admitted to the

labor room with backache and pain in the lower abdomen. She had
noticed blood-stained vaginal discharge, and the pain was intermit-
tent, but progressively becoming more frequent and more severe.
Introduction Diagnosis of labor

Most labors progress normally and have a good Accurate diagnosis of labor is difficult especially
maternal and perinatal outcome. This, however, if the woman is in the latent phase of labor. False
is dependent on prompt diagnosis of labor, ade- labor is common and admitting women in false
quate monitoring, and appropriate management. labor must be avoided since it can lead to unnec-
Complications in labor occur at the most unex- essary intervention. Differences between true
pected moments, and the obstetrician has to be and false labor are listed in Table 15.1. If a diag-
vigilant. Adherence to protocols, adequate staff- nosis cannot be made with certainty, the parturi-
ing, and facilities to handle emergencies swiftly ent may be observed for a few hours.
are essential for ensuring good outcome.
Clinical evaluation
Procedures at admission istory
It is essential to first establish the diagnosis of A review of antenatal records is mandatory.
labor. The stage of labor and fetal and maternal Risk factors in the present pregnancy and com-
condition should also be assessed. plications during the previous pregnancy and
CH 15_p208-225_v3.indd 208 17-07-2015 12:41:16

Management of Normal Labor and Delivery 209
Table 15.1 Differences between true and false labor
True labor False labor

Uterine contractions • Regular • Irregular
• Increasing frequency • Variable intervals
• Increasing intensity • Variable intensity
Location of pain Low back and abdomen Lower abdomen
Cervical effacement and dilatation Present Absent or not progressive and dilatation
Show Present Absent
Sedation No effect Relieved
delivery should be noted (see Chapter 8, History maneuver (see Chapter 14, Normal labor:
taking and examination of the obstetric patient). Mechanics, mechanism, and stages) should be
Details regarding time of onset of contractions, performed to assess flexion or deflexion, engage-
their frequency, duration, presence of show, ment and descent of fetal head. Fetal heart
leakage of fluid, bleeding, and fetal movements sounds should be checked by auscultation.
should be obtained (Box 15.1). Routine enema and shaving of pubic hair
are no longer recommended. Pubic hair may be
Physical examination clipped if necessary.
This consists of recording vital signs, including

maternal pulse, blood pressure, and tempera- aginal examination
ture. Uterine contractions, fetal lie, presentation,
This is performed with the parturient in the dor-
and position should be assessed by abdominal
sal position, with the hips and knees flexed, and
examination. Second pelvic grip and Crichton’s
the hips slightly abducted. Aseptic precautions
must be taken and the index and middle fin-
Box 15.1 Clinical evaluation gers of the gloved right hand are used. (Vaginal
examination should not be performed if there is
• Review antenatal records
Ŧ Antenatal risk factors
significant active bleeding.) On vaginal examina-
Ŧ Complications in previous pregnancy/labor tion, cervical effacement, dilatation, consistency,
• History position, status of membranes, fetal presenta-
Ŧ Labor pains tion, and position and station of the presenting
Time of onset part should be noted. If the membranes are rup-
Frequency tured, presence of meconium should be looked
Duration for (Box 15.2). Lastly, the type of pelvis should be
Ŧ Presence of show determined, and contracted pelvis excluded.
Ŧ .GCMCIGQHƀWKF Consistency of the cervix may be firm,
Ŧ Fetal movements
medium, or soft, depending on the prelabor rip-
• General examination
ening. Position of the cervix is in relation to the
Ŧ Vital signs
fetal head and can be anterior, midposition, or
Pulse
Blood pressure posterior.
Temperature Fetal position is the relationship of the occiput
• Abdominal examination to the quadrant of the pelvis, for example, left
Ŧ Uterine contractions occipitoanterior (LOA) or right occipitoante-
Duration rior (ROA) (Fig. 15.1). Flexion is determined by
Frequency the portion of the sagittal suture and the fon-
Intensity tanel that is felt on vaginal examination. When
Ŧ Fetal presentation the head is well flexed, the posterior fontanel is
Ŧ Position easily felt and the anterior fontanel is not felt
Ŧ Descent
or felt with difficulty (Fig. 15.2). If the anterior
Ŧ Fetal heart sounds
and posterior fontanels are felt with equal ease
CH 15_p208-225_v3.indd 209 17-07-2015 12:41:16

Box 15.2 aginal examination

• Cervix
Ŧ %QPUKUVGPE[5QHVOGFKWOſTO
Ŧ Effacement (in centimeters of length of cervix)
Ŧ Dilatation (in centimeters)
lexio e lexio
Ŧ Position: Anterior/midposition/posterior
• Status of membranes Figure 15.2 Flexion of the fetal head as determined by
Ŧ Intact XCIKPCNGZCOKPCVKQP9JGPJGCFKUYGNNƀGZGF
XGTVGZ
Ŧ Ruptured presentation), the posterior fontanel is well felt and anterior
• Meconium, if membranes ruptured HQPVCPGNKUHGNVYKVJFKHſEWNV[9JGPJGCFKUFGƀGZGF
• Fetus anterior and posterior fontanels are felt with equal ease.
Ŧ Presentation
Ŧ Position
Ŧ (NGZKQP(NGZGFFGƀGZGFGZVGPFGF
Ŧ Station
• Assessment of bony pelvis
Ŧ Shape cm
Ŧ Any abnormality
at either end of the sagittal suture or if the ante-

rior fontanel is felt more easily, then the head is
deflexed. The head is extended if the presenta- Figure 15.3 Station of the presenting part as determined
tion is brow or face (see Chapter 41, Abnormal by vaginal examination. The level of the ischial spines is
labor: Malposition and malpresentations). considered as ‘0’. There are 5 levels above and below, as
Station or level of the vertex (or other pre- minus (–) 1–5 and plus (+) 1–5.
senting part) is determined by the relationship
of the leading part to the ischial spines. The level of the ischial spines is considered ‘0’ station. The
portion of the pelvis from the inlet to the ischial
spines is divided into five levels, each 1 cm above
the other, designated as stations –1, –2, –3, –4,
and –5. Similarly, the part of the pelvis below is
divided into five levels, designated as +1, +2, +3,
+4, and +5. Minus 5 is at the level of the inlet or
L pelvic brim and +5 at the introitus (Fig. 15.3).
Caput succedaneum
A caput succed aneum develops on the fetal
scalp when labor is prolonged. The area of the
scalp that is pressed against the cervix becomes
L
edematous (Box 15.3; Fig. 15.4a and b). An exten-
sive and thick caput forms in the most depen-
dent part of the vertex when there is obstructed
labor or prolonged labor. The caput appears as a
diffuse swelling, and the location depends on the
position of fetal head. It may be difficult to feel
L P P the sutures of the vertex and ascertain position
Figure 15.1 Fetal position. On vaginal examination, and flexion when there is a large caput. The sta-
position is determined by the relationship of the occiput tion of the fetal head may also appear to be lower
to the quadrants of the pelvis. In occiput transverse if the vertex is not carefully palpated through the
positions, the occiput is pointing directly to the left or caput. The caput is present at birth but disap-
right side of the pelvis. pears in 24–48 hours.
CH 15_p208-225_v3.indd 210 17-07-2015 12:41:16

Box 15.3 Caput succedaneum Box 15.4 Molding

• Localized edema of fetal scalp • Coming together/overlapping of skull bones
• Appears as diffuse swelling • Occurs in occipitoparietal and parietoparietal sutures
• Subsides 1–2 days after delivery • Reduces diameters of the fetal skull
• If cervix is thick • Expressed as
Ŧ forms where fetal scalp presses against the cervix Ŧ 1+: Bones touch each other
Ŧ is few millimeters thick Ŧ $QPGUQXGTNCRDWVUGRCTCVGQPſPIGTRTGUUWTG
• In prolonged/obstructed labor Ŧ $QPGU QXGTNCR CPF FQ PQV UGRCTCVG QP ſPIGT
Ŧ covers larger area pressure
Ŧ thicker and more edematous • Physiological when mild (1+)
Ŧ forms in the most dependent area of scalp • Indicates obstructed labor when severe (2+/3+)
Ŧ UWVWTGUCPFHQPVCPGNDGEQOGFKHſEWNVVQRCNRCVG
Caput
agittal suture
nterior fontanel
a.
Figure 15.5 Molding. When resistance is encountered
Caput in the bony pelvis, the fetal skull bones come together or
even overlap.
Periosteum
agittal suture other; therefore, there is molding at the occipito-
parietal suture and the sagittal (parietoparietal)
suture. The degree of molding is expressed as
calp
follows (Fig. 15.5):
alea aponeurotica
ull bone • 1+: The bones touch each other.
b. • 2+: The bones overlap but separate on pres-
sure by finger (reducible).
Figure 15.4 Caput succedaneum.a. Caput succedaneum.
The area of the scalp that is pressed against the cervix
• 3+: The bones overlap and do not separate
becomes edematous. b.6JGƀWKFKUUWRGTſEKCNVQVJG with pressure by finger (irreducible).
periosteum and goes across the suture lines. In mild degrees of cephalopelvic disproportion,
molding may reduce the suboccipitobregmatic
Molding diameter and facilitate vaginal delivery. Some
degree of molding is physiological and occurs in
The sutures joining the skull bones of the fetus most women in labor when the head negotiates
are quite flexible. The fetal skull bones come the midpelvis.
together or even overlap when resistance is
encountered in the maternal bony pelvis, thus
Assessment of the bony pelvis
reducing the diameters of the skull and enabling
normal delivery. The extent of overlapping of Assessment of the bony pelvis is described in
skull bones is called molding (Box 15.4). During detail in Chapter 8, History taking and exam-
molding, the occipital bone slips under the pari- ination of the obstetric patient. The type of
etal bones and one parietal bone slips under the pelvis should be determined by noting its
CH 15_p208-225_v3.indd 211 17-07-2015 12:41:17

characteristic features. The diagonal conjugate Bladder function

should be measured if the sacrum is tipped. A
decrease in any diameter at any level should be Women in labor should be encouraged to void
documented. frequently. As the head descends, women may
find it difficult to void. If the bladder is distended
and the woman cannot void, catheterization
Admission test may be required.
A short nonstress test for 20 minutes, using
cardiotocography, is performed at admission in Analgesia
some centers. Women with a normal trace are Analgesia is administered to relieve pain.
then monitored by intermittent auscultation. Epidural analgesia, where available, is a good
Several studies have concluded that admission means of providing analgesia without interfering
cardiotocography is not useful in low-risk women. with uterine contractions.
Method of pain relief in labor should be
discussed during the antenatal period. Labor
analgesia is discussed in Chapter 18, Obstetric
Management of analgesia and anaesthesia. Administration of
ſTUVUVCIGQHNCDQT analgesia should not be delayed too long but
administration in early latent phase can result in
During the first stage of labor, uterine contrac- prolongation of the latent phase of labor.
tions become progressively stronger, the cervix General management of normal labor is out-
dilates and the presenting part descends. Close lined in Box 15.5.
monitoring of these is essential to ensure that
the events are progressing normally. Box 15.5 General management of normal labor
• Ambulation/maternal position
Ŧ Early labor
Supportive measures Ambulation
in labor Ŧ Active phase
Lying in lateral position
The first stage of labor usually extends for a few Ŧ Oral intake
hours. It is important that the parturient be Frequent clear fluids
made comfortable during this time and the nec- No solids
essary pain relief and support provided. Ŧ +PVTCXGPQWUƀWKFU
Dextrose saline in prolonged labor
Ŧ Bladder function
Ambulation maternal position Frequent voiding
During the early stage of labor, women may be Catheterization if unable to void
Ŧ Analgesia
allowed to walk about or sit in a comfortable
Parenteral or epidural
chair. In the active phase of labor, most women
prefer to lie down. When they lie down, they
must be encouraged to lie in the lateral position Monitoring
to avoid supine hypotension.
Maternal monitoring
ral intake Pulse, blood pressure, and temperature should
be recorded hourly and more frequently, if there
Gastric emptying is delayed in labor. Vomiting
are indications. If labor is prolonged, look for
and aspiration are common. Solid food is, there-
signs of dehydration.
fore, not recommended during labor. Clear fluids
should be given orally, and the woman should
remain well hydrated. If labor is prolonged,
terine contractions
intravenous (IV) dextrose saline may be admin- Uterine contractions are monitored with the
istered to prevent dehydration and acidosis. palm of the hand on the abdomen. The duration,
CH 15_p208-225_v3.indd 212 17-07-2015 12:41:17

interval between contractions (frequency),

Box 15.7 Assessment of progress in labor
and intensity should be noted. As described in
Chapter 14, Normal labor: Mechanics, mecha- • Abdominal examination
nism, and stages, the examining fingers cannot Ŧ &GUEGPVQHHGVCNJGCFKPŎſHVJUŏ
• Vaginal examination
indent the uterus when the contraction is of
Ŧ Cervical effacement, dilatation
adequate intensity. If cardiotocography is used,
Ŧ 2TGUGPVKPIRCTV5VCVKQPƀGZKQP
contractions can be recorded on the trace. Ŧ Status of membranes
Ŧ 2GTHQTOGFGXGT[JQWTUKPſTUVUVCIG
Fetal monitoring Ŧ Performed when membranes rupture and head not
engaged
In low-risk pregnancies, during the first stage
Ŧ Frequency variable
of labor, fetal heart rate should be checked after
a contraction, by intermittent auscultation,
every 30 minutes. During the second stage, membranes rupture, especially if the head is
monitoring should be every 15 minutes. When not engaged.
the laboring woman is pushing, the fetal heart
rate should be monitored more frequently. If
electronic fetal monitoring is used, the trace
Amniotomy
should be reviewed every 30 minutes in the first Membranes usually rupture at or near full dil-
stage and every 15 minutes in the second stage. atation of the cervix but can rupture earlier.
Monitoring should be more frequent in high- Membranes are sometimes ruptured electively
risk women. when the cervix is >4-cm dilated, with the inten-
Monitoring in labor is outlined in Box 15.6. tion of accelerating labor. Randomized trials
have shown that artificial amniotomy is not
Box 15.6 Monitoring in labor associated with significant reduction in dura-
tion of labor, need for oxytocin, or cesarean sec-
• Maternal
tion rate. Routine amniotomy is, therefore, not
Ŧ Pulse, blood pressure, temperature (4 hourly)
recommended.
Ŧ With palm of hand on abdomen The advantages and disadvantages of amniot-
Ŧ Frequency omy are enumerated in Box 15.8.
Ŧ Duration
Ŧ Intensity Box 15.8 Amniotomy
• Fetal heart
Ŧ Intermittent auscultation/electronic fetal monitor • Elective amniotomy
Every 30 minutes during first stage Ŧ Performed in spontaneous labor
Every 15 minutes during second stage Ŧ After 4–5 cm dilatation
More frequently while pushing • Advantages
Ŧ Can diagnose meconium staining
Ŧ (CEKNKVCVGUſZKPIQHHGVCNUECNRGNGEVTQFG
Assessment of • Complications
Ŧ Chorioamnionitis
progress in labor Ŧ Cord prolapse
• No difference in
Progress in labor is assessed by abdominal and
Ŧ duration of labor
vaginal examination (Box 15.7). Descent of the Ŧ need for oxytocin
head in fifths should be recorded by abdominal Ŧ cesarean section rate
palpation. On vaginal examination, effacement
and dilatation of cervix, station of present-
ing part, degree of flexion, caput formation,
molding, and status of membranes should be
Partograph (or partogram)
noted. Frequency of vaginal examination must A partograph (or partogram) is a simple, inex-
be individualized but 4-hourly examination is pensive tool that provides a graphic documen-
the norm in the first stage of labor. In addition, tation of progress in labor and that allows early
a vaginal examination may be required when recognition of dysfunctional labor.
CH 15_p208-225_v3.indd 213 17-07-2015 12:41:17

Friedman, in 1955, found that the least rate of contractions, maternal vital signs, oxytocin aug-
cervical dilatation in the active phase of labor in mentation, and fetal parameters such as fetal
multigravidas is 1.5 cm/hour and in primigravi- heart rate, presence of meconium, and molding
das it is 1.2 cm/hour. The minimum acceptable of the head are recorded in the graph, which is
rate of dilatation is 1cm/hour for both multipara known as the composite partograph (Fig. 15.7).
and primigravida; below this, progress is consid- The first composite WHO partograph included a
ered abnormal. latent phase of 8 hours and the alert line began
Philpott and Castle, in 1972, introduced alert at 3-cm dilatation (beginning of active phase).
and action lines based on Friedman’s data. The A modified WHO partograph was introduced in
alert line is drawn from 3-cm dilatation (when 2000. This does not include the latent phase and
active phase begins, as per Friedman's defini- the alert line (and active phase) begins at 4-cm
tion). The alert line represents a progress rate of dilatation.
1 cm/hour, until full dilatation. Any labor where The features of modified WHO partograph are
the graph is to the left of this line is normal. listed in Box 15.9.
When the graph crosses the alert line, progress
is considered to be slow and the obstetrician is Advantages of partograph
alerted to the possibility of dysfunctional labor.
If the parturient is in a primary or secondary care The partograph has proved valuable in both
center, she may be transferred to a tertiary cen- resource-rich and resource-poor areas for early
ter. An action line is drawn 4 hours to the right of recognition of prolonged labor.
the alert line. When the graph crosses the action The advantages of partograph are listed in
line, definitive action to prevent prolonged/ Box 15.10.
obstructed labor is indicated (Fig. 15.6).
Management of
The W composite second stage of labor
partograph After full cervical dilatation, descent and deliv-
Subsequently, as per the recommendations of the ery of the fetus occur in the second stage.
Safe Motherhood Conference, WHO introduced Management of this stage consists of the identi-
a partograph in 1990. In addition to cervical dil- fication of onset of the second stage, preparation
atation, descent of the presenting part, uterine for delivery, and conduct of delivery.
cti e phase
n
io
rt
ct
le
Cer i cm
Plot
escent
of hea Latent phase
Plot
ime Hours
Figure 15.6 The partograph. Duration of labor in hours is marked on the X axis and cervical dilatation and descent of the
fetal head are marked on the Y axis. Alert line begins at 3-cm dilatation and action line begins 4 hours to the right.
CH 15_p208-225_v3.indd 214 17-07-2015 12:41:17

ame ra i a Para Hospital number

ate of a mission ime of a mission upture membranes hours
etal
heart
rate
mniotic flui
Mol ing
t n
ler ctio
Cer i cm
Plot
escent
of hea
Plot
Hours
ime
Contractions
per mins
ytocin U L
rops min
rugs gi en
an V flui s
Pulse
an
P
emp C
protein
Urine acetone
olume
Figure 15.7 Composite partograph. In this, in addition to cervical dilatation and fetal decent, uterine contractions, maternal
vital signs, urine output oxytocin augmentation, fetal heart rate, presence of meconium, and molding of the head are
recorded.
CH 15_p208-225_v3.indd 215 17-07-2015 12:41:17

Box 15.9 (GCVWTGUQHOQFKſGF9*1RCTVQITCRJ Box 15.11 Preparations for delivery

Components • Maternal position
• Cervical dilatation and descent Ŧ Dorsal/semirecumbent/dorsal lithotomy
• Latent phase not included Clean the vulva
• Cervical dilatation plotted against time Sterile drapes
• Minimum rate of dilatation: 1 cm/hour Keep local anesthetic ready, if required
• Alert line: Begins at 4-cm dilatation Delivery tray to be opened and ready
• Action line: 4 hours to the right of alert line Keep 10 units of oxytocin ready for use in third
• Fetal parameters stage
Ŧ Fetal heart rate
Ŧ Liquor
Ŧ Molding commonly used. When the woman is brought
• Maternal parameters down to the edge of the cot, soiling of obste-
Ŧ Vital signs trician’s clothes and feet by amniotic fluid and
Ŧ Urine output/protein blood is more. Mid-cot delivery (delivering in
Ŧ +8ƀWKFU the middle of the cot) is recommended for nor-
Ŧ Drugs mal delivery to avoid this. A semirecumbent
Ŧ Uterine contractions position with head and shoulders elevated to
Ŧ Oxytocin dose
45 degrees may also be used. A lithotomy posi-
tion with the legs in stirrups and the buttocks
at the edge of the delivery table is preferred if
Box 15.10 Advantages of partograph
instrumental delivery is anticipated. The lat-
• Effective tool to eral position does not interfere with venous
Ŧ document events in labor return and is preferred in women with cardiac
Ŧ assess progress of labor valvular disease. Preparations for delivery are
Ŧ diagnose dysfunctional labor early listed in Box 15.11.
Ŧ prevent obstructed labor
• Assists in
Ŧ early augmentation of labor Delivery of the head
Ŧ early termination of labor
Ŧ early transfer of the parturient to tertiary center The head descends and is seen at the vulva,
initially during contractions and later in
between contractions as well. When the head
Watching for bearing is seen at the vulval outlet and does not recede
between contractions, crowning is said to have
down pains occurred (Fig. 15.8). The anus is stretched and
When the cervix is fully dilated and the fetal head the anal opening appears prominent. If an
descends low into the vagina, the woman has
an uncontrollable urge to bear down. She usu-
ally will flex her knees and bear down. Uterine
contractions increase in duration, last for 1–1.5
minutes and the interval between contractions
decreases to 1 minute. When the fetal head
presses on the rectum, the woman has an urge to
defecate. At this time, preparations for delivery
should be made.
Preparations for delivery

Maternal position
Figure 15.8 Crowning of the fetal head. When the fetal
The dorsal position with flexion at hips and head is visible at the vulval outlet and does not recede
knees and abduction of the thighs is most between contractions, crowning is said to have occurred.
CH 15_p208-225_v3.indd 216 17-07-2015 12:41:18

episiotomy is indicated, it should be performed Suctioning the baby’s nose and mouth when
at this time; however, routine episiotomy is not the head is at the perineum is not recommended
recommended. irrespective of meconium staining of amniotic
A sterile towel or pad is held in the right hand fluid.
and placed over the perineum. The left hand
is placed on the occiput to apply gentle down-
ward pressure to promote flexion and con-
Delivery of the shoulders
trolled delivery of the head. This ensures that With external rotation of the fetal head, the
the smallest diameter of the fetal head presents shoulders rotate to lie in the anteroposterior
at the outlet. Simultaneously, the perineum is diameter of the pelvis. The anterior shoulder is
supported with the right hand through the towel delivered first by downward traction and then
to reduce the incidence of perineal lacerations, the posterior shoulder by an upward sweeping
especially third and fourth degree perineal movement (Fig. 15.10). The rest of the body usu-
tears. Once the occiput is born, gentle pressure ally slips out immediately. Management of the
is exerted on the chin of the fetus with the right second stage is outlined in Box 15.12.
hand, to promote extension of the head; the
forehead, nose, mouth, and chin are born. This
procedure is called the modified Ritgen maneu-
ver (Fig. 15.9). The hands poised technique
involves waiting and watching without touch-
ing the fetal head or perineum. Randomized
trials have not shown any difference in inci-
dence of perineal lacerations between the two
methods of delivery.
Once delivered, the head undergoes restitu-
tion and external rotation. The infant’s face is
turned toward the maternal thigh. The infant’s
neck should be palpated and if the umbili- Figure 15.10 Delivery of shoulders. The anterior shoulder
is delivered by downward traction and posterior shoulder
cal cord is wound around the neck of the fetus
by an upward lifting of the fetus.
(nuchal cord), it can be slipped over the head.
If the cord is tight around the neck, two clamps
are placed on it and the cord is cut between the Box 15.12 Management of second stage
clamps to facilitate delivery. • Delivery of the head
Ŧ Wait for crowning
Ŧ /QFKſGF4KVIGPOCPGWXGT
Support perineum with towel/pad in right hand
- Prevents perineal laceration
Downward pressure with left hand on occiput
- Promotes flexion
- Controlled delivery
Upward pressure on chin through perineum
- Promotes extension and delivery of face
Ŧ Delivery of shoulders
Wait for external rotation of head
Downward traction to deliver anterior shoulder
Upward movement for delivery of posterior
shoulder
Prophylactic uterotonics
Figure 15.9 /QFKſGF4KVIGPOCPGWXGT1PGJCPFKU
placed on the occiput to prevent rapid delivery, the The oxytocics used for prophylaxis against post-
other hand supports the perineum to prevent perineal partum hemorrhage are methyl ergometrine
lacerations and promote extension of the fetal head. (methergine) and oxytocin.
CH 15_p208-225_v3.indd 217 17-07-2015 12:41:18

xytocin hemorrhage. Misoprostol can be used orally or

rectally in a dose of 600–800 mg when oxytocin
Oxytocin is the drug of choice and can be ad- and ergometrine are not available. Its advantage
ministered intramuscularly or intravenously. is that refrigeration is not required because it is
The current recommendation is to adminis- stable at room temperature, but it is less effec-
ter 10 units of oxytocin intramuscularly (IM) tive than ergometrine and oxytocin. It is recom-
with the anterior shoulder or within 1 minute mended for use in resource-poor settings, where
of delivery of the baby. It may also be given as refrigeration facilities for drug storage and skilled
an IV infusion in doses of 10–20 units in 500 mL birth attendants who can administer injections
of saline over a period of 2 hours if an IV line is are not available.
already in place. Intravenous bolus injection of Prophylactic uterotonics are listed in Table 15.2.
10 units can cause hypotension. Side effects are
uncommon with IM use. Unlike methergine, the
need for manual removal of placenta is not in- Clamping of umbilical cord
creased with IM oxytocin, even when adminis-
tered before placental delivery. Timing of clamping
Early cord clamping, as soon as the baby is
Ergometrine delivered, reduces the amount of blood return-
Methyl ergometrine should be administered ing to the fetus from the placenta. About 80 mL
intravenously, in a dose of 0.25 mg, at the delivery of blood flows into the fetus if cord clamping is
of the anterior shoulder. If administered after delayed by 3 minutes. This increases the baby’s
delivery of the fetus but before placental delivery, iron stores and reduces the risk of neonatal
hourglass contraction of the uterus, retention of anemia. However, delaying cord clamping can
the placenta, and the need for manual removal cause hyperbilirubinemia, necessitating photo-
can occur. It can also cause a sudden increase in therapy. Therefore, it is recommended that the
blood pressure, nausea, and vomiting. It is, there- cord should be clamped 1–3 minutes after the
fore, contraindicated in hypertensive disorders of delivery of the baby. In preterm babies delayed
pregnancy and cardiac valvular disease. clamping can cause cardiac overload and there-
A combination of ergometrine 0.5 mg and fore, the cord should be clamped immediately in
oxytocin 5 units, known as syntometrine, is also preterm births (Box 15.13).
available and equally effective but can cause
hypertension. Site of clamping
The cord is usually clamped 5–6 cm from the
Prostaglandins fetal abdomen. Two clamps are placed 3–4 cm
PGF2D is not used for prophylaxis though it is apart and the cord cut between the two. The cord
useful for the treatment of atonic postpartum should be milked after placing the first clamp,
Table 15.2 Prophylactic uterotonics
Drug characteristic Ergometrine xytocin Misoprostol

'HſECE[ Effective Effective Less effective
Route of administration IV/IM IM/IV/infusion Oral/rectal
Timing of administration At anterior shoulder or At anterior shoulder or after After delivery
after placental delivery delivery of baby of placenta
Dose 0.25 mg 10 units 600–800 mg
Side effects • Sudden hypertension Rarely hypotension • Nausea, vomiting
• Nausea, vomiting • Pyrexia
• Hourglass contraction
• Retained placenta
Refrigeration Not required Required Not required
CH 15_p208-225_v3.indd 218 17-07-2015 12:41:18

Box 15.13 Clamping of umbilical cord Box 15.14 Signs of placental separation
• Early clamping • 7VGTWUDGEQOGUſTOCPFINQDWNCT
Ŧ Reduces blood to fetus from placenta • Gush of blood from vagina
Ŧ No gain in hematocrit • Increase in the extravulval portion of the cord
Ŧ No hyperbilirubinemia • Appearance of suprapubic bulge
Ŧ Preferred in preterm births • Uterus pushed upward by placenta in lower segment
• Late clamping • When uterine fundus is pushed up, cord does not
Ŧ +PETGCUGUDNQQFƀQYHTQORNCEGPVCVQHGVWU recede
80 mL in 3 minutes
Improves fetal iron stores and reduces fetal anemia
Ŧ Increased risk of hyperbilirubinemia
The placenta separates within 5 minutes of
• Recommendation
delivery of the baby. Once signs of placenta sep-
Ŧ 1–3 minutes after delivery of the baby
• Site of clamping
aration appear, the uterus is pushed upward
Ŧ 5–6 cm from umbilicus (cephalad) with the left hand on the abdomen
and the cord is held taut with the right hand.
This is called controlled cord traction or mod-
ified Brandt–Andrews maneuver (Box 15.15;
and the second clamp should be placed just Fig. 15.11). This method of placental delivery
beyond the milked segment, so that a bloodless prevents uterine inversion since there is no
field is obtained for dividing the cord. After the downward pressure on the uterine fundus. Once
baby is handed over to the nurse/pediatrician, the placenta appears at the vulva, it is grasped
and immediate baby care has been provided, a with both hands and gently removed, taking care
disposable cord clamp is placed 2–3 cm distal to to remove the membranes as well.
the umbilicus.
If blood is being drawn for umbilical cord
blood banking (for stem cells), it has to be done
before cord clamping. Box 15.15 /QFKſGF$TCPFV–Andrews technique
• Controlled cord traction
• Left hand grasps uterine fundus through abdomen
• Right hand holds cord taut
Management of third stage • Left hand pushes uterus upward (cephalad)
Placental separation and expulsion occur in the

third stage of labor.
Signs of placental separation

When the placenta separates, there is a gush of
blood, especially if the separation is marginal
(Chapter 14, Normal labor: Mechanics, mech-
anism, and stages). The uterus contracts and
retracts. The placenta comes to lie in the lower
uterine segment and the vagina, forming a bulge
in the suprapubic area and pushing the uterus
upward. The part of the cord protruding out-
side the vulva lengthens, and on pushing the
uterus upward, the cord does not recede into the Figure 15.11 /QFKſGF$TCPFV–Andrews maneuver. The
vagina since the placenta is no longer attached placenta is delivered by controlled cord traction wherein
to the uterus. the uterus is pushed upward with the left hand and
Signs of placental separation are listed in gentle, steady traction is applied with the right hand in the
Box 15.14. direction indicated by the arrow.
CH 15_p208-225_v3.indd 219 17-07-2015 12:41:18

Active management of cord is 50–60 cm long. The normal cord should

have two arteries and one vein. The maternal
third stage of labor (AMTSL) and fetal surfaces of the placenta should be
Active management of the third stage is aimed at examined for abnormalities (see Chapter 46,
preventing the two main complications of third Abnormalities of the placenta: Cord and fetal
stage: postpartum hemorrhage and retained pla- membranes). Missing cotyledons must be looked
centa. The active management of the third stage for and membranes examined to ensure that the
consists of the following: placenta is complete.
• Administration of uterotonic agent

Oxytocin 10 units IM is administered with the
anterior shoulder or within 1 minute of deliv-
Management of
ery of the baby. fourth stage
• Delivery of placenta by controlled cord traction
The delivered woman should be monitored
Controlled cord traction following oxyto- closely during the fourth stage of labor, which
cin administration prevents postpartum extends over 1–2 hours after delivery. Postpartum
hemorrhage. hemorrhage, vulval hematoma, and postpartum
collapse can occur during this time. The pulse
• Assessment of uterine tone and size
should be checked every 30 minutes and blood
The uterus is assessed intermittently to see if it pressure monitored every hour. A distended
is well contracted by placing the left hand on the bladder should be watched for as it may indicate
fundus, abdominally. a vulval hematoma. The urine output should be
monitored (Box 15.17).
Uterine massage to promote uterine con-
traction and prevent excessive bleeding was
Box 15.17 Fourth stage of labor
a common practice earlier. However, uter-
ine massage causes discomfort and does not • Watch for complications
reduce blood loss. It is therefore not recom- Ŧ Postpartum hemorrhage
mended currently. Ŧ Vulval hematoma
Ŧ Postpartum collapse
Early clamping of the cord does not contrib- • Monitor
ute much to prevention of postpartum hemor- Ŧ Pulse half-hourly
rhage; therefore, this is not included in active Ŧ Blood pressure hourly
management of the third stage. Ŧ Voiding and urine output
Examination of the placenta Episiotomy

The placenta, fetal membranes, and umbilical
Episiotomy is the surgical incision on the
cord must be examined after delivery (Box 15.16).
perineum to enlarge the vaginal introitus and
The normal placenta weighs about one-sixth the
facilitate delivery. There are two types of episi-
weight of the baby and the normal umbilical
otomy (Fig. 15.12):
• Median: In the midline, extending from the
Box 15.16 Examination of the placenta posterior fourchette toward the anus
• Mediolateral: Extending laterally from the pos-
• Weight: One-sixth the baby’s weight (500–600 g)
• Cord length: 50–60 cm
terior fourchette in the midline, at an angle of
• Vessels in the cord: Two arteries, one vein 45 degrees
• Look for The incision involves the vaginal wall, per-
Ŧ missing cotyledons
ineal muscles, and skin and is about 3–4 cm in
Ŧ completeness of membranes
length. Episiotomy was routine practice for all
Ŧ other abnormalities
nullipara and most multipara. With increasing
CH 15_p208-225_v3.indd 220 17-07-2015 12:41:18

Box 15.19 Indications for episiotomy

• When failure to perform episiotomy will result in tear
Hea of baby • Large baby
• Delivery as occipitoposterior
• Operative vaginal deliveries
Mi iline Ŧ Forceps
Ŧ Vacuum extraction
Me iolateral • Shoulder dystocia
• Vaginal breech delivery
Figure 15.12 Types of episiotomy. Episiotomy can be

median or mediolateral; both begin at the midline and to the convenience of the obstetrician. Median
extend either vertically toward the anus or laterally at episiotomy is not recommended because of risk
45 degrees. of the extension to the anus and the rectum.
However, a midline episiotomy is associated
Box 15.18 2TQRQUGFDGPGſVUQHGRKUKQVQO[ with less blood loss, better healing, easier repair,
and less postoperative dyspareunia.
• Maternal
Ŧ Slightly shorter second stage
Ŧ Surgical incision rather than tear Timing of episiotomy
Ŧ 2TGXGPVKQPQHRGNXKEƀQQTTGNCZCVKQP
Less urinary incontinence The timing for episiotomy is given in Box 15.20.
Less fecal incontinence
Ŧ Less anal sphincter injury
Ŧ Less sexual dysfunction Box 15.20 ecommended type and timing
• Neonatal of episiotomy
Ŧ Less intracranial hemorrhage in preterms • Type
Ŧ Mediolateral
• Timing
awareness regarding the complications of episi- Ŧ When head is ‘crowning’
otomy, the benefits of routine episiotomy have Ŧ When breech is climbing the perineum
been questioned. The proposed benefits of epi- Ŧ Before or after blades of forceps are placed but
before traction
siotomy are listed in Box 15.18.
A review of randomized trials has found no
difference in healing or postoperative pain with
lacerations, an increase in anal sphincter injury Procedure
with median episiotomies, and no increase in The procedure for an episitomy is as follows:
sexual dysfunction or urinary and fecal incon-
tinence without episiotomies. The American • Local anesthetic is infiltrated at the site of the
College of Obstetricians and Gynecologists episiotomy, if the woman is not on epidural
and the Royal College of Obstetricians and analgesia.
Gynaecologists currently recommend selective • Index and middle fingers are inserted between
(restrictive) episiotomy only if failure to per- fetal scalp and perineum to protect the scalp.
form episiotomy will result in perineal tear. • Knife or scissors may be used.
• Should start at midline of posterior fourchette.
• Should be cut
Indications – at 45 degrees for mediolateral (Fig. 15.13) and
Indications for episiotomy are listed in Box 15.19. – directly downward for median.
Types of episiotomy epair of episiotomy

A mediolateral episiotomy is the preferred type. This is performed after the placenta is delivered
Left or right mediolateral may be used according (Box 15.21).
CH 15_p208-225_v3.indd 221 17-07-2015 12:41:19

Me iolateral
episiotomy
Mi line
episiotomy
Figure 15.13 'RKUKQVQO[RTQEGFWTG+PFGZCPFOKFFNGſPIGTUCTGKPUGTVGFDGVYGGPVJGHGVCNUECNRCPFRGTKPGWOVQ

protect the scalp and the cut is made with scissors or a knife.
Box 15.21 epair of episiotomy Postoperative care

• After delivery of placenta This includes a nonsteroidal anti-inflammatory
• 2–0 chromic catgut or rapidly absorbable polyglactin agent orally or as a suppository. Local hygiene is
• Continuous suturing preferred maintained with regular cleaning with soap and
• Adequate exposure of apex water. Infrared or dry heat may be used for pain
• Suture in three layers relief. Sitz baths are soothing. Antibiotics are not
Ŧ Vaginal mucosa
recommended.
Ŧ Perineal muscle
Ŧ Skin
• Start with vaginal mucosa at apex
• Continue through muscle layer
Perineal lacerations
• Continue through skin Perineal lacerations are classified as follows:
• First degree: Involves skin and vaginal mucosa
• Second degree: Involves skin, vaginal mucosa,
If the three layers are sutured independently, and muscle (like an episiotomy)
continuous sutures are used for vaginal mucosa, • Third degree: Involves the anal sphincter
interrupted sutures for muscle layer, and either • Fourth degree: Involves the rectal mucosa
continuous or interrupted for skin (Fig. 15.14). (Fig. 15.15)
a i al
mucosa
Peri eal i suture
muscles
i
a i al Peri eal
muscles suture muscles suture
Figure 15.14 Suturing the episiotomy. Suturing is performed in three layers but with a continuous stitch, beginning with
the apex of vaginal mucosa and continued through the muscle layer and skin.
CH 15_p208-225_v3.indd 222 17-07-2015 12:41:19

Vaginal Vaginal mucosa

mucosa
Perineal Perineal muscles
in muscles
nal ectal mucosa
sphincter
a. b. . .
Figure 15.15 Perineal lacerations. a. First degree laceration involves skin and vaginal mucosa. b. Second degree
laceration involves muscle layers as well. c. Third degree lacerations involve the anal sphincter. d. Fourth degree
lacerations involve rectal mucosa.
isk factors Box 15.23 Management of perineal lacerations

Risk factors for perineal laceration are listed in • First degree: No repair required unless bleeding
Box 15.22. When laceration is anticipated, episi- • Second degree: Similar to episiotomy
otomy should be performed to avoid it. • Third and fourth degree
Ŧ Repair in operating room
Ŧ Regional or general anesthesia
Box 15.22 isk factors for perineal laceration Ŧ Lithotomy position
• Nulliparity Ŧ Adequate lighting
• Delivery as occipitoposterior Ŧ Adequate exposure
• Large baby Ŧ Interrupted sutures: 2-0 rapidly absorbable poly-
glactin
• Midline episiotomy
Ŧ Anal mucosa: Interrupted sutures
• Instrumental delivery
Ŧ Anal sphincters: Overlap or end-to-end approxi-
• Vaginal breech delivery
mation
Ŧ Vaginal mucosa, muscle layer, and skin: As in
episiotomy
Management of Ŧ Postoperative
Laxatives: 3–4 days
perineal lacerations Antibiotics: 5 days
First degree lacerations do not require repair
unless there is bleeding. Second degree lacera-
tions are repaired in the same way as an episiot- muscle layer, and skin are then sutured as done
omy. Local anesthetic should be injected before in an episiotomy (Fig. 15.16).
suturing. Third and fourth degree lacerations
should be repaired preferably in the operating
room, under adequate anesthesia, good expo-
Postoperative care
sure, proper positioning, and adequate lighting After the repair of third and fourth degree lac-
(Box 15.23). erations, stool softeners are given for 3–4 days
The repair is started initially with the anal postoperatively to reduce the incidence of
mucosa. The mucosa is approximated with 2–0 wound dehiscence. Antibiotics (third-gener-
rapidly absorbable polyglactin or chromic cat- ation cephalosporin + metronidazole) should
gut. The internal and external anal sphincters are be administered for 5 days. Infrared, dry heat,
approximated next, using overlap or end-to-end and oral analgesics should be administered
approximation technique. The vaginal mucosa, for pain relief.
CH 15_p208-225_v3.indd 223 17-07-2015 12:41:19

Vaginal mucosa
Perineal muscles nal mucosa

nal mucosa suture
nal sphincter
nal sphincter suture
a. b. .
Perineal muscles Vaginal mucosa

suture an s in suture
. .
Figure 15.16 Suturing of the fourth degree laceration. a. Fourth degree laceration. b. Suturing begins with rectal mucosa.
c. 6JGCPCNURJKPEVGTſDGTUCTGCRRTQZKOCVGFPGZVd. Perineal muscles sutured next. e. Finally, vaginal mucosa and skin
are sutured.
Key points
• Management of labor begins with the diagnosis of pressure of the left hand on the occiput and extension
labor. True labor must be differentiated from false labor. aided by the right hand on the perineum.
The woman should be admitted to the labor room only if
• Shoulders are delivered by downward traction to
the diagnosis of labor is reasonably certain.
deliver the anterior shoulder and upward movement to
• The woman’s antenatal records must be reviewed and deliver the posterior shoulder.
risk factors noted.
• Prophylactic oxytocin (10 units IM) should be ad-
• Physical examination includes checking vital signs, ministered at the delivery of the anterior shoulder
abdominal palpation to ascertain frequency, duration or after delivery of the baby, to prevent postpartum
and interval between contractions, presentation, posi- hemorrhage.
tion, and descent of fetal head, and fetal heart sounds.
• The cord should be clamped 30 seconds to 1 minute
• Vaginal examination to assess the cervix, status of after the delivery of the baby, about 5–6 cm from the
membranes, and level and position of fetal head is baby’s umbilicus. The cord should be cut between
the next step. The pelvis should be assessed for any clamps.
abnormality. • Monitoring of the mother should continue for 2 hours
• The presence of caput and molding should be looked after delivery.
for. The degree of molding should be noted.
• 2NCEGPVCNUGRCTCVKQPKUKFGPVKſGFD[QDUGTXKPIVJG
• &WTKPIVJGſTUVUVCIGQHNCDQTVJGYQOCPOC[DGCO- signs. Placenta is delivered by controlled cord traction
DWNCVGF(TGSWGPVENGCTƀWKFUUJQWNFDGIKXGPQTCNN[
OQFKſGF$TCPFVŌ#PFTGYUVGEJPKSWG
and voiding encouraged. Uterine contractions and • Placenta and membranes should be examined for
fetal heart rate should be monitored. completeness. The woman should be monitored for
• Progress in labor is assessed by Crichton’s maneuver 1–2 hours after delivery.
and vaginal examination.
• Routine episiotomy is not recommended for all
• Partograph is the graphic documentation of progress women. Use of episiotomy should be selective and
in labor. Cervical dilatation is plotted against time. only when indicated.
Other maternal and fetal parameters are also recorded • Suturing of episiotomy should be in layers—vaginal
in the WHO composite partogram. mucosa, perineal muscles, and skin.
• Taking the minimum rate of dilatation as 1 cm/hour,
• 2GTKPGCNNCEGTCVKQPUCTGENCUUKſGFCUſTUVUGEQPF
the alert line is drawn beginning at 4-cm dilatation.
third, and fourth degree lacerations. Third and fourth
The action line is drawn 4 hours to the right.
degree lacerations involve the rectal sphincter and
• Once the woman reaches the second stage of labor, mucosa and should be sutured under regional or
preparations for delivery are made. general anesthesia in an operating theater under
• 6JGJGCFKUFGNKXGTGFD[VJGOQFKſGF4KVIGPOC- good light.
PGWXGTKPYJKEJƀGZKQPKURTQOQVGFD[VJGFQYPYCTF
CH 15_p208-225_v3.indd 224 17-07-2015 12:41:20

Self-Assessment
Case-based questions rate, meconium, and maternal parameters should be
noted in the composite partograph.
Case 1 4. The alert line is drawn from 4 cm dilatation, taking
minimum rate of dilatation as 1 cm/hour. The action
Mrs. CA, 22, primigravida, is admitted to the labor room line is drawn 4 hours to the right. If the graph crosses
with backache and pain in the lower abdomen. She has the alert line, progress is slow and labor is abnormal.
blood-stained discharge, and the pain is intermittent, pro- +HKVETQUUGUVJGCEVKQPNKPGFGſPKVKXGUVGRUUJQWNFDG
gressively increasing in severity. taken to rectify the problem and expedite delivery.
1. Is she in labor? How will you differentiate true from
false labor? Case 2
2. What physical examination will you perform at
admission? 1. Ambulate the parturient, maintain hydration by
3. How will you assess and document progress in HTGSWGPVENGCTƀWKFUQTCNN[CPFGPEQWTCIGXQKFKPI
labor? Administer analgesia. Monitor progress in labor and
4. What are the alert and action lines on the maternal and fetal well-being.
partograph? 2. When in the second stage, the parturient should be
put in dorsal position, vulva and perineum cleaned
with antiseptic, and draped. The head is delivered by
Case 2 OQFKſGF4KVIGPOCPGWXGTD[FQYPYCTFRTGUUWTGQP
the occiput with the left hand and gentle upward pres-
Mrs. DA, 27, second gravida, is admitted in labor. Her sure on the chin through the perineum with the right
contractions are every 7 minutes, lasting for 30–40 sec- hand. Perineal support should be given to prevent
QPFU+VKUCXGTVGZRTGUGPVCVKQPJGCFVYQſHVJURCNRCDNG lacerations. Shoulders are delivered by downward
cervix 5-cm dilated, vertex at -1 station, left occipitoante- traction to deliver the anterior shoulder and upward
rior position. Membranes present. Fetal heart rate is 130/ movement to deliver the posterior shoulder.
min. 3. Administer prophylactic oxytocin 10 units IM, look for
1. *QYYKNN[QWOCPCIGVJGſTUVUVCIGQHNCDQT! signs of placental separation, and deliver placenta by
2. How will you prepare for and conduct delivery? controlled cord traction. Monitor the tone and size of
uterus with the left hand on the abdomen.
3. How will you manage the third stage?
4. If the baby is large, perineal tear imminent, or shoul-
4. What would be the indications for episiotomy in this
der dystocia.
woman?
Sample questions
Answers
Case 1
1. &GſPGPQTOCNNCDQT&KUEWUUVJGdiscuss the stages
1. Yes, she is in labor, because she has backache and of labor and their management.
lower abdominal pain, the uterine contractions are
2. What is partograph? How will you monitor a
increasing in frequency and intensity, and there is
woman in labor and document the progress
associated show. Further signs to look for would be
of labor?
dilatation and effacement of the cervix.
2. General examination for vital signs such as pulse and
blood pressure, abdominal examination for uterine Short-answer questions
contractions, duration, frequency, presentation, and
position of presenting part, descent of head, and fetal 1. False labor
heart rate. Vaginal examination for effacement and 2. Partograph
dilatation of cervix, presentation, position, station of 3. First stage of labor
presenting part, status of membranes, and type of 4. Delivery of placenta
pelvis. 5. Episiotomy
3. Dilatation of cervix and descent of head should be 6. Perineal laceration
evaluated by abdominal and vaginal examination 7. Caput succedaneum
every 4 hours. This should be plotted on a parto-
8. Molding of fetal head
graph. In addition, uterine contractions, fetal heart
CH 15_p208-225_v3.indd 225 17-07-2015 12:41:20

Induction
16 of Labor
Case scenario
Mrs. MN, 25, was admitted to the hospital in the 37th week of preg-
nancy. She had developed pregnancy induced hypertension at 36 weeks.
Within a week, her blood pressure went up to 160/100 mm Hg and a
urine test revealed 2 albumin. Delivery of the baby would be the best
treatment for her condition. She needed induction of labor.
Introduction Indications
Induction of labor is a therapeutic option when Labor may be induced because of maternal or
the benefits of delivery outweigh the risks of fetal indications (Box 16.1). In some cases, the
continuing the pregnancy. Induction is indi- indications may overlap.
cated when complications of pregnancy may
have a negative impact on the health of the
mother, the fetus, or both. The decision to Contraindications
induce labor must take into consideration the
potential maternal and fetal risks associated Induction of labor is contraindicated generally in
with this procedure. the same situations where spontaneous labor and
vaginal delivery are contraindicated (Box 16.2).
&GſPKVKQP Prerequisites for induction

Before a decision is made to induce labor, cer-
Induction of labor refers to methods used for
tain prerequisites should be met:
the stimulation of uterine contractions to bring
about delivery before the onset of spontaneous • The indication for the induction must be
labor or after the period of viability. assessed and discussed.
CH 16_p226-237_v3.indd 226 17-07-2015 12:59:37

Induction of Labor 227
Box 16.1 Indications for induction of labor Box 16.3 Checklist for induction of labor
aternal • Review indication
• Postdated or postterm pregnancy • Assess and discuss
• Preterm, prelabor rupture of membranes Ŧ Indication
• Prelabor rupture of membranes at term Ŧ Probability of failed induction
• Placental abruption • %QPſTOIGUVCVKQPCNCIG
• Hypertensive disorders Ŧ LMP
Ŧ Gestational hypertension Ŧ Ultrasound scan before 20 weeks
Ŧ Preeclampsia • Evaluate fetal well-being
Ŧ Eclampsia Ŧ Cardiotocography
Ŧ Chronic hypertension Ŧ $KQRJ[UKECNRTQſNG&QRRNGTKHTGSWKTGF
• Diabetes mellitus • Abdominal examination
• Antiphospholipid syndrome Ŧ Fetal size
• Intrauterine fetal demise Ŧ Presentation
Ŧ Descent of presenting part
etal
• Pelvic examination
• Fetal growth restriction Ŧ Favorability of cervix
• Oligohydramnios Effacement
• Rh alloimmunization Dilatation
• Nonreassuring fetal testing Consistency
Ŧ Station of presenting part
Ŧ #FGSWCE[QHRGNXKU
Box 16.2 Contraindications for induction
of labor P, last menstrual period.
• Abnormal fetal presentation

Ŧ Breech
Ŧ Brow Prediction of success
Ŧ Face
Ŧ Transverse lie of induction of labor
• Suspected cephalopelvic disproportion/contracted
pelvis It is difficult to predict the success of labor
• Placenta previa induction. When a vaginal delivery follows labor
• Umbilical cord presentation induction, the induction is considered successful.
• Severe fetal growth restriction with signs of fetal Failed induction results in cesarean section.
compromise Some patient characteristics have been found
• Previous uterine rupture to be associated with a higher rate of vaginal
• Surgical scar on the uterus
delivery (Box 16.4). They are not specific pre-
Ŧ Previous classical cesarean section
dictors, since they are indicative of likelihood
Ŧ Previous inverted T incision
Ŧ Previous myomectomy scar entering the endome-
of vaginal delivery in spontaneous labor as well.
trial cavity The only method that is currently in use to pre-
• Active maternal genital herpes infection dict the success of labor induction is the modi-
• Invasive cervical cancer fied Bishop score.
• Any contraindication must be ruled out.

• The cervix must be assessed to see if it is Box 16.4 Predictors of success of induction
favorable for induction (Bishop score). of labor
• The pelvis must be assessed to rule out the • Patient characteristics
possibility of fetopelvic disproportion or Ŧ Gestational age close to term
dystocia. Ŧ (CXQTCDNGRGNXKEEQPſIWTCVKQP
• Fetal size and presentation must be assessed. Ŧ Multiparity
• Fetal well-being must be assessed prior to Ŧ Fetal weight <3.5 kg
induction. Ŧ Tall stature
Ŧ Normal body mass index
The checklist for induction of labor is enu- • High Bishop score
merated in Box 16.3.
CH 16_p226-237_v3.indd 227 17-07-2015 12:59:37

Bishop score for Preinduction cervical

assessment of ripening
the cervix Induction may be indicated even when the cer-
vix is unfavorable or unripe (Bishop score <6).
The most important predictor of the success of In these cases, techniques for cervical ripen-
induction of labor is the status of the cervix. To ing are utilized. The methods used include the
assess if the cervix is favorable (ripe) or unfavor- following:
able (unripe), the Bishop score, first described in
1964, is used. • Sweeping of membranes
The modified Bishop score (Table 16.1) is • Pharmacological
based on a pelvic examination to assess the sta- • Mechanical
tus of the cervix and the station of the vertex. The The methods of cervical ripening are summa-
five parameters assessed are as follows: rized in Box 16.5.
• Dilatation of the cervix (cm)
• Effacement of the cervix (%) Box 16.5 Methods for cervical ripening
• Station of the vertex (from –3 to +2) • Sweeping of membranes
• Consistency (firm, medium, or soft) • Pharmacological
• The position of the external os (posterior, mid, Ŧ Prostaglandin E2 (intracervical, intravaginal)
or anterior) Ŧ Prostaglandin E1 (vaginal, oral)
• Mechanical
Effacement may also be assessed by the length Ŧ Transcervical balloon catheter
of the cervix since the cervix becomes shorter as Foley catheter
it effaces. This is a more objective assessment of Double balloon catheter
effacement. Transcervical catheters with extra-amniotic
Each parameter is given a score and the total saline instillation (EASI)
is called the Bishop score. The cervix is consid- Ŧ Laminaria
ered unfavorable if the score is 6 or less.
A high Bishop score prior to induction (8
or more) predicts that the likelihood of vagi-
nal delivery is similar to spontaneous onset of
Sweeping of fetal membranes
labor. A low Bishop score (6 or less) predicts an Sweeping of fetal membranes is also called
increased rate of failed induction, resulting in stripping of membranes. It is an outpatient pro-
cesarean section. When the Bishop score is low, cedure. It can only be performed if the cervix is
cervical ripening is performed to improve the dilated enough to allow insertion of a finger. This
score, prior to induction. method should only be offered if the indication
Table 16.1 Bishop score
Parameter Bishop score

0 1 2 3
Dilatation (cm) 0 1–2 3–4 5–6
Length of cervix/ >4 cm/0% – 3 0% 2–4 cm/40% – 50 % 1–2 cm/60% – 7 0% <1cm/80%
effacement
Station –3 –2 –1 or 0 +1 or +2
Consistency Firm Medium Soft –
Position Posterior Mid Anterior –
*Each parameter gets 0–3 points and the cumulative points give the Bishop score.
CH 16_p226-237_v3.indd 228 17-07-2015 12:59:37

prostaglandins and misoprostol. Other phar-

Box 16.6 Sweeping of membranes
macological agents, including oxytocin, are less
• Outpatient procedure commonly used.
• For nonurgent induction
• More effective in multigravidas than in primigravidas
• Works by releasing prostaglandin F2D Prostaglandins
• May result in rupture of membranes
Prostaglandins are most commonly used for
cervical ripening in an unscarred uterus. Quite
for induction is nonurgent because the response often, prostaglandins not only improve the cer-
to membrane sweeping is unpredictable and vical score and cause ripening, they also initiate
slow (Box 16.6). labor. The need for oxytocin to induce or aug-
The sweeping is done by gently inserting a fin- ment labor is thus reduced. The commonly used
ger through the open external os into the space prostaglandins are prostaglandin E2 (PGE2) and
between the membranes and the lower uterine prostaglandin E1 (PGE1). See Table 16.2 for pros-
segment. The finger is then swept in a circular taglandin regimens for cervical ripening.
motion through 360 degrees. Care is taken to
keep the finger close to the uterine wall. The pro- rostaglan in ( inoprostone)
cess strips the amniotic membrane off the lower There are two PGE2 preparations available
uterine segment. (Box 16.7). One is in the form of a preloaded
Sweeping the membrane from the uterine wall intracervical gel which contains 0.5 mg of dino-
causes increased local production and release of prostone in 2.5 mL of gel. The other is an intra-
prostaglandin F2D(PGF2D) from the decidua and vaginal insert which contains 10 mg of dinopros-
adjacent membrane, thereby leading to onset tone in a timed-released formulation.
of labor. Following sweeping of membranes, Intracervical gel (Box 16.8): The pre-
women must be counseled that there may be loaded syringe comes with a plastic insertor,
bleeding, discomfort, and contractions that may which is placed into the cervical canal under
not lead to labor in the next 24 hours. direct vision. 0.5 mg of the intracervical gel
Sweeping of membranes may result in pre-
labor rupture of membranes. Bleeding can be a
serious complication if sweeping is done in an Box 16.7 Prostaglandin E2
undiagnosed placenta previa or vasaprevia.
• Route
Ŧ Intracervical
Pharmacological methods Ŧ Intravaginal
• Induces cervical ripening
of cervical ripening • Reduces failed induction rate
Pharmacological agents available for cervical • Reduces the need for oxytocin
• Shortens induction-delivery interval
ripening and labor induction currently include
Table 16.2 Prostaglandin regimens for cervical ripening (in unscarred uterus)
Drug oute dose Caution
Dinoprostone gel (PGE2) 0.5 mg Cervical insertion every 6 hours for a Interval of 6 hours from last dose before
maximum of 3 doses in a 24-hour oxytocin is started
period
Dinoprostone (PGE2) insert 10 mg Placed high in posterior fornix Easy to remove in case of tachy-systole
Misoprostol (PGE1) Vaginal: 25 μg tablet every 3–6 • Tachysystole common with vaginal dose
hours of >25 μg
Oral: 50 μg every 3–6 hours • Interval of 4 hours after the last dose
before oxytocin is started
P , prostaglandin E.
CH 16_p226-237_v3.indd 229 17-07-2015 12:59:37

Box 16.8 Prostaglandin E2 intracervical gel Box 16.11 aginal misoprostol (prostaglandin
E1) for cervical ripening
• 0.5 mg
• Inside cervical canal • 25 μg
• Every 6 hours • Placed high in vagina
• Maximum of 3 doses in 24 hours • Can be repeated every 3–6 hours
• Maximum 6 doses
is administered into the cervical canal every

6 hours up to a maximum of three doses in a
Box 16.12 ral misoprostol (prostaglandin E1)
24-hour period.
for cervical ripening
Intravaginal insert (Box 16.9): This contains
10 mg of dinoprostone in a small white polymer • 50 μg
mesh sac and has an attached tape that helps • Can be repeated every 4–6 hours
during removal. It is left in the vagina until active • Not used routinely for cervical ripening
labor starts or for 12 hours.
Vaginally administered PGE2 is associated
rostaglan in (misoprostol) with tachysystole (six or more contractions in
Misoprostol is available as a 25 Pg or 100 Pg tab- 10 minutes) in 1%–5% of women. Misoprostol
let. The 100 g tablet can be broken into four equal has been associated with uterine hyperstimula-
pieces for cervical ripening. The tablets can tion (tachysystole leading to nonreassuring fetal
be administered both vaginally and orally heart rate pattern). A summary of side effects of
(Box 16.10). The dosages for the vaginal and oral prostaglandins used for cervical ripening is pre-
routes are summarized in Boxes 16.11 and 16.12, sented in Box 16.13.
respectively. Prostaglandins (especially misoprostol) are
contraindicated in a woman with a previous
Si e e ects o prostaglan ins cesarean section, due to the increased risk of
Though prostaglandins have minimal systemic uterine rupture.
side effects, they are associated with tachysys-
tole and uterine hyperstimulation. ther pharmacological agents
Oxytocin has been extensively used in the past
Box 16.9 Prostaglandin E2 intravaginal insert for cervical ripening. Since PGE2 and PGE1
• 10 mg have been found to be better than oxytocin in
• In posterior fornix randomized trials, it is now used only for labor
• Left for 12 hours or until labor starts induction. Relaxin, hyaluronidase, and other
• Expensive agents such as glyceryl trinitrate and isosorbide
mononitrate have been tried. Success rates vary
and their safety profiles are not known (Box 16.14).
Box 16.10 Prostaglandin E1 Nipple stimulation (to induce oxytocin release
• Route from the pituitary gland) and sexual intercourse
Ŧ Vaginal
Ŧ Oral
• Induces cervical ripening
• More effective than PGE2 Box 16.13 Side effects of prostaglandins used
• Associated with for cervical ripening
Ŧ tachysystole • Vaginal prostaglandin E2
Ŧ fetal heart rate abnormalities Ŧ Tachysystole (6 or more contractions in 10 min-
Ŧ meconium staining utes)
• Can cause uterine rupture Ŧ Affects 1%–5% of women
• Contraindicated in scarred uterus (previous cesarean • Misoprostol
or myomectomy) Ŧ Hyperstimulation (tachysystole leading to non-
• No increase in cesarean section rate reassuring fetal heart rate pattern)
• Effects are dose related Ŧ Contraindicated in previous cesarean section
CH 16_p226-237_v3.indd 230 17-07-2015 12:59:37

Box 16.14 Pharmacological agents not recom-

mended for cervical ripening
• Oxytocin
• Relaxin
• Mifepristone
• Hyaluronidase
• Nitric oxide donors
Ŧ Glyceryl trinitrate
Ŧ Isosorbide mononitrate
a.
have also been described but are not methods of
choice (Box 16.15).
Mechanical methods
of cervical ripening
The common methods used for mechanically
stimulating cervical ripening are as follows:
• Transcervical catheter
– Foley
– Double balloon catheter
• Transcervical catheter with extra-amniotic
saline infusion (EASI) b.
• Laminaria
Figure 16.1 Transcervical Foley catheter for cervical
ripening. a. Foley catheter being introduced into the extra-
Transcervical Foley catheter amniotic space. b.(QNG[DWNDKPƀCVGFCPFRNCEGFUPWIN[
against the internal os.
A #16 Foley catheter with a 30 mL bulb and with
the tip cut off is used. It is passed through the
cervical canal, past the internal os, and into the
extra-amniotic space. The bulb is then filled with Transcervical double balloon
30 mL of saline and the Foley catheter is pulled catheter
back gently so that the bulb rests against the
internal os (Fig. 16.1). The catheter is taped to Double balloon catheters with one balloon
the woman's thigh. placed below and the other above the inter-
The catheter is left in place till it is extruded nal os are available (Fig. 16.2). The first (distal)
or for 12 hours. Cervical ripening is usually balloon is inserted beyond the internal os and
achieved with this method and may also result in inflated with 40 mL of saline, and gentle traction
the onset of labor. is applied to the catheter. The second (proxi-
mal) balloon appears below the external os and
is inflated. When inflated, the two balloons are
above and below the cervical canal. As the cer-
Box 16.15 Methods not recommended for vix effaces, the two balloons come together. The
cervical ripening
cervix dilates simultaneously. Success rates have
• Nipple stimulation been higher with the double balloon catheters
• Sexual intercourse but they are not in common use.
• Castor oil Extra-amniotic saline infusion (EASI) is a
• Acupuncture
modification of this method (Fig. 16.3). Room
• Hot baths
temperature saline is infused through the cath-
• Enema
eter port. This method has not been shown to
CH 16_p226-237_v3.indd 231 17-07-2015 12:59:37

mnion
mL
tra amniotic
saline
Figure 16.2 Transcervical double balloon catheter being

placed in the extra-amniotic space. Figure 16.3 Extra-amniotic saline infusion.
Box 16.16 Complications of catheter insertion cervical ripening are usually followed by oxy-
for cervical ripening tocin to induce labor. The terminology used
• Rupture of membranes
to describe uterine contractions during labor
• Febrile morbidity induction is listed in Box 16.17.
• Displacement of the presenting part
• 5KIPKſECPVXCIKPCNDNGGFKPIKPYQOGPYKVJCNQYN[KPI
placenta
Methods of induction
The available methods of labor induction are as
follows:
have a major advantage over other methods of
cervical ripening. • Intravenous oxytocin
The complications of catheter insertion for • Amniotomy
cervical ripening are summarized in Box 16.16.
Box 16.17 Terminology used to describe
Laminaria uterine contractions during labor
Laminaria tents are usually used for pregnancy induction
termination rather than for preinduction cervi- • Uterine contractions
cal ripening. They are hygroscopic, that is, they Ŧ (TGSWGPE[
absorb moisture. Once they are placed in the Ŧ Duration
cervix, they slowly expand due to the absorp- Ŧ Intensity
tion of moisture. By disrupting the chorioamni- Ŧ Relaxation time between contractions
• &GUKTGFHTGSWGPE[
otic decidual surface, they cause the release of
Ŧ 3–5 contractions in 10 minutes
endogenous prostaglandins and result in cervi-
• Effective duration
cal ripening. Laminaria are removed 12–24 hours Ŧ 30–60 seconds
after placement. • Desired intensity
Ŧ 7VGTWUECPPQVDGKPFGPVGFD[RCNRCVKPIſPIGTUCV
the peak of the contraction
Labor induction • Optimal relaxation time between contractions
Ŧ ŮOKPWVGU
Once the cervix becomes favorable, labor is • Tachysystole
induced, usually with oxytocin. Amniotomy Ŧ >6 contractions in 10 minutes
(artificial rupture of membranes or AROM) may • Uterine hypertonus
or may not be performed along with oxytocin Ŧ Single contraction lasting >2 minutes
infusion. Prostaglandins used for ripening the • Hyperstimulation
Ŧ Tachysystole or hypertonus associated with nonre-
cervix may also stimulate uterine contraction,
assuring fetal heart rate pattern
and labor may follow. Mechanical methods of
CH 16_p226-237_v3.indd 232 17-07-2015 12:59:38

• Prostaglandins • Less occurrence of uterine tachysystole and

• Sweeping (or stripping) of membranes associated fetal heart rate changes
igh-dose regimens
xytocin • High dose of oxytocin
Oxytocin is an octapeptide which is available in • More frequent dose increases (every 20 minutes)
its synthetic form. Oxytocin was the first poly- • Associated with shorter labor
peptide hormone to be sequenced and synthe- • Lower rates of cesarean delivery for dystocia
sized and won Vincent du Vigneaud a Nobel • Increased rates of uterine tachysystole with
Prize in 1953. associated fetal heart rate changes
Oxytocin is the most common drug used for
Box 16.18 lists the optimal end points looked
the induction of labor. It is administered intra-
for in induction with oxytocin.
venously. It is not used orally since it is degraded
to inactive form when administered orally. In a imum ose o o ytocin
the presence of a ripe cervix, induction of labor
with oxytocin has a high rate of success. If the The maximum dose recommended for oxytocin
cervix is not favorable (Bishop score of 6 or less), varies from 32 mU/min to 40 mU/min. If the
cervical ripening will improve the success of uterus does not respond to 32 mU/min, it prob-
induction, as described previously. ably is prudent not to increase the dose beyond
When oxytocin is administered, uterine that. Oxytocin dosage in mU, drops/min, and
activity and fetal heart rate must be continu- mL/hour (using 5 units in 500 mL of normal
ously monitored. saline) is given in Table 16.4.
Intravenous o ytocin a ministration Si e e ects o o ytocin

• 5 units of oxytocin are diluted in 500 mL of The side effects of oxytocin are enumerated in
normal saline. Box 16.19.
• Ideally, it should be administered with an infu- yponatremia (water intoxication)
sion pump. Hyponatremia occurs when high doses of oxyto-
• If an infusion pump is not available, the rate of cin (e.g., 40 mU/min) are administered in large
infusion must be monitored manually. quantities of hypotonic solutions such as dex-
• 5 units of oxytocin in 500 mL gives a concen- trose in water. This results in excessive water
tration of 10 mU/mL (or 0.5 mU in 1 drop of retention and ends in severe, symptomatic
the infusion, calculated at 20 drops/mL). hyponatremia. It can be avoided by using more
concentrated solutions of oxytocin (5 units in
Dosage o o ytocin
Two regimens are described for the administra-
tion of intravenous oxytocin: low dose and high Box 16.18 ptimal end points with
dose (Table 16.3). oxytocin induction
Low-dose regimens • Strong contractions
• At intervals of 2-3 minutes
• Low dose of oxytocin
• Lasting 45–60 seconds
• Less frequent increases in dose (every 40
• Progressive cervical dilatation
minutes)
Table 16.3 Low- and high-dose regimens for oxytocin administration
egimen Starting dose Incremental Dosage interval in

(m ) increase (m min) minutes
Low dose 0.5–2 1–2 15–40

High dose 6 3–6 15–40
CH 16_p226-237_v3.indd 233 17-07-2015 12:59:38

Table 16.4 Dosage of oxytocin for induction

Augmentation o labor ith o ytocin
of labor Oxytocin is used to augment labor in women
who have a protracted latent phase or protracted
m of oxytocin Drops min mL hour (infusion
active phase of labor. The dosage regimens used
(manual) pump)
are similar to the dosage used for induction of
0.5 1 3.75 labor. However, since the woman is already in
2 4 15 labor, the uterus might respond at lower doses.
4 8 30
6 12 45 #OPKQVQO[QTCTVKſEKCNTWRVWTG
8 16 60 of membranes (A M)
10 20 75
14 24 90
The combination of amniotomy plus intrave-
16 28 105
nous oxytocin administration is more effective
than amniotomy alone. During oxytocin induc-
18 32 120
tion, early amniotomy at a cervical dilatation
20 36 135
of 4 cm or more is an effective way of hastening
24 40 150
labor. The other advantage of early amniotomy
28 44 165
is that it helps in the assessment of the liquor,
30 48 180
particularly for the presence of meconium. The
32 52 195
fetal heart rate should be auscultated/monitored
soon after amniotomy to look for fetal heart rate
decelerations, which may signal occult cord pro-
Box 16.19 Side effects of oxytocin lapse (Box 16.20).
• Hyponatremia (water intoxication) Amniotomy may be performed
Ŧ Anorexia
• to induce labor;
Ŧ Nausea and vomiting
• to augment labor when progress of labor is slow;
Ŧ Abdominal pain
Ŧ Lethargy, drowsiness, unconsciousness
• as an elective procedure after 4-cm dilatation.
Ŧ Grand mal seizures
• Hypotension (rare) roce ure
• Neonatal hyperbilirubinemia Under aseptic conditions, two fingers are
inserted into the cervix and the membranes are
palpated (Fig. 16.4). Using a sharp instrument
500 mL of normal saline) and avoiding oxytocin such as an artery forceps, Kocher’s forceps, or
dose of more than 32 mU/min. a sterile plastic hook called an amnihook, the
Treatment of water intoxication includes membranes are ruptured. It helps to wait for a
immediate stopping of oxytocin and any hypo- contraction, so that the membranes bulge a little,
tonic solutions. Correction of hyponatremia making it easier to rupture them. Any meconium
must be performed carefully and consists of staining of the amniotic fluid should be noted.
restricting water intake and careful adminis- Cord prolapse must be looked for before the
tration of hypertonic saline if the woman is hand is withdrawn.
symptomatic.
ypotension Box 16.20 Amniotomy

This is a very rare complication and may occur • Reduces the duration of labor
with rapid infusion of oxytocin. • *GNRUKPCUUGUUKPINKSWQTHQTOGEQPKWO
• Needs monitoring for occult cord prolapse
eonatal hyperbilirubinemia • Should be done only when
Ŧ cervix is partially effaced and dilated
Though the induction of labor with oxytocin is
Ŧ vertex has descended into the pelvis
associated with an increased rate of hyperbil-
Ŧ decision has been made to deliver within 12–24
irubinemia in the neonate, it is probably not a hours of amniotomy
direct side effect of oxytocin.
CH 16_p226-237_v3.indd 234 17-07-2015 12:59:38

intrauterine fetal death, prostaglandins are the

drugs of choice for inducing labor (Box 16.21).
mniotic sac
Sweeping (or stripping)

mnihoo
of membranes
Routine stripping of membranes at 38 weeks to
induce labor is of limited benefit, when com-
pared to prostaglandins.
Complications of labor
Figure 16.4 #OPKQVQO[
CTVKſEKCNTWRVWTGQHOGODTCPGU
induction
Complications o amniotomy Induction of labor can be associated with certain
Complications include the following: complications (Box 16.22).
• Cord prolapse
• Chorioamnionitis, if labor is prolonged Management of tachysystole,
• Fetal heart decelerations due to cord com-
pression
hypertonus, and uterine
hyperstimulation
Prostaglandins If excessive uterine activity (>6 contractions in
10 minutes or contractions lasting longer than 2
Prostaglandins E2 and E1 are typically used for
minutes) occurs, with or without a nonreassur-
cervical ripening, as mentioned previously. The
ing fetal heart rate pattern,
role of prostaglandins in the presence of a favor-
able cervix in a term pregnancy is not clear, and • Discontinue intravenous oxytocin infusion.
oxytocin is preferred in that situation. • Reposition the woman in the lateral position.
• Administer oxygen by face mask (at 10 L/min).
ole o prostaglan ins in intrauterine • Increase intravenous hydration if not contrain-
etal emise (I D) dicated by the maternal condition (a bolus of
If pregnancy needs to be terminated in the 500 mL of Ringer’s solution).
second or third trimester in the presence of an • Assess blood pressure.
• Perform pelvic examination to assess cervical
dilation and rule out cord prolapse.
Box 16.21 Prostaglandins for pregnancy termi- • Administer a tocolytic, such as terbutaline
nation in intrauterine fetal demise 250 μg, subcutaneously or intravenously, if
weeks hypertonus does not respond to the above
measures.
• Mifepristone (200 mg) administered orally
• Misoprostol
Ŧ 48 hours after mifepristone
Ŧ 600–800 Pg intravaginally Box 16.22 Complications of induction
Ŧ Followed by
400 Pg orally or intravaginally • Tachysystole, hypertonus, and uterine hyperstimulation
Every 3 hours up to 4 doses. • Uterine rupture (in women with previous cesarean
section)
hird trimester • #OPKQVKEƀWKFGODQNKUO
• Prostaglandin E2 or misoprostol • Chorioamnionitis
Ŧ For cervical ripening • Risk of cesarean section
Ŧ Followed by oxytocin for induction of labor • Atonic postpartum hemorrhage
CH 16_p226-237_v3.indd 235 17-07-2015 12:59:38

estarting oxytocin after The rate of cesarean delivery is increased

tachysystole approximately twofold in nulliparous women
undergoing elective induction as compared to
Oxytocin should be restarted carefully after those women in spontaneous labor. With opti-
an episode of tachysystole. If there are no per- mal cervical ripening, this difference in rate
sistent abnormal changes in fetal heart rate, comes down considerably.
the oxytocin is restarted at a lower dosage.
The incremental increase should be reduced
to 3 mU/min if hyperstimulation is present
Postpartum hemorrhage
and reduced to 1 mU/min if there is recurrent The risk of postpartum hemorrhage increases
hyperstimulation. with induction of labor. Prophylactic measures
must be taken to avoid postpartum hemorrhage
terine rupture in women undergoing induction of labor.
Though the risk of uterine rupture is very low

with induction, care must be taken in the case of Failed induction
a grand multipara. Most cases of uterine rupture
occur in women with a scarred uterus and there- When, following induction, labor does not enter
fore special care must be taken in women with a the active phase (failure to generate regular con-
previous cesarean section. tractions and cervical change) or, in the pres-
ence of regular contractions, vaginal delivery is
#OPKQVKEƀWKFGODQNKUO not achieved, it is termed a failed induction. This
term must only be used in the following cases:
This is a very rare complication of labor induc-
tion. Its incidence has been reported as 10.3 • Adequate measures have been taken to achieve
per 100,000 births with medical induction cervical ripening.
versus 5.2 per 100,000 births without medical • Adequate dosage of oxytocin has failed to gen-
induction. erate regular contractions.
• Regular contractions have failed to establish
active phase of labor.
Chorioamnionitis
Causes of failed induction are given in
If the interval between the onset of induction Box 16.23.
and delivery is prolonged, the risk of chorioam-
nionitis increases. Once membranes are rup-
tured, the risk of chorioamnionitis will increase Box 16.23 Causes of failure to progress with
induction
with increase in the duration between amniot-
omy and delivery. • +PCFGSWCVGEGTXKECNTKRGPKPI
• +PCFGSWCVGFQUCIGQHQZ[VQEKP
• Large baby
isk of cesarean section • Malposition
• &GƀGZKQPQHXGTVGZ
Any increase in the risk of cesarean delivery
• Small pelvis
related to induction appears to be associated pri-
• Cervical dystocia
marily with an unfavorable cervix at admission.
CH 16_p226-237_v3.indd 236 17-07-2015 12:59:38

Key points
• The decision to induce labor is taken when the bene- • High doses of oxytocin should not be administered
ſVUQHFGNKXGT[QWVYGKIJVJGRQVGPVKCNTKUMUQHKPFWEVKQP in hypotonic solutions, as this can lead to
to the mother and fetus, and there are no contraindica- excessive water retention and dilutional
tions to induction. hyponatremia.
• Assessing the cervix with the Bishop score is the best • Early amniotomy (at a cervical dilatation of 4 cm or
predictor of the success of induction. more) is an effective way of hastening labor. Amni-
• In the presence of an unfavorable cervix, cervical QVQO[CNUQCNNQYUCUUGUUOGPVQHVJGCOPKQVKEƀWKFHQT
ripening with prostaglandins or mechanical methods the presence of meconium.
improves the success rate of induction. • The side effects of labor induction include
• Prostaglandins should be avoided in a uterus with a tachysystole, hypertonus, uterine hyperstimulation,
scar (previous cesarean section). uterine rupture (in women with previous cesarean
• Oxytocin is the drug of choice for induction of labor in section), amniotic fluid embolism, chorioamnionitis,
the presence of a favorable cervix. risk of cesarean section, and atonic postpartum
hemorrhage.
• Oxytocin may be administered with a low-dose regi-
OGPQTCJKIJFQUGTGIKOGPCUNQPICUCURGEKſE
protocol is followed.
Self-Assessment
3. Foley catheter does not result in hyperstimulation.
Case-based questions 4. Misoprostol should not be used in a scarred uterus.
Case 1
Mrs. MN, 25, primigravida, was admitted to the hospital Case 2
in the 37th week of pregnancy. She had developed preg- 1. Oxytocin is an octapeptide which is available in its
nancy induced hypertension at 36 weeks. Within a week, synthetic form.
her blood pressure went up to 160/100 mm Hg and the 2. Low-dose regimen: 0.5–2 mU
urine test revealed 2+ albumin. Her Bishop score was 4.
High-dose regimen: 6 mU
1. What is a favorable Bishop score? 3. a. Stop the oxytocin infusion.
2. Mention three methods of cervical ripening. b. Turn the patient to the lateral position.
3. Which cervical ripening agent does not result in 4. When high doses of oxytocin (e.g., 40 mU/min) are
hyperstimulation? CFOKPKUVGTGFKPNCTIGSWCPVKVKGUQHJ[RQVQPKEUQNWVKQPU
4. What is the contraindication to the use of misoprostol? such as dextrose in water, it results in excessive water
retention and ends in severe, symptomatic hypo-
natremia (water intoxication).
Case 2
Mrs. JK, 26, gravida 2, para 1, was admitted in labor. Due
to nonprogress of labor, augmentation was started with
Sample uestions
oxytocin.
1. What is oxytocin?
1. Mention indications, contraindications, and complica-
2. What are the starting doses of oxytocin for the low-
tions of induction of labor.
dose and high-dose regimens?
3. Mention two interventions for hyperstimulation with
oxytocin. Short-answer questions
4. What is water intoxication?
1. Cervical ripening
2. Bishop score
Answers
Case 1
1. #$KUJQRUEQTGQHŮKUEQPUKFGTGFHCXQTCDNG
2. Foley catheter, PGE2 gel, and PGE1.
CH 16_p226-237_v3.indd 237 17-07-2015 12:59:38

Intrapartum Fetal
17 Surveillance
Case scenario
Mrs. MG, 25, came in labor at 38 weeks’ gestation. She was having
contractions every 3–4 minutes and the contractions were lasting
40–50 seconds. She was a known hypertensive. At 4-cm cervical dilata-
tion, membranes ruptured spontaneously and the amniotic fluid was
meconium stained. She needed intrapartum evaluation to make sure
that the fetus was tolerating labor well and there was no fetal hypoxia.
Introduction
In the normal course of labor, uterine con-
It is the goal of every obstetrician to ensure tractions cause a decrease in uteroplacental
that the mother and fetus tolerate labor well. blood flow and therefore a decrease in oxygen
However, assessing the fetal response to labor is delivery to the fetus. A well-oxygenated term
a challenge. Intrapartum fetal surveillance aims fetus usually tolerates this and shows no adverse
to prevent adverse perinatal outcomes arising effect. Even a well-compensated, term fetus
from fetal metabolic acidosis related to labor. may respond poorly to a prolonged period of
Monitoring of the fetal heart is an integral part of decreased oxygenation as may occur in abrup-
the care of the fetus in labor. tion, bleeding due to placenta previa, supine
hypotension, and hypotension associated with
epidural analgesia.
ationale for intrapartum In conditions with chronic placental insuf-
ficiency such as hypertension, diabetes, and
fetal surveillance antiphospholipid antibody syndrome where
there is fetal growth restriction, the fetus may
Two major factors affect fetal oxygenation in labor:
not tolerate the decrease in oxygenation and
• Placental blood flow may show signs of hypoxia. The preterm fetus
• Blood flow through the umbilical cord too tolerates hypoxia poorly (Fig. 17.1).
CH 17_p238-252_v3.indd 238 17-07-2015 13:49:36

Intrapartum Fetal Surveillance 239
Box 17.1 Aim of fetal surveillance in labor

Uterine
contraction • +FGPVKſECVKQPQHFGETGCUGFHGVCNQZ[IGPCVKQP
• Timely and effective intervention
• Prevention of brain injury
ecrease
utero placental Decreased oxygenation may result in brain
bloo flo injury. At present no technology is available to
directly assess brain injury during labor. Certain
fetal heart rate changes occur prior to brain
ntermittently injury. Recognition of fetal heart rate changes is
ecrease the basis for fetal monitoring in labor. Therefore,
fetal o ygenation the aim of intrapartum fetal surveillance is
to identify abnormal fetal heart patterns and
implement timely and effective interventions to
Prolonge insult prevent brain injury (Box 17.1).
erm
ro th restricte fetus
ell o ygenate fetus
Preterm fetus
ypoxia and hypoxic
in uries to the fetus
nsult tolerate nsult not tolerate
When there is decreased oxygenation to the
fetus, there is a chain of events that leads to long-
term neurological sequelae (Fig. 17.2).
Hypoxic injury affects the fetus in several
o hypo ia etal hypo ia ways. Multiorgan dysfunction may result, but
the fetal nervous system is the most vulnerable
to long-term injury. The types of hypoxic injuries
Possible brain injury
Causes of intrapartum hypoxia
Figure 17.1 Response of the fetus to intermittent Any interference with the uterine blood flow due
decrease in oxygenation during a uterine contraction. to maternal factors, placental dysfunction, or
fetal factors can lead to compromise of fetal oxy-
genation in labor (Box 17.3).
Aim of intrapartum fetal
surveillance
Intrapartum fetal surveillance aims to detect
Methods of intrapartum
potential fetal harm due to decreased oxygen- fetal surveillance
ation during labor. Timely detection allows for
prompt and effective intervention, leading to a The methods available for evaluating and
decrease in perinatal/neonatal morbidity and assessing the fetal response to labor include the
mortality. following:
ypoxic etabolic eo atal o term

aci emia aci osis e cephalopathy se uelae
Figure 17.2 Chain of events leading to hypoxic brain injury.
CH 17_p238-252_v3.indd 239 17-07-2015 13:49:36

Box 17.2 ypoxic fetal in uries Box 17.3 Causes for decreased fetal
oxygenation in labor
• Hypoxic ischemic encephalopathy (HIE)
Ŧ Due to intrapartum hypoxia aternal factors
Ŧ Can be mild, moderate, or severe • Chronic maternal conditions
Ŧ 5GXGTG*+'ECPDGCUUQEKCVGFYKVJ Ŧ Chronic hypertension
neonatal death Ŧ Type I diabetes
disabilities in survivors Ŧ Antiphospholipid syndrome
• Neonatal encephalopathy • &GETGCUGFWVGTKPGDNQQFƀQY
Ŧ Majority due to conditions that occur before labor Ŧ Hypotension (e.g., acute blood loss)
Prenatal stroke Ŧ Regional anesthesia (epidural, spinal)
Infection Ŧ Maternal positioning (supine hypotension)
Cerebral malformation • 5KIPKſECPVCPGOKC
Genetic disorders
Ŧ Small percentage occur due to teroplacental factors
intrapartum asphyxia • Excessive uterine activity or tone
hypoxemic insult to the brain Ŧ Hyperstimulation
• Cerebral palsy (CP) Ŧ Placental abruption
Ŧ Majority not due to asphyxia during labor • Uteroplacental dysfunction
Ŧ Majority due to Ŧ (GVCNITQYVJTGVCTFCVKQP
insult occuring in the antenatal period Ŧ Postterm pregnancy
genetic or environmental factors Ŧ Oligohydramnios
Ŧ Small percentage etal factors
Due to acute intrapartum hypoxia
• Cord compression
Results in spastic quadriplegic CP
Ŧ Oligohydramnios
Ŧ Cord prolapse or entanglement
• Decreased fetal oxygen-carrying capacity
• Intermittent auscultation (IA) Ŧ 5KIPKſECPVCPGOKC
– Pinard fetoscope Rh alloimmunization
– Stethoscope Maternal–fetal bleed
– Handheld Doppler device Ruptured vasa previa
• Cardiotocography (CTG) or electronic fetal
monitoring (EFM)
with the other two methods because it amplifies
– Intermittent (when required)
sound. This is an advantage, especially in obese
– Continuous
women, in the presence of polyhydramnios, or
• Fetal scalp blood sampling
an actively moving fetus.
– Scalp pH
– Fetal lactate concentration
• Fetal electrocardiography Frequency of auscultation for fetal
• Pulse oximetry
heart rate in labor
Intermittent auscultation There are established protocols for the frequency
of assessment of the fetal heart rate by ausculta-
Using a device such as a Pinard fetoscope, a tion to determine fetal status during labor.
stethoscope, or a handheld Doppler device, the
obstetrician or nurse listens to the fetal heart- irst stage o labor (till complete
beat through the maternal abdomen. The heart- cervical ilation)
beats are usually counted for 30 or 60 seconds
The recommendation for frequency of auscul-
and the baseline fetal heart rate calculated.
tation of the fetal heart rate in the first stage
In the absence of maternal and fetal risk
of labor (till complete cervical dilation) are as
factors, intermittent auscultation is the recom-
follows:
mended fetal surveillance method during labor
(Fig. 17.3). The fetal heart rate is better assessed • Auscultate every 15 minutes during the active
with the handheld Doppler device as compared phase of the first stage of labor.
CH 17_p238-252_v3.indd 240 17-07-2015 13:49:36

during a contraction. If there is any abnor-

mal change, it will alert the obstetrician to the
presence of fetal distress.
Secon stage o labor ( rom complete

cervical ilation to elivery o the etus)
The recommendations for frequency of auscul-
tation of the FHR in the second stage of labor
(from complete cervical dilation to delivery) are
as follows:
a. • Every 5 minutes during the second stage of labor
• After every contraction during the pushing
phase of labor
Interpretation of fetal heart rate by

auscultation
aseline etal heart rate
The fetal heartbeats are counted between con-
tractions for 60 seconds, at least for the first time,
to establish the baseline fetal heart rate. The fetal
heart rate is expressed as beats per minute (bpm).
The normal baseline fetal heart rate is 110–160
bpm.
Following the initial counting, the fetal heart
rate can be intermittently counted for 15–30
b. seconds (and multiplied by 4 or 2, respectively),
to continue monitoring the heart rate. The fre-
quency of counting should follow a set protocol
(Box 17.4).
etal heart rate changes

Once a baseline fetal heart rate has been estab-
lished, it is easy to identify changes from the
baseline by auscultation. There can be acceler-
ations (the fetal heart rate abruptly rising above
baseline for 15–60 seconds) or decelerations
(the fetal heart rate abruptly dropping below
baseline for 15–60 seconds). Accelerations are a
reassuring sign of fetal well-being. There can be
.
tachycardia, defined as a fetal heart rate above
Figure 17.3 .KUVGPKPIVQHGVCNJGCTVDGCVYKVJ 160 bpm for >10 minutes, or bradycardia, which
a. Pinard fetoscope. b. Stethoscope. c. Handheld
Doppler device.
Box 17.4 Establishing baseline fetal heart rate
by intermittent auscultation
• Auscultate from before the start of the con-
traction to after the contraction is over. This • Initial counting for 60 seconds
• $GVYGGPEQPVTCEVKQPU
is important because it will help pick up any
• (QNNQYWRCUUGUUOGPVHQTŌUGEQPFU
change in the heart rate after the contraction
• Normal baseline fetal heart rate 110–160 bpm
since oxygenation to the fetus is decreased
CH 17_p238-252_v3.indd 241 17-07-2015 13:49:38

continuous electronic recording of the fetal heart

Box 17.5 Intermittent auscultation
rate on a graph paper, known as electronic fetal
• Baseline fetal heart rate monitoring, was introduced for obtaining more
Ŧ Normal: 110–160 bpm accurate information, early diagnosis of fetal
• Accelerations
hypoxia, and immediate intervention.
Ŧ Abrupt rise
However, randomized controlled trials com-
Ŧ >15 bpm above baseline
Ŧ Lasting 15–60 seconds
paring electronic fetal monitoring, with intermit-
Ŧ Reassuring sign tent auscultation have shown that the reduction
• Decelerations in perinatal mortality is not statistically signifi-
Ŧ #DTWRVFTQRDGNQYDCUGNKPG cant. There is no reduction in cerebral palsy when
Ŧ Lasting 15–60 seconds electronic fetal monitoring is used. A decrease
Ŧ Cannot diagnose etiology in neonatal seizures has been reported. On the
• Tachycardia other hand, electronic fetal monitoring is associ-
Ŧ Fetal heart rate above 160 bpm for >10 minutes ated with an increase in interventions, including
• Bradycardia cesarean section, vaginal operative delivery, and
Ŧ (GVCNJGCTVTCVGDGNQYDROHQT OKPWVGU the use of anesthesia. No difference in the long-
term outcome has been demonstrated.
is a fetal heart rate below 110 bpm for >10 min- Electronic fetal monitoring is useful in assess-
utes (Box 17.5). It is important to compare the ing fetal heart rate patterns when intermittent
fetal heart rate with the maternal pulse to ensure auscultation picks up abnormalities or there is
that there is no confusion between the two. meconium present in the amniotic fluid. In these
These changes are best looked for after a con- situations, a reassuring fetal heart rate tracing
traction, when the fetus has been subjected to a allows the obstetrician to continue monitoring
temporary decrease in oxygenation. When there labor without any major intervention.
is no drop in the baseline fetal heart rate following It is reasonable clinical practice to use inter-
a contraction, it establishes the ability of the fetus mittent auscultation followed by electronic
to withstand labor contractions. In a decompen- fetal monitoring if fetal heart rate abnormali-
sated fetus, the fetal heart rate will drop following ties are recognized on intermittent auscultation.
a contraction. Continuous electronic fetal monitoring has not
been shown to improve perinatal outcomes in
low-risk women.
Drawbacks
The drawbacks of auscultation of the fetal heart
rate are as follows: Indications for electronic fetal
• It is often difficult to auscultate the fetal heart monitoring
rate in an obese woman or in a woman with Electronic fetal monitoring (if available) is indi-
polyhydramnios. cated in pregnancies at high risk for adverse
• It is also not possible to distinguish between perinatal outcome. Some of the indications for
decelerations caused by cord compression or electronic fetal monitoring are mentioned in
by placental insufficiency. Box 17.6.
• Baseline variability, which can be seen on
electronic fetal monitoring and is a good
marker for the presence or absence of fetal Equipment for electronic fetal
hypoxia, cannot be made out with intermit- monitoring
tent auscultation. Electronic fetal monitoring may be performed
by the following methods:
Electronic fetal monitoring • External electronic monitoring
• Internal electronic monitoring
From the beginning of the 20th century, intermit-
tent auscultation has been the method of assess- The external electronic monitoring equip-
ing the fetal heart rate during labor. In the 1960s, ment consists of the following (Fig. 17.4):
CH 17_p238-252_v3.indd 242 17-07-2015 13:49:39

External fetal heart rate monitoring is used for

Box 17.6 Indications for electronic fetal
monitoring nonstress testing in the antenatal period and for
monitoring women in labor. In active labor, fetal
• Maternal and maternal movements may make it difficult to
Ŧ Hypertension
use.
Ŧ Pregestational diabetes
The internal electronic monitoring equip-
Ŧ Induced or augmented labor
ment consists of the following:
Ŧ Chorioamnionitis • Internal fetal heart rate monitor—a spiral
Ŧ Antiphospholipid antibody syndrome electrode that is fixed to the fetal scalp. The
Ŧ Oligohydramnios
membranes must be ruptured for the insertion
• Fetal
of the electrode. The signal processor counts
Ŧ /GEQPKWOUVCKPGFCOPKQVKEƀWKF
Ŧ (GVCNITQYVJTGUVTKEVKQP
every R–R interval of the fetal ECG and displays
Ŧ Multiple pregnancy it on a fetal monitor recording paper.
Ŧ Prematurity • Uterine contractions are monitored by external
Ŧ Postterm tocodynamometer as in external monitoring.
Ŧ Previous intrapartum asphyxia/death • Intrauterine pressure catheters provide a
more accurate measurement of uterine activ-
• The external monitor: An ultrasound trans- ity but are not often used.
ducer that detects the fetal heart rate. Advantages of internal fetal heart rate moni-
• The external tocotransducer: A pressure-sensitive toring are as follows:
device that demonstrates the beginning and the
end of the contraction and shows the relation- • It can be used in active labor when maternal
ship between contractions and fetal heart accel- movements may make it difficult to use an
erations/decelerations. This however does not external monitor.
reflect the actual intrauterine pressure. • It can be used in obese women.
• The fetal heart rate monitoring is more accurate.
Both monitors are placed on the maternal
abdomen with the help of two elastic belts.
• Graphic tracing: This provides a permanent
record of the fetal heart rate and uterine
contractions.
Figure 17.4 External fetal monitoring. The ultrasound transducer and the external tocotransducer are placed on the
maternal abdomen. A graphic tracing is being obtained.
CH 17_p238-252_v3.indd 243 17-07-2015 13:49:39

Interpretation of fetal heart rate pattern Box 17.7 The causes for fetal tachycardia and
on electronic fetal monitoring bradycardia
• Tachycardia (heart rate of >160 bpm)
erminology
Ŧ Causes of tachycardia
Fetal heart rate patterns are described using the Maternal fever
following terms: Chorioamnionitis
E-Sympathomimetics
• Baseline fetal heart rate
Fetal compromise
• Baseline variability • Bradycardia (heart rate of <110 bpm)
• Periodic changes Ŧ Causes of bradycardia
– Accelerations Head compression
– Decelerations Fetal compromise
Baseline fetal heart rate

The normal baseline fetal heart rate is 110–160 Baseline variability
bpm. It can be interpreted only in a segment of a Baseline variability refers to the fluctuations in
minimum of 2-minute duration with no periodic the baseline fetal heart rate that are irregular in
changes. Figure 17.5 shows the baseline fetal amplitude and frequency. The normal baseline
heart rate and baseline variability. variability has an amplitude range of 6–25 bpm.
When the fetal heart rate exceeds 160 bpm It is measured from peak to trough. The fetal
for 10 minutes or more, it is called tachycardia. heart rate variability is a reflection of modula-
When the fetal heart rate is below 110 bpm for tion of the heart rate by the central and the auto-
10 minutes or more, it is called bradycardia. The nomic nervous systems. It is said to be minimal
causes for fetal tachycardia and bradycardia are when it is <5 bpm, moderate or normal when
listed in Box 17.7. it is 5–25 bpm, and marked when it is >25 bpm.
Figure 17.5 'NGEVTQPKEHGVCNOQPKVQTKPI(GVCNJGCTVTCVGVTCEKPIUJQYKPICDCUGNKPGHGVCNJGCTVTCVGQHDRO$CUGNKPG

XCTKCDKNKV[KUIQQF
CTTQYU
CH 17_p238-252_v3.indd 244 17-07-2015 13:49:40

Box 17.8 Causes of decreased or absent base-

line variability
• Maternal administration of
Ŧ analgesics
Ŧ sedatives
Ŧ magnesium sulfate
• Fetal hypoxia
Decreased variability is an important sign of fetal

hypoxia (Box 17.8).
Periodic changes
Accelerations
Accelerations are transient increases in the basal
heart rate by >15 bpm, lasting for at least 15 sec-
onds (Fig. 17.6). They are a reassuring sign, and Figure 17.6 Fetal heart rate monitoring graph.
the presence of accelerations rules out fetal #EEGNGTCVKQPUCTGUGGP
CTTQYU
hypoxia.
The following types of decelerations may also
Decelerations
occur:
Electronic fetal monitoring can differentiate
decelerations into three types based on their • Prolonged deceleration: Prolonged deceleration
relationship to uterine contractions. A decelera- is one where the deceleration lasts >2 minutes
tion is considered significant if it decreases >15 but <10 minutes. If it continues for >10 minutes,
bpm below baseline, lasts for >15 seconds, and it is considered a shift of the baseline fetal heart
is repetitive. rate (bradycardia). It is indicative of prolonged
cord compression, hypotension, or severe, acute
• Early decelerations: They are symmetric grad- placental insufficiency.
ual drops in the fetal heart rate that mirror • Sinusoidal pattern: This is a smooth, sine wave–
the uterine contraction. The nadir (the low- like undulating pattern in the baseline fetal heart
est point) of the deceleration coincides with rate with a cycle frequency of 3–5 per minute
the peak of the contraction. These are caused that persists for 20 minutes or more (Fig. 17.7d).
by head compression and do not denote fetal The characteristic features are as follows:
hypoxia (Fig. 17.7a). – Baseline fetal heart rate is 120–160 bpm.
• Late decelerations: They commence after the – Variability is markedly decreased or absent.
start of the contraction and return to the base- – The oscillations are 5–15 bpm,
line after the contraction is over. The nadir of – Cycle frequency is 3–5 times/min.
the deceleration occurs after the peak of the – There are no accelerations.
contraction. They are caused by placental Sinusoidal pattern indicates
insufficiency (Fig. 17.7b).
• Variable decelerations: They are characteristi- • fetal anemia,
cally variable in duration, intensity, and tim- • severe hypoxia/acidosis.
ing. They are caused by cord compression. Interpretation of the electronic fetal monitor-
They resemble the letters ‘U,’ ‘V,’ or ‘W’ and ing graph is summarized in Box 17.9.
may be variable even in relation to the uterine
contraction (Fig. 17.7c). Intermittent variable
decelerations are often seen even in a nor-
etal heart rate patterns in the secon
mal labor tracing, but the fetus tolerates tran- stage o labor
sient cord compression. However, persistent, Variable decelerations may be associated with
deep, and recurrent variable decelerations are almost every contraction in the second stage
indicative of fetal acidosis. They vary in onset, because the fetal head and cord are compressed.
depth, and duration. This makes it difficult to interpret the electronic
CH 17_p238-252_v3.indd 245 17-07-2015 13:49:40

a. b.
. .
Figure 17.7 'NGEVTQPKEHGVCNOQPKVQTKPIUJQYKPIa. Early decelerations. The decelerations are symmetric and mirror the
contraction. b. Late decelerations. Onset occurs at the peak of contraction and returns to normal after contraction ends.
c. Variable decelerations. Abrupt decrease from baseline and onset is variable. d. Sinusoidal pattern.
fetal monitoring trace. Patterns suggestive of • Reassuring (Category I by ACOG or Normal by

fetal hypoxia are as follows: RCOG)
• Indeterminate (Category II by ACOG or
• Decelerations to <70 bpm Suspicious by RCOG)
• Loss of variability • Nonreassuring (Category III by ACOG or
• Persistent baseline bradycardia/tachycardia Pathological by RCOG)
Category I or reassuring tracings are consid-
hree tiere etal heart rate ered ‘normal’ since they are associated with a
interpretation system normal fetus that is tolerating labor well. There is
Electronic fetal monitoring tracings are classi- no fetal acidemia. A Category I tracing (Fig. 17.8)
fied as follows: will have all of the following:
CH 17_p238-252_v3.indd 246 17-07-2015 13:49:41

Category II tracings or indeterminate fetal

Box 17.9 Interpretation of an electronic fetal
monitoring graph heart rate patterns (Fig. 17.9) neither suggest
acidosis nor give a clear indication of fetal well-
Interpretation of an electronic fetal monitoring graph being. They include the following:
TGSWKTGUOGPVKQPQHVJGHQNNQYKPI
• Baseline fetal heart rate (in bpm) • Tachycardia
• Baseline variability (normal, decreased, absent) • Bradycardia without absent variability
• Presence of accelerations (duration and elevation • Minimal or marked variability
above baseline) • Absent variability without recurrent decel-
• 2TGUGPEGQHFGEGNGTCVKQPU
FWTCVKQPFGETGCUGDGNQY erations
baseline, and relation to contraction)
• Absence of accelerations without absent varia-
Ŧ Early
bility
Ŧ Late
Ŧ Variable
• Recurrent, variable, or late decelerations with
moderate variability
• Prolonged decelerations t2 minutes but <10
minutes
• A baseline fetal heart rate of 110–160 bpm
• Absence of late or variable fetal heart rate Category III or nonreassuring tracings
decelerations (Fig. 17.10) are considered ‘abnormal’ because
• Moderate fetal heart rate variability (6–25 bpm) they are associated with an increased risk of fetal
• Fetal heart rate accelerations—present or hypoxic acidemia, which can lead to cerebral palsy
absent and neonatal hypoxic ischemic encephalopathy.
• Early decelerations—present or absent Findings on the tracings include the following:
Figure 17.8 %CVGIQT[+VTCEKPI$CUGNKPGHGVCNJGCTVTCVGQHDROCPFOQFGTCVGDCUGNKPGXCTKCDKNKV[KUUGGPYKVJPQ

decelerations.
CH 17_p238-252_v3.indd 247 17-07-2015 13:49:43

Figure 17.9 %CVGIQT[++VTCEKPI4GEWTTGPVXCTKCDNGFGEGNGTCVKQPU

CTTQYUCTGUGGPYKVJOQFGTCVGXCTKCDKNKV[
Figure 17.10 %CVGIQT[+++VTCEKPI2QQTDCUGNKPGXCTKCDKNKV[YKVJUGXGTGTGEWTTGPVXCTKCDNGFGEGNGTCVKQPUUGGP
CH 17_p238-252_v3.indd 248 17-07-2015 13:49:46

• Absent baseline fetal heart rate variability with If membranes are not ruptured yet, artificial
any of the following: rupture of membranes (ARM) would help assess
– Recurrent late deceleration the amniotic fluid. Thick meconium adds to
– Recurrent variable decelerations the seriousness of the situation. Transcervical
– Bradycardia amnioinfusion may be attempted to decrease
• Sinusoidal pattern cord compression by increasing the amniotic
fluid. It also helps to dilute the meconium.
urther evaluation o Category II an Amnioinfusion
Category III tracings
After rupture of the fetal membranes, a pediat-
In the presence of a Category II or Category III ric nasogastric feeding tube is inserted using
tracing, it is important to try and assess the degree standard technique and attached to intravenous
of fetal acidemia. The tests mentioned below may extension tubing. Normal saline (without dex-
be done. trose), at body temperature, is infused through
Fetal scalp stimulation test the catheter. Usually a bolus of 50–1000 mL is
given, followed by a constant infusion.
The fetal scalp stimulation test is a reassuring
The following steps should be taken for man-
technique for determining fetal reserves and to
aging Category II and III tracings:
rule out hypoxia and acidemia. It is easily per-
formed and immediately reassuring. During a • Step 1: Immediate evaluation for the likely
vaginal examination, the examiner strokes the cause of the abnormality such as rapid descent
fetal scalp with firm digital pressure. This should of fetal head, tachysystole, cord compression,
elicit a fetal heart rate acceleration of t15 bpm cord prolapse, placental abruption, or maternal
above the baseline and lasting for t15 seconds. medication.
A positive test rules out fetal acidemia in 90% of • Step 2: Correction of the problem by attempt-
cases, and a negative test may indicate fetal aci- ing to improve fetal oxygenation
demia in 50% of fetuses. – Change maternal position
Fetal scalp blood sampling – Provide oxygen by mask or nasal prongs
– Amnioinfusion, if indicated
The methodology and interpretation of this test – Stop oxytocics.
are described later in this chapter. If the pH is 7.2 • Step 3: Fetal scalp stimulation test to deter-
or less, it is indicative of acidemia and requires mine fetal reserve and signs of acidosis.
immediate delivery (see below). • Step 4: Make a decision whether operative
intervention (cesarean or instrumental vaginal
anagement o Category I Category II delivery) is required.
an Category III tracings The management of Category II and Category
Category I III tracings is summarized in Box 17.10.
Since Category I tracings denote a normal fetus
that is tolerating labor well, no intervention is
A mission test
required. The electronic fetal monitoring trac- On admission to the labor room, all pregnancies
ing may be reviewed every 30 minutes in the first are monitored by electronic fetal monitoring for
stage and every 15 minutes in the second stage 20 minutes. This is called the admission test.
of labor. Based on this trace, a decision is made regarding
the need for continuous electronic fetal mon-
Category II and Category III
itoring in labor. The fetus is considered to be
Category II tracings are suspicious and need to be healthy and capable of withstanding labor if
managed before acidemia sets in. Since Category
III tracings indicate fetal acidemia, preparations • the baseline variability is good,
for delivery should be made while simultane- • there are at least two accelerations in 20 min-
ously initiating steps to improve uteroplacental utes, and
perfusion and oxygen delivery. • there are no decelerations.
CH 17_p238-252_v3.indd 249 17-07-2015 13:49:46

prediction of acidemia. However, randomized

Box 17.10 Interventions in Category II and
Category III tracings trials have not found this to be superior to fetal
scalp pH measurements.
• Decrease uterine activity
Ŧ Stop oxytocin infusion (if there is one)
Ŧ 6QEQN[UKUYKVJVGTDWVCNKPGKPVJGRTGUGPEGQHJ[RGT- Disadvantages
stimulation
• +ORTQXGWVGTKPGDNQQFƀQY The disadvantages of fetal scalp blood sampling
Ŧ Turn the mother to the lateral recumbent position are as follows:
• +ORTQXGWODKNKECNCTVGT[DNQQFƀQY
Ŧ Reposition the mother to relieve cord compression • The test is cumbersome, requires special
Ŧ Amnioinfusion, if indicated equipment, and is expensive.
• Improve maternal/fetal oxygenation • It has poor sensitivity and positive predictive
Ŧ Institute oxygen by mask/nasal prongs value for identification of HIE.
• Perform vaginal examination • The test is not used commonly in many
Ŧ Assess progress of labor institutions.
Ŧ Stimulate the scalp to induce accelerations
• Prepare for delivery
Fetal electrocardiography
However, there is no difference in neonatal Fetal electrocardiography can be recorded by
outcome when this test is used in low-risk preg- internal fetal monitoring with special equipment
nancies. Its value in high-risk pregnancies is not that processes fetal ECG, known as the STAN
proven. Admission test, therefore, is not rou- system. Fetal hypoxia causes ST segment and T
tinely recommended. wave changes in the fetal ECG. Randomized tri-
als have shown that when STAN was used as an
adjunct to electronic fetal monitoring, there is a
ther methods of significant reduction in neonatal acidosis. This
technique of fetal monitoring is being evaluated
intrapartum fetal further.
surveillance
Fetal scalp blood sampling Fetal pulse oximetry
Fetal scalp blood sampling is carried out if there Fetal oxygen saturation (SpO2) of <30% for >2
is an abnormality in the fetal heart rate. It is done minutes has been shown to be associated with
to confirm the presence of fetal hypoxia and/or fetal acidosis. Fetal SpO2 can be measured using
acidemia. The cervix must be at least 4–5 cm a sensor introduced transcervically and posi-
dilated and the vertex at least at –1 station. Using tioned against the fetal face. Initial trials showed
a lancet, a blood sample is obtained from the a reduction in cesarean section rate for fetal dis-
fetal scalp. The blood sample is then checked for tress with the use of this technique, but larger
pH. The pH values are interpreted as follows: randomized trials later have failed to show
any benefit. Fetal pulse oximetry is not used
• >7.25: Normal, continue monitoring with elec- currently.
tronic fetal monitoring The fetus faces stress during labor. Fetal surveil-
• 7.25–7.2: Borderline, repeat test in 20–30 lance during labor helps in recognizing the fetus
minutes that is not tolerating labor well and is hypoxic/
• <7.2: Acidemia, immediate delivery indicated acidemic. Recognition of fetal compromise
guides decisions about appropriate intervention
Fetal lactate concentration so that short- and long-term neurological dam-
age may be avoided.
Using the fetal scalp blood, blood lactate can
also be determined. Lactate levels are used for
CH 17_p238-252_v3.indd 250 17-07-2015 13:49:46

Key points
• In the normal course of labor, uterine contractions • Interpretation of the electronic fetal monitoring
ECWUGCFGETGCUGKPWVGTQRNCEGPVCNDNQQFƀQYCPF requires a mention of the baseline fetal heart rate,
therefore a decrease in oxygen delivery to the fetus. baseline variability, presence of accelerations,
• Intrapartum fetal surveillance aims to detect potential and presence of decelerations (early, late, and
fetal harm due to decreased oxygenation. variable).
• Certain fetal heart rate changes occur prior to brain • 'NGEVTQPKEHGVCNOQPKVQTKPIVTCEKPIUECPDGENCUUKſGF

injury. Recognition of these heart rate changes is the as Category I (reassuring), Category II (suspicious), or
basis for fetal monitoring in labor. Category III (nonreassuring).
• Fetal scalp stimulation is a simple clinical test for
• The aim of intrapartum fetal surveillance is to identify
ruling out fetal acidemia.
abnormal fetal heart patterns and provide timely and
effective response to prevent brain injury. • Fetal scalp blood sampling is carried out (if available)
• In the absence of maternal and fetal risk factors, in the presence of an abnormality in the fetal heart
intermittent auscultation is the recommended fetal rate. A pH of 7.2 or less is an indication for immediate
surveillance method during labor. delivery.
• The admission electronic fetal monitoring has a
• Fetal heart rate changes are best looked for after a
doubtful value in high-risk pregnancies and is not
EQPVTCEVKQPYJGPVJGHGVWUJCUDGGPUWDLGEVGFVQC
TGEQOOGPFGFTQWVKPGN[KPNQYTKUMRTGIPCPEKGU
temporary decrease in oxygenation.
• When there is no drop in the baseline fetal heart rate • In the presence of a persistent or repetitive fetal heart
HQNNQYKPICEQPVTCEVKQPKVGUVCDNKUJGUVJGCDKNKV[QHVJG rate abnormality, oxytocin is stopped, the mother is
HGVWUVQYKVJUVCPFNCDQTEQPVTCEVKQPU+PCFGEQORGP- placed in the lateral recumbent position, oxygen is
UCVGFHGVWUVJGHGVCNJGCTVTCVGYKNNFTQRHQNNQYKPIC given by mask, a vaginal examination is done, and
contraction. preparations are made for delivery.
• Electronic fetal monitoring, if available, is indicated in

pregnancies at high risk for adverse perinatal outcome.
Self-Assessment
Case-based questions VJGTG YGTG FGEGNGTCVKQPU YKVJ VJG HGVCN JGCTV TCVG FTQR-
ping to 80 bpm after contractions.
Case 1 1. 9JCVKUVJGſTUVUVGRKPVJGOCPCIGOGPVQHVJGCD-
PQTOCNHGVCNJGCTVTCVG!
/TU/)ECOGKPNCDQTCVYGGMUŏIGUVCVKQP5JGYCU
having contractions every 3–4 minutes and the contrac- 2. *QYECPOCVGTPCNCPFHGVCNQZ[IGPCVKQPDGKO-
VKQPUYGTGNCUVKPIŌUGEQPFU5JGYCUCMPQYPJ[RGT- RTQXGF!
tensive. At 4-cm dilatation, membranes ruptured spontane- 3. +UVJGTGCUKORNGVGUVVQEJGEMHQTHGVCNYGNNDGKPI!
QWUN[CPFVJGCOPKQVKEƀWKFYCUOGEQPKWOUVCKPGF
1. *QYQHVGPYKNN[QWCWUEWNVCVGVJGHGVCNJGCTVTCVGKP Answers
VJGſTUVUVCIGCPFVJGUGEQPFUVCIG!9JKEJKUVJG
DGUVVKOGVQRKEMWRCPCDPQTOCNHGVCNJGCTVTCVG! Case 1
2. 9JCVKUVJGPQTOCNDCUGNKPGHGVCNJGCTVTCVG!
3. Describe late decelerations. What causes late 1. The fetal heart is auscultated every 15–30 minutes
FGEGNGTCVKQPU! KPVJGſTUVUVCIGCPFGXGT[OKPWVGUKPVJGUGEQPF
stage. It is best to listen immediately after the con-
4. 9JCVCTGXCTKCDNGFGEGNGTCVKQPUCPFYJCVECWUGU
traction.
VJGO!
2. The normal baseline fetal heart rate is 110–160 bpm.
3. Late decelerations commence after the start of
Case 2 the contraction and return to the baseline after the
contraction is over. They are caused by placental
/TU56ITCXKFCRCTCYCUKPCEVKXGNCDQT5JG KPUWHſEKGPE[
YCUEOFKNCVGFCPFVJGXGTVGZYCUCVUVCVKQP5JGYCU 4. Variable decelerations are characteristically variable
QPQZ[VQEKPCWIOGPVCVKQP5JGYCUJCXKPIEQPVTCEVKQPU in duration, intensity, and timing. They are caused by
every 2–3 minutes, lasting 45 seconds. On auscultation, cord compression.
CH 17_p238-252_v3.indd 251 17-07-2015 13:49:46

Case 2 Short-answer questions

1. Decrease uterine activity by stopping oxytocin 1. Early, late, and variable decelerations
infusion. 2. Fetal scalp blood sampling
2. Maternal and fetal oxygenation can be improved by 3. Sinusoidal pattern
turning the mother to a lateral recumbent position and 4. Fetal pulse oximetry
by giving oxygen by mask. 5. Admission test
3. 6JGUECNRUVKOWNCVKQPVGUVYKNNGNKEKVHGVCNJGCTVTCVG
acceleration in a healthy fetus. It is a reassuring sign.
Sample questions
1. 9JCVCTGVJGOGVJQFUQHCUUGUUKPIHGVCNYGNNDGKPI
KPNCDQT!
2. What are reassuring and nonreassuring signs of
HGVCNUVCVWU!*QYCTG%CVGIQT[+++VTCEKPIU
OCPCIGF!
CH 17_p238-252_v3.indd 252 17-07-2015 13:49:46

Obstetric Analgesia
18 and Anesthesia
Case scenario
Mrs. JR, 23, went to the hospital in active labor. It was her first pregnancy
and she was in severe pain. She requested pain relief.
Introduction triggers various systemic responses: tachy-

cardia, hypertension, increased cardiac out-
Labor pain is the most severe pain a woman will put, and increased oxygen consumption.
ever experience in her life. In no other situation • Hyperventilation and resultant hypocarbia
involving so much pain is one expected to man- – The pain pushes the woman into hyper-
age without pain relief. ventilation–hypoventilation–apnea cycles
It is difficult for the obstetrician and the during contractions. This results in mater-
woman herself to predict her reaction to labor nal respiratory alkalosis and fetal aci-
pain. Women tend to underestimate the level of demia, both of which are tolerated by
pain they will experience in labor and therefore healthy mothers and fetuses. However, in
may lose control when the pains continue to the presence of fetal or maternal compro-
intensify. It is the responsibility of the obstetric mise, this may lead to maternal or fetal
team to alleviate pain by providing all laboring decompensation.
women with options for pain relief. • Psychological effects
– Unrelieved pain during labor can contribute
to the development of postpartum depres-
Effect of pain on labor sion and posttraumatic stress disorder.
and the laboring woman
Pain has the following effects on labor (Fig. 18.1): Pain pathways
• Neurohormonal response to stress and release Somatic and autonomic innervation of the female
of catecholamines reproductive tract is discussed in Chapter 1,
– The intensity of labor pains causes stress and Anatomy of the female reproductive tract. Pain
the release of catecholamines. This in turn from the uterus and cervix is transmitted through
CH 18_p253-265_v3.indd 253 17-07-2015 15:39:22

Pain
ncrease
ncrease car iac output
respiratory rate
ncrease bloo pressure
Hypocarbia
Catecholamine ympathetic ecrease gastric

releases stimulation emptying
ncrease free
fatty aci s
Lactic aci osis
ecrease placental etal hypo ia

Metabolic aci osis
perfusion etal aci osis
Figure 18.1 Effect of pain on labor.
sympathetic and parasympathetic nerve fibers. upper vagina pass through the pelvic splanchnic
The sympathetic nerve fibers carry the pain from nerves to the second, third, and fourth sacral
the uterus to spinal levels T10–L1. Therefore, pain nerves. Pain from the perineum is transmitted
of uterine contractions is felt in the lumbosacral through somatic fibers of the pudendal nerve to
area. The sensory pain fibers from the cervix and the same sacral segments (Fig. 18.2).
irst phase
isceral pai
ympathetic
path ay
pi al cor
Cer ix eco phase

somatic pai
Pu e al
er e
a i a
Figure 18.2 Pain pathways in labor.
CH 18_p253-265_v3.indd 254 17-07-2015 15:39:23

Obstetric Analgesia and Anesthesia 255
Causes of labor pain methods. Anesthesia refers to complete block

of pain sensation with or without loss of
The causes of labor differ in the different stages consciousness. This is used during cesarean
of labor. delivery and for some obstetric procedures
(Box 18.3).
First stage of labor
In the first stage of labor, the pain results from onpharmacological methods
uterine contractions. It is described as severe for labor analgesia
cramping in the uterus and may radiate to the
abdominal wall, low back, gluteal areas, and Nonpharmacological approaches to labor pain
thighs. As mentioned earlier, it involves spinal management do not aim to make pain disappear.
roots T10–L1 (Fig. 18.2). It is caused by both dis- They give the laboring mother means for coping
tension of the uterus and ischemia of cervical with the pain and therefore maintain a sense of
and uterine tissues (Box 18.1). personal control over the birth process.
Second stage of labor Prenatal or antenatal education

In addition to the pain originating from the When a woman is well informed about the labor
uterus and cervix, the laboring woman now starts process and what to expect during labor, she will
to experience somatic pain from distension of be able to cope better with labor pains. Antenatal
the vagina, perineum, and pelvic floor as the fetal classes can be used to educate the couple and
head passes through the pelvis (Box 18.2). teach methods for managing pain.
The ideal labor analgesic would decrease both
visceral and somatic pain.
Box 18.3 ptions for obstetric analgesia and
anesthesia
ptions for obstetric abor analgesia
analgesia and anesthesia • Nonpharmacological
Ŧ Prenatal/antenatal education
Labor analgesia refers to relief of pain in labor Ŧ Rhythmic breathing techniques
with pharmacological and nonpharmacological Ŧ Continuous labor support
Ŧ Touch and massage
Ŧ Warm water baths
Box 18.1 2CKPKPVJGſTUVUVCIGQHNCDQT
Ŧ Transcutaneous electrical nerve stimulation (TENS)
• Visceral pain (uterus and cervix) Ŧ Music
• Occurs with Ŧ Acupuncture
Ŧ uterine contractions Ŧ Hypnosis
Ŧ cervical dilatation • Pharmacological
• Caused by Ŧ Opioids
Ŧ distension of uterus Ŧ Inhalational analgesia (Entonox)
Ŧ ischemia of uterine and cervical tissues Ŧ Neuraxial analgesia
• Mediated through T10–L1 spinal root Epidural
Ŧ Local analgesia
Pudendal block
Box 18.2 Pain in the second stage of labor Paracervical block
• Somatic pain in addition to visceral pain Perineal infiltration
• 9QTUGVJCPſTUVUVCIGRCKP Anesthesia
• Caused by distension of • Without loss of consciousness
Ŧ vagina Ŧ Spinal
Ŧ perineum Ŧ Epidural
Ŧ RGNXKEƀQQT Ŧ Combined spinal–epidural
• Transmitted by pudendal nerve (S2, S3, S4) • With loss of consciousness
• Rectal pressure and ‘bearing down’ sensation Ŧ General
CH 18_p253-265_v3.indd 255 17-07-2015 15:39:23

hythmic breathing techniques (instead of needles) at specific points. Studies

have shown a modest benefit.
Rhythmic, controlled breathing allows the
woman to divert her mind from the pain. This
contributes to her ability to cope with labor pain. Music
Women express high satisfaction with breathing Music has been shown to have a great influence
techniques, and it should be taught to them in on mood and emotional well-being. Playing
antenatal classes or even during labor. music in the labor room helps divert the woman’s
mind from the pain and helps her cope better.
Continuous labor support Application of heat and cold, hypnosis, and
aromatherapy are other nonpharmacological
The term continuous labor support refers to the methods that have been tried.
use of a companion to provide nonmedical care
of the laboring woman throughout labor and
birth. Husbands, in the labor room, can provide Pharmacological agents
emotional support during labor and help the for labor analgesia
woman cope.
pioids
Touch and massage Opioids have been safely used for many decades
for labor analgesia. However, only 50% of women
When a woman is feeling helpless in labor, a car- will report adequate pain relief. The decrease in
ing and reassuring touch by another person can pain perception is mostly mediated by inducing
be very comforting. Massage of the low back and sedation. Although opioids are usually adminis-
thighs also helps relieve some of the pain. tered as intramuscular (IM) or intravenous (IV)
injections, they may also be administered with a
Warm water baths pump [patient-controlled analgesia (PCA)].
In countries with the necessary facilities, immer- Commonly use opioi s

sion in a warm water bath has been shown to be
soothing. The commonly used opioids are listed in
Table 18.1.
Transcutaneous electrical Meperidine (pethidine)

nerve stimulation Meperidine (pethidine) is the most commonly
used, cost-effective opioid for labor analgesia
Low-voltage electrical impulses (mild shocks) (Box 18.4). The dose is 50 mg IM (or 1–2 mg/kg
from a handheld battery-powered unit are trans- body weight), which can be repeated after 4–
mitted to the skin via surface electrodes. One 6 hours if the woman has not delivered yet. It
pair of electrodes is usually placed paraverte- can also be used IV at the dose of 25 mg every
brally at the level of T10–L1 and another at the 2 hours. The onset of action is within 45 minutes
level of S2–S4. The woman controls the intensity after IM administration and almost immediate
of the current by turning a dial. The mild shocks
supposedly reduce the awareness of contraction
pain. There is no strong evidence that transcuta-
neous electrical nerve stimulation (TENS) pro- Box 18.4 Pethidine (meperidine) for labor
vides significant pain relief in labor. analgesia
• 50 mg IM repeated 4–6 hourly
• Onset of action 45 minutes
Acupuncture and acupressure • Antiemetic may be given for nausea
In acupuncture, needles are placed at specific • Infant preferably to be delivered
points on the body depending on the location of Ŧ Within 1 hour of maternal dosing or
Ŧ After 4 hours of maternal dosing
pain. There is a high level of satisfaction and
• Does not facilitate cervical dilatation
reduction in dosage of analgesics used with this
• Decreased beat-to-beat variability on fetal heart tracing
method. Acupressure involves applying pressure
CH 18_p253-265_v3.indd 256 17-07-2015 15:39:23

Table 18.1 pioids used in labor
Drug Dose nset (Minutes) Duration ( ours) Comments

Pethidine • 50–100 mg IM 40 2–3 • Respiratory depressant
• Can be repeated • Neonatal effects seen
at intervals of if delivery occurs between 1
4–6 hours and 4 hours after administration
Fentanyl • 25–50 μg IV (given 2–3 0.45–1 • #PCNIGUKEGHſECE[PQVCU
slowly over effective as pethidine
1–2 minutes) • Less side effects than opioid
• Short acting
• Potent respiratory depressant
Butorphanol • 1–2 mg IM 10–15 3–4 • Not commonly used in labor
• Excessive sedation
after IV administration. The IM route is most minutes) every hour. Compared with pethidine, it
commonly used. Since nausea is one of the most performs better in terms of pain scores in women
common side effects of pethidine, an antiemetic in labor. Remifentanil is also gaining popularity,
is often administered along with it. especially for PCA.
It is recommended that the infant be deliv-
ered within 1 hour of, or >4 hours after, a dose of Butorphanol
pethidine, as pethidine reaches a maximal con- Butorphanol is an opioid that is 5 times as potent
centration in the fetus from 2 to 3 hours after as morphine and 40 times as potent as pethidine.
maternal dosing. Delivering the infant 2–3 hours It offers analgesia with sedation. The dose of
after the administration of pethidine may result butorphanol is 1–2 mg IM. It is not used fre-
in neonatal respiratory depression. quently for labor analgesia as it produces exces-
Pethidine does not facilitate cervical dilata- sive sedation.
tion in cervical dystocia and has been shown to
worsen neonatal outcomes when given for that Si e e ects o opioi s
indication. Decrease in beat-to-beat variability Opioids are associated with side effects, espe-
of the fetal heart tracing can also occur with cially nausea, vomiting, and neonatal respiratory
pethidine, and the obstetrician should be aware depression. Box 18.5 lists the common side effects
of this while interpreting the trace. of opioids.
Tramadol
atient controlle analgesia
Tramadol is a synthetic opioid analgesic. It is
Intravenous analgesia, where the woman herself
administered at a dose of 100 mg IM (or 1–2 mg/
controls the frequency of administration, pro-
kg body weight). Its potency is 10% of pethidine.
vides good pain relief in labor. It is used in women
It causes no clinically significant respiratory
who desire continuous analgesia but where epi-
depression. The onset of action is within 10 min-
dural analgesia is contraindicated. Maternal res-
utes of IM administration, and the effect lasts for
piration should be closely monitored when PCA
2–3 hours. It is not as effective as pethidine.
Fentanyl
Box 18.5 Common side effects of opioids
Fentanyl has a rapid onset of action (within 2–3
minutes after IV administration) with a short dura- • Nausea and vomiting
tion of action, making it useful for labor analgesia. • Drowsiness
It is a highly lipid-soluble synthetic opioid, with • Respiratory depression
• Delayed gastric emptying
analgesic potency 100 times that of morphine and
• Decreased variability on fetal heart tracing
800 times that of pethidine. It can be administered
• Neonatal respiratory depression
in IV boluses of 25–50 μg (given slowly over 1–2
CH 18_p253-265_v3.indd 257 17-07-2015 15:39:23

is administered. Fentanyl and remifentanil are euraxial analgesia

the drugs used in the dosage given as follows:
Neuraxial analgesia provides the best pain relief in
Fentanyl labor and is widely used. It is also beneficial to the
Loading dose: 50–100 μg mother in certain clinical situations. A local anes-
Patient-controlled 20–60 μg every thetic with or without an opioid is injected into the
dose: 5–10 minutes epidural or intrathecal space close to the spinal
Remifentanil nerves that transmit pain from the uterus to the
spinal column (T10–L1). The dose is adjusted to
Patient-controlled 25–50 μg every
provide analgesia without affecting motor function
dose: 5–10 minutes
and appreciation of pressure during uterine con-
tractions. Neuraxial analgesia may be epidural, spi-
onopioid analgesics nal, or combined epidural and spinal analgesia.
Barbiturates and benzodiazepines such as mid-
azolam and diazepam are used as anxiolytics in Epidural analgesia
early labor. They do not provide adequate anal- Epidural analgesia is a central nerve block tech-
gesia and can cause neonatal respiratory nique accomplished by injecting a local anes-
depression. thetic (Box 18.7). It is widely used as a form of
pain relief in labor. The primary goal of neuraxial
Inhalational analgesia analgesia during labor or vaginal delivery is to
provide adequate maternal analgesia with mini-
itrous oxide mal motor block. Epidural analgesia achieves
Nitrous oxide inhalation analgesia is adminis- this when a local anesthetic (e.g., bupivacaine) is
tered as a blend of 50% nitrous oxide and 50% used at low concentrations with or without
oxygen (Entonox). The laboring woman uses a opioids (e.g., fentanyl).
handheld face mask to self-administer the The contraindications to epidural analgesia
anesthetic gas. Since Entonox takes 50 sec- are listed in Box 18.8.
onds to take effect, the woman is instructed
on correctly timing each inhalation. She Epidural for cesarean section
should start with the onset of contraction so With a larger dose of anesthetic and opioid, an
that the analgesia is effective at the peak of the epidural can also be used for a cesarean section.
contraction.
It is safe because when the woman becomes
too drowsy, she will automatically drop the Box 18.7 Epidural analgesia
mask. Entonox provides women with a signifi- • Commonest neuraxial block in labor
cant degree of pain relief, and may be useful in • Most effective method for pain relief
situations where epidural analgesia is not • 2TGNQCFYKVJ+8ƀWKFUVQCXQKFJ[RQVGPUKQP
available. It does not cause neonatal respira- • Bupivacaine and fentanyl commonly used
tory depression or affect uterine contractility • Repeated bolus doses or continuous infusion
(Box 18.6). • Can be used for cesarean section
Box 18.6 Entonox for labor analgesia Box 18.8 Contraindications to epidural
• Inhalation analgesia analgesia
• 50% nitrous oxide and 50% oxygen • Coagulopathy
• Self-administered • Thrombocytopenia
• Through handheld mask • Raised intracranial pressure
• Taken with start of contraction • Skin or soft tissue infection at the site of the epidural
• 5KIPKſECPVRCKPTGNKGH placement
• No neonatal respiratory depression • Anticoagulant therapy
• No effect on uterine contractility Ŧ Within 6–12 hours after the last dose
CH 18_p253-265_v3.indd 258 17-07-2015 15:39:23

If a woman has been receiving epidural analge- recautions

sia during labor, it can be continued in case she The following precautions need to be taken in
undergoes a cesarean section. the case of epidural analgesia:
• Blood pressure should be recorded prior to
Procedure
administration of an epidural. Thereafter it
Epidural analgesia is administered as follows: should be checked at 5- to 15-minute intervals.
• Continuous fetal heart rate monitoring should
• A preload of 500 mL of IV fluids should be
be done since the epidural may cause mater-
given prior to administering epidural anal-
nal hypotension, leading to fetal heart rate
gesia since the procedure is often associated
abnormalities.
with hypotension.
• Aseptic precautions must be used (gown,
gloves, masks, and povidone–iodine skin Drugs used for epidural analgesia
prep). The following drugs are used for epidural
• Epidural block can be performed in the lateral analgesia:
or sitting position (Fig. 18.3).
• The lumbar spinous process is palpated and • Local anesthetic: Bupivacaine is the most com-
the widest interspace below L3 is chosen. monly used anesthetic for epidural analgesia.
• A local anesthetic is used to numb the skin. • Opioid: Fentanyl is the most commonly used
• A spinal needle is slowly advanced while opioid for epidural analgesia.
feeling for resistance. A sudden loss of resist- Commonly, bupivacaine is combined with
ance is felt as the epidural needle enters fentanyl. Epidural analgesia usually starts tak-
the epidural space. Care is taken not to ing effect 5–10 minutes after injection. The
puncture the dura. An epidural catheter is maximal effect may not be achieved for 15–20
threaded through the needle and the needle minutes.
is removed.
• The catheter is fixed in place.
• A combination of low-concentration bupi- Complications of epidural analgesia
vacaine and fentanyl is given as bolus every Complications associated with epidural analge-
2 hours or as needed to maintain mater- sia are listed in Box 18.9.
nal comfort. Continuous infusion may also
be used.
Effect of epidural analgesia on labor
Epidural analgesia has the following effects on
labor:
• Timing of epidural analgesia has no effect on
labor progression; therefore, it is not necessary
Box 18.9 Complications associated with

epidural analgesia
• Hypotension
• Nausea and vomiting
• Inadequate or failed analgesia
• Fetal heart rate abnormalities (due to maternal
hypotension)
• Prolonged labor leading to increase in instrumental
Figure 18.3 Administration of epidural analgesia. delivery
• Fever
The laboring woman is sitting up and arching her
• Postdural puncture headache (PDPH) due to inadver-
back. The epidural needle is being inserted into the
tent dural tear
L2–L3 space.
CH 18_p253-265_v3.indd 259 17-07-2015 15:39:24

to wait until the active phase of labor for Indications for a pudendal block are as
administration of epidural analgesia. follows:
• Epidural analgesia prolongs active phase of
• Outlet forceps delivery
labor by 1 hour.
• Assisted breech delivery
• Due to the motor blockade induced by the
• Repair of episiotomy and perineal lacerations
analgesic, the duration of the second stage is
prolonged.
• The need for operative vaginal delivery for Procedure for pudendal block
prolonged stage is higher. Discontinuation of A pudendal block is administered as follows:
epidural analgesia in the second stage of labor
does not reduce the likelihood of instrumental • The procedure should be performed with all
delivery but increases pain. aseptic precautions.
• There is no increase in the cesarean section • The woman is placed in a dorsolithotomy
rate. position.
• Epidural analgesia is not associated with any • The perineum should be prepped with povi-
increase in adverse neonatal outcome. done–iodine solution.
• Sterile gloves must be used.
• 1% solution of lidocaine (Xylocaine) is used.
Patient-controlled • The anesthetic solution is drawn up into a
epidural analgesia 10-mL syringe.
Patient-controlled epidural analgesia (PCEA) • A 20-gauge, 15-cm spinal needle is used.
gives women a feeling of being in control of their • Usually a transvaginal approach is used (Fig.
own pain relief, and results in a lower total dose 18.4), although a transperineal approach has
of the local anesthetic used and less motor block- been described.
ade. This must be combined with a continuous • The pudendal nerve lies behind the sacros-
epidural infusion for best results. The same pinous ligament that stretches between the
drugs are used. ischial spine and the sacrum.
• The ischial spine is palpated with the index
and middle fingers and the needle advanced
Pudendal block for a distance of 1 cm through the vaginal
A pudendal block provides relief of pain resulting mucosa into the sacrospinous ligament. A
from the stretching of the vagina and perineum needle guide may be used, if available.
by the descending fetal presenting part in the • The syringe is aspirated to ensure that the
second stage of labor. The pain of the second needle has not entered a blood vessel.
stage of labor is mediated through the pudendal
nerve. The sacral nerve roots 2, 3, and 4 (via the
pudendal nerve) provide sensory and motor
innervation to the lower vagina, perineum, and
vulva, respectively. Analgesia over these areas is
obtained by infiltrating a local anesthetic around
the trunk of the pudendal nerve.
A pudendal block also provides analgesia Pu en al ner e
during the surgical repair of vaginal and perineal
tears and/or episiotomy. It is important to
remember that the pudendal block does not
abolish sensation to the anterior part of the
perineum because branches of the ilioinguinal
and genitofemoral nerves supply this region.
Therefore, lacerations in this area will require acrospinous ligament
local infiltration with additional medication. A Figure 18.4 Transvaginal pudendal block. The needle is
pudendal block has no adverse effects on the advanced through the sacrospinous ligament into the loose
neonate. areolar tissue around the pudendal nerve.
CH 18_p253-265_v3.indd 260 17-07-2015 15:39:25

• If there is no backflow of blood, 3 mL of the • Two fingers are used to direct the tip of the
anesthetic solution is injected into the sacros- guide into the lateral vaginal fornix. Care must
pinous ligament. be taken to interpose the fingers between the
• The needle is then advanced through the cervix or fetal head and the needle. A needle
sacrospinous ligament into the loose areolar guide may be used, if available.
tissue around the pudendal nerve. • The needle is usually inserted close to the cer-
• After aspirating to ensure no vascular punc- vix at the 3 and 9 o’clock positions in the lateral
ture, another 7 mL of the anesthetic solution is fornix (imagining the cervix as a clock face).
injected into this area. Some authors suggest 4 and 8 o’clock positions
• The procedure is repeated on the other side. to avoid blood vessels (Fig. 18.5).
• The needle is inserted into the vaginal mucosa
Complications of pudendal block for a depth of 3–5 mm (Fig. 18.6).
• The syringe is aspirated to rule out needle
Complications of a pudendal block are rare but position inside a blood vessel.
include the following: • If there is no backflow of blood, 5 mL of the
• Hematoma formation from perforation of a anesthetic solution is injected into the vagi-
blood vessel during needle insertion nal submucosa. Injection is avoided during
• Infection at the site of injection contractions.
• Ischial region paresthesias and sacral • The process is repeated on the other side.
neuropathy
• Seizures, hypotension, and cardiac arrhyth- Complications of paracervical block
mias after intravascular administration The following are the complications of a para-
cervical block:
Paracervical block • Postblock fetal bradycardia is one of the rea-
A paracervical block relieves the pain caused by sons that paracervical blocks are not popular.
cervical dilatation during the first stage of labor.
The anesthetic blocks the visceral sensory fibers
of the lower uterus, cervix, and upper vagina
(T10–L1) as they pass through the uterovaginal
plexus (Frankenhäuser’s plexus) on each side of
the cervix. It does not significantly affect the pro-
gression of labor. A paracervical block does not
block the sensory nerves from the perineum, so it
is ineffective during the second stage of labor.
Paracervical blocks can be given only after a
cervical dilatation of 4 cm and may need to be
repeated every 1–2 hours depending on the 9 3
8 o’Clock 4 o’Clock
anesthetic agent used. The pain relief has been
reported to be effective. Paracervical blocks are 7 5
no longer used commonly for pain relief during 6
labor.
Procedure
A paracervical block is administered as follows:
• The procedure is done under aseptic conditions. Figure 18.5 Sites for paracervical block. The needle is
• The woman is placed in a dorsolithotomy usually inserted close to the cervix at the 3 and 9 o’clock
position. positions in the lateral fornix (imagining the cervix as
• The perineum and vagina are prepped with a clock face). Some authors suggest 4 and 8 o’clock
povidone–iodine solution. RQUKVKQPUVQCXQKFDNQQFXGUUGNU
CUUJQYPKPVJGſIWTG
CH 18_p253-265_v3.indd 261 17-07-2015 15:39:25

because the effect lasts only for a short time

(90–120 minutes). It may be used for short
obstetric procedures such as forceps, vacuum
delivery, or manual removal of placenta in the
case of a retained placenta. However, spinal
anesthesia is the anesthesia of choice for a
cesarean section.
Spinal anesthesia is achieved by a subarach-
noid injection of a local anesthetic (bupiva-
caine) and an opioid (fentanyl). It is usually
given in the L3/L4 interspace or the one above
or below it. It blocks the sensation of pain below
the level of the umbilicus. The motor pathways
Figure 18.6 Paracervical block. The needle is inserted into
are also affected, so the woman will not be able
the vaginal mucosa for a depth of 3–5 mm.
to move her lower limbs till the anesthetic
wears off.
It may occur within 10 minutes of the injec- Its advantages over epidural analgesia include
tion. It is usually transient, but can last as long the following:
as 40 minutes. The mechanism of postblock
fetal bradycardia is unclear. • Short procedure time
• Systemic toxicity after intravascular admin- • Rapid onset of the block (within 5 minutes)
istration may result in excessive sedation, • High success rate
generalized convulsions, and cardiovascular Spinal anesthesia in a pregnant woman dif-
collapse. fers from spinal anesthesia in the nonpregnant
• Lower extremity paresthesias have been woman. The differences are summarized in
reported. Table 18.2.
• Vaginal/broad ligament hematoma or infec-
tion is a rare complication.
Procedure
Spinal anesthesia is administered as follows:
Anesthesia for • A preload of 500–1000 mL of IV fluids is given
labor and delivery to prevent hypotension resulting from sym-
pathetic block that may result from spinal
anesthesia.
Spinal anesthesia • The procedure is done under complete aseptic
In a woman undergoing a vaginal delivery, spi- precautions.
nal anesthesia is not used for labor analgesia • The woman can be sitting or lying on her side.
Table 18.2 Differences between spinal anesthesia in pregnant and

nonpregnant women
In pregnant In nonpregnant
women women
Dose of anesthetic Smaller Larger
Risk of high block More common Less common
Hypotension More common Less common
Spinal headache More common Less common
6GEJPKECNFKHſEWNV[KPſPFKPI More Less
subarachnoid space
Fetal adverse effects Secondary to maternal –
hypotension
CH 18_p253-265_v3.indd 262 17-07-2015 15:39:25

pinous process
ura
Figure 18.7 Positioning for spinal anesthesia and placement of spinal needle.
• The woman is instructed to arch her back ost ural puncture hea ache
since flexion of the spine opens the interver- A postdural puncture headache (PDPH) is an
tebral spaces. extremely distressing complication of spinal anes-
• The L3/4, L4/5, or L5/S1 interspace is identified. thesia. It is caused by leakage of the CSF through
• The chosen interspace is infiltrated with a the dural rent made by the spinal needle. The
local anesthetic. resultant traction on cranial structures and
• The spinal needle is inserted in the midline, accompanying cerebral vasodilation cause a
aiming slightly cranially (Fig. 18.7). severe headache that is worsened by sitting or
• Resistance increases as the ligamentum flavum standing and relieved by lying down.
is entered and when the dura is encountered, CSF leakage can be avoided or reduced by
with a sudden ‘give’ as the dura is pierced. using a 26- or 27-gauge spinal needle with a short
• Correct placement of the needle is confirmed bevel or a pencil point.
by a drop of clear cerebrospinal fluid (CSF) The headache is treated with oral or parenteral
appearing at the hub of the needle when the analgesics and caffeine. If the headache is very
stilette is removed. severe and does not respond to conventional
treatment, it can be treated with an epidural blood
Complications patch. The epidural blood patch is performed by
injecting 10–20 mL of the woman's blood into the
Complications associated with spinal anesthesia epidural space, thereby sealing the dural defect.
Combined spinal epidural

Box 18.10 Complications associated with spinal
anesthesia anesthesia
• Hypotension Combining spinal with epidural anesthesia pro-
• Nausea and vomiting vides the rapid onset of action of a spinal and the
• High spinal (cephalad progression of the level of longer duration of action of an epidural. It is not
anesthesia)
a routinely practiced technique.
• Pruritus
The technique involves placing a needle into
• Postdural puncture headache (PDPH)
the epidural space. Another smaller-gauge needle
CH 18_p253-265_v3.indd 263 17-07-2015 15:39:25

is then threaded through this into the subarach- – Profound maternal hypovolemia
noid space. After injecting the required drugs into – Certain maternal medical conditions
the spinal space, a catheter is inserted into the – Skin infection in the lower back
epidural space for additional drug injection. • Mother unwilling to have spinal/epidural
anesthesia
General anesthesia
Procedure
Indications for general anesthesia
Preoxygenation with 100% oxygen for 3–5
in the peripartum period minutes is recommended. Anesthesia is
The indications for general anesthesia in the induced with IV sodium pentothal or propofol.
peripartum period are as follows: Succinylcholine is the most commonly used
muscle relaxant. The woman is intubated with
• Cesarean section
an endotracheal tube to maintain the airway.
• Suturing of extensive vaginal or perineal tears
Inhalation agents such as sevoflurane or iso-
after vaginal delivery
flurane, with or without nitrous oxide, are used
• Removal of retained placenta
to maintain anesthesia.
• Management of acute uterine inversion
General anesthesia is indicated for a cesarean eonatal effect
section in the following situations:
• Emergency cesarean section where anesthesia General anesthesia can cause respiratory depres-
has to be induced without delay due to fetal sion in the neonate. To avoid exposing the fetus
condition to anesthetic agents for a longer time, it is rec-
• Failed/inadequate spinal or epidural anesthesia ommended that the woman have the skin
• Contraindications to spinal or epidural prepped and the abdomen draped before anes-
anesthesia thesia is induced. The skin incision is made as
– Coagulopathy soon as anesthesia is induced.
– Anticoagulant therapy
Key points
• Labor pain is the most severe pain a woman will ever • Epidural analgesia is the most effective technique for
experience in her life. It is the responsibility of the ob- labor analgesia.
stetric team to alleviate pain by providing all laboring
• Epidural analgesia is a central nerve block technique
women with options for pain relief.
accomplished by injecting a local anesthetic close
• Labor pain, by causing maternal respiratory alkalosis VQVJGPGTXGUVJCVVTCPUOKVNCDQTRCKPKPVJGſTUVCPF
and fetal acidemia, can have deleterious effects on the second stages of labor.
mother and fetus.
• Hypotension, which is the commonest complication
• 2CKPKPVJGſTUVUVCIGQHNCDQTKUXKUEGTCNKPPCVWTGCPF of epidural, can be avoided by preloading the mother
is mediated by T10–L1 nerve roots. with 500–1000 mL of IV crystalloid solution.
• Pain in the second stage is somatic and is mediated by • A pudendal block provides relief of pain resulting
the splanchnic nerves and the pudendal nerve (S2–S4). from the stretching of the vagina and perineum by the
• Labor analgesia refers to relief of pain in labor with descending fetal presenting part in the second stage of
pharmacological and nonpharmacological methods. labor.
• Anesthesia refers to complete block of pain sensation • Complications of a pudendal block are rare but include
with or without loss of consciousness. hematoma formation, infection at the site of injection,
ischial region paresthesias, and sacral neuropathy.
• Pain relief in labor can be provided by nonpharmaco-
logical or pharmacological techniques. • A paracervical block relieves the pain caused by
EGTXKECNFKNCVCVKQPFWTKPIVJGſTUVUVCIGQHNCDQT
• The commonest pharmacological techniques used in Paracervical blocks are not commonly used for
labor are opioids, Entonox, and epidural analgesia. pain relief during labor.
(Continued)
CH 18_p253-265_v3.indd 264 17-07-2015 15:39:25


• In a woman undergoing a vaginal delivery, spi- • Complications of spinal anesthesia include hypoten-
nal anesthesia is not used for labor analgesia sion, nausea and vomiting, high spinal (cephalad
because the effect lasts only for a short time progression of the level of anesthesia), pruritus, and
(90–120 minutes). postdural puncture headache (PDPH).
• Spinal anesthesia may be used for short obstet- • General anesthesia is used for a cesarean section
ric procedures such as forceps, vacuum delivery, in situations where delivery is urgent due to fetal
or manual removal of placenta in the case of a condition, in failed neuraxial anesthesia, in cases
retained placenta. where there is a contraindication to neuraxial
• Spinal anesthesia is the anesthesia of choice for a anesthesia, or if the woman is unwilling for neuraxial
cesarean section. anesthesia.
Self-Assessment
3. Epidural analgesia is ideal to relieve the pain of both
Case-based questions VJGſTUVCPFUGEQPFUVCIGUQHNCDQT
4. A pudendal block may be given in the second stage
Case 1 to relieve the pain from cervical dilatation and for
Mrs. JR, 23, came to the hospital in active labor. This analgesia during suturing of lacerations/episiotomy.
YCUJGTſTUVRTGIPCPE[CPFUJGYCUKPUGXGTGRCKP5JG
requested pain relief.
Case 2
1. 9JCVKUVJGECWUGQHRCKPKPVJGſTUVUVCIGQHNCDQT!
2. What is the cause of pain in the second stage of 1. Maternal hypotension is a major complication fol-
NCDQT! lowing epidural analgesia. This leads to decreased
placental perfusion and heart rate abnormalities.
3. 9JKEJKUVJGKFGCNNCDQTCPCNIGUKCHQTDQVJVJGſTUV
CPFUGEQPFUVCIGUQHNCDQT! 2. 2TGNQCFKPIYKVJŌO.QH+8ƀWKFUDGHQTG
administering the epidural can decrease the risk of
4. Which block would be useful in the second stage of
hypotension.
NCDQTKHVJGYQOCPFQGUPQVYCPVGRKFWTCNCPCNIGUKC!
3. A postdural puncture headache can result from an
accidental dural rent while administering the epidural.
Case 2 .GCMCIGQHVJGEGTGDTQURKPCNƀWKFNGCFUVQVTCEVKQPQP
cranial structures and, along with cerebral vasodila-
Mrs. RJ, 28, requested epidural analgesia in labor. Soon tion, results in a severe headache.
after the epidural was given, there was fetal bradycardia. 4. The postdural puncture headache is treated with
1. What causes fetal heart rate abnormalities following analgesics and oral hydration. If unrelieved and severe,
GRKFWTCNCPCNIGUKC! an epidural blood patch is used. This is achieved by
injecting 10–20 mL of the woman’s blood into the
2. What are the measures for avoiding hypotension fol-
epidural space.
NQYKPICPGRKFWTCN!
3. 9JCVKUCRQUVFWTCNRWPEVWTGJGCFCEJG!
4. *QYKUCRQUVFWTCNRWPEVWTGJGCFCEJGOCPCIGF!
Sample questions
Answers Long-answer questions
1. What are the nonpharmacological and pharmacologi-
Case 1 ECNOGVJQFUQHNCDQTCPCNIGUKC!
2. List and explain the different methods of neuraxial
1. 6JGRCKPKPVJGſTUVUVCIGQHNCDQTKUECWUGFD[
analgesia used in labor.
distension of the uterus and ischemia of the uterine
and cervical tissues. It is mediated through T10–L1
spinal roots. Short-answer questions
2. The pain in the second stage of labor is caused by
distension of the vagina, perineum, and pelvic 1. Pudendal block
ƀQQTCPFKUVTCPUOKVVGFD[VJGRWFGPFCNPGTXG 2. Complications of epidural analgesia in labor
(S2, S3, S4). 3. Spinal anesthesia for labor and delivery
CH 18_p253-265_v3.indd 265 17-07-2015 15:39:25

Operative Vaginal
Delivery and
19 Destructive
Operations
Case scenario
Mrs. BN, a primigravida at term, was admitted to the labor room with
pains. Labor progressed normally and a vaginal examination revealed
that the cervix was fully dilated. An hour later, she had pushing pains.
The fetal heart rate was found to be 100 bpm and continued at that rate
for 3 minutes. She was delivered by forceps and a live, term, girl baby
was born. The newborn’s cry was initially feeble, but the baby recovered
rapidly after oxygen administration by mask.
Introduction perative vaginal delivery

Once the first stage of labor proceeds normally
and the cervix is fully dilated, delivery of the fetus Operative vaginal delivery refers to a procedure
takes place spontaneously in most situations. where the mother is assisted in the delivery of
However, when the mother’s expulsive efforts the fetal head by the use of a forceps or vacuum
are inadequate or when there is a possible com- device.
promise to the fetus while waiting for normal
delivery, operative vaginal delivery is required.
Operative vaginal delivery is an art. When the
Incidence
instruments are used appropriately, the proce- The incidence of operative vaginal delivery varies
dure is simple and there is no injury to mother widely. It is about 5%–10% globally. Vacuum is
of fetus. Training in the technique operative vag- used more frequently than forceps.
inal delivery is essential for every obstetrician to
avoid high cesarean section rates.
CH 19_p266-281_v3.indd 266 17-07-2015 16:50:17

Operative Vaginal Delivery 267
The obstetric forceps

The obstetric forceps are an instrument used to
assist in the delivery of the fetal head. The for-
ceps may be used for traction, rotation, or simple
‘lift out’.
istory
Paired instruments similar to obstetric forceps
were used in 1500 BCE in Egypt, Greece, and Persia.
The modern forceps, however, were invented by
Peter Chamberlen of England in the 17th cen-
tury. The instrument was kept secret for nearly
Figure 19.1 Parts of a forceps. The forceps consist of two
150 years and surfaced in 1813. Chamberlen’s
branches. Each branch has a blade (black arrow), shank
forceps did not have a pelvic curve and were

QTCPIGCTTQYJCPFNG
YJKVGCTTQYſPIGTIWCTFCPF
associated with high perinatal mortality. In 1723, lock (red arrow).
Jean Palfyn presented forceps invented by him in
the Academy of Sciences in Paris. These forceps
had parallel blades. The pelvic curve was intro- Box 19.1 Parts of the obstetric forceps
duced by Andre Levret in France in 1747 and • Two halves with a lock
William Smellie in England in 1751. With this, Ŧ Each half consists of
the application of forceps became easier. Tarnier fenestrated blade
later introduced a traction system (axis traction). shank
The forceps with cephalic and pelvic curves were lock
developed by Sir James Simpson in 1845. Milne handle
Murray (1891) and Neville (1886) introduced the finger guard
detachable angled traction rods and traction • Cephalic curve
handles. This facilitated traction in the axis of the • Pelvic curve
• Perineal curve
birth canal. More than 700 types of forceps have
• Locking system
been developed subsequently.
Ŧ English lock
Ŧ French lock
Description and design Ŧ Sliding lock
Forceps consist of two crossing halves or branches

with a locking mechanism in the center. Each (Fig. 19.2a). The curvature helps to grasp the fetal
branch of the forceps consists of a blade, shank, head and distribute the force evenly.
handle, finger guards, and lock (Fig. 19.1; Box 19.1). The pelvic curve is the curvature along the
The blade is the part that hugs the fetal skull. long axis of the blade that conforms to the axis of
It is usually fenestrated but may be solid or the birth canal and facilitates the application of
pseudofenestrated. The blade joins the shank. the forceps along this axis (Fig. 19.2b).
The lock is located at the point where the shank The perineal curve is unique to some types of
joins the handle. The handles are used to grasp forceps and is the curvature on the lower border
the forceps to apply traction. The blades are of the shank as in Piper’s forceps or in the trac-
referred to as right and left blades corresponding tion rods of axis traction forceps (Fig. 19.2c).
to the side of the maternal pelvis into which they The lock is the fulcrum. The sliding lock allows
are inserted. one branch of the forceps to slide up and down
The cephalic curve is the curvature on the inner along the other (Keilland’s forceps) and is use-
surface of the blades and can be measured by the ful for correcting asynclitism. Axis traction for-
radius of the blades when they are in opposition ceps have a nut and screw system that locks one
CH 19_p266-281_v3.indd 267 17-07-2015 16:50:17

a.
a. b. .
Figure 19.3 Locks on the forceps. a. Sliding lock allows one

branch of the forceps to slide along the other. b. Nut and
screw system locks one branch to the other. c. English lock
b. JCUCUQEMGVVJCVſVUKPVQVJGUQEMGVQHVJGQRRQUKVGUJCPM
Types of forceps
The types of forceps are listed in Table 19.1 and
shown in Figure 19.4.
%NCUUKſECVKQPQHQRGTCVKXG
.
vaginal delivery
Figure 19.2 Cephalic, pelvic, and perineal curves. a. The
cephalic curve is the curvature on the inner surface of the The American College of Obstetricians and
blades (arrow). b. The pelvic curve is the curvature along Gynecologists (ACOG) has classified forceps and
the upper border of the blades (arrow). c. The perineal vacuum delivery according to station and posi-
curve is unique to some forceps and is the curvature on tion, as given in Box 19.2.
the lower border of the shank (arrow). (Photo courtesy: High forceps delivery is not included in the
Dr Rajnish Samal.) above classification because of the following
reasons:
• Head is >two-fifth palpable per abdomen
branch firmly on to the other. The English lock • Presenting part above ischial spines
is most common and consists of a socket at the • Not practiced in modern obstetrics
base of one shank that fits into the socket at the
base of the opposite shank (Fig. 19.3).
Indications for forceps
Functions of forceps delivery
The functions of forceps are as follows:
Forceps delivery is used when delivery needs
• Traction to be expedited due to fetal compromise,
• Rotation maternal exhaustion, or to shorten the second
CH 19_p266-281_v3.indd 268 17-07-2015 16:50:18

Table 19.1 Types of forceps
ame of forceps Level se Features

raction orceps
Wrigley’s forceps • Outlet forceps Short, light forceps
• Simple lift out Cephalic and pelvic curves
• Cesarean section English lock
Simpson’s forceps • Longer forceps
Low forceps
Elliot’s forceps • Cephalic and pelvic curves
• English lock
Milne Murray’s forceps • Axis traction forceps
Low/mid forceps
Tarnier’s forceps • Has traction rods and handle
• Has cephalic, pelvic, and perineal curves
• English lock, nut, and screw
• Traction along axis of birth canal
otational orceps
Kielland’s forceps Midforceps • Cephalic and minimal pelvic curves
• Sliding lock
• Used in occipitotransverse position
• Corrects asynclitism
Barton’s forceps Midforceps • One blade hinged
• Sliding lock
• Cephalic curve
Special orceps
Piper’s forceps • Aftercoming head • Long shaft
• In breech delivery • Cephalic, pelvic, and perineal curves
• English lock
Box 19.2 #
%1)ENCUUKſECVKQPQHQRGTCVKXG stage in case of maternal medical conditions.
vaginal delivery
Terms such as prophylactic and elective for-
utlet ceps are not used in modern obstetrics. The
• Scalp visible at introitus without separating labia indications for forceps delivery are given in
• (GVCNUMWNNJCUTGCEJGFVJGRGNXKEƀQQT Box 19.3.
• Sagittal suture is in the AP diameter, or occiput in
LOA, LOP, ROA, or ROP position.
• Fetal head is at or on the perineum
• Rotation does not exceed 45 degrees Contraindications
Low forceps
There are very few contraindications to for-
• .GCFKPIRQKPVQHHGVCNUMWNNKUCVŮ EOUVCVKQPCPF ceps delivery, usually pertaining to poten-
PQVQPVJGRGNXKEƀQQT
tial harm to the fetus. An unengaged head,
Ŧ 4QVCVKQP ŭ FGITGGU
VQ .1#41# VQ 1# QT
LOP/ROP to OP), or unknown fetal position, malpresentation (e.g.,
Ŧ 4QVCVKQPŮFGITGGUKPENWFKPI12RQUKVKQP brow, mentoposterior) are contraindications.
Fetal prematurity is a relative contraindica-
Midforceps
tion. Suspected fetal bleeding disorders such
• 5VCVKQPCDQXG EODWVJGCFGPICIGF as thrombocytopenia and maternal human
Ŧ 4QVCVKQP ŭ FGITGGU
VQ .1#41# VQ 1# QT immunodeficiency virus (HIV) infection (to
LOP/ROP to OP), or
avoid scalp abrasion) are relative contraindica-
Ŧ 4QVCVKQPŮFGITGGUKPENWFKPI12RQUKVKQP
tions. Forceps delivery should not be attempted
AC American College of Obstetricians and Gynecologists; in suspected cephalopelvic disproportion and
AP anteroposterior; A left occipitoanterior; P left
occipitoposterior; A occipitoanterior; P occipitoposterior; mentoposterior position.
A right occipitoanterior; P right occipitoposterior.
CH 19_p266-281_v3.indd 269 17-07-2015 16:50:18

Box 19.3 Indications for forceps delivery

• Maternal
Ŧ Prolonged second stage
Without epidural analgesia
- Nullipara >2 hours
- Multipara >1 hour
With epidural analgesia
- Nullipara >3 hours
- Multipara >2 hours
Ŧ Maternal exhaustion
• Fetal
Ŧ Nonreassuring fetal heart pattern
Ŧ Malpositions
Occipitoposterior
Occipitotransverse
Ŧ Malpresentations
Breech: Aftercoming head
a. b.
Face: Mentoanterior
• To shorten second stage
Ŧ Cardiac disease class III/IV
Ŧ Severe preeclampsia/hypertension
Ŧ Myasthenia gravis
.
Morbidity
Maternal and perinatal morbidities increase
with (a) higher station of the fetal head and (b)
rotational forceps. When outlet or low forceps
are properly applied, perinatal mortality is low.
The benefits clearly outweigh the risks. Causes of
morbidity are given in Box 19.4.
Box 19.4 Morbidity from forceps delivery

• Maternal
Ŧ Injuries
Perineal lacerations
Need for episiotomy
Vaginal and cervical tears
Traumatic postpartum hemorrhage
Long-term
- Urinary incontinence
- Anal sphincter dysfunction
Ŧ Puerperal endometritis
• Perinatal
. . Ŧ Soft tissue injury to face
Ŧ Facial nerve palsy
Figure 19.4 Types of forceps. a. Wrigley’s forceps.
Ŧ Intracranial hemorrhage
b. Simpson’s forceps. c. Milne Murray’s axis traction
Ŧ Cephalhematoma
forceps. d. Kielland’s forceps. e. Piper’s forceps. (Photo
courtesy: Dr Rajnish Samal.)
CH 19_p266-281_v3.indd 270 17-07-2015 16:50:19

Maternal and fetal Box 19.6 Prerequisites for forceps delivery
evaluation •
•
Head must be engaged
Cervix must be fully dilated
Forceps delivery should be undertaken only • Membranes must be ruptured
after careful assessment of the mother and fetus • Presentation must be vertex or mentoanterior
• Position must be precisely known
(Box 19.5). History of maternal medical condi-
• There should be no cephalopelvic disproportion
tion, progress in labor, duration of second stage,
• Bladder must be empty
and indication for forceps delivery must be • Informed consent must be obtained from the mother
reviewed. Routine ultrasonography for assess-
ment of fetal position is not recommended.
Application of forceps
Prerequisites for forceps
• Aseptic technique must be used. Prophylactic
delivery antibiotics are not recommended.
• The mother should be in the lithotomy posi-
Forceps should only be applied if the head is tion (dorsal position may be sufficient for out-
engaged, cervix fully dilated, membranes rup- let forceps).
tured, bladder empty, and vertex or mentoante- • A pudendal block is recommended for low and
rior presentation, and when the position of the midforceps delivery. In addition, the perineum
presenting part is precisely known (Fig. 19.5). should be infiltrated with local anesthetic for
Forceps should not be applied if there is ceph- episiotomy.
alopelvic disproportion. These prerequisites are • The bladder should be empty. Catheterize if
listed in Box 19.6. bladder is full.
• Reevaluate station, position, and rotation of
vertex.
Procedure • Forceps should be selected according to sta-
tion of vertex:
The procedure of forceps delivery consists of – +3 cm: Wrigley’s
application, traction, and delivery of the fetal – +2 cm: Simpson’s
head. – Above +2 cm: Simpson’s or Milne Murray’s
• The left blade is inserted first. This should be
held in the left hand, using the thumb and two
Box 19.5 Assessment before forceps delivery fingers, with the shank and handle held ver-
tical, with the tip of the blade pointing to the
• Abdominal examination
floor (Fig. 19.5).
Ŧ Uterine contractions
• The index and middle fingers of the right hand
Ŧ Descent of the head
Ŧ Fetal heart rate
are introduced into the posterior aspect of the
Ŧ Weight of the baby vagina toward the left, between the fetal head
• Vaginal examination and the vaginal wall.
Ŧ Cervical dilatation • The left blade is guided along the palmar sur-
Ŧ Rupture of membranes face of the fingers of the right hand, initially
Ŧ %QNQTQHCOPKQVKEƀWKF into the posterior part of the vagina, gradually
Ŧ Presenting part rotating it to the left, and finally placing it hori-
Station zontally on the left side of the pelvis.
Flexion • The handle is depressed and held in place by
Asynclitism the assistant.
Position
• The right blade is held in the right hand. Two
Degree of molding
fingers of the left hand are introduced into the
Ŧ Caput succedaneum
right posterior aspect of the vagina.
CH 19_p266-281_v3.indd 271 17-07-2015 16:50:20

Figure 19.7 Locking the forceps. The handles of the

Figure 19.5 Application of the left blade. The left blade is blades are approximated and the forceps are locked.
JGNFKPVJGNGHVJCPFYKVJVJGVJWODCPFſPIGTUVJGUJCPM
CPFJCPFNGKUJGNFXGTVKECNYKVJVJGVKRRQKPVKPIVQVJGƀQQT
This is guided along the palmar surface of the right hand • The right blade is introduced along the fingers
into the posterior aspect of the vagina. of the left hand and the procedure is repeated
(Fig. 19.6).
• The handles are approximated, and the blades
are locked (Fig. 19.7).
Checking for accurate

application
• The sagittal suture should be perpendicular to
the plane of the shanks and equidistant from
the two blades.
• The posterior fontanel should be midway
between the blades and one finger breadth
anterior to the line joining the shanks.
• A small part of the fenestration of the blade
may be felt on either side.
When correctly applied, and the above crite-
ria are satisfied, the forceps grasp the head in the
occipitomental diameter. In the occipitoanterior
position, the major part of the blade is on the
fetal face (Fig. 19.8).
If rotation is not complete

• If the sagittal suture is <45 degrees short of
Figure 19.6 Application of the right blade. The right blade full rotation, the blades should be applied in
is held in the right hand and introduced along the palmar the same order but the application should be
aspect of the left hand into the right posterior aspect of cephalic, with the blades over the parietal bones.
the vagina. The vertex rotates when traction is applied.
CH 19_p266-281_v3.indd 272 17-07-2015 16:50:23

Figure 19.9 Traction. When forceps are applied at the

outlet, upward traction completes the extension of and
ccipitomental iameter delivery of the head.
Figure 19.8 Correct application of forceps. When the
forceps are applied and blades are locked, the head is
Episiotomy should be performed when the
grasped in the occipitomental diameter with the major part perineum bulges and the head crowns.
of the blade on the fetal face.
• If the sagittal suture is >45 degrees from the mid-

ccipitotransverse
line (low or midforceps), manual rotation may positions
be tried first. If not successful, forceps can be
applied and rotation takes place during traction. When the vertex is in occipitotransverse posi-
tion, delivery is by one of the following methods:
Traction • Manual rotation and forceps delivery
• Forceps rotation and delivery
Traction should be applied during contraction.
• Vacuum extraction
Direction of traction depends on station and
position. It should be in the axis of the birth
canal, along the curve of Carus. From the level of Manual rotation is discussed in Chapter 41,
ischial spines, the maternal pelvis is ‘J’ shaped. Abnormal labor: Malposition and malpresentations.
Hence, the direction of traction is as given below:
• Outlet forceps: Upward to complete extension otational forceps
of head (Fig. 19.9). This requires specialized skill and training.
• Low forceps: Horizontal until head crowns and Kielland’s or Barton’s forceps must be used. The
perineum bulges, followed by upward traction Kielland’s forceps have minimal pelvic curve to
• Midforceps: Downward and backward initially, facilitate rotation. The blades are referred to as
followed by upward and forward and finally anterior and posterior blades. The forceps should
upward. be assembled and held in front of the patient with
• Delivery as occipitoposterior: Horizontal until the knob on the lock pointing in the direction of the
the root of the nose hitches under the pubic occiput; in this position, the anterior and posterior
symphysis, upward and forward until occiput blades are determined. There are three methods of
is born, and downward and backward for the application of the anterior blade (Fig. 19.10).
nose, face, and chin to be born.
Classical method
Episiotomy The anterior blade is introduced between the
Although routine episiotomy is not recom- head and the uterine wall under the pubic sym-
mended, it is required in most forceps deliveries. physis, with the cephalic curve facing upward.
CH 19_p266-281_v3.indd 273 17-07-2015 16:50:23

a. b.
. .
.
Figure 19.10 Methods of application of Keilland’s forceps. a.+FGPVKſECVKQPQHCPVGTKQTCPFRQUVGTKQTDNCFGUD[
assembling the forceps in front of the patient. b. Classical method. The anterior blade is inserted with the cephalic
curve facing upward. c. Wandering method. The anterior blade is inserted along the posterior aspect of the head and
swept over the face to anterior position. d. Direct method. The anterior blade is applied directly anteriorly with the
cephalic curve facing the fetal head. e. The posterior blade is applied directly and the blades are locked.
The blade is turned 180 degrees after it is in the Direct method

uterine cavity, to grip the fetal head.
The anterior blade is inserted directly behind the
pubic symphysis with the cephalic curve facing
Wandering method downward and is slipped over the fetal head.
The anterior blade is inserted posterior to the In all the three methods, the posterior blade is
head and swept over the face to the anterior inserted directly behind the head and the head is
position. grasped. Traction is applied during contraction,
CH 19_p266-281_v3.indd 274 17-07-2015 16:50:23

and rotation is performed between contractions. Negative pressure is created between the cup
Gradually, the head is rotated and delivery is and the fetal scalp by the pump, and traction is
completed. applied to the scalp to pull the fetus.
Rotational forceps are associated with
higher rate of maternal and fetal complications.
Spiral tears of the vagina, and uterine rupture,
Description and design
especially with the classical method of applica- Vacuum extractors are classified into two
tion, are well-known complications. Therefore, types according to the material used to make
rotational forceps have been replaced by vac- the cup:
uum delivery and cesarean section in modern
• Rigid cups
obstetrics.
– Rigid metal cups
Forceps for the aftercoming head in breech is
– Rigid plastic, polyurethane, or polyethylene
discussed in Chapter 42, Abnormal labor: Breech
cups
presentation and shoulder dystocia.
• Soft cups
– Soft silastic/plastic cups
Trial of forceps
When difficulty is anticipated in vaginal delivery
igid cups
with forceps, an attempt is made in the operating The traditional metal cup is the Malmström cup.
room, fully equipped with facilities for immediate
• The cup is made of stainless steel. It is mush-
cesarean section. This is known as trial of forceps.
room shaped with a smaller diameter at the
This should be attempted only when the likelihood
rim than above the rim (Fig. 19.11). This shape
of success is high. If difficulty is encountered in
helps in drawing the scalp into the cup to cre-
application, locking, or traction, immediate cesar-
ate an artificial caput succedaneum (chignon)
ean section should be proceeded with. Neonatal
(Fig. 19.12) and allows a firm grip. The diameter
outcome in the trial of forceps, when attempted in
of the cup may be 40, 50, or 60 mm.
selected cases, is similar to elective cesarean section.
• A metallic disk is attached to a traction chain
that goes through the tubing.
Failed forceps
When difficulty is not anticipated in forceps
delivery but the attempt fails, it is known as failed
forceps. Neonatal morbidity is much higher with
failed forceps delivery. Maternal morbidity also
increases when cesarean section is performed
in the second stage with the fetal head jammed
in the pelvis. Forceps delivery should be aban-
doned in the following situations:
• There is difficulty is application of the blades.
• There is no progressive descent with moderate
traction.
• Delivery is not imminent after three pulls.
The vacuum extractor

(ventouse)
The vacuum extractor was first devised by Tage Figure 19.11 Vacuum extractor—the metal cup. The cup
Malmström in 1953. The instrument consists of a is mushroom shaped, with a smaller diameter at the brim
metal cup attached to a pump by suction tubing. rather than above the brim.
CH 19_p266-281_v3.indd 275 17-07-2015 16:50:23

Figure 19.12 Chignon. This is formed on the fetal scalp

when it is drawn into the metal cup by negative pressure.
• The rubber tubing connects the center of the Figure 19.13 The vacuum extractor—Silastic cup. The
EWRKUHWPPGNUJCRGFCPFſVUQXGTVJGUECNRYKVJQWVVJG
cup to the suction pump.
need for the formation of a chignon.
• The suction pump may be a handheld pump
or wall suction.
Bird’s cup is a modification in which the tube Table 19.2 Differences between soft and rigid
is attached eccentrically near the rim of the cup. cups
This is particularly useful for occipitoposterior
Soft cups igid cups
and transverse positions.
More likely to fail Less likely to fail
Less scalp injuries More scalp injuries
Soft cups More suitable for More suitable for OP positions,
OA positions asynclitism and larger fetus
The Silastic cup was first introduced by
Kobayashi in 1973. A occipitoanterior; P occipitoposterior.
• The cup has a diameter of 65 mm and is fun-

nel shaped (Fig. 19.13). Smaller sizes of 50 mm Functions
and 60 mm are also available
Functions of the vacuum extractor are as follows:
• The cup fits over the occiput without the need
for the formation of a chignon. • Traction
• There is less scalp trauma but more failure due • Rotation
to the slipping of the cup.
There are several modifications of this cup. Indications for vacuum
The most commonly used one is the Kiwi cup,
which consists of a Silastic cup attached directly
delivery
to a hand pump. The traction handle may be The indications for vacuum delivery are the
flexible to allow easy placement and lateral trac- same as for forceps delivery. However, it must
tion as in Bird’s cup. be remembered that vacuum cannot be used in
malpresentations.
igid versus soft cups
The rigid cups generate more traction force by
Contraindications
creating a good chignon. The traction force is, Since the formation of chignon and traction on
therefore, more with metal cups. The differences the scalp can result in trauma to the scalp, there
between soft and rigid cups are given in Table 19. 2. are a few contraindications (Box 19.7).
CH 19_p266-281_v3.indd 276 17-07-2015 16:50:24

Box 19.7 Contraindications for vacuum Prerequisites for vacuum

extraction
delivery
• Gestational age <34 weeks
Ŧ Risk of fetal intraventricular hemorrhage
The prerequisites for vacuum extraction are
• Malpresentations similar to those for forceps delivery and are
• Cephalopelvic disproportion listed below:
• Fetal bleeding disorders • Presentation must be cephalic.
• Maternal HIV infection
• Head must be engaged; station should be +2 cm
JWOCPKOOWPQFGſEKGPE[XKTWU or below.
• Cervix should be fully dilated.
• There should be no cephalopelvic dispro-
Morbidity from vacuum portion.
delivery • Bladder should be empty.
The morbidity from vacuum delivery is similar to

that seen with forceps delivery. The risk of sub- Procedure
aponeurotic hemorrhage and scalp lacerations Before vacuum delivery, progress in labor,
is higher. fetal heart tracing, engagement of the head,
and uterine contractions must be evaluated.
Forceps versus vacuum Indication for vacuum delivery should be clearly
documented.
delivery
• The mother should preferably be in the lithot-
Vacuum delivery has advantages and disadvan- omy position. Dorsal position can also be used.
tages over forceps delivery (Box 19.8). The vac- • Prophylactic antibiotics are not recommended.
uum extractor is preferred to forceps in many • Pudendal block anesthesia is recommended.
centers, but the decision rests on the operator’s • Vaginal examination is performed to assess the
experience and personal preferences. position and station of the head and ensure
that the cervix is fully dilated.
• The largest cup that can be applied should be
Box 19.8 Advantages and disadvantages selected.
of vacuum over forceps • The cup should be placed at the flexion point
• Advantages (point on the fetal skull where the suction cup
Ŧ The cup does not occupy space in the pelvis is placed, so that appropriate flexion can be
Ŧ Precise positioning on the head not mandatory achieved). In occipitoanterior positions, the
Ŧ Less maternal injury flexion point is located on the sagittal suture,
Third and fourth degree perineal tears 6 cm from the anterior fontanel and 3 cm from
Vaginal lacerations
the posterior fontanel. The center of the cup
Ŧ No compression of fetal head
should be over this point; the posterior edge of
Ŧ Less risk of
Birth injuries
the cup should be just at the edge of the poste-
Seizures rior fontanel (Fig. 19.14).
Assisted ventilation • If using a soft Silastic cup, the cup can be
• Disadvantages folded for easy insertion into the vagina.
Ŧ More failure rate • Once the cup is placed on the scalp, two fingers
Ŧ Cannot be used in should be inserted into the vagina to check all
Preterm fetuses around the cup to ensure that vaginal or cervi-
Malpresentations cal tissue is not trapped in the cup.
Ŧ Higher risk of • Negative pressure is created using the pump
Subgaleal hemorrhage and the pressure is raised to 0.2 kg/cm2. The
Retinal hemorrhage
perimeter of the cup is checked again to ensure
Cephalhematoma
that vaginal or cervical tissue is not trapped in
Shoulder dystocia
the cup.
CH 19_p266-281_v3.indd 277 17-07-2015 16:50:24

• Faulty direction of traction

• Cephalopelvic disproportion
The cup may be reapplied two to three times.
However, there should be descent with each pull.
If no descent occurs after three pulls, vacuum
extraction should be abandoned. Detachment
of the cup can cause lacerations on the scalp.
Sequential use of
vacuum and forceps
Figure 19.14 Flexion point. This is the point on the fetal Often, when the vacuum extractor detaches,
skull where the suction cup is placed so that appropriate the vertex may have rotated and some descent
ƀGZKQPKUCEJKGXGF+PQEEKRKVQCPVGTKQTRQUKVKQPKVKUQPVJG also may have occurred. Delivery at this stage
sagittal suture, 6 cm from the anterior fontanel and 3 cm can be completed by outlet forceps if the head
from posterior fontanel. is on the pelvic floor. However, if the cup had
detached because of excessive force being
• Negative pressure is raised rapidly to 0.8 kg/cm2. applied during traction, and there is no descent
Slow, gradual increase was practiced earlier, of the head, sequential use of instruments is
but randomized trials have shown that rapid associated with an increase in neonatal mor-
increase reduces the duration of application bidity, trauma, intracranial hemorrhage, and
without compromising effectiveness and safety. asphyxia. Cesarean section is a safer alternative
• Traction is applied during contractions, with and should be resorted in this situation.
the right hand, with the direction of traction
perpendicular to the surface of the cup. Two
fingers of the left hand should be placed on the
scalp and the thumb on the cup to exert coun-
Destructive operations
ter traction and prevent the cup from slipping.
Destructive operations are performed to reduce
The woman should be encouraged to push
the fetal size or skull diameter to relieve obstruc-
when traction is being applied.
tion and achieve vaginal delivery of a dead fetus or
• Traction should be in the direction of the birth
one with lethal malformation. These are seldom
canal, that is, downward and backward ini-
performed in modern obstetrics for the following
tially followed by upward and forward as the
reasons:
head crowns.
• If the vertex is in the occipitoposterior or • The majority of lethal fetal malformations are
transverse position, rotation takes place auto- diagnosed early by ultrasonography and the
matically as traction is applied and progressive pregnancy terminated.
descent occurs. • Obstructed labor with fetal death is rarely
• A maximum of three pulls during descent and encountered in developed countries.
three pulls during crowning and delivery are • Lack of expertise and experience in these
acceptable. Usually the baby is delivered with procedures.
three pulls. The total duration of the procedure • Risk of maternal complications.
should not exceed 20 minutes.
Detachment of the cup Types of destructive

Detachment or slipping of the cup can occur due operations
to the following reasons:
Several destructive operations have been
• Large caput succedaneum described and have been performed in the past.
• Faulty application These are listed in Table 19.3. Perforation of the
CH 19_p266-281_v3.indd 278 17-07-2015 16:50:24

Table 19.3 Destructive operations
Terminology Procedure Indication

Craniotomy Removal of intracranial contents Hydrocephalus
by making an opening in the skull Obstructed labor with CPD
Cleidotomy Dividing the clavicle(s) Shoulder dystocia with or without
anencephaly
Decapitation Separating the head from the trunk Transverse lie
Spondylotomy Dividing the fetal trunk Transverse lie
Evisceration Removal of abdominal contents Macrosomia
CPD cephalopelvic disproportion.
fetal skull in a hydrocephalic fetus is the only pro- anteriorly, with palm facing down, to protect
cedure performed with any frequency currently. the bladder.
Cleidotomy may occasionally be undertaken in • The Simpson’s or Oldham’s perforator (Fig.
shoulder dystocia in a fetus with anencephaly. 19.15) is introduced along the palmar aspect
of the left hand into the vagina and cervix
(Fig. 19.16).
Craniotomy • The perforator should be pushed into the fetal
This procedure is most commonly indicated in skull after steadying the head by suprapubic
following conditions:
• Fetus with gross hydrocephalus, even if alive
• Obstructed labor
– Cephalopelvic disproportion
– Dead fetus
– No threatened or suspected rupture
Procedure Figure 19.15 Simpson’s perforator. This is used for

• General or regional anaesthesia is recom- perforating the head of a dead fetus or a fetus with
mended. lethal malformation.
• The woman should be in a lithotomy position.
• The bladder should be catheterized.
• The cervix should be fully dilated for per-
foration in a normally formed dead fetus. If
the fetus is hydrocephalic, this can be done
through an incompletely dilated cervix.
• In a fetus with hydrocephalus, the skull bones
may be thin, and any skull bone that is within
reach or a fontanel may be perforated. The
fluid is drained and the head delivered with
further uterine contractions.
• In obstructed labor, the site of perforation
depends on the fetal presentation
– Vertex presentation — parietal bones
– Brow presentation — frontal bone
– Face presentation — roof of the mouth or orbit Figure 19.16 Perforation of the fetal head. The index
– Aftercoming head of breech — occipital bone CPFOKFFNGſPIGTQHVJGNGHVJCPFCTGRNCEGFCPVGTKQTN[VQ
• The index and middle fingers of the left protect the bladder. The perforator is introduced along the
hand should introduced into the vagina palmar aspect of the left hand.
CH 19_p266-281_v3.indd 279 17-07-2015 16:50:24

pressure. The scalp may have to be incised with drained by thrusting the perforator into the
a knife before this. The perforator is opened in skull and breaking it up.
one direction and then at right angles to make • Delivery is completed with traction by volsel-
a cruciate incision. Brain matter should be lum as the skull diameter reduces.
Key points
• Operative vaginal delivery can be by forceps or • Guidelines and appropriate procedures should be
vacuum extraction. followed for application, traction, and rotation.
• The obstetric forceps consist of two branches with a • 8CEWWOGZVTCEVQTUCTGENCUUKſGFCUTKIKFCPFUQHVEWRU
locking mechanism. according to the material used to make the cup.
• Each branch of the forceps has a cephalic and a pel- • Indications and risks for vacuum extraction are the
vic curve. Some forceps have a perineal curve as well. same as for forceps delivery. However, vacuum
• Functions of the forceps are traction, rotation, extraction should not be used in preterm delivery and
and minimal compression of fetal skull to facilitate malpresentations.
delivery. • Risk of subgaleal hemorrhage is higher with vacuum
extraction.
• There are different types of forceps, broadly classi-
ſGFCUVTCEVKQPHQTEGRUTQVCVKQPCNHQTEGRUCPFURGEKCN • Evaluation of the mother and fetus and adherence to
forceps. guidelines and appropriate procedure are mandatory
• Indications for operative vaginal delivery are pro- for vacuum delivery as well.
longed second stage, nonreassuring fetal status, and • Sequential use of vacuum and forceps is associ-
necessity to shorten the second stage due to maternal ated with a high neonatal morbidity and should be
medical conditions. avoided.
• Instrumental delivery is associated with maternal and • Destructive operations are not commonly performed
PGQPCVCNOQTDKFKV[*QYGXGTVJGDGPGſVUQWVYGKIJ in modern obstetrics. Perforation of the fetal head in
the risks. cases of hydrocephalus or obstructed labor with a
• There are prerequisites for application of forceps. The dead fetus is the only one that is undertaken in some
mother and fetus should be clinically evaluated before centers.
forceps delivery is attempted.
Self-Assessment
Mrs. VM, 25, third gravida at term, was admitted to the
Case 1 labor room with pains. Pelvic examination revealed that
Mrs. BN, a primigravida at term, was admitted to the labor the vertex was in right occipitoposterior position. Pelvic
room with pains. Labor progressed normally and vaginal EQPſIWTCVKQP YCU PQTOCN .CDQT RTQITGUUGF PQTOCNN[
examination revealed that the cervix was fully dilated. An and cervix was fully dilated at 8 PM. Two hours later, on
hour later, she had pushing pains, and the fetal heart rate vaginal examination, vertex was in occipitotransverse
was found to be 100 bpm. It continued at that rate for 3 position.
minutes. 1. What is the diagnosis?
1. What is the diagnosis? 2. How will you make a decision regarding the mode of
2. How will you make a decision regarding the mode of delivery?
delivery? 3. If the vacuum cup detaches during traction, what will
3. How will you make a decision regarding the type of you do?
forceps to be used? 4. What is the most common neonatal morbidity?
4. If the position is direct occipitoposterior, what is the
direction of traction?
CH 19_p266-281_v3.indd 280 17-07-2015 16:50:24

3. Reevaluate the station of the presenting part, the

Answers rotation, and the location of the cup. One more at-
tempt can be made, making sure that the direction of
Case 1 traction is perpendicular to the surface of the cup.
1. Nonreassuring fetal status. 4. Subgaleal hemorrhage and scalp lacerations,
2. If the vertex is fully rotated or <45 degrees especially when the cup detaches.
short of rotation and station is > EOHQTEGRU
or vacuum delivery may be attempted. If the
station is higher, cesarean section is the best Sample questions
option.
3. If the station is > QWVNGVHQTEGRUCPFKH Long-answer question
DGVYGGP CPF OKFHQTEGRUUJQWNFDGWUGF
1. Describe the procedure for forceps delivery and
4. Horizontal traction until root of the nose is born,
vacuum extraction. What are the advantages and
followed by upward and forward until occiput is
disadvantages of both?
DQTPCPFſPCNN[FQYPYCTFCPFDCEMYCTF

1. Outlet forceps
1. Deep transverse arrest.
2. Chignon
2. +HVJGXGTVGZKUŮ EODGNQYVJGURKPGUCPFVJGTG
3. Prerequisites for forceps delivery
is caput or molding, delivery may be instrumental,
preferably vacuum extraction. Keilland’s rotational 4. Advantages of vacuum over forceps
forceps are an option but are not commonly used 5. Rotational forceps
PQY+HVJGXGTVGZKUCDQXG UVCVKQPCPFQTVJGTG
KUUKIPKſECPVOQNFKPIEGUCTGCPUGEVKQPUJQWNFDG
performed.
CH 19_p266-281_v3.indd 281 17-07-2015 16:50:24

Cesarean Section
and Management
20 of Pregnancy with
Previous Cesarean
Case scenario
Mrs. SS, 25, was a short primigravida (149 cm). She presented at
38 weeks’ gestation in spontaneous labor. Labor did not progress due to
cephalopelvic disproportion. She delivered a 3.6-kg baby by a cesarean
section.
Introduction Incidence
Globally, at least one in five women delivers Over the past 20 years, there has been a dis-
by a cesarean section. When done for the turbing increase in the rate of cesarean sections
right indications, cesarean sections are life- around the world, including India. Some stud-
saving procedures that benefit mothers and ies in urban India have shown the rate to be as
babies. Advances in anesthetic services and high as one out of two women. At the other end
improved surgical techniques have consider- of the spectrum, cesarean sections are very low
ably reduced the morbidity and mortality of in underresourced areas in India due to lack of
this procedure. facilities, leading to increased maternal and
perinatal mortality. Women are more likely to
have a cesarean section if they have had a pre-
vious cesarean section or have a baby with a
Cesarean section breech presentation.
&GſPKVKQP Do increasing rates of cesarean

A cesarean delivery is defined as the birth of a decrease perinatal mortality
fetus through an incision in the abdominal wall
(laparotomy) followed by another incision in The increased rate of cesarean sections does not
the uterus (hysterotomy). decrease perinatal deaths in low risk pregnancies.
CH 20_p282-299_v3.indd 282 17-07-2015 16:42:57

Cesarean Section and Management of Pregnancy with Previous Cesarean 283
On the other hand, in a low-risk, uncomplicated • Elective or planned cesarean section: An elec-
pregnancy, a cesarean section has an eight-fold tive cesarean section is a planned cesarean for
higher maternal mortality than a vaginal deliv- maternal or fetal indications that arise in the
ery and an 8–12 times higher morbidity. There is antepartum period. It is done in a woman who
also a higher incidence of complications in sub- has not gone into labor.
sequent pregnancies. • Emergency cesarean section: A cesarean sec-
tion done for indications arising during labor
Types of cesarean section is known as an emergency cesarean section.
• Cesarean on demand: A cesarean done at the
A woman may undergo a cesarean section for
woman’s request is known as cesarean on
the first time or have a repeat cesarean section.
demand.
• Primary cesarean section: When a cesarean
section is performed for the first time on a
pregnant woman, it is called a primary cesar-
Indications for
ean section. cesarean section
• Repeat cesarean section: When a woman has
had one or more previous cesarean sections, it Elective cesarean section
is known as a repeat cesarean section.
• Lower segment cesarean section (LSCS): In There are both maternal and fetal indications for
modern obstetrics, the uterine incision is elective cesarean section.
made in the lower uterine segment. The lower
uterine segment is the thinner, less active part Maternal indications
of the uterus. The advantages of the lower uter- • Previous cesarean section is a leading indi-
ine segment transverse incision are as follows: cation for elective cesarean sections. A previ-
– Ease of suturing ous classical cesarean section is an absolute
– Decreased bleeding indication for an elective cesarean section.
– Decreased risk of uterine rupture in subse- However, in a woman with a previous LSCS,
quent pregnancies an elective cesarean section is done only after
– Decreased risk of bowel/bladder adhering assessing that the chances for a successful vag-
to the uterine scar inal delivery are low.
• Classical cesarean section: In rare cases, a ver- • Placenta previa partially or completely cover-
tical incision is made in the upper uterine ing the internal os is an indication for a cesar-
segment. This is called a classical cesarean ean section.
section. It is not routinely used in modern • Maternal HIV is an indication for a cesarean
obstetrics because of the increased risk of section, to minimize transmission to the baby.
uterine rupture in a subsequent pregnancy. • Primary genital herpes with visible lesions
• Extraperitoneal cesarean section or Porro’s at the time of labor or ruptured membranes
technique: This technique is not routinely requires a cesarean section to prevent congen-
used. It was described in an era where there ital herpes in the infant.
was an increased risk of peritoneal infection. • An elderly primigravida who has conceived
• Cesarean hysterectomy: This procedure is done after extensive infertility treatment may be
in rare situations. The most common indica- offered an elective cesarean delivery. She
tions are intractable hemorrhage due to uter- may also have associated complications such
ine atony, placenta percreta or increta, and as gestational and pregestational diabetes,
uterine rupture. hypertension, and fetal macrosomia.
• Dystocia may be an indication for planned
%NCUUKſECVKQPQHEGUCTGCP cesarean section. Dystocia may be due to
– pelvic deformity or abnormal pelvic
sections (based on indication) configuration;
Cesarean sections may be classified under three – soft tissue dystocia resulting from uterine
categories, depending on the indication, as follows: fibroids or ovarian tumors obstructing labor.
CH 20_p282-299_v3.indd 283 17-07-2015 16:42:57

• Anomalies of the lower genital tract such as

Box 20.1 Indications for elective cesarean
vaginal septum and scarring of the vagina or section
cervix are also indications for planned cesar-
ean section. aternal
• Previous vaginal surgery for pelvic organ pro- • Previous cesarean
lapse or extensive vaginal lacerations after a Ŧ Classical
previous vaginal delivery may be an indication Ŧ Lower segment
• Placenta previa
for an elective cesarean section.
• Infections
• Cervical cancer necessitates a cesarean sec-
Ŧ Maternal HIV
tion because a vaginal delivery can pose a risk Ŧ Primary herpes with visible vesicles
for hemorrhage and dissemination of disease. • Elderly primigravida with treatment for infertility
• Previous vaginal surgery
Ŧ Pelvic organ prolapse
Fetal indications Ŧ Third- or fourth-degree perineal lacerations
• Fetal growth restriction with oligohydram- • Dystocia
nios/abnormal Doppler findings requires a Ŧ #DPQTOCNRGNXKEEQPſIWTCVKQP
Ŧ Pelvic deformity
cesarean delivery to prevent fetal compromise.
Ŧ Soft tissue dystocia
• Multiple gestations with the first baby in a
Pelvic tumors
noncephalic presentation is an indication. • Vaginal septum
• Malpresentations • Cervical cancer
– Term singleton breech, if external cephalic
etal
version is contraindicated or has failed, is
considered an indication for an elective • Fetal growth restriction with fetal compromise
• Twin pregnancy
cesarean section in some obstetric units.
Ŧ First twin noncephalic
However, each obstetric unit needs to work
• Malpresentation (breech or transverse presentation)
out its policy for allowing a vaginal delivery • Macrosomia
in selected cases of breech presentation (see • Fetal anomalies, e.g., severe hydrocephalus
Chapter 42, Abnormal labor: Breech presen- • Previous adverse perinatal event, e.g., stillbirth
tation and shoulder dystocia).
– A fetus in a transverse lie will need a cesar-
ean delivery.
• Suspected macrosomia (estimated fetal Maternal indications
weight >4000 g), especially in diabetic moth-
ers, is an indication to avoid shoulder dystocia • Dystocia is one of the commonest indications
and maternal trauma. for an emergency cesarean section done for
• Fetal anomalies such as severe hydrocephalus a laboring woman (see Chapter 40, Abnormal
may necessitate a cesarean section. labor: Abnormalities in passage and powers).
• A previous adverse perinatal event, for • Cephalopelvic disproportion (CPD) is one
example, stillbirth or a difficult vaginal deliv- of the reasons for failure to progress in labor.
ery resulting in a severely asphyxiated infant, This may be due to a malformed or inadequate
may be considered an indication for an elec- maternal pelvis resulting in CPD. Although it
tive cesarean section. can be suspected prior to labor, it is usually
diagnosed during labor.
The indications for an elective cesarean section • Dysfunctional labor, resulting from abnormal
are summarized in Box 20.1. uterine action, protraction, and arrest disorders,
may require a cesarean section if other treat-
Emergency cesarean ment modalities fail (see Chapter 40, Abnormal
labor: Abnormalities in passage and powers).
section (during labor) • When labor has been induced but does not
The majority of primary cesarean sections are progress to a vaginal delivery, it is termed
performed as an emergency due to problems failed induction. A cesarean section is indi-
that arise in labor. cated in this situation.
CH 20_p282-299_v3.indd 284 17-07-2015 16:42:57

Fetal indications avoiding injury to the perineum, which may

lead to sexual or bladder dysfunction, are
• Nonreassuring fetal status is a common indi- some of the reasons quoted. Advantages of
cation for cesarean sections. In the presence of cesarean section on maternal request are con-
abnormal fetal heart rate on auscultation (per- venience, prevention of postmaturity, reduced
sistent tachycardia or bradycardia) or abnor- risk of pelvic floor injury, and prevention of
mal fetal heart tracing on an electronic fetal late stillbirths. However, these should be
monitor (absent baseline variability, recurrent weighed against the disadvantages, which are
variable decelerations, recurrent late decelera- maternal morbidity, prematurity, increase in
tions, or bradycardia), a timely cesarean sec- neonatal respiratory problems, and risk of
tion will reduce perinatal morbidity and mor- scar rupture in future pregnancies. These have
tality. Compression of a prolapsed umbilical to be discussed in detail with the woman and
cord can also be a cause of fetal distress. her partner before decisions are made.
• Placental abruption occurring during labor Cesareans on demand cannot be supported,
can be an acute indication for a cesarean secon either ethical or medical grounds.
tion (see Chapter 39, Antepartum hemorrhage).
• Fetal macrosomia leading to CPD and pro-
longed labor is an indication for a cesarean
section.
Timing of cesarean delivery
• Difficulty in delivery of the second twin may Planned cesarean sections should be per-
also necessitate a cesarean section. formed after 39 weeks’ gestation. Delivery
The indications for emergency cesarean sec- earlier than this gestation increases the risk of
tion are summarized in Box 20.2. transient tachypnea (TTN) of the newborn and
other complications.
Cesarean section on demand

Patient demand has complicated the already Technique of
complex issue of rising cesarean section rates. cesarean delivery
This is also known as cesarean section on
maternal request. Fear of the pain of labor and Being the most common surgical procedure in
obstetrics, the steps of a cesarean section have
been standardized over the years.
Box 20.2 Indications for emergency cesarean
section
aternal
Preoperative care
• Dystocia
Ŧ Cephalopelvic disproportion ral intake
• Dysfunctional labor
It is preferable to stop oral intake for at least 8
Ŧ Abnormal uterine action
hours prior to an elective cesarean section.
Ŧ Protraction disorders
Ŧ Arrest disorders
Women who have been in labor should ideally
• Failed induction have been on clear liquids. In women who need
• Soft tissue dystocia to undergo an emergency cesarean section soon
etal
after a meal, steps should be taken to prevent
acid aspiration syndrome, which results from
• Fetal distress
pulmonary aspiration of gastric contents if gen-
Ŧ 2NCEGPVCNKPUWHſEKGPE[
eral anesthesia is used (Box 20.3).
Ŧ Cord compression
Ŧ Cord prolapse
• Placental abruption Shaving
• Macrosomia
• &KHſEWNV[KPFGNKXGT[QHUGEQPFVYKP Only hair that will interfere with the operative
area is shaved on the day of surgery. Extensive
CH 20_p282-299_v3.indd 285 17-07-2015 16:42:57

sections in low-risk pregnancies. It may be used

Box 20.3 Prevention of acid aspiration syndrome
in women at high risk for VTE. This includes
• Regional anesthesia (spinal or epidural) preferred women with previous VTE, high-risk thrombo-
• General anesthesia avoided philia (inherited or acquired), or body mass
• Gastric pH increased
index (BMI) >40 kg/m2.
Ŧ Nonparticulate antacids (sodium citrate 30 mL)
Anticoagulation is begun 6–12 hours postop-
Ŧ Intravenous ranitidine
eratively, after risk of hemorrhage has decreased
and is continued till ambulation. Unfractionated
heparin, 5000 units every 12 hours, or low-mo-
shaving is not necessary. Shaving on the night lecular-weight heparin (enoxaparin) 40 mg daily
before surgery increases the risk of wound infec- can be used.
tion and should be avoided.
Chlorhexidine bath Anesthesia

In elective cesarean sections, bathing with chlor-
hexidine on the day of surgery has been shown egional anesthesia
to decrease surgical site infection. 100-mL bot- Spinal anesthesia is the most common type of
tles of chlorhexidine are available commercially anesthesia used for a cesarean delivery. It has the
and may be used for this purpose. advantage of quick placement and rapid onset of
anesthesia. Epidural anesthesia is used when an
epidural catheter is already in place for labor
Bladder drainage analgesia, or when the cesarean section is not an
An indwelling Foley catheter is inserted just emergency. Combined spinal–epidural anes-
before starting the surgery and is usually thesia is preferred by some anesthetists.
removed 24 hours after surgery.
General anesthesia
Prophylactic antibiotics The indications for general anesthesia are as
Prophylactic antibiotics have conclusively been follows:
shown to decrease wound infection and endo-
• Urgency for delivery of baby
metritis following a cesarean section (Box 20.4).
• Inadequate or failed regional anesthesia
A single dose of a first-generation cephalosporin
• Coagulation disorders
(cefazolin) is commonly recommended. Women
• Spinal abnormalities (preventing spinal
with a documented history of penicillin allergy
anesthesia)
may receive IV clindamycin or IV erythromycin.
General anesthesia is induced with propofol
and succinylcholine. After endotracheal intuba-
Prophylactic anticoagulation tion, anesthesia is maintained by an inhalational
Anticoagulation to prevent venous thromboem- agent such as sevoflurane.
bolism (VTE) is not recommended for cesarean
Box 20.4 Prophylactic antibiotics for cesarean

perative techniques
section
Positioning of the woman
• Administered within 60 minutes before making
incision The gravid uterus may cause aortocaval compres-
• Cefazolin 2 g IV as single dose sion and cardiovascular compromise. Therefore,
• Clindamycin 600 mg IV or erythromycin 500 mg IV the woman should be positioned supine with a
(single dose) in women with a documented history of 15% left lateral tilt. Alternatively, a wedge may be
penicillin anaphylaxis
placed under the right hip.
CH 20_p282-299_v3.indd 286 17-07-2015 16:42:57

Figure 20.1 Skin cleansing. The abdominal skin is

cleansed with povidone-iodine solution.
a.
Skin cleansing
The skin is cleansed with 10% povidone–iodine
solution (Fig. 20.1).
Skin incision
The commonly used skin incisions for a cesarean
delivery include the following:
• Vertical (midline) incision
• Transverse incisions (Pfannenstiel, Joel-Cohen,
Maylard)
The type of incision usually is dictated by the
b.
clinical situation and the preferences of the
operator (Fig. 20.2). Figure 20.3 Joel–Cohen type of transverse incision.
a.6JGCPVGTKQTUWRGTKQTKNKCEURKPGUCTGDGKPIKFGPVKſGF
ransverse s in incision on either side (arrows). b. A straight transverse incision is
made, 3 cm below the line joining the two anterior superior
A low transverse skin incision is most commonly
iliac spines.
used for a cesarean delivery. The Pfannenstiel
incision is usually 2–3 cm above the pubic sym-
The advantages and disadvantage of a trans-
physis and placed in a natural fold of skin (the
verse skin incision are listed in Box 20.5.
‘smile’ or ‘bikini’ incision). The Joel–Cohen type
The types of transverse abdominal incisions
incision is straight, 3 cm below the line that joins
commonly used are listed in Box 20.6.
the anterior superior iliac spines, and slightly more
cephalad than Pfannenstiel (Fig. 20.3a and b). ertical s in incision
The vertical skin incision is less commonly used
for cesarean sections. The advantages and disad-
vantages of a vertical skin incision are listed in
Box 20.5 Advantages and disadvantage

of transverse skin incision
• Advantages
Ŧ Less postoperative pain
Ŧ Greater wound strength
a. b. Ŧ Better cosmetic results
• Disadvantage
Figure 20.2 Incision for cesarean section. a. Low
Ŧ Does not allow access to the upper abdomen
transverse incision (Pfannenstiel). b. Low midline incision.
CH 20_p282-299_v3.indd 287 17-07-2015 16:42:58

Box 20.6 Types of transverse abdominal

incisions for cesarean section
• Pfannenstiel incision
Ŧ Curved
Ŧ 2–3 cm above the symphysis pubis
Ŧ Midportion of the incision within the shaved area
of the pubic hair
• Joel-Cohen incision
Ŧ Straight
Ŧ 3 cm below the line that joins the anterior superior
iliac spines
Ŧ Higher than Pfannenstiel incision
Ŧ Associated with Figure 20.4 Pfannenstiel incision. The fascia has been
less pain and analgesic requirements EWVVTCPUXGTUGN[CPFTCKUGFCUƀCRU
less blood loss
shorter duration of surgery
Box 20.7. Paramedian incisions are not recom-

mended in modern surgery.
ascia an muscle
The important differences in the incisions are as
follows:
• In the Pfannenstiel incision, the fascia is cut
with a transverse incision and raised as flaps a.
(Fig. 20.4). The rectus muscles are separated in
the midline with blunt finger dissection.
• In the Joel-Cohen incision, the fascia is nicked
in the midline and opened transversely with
blunt finger dissection (Fig. 20.5a and b) or by
pushing laterally with slightly opened scissor
tips. The rectus muscles are then separated by
finger traction.
• In the Maylard technique, the rectus mus-
cles are cut 2 cm above the insertion into the
pubic bone, using a knife or electrocautery b.
(Fig. 20.6). This has the advantage of providing
Figure 20.5 Joel–Cohen incision. a. A nick is made in the
more operative space.
fascia in the midline. b. The fascia is opened transversely
YKVJDNWPVſPIGTFKUUGEVKQP
Box 20.7 ertical skin incision

• Advantages Entering the peritoneal cavity
Ŧ Faster abdominal entry
Ŧ Less bleeding and nerve injury After lifting the peritoneum with toothed for-
Ŧ Can be easily extended upward if more space is ceps, a small incision is made in the peritoneum
required for access to the upper abdomen and the incision is extended transversely with
• Disadvantages blunt or sharp dissection (Fig. 20.7a–c). Using
Ŧ Greater risk of postoperative wound dehiscence the fingers to bluntly open the peritoneum may
and incisional hernia
minimize the risk of inadvertent injury to the
Ŧ Greater postoperative pain
bowel or other organs that may be adherent to
Ŧ Scar cosmetically less pleasing
the underlying surface.
CH 20_p282-299_v3.indd 288 17-07-2015 16:42:58

a.
Figure 20.6 Maylard incision. The rectus muscle is

lifted up and divided 2 cm above its insertion, using
electrocautery.
On entering the peritoneal cavity, the lower

part of the uterus is exposed. The uterus is
often tilted to the right (dextrorotated), due to
presence of the rectosigmoid colon on the left
side. The left round ligament will be found
lying more anterior and nearer the midline b.
than the right round ligament. This dextrorota-
tion can be quickly corrected by inserting a
hand between the uterus and the right pelvic
sidewall and lifting the uterus gently upward
and to the left.
4CKUKPIVJGDNCFFGTƀCR
The uterovesical fold of peritoneum is grasped
with toothed forceps, just above the upper mar-
gin of the bladder, and a small nick is made in .
the midline with fine scissors (Fig. 20.8). The Figure 20.7 Opening the peritoneal cavity. a. After lifting
peritoneum is then cut sharply to both sides, the peritoneum with toothed forceps, a small incision
taking care to cut so that the incision forms a is made in the peritoneum. b. The incision is extended
curve, with the lateral ends curving upward. transversely with sharp or c. Blunt dissection.
The lower edge of the peritoneal flap is then
grasped with a toothed forceps or artery clamp,
and the bladder is separated gently by blunt incision, especially if an ultrasound scan has
dissection. indicated a low-lying placenta or placenta previa.
terine incision Transverse incision

The uterine incision is made in the lower uterine A transverse uterine incision (Munro Kerr inci-
segment. It must be large enough to allow sion) is used most commonly. The advantages of
atraumatic delivery of the fetal head and trunk a low transverse uterine incision are mentioned
without either tearing into or having to cut the in Box 20.8.
uterine vessels at the lateral margins of the A small incision is made in the midline with
uterus. It is important to be aware of the placen- the scalpel. Care must be taken not to nick the
tal position at the time of making the uterine baby’s skin. When entry into the uterine cavity
CH 20_p282-299_v3.indd 289 17-07-2015 16:42:58

Figure 20.8 4CKUKPIVJGDNCFFGTƀCR6JGWVGTQXGUKECNHQNF

of peritoneum is grasped with toothed forceps, just above a.
the upper margin of the bladder, and a small nick is made
KPVJGOKFNKPGYKVJſPGUEKUUQTU
Box 20.8 Advantages of transverse uterine

incision
• Less blood loss
• Less need for bladder dissection
• Easier reapproximation
• Lower risk of rupture in subsequent pregnancies
b.
is achieved, the incision can be extended using

blunt expansion with the surgeon’s fingers or
by sharp dissection with scissors (Fig. 20.9).
Blunt expansion is fast, has less chance of lat-
eral extension, and has less risk of inadvertent
trauma to the fetus as compared with sharp
dissection.
In certain situations, when more space is
required to deliver the baby, a ‘J’ (vertical exten-
sion in one lateral angle) or inverted midline ‘T’
extension is used (Fig. 20.10). If these incisions
have been made during the cesarean section, it is .
important to document them because of Figure 20.9 Transverse incision in the lower uterine
increased risk of uterine rupture in a subsequent segment (Munro Kerr incision). a. Diagrammatic
pregnancy. representation. b. A small incision is made with a
scalpel in the lower part of the lower uterine
segment. c. The incision is expanded by blunt
ertical incision dissection.
The low vertical incision (Kronig, De Lee, or
Cornell) is performed in the lower, noncontractile
Classical cesarean incision
uterine segment (Fig. 20.11). The low vertical inci-
sion has not found much favor in practice because A vertical incision that extends into the upper
of the possibility of extension upward into the uterine segment/fundus is termed a ‘classical’
uterine fundus or downwards into the bladder. incision (Fig. 20.12).
CH 20_p282-299_v3.indd 290 17-07-2015 16:42:58

a.
Figure 20.12 Classical cesarean section: The vertical

incision is in the upper uterine segment.
b.
Figure 20.10 Extending the transverse uterine incision. a. Delivery of fetus

‘J’ incision extending up one of the lateral edges of uterus.
b. Inverted T-shaped incision extending into the upper After the uterine cavity is entered, the mem-
muscular segment of uterus. branes (if still intact) are ruptured. The presenta-
tion of the fetus is assessed.
In a cephalic presentation, the operator’s
hand is used to scoop the head up and bring it to
the level of the uterine incision. The head is then
extracted through the uterine incision
(Fig. 20.13). To facilitate the delivery of the head
through the uterine incision, the surgical assis-
tant applies appropriate transabdominal fundal
pressure. The shoulders are then delivered by
gentle traction, and the rest of the body will read-
ily follow. Once the infant’s cord is clamped and
cut, it is handed over to trained personnel who
will take over the care of the infant.
Figure 20.11 Low vertical uterine incision.
This incision is not performed in modern

obstetrics because of the high frequency of cat-
astrophic uterine rupture in a subsequent
pregnancy. The only indications for a classical
cesarean incision may be invasive cervical can-
cer or the need for a quick delivery where the Figure 20.13 Delivery of the fetal head through the lower
woman will also be undergoing tubal ligation. uterine segment incision.
CH 20_p282-299_v3.indd 291 17-07-2015 16:42:59

Although forceps and ventouse have been

used to deliver the fetal head at a cesarean sec-
tion, the current recommendations favor a man-
ual delivery.
Delivery of the breech at a cesarean section is
described in Chapter 42, Abnormal labor: Breech
presentation and shoulder dystocia.
Delivering the placenta

Spontaneous delivery of the placenta is encour-
aged with gentle traction on the cord and use of
oxytocin to enhance uterine expulsive forces. Figure 20.14 Exteriorization of uterus. The uterus has
been exteriorized by lifting it out of the pelvic cavity.
Although many obstetricians remove the pla-
centa manually, waiting for the spontaneous
Technique for closure of the
expulsion of the placenta is recommended. The
placenta is inspected, and it is ensured that the uterine incision
entire placenta has been removed with the The uterine incision is closed with a two-layer
membranes. After delivering the placenta, the repair (Fig. 20.15). The first layer is closed with a
uterine cavity is explored or wiped with a locking suture that ensures hemostasis. This is
sponge. followed by an imbricating layer.
Prophylaxis against
postpartum hemorrhage
The uterus is massaged immediately after the
delivery of the placenta to facilitate uterine con-
traction. Oxytocin is the commonest uterotonic
drug used to promote uterine contraction. 10–20
units of oxytocin are added to 500 mL of normal
saline and infused over 30 minutes immediately
after the cord is clamped. This is followed by two
more bottles of 500 mL of dextrose saline or lac-
tated Ringer’s with 10–20 units of oxytocin in
a.
each bottle, given as an infusion at the rate of
125 mL/hour.
Closing the uterine incision

Temporary lifting up of the uterus from the pel-
vic cavity (exteriorization of the uterus) to facil-
itate repair of the uterine incision may be a good
technique and is practiced by many obstetri-
cians (Fig. 20.14). If the cesarean section has
been done under regional anesthesia, the mother
may experience discomfort and vomiting when
the uterus is exteriorized.
Apart from providing good exposure for sutur- b.
ing the angles of the uterine incision, exterioriza- Figure 20.15 Closure of the uterine incision. a. The
tion allows visualization of the ovaries and also ſTUVNC[GTKUENQUGFYKVJCNQEMKPIUWVWTGVJCVGPUWTGU
facilitates tubal ligation. hemostasis. b. The second layer is an imbricating layer.
CH 20_p282-299_v3.indd 292 17-07-2015 16:42:59

A single-layer closure has been described and

saves time. However, due to the increased risk of
uterine rupture in a subsequent pregnancy, a
single-layer technique is reserved for women
who undergo tubal sterilization at the same time.
Polyglactin 910 (Vicryl®) or chromic catgut may
be used for suturing.
Abdominal irrigation
Intra-abdominal irrigation is not recommended.
The excessive amniotic fluid and blood that may
have collected in the peritoneal cavity may be Figure 20.16 Closure of rectus fascia. The fascial edges
suctioned out. (arrows) have been grasped with Allis clamps and suturing
has started from the left angle.
Inspection of adnexae Closure of the

Examining the adnexae during a caesarean sec- subcutaneous tissue
tion is a good clinical practice. This ensures that
an ovarian cyst or mass is not missed. Routine subcutaneous tissue closure in women
with a depth <2 cm cannot be recommended.
However, when the subcutaneous tissue is
Closure of peritoneum >2 cm, closure with an interrupted delayed
absorbable suture prevents formation of seroma
There is currently no evidence to justify the
and subsequent wound breakdown. Placing a
time taken and cost of peritoneal closure.
drain in the subcutaneous tissue is unnecessary
Nonclosure of visceral and parietal peritoneum
and may lead to infection.
results in significantly fewer adhesions at sub-
sequent surgery.
Closure of skin
ectus muscles The skin can be closed with vertical mattress
sutures using fine nylon. Better cosmetic results
Reapproximation of the rectus muscles is not and patient satisfaction can be achieved with
recommended. When the edges of the rectus fas- subcuticular sutures using a delayed absorbable
cia are approximated, the muscles will come suture. Adhesive paper strips are the least painful
together naturally. and have excellent cosmetic results (Fig. 20.17).
Closure of rectus fascia

This is probably the most important step in
closure of the abdomen. A properly done fascial
closure is essential in preventing the occurrence
of incisional hernia. The recommendation for
fascial closure is a continuous nonlocking tech-
nique, with the sutures placed 1 cm from the edge
of the fascia and placed 1 cm apart (Fig. 20.16).
The fascial closure can be done using a
delayed absorbable suture such as polydioxa-
none or polyglactin. A permanent suture such as
1-0 nylon has also been recommended and may Figure 20.17 Closure of skin. Adhesive paper strips have
be cost-effective for developing countries. been used to approximate the skin edges.
CH 20_p282-299_v3.indd 293 17-07-2015 16:42:59

Wound dressing Difficulties and the measures to manage these

are listed in Table 20.1. If a prominent scar or
A light protective gauze dressing is recom- keloid is present, the incision may be made
mended. One or two narrow strips of tape can above or below it and the scar excised after the
hold the dressing in place. An occlusive dressing cesarean section is completed. Intra-abdominal
is not necessary. The dressing can be removed adhesions should be released only if the lower
after 24–48 hours. segment cannot be accessed. The bladder may
be pulled up and edematous in prolonged and
Incidental surgery obstructed labor. If the peritoneum is opened at
the usual level, there is a risk of entering the
during cesarean section bladder. Hence, care must be taken to open the
The two common incidental findings at cesarean peritoneum at a higher level. Large veins on the
section are adnexal masses and fibroids. lower segment may be ligated or cauterized.
Difficulties in delivering the head can arise due
• Inspecting the adnexae after closing the uter- to a deeply engaged head or mobile head. A
ine incision is good clinical practice. If an deeply engaged head may be delivered by
ovarian mass is found during a cesarean sec-
tion, and the mass is suspected of being a neo- • An assistant pushing the head up from the vagina
plasm, excision may be required. • Delivery as a breech by bringing the feet down
• Myomectomy in the pregnant uterus has the into the incision
potential for severe blood loss. Myomectomy • Delivering the shoulders first, followed by
is generally contraindicated for this reason. the breech and then the head (Patwardhan’s
Pedunculated myomas, however, can usually method)
be removed safely during a cesarean section. Extension of the incision to the vagina, upper
segment or laterally involving the uterine ves-
&KHſEWNVKGUGPEQWPVGTGF sels, must be managed by careful suturing and
ligation of uterine vessels.
at cesarean section
Difficulties may be encountered at any stage
during surgery. The common problems encoun-
Postoperative care
tered are skin scar, intra-abdominal adhesions, Postoperatively, pulse, BP, and urine output
delivery of the head, extension of the uterine should be monitored. A watch must be kept for
incision, and atonic uterus. uterine atony and vaginal bleeding (Box 20.9).
Table 20.1 &KHſEWNVKGUGPEQWPVGTGFFWTKPIEGUCTGCPUGEVKQPCPFVJGKTOCPCIGOGPV
Stage of surgery &KHſEWNV[ Management

At incision Previous scar/keloid • Incision above or below scar
• Excise scar before or after surgery
Opening abdomen Adhesions Release if lower segment not accessible
Incision of UV peritoneum Bladder edematous and pulled up Incise higher up to avoid the bladder
Incision on uterus Engorged veins on lower segment Ligate/cauterize if required
Placenta previa • Cut through the placenta
• Separate the placenta and enter from above
&KHſEWNV[KPFGNKXGTKPIJGCF Deeply engaged • Push up by hand in vagina
• Deliver as breech
• &GNKXGTUJQWNFGTUſTUV
Mobile head Use forceps/vacuum
Closure of uterine incision Extension of uterine incision Suture with care
Extension to uterine vessels Avoid bladder, ureter
Atonic uterus Postpartum hemorrhage • Ligate uterine vessels
• B-Lynch or hysterectomy
CH 20_p282-299_v3.indd 294 17-07-2015 16:42:59

Box 20.9 Postoperative care Intraoperative complications

• Monitor at cesarean section
Ŧ Pulse: half-hourly
Ŧ BP hourly
Intraoperative surgical complications occur
Ŧ Urine output 4 hourly more often in an emergency cesarean section
Ŧ Uterine atony than in an elective cesarean section. These
Ŧ Vaginal bleeding include damage to adjacent organs, including
• +PVTCXGPQWUƀWKFU bladder, urinary tract, or bowel, bleeding >1000
Ŧ Dextrose saline/lactated Ringer’s mL, and lacerations of the uterus or cervix.
Ŧ 500 mL 4 hourly for 12 hours Injuries to the fetus may also occur during uter-
• Oral intake ine incision or fetal extraction (Box 20.10).
Ŧ Fluids and soft solids within 6–8 hours
• Analgesia
Ŧ Pethidine/buprenorphine 6 hourly for 24 hours Postoperative complications
• Oral NSAIDs after 24 hours
Ŧ Catheter removed after 12–24 hours
after cesarean section
Postoperative complications following a cesar-
ean section include wound infection, endome-
+PVTCXGPQWUƀWKFU tritis, and hemorrhage (Box 20.10).
Intravenous fluids are continued for 12–14 hours Long-term complications of a cesarean
after a cesarean section till the mother is able to section include abnormal placentation in the
tolerate and retain oral feeding. Lactated Ringer’s subsequent pregnancy, scar dehiscence or rup-
solution or normal saline solution containing 5% ture in the next pregnancy, and subfertility.
dextrose is used. The usual amount adminis- Complications related to the uterine and abdom-
tered is 500 mL every 4 hours. inal scar include pregnancy in the hysterotomy
Feeding after cesarean section

Box 20.10 Intraoperative and postoperative
Early oral fluids or food intake is encouraged. complications of cesarean section
Early intake of oral fluids or food is associated ntraoperative
with the following:
• Damage to adjacent organs
• Reduced time to first food intake Ŧ Bladder
• Reduced time to return of bowel sounds Ŧ Urinary tract
• Reduced postoperative hospital stay Ŧ Bowel
• Bleeding >1L
Resumption of feeding (clear liquids or solids • Lacerations of uterus and cervix
according to the mother’s preference) within 8 • Injuries to fetus
hours of surgery is recommended. Ŧ At uterine incision
Ŧ During fetal extraction
Pain relief Postoperative
Pain relief is provided by narcotic analgesics • Wound infection
such as meperidine (pethidine) 75–100 mg • Endometritis
every 6 hours, according to requirement. • Subsequent pregnancy
Ŧ Abnormal placentation
Buprenorphine is also a good choice for post-
Ŧ Scar dehiscence or rupture
operative pain and can be given in the dosage
• Subfertility
of 0.3–0.6 mg intramuscularly every 6–8 hours. • Uterine scar
Oral nonsteroidal anti-inflammatory agents Ŧ Hysterotomy scar pregnancy
should suffice after 24 hours. • Abdominal scar
Ŧ Numbness and pain
rinary catheter Ŧ Scar endometriosis
• Neonatal
The urinary catheter may be removed after 12–24
Ŧ Transient tachypnea
hours. Routine urine culture after catheteriza-
Ŧ Respiratory distress syndrome
tion is not recommended.
CH 20_p282-299_v3.indd 295 17-07-2015 16:42:59

scar pregnancy, pain and numbness over the remains intact. It may go unrecognized if the
abdominal scar, and scar endometriosis. uterine scar is not explored after the vaginal
Neonatal complications include transient delivery. The risk of hemorrhage or adverse
tachypnoea of the newborn or respiratory distress maternal or perinatal outcomes is low.
syndrome (due to unexpected prematurity). Uterine rupture is defined as the complete
Intraoperative and postoperative complica- disruption of the uterine scar, including the
tions of a cesarean section are listed in Box 20.10. visceral peritoneum. It is a catastrophic event,
jeopardizing the life of the mother and fetus. It
may be associated with severe hemorrhage and
Management of bladder laceration, and may often necessitate
hysterectomy. Perinatal morbidity and mortality
pregnancy with previous may result from intrauterine hypoxia.
cesarean section
Maternal and
All women who have had a prior cesarean deliv-
ery should be counseled about the maternal and perinatal morbidity
perinatal risks and benefits of either a planned Risk of hemorrhage, infection, hysterectomy, and
vaginal birth or an elective repeat cesarean sec- perinatal asphyxia are higher in women undergo-
tion. The risk of uterine rupture while attempting TOLAC if the attempt is unsuccessful and scar
ing a vaginal delivery following a prior cesarean dehiscence or rupture results. On the other hand,
section is 7 per 1000 as compared with 0.2 per uterine rupture and other complications are
1000 in an unscarred uterus. This has a major fewer in women who undergo an elective repeat
influence on the decisions made by women and cesarean section. However, the absolute risk of
their obstetricians. these complications is low. Silent scar dehiscence
The decision to be made involves the may be seen even during elective cesarean sec-
following: tions, and morbidities associated with a cesarean
• Should she have an elective repeat cesarean section should also be considered. The morbidity
section? with a failed VBAC varies with the facilities avail-
• Should she have a trial of labor after cesarean able for an immediate cesarean section.
(TOLAC)?
• Would she be able to have a successful vaginal
birth after cesarean (VBAC)? Candidates for trial of labor
In a woman who has had one previous low Factors that can predict a successful TOLAC in a
transverse uterine incision, the chances of a suc- woman are
cessful vaginal delivery in a subsequent preg- • History of a vaginal delivery (before or after the
nancy are approximately 50%–60%. However, a cesarean section)
careful selection of the ideal candidate for • Onset of active spontaneous labor at d40
TOLAC will ensure success. weeks’ gestation
• Fetal weight not suggestive of macrosomia
terine dehiscence • Nonrecurrent indication for a previous cesar-
ean section, for example, fetal malpresenta-
and uterine rupture tion or fetal distress
Uterine dehiscence and uterine rupture are major
Factors that decrease chances for a successful
complications of TOLAC. Uterine rupture may
VBAC are
occur in 0.9%–1.5% of women attempting vaginal
delivery following LSCS. The occurrence is 4%–5% • Induced labor
with J-shaped or lower segment vertical incisions • No previous vaginal birth
and much higher with classical sections. • Previous cesarean section for dystocia
Uterine dehiscence is an incomplete uterine • Postdates
scar separation where the visceral peritoneum • Estimated fetal weight >4000 g
CH 20_p282-299_v3.indd 296 17-07-2015 16:42:59

• Occipitoposterior position and deflexion Uterine contractions should be noted. Pelvic

• Interdelivery interval <18 months examination should be performed to assess the
• Interpregnancy interval <6 months pelvic configuration, cervical effacement, and
• Advanced maternal age dilatation.
• Cervical dilatation <4 cm on admission in labor Recognition and management of uterine rup-
• BMI >30 kg/m2 ture is the most important aspect of the care of a
woman undergoing TOLAC. The following are
guidelines to be followed for a successful VBAC:
Contraindications to BAC • Facilities and personnel for an immediate
Certain factors increase the risk of uterine rup- cesarean section should be available.
ture when attempting VBAC. These are therefore • Labor should be monitored carefully. Electronic
considered contraindications to TOLAC, and the fetal monitoring of the fetal heart rate is
woman should be directly offered an elective recommended.
repeat cesarean section. These factors are • Induction of labor should be avoided.
Misoprostol for cervical ripening is contrain-
• High risk uterine scars
dicated with a previous cesarean scar. Many
– Two or more previous cesarean scars
units will not use any prostaglandins with a
– Inverted T incision or J incision
previous cesarean scar. Use of prostaglandins
– Classical cesarean
followed by oxytocin is not recommended.
– Myomectomy scar extending deep into the
• Augmentation of labor can be carried out with
myometrium
judicious use of oxytocin. There should be a
• Previous uterine rupture
lower threshold to intervene with a cesarean
• Obstetric complications, for example, placenta
section if labor does not progress normally.
previa and breech presentation
• Epidural analgesia may mask the signs and
• Limited facilities
symptoms of uterine rupture. However, it may
– Surgical, anesthetic, nursing, and pediatric
be used with close fetal monitoring and is not
staff
contraindicated.
– Blood and blood products
• The parturient should be monitored during
labor
Prediction of scar rupture – Half-hourly pulse
Although attempts have been made to predict – Hourly BP
the risk of scar dehiscence using ultrasono- – Electronic fetal monitoring if available
graphic measurement of the thickness of the • Abnormal fetal heart tracing, including base-
lower uterine segment, it has not proved useful. line bradycardia, tachycardia, variable and
Measurement is taken from the amniotic fluid to late decelerations, and maternal tachycardia,
the bladder, and the normal scar thickness is is suggestive of scar dehiscence and warrants
2–3.5 mm. Although the risk of rupture increases an immediate cesarean section.
with thin scars, there is no established cutoff • Maternal hypotension is a late sign and indi-
value and the predictive value of the test is low. cates rupture with internal hemorrhage.
• Following a successful VBAC, exploration of
the uterine cavity is practiced by many, but
Management of labor the benefits of this procedure are not clear.
and delivery in a woman Moreover, surgical intervention is not required
for asymptomatic dehiscence. Hence, there is
with a previous cesarean scar no recommendation regarding routine scar
The risks and benefits of TOLAC should be dis- exploration.
cussed with the mother and her partner. The
possibility of a successful vaginal delivery should
be estimated and contraindications excluded.
Cesarean hysterectomy
Ultrasonography should be performed to esti- Surgical removal of the uterus at the time of a
mate the weight of the baby and the placental cesarean delivery is called cesarean hysterec-
location. tomy (see Chapter 43, Complications of third
CH 20_p282-299_v3.indd 297 17-07-2015 16:42:59

stage of labor). It is not only a surgically challeng- Postpartum hemorrhage during a cesarean
ing procedure but also an emotionally challeng- section can result in a cesarean hysterectomy, if
ing one because it ends the fertility potential of all other interventions fail (see Chapter 43,
the woman. Complications of third stage of labor).
Cervical cancer is a rare indication for a cesar-
Indications ean hysterectomy.
A cesarean hysterectomy is technically chal-
Abnormal placentation (placenta accreta, pla- lenging due to the following factors:
centa percreta, and placenta increta) is the com-
monest indication for cesarean hysterectomy • It is usually done as an emergency, when the
(Box 20.11; see Chapter 46, Abnormalities of the woman may not be hemodynamically stable
placenta, umbilical cord, and fetal membranes). and her life may be in danger.
The increased incidence of cesarean sections is • Increased vascularity from the pregnancy may
one of the reasons for the increasing incidence of result in excessive bleeding.
abnormal placentation. • The cervix may be effaced due to labor, and
there may be difficulty in differentiating it
from the lower part of the uterus.
Box 20.11 Indications for cesarean hysterectomy • A subtotal hysterectomy (removing the uterus
• Abnormal placentation and leaving the cervix behind) may be an
Ŧ Placenta accreta, increta, and percreta option to cut short the operating time.
• Postpartum hemorrhage
• Cervical cancer
Key points
• #EGUCTGCPFGNKXGT[KUFGſPGFCUVJGDKTVJQHCHGVWU reserved for situations where fast abdominal
through an incision in the abdominal wall (laparotomy) entry is required. Paramedian incisions are
followed by an incision in the uterus (hysterotomy). not used.
• The commonest type of cesarean section done is • The commonest uterine incision is the transverse
a lower segment cesarean section (LSCS) through a incision in the lower uterine segment.
transverse uterine incision.
• The uterine incision is closed in two layers. A
• Classical cesarean and extraperitoneal cesarean are single-layer closure is used when a tubal ligation
rarely done. is being done concomitantly since a single-layer
closure is associated with an increased risk of
• %GUCTGCPUGEVKQPUCTGENCUUKſGFCUGNGEVKXGGOGT- rupture in a subsequent pregnancy.
gency, or on demand.
• 2QUVQRGTCVKXGN[+8ƀWKFUCTGEQPVKPWGFHQTJQWTUC
• Previous cesarean section, failure to progress in labor Foley is left in situ for 12–24 hours, and early feeding
or dystocia, and fetal distress are the three common- (by 6–8 hours) is encouraged.
est indications for cesarean section.
• In a woman who has had a previous cesarean section,
• Spinal anesthesia is the preferred mode of anesthesia the decision for the route of delivery depends on the
for a cesarean section. If a woman has had epidural risk factors for uterine rupture.
analgesia during labor, it can be continued for provid-
ing anesthesia. • Trial of labor after a cesarean section should follow
recommended guidelines. Close monitoring is manda-
• #UKPINGFQUGQHCſTUVIGPGTCVKQPEGRJCNQURQTKP tory and facilities for an immediate cesarean section
(cefazolin) is most commonly used as a prophylactic should be available.
antibiotic. A single dose of metronidazole may be
given in addition. • A cesarean hysterectomy is usually an emergency
and can be technically challenging.
• A transverse skin incision (Pfannenstiel or Joel–
Cohen) is usually used. A vertical skin incision is
CH 20_p282-299_v3.indd 298 17-07-2015 16:43:00

Self-Assessment
3. The uterine incision can be extended along the lateral
Case-based questions edge of the uterus as a ‘J’ incision or in the midline as
an inverted ‘T.’
Case 1 4. The classical cesarean section is associated with
Mrs. SS, 25, is a short primigravida (149 cm). She pre- a high incidence of uterine rupture in a subsequent
sents at 38 weeks’ gestation in spontaneous labor. Labor pregnancy.
does not progress due to cephalopelvic disproportion.
She delivers a 3.6-kg baby by cesarean section.
Case 2
1. What are the risk factors for possible cesarean sec-
tion in this woman? 1. The risk of uterine rupture is 0.9%–1.5%.
2. Which is the most commonly used uterine incision? 2. The chances for a successful VBAC are 50%–60%.
3. If the uterine incision has to be extended to deliver 3. Two or more uterine scars, previous uterine rup-
the large baby, what are the options? VWTGHGVCNOCETQUQOKCCDPQTOCNRGNXKEEQPſIWTC-
4. Why has the classical cesarean section been given up? tion, previous classical, J-shaped, or T-shaped
incision, and obstetric complications such as
malpresentations.
Case 2 4. A history of vaginal delivery, nonrecurrent indication,
Mrs. JK, 31, gravida 2, para 1, live 1, has had a lower spontaneous labor, gestational age <40 weeks, and
segment cesarean section for a breech presentation 3 average fetal weight.
years ago. She is now 36 weeks’ pregnant with a vertex
presentation. The estimated fetal weight is 2.9 kg. She
has been counseled for a vaginal delivery. Sample questions
1. What is the risk of uterine rupture in a woman with a
previous lower segment cesarean scar?
2. What are the chances for a successful VBAC in a 1. Enumerate the indication for LSCS.
woman attempting a trial of labor after a cesarean Discuss the management of a case of
section? previous LSCS.
3. What are the contraindications to attempting a trial of
labor in a woman with a previous cesarean section?
4. What are the indicators for a successful VBAC? Short-answer questions
1. Advantages of LSCS over classical section
Answers 2. Indications for emergency cesarean section
3. Advantages of elective cesarean section
Case 1 4. Scar dehiscence
1. Short primigravida and large baby. 5. Trial of vaginal delivery after cesarean section
2. Transverse incision in the lower segment. 6. Complications of VBAC
CH 20_p282-299_v3.indd 299 17-07-2015 16:43:00

Section 4
Postpartum
Management
CH 21_p300-307_v3.indd 300 17-07-2015 17:59:35

The Normal
21 Puerperium
Case scenario
Mrs. KM, 30, delivered normally. On the second postnatal day, she found
that her abdomen was flabby, her breasts were full, and she had vaginal
bleeding. She felt inadequate to take care of the baby. She also received
conflicting suggestions about food, clothing, breastfeeding, and medi-
cations from her parents, in-laws, and friends. She was confused and
wanted help.
Introduction during pregnancy revert to the normal prepreg-

nancy state. It may take up to 8–12 weeks for
There are several cultural practices, traditional some organ systems to return to baseline.
rituals, and religious beliefs about how the
postnatal mother and the newborn should be
managed. The mother goes through physiolog-
ical and emotional changes during this period.
Immediate postnatal
Obstetricians, nurses, and other health care pro- period
viders must be aware of the local practices and
mother’s medical and psychological needs and The first few hours after delivery are referred to
provide support and appropriate advice. as immediate postnatal period. During this time
the woman recovers from the strain of labor and
the infant may be put to the breast.
&GſPKVKQP Postpartum chills

The puerperium is the period from the delivery This occurs in 25%–50% of women. The shiv-
of placenta till 6 weeks postpartum. This is the ering or chills start soon after delivery and may
time during which the physiological changes last up to 1 hour. The etiology is not known. It
CH 21_p300-307_v3.indd 301 17-07-2015 17:59:35

is self-limiting and only supportive treatment

Box 21.1 Changes in the uterus during
(warm blankets) is required. puerperium
• Uterus
Anatomical and physiological Ŧ Involution
After third stage
changes - At the level of umbilicus, weighs 1000 g
During the days following delivery, several After 1 week
changes occur in the various organ systems. - Midway between umbilicus and pubic sym-
physis, weighs 500 g
After 2 weeks
terus - Within the pelvis, weighs 300 g
After 6 weeks
The uterus is well contracted and has the con-
- Prepregnant size, weighs 100 g
sistency of ‘cricket ball’ soon after expulsion of
• Lower segment
the placenta. The fundus is at the level of the Ŧ Contracts and becomes isthmus
umbilicus. Involution of the uterus occurs in the • Cervix
puerperium, and the fundal height decreases by Ŧ Contracts and thickens
1 cm (one fingerbreadth) every day (Fig. 21.1). Ŧ Becomes a transverse slit
The fundus lies midway between umbilicus and • Endometrium
pubic symphysis 1 week after delivery and is not Ŧ 5WRGTſEKCNFGEKFWCUNQWIJU
palpable after 2 weeks (Box 21.1). By 6 weeks, the Ŧ New endometrium from basal layer of decidua
uterus returns to its prepregnant size. The weight Ŧ .GWMQE[VKEKPſNVTCVKQP
decreases from 1000 g postdelivery to 500 g
after a week, 300 g after 2 weeks, and 100 g after
6 weeks. The process of involution is by reduc- is round in the nulliparous woman, becomes a
tion in size of individual muscle cells and not by transverse slit in multipara. This differentiates
reduction in number of cells. Lower segment of the parous cervix from the nulliparous one.
the uterus also contracts and becomes the isth- Hyperplasia and hypertrophy of the glands,
mus. The placental site vessels undergo throm- edema, and hemorrhage begin to regress a few
bosis and hyalinization. days after delivery and the regression is com-
plete by 6 weeks.
Cervix
The cervix, which was dilated to 10 cm, contracts
Endometrial changes
gradually and thickens. The external os, which The decidua differentiates into two layers. The
superficial layer becomes necrotic, sloughs, and
is expelled with the lochia. The deeper layer of
decidua (basal layer) remains and is the source
of new endometrium. The placental site and the
rest of the regenerating endometrium are infil-
t umbilicus
trated with granulocytes and lymphocytes. After
after eli ery Day 10, the leukocytic infiltration decreases.
Plasma cells appear and may be seen in the
fter endometrium for a few months.
ee
Changes in the uterus during puerperium are
fter
ee s
Lochia
Figure 21.1 Involution of the uterus. The uterus shrinks The discharge from the uterus in the postpartum
by 1 cm/day and lies midway between umbilicus and pubic period is known as lochia. It begins as bleeding
symphysis 1 week after delivery and becomes a pelvic following delivery of placenta and decreases
organ (not palpable) by 2 weeks. during the next 4–5 days. This bloody discharge,
CH 21_p300-307_v3.indd 302 17-07-2015 17:59:35

The Normal Puerperium 303
Box 21.2 Lochia Box 21.3 Changes in vagina, vulva, and ovarian
function during puerperium
• Discharge from the uterus in the puerperium
• Consists of • Vagina
Ŧ decidua Ŧ Decrease in vascularity
Ŧ blood Ŧ Reappearance of rugae
Ŧ leukocytes • Vulva
Ŧ exudates Ŧ Partial/complete regression of
• First 4–5 days: Lochia rubra relaxation/enlargement of introitus
• Next 2–3 weeks: Lochia serosa relaxation of pelvic muscles/ligaments/fascia
• Till 6–8 weeks: Lochia alba • Ovarian function
Ŧ Suppression of ovulation due to
high prolactin
suppression of pulsatile GnRH release
which consists of blood and sloughed decidua, Ŧ Return of ovulation
is known as lochia rubra (Box 21.2). During the Nonlactating: Mean 75 days
following 2–3 weeks, the discharge is pale, thin- Lactating: Mean 6 months
ner, and blood stained and is known as lochia Ŧ Return of menstruation
serosa. Lochia rubra and serosa have a unique Nonlactating: 8–12 weeks
offensive mildly fishy odor. Following this, yel- Lactating: Depends on duration of breastfeeding
lowish-white discharge consisting of leukocytes n gonadotropin-releasing hormone.
and exudates persists for a few days, referred
to as lochia alba. Total duration of lochial dis-
charge is 6–8 weeks.
menstruation may resume by 8–12 weeks. In
women who breastfeed, ovulation may resume
Afterpains by 6 months but amenorrhea can continue for
The uterus contracts intermittently, giving rise 1–2 years depending on the duration of lactation.
to pain similar to but milder than labor pains. Changes in the vulva, vagina, and ovarian
During suckling, oxytocin is released by the pitu- function are summarized in Box 21.3.
itary and the afterpains are more pronounced.
They usually subside within 3–4 days. Abdominal wall
The abdominal wall is flabby and the muscles
agina and vulva are lax in the immediate postnatal period. The
The vagina becomes vascular from first tri- muscles regain their tone over a period of time
mester and enlarges during delivery, especially and can be aided by exercises. Divarication of
second stage. It contracts and vaginal rugae recti may persist. The rupture of elastic fibers of
gradually appear in the puerperium. The vascu- the skin results in striae gravidarum, which is
larity decreases. The stretching ligaments, fas- permanent.
cia, levator ani, and other pelvic muscles may
result in pelvic floor relaxation. Changes in the urinary tract
The dilatation of the renal pelvis and ureter,
varian function changes in renal plasma flow, and glomerular
In lactating women, prolactin levels remain ele- filtration rate return to normal by 6–8 weeks
vated and estrogen levels decreased till about postpartum. Following vaginal delivery, there is
6 weeks. In nonlactating women, the levels edema and submucosal hemorrhage in the blad-
normalize after 2–3 weeks. Follicle-stimulating der with associated increase in bladder capacity
hormone (FSH) levels are normal but the and mild reduction in bladder sensation. Due to
ovary is unresponsive to FSH. These hormonal these changes, stasis of urine, incomplete void-
changes form the basis of ovulation suppres- ing, and bladder distension can occur (Box 21.4).
sion and amenorrhea. Nonlactating women Epidural analgesia and reflex spasm of urethra
begin ovulating about 75 days after delivery and due to pain at the episiotomy/perineal tear can
CH 21_p300-307_v3.indd 303 17-07-2015 17:59:35

Box 21.4 Changes in the urinary tract during Box 21.6 Changes in other systems during
puerperium puerperium
• 4GPCNRNCUOCƀQY • Hematological changes
• )NQOGTWNCTſNVTCVKQP 4GVWTPVQPQTOCND[ Ŧ Leukocytes
rate 6–8 weeks Increase immediately after delivery
• Dilatation of renal Decrease soon after
pelvis and ureter Ŧ Hemoglobin
• Postnatal urinary retention and stasis due to Fluctuates
Ŧ increased bladder capacity Rises after 1 week
Ŧ reduced bladder sensation Ŧ Increase in blood coagulability
Edema of bladder base Thrombocytosis
Submucosal hemorrhage Increased platelet adhesiveness
Ŧ TGƀGZWTKPCT[URCUOFWGVQRCKP Increase in fibrinogen
Ŧ epidural analgesia Persistence of increase in other coagulation factors
• Cardiovascular system
Ŧ Fall in cardiac output
worsen these. Urinary incontinence can occur Ŧ Decrease in blood volume Occur within a week
following prolonged labor or instrumental deliv- Ŧ Fall in heart rate
ery, due to stretching and damage to the pelvic Ŧ Peripheral resistance increases
muscles and fascia. Ŧ Blood pressure returns to normal
Ŧ Third heart sound and functional systolic murmurs
disappear
Weight loss
Delivery of the fetus, placenta, and amniotic fluid
results in a weight loss of 5–6 kg (11–13 lbs) in the
immediate postpartum period (Box 21.5). There is asymptomatic. A small percentage of affected
some water retention in the intra- and extravascu- women can present with symptoms of transient
lar compartments in the immediate postpartum hypo- or hyperthyroidism. Symptomatic women
period, and the water is mobilized and excreted should be evaluated and treated with appropri-
gradually. This leads to further weight reduction ate medications.
of about 2–5 kg. Women who had excessive weight
gain in pregnancy have a net weight gain which
has to be shed by diet and exercise.
Management of
ther systems puerperium
Changes in the other systems are summarized in
Box 21.6. This consists of monitoring the mother and baby
for complications and providing care, support,
hyroi ys unction and advise.
Postpartum thyroiditis occurs in about 10% of
women. Etiology is autoimmune and it is largely Maternal monitoring
After delivery, mother should be closely moni-
tored in the labor room for 2 hours (Table 21.1).
Box 21.5 Weight loss during puerperium
She should be shifted to the postnatal ward only
• Immediate postpartum: 5–6 kg after ensuring that all parameters are normal.
Ŧ Fetus
Ŧ Placenta
Ŧ #OPKQVKEƀWKF Subsequent care
Ŧ Blood
Subsequent care should include care of the
• Subsequent loss: 2–5 kg
mother, neonate, breastfeeding, and advice at
Ŧ 'ZVTCCPFKPVTCXCUEWNCTƀWKF
discharge (Box 21.7).
CH 21_p300-307_v3.indd 304 17-07-2015 17:59:35

Constipation is common. Plenty of fluids, high

Table 21.1 Maternal monitoring after delivery
residue diet, and, if required, mild laxatives are
Clinical parameters To detect recommended. Thrombosed external hemor-
Pulse
rhoids may appear during the postnatal period.
Atonic/traumatic PPH They should be treated with laxatives and local
Blood pressure
ointments. If persistent, surgical intervention is
Temperature Sepsis
required.
Vaginal bleeding PPH
Fundal height/consistency Uterine atony
Voiding of urine Care of the perineum
Urinary retention
Distension of bladder
Perineal hygiene is important. Cleaning the vulva
Dyspnea Pulmonary embolism
should be from anterior to posterior toward the
Perineal pain Vulval hematoma
anus, in order to avoid bacteria from the perianal
PP , postpartum hemorrhage. region contaminating the vulva. Moist heat, iced
sitz bath, and rectal or oral analgesics may be
required for painful episiotomy or lacerations.
Lochia must be checked for abnormal foul odor.
Box 21.7 Subsequent care after the delivery
• Mother
Ŧ Ambulation Diet and supplements
Ŧ Perineal care Normal diet (30 cal/kg ideal body weight) with
Ŧ Care of the bladder and bowel
extra 500 kcal for lactation is recommended.
Ŧ Diet
Iron supplementation should be continued for
Ŧ Breastfeeding and care of the breast
• Neonate
3 months and calcium supplements as long as
Ŧ Feeding breastfeeding continues.
Ŧ Immunization
• Advice at discharge Breastfeeding and care
Ŧ Contraception
Ŧ Exercises of the breast
Breastfeeding is discussed in Chapter 25,
Lactation and breastfeeding. Breastfeeding
should begin within an hour of delivery.
Ambulation Rooming in and skin-to-skin contact are essen-
Early ambulation, few hours after delivery, is tial. Nulliparous women must be given instruc-
important to facilitate bowel movement and tions regarding proper positioning of the mother
reduce the risk of venous thrombosis and embo- and infant and the technique of breastfeeding.
lism. The mother and child can be discharged Nipples should cleaned before and after
48 hours after delivery. each feed. Breast supports must be encouraged.
Retracted nipples are common and must be
Care of the bladder and bowel attended to in the antenatal period. Drawing out
the nipples using fingers or the reverse end of a
Reduction in bladder sensation, increase in syringe may be necessary. In case of cracked nip-
bladder capacity, epidural analgesia, and peri- ples, local application of breast milk or lanolin
neal pain due to tears or episiotomy can cause and using a nipple shield are recommended.
urinary retention. Large doses of oxytocin have
antidiuretic effect and the mother may not be
hydrated adequately. These factors reduce the
Care of the neonate
urine output. Hence, women should be encour- The neonate is usually weighed, swaddled, and
aged to void. If bladder is distended and woman kept warm. The cut end of the umbilical cord
does not void in 6–8 hours, an indwelling cath- should be kept clean. The cord usually shriv-
eter should be introduced and left in place for els and falls off in a week. Demand feeding is
24 hours. recommended.
CH 21_p300-307_v3.indd 305 17-07-2015 17:59:35

Immuni ation Box 21. 8 Postnatal checkup

Mother must be counseled regarding the impor- • History
tance of immunization and the schedule should Ŧ Vaginal bleeding/discharge
be given. BCG vaccine may be administered Ŧ Breastfeeding
before mother and baby are discharged. • General examination
Ŧ Blood pressure
Ŧ Pallor
Advice at discharge
• Breast examination
Mother should be advised regarding exercises Ŧ Engorgement
and contraception. Pelvic floor exercises and Ŧ Cracked nipple
abdominal exercises can be started after a week • Abdominal examination
in case of normal delivery. Contraception is dis- Ŧ Involution of uterus
• Local and pelvic examination
cussed in Chapters 26, Contraception: Temporary
Ŧ Episiotomy/laceration
methods and Chapter 27, Emergency contracep-
Ŧ Lochia
tion and sterilization. Ŧ Uterine size
• Investigations
Follow-up Ŧ Oral GTT if gestational diabetic
• Advice
First postnatal follow-up is at 6 weeks (Box 21.8).
Ŧ Contraception
Ŧ Resumption of sexual activity
esumption of sexual activity Ŧ Postnatal exercises
Ŧ Weight reduction
Mother may resume sexual activity about 2–3
weeks after delivery or whenever she is comfort- , glucose tolerance test.
able. Decrease in libido is often noticed. This is
due to hormonal changes, postpartum blues,
and depression. Dyspareunia due to episiotomy
or perineal laceration and vaginal dryness due to Postnatal exercises
estrogen deficiency are also common. Pelvic floor exercises and exercises for toning up
the back and abdominal muscles can be started
Weight reduction 4–6 weeks after normal delivery and 8 weeks
Women who have gained weight excessively after cesarean section. These exercises can pre-
must be advised regarding diet, regular exercises, vent urinary incontinence, chronic backache,
and return to normal weight before embarking and lax abdominal wall.
on next pregnancy.
Key points
• Puerperium is the period from delivery of the placenta symphysis 1 week later, and not palpable 2 weeks
to 6 weeks postpartum. The physiological changes later.
during pregnancy revert to normal during this period.
• 6JGUWRGTſEKCNNC[GTQHFGEKFWCUNQWIJUQHHCPFKU
• In the immediate postpartum period, mother should expelled with lochia. The deeper layer is the source
be monitored closely. Pulse, blood pressure, QHPGYGPFQOGVTKWO6JGTGKUNGWMQE[VKEKPſNVTCVKQPQH
temperature, fundal height and consistency, bladder decidua during puerperium.
distension, perineal pain, and vaginal bleeding should • Lochia is the discharge from uterus. This consists
be monitored.
of decidua, blood, leukocytes, and exudates. The
• The uterus undergoes involution during this period. discharge persists for 6–8 weeks.
The fundus is at the level of umbilicus immediately
• Changes in the vagina, vulva, and abdominal wall
after delivery, midway between umbilicus and pubic
regress. The striae gravidarum persist.
(Continued)
CH 21_p300-307_v3.indd 306 17-07-2015 17:59:35


• Changes in the urinary system regress gradually. • Advice regarding care of the neonate and breastfeed-
Cardiac output, blood volume, and heart rate fall within ing should be given.
1 week.
• During follow-up at 6 weeks, clinical examination
• Mother should be ambulated early and discharged should be performed to exclude cracked nipples, breast
after 48 hours of vaginal delivery. engorgement, anemia, and episiotomy breakdown.
Advice regarding contraception, exercises, immunization,
• Normal diet and extra 500 kcal for lactation should be
and return to sexual activity are mandatory.
advised and perineal care should be given.
Self-Assessment
normal prepregnant conditions is uterine involution.
Case-based questions 6JGUK\GTGFWEGUD[QPGſPIGTDTGCFVJGXGT[FC[
1P&C[KVUJQWNFDGQPGſPIGTDTGCFVJDGNQYVJG
Case 1 umbilicus.
Mrs. KM, 30, delivered normally. On the second postnatal 3. Normal diet with extra 500 kcal for lactation.
FC[UJGHQWPFVJCVJGTCDFQOGPYCUƀCDD[JGTDTGCUVU 4. Iron supplementation for 3 months and calcium
were full, and she had vaginal bleeding. She was not sure supplementation as long as breastfeeding continues.
about how to take care of the baby.She also received con- Analgesics for afterpains and perineal pain.
ƀKEVKPI UWIIGUVKQPU CDQWV HQQF ENQVJKPI DTGCUVHGGFKPI
and medications from her parents, in-laws, and friends.
Case 2
1. 9JCVCTGVJGENKPKECNſPFKPIU[QWYQWNFNQQMHQTQP
routine postnatal evaluation? 1. General examination for pallor and blood pressure,
2. What is uterine involution? Where would you expect breast examination, abdominal examination for uter-
the uterine fundus to be on the second postnatal day? ine involution, pelvic examination for uterine size and
3. What dietary advice would you give her? examination of lochia for color and odor.
4. What medications are recommended in the puer- 2. 2QUVPCVCNRGNXKEƀQQTGZGTEKUGUCPFGZGTEKUGUVQ
perium? tone up back and abdominal muscles can be started
2–4 weeks after vaginal delivery and 8 weeks after
cesarean section.
Case 2 3. #FXKEGQPNKHGUV[NGOQFKſECVKQPECNYGKIJV
reducing diet, and regular exercises. The goal is to
Mrs. NC, 29, mother of one child, postnatal 6 weeks, reduce 1–1.5 kg/month and get back to normal BMI
came for routine checkup. before embarking on next pregnancy.
1. What clinical evaluation will you do?
2. What advice will you give her regarding postnatal
exercises? Sample questions
3. Her body mass index (BMI) is 30. What advice will
you give her?
Long answer question
&GſPGRWGTRGTKWO&KUEWUUVJGRJ[UKQNQIKECNEJCPIGU
Answers in purperium.

1. Temperature and pulse, for puerperal fever; blood
1. Care of the mother in the puerperium
pressure, for hypertension; fundal height, for
2. Lochia
involution; lochia, for color and odor; perineum,
for episiotomy and laceration; and breasts, for 3. Involution of the uterus
engorgement, cracked nipples, and abscess. 4. Postnatal checkup
2. The gradual reduction in size of the uterus and
regression of changes of pregnancy and return to
CH 21_p300-307_v3.indd 307 17-07-2015 17:59:35

The Abnormal
22 Puerperium
Case scenario
Mrs. RM, 28, presented with fever after having delivered 5 days ago at
a local hospital. She was feeling ill, had lower abdominal pain, and a
slight increase in vaginal bleeding. Her husband was worried since she
had just delivered and had to take care of the baby as well.
Introduction Box 22.1 Postpartum complications

• Secondary postpartum hemorrhage
Most women have an uncomplicated recovery
• Puerperal pyrexia
after delivery but postpartum complications do
• Thromboembolism
occur. Puerperal infection is a common cause • Postpartum neuropathy
of febrile morbidity. Though it is a time of hap- • Musculoskeletal pain
piness for the entire family, the woman can feel • Mental health issues
overwhelmed and inadequate and develop men-
tal health problems, which may enhance the
severity of physical symptoms. The obstetrician
should recognize these complications early and Secondary postpartum
treat them appropriately.
hemorrhage
Excessive vaginal bleeding that occurs between
Postpartum complications 24 hours and 12 weeks after delivery is known
as secondary postpartum hemorrhage (PPH). It
Several complications can develop in the puer- most often occurs within the first 3–4 weeks after
perium. These are listed in Box 22.1. delivery.
CH 22_p308-319_v3.indd 308 17-07-2015 18:21:56

The Abnormal Puerperium 309
Box 22.2 Causes of secondary postpartum

hemorrhage
• Retained placental tissue
Ŧ Cotyledons
Ŧ Membranes
• Infection
Ŧ Endometritis
• Arteriovenous malformations
• Choriocarcinoma/placental site trophoblastic tumor
Box 22.3 Clinical features and diagnosis of sec- a.

ondary postpartum hemorrhage
• Clinical features
Ŧ Bleeding excessive but not profuse
Ŧ Fever, constitutional symptoms
Ŧ Foul-smelling lochia
Ŧ Uterine subinvolution
Ŧ Uterine tenderness
• Diagnosis
Ŧ Clinical examination
Ŧ Ultrasonography
Placental tissue
GTN/Choriocarcinoma
Ŧ Color Doppler
Arteriovenous malformations b.
Ŧ If >4 weeks after delivery
Figure 22 .1 Ultrasonographic images of retained
Serum E hCG to rule out GTN
placental tissue. a. Placental tissue visible in the uterine
gestational trophoblastic neoplasm. cavity. b. Color Doppler shows vascularity in the periphery
of the tissue.
Curettage is indicated if ultrasonography

Causes reveals retained placental tissue (Fig. 22.1).
Causes of secondary PPH are listed in Box 22.2. Curettage should be performed with caution to
avoid uterine perforation.
Clinical features and diagnosis
The clinical features and diagnosis of secondary Puerperal pyrexia
PPH are listed in Box 22.3. Pyrexia or fever in the puerperium can occur due
to several causes. Clinical evaluation of symp-
Management toms and signs and appropriate investigations
are necessary to arrive at a diagnosis.
Since secondary PPH usually occurs in the pres-
ence of infection (endometritis), antibiotics
&GſPKVKQP
must be administered to all women with second-
ary PPH. The offending organisms are a combi- Puerperal pyrexia (puerperal febrile morbidity)
nation of aerobic gram-negative and anaerobic is defined as oral temperature of 380C (100.40F)
bacteria. Hence, a combination of antibiotics or higher, on any 2 of the first 10 days postpar-
that cover these organisms should be used. Oral tum, exclusive of the first 24 hours. Low-grade
amoxicillin/clavulinic acid and metronidazole fever in the first 24 hours after delivery is com-
are commonly used. mon and therefore not included.
CH 22_p308-319_v3.indd 309 17-07-2015 18:21:56

Box 22.4 Etiology of puerperal fever Box 22.6 Common pathogens causing uterine
infections
• Genital tract infection
Ŧ Uterine infection • Aerobes
Ŧ Pelvic cellulitis Ŧ Gram positive
Ŧ Peritonitis Streptococcus—group A, B, and D
Ŧ Septicemia Staphylococcus aureus
Ŧ Septic pelvic thrombophlebitis nterococcus
• Wound infections Ŧ Gram negative
• Urinary tract infection scherichia coli
• Mastitis/breast abscess lebsiella pneumonia
• Respiratory tract infections Proteus species
eisseria gonorrheae
Ŧ Others
Etiology ardnerella vaginalis
ycoplasma hominis
Causes of puerperal fever are listed in Box 22.4. Chlamydia trachomatis
• Anaerobes
terine infection Ŧ Peptostreptococci and peptococci
Ŧ Bacteroides species
Puerperal uterine infection usually involves
Ŧ Clostridium sordellii and C perfringens
the endometrium, myometrium, and parame-
Ŧ usobacterium and obiluncus
trium and is therefore better described as endo-
paramyometritis or metritis with pelvic cellulitis.
icrobiology
is actors The infection is usually polymicrobial and a
The most important risk factor for puerperal combination of gram-negative, gram-positive,
infection is cesarean section. Without antibiotic and anaerobic bacteria are involved. Most infec-
prophylaxis, the risk is 8–10 times higher with tions are caused by organisms that colonize the
cesarean delivery, and mortality due to sepsis is genital tract. In women infected with HIV, other
25 times higher as compared with vaginal deliv- less likely pathogens, such as herpes simplex
ery. Other risk factors are listed in Box 22.5. virus and cytomegalovirus, may also play a role.
The common pathogens are listed in Box 22.6.
Box 22.5 isk factors for uterine infection
athogenesis
The organisms from the lower genital tract enter
• Prolonged labor
• Prolonged rupture of membranes
the amniotic fluid when the membrane ruptures.
• Multiple vaginal examinations Given the right conditions, they invade the site
• Internal fetal monitoring of placental attachment or the uterine incision.
• /GEQPKWOUVCKPGFCOPKQVKEƀWKF The infection subsequently spreads to the para-
• Vaginal colonization with metrial connective tissue (pelvic cellulitis) and
Ŧ Group B Streptococcus can later involve the adnexae (Fig. 22.2). Pelvic
Ŧ ycoplasma hominis and general peritonitis and pelvic abscess can
Ŧ reaplasma urealyticum result. Septicemia can occur at any time during
Ŧ ardnerella vaginalis the process of spread of infection.
Ŧ Chlamydia trachomatis The spread of infection is by
• Low socioeconomic status
• Operative vaginal delivery • contiguous spread from uterus,
• Intrapartum chorioamnionitis • bloodstream (hematogenous), and
• Maternal anemia, diabetes • lymphatics.
• Manual removal of placenta
• Younger age, nulliparity Clinical eatures
• HIV infection
Fever is the most predominant symptom. Other
JWOCPKOOWPQFGſEKGPE[XKTWU
symptoms and signs are listed in Box 22.7.
CH 22_p308-319_v3.indd 310 17-07-2015 18:21:56

rganisms in agina cer i
is factors
Multiple aginal e amination
P M prolonge labor an
cesarean section
Placental site uterine incision
Pel ic general
Myometrium Parametrium loo stream
peritoneum
Figure 22. 2 Pathogenesis of puerperal infection. P , prelabor rupture of membranes.
• Antibiotic prophylaxis at cesarean section: A

Box 22.7 Clinical features of puerperal infection
single dose of ampicillin 2 g IV or first-genera-
• Symptoms tion cephalosporin (cefazoline) 1–2 g IV given
Ŧ Fever, chills not more than 30 minutes before skin inci-
Ŧ Lower abdominal pain
sion has been found to reduce the incidence
Ŧ Headache, malaise
of infection.
Ŧ Malodorous lochia
Ŧ Excessive vaginal bleeding
• Spontaneous delivery of the placenta at cesar-
• Signs ean section reduces the incidence of infection.
Ŧ Tachycardia Antibiotic prophylaxis is not recommended
for vaginal delivery. Cleansing the vagina with
Ŧ Subinvolution of uterus
chlorhexidine or providone-iodine prior to labor
Ŧ Purulent lochia
or cesarean section has not been found to be
Ŧ Parametrial tenderness
useful in reducing infection rates.
reatment
Diagnosis Treatment should include antibiotics to cover
In women who present with puerperal fever, a aerobic gram-positive, gram-negative, and
detailed history of risk factors for uterine infec- anaerobic organisms.
tion should be asked for. Clinical evaluation is Mild endometritis following vaginal delivery
important to look for the symptoms and signs can be treated with oral amoxicillin-clavulanic
of uterine infection and to exclude other causes acid and oral metronidazole.
of puerperal fever. Routine cultures from Infection following cesarean sections and
the vagina or endometrium are not recom- more severe infections with fever, chills, abdom-
mended. Blood culture is recommended when inal pain, and purulent discharge that occur after
the woman appears acutely ill with sepsis syn- vaginal delivery should be treated with paren-
drome, the fever does not respond to treatment, teral antibiotics. A combination of clindamycin
or the woman is immunocompromised. and gentamycin has a 95% cure rate and is the
recommended first-line treatment (Table 22.1).
revention Other antibiotics that have an equivalent
Postpartum uterine infection and its com- efficacy are third-generation cephalosporins
plications can be prevented by the following (cefotetan, cefoxitin, and ceftizoxime), piperacil-
strategies: lin, and ampicillin-sulbactam. Women who are
CH 22_p308-319_v3.indd 311 17-07-2015 18:21:57

Table 22.1 Antimicrobial treatment of puerperal uterine infection
Severity of infection Antibiotic Dose Frequency oute

Mild infection, Amoxicillin/clavulanic acid 625 mg 12 hourly Oral
vaginal delivery + metronidazole 400 mg 8 hourly Oral
Moderate-to-severe,
infection, vaginal delivery; Clindamycin 900 mg 8 hourly IV
infection following + Gentamycin 5 mg/kg Once daily IV
cesarean section
known to be colonized with group B streptococ- Pelvic cellulitis

cus on antepartum screening should be treated
with ampicillin-sulbactam alone or in combina- Spread of infection to the retroperitoneal con-
tion with clindamycin and gentamycin. nective tissue between the layers of the broad
ligament is also known as pelvic cellulitis or
parametrial phlegmon (Fig. 22.3). The uterine
Duration o therapy incision may also undergo necrosis.
Clinical response is usually evident within 48 Clinically, prolonged fever persists in spite of
hours of initiation of treatment. IV antibiotics antibiotic therapy. Pelvic examination reveals
must be continued for 24 hours after the patient induration in the parametrium. CT scan clinches
becomes afebrile. In women with positive blood the diagnosis.
culture, parenteral antibiotics should be contin- If uterine wound dehiscence is diagnosed,
ued for a total period of 2 weeks. laparotomy, resuturing of the wound, or hyster-
If there is no response to treatment in 48–72 ectomy is indicated. Clinical features and man-
hours, consider the following: agement of pelvic cellulitis are summarized in
Box 22.8.
• Other causes of fever: Evaluate
• Drug resistance: Change antibiotics
Adnexal infection
• Pelvic cellulitis, abscess, and uterine wound
dehiscence: Perform imaging and surgery as The infection can spread from the uterus to the
required adnexa and an ovarian abscess may develop.
• Unusual organisms: Treat according to blood Rupture of an ovarian abscess results in peri-
culture tonitis and septicemia (Box 22.9). A high index
• Retained products: Perform ultrasonography of suspicion is necessary for the diagnosis.
and curettage Imaging by ultrasonography and/or CT is
allopian tube
ary
Pel ic cellulitis
Figure 22.3 Pelvic cellulitis. The infection spreads between the layers of the broad ligament.
CH 22_p308-319_v3.indd 312 17-07-2015 18:21:57

Box 22.8 Pelvic cellulitis Box 22.10 Clinical features and management
of peritonitis
• Infection of tissue between layers of broad ligament
• Can be associated with uterine wound dehiscence • Occurs following
• Spread of infection from uterus Ŧ uterine infection
• Symptoms Ŧ uterine wound dehiscence
Ŧ Persistent fever Ŧ pelvic cellulitis
Ŧ Parametrial tenderness • Clinical features
• 75%6HQTEQPſTOCVKQP Ŧ Persistent fever
• Treatment Ŧ Abdominal pain
Ŧ Antibiotics Ŧ Abdominal tenderness and rigidity
Ŧ Surgery, if uterine wound dehiscence present Ŧ Paralytic ileus
C computerized tomography; S, ultrasound scan.
• Treatment
Ŧ Intravenous antibiotics
Ŧ Conservative management of paralytic ileus
Ŧ Surgical intervention in case of
uterine wound dehiscence
Box 22.9 Adnexal infections
bowel perforation
• Spread from uterus
• Can result in ovarian abscess
• Rupture of ovarian abscess results in Pelvic abscess
Ŧ Peritonitis
Ŧ Septicemia Following peritonitis, pus may collect in the
• Diagnosis by U/S, CT broad ligament, between bowel loops or in the
• Treatment pouch of Douglas (Fig. 22.4). If the abscess is
Ŧ Antibiotics in the pouch of Douglas and can be accessed
Ŧ Surgical excision of ovary through the posterior fornix, it should be
C computerized tomography; S ultrasound scan. drained by colpotomy. Others can be managed
by ultrasound-guided or CT-guided aspiration.
Antibiotics must be administered.
usually required. Treatment is by resection of
the ovarian abscess. Septicemia
Once the bacteria enters the bloodstream, sep-
ticemia results. Gram-negative septicemia can
Peritonitis
lead to septic shock with associated hypoten-
This may occur following endomyometritis, sion, respiratory distress syndrome, and renal
uterine wound dehiscence, or pelvic cellulitis. failure, and is associated with high mortal-
Clinical features and management of peritonitis ity. Septic shock is discussed in Chapter 45,
are given in Box 22.10. Nonhemorrhagic shock in pregnancy.
la er
Pel ic abscess
Pouch of ouglas
Posterior forni
ectum
Figure 22.4 Pelvic abscess. The pus collects in the pouch of Douglas and can be drained through the posterior fornix.
CH 22_p308-319_v3.indd 313 17-07-2015 18:21:57

Septic pelvic thrombophlebitis intravascular coagulation, and hepatic failure.

Mortality is high in this condition. Management
This is a rare complication of puerperal uterine consists of early diagnosis, inotropic support,
infection. Incidence has declined remarkably appropriate antibiotics, and management of
with the use of prophylactic antibiotics during renal failure.
cesarean section. The infection spreads along
the veins and causes thrombosis. The thrombo-
sis may extend upwards from the uterine veins Wound infections
to the internal and common iliac veins, ovarian
veins and occasionally, to the inferior vena cava Abdominal wound infection may be associ-
and renal vein (Fig. 22.5). ated with uterine infection or may occur alone.
Clinical presentation includes fever, pelvic Wound infection with collection of pus is man-
pain, tachycardia, abdominal tenderness, and aged as given in Box 22.11.
guarding. Diagnosis is by ultrasonography, CT, Necrotizing fasciitis with extensive tissue ne-
or MRI. Treatment is by broad-spectrum antibi- crosis is a rare wound infection, associated with
otics. Use of anticoagulants is controversial.
Box 22.11 Management of abdominal wound
Toxic shock syndrome infection
Rarely, endotoxins released by Staphylococcus • Antibiotics as for endometritis

aureus or beta-hemolytic streptococci give rise • Surgical drainage of wound
to a clinical condition called toxic shock syn- • Daily dressing
• Single layer closure after healthy granulation tissue
drome. Clinical features include fever, headache,
seen
vomiting, diarrhea, renal failure, disseminated
nferior ena ca a
arian
ein
Common
iliac ein
Uterine eins
Figure 22.5 Septic pelvic thrombophlebitis. The thrombosis extends from the uterine veins to internal and common iliac
veins, ovarian veins, inferior vena cava, and renal vein.
CH 22_p308-319_v3.indd 314 17-07-2015 18:21:57

high mortality. It is usually seen in women with di- anagement

abetes, hypertension, and obesity. Antibiotics and Since most infections are caused by E. coli, treat-
excision of the necrotic tissue is the treatment. ment can be started based on clinical symp-
toms and signs. The urine sample should be
In ection o episiotomy an sent for culture prior to the initiation of therapy.
perineal tears Diagnosis and management of urinary tract
Infection may involve the skin and subcutaneous infections is discussed in Chapter 55, Renal and
tissue alone or the muscle layer as well, result- urinary tract disorders.
ing in episitomy breakdown. The entire wound
should be opened and allowed to granulate.
Antibiotics are not recommended. Analgesics
Breast engorgement, mastitis, and
and warm Sitz bath relieve pain, and wound breast abscess
debridement assists in healing. Large deep These are common causes of puerperal pyrexia
wound breakdown should be resutured after 6–7 and are discussed in Chapter 25, Lactation and
days. Closure is performed in layers as for pri- breastfeeding.
mary repair of episiotomy.
rinary tract infections espiratory infections

Urinary tract infection is a common cause of puer- Respiratory infections are usually seen after
peral pyrexia. Cystitis occurs mainly due to incom- cesarean section, especially if general anesthesia
plete emptying of the bladder (urinary stasis). The has been used. Stasis and aspiration are the lead-
infection ascends easily since the physiological ing causes of pneumonitis.
dilatation of the ureters takes a few days to regress.
Differential diagnosis of puerperal
athogenesis pyrexia
The predisposing factors for urinary tract infec-
tions in the puerperium are listed in Box 22.12. Arriving at the right diagnosis requires a careful
history, physical examination, and appropriate
athogens investigations (Table 22.2). Fever, chills, malaise,
and headache are common to all conditions
The most common organism is E. coli. Proteus,
causing puerperal pyrexia. Leukocytosis is usu-
Klebsiella, Enterobacter, and Staphylococci are
ally present.
the other organisms responsible for UTI.
Clinical eatures Thromboembolic disease

The most common presentation is fever, chills,
Puerperal thromboembolism commonly occurs
and dysuria. Presence of renal angle tenderness
in women with prior history of thrombosis or
and high fever indicates pyelonephritis.
inherited thrombophilias. Occasionally, it can
occur in women with other high risk factors but
without inherited thrombophilias. The increase
Box 22.12 Predisposing factors for urinary tract
infections
in clotting factors, pressure on the vena cava
by the enlarging uterus, and the resultant stasis
• Decreased bladder sensation are contributing factors. It may present as the
Ŧ Pressure on the bladder by fetal head following:
Ŧ Epidural analgesia
• 8QKFKPIFKHſEWNV[
WTKPCT[UVCUKU • Thrombophlebitis
Ŧ Pain of episiotomy/perineal tear
• Deep vein thrombosis
Ŧ Vaginal/vulval hematoma
• Pulmonary embolism
• Catheterization during labor/postpartum
CH 22_p308-319_v3.indd 315 17-07-2015 18:21:58

Table 22.2 Differential diagnosis of puerperal pyrexia
istory Physical examination Investigations Diagnosis

Risk factors, Uterine tenderness, Uterine infection
lower abdominal pain, subinvolution,
malodorous lochia, malodorous lochia
excessive vaginal bleeding
Persistent fever Parametrial tenderness, U/S Pelvic cellulitis
induration
Adnexal mass, tenderness U/S Adnexal infection
Abdominal tenderness Peritonitis
rigidity, paralytic ileus
Mass in POD U/S, CT Pelvic abscess
Pelvic pain CT/MRI Septic pelvic
thrombophlebitis
Pain at operative site or Erythema, induration, Wound infection
perineum tenderness, discharge
Dysuria, frequency, Suprapubic/renal angle Urine culture Urinary tract infection
loin pain tenderness
Pain in the breast Breast engorgement, Mastitis, breast abscess
cracked nipple, tenderness,
erythema
Cough, purulent sputum Respiratory signs Chest X-ray Respiratory infection
C , computerized tomography; , magnetic resonance imaging; P D, pouch of Douglas; S, ultrasound scan.
Thrombophlebitis • Unfractionated heparin (UFH)

– Weight-adjusted full dose
It is thrombosis with associated inflammation or – 10,000 units 12 hourly
infection. It can affect the superficial veins of the – Dose adjusted according to activated partial
leg but more often is deep seated. Septic pelvic thromboplastin time (aPTT)
thrombophlebitis extends retrograde to involve • Low molecular weight heparin (LMWH)
the ileofemoral veins. The leg is swollen and – Weight-adjusted full dose
edematous. If the collateral veins are open and – Dalteparin 100 U/kg 12 hourly
there is no venous congestion, the leg is pale and • UFH followed by oral anticoagulants:
swollen, described as phlegmasia alba dolens. If – Warfarin 7 mg started along with UFH
collateral veins are involved, the leg is congested – UFH stopped after 3 days
and edematous, described as phlegmasia cerulia – Warfarin dose adjusted to 2–3 mg daily
dolens. Treatment is the same as for septic pelvic according to INR (international normalized
thrombophlebitis. ratio)
Deep vein thrombosis

It affects the left leg more often (Fig. 22.6). The
leg may be swollen and painful, and calf muscle
tenderness is present. Homan’s sign is usually
positive (pain in the calf muscle on dorsiflexion
of the foot). Diagnosis is by ultrasonography and
Doppler imaging. Bed rest, elastic stockings, anal-
gesics, and therapeutic doses of anticoagulants Figure 22.6 Deep vein thrombosis. The affected leg is
are indicated. swollen, discoloured, and tender.
CH 22_p308-319_v3.indd 316 17-07-2015 18:21:58

Pulmonary embolism Musculoskeletal pain

Pulmonary embolism is associated with high The most common musculoskeletal problems
maternal mortality. It may follow deep vein in the puerperium are sacroiliac joint pain and
thrombosis of the leg or can occur without any separation (diastasis) of the pubic symphysis.
prior symptoms. Dyspnea, cough, and chest Sacroiliac joint pain can occur during preg-
pain are the usual symptoms. nancy or puerperium and is due to hormonal
Diagnosis requires a high index of suspicion. changes resulting in lax joint ligaments, lum-
Chest X-ray, arterial blood gas analysis, ven- bar lordosis, and position in labor. It is man-
tilation/perfusion scan, and MRI are helpful. aged by rest, analgesics, and physiotherapy.
Treatment is by immediate anticoagulation. Separation of pubic symphysis is summarized
Intracaval filters may be inserted into the inferior in Box 22.14.
vena cava to prevent recurrent emboli reaching
the lungs from the legs or pelvis.
Mental health issues
Postpartum neuropathy Mood disturbances, depression, and psycho-
sis are experienced by many women during the
Neuropathies occur in the postpartum period postpartum period. Preexisting anxiety disor-
due to traction, compression, or vascular injury. ders, obsessive disorders, and depressive illness
The incidence is less in modern obstetric prac- can exacerbate or recur in the postnatal period.
tice. The weakness and paralysis are usually The common disorders that occur in puerpe-
transient; most women recover within 72 hours. rium are postpartum ‘blues,’ depression, and
Foot drop may persist for longer and requires psychosis. Posttraumatic stress disorder can also
physiotherapy. The etiology and management occur in the postpartum period.
Etiology
Box 22.13 Postpartum neuropathy Hormonal changes in pregnancy and puerpe-
rium have been implicated in the causation.
• Risk factors
Interaction between various steroid hormones,
Ŧ Fetal macrosomia
Ŧ Malpresentations
genetic predisposition, and environmental
Ŧ Prolonged labor
Ŧ Mid/high forceps delivery
Ŧ Prolonged lithotomy position
Box 22.14 Separation (diastasis) of pubic
Ŧ Improper use of stirrups
symphysis
Ŧ *[RGTƀGZKQPQHVJKIJU
Ŧ Epidural analgesia • Can occur in late pregnancy or during delivery
• Involves • Etiology
Ŧ Lumbosacral trunk Ŧ Hormonal changes in pregnancy
Ŧ Femoral nerve Ŧ Delivery of large baby
Ŧ Lateral cutaneous nerve of thigh Ŧ Position in labor
Ŧ Pudendal nerve • Clinical features
Ŧ Peroneal nerve Ŧ &KHſEWNV[KPYCNMKPI
• Clinical features Ŧ Severe pain
Ŧ Pain Ŧ Tenderness over pubic symphysis
Ŧ Weakness of leg Ŧ Palpable joint defect
Ŧ Foot drop • Management
• Management Ŧ Bed rest
Ŧ Physiotherapy Ŧ Analgesics
Ŧ Splinting Ŧ Binders
Ŧ Electrical nerve stimulation Ŧ Injection of local anesthetics
CH 22_p308-319_v3.indd 317 17-07-2015 18:21:58

Box 22.15 Predisposing factors for mental Postpartum depression

health problems If the postpartum ‘blues’ last for longer than 2
• History of depression weeks, postpartum depression must be suspected.
Ŧ Family history Depression occurs within the first 1 month but
Ŧ Past history later than postpartum ‘blues’. This is one of the dif-
• Stressful environment ferentiating features. Criteria for diagnosis are the
Ŧ At home same as in nonpregnant women. Insomnia, low
Ŧ At work
energy level, loss of appetite and weight, anger,
• /CTKVCNEQPƀKEVU
feeling of being overwhelmed or inadequate, and
• Malformed infant
obsessional thoughts are the usual symptoms.
Treatment is by supportive therapy and antide-
pressants. Selective serotonin reuptake inhibitors
are the drugs of choice.
factors may explain the onset of these mental
health problems, but definite proof is lacking.
Predisposing factors are listed in Box 22.15. Postpartum psychosis
Some women develop delusions, hallucinations,
Postpartum blues
and psychotic behavior in the postnatal period.
Postpartum ‘blues’ occur in almost 50% of Usually, there is a past history of schizophrenia
women. The condition is self-limiting. It is char- or bipolar disorder. The condition is uncom-
acterized by mood swings, insomnia, anxiety, mon but can recur in a subsequent pregnancy.
and crying spells that occur by 2–3 days after Hospitalization, antipsychotic therapy, and occa-
delivery, peak by the fifth day, and resolve within sionally electroconvulsive therapy are required.
2 weeks. The condition is treated by supportive Mental health issues in the puerperium are
therapy and minor tranquilizers. summarized in Table 22.3.
Table 22.3 Mental health problems in puerperium
Condition Timing Clinical features Management

Postpartum blues Begin 2–3 days after delivery, Mood swings, anxiety, crying spells Supportive, mild
RGCMD[ſHVJFC[ tranquilizers
subside by 2 weeks
Depression 2 weeks after delivery Insomnia, low energy levels, Supportive,
loss of appetite/weight, anger, antidepressants
feeling of inadequacy
Psychosis 9KVJKPſTUVOQPVJ Mania, hallucinations, delusions, Hospitalization,
psychotic behavior antipsychotics, electro-
convulsive therapy
Key points
• The most common postpartum complications are • Puerperal pyrexia is caused by uterine infection or its
puerperal pyrexia and secondary postpartum hemor- complications, wound infection, urinary tract infection,
TJCIG
22* or mastitis.
• Secondary PPH occurs due to endometritis or retained • Uterine infection occurs in women with risk factors.
placental tissue. Antibiotics must be administered to The infection is polymicrobial, caused by aerobic and
all women with secondary PPH. If ultrasonography anaerobic organisms.
shows retained placental tissue, curettage is required.
• Infection spreads from the uterus to the parametrium,
• Puerperal pyrexia is a temperature of 100.4°F or adnexa, and peritoneal cavity or enters the blood
JKIJGTQPCP[VYQQEECUKQPUKPVJGſTUVFC[URQUV- stream.
RCTVWOGZENWFKPIVJGſTUVJQWTU
(Continued)
CH 22_p308-319_v3.indd 318 17-07-2015 18:21:58


• Treatment is by antibiotics to cover polymicrobial • Postpartum neuropathy is caused by traction, com-
infection. Cultures are not necessary. Severe infection pression, or occlusion of blood supply to the nerves.
warrants hospitalization and IV antibiotics. Clindamy- Most neuropathies are self-limiting. Foot drop may
cin and gentamycin are the antibiotics of choice. take time to resolve.
• Cesarean wound infection and episiotomy breakdown • Musculoskeletal pain involves the pubic symphysis
should be managed by wound debridement, antibiot- or sacroiliac joint. Diastasis of the pubic symphysis is
ics, and resuturing if required. treated by rest, strapping, and analgesics.
• The most common organism involved in urinary tract • The mental health issues encountered in the
infection is coli. puerperium are postpartum ‘blues’, depression,
and psychosis. All require supportive therapy.
• Thromboembolic disease may be thrombophlebitis,
Depression and psychosis should be treated with
deep vein thrombosis, or pulmonary embolism. Deep
medications.
vein thrombosis and pulmonary embolism should be
treated by prompt anticoagulation.
Self-Assessment
4. Since the patient presents with vaginal bleeding, she
Case-based questions should be hospitalized.
a. If the temperature is mild to moderately high, bleed-
Case 1 ing is not profuse, and the patient is otherwise well,
Mrs. RM, 28, presented with fever after having delivered oral amoxicillin with clavulanic acid 625 mg 12 hourly
5 days ago at a local hospital. She was feeling ill, had lower with metronidazole 400 mg 8 hourly is indicated.
abdominal pain, and a slight increase in vaginal bleeding. b. If bleeding is moderate, the temperature is high
and the condition is suggestive of moderate
1. What is the diagnosis? to severe infection, IV clindamycin 900 mg 8 hourly
2. How will you ascertain the cause of fever? and gentamycin 5 mg/kg daily are indicated.
3. What is the most likely cause? Why?
4. What is the management?
Case 2
Case 2 1. Diastasis of pubic symphysis.
2. Delivery of large baby, instrumental delivery, and
Mrs. MS, 20, was delivered by forceps for prolonged sec- positioning in labor. Hormonal changes of pregnancy
ond stage. She developed acute pain in the pubic area may also contribute.
CPFFKHſEWNV[KPYCNMKPICHVGTFGNKXGT[ 3. Bed rest, analgesics, and strapping. Gradual
1. What is the most likely diagnosis? ambulation after a few days.
2. What are the risk factors?
3. How will you manage this condition?
Sample questions
Answers Long-answer questions
1. Discuss the importance of postnatal care. Describe
Case 1 the clinical features, diagnosis, and management of
puerperal sepsis.
1. Puerperal pyrexia
2. What is puerperium? Describe the complications of
2. a. History: Degree of fever, risk factors for infection,
puerperium and their management.
FKHſEWNV[KPDTGCUVHGGFKPICUUQEKCVGFEJKNNUCD-
dominal pain, dysuria, excessive vaginal bleeding.
b. Look for any of the following: Uterine tenderness, Short-answer questions
subinvolution, foul-smelling lochia, adnexal mass
or tenderness, cracked nipple, breast engorge- 1. Secondary postpartum hemorrhage
ment or abscess, wound breakdown. 2. Prevention of puerperal sepsis
3. Endometritis, because the patient presented with 3. Predisposing causes for puerperal sepsis
lower abdominal pain and vaginal bleeding along with 4. Septic pelvic thrombophlebitis
the fever. 5. Deep vein thrombosis.
CH 22_p308-319_v3.indd 319 17-07-2015 18:21:58

23 The Newborn
Case scenario
Mrs. NK, 32, a multigravida, was delivered by forceps at term. The baby
did not cry at birth and was limp and pale.
Introduction transition and has adapted to extrauterine life.

When the baby struggles to take its first breath or
The first few breaths in an infant’s life are repre- does not attempt to take a breath, it indicates fail-
sentative of a profound and challenging mecha- ure of a process. The baby needs assistance from
nism that marks the remarkable transition from the obstetrician and neonatologist.
intrauterine to extrauterine life. After depend- The transition involves:
ing entirely on the mother during fetal life for • Pulmonary adaptation and
thermoregulation, metabolic homeostasis, and • Circulatory adaptation.
respiratory gas exchange, the fetus has to transi-
tion effectively and rapidly to postnatal respira-
tory and circulatory pathways. Pulmonary adaptation
and changes
Pulmonary adaptation involves clearance of
Transition from intrauterine fluid from the alveoli and expansion of the lungs,
with air completely replacing fluid. Surfactant
to extrauterine life plays a major role in the transition.
The transition from intrauterine to extrauterine life

is a complex process, the failure of which can jeop-
#NXGQNCTƀWKFENGCTCPEG
ardize the infant’s life. In simple terms, the baby’s During fetal life, the lungs are filled with a fluid
first cry reassures the mother and the obstetrician that is essential for normal growth and develop-
that the baby has had a smooth, uncomplicated ment of the lungs. Transition from intrauterine
CH 23_p320-331_v3.indd 320 17-07-2015 18:42:37

The Newborn 321
to extrauterine life involves a smooth process of

Box 23.1 Pulmonary adaptation and changes
converting the fluid-filled lungs into an organ
capable of gas exchange. This transition hap- • Fetal life
pens during labor, delivery, and in the first few Ŧ .WPIUſNNGFYKVJƀWKF
• During labor
instants of extrauterine life.
Ŧ 2TQFWEVKQPQHNWPIƀWKFUVQRU
Ŧ 4GCDUQTRVKQPQHNWPIƀWKFDGIKPU
During labor
• Vaginal delivery
During labor, the following two mechanisms go Ŧ Fluid squeezed out mechanically
into action: • First breath
Ŧ Quick inspiration
• Production of lung fluid stops.
Ŧ Short expiration
• Reabsorption of lung fluid begins. Ŧ (NWKFſNNGFURCEGDGEQOGUCKTſNNGF
• Lung expansion
During vaginal elivery Ŧ Due to fall in intrathoracic pressure
During vaginal delivery, one more mechanism Ŧ Leads to stimulation of surfactant production
comes into play:
• Fluid is mechanically squeezed out of the lungs.
Delivery of the head causes the expulsion of ole of surfactant
tracheal fluid. The amount of fluid squeezed out When the infant takes its first breath, air rushes
from the lungs during vaginal delivery is much into the pulmonary alveoli. The alveoli are the
more than that during a cesarean delivery. primary site of gas exchange with the blood and
consist of an epithelial layer and extracellular
6JGſTUVDTGCVJ matrix surrounded by capillaries. During expi-
The baby’s first breath establishes an air–liquid ration the alveoli have a tendency to collapse.
interface that rapidly involves the major part If this happens, then a much greater inspiratory
of the lungs and the lungs fill with air. The first effort is required to open them with the next
breath of air after birth is typically a quick inspi- breath. Surfactant is essential to prevent the
ration, followed by constriction of the larynx that alveoli from collapsing after they have expanded
holds air within the lungs with a positive intra- with the first few breaths (Box 23.2).
thoracic pressure. This is followed by a short
active expiration through a narrowed larynx with • Surfactant forms a very thin film that covers
an immediate inspiration. This results in the first the surface of the alveolar cells and acts by
burst of crying by the baby. reducing the surface tension at the air–liquid
interface of the alveolus, thus preventing its
2QUVPCVCNN[ collapse during end-exhalation. Surfactant is a
The lymphatics and pulmonary capillaries absorb
the remaining minimal amount of lung liquid.
Box 23.2 Pulmonary surfactant
Lung expansion • Phospholipids and 4 surfactant proteins
As the newborn initiates the first breath, intra- • Produced by type II alveolar epithelial cells (pneumo-
cytes)
thoracic pressure falls and air starts moving
Ŧ Production initiated by 20 weeks’ gestation
into the lungs. Increasing inspiratory pressure Ŧ Increased production by 30–32 weeks
expands the alveolar air spaces and establishes Ŧ Production stimulated by glucocorticoids
functional residual capacity (FRC). Expansion Ŧ Low production in preterm infants
of the alveoli also stimulates surfactant release, • (QTOUVJKPſNOEQXGTKPIUWTHCEGQHCNXGQNCTEGNNU
which has an important role in reducing alveo- Ŧ Reduces surface tension at air–liquid interface
lar surface tension, increasing lung compliance, Ŧ Prevents alveolar collapse during end-exhalation
and stabilizing the functional residual capacity. • Natural or synthetic surfactant used in treatment/preven-
Pulmonary adaptation and changes are summa- tion of RDS
rized in Box 23.1. DS respiratory distress syndrome.
CH 23_p320-331_v3.indd 321 17-07-2015 18:42:37

complex substance containing phospholipids stimulates closure of the ductus arteriosus. The
and four different types of surfactant proteins. ductus arteriosus is functionally closed within
• Surfactant is produced in the fetal lungs by type 4 days of birth.
II alveolar epithelial cells, also called pneumo- Failure of closure of the ductus arteriosus
cytes. At approximately 20 weeks’ gestation, results in a condition called patent ductus arteri-
the components start to appear. The natural osus (PDA) and will require medical and/or sur-
production of surfactant increases at approxi- gical intervention.
mately 30–32 weeks, and adequate amounts
are produced by 34 weeks’ gestation.
Closure of the foramen ovale
• Surfactant production is stimulated by several
hormones and growth factors: glucocorticoids, The increased pulmonary arterial blood flow
thyroid hormone, thyrotropin-releasing hor- raises pulmonary venous return to the left
mone, and others. Glucocorticoids are the most atrium. As the left atrial pressure increases and
important stimulating factors and are used in the right atrial pressure falls, right-to-left shunt-
clinical practice to accelerate fetal lung maturity. ing across the foramen ovale decreases. Closure
• Preterm infants may have low amounts of of the foramen ovale occurs when the left atrial
surfactant, and this may result in respiratory pressure exceeds the right atrial pressure.
distress syndrome (RDS). Aspiration of meco- The transition of intrauterine to extrauterine
nium into the fetal lungs is known to inactivate life is summarized in Figure 23.1.
surfactant and may lead to meconium aspira-
tion syndrome.
• Both natural and synthetic surfactants are
effective in the treatment and prevention of
Immediate assessment
RDS. The management of RDS is described of the newborn in the
later in this chapter.
delivery room
Circulatory adaptation Delivery room assessment of the clinical status
of the newborn includes the following:
The following two important circulatory changes
occur during the transition from intrauterine to • Clinical estimation of the infant’s age (term or
extrauterine life: preterm)
• Apgar score
• There is a rise in neonatal systemic blood
pressure. This happens when the placenta is
abruptly removed from the neonatal circula- Apgar score
tion with the clamping of the umbilical cord.
• Both pulmonary vascular resistance and the Dr. Virginia Apgar, an anesthetist, introduced the
pulmonary artery pressure drop significantly Apgar score in 1952. The Apgar score is a quick
with the expansion of the lungs. screening test used worldwide to assess the
health of the newborn infant at 1 and 5 minutes
These two changes in turn result in the after birth. The Apgar score is a convenient way
following: of determining whether the infant needs prompt
intervention to establish breathing.
• Increased left-to-right shunt at the ductus
arteriosus • The 1-minute Apgar score measures how well
– Increased ventricular stroke volume the newborn tolerated labor and delivery.
– Increased cerebral oxygen saturation • The 5-minute Apgar score assesses how well
• Increased blood flow through the pulmonary the newborn is adapting to the extrauterine
arteries and lungs environment.
Assignment of the Apgar score is detailed in
Closure of ductus arteriosus
Table 23.1.
As lung perfusion and expansion increase, neo- Scores of 7 and above are generally con-
natal oxygenation saturation is increased, which sidered normal, 4–6 low, and 3 and below are
CH 23_p320-331_v3.indd 322 17-07-2015 18:42:37

The Newborn 323
ransition from intrauterine

to e trauterine life
Pulmonary Circulatory
a aptation a aptation
Labor an Cor clamping cuts off

irst breath Postnatal
eli ery placental circulation
Lung flui ncrease in systemic

pro uction stops bsorption bloo pressure
Lung e pan s
Lung flui Lungs fill of flui by ecrease in pulmonary
urfactant
reabsorbe ith air lymphatics ascular resistance an
release
lui s uee e an capillarls pulmonary artery
out pressure
ncrease in
ncrease in left
lui fille space p in pulmonary
to right shunt
becomes air fille ascular be
Closure of uctus Closure of

arteriosus foramen o ale
Figure 23.1 The transition of intrauterine to extrauterine life.
Table 23.1 Assignment of Apgar score
Score
0 1 2
A: Appearance Pale or blue Pink with blue Pink all over
extremities
P: Pulse rate Absent <100 bpm >100 bpm
G: Grimace Nil Grimace Cry or cough
(response to
stimulation)
A: Activity (muscle Limp 5QOGƀGZKQP 9GNNƀGZGF
tone) active
movement
R: Respiratory effort Absent Gasping or Regular or
irregular strong cry
generally regarded as critically low. However,

the Apgar score should not be used as the only
Examination of the normal
measure to evaluate the possibility that neu- newborn
rological damage occurred during the birthing
process. A term infant with good respiratory effort, mus-
The clinical significance of the Apgar score cle tone, and good Apgar score does not require
and association with morbidity are listed in further treatment and, after the initial care, can
Box 23.3. remain with the mother to encourage
CH 23_p320-331_v3.indd 323 17-07-2015 18:42:37

be documented. A checklist should contain the

Box 23.3 6
JGENKPKECNUKIPKſECPEGQHVJG#RICT
score following:
• Low score at 1 minute • Head

Ŧ Medical attention required by the neonate – Shape of head
Ŧ Does not necessarily indicate a long-term problem – Fontanel: normal, sunken, or bulging
If the score improves at the 5-minute test – Sutures: molding, fused sutures
• Low score at 5 minutes (0–3) – Facial appearance and eye position
Ŧ May have poor outcome/cerebral palsy – Asymmetry or abnormality of facial form
Ŧ Associated with neonatal seizures • Face
• 5EQTGDGNQYCVQTOKPWVGU
– Asymmetry
Ŧ Indicates long-term neurological damage
– Facial palsy
Ŧ Must be correlated with fetal hypoxemia and
hypercarbia • Eyes
– Normal shape and appearance
– Movement
• infant–maternal bonding by skin-to-skin con- – Ophthalmoscope exam for presence of red
tact and reflex
• early initiation of breastfeeding. Present: Normal
Every newborn should be examined in the Abnormal: Rule out
neonatal period. This allows confirmation of - Retinoblastoma
normalcy and also the detection of any minor or - Cataracts
major abnormality. The physician’s hands must - Retinal dysplasia
be washed thoroughly before examining the • Ears
baby to reduce the risk of cross-infection. – Shape, size, malformed
– Set at the normal level or ‘low-set’
– Patency of external auditory meatus
istory • Mouth
History should include the following: – Color of the mucous membrane
– Tongue
• History of neonatal problems in previous
Freely mobile
siblings
Tethered (tongue-tie)
• Family history of inherited disorders
– Palate
• Antenatal history—high-risk factors, medica-
High palate
tions, and intrapartum complications
Cleft palate
• Mode of delivery
– Lips
Cleft lip
Documentation of physical – Suckling reflex present
parameters • Neck
– Masses (e.g., cystic hygroma)
The following must be documented for the infant: – Torticollis (head tipped to one side and chin
• Gender of the infant rotated toward the other)
• Weight • Arms and legs
• Temperature – Normal length and shape, and moving
• Length (from top of the head to the heels) normally
• Head circumference – Hands and feet
Polydactyly (extra digits)
Syndactyly (fused digits)
Palmar creases—multiple or single
Systematic head-to-toe - Single palmar crease may be normal or
examination sign of Down syndrome
• Peripheral pulses
The infant should have a complete examination, – Brachial, radial, and femoral pulses for rate,
and both normal and abnormal findings should rhythm, and volume
CH 23_p320-331_v3.indd 324 17-07-2015 18:42:37

The Newborn 325
– Hyperdynamic suggestive of patent ductus Further examination should be conducted as

arteriosus necessary according to any abnormalities that
– Radial–femoral delay suggestive of aortic are detected, or suspicions of undetected ill-
coarctation ness in the baby. Depending on the abnormality
• Heart found, the appropriate specialist can be called in.
– Palpation
Cardiac position
Thrill or heave
– Auscultation
outine care of the
Added sounds newborn
Murmurs
• Lungs Following birth, the routine care of the newborn
– Respiratory rate, pattern, and depth usually includes the following:
– Intercostal retraction • Prophylactic eye care
– Stridor or grunting • Administration of vitamin K
– Auscultation of lung fields for added • Breastfeeding
sounds • Care of the skin
• Abdomen • Meconium passage and voiding
– Abdominal distension • Umbilical cord care
– Scaphoid abdomen—suggestive of dia- • Hepatitis B vaccination
phragmatic hernia
– Umbilical stump for infection or hernia
– Gentle palpation for organs, masses, or Prophylactic eye care
herniae
Prophylactic eye care is given shortly after birth
– Liver and spleen palpable in newborn
as a preventive measure against developing
• External genitalia
gonococcal conjunctivitis. The commonly used
– Female infant
medications are one of the following:
Size and location of
- Labia, clitoris, urethral meatus, vaginal • Silver nitrate solution
opening • Erythromycin ointment 0.5%
– Male infant • Tetracycline ointment 1%
Presence of testes • Povidone–iodine solution 2.5%
Location of urethral meatus
Appearance of scrotum
– Ambiguous genitalia
itamin K
• Anus Prophylactic vitamin K is given intramuscularly
– Location to newborns shortly after birth to prevent vita-
– Patency (establish whether meconium min K–deficient bleeding, previously known as
passed) hemorrhagic disease of the newborn. Vitamin K
• Back should be given to all newborns as a single intra-
– Spinal curvature/symmetry muscular dose of 0.5–1 mg.
– Neural tube defect
– Deep sacral dimple (spina bifida occulta)
• Hips
mbilical cord care
– Test for congenital dislocation of the hip If the umbilical cord has been cut under asep-
• Central nervous system tic conditions, no further treatment is required.
– Level of alertness However, in underresourced areas, cord care helps
– Spontaneous motor activity in reducing neonatal morbidity and mortality due
– Tone to cord stump sepsis. Use of antiseptic agents
– Muscle strength (alcohol, silver sulfadiazine, or chlorhexidine) for
– Primitive reflex responses cord care is recommended in this situation.
CH 23_p320-331_v3.indd 325 17-07-2015 18:42:37

Care of the skin CQOOQPſPFKPIUUGGP

Vernix and blood should be gently wiped off. in the newborn
Bathing should be delayed till the baby’s tem-
perature stabilizes. The following are the common findings seen in
the newborn:
Meconium passage and • Hemangiomas (‘strawberry hemangioma’) are
voiding of urine seen around the eyes and nape of the neck.
They usually disappear within a year.
Using a rubber catheter, the patency of the anal • Mongolian spots are blue-black pigmented areas
canal and rectum should be checked in all neo- seen at the base of the back and on the buttocks.
nates. The baby usually passes meconium at These are common in dark-skinned babies and
birth or soon after. If meconium passage does normally disappear over the first year.
not occur by 48 hours, further evaluation is rec- • Urticaria of the newborn is most evident on
ommended. The color of the stools gradually Day 2 as a fluctuating, widespread erythema-
changes to yellow over the next few days. tous rash with a raised white/cream dot at the
The baby usually voids urine immediately center of a red flare, mostly apparent on the
after delivery. If urine is not passed by 48 hours, trunk. This disappears spontaneously without
evaluation is indicated. treatment.
• Miliaria may appear as either red, macular
Breastfeeding patches or superficial, clear vesicles that are
most marked on the forehead and around the
Breastfeeding should be initiated in the labor neck. It is associated with warm humid environ-
room as soon as the mother is made comfort- ments and will clear in cooler, drier conditions.
able. The mother should be advised regarding • Breast enlargement can be seen in both girls
the techniques for holding the baby, and should and boys; occasionally there might be secre-
be helped in having the baby latch on and begin tion of a small amount of milk. This occurs as a
proper sucking. Breastfeeding is discussed fur- result of circulating maternal hormones. It will
ther in Chapter 25, Lactation and breastfeeding. subside spontaneously.
• Milia or white pimples are seen on the nose
epatitis B vaccination and cheeks and are found in approximately
40% of newborns, due to blocked sebaceous
Universal vaccination of newborns, regardless of glands. These clear spontaneously.
maternal hepatitis B virus surface antigen (HBsAg) • Natal teeth can be present at birth. No action
status, is recommended. In addition to hepatitis B is required unless they are loose or abnormal,
vaccine (HBV), infants of HBsAg-positive moth- in which case they may have to be extracted..
ers should receive hepatitis B immunoglobulin • Accessory skin tags are often seen on the face as
(HBIG) shortly after birth, preferably within 12 accessory auricles anterior to the ears.
hours of birth. • Vestigial extra digits can usually be excised
easily.
epatitis B vaccine schedule
The schedule for Hepatitis B vaccine is as follows: %QOOQPTGƀGZGUQHVJG
• First dose 0.5 mL at birth newborn
• Second dose 0.5 mL at 1–2 months
The presence of the following reflexes is reassur-
• Third dose 0.5 mL at 6 months
ing and usually denotes an intact neurological
system.
epatitis B immunoglobulin
One dose of HBIG should be given within /QTQTGƀGZ
12 hours of birth (for infants of HBsAg-positive When newborns are startled, their arms and legs
mothers). swing out and forward with fingers outstretched.
CH 23_p320-331_v3.indd 326 17-07-2015 18:42:37

The Newborn 327
4QQVKPITGƀGZ Box 23.4 Conditions where the infant is likely to

When either side of the mouth is touched, new- require resuscitation
borns turn their head toward that side. This reflex • Maternal complications
enables newborns to find the nipple. Ŧ Advanced or very young maternal age
Ŧ Maternal diabetes mellitus or hypertension
5WEMKPITGƀGZ Ŧ 2TGXKQWUJKUVQT[QHUVKNNDKTVJHGVCNNQUUQTGCTN[PGQ-
When an object is placed in their mouth, new- natal death
borns begin sucking immediately. • Fetal factors
Ŧ Prematurity
Ŧ Postmaturity
ewborn metabolic Ŧ Congenital anomalies
Ŧ Multiple gestation
screening • Antepartum complications
Ŧ Placenta previa or placental abruption
Newborn metabolic screening is done to screen Ŧ Oligohydramnios or polyhydramnios
infants shortly after birth for metabolic condi- • Delivery complications
tions that are treatable, but not clinically evident Ŧ Abnormal fetal heart rate pattern
in the newborn period. Newborn screening tests Ŧ Instrumental delivery
Ŧ Cesarean delivery
are most commonly done from whole blood sam-
Ŧ Malpresentation
ples obtained from a heel prick and collected on
Ŧ Chorioamnionitis
specially designed filter paper. The infant should Ŧ Maternal administration of opioid <4 hours of birth
have been fed at least once. Usually the sample is
collected 2–4 days after birth.
The common disorders that are screened for 2. The infant requires some assistance in
are: breathing.
• Phenylketonuria 3. The infant requires prompt resuscitation.
• Congenital adrenal hyperplasia
• Congenital hypothyroidism Category 1
• Galactosemia
Category 1 comprises infants with the following
Other conditions screened for in high-risk characteristics:
populations are:
• Healthy term baby
• Cystic fibrosis • Cries within seconds
• Sickle cell anemia • Good tone and activity
• Heart rate of >100 bpm
• Rapidly turns pink
esuscitation of the
This baby only needs to be dry, wrapped in a
newborn towel, and handed over to the mother. Routine
When an infant is unable to make a smooth tran- neonatal examination can be performed accord-
sition to extrauterine life, it needs resuscitation. ing to hospital protocol.
Approximately 10% of infants will require some
form of intervention, and only 1% will require Category 2
major resuscitative efforts.
Category 2 comprises infants with the following
Certain high-risk pregnancies should alert the
characteristics:
obstetrician to anticipate the need for resuscita-
tion in the newborn. These factors are listed in • Not breathing regularly
Box 23.4. • Heart rate of >100 bpm
Immediately after delivery, infants are assessed • Centrally cyanosed
and placed into three categories. These are:
This baby needs to be rubbed dry, which
1. The infant can be left alone. might provide enough stimulation to induce
CH 23_p320-331_v3.indd 327 17-07-2015 18:42:37

breathing. The baby should be placed under a • Stimulation

heat source. Active resuscitation is needed if – Rub infant’s back
there is no response to these simple measures. – Gently slap or flick infant’s soles of feet
Subsequent resuscitative steps

Category 3 The subsequent resuscitative steps consist of the
Category 3 comprises infants with the following following:
characteristics:
• Supplemental oxygen
• Not breathing – Blended oxygen or room air recommended
• Heart rate of <100 bpm – 100% oxygen not recommended
• Pale • Positive pressure ventilation
• Poor tone/floppy – Required when
infant is gasping or apneic
This baby needs prompt resuscitation and heart rate is <100 bpm
will deteriorate without it. – Equipment
Bag-mask ventilation (BMV)
- 40–60 times/min for 30 seconds
esuscitative steps - Check heart rate
The ABCDs of resuscitation can be applied to the Continuous positive pressure ventilation
neonate, with some modification. (CPAP)
The 2010 American Heart Association (AHA)/ • Endotracheal intubation indicated if
American Academy of Pediatrics (AAP)/Inter- – BMV is ineffective or prolonged
national Liaison Committee on Resuscitation – chest compressions are being performed
(ILCOR) guidelines recommend the following – tracheal suctioning for meconium is required
approach: • Chest compression initiated if
– infant’s heart rate remains <60 bpm despite
• Initial steps (provide warmth, clear Airway if adequate ventilation for 30 seconds
necessary, dry, and stimulate) • Drugs
• Breathing (ventilation) – Used only if required
• Chest compressions – Epinephrine if heart rate <60 bpm
• Administration of Drugs, such as epinephrine – Naloxone not recommended
and/or volume expansion – Sodium bicarbonate no longer recommended
The guidelines for neonatal resuscitation are
Initial steps given in Figure 23.2.
The following are the initial steps:
• Provide warmth (avoiding hypothermia)
Discontinuing resuscitation
– Dry and wrap in cloth or towel Resuscitative procedures may be discontinued
– Ensure skin-to-skin contact with mother after 10 minutes of resuscitation if the neonate
and cover with blanket has demonstrated no signs of life:
– Polyurethane bags or wraps for infants
<1500 g • No heartbeat
– Raise room temperature (turn off air • No respiratory effort for >10 minutes
conditioning) The outcome in these infants is associated
– Use warming lamps/pads with high early mortality and unacceptably
• Airway severe motor and sensory disabilities.
– Place flat on back
– Neck in neutral or slightly extended position
– Suction secretions if required
oninitiation of resuscitation
Bulb syringe In some situations, resuscitation may not be
Mechanical suction device initiated because of the poor prognosis for the
CH 23_p320-331_v3.indd 328 17-07-2015 18:42:37

The Newborn 329
aluate cry
aluate muscle tone
aluate respirations
o respiratory effort e uate respiratory

asping effort
PPV
p monitoring
aluate H e ery secon s
CP ith PPV aluate color

PPV till H
consi er P P Continue
hen ongoing care
or CP P bser e an monitor
H persists at H top CP
V access
pinephrine
ntubation
Figure 23. 2 Algorithm for resuscitating the neonate. CPAPEQPVKPWQWURQUKVKXGCKTYC[RTGUUWTGCP ECTFKQRWNOQPCT[

TGUWUEKVCVKQP JGCTVTCVG KPVTCXGPQWUP PRQUKVKXGGPFGZRKTCVQT[RTGUUWTGPP RQUKVKXGRTGUUWTGXGPVKNCVKQP
Sp QZ[IGPUCVWTCVKQP
infant. This decision must be taken in consulta- the goal of reducing infant mortality rates by
tion with the parents. These conditions include promoting breastfeeding practices in hospitals,
the following: both in government and private sectors.
The initiative is a global effort for educating
• Gestational age <24 weeks
mothers about the benefits of breastfeeding
• Birth weight <500 g
and improving the role of maternity services to
• Anencephaly or other lethal anomaly
enable mothers to breastfeed babies for the best
• Chromosomal abnormalities incompatible with
start in life. Maternity services are encouraged
life
to protect, promote, and support breastfeeding.
– Trisomy 13 or 18
ecommendations of the BF I
Baby Friendly ospital Recommendations of the BFHI are as follows:
Initiative • Babies should be breastfed exclusively for the

first 6 months of life.
The Baby Friendly Hospital Initiative (BFHI) is • Breastfeeding should be initiated within 1 hour
a worldwide program launched in 1991 by the of birth. Early skin-to-skin contact between
World Health Organization (WHO) and UNICEF. mother and baby encourages this practice.
It was launched in India in 1993. It is considered • No prelacteal feeds (e.g., glucose water, honey,
one of the key interventions toward achieving plain water) should be given.
CH 23_p320-331_v3.indd 329 17-07-2015 18:42:38

• No supplemental feeds should be given, espe- • Eczema

cially formula. • Respiratory and ear infections
• Pacifiers or teats should not be used.
$GPGſVUQHDTGCUVHGGFKPI
Achieving the goals of the BF I for the mother
Achieving the goals of the BFHI requires the
Women who breastfeed have decreased risk of
following:
developing the following:
• Doctors and nurses should receive training in
• Metabolic syndrome (heart disease, hyperten-
breastfeeding practices.
sion, diabetes, high cholesterol)
• Breastfeeding practices should be taught in
• Breast cancer
the antenatal period.
• Ovarian cancer
• Adequate support should be received from
• Hip fractures in later life
lactational specialists/nurses to help women
with breastfeeding problems (see Chapter 25, The aim of BFHI is to increase the numbers of
Lactation and breastfeeding). babies who are exclusively breastfed worldwide,
• Rooming-in and demand feeding should be a goal which the WHO estimates could contrib-
encouraged. ute to avoiding >1 million child deaths each
year, and potentially many premature maternal
deaths as well.
Advantages of breastfeeding
for the infant
Studies have shown that breastfed babies are less
likely to suffer from the following:
• Gastroenteritis
• Asthma
Key points
• 6JGſTUVHGYDTGCVJUKPCPKPHCPVŏUNKHGCTGTGRTGUGPVC- VKQPQHXKVCOKP-WODKNKECNEQTFECTGCPFJGRCVKVKU$
tive of a profound and challenging mechanism that vaccination.
marks the remarkable transition from intrauterine to • Every newborn should be examined in the neonatal
extrauterine life.
RGTKQFCPFVJGIGPFGTQHVJGKPHCPVYGKIJVNGPIVJ
• The transition from intrauterine to extrauterine life is a and head circumference must be documented for the
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the infant’s life. The transition involves both pulmonary • 6JGKPHCPVUJQWNFJCXGCEQORNGVGGZCOKPCVKQP
and circulatory adaptation. CPFDQVJPQTOCNCPFCDPQTOCNſPFKPIUUJQWNFDG
• Surfactant is essential for normal breathing. It is documented.
produced in the fetal lungs by type II alveolar epithelial • 6JGRTGUGPEGQHVJGHQNNQYKPITGƀGZGUKUTGCUUWTKPI
EGNNUCNUQECNNGFRPGWOQE[VGU+VRTGXGPVUVJGCNXGQNK and usually denotes an intact neurological system:
HTQOEQNNCRUKPICHVGTVJG[JCXGGZRCPFGFYKVJVJGſTUV /QTQTGƀGZTQQVKPITGƀGZCPFUWEMKPITGƀGZ
few breaths.
• Newborn screening for hearing loss is important since
• The Apgar score is a quick screening test used world- hearing loss is one of the most common congenital
wide to assess the health of the newborn infant at anomalies and occurs in approximately 2–4 infants per
1 and 5 minutes after birth. 5-minute scores of 7 and 1000.
CDQXGCTGIGPGTCNN[EQPUKFGTGFPQTOCNŌNQYCPF
3 and below are generally regarded as critically low. • Newborn metabolic screening is done to screen infants
shortly after birth for metabolic conditions that are treat-
• (QNNQYKPIDKTVJVJGTQWVKPGECTGQHVJGPGYDQTP CDNGDWVPQVENKPKECNN[GXKFGPVKPVJGPGYDQTPRGTKQF
WUWCNN[KPENWFGURTQRJ[NCEVKEG[GECTGCFOKPKUVTC-
(Continued)
CH 23_p320-331_v3.indd 330 17-07-2015 18:42:38

The Newborn 331

• +OOGFKCVGN[CHVGTFGNKXGT[KPHCPVUCTGCUUGUUGFCPF • The subsequent steps in resuscitation include
placed into three categories. This helps determine UWRRNGOGPVCNQZ[IGPRQUKVKXGRTGUUWTGXGPVKNCVKQP
YJKEJKPHCPVECPDGNGHVCNQPGYJKEJKPHCPVTGSWKTGU GPFQVTCEJGCNKPVWDCVKQPYJGPTGSWKTGFEJGUVEQO-
UQOGCUUKUVCPEGKPDTGCVJKPICPFYJKEJKPHCPVTG- RTGUUKQPCPFFTWIUUWEJCUGRKPGRJTKPG
quires prompt resuscitation.
• 6JG$CD[(TKGPFN[*QURKVCN+PKVKCVKXG
$(*+KUEQPUKF-
• 0GQPCVCNTGUWUEKVCVKQPKPXQNXGU#$%&UKPKVKCNUVGRU ered one of the key interventions toward achieving the

RTQXKFGYCTOVJENGCTaKTYC[KHPGEGUUCT[FT[CPF goal of reducing infant mortality rates by promoting
UVKOWNCVGbTGCVJKPI
XGPVKNCVKQPchest compres- DTGCUVHGGFKPIRTCEVKEGUKPJQURKVCNUDQVJKPIQXGTP-
UKQPUCPFCFOKPKUVTCVKQPQH TWIUUWEJCUGRKPGRJ- ment and private sectors.
rine and/or volume expansion.
Self-Assessment
UJQWNFDGRNCEGFWPFGTCYCTOKPINCORIGPVNGUVKOWNK
Case-based questions UJQWNFDGIKXGPſTUV5GETGVKQPUUJQWNFDGUWEVKQPGF
and oxygen administered. Heart rate should be
Case 1 EQWPVGFCPFKHDRORQUKVKXGRTGUUWTGXGPVKNCVKQP
/TU0-COWNVKITCXKFCYCUFGNKXGTGFD[HQTEGRUCV KUTGSWKTGFYKVJDCICPFOCUM+HTGEQXGT[KUFGNC[GF
term. The baby did not cry at birth and was limp and pale. the baby should be intubated and ventilated.
1. How will you assess the condition of the baby?

2. How will you categorize a newborn in relation to Case 2
resuscitation?
1. Routine examination consists of history and documen-
3. What are the basic steps of resuscitation?
VCVKQPQHIGPFGTYGKIJVVGORGTCVWTGNGPIVJCPFJGCF
4. How will you resuscitate this baby? circumference. This should be followed by systematic
head-to-toe examination of all organs and systems.
Case 2 2. Routine newborn care consists of prophylactic eye
ECTGCFOKPKUVTCVKQPQHXKVCOKP-WODKNKECNEQTF
Mrs. MT had a vaginal delivery of a term baby that ECTGECTGQHVJGUMKPDTGCUVHGGFKPIEJGEMKPIHQT
breathed and cried immediately after birth. RCUUCIGQHOGEQPKWOCPFXQKFKPIQHWTKPGCPF
JGRCVKVKU$XCEEKPCVKQP
1. What routine examination will you do?
3. This is common in newborns and is due to maternal
2. What is routine newborn care? hormones. The condition will subside in a few days.
3. The baby had some milky discharge from the breast 4. Although the baby usually passes meconium and
on the third postnatal day. How will you counsel? XQKFUWTKPGYKVJKPCHGYJQWTUCHVGTDKTVJVJGRTQEGUU
4. The mother complained that the baby did not pass may take up to 48 hours. If rectal patency has been
meconium or urine for 6 hours after delivery. What EJGEMGFHWTVJGTGXCNWCVKQPECPYCKVVKNNJQWTU
will you do?
Sample questions
Answers
Case 1
1. What is Apgar score? How will you resuscitate a
1. $[PQVKPIVJGEQNQTTGURKTCVKQPOWUENGVQPGJGCTV newborn baby?
TCVGCPFET[CVCPFOKPWVGUCPFECNEWNCVKPI
Apgar score.
2. 0GYDQTPUECPDGRNCEGFKPVQECVGIQT[QT%CV- Short-answer questions
GIQT[PGGFUPQTGUWUEKVCVKXGOGCUWTGUECVGIQT[
TGSWKTGUYCTOVJCPFUVKOWNCVKQPCPFECVGIQT[ 1. Surfactant
requires prompt active resuscitation. 2. Care of a healthy newborn
3. 6JGUGCTGCKTYC[DTGCVJKPIEJGUVEQORTGUUKQPCPF 3. $CD[(TKGPFN[*QURKVCN+PKVKCVKXG
FTWIU
#$%&
4. This baby probably belongs to category 3. The baby
should be wiped dry and wrapped in a towel and
CH 23_p320-331_v3.indd 331 17-07-2015 18:42:38

Common Problems
24 of the Newborn
Case scenario
Mrs. KL, 27, delivered her baby at 35 weeks + 4 days. The baby developed
high levels of bilirubin on the second day of life. The parents were very
concerned and were anxious about the prognosis.
Introduction serious condition that may result in neurological

sequelae in the neonate.
The first 4 weeks are the most challenging period
in an infant’s life. During this time, the neonate eonatal or physiological
faces the highest mortality rate in all of childhood. aundice
The greatest risk occurs during the first few days
after birth. Management of neonatal problems is Newborn infants commonly develop a total
challenging and requires a trained neonatologist serum or plasma bilirubin level >1 mg/dL, which
and a well-equipped neonatal care facility. is the upper limit of normal for adults. This
results in neonatal jaundice. There is yellowish
discoloration of the skin and/or sclera due to the
deposition of unconjugated bilirubin. Neonatal
jaundice first becomes visible on the face and
Common metabolic forehead. Identification is aided by gentle pres-
disorders in the newborn sure on the skin (especially tip of the nose), since
blanching reveals the underlying color.
The risk of developing significant neonatal
eonatal aundice and jaundice is higher in male infants and preterm
hyperbilirubinemia infants.
Neonatal physiological jaundice results due
It is common for neonates to develop jaun-
to the following:
dice, which is the yellowish discoloration of
the skin and/or conjunctiva caused by biliru- • Since newborns have more red blood cells
bin deposition. Hyperbilirubinemia is a more (hematocrit between 50% and 60%) and fetal
CH 24_p332-345_v3.indd 332 17-07-2015 20:08:41

Common Problems of the Newborn 333
red blood cells have a shorter life span (approx-

Box 24.2 Signs suggestive of bilirubin-induced
imately 85 days) than those in adults, the rapid neurologic dysfunction
turnover of red blood cells produces more
bilirubin. • Intense yellow discoloration (lemon yellow or orange
yellow)
• The immature neonatal liver is unable to pro-
• Infant refuses feeds
cess bilirubin because of • Infant not rousable
– insufficient concentrations of the binding • Infant irritable, with a continuous, high-pitched cry
protein ligand in the hepatocytes and • Infant arches neck or body backward
– low activity of glucuronyl transferase, the
enzyme responsible for binding bilirubin
to glucuronic acid, making bilirubin water
soluble or conjugated. Causes of severe
hyperbilirubinemia
is actors or neonatal jaun ice
The important causes of pathologically high
The risk factors for neonatal jaundice are listed levels of bilirubin are listed in Box 24.3.
in Box 24.1.
Treatment of severe
yperbilirubinemia
hyperbilirubinemia
Hyperbilirubinemia or high levels of serum bil-
irubin, >25–30 mg/dL (in a term infant), are Therapeutic interventions for infants with
associated with an increased risk for bilirubin- hyperbilirubinemia include the following:
induced neurologic dysfunction (BIND). In • Improving the frequency and efficacy of
preterm infants, these sequelae can arise at levels breastfeeding
of 20 mg/dL. This occurs when bilirubin crosses • Phototherapy
the blood–brain barrier and binds to brain tissue. • Exchange transfusion
The chronic and permanent sequelae of BIND are
called kernicterus, a devastating chronic con- hototherapy
dition in which bilirubin-mediated irreversible The following points should be noted regarding
brain damage results in cerebral palsy and loss of phototherapy:
hearing. This is why neonates must be monitored
for hyperbilirubinemia. • Phototherapy acts principally by converting
Severe hyperbilirubinemia must be suspected bilirubin to lumirubin, which is more soluble
in the following cases: than bilirubin and is easily excreted into bile
and urine.
• Jaundice occurs in the first 24 hours.
• Effectiveness of phototherapy depends on the
• Total bilirubin is >15 mg/dL and continues
type of the light used, distance between the
to rise.
light and infant, and the exposed surface area
• Rate of rise of total bilirubin is >0.2 mg/dL/
of the infant.
hour.
• Lamps with output predominantly in the blue
• Jaundice in a term newborn after 2 weeks of age.
region of the spectrum (460–490 nm) are most
Signs of worsening jaundice that suggest
BIND and require immediate intervention are
enumerated in Box 24.2. Box 24.3 Causes of pathologically high levels
of bilirubin
Box 24.1 eonates at risk for developing aun- • ABO incompatibility (mother O blood group, baby
dice A or B blood group)
• Rh incompatibility (see Chapter 38, ed cell alloim-
• Infants of diabetic mothers muni ation)
• Preterm infants/low-birth-weight infants • )NWEQUGRJQURJCVG FGJ[FTQIGPCUG
)2& FGſ-
• Babies born at high altitudes ciency
• Breastfed infants • Hereditary spherocytosis/elliptocytosis
• Underfed infants • Sepsis
CH 24_p332-345_v3.indd 333 17-07-2015 20:08:41

effective. Fluorescent blue light or halogen

Box 24.4 eonates at risk for developing
white light is commonly used. hypoglycemia
• The baby is exposed to phototherapy wear-
ing only a diaper and an opaque blindfold to • Infants of diabetic mothers
• Preterm or low-birth-weight infants
shield the eyes.
• Growth-restricted infants
• Continuous phototherapy is recommended
• Infants with sepsis
for bilirubin levels of t20 mg/dL. Below this
level, phototherapy can be interrupted for
breastfeeding. isk factors for hypoglycemia
Exposure to early morning and late eve- Certain neonates are at risk for hypoglycemia
ning sunlight is useful for neonatal jaundice in (Box 24.4), and it is important to monitor their
under-resourced areas but is not effective for blood glucose levels.
severe hyperbilirubinemia.
Signs of hypoglycemia
change trans usion
Many infants remain asymptomatic and that is
Exchange transfusion is used to remove bilirubin why blood glucose levels should be monitored,
from the circulation in severe hyperbilirubin- especially in high-risk infants. The immediate
emia. The indications are as follows: consequences of prolonged or severe hypoglyce-
• Intensive phototherapy fails to bring down the mia are listed in Box 24.5.
bilirubin level
– Below 25 mg/dL in term infants Long-term consequences
– Below 20 mg/dL in preterm or very-low- of severe hypoglycemia
birth-weight infants
• Infants with signs of BIND Major long-term sequelae include neurologic
damage resulting in mental disability, recurrent
Rh incompatibility and ABO incompatibility seizure activity, developmental delay, and per-
are two of the more common reasons for per- sonality disorders.
forming exchange transfusion. With the advent
of anti-D prophylaxis, the incidence of exchange Management
transfusion has declined due to the decline in
Management of hypoglycemia involves the fol-
hemolytic disease of the newborn.
lowing measures:
Procedure
• Frequent feeds in asymptomatic infants
A double-volume exchange transfusion (160–180 • Parenteral glucose infusions in symptomatic
mL/kg) is performed with appropriately cross- infants
matched blood reconstituted from packed red
blood cells and fresh frozen plasma. This will
replace approximately 85% of the infant’s circu-
eonatal hypocalcemia
lating red blood cells. Hypocalcemia is defined as serum total cal-
cium concentration <8 mg/dL in term infants or
eonatal hypoglycemia
Box 24.5 Short-term consequences of prolonged
Transient low blood glucose levels are common or severe hypoglycemia
after birth as the continuous transplacental glucose
• Jitteriness/tremors
infusion from the mother is replaced by an inter-
• Hypotonia
mittent supply from feeds. Persistent or recurrent
• Changes in level of consciousness
hypoglycemia can result in neurologic sequelae. • Apnea/bradycardia
Neonatal hypoglycemia is the most common • Cyanosis
metabolic problem in newborns. It is defined as • Tachypnea
a plasma glucose level of • Poor feeding
• Hypothermia
• <30 mg/dL in the first 24 hours of life
• Seizures
• <45 mg/dL thereafter
CH 24_p332-345_v3.indd 334 17-07-2015 20:08:41

<7 mg/dL in preterm infants. Risk factors for gestation. The lesser the gestational age, the
hypocalcemia include the following: greater is the risk of RDS. The risk is the highest
in extremely preterm infants.
• Preterm infant
Though less common, RDS may also occur in
• Infant of diabetic mother
late preterm infants (34–36+6 weeks).
• Growth-restricted or low-birth-weight infant
Deficiency of pulmonary surfactant in an
• Perinatal asphyxia
immature lung is the main reason for preterm
Signs of hypocalcemia are similar to those for infants developing this condition. RDS can be a
hypoglycemia. In an infant with neonatal sei- major cause of morbidity and mortality in pre-
zures, serum calcium level should be included in term infants.
the workup.
Treatment is by a slow IV infusion of 10% cal-
Pathophysiology
cium gluconate. This is followed up with oral
calcium. Surfactant deficiency leads to the following:
• Higher surface tension in the alveoli
Common respiratory • Collapse of large portions of the lung
(atelectasis)
disorders of the newborn • Lung inflammation and respiratory epithelial
injury causing
Transient tachypnea – Pulmonary edema
– Increased airway resistance
of the newborn
In addition to the problems resulting from
Transient tachypnea of the newborn (TTN) is surfactant deficiency, there is hypoxemia due
a benign disorder that causes respiratory dis- to intrapulmonary and extrapulmonary right-
tress in the neonate. It occurs due to pulmonary to-left shunts. Extrapulmonary shunting occurs
edema resulting from delayed resorption and typically across the foramen ovale and patent
clearance of fetal alveolar fluid. The risk factors ductus arteriosus (PDA).
for TTN are listed in Box 24.6.
Transient tachypnea of the newborn presents
as tachypnea within 2 hours after delivery. The Signs of respiratory distress
infant has nasal flaring, intercostal and subcostal syndrome
retractions, and expiratory grunting. Symptoms
The signs of RDS in preterm infants are listed in
usually disappear after 12–24 hours, but may
Box 24.7.
persist for as long as 72 hours.
Management Diagnosis
Transient tachypnea of the newborn is a benign, The results of diagnostic tests include the
self-limited condition and management is sup- following:
portive. Supplemental oxygen may be required. • Chest X-ray
– Reticulogranular ground-glass appearance
espiratory distress syndrome – Air bronchograms
Respiratory distress syndrome (RDS) is a com-
mon problem in preterm infants of <34 weeks’
Box 24.7 Signs of respiratory distress syndrome
• Tachypnea
Box 24.6 isk factors for transient tachypnea
• 0CUCNƀCTKPI
of the newborn
• Use of accessory respiratory muscles
• Prematurity • Expiratory grunting
• Cesarean delivery • Intercostal, subxiphoid, and subcostal retractions
• Maternal diabetes • Cyanosis due to right-to-left intrapulmonary and
• Maternal asthma extrapulmonary shunting
CH 24_p332-345_v3.indd 335 17-07-2015 20:08:41

• Arterial blood gas measurement obstruction, air trapping and hyperdistention

– Hypoxemia of the alveoli occur. The gas that is trapped may
– High levels of CO2 as disease worsens rupture into the pleura (pneumothorax), medi-
astinum (pneumomediastinum), or pericardium
Treatment (pneumopericardium).
Exogenous surfactant replacement therapy is Sur actant ys unction

effective in reducing RDS mortality and mor- Meconium deactivates surfactant and may also
bidity in preterm infants. Both natural and inhibit surfactant synthesis. The end result is
synthetic surfactants are effective, but natural diffuse atelectasis.
surfactants have been shown to be superior to
synthetic preparations. Chemical pneumonitis
Continuous positive airway pressure (CPAP)
Enzymes, bile salts, and free fatty acids in meco-
is the preferred initial therapy for neonates with
nium irritate the airways and parenchyma,
respiratory distress. If CPAP fails, endotracheal
initiating a diffuse pneumonitis that may begin
intubation is performed and surfactant ther-
within a few hours of aspiration.
apy is administered. Surfactant therapy should
be administered within 30–60 minutes after
ulmonary hypertension
delivery.
Many infants with MAS have primary or second-
ary persistent pulmonary hypertension of the
Meconium aspiration newborn (PPHN) resulting from chronic in utero
syndrome stress. PPHN further contributes to the hypox-
emia caused by MAS.
In utero meconium passage usually results from The pathophysiology of MAS is summarized
fetal hypoxic stress. The most severe complica- in Box 24.8.
tion of this is aspiration of meconium-stained
amniotic fluid before, during, and after birth. The
diagnosis of meconium aspiration syndrome
(MAS) is made when there is neonatal respiratory Box 24.8 The pathophysiology of meconium
distress in the presence of meconium-stained aspiration syndrome
amniotic fluid. It is confirmed by characteristic • Airway obstruction
radiographic abnormalities. Meconium aspira- • Complete obstruction
tion syndrome can result in significant neonatal Ŧ Atelectasis
morbidity and mortality. Ŧ Partial obstruction
Routine infusion of warm, sterile saline to Air trapping and hyperdistention of alveoli
dilute the meconium in amniotic fluid (amnio- - Pneumothorax
- Pneumomediastinum
infusion) has not been shown to prevent MAS.
- Pneumopericardium
Suctioning of the infant above the vocal cords,
• Surfactant dysfunction
as soon as the head is delivered, is also currently Ŧ Meconium
not recommended in the presence of meconium- Deactivates surfactant
stained amniotic fluid. This procedure has not Inhibits surfactant synthesis
shown to decrease MAS. - Diffuse atelectasis
• Chemical pneumonitis
Pathophysiology Ŧ Caused by meconium which contains
enzymes
Meconium aspiration causes neonatal hypoxia bile salts
through the following pulmonary effects: free fatty acids
• Pulmonary hypertension
Air ay obstruction Ŧ PPHN
Meconium may completely obstruct the airways, Ŧ Worsens hypoxemia
resulting in atelectasis. When there is partial PP , persistent pulmonary hypertension of the newborn.
CH 24_p332-345_v3.indd 336 17-07-2015 20:08:41

Signs of MAS Bruising, petechiae,

Infants who develop MAS exhibit the following lacerations
signs of respiratory distress immediately after
Difficult deliveries and instrumental deliver-
birth:
ies may be associated with soft tissue injuries.
• Barrel-shaped chest Lacerations are the most common birth injury
• Rales and rhonchi on auscultation occurring during a cesarean section.
Diagnosis cular in uries

Diagnosis is made from the immediate onset
Minor injuries, in and around the eye, such as
of respiratory distress with a history of meconi-
retinal and subconjunctival hemorrhages, and lid
um-stained amniotic fluid at birth. The diagnosis
edema, are commonly encountered and resolve
is confirmed by the chest X-ray that demonstrates
spontaneously without affecting the infant.
the following:
• Streaky, linear densities
• Hyperinflated lungs with flattening of the Extracranial in uries
diaphragms The passage through the vaginal canal and the
• Diffuse patchy densities alternating with areas process of birth may result in swelling over the
of expansion head. Application of a vacuum cup for delivery
may also result in an asymmetrical swelling over
Management the head.
The three common causes of swelling over the
The approach to the management of MAS is newborn’s head are as follows:
listed in Box 24.9.
• Caput succedaneum
• Chignon
• Cephalhematoma
Common birth in uries
Minor or major birth injuries may occur during
Caput succedaneum
delivery. These may be due to the following A caput succedaneum is a subcutaneous, extra-
reasons: periosteal fluid collection with poorly defined
margins on the scalp over the neonatal head. It
• Fetal macrosomia
may occasionally be hemorrhagic. It is caused by
• Shoulder dystocia
the pressure of the presenting part of the scalp
• Fetal breech presentation
against the dilating cervix during labor. The
edema in caput succedaneum crosses the suture
• Cesarean delivery
lines (Fig. 24.1a). It may involve a large area of
• Maternal morbid obesity
the head or it may just be the size of a large egg.
Causes
Box 24.9 Management of meconium aspiration Causes include the following:
syndrome
• Mechanical trauma of the initial portion of the
• Maintenance of adequate oxygenation and ventilation
• Maintenance of adequate blood pressure and perfusion
scalp pushing against the undilated cervix
• Correction of hypoglycemia and acidosis • Prolonged or difficult delivery
• Empirical antibiotic therapy
• Minimal handling of the infant to anagement
Ŧ avoid agitation A caput succedaneum needs no treatment. The
Ŧ exacerbation of PPHN edema is gradually absorbed and disappears
PP persistent pulmonary hypertension of the newborn. within a few days.
CH 24_p332-345_v3.indd 337 17-07-2015 20:08:41

calp
Periosteum
ull
a.
Cephalhematoma
calp
Periosteum
ull
b.
Figure 24.1 Difference between caput succedaneum and cephalhematoma. a. Caput succedaneum showing the edematous
ƀWKFTCKUKPIVJGUECNRCPFETQUUKPIVJGUWVWTGNKPGb. Cephalhematoma is raising the periosteum and does not cross the
suture line.
Chignon delivery. It is not commonly associated with sig-

nificant blood loss.
A chignon is an iatrogenic caput succedaneum
that develops after the application of a vac- Causes
uum cup for delivery. It is an edematous swell-
Causes are as follows:
ing that develops due to the suction applied by
the vacuum cup to the scalp. It may take as lit- • Rupture of a periosteal capillary due to the
tle as 2 hours or as long as 2 weeks to resolve. A pressure of birth
chignon is associated with a higher incidence of • Instrumental delivery
neonatal jaundice.
anagement
The majority of cephalohematomas will resolve
Cephalhematoma
spontaneously in a few weeks without any inter-
Cephalhematoma is a collection of blood under vention. Occasionally, calcification of the hema-
the periosteum of the skull. It is estimated to toma can occur with a subsequent bony swell-
occur in 1%–2% of all deliveries and is much ing that may persist for months.
more common when forceps or vacuum delivery Resorption of the blood from a large cephal-
is performed. hematoma may cause hyperbilirubinemia.
The swelling does not cross suture lines (Fig. The differences between a caput succe-
24.1b). It may or may not be accompanied by daneum and a cephalhematoma are illustrated
discoloration and usually does not expand after in Figure 24.1 and enumerated in Table 24.1.
Table 24.1 Differences between caput succedaneum and cephalhematoma
Presentation Caput succedaneum Cephalhematoma

Location Above the periosteum Subperiosteal
Extent of involvement One or both hemispheres Usually occipital or parietal bone
Relation to suture line Crosses the suture lines Does not cross the suture lines
Period of absorption 3–4 days Few weeks
Treatment None Supportive
CH 24_p332-345_v3.indd 338 17-07-2015 20:08:41

eurologic in uries Fractures

Brachial plexus injury and facial nerve injury Fractures are uncommon in modern obstetrics.
are neurologic injuries that can occur in the However, they may occur in difficult vaginal
newborn. deliveries. Four of the more common fractures
are described here.
Brachial plexus in ury
Brachial plexus injury is rare, although among
Clavicular fractures
neonatal neurologic birth injuries, it is one of the Clavicular fractures are the most commonly
most common. The only established risk factor for reported fractures in neonates. They can occur
neonatal brachial plexus palsy (NBPP) is shoulder in the following conditions:
dystocia. It occurs when there is excessive lateral • Shoulder dystocia
traction on the fetal head. There are no proven • Instrumental delivery
measures that can predict or prevent NBPP. The • Macrosomia
clinical classification of NBPP is given in Box 24.10.
Clavicular fractures in infants heal sponta-
neously with no long-term sequelae.
Facial nerve in ury Symptoms of neonatal clavicular fracture are
Facial nerve injury is usually due to traumatic enumerated in Box 24.12.
compression of the nerve by
umeral fractures
• forceps or
• prominent maternal sacral promontory (rare). Humeral fractures are rare. They may occur with
the following:
Commonly, only the mandibular branch of
the facial nerve is affected. The clinical features • Shoulder dystocia
of facial palsy are listed in Box 24.11. • Macrosomia
Traumatic facial nerve palsy has an excellent • Cesarean delivery
outcome. Spontaneous resolution usually occurs • Breech delivery
within the first 2 weeks of life. After radiographic confirmation, treatment
of humeral fractures consists of immobilization
of the affected arm with the elbow in 90 degrees
Box 24.10 %
NKPKECNENCUUKſECVKQPQHPGQPCVCN
brachial plexus palsy flexion to prevent rotational deformities.
• Upper brachial plexus palsy (Erb’s palsy) Femoral fractures

Ŧ Involves injury to C5, C6, and occasionally C7
Ŧ C5 and C6 injury Fractures of the femur as a result of birth trauma
Adduction and internal rotation of the arm are very rare. They may occur during delivery of
Forearm extension twins or in breech presentation.
Ŧ C7 additionally involved
Flexion of wrists and fingers in addition to the Skull fractures
above features
• Total brachial plexus palsy (not common) Skull fractures as a result of birth trauma are
Ŧ Involves all the roots from C5 to T1 usually depressed skull fractures. These are often
Arm paralysis associated with forceps-assisted deliveries.
Box 24.11 Clinical features of facial palsy Box 24.12 Symptoms of neonatal clavicular
fracture
• Diminished movement on affected side of the face
• Loss of nasolabial fold • Crepitus and edema over affected clavicle
• Partial closing of eye • Lack of movement of affected extremity
• Inability to contract lower facial muscles on affected side • Asymmetrical bone contour
• Mouth being drawn over to unaffected side when crying • Crying with passive motion
CH 24_p332-345_v3.indd 339 17-07-2015 20:08:41

Complications of incidence of PDA in preterm infants may be

explained by the effect of prematurity and may
prematurity in the neonate also be precipitated by RDS.
In infants with a PDA, the left-to-right
Complications resulting from prematurity con- shunting of blood results in an excessive blood
tribute to the higher rate of infant mortality and flow through the pulmonary circulation and
morbidity in preterm infants, compared with that hypoperfusion of the systemic circulation.
in infants born at term. The greater the immatu- The physiological consequences of the shunt-
rity, the greater is the risk of complications. ing depend on the size of the shunt and the
Complications of the premature infant are response of the heart, lungs, and other organs to
listed in Box 24.13. the shunt. Moderate-to-large shunts may result
in the following:
ypothermia • Pulmonary edema and hemorrhage
The low-birth-weight premature infant is sus- • Bronchopulmonary dysplasia
ceptible to hypothermia. Hypothermia is man- • Decreased perfusion and oxygen delivery to
aged by drying and wrapping the baby in cloth end-organs
or towel, skin-to-skin contact with the mother The treatment modalities for PDA are summa-
and covering with blanket, polyurethane bags, rized in Box 24.14.
or wraps in infants <1500 g (very effective in
developing countries), raising room tempera-
ture (turn off air-conditioning), and the use of Intraventricular hemorrhage
warming lamps/pads. Intraventricular hemorrhage is an important
cause of brain injury in premature infants. It
espiratory distress syndrome occurs most frequently in infants born before
32 weeks’ gestation or <1500 g birth weight.
It is the result of low levels of surfactant in the Improved survival of extremely premature
premature lung. It is discussed in greater detail infants has resulted in a greater number of
in the section Common respiratory disorders of survivors with this condition, and, therefore, a
the newborn. greater number of infants with neurodevelop-
mental disabilities.
Patent ductus arteriosus In preterm infants, hemorrhage is primarily
within the capillary network, which freely commu-
Ductal closure is delayed in preterm infants nicates with the venous system, although bleeding
(see Transition from intrauterine to extrauter- can also occur from the arterial circulation.
ine life in Chapter 23, The newborn). The higher
Severity and grading of I

Box 24.13 Short-term and long-term
complications of the premature infant Severity of hemorrhage is based on the extent of
spread into the adjacent ventricular system or
• Short-term complications in the neonatal period white matter (intraparenchymal). The following
Ŧ Hypothermia
Ŧ Respiratory distress syndrome
Ŧ Patent ductus arteriosus
Ŧ Intraventricular hemorrhage
Box 24.14 Treatment modalities for PDA
Ŧ Hypoglycemia • Medical intervention
Ŧ Necrotizing enterocolitis Ŧ Indomethacin
Ŧ Infection Ŧ Ibuprofen
Ŧ Retinopathy of prematurity PDA closes within 24 hours of administration
• Long-term sequelae in neonates who survive and are • Surgical ligation
discharged from the neonatal intensive care unit Ŧ When medical therapy fails
Ŧ Neurodevelopmental disabilities such as cerebral Ŧ Large PDA
palsy
PDA, patent ductus arteriosus.
CH 24_p332-345_v3.indd 340 17-07-2015 20:08:41

grading system is used to define the extent of

Box 24.15 Clinical presentations of I
bleeding:
• Silent
• Grade I: Bleeding is confined to the germinal Ŧ 25%–50% of cases of IVH
matrix. Ŧ Diagnosed only on routine ultrasonography
• Grade II: IVH occupies 50% or less of the lateral • Saltatory or stuttering course
ventricle volume. Ŧ Most common presentation
• Grade III: IVH occupies >50% of the lateral Ŧ Evolves over hours to several days.
ventricle volume. Ŧ Associated with
• Grade IV: Hemorrhagic infarction in periven- altered level of consciousness
tricular white matter ipsilateral to large IVH. hypotonia
decreased spontaneous and elicited movements
subtle changes in eye position and movement
Diagnosis • Catastrophic
Cranial ultrasonography is the most sensi- Ŧ Uncommon presentation
tive diagnostic modality for IVH. Coronal and Ŧ Can deteriorate over minutes to hours
Ŧ Infant may have
parasagittal views are performed to identify
stupor or coma
blood in the germinal matrix, ventricles, or
generalized seizures, especially tonic seizures
cerebral parenchyma, and any other echogenic irregular respirations, hypoventilation, or apnea
abnormalities. Ultrasonography can accurately cranial nerve abnormalities
grade the severity of IVH. Since 25%–50% of the decerebrate posturing
IVH cases are clinically silent, routine ultra- flaccid weakness
sound screening should be performed in pre- bulging anterior fontanel
mature infants. circulatory failure
metabolic acidosis
Clinical presentation , intraventricular hemorrhage.
The various clinical presentations of IVH are – Preservation of cerebral blood flow
given in Box. 24.15. • Adequate oxygenation and ventilation
– Avoidance of hypocarbia, hypercarbia, and
Prevention of I acidosis
• Appropriate fluid, metabolic, and nutritional
Antenatal corticosteroi s support
Antenatal corticosteroids given before preterm • Treatment of seizures
birth reduce the risk of IVH.
Delaye clamping o the umbilical cor Sequelae

A delay of 30–60 seconds in umbilical cord Posthemorrhagic hydrocephalus (PHH), periven-
clamping is associated with up to 50% reduction tricular hemorrhagic infarction, and periventric-
in IVH in preterm infants. ular leukomalacia are major sequelae of IVH.
In utero trans er to tertiary center osthemorrhagic hy rocephalus

Premature infants whose mothers are trans- PHH is the major complication of IVH. Serial
ported to a tertiary center prior to delivery are studies with weekly cranial ultrasound can help
less likely to have IVH than similar infants who detect early asymptomatic PHH. Other assess-
are transported after delivery, because of prompt ments include daily head measurement and
management. monitoring for signs and symptoms of increased
intracranial pressure (relatively uncommon).
Management
Management to decrease the consequences of ecroti ing enterocolitis
IVH includes the following:
Necrotizing enterocolitis (NEC) is one of the
• Maintenance of arterial perfusion most common gastrointestinal emergencies in
– Avoidance of hypotension or hypertension the preterm neonate. The incidence is highest
CH 24_p332-345_v3.indd 341 17-07-2015 20:08:41

(approximately 6%–7%) in very-low-birth-weight Management

infants (<1500 g).
e ical management
Pathogenesis Medical management consists of discontinuation
of enteral feeds, parenteral nutrition, and correc-
Necrotizing enterocolitis occurs in low- tion of metabolic and hematologic abnormali-
birth-weight premature infants after starting ties. Antibiotic therapy is initiated with a course
milk feeds. The terminal ileum and colon are of parenteral antibiotics that cover a broad range
involved in the majority of cases. of aerobic and anaerobic intestinal bacteria.
The majority (90%) of cases occur following
initiation of milk feeds. Immaturity of the gastro- Surgical management
intestinal tract in premature infants predisposes
Surgical management is indicated only when
to NEC because of the following:
there is an intestinal perforation or extensive
• Impaired mucosal defense necrosis.
• Impaired intestinal motility and function
– Microbial overgrowth inflammation
– Ischemia and gangrenous necrosis of intes-
etinopathy of prematurity
tinal mucosa Retinopathy of prematurity (ROP) is a potentially
blinding eye disorder that primarily affects pre-
Clinical presentation mature infants weighing <1500 g or of <32 weeks’
gestation. The incidence and severity of ROP
NEC may present with both nonspecific systemic increase with decreasing gestational age and
signs and abdominal signs. The signs of NEC are birth weight. This disorder is usually bilateral
enumerated in Box 24.16. and is one of the most common causes of visual
loss in childhood and can lead to lifelong vision
Diagnosis impairment and blindness.
Diagnosis is based on the clinical signs of

abdominal distension and rectal bleeding.
Pathogenesis
Abdominal X-ray will show the following: Retinopathy of prematurity is a developmental
proliferative vascular disorder that occurs in the
• Dilated loops of bowel consistent with ileus, in
retina of preterm infants with incomplete retinal
the early stages of NEC
vascularization.
• Pneumatosis intestinalis, which is the hall-
Neovascularization then involves the entire
mark of NEC, appears as bubbles of gas in the
retina. Hypotension, hypoxia, or hyperoxia, with
small bowel wall, and is seen in the later stages
free radical formation, affects these newly form-
of NEC
ing vessels. These abnormal blood vessels are
fragile and can leak, scarring the retina, and can
lead to retinal detachment. Retinal detachment
Box 24.16 The clinical signs of necroti ing is the leading cause of visual impairment and
enterocolitis blindness in ROP.
• 0QPURGEKſEU[UVGOKEUKIPU High levels of oxygen given to preterm infants
Ŧ Apnea have been implicated in the pathogenesis of ROP.
Ŧ Respiratory failure It is therefore important not to use 100% oxygen
Ŧ Poor feeding for resuscitation.
Ŧ Lethargy, or temperature instability
• Abdominal signs
Ŧ Abdominal distension
Management
Ŧ Gastric retention All premature infants must be screened for ROP,
Ŧ Tenderness 4–6 weeks after birth.
Ŧ Vomiting
Ninety percent of infants with ROP have only
Ŧ Rectal bleeding
the mild degree of disease and will recover sponta-
Ŧ Diarrhea
neously. The infants with severe degree of disease
CH 24_p332-345_v3.indd 342 17-07-2015 20:08:42

will require ablation of the peripheral avascular Management

retina, usually by laser photocoagulation.
The supportive management of moderate and
severe neonatal encephalopathy should take
eonatal sei ures place in an NICU.
Management of HIE is summarized in Box
The occurrence of neonatal seizures may be the 24.18.
first clinical sign of a central nervous system
(CNS) disorder in the neonate. Seizures may be
the indication of a potentially treatable etiology. Metabolic causes of sei ures
Immediate evaluation for the cause will help in Metabolic etiologies include the following:
instituting specific therapy.
There is a high incidence of early death asso- • Hypocalcemia
ciated with neonatal seizures. Survivors have a • Hypoglycemia
greatly increased risk of the following: These disorders are discussed earlier in this
• Neurologic impairments chapter.
• Developmental delay
• Postneonatal epilepsy Inborn errors of metabolism
Although neonatal seizures may have mul- Inborn errors of metabolism, for example,
tiple etiologies (Box 24.17), the causes can be aminoacidurias, urea cycle defects, or organic
broadly classified as follows: acidurias, may result in neonatal seizures. These
• Hypoxic-ischemic encephalopathy (HIE) disorders should be suspected when seizures do
• Metabolic disturbances not respond to conventional treatment and are
• CNS or systemic infections associated with progressive clinical and electro-
• Neonatal epileptic syndromes encephalographic worsening.
ypoxic-ischemic Infections
encephalopathy Bacterial meningitis is an important cause of
Hypoxic-ischemic encephalopathy (see Chapter neonatal seizures. Fever associated with irrita-
17, Intrapartum fetal surveillance) is the most bility, seizures, and poor feeding should raise a
common cause of neonatal seizures. The seizures suspicion of bacterial meningitis.
usually occur within the first 1–2 days of birth. Infections occurring in the first 3–6 days after
Neonatal seizures with HIE can be anticipated birth, and especially those in the first 2 days after
with the following: birth, are usually vertically transmitted from the
maternal genital tract flora. Late-onset infec-
• Apgar score <5 at 5 minutes tions occurring after the first week of life suggest
• Umbilical cord pH <7.0 nosocomial (hospital-acquired) or community-
• Intubation required in the delivery room acquired infections.
Box 24.17 Common etiologies of neonatal

sei ures Box 24.18 Management of hypoxic-ischemic
encephalopathy
• Hypoxic-ischemic encephalopathy
• Metabolic disturbances • Therapeutic hypothermia
Ŧ Hypocalcemia Ŧ +PVJGſTUVJQWTUCHVGTDKTVJ
Ŧ Hypoglycemia Ŧ Treatment of choice
Ŧ Hypomagnesemia • Maintenance of adequate ventilation
Ŧ Inborn errors of metabolism • Avoidance of systemic hypotension or hypertension
• Central nervous system infection • Maintenance of normal metabolic status
Ŧ Bacterial meningitis • Control of seizures
• Neonatal epileptic syndromes • Control of brain edema
CH 24_p332-345_v3.indd 343 17-07-2015 20:08:42

Neonatal risk factors for developing meningi- • Third-generation cephalosporin (e.g., ceftriax-
tis include the following: one or cefotaxime)
• Low birth weight However, resistance to commonly used antibi-
• Prematurity otics is now a global problem. Most gram-negative
• Prelabor rupture of membranes bacilli are now resistant to ampicillin and increas-
• Prolonged rupture of membranes (>18 hours) ingly to gentamicin.
• Maternal chorioamnionitis Further antibiotic management depends
• Low socioeconomic status on the culture and sensitivity reports from the
cerebrospinal fluid obtained from a spinal tap.
Pathogens causing meningitis in develop-
ing countries differ from the ones in developed
countries. The pathogens more commonly iden- eonatal epileptic
tified within developing countries, including
India, are as follows:
syndromes
Neonatal epileptic syndromes are rare. Four
• Gram-negative bacilli (excluding E. coli)
distinct neonatal epileptic syndromes have been
• Streptococcus pneumoniae
described:
• S. aureus
• Hemophilus influenza • Benign neonatal convulsions
• Klebsiella pneumoniae • Benign neonatal familial convulsions
• Early myoclonic encephalopathy
Management • Early infantile epileptic encephalopathy
In developing countries, the World Health Antiepileptic drugs, particularly phenobarbi-

Organization (WHO) recommends initial antibi- tal, phenytoin, and benzodiazepines, are used in
otic therapy with either of the following: the management of these cases.
• Ampicillin and an aminoglycoside (e.g.,

gentamicin)
Key points
• 6JGſTUVYGGMUCTGVJGOQUVEJCNNGPIKPIRGTKQFKP • Neonatal hypoglycemia is the most common meta-
an infant’s life. DQNKERTQDNGOKPPGYDQTPU+VKUFGſPGFCUCRNCUOC
• Neonatal physiological jaundice results from rapid INWEQUGNGXGNQHOIF.KPVJGſTUVJQWTUQHNKHG
turnover of fetal red blood cells and the inability of the and <45 mg/dL thereafter.
immature liver to metabolize the bilirubin. • *[RQECNEGOKCKUFGſPGFCUUGTWOVQVCNECNEKWO
concentration <8 mg/dL in term infants or <7 mg/dL
• Severe hyperbilirubinemia with serum bilirubin levels
in preterm infants. Risk factors for hypocalcemia
>25–30 mg/dL is associated with an increased risk for
include preterm infant, infant of diabetic mother,
bilirubin-induced neurologic dysfunction (BIND). The
growth-restricted or low-birth-weight infant, and perina-
chronic and permanent sequelae of BIND result in
tal asphyxia.
kernicterus.
• The important causes of pathologically high levels of • Common respiratory disorders of the newborn include
bilirubin are ABO incompatibility, Rh incompatibility, transient tachypnea of the newborn, respiratory dis-
INWEQUGRJQURJCVGFGJ[FTQIGPCUGFGſEKGPE[JG- tress syndrome, and meconium aspiration syndrome.
reditary spherocytosis/elliptocytosis, and sepsis. • Common birth injuries include bruising, petechiae,
lacerations, ocular injuries, extracranial injuries, neuro-
• Phototherapy acts principally by converting bilirubin to
logic injuries, and fractures.
lumirubin, which is more soluble than bilirubin and is
easily excreted into the bile and urine. • Complications resulting from prematurity contribute
• Exchange transfusion is used to remove bilirubin from to the higher rate of infant mortality and morbidity in
the circulation in severe hyperbilirubinemia. preterm infants.
(Continued)
CH 24_p332-345_v3.indd 344 17-07-2015 20:08:42


• Complications of the premature infant are divided der in the neonate. Seizures may be the indication of a
into short-term complications (hypothermia, RDS, potentially treatable etiology. Immediate evaluation for
patent ductus arteriosus, intraventricular hemorrhage, VJGECWUGYKNNJGNRKPKPUVKVWVKPIURGEKſEVJGTCR[
hypoglycemia, necrotizing enterocolitis, infection, and
• Although neonatal seizures may have multiple etiolo-
retinopathy of prematurity) and long-term sequelae
IKGUVJGECWUGUECPDGDTQCFN[ENCUUKſGFCUJ[RQZKE
(cerebral palsy).
ischemic encephalopathy, metabolic disturbances,
• 6JGQEEWTTGPEGQHPGQPCVCNUGK\WTGUOC[DGVJGſTUV CNS or systemic infections, and neonatal epileptic
clinical sign of a central nervous system (CNS) disor- syndromes.
Self-Assessment
condition in which bilirubin-mediated irreversible brain
Case-based questions damage results in cerebral palsy and loss of hearing.
4. Exchange transfusion is indicated when intensive
Case 1 phototherapy fails or the infant exhibits signs of BIND.
Mrs. KL, 27, delivered her baby at 35+4 weeks. The baby
weighed 1.6 kg. It developed high levels of bilirubin on the
second day of life. The parents were very concerned and
Case 2
were anxious about the prognosis. 1. A history of birth asphyxia and family history of epilepsy
should be asked for. Blood glucose and calcium levels
1. What is the reason in this case for neonatal jaundice?
should be obtained because she is a diabetic and the
2. What would be the initial treatment for the hyperbili- infant could have low levels of glucose or calcium.
rubinemia?
2. Hypoglycemia: plasma glucose level of <30 mg/dL
3. What are the consequences of high levels of bilirubin? KPVJGſTUVJQWTUQHNKHGCPFOIF.VJGTGCHVGT
4. What are the indications for exchange transfusion? Hypocalcemia: serum total Ca concentration <8 mg/
dL in term infants or <7 mg/dL in preterm infants.
3. Parenteral glucose infusions should be started im-
Case 2 mediately in the case of hypoglycemia and followed
Mrs. BV, 32, a known diabetic on insulin, delivered at with frequent feeds. Treatment of hypocalcemia is by
37 weeks. On the second day of life, the baby developed a slow IV infusion of 10% calcium gluconate. This is
seizures. followed up with oral calcium.
4. Other causes of neonatal seizures: hypoxic-ischemic
1. How would you investigate the baby? encephalopathy, CNS or systemic infections, and
2. &GſPGJ[RQIN[EGOKCCPFJ[RQECNEGOKCKPVJG neonatal epileptic syndromes.
neonate.
3. What is the management for hypoglycemia and
hypocalcemia? Sample questions
4. What are the other causes of neonatal
seizures? Long-answer questions
1. What is physiological jaundice? Enumerate the
Answers causes and management of hyperbilirubinemia.
2. What is respiratory distress syndrome? Discuss
Case 1 prevention and treatment of RDS.
3. What are the complications associated with
1. The baby is preterm and low birth weight. The im- prematurity?
mature liver is unable to metabolize the bilirubin
produced by the rapid turnover of RBCs.
2. Phototherapy would be the initial treatment. It acts Short-answer questions
principally by converting bilirubin to lumirubin, which
1. Cephalhematoma
is more soluble than bilirubin and is easily excreted
into bile and urine. 2. Caput succedaneum
3. Hyperbilirubinemia is associated with an increased 3. Physiological jaundice
risk for bilirubin-induced neurologic dysfunction 4. Neonatal convulsions
(BIND). The chronic and permanent sequelae of 5. Meconium aspiration syndrome
BIND are called kernicterus, a devastating chronic 6. Prematurity
CH 24_p332-345_v3.indd 345 17-07-2015 20:08:42

Lactation and
25 Breastfeeding
Case scenario
Mrs. AS, 23, had a cesarean section 3 days ago. She had been trying to
breastfeed but felt that the baby was not getting enough milk. She and
her family were anxious that the baby may not be receiving the nutri-
tion it needed.
Introduction Anatomy and development

It is clearly established that breast milk is the of the breast
best form of nutrition for neonates and infants.
Breast milk has unique properties and is com- The breast is made up of many lobules, and
posed of a combination of nutrients essential to each lobule consists of alveoli drained by duct-
a child’s health. In the first 6 months, the baby ules. The ductules unite to form lactiferous
should be nourished exclusively by breast milk. ducts. The ducts converge to open at the nipple.
It is recommended that mothers breastfeed for Proximal to the opening, they dilate to form lac-
at least the first year of a child’s life. tiferous sinuses where milk is stored (Fig. 25.1).
Human milk provides a diverse array of bioac- The space between the glandular tissue is filled
tive substances during critical periods of devel- with fat. Estrogen stimulates development of
opment of the brain, immune system, and gut in the ductal system of the breast, whereas pro-
the growing infant. Obstetricians and other care- gesterone is responsible for the alveolar devel-
takers play a crucial role in facilitating the moth- opment. Together, the two hormones facilitate
er’s success in lactation. Not only is lactation the formation of the adult breast. Full alveolar
important for infant nutrition, it also influences development and maturation occurs only with
bonding between mother and newborn. hormonal changes in pregnancy.
CH 25_p346-354_v3.indd 346 17-07-2015 19:13:38

Lactation and Breastfeeding 347
Box 25.1 Mammogenesis

• Breast growth
• Size and weight increase
• Increased volume due to
uctule
Ŧ Development and proliferation of secretory tissue
uct
• Estrogen
l eoli Ŧ Ductal development
• Progesterone
reola Ŧ Alveolar development
Lactiferous
sinus
pregnant breast that transform it into an organ
capable of lactation. There are three stages of
lactogenesis.
Figure 25.1 Anatomy of the breast. Stage 1 or secretory initiation (occurs by
midpregnancy)
• The mammary glands become sufficiently dif-
ferentiated and become capable of secreting
The physiology of lactation milk. Women may notice drops of colostrum on
During pregnancy, changes occur in the breast their nipples in the second or third trimester.
(mammogenesis) that prepare it for the secre- • Lactose, total protein, and immunoglobulin
tion of milk (lactogenesis) followed by the estab- concentrations increase within the secreted
lishment and maintenance of milk secretion glandular fluid.
(galactopoiesis or lactation). After breastfeed- • Sodium and chloride concentrations decrease.
ing has been stopped, involution occurs. • High circulating levels of progesterone and
estrogen inhibit the secretion of milk.
Stage 2 or secretory activation (after delivery)

Mammogenesis
• It is defined as the onset of copious milk
Mammogenesis includes the following changes secretion.
in the breast: • In the majority of women, this occurs 2–3 days
• Mammary (breast) growth occurs. The size postpartum.
and weight of the breast increase. • There is swelling of the breasts and secretion
• The increased volume of breast tissue during of colostrum until this stage begins.
pregnancy results from the development and • Blood flow in the breasts increases.
proliferation of secretory tissue. • This stage is triggered by the rapid decline
• Hormonal changes of pregnancy promote in progesterone that follows delivery of the
alveolar development and maturation of the placenta.
epithelium. • Elevated levels of prolactin, cortisol, and insu-
• Progesterone plays an important role in stimu- lin play an important role.
lating alveolar development during this phase.
Stage 3 or galactopoiesis lactation
Mammogenesis is summarized in Box 25.1.
The stage of galactopoiesis begins 4–6 days
postpartum. Milk production continues at the
established rate during this period till weaning
Lactogenesis is started.
In lactogenesis, the breasts develop the capa- The stages of lactogenesis are summarized in
city to secrete milk. Processes occur in the Box 25.2.
CH 25_p346-354_v3.indd 347 17-07-2015 19:13:38

Box 25.2 Stages of lactogenesis *QTOQPCNKPƀWGPEG

• Stage 1 or secretory initiation on lactation
Ŧ Mammary glands differentiate
Ŧ Colostrum produced
For the continuing synthesis and secretion of
Ŧ Increase in human milk, the mammary gland responds to
lactose hormonal signals. Stimulation of the nipple and
total protein areola during suckling sets off these signals. The
immunoglobulins signals are then relayed to the central nervous
Ŧ Decrease in system. This cyclical process of milk synthesis
sodium and chloride and secretion is termed lactation.
Ŧ High levels of estrogen and progesterone The following two hormones are essential for
inhibit milk secretion the initiation and maintenance of lactation:
• Stage 2 or secretory initiation
Ŧ Onset of milk secretion • Prolactin
Ŧ Occurs 2–3 days postpartum • Oxytocin
Ŧ $NQQFƀQYKPDTGCUVKPETGCUGU
Ŧ Triggered by Prolactin and oxytocin act independently
drop in progesterone level on different cellular receptors, but their com-
elevated levels of prolactin, cortisol, insulin bined actions are critical for successful lacta-
• Stage 3 or galactopoiesis/ lactation tion (Fig. 25.2).
Ŧ Begins 4–6 days postpartum
Ŧ Milk production continues till weaning
oun of chil s cry
ytocin
Hypothalamus synthesi e
Para entricular nucleus
upraoptic nucleus
opamine
inhibition remo e
scen ing sensory

nterior information
pituitary
Prolactin Posterior
pituitary
ytocin store
Prolacting le el
increase
ytocin le el
increase
Mil synthesis in
Mil ejecte
mammary glan s
aby suc ling
Figure 25.2 *QTOQPCNKPƀWGPEGQPNCEVCVKQP6JGUQWPFQHVJGDCD[ŏUET[TGOQXGUVJGRTQNCEVKPKPJKDKVQT[HCEVQTU

(dopamine). Prolactin levels increase and lead to milk synthesis. Suckling sends afferent impulses to the hypothalamus
and oxytocin is synthesized. Impulses to the posterior pituitary release the stored oxytocin that stimulates ejection of milk.
CH 25_p346-354_v3.indd 348 17-07-2015 19:13:39

Box 25.3 Characteristics of prolactin egulation of milk

• Polypeptide hormone from anterior pituitary
• Synthesized by lactotrophic cells
synthesis
• Structurally similar to The regulation of milk synthesis is an efficient
Ŧ growth hormone mechanism. The actual volume of milk secreted
Ŧ human placental lactogen
may be adjusted to the requirement of the infant
• Acts on prolactin receptors in epithelial cells
by feedback inhibitor of lactation, a local factor
• Stimulates secretion of milk
• Under inhibitory control of hypothalamus through
secreted into the milk. The rate of milk synthe-
dopamine sis is related to the degree of breast emptiness
• +PJKDKVKQPTGOQXGFD[VJGUQWPFQHDCD[ŏUET[ or fullness.
• Increased suckling of the hungry infant, lead-
ing to increased emptying of the breast, is
Prolactin associated with increased milk volume.
• If the breast remains full due to decreased
Prolactin is the most important hormone for interfeeding intervals, breast milk production
continued lactation. The characteristics of pro- is decreased.
lactin are summarized in Box 25.3.
Milk production is also affected by mater-
nal stress and fatigue. The mechanism for this
xytocin effect is the down–regulation of milk synthesis
Oxytocin is responsible for milk ejection or the with increased levels of dopamine, norepi-
‘letdown’ reflex. Characteristics of oxytocin are nephrine, or both, which inhibit prolactin syn-
listed in Box 25.4. thesis. The more anxious a mother is about her
The infant’s suckling stimulates nerve end- ability to feed the baby, the less the production
ings in the areola. The afferent impulses reach of milk. Relaxation is essential for successful
the pituitary gland through the spinal cord. This lactation.
releases oxytocin in a pulsatile fashion to adja-
cent capillaries, traveling to the mammary myo-
epithelial cell receptors.
Oxytocin causes contraction of the myoep-
Composition and
ithelial cells that line the ducts of the breast. properties of human milk
These smooth muscle-like cells, when stimu-
lated, expel milk from the alveoli into ducts and Human milk is a unique, complex fluid with
subareolar sinuses that empty through a nipple nutritional qualities, immunologic properties,
pore (Fig. 25.2). and growth-promoting characteristics essential
for the healthy growth of the infant. Milk actually
changes its composition to meet the changing
Involution needs of the baby during growth and matura-
Involution begins approximately 40 days after tion. Colostrum has lower concentrations of fat
last breastfeeding. Milk secretion decreases due than mature milk but higher concentrations of
to the buildup of inhibiting peptides and lack of protein and minerals. The composition of milk
production of stimulatory hormones. reverses as the infant matures.
Characteristics of colostrum
Box 25.4 Characteristics of oxytocin
Colostrum is secreted by the breasts in the first
• Synthesized by hypothalamus 24–48 hours after delivery, till stage 2 of lacto-
• Stored in posterior pituitary gland genesis begins. It is a thin fluid and contains fat
• Stimulated by suckling
globules, acinar cells, and colostrum corpuscles.
• Acts on
The colostrum corpuscles are large, round poly-
Ŧ myoepithelial cells of lactiferous ducts
morphonuclear leukocytes.
CH 25_p346-354_v3.indd 349 17-07-2015 19:13:39

Box 25.5 Characteristics of colostrum Box 25.6 Essential nutrients in human

breast milk
• 5GETGVGFKPVJGſTUVŌJQWTUCHVGTFGNKXGT[
• 6JKPƀWKF • Proteins (primarily D-lactalbumin and whey)
• Contains • Carbohydrates (lactose)
Ŧ Fat globules • Minerals, vitamins
Ŧ Acinar cells • Fats
Ŧ Colostrum corpuscles Ŧ Cholesterol
Ŧ Protein Ŧ Triglycerides
Ŧ Immunoglobulins Ŧ Short-chain fatty acids
Ŧ Long-chain polyunsaturated fatty acids
Arachidonic acid
The colostrum has higher protein content Docosahexaenoic acid
than breast milk. It also contains immunoglobu-
lin A (IgA), immunoglobulin G (IgG), and immu-
noglobulin M (IgM). The IgA protects the neo-
nate gastrointestinal infections. growth. These two fatty acids may be considered
The characteristics of colostrum are listed in essential fatty acids. Many infant formulas have
Box 25.5. supplemental AA, DHA, or both, although the
benefits of this are doubtful.
nique characteristics assive immunity rom mother to
of human milk breast e in ant
oremil an hin mil Breastfeeding is important for the passive
immunity that is passed on to the infant from
The quality of milk varies within a given breast- the mother.
feeding session.
• Mother’s milk contains immunoglobulins that
• Foremilk is the milk first ingested by the infant. passively immunize the infant.
– Lower fat content • There is decreased risk for gastrointestinal
• Hindmilk is produced as the infant continues infections by E. coli and rotavirus, dermatitis,
to breastfeed over the next several minutes. allergies, and respiratory infections in breastfed
– Fat content increases infants, particularly during the first year of life.
– Facilitates satiety in the infant
• Diurnal variations in breast milk depend on the
maternal diet and daily hormonal fluctuations.
Breastfeeding
n ymes to ai neonatal igestion Suckling and breastfeeding are areas that new
Human milk contains various enzymes. mothers frequently struggle with. It is often
taken for granted that the newborn infant will
• They are specific for the digestion of pro-
instinctively take to breastfeeding or that the
teins, fats, and carbohydrates that facilitate
mother will be able to successfully feed her baby.
the infant’s ability to break down food and to
However, it is important to instruct all mothers
absorb human milk.
on the proper techniques for breastfeeding to
• They serve as transport moieties for other
ensure a successful and uncomplicated breast-
substances, such as zinc, selenium, and
feeding experience.
magnesium.
ssential nutrients Baby-friendly hospital

Human milk provides appropriate amounts of
essential nutrients as shown in Box 25.6.
initiative
Arachidonic acid (AA) and docosahexaenoic The Ten Steps to Successful Breastfeeding devel-
acid (DHA) are deposited in the developing brain oped by the World Health Organization (WHO)
and retina during prenatal and early postnatal and the United Nations Children’s Fund
CH 25_p346-354_v3.indd 350 17-07-2015 19:13:39

(UNICEF) as criteria for a Baby-Friendly Hospital • Rooming-in and demand feeding are two
include the following: crucial methods to help in establishing
breastfeeding.
1. Have a written policy on breastfeeding that
is communicated routinely to all staff.
2. Train all health care staff in the skills needed
to implement the policy. Mechanics of breastfeeding
3. Inform all pregnant women of the benefits
To ensure successful breastfeeding, the two
and management of breastfeeding.
important factors are as follows:
4. Help mothers start breastfeeding within 1
hour after birth. • Positioning of the infant
5. Show mothers how to breastfeed and main- • Latching-on
tain lactation, even if they are separated
from their infants.
6. Give newborns only breast milk, unless other Positioning
feedings are medically indicated. Hospitals
The correct positioning of the infant facilitates
must pay a fair market price for formula and
successful breastfeeding.
feeding supplies.
7. Allow mothers and infants to remain together • The mother must be in a comfortable position
at all times (continuous rooming-in). while breastfeeding her infant.
8. Encourage breastfeeding on demand. • The infant should be positioned to face the
9. Provide no pacifiers or artificial teats to mother’s body.
nursing infants. • The mouth of the infant should be opposite
10. Foster the establishment of breastfeeding the mother’s nipple.
support groups and refer mothers to them. • The infant’s neck should be slightly extended.
• The head, shoulders, and hips of the infant
should be in alignment.
Early initiation of breastfeeding Latching-on

It is crucial for sustained breastfeeding to initi-
Latching-on refers to the formation of a tight
ate the process immediately after delivery, be it a
seal of the infant’s lips around the nipple and
vaginal or cesarean delivery.
a sufficient portion of the surrounding are-
• Unless there are neonatal complications, the ola. This facilitates efficient extraction of milk
baby should be given to the mother immedi- during suckling.
ately after birth, in the delivery room. This has It is normal instinct for the baby to open
two advantages: its mouth wide when the nipple touches its
– The infant is still alert soon after delivery. upper or lower lip. The tongue extends under
Approximately 6–12 hours after birth, the the nipple, and the nipple is drawn into the
baby enters a deep sleep period and will not mouth, initiating the suckling reflex. The moth-
be interested in feeding. er’s nipple and areola should be maneuvered
– The mother’s oxytocin levels are still high, to the infant’s open mouth instead of pushing
and this has been shown to help in the infant’s head toward the breast. This sim-
milk letdown ple maneuver may seem difficult to an anxious
bonding with the infant first-time mother.
• Physical contact between the mother and the When the latching-on is correct, the nipple
infant, and placing the baby on the breast and areola extend as far as the junction between
are associated with increased duration of the infant’s hard and soft palates. The infant’s
breastfeeding. jaw then moves the tongue toward the areola,
• Weighing, measuring, and routine care for the compressing it. This process causes the milk
infant should be delayed until the first feeding to travel from the lactiferous sinuses into the
is completed. infant’s mouth.
CH 25_p346-354_v3.indd 351 17-07-2015 19:13:39

Assessing adequacy Table 25.1 Advantages of breastfeeding

of infant intake Nutritional Has all essential nutrients in the
right proportion
Adequacy of intake is assessed based on the
Economical Economical when compared with
following: formula feed
• Frequency and duration of feeding Immunologic • Immunoglobulins protect against
infections
– There should be an average of 8–12 feeds in
• Reduced allergies, respiratory,
24 hours, for 10–15 minutes per feed. and gastrointestinal infections
• Urine and stool output Psychological Better mother to child bonding
– Voiding of urine occurs 4–6 times during Developmental • Better physical and psychological
the third and fourth days, and increases to development
6–8 times on day 5 and after, with adequate • IQ and mental development
feeds. better
– Meconium changes to transitional stools Socioeconomic • Cost-effective for family and
within approximately 3 days of birth. The society
• Best for low-resource countries
baby has 3-4 stools per day after day 4, with
Protection Lowers risk of breast cancer
adequate feeds. against cancer in mother
• Weight of the infant
– Weight loss is normal after delivery, and
infants lose 5%–7% of birth weight soon
after birth. lubricant applied to the fingers, is sufficient. If
– Usually infants stop losing weight by 5 days retracted nipple persists, the nipple should be
after birth and will regain their birth weight pulled out by the inverted syringe technique.
by 1–2 weeks of age. The nozzle of a 10-mL syringe is cut off and the
– If the breastfeeding is adequate, infants gain piston introduced through the cut end. The
15–40 g/day. smooth end is placed on the breast, around
the nipple, and the piston withdrawn slowly.
Maternal nutrition during This procedure should be performed daily
before each feed for a few days.
breastfeeding • Engorgement: This can occur due to interstitial
The mother needs an additional 500–700 kcal/ edema or excessive milk. The breasts become
day during breastfeeding. Protein intake should swollen and painful. The treatment is preven-
be 25 g/day. Iron and calcium supplementation tion with frequent breastfeeding. Pumping
must be continued throughout the duration of of milk may be required to soften the areola
breastfeeding. Vitamins and minerals should and allow better latch-on. Analgesics and firm
also be supplemented. support with well-fitting underclothes are
recommended.
• Sore nipple and cracked nipple: This problem is
Advantages of breastfeeding commonly associated with improper latch-on.
Breastfeeding has several advantages as listed in Proper technique should be taught. Placing a
Table 25.1. drop of milk on each nipple and allowing this
to air dry after breastfeeding may help.
• Mastitis: Mastitis is a localized inflammation
Common problems during of the breast that is associated with fever,
breastfeeding myalgia, breast pain, and redness. It is usually
caused by organisms from the infant’s mouth.
The following are some of the common prob-
It is treated with antibiotics. Analgesics may be
lems encountered during breastfeeding:
required. Breastfeeding should be continued.
• Retracted nipple: This should be identified • Breast abscess: Mastalgia may progress to a
during the antenatal period and treated. breast abscess. Clinically, there is redness, ten-
Drawing out the nipple daily during bath, with derness, and induration. High spiking fever
CH 25_p346-354_v3.indd 352 17-07-2015 19:13:39

is characteristic. Treatment is with antibiot- Galactogogues

ics. Oral cloxacillin (500 mg 6 hourly) is rec-
ommended since the infection is most often Some women have a problem with establishment
staphylococcal or streptococcal. Drainage of of adequate lactation. If there is no improve-
the abscess may be required by ment with proper techniques of breastfeeding,
– ultrasound-guided aspiration of the pus galactogogues may be used. Galactagogues are
– surgical incision and drainage drugs that facilitate milk production. The agents
The mother should continue to breastfeed on most commonly used are dopamine receptor
the unaffected side and pump the affected side antagonists: metoclopramide and domperi-
to relieve pressure and facilitate recovery. done. These are particularly useful for mothers
of preterm infants.
The common problems encountered during
breastfeeding are listed in Box 25.7.
Suppression of lactation
Box 25.7 Common problems encountered Suppression of lactation may be required in cer-
during breastfeeding tain situations. The indications are enumerated
• Retracted nipple in Box 25.8.
Ŧ 5JQWNFDGKFGPVKſGFKPCPVGPCVCNRGTKQF
Ŧ Corrected
Manually Drugs for suppression of lactation
Inverted syringe technique
Cabergoline is the drug of choice as it is well tol-
• Engorgement
erated. It can be given as
Ŧ Caused by
interstitial edema • a single dose of 1 mg or two doses of 0.5 mg
excessive milk 12 hourly.
Ŧ Breasts swollen and painful
Ŧ Treated with Bromocriptine was used earlier but is not
frequent breastfeeding recommended now due to the high risk of vom-
mechanical pumping iting, seizures, hypertension, and thrombo-
analgesics embolism. There is currently no evidence that
firm support nonpharmacologic methods (e.g., jasmine flow-
• Sore/cracked nipple ers or cabbage leaves) are better than placebo in
Ŧ Due to improper latching-on lactation suppression.
Ŧ Proper technique advised
Ŧ Drops of milk applied to nipple
• Mastitis
Ŧ .QECNK\GFKPƀCOOCVKQP Box 25.8 Indications for suppression
Ŧ Associated with of lactation
fever
• Stillbirth
myalgia
• Mother decides against breastfeeding
breast pain
• Contraindications to breastfeeding
redness
Ŧ HIV positive mother
Ŧ Treated with antibiotics
Ŧ Active pulmonary tuberculosis
• Breast abscess
Ŧ Puerperal psychosis
Ŧ Redness, tenderness, induration
Ŧ Mother on drugs secreted in breast milk
Ŧ High spiking fever
Ŧ Oral cloxacillin 500 mg 6 hourly
Ŧ Drainage
Ultrasound guided
Surgical incision and drainage
CH 25_p346-354_v3.indd 353 17-07-2015 19:13:39

Key points
• Breast milk is the best form of nutrition for neonates • 6JGTGIWNCVKQPQHOKNMU[PVJGUKUKUCPGHſEKGPVOGEJC-
and infants. nism. The actual volume of milk secreted may be
• +PVJGſTUVOQPVJUVJGDCD[UJQWNFDGPQWTKUJGF adjusted to the requirement of the infant by feedback
exclusively by breast milk. It is recommended that inhibitor of lactation, a local factor secreted into the milk.
OQVJGTUDTGCUVHGGFHQTCVNGCUVVJGſTUV[GCTQHC • *WOCPOKNMKUCWPKSWGEQORNGZƀWKFYKVJPWVTKVKQPCN
EJKNFŏUNKHG qualities, immunologic properties, and growth-promoting
• During pregnancy, changes occur in the breast characteristics essential for the healthy growth of the
(mammogenesis) that prepare it for the secretion of infant.
milk (lactogenesis) followed by the establishment • Colostrum has lower concentrations of fat than mature
and maintenance of milk secretion (galactopoiesis milk but higher concentrations of protein and minerals.
or lactation). After breastfeeding has been stopped, The composition of milk reverses as the infant matures.
involution occurs.
• Suckling and breastfeeding are areas that new
• The two hormones essential for the initiation mothers frequently struggle with.
and maintenance of lactation are prolactin and • It is crucial for sustained breastfeeding to initiate the
oxytocin. process immediately after delivery, be it a vaginal or
• Prolactin and oxytocin act independently on different cesarean delivery.
cellular receptors, but their combined actions are criti-
• Common problems during breastfeeding include
cal for successful lactation.
retracted nipple, engorgement, sore and cracked
• Prolactin is responsible for synthesis of milk protein in nipple, mastitis, and breast abscess.
the mammary glands. • If there is no improvement with proper techniques of
• Oxytocin is responsible for milk ejection or the breastfeeding, galactogogues may be used. Galacta-
ŎNGVFQYPŏTGƀGZ gogues are drugs that facilitate milk production.
Self-Assessment
minerals. The composition of milk reverses as the
Case-based questions infant matures.
Mrs. AS, 23, had a cesarean section 3 days ago. She 3. Prolactin is responsible for synthesis of milk protein in
had been trying to breastfeed but felt that the baby was the mammary glands. Oxytocin is responsible for milk
not getting enough milk. She and her family were anxious GLGEVKQPQTVJGŎNGVFQYPŏTGƀGZ
that the baby may not be receiving the nutrition it needed. 4. Common problems during breastfeeding include
retracted nipple, engorgement, sore and cracked
1. How would you reassure the couple and assess the
nipple, mastitis, and breast abscess.
CFGSWCE[QHVJGKPHCPVŏUKPVCMG!
2. *QYFQGUEQNQUVTWOFKHHGTHTQOOCVWTGOKNM!
3. 9JCVKUVJGTQNGQHRTQNCEVKPCPFQZ[VQEKPKPNCEVCVKQP! Sample questions
4. Name common problems during breastfeeding.
Answers 1. Describe the physiology of lactation.
1. The couple should be reassured that it takes

3–4 days for lactation to set in. Adequacy of feeds is Short-answer questions
assessed by frequency and duration of breastfeeding,
VJGKPHCPVŏUWTKPGCPFUVQQNQWVRWVCPFCUUGUUOGPVQH 1. Breastfeeding
fetal weight. 2. Colostrum
2. Colostrum has lower concentrations of fat than 3. Common problems with breastfeeding
mature milk but higher concentrations of protein and 4. Galactogogues
CH 25_p346-354_v3.indd 354 17-07-2015 19:13:39

Contraception:
26 Temporary Methods
Case scenario
Ms. YT, 24, was about to get married in 2 months and wanted to avoid
pregnancy for the next 2 years till she finished her higher studies. She
and her fiancé had come for contraceptive advice.
Introduction &GſPKVKQP
The freedom of couples to plan the number, spac- Contraception is the planned use of temporary
ing, and timing of births is a fundamental human or permanent artificial measures to prevent
reproductive right. India was the first country in the pregnancy as an outcome of sexual intercourse.
world to initiate a nationwide family planning pro- A person’s choice of contraceptive method
gram in 1952. However, the number of unintended depends on his or her concern regarding its effi-
pregnancies is unacceptably high in developing cacy, side effects, and cost. The physician’s role is
countries, particularly in India. Since India has a to advice the right fit of contraceptive to the per-
very liberal Medical Termination of Pregnancy Act, ceived need of the individual.
unintended pregnancies lead to therapeutic abor-
tions, many of which are unsafe. Repeated thera-
peutic terminations also have a short- and a long-
Ideal contraceptive method
term effect on the mother’s health. An ideal contraceptive is one that is easy to use,
Therefore, contraceptive advice and counsel- cheap, easily available, safe, effective, and requires
ing should be an important part of an obstetri- minimum motivation, supervision, and mainte-
cian’s responsibility. nance. Although there are many contraceptive
CH 26_p355-377_v3.indd 355 17-07-2015 19:43:50

options available at present, none of them have to have a clear understanding of the advantages
all the characteristics of an ideal contraceptive. and disadvantages of the method so that appro-
priate counseling can be done.
%NCUUKſECVKQPQHCXCKNCDNG 'HſECE[QHVJGEQPVTCEGRVKXG
method
contraceptive methods
The number of pregnancies that occur in spite of
The array of available contraceptive choices is using the method correctly is called failure rate.
impressive (Box 26.1). However, both the indi- The efficacy can be judged by perfect-use rate
vidual and the physician need to make a decision (used consistently with strict adherence to all
on the best choice for that particular individual, instructions) and typical-use rate (not used every
based on his or her requirement. time and not according to instructions, which is
what the average couple will do). The lower the
failure rate, the more acceptable is the method.
The efficacy also depends on frequency of inter-
Making the right choice course, age, and regularity of menstrual cycles.
Failure rates can result from the following:
When considering the ideal method of contra-
ception for an individual, several factors should • Improper instructions being given on how to
be taken into consideration. The physician needs use the method
• Improper usage by the woman/man
• Noncompliance with method
Box 26.1 %NCUUKſECVKQPQHEQPVTCEGRVKXGU
Failure rate of any contraceptive method
emporary should be weighed against nonuse of contra-
• Natural methods ception. Unprotected intercourse has an unin-
Ŧ Coitus interruptus
tended pregnancy rate of 85%.
Ŧ Lactational amenorrhea
Ŧ Periodic abstinence
• Mechanical barriers
he earl In e
Ŧ Male condom The Pearl Index is the most common technique
Ŧ Female condom used for reporting the effectiveness of a contracep-
Ŧ Diaphragm tive method. It is defined as the number of unin-
Ŧ Cervical cap tended pregnancies per 100 women-years (HWY).
Ŧ Spermicidal agent The Pearl Index is calculated as
• Hormonal contraceptives
number of accidental pregnancies × 1200
Ŧ Combination oral contraceptives Pearl Index =
number of patients observed × total months of use
Ŧ Progestin-only oral contraceptives
Ŧ Implants The higher the Pearl Index, the greater is the
Ŧ Injectable depot medroxyprogesterone
chance of an unintended pregnancy. For exam-
Ŧ Combination patch contraceptive
ple, the Pearl Index for combined contraceptive
Ŧ Contraceptive vaginal ring
• Intrauterine devices (IUDs)
pills is 2.18 per 100 women-years of use (effec-
Ŧ Copper T tive) as compared with 20 per 100 women-years
Ŧ Levonorgestrel intrauterine system (IUS) of use (least effective) for natural methods.
In clinical practice, contraceptive methods
ermanent
may be classified according to effectiveness
• Female sterilization
• Male sterilization (vasectomy)
(Table 26.1). This makes it easier to counsel the
patient.
mergency postcoital contraception
• Emergency contraceptive pills (ECP)
• Copper T %QPXGPKGPEGQHWUG
• Minipill emergency contraception method (MECM)
If the contraceptive is inconvenient or difficult to
• Progesterone agonist/antagonist
use, compliance will be poor.
CH 26_p355-377_v3.indd 356 17-07-2015 19:43:50

Contraception: Temporary Methods 357
6CDNG %QPVTCEGRVKXGOGVJQFUCPFVJGKTHCKNWTGTCVGU
Contraceptive method Failure rate ( )

ost e ective
LARC
• Intrauterine contraceptive devices 0.5–2
• Implants 0.05–0.1
• LNg-IUS 0.2
Sterilization (male or female) 0.1–0.5
ective
Injectable contraceptives 0.3
Oral contraceptives 0.3
Transdermal contraceptive patches 0.3
Vaginal ring 0.3
In these methods, unintended pregnancy may occur due to incorrect or inconsistent use.
east e ective
Barrier methods 15
Periodic abstinence 25
A C, long-acting reversible contraceptive; g- S, levonorgestrel-releasing intrauterine system.
4GXGTUKDKNKV[CPFVKOGVQTGVWTP may be used in conjunction with other, more

effective contraceptive methods.
VQHGTVKNKV[
A reversible contraceptive that has a quick return
to fertility is highly desirable. Of the women try-
ing to conceive, 70%–95% will become pregnant
6GORQTCT[OGVJQFUQH
within 12 months following the use of contraception
• oral contraceptives (OCs)
Pregnancy spacing is an essential part of family
• intrauterine devices (IUDs)
planning. Temporary methods of contracep-
• progestin-only pills
tion allow couples to space their pregnancies
However, the time to conception is delayed up and give them the freedom to choose when they
to 2 years after want to have a child, without jeopardizing their
• progestin-only injections. fertility. Temporary methods are also used until
the couple decides on a permanent form of fam-
'HHGEVQPWVGTKPGDNGGFKPI ily planning. This chapter deals with temporary
methods of contraception.
Compliance will be affected and patients may
discontinue contraception if it is associated with
changes in the bleeding pattern (Box 26.2).
Box 26.2 %
JCPIGUKPDNGGFKPIRCVVGTPYKVJ
Cost contraceptives
• Heavy bleeding (IUDs)
High cost of a contraceptive method is a deter- • Scanty bleeding (OCPs)
rent in developing countries. • Breakthrough bleeding
Ŧ Low-dose OCPs
2TQVGEVKQPCICKPUVUGZWCNN[ Ŧ Progestin-only pills
Ŧ Progestin-only injectable
transmitted diseases Ŧ Progesterone-only ring
Condoms provide protection against sexually Ds, intrauterine contraceptive devices; CPs, oral contraceptive
transmitted diseases (STDs) and for this reason pills.
CH 26_p355-377_v3.indd 357 17-07-2015 19:43:50

atural methods Box 26.3 %

CWUGUHQTCPQXWNCVKQPKPNCEVCVKQPCN
amenorrhea
Natural methods are methods where no medi-
• Elevated prolactin levels
cations or contraceptive devices are used. Since
• Reduction of gonadotropin-releasing hormone from
conception requires the sperm to reach the the hypothalamus
ovum, methods of naturally avoiding the sperm • Decreased levels of LH
from reaching the ovum work as contraception. • Lack of follicular maturation
, luteinizing hormone.
Coitus interruptus
Coitus interruptus involves withdrawing the • This method cannot be used if the mother has
entire penis from the vagina prior to ejaculation. human immunodeficiency virus (HIV) infection.
This prevents contact between the sperm and
the ovum. This method of contraception contin-
ues to be an important means of fertility control 0CVWTCNOGVJQFUDCUGFQP
in the developing world. HGTVKNGFC[U
'HſECE[ Natural methods of pregnancy prevention based
Coitus interruptus fails mainly because of the on fertile days are some of the most commonly
man’s inability to judge the timing of ejaculation used methods of fertility regulation. They involve
and failure to withdraw prior to ejaculation. The identifying the woman’s fertile days during the
failure rate is estimated to be approximately 20% menstrual cycle and then avoiding unprotected
during the first year of use. sexual intercourse on those days.
Techniques to determine the fertile period
Lactational amenorrhea include the following:
After delivery, when a woman is actively breast- • The calendar method
feeding, ovulation is suppressed due to factors • Cervical mucus method
listed in Box 26.3. • The sympto-thermal method
Anovulation from lactational amenorrhea var-
ies in duration. There can be breakthrough ovu- he rhythm metho or calen ar
lation. Once the first menses has resumed follow- metho
ing childbirth, this method is no longer safe and
The rhythm method or calendar method is based
another contraceptive method must be adopted.
on the following assumptions:
'HſECE[
• The ovum can be fertilized only 12–24 hours
The failure rate within the first 6 months in a after release.
woman who is exclusively breastfeeding and is • The sperm is viable for only 3–5 days in the
amenorrheic is 2%. cervical mucus and the upper genital tract.
Advantages • Ovulation occurs 12–16 days prior to the next
The following are the advantages of lactational menses.
amenorrhea as contraception: Intercourse is avoided on the days calculated
• The woman has complete control. to be the ovulation time.
• There is no requirement for exogenous contra- 6JGUVCPFCTFFC[UOGVJQF
ceptive methods.
Women with regular cycles of 26–32 days are
Disadvantages asked to avoid unprotected intercourse from days
The following are the disadvantages of lacta- 8 through 19. The user abstains completely or
tional amenorrhea as contraception: uses a barrier method on those 12 days.
• Return to fertility is uncertain. 6YQ&C[OGVJQF

• Pregnancy may occur during the period of Women using the Two Day method are counseled
amenorrhea. to avoid unprotected intercourse on days when
CH 26_p355-377_v3.indd 358 17-07-2015 19:43:50

they note cervical secretions and on the first day

Box 26.5 &KUCFXCPVCIGUQHVJGPCVWTCNOGVJQFU
after a day with cervical secretions. The advantage
of the Two Day method is that it can be used by • Most suitable for women with regular and predictable
cycles
women with short, long, or irregular cycles. With
• Require complete abstinence during the fertile period
this method most women will abstain or use a bar- unless backup contraception is used
rier method for approximately 13 days in a cycle. • Require discipline
• Relatively high failure rate
Cervical mucus or illings metho • Do not protect against STDs
Under the influence of estrogen, the mucus
increases in quantity and becomes progres-
sively more copious, clear, and stretchy until it
peaks for 3–4 days immediately before, during,
Barrier methods
and immediately after ovulation. The woman is Barrier methods prevent the sperm from com-
taught to test her cervical mucus several times ing in contact with the cervix. Barrier meth-
each day and avoid intercourse on the days when ods include male condom, female condom,
the secretions suggest ovulation. diaphragm, cervical cap, and spermicidal
agents. Unlike other methods of birth control,
he sympto thermal metho barrier methods are used only during sexual
The sympto-thermal method combines the tem- intercourse.
perature method, the cervical mucus method,
and the calendar method. Male condom
The first day of the fertile period is calculated The male condom is one of the most popular
by either the calendar method or the first day the mechanical barriers used globally. The condom
mucus is detected. consists of a thin sheath placed over the glans
The end of the fertile period is predicted by and the shaft of the penis. It is most effective
a slight rise (0.2°C – 0.5°C), in the basal body when applied before any vaginal insertion. It
temperature (BBT). A special thermometer is prevents pregnancy by acting as a barrier to the
required to measure the BBT. Intercourse can passage of semen into the vagina.
resume 3 days after the rise in temperature. The leading noncontraceptive benefit of con-
The characteristics of the basal body temper- dom use is the protection offered against STDs,
ature of a woman are enumerated in Box 26.4. including HIV.
'HſECE[
The failure rate for the natural methods is high 6[RGUQHEQPFQOU
and is approximately 25%. The 1-year Pearl Index
Condoms are made of latex rubber or polyure-
is 20 per 100 women-years of use.
thane and other synthetic material.
Disadvantages
The disadvantages of natural methods of contra- 0CVWTCNTWDDGTNCVGZ
ception are listed in Box 26.5. The majority of male condoms are manufac-
tured from natural rubber latex. Latex condoms,
however, can cause latex sensitivity or allergy.
Box 26.4 $
CUCNDQF[VGORGTCVWTGCPFHGTVKNG
They also have a tendency to tear with oil-based
period
lubricants.
• BBT
Ŧ Relatively low during the follicular phase 2QN[WTGVJCPGCPFQVJGTU[PVJGVKEOCVGTKCNU
Ŧ Rises in the luteal phase of the menstrual cycle Polyurethane condoms are generally non-
due to progesterone allergenic, are compatible with both oil-based
Ŧ Begins to elevate 1–2 days after ovulation and water-based lubricants, and have a longer
Ŧ Changes vary from 0.2°C to 0.5°C
shelf life than latex condoms. Since they are
• Fertile period ends 3 days after rise in temperature
more expensive, they are usually prescribed only
BB , basal body temperature. for men with latex allergy.
CH 26_p355-377_v3.indd 359 17-07-2015 19:43:50

Spermicide-coated condoms sexual intercourse. All female condoms have

Spermicide-coated condoms are not recom- two anchors (a ring or frame). The inner smaller
mended as they are not more effective than reg- ring fits high up in the vagina and the outer ring
ular condoms and are associated with adverse lies outside the vagina to prevent the condom
effects for the user. from being pushed inside the vagina during use
(Fig. 26.1). The female condoms available in
'HſECE[ India are Femidom and Femshield.
The failure rate for male condoms is esti- Like the male condom, the female condom is
mated to be approximately 18%. The reason for designed to protect against both pregnancy and
contraceptive failure with condoms is given in STDs. However, because it is not easy to use and
Box 26.6. women find it cumbersome, the female con-
dom accounts for <1% of condoms produced
Advantages
globally.
The advantages of male condoms are enumer-
'HſECE[
ated in Box 26.7.
Efficacy trials are limited. Initial trials have
Disadvantages
demonstrated a pregnancy rate of 20% with typ-
There are some disadvantages associated with ical use.
the use of male condoms (Box 26.8).
Advantages
There are several advantages of the female con-
Female condom doms (Box 26.9).
The female condom is a polyurethane sheath
intended for one-time use. It is approximately
17 cm in length. It covers the cervix, lines the
vagina, and shields the introitus, thus providing
a physical barrier to sperm and secretions during n e finger
Box 26.6 %
CWUGUHQTEQPVTCEGRVKXGHCKNWTGYKVJ nner ring
condoms
• Not using condoms with every act of intercourse and pening
throughout intercourse a.
• Using oil-based lubricants with latex condoms
• Incorrect placement of the condom on the penis
• Poor withdrawal technique
Box 26.7 #FXCPVCIGUQHOCNGEQPFQOU

• Easy availability
• Inexpensive
• Easy to use
• No side effects
• 0QPEQPVTCEGRVKXGDGPGſVU
Ŧ Effective against STDs including HIV b. .
Figure 26.1 +PUGTVKPICHGOCNGEQPFQOa. Correct way
of holding the condom prior to insertion. D Using the index
Box 26.8 &KUCFXCPVCIGUQHOCNGEQPFQOU
ſPIGTVQKPUGTVVJGEQPFQOc. The condom in position.
• Leave contraceptive choice to male partner
• Possibly decrease enjoyment of sex
Box 26.9 #FXCPVCIGUQHVJGHGOCNGEQPFQOU
• Possibility of latex allergy
• Effectiveness decreased due to condom breakage • Safe, effective, and reversible method of contraception
and slippage • Effective against both pregnancy and STDs
• Possible damage to condom from oil-based lubricants • Can be placed before intercourse
CH 26_p355-377_v3.indd 360 17-07-2015 19:43:51

Box 26.10 &KUCFXCPVCIGUQHHGOCNGEQPFQOU

• &KHſEWNVVQKPUGTVCPFTGOQXG
• More expensive than male condoms
Uterus
• Higher failure rate than nonbarrier methods and the
male condom
• Cannot be used in women with pelvic organ prolapse
• Associated with urinary tract infections and, rarely, iaphragm
toxic shock syndrome
Disadvantages
Female condoms are not popular because of the
disadvantages associated with them (Box 26.10). Figure 26.3 The female diaphragm. The diaphragm is
ſVVKPIRTQRGTN[KPVJGXCIKPCCPFEQXGTKPIVJGEGTXKZ
Diaphragm
The diaphragm is a shallow latex cup with a effectiveness. The diaphragm should be inserted
spring mechanism in its rim to hold it in place in at least 3 hours prior to sexual intercourse. Once
the vagina (Fig. 26.2). Diaphragms come in dif- placed in the right position, the diaphragm is
ferent sizes so the gynecologist examines and fits effective for 6 hours. After intercourse, the dia-
the woman for the size appropriate for her. The phragm should not be removed immediately and
diagonal length of the vaginal canal is measured must be left in place for at least 6 hours.
during a pelvic examination and the correct dia- 'HſECE[
phragm size is determined. The diaphragm is The typical-use failure rate within the first year is
not available in India. estimated to be 15%–20%. Failure rate is higher
Spermicidal cream or jelly (commonly non- than hormonal methods and the IUD.
oxynol-9) is applied to the inside of the dome,
which is then inserted into the vagina before Advantages
intercourse. Care must be taken to fit the poste- The advantages of the diaphragm are listed in
rior rim into the posterior fornix and the anterior Box 26.11.
rim behind the pubic bone. This way the entire
Disadvantages
dome covers the cervix (Fig. 26.3).
The diaphragm prevents pregnancy by acting The disadvantages of the diaphragm are listed in
as a barrier to the passage of sperm into the cervix. Box 26.12.
The spermicide used along with it enhances its
Box 26.11 #FXCPVCIGUQHFKCRJTCIO

• Safe, effective, and reversible method of contraception
• Leaves contraceptive control to the woman
• Reusable
• Can be placed before intercourse
Box 26.12 &KUCFXCPVCIGUQHFKCRJTCIO

• 4GSWKTGUUK\KPICPFſVVKPID[I[PGEQNQIKUV
• Must be inserted before each episode of intercourse
• Does not protect against STDs, including HIV
• Must be used with a spermicide
• &KHſEWNV VQ WUG KP VJG RTGUGPEG QH UKIPKſECPV RGNXKE
relaxation and pelvic organ prolapse
Figure 26.2 The female diaphragm and the cervical cap.
• Frequent urinary tract infections and, rarely, toxic
The diaphragm is wider compared with the cervical cap.
shock syndrome
6JGEGTXKECNECRſVUUPWIN[QXGTVJGEGTXKZ
CH 26_p355-377_v3.indd 361 17-07-2015 19:43:51

Cervical cap
The cervical cap is similar to a diaphragm, only
smaller in size, cup shaped, and made out of latex
rubber instead of silicone. A groove along the
inner circumference of the rim improves the seal
between the inner rim of the cap and the base of
the cervix (Figs 26.2 and 26.4). The cap is filled
one-third full with spermicide prior to insertion.
It may be inserted as long as 8 hours before inter- Figure 26.4 The cervical cap. The cervical cap is shown
course and can be left in place for as long as 48 ſVVKPIUPWIN[QPVJGEGTXKZ
hours. The cervical cap is not available in India.
A cervical cap provides a mechanical barrier to Spermicides must be inserted into the vagina
sperm entering the cervical canal. The spermici- prior to each intercourse. They are also used
dal used along with it increases its effectiveness. along with diaphragms and cervical caps.
'HſECE[ 'HſECE[
The effectiveness of the cervical cap depends on The typical-use failure rate is 25%.
parity, which changes the shape of the cervical
Advantages and disadvantages
os. With typical use within the first year, the fail-
ure rate is 20% in nulliparous women and 40% in Box 26.13 lists the advantages and disadvantages
parous women. of spermicides.
Advantages
Box 26.13 #
FXCPVCIGUCPFFKUCFXCPVCIGUQH
The following are the advantages of the cervical
spermicides
cap:
Advantages
• Provides continuous contraceptive protection
• Ease of application
for its duration of use • May provide lubrication
• Can be left in place for 48 hours • Relatively inexpensive
• #WIOGPV EQPVTCEGRVKXG GHſECE[ QH VJG EGTXKECN ECR
Disadvantages and diaphragm
The following are the disadvantages of the cer- Disadvantages
vical cap: • Possibility of vaginal irritation
• High failure rate
• Like the diaphragm, requires fitting by
• Provide minimal protection from STDs
gynecologist
• Relatively high failure rate, especially in parous
women
ormonal contraceptives
Spermicidal agents Hormonal methods of birth control contain
estrogen and progestin, or progestin only. They
Spermicides are among the least effective methods
have been established as a safe and reliable way
of contraception. They consist of a base combined
to prevent pregnancy in the majority of women.
with either nonoxynol-9 or octoxynol. They are
The following kinds of hormonal contracep-
commercially available as vaginal foams, suppos-
tives are available:
itories, jellies, films, foaming tablets, and creams.
Vaginal spermicides consist of a surfactant • Combination oral contraceptive pills (COCPs)
that destroys the sperm cell membrane and • Progestin-only oral contraceptive pills (POPs)
attacks the sperm’s flagella and body. The sperm • Implants
mobility is adversely affected. The sperm’s fructo- • Injectable depot medroxyprogesterone
lytic activity is also disrupted, thereby inhibiting • Combination patch contraceptive
their nourishment. • Contraceptive vaginal ring
CH 26_p355-377_v3.indd 362 17-07-2015 19:43:51

%QODKPCVKQPQTCN levonorgestrel have the highest androgenic prop-

erties. This can result in adverse metabolic effects
contraceptives such as lowering serum high-density lipoprotein
The oral contraceptive pill (OCP) has been in use (HDL) cholesterol concentrations.
for more than five decades. It is a reliable form Third-generation progestins have been
of contraception and also has noncontraceptive developed that have structural modifications that
benefits. The past decade has seen a reduction in lower their androgenic activity, in spite of being
the estrogen content and the introduction of pro- 19-nortestosterone derivatives. These include
gestins with fewer side effects. This has resulted norgestimate, desogestrel, and gestodene.
in improving the safety profile of OCPs and made The commonly used progestins and their level
them a dependable option for many women. of androgenic activity are tabulated in Table 26.2.
/GEJCPKUOQHCEVKQP
%QORQUKVKQPQH%1%2U
There are several mechanisms by which combi-
The combination oral contraceptive contains nation OCPs provide contraception. The estro-
• Ethinyl estradiol (EE) gen and progestin components have different
• Progestin actions. The main mechanism of action is sup-
pression of ovulation.
thinyl estra iol The mechanism of action is summarized in
Box 26.14.
The addition of an ethinyl group to estradiol
resulted in both an orally active estrogen com-
pound and a dramatic increase in estrogenic
5KFGGHHGEVUQHQTCNEQPVTCEGRVKXGRKNNU
potency. Ethinyl estradiol is the estrogen in oral The side effects can be minor or major.
contraceptives currently used.
&QUCIGQH''KP1%2U
inor si e e ects
Minor side effects are dependent on the prepa-
The dosage of EE in OCPs is as follows:
ration of estrogen and progestin in the pill and
• Standard dose their dosage. The side effects are usually expe-
– 30–35 Pg rienced during the initial 2–3 months of use.
Changing to a lower dose of estrogen or chang-
• Low dose
ing to a preparation with less androgenic proges-
– 20–25 Pg
tin relieves the symptoms. The minor side effects
– Less risk of
of OCPs are listed in Table 26.3.
minor side effects
thromboembolism
Box 26.14 6
JGOGEJCPKUOQHCEVKQPQH
The lower dose of EE is associated with a
EQODKPCVKQPQTCNEQPVTCEGRVKXGRKNNU
decrease in the incidence of estrogen-related
adverse effects such as bloating, breast tender- 'HHGEVUQHGUVTQIGPEQORQPGPV
ness, and nausea. Although venous thromboem- • Inhibition of the midcycle luteinising hormone (LH) surge
bolism (VTE) is an uncommon risk, the risk is least Ŧ Prevention of ovulation
• Suppression of pituitary follicle-stimulating hormone
with the lower dose.
(FSH) secretion
Ŧ Suppression of ovarian folliculogenesis
rogestins • Suppression of gonadotropin secretion
Most available progestins are derived from Ŧ Suppression of ovarian steroid production
testosterone and bind to both the progester- 'HHGEVUQHRTQIGUVKPEQORQPGPV
one and androgen receptors. Norethindrone, • Effects on the endometrium
lynestrol, and ethynodiol diacetate are first- Ŧ Decidualization and eventual atrophy
generation progestins. Norgestrel and levonorge- Ŧ Less suitable for implantation
• Alterations in cervical mucus
strel are second-generation progestins. Being
Ŧ Less permeable to penetration by sperm
19-nortestosterone derivatives, they have unde-
• Impairment of normal tubal motility and peristalsis
sirable androgenic properties. Norgestrel and
CH 26_p355-377_v3.indd 363 17-07-2015 19:43:51

6CDNG %NCUUKſECVKQP QH RTQIGUVKPU KP EQODKPCVKQP

YKVJ QTCN EQPVTCEGRVKXG RKNNU CPF VJGKT NGXGN QH
CPFTQIGPKECEVKXKV[
Progestin #PFTQIGPKECEVKXKV[
irst generation
• Norethindrone acetate Middle
• Ethynodiol diacetate
• Lynestrenol
• Norethynodrel
Secon generation
• Norgestrel Highest
• Levonorgestrel
hir generation
• Desogestrel Lowest
• Gestodene
• Norgestimate
7PENCUUKſGF
• Drospirenone Has mineral ocorticoid activity
• Cyproterone acetate Antiandrogenic properties
ajor si e e ects 6CDNG /KPQTUKFGGHHGEVUQHEQODKPCVKQPQTCN

Major cardiovascular and cerebrovascular contraceptive pills
side effects were reported when higher doses
5KFGGHHGEVU %CWUGFD[
(30–50 Pg) of estrogen were used. The risk is
very low with low-dose preparations and newer Nausea, vomiting Estrogen
progestins. However, these adverse effects more Headache and migraine Estrogen
commonly occur in women who are older than Chloasma Estrogen
35 years of age, smokers, obese, or have uncon- Water retention, edema Progestin
trolled diabetes, hypertension, or dyslipidemia. Weight gain Progestin
Prolonged immobilization, past or family history Acne Progestin
of thromboembolism, and cardiovascular dis- Decreased libido Progestin
ease also increase the risk. Major side effects of Mental depression Progestin
OCPs are listed in Table 26.4. Breast tenderness Estrogen and progestin
Breakthrough bleeding Estrogen and progestin
is o cancers
The association between combined OCPs and
cancers has been studied extensively. There is a Stan ar ose or lo ose
small increase in breast cancer in current users Both standard-dose pills (containing 30 Pg of
with prolonged duration of use. Although asso- EE) and low-dose pills (contain 20 Pg of EE) are
ciation with cervical cancer has not been proven, equally effective contraceptives. The aim of low-
regular cytologic screening is recommended in dose pills is to decrease side effects.
pill users. It is common practice to start with low-dose
pills when prescribing COCPs.
#XCKNCDNGRTGRCTCVKQPU Standard dose should be avoided with
Combination pills are available as follows: • obesity (BMI >30 kg/m2)
• age >45 years
• Standard dose or low dose
• 21- or 28-day packets Standard dose is more often prescribed for
• Monophasic, biphasic, or triphasic noncontraceptive indications (discussed in
• Extended-cycle preparations detail later in this chapter).
CH 26_p355-377_v3.indd 364 17-07-2015 19:43:51

6CDNG /CLQTUKFGGHHGEVUQHEQODKPCVKQPQTCNEQPVTCEGRVKXGRKNNU
Car iovascular e ects

Venous thrombosis • Increased risk (3/10,000)
• More in thrombophilias
• More in COCPs with newer progestins
Ischemic heart disease Risk in heavy smokers
Stroke • Increased if smoker, diabetic, hypertensive
• Increased in migraine with aura
Blood pressure Minimal effect—monitoring recommended
etabolic e ects
Protein metabolism • Increase in SHBG
• Increase in angiotensinogen
• Increase in clotting factors
Liver • Cholestasis—uncommon
• Hepatocellular adenoma
C CPs, combination oral contraceptive pills; S B , sex hormone–binding globulin.
or ay pac et The noncontraceptive indications for extended-

OCPs are available in a 21-or 28-day packet. cycle preparations are given in Box 26.16.
Estrogen/progestin is present only in the first
21 tablets. In the 28-day packet, the last seven 5ETGGPKPIQHRCVKGPVRTKQTVQUVCTVKPI
pills contain a placebo. Some brands add iron 1%2U
and/or folic acid to the last seven pills.
The 28-day packet is supposed to make it Minimal medical screening is required before
easier for the woman to take the pills without a starting a woman on OCPs. The important
pill-free interval. However, in studies it has been screening tests are listed in Box 26.17.
shown that women are quite comfortable taking
Box 26.15 /
QPQRJCUKEDKRJCUKECPFVTKRJCUKE
a 21-day packet and having a pill-free break.
oral contraception pills
onophasic biphasic an triphasicOC s • Monophasic pills

Ŧ Same dose of EE and progestin in each
Monophasic, biphasic, and triphasic pills have
• Biphasic pills contain
21 hormonally active pills. While multiphasic Ŧ ſZGFFQUGQHPg of EE
regimens slightly decrease total steroid content Ŧ increasing dose of progestin
over the month, they have no proven clinical 0.5 mg for 10 days
advantage over monophasic preparations. 1.0 mg for remaining 11 days
The characteristics of monophasic, biphasic, • Triphasic pills
and triphasic OCPs are summarized in Box 26.15. Ŧ Varying doses of EE plus progestin
Ŧ Gradually increasing dose of EE
ten e cycle preparations or 20 Pg on cycle days 1–5
continuous pills 30 Pg on days 6–12
35 Pg on days 13–21
Extended-cycle preparations include 7-day Ŧ Gradually increasing dose of progestin
interval of placebo pills approximately every
3 months. For example, there are 84 estrogen/ , ethinyl estradiol.
progestin tablets followed by 7 days of placebo Box 26.16 0

QPEQPVTCEGRVKXGKPFKECVKQPUHQT
pills. The woman takes a tablet every day contin- GZVGPFGFE[ENGRTGRCTCVKQPU
uously. She will have approximately four periods
• Endometriosis
in a year. Extended-cycle preparations are not
• Hyperandrogenism
available in India, but using four 21-day pill pack-
• Lifestyle reasons (patient does not want frequent periods)
ets continuously will achieve the same effect.
CH 26_p355-377_v3.indd 365 17-07-2015 19:43:51

Backup contraception is needed for the first

Box 26.17 Patient screening prior to starting
%1%2U 7 days of use if the pill is started 5 days after onset
of menses, which may be the case in Sunday start
• History and quick start methods. Condoms may be used.
Ŧ Age
One pill a day is continued for 21 days. There is
Ŧ Breastfeeding
a 7-day pill-free interval. The woman will get her
Ŧ Past/family history of venous thromboembolism
Ŧ Diabetes and hypertension
period either during or at the end of the 7 days,
Ŧ Family h/o of hypertriglyceridemia, diabetes, or depending on when she started the pills. The
coronary artery disease pills are then started again on the first Sunday
• Physical examination or the first day of the period. There are newer
Ŧ BMI preparations available with less pill-free days.
Ŧ Blood pressure With the 28-day packet, there is no pill-free
Ŧ Breast examination interval. The period will start usually during or at
Ŧ Pelvic examination the end of the placebo pills.
Ŧ Pap smear
B , body mass index; C CPs, combination oral contraceptive pills. 6KOGQHFC[

The pill should preferably be taken at a fixed
+PKVKCVKQPQHEQODKPCVKQP1%2U part of each day, for example, at bedtime or with
morning coffee, so that it can become part of the
Women desiring contraception can start OCPs
daily routine. This means that the chances of for-
at their convenience. Following a miscarriage or
getting decrease. It is also important to take the
delivery, the following considerations apply:
pill around the same time each day. This is par-
• Following first or second trimester miscar- ticularly important for the low-dose pills.
riage, the pill can be started immediately.
• COCPs reduce breast milk; therefore, proges- Missed pills
terone-only pills or IUDs are recommended
in breastfeeding women till 6 months after Missed pills are a common cause of unintended
delivery. pregnancy while on the pill.
• Nonbreastfeeding women can start the pill The management of missed pills is summa-
21 days after delivery. rized in Box 26.18. This does not apply to the
placebo pills in the 28-day packet.
/GVJQFUQHKPKVKCVKQP Drug interactions

There are three methods commonly used to start Some drugs reduce the efficacy of COCPs. This
OCPs (Table 26.5). It is important to choose one must be kept in mind when prescribing these
method that is suitable and explain it properly to
the woman. Starting pills can be confusing, and Box 26.18 /CPCIGOGPVQHOKUUGFRKNNU
if the woman does not understand the instruc-
tions, she might get pregnant unintentionally. • Single pill missed anywhere in the packet
Ŧ Forgotten pill to be taken when noticed
Ŧ Next pill taken when it is due (may mean taking two
6CDNG /GVJQFU HQT KPKVKCVKPI QTCN EQPVTCEGR- pills on the same day)
tive pills Ŧ No backup contraception required
• Two or more consecutive pills missed
Sunday start (KTUVRKNNUVCTVGFQPVJGſTUV
Sunday after her period Ŧ One of the missed pills taken as soon as possible
(even if it is the next Ŧ One pill each day continued as prescribed
day) Ŧ Backup contraception generally needed
First day start (KTUVRKNNQPVJGſTUVFC[QH • Two or more consecutive hormonal pills missed
menses Ŧ +P ſTUV YGGM QH VJG E[ENG CPF WPRTQVGEVGF KPVGT-
Quick start First pill started on the course occurs during this week
day she is given the Emergency contraception could decrease risk of
prescription pregnancy
CH 26_p355-377_v3.indd 366 17-07-2015 19:43:51

drugs to women on OCPs. The dose of estrogen 4GVWTPQHOGPUGUCPFHGTVKNKV[

has to be increased in these situations.
In a large number of women, menses returns
• Impaired absorption of COCPs within 30 days after stopping the pill. In the
– Antibiotics such as ampicillin and majority of women, menses and fertility should
cephalosporins return to normal by 90 days. If amenorrhea per-
• Rapid degradation of COCPs sists for 6 months after discontinuation of the
– Enzyme-inducing drugs pills, the woman needs to be investigated.
Phenobarbitone, sodium valproate,
rifampicin, clonazepam, griseofulvin and
%QPVTCKPFKECVKQPUVQVJGWUGQH%1%2U
ketoconazole, warfarin, antiretrovirals
Contraindications to use include the following:
0QPEQPVTCEGRVKXGDGPGſVUCPF • Age >35 years and smoking >35 cigarettes/day
WUGUQHQTCNEQPVTCEGRVKXGU • Undiagnosed abnormal vaginal bleeding
• Known or suspected pregnancy
Not only do COCPs have high contraceptive effi- • Untreated hypertension
cacy, they also have noncontraceptive benefits • Diabetes with vascular complications
(Box 26.19). • Estrogen-dependent neoplasia
• History of deep vein thrombosis, pulmonary
Box 26.19 0
QPEQPVTCEGRVKXGDGPGſVUCPFWUGU
embolism, or congestive heart failure
QHQTCNEQPVTCEGRVKXGU
• Cerebrovascular disease
• Menstrual cycle disorders • Significant structural heart disease, pulmo-
Ŧ /GPQTTJCIKC
TGFWEVKQPKPOGPUVTWCNƀQYD[ nary hypertension, or coronary artery disease
Ŧ Dysmenorrhea (by inducing anovulation) • Atherogenic lipid disorders
Ŧ 2TGOGPUVTWCNU[PFTQOG
PQVſTUVNKPGQHVTGCVOGPV
• Breast cancer
Ŧ Prevention of menstrual migraine (with the use of
extended-cycle preparation or continuous pills)
• Active liver disease
• Hyperandrogenism • Protein C, protein S, and antithrombin
Ŧ Acne deficiencies
Ŧ Hirsutism • Prolonged immobilization and major surgery
• Gynecologic disorders
Age beyond 40 years is no longer considered a
Ŧ Endometriosis and adenomyosis
Ŧ Polycystic ovarian syndrome
contraindication to taking low-dose OCPs.
Ŧ 2GTKOGPQRCWUCNJQVƀWUJGU
• Cancer risk reduction 'HſECE[
Ŧ Decreased risk of developing Combination OCPs are very effective, but failure
'PFQOGVTKCNECPEGT
TGFWEVKQPQHTKUM rates are dependent on individual compliance.
1XCTKCPECPEGT
TGFWEVKQPQHTKUM Rates range from 0.1% with perfect use to 5%
Colon cancer
with typical use.
Ŧ Protection
Lasts for at least 15 years following discontinu-
Advantages
ation of use
Increases with duration of use The advantages of combination OCPs are listed
• 1VJGTDGPGſVUQHWUKPI%1%2U in Box 26.20.
Ŧ Reduction of occurrence of anemia (due to de-
ETGCUGFOGPUVTWCNƀQY
Ŧ Protection against
Pelvic inflammatory disease (thickened cervical
mucus provides barrier against bacteria)
Box 26.20 #FXCPVCIGUQHEQODKPCVKQP1%2U
Ectopic pregnancy
Benign breast disease • Ease of use
Osteoporosis • Low failure rate
Functional ovarian cysts • Reversible with quick return of fertility
• Improvement in rheumatoid arthritis • 0QPEQPVTCEGRVKXGDGPGſVU
CH 26_p355-377_v3.indd 367 17-07-2015 19:43:52

Disadvantages &GNC[GFQTOKUUGFRKNN
The disadvantages of combination OCPs are Abstention or backup contraception must be
listed in Box 26.21. used for 2 days if
Box 26.21 &KUCFXCPVCIGUQHEQODKPCVKQP1%2U • norethindrone-containing pill is taken 3 hours
• Daily ingestion necessary late or missed for a day,
• Side effects • desogestrel-containing pill is taken 12 hours
Ŧ Nausea late or missed for a day.
Ŧ Breast tenderness
Ŧ Breakthrough bleeding The pill must be resumed as soon as possible
Ŧ Headaches and continued daily.
Ŧ Postpill amenorrhea due to anovulation 'HſECE[
• May decrease lactation
Failure rates with typical use are estimated to be
7% in the first year of use.
2TQIGUVKPQPN[QTCN Advantages
The advantages of POPs are enumerated in
contraceptives Box 26.22.
Progestin-only oral contraceptive pills (POPs) Disadvantages
are also known as minipills. They are indicated in
The disadvantages of POPs are enumerated in
women who are breastfeeding and women who
Box 26.23.
have a contraindication to the use of estrogen.
The progestins used for the minipill are as
follows: Contraceptive implants
• Norethindrone (Micronor) 0.35 mg In recent years, contraceptive research has
• Norgestrel (Ovrette) 0.75 mg focused on the development of a range of con-
• Levonorgestrel (Microval) 0.30 mg traceptive methods designed to provide
• Desogestrel (Cerazette) 0.75 mg • maximum efficacy,
• nondependence on user compliance, and
/GEJCPKUOQHCEVKQP • prompt return of fertility after removal.
Progestin-only oral contraceptive work by
Box 26.22 #FXCPVCIGUQHRTQIGUVKPQPN[RKNNU
• inhibition of ovulation,
• thickening of cervical mucus, • Safe in breastfeeding mothers
Ŧ POPs do not reduce breast milk
• thinning of endometrium,
• Absence of estrogen-dependent complications such
as VTE
Administration • Can be used in obese, hypertensive, and diabetic women
• 0QPEQPVTCEGRVKXGDGPGſVU
Progestin-only oral contraceptives are started Ŧ Decreased dysmenorrhea
the same way as COCPs. In the postpartum Ŧ Decreased menstrual blood loss
period, if the woman is breastfeeding, the pill Ŧ Decreased premenstrual syndrome symptoms
can be started within 3–4 weeks of giving birth. It Ŧ Fertility immediately reestablished after cessation
has no deleterious effect on lactation. of pills
POPs come in a 28-day packet. One pill is
VTE, venous thromboembolism.
taken daily. There is no pill-free interval. The pill
must be taken at the same time each day for
Box 26.23 &KUCFXCPVCIGUQHRTQIGUVKPQPN[RKNNU
maximum efficacy. This is because of the short
duration of action and the short half-life of POPs. • Need for complete compliance with usage
The patient must be instructed that she will • Amenorrhea and unscheduled bleeding/spotting, which
may bother some women
have amenorrhea while on the POP. There can be
• Breast tenderness
spotting and unscheduled bleeding, which may
• Headache
bother some women.
CH 26_p355-377_v3.indd 368 17-07-2015 19:43:52

Implants are long-acting reversible contra- anesthesia. Implanon is most commonly used at
ceptives (LARCs) that meet these requirements. present (Fig. 26.6).
Synthetic polymers have made it possible to Contraceptive implants are ideal for women
develop delivery systems with a long duration of who are
action, which continuously release low amounts
• postpartum or breastfeeding and
of hormones. Initially, the Norplant implant
• poor compliers.
was introduced. It consisted of six levonorge-
strel-containing capsules for subdermal inser- Contraceptive implants are also useful in
tion (Fig. 26.5). It became unpopular because of women who have contraindications to
the difficulty in removal of the implant.
• pregnancy (due to a medical condition) and
Currently, the available implants are
• the use of estrogen.
Norplant 1, Norplant 2, and Implanon. All are
placed subdermally in the arm under local The features of subdermal implants are given
in Table 26.6.
/GEJCPKUOQHCEVKQP
The mechanism of action of contraceptive
implants is summarized in Box 26.24.
'HſECE[
The implant is as efficient as female sterilization
in preventing pregnancy. The rate of pregnancy
with typical-use is <1%. The Pearl Index is 0.38
pregnancies per 100 women-years of use.
Figure 26.5 Norplant subdermal implant. Six rods are
implanted in the upper inner arm. Advantages and disadvantages
Contraceptive implants have not become a pop-
ular form of contraception. The advantages and
disadvantages of contraceptive implants are
listed in Box 26.25.
mplant place un er
the s in sub ermal Box 26.24 /
GEJCPKUOQHCEVKQPQHEQPVTCEGRVKXG
implants
Progestogen in the implant acts by the following:
• Suppression of the LH surge
mplanon implant Ŧ Suppression of ovulation
• Making cervical mucus thick and scant
Ŧ Deters sperm penetration
• Decreasing tubal motility
Ŧ Prevents fertilization
Figure 26.6 Implanon implant. One rod is placed
• Thinning endometrium
subdermally in the upper inner arm.
6CDNG %QPVTCEGRVKXGUWDFGTOCNKORNCPVU(GCVWTGUFQUCIGCPFFWTCVKQPQHCEVKQP
orplant 1 orplant 2 Implanon

6 Silastic rods 2 Silastic rods Single polymer rod
34 mm long, 2.4 mm wide 43 mm long, 2.5 mm wide 40 mm long, 2 mm wide
Levonorgestrel 36 mg each Levonorgestrel 70 mg each Etonogestrel 68 mg each
Releases 85 μg/day for 6 months, 50 μg/day for 15 Releases 50 μg/day Releases 30 μg/day
months, 30 μg/day thereafter
Effective for 5 years Effective for 3–5 years Effective for 3 years
CH 26_p355-377_v3.indd 369 17-07-2015 19:43:52

or abstinence is indicated for 7 days if it is not

Box 26.25 #
contraceptive implants started in the first 7 days of the cycle.
Repeat injections are given every 3 months.
Advantages
• Long acting
• Quick return to fertility
4GVWTPVQHGTVKNKV[
Ŧ Ovulation within 3 weeks The return to fertility (ovulation) may be delayed
• No exogenous estrogen for up to 1 year after DMPA is stopped. Women
• No adverse effect on lactation with higher BMIs take longer to ovulate.
Disadvantages
'HſECE[
• A minor surgical procedure is necessary for insertion
and removal DMPA is an extremely effective contraceptive
• Amenorrhea and unscheduled bleeding may occur option. The Pearl Index is 0–0.7 per 100
• Associated with women-years.
Ŧ headaches, mood changes, weight gain, breast
tenderness, acne
The advantages and disadvantages of DMPA are
+PLGEVCDNGFGRQV
OGFTQZ[RTQIGUVGTQPGCEGVCVG +PLGEVCDNGGUVTQIGPŌ
Depot medroxyprogesterone acetate (DMPA) is RTQIGUVGTQPGEQODKPCVKQPU
an injectable, progestin-only contraceptive that
Depot medroxyprogesterone is associated with
provides highly effective, reversible contraception
irregular bleeding. Combining it with estrogen
for 3 months at a time. Pharmacologically active
reduces this inconvenience. The two available
blood levels are achieved within 24 hours after
preparations are used as a monthly injection.
injection, and are maintained for 3 months. A dose
of 150 mg of DMPA suppresses ovulation in most • Cyclo-Provera is a combination of DMPA and
women for as long as 14 weeks. The contraceptive estradiol propionate.
regimen consists of one dose every 3 months. • Norigynon is a combination of 50 mg of nore-
DMPA is ideal for women who do not want thindrone enanthate and 5 mg of estradiol
valerate.
• to take a contraceptive pill daily,
• an estrogen-containing contraceptive, and
• monthly periods. Box 26.26 #
DMPA
However, the discontinuation rate for DMPA Advantages
within 6–12 months is high globally. It might be
• Can be used by lactating mothers
due to the concern women have about the asso-
• Not affected by high BMI
ciated amenorrhea.
• Does not have adverse effects of estrogen
• Dysmenorrhea decreased
/GEJCPKUOQHCEVKQP • Can be used for treatment of endometriosis
DMPA creates a relative hypoestrogenic state. It Disadvantages

acts by • Disruption of the menstrual cycle leading to amenorrhea
• Persistent irregular bleeding
• suppressing FSH and LH levels, • Delay in return to fertility
• eliminating the LH surge, and • Weight gain
• suppressing folliculogenesis and ovulation. • Reduction of bone mineral density when used for >2
years
Ŧ Due to suppression of gonadotropins
Administration Ŧ Does not necessitate stopping DMPA
Ŧ Reversible after DMPA stopped
The first DMPA injection can be given within 7
days of the start of menses. Backup contraception D PA, depot medroxyprogesterone acetate.
CH 26_p355-377_v3.indd 370 17-07-2015 19:43:52

The injectable combinations are highly effec-

tive (failure rate 0.2–0.4 per HWY) and easy to use.
st Patch
Patch
%QODKPCVKQPRCVEJ
r Patch
contraceptive o Patch
The transdermal contraceptive patch has similar
Figure 26.8 Calendar depicting usage schedule for
benefits, risks, and contraindications as com-
contraceptive patch. The patch is changed once a week
bined hormonal OCPs. The difference is that the
for three weeks (21 total days), followed by one week that
contraceptive transdermal patch releases estro-
is patch free.
gen and progesterone directly into the skin and
is used only once a week. The transdermal patch
is not available in India. 'HſECE[
The patch is a small 20 cm2 square that has an The failure rate for the patch is 5% with typi-
outer waterproof layer and an active layer that cal-use, similar to that of other combination hor-
is medicated and adhesive. The patch contra- mone methods.
ceptive is most commonly applied on the upper
Advantages
arm, hip, thigh, buttock, or lower abdomen
(Fig. 26.7). It should not be applied anywhere • Greater compliance
near the breast. • Less nausea
Each patch contains a 1-week supply of
norelgestromin (150 Pg) and EE (20 Pg). A sus- Disadvantages and contraindications
tained low dose of hormones is released daily, • Similar to those of COCPs
equivalent to the lowest-dose OC. • Irritation over the patch site
/GEJCPKUOQHCEVKQP
The mechanism of action is the same as that of %QODKPCVKQPEQPVTCEGRVKXG
combined OCPs. vaginal ring
Administration
The contraceptive vaginal ring offers the same
The patch is initiated the same way as COCPs— benefits as OCPs, but has the advantage that the
first day, first Sunday, or quick start. The patch is woman does not have to remember to use the con-
changed once a week for 3 weeks (21 total days), traceptive daily. The ring is left in place for 3 weeks
followed by 1 week that is patch free (Fig. 26.8). It and then removed for a single ring-free week.
should always be changed/applied on the same The contraceptive vaginal ring is a latex-free,
day of the week. flexible device measuring 54 mm in diameter and
4 mm in cross-section (Fig. 26.9). The outer ring
is composed of EE and an ethylene vinyl acetate
Uterus
Vaginal
ring
a. b.
Figure 26.7 Transdermal combination patch Figure 26.9 a. Combination contraceptive vaginal ring.
contraceptive. It is most commonly applied on the upper D6JGƀGZKDNGEQPVTCEGRVKXGXCIKPCNTKPIKUNGHVKPVJG
arm, hip, thigh, buttock, or lower abdomen. vagina for 3 weeks and removed for 1 week.
CH 26_p355-377_v3.indd 371 17-07-2015 19:43:53

copolymer that is embedded with crystals of Saheli. It is a once-a-week contraceptive that

etonogestrel. The dose of hormones released acts by causing asynchrony between ovulation
each day is 15 Pg of EE and 120 Pg of etonogestrel. and endometrial changes, thereby preventing
implantation. Initial dose is 30 mg twice a week
/GEJCPKUOQHCEVKQP for 3 months followed by once a week thereafter.
It is contraindicated during breastfeeding and in
The mechanism of action is the same as COCPs. hepatic dysfunction. Ormeloxifene is marketed
only in India as a contraceptive. The failure rate
Administration with typical use is 9%.
The use of the vaginal ring is initiated in the
same way as COCPs.
The sides of the ring are pressed together Intrauterine devices
and then the ring is inserted into the vagina as
Intrauterine contraceptive devices are the most
high as possible for comfort and to decrease the
accepted reversible method of contraception
chance of expulsion. The ring can be placed in
available globally. They are among the safest and
the vagina even if the woman has not finished
most effective methods existing today and rank
bleeding.
alongside implants and sterilization in efficacy.
The ring is left in place for 3 weeks and then
The copper-based devices are also extremely
removed for 1 ring-free week to allow withdrawal
cost-effective. Acceptance rates are high among
bleeding. The new cycle is inserted on the same
women and continuance rates are as high as 80%
day of the week that the old ring was removed
after 1 year of use, placing them in the top tier of
the previous week.
contraceptives.
'HſECE[ Modern devices for intrauterine contracep-
If used properly, it is as effective as COCPs with a tion are made of plastic and release either cop-
failure rate of 5% with typical use. per or a progestin to enhance the contraceptive
action of the device.
The advantages and disadvantages of combina-
tion contraceptive vaginal ring are summarized
6[RGUQH+7&U
in Box 26.27. Modern IUDs fall under two categories depend-
ing on the chemical component involved:
• Copper IUDs
1TOGNQZKHGPG • Levonorgestrel-releasing IUDs (LNg-IUS)
Ormeloxifene is a nonhormonal contraceptive. It Inert or nonmedicated IUDs are available in
is a selective estrogen receptor modulator (SERM) certain countries but are not available in India.
sold commercially in India as Centchroman or All IUDs have monofilament plastic/nylon
strings attached to one end. These strings are
used both by the patient and obstetrician to
Box 26.27 #FXCPVCIGUCPFFKUCFXCPVCIGUQH check that the IUD is in position. They are also
EQODKPCVKQPEQPVTCEGRVKXGXCIKPCNTKPI
used to remove the IUD from the uterine cavity.
Advantages
• Daily compliance not required %QRRGT+7&U
• Ease of use
• Rapid return of fertility The copper T device is a T-shaped polyethylene
• Lowest dose of EE compared with other combined frame with fine copper wire wound around the
hormonal contraceptives vertical stem (Fig. 26.10).
Disadvantages
In India, the commonly available devices are
CuT 250, CuT 375, and CuT 380A, which, in addi-
• Increased vaginitis, vaginal wetness, and leukorrhea
tion to the copper wire, also has copper collars
• Expulsion
on each of the horizontal arms.
CH 26_p355-377_v3.indd 372 17-07-2015 19:43:53

.GXQPQTIGUVTGNTGNGCUKPI+7&
Levonorgestrel-releasing IUD is marketed as an
intrauterine system (LNg-IUS). It consists of a
small T-shaped frame with a reservoir that con-
tains 52 mg of levonorgestrel. The levonorgestrel
has a release rate of 20 Pg/day. The progestin acts
locally on the endometrium. There is little or no
systemic circulation of the progestin.
The very high cost of the LNg-IUS prevents it
from being used commonly as an IUD in devel-
oping countries.
Duration o use
Figure 26.10 Copper T device. Copper wire is wound The LNg-IUS is approved for up to 5 years of use.
around the vertical stem. Copper collars are seen on each
of the horizontal arms. There are plastic/nylon strings echanism o action
attached to one end. Like any progestin, levonorgestrel acts on the
cervical mucus and locally on the endometrium.
The mechanism of action is given in Box 26.29.
Since the copper ions released by the copper The features of the LNg-IUS are summarized
wires play a major role in providing contracep- in Box 26.30.
tion, the amount of copper available in the IUD Box 26.29 .0I+75/GEJCPKUOQHCEVKQP
determines the duration of use. The numbers
250, 375, and 380 refer to the mm2 of exposed • Changes in cervical mucus
Ŧ Thickening of mucus
surface of copper wire (Table 26.7).
Ŧ Inhibit sperm transport
• Changes in endometrium
echanism o action Ŧ Decidualization and glandular atrophy
The exact mechanism of action of copper IUDs Ŧ Hostile to implantation
is not known. They primarily prevent fertiliza-
g- S, levonorgestrel-releasing intrauterine system.
tion. The factors involved are summarized in
Box 26.28. Box 26.30 (GCVWTGUQHVJG.0I+75
• Contains 52 mg of levonorgestrel
• Releases 20 μg daily
Box 26.28 %QRRGT+7&/GEJCPKUOQHCEVKQP • Effective for 5 years
• Causes amenorrhea
• Changes in cervical mucus • Reduces ectopic pregnancy, PID
Ŧ Due to increased Cu concentration • (CKNWTGTCVG
Ŧ Inhibit sperm transport • Side effects
• Changes in endometrium and fallopian tubes Ŧ Irregular bleeding
Ŧ %JTQPKECUGRVKEKPƀCOOCVQT[EJCPIGU Ŧ Uterine cramping
Toxic to sperm and ova
Inhibit fertilization and implantation g- S, levonorgestrel-releasing intrauterine system; P D, pelvic
KPƀCOOCVQT[FKUGCUG
6CDNG %QRRGTKPVTCWVGTKPGFGXKEGUYKVJCXCKNCDNGEQRRGTCPFFWTCVKQPQHCEVKQP
Device 5WTHCEGCTGCQHEQRRGT
OO2) %QRRGTTGNGCUGFFC[
zI &WTCVKQPQHCEVKQP
[GCTU
Copper T 200 200 50 3
Copper T 200B 215 50 4
Multiload Cu 250 250 60–100 3
Multiload 375 375 30 5
CuT 380A 380 30 10
CH 26_p355-377_v3.indd 373 17-07-2015 19:43:53

iming o insertion o I Ds 6GEJPKSWGQHKPUGTVKQP

The following points should be noted regarding
Insertion o Cu
timing of insertion:
The insertion should be done under aseptic con-
• The IUD is best inserted immediately after ditions. Sterile gloves must be used. The IUDs
the period. This excludes pregnancy and also come with special inserters (Fig. 26.11).
makes insertion easier.
• Insertion can also be done at any time dur- • No anesthesia is required and the procedure is
ing the menstrual cycle if pregnancy can be an outpatient procedure.
excluded before insertion. • ‘No touch’ technique should be used while
• Following miscarriage or induced abortion, loading the device into the inserter, cleaning,
the IUD can be inserted immediately or any- and introducing the speculum and the inserter
time thereafter. with device.
• Following delivery, it can be inserted 6 weeks • The woman should be in the lithotomy posi-
postpartum. tion. Pelvic examination should be performed
• Postpartum or placental insertion is being pop- to assess uterine size and anteversion.
ularized by the Government of India. The cop- • The cervix should be visualized using a Sims
per-bearing device can be inserted immediately speculum. The anterior lip is held with a
after placental delivery using a sponge holding tenaculum, and the uterus should be sounded
forceps. However, the expulsion rate is higher. to measure the uterocervical length.
• CuT IUDs are also used for emergency contra- • The device should be loaded into the inserter
ception, following unprotected sexual inter- by bending the horizontal arms (Fig. 26.12).
course (see Chapter 27, Emergency contracep-
tion and sterilization).
Figure 26.12 Preparation for insertion of Copper T.

The device should be loaded into the inserter by bending
Figure 26.11 Copper T with inserter and plunger. the horizontal arms.
CH 26_p355-377_v3.indd 374 17-07-2015 19:43:53

• The guard on the inserter should be adjusted into the inserter by traction on the threads. The
according to the uterocervical length. The guard is held 1.5 cm below the cervical os; the
plunger is carefully placed inside the inserter. device is released, and the inserter is pushed up
• The inserter with the plunger should be intro- to the fundus. The rest of the steps of insertion
duced into the uterine cavity till it reaches just are similar to CuT.
below the fundus and the guard is just below
the cervix. 4GOQXCNQH+7&U
• The plunger is kept steady and the inserter is
withdrawn, releasing the device into the uter- An IUD can be removed any time during the
ine cavity (Fig. 26.13). menstrual cycle. The patient should be informed
• After proper placement is confirmed, the that fertility may return quickly. A new IUD can
strings are trimmed to approximately 2–3 cm. be placed immediately after removal of the old
device, if the patient wants to continue the same
form of contraception.
Insertion o gI S
The LNg-IUS comes with an inserter, plunger, Discontinuation rates
guard, and a slider to push the device out of the
inserter (Fig. 26.14). The device can be pulled Women are very satisfied with IUDs, and the per-
centage of women who continue to use them is
approximately 80% after 1 year of use.
'HſECE[QH+7&U
IUDs have a very low failure rate. The typical-use
failure rate is 0.6% with the CuT 380, and 0.1%
with LNg-IUS. The failure rate is slightly higher
with CuT 250 and CuT 375.
#FXCPVCIGUCPFFKUCFXCPVCIGUQH+7&U
The advantages and disadvantages of IUDs are
enumerated in Box 26.31.
Box 26.31 #FXCPVCIGUCPFFKUCFXCPVCIGUQH+7&U

Advantages
• No adverse systemic effects
• Long acting
• Reversible
Ŧ Immediate return of fertility
• Reduced chance of
Ŧ intrauterine and ectopic pregnancies
Figure 26.13 Demonstration of IUD insertion in plastic • 5KIPKſECPV FGETGCUG KP DNGGFKPI
GXGP COGPQTTJGC
model. The inserter with the plunger is introduced into the with LNg-IUS
uterine cavity till it reaches just below the fundus and the
Disadvantages
guard is just below the cervix. The plunger is kept steady
and the inserter is withdrawn, releasing the device into the • Uterine cramps
uterine cavity. Ŧ Can occur immediately after insertion
Ŧ Usually respond to NSAIDs
• Menorrhagia and dysmenorrhea
Ŧ 7UWCNN[KPVJGſTUVŌOQPVJUCHVGTKPUGTVKQP
Ŧ Reduces gradually
Ŧ Respond to oral mefenamic acid or tranexamic
acid
• Increased vaginal discharge
g- S, levonorgestrel intrauterine system; SA Ds, nonsteroidal

Figure 26.14 LNg-IUS shown with inserter. CPVKKPƀCOOCVQT[FTWIU
CH 26_p355-377_v3.indd 375 17-07-2015 19:43:53

Box 26.32 %QORNKECVKQPUCUUQEKCVGFYKVJ+7&U %QORNKECVKQPUQH+7&U

• Expulsion of IUD The complications associated with IUDs are
Ŧ )TGCVGUVKPVJGſTUV[GCTQHWUG enumerated in Box 26.32.
Ŧ ŌYKVJ%W6
Ŧ ŌYKVJ.0I+75
• Perforation of uterus
Ŧ 1 in 1000 chance of perforation during insertion 2QUVRCTVWO+7&RTQITCOU
• Malposition
Ŧ Contraception not effective if not positioned in fundus Governmental programs have been initiated
• Infection and PID in many developing countries to insert an IUD
• Migration into the peritoneal cavity immediately postpartum (PPIUD). This gives
Ŧ Diagnosed by X-ray or ultrasonography women an option for a long-acting, highly effec-
Ŧ IUD must be removed
tive, and ‘forgettable’ method of contraception to
Ŧ Removal can be by laparoscopy or laparotomy
meet their reproductive health needs. However,
• Nonvisualization of thread
Ŧ Device expelled, embedded in uterine wall, or
the conventional IUDs come with inserters
migrated which are too short for this purpose. The uterus
Ŧ Diagnosed by ultrasonography immediately postpartum is still enlarged signifi-
Ŧ Removed by hysteroscopy cantly and a longer inserter is required to reach
the fundus of the uterine cavity. Newer IUDs
Cu , copper T; D, intrauterine device; g- S, levonorgestrel
intrauterine system; P DRGNXKEKPƀCOOCVQT[FKUGCUG
have been manufactured for this purpose with
longer inserters and strings.
-G[RQKPVU
• %QPVTCEGRVKQPKUVJGRNCPPGFWUGQHCTVKſEKCNOGVJQFU • The female condom is a polyurethane sheath intended
or other techniques to prevent pregnancy as an out- for one-time use. It covers the cervix, lines the vagina,
come of sexual intercourse. CPFUJKGNFUVJGKPVTQKVWU6JGHCKNWTGTCVGKU
• Temporary forms of contraception are periodic absti- • The diaphragm is a shallow latex cup with a spring
nence, mechanical barriers, hormonal contraceptives, mechanism in its rim to hold it in place in the vagina.
and intrauterine devices. #YQOCPJCUVQDGſVVGFHQTCFKCRJTCIOUKPEGKVKU
• Unprotected intercourse has an unintended pregnancy manufactured in different diameters.
TCVGQH • The cervical cap is similar to a diaphragm, only
• The number of pregnancies that occur in spite of using UOCNNGTKPUK\GCPFſVUUPWIN[CTQWPFVJGEGTXKZ
the method correctly is called failure rate. • Hormonal contraceptives include combination oral
• The Pearl Index is the most common technique used contraceptives, progestin-only oral contraceptives,
for reporting the effectiveness of a contraceptive implants, injectable depot medroxyprogesterone,
OGVJQF+VKUFGſPGFCUVJGPWODGTQHWPKPVGPFGF combination patch contraceptive, and contraceptive
pregnancies per 100 women per year. vaginal ring.
• Natural methods include periodic abstinence, coitus • Intrauterine devices are long-acting reversible con-
interruptus, lactational amenorrhea, and methods traceptives. The two kinds available are copper T
based on fertile days. devices and the levonorgestrel-releasing device.
• The male condom is one of the most popular mechani-

cal barriers used globally. The failure rate is estimated
VQDGCRRTQZKOCVGN[
CH 26_p355-377_v3.indd 376 17-07-2015 19:43:53

5GNH#UUGUUOGPV
%CUGDCUGFSWGUVKQPU Case 2
1. Since she is breastfeeding, COCPs cannot be
Case 1 prescribed. She can be placed on POPs or injectable
Ms. YT, 24, is getting married in 2 months. She wants to DMPA. The contraception can be started immedi-
CXQKFCRTGIPCPE[HQTVJGPGZV[GCTUVKNNUJGſPKUJGUJGT ately.
higher studies. She has regular periods. Her last period 2. POPs can result in amenorrhea and unscheduled
was 3 weeks ago. She is not sexually active. She and her bleeding, and she should be instructed about it.
ſCPEÃJCXGEQOGHQTEQPVTCEGRVKXGCFXKEG 3. She has heavy periods, and although an IUD would be
ideal for her, she runs the risk of having menorrhagia.
1. Which contraceptive would you advise her and why?
If she can afford it, an LNg-IUS would be ideal since it
2. How will you initiate combination oral contraceptive leads to oligomenorrhea and even amenorrhea.
pills?
4. DMPA can be used by lactating mothers, is not
3. What should she do if she misses a pill? affected by high BMI, and does not have adverse
4. When will fertility return when she stops COCPs? effects of estrogen. It can, however, cause disruption
of the menstrual cycle, leading to amenorrhea and
persistent irregular bleeding. There may be a delay in
Case 2 return to fertility. It can cause weight gain and result
Mrs. VC, 34, has delivered her second baby 2 months in reduction of bone mineral density.
ago. She is breastfeeding. She has come for contracep-
tive advice. She usually has regular periods with heavy
bleeding. She has not resumed her periods yet. Sample questions
1. What contraceptive options can be offered to her? .QPICPUYGTSWGUVKQPU
2. What are the complications encountered with
progestin-only pills? 1. What is the mechanism of action, method of admin-
KUVTCVKQPGHſECE[CFXCPVCIGUCPFEQORNKECVKQPUQH
3. What are the disadvantages of IUD in her case?
combination oral contraceptive pills?
4. What are the advantages and disadvantages of
2. What are the types of intrauterine devices? How do
injectable DMPA?
they work? What are the complications of IUDs?
#PUYGTU 5JQTVCPUYGTSWGUVKQPU
Case 1 1. Pearl Index
2. Natural methods of contraception
1. COCPs would be ideal for her. She needs revers-
ible contraception, and an IUD cannot be inserted 3. Barrier contraception
because she is not sexually active. 4. 0QPEQPVTCEGRVKXGDGPGſVUQHQTCNEQPVTCEGRVKXGRKNNU
2. Since she had her period 3 weeks ago, she can wait 5. Major and minor side effects of combined oral con-
HQTJGTPGZVRGTKQFCPFUVCTVHTQOVJGſTUVFC[QHVJG traceptive pills
RGTKQF$CEMWREQPVTCEGRVKQPHQTVJGſTUVFC[UQH 6. The minipill
use is not needed. 7. Contraception during lactation
3. If a single pill is missed anywhere in the packet, the 8. Contraceptive implants
forgotten pill is to be taken when noticed and the next 9. Contraceptive vaginal ring
pill taken when it is due (may mean taking two pills 10. Injectable hormonal contraception
on the same day). No backup contraception required. 11. Levonorgestrel intrauterine system
If two or more consecutive pills are missed, then one 12. Centchroman
of the missed pills is to be taken as soon as pos-
sible and one pill each day continued as prescribed.
Backup contraception needed.
4. In the majority of women, menses and fertility return
to normal by 90 days. If amenorrhea persists for 6
months after discontinuation of the pills, the woman
needs to be investigated.
CH 26_p355-377_v3.indd 377 17-07-2015 19:43:53

Emergency
27 Contraception and
Sterilization
Case scenarios
Mrs. JK, 24, and her husband were very worried. They were married
for 3 months and were using condom for contraception but the con-
dom slipped. They were not willing for a pregnancy. They had come for
advice on how to proceed.
Mrs. RE, 26, was pregnant for the second time and at 36 weeks’ gesta-
tion. Her first child was 3 years old and healthy. She and her husband
were very sure that they did not want any further pregnancies and
wanted advice on a permanent method of contraception.
Introduction Emergency contraception

Emergency contraception or postcoital con- Women who have had recent unprotected or
traception refers to the use of drugs or a device inadequately protected intercourse require
as an emergency approach to preventing preg- emergency contraception (EC). Emergency con-
nancy. Emergency contraception can prevent traception is also useful for couples who have had
most pregnancies when taken after intercourse. a failure of some other form of contraception.
Currently, there is increased awareness about
the advantages of a small family. Most couples
consider stopping with one or two children.
Using temporary methods is cumbersome and
Indications
the chances of failure are a cause for anxiety. Common indications for emergency contracep-
Hence, many couples prefer permanent meth- tion are enumerated in Box 27.1.
ods of contraception. These include male and Emergency contraception prevents preg-
female sterilization. nancy. There are no conditions in which the risks
CH 27_p378-396_v3.indd 378 17-07-2015 19:58:18

Emergency Contraception and Sterilization 379
Box 27.1 Indications for emergency Screening prior to

contraception
• No contraceptive used during sexual intercourse
prescribing emergency
Ŧ Within the previous 120 hours (5 days) contraception
• Contraceptive failure or incorrect use of a contraceptive
Ŧ Within the previous 120 hours (5 days), including There is no necessity for a clinical examination or a
condom breakage, slippage, or incorrect use pregnancy test before prescribing emergency con-
3 or more consecutively missed combination oral traception. Emergency contraception should not
contraceptive pills
be withheld or delayed for the following reasons:
dislodgment, delay in placing, or early removal
of contraceptive patch or vaginal ring • To test for pregnancy
norethindrone-containing progestin-only pill (min- • Because the unprotected event did not occur
ipill) taken more than 3 hours late
during the fertile time of the cycle
desogestrel-containing progestin-only pill (min-
ipill) taken more than 12 hours late
>2 weeks late for injection of depot medroxypro-
gesterone acetate
expulsion of intrauterine contraception
Methods available for
• Victim of sexual assault emergency contraception
The different methods available for emergency
of emergency contraception use outweigh the contraception are as follows:
benefits. Emergency contraception should be • Levonorgestrel alone
offered to any woman in need of it. Medical eligi- • Levonorgestrel with ethinyl estradiol (EE)
bility for emergency contraception includes the • Copper intrauterine device (IUD)
following: • Antiprogestins
• Women with previous ectopic pregnancy – Mifepristone
• Women with cardiovascular disease – Ulipristal
• Women with migraines
• Women with liver disease Levonorgestrel
• Breastfeeding women
Levonorgestrel can be administered as follows:
• 1.5-mg tablet taken as a single dose (more con-
venient and as effective as the split dose)
Contraindications to • 0.75-mg tablet taken in two doses 12 hours
emergency contraception apart
The only reason not to give emergency contracep- echanism o action

tion is in a woman with a confirmed pregnancy. Levonorgestrel emergency contraceptive pills
However, if a woman inadvertently takes emer- act by
gency contraceptive pills after she becomes preg-
nant, the available evidence suggests that the pills • preventing or delaying ovulation
will not harm either the mother or her fetus. • preventing fertilization of the ovum
It is important to emphasize to women that – by affecting the cervical mucus
emergency contraceptive pills are for emergency – by affecting the ability of the sperm to bind
use only and are not intended for regular use as to the egg
an ongoing contraceptive method. There is a
higher possibility of failure compared with non- 'HſECE[
emergency contraceptives. Frequent use of emer- When used within 72 hours of intercourse, lev-
gency contraception can also result in menstrual onorgestrel is 50% effective in preventing preg-
irregularities, although their repeated use is not nancy. The regimen is more effective the sooner
associated with any known health risks. after intercourse it is taken.
CH 27_p378-396_v3.indd 379 17-07-2015 19:58:18

5CHGV[ mg has been studied and has been found to be

Levonorgestrel-alone emergency contraception equally effective with fewer side effects. It is better
is very safe and does not cause miscarriage or tolerated and more effective than the Yuzpe regi-
affect future fertility. There are no medical con- men. However, there may be a delay in the timing
traindications to the use of levonorgestrel emer- of the next menstrual period with mifepristone
gency contraception pills. especially with the higher dose, which is not usu-
ally seen with the lower dose. Low-dose mifepri-
Si e e ects stone is currently recommended as the drug of
choice for emergency contraception by the World
Side effects are not common and generally mild:
Health Organization (WHO).
• Nausea and rarely vomiting
• Irregular bleeding echanism o action
– Period may occur within 1 week before or The main action of mifepristone is through its anti-
after the expected time progestenic effect. Withdrawal of progesterone
• Breast tenderness, abdominal pain, dizziness,
• disrupts or prevents implantation of a ferti-
headache, and fatigue
lized ovum and
• prevents further development of an implanted
Combined ethinyl estradiol embryo.
levonorgestrel ( u pe regimen) Due to this dual action, mifepristone is an

effective emergency contraceptive when given
Unlike the levonorgestrel pills, the estrogen– before or after implantation has occurred.
progestin combination is not available in pill
packets specifically intended for emergency 'HſECE[
contraception. The patient is instructed to take Mifepristone is 99%–100% effective in prevent-
multiple oral contraceptive pills (OCPs) from ing pregnancy after a single episode of unpro-
packets of combined OCPs. The number of pills tected intercourse, when administered within 72
to be taken should have the equivalent of hours. It may be effective up to 12–17 days.
• 100 Pg of EE plus 0.50 Pg of levonorgestrel.
• This is repeated 12 hours later.
Si e e ects
Mifepristone can cause nausea and vomiting,
echanism o action but to a lesser degree than the Yuzpe regimen.
Combined contraceptive pills, such as levonorg-
estrel alone, prevent pregnancy by preventing or lipristal
delaying ovulation. Ulipristal has primarily an antiprogestin activ-
ity. It can delay ovulation by as much as 5 days.
Si e e ects Like mifepristone, it appears to be effective in the
Because of the high dose of EE, approximately advanced follicular phase, including after lutein-
50% of women taking the combined contracep- izing hormone (LH) levels have begun to rise but
tive pills will experience nausea and vomiting. not peaked (when levonorgestrel may not be
An antiemetic taken an hour before the first dose effective).
will help in reducing the nausea.
'HſECE[
Antiprogestins Mifepristone When used within 72 hours of intercourse, uli-
pristal is 60–70% effective in preventing preg-
and ulipristal nancy. It can be used for emergency contracep-
Mifepristone tion up to 120 hours after intercourse.
Mifepristone (RU-486) is a progesterone and glu-

cocorticoid antagonist. A single dose of mifepris-
Copper intrauterine device
tone 600 mg was initially found to be effective for It is recommended that for emergency contra-
emergency contraception. A lower dose of 25–50 ception, a copper IUD be inserted within 5 days
CH 27_p378-396_v3.indd 380 17-07-2015 19:58:18

of unprotected intercourse. This has the added

Box 27.2 6
KOKPICPFGHſECE[QHGOGTIGPE[
advantage of providing an ongoing, highly effec- contraception after unprotected or
tive contraceptive method. inadequately protected intercourse
The copper IUD primarily prevents fertiliza-
• Levonorgestrel or levonorgestrel + EE
tion by causing a chemical change that damages
Ŧ Most effective
both the sperm and the ovum.
Immediately after intercourse
Up to 72 hours after intercourse
'HſECE[ Ŧ Moderately effective
A copper IUD is >99% effective in prevent- If first dose is taken after 72 hours and up to 5
ing pregnancy when inserted within 5 days of days after intercourse
unprotected intercourse. This is the most effec- Ŧ 7PMPQYPGHſECE[
tive form of emergency contraception available. If taken >5 days after intercourse
• Mifepristone
Once inserted, a woman can continue to use the
Ŧ Effective if taken within 72 hours
IUD as an ongoing method of contraception.
Ŧ May be effective up to 12–17 days
More than 80% of women choose to continue • Ulipristal
with the copper IUD as long-term contraception. Ŧ Effective if taken within 72 hours
Ŧ Also effective between 72 and 120 hours
5CHGV[ • Copper IUD
A copper IUD is very safe for providing emer- Ŧ Inserted within 5 days after intercourse
gency contraception. The risks of infection, Ŧ >99% effective
expulsion, or perforation are low. ethinyl estradiol; D intrauterine device.
Timing of emergency regimens) usually occurs within 1 week of

the expected time. Menstrual periods may be
contraception delayed more than 1 week with antiprogestins.
With any form of emergency contraception, a
Treatment is most efficacious when initiated as pregnancy test should be performed to exclude
soon as possible after the unprotected or inade- the possibility of an intrauterine or ectopic preg-
quately protected intercourse. nancy if
Timing of emergency contraception is sum-
marized in Box 27.2. • bleeding has not occurred within 3–4 weeks;
• there is abdominal pain or irregular bleeding.
Couples who come for emergency contracep-
tion should also be advised a more reliable and
easons for failure of long-term plan for contraception.
emergency contraception
Emergency contraception may be less effective
in the following situations: Pregnancy following
• Obese women [body mass index (BMI)t30 kg/m2] use of emergency
• Intercourse on the day before ovulation
– Probability of conception high contraception
• Further acts of unprotected intercourse after
If a woman finds that she is pregnant after tak-
using emergency contraception
ing emergency contraception, she can choose to
continue or terminate the pregnancy, depending
on her wish for a child.
Follow-up Levonorgestrel or levonorgestrel + EE used
for emergency contraception have no terato-
Menstrual bleeding after emergency contracep- genic effects. The rate of major malformations
tion (progestin-only and estrogen–progestin after first trimester exposure to mifepristone or
CH 27_p378-396_v3.indd 381 17-07-2015 19:58:18

ulipristal is only slightly higher than the expected • The ampulla is wide, thin-walled, somewhat
2%–3% rate in the general population. tortuous and is the largest portion of the tube,
in both length and caliber.
• The isthmus is a narrow, straight, thin-walled
portion of the tube immediately adjacent to
Sterili ation the uterus. The isthmic portion of the fallo-
pian tube is the site for intra-abdominal tubal
Sterilization is a permanent form of contracep- occlusion. Tubal sterilization by the Pomeroy
tion, used in both women and men. Surgical technique should be performed at the isth-
advances have resulted in safe, less invasive ster- mus. If a reversal of the tubal ligation is
ilization procedures, for both females and males. required, the size of the lumen on either side
This safe and highly effective method has been of the cut ends is similar, making reanasto-
accepted as the commonest form of contracep- mosis feasible.
tion globally. Female sterilization is one of the • In the interstitial portion of the tube, the lumen
most popular methods of permanent steriliza- narrows to approximately 1 mm or less as it
tion. The majority of sterilization procedures are passes through the uterine wall, terminating in
done in the postpartum period. Couples also opt the tubal ostium, which opens out in the supero-
for interval procedures. lateral aspect of the uterine cavity. Hysteroscopic
occlusion utilizes this portion of the tube.
Female sterili ation Consent and counseling

Women who are sure that they do not want Sterilization requires informed consent since it
any more children or want to remain childless is a surgical procedure. It is a permanent proce-
opt for female sterilization. It involves surgical dure and this should be explained to the couple.
occlusion of the fallopian tubes bilaterally. It can Only the woman who will be undergoing the
be performed at any time prior to conceiving operation needs to give consent. Consent of the
(interval sterilization) or soon after a pregnancy spouse is not mandatory. The woman’s right to
(postpartum). privacy must be respected. However, it is proba-
bly prudent to involve both partners.
If there is any question of a person not having
Mechanism of action the mental capacity to consent to a procedure
Tubal ligation techniques result in the perma- that will permanently remove their fertility, the
nent occlusion of the fallopian tubes, prevent- case should be referred to a committee in the
ing the ovum and spermatozoa from coming hospital (set up for this issue) or the court.
together. The choice of occlusion method
depends on the surgeon’s training, personal nterstitial
experience, and the technical facilities available. sthmus segment
mpulla
elevant anatomy
The two fallopian tubes lie on either side of the
uterus in the upper margin (mesosalpinx) of the
broad ligament. Each tube is divided into four
parts (Fig. 27.1).
Starting from the lateral end, the parts are as imbrial en
follows:
• The fimbrial end (infundibulum). Fimb- Figure 27.1 Anatomy of the fallopian tube. The isthmic
riectomy was used as a procedure for steriliza- portion of the fallopian tube is the site used for intra-
tion earlier, but it has been given up due to the abdominal tubal occlusion. The interstitial portion is the
high risk of subsequent ectopic pregnancy. site for hysteroscopic occlusion.
CH 27_p378-396_v3.indd 382 17-07-2015 19:58:18

Timing of sterili ation Minilaparotomy sterili ation

The surgical approach and the method chosen A minilaparotomy, often referred to as ‘minilap,’
for the tubal ligation depend on the timing of is an abdominal surgical approach to the fallo-
the procedure. Sterilization can be of the follow- pian tubes through an incision 2–3 cm in length.
ing types: It is employed for PS and may also be used for
interval sterilization if facilities for laparoscopy
• Postpartum sterilization (PS) is done usually
are not available.
within 48 hours of vaginal delivery or along
The minilap may be through two types of
with a cesarean delivery. It is referred to as
approaches:
postpartum sterilization when performed
within 7 days of delivery. • Subumbilical approach (postpartum sterili-
– Immediately postpartum the uterus is still zation)
enlarged and the subumbilical region is • Suprapubic approach (interval sterilization)
thinned out. This facilitates access to the
tubes. A laparoscopic approach is not pos- Postpartum sterili ation
sible in the immediate postpartum period. (subumbilical approach)
– Hospital stay is only a little more than what
is required for a normal delivery (72 hours). As already discussed, this is performed within 48
hours and up to 7 days after delivery.
• Interval sterilization is preferably done imme-
diately after a menstrual period to ensure that reoperative preparation
there is no existing pregnancy. It can be done at Preoperative counseling and informed consent
any time of the menstrual cycle if the woman is are mandatory. History and physical examination
using reliable contraception. must be performed and minimal investigations
• Postabortal sterilization can be performed are required. Hemoglobin should be >8 g/dL.
immediately or within 48 hours following mis-
carriage or induced abortion. Anesthesia
The types of sterilization based on timing are The procedure can be performed under short
listed in Box 27.3. general, spinal, or local anesthesia. Intravenous
sedation with pethidine and promethazine along
with local infiltration with lidocaine is also rec-
oute of sterili ation ommended in under-resourced areas.
Sterilization can be done by
roce ure
• minilaparotomy
• laparoscopy The procedure includes the following steps:
• colpotomy • The patient must be asked to void before the
• hysteroscopy procedure.
• The uterine fundus is palpated and a 2-cm
incision is made 2 cm below the fundus.
Box 27.3 Types of sterili ation • The index finger is introduced into the perito-
• Postpartum sterilization (PS) neal cavity, run along the uterine fundus, pos-
Ŧ Vaginal delivery terior uterine surface and broad ligament, and
Within 48 hours up to 7 days the tube is hooked out.
Ŧ Cesarean section • The tubes should be traced laterally and fim-
Along with cesarean section briae visualized to differentiate it from the
• Interval sterilization round ligament.
Ŧ Immediately after period • A loop of 2–3 cm of tube is picked up with
Ŧ Any time if on contraception Babcock clamp at the isthmus (2–3 cm from
• Postabortal sterilization
the cornua). An avascular area on the mesosal-
Ŧ Immediately
pinx should be selected for application of the
Ŧ Within 48 hours
Babcock clamp.
CH 27_p378-396_v3.indd 383 17-07-2015 19:58:18

• Sterilization is performed by the modified

Box 27.4 Methods of tubal ligation
Pomeroy technique (described later), and
approximately 1 cm of tube is excised. The • Pomeroy method
procedure is repeated on the opposite side. • /QFKſGF2QOGTQ[OGVJQF
• Parkland method
• The ovaries are inspected. The tube is returned
• Other less commonly used methods are
into the abdomen and the abdomen closed.
Ŧ Irving method
• Prophylactic antibiotics are not recommended. Ŧ Uchida method
• Abandoned methods include
Ŧ Madlener technique
Interval sterili ation (suprapubic Ŧ Kroener technique
incision)
Interval sterilization (suprapubic incision) is
performed when the woman is not pregnant, be absorbable so that the cut ends of the tubes
or immediately after a miscarriage or induced separate, reducing chances of recanalization.
abortion. The ligated segment of the fallopian tube is then
excised (Fig. 27.2c). The ligated ends should be
reoperative preparation an anesthesia inspected for hemostasis and the presence of the
The preoperative preparation and anesthesia tubal lumen confirmed. The same procedure is
are the same as for PS. completed on the contralateral side.
The catgut suture resorbs in a few days, and
Incision the two ends of the cut tube separate (Fig. 27.2d).
A 2- to 3-cm transverse incision is made 2–3 cm Permanent suture material increases the chance
above the upper border of the pubic symphysis. of fistula formation and sterilization failure and
so it should not be used.
roce ure
/QFKſGF2QOGTQ[OGVJQF
The procedure includes the following steps:
The modified Pomeroy method differs from the
• The bladder may be catheterized or the patient Pomeroy method in that after the knuckle of the
asked to void just before surgery. tube is ligated, the proximal and distal segments
• The procedure can be performed in the are ligated separately before excising the knuckle
dorsal position. However, if the uterus is of tube. The cut ends separate after a few days.
elevated with a uterine manipulator to the
level of the incision, it is easier to access the ar lan metho
fallopian tube. The patient has to be placed An opening is made in an avascular portion of
in a semilithotomy position for vaginal the mesosalpinx. 0 or 2-0 chromic catgut sutures
manipulation. are passed through the opening. The proxi-
• The rest of the procedure is the same as for PS. mal and distal portions of the tube are ligated.
The intervening segment of the tube is excised
Methods of tubal ligation (Fig. 27.3). The cut ends separate immediately.
The same procedure is completed on the contra-
The commonest methods of tubal ligation are
lateral side.
listed in Box 27.4.
Failure rate: The failure rate for the Pomeroy and
2QOGTQ[OGVJQF modified Pomeroy methods is 5–6 per 1000 pro-
The Pomeroy method is the commonest cedures (0.5%).
method used for tubal occlusion worldwide.
The isthmic portion of the Fallopian tube is Irving metho
identified and grasped with a Babcock clamp The Irving technique can be performed at the
(Fig. 27.2a). The knuckle of the tube is then time of cesarean section. It is time-consuming
ligated with 0 or 2-0 plain or chromic catgut and is associated with more blood loss. A similar
suture (Fig. 27.2b). The suture material should procedure can be accomplished at laparoscopy.
CH 27_p378-396_v3.indd 384 17-07-2015 19:58:18

a. b.
. .
Figure 27.2 Pomeroy method of tubal sterilization. a. The tube is grasped at the isthmic portion. b. The knuckle of the
tube is then ligated with 0 or 2-0 plain or chromic catgut. c. The ligated segment of the fallopian tube is excised. d. The
two ends of the cut tube separate after a few days.
a. b.
Figure 27.3 Parkland method of tubal sterilization. a. An avascular portion of the mesosalpinx is entered and the tube is
separated from the mesosalpinx. b. A 2-cm segment of the midportion of the tube is ligated proximally and distally with
0 chromic catgut. The intervening segment is then excised.
CH 27_p378-396_v3.indd 385 17-07-2015 19:58:19

After ligating the tube and excising a portion, roener techni ue

the proximal end of the tube is buried into the A fimbriectomy is done by clamping the mesos-
posterior myometrium (Fig. 27.4). alpinx and outer third of the tube, and doubly
Failure rate: The Irving sterilization technique ligating it with synthetic absorbable suture. The
has a failure rate of <1 per 1000 cases (0.1%). tube is then excised to make certain that the
entire fimbriated end of the tube (and a portion
chi a metho of ampulla) is removed. The most common com-
The Uchida method is the most complicated ster- plication is incomplete excision of the fimbriae,
ilization procedure and very time-consuming. resulting in sterilization failure. This method is
The tube is separated from the overlying serosa. now abandoned.
After ligation and excision of a portion of the tube, The failure rates of the various methods of
the proximal end is buried inside the mesosalpinx tubal sterilization are enumerated in Box 27.5.
and the distal stump is exteriorized (Fig. 27.5).
Challenges of sterili ation
Failure rate: The failure rate for the Uchida
method is reported to be nil.
techniques done through
minilaparotomy
ther methods Sterilization done through minilaparotomy may
Methods of sterilization that have been aban- be associated with certain operative challenges
doned include the Madlener method and the and complications (Box 27.6).
Kroener technique.
Laparoscopic sterili ation
a lener metho Laparoscopic sterilization is the most commonly
A loop of the ampullary portion of the tube is employed method for interval sterilization.
crushed with a hemostat. The tube is then ligated
with nonabsorbable suture material without Box 27.5 Failure rates for tubal sterili ation
excision of a tubal segment. The Madlener • 2QOGTQ[CPFOQFKſGF2QOGTQ[OGVJQFU
method has been abandoned due to the very Ŧ 5–6 per 1000 procedures (0.5%)
high failure rate resulting from fistula formation • Irving method
beneath the permanent suture material. Ŧ <1 per 1000 cases (0.1%).
• Uchida method
Ŧ Nil
Box 27.6 perative challenges and complica-

tions of sterili ation done through
minilaparatomy
• &KHſEWNV[ in accessing tubes due to adhesions from
Ŧ previous surgery
Ŧ previous cesarean section
• Slippage of suture from tied tubes
Ŧ Prevented by
ligating suture firmly and snugly
not applying unnecessary traction on the suture
• Ligation of round or utero-ovarian ligament instead of tube
Ŧ Prevented by
identification of fimbrial ends of both tubes
• Broad ligament hematoma
• Bowel/bladder injuries
• Infection
Ŧ Wound infection
Figure 27.4 Irving technique for sterilization. The Ŧ Peritonitis
proximal ends of the cut tubes are buried into the posterior Ŧ Pelvic infection
myometrium.
CH 27_p378-396_v3.indd 386 17-07-2015 19:58:19

a. b.
. .
Figure 27.5 Uchida method of sterilization. a. Saline injected into the serosa. b. Segment of the tube isolated.
c. Segment of the tube ligated and excised. d. The serosa is reapproximated so that the proximal stump is buried within
the mesosalpinx and the distal stump is exteriorized.
This is also the method chosen most often for

Box 27.7 Advantages of laparoscopic
post-abortal sterilization. The small incision and sterili ation
rapid recovery make it a very acceptable proce-
dure for women. • Requires small incisions
• Provides opportunity to inspect abdominal and pelvic
organs
• Immediately effective
Advantages of laparoscopic • Rapid return to full activity
• Well accepted by women
sterili ation
Laparoscopic sterilization has several advan-
tages (Box 27.7). However, unexpected findings Procedure for laparoscopy
of dense adhesions or other complications may
necessitate conversion to laparotomy. Laparoscopic sterilization includes the following
steps:
• The patient is placed in the dorsolithotomy
Anesthesia position.
General or spinal anesthesia can be used. • The bladder should be catheterized.
CH 27_p378-396_v3.indd 387 17-07-2015 19:58:19

• A speculum assists in direct visualization of

the cervix.
• The cervix is cleaned with a povidone–iodine
solution and a uterine manipulator is placed
in position. This helps in anteverting a retro-
verted uterus and in bringing the tubes and
ovaries into the operative field.
• An incision is made subumbilically for the
main port.
• Another incision is made for a side port
through which the second laparoscopic instru-
ment is introduced.
• After insertion of the laparoscope, the pelvis is
examined for any pelvic pathology.
• Adhesions are released if present.
a.
Methods for laparoscopic sterili ation

The available methods for laparoscopic steriliza-
tion are listed in Box 27.8.
ipolar electrocoagulation
Bipolar electrocoagulation is safer and has a
lower failure rate than unipolar electrocoag-
ulation. It is therefore preferred over unipolar
electrocoagulation.
Procedure
The procedure consists of the following steps:
• The fallopian tube is grasped and maneuvered
until the fimbrial end is identified. This step is b.
essential to confirm that the tube is the struc- Figure 27.6 Bipolar electrocoagulation of the fallopian
ture that will be coagulated, and not the round tube. a. The left tube is grasped at the isthmic portion with
or utero-ovarian ligament. the bipolar forceps and elevated. b. Bipolar cautery is
• The tube is grasped with bipolar forceps used to coagulate the tube, including the mesosalpinx.
approximately 2–3 cm from the uterine cornu.
A few millimeters of the mesosalpinx should
also be held by the forceps to ensure that the • Current is applied until visual inspection
blades of the forceps have completely encir- shows the tissue grasped has been completely
cled the tube. coagulated and can no longer transmit an
• The tube is lifted up and away to ensure that electrical current.
the forceps are not in contact with any other • The tube is then regrasped and desiccated at
structures (Fig. 27.6). the immediately adjacent sites to coagulate
3 cm of contiguous tube.
Box 27.8 Methods of laparoscopic sterili ation
• The same procedure is repeated on the oppo-
site side.
• Bipolar electrocoagulation
• Banding
Ŧ Falope ring an ing proce ures
• Clip application
Banding procedures are nonthermal methods
Ŧ Hulka-Clemens clip
that use a ring or clip to occlude the tube. Correct
Ŧ Filshie clip
placement is important because full necrosis of
CH 27_p378-396_v3.indd 388 17-07-2015 19:58:19

the tube only occurs after a few days and early

slippage of the ring may lead to failure.
Falope ( oon) ring
The Falope (Yoon) ring is made of a nonreactive
silicone rubber. It is radiopaque, that is, it can be
identified on an X-ray.
The applicator consists of inner grasping
prongs and an outer double-barreled sheath. The
Falope ring is stretched around the base of the
applicator sheath. Some devices allow for double
loading of the rings so that the applicator need
not be inserted into the abdominal cavity twice.
Procedure
The procedure consists of the following steps: a.
• The preloaded ring applicator is placed

through the operating channel of an operating
laparoscope or through a side port.
• The grasping forceps is extended, and the fal-
lopian tube is grasped approximately 2–3 cm
distal to the uterotubal junction (Fig. 27.7a).
• The applicator is designed to draw a
2.5-cm tubal segment into the inner cylinder
(Fig. 27.7b). If the tube is thickened, a complete
knuckle of the tube may be difficult to pull
through.
• Once the tube has been pulled in, the surgeon
squeezes the handle to push the ring over the
drawn-up tubal segment.
• With correct application, a 1.0-cm high knuckle
of the tube will be seen above the ring and both b.
the distal and proximal tubal segments can
be observed entering the tubal ring (Fig. 27.7c).
• The ring cuts off the blood supply to the tubal
knuckle and it will necrose. Following this, the
tubal segments separate.
Clips
The two common clips used for sterilization are
as follows:
• Hulka-Clemens clip
• Filshie clip
ulka-Clemens clip
The Hulka-Clemens clip consists of two toothed .
jaws made of Lexan plastic, joined by a metal Figure 27.7 Application of the Falope ring. a. The
hinge pin. The lower jaw possesses a distal hook. fallopian tube is grasped. b. A 2.5-cm tubal segment is
A gold-plated spring maintains the clip in an drawn into the inner cylinder. c. The Falope ring has been
open position. When completely advanced, the applied on both tubes (arrows) and a 1.0-cm high knuckle
spring closes and locks the jaws. of the tube is seen above the ring.
CH 27_p378-396_v3.indd 389 17-07-2015 19:58:20

The Hulka applicator is specifically designed

to open, close, and lock the clip. It is used
through a laparoscope.
Procedure
The procedure consists of the following steps:
• The fallopian tubes are identified Figure 27.8 Hulka clip applied at a right angle to the
laparoscopically. isthmic portion of the fallopian tube, 2–3 cm from the
• The Hulka clip applicator is introduced with uterotubal junction.
the clip in the closed position.
• The clip is opened after the applicator is intra-
laparoscopic route. The laparoscopic route
abdominal in position.
came to be preferred because of the risk of pelvic
• The hook of the lower jaw is placed against
infection with the transvaginal route. However,
the posterior mesosalpinx, the tube is pulled
routine use of prophylactic antibiotics decreases
slightly upwards, and the clip is applied at
this risk.
right angles to the tube.
The vaginal approach is useful in following
• The clip may be opened and repositioned until
cases:
the correct position is achieved.
• The center piston is now advanced to per- • Very obese patients
manently lock the clip and release it from the • Women with an umbilical hernia
applicator (Fig. 27.8). • Women with a previous umbilical hernia repair
• If the clip has not been applied satisfactorily, a
second clip is placed close to the first. Contraindications to the colpotomy
• The procedure is repeated on the opposite side.
route
Filshie clip
The contraindications to transvaginal tubec-
The Filshie clip is a 2.7-mm long clip made of
tomy are listed in Box 27.9.
titanium with a silicone rubber lining. The clip
is applied laparoscopically with an applicator,
similar to the Hulka spring clip. It is also applied Procedure
at right angles to the isthmus, approximately The procedure includes the following steps:
2–3 cm from the uterotubal junction. The proce-
dure is repeated on the contralateral side. • The woman is placed in the dorsal lithotomy
Initially, the clip occludes the tubal lumen position.
by pressure. As tubal necrosis occurs, the rub- • A retractor is used to expose the cervix. The
ber expands and keeps the lumen blocked. The posterior lip of the cervix is grasped with a
tube eventually divides, and the stumps close as tenaculum.
they heal. • The posterior cul-de-sac (pouch of Douglas)
is exposed. The vaginal wall is held with tissue
forceps and a transverse incision is made in the
Failure rate of laparoscopic vaginal mucosa (colpotomy), along the line of
methods of sterili ation junction of the vaginal wall and the cervix.
• The edge of the vaginal wall is held with tissue
The failure rate of the different laparoscopic forceps that puts the peritoneum on stretch,
methods of sterilization is approximately 2–3
per 1000 (0.2–0.3%).
Box 27.9 Contraindications to transvaginal
tubectomy
Transvaginal tubectomy • Multiple pelvic surgical procedures
• Known endometriosis
Transvaginal tubectomy (TVT) for interval
• Known pelvic adhesive disease
and postabortal sterilization, through a colpo-
• Uterine immobility on examination
tomy, was very popular till the advent of the
CH 27_p378-396_v3.indd 390 17-07-2015 19:58:20

and the peritoneum is cut with scissors. The

opening is enlarged to 2–2.5 cm.
• The retractor is then introduced posterior to
the cervix, just inside the incision. A narrow
moistened pack is introduced into the perito-
neal cavity to keep the bowel out of the opera-
tive field.
a.
• The fallopian tube is visualized and grasped
with a Babcock clamp and brought into the
operative field.
• The sterilization is most commonly done using
the Pomeroy technique.
• After doing the procedure on the contralateral
tube, the colpotomy incision is closed using
interrupted figure-of-eight sutures or a single
running suture of an absorbable material. b.
Complications
Pelvic infection is the most serious postoperative
complication. A single dose of a prophylactic anti-
biotic should be administered within 15 minutes
before the incison, to prevent this complication. .
Figure 27.9 Hysteroscopic insertion of Essure® tubal
ysteroscopic sterili ation occlusion system. a. The device delivery system is
threaded into the tube through the ostium. b. A micro-insert
The principle behind hysteroscopic sterilization
KURNCEGFKPVJGVWDG+VGZRCPFUCPFſNNUVJGVWDGc. Scar
is the blocking of the interstitial portion of the fal-
tissue forms around the micro-insert and blocks the tube.
lopian tubes. The approach is through the ostia,
which are visualized using the hysteroscope. • Quinacrine pellets: Quinacrine scleroses the
interstitial portion of the tube. Pellets of quin-
Methods currently available acrine are placed into the uterus using a tube
similar to a copper T IUD inserter, for two to
ranscervical tubal occlusion three doses 1 month apart.
Transcervical tubal occlusion consists of the fol-
Quinacrine is inexpensive and a good option
lowing steps:
for developing countries. However, the failure
• A metal microinsert (Essure®) is placed under rates are high compared with other methods
hysteroscopic guidance into the interstitial por- of sterilization. There have also been questions
tion of each fallopian tube. The insert consists raised about quinacrine being a carcinogen.
of an inner coil of stainless steel and polyeth-
ylene terephthalate (PET) fibers and an outer Advantages of hysteroscopic
coil of nickel–titanium (nitinol). Following sterili ation
placement, the PET fibers incite a benign tissue
The advantages and disadvantages of hystero-
response and within several weeks, the fibrotic
scopic sterilization are enumerated in Box 27.10.
reaction around the device results in complete
tubal occlusion (Fig. 27.9).
• The Adiana® sterilization method combines
Complications of tubal ligation
controlled thermal damage to the lining of the Tubal ligation is the commonest permanent
fallopian tube with insertion of a nonabsorb- method of sterilization globally. Though they are
able silicone elastomer matrix within the tubal rare (<1%), complications have been reported
lumen. (Box 27.11).
CH 27_p378-396_v3.indd 391 17-07-2015 19:58:20

Box 27.10 Advantages and disadvantages of equest for restoration of

hysteroscopic sterili ation
fertility
Advantages
A couple may request reversal of sterilization.
• No incision
This usually follows the loss of a child. The two
• Less postoperative pain
choices are as follows:
• Can be performed in women
Ŧ With extensive pelvic adhesions • Tubal reanastomosis
Ŧ With contraindications to laparoscopy and laparotomy • In vitro fertilization (IVF)
Disadvantages
Both have approximately 60% chance of a
• Need for contraception for 3 months postprocedure
live pregnancy, although surgical reversal is less
Ŧ 7PVKNVWDCNQEENWUKQPKUEQPſTOGF
expensive.
• 0GGFHQTKOCIKPIUVWF[VQEQPſTOVWDCNQEENWUKQP
• Higher risk of unilateral tubal occlusion
Tubal reanastomosis
Box 27.11 Complications of tubal ligation roce ure o reanastomosis
• Intraoperative and postoperative complications Tubal reanastomosis includes the following
Ŧ Wound infection steps:
Ŧ Hematoma
Ŧ Perforation of the uterus, bladder, or intestine
• The technique involves microsuturing using
Ŧ Complications related to the mode of sterilization 6-0 to 10-0 sutures.
Laparoscopy • The damaged and scarred portions of the
Hysteroscopy tubes are excised.
Colpotomy • The healthy tubal segments are reapproxi-
• Factors that increase the risk of complications mated with as little adhesion formation as
Ŧ Diabetes mellitus possible.
Ŧ General anesthesia
Ŧ Previous abdominal or pelvic surgery Indicators for success of reanastomosis are
Ŧ Obesity listed in Table 27.1.
• Mortality rate of tubal sterilization
Ŧ 4.7 per 100,000 procedures
Ŧ Mostly due to anesthetic complications
Ŧ Lower than pregnancy-associated maternal mortality
Male sterili ation
Vasectomy is among the most reliable and
cost-effective methods of contraception. The
utcomes of sterili ation procedure involves interruption or occlusion of
the vas deferens, and can be performed in an
The following are the outcomes of sterilization:
outpatient setting, under local anesthesia. It has
• Pregnancy is uncommon after tubal steriliza- a 98% success rate. Failure rates of vasectomy
tion. It is highest after clip sterilization, and low- and tubal sterilization are comparable, as are
est after Pomeroy or modified Pomeroy method. their rates of successful reversal.
• When pregnancy does occur, there is a greater Although vasectomy is safer, less costly,
risk that it will be an ectopic pregnancy. and has a significantly shorter postprocedure
Table 27.1 Indicators for success of reanastomosis
Factor Most successful Least successful

Age (years) <35 >35
Type of sterilization Clips, band Electrocautery
Length of residual tube (cm) >6 <6
Years since tubal ligation <10 >10
CH 27_p378-396_v3.indd 392 17-07-2015 19:58:20

recovery time than tubal ligation, tubal ligation • He should not eat for 2 hours before the
is performed five times more often than vasec- procedure.
tomy, worldwide. This resistance to vasectomy is • Aspirin should not be taken for 1–2 weeks
mostly from the husband, due to misperceptions before the procedure.
regarding its effects on male libido and virility. • Nonsteroidal anti-inflammatory agents, plate-
let inhibitors, and anticoagulants should be
Consent and counseling withheld for 3–4 days before the procedure.
Vasectomy requires informed consent since it

is a surgical procedure. It is a permanent proce- Anesthesia
dure and this should be explained to the couple. Vasectomy is done under local anesthesia.
Counseling for a vasectomy should stress that • Before administration of local anesthe-
it has no deleterious effect on male libido or sia, a rapid examination of the genital area
virility. should be performed to confirm anatomic
landmarks.
Methods of vasectomy • For providing anesthesia, a 1- to 2-cm wheal
The following are the methods of vasectomy: should be made at the desired incision site,
usually at the junction of the middle and upper
• Conventional vasectomy one-third of the scrotum bilaterally.
• No-scalpel vasectomy • The needle is advanced through the wheal,
without injecting the anesthetic, parallel and
Conventional vasectomy adjacent to the vas and toward the external
inguinal ring.
Traditionally, a vasectomy involves bilateral
• After gentle aspiration, 2–5 mL of 1% lidocaine
small scrotal incisions through which the vas
(without epinephrine) is injected into the
deferens is visualized and mobilized. A portion
external spermatic fascia.
of the vas is removed and the resulting end or
ends are occluded.
roce ure
reoperative preparation The procedure of vasectomy involves three steps
Preoperative preparation involves the following: (Fig. 27.10):
• The patient should be instructed to shower • Isolation of the vas
and cleanse the genital area thoroughly on the • Interruption of the vas
day of surgery. • Management of the vasal ends
a. b. . .
Figure 27.10 Surgical procedure for vasectomy. a. Incision exposes sheath, which is then opened. b. Vas is exposed and
occluded. c. Segment of approximately 1.5 cm is excised. d. Vas is replaced in sheath after intraluminal fulguration and
sealing of both ends, and skin is sutured.
CH 27_p378-396_v3.indd 393 17-07-2015 19:58:20

Isolation of the vas deferens for transection. The remainder of the

The vas needs to be isolated and maneuvered procedure is performed in a similar fashion to the
subcutaneously to the desired operative site, open incision method. The no-scalpel approach
which is usually at the junction of the middle is associated with less bleeding, infection, and
and upper one-third of the scrotum bilaterally. pain.
• Isolation of the vas utilizes a ‘three-finger tech-

nique’ in which the nondominant hand is used
asal occlusion
to manipulate the vas into a subcutaneous Vasal occlusion with a plug (made of medical
position. grade silicone rubber) requires microsurgery for
• A modification of this technique is to place the implantation and later removal. Either a conven-
thumb of the nondominant hand posterior to tional open or a no-scalpel technique may be
the cord and scrotum, and trapping the vas used to isolate the vas deferens for the implanta-
between the posterior thumb and the middle tion of these devices. Vasal occlusion procedures
finger in a pincer grasp. are still in the experimental stage.
• The index finger is then used to retract the
skin, yielding improved exposure of the vas. Postoperative instructions
• Ligatures and clips should be avoided because
of increased risk of vasectomy failure. It is essential to perform a semen analysis 3
months after the procedure to check for azo-
Interruption of the vas ospermia. Backup contraception should be used
till sterility is confirmed.
The vas is interrupted in the following manner:
• After the vas is maneuvered to the desired Complications of vasectomy
location, a 1- to 2-cm horizontal or vertical
skin incision is made. The complications following vasectomy are
• The vas is grasped with an Allis clamp. listed in Box 27.12.
• After further blunt dissection, the vas is fully Failure rate: The failure rate of vasectomy is very
isolated and is ready for division. low: 1 in 2000 or 0.2%.
• Removal of at least 15 mm length of vas is
recommended. easons for failure
Management of the vasal ends

The following are the various reasons for failure:
Occlusion of the vasal ends is an important step • Pregnancy occurs after a vasectomy in most
in vasectomy. cases because the couple has sexual inter-
course before azoospermia is confirmed.
• Intraluminal fulguration of 1.5 cm of the pro- • True early failure, defined as the presence of
static end of the vas with fascial interposition motile spermatozoa in the ejaculate 4 months
between the prostatic and testicular vasal end after surgery, is usually due to
appears to be the most effective method for – technical error
managing the two cut ends of the vas. – early recanalization of the vas
o-scalpel vasectomy
Box 27.12 Complications following vasectomy
This is the commonest method used for vasec-
tomy. Instead of an incision, the no-scalpel tech- • Hematoma
• Infection
nique uses a puncture made through the scrotal
• Sperm granuloma
skin overlying the vas deferens. The puncture
• Persistent postvasectomy pain
is widened just enough to exteriorize the vas
CH 27_p378-396_v3.indd 394 17-07-2015 19:58:20

Key points
Emergency contraception • Sterilization requires informed consent since it is a

surgical procedure.
• Emergency or postcoital contraception refers to the • Sterilization can be postpartum, postabortion, or an
use of drugs or a device as an emergency approach to interval procedure (unrelated to pregnancy).
preventing pregnancy.
• A minilaparotomy sterilization is employed for post-
• Common indications for emergency contraception partum sterilization and may also be used for interval
include contraceptive failure and failure to use any sterilization if facilities for laparoscopy are not avail-
form of contraception. able.
• The only reason not to give emergency contraception • The commonest methods of tubal ligation are
KUKPCYQOCPYKVJCEQPſTOGFRTGIPCPE[*QYGXGT 2QOGTQ[OGVJQFOQFKſGF2QOGTQ[OGVJQFCPFVJG
if a woman inadvertently takes emergency contracep- Parkland method.
tive pills after she becomes pregnant, the available
evidence suggests that the pills will not harm either • Other less commonly used methods are the Irving
the mother or her fetus. method and the Uchida method. The Madlener meth-
od and the Kroener technique have been abandoned.
• The different methods available for emergency
contraception are levonorgestrel alone, levonorgestrel • 2TQDCDKNKV[QHRTGIPCPE[HQTVJG2QOGTQ[CPFOQFKſGF
with ethinyl estradiol, copper intrauterine device, and Pomeroy methods is 5–6 per 1000 procedures (0.5%).
antiprogestins. • Laparoscopic sterilization is the most commonly em-
• Emergency contraception pills are most effective when ployed method for interval sterilization and postabortal
taken within 72 hours of unprotected intercourse. sterilization. The small incision and rapid recovery
make it a very acceptable procedure for women.
• For emergency contraception, a copper intrauterine
device should be inserted within 5 days of unprotected • Methods for laparoscopic sterilization include bipolar
intercourse. This has the added advantage of provid- electrocoagulation, banding (Falope ring), and clip ap-
ing an ongoing, highly effective contraceptive method. plication (Hulka-Clemens clip, Filshie clip).
• With any form of emergency contraception, a pregnan- • The failure rate of the different laparoscopic methods
cy test should be performed to exclude the possibility of sterilization is approximately 2–3 per 1000.
of an intrauterine or ectopic pregnancy if bleeding has • Transvaginal tubectomy (TVT) for interval and post-
not occurred within 3–4 weeks or if there is abdominal abortal sterilization was very popular till the advent of
pain or irregular bleeding. the laparoscopic route.
• Levonorgestrel or levonorgestrel + ethinyl estradiol • The principle behind hysteroscopic sterilization is the
used for emergency contraception has no teratogenic blocking of the interstitial portion of the fallopian tubes.
GHHGEVU6JGTCVGQHOCLQTOCNHQTOCVKQPUCHVGTſTUV The approach is through the ostia, which are visual-
trimester exposure to mifepristone or ulipristal is only ized using the hysteroscope.
slightly higher than the expected 2%–3% rate in the
general population. • Pregnancy is uncommon after tubal sterilization. It is
highest after clip sterilization, and lowest after post-
Sterilization (for women and men) RCTVWOUVGTKNK\CVKQPWUKPIVJG2QOGTQ[CPFOQFKſGF
Pomeroy methods.
• Sterilization is a permanent form of contraception. It • When pregnancy does occur, there is a greater risk
is a safe and highly effective method that has been that it will be an ectopic pregnancy.
accepted as the commonest form of contraception
globally. • Vasectomy is among the most reliable and cost-effec-
tive methods of contraception. The procedure involves
• Female sterilization involves surgical occlusion of the interruption or occlusion of the vas deferens, and can
fallopian tubes bilaterally. It can be performed at any be performed in an outpatient setting, under local
time prior to conceiving or soon after a pregnancy. anesthesia. It has a 98% success rate.
CH 27_p378-396_v3.indd 395 17-07-2015 19:58:20

Self-Assessment
3. A copper intrauterine device is >99% effective in
Case-based questions preventing pregnancy when inserted within 5 days of
unprotected intercourse.
Case 1 4. +HUJGſPFUVJCVUJGKURTGIPCPVCHVGTVCMKPI
Mrs. JK, 24, and her husband are very worried. They emergency contraception, she can choose to
have been married for 3 months. They were using a con- continue or terminate the pregnancy, depending on
dom for contraception but the condom slipped. her wish for a child. Levonorgestrel or levonorgestrel
+ EE used for emergency contraception has no
1. What would you advise the couple? teratogenic effects.
2. How does levonorgestrel work and what is the dose
for emergency contraception?
3. Which would be the best choice of emergency contra- Case 2
ception if the unprotected intercourse had occurred 4
1. Postpartum sterilization through a minilaparotomy
days ago?
would be the best option for her. A Pomeroy or
4. 9JCVYQWNF[QWCFXKUGVJGEQWRNGKHUJGſPFUJGTUGNH
OQFKſGF2QOGTQ[OGVJQFQHUVGTKNK\CVKQPUJQWNFDG
pregnant after taking the pills?
used.
2. Probability of pregnancy for the Pomeroy and modi-
Case 2 ſGF2QOGTQ[OGVJQFUKUŌRGTRTQEGFWTGU
(0.5%).
Mrs. RE, 26, is pregnant for the second time and is at 3. Laparoscopic sterilization can be done using bipolar
YGGMUŏ IGUVCVKQP *GT ſTUV EJKNF KU [GCTU QNF CPF electrocoagulation, Falope ring, or clip application
healthy. She and her husband are very sure that they do (Hulka-Clemens clip or Filshie clip).
not want any further pregnancies and want a permanent 4. She can undergo a tubal reanastomosis or an in vitro
method. fertilization procedure.
1. Which method of sterilization would be the best op-
tion for her?
2. 9JCVKUVJGHCKNWTGTCVGHQTVJG2QOGTQ[CPFOQFKſGF Sample questions
Pomeroy procedures?
3. What are the methods available for laparoscopic Long-answer questions
sterilization? 1. What is emergency contraception? Describe the
4. If this couple wanted to have another child 5 years options available.
from now, what would be the options? 2. Discuss the methods of tubal sterilization. What are
the advantages, disadvantages, and complications of
the various methods?
Answers 3. What is laparoscopic sterilization? Enumerate the
methods used.
Case 1
1. Advise them a choice of levonorgestrel pills or a Short-answer questions
copper intrauterine device immediately.
2. Levonorgestrel emergency contraceptive pills pre- 1. Timing of emergency contraception
vent pregnancy primarily by preventing or delaying 2. Minilaparotomy
ovulation. They may also prevent fertilization of the 3. Transvaginal (colpotomy) sterilization
ovum by affecting the cervical mucus and the ability 4. Vasectomy
of the sperm to bind to the egg. The dose is a 1.5-mg
tablet taken as a single dose or a 0.75-mg tablet
taken in two doses 12 hours apart.
CH 27_p378-396_v3.indd 396 17-07-2015 19:58:20

Section 5
Obstetric
Complications:
Antepartum
CH 28_p397-404_v3.indd 397 17-07-2015 21:15:03

Hyperemesis
28 Gravidarum
Case scenario
Mrs. GN, 20, had missed her periods and the pregnancy test was posi-
tive. She had experienced mild nausea a week after the expected date of
menstruation but this progressed to vomiting three to four times a day.
She was currently unable to retain even fluids, was weak and tired, and
felt faint on standing. Her concerned husband brought her to the clinic.
She was found to be dehydrated and had a weight loss of 4 kg. She was
immediately hospitalized and necessary treatment was started.
Nausea and vomiting is common in the first tri- Hyperemesis gravidarum is defined as per-
mester of pregnancy and is considered physiolog- sistent, severe vomiting in pregnancy, associated
ical. It usually responds to home remedies, dietary with weight loss of >5% of prepregnancy weight,
modifications, and reassurance. Though often dehydration, and ketonuria. Hypokalemia and
referred to as ‘morning sickness’, symptoms can hypochloremic alkalosis due to loss of potassium
occur at any time. Moderate symptoms can be and hydrochloric acid in the vomitus are also usu-
controlled with oral medication. However, nau- ally present. Distinction between physiological
sea and vomiting maybe severe in some women nausea and vomiting and hyperemesis is import-
and can progress to dehydration and weight loss, ant. Hyperemesis interferes with the quality of
necessitating hospitalization and parenteral med- life.
ications. This severe form of nausea and vomiting
is referred to as hyperemesis gravidarum.
CH 28_p397-404_v3.indd 398 17-07-2015 21:15:03

Hyperemesis Gravidarum 399
Incidence Box 28.3 ormonal changes implicated

in hyperemesis
The incidence of hypermesis varies with ethnic
Elevated levels of
groups and ranges from 0.2% to 2%. Recurrence
of hyperemesis in subsequent pregnancies is as • Estrogen
• Progesterone
high as 15%–20%. Nausea and vomiting begins
• Human chorionic gonadotropin
at 5–6 weeks, peaks at 9–10 weeks, and subsides
• Thyroxine
by 12–14 weeks in 70% of women and by 16–20 • Placental growth hormone
weeks in 90%. • Adrenocortical hormones
• Prolactin
isk factors
Risk factors for hyperemesis are listed in Box 28.1.
ormonal changes
Pathophysiology Several hormones have been implicated in the
pathogenesis of hyperemesis (Box 28.3).
There are several theories regarding the causation Estrogen and progesterone levels are ele-
of hyperemesis but the exact mechanism is not vated in pregnancy and may be implicated in
known. There is a complex interaction between the causation of nausea and vomiting. Human
sociocultural, psychological, and biological fac- chorionic gonadotropin (hCG) increases rap-
tors. The factors involved are given in Box 28.2. idly in the first trimester. Moreover, hypereme-
sis is more common in hydatidiform mole and
multifetal pregnancy, both conditions asso-
Box 28.1 isk factors for hyperemesis ciated with high hCG levels. hCG can stimu-
gravidarum late the thyroid-stimulating hormone (TSH)
• Primigravida
receptors and stimulate production of thyrox-
• Younger age ine. Transient elevation of T4 and suppression
• Multifetal pregnancy of TSH occurs in many women in the first tri-
• Hydatidiform mole mester. These women are clinically euthyroid
• Genetic factors (euthyroid hyperthyroxinemia), have no thy-
• Past history roid enlargement or thyroid antibodies, but
Ŧ Motion sickness may present with hyperemesis. Hyperemesis is
Ŧ Migraine also more common in women who have nausea
Ŧ Hyperemesis in previous pregnancy and vomiting when they are on oral contracep-
Ŧ Female fetus
tives. So far, studies have not proved a causal
association between hormonal changes and
hyperemesis gravidarum.
Box 28.2 Factors involved in causation
of hyperemesis
• Hormonal changes
Gastrointestinal dysfunction
• Gastrointestinal dysfunction Gastric dysmotility induced by progesterone,
• Hepatic dysfunction abnormal vagal and sympathetic tone, and
• Infection thyroxine has also been considered to play a
• Vestibular and olfactory stimuli
causative role. Relaxation of the lower esopha-
• Psychological factors
geal sphincter and the resultant reflux can also
• Genetic factors
give rise to nausea and vomiting.
CH 28_p397-404_v3.indd 399 17-07-2015 21:15:03

epatic dysfunction Box 28.4 Complications of hyperemesis

Mild elevation in serum transaminase levels • Ketosis
occurs in hyperemesis. Impairment of mito- • Hypochloremic alkalosis
chondrial fatty acid oxidation has been found in • Hypokalemia
some women. • 8KVCOKP-FGſEKGPE[*[RQRTQVJTQODKPGOKC
• 6JKCOKPGFGſEKGPE[9GTPKEMGŏUGPEGRJCNQRCVJ[
• /CNNQT[Ō9GKUUVGCTUGUQRJCIGCNTWRVWTG
Infection • &GJ[FTCVKQPJ[RQXQNGOKCRTGTGPCNCPFNCVGTTGPCNHCKNWTG
Infection with Helicobacter pylori may also

play a role. Epidemiological studies have found
an association and treatment of this infection poor renal perfusion, and prerenal failure, which
improves symptoms. if not corrected in a timely fashion can lead to
acute renal failure. Severe retching and vomiting
can cause Mallory–Weiss tears in the esophagus,
estibular and olfactory hematemesis and, rarely, esophageal rupture.
stimuli
Abnormal response to vestibular and olfactory
stimuli has also been thought to cause vomiting. Clinical features
Women who have motion sickness have a hyper-
sensitive labyrinth and a tendency to develop Symptoms
hyperemesis. Many olfactory stimuli such as oily
food and strong perfumes can also trigger vom- The severe nausea of hyperemesis usually begins
iting in pregnancy. by 5–6 weeks and resolves by 12–14 weeks.
Symptoms continue till term or puerperium in 5%
of women. Clinical features are listed in Box 28.5.
Genetic factors
Mothers and sisters of women with hyper-
emesis have a history of the same disorder in
their pregnancies. This may indicate a genetic Clinical evaluation
predisposition.
Clinical evaluation of hyperemesis should begin
with a detailed history (Box 28.6).
Psychological factors
Psychological factors are thought to play a major Physical examination
role. Hyperemesis may be a response to stress or
Physical examination in women with hyperem-
a somatization disorder. The woman’s attitude
esis may reveal signs of dehydration. Physical
toward the pregnancy, environment, and lack of
examination should be as given in Box 28.7.
emotional support may also be underlying factors.
Complications Box 28.5 Clinical features of hyperemesis

Hyperemesis usually responds to treatment gravidarum
and runs a benign course. But, in refractory and • Nausea and vomiting >3 times a day
severe cases, complications can occur (Box 28.4). • Begin at 5–6 weeks
Loss of potassium, hydrogen, and chloride due • Peak at 8–9 weeks
to vomiting can lead to hypokalemia and hypo- • Resolve by 12–14 weeks
chloremic alkalosis. Starvation leads to ketosis. • Fatigue
• Ptyalism (excessive salivation)
Chronic vomiting and poor intake can cause
• 9GKIJVNQUU QT MI
vitamin K and vitamin B1 (thiamine) deficiency.
• Orthostatic hypotension
Persistent dehydration can lead to hypovolemia,
CH 28_p397-404_v3.indd 400 17-07-2015 21:15:04

severe vomiting, liver enzymes can be elevated.

Box 28.6 istory in hyperemesis gravidarum
Hyperthyroxinemia is usually transient and is
• Gestational age at onset not associated with signs of hyperthyroidism.
• Severity Antithyroid medications should not be admin-
• Triggering factors
istered and there is no need for routine thyroid
• History of hematemesis
function tests.
• Past history
Ŧ Hyperemesis in previous pregnancy
Ŧ Motion sickness/migraine
Ŧ Gastrointestinal disorders
Ŧ Vomiting with oral contraceptives Differential diagnosis
• Family history
• Social history
The diagnosis is fairly straightforward in uncom-
plicated cases. Disorders other than hyperemesis
should be considered if the symptoms develop
after 10 weeks, persist after 20 weeks, and are
Box 28.7 Physical examination in hyperemesis
associated with hematemesis, abdominal pain,
gravidarum
fever, elevated blood pressure, and jaundice.
• Vital signs The differential diagnosis is listed in Box 28.9.
Ŧ Pulse
Ŧ Blood pressure—lying and standing
• Signs of dehydration
Ŧ Dry tongue
Ŧ Skin turgor
Management
• 9GKIJV Management consists of dietary modification,
• Urine output
supportive therapy and psychotherapy, and
medical management.
Ŧ Size of uterus
Ŧ To exclude other causes
• Vaginal examination Initial management
Ŧ Size of uterus
Initial management, when the woman is not
dehydrated, is by simple measures such as modifi-
cation of diet, avoidance of triggers, and support-
Investigations ive therapy. Pyridoxine with doxylamine is usually
prescribed as an initial measure (Box 28.10).
Investigations should be aimed at assessing the
severity of the problem and excluding other
causes (Box 28.8). Rise in hematocrit indicates
Diet
dehydration and hemoconcentration. In case of Small meals at 2–3 hourly intervals should be
recommended. Both an empty stomach and
large meals leading to a full stomach can induce
Box 28.8 Investigations in hyperemesis nausea and vomiting. Oily, spicy, and acidic
gravidarum
• Serum electrolytes
• Urine for ketone bodies
Box 28.9 Differential diagnosis
• Hematocrit • Hepatitis
• Ultrasonography to rule out • Gastroenteritis
Ŧ multifetal pregnancy • Cholecystitis
Ŧ hydatidiform mole • Pancreatitis
• If vomiting severe • Peptic ulcer
Ŧ Liver function tests • Preeclampsia
Ŧ Serum creatinine • HELLP syndrome
Ŧ Thyroid function tests
P JGOQN[UKUGNGXCVGFNKXGTGP\[OGUCPFNQYRNCVGNGVU
CH 28_p397-404_v3.indd 401 17-07-2015 21:15:04

carbohydrates, proteins, and fats. It reduces

Box 28.10 Initial management in hyperemesis
gravidarum nausea and may be used alone in doses of 25 mg
four to six times a day. Doxylamine succinate is
• Diet an antihistamine which, when used along with
Ŧ Small meals at 2–3 hourly intervals
pyridoxine, is very effective in the treatment of
Ŧ Fluids with lime/mint and electrolytes
nausea and vomiting and has no teratogenic
Ŧ #XQKFQKN[URKE[CEKFKECPFUYGGVHQQFU
• Avoidance of triggers
effect on the fetus.
• Supportive therapy
• Acupressure Subsequent management
• Medications: Pyridoxine 10 mg + doxylamine 10 mg
Women with hyperemesis not responding to
general measures and those who present with
moderate-to-severe dehydration, ketosis, and
foods and sweets should be avoided. Low-fat, electrolyte disturbances must be hospitalized.
bland, and dry snacks and meals are preferable.
Oral fluids containing lemon, mint, and electro- • Other causes of vomiting should be excluded
lytes should be advised in small quantities but at by clinical examination and investigations.
frequent intervals. • Intravenous thiamine 100 mg should be con-
sidered before initiating IV dextrose, if vitamin
B deficiency is suspected.
Avoidance of triggers • Fluids and electrolytes should be replaced.
The common triggers for vomiting are coffee, Dextrose saline replaces the sodium and chlo-
tea, smell of oil, some spices, and smell of cook- ride loss due to vomiting. Dextrose provides
ing, especially frying foods. These should be carbohydrates and prevents utilization of fat
avoided. In addition, other activities, such as and resultant ketosis.
lying down after food, that are associated with • If serum potassium is low, additional potas-
vomiting should be avoided. sium is added to the IV fluids (20 mmol of
potassium [1.5 g KCl]) to each bottle of IV
fluid.
Supportive therapy • Ringer lactate can also be used initially and
switched to dextrose saline after 6 hours.
Counseling and reassurance that the problem is
• Dextrose saline should be continued till urine
self-limiting, resolves by 12–14 weeks, and does
is free of ketone bodies.
not harm the fetus are helpful. Change of envi-
• Hypomagnesemia and hypocalcemia also
ronment is also recommended.
should be looked for and corrected.
• Oral fluids should be introduced gradually.
Acupressure
Acupressure on the P6 point on the wrist has
been found to be helpful. Randomized trials have Pharmacotherapy
revealed contradicting results. Some women
benefit from it, though it is not certain if it is a Medications are required in most women to con-
placebo effect. trol vomiting. In addition, adjunctive therapy is
used to reduce acid reflux.
Medications
A combination of 10 mg of pyridoxine with
Antiemetic therapy
10 mg of doxylamine is the first-line treatment of If pyridoxine with doxylamine is not effective,
choice for nausea and vomiting in pregnancy. It other drugs may be tried (Table 28.1). Each
relieves symptoms in 70% of women. Pyridoxine drug should be continued for a few days before
is a coenzyme involved in the metabolism of switching to the next.
CH 28_p397-404_v3.indd 402 17-07-2015 21:15:04

Table 28.1 Pharmacotherapy
Drug Dosage oute

Antihistamines
• Doxylamine succinate 10 mg one to two times daily Oral
• Diphenhydramine 25 mg 6 hourly Oral
• Meclizine 25 mg 6 hourly Oral
Dopamine antagonists
• Metoclopramide 10 mg 8 hourly Oral/IV
• Promethazine 12.5–25 mg 4 hourly Oral/rectal/IM
Serotonin antagonists
• Ondansetron 4–8 mg 8 hourly Oral/IV
Ad unctive therapy Treatment of refractory cases consists of the

following:
To reduce gastric acidity, H2 blockers such as
ranitidine or proton pump inhibitors such as • Total parenteral nutrition till vomiting stops
pantoprazole or omeprazole can be combined • Intravenous or intramuscular chlorpromazine
with antiemetics. This combination is effective 25–50 mg 4–6 hourly
in women with heartburn and acid reflux. • Intravenous methyl prednisolone 16 mg
8 hourly for 48–72 hours. This is rarely required
Termination of pregnancy is rarely indicated
Management of refractory in refractory cases not responding to above
measures.
cases
Refractory hyperemesis is rare. Other under-
lying causes for vomiting should be excluded.
Key points
• Nausea and vomiting is common in pregnancy; it ICUVTQKPVGUVKPCNCPFJGRCVKEF[UHWPEVKQPCPFIGPGVKE
DGIKPUD[ŌYGGMURGCMUD[ŌYGGMUCPF factors have been implicated.
subsides by 12–14 weeks. • %QORNKECVKQPUQHJ[RGTGOGUKUKPENWFGMGVQUKU
• Hyperemesis gravidarum is persistent vomiting J[RQEJNQTGOKECNMCNQUKUTGPCNHCKNWTGVJKCOKPG
CUUQEKCVGFYKVJYGKIJVNQUUQH FGJ[FTCVKQP FGſEKGPE[CPF/CNNQT[Ō9GKUUVGCTU
MGVQPWTKCCPFGNGEVTQN[VGFKUVWTDCPEGU • %NKPKECNGXCNWCVKQPEQPUKUVUQHJKUVQT[VTKIIGTHCEVQTU
• 4KUMHCEVQTUHQTJ[RGTGOGUKUCTG[QWPIGTCIGſTUV RCUVJKUVQT[QHOKITCKPGQTOQVKQPUKEMPGUUCPFHCOKN[
RTGIPCPE[J[FCVKFKHQTOOQNGOWNVKHGVCNRTGIPCPE[ and social history.
IGPGVKEHCEVQTUHGOCNGHGVWUCPFRCUVJKUVQT[QH • 8KVCNUKIPUUMKPVWTIQTYGKIJVWTKPGQWVRWVCPFWVGT-
J[RGTGOGUKUOQVKQPUKEMPGUUQTOKITCKPG ine size should be checked.
• There are several theories regarding the causation • $NQQFVGUVUHQTUGTWOGNGEVTQN[VGUCPFJGOCVQETKVWTKPG
of hyperemesis. Hormonal changes such as increase GZCOKPCVKQPHQTMGVQPGDQFKGUCPFWNVTCUQPQITCRJ[VQ
KPJWOCPEJQTKQPKEIQPCFQVTQRKP
J%)VJ[TQZKPG rule out hydatidiform mole and multiple pregnancy are
GUVTQIGPCPFRTQIGUVGTQPG elicobacterKPHGEVKQP essential investigations in hyperemesis.
(Continued)
CH 28_p397-404_v3.indd 403 17-07-2015 21:15:04


• &KHHGTGPVKCNFKCIPQUKUKPENWFGUEJQNGE[UVKVKU • +HVJGTGKUPQTGURQPUGCPFVJGYQOCPKUFGJ[FTCVGF
ICUVTQGPVGTKVKURCPETGCVKVKUJGRCVKVKURGRVKEWNEGT JQURKVCNK\CVKQPKPXGUVKICVKQPUVQGZENWFGQVJGTECWUGU
RTGGENCORUKCCPF*'..2U[PFTQOG intravenous dextrose saline with potassium supplemen-
VCVKQPCPFCFFKVKQPCNRJCTOCEQVJGTCR[CTGKPFKECVGF
• +PKVKCNOCPCIGOGPVKUD[FKGVCT[OQFKſECVKQP
CXQKFCPEGQHVTKIIGTUUWRRQTVKXGVJGTCR[CPF • Refractory cases are rare and may require chlorproma-
doxylamine and pyridoxine. zine or methylprednisolone with total parenteral nutrition.
Self-Assessment
2. &KGVCT[CFLWUVOGPVYKVJHTGSWGPVUOCNNSWCPVK-
Case-based question VKGUQHHQQFCXQKFCPEGQHQKN[CPFURKE[HQQFUCPF
/TU)0JCFOKUUGFJGTRGTKQFUCPFRTGIPCPE[VGUV CXQKFCPEGQHVTKIIGTUCPFFQZ[NCOKPGOIYKVJ
was positive. She had experienced mild nausea a week pyridoxine 10 mg twice daily should be advised.
after the expected date of menstruation but this pro- 3. *QURKVCNK\CVKQPKPVTCXGPQWUFGZVTQUGUCNKPGKPHWUKQP
gressed to vomiting three to four times a day. She was RQVCUUKWOUWRRNGOGPVCVKQPKPVTCXGPQWUVJ[OKPG
PQYPQVCDNGVQTGVCKPGXGPƀWKFUYCUYGCMCPFVKTGFCPF OIKPVTCXGPQWUQPFCPUGVTQPŌOIJQWTN[
felt faint on standing. Her concerned husband brought her 4. 5GTWOGNGEVTQN[VGUWTKPGHQTMGVQPGDQFKGUCPFWNVTC-
to the clinic. She was found to be dehydrated and had a sonography to exclude hydatidiform mole or multifetal
weight loss of 4 kg. RTGIPCPE[+HXQOKVKPIKUUGXGTGCPFRGTUKUVGPVNKXGT
HWPEVKQPVGUVUUGTWOETGCVKPKPGCPFVJ[TQKFHWPEVKQP
1. 9JCVKUVJGFKCIPQUKUNKMGN[VQDG!*QYYKNN[QW
tests are required.
differentiate it from simple nausea and vomiting of
RTGIPCPE[!
2. 9JCVKUVJGKPKVKCNOCPCIGOGPVKHUJGKUPQV
FGJ[FTCVGF!
Sample questions
3. If she does not respond to treatment and presents
YKVJFGJ[FTCVKQPJQYYKNN[QWOCPCIG!
4. 9JCVKPXGUVKICVKQPUYKNN[QWQTFGT! 1. &KUEWUUVJGRCVJQNQI[GVKQNQI[ENKPKECNHGCVWTGUCPF
management of hyperemesis gravidarum.
Answers
1. Hyperemesis gravidarum. If clinical examination
TGXGCNUUKIPUQHFGJ[FTCVKQPQTVJQUVCVKEJ[RQVGPUKQP 1. Etiology of hyperemesis gravidarum
WTKPGKURQUKVKXGHQTMGVQPGDQFKGUCPFGNGEVTQN[VG 2. Complications of hyperemesis gravidarum
CDPQTOCNKVKGUCTGRTGUGPVKVKUPQVUKORNGPCWUGCCPF
vomiting of pregnancy.
CH 28_p397-404_v3.indd 404 17-07-2015 21:15:04

Miscarriage
29 and Recurrent
Pregnancy Loss
Case scenario
Mrs. HR, 31, gravida 3, para 0, Ab 3, live 0, had three early miscarriages.
She reported no medical problems or previous surgeries. She had recur-
rent pregnancy loss and needed investigation for the cause so that
appropriate treatment, if any, could be offered.
Introduction or spontaneous abortion. The World Health

Organization (WHO) defines miscarriage as
Miscarriages are quite common, as human expulsion or extraction of an embryo (at or
reproduction is surprisingly inefficient and before 10 weeks) or fetus (after 10 weeks),
wasteful. Miscarriages occur in approximately weighing 500 g or less.
15% of confirmed pregnancies.
Recurrent pregnancy loss is a common clin-
ical problem, occurring in approximately 1%
Incidence
of reproductive-aged women. Unfortunately, a Miscarriages occur in approximately 15% of
definite cause can be established only in 50% confirmed pregnancies. If the loss of unrecog-
of couples. Many supposed causes of recurrent nized or subclinical pregnancy losses is taken
pregnancy loss are controversial. Out of des- into consideration, the rate of loss is estimated
peration, both the affected couples and their to be as high as 30% of all pregnancies. The
physicians sometimes turn to untested and con- risk of pregnancy loss decreases with increas-
troversial treatment options. ing gestational age. Although the miscarriage
rate up to 20 weeks varies between 8% and
20%, having had a child in a previous preg-
Miscarriage nancy reduces a woman’s risk of miscarriage
to 5%. The risk of miscarriage increases with
&GſPKVKQP increasing maternal age. It is 10% in women
aged 20–24 years, 50% in women aged 40–44
The loss of a pregnancy before 20 weeks is years, and 80% in women aged 45 years or
called miscarriage, early pregnancy loss, older (Table 29.1).
CH 29_p405_427_v3.indd 405 17-07-2015 21:45:05

Table 29.1 Incidence of miscarriage in relation

ecurrent miscarriage
to gestational age and maternal age Known earlier as habitual abortion, recurrent
Miscarriage Incidence rate ( ) miscarriage is defined as three or more consecu-
tive pregnancy losses before 20 weeks’ gestation.
+PEQPſTOGFRTGIPCPEKGU 15
Up to 20 weeks 8–20
+PWPTGEQIPK\GFQTUWDENKPKECN 30
RTGIPCPEKGU
isk factors for miscarriage
9QOCPYKVJRTGXKQWUEJKNF 5 The best predictors for miscarriage are maternal
9QOGPCIGFŌ[GCTU 10 age and previous history of miscarriage.
9QOGPCIGFŌ[GCTU 50
9QOGPCIGFŮ[GCTU 80
Advanced maternal age
Advancing maternal age has an effect on miscar-
riage rate. Age primarily affects the oocyte. Older
Terminology used oocytes tend to result in chromosomal abnor-
malities, and therefore the pregnancies resulting
for miscarriages from them tend to miscarry. This is proved by
the fact that when oocytes from young women
Miscarriage is the commonest complication of are used to create embryos for transfer to older
early pregnancy. It denotes failure of abnormal recipients, implantation and pregnancy rates
embryos or fetuses to progress to viability. match those seen in younger women.
Biochemical loss Previous spontaneous miscarriage

Biochemical loss is a pregnancy loss that occurs Having had one miscarriage increases the risk
after a positive pregnancy test [urinary or serum of miscarriage in subsequent pregnancies. The
E-human chorionic gonadotropin (EhCG)] but risk of miscarriage in future pregnancy increases
before ultrasound or histological verification. exponentially with increasing number of mis-
This usually occurs before 6 weeks’ gestation. carriages (Table 29.2). This is because of the
increased probability of an underlying cause for
the miscarriage.
Clinical miscarriage
The term ‘clinical miscarriage’ is used when the ther risk factors
presence of an intrauterine pregnancy has been
The effect of caffeine on spontaneous miscar-
confirmed by ultrasound examination or histo-
riage is controversial, but one to two cups of cof-
logical evidence. Depending on the gestational
fee or the equivalent of 200–300 mg of caffeine/
age that the miscarriage occurs at, it may be sub-
day as coffee, tea, or hot chocolate is considered
divided into the following:
safe. The risk increases with very high levels of
• Early clinical pregnancy loss (before gesta- intake (1000 mg/day or more).
tional week 10) and
• Late clinical pregnancy loss (gestational weeks Table 29.2 isk of miscarriage in a future
10–20) pregnancy
umber of isk of miscarriage in

Missed miscarriage miscarriages future pregnancy ( )
(missed abortion) 0 5
1 20
A missed miscarriage in the first trimester is
EQPUGEWVKXGOKUECTTKCIGU 28
characterized by the arrest of embryonic or fetal
development. The cervix is closed and there is no QTOQTGEQPUGEWVKXG 43
OKUECTTKCIGU
or only slight bleeding.
CH 29_p405_427_v3.indd 406 17-07-2015 21:45:05

/KUECTTKCIGCPF4GEWTTGPV2TGIPCPE[.QUU 407
Nonsteroidal anti-inflammatory drugs

Box 29.2 Etiology of miscarriage
(NSAIDs), if used around the time of concep-
ſTUVCPFUGEQPFVTKOGUVGTU
tion, are associated with an increased risk of
miscarriage. These are, therefore, best avoided in • %JTQOQUQOCNFGHGEVU
Ŧ #PGWRNQKF[
VTKUQO[EQOOQPGUV
women trying for a pregnancy.
Ŧ Structural aberrations
Low levels of folate are associated with a
Ŧ /QUCKEKUO
higher rate of miscarriage, in the presence of • %QPIGPKVCNCPQOCNKGU
chromosomal abnormality. If the fetus has no • 7VGTKPGCDPQTOCNKVKGU
aneuploidy, folate levels have no effect on mis- Ŧ 7VGTKPGUGRVWO
carriage rate. Ŧ 5WDOWEQWUſDTQKF
Very low and very high body mass index (BMI) • %GTXKECNKPUWHſEKGPE[
KPEQORGVGPEG
are also risk factors. Other risk factors include Ŧ 1PN[KPUGEQPFVTKOGUVGT
smoking (Box 29.1). • Infections
Ŧ isteria monocytogenes
Ŧ o oplasma gondii
Ŧ 2CTXQXKTWU$
Etiology of spontaneous Ŧ 4WDGNNC
OKUECTTKCIG
ſTUVCPF Ŧ *GTRGUUKORNGZ
Ŧ %[VQOGICNQXKTWU
second trimesters) • /CVGTPCNOGFKECNEQPFKVKQPU
Ŧ 6J[TQKFF[UHWPEVKQP
Although most etiological factors can cause first Ŧ 2QN[E[UVKEQXCTKCPU[PFTQOG
and second trimester losses, some factors are Ŧ Uncontrolled diabetes
more commonly associated with first trimester Ŧ %WUJKPIU[PFTQOG
losses and some with second trimester miscar- • +OOWPQNQIKECNHCEVQTU
Ŧ 5.'
riages (Box 29.2).
Ŧ #PVKRJQURJQNKRKFCPVKDQF[U[PFTQOG
• Chromosomal and congenital anomalies, • 2TGPCVCNRTQEGFWTGU
maternal infections, medical disorders, and Ŧ %JQTKQPKEXKNNWUUCORNKPI
antiphospholipid antibody (APA) syndrome Ŧ #OPKQEGPVGUKU
can cause miscarriage in the first or second S U[UVGOKENWRWUGT[VJGOCVQUWU
trimester.
• Uterine anomalies, cervical incompetence, anomaly most often associated with miscar-
and thrombophilias are associated more often riage. Structural chromosomal aberrations and
with second trimester losses. mosaicism account for a small number of mis-
carriages. The earlier the pregnancy loss occurs,
Chromosomal defects the higher the chance of chromosomal defect as
the cause (Table 29.3).
Approximately 50% of miscarriages are caused
by chromosomal defects. Aneuploidy (of which
trisomy is the commonest) is the chromosomal Congenital anomalies
Major anatomic defects in the fetus, whether
Box 29.1 isk factors for spontaneous resulting from chromosomal or genetic causes,
miscarriage
• /CVGTPCNCIG
Table 29.3 Correlation of chromosomal defects
• 2TGXKQWUURQPVCPGQWUOKUECTTKCIG with weeks of miscarriage
• .QYHQNCVGNGXGNU
• *KIJEQPUWORVKQPQHECHHGKPG Week of Prevalence of
• 05#+&UCVVKOGQHEQPEGRVKQP miscarriage chromosomal defect ( )
• 8GT[JKIJQTXGT[NQY$/+
GORV[UCE 90
• 5OQMKPI
Between 8 and 11 50
B DQF[OCUUKPFGZ SA DsPQPUVGTQKFCNCPVKKPƀCOOCVQT[ Between 16 and 19 30
FTWIU
CH 29_p405_427_v3.indd 407 17-07-2015 21:45:06

are usually lethal and can result in spontaneous spontaneous miscarriages. Women with and
miscarriages. Almost 20% of morphologically without SLE, who have antiphospholipid anti-
abnormal fetuses have a normal karyotype, and bodies, are at a high risk of miscarriage in the
there is no known explanation for why these first or second trimester. Antiphospholipid anti-
anatomic defects arise. body syndrome is discussed further in Chapter
54, Thromboembolic disorders.
terine abnormalities
A uterine septum may lead to defective implan- Prenatal procedures
tation and has been associated with miscarriage. Invasive procedures such as chorionic villus
Other Müllerian anomalies such as bicornuate sampling or amniocentesis can result in a mis-
and unicornuate uterus are also associated with carriage in 0.5%–1% of cases.
second trimester miscarriages. Similarly, a sub-
mucosal fibroid can interfere with implantation
and growth and may result in miscarriage. atural progression
%GTXKECNKPUWHſEKGPE[ of miscarriage
(incompetence) A spontaneous miscarriage is a process that can
progress through four stages but may not always
Congenital or acquired structural weakness of
go through each stage. The natural progres-
the cervix is called cervical insufficiency (ear-
sion of a miscarriage is threatened, inevitable,
lier known as cervical incompetence). Cervical
incomplete, and complete.
insufficiency can lead to recurrent second tri-
mester losses/preterm births. It is not associ-
ated with early pregnancy loss (see the Section, Threatened miscarriage
Recurrent pregnancy loss).
Approximately 25% of all pregnant women have
some degree of vaginal bleeding during the first
Infectious causes two trimesters. Only half of these cases progress
to an actual miscarriage.
Many acute maternal infections have been impli-
A threatened miscarriage (Fig. 29.1) con-
cated in miscarriage. Some of the organisms
sists of vaginal bleeding, with or without mild
known to cause miscarriage are Listeria mono-
abdominal/pelvic pain, in the presence of a
cytogenes, Toxoplasma gondii, parvovirus B19,
rubella, herpes simplex, or cytomegalovirus. It is
important to remember that these do not cause
recurrent pregnancy loss (RPL).
Maternal medical conditions

Endocrine disorders such as thyroid dysfunction,
polycystic ovarian syndrome, uncontrolled dia-
Uterus
betes, and Cushing syndrome have been impli-
cated in miscarriage. Progesterone deficiency
has been studied as an etiological factor, but
there is no evidence that there is a difference in
progesterone levels in normal pregnancies or
failed pregnancies. Cer i
Immunological factors
Figure 29.1 6JTGCVGPGFOKUECTTKCIG8CIKPCNDNGGFKPIKU
Autoimmune diseases such as systemic lupus RTGUGPVVJGEGTXKZKUENQUGFCPFVJGRTGIPCPE[CRRGCTU
erythematosus (SLE) are associated with PQTOCNQPWNVTCUQWPF
CH 29_p405_427_v3.indd 408 17-07-2015 21:45:06

live pregnancy. On abdominal examination, to an incomplete or complete miscarriage (Fig.

the uterus might be diffusely tender. On vaginal 29.2a). The vaginal bleeding is significant and is
examination, the definitive diagnostic sign is a accompanied with cramping pelvic pains. The
closed cervical os. The uterine size corresponds uterine size may or may not correspond to the
to period of gestation. Movement of the cervix gestational age. The cervical os is open, and the
does not elicit significant pain, thus ruling out products of conception are felt at the level of the
ectopic pregnancy. The bleeding accompanying internal os or even in the cervical canal (Box 29.4).
a threatened miscarriage is usually not very sig- The ultrasound examination will reveal the preg-
nificant and is rarely severe (Box 29.3). An ultra- nancy in the lower portion of the uterus (close to
sound examination will reveal an intrauterine the internal os) or in the cervical canal (Fig. 29.2b).
pregnancy consistent with the gestational age.
If the gestational age is 6 weeks or more, cardiac
activity will be identified.
Incomplete miscarriage
When a miscarriage occurs but portions of the
Inevitable miscarriage products of conception are still retained in the
Like the name suggests, this stage of a miscarriage

cannot be stopped and will inevitably proceed
Box 29.4 Diagnosis of inevitable miscarriage
• #DFQOKPCNGZCOKPCVKQP
Box 29.3 Diagnosis of threatened miscarriage Ŧ Uterine tenderness
Ŧ 7VGTWU KPVGTOKVVGPVN[ JCTF CPF INQDWNCT
EQPVTCEV-
• #DFQOKPCNGZCOKPCVKQP KPI
Ŧ Diffuse uterine tenderness • 8CIKPCNGZCOKPCVKQP
• 8CIKPCNGZCOKPCVKQP Ŧ 8CIKPCNDNGGFKPI
Ŧ 8CIKPCNDNGGFKPI
WUWCNN[OKNF Ŧ Open cervical os and cervical canal
Ŧ Closed cervical os Ŧ 2TQFWEVUQHEQPEGRVKQPHGNV
Ŧ 7VGTKPGUK\GEQTTGURQPFKPIVQRGTKQFQHIGUVCVKQP VJTQWIJVJGKPVGTPCNQU
Ŧ No products of conception passed KPVJGEGTXKECNECPCN
Ŧ 0QVGPFGTPGUUQPOQXGOGPVQHEGTXKZ • 7NVTCUQWPFGZCOKPCVKQP
• 7NVTCUQWPFGZCOKPCVKQP Ŧ 2TQFWEVUQHEQPEGRVKQPGPVGTKPIQTN[KPIKPEGTXKECN
Ŧ +PVTCWVGTKPGRTGIPCPE[YKVJECTFKCECEVKXKV[ ECPCN
(KI
ilate cer i ith

lo lying pro ucts
an acti e blee ing
a. b.
Figure 29.2 +PGXKVCDNGOKUECTTKCIGa.%GTXKZKUFKNCVGFCPFRTQFWEVUCTGHGNVCVVJGKPVGTPCNQUQTKPVJGEGTXKECNECPCN

b.7NVTCUQWPFKOCIGUJQYKPIVJGRTQFWEVUQHEQPEGRVKQPN[KPIKPVJGEGTXKECNECPCN
Photo courtesy/GFKUECP5[UVGOU
%JGPPCK
CH 29_p405_427_v3.indd 409 17-07-2015 21:45:06

uterus, it is called an incomplete miscarriage.

Box 29.5 Diagnosis of incomplete miscarriage
Since the uterus is not able to contract down
completely, these retained bits may result in • *KUVQT[
severe bleeding that can sometimes be massive Ŧ $NGGFKPICPFRCKP
Ŧ 2CUUCIGQHVKUUWG
enough to cause hypovolemic shock. In an effort
to push out the retained products of conception,
the uterus may continue to contract and this • 8CIKPCNGZCOKPCVKQP
results in abdominal pain. Ŧ 7VGTKPGUK\GUOCNNGTVJCPGZRGEVGF
Incomplete miscarriages tend to occur after Ŧ Open or closed internal os
12 weeks. In earlier pregnancies, the entire ges- Ŧ 2CTVKCNRTQFWEVUQHEQPEGRVKQP
tation will be expelled. After 12 weeks, the mem- $GKPIRCUUGF
branes may rupture and the fetus expelled but .[KPIKPVJGXCIKPC
the placental tissue may still be retained, result- • 7NVTCUQWPFGZCOKPCVKQP
ing in an incomplete miscarriage (Fig. 29.3a). Ŧ 4GVCKPGFRTQFWEVUQHEQPEGRVKQP
An incomplete miscarriage is diagnosed from 'PFQOGVTKWO OO
the history of passage of tissue with continued 'EJQIGPKEQTJGVGTQIGPGQWUOCVGTKCN
8CUEWNCTKV[RTGUGPV
bleeding. Examination of the uterus will reveal
a uterine size smaller than expected for the ges-
tational age, but the uterus may still be bulky
and boggy (not well contracted). The cervical os
Complete miscarriage
may be open with products of conception being In a complete miscarriage, the products of con-
passed, or the internal cervical os may be closed. ception have been totally expelled from the
Ultrasonography will help confirm the pres- uterine cavity and cervix. The woman usually
ence of retained products of conception in the gives a history of several hours of vaginal bleed-
uterus (Fig. 29.3b). Retained products are sus- ing with severe pelvic cramping, followed by
pected if the endometrium is >5 mm and a vari- passage of tissue, which eases the bleeding and
able amount of echogenic or heterogeneous cramping (Box 29.6). Commonly, this event hap-
material is imaged within the endometrial cavity. pens at home.
There will be vascularity that confirms the diag- On examination, the uterus is smaller than the
nosis and helps to differentiate it from an intra- gestational age and well contracted. The cervix is
uterine blood clot (Box 29.5). closed. Since the process has resolved, vaginal
a. b.
Figure 29.3 +PEQORNGVGOKUECTTKCIGa.2TQFWEVUQHEQPEGRVKQPJCXGDGGPRCTVKCNN[GZRGNNGFb.7NVTCUQWPFKOCIG
UJQYKPITGVCKPGFRTQFWEVUQHEQPEGRVKQPKPVJGWRRGTRCTVQHVJGWVGTKPGECXKV[
Photo courtesy/GFKUECP5[UVGOU
%JGPPCK
CH 29_p405_427_v3.indd 410 17-07-2015 21:45:06

Box 29.6 Diagnosis of complete miscarriage

• *KUVQT[
Ŧ 5GXGTCNJQWTUQHDNGGFKPICPFRCKP
Ŧ 'CUKPIQHHQHRCKPCHVGTRCUUCIGQHVKUUWG
Ŧ Mild uterine tenderness
• 8CIKPCNGZCOKPCVKQP
Ŧ 7VGTWUUOCNNCPFEQPVTCEVGF
Ŧ %GTXKZENQUGF
• 7NVTCUQWPFGZCOKPCVKQP
Ŧ 'ORV[WVGTKPGECXKV[
• 'ZCOKPCVKQPQHCDQTVWU
Figure 29.4 /KUUGFOKUECTTKCIGYKVJCPGORV[UCEQP

WNVTCUQWPFGZCOKPCVKQP6JGUCEFKCOGVGTKU OO
bleeding might be minimal and the abdomi- YKVJPQ[QNMUCEQTGODT[QUGGPYKVJKPVJGUCE
mage
nal pain may have subsided. Ultrasonography courtesy/GFKUECP5[UVGOU%JGPPCK
reveals an empty uterine cavity. Diagnosis may
also be confirmed by examining the abortus.
Missed miscarriage developed than its calculated gestational age

and has no cardiac activity. It may also present as
A missed miscarriage in the first trimester is
an empty gestational sac.
characterized by the arrest of embryonic or fetal
development. The cervix is closed and there is no
or only slight bleeding. Usually the bleeding is in Empty sac (anembryonic
the form of brownish altered blood. The symp- pregnancy, blighted ovum )
toms of pregnancy (nausea, breast tenderness,
tiredness) may persist for some time after the fetal A missed abortion could present sonographi-
demise, but soon the woman may find that they cally as an empty sac (Fig. 29.4). This is defined
disappear (Box 29.7). It is better termed delayed as a gestational sac >25 mm without evidence of
miscarriage or silent miscarriage, although this embryonic tissues (yolk sac or embryo). The term
terminology has not been adopted widely. ‘blighted ovum’ should not be used any longer.
The diagnosis is made on routine ultraso- Differences between different types of mis-
nography when the fetus is found to be less carriage are given in Table 29.4.
Diagnosis and
Box 29.7 Diagnosis of missed miscarriage
• *KUVQT[
evaluation
Ŧ 6JGTG CTG OKPKOCN QT PQ U[ORVQOU QH DNGGFKPI The diagnosis of miscarriage necessitates care-
pain
ful elicitation of history. A clinical examination
Ŧ 5[ORVQOUQHRTGIPCPE[OC[FKUCRRGCT
along with an ultrasound examination will help
Ŧ 7VGTWUOC[QTOC[PQVDGRCNRCDNG define the type of miscarriage (Box 29.8).
Ŧ (GVCNJGCTVVQPGUCTGKPCWFKDNG
• 8CIKPCNGZCOKPCVKQP
Ŧ 7VGTKPGUK\GKUUOCNNGTVJCPGZRGEVGF
istory
• 7NVTCUQWPFGZCOKPCVKQP It is important to obtain a detailed history regard-
Ŧ 'ORV[UCEKURTGUGPV ing abdominal pain and its severity, amount of
Ŧ If fetus present
bleeding and color of blood, passage of prod-
7PFGXGNQRGFQTUOCNNGTVJCPFCVGU
ucts, and disappearance of symptoms of preg-
%CTFKCECEVKXKV[KUCDUGPV
nancy such as nausea and vomiting.
CH 29_p405_427_v3.indd 411 17-07-2015 21:45:06

Table 29.4 Differences between various stages types of miscarriage
Threatened Inevitable Incomplete Complete Missed

miscarriage miscarriage miscarriage miscarriage miscarriage
$NGGFKPI Mild *GCX[RTQHWUG *GCX[RTQHWUG *GCX[RTQHWUG /KPKOCN
DTQYPKUJ
#DFQOKPCNRCKP Mild Moderate Moderate Moderate Absent
7VGTKPGUK\G Corresponds Corresponds to )GUVCVKQPCNCIG )GUVCVKQPCNCIG )GUVCVKQPCNCIG
ŭIGUVCVKQPCN VQIGUVCVKQPCN IGUVCVKQPCNCIG
CIG CIG
Cervical os Closed Open Open %NQUGFQRGP Closed
Ultrasound .KXGHGVWU 2TQFWEVUNQYKP 5OCNNDKVUQH %CXKV[GORV[ &GCFHGVWU
ECXKV[ products seen CPGODT[QPKEUCE
KPVJGECXKV[
had an antenatal checkup where these tests have

Box 29.8 Examination and investigations
in miscarraige already been done, it is important to check hemo-
globin and hematocrit because severe anemia
• *KUVQT[ due to ongoing bleeding may indicate need for
Ŧ #DFQOKPCNRCKP
transfusion. The Rh type should be known since
Ŧ $NGGFKPI
a woman who is Rh negative will require anti-D
#OQWPV
Color
to prevent Rh alloimmunization. Serology should
Ŧ 5[ORVQOUQHRTGIPCPE[ be done to rule out the presence of syphilis or
• 2J[UKECNGZCOKPCVKQP human immunodeficiency virus (HIV).
Ŧ 8KVCNUKIPU
Ŧ 7VGTKPGUK\G
Ŧ Condition of cervical os
ltrasound examination
Ŧ 2TGUGPEGQHRTQFWEVUQHEQPEGRVKQP An ultrasound examination plays an important
• +PXGUVKICVKQPU role in diagnosing and classifying miscarriages.
Ŧ *GOQINQDKPCPFJGOCVQETKV
5GXGTG CPGOKC OC[ KPFKECVG PGGF HQT VTCPUHW-
sion
Ŧ 4JV[RG
ltrasound diagnosis
4JPGICVKXG of miscarriage
- #PVK&VQRTGXGPV4JCNNQKOOWPK\CVKQP
Ŧ 5GTQNQI[ In early pregnancy a failed pregnancy can be
8&4.424 suspected when certain sonographic criteria
HIV 1 and 2 are not met using transvaginal scan (TVS). This
• 7NVTCUQWPFGZCOKPCVKQP is called ‘discriminatory level’ and the absence
JWOCPKOOWPQFGſEKGPE[XKTWU P TCRKFRNCUOCTGCIKP of a finding at the discriminatory level predicts a
VGUVHQTU[RJKNKU D XGPGTGCNFKUGCUGTGUGCTEJNCDQTCVQT[VGUV
nonviable pregnancy (Table 29.5).
HQTU[RJKNKU
Clinical evaluation Table 29.5 Discriminatory levels for early

pregnancy events
ital signs
Time of visuali ation 'ZRGEVGFſPFKPI
Initial examination should include recording on transvaginal scan
of pulse rate and blood pressure, especially if OGPUVTWCNYGGMU Gestational sac
bleeding is heavy. OGPUVTWCNYGGMU 'ODT[QPKERQNG
/GCPUCEFKCOGVGT Yolk sac
Blood tests ŌOO
Certain blood tests are essential when a woman %TQYPŌTWORNGPIVJ %CTFKCECEVKXKV[
OO
presents with a miscarriage. If she has not recently
CH 29_p405_427_v3.indd 412 17-07-2015 21:45:06

ltrasound criteria for • Free floating in the gestational sac rather than
at the periphery
failed early pregnancy • Calcified
The diagnosis of a failed early pregnancy can be
based on the following criteria: Fetal bradycardia
• Gestational sac When a first trimester ultrasound is done, cardiac
– No fetal pole or yolk sac in a gestational sac activity can be identified at t6 weeks’ gestation.
with mean sac diameter (MSD) t25 mm The normal fetal heart rate in early pregnancy is
– No change in MSD on consecutive scans 120–140 bpm. A fetal heart rate <100 bpm at 6–7
7 days apart weeks is considered to be bradycardia. This is
• Crown–rump length (CRL) associated with a 40% risk of fetal loss. When the
– Either of the following findings fetal heart rate is <70 bpm at 6–8 weeks, it pre-
No heartbeat in an embryo with CRL dicts a 100% risk of fetal loss.
t7 mm When fetal bradycardia is observed in early
CRL <7 mm and no interval growth over pregnancy, it is important to perform a follow-up
5–7 days ultrasound examination in 1 week to confirm or
rule out early fetal demise.
If there is any doubt about the viability of the
fetus, it is better to give the pregnancy the benefit
of the doubt. The ultrasound should be repeated Subchorionic hematoma
after 5–7 days, unless there is heavy bleeding and A subchorionic hematoma is a collection of
signs of an inevitable miscarriage. If there is no blood between the chorion and the endome-
growth, or if cardiac activity does not appear, then trium (Fig. 29.5). This may occur spontaneously
the final diagnosis of missed miscarriage is made. and is usually associated with vaginal bleeding.
In the presence of vaginal bleeding, an important
finding on ultrasound examination is a subcho-
7NVTCUQWPFſPFKPIUVJCV rionic hematoma (Fig. 29.6). Although a small
may predict miscarriage hematoma does not increase the risk of miscar-
riage, larger hematomas have been implicated in
Certain ultrasound findings are predictors of a an increased risk of miscarriage and other poor
failed pregnancy. pregnancy outcomes such as placental abrup-
tion, preterm prelabor rupture of membranes,
Abnormal gestational sac preterm labor, and stillbirth (Box 29.9).
The following abnormalities in the gestational
sac may predict a poor outcome and an increased
risk of miscarriage:
• A gestational sac that is abnormally small (the Placenta
amnion is snug around the embryo) or abnor-
mally large (the embryo seems to be floating ubchorionic
hematoma
in the fluid)
• A gestational sac with an irregular contour
• Absence of the double decidual sac sign Chorion
• Low sac position in the uterus
Abnormal yolk sac mniotic ca ity
A yolk sac with the following characteristics may

be predictive of a pregnancy loss:
• Large for gestational age Figure 29.5 5WDEJQTKQPKEJGOCVQOC%QNNGEVKQPQHDNQQF
• Irregular DGVYGGPVJGEJQTKQPCPFVJGGPFQOGVTKWO
CH 29_p405_427_v3.indd 413 17-07-2015 21:45:07

are caused by fetal chromosomal abnormali-

ties, it seems unlikely that progestogens could
prevent a miscarriage. At present there is no
strong evidence to support its use.
• Human chorionic gonadotropin and uterine
muscle relaxants (e.g., tocolytics, E-agonists)
have not been found to be useful and are not
recommended.
Inevitable and
incomplete miscarriage
Women with an inevitable or incomplete mis-
carriage may present with profuse bleeding.
Figure 29. 6 7NVTCUQWPFKOCIGQHCNCTIGUWDEJQTKQPKE
JGOCVQOCN[KPICFLCEGPVVQVJGIGUVCVKQPCNUCE
+OCIG emodynamic instability
EQWTVGU[/GFKUECP5[UVGOU%JGPPCK and hypovolemic shock
If the woman is in hypovolemic shock, resusci-
Box 29.9 Subchorionic hematoma tation with intravenous fluids should be started
• 5OCNNJGOCVQOC and blood products may be required. After the
Ŧ 0QKPETGCUGFTKUMQHOKUECTTKCIG patient is stabilized, surgical evacuation should
• .CTIGJGOCVQOCŮQHIGUVCVKQPCNUCE be proceeded with, as described later.
Ŧ Increased risk of
OKUECTTKCIG
placental abruption Expectant management
RTGVGTORTGNCDQTTWRVWTGQHOGODTCPGU
If the bleeding is minimal and the ultrasound
RTGVGTONCDQT
reveals a negligible amount of products in the
UVKNNDKTVJ
cavity or cervical canal, expectant management
may be advised. The miscarriage will become
complete in a few days. The bleeding will reduce
or stop, and the abdominal discomfort will dis-
Management appear. The complete expulsion of the products
of miscarriage should be confirmed with an ultrasound.
Threatened miscarriage Medical evacuation

In women with threatened miscarriage, the pres- If the patient is not bleeding heavily, is not in
ence of cardiac activity with a fetal heart rate pain, and products are seen in the uterine cav-
t120 bpm is a strong predictor that the preg- ity, then medical evacuation with misoprostol
nancy will proceed normally. is recommended as an outpatient procedure
The management of a threatened miscarriage (Box 29.10; see Chapter 13, Medical termination
is expectant. of pregnancy).
• The patient is reassured. She is placed on
restricted physical activity and advised to Surgical evacuation of uterus
avoid sexual intercourse for 2 weeks. She is also
Surgical evacuation is indicated when there is no
asked to report back if the bleeding becomes
spontaneous expulsion of products or medical
heavy, or if there is increasing abdominal/pel-
evacuation has failed.
vic cramping or passage of tissue.
• Progestogens have been used for threatened • The aim of intervention is to remove the prod-
miscarriage. However, since many miscarriages ucts of conception and empty the uterine cavity
CH 29_p405_427_v3.indd 414 17-07-2015 21:45:07

Box 29.10 Medical evacuation for inevitable,

incomplete, or missed miscarriages
• Misoprostol
Ŧ ŌzIXCIKPCNN[
• 7NVTCUQWPFGXCNWCVKQPCHVGTŌJQWTU
Ŧ %CXKV[GORV[
0QHWTVJGTKPVGTXGPVKQP
Ŧ 2TQFWEVUTGVCKPGF
Misoprostol repeated
Ŧ 2TQFWEVUUVKNNTGVCKPGFCHVGTŌFC[U
5WTIKECNGXCEWCVKQP
• Medications for
Ŧ PCWUGCCPFXQOKVKPI
Ŧ FKCTTJGC Figure 29.8 )GPVNGEWTGVVCIG
Ŧ pain
– The procedure should be performed under

so that further bleeding does not occur. If the intravenous sedation, spinal, or short gen-
products are accessible (lying in the cervical eral anesthesia.
canal or partly in the vagina), they are grasped – After all the tissue is suctioned out, a gen-
with an artery forceps or sponge holding for- tle sharp curettage may be performed to
ceps and gently teased out. If the products are ensure that the uterine cavity is completely
mostly expelled, evacuation of the uterus can empty (Fig. 29.8). A single dose of prophy-
even be done on an outpatient basis. lactic antibiotic is administered (Box 29.11).
• If the gestational age is <6 weeks and the
products are not easily accessible or very
small amounts of products are left in the Missed miscarriage
uterus, manual vacuum aspiration can be Medical evacuation
performed (see Chapter 13, Medical termina-
tion of pregnancy). The same protocol is used for medical evacua-
• If a large amount of products are retained in tion of a missed miscarriage as for inevitable or
the uterine cavity, suction curettage may be incomplete miscarriage (see above). This is the
utilized (Fig. 29.7).
– The uterine evacuation can be done in an
operating room or procedure room. Box 29.11 Surgical evacuation of inevitable or
incomplete miscarriage
• )GUVCVKQPCNCIGYGGMU
Ŧ MVA as outpatient procedure
• )GUVCVKQPCNCIG YGGMU
Ŧ Inpatient procedure
Ŧ +PVTCXGPQWUUGFCVKQPURKPCNIGPGTCNCPGUVJGUKC
• &KNCVCVKQPPQVTGSWKTGF
QUQRGP
• Evacuation of products
Ŧ 5KORNGTGOQXCNQHRTQFWEVU
Ŧ Suction evacuation
Ŧ 5JCTREWTGVVCIGKHPGGFGF
• 5KPINGFQUGQHRTQRJ[NCEVKECPVKDKQVKE
• 9CVEJHQT
Ŧ perforation
Ŧ EGTXKECNVTCWOC
Ŧ infection
Figure 29.7 5WEVKQPEWTGVVCIGHQTKPGXKVCDNGKPEQORNGVG Ŧ KPVTCWVGTKPGCFJGUKQPU
NCVGEQORNKECVKQP
QTOKUUGFOKUECTTKCIG AOCPWCNXCEWWOCURKTCVKQP
CH 29_p405_427_v3.indd 415 17-07-2015 21:45:07

preferred method unless there is heavy bleeding A complete miscarriage does not require any
or the patient is not willing to wait for expulsion intervention. The woman is reassured that she
of the products. has expelled the products completely. An oral
uterotonic may be prescribed for 24–48 hours.
Surgical evacuation
Three methods can be used to dilate the cervix, Prevention of h
prior to suction curettage:
alloimmuni ation
• Manual dilatation using cervical dilators
If a woman is Rh negative and undergoes a mis-
• Mechanical dilatation using osmotic dilators
carriage, there is a small chance of develop-
(e.g., laminaria)
ing Rh alloimmunization. The requirement for
• Physiological dilatation using prostaglandins
anti-D immunoglobulin following miscarriage is
Since the latter two require a few hours to a as given in Box 29.12.
day to accomplish, in early pregnancy, cervical A dose of 50 μg of anti-D immunoglobulin
dilatation is usually done with manual dila- is effective through the 12th week of gestation,
tors (Fig. 29.9). After the dilatation is accom- although the standard 300 μg dose may also be
plished, surgical evacuation is carried out in given, because it is more readily available.
the same way as for inevitable or incomplete
miscarriage.
Postmiscarriage instructions
Postmiscarriage instructions include the fol-
Complete miscarriage lowing:
Clinical examination will confirm a complete
• Activity is restricted for 2 weeks.
miscarriage by the normal or slightly bulky
• Intercourse is avoided for 2 weeks.
size of the uterus, a closed cervix, minimal or
• Review is performed after 4–6 weeks.
no vaginal bleeding, and cessation of abdom-
• Counseling is provided regarding contracep-
inal pain. If there is any doubt about retained
tion. Intrauterine devices may be inserted or
tissue, an ultrasound examination will confirm
oral contraceptives initiated 4 weeks after the
the presence or absence of products in the
miscarriage.
uterine cavity.
• Interval to next pregnancy may be 2–3 months.
• Iron supplementation is recommended for
4–12 weeks.
• Emotional support is required for all women
la er after the miscarriage.
• Reassurance to the woman that she is not
responsible for the event is essential.
ilator
Box 29.12 ecommendations for anti-D immu-

noglobulin following miscarriage
• 0QCPVK&KOOWPQINQDWNKPKUTGSWKTGFHQT
Ŧ IGUVCVKQPCNCIGYGGMU
ectum Ŧ URQPVCPGQWUOKUECTTKCIGYKVJPQKPUVTWOGPVCVKQP
Ŧ VJTGCVGPGFOKUECTTKCIGYKVJNKXGHGVWU
• zIQHCPVK&KOOWPQINQDWNKPKUTGEQOOGPFGFHQT
Ŧ IGUVCVKQPCN CIG YGGMU YKVJ TGEWTTGPV JGCX[
DNGGFKPIQTKPUVTWOGPVCVKQP
• #PVK&KOOWPQINQDWNKPKUTGEQOOGPFGFHQT
Ŧ CNNRTGIPCPEKGUCVIGUVCVKQPCNCIG YGGMU
Figure 29.9 &KNCVCVKQPQHVJGEGTXKZWUKPIEGTXKECNFKNCVQTU
CH 29_p405_427_v3.indd 416 17-07-2015 21:45:07

Complications ecurrent pregnancy loss

of miscarriage
The risk of complications following a miscar- &GſPKVKQP
riage increases as the gestational age increases.
The term recurrent pregnancy loss is used
It is <1% in pregnancies at 6 weeks or below
when miscarriage occurs consecutively in
and increases to 3%–6% at the end of the first
three or more pregnancies, prior to the 20th
trimester.
week of pregnancy. Many experts consider two
The complications may arise due to the fol-
consecutive losses as sufficient for the diagno-
lowing etiologies (Box 29.13):
sis of recurrent miscarriage because the recur-
• Incomplete evacuation of the uterus with rence rate is similar to that after three losses.
retained products may lead to hemorrhage, When the miscarriages occur before 10 weeks’
lower abdominal cramping and pain, and, gestation, they are classified as recurrent ‘early’
occasionally, low-grade fever. pregnancy loss. A smaller proportion of women
• Injury may result from instruments used dur- with recurrent miscarriage have a ‘late’ mis-
ing the procedure. Forcible dilatation of the carriage (after 10 weeks’ gestation and usually
cervix can lead to cervical trauma and uterine before 20 weeks). Causes and recurrence rates
perforation may occur because the pregnant may differ between recurrent early miscarriage
uterus has a soft myometrium that does not and recurrent late miscarriage.
require much force to pierce or perforate.
• Infection may result from retained products
and may lead to septic abortion. Infection Incidence
usually begins as endometritis (involving the
endometrium). Untreated, the infection may Recurrent miscarriage occurs in 1% of couples
spread further into the myometrium and para- attempting to have a baby. If the definition of
metrium. Parametritis may rapidly progress to RPL is reduced to two consecutive miscarriages,
peritonitis. The patient may develop bactere- then 2%–5% of couples will face this problem.
mia and sepsis at any stage of septic abortion. In women older than 35 years of age, the risk
• Vigorous curettage may damage the basal increases even more.
layer of the endometrium leading to formation Evaluation is commonly started after the third
of granulation tissue that causes intrauterine pregnancy loss but, depending on the nature of
synechiae (Asherman syndrome). This can the losses and presence of other factors such
result in secondary amenorrhea and infertility. as maternal age, can start after two pregnancy
losses, as the prevalence and frequency of causes
found are similar in both groups.
Box 29.13 Complications of miscarriage
• +PEQORNGVGGXCEWCVKQPQHVJGWVGTWU
Ŧ *GOQTTJCIG Primary and
Ŧ #DFQOKPCNRCKP
Ŧ .QYITCFGHGXGT secondary PL
• +PLWT[FWGVQKPUVTWOGPVU
Ŧ %GTXKECNVTCWOC Two major groups of RPL patients can be iden-
Ŧ Uterine perforation tified and they should be assessed separately,
• Infection because the risk of subsequent miscarriage
Ŧ Septic abortion among these groups varies.
'PFQOGVTKVKURCTCOGVTKVKURGTKVQPKVKU
5GRVKEGOKC
• 8KIQTQWUEWTGVVCIG Primary PL
Ŧ +PVTCWVGTKPGU[PGEJKCG
#UJGTOCPU[PFTQOG
Primary RPL patients are those with at least three
5GEQPFCT[COGPQTTJGC
consecutive miscarriages with no pregnancy
+PHGTVKNKV[
being carried to viability.
CH 29_p405_427_v3.indd 417 17-07-2015 21:45:07

Secondary PL Epidemiological factors

Secondary RPL patients are those with at least Maternal age
three miscarriages who have had a live birth at
some time. These patients have a better progno- The risk of miscarriage increases with increasing
sis for a successful pregnancy. maternal age. Paternal age has also been impli-
The majority of investigations and treatments cated. The risk of miscarriage is highest when the
offered to women with RPL are not evidence maternal age is t35 years and the paternal age is
based. Some contributing factors are known, t40 years.
but in several couples it is difficult to identify the
specific problem leading to RPL.
Previous history
of miscarriage
Factors implicated in
The risk of further miscarriage increases with
recurrent miscarriage each pregnancy loss and can be as high as 40%
after three consecutive pregnancy losses.
There are several factors which have been impli-
cated in the causation of RPL (Box 29.14).
besity
Box 29.14 Factors implicated in recurrent
miscarriage Recent studies have linked a BMI t30 kg/m2 with
recurrent miscarriage.
• 'RKFGOKQNQIKECNHCEVQTU
Ŧ /CVGTPCNCIGŮ
Ŧ 2TGXKQWUJKUVQT[QHOKUECTTKCIG
Ŧ 1DGUKV[
Antiphospholipid
• #PVKRJQURJQNKRKFCPVKDQF[U[PFTQOG antibody syndrome
Ŧ +PQHYQOGPYKVJ42.
Ŧ 7PVTGCVGFECPECWUGHGVCNNQUU Antiphospholipid antibody syndrome is the
• Genetic factors association between antiphospholipid anti-
Ŧ 2CTGPVCN bodies and several adverse pregnancy out-
Balanced reciprocal translocation comes. This is the most important treatable
$CNCPEGF4QDGTVUQPKCPVTCPUNQECVKQP cause of RPL.
Ŧ 'ODT[QPKECPGWRNQKF[ Adverse pregnancy outcomes include the
• Uterine factors following:
Ŧ 5VTWEVWTCNCDPQTOCNKVKGU
+PVTCWVGTKPGCFJGUKQPU • Three or more unexplained consecutive spon-
5WDOWEQWUHKDTQKF taneous abortions before the 10th week of
Cervical laceration
gestation
Ŧ %QPIGPKVCNWVGTKPGOCNHQTOCVKQPU
• One or more morphologically normal fetal loss
Septate uterus
- &GHGEVKXGKORNCPVCVKQP
at or beyond the 10th week of gestation
%GTXKECNKPUWHHKEKGPE[
KPEQORGVGPEG • One or more premature births of a morpho-
- 5GEQPFVTKOGUVGT42. logically normal neonate before the 34th week
• Endocrine factors of gestation because of placental disease
Ŧ Uncontrolled diabetes
Ŧ 7PVTGCVGFVJ[TQKFF[UHWPEVKQP Antiphospholipid antibodies may be present
• +OOWPGHCEVQTU in 2%–5% of women with uncomplicated preg-
Ŧ Not proven nancies as compared with 15% of women with
• Infections recurrent miscarriage. Fetal losses rise from
Ŧ 0QVKORNKECVGFKP42. 25%–30% in the absence of APA to 90% in cases
• +PJGTKVGFVJTQODQRJKNKCU of untreated APA syndrome. Evaluation and
Ŧ Not proven management of APA syndrome is discussed in
P TGEWTTGPVRTGIPCPE[NQUU Chapter 54, Thromboembolic disorders.
CH 29_p405_427_v3.indd 418 17-07-2015 21:45:07

Genetic factors
Parental chromosomal
rearrangement
Two to five percent of couples with recurrent
miscarriage exhibit a balanced reciprocal or
Robertsonian translocation in one partner.
Reciprocal translocation occurs between homol- a. b.
ogous chromosomes. Robertsonian transloca- Figure 29.10 4QDGTVUQPKCPVTCPUNQECVKQPUa. Balanced
tion is a form of chromosomal rearrangement 4QDGTVUQPKCPVTCPUNQECVKQPDGVYGGPEJTQOQUQOGUCPF
that occurs in the five acrocentric chromosome 21 in parent. b.6JGGZVTCEJTQOQUQOCNOCVGTKCNQPKU
pairs, namely, 13, 14, 15, 21, and 22. A balanced RCUUGFQPVQVJGHGVWUCPFTGUWNVUKPVTKUQO[
&QYP
Robertsonian translocation results in no excess U[PFTQOG
or deficit of genetic material and therefore
causes no abnormalities in the parent who has
it. When this translocation is passed on to the Congenital uterine malformations
fetus, it might be unbalanced. In unbalanced Congenital uterine anomalies are implicated
forms, Robertsonian translocations cause chro- in 10%–15% of women with RPL. The septate
mosomal deletions or additions, resulting in uterus (Fig. 29.11) is the most common uter-
trisomies (Fig. 29.10). When this happens con- ine abnormality associated with RPL, although
sistently, it results in recurrent miscarriage. other Müllerian anomalies such as bicornuate
and unicornuate uterus have also been impli-
Embryonic aneuploidy cated. The longer the uterine septum, the greater
is the chance of pregnancy loss. The mechanism
Embryonic aneuploidy is usually implicated in
by which a septate uterus causes pregnancy loss
sporadic miscarriages. However, it can also result
is not clearly understood, but defective implan-
in recurrent miscarriage. In couples with recur-
tation into the poorly vascularized septum is a
rent miscarriage, 30%–60% of embryos exhibit
possibility.
aneuploidies in further miscarriages.
%GTXKECNKPUWHſEKGPE[
terine factors
(incompetence)
Structural uterine abnormalities can interfere
with implantation and early pregnancy during Cervical insufficiency is defined as the inabil-
the first or second trimester. This may lead to ity of the uterine cervix to retain pregnancy
fetal loss. in the second trimester, in the absence of
uterine contractions. Congenital or acquired
structural weakness of the cervix contributes
allopian tube to cervical insufficiency (earlier known as
cervical incompetence). Although this tends
to be a congenital condition, cervical injury
during a surgical procedure or laceration in a
eptum previous pregnancy may also lead to cervical
Uterus insufficiency.
Cervical insufficiency can lead to recurrent
second trimester losses/preterm births. It is not
Cer i associated with early pregnancy loss.
The typical history is of painless expulsion
Vagina
of the fetus in the second trimester. The expul-
Figure 29.11 5GRVCVGWVGTWU7VGTKPGUGRVWOKU sion could be preceded by pelvic heaviness/
VJGEQOOQPGUVWVGTKPGCDPQTOCNKV[CUUQEKCVGFYKVJ pressure, profuse mucous discharge, or preterm
TGEWTTGPVRTGIPCPE[NQUU prelabor rupture of membranes. Preterm labor is
CH 29_p405_427_v3.indd 419 17-07-2015 21:45:08

also known to occur with cervical insufficiency. Although certain other endocrine factors have
Miscarriage typically occurs at 16–24 weeks. been associated with miscarriage, it is difficult to
implicate them in recurrent miscarriage.
%CWUGUQHEGTXKECNKPUWHſEKGPE[ • Progesterone deficiency is not predictive of preg-
Cervical insufficiency may be congenital or nancy outcome, and there is no high-quality
acquired following surgical procedures on the evidence to support the use of oral or vaginal
cervix (Box 29.15). progesterone to prevent early miscarriage.
• Women with polycystic ovarian syndrome
Diagnosis have a higher rate of miscarriage. This may be
The diagnosis of cervical insufficiency is primar- related to insulin resistance, hyperinsuline-
ily clinical, based on history. mia, and hyperandrogenemia.
• Speculum examination may reveal a short

cervix, evidence of prior surgery, or old tears.
Immune factors
If the process of abortion has begun, bulging Since the fetus is a foreign graft, it is tempting
membranes may be visible through the exter- to implicate a host-versus-graft reaction as a
nal os reason for RPL. However, there is no evidence
• Criteria used for ultrasonographic diagnosis of to support the hypothesis of human leucocyte
cervical insufficiency: antigen (HLA) incompatibility between couples.
– Cervical length of <25 mm between 16 and Therefore, this should not be offered routinely
24 weeks’ gestation in the investigation of couples with recurrent
– Funneling at the internal os miscarriage.
– Funneling in response to fundal pressure
Infections
Endocrine factors Although any bacterial or viral infection that
Endocrine disorders have been associated with spreads to the uterus may potentially cause spo-
RPL. radic miscarriage, there is no proven infectious
cause of recurrent miscarriage. Thus, screen-
• Uncontrolled diabetes mellitus with high ing tests for ureaplasma, chlamydia, and other
hemoglobin A1c levels can give rise to RPL. infectious agents such as toxoplasmosis, rubella,
• Untreated thyroid dysfunction is also a known cytomegalovirus, herpes, and listeria are not
etiological factor. recommended in the evaluation of recurrent
miscarriage. Routine screening for TORCH infec-
Since symptomatic women with diabetes or
tions (toxoplasmosis, other, rubella, cytomegalo-
thyroid dysfunction will seek treatment or will be
virus and herpes simplex) should be abandoned
treated after a miscarriage, it is unusual for them
in the investigation of RPL.
to have recurrent miscarriage.
Inherited thrombophilias
Box 29.15 %CWUGUQHEGTXKECNKPUWHſEKGPE[ Inherited thrombophilias include activated pro-
• %QPIGPKVCN
tein C resistance (most commonly due to factor V
• Acquired Leiden mutation), deficiencies of protein C, pro-
Ŧ (QTEGHWNFKNCVCVKQPQHEGTXKZ tein S, and antithrombin III, hyperhomo-cystein-
Ŧ Cervical tears emia, and prothrombin gene mutation. They are
Ŧ %GTXKECNCORWVCVKQP associated with venous thromboembolism and
Ŧ %QPK\CVKQP also have been associated with adverse outcomes
Ŧ 6TCEJGNGEVQO[ in pregnancies, including fetal loss, preeclampsia,
Ŧ (QVJGTIKNNUWTIGT[ fetal growth restriction, and placental abruption.
Ŧ .''2 However, it is controversial whether there is an
P NQQRGNGEVTQGZEKUKQPRTQEGFWTG association between inherited thrombophilias
CH 29_p405_427_v3.indd 420 17-07-2015 21:45:08

and uteroplacental thrombosis that leads to remain unexplained. These couples can be reas-
recurrent early pregnancy loss. sured that the chance for a successful future preg-
Box 29.16 summarizes factors implicated in nancy with supportive care alone is close to 70%.
recurrent miscarriage.
istory and physical
Evaluation of a couple examination
A careful history will contribute information that
with PL may help in diagnosing the cause of RPL. The
The evaluation of a couple with RPL aims to history should include the following:
• find factors that have contributed to the RPL, • Gestational age at which the previous preg-
• provide prognostic value in the subsequent nancy losses occurred: This is of importance
pregnancy, and because RPL typically occurs at a similar gesta-
• help choose treatment of proven benefit to tional age in consecutive pregnancies and the
improve live birth rates. most common causes of RPL vary by trimester.
• The specifics of each pregnancy (anembryonic
In spite of detailed evaluation, a significant pregnancy or live embryo): A live abortus is
proportion of cases of recurrent miscarriage indicative of structural uterine malformation,
whereas in conditions interfering with placen-
tal blood flow such as APA syndrome, the fetus
Box 29.16 Factors implicated in PL is usually dead.
• 'RKFGOKQNQIKECNHCEVQTU • Associated pain: A painless expulsion of the
Ŧ /CVGTPCNCIG fetus occurring consistently in the second tri-
Ŧ 2TGXKQWUJKUVQT[QHOKUECTTKCIG mester is suggestive of cervical insufficiency.
Ŧ 1DGUKV[
• #PVKRJQURJQNKRKFCPVKDQF[U[PFTQOG Physical examination should include a gen-
Ŧ +PQHYQOGPYKVJ42. eral physical assessment with attention to BMI
Ŧ 7PVTGCVGFECPECWUGHGVCNNQUU and pelvic organ abnormalities (e.g., uterine
• Genetic factors malformation or cervical laceration).
Ŧ 2CTGPVCN
Balanced reciprocal translocation
$CNCPEGF4QDGTVUQPKCPVTCPUNQECVKQP Testing for APA syndrome
Ŧ 'ODT[QPKECPGWRNQKF[ It is recommended that all women with recur-
• Uterinefactors rent first trimester miscarriage and all women
Ŧ 5VTWEVWTCNCDPQTOCNKVKGU
with one or more second trimester miscar-
+PVTCWVGTKPGCFJGUKQPU
riages should be screened before pregnancy for
5WDOWEQWUHKDTQKF
Cervical laceration the presence of antiphospholipid antibodies.
Ŧ %QPIGPKVCNWVGTKPGOCNHQTOCVKQPU Anticardiolipin antibody, lupus anticoagulant,
Septate uterus and anti-E-2 glycoprotein1 are antiphospholipid
- &GHGEVKXGKORNCPVCVKQP antibodies that have established assays.
%GTXKECNKPUWHHKEKGPE[
KPEQORGVGPEG Antiphospholipid syndrome is confirmed
- 5GEQPFVTKOGUVGT42. when the woman has two positive tests at least
• Endocrine factors 12 weeks apart for either lupus anticoagulant or
Ŧ Uncontrolled diabetes anticardiolipin antibodies. This is discussed in
Ŧ 7PVTGCVGFVJ[TQKFF[UHWPEVKQP detail in Chapter 54, Thromboembolic disorders.
• +OOWPGHCEVQTU
Ŧ Not proven
• Infections Structural uterine
Ŧ 0QVKORNKECVGFKP42.
• +PJGTKVGFVJTQODQRJKNKCU
abnormalities
Ŧ Not proven Anatomic causes of RPL are typically diag-
P TGEWTTGPVRTGIPCPE[NQUU nosed using hysterosalpingography (HSG) or
CH 29_p405_427_v3.indd 421 17-07-2015 21:45:08

recurrent miscarriage. This recommendation

is based on the argument that if the abortus is
aneuploid, the physician and the patient can
conclude that a maternal cause is excluded.
Screening for diabetes

and thyroid dysfunction
Routine testing for diabetes is not recom-
mended in the evaluation of recurrent mis-
carriage unless symptoms or clinical findings
warrant testing. Some studies have shown an
increased risk of RPL in women with subclin-
ical hypothyroidism and presence of thyroid
peroxidase (TPO) antibodies. Therefore, some
centers perform thyroid function tests and TPO
antibody testing, but these are not routinely
recommended.
Figure 29.12 &WNVTCUQWPFKOCIGQHCUGRVCVGWVGTWU Inherited thrombophilias

6JGUGRVWOKUURNKVVKPIVJGWRRGTRCTVQHVJGECXKV[KPVQVYQ
Screening for inherited thrombophilias is not
(Photo courtesy/GFKUECP5[UVGOU%JGPPCK
recommended as their role in recurrent early
pregnancy loss is uncertain, and there is no evi-
sonohysterography (Fig. 29.12). Sonohysterography dence that antithrombotic therapy for this rea-
is a technique in which saline is injected through son effectively prevents miscarriage.
the cervix into the uterus, and an ultrasound Evaluation of a couple with recurrent miscar-
image is obtained of the uterine cavity. The fluid riage is given in Box 29.17.
reveals more detail of the uterine cavity than
when ultrasound is used alone.
Hysteroscopy, 3D ultrasound, or magnetic Box 29.17 Evaluation of couple with recurrent
resonance imaging (MRI) may also be useful in miscarriage
defining the abnormality but are more expensive • *KUVQT[
modalities. Ŧ Obstetric
)GUVCVKQPCNCIGCVOKUECTTKCIG
.KXGFGCFHGVWU
Parental karyotype and Associated pain
karyotype of the abortus Ŧ (COKN[RCUVJKUVQT[
Diabetes
If the previous two tests are normal, then genetic 6J[TQKFF[UHWPEVKQP
testing may be done. • 2J[UKECNGZCOKPCVKQP
Ŧ $QF[OCUUKPFGZ
• Karyotyping of both partners has been
Ŧ 2GNXKEGZCOKPCVKQP
found to be helpful in predicting future RPL. )GPKVCNVTCEVCPQOCNKGU
Chromosomal abnormalities implicated in • #PVKRJQURJQNKRKFCPVKDQFKGU
RPL are balanced reciprocal or Robertsonian Ŧ .WRWUCPVKEQCIWNCPV
translocation in one partner. Couples found to Ŧ #PVKECTFKQNKRKP+I)CPF+I/
have these should receive genetic counseling. Ŧ Anti-EIN[EQRTQVGKP
• Chromosomal analysis of the products of • *[UVGTQUCNRKPIQITCRJ[QTUQPQJ[UVGTQITCRJ[
conception is debatable, as some conditions • %JTQOQUQOCNCUUGUUOGPV
may occur spontaneously. Although contro- Ŧ 2CTGPVCNMCT[QV[RKPI
versial, some experts recommend karyotype Ŧ -CT[QV[RKPIQHCDQTVWUEQPVTQXGTUKCN
analysis of the conceptus in couples with g KOOWPQINQDWNKP) g KOOWPQINQDWNKP/
CH 29_p405_427_v3.indd 422 17-07-2015 21:45:08

Treatment options Septate uterus

for PL Of the congenital uterine anomalies, uterine
septum is the only one that can be treated and
It is important to remember that the progno- corrected by hysteroscopic surgery. A resecto-
sis for a successful future pregnancy, even after scope is introduced into the uterine cavity, and
three early pregnancy losses, is generally good. the location as well as the length of the septum is
With or without a known cause for the RPL, the confirmed. The septum is then incised by needle
overall live birth rates are still 70%. This means electrode till a single uterine cavity results.
that three out of four couples with RPL will suc-
ceed when they try for a live birth. Increasing
maternal age and a higher number of miscar- %GTXKECNKPUWHſEKGPE[
riages at the time of initial visit decrease the like- Ultrasonography should be performed to con-
lihood of having a live birth. firm intrauterine pregnancy. Infection should
One of the important lessons that has emerged be excluded. Cervical cerclage is the recom-
is that providing emotional support from the mended treatment for cervical insufficiency.
beginning of pregnancy enhances the effect of The indication for the cerclage helps in classi-
therapeutic measures. fying cerclages.
• History-indicated cerclage: A history-indicated

Treatment of APA cervical cerclage is offered between 12 and 14
syndrome weeks’ gestation in women with a history sug-
gestive of cervical insufficiency. There are no
Combined therapy with low-dose aspirin and
tests that can be done prior to pregnancy to
prophylactic dose heparin is the choice for
confirm this diagnosis.
recurrent miscarriage caused by APA syndrome.
• Ultrasound-indicated cerclage: This is per-
Low-dose aspirin (50–100 mg/day) is started
formed at 14–24 weeks in women with cervical
at the earliest confirmation of pregnancy. The
length <25 cm before 24 weeks’ gestation, with
heparin is started on ultrasound confirmation of
prior pregnancy loss or preterm labor.
viable intrauterine pregnancy. Either unfraction-
• Physical examination–indicated cerclage: This
ated or low-molecular-weight heparin (LMWH)
is performed at 16–28 weeks when the cervix is
may be used (Table 29.6).
>1 cm dilated and membranes have prolapsed.
• Emergency cerclage: This is indicated in
Treatment of uterine women in whom the diagnosis was not made
or suspected earlier and who present with the
abnormality cervix dilated <4 cm and bulging membranes.
Septate uterus, intrauterine adhesions, and sub- Rupture of membranes, cervical dilatation >4
mucous fibroid can be treated with hysteroscopic cm, and evidence of infection are contraindi-
resection. cations to this procedure.
Table 29.6 Drugs for the treatment of antiphospholipid antibody syndrome causing recurrent
pregnancy loss
Medication Dosage Time of initiating treatment

.QYFQUGCURKTKP ŌOIQTCNFCKN[ #VVJGGCTNKGUVEQPſTOCVKQPQHRTGIPCPE[
7PHTCEVKQPCVGFJGRCTKP 7PKVU5%JQWTN[ 1PWNVTCUQWPFEQPſTOCVKQPQHXKCDNG
KPVTCWVGTKPGRTGIPCPE[
./9* 'PQZCRCTKPOI5%QPEGFCKN[ 1PWNVTCUQWPFEQPſTOCVKQPQHXKCDNG
&CNVGRCTKP7PKVU5%QPEGFCKN[ KPVTCWVGTKPGRTGIPCPE[
.QYOQNGEWNCTYGKIJVJGRCTKPSC subcutaneous.
CH 29_p405_427_v3.indd 423 17-07-2015 21:45:08

Techniques for cervical cerclage are as follows: cerclage or an emergency cerclage done in the
second trimester.
• Transvaginal cerclage
• The suture is usually removed at 38 weeks’
– McDonald suture
gestation.
– Shirodkar procedure
• Transabdominal cerclage
Shiro ar proce ure
cDonal proce ure A Shirodkar cerclage (Fig. 29.14) is indicated in
women with previous failed McDonald cerclage.
McDonald procedure is the procedure of In this procedure, the bladder is dissected and
choice for cervical cerclage (Fig. 29.13). The pushed up and the suture is placed at the level
procedure is performed under spinal or general of the internal os. A Mersilene tape is used and
anesthesia. is passed around the cervix using a specially
• The patient is placed in a dorsolithotomy designed Shirodkar needle.
position.
• The lips of the cervix are held with sponge ransab ominal cerclage
holding forceps. Transabdominal cerclage (Fig. 29.15) is used
• A purse string suture is applied around the cer- when vaginal procedures fail or are difficult to
vix, the suture passing through the substance perform due to unfavorable cervical anatomy
of the cervix, using a nonabsorbable synthetic (e.g., a very short cervix). Delivery after trans-
suture such as polypropylene (Prolene). The abdominal cerclage is by cesarean section.
knot is tied anteriorly or posteriorly.
• In an emergency cerclage, if the cervix is dilated
and the membrane is bulging, it is pushed up Management of parental
gently with a sponge on a holder. Head-down
tilt may also be useful in this situation.
karyotype abnormality
• Tocolytics are not administered in a history- When one of the parents is found to have a bal-
indicated cerclage. They may be given for anced translocation, genetic counseling must be
48 hours in a physical examination–indicated offered.
Figure 29.13 #/E&QPCNFUWVWTG+VKUCRWTUGUVTKPIUWVWTGWUKPIPQPCDUQTDCDNGU[PVJGVKEUWVWTGRNCEGFVTCPUXCIKPCNN[

JKIJQPVJGEGTXKZ
CUENQUGVQVJGNGXGNQHVJGKPVGTPCNQUCURQUUKDNG+VKUTGOQXGFCVŌYGGMUŏIGUVCVKQP
CH 29_p405_427_v3.indd 424 17-07-2015 21:45:08

Figure 29.14 #5JKTQFMCTUWVWTG+VKURNCEGFCVVJGNGXGNQHVJGKPVGTPCNQUCHVGTFKUUGEVKPIVJGXCIKPCNOWEQUCWRYCTFU

6JGDNCFFGTKUTGVTCEVGFCPFC/GTUKNGPGVCRGKURNCEGFWPFGTVJGXCIKPCNOWEQUCVKIJVGPGFCPFMPQVVGF
The following pregnancy outcomes are to determine fetal karyotype. If the fetus has a
possible: trisomy, the couple may choose termination.
In vitro fertilization (IVF) with preimplantation
• Normal pregnancy and normal fetus
genetic diagnosis (PGD) can be used to select a
• Normal pregnancy with fetus having a bal-
normal embryo.
anced translocation (carrier)
• Fetus with trisomy (e.g., trisomy 21 or Down
syndrome) Treatment modalities
• Failure to establish a pregnancy of doubtful value
• Pregnancy loss
Couples with balanced translocation should
Bed rest
be offered prenatal diagnostic procedures, such There is insufficient evidence to support a pol-
as amniocentesis or chorionic villus sampling, icy of bed rest in order to prevent miscarriage in
women who have had RPL. Neither bed rest in
hospital nor bed rest at home shows a significant
difference in the prevention of miscarriage.
Empirical aspirin
with or without heparin
The empirical use of low-dose aspirin, with
or without heparin, in the absence of estab-
lished APA syndrome, has shown no benefit in
improving live birth rates in women with RPL.
Thus, there is no evidence for this treatment in
unexplained RPL. Aspirin and LMWH have also
not been shown to be of therapeutic benefit in
women with thrombophilia.
Figure 29.15 6TCPUCDFQOKPCNEGTENCIG6JGUWVWTGKU uman chorionic gonadotropin
RNCEGFCVVJGNGXGNQHVJGKPVGTPCNQUWUKPIC/GTUKNGPG
VCRG+VECPDGFQPGD[NCRCTQVQO[
CVŌYGGMUŏ Currently, the use of hCG to prevent pregnancy
IGUVCVKQPQTNCRCTQUEQRKECNN[
RTGEQPEGRVKQPCN6JGUWVWTG loss in women with a history of unexplained RPL
KURGTOCPGPVCPFFGNKXGT[KUCNYC[UD[EGUCTGCPUGEVKQP is not recommended.
CH 29_p405_427_v3.indd 425 17-07-2015 21:45:09

Progesterone Immunotherapy
In women with recurrent miscarriage, there is Immunotherapy (e.g., paternal cell immuniza-
not enough evidence to evaluate the effect of tion, third-party donor leucocytes, trophoblast
progesterone supplementation in pregnancy to membranes, and intravenous immunoglobulin)
prevent a miscarriage. It is of no benefit after 10 has not been shown to be of benefit in women
weeks’ gestation, after the placental production with unexplained recurrent miscarriage.
of progesterone begins. Treatment options for RPL are given in Box 29.18.
Box 29.18 Treatment options for recurrent pregnancy loss

• 'OQVKQPCNUWRRQTV • 2CTGPVCNMCT[QV[RKPICDPQTOCNKV[
• #PVKRJQURJQNKRKFCPVKDQF[U[PFTQOG Ŧ )GPGVKEEQWPUGNKPI
Ŧ .QYFQUGCURKTKP Ŧ #OPKQEGPVGUKUQT%85HQTVTKUQO[
Ŧ Heparin Ŧ +8(CPF2)&
7PHTCEVKQPCVGFJGRCTKP • 6TGCVOGPVOQFCNKVKGUQHFQWDVHWNQTPQXCNWG
.QYOQNGEWNCTYGKIJVJGRCTKP Ŧ Bed rest
• 7VGTKPGCDPQTOCNKVKGU Ŧ #URKTKPvJGRCTKPKP
Ŧ *[UVGTQUEQRKETGUGEVKQP 7PGZRNCKPGF42.
+PVTCWVGTKPGCFJGUKQPU 6JTQODQRJKNKCU
5WDOWEQWUHKDTQKF Ŧ *WOCPEJQTKQPKEIQPCFQVTQRKP
5GRVWO Ŧ 2TQIGUVGTQPG
Ŧ %GTXKECNKPUWHſEKGPE[ Ŧ +OOWPQVJGTCR[
McDonald suture
5JKTQFMCTUWVWTG
6TCPUCDFQOKPCNEGTENCIG
C S EJQTKQPKEXKNNWUUCORNKPI KPXKVTQHGTVKNK\CVKQPP D RTGKORNCPVCVKQPIGPGVKEFKCIPQUKU P TGEWTTGPVRTGIPCPE[NQUU
Key points
Miscarriage • 7NVTCUQWPFſPFKPIUVJCVOC[RTGFKEVCOKUECT-
TKCIGKPENWFGCDPQTOCNIGUVCVKQPCNUCECDPQTOCN
• 6JGNQUUQHCRTGIPCPE[DGHQTGYGGMUKUECNNGFOKU- [QNMUCEHGVCNDTCF[ECTFKCCPFNCTIGUWDEJQTKQPKE
ECTTKCIGGCTN[RTGIPCPE[NQUUQTURQPVCPGQWUCDQTVKQP JGOCVQOC
• 6JG9QTNF*GCNVJ1TICPK\CVKQP
9*1FGſPGUOKUECT- • +HVJGTGKUCP[FQWDVCDQWVVJGXKCDKNKV[QHVJGHGVWUVJG
TKCIGCUGZRWNUKQPQTGZVTCEVKQPQHCPGODT[Q
CVQT WNVTCUQWPFUJQWNFDGTGRGCVGFCHVGTŌFC[UWPNGUU
DGHQTGYGGMUQTHGVWU
CHVGTYGGMUYGKIJKPI VJGTGKUJGCX[DNGGFKPICPFUKIPUQHCPKPGXKVCDNG
IQTNGUU OKUECTTKCIG
• $KQEJGOKECNNQUUKUCRTGIPCPE[NQUUVJCVQEEWTUCHVGT • /CPCIGOGPVQHOKUECTTKCIGFGRGPFUQPYJCVUVCIG
CRQUKVKXGRTGIPCPE[VGUVDWVDGHQTGWNVTCUQWPFQT KVKUCV6JTGCVGPGFOKUECTTKCIGECPDGOCPCIGF
JKUVQNQIKECNXGTKſECVKQP GZRGEVCPVN[+PGXKVCDNGKPEQORNGVGCPFOKUUGFOKU-
ECTTKCIGUECPDGOCPCIGFOGFKECNN[QTUWTIKECNN[
• /KUUGFOKUECTTKCIGKPVJGſTUVVTKOGUVGTKUEJCTCEVGTK\GF
D[VJGCTTGUVQHGODT[QPKEQTHGVCNFGXGNQROGPV6JG • 2QUVOKUECTTKCIGECTGKPENWFGUGOQVKQPCNUWRRQTVKTQP
EGTXKZKUENQUGFCPFVJGTGKUPQQTQPN[UNKIJVDNGGFKPI UWRRNGOGPVCVKQP4JRTQRJ[NCZKUCPFEQPVTCEGRVKQP
• -PQYPGCTNKGTCUJCDKVWCNCDQTVKQPTGEWTTGPVOKUECT- • %QORNKECVKQPUQHOKUECTTKCIGKPENWFGJGOQTTJCIG
TKCIGKUFGſPGFCUVJTGGQTOQTGEQPUGEWVKXGRTGI- KPLWT[CPFKPHGEVKQP
PCPE[NQUUGUDGHQTGYGGMUŏIGUVCVKQP
Recurrent pregnancy loss
• #URQPVCPGQWUOKUECTTKCIGKUCRTQEGUUVJCVECPRTQ-
ITGUUVJTQWIJHQWTUVCIGUDWVOC[PQVCNYC[UIQVJTQWIJ • 6JGVGTOTGEWTTGPVRTGIPCPE[NQUU
42.KUWUGFYJGP
GCEJUVCIG6JGPCVWTCNRTQITGUUKQPQHOKUECTTKCIGKU OKUECTTKCIGQEEWTUEQPUGEWVKXGN[KPVYQQTVJTGGQT
VJTGCVGPGFKPGXKVCDNGKPEQORNGVGCPFEQORNGVG OQTGRTGIPCPEKGURTKQTVQVJGVJYGGMQHRTGIPCPE[
(Continued)
CH 29_p405_427_v3.indd 426 17-07-2015 21:45:09


• 2CVKGPVUYKVJRTKOCT[42.JCXGJCFPQRTGIPCPE[ • 'XCNWCVKQPQH42.KPENWFGUCVJQTQWIJJKUVQT[CPF
DGKPIECTTKGFVQXKCDKNKV[ RJ[UKECNGZCOKPCVKQPVGUVUHQTVJGRTGUGPEGQHCPVK-
• 2CVKGPVUYKVJUGEQPFCT[42.JCXGJCFCNKXGDKTVJCV ECTFKQNKRKPCPVKDQFKGUNWRWUCPVKEQCIWNCPVCPFCPVK
UQOGVKOG6JGUGRCVKGPVUJCXGCDGVVGTRTQIPQUKUHQT IN[EQRTQVGKPWVGTKPGECXKV[GXCNWCVKQPCPFRCTGPVCN
CUWEEGUUHWNRTGIPCPE[ MCT[QV[RKPI-CT[QV[RKPIQHVJGCDQTVWUKUTGEQO-
OGPFGFD[UQOG
• (CEVQTUKORNKECVGFKPVJGGVKQNQI[QH42.CTGOCVGTPCN
CIGRTGXKQWUOKUECTTKCIGQDGUKV[CPVKECTFKQNKRKP • 6TGCVOGPVQH42.FGRGPFUQPVJGWPFGTN[KPIECWUG
CPVKDQF[U[PFTQOGRCTGPVCNDCNCPEGFVTCPUNQECVKQP %GTXKECNKPUWHſEKGPE[YKNNTGSWKTGEGTXKECNEGTENCIG
GODT[QPKECPGWRNQKF[CPFWVGTKPGCDPQTOCNKVKGU
• %GTXKECNKPUWHſEKGPE[
KPEQORGVGPEGKUKORNKECVGFKP
TGEWTTGPVUGEQPFVTKOGUVGTOKUECTTKCIGU
Self-Assessment
4. #OKUUGFOKUECTTKCIGECPDGOCPCIGFYKVJOGFKECN
Case-based questions GXCEWCVKQPWUKPIOKUQRTQUVQN+HVJGDNGGFKPIKUJGCX[
QTVJGRCVKGPVKUWPYKNNKPIVQYCKVVJGPCUWEVKQP
Case 1 evacuation can be done.
/TU;6CRTKOKITCXKFCRTGUGPVGFCVYGGMUŏIGUVC-
VKQPYKVJOQFGTCVGXCIKPCNDNGGFKPICPFOKNFRGNXKEETCOR- Case 2
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VTCPUNQECVKQPEGTXKECNKPUWHſEKGPE[EJTQOQUQOCN
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CPFYGGMUVQOGCUWTGVJGEGTXKECNNGPIVJ
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CDQTVWUGU5JGTGRQTVGFPQOGFKECNRTQDNGOUQTRTGXKQWU EGTENCIGQTCPCDFQOKPCNEGTENCIGECPDGFQPGKH
UWTIGTKGU C/E&QPCNFEGTENCIGHCKNU
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2. 9JCVKUVJGNKMGN[ECWUGKPVJKUYQOCP!9J[!
3. *QYYKNN[QWEQPſTOVJGFKCIPQUKU!
Sample questions
4. *QYYKNN[QWOCPCIGVJKUECUGQH42.!
1. 9JCVCTGVJGECWUGUQHUGEQPFVTKOGUVGTOKUECT-
Answers TKCIG!*QYFQ[QWFKCIPQUGCPFOCPCIGCECUGQH
EGTXKECNKPUWHſEKGPE[!
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UGZWCNKPVGTEQWTUGHQTYGGMU0QOGFKECVKQPUCTGTG- Short-answer questions
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1. +PEQORNGVGOKUECTTKCIG
3. 6JGWVGTWUYQWNFDGUOCNNGTVJCPGZRGEVGFHQTVJG
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CH 29_p405_427_v3.indd 427 17-07-2015 21:45:09

Ectopic
30 Pregnancy
Case scenario
Mrs. HG, 29, had been attempting to conceive for the past 3 years. She
had a missed miscarriage 2 years ago and underwent surgical evacua-
tion. She presented at 6 weeks’ amenorrhea with intermittent, cramping
abdominal pain on the left side. She also had some vaginal spotting
and fainted once when she tried to stand up. She was brought to the
hospital to check if the pregnancy was proceeding normally.
Introduction cesarean scar is reported more often now. It

occurs in approximately 1 in 2000 pregnancies
Ectopic pregnancy, though infrequent, can be and accounts for 6% of ectopic pregnancies
a life-threatening obstetric condition. Without among women who have undergone a previous
prompt diagnosis and treatment, it can lead to cesarean section.
significant maternal morbidity and mortality. In the fallopian tube, approximately 80% of
Newer diagnostic methods and a more conser- pregnancies occur in the ampullary region, and
vative therapeutic approach have led to lesser the remaining in other sites, including the isthmus
mortality and better future fertility. and the interstitial (cornual) portion of the fallo-
pian tube. The interstitial portion of the fallopian
tube is the proximal segment that is embedded
&GſPKVKQP within the muscular wall of the uterus. A hetero-
topic pregnancy is one in which there is an intra-
A pregnancy that occurs in a site outside the uterine pregnancy as well as an ectopic pregnancy.
uterine cavity is called ectopic pregnancy.
Almost all ectopic pregnancies (98%) are sited
in the fallopian tube (Fig. 30.1). The remaining Incidence
2% occur in the abdominal cavity, the ovary,
or the cervix. With the increasing rate of cesar- The incidence of ectopic pregnancies is increasing
ean sections, ectopic pregnancy in a previous worldwide, partly due to increasing incidence of
CH 30_p428-446_v3.indd 428 17-07-2015 22:32:53

Ectopic Pregnancy 429
sthmic
allopian tube
Cornual
arian artery
ary
arian
mpullary Uterus
Cer ical
Cer i
Vagina
Figure 30.1 Sites of ectopic pregnancy.
pelvic infections and partly due to increasing num- structural damage to the tube (obstruction or
bers of assisted reproductive techniques being adhesions), pelvic infections alter tubal func-
utilized. The incidence ranges from 6 per 1000 in tion, thus delaying the passage of the blastocyst,
India to 16 per 1000 in developed countries. which then implants in the tube.
isk factors Infertility

Women undergoing treatment for infertility have a
Even though some women with ectopic preg- fourfold increase in the incidence of ectopic preg-
nancy will have no identifiable risk factors, sev- nancy. This is partly due to the higher incidence
eral conditions increase the probability of its of tubal abnormality in infertile women. There is
occurrence. also an association between fertility drugs and an
increased occurrence of ectopic pregnancy.
Previous ectopic pregnancy
The history of treatment for a previous ectopic In vitro fertili ation
pregnancy increases the risk for an ectopic preg- Women undergoing in vitro fertilization (IVF)
nancy in the next pregnancy. One-third of preg- have a two to three times increased risk of both
nancies following a previous ectopic pregnancy ectopic and heterotopic pregnancy. Cervical and
are in an ectopic location. The risk also is modi- interstitial (cornual) pregnancies are more often
fied by whether the ectopic pregnancy was treated seen following IVF.
medically with methotrexate (MTX) or surgically.
Tubal surgery
Pelvic infection
Since ectopic pregnancies result from tubal dam-
Nonspecific salpingitis and chlamydial and gon- age, it follows that tubal surgery will increase the
orrheal infections (especially when recurrent) incidence of tubal ectopic pregnancy.
lead to tubal damage and therefore have been
implicated in the causation of ectopic pregnancy.
Tubal reconstructive surgery
The rise in chlamydial infection worldwide has
been reflected in the increasing numbers of ecto- Women who have undergone reconstructive sur-
pic pregnancy. gery for obstructed tubes have an increased risk
After acute salpingitis, the risk of an ectopic of tubal implantation. The previous infection or
pregnancy is increased sevenfold. In addition to ectopic pregnancy that caused the obstruction,
CH 30_p428-446_v3.indd 429 17-07-2015 22:32:53

rather than the surgery itself, is believed to be the

Box 30.1 isk factors for ectopic pregnancy
main reason for an ectopic pregnancy following
tubal surgery. • Previous ectopic pregnancy
• Pelvic infection
Ŧ 0QPURGEKſEUCNRKPIKVKU
Tubal sterili ation Ŧ Chlamydia
Ŧ Gonorrhea
Although the failure rate following tubal steril- • Infertility
ization is low, 30% of tubal failures are ectopic Ŧ Tubal factors
implantations. Bipolar coagulation is associ- Ŧ Fertility drugs
ated with a much higher risk of ectopic preg- • In vitro fertilization
nancy than the traditional postpartum tubal Ŧ Heterotopic pregnancy
ligation. Ŧ Cervical pregnancy
Ŧ Interstitial (cornual) pregnancy
• Tubal surgery
Ŧ Tubal reconstructive surgery
Intrauterine devices Ŧ Tubal sterilization
Since the incidence of any pregnancy is lower • IUD
in women using intrauterine contraceptive Ŧ Levonorgestrel IUD
Ŧ Copper IUD
devices (IUDs), the incidence of ectopic preg-
• Tubal pathology
nancy is also lower in these women. However,
Ŧ Developmental anomalies
if a pregnancy does occur, the risk of ectopic Ŧ Salpingitis isthmica nodosa
pregnancy is higher. The incidence is higher
with levonorgestrel IUDs as compared with D, intrauterine device.
copper IUDs.
around the gestational sac. The tubal wall is

Tubal conditions stretched and thinned out, and finally ruptures,
Developmental anomalies of the tube such as a resulting in hemoperitoneum.
diverticulum can be associated with a tubal preg- Intermittent pain occurs when the tube dis-
nancy. Salpingitis isthmica nodosa, an inflam- tends; when blood escapes into the peritoneal
matory condition associated with nodularity and cavity, the pain is acute and severe.
hyperplasia of the muscular layer of the tube, also
increases the risk of ectopic pregnancy.
Risk factors for ectopic pregnancy are sum-
terine changes
marized in Box 30.1. The uterus enlarges marginally under the
influence of progesterone and human chori-
onic gonadotropin (hCG). The endometrium
Pathology undergoes decidualization. However, since the
implantation is ectopic, chorionic villi are not
An ectopic pregnancy demonstrates not only found in the decidua. A fall in progesterone lev-
tubal changes but will also be accompanied by els leads to bleeding into the uterine cavity and
uterine changes (Box 30.2). the appearance of a pseudosac. The decidua may
be expelled, leading to external hemorrhage.
Tubal changes Occasionally, the entire decidua is expelled as a
decidual cast.
When implantation occurs in the tube, there is In 10%–15% of cases, the endometrial glands
minimal decidual reaction and increase in vas- undergo adenomatous changes under the influence
cularity. The blastocyst burrows into the tubal of progesterone. The lining cells are pleomorphic,
wall. The engorged blood vessels are eroded with vacuolated cytoplasm and hyperchromatic
by the chorionic villi, and there is hemorrhage nuclei. This is known as the Arias–Stella reaction.
CH 30_p428-446_v3.indd 430 17-07-2015 22:32:53

Occasionally, the rupture is between the layers

Box 30.2 Pathology of ectopic pregnancy
of the broad ligament, with formation of a broad
• Tubal changes ligament hematoma. Rarely, the pregnancy that
Ŧ Minimal decidual reaction is extruded into the abdomen attaches itself
Ŧ Increased vascularity
to other organs and continues as a secondary
Ŧ Blastocyst burrows into tubal wall
abdominal pregnancy.
Ŧ Stretching and thinning of the tubal wall
Ŧ Erosion of the vessels by chorionic villi
Ŧ Tubal rupture Chronic ectopic pregnancy
• Uterine changes
Ŧ Enlargement The tubal pregnancy may perforate through the
Ŧ Decidualization of endometrium wall but be walled off by omentum and loops of
Ŧ Expulsion of decidua bowel, forming a pelvic mass. Acute pain and
Ŧ Pseudosac formation bleeding may subside, but the woman continues
Ŧ Arias–Stella reaction to have chronic pain and a pelvic mass.
The natural progression of a tubal pregnancy
is summarized in Box 30.3.
atural progression
of tubal pregnancy Presenting symptoms
Complete expulsion Physicians must have a high degree of suspi-
absorption cion for ectopic pregnancy if a woman presents
with amenorrhea, abdominal pain, and vaginal
Very early in gestation, the pregnancy may be bleeding. In other words, any sexually active
absorbed entirely or expelled through the uterus. woman presenting with abdominal pain and
Some intraperitoneal bleeding may occur, but vaginal bleeding after an interval of amenorrhea
the hemoperitoneum gets absorbed gradually. should be presumed to have an ectopic preg-
nancy until proved otherwise. Very often with
Tubal abortion an ectopic pregnancy, the usual symptoms of
pregnancy (nausea, vomiting, breast tenderness,
When implantation occurs in the infundibu- fatigue) may not be pronounced.
lum of the tube, the products are extruded into
the abdomen through the tubal ostium. This is
known as tubal abortion. Blood collects in the Amenorrhea
pouch of Douglas, leading to the formation of a Women with ectopic pregnancy typically present
pelvic hematocele. 6–8 weeks after the last normal menstrual period.
However, if the pregnancy is in an extrauterine
Tubal rupture site other than the fallopian tube, the symptoms
As already described, the tubal wall is stretched may occur later than 8 weeks.
and thinned out and may ultimately rupture. This
is common with pregnancies implanted in the
isthmus since the lumen is narrow. Rupture occurs Box 30.3 The natural progression of tubal
pregnancy
by 6 weeks or sometimes earlier when implanta-
tion is in the isthmus, and there may be no history • Complete expulsion or absorption
of a missed period. Ampullary pregnancies usu- • Tubal abortion
ally rupture by 8–10 weeks because there is more • Rupture
space to expand. Blood collects in the pouch of Ŧ Pelvic hematocele
Ŧ Broad ligament hematoma
Douglas and a large pelvic hematocele is usu-
Ŧ Secondary abdominal pregnancy
ally formed. Continued bleeding can give rise to
• Formation of chronic ectopic pregnancy
hemoperitoneum, shock, and collapse.
CH 30_p428-446_v3.indd 431 17-07-2015 22:32:53

Abdominal pain Box 30.4 Presenting symptoms of ectopic

The majority of women (95%) with ectopic preg- pregnancy
nancy present with abdominal pain. Abdominal • Amenorrhea
pain associated with ectopic pregnancy may be Ŧ Usually 6–8 weeks
diffuse but could also be localized to one side. The • Abdominal pain
woman may give a history of mild cramping pain Ŧ Diffuse or localized
that slowly increases in intensity. The onset of the Ŧ Onset slow or acute
Ŧ Dull or sharp
pain may be acute. The pain may be continuous or
Ŧ Maybe accompanied by
intermittent, dull, or sharp. Often, rupture of the
Fainting
tube may be accompanied by a sudden increase Shoulder pain
in the severity of pain. It may also be accompanied Urge to defecate
by fainting (syncope). • Vaginal bleeding
Ŧ Variable quantity
Accompanying symptoms Ŧ May be mistaken for menstrual period
When the tube has ruptured and there is increas-

ing collection of blood in the peritoneal cavity,
the pain may start radiating upward to the mid- In the early stages, when the bleeding from
dle or upper abdomen. the tube into the peritoneal cavity is not signif-
When the collection of intraperitoneal blood icant enough, the woman will have stable vital
irritates the inferior surface of the diaphragm, signs. As the bleeding increases, there may be
pain may be referred to the tip of the shoulder. an increase in the pulse rate (tachycardia) and
Pooling of blood in the pouch of Douglas (pelvic hypotension. She may appear pale.
hematocele) may cause an urge to defecate. Since most women with ectopic pregnancy are
young and healthy, compensatory mechanisms
may keep the vital signs stable. If intra-abdominal
aginal bleeding bleeding is suspected, postural changes in blood
Since vaginal bleeding occurs in other conditions pressure should be checked for. With significant
in early pregnancy, it is not specific to ectopic bleeding, the woman may have normal blood
pregnancy. It may vary from brownish staining pressure while lying down, but she will have
to heavy bleeding and may also be intermittent hypotension when she is made to sit up (postural
or continuous. hypotension).
Women may misinterpret vaginal bleeding A ruptured ectopic pregnancy can result in
as a normal period, and an ectopic pregnancy life-threatening intra-abdominal hemorrhage.
may only be suspected when they present with Acute rupture of the tubal pregnancy can result
abdominal pain, fainting, and/or shoulder pain. in acute hypotension and hypovolemic shock. It
The presenting symptoms of ectopic preg- is important to remember that most women will
nancy are listed in Box 30.4. have prodromal symptoms and a high index of
suspicion will help diagnose an ectopic preg-
nancy before it ruptures.
Signs suggestive of Abdominal palpation
ectopic pregnancy Abdominal tenderness is elicited in 90% of
women. Unilateral iliac fossa pain is common
General examination in an ectopic pregnancy, but due to peritoneal
irritation from the blood, bilateral pain is not
and vital signs unusual. Abdominal guarding, rigidity, and
The general condition of the woman depends on rebound tenderness are signs of peritoneal irri-
whether the ectopic pregnancy is unruptured or tation. When hemoperitoneum is present, shift-
ruptured at the time of presentation. ing dullness may be elicited.
CH 30_p428-446_v3.indd 432 17-07-2015 22:32:53

aginal examination unruptured ectopic pregnancy can be treated

conservatively, whereas a ruptured ectopic preg-
The uterus may feel soft and slightly enlarged in nancy will require surgical intervention. When
the presence of an ectopic pregnancy. This is a an ectopic pregnancy ruptures, it becomes a
consequence of the raised levels of progesterone life-threatening emergency.
in pregnancy leading to myometrial hyperplasia.
Adnexal tenderness may be elicited, although
care must be taken not to palpate too deeply Early diagnosis
because that might lead to rupture of an unrup- Diagnosing an ectopic pregnancy before
tured ectopic pregnancy. The classic sign of a it ruptures requires a high index of suspi-
tubal pregnancy is elicitation of pain on the cion. Every sexually active reproductive-aged
affected adnexal side on movement of the cervix. woman who presents with abdominal pain or
Boggy fullness can be felt in the posterior fornix vaginal bleeding should be screened carefully
when blood is collected in the pouch of Douglas. for history suggestive of pregnancy symp-
This may push the uterus up and anteriorly against toms, history that places her at high risk for
the bladder and cause urinary retention. an ectopic pregnancy, and history suggestive
Signs suggestive of ectopic pregnancy are of intra-abdominal bleeding (abdominal pain,
summarized in Box 30.5. feeling faint).
A combination of serum hCG and transvagi-
nal ultrasonography is the best method for diag-
Diagnosis of ectopic nosing an ectopic pregnancy.
pregnancy
The aim of good clinical practice is to diagnose Serum hCG and discriminatory
an ectopic pregnancy before it ruptures. An one
If the urine pregnancy test is positive but an
Box 30.5 Signs suggestive of ectopic
pregnancy intrauterine pregnancy is not demonstrated on
transvaginal ultrasonography (TVUS), then it is
• General examination mandatory to obtain a serum hCG level.
Ŧ Vital signs
Commonly, with a serum hCG level of 1500
Early unruptured
or 2000 mIU/mL, an intrauterine pregnancy
- Stable in early stages
- Postural hypotension
should be demonstrated using TVUS. This is
Ruptured known as the discriminatory zone of serum
- Frank hypotension hCG level.
- Hypovolemic shock If the serum hCG level is lower than 1500 mIU/
• Abdominal palpation mL, the test is repeated in 48 hours. In a normal
Ŧ Tenderness intrauterine pregnancy, the hCG level will dou-
Diffuse ble in 48 hours. At this point an intrauterine
Unilateral pregnancy should be demonstrable. If the hCG
Bilateral level does not double, TVUS must be repeated
Ŧ Peritoneal irritation from bleeding to demonstrate a failing intrauterine pregnancy
Abdominal guarding
(miscarriage) or an ectopic pregnancy.
Rigidity
Rebound tenderness
Shifting dullness
• Vaginal examination
Transvaginal ultrasonography
Ŧ Uterus Transvaginal ultrasonography is the gold stan-
Soft dard for the evaluation of suspected ectopic
Slightly enlarged pregnancy. A transvaginal ultrasound exam-
Ŧ Adnexal tenderness ination may demonstrate an intrauterine preg-
Ŧ Pain on movement of cervix
nancy or an extrauterine pregnancy, or may be
Ŧ Bogginess/fullness in posterior fornix
nondiagnostic.
CH 30_p428-446_v3.indd 433 17-07-2015 22:32:54

Intrauterine pregnancy
The visualization of an intrauterine pregnancy
rules out an ectopic pregnancy. However, in a
woman who has undergone IVF, a heterotopic
pregnancy must be excluded.
Extrauterine pregnancy
A mass lying between the ovary and the uterus
is the most common finding in an ectopic preg-
nancy. The mass could be cystic or solid.
• Pseudogestational sac: In the presence of an
ectopic pregnancy, the uterine cavity may con-
tain a pseudogestational sac (Fig. 30.2). A pseu- Figure 30.3 Transvaginal ultrasound image of adnexa.
dogestational sac is a small fluid collection that Empty gestational sac or tubal ring (arrow) seen in the
is centrally located within the endometrial cav- CFPGZC0Q[QNMUCEQTGODT[QECPDGKFGPVKſGFKPVJG
ity and is surrounded by a thick decidual reac- sac. (Photo courtesy: Mediscan Systems, Chennai.)
tion. This may be demonstrated in up to 20% of
women with an ectopic pregnancy.
• Decidual cysts: These can be present in both seeing a gestational sac in the adnexa that con-
intrauterine and ectopic pregnancies and mimic tains a yolk sac and embryo (Fig. 30.4). Cardiac
a gestational sac. They have a thin wall, can be activity may or may not be seen. Identification
multiple, and are generally located in the periph- of cardiac activity in an adnexal cystic lesion is
eral endometrium at the myometrial junction. 100% pathognomonic of an ectopic pregnancy.
• Empty gestational sac or tubal ring: This is an • Solid adnexal mass: An ectopic pregnancy may
adnexal finding that is suggestive, but not diag- also be seen as a solid mass in the adnexa. This
nostic, of a tubal pregnancy. The cystic center usually happens because of hemorrhage into
represents the sac and the echogenic ring rep- the ectopic pregnancy, which then loses its
resents the trophoblastic tissue (Fig. 30.3). cystic appearance and appears solid (Fig. 30.5).
• Gestational sac with yolk sac and embryo: • Peritoneal fluid: If echogenic fluid is seen in
Tubal pregnancy may also be identified by the cul-de-sac in a pregnant woman with no
Figure 30.2 Transvaginal ultrasound image of the uterine Figure 30.4 Transvaginal ultrasound image of adnexa.
ECXKV[6JGEGPVTCNN[NQECVGFƀWKFEQNNGEVKQPYKVJQWVCP Viable tubal pregnancy seen with yolk sac. S gestational
echogenic ring (arrow) represents a pseudogestational sac; S yolk sac. (Photo courtesy: Mediscan Systems,
sac. (Photo courtesy: Mediscan Systems, Chennai.) Chennai.)
CH 30_p428-446_v3.indd 434 17-07-2015 22:32:54

Figure 30.7 6TCPUXCIKPCNWNVTCUQWPFYKVJEQNQTƀQY

Figure 30.5 Transvaginal ultrasound image of adnexa. &QRRNGTKOCIKPI+PETGCUGFDNQQFƀQY
ŎTKPIQHſTGŏ
Ectopic pregnancy seen as a solid mass (indicated by appearance) seen around the ectopic pregnancy. (Photo
arrows) lying adjacent to the ovary. (Photo courtesy: courtesy: Mediscan Systems, Chennai.)
increased blood flow around an ectopic preg-
evidence of an intrauterine pregnancy, it could nancy. This is called the ‘ring of fire’ appearance
be suggestive of an ectopic pregnancy. Clear fluid (Fig. 30.7). However, this does not help differen-
can be considered physiologic, but complex or tiate a tubal pregnancy from a corpus luteum,
echogenic fluid is always pathological (Fig. 30.6). since a ‘ring of fire’ appearance can be seen in
With a ruptured ectopic pregnancy, a large quan- either condition.
tity of echogenic fluid can be demonstrated in The ultrasonographic findings suggestive of
the peritoneal cavity and the pelvic organs and an ectopic pregnancy are listed in Box 30.6.
bowel can be seen floating in the fluid.
Culdocentesis
Doppler imaging Culdocentesis is aspiration of the contents of
Due to the increased vascularity in an ectopic the cul-de-sac (pouch of Douglas) to determine
pregnancy, color flow Doppler may demonstrate whether blood is present. It is a diagnostic pro-
cedure where a long 18-gauge needle is inserted
Box 30.6 7
NVTCUQWPFſPFKPIUUWIIGUVKXGQH
ectopic pregnancy in a serum hCG-
positive (1500 2000 mI mL) woman
• terus
Ŧ Empty uterine cavity/no evidence of intrauterine
pregnancy
Ŧ Pseudogestational sac/decidual cyst
• Adne ae
Ŧ Simple adnexal cyst
Ŧ Empty gestational sac (tubal ring)
Ŧ Gestational sac with yolk sac and embryo
Ŧ %CTFKCECEVKXKV[URGEKſE
Ŧ Complex/ solid adnexal cyst/mass
• Peritoneal cavity
Figure 30.6 Transvaginal ultrasound image. Echogenic Ŧ 'EJQIGPKERGTKVQPGCNƀWKFKPVJGEWNFGUCE
• &QRRNGTEQNQTƀQYKOCIKPI
RGTKVQPGCNƀWKFUGGPKPVJGEWNFGUCEKUUWIIGUVKXG
Ŧ Ŏ4KPIQHſTGŏUKIPPQVURGEKſE
of unruptured or ruptured ectopic pregnancy. (Photo
courtesy: Mediscan Systems, Chennai.) hC , human chorionic gonadotropin.
CH 30_p428-446_v3.indd 435 17-07-2015 22:32:54

through the posterior vaginal fornix into the cul-

de-sac and fluid is withdrawn (Fig. 30.8). This is
performed when pelvic hematocele is detected
clinically or on ultrasonography.
A culdocentesis that is positive for nonclotting
bloody fluid strongly suggests the presence of a
bleeding ectopic pregnancy. The finding of yel-
low or straw-colored fluid is more suggestive of
a ruptured ovarian cyst rather than of an ectopic
pregnancy.
Culdocentesis is not commonly performed
now because ultrasonography can demonstrate
the presence of fluid in the pelvis. The proce-
dure is used when ultrasonography is not readily
available or when a rapid confirmation of diag- Figure 30.9 Unruptured ectopic pregnancy (arrow) in the
nosis is required in a woman in shock from intra- right fallopian tube seen on laparoscopy. (Photo courtesy:
peritoneal hemorrhage. Dr Sandip Dutta Roy.)
Diagnostic laparoscopy pregnancy, surgical treatment can be carried out

laparoscopically (see the section, Surgical man-
If the ultrasound examination does not give a agement of tubal ectopic pregnancy).
specific diagnosis or is unable to differentiate
between an ectopic pregnancy and a bleeding
ovarian cyst, or the woman’s condition is hemo-
Curettage
dynamically unstable, a laparoscopy can be Presence of trophoblastic villi on endometrial
performed to confirm the diagnosis (Fig. 30.9). curetting is diagnostic of an intrauterine preg-
If there is an unruptured or ruptured ectopic nancy. This may help in diagnosis when a viable
Figure 30.8 Culdocentesis. A long needle is introduced into the cul-de-sac through the posterior vaginal fornix.
CH 30_p428-446_v3.indd 436 17-07-2015 22:32:54

intrauterine pregnancy has been excluded. If cho- Management of ectopic

rionic villi are present, in the presence of falling
hCG levels, a diagnosis of failing intrauterine pregnancy
pregnancy may be made and unnecessary inter-
ventions avoided. Curettage, however, is not often There are three options for the management of
used in the diagnosis of an ectopic pregnancy. an ectopic pregnancy:
• Expectant management
• Medical management with methotrexate (MTX)
Serum progesterone • Surgical management
Serum progesterone level of >25 ng/mL suggests The choice of modality of management
an intrauterine pregnancy. Levels <5 ng/mL depends on the clinical situation. Women who
indicate a nonviable intrauterine pregnancy or are hemodynamically unstable must be oper-
an ectopic pregnancy. The clinical usefulness of ated upon immediately, whereas in women with
this test is limited. an unruptured ectopic pregnancy, other meth-
The suggested algorithm for the diagnosis of ods may be appropriate. The decision is based
an ectopic pregnancy is given in Figure 30.10. on initial evaluation.
Positi e pregnancy test

b ominal pain
Vaginal blee ing
rans aginal
ultrasoun
UP seen UP not seen
nconclusi e
ormal failing
ne al mass ultrasoun erum hC
pregnancy
fin ings
ctopic
pregnancy m U mL m U mL
uspect erial hC
ectopic testing
ormal hC bnormal hC
oubling time oubling time
rans aginal ultrasoun hen

hC m U mL ctopic
ailing UP
pregnancy
ctopic
UP
pregnancy
Figure 30.10 Diagnostic pathway for ectopic pregnancy. hC , human chorionic gonadotropin; P, intrauterine pregnancy.
CH 30_p428-446_v3.indd 437 17-07-2015 22:32:54

Box 30.7 Initial evaluation in ectopic Management of women who

pregnancy
are hemodynamically unstable
• History
Ŧ Risk factors
Management of women who are hemodynami-
Ŧ Duration of symptoms cally unstable includes concomitant supportive
Ŧ Amenorrhea and definitive measures.
Ŧ Bleeding
• If the woman has tachycardia and hypoten-
Ŧ Pain
sion, intravenous access should be obtained
Severity
Ŧ Syncope
with a large-bore needle, and IV fluids must be
Ŧ Urinary/bowel symptoms started.
• Examination • Blood should be sent for hematocrit, grouping,
Ŧ Pulse/BP/respiration and cross-matching.
Ŧ Abdomen • Transfusion of packed cells or whole blood
Tenderness/rigidity/shifting dullness must be started as soon as possible.
Abdominal mass • TVUS, if readily available, should be per-
Ŧ Pelvic examination formed to confirm diagnosis. Culdocentesis
Adnexal mass/tenderness may be performed if TVUS is not available.
Fullness in pouch of Douglas • The woman should be prepared for laparotomy.
• Ultrasonography
Ŧ Hemoperitoneum
Ŧ Adnexal mass with or without embryo Management options
Ŧ Fetal pole with cardiac activity
• Serum EhCG levels in women who are
BP, blood pressure; hC , human chorionic gonadotropin. hemodynamically stable
Women with an ectopic pregnancy who are hemo-
dynamically stable can be managed expectantly if
Initial evaluation the hCG levels are low. Medical management is
indicated in women wih hCG levels <5000 mIU/
Initial evaluation consists of history, clinical mL and who are compliant with instructions.
examination, and investigations as given in
Box 30.7.
Expectant management
Following the initial evaluation, women
may be categorized as given in Table 30.1. This Some ectopic pregnancies resolve sponta-
helps in choosing the appropriate management neously. In hemodynamically stable women,
option. expectant management is a good option.
Table 30.1 Categori ation of women according to hemodynamic

stability, status of ectopic pregnancy, and hCG levels
emodynamic Status of ectopic
stability pregnancy Serum EhCG level
No gestational sac Low
or adnexal mass
Gestational sac/adnexal mass Moderately high
Stable
pesent
Unruptured ectopic gestation Moderately high
with cardiac activity
Hemodynamically Ruptured ectopic pregnancy Variable
Unstable
hC , human chorionic gonadotropin.
CH 30_p428-446_v3.indd 438 17-07-2015 22:32:54

The cases selected for expectant management of trophoblastic cells and leads to tubal abor-
are not chosen by the size of the ectopic preg- tion. Since it is used at a much lower dose than
nancy on TVUS. The decision depends on the that used for treatment of malignancy, the side
initial hCG titer and whether repeated hCG titers effects are fewer than with higher doses.
are trending down. In spite of giving MTX, some ectopic pregnan-
It is important, therefore, to serially monitor cies may go on to rupture. This must be explained
serum titers of hCG in women who are being to the woman, and she should be counseled
managed expectantly. The higher the serum con- about the symptoms of impending rupture (sud-
centration, the more likely that expectant man- den increase in abdominal pain, fainting). She
agement will fail. should have rapid access to a medical institution
The candidates for expectant management with surgical facilities.
are chosen if:
Selection o omen or treatment ith
• transvaginal ultrasonography does not show a
gestational sac or demonstrates an extrauterine
methotre ate
mass suspicious for an ectopic pregnancy and The criteria for the optimal candidate for MTX
• the hCG concentration is low (d200 mIU/mL) treatment of ectopic pregnancy are enumerated
and declining on serial monitoring. in Box 30.9.
The woman must be informed about signs Contrain ications to the use o metho
of impending rupture and asked to report back tre ate
immediately at the appearance of any symptoms
or signs of rupture. If hCG levels are increasing The contraindications for the use of MTX are
or if there are signs of tubal rupture, the woman listed in Box 30.10.
should be treated medically or surgically.
The prerequisites for expectant management Treatment protocols for
are listed in Box 30.8. methotrexate
Two regimens have been described: single-dose
Medical management with and multidose. Both have a success rate of 90%,
methotrexate although the multidose regimen results in more
The advantage of early diagnosis of an unrup- side effects.
tured ectopic pregnancy is that it can be man-
aged medically with MTX. Selecting the right
candidates for medical management can yield a Box 30.9 ptimal candidate for methotrexate
therapy
success rate of nearly 90%.
Methotrexate is a folic acid antagonist that • Hemodynamically stable
inhibits DNA synthesis and cell reproduction, • Willing and compliant with follow-up
primarily in actively proliferating cells such as • 5GTWOJ%)NGXGNŭO+7O.
malignant cells, trophoblasts, and fetal cells. Its • No fetal cardiac activity
cytotoxic effect prevents further proliferation • Ectopic mass size <3–4 cm
hC , human chorionic gonadotropin.
Box 30.8 Prerequisites for expectant manage- Box 30.10 Contraindications to methotrexate
ment of woman with ectopic pregnancy • Hemodynamic instability
• Hemodynamically stable • Signs of impending or ongoing rupture
• On TVUS Ŧ Severe or persistent abdominal pain
Ŧ No gestational sac Ŧ O.QHHTGGRGTKVQPGCNƀWKFQWVUKFGVJGRGNXKE
Ŧ No extrauterine mass cavity
• J%)NGXGNŭO+7O.CPFFGENKPKPI • Hepatic, renal, or hematologic dysfunction
• Poor access to medical facilities
hC , human chorionic gonadotropin; S, transvaginal ultra- • Not compliant with follow-up
sonography.
CH 30_p428-446_v3.indd 439 17-07-2015 22:32:54

Single ose regimen i e multi ose regimen

A single intramuscular (IM) dose of MTX is the In the most common protocol used for the mul-
simplest and most convenient protocol for tidose regimen, MTX is alternated with folinic
MTX therapy. Although 15%–20% of women will acid (‘folinic acid rescue’). Folinic acid bypasses
require a second dose, <1% of women need more the metabolic block induced by MTX, and thus
than two doses. rescues normal cells from toxicity.
Calculation of dose Protocol
The dose of MTX is based on body surface area The following protocol is used for the multidose
(in m2). An average Indian woman has a body regimen (Table 30.3):
surface area of 1.5–1.6 m2. The dose given for a
• MTX at the dose of 1 mg/kg IM or IV is given on
tubal ectopic pregnancy is 50 mg/m2. For the
Days 1, 3, 5, and 7.
average Indian woman the dose of MTX is 75–80
• Oral folinic acid at the dose of 0.1 mg/kg is
mg IM, based on the body surface area.
given on Days 2, 4, 6, and 8.
Protocol • Serum hCG levels are checked on Days 1, 3, 5,
The following protocol is used for the single-dose and 7 (the days on which MTX is given).
regimen (Table 30.2): • If the serum hCG declines >15% from the pre-
vious measurement, treatment is stopped and
• The baseline hCG level prior to administering hCG levels are checked weekly.
MTX is an important number because further • If the hCG declines <15% from the previous
management is based on this value. level, the woman is given an additional dose of
• The day the first dose is given is counted as Day 1. MTX (1 mg/kg IM) followed by a dose of oral
• The commonest protocol measures the serum folinic acid (0.1 mg/kg) the next day.
hCG levels on Days 4 and 7. • The hCG levels are checked till a nonpregnant
• If the decrease in hCG between Days 4 and 7 is level is reached.
<15%, a second dose of MTX 50 mg/m2 IM is
administered. It is not uncommon to observe onitoring the oman
an increase in hCG levels until Day 4. This is on methotre ate therapy
due to continued hCG production by the syn-
The woman is monitored for the following:
cytiotrophoblast despite cessation of produc-
tion by the cytotrophoblast. • Signs of worsening disease
• Some protocols recommend only one measure- – Abdominal pain
ment of serum hCG on Day 7. In that case, a sec- – Fluid in pelvis on TVUS
ond dose of MTX is administered if the serum – Fall in hemoglobin levels to <10 g/dL
hCG concentration on Day 7 has not declined by • Effectiveness of therapy
at least 25% from the Day 1 level. • Side effects of MTX
Table 30.2 Single-dose regimen of methotrexate therapy for tubal

ectopic pregnancy
Day Serum hCG level Methotrexate
Day 1 Note the base-line level 50 mg/m2 (approximately
75–80 mg IM)
Day 4 Check the level (remained the Methotrexate not given
same/increased/ decreased)
Day 7 %JGEMVJGNGXGN
ŮFGETGCUG Repeat dose if hCG level decreases
HTQO&C[NGXGNŮFGETGCUG <15% from Day-4 level or
from Day-1 level) <25% from Day-1 level
Weekly Check levels until nonpregnant If hCG levels plateau or increase,
levels are reached dose may be repeated
hC , human chorionic gonadotropin; , intramuscular.
CH 30_p428-446_v3.indd 440 17-07-2015 22:32:54

Table 30.3 Multidose regimen of methotrexate therapy with folinic acid recue for tubal
ectopic pregnancy
Day on which Days on which
methotrexate given folinic acid given Days on which
(1 mg kg IM or I ) (0.1 mg kg orally) hCG checked Stop treatment Follow-up
1, 3, 5, 7 2, 4, 6, 8 1, 3, 5, 7 When hCG level Weekly until
FTQRUŮ hCG level is
from previous not detected
level
hC , human chorionic gonadotropin; , intramuscular.
Signs of worsening disease The common side effects of MTX are listed in
It is important to remember that with MTX Box 30.12.
therapy, the woman may experience increase
in pain from days 4–7 of therapy. This is usu-
ally due to tubal abortion or hemorrhage into Surgical management of tubal
the ectopic pregnancy. The pain can be man- ectopic pregnancy
aged with paracetamol. Nonsteroidal anti-in-
flammatory drugs (NSAIDs) should not be Medical therapy is the treatment of choice for an
used along with MTX due to significant drug unruptured tubal ectopic pregnancy. However,
interaction. there are clinical situations where surgical inter-
If the abdominal pain is severe, the woman vention is required. The indications for surgical
must be evaluated with TVUS for intra-abdom- therapy are summarized in Box 30.13.
inal bleeding or rupture.
Therapy with MTX is summarized in Box 30.11.
Box 30.12 Side-effects of methotrexate
Side effects of methotrexate
The single-dose regimen has fewer side effects • Stomatitis
than the multidose regimen. However, due to • Conjunctivitis
the low dose of MTX used (as compared with the • Rare side effects
dose used for malignancy), the side effects are Ŧ Gastritis
usually mild and transient. Ŧ Enteritis
Ŧ Dermatitis
Ŧ Pneumonitis
Ŧ Alopecia
Box 30.11 Therapy with methotrexate Ŧ Elevated liver enzymes
• Methotrexate Ŧ Bone marrow suppression
Ŧ Folic acid antagonist
Ŧ Inhibits DNA synthesis and cell reproduction
Ŧ Affects trophoblasts and fetal cells Box 30.13 Indications for surgical therapy
• Single-dose therapy
Ŧ 50 mg/m2 IM • Hemodynamic instability
Ŧ hCG level checked on Days 4 and 7 • Suspected rupture
Ŧ Dose repeated if needed • When MTX is likely to fail
• Multidose therapy Ŧ hCG >5000 mIU/mL
Ŧ Methotrexate on Days 1, 3, 5, and 7 Ŧ Sac size >4 cm
Ŧ Folinic acid on Days 2, 4, 6, and 8 Ŧ Cardiac activity demonstrated
• hCG levels followed weekly till undetectable • Other contraindications to MTX
• Signs of tubal rupture watched for • Failed medical therapy
hC , human chorionic gonadotropin; , intramuscular. hC human chorionic gonadotropin; methotrexate.
CH 30_p428-446_v3.indd 441 17-07-2015 22:32:55

Surgical options for unruptured • A 1- to 2-cm incision (called a linear salpin-

ectopic pregnancy gostomy) is made through the antimesenteric
wall of the tube, overlying the ectopic preg-
The two surgical options for the management of nancy (Fig. 30.11b).
an unruptured tubal ectopic pregnancy are as • The products of conception are then flushed
follows: out of the tube with gentle mechanical pres-
sure (Fig. 30.11c).
• Salpingostomy
• Alternatively, aquadissection (pressurized irri-
• Salpingectomy
gation) is used. The aquadissector, or a syringe
Both procedures can be done either by lapa- filled with saline, is inserted deep into the inci-
roscopy or by laparotomy. sion. The pressurized fluid dissects and dis-
lodges the ectopic pregnancy and clots.
Salpingostomy • Any bleeding sites are treated by applying
A salpingostomy involves the following steps: pressure with forceps or by cauterizing the
bleeding points. The incision is not sutured
• To minimize bleeding, a dilute solution con- but instead left to heal on its own (closure by
taining vasopressin may be injected into the secondary intent (Fig. 30.11d).
mesosalpinx just below the ectopic pregnancy
and on the overlying serosa (Fig. 30.11a).
a. b.
. .
Figure 30.11 Salpingostomy. a.8CUQRTGUUKPDGKPIKPſNVTCVGFKPVQVJGUGTQUCb. Incision being made with monopolar
L-hook on anti-mesenteric border. c. Ectopic mass extruding through the salpingostomy. d. The incision is left unsutured.
(Photo courtesy: Dr Sandip Dutta Roy.)
CH 30_p428-446_v3.indd 442 17-07-2015 22:32:55

Drawbacks of salpingostomy
Box 30.14 Drawbacks of salpingostomy
Although salpingostomy conserves the tube, there
• 20% converted to salpingectomy because of uncon-
are some drawbacks associated with the procedure. trolled bleeding
These drawbacks are summarized in Box 30.14. • Increased risk of recurrent ectopic pregnancy in the
same tube
Salpingectomy • No increase in fertility when compared with sal-
Excision of the affected tube is called salpingec- pingectomy
• Small risk of persistent trophoblastic tissue in tube
tomy. The procedure is usually done laparoscop-
ically but may require a laparotomy in certain
situations.
Salpingectomy may be
Box 30.15 Indications for salpingectomy
• total or
• Ruptured ectopic pregnancy
• partial. • Uncontrolled hemorrhage
• Further fertility not desired by the woman
Total salpingectomy • Failed tubal sterilization/reconstruction followed by
Total salpingectomy is preferred to partial sal- ectopic pregnancy
pingectomy. This can be achieved by progres- • Chronic tubal pregnancy
sively coagulating or clamping and cutting the • Severely damaged tube
mesosalpinx, starting from the fimbrial end and
advancing toward the proximal isthmic portion
of the tube (Fig. 30.12a and b). At this point, the
tube is separated from the uterus by coagulating In ications or laparotomy
or ligating and excising with scissors. Although laparoscopy is the preferred route for
the surgical management of a tubal ectopic preg-
Partial salpingectomy nancy, there are certain situations where a lapa-
A partial salpingectomy is sometimes done by rotomy is the better choice.
removing only the ectopic pregnancy and the The indications for a laparotomy are enumer-
portion of the tube distal to it. Since there is a risk ated in Box 30.16.
of recurrent ectopic pregnancy in the same tube, Surgical management for ectopic pregnancy
a complete salpingectomy is a better option. is summarized in Box 30.17.
The indications for salpingectomy are listed Management of ectopic pregnancy is outlined
in Box 30.15. in Figure 30.13.
a. b.
Figure 30.12 Laparoscopic salpingectomy. a. The mesosalpinx is being progressively coagulated. b. The mesosalpinx is
being cut till the proximal isthmic end of the tube is reached. (Photo courtesy: Dr Sandip Dutta Roy.)
CH 30_p428-446_v3.indd 443 17-07-2015 22:32:55

Box 30.16 Indications for laparotomy Follow-up of surgery for ectopic

• Hemodynamically unstable woman
pregnancy
Ŧ Severe intra-abdominal bleeding The incidence of persistent trophoblastic tissue is
• Cornual ectopic pregnancy greater with salpingostomy, especially if the initial
• .CRCTQUEQRKECRRTQCEJVGEJPKECNN[FKHſEWNVFWGVQ
hCG level was >3000 mIU/mL. After salpingos-
Ŧ Multiple dense adhesions
tomy, the woman should be followed with serum
Ŧ Obesity
hCG levels till the level becomes undetectable.
Contraceptive advice should be given and
effective contraception should be used for
Box 30.17 Surgical therapy for ectopic 3–6 months.
pregnancy
• Laparoscopy or laparotomy
• Salpingostomy
Interstitial (cornual)
Ŧ Unruptured tubal ectopic pregnancy
Ŧ Conserves tube
pregnancy
• Salpingectomy Pregnancy may be implanted in the portion
Ŧ Ruptured tubal ectopic of the tube that traverses the myometrium.
Ŧ Hemodynamically unstable woman
Diagnosis may be delayed due to its unusual
Ŧ Preferred option if other tube is healthy
location. These women present later in gestation
Ŧ Total salpingectomy preferred to partial
than those with pregnancy in the other parts of
ctopic pregnancy
iagnose
nitial e aluation
Vital signs
Clinical e amination
Hemo ynamically Hemo ynamically

unstable stable
Correct hypo olemlia hC m U mL

hC m U mL
loo transfusion hC m U mL ac cm
ac cm
rans aginal ultrasoun o e trauterine sac Car iac acti ity present
o car iac acti ity
f no VU cul ocentesis uspecte rupture
pectant Me ical therapy

Laparotomy Laparoscopy
management ith methotre ate
alpingostomy alpingectomy
Figure 30.13 Suggested management algorithm for ectopic pregnancy. hC , human chorionic gonadotropin; S,
transvaginal ultrasonography.
CH 30_p428-446_v3.indd 444 17-07-2015 22:32:55

the tube. Rupture with profuse intra-abdomi- difficult and may be mistaken for other lesions
nal bleeding is the usual clinical presentation. in the cervix. Management is with MTX. Uterine
Laparotomy is indicated in most, although some artery embolization may be required for control
women may be managed by laparoscopic sur- of bleeding. Hysterectomy is an option in multipa-
gery. Cornuostomy or removal of the intersti- rous women.
tial portion of the tube should be performed.
Rupture of the uterus is known to occur during
subsequent pregnancy.
Pregnancy in other sites
Ovarian, broad ligament, and secondary abdom-
Cervical pregnancy inal pregnancies have been reported but are
uncommon.
Cervical pregnancy is rare. Women usually
present with massive hemorrhage. Diagnosis is
Key points
• A pregnancy that occurs in a site outside the uterine TVUS. This is known as the iscriminatory one of
cavity is called GEVQRKERTGIPCPE[. The majority of ec- serum hCG level.
topic pregnancies (98%) are sited in the fallopian tube.
• TVUS is the gold standard for the evaluation of a
• In the fallopian tube, approximately 80% of the preg- suspected ectopic pregnancy. A TVUS examination
nancies occur in the ampullary region. may demonstrate an intrauterine pregnancy, or an
• The history of treatment for a previous ectopic preg- extrauterine pregnancy, or could be nondiagnostic.
nancy increases the risk for an ectopic pregnancy in • Culdocentesis is a diagnostic procedure where a long
the next pregnancy. 18-gauge needle is inserted through the posterior
• 0QPURGEKſEUCNRKPIKVKUCPFEJNCO[FKCNCPFIQPQTTJGCN XCIKPCNHQTPKZKPVQVJGEWNFGUCECPFƀWKFKUYKVJFTCYP
infections (especially when recurrent) lead to tubal to test for the presence of blood. It is done only if
damage and therefore have been implicated in the ultrasound imaging is not available.
causation of ectopic pregnancy. • There are three options for the management of an
• Women undergoing treatment for infertility have ectopic pregnancy: expectant management, medical
a fourfold increase in the incidence of an ectopic management with methotrexate (MTX), or surgical
pregnancy. management.
• Women undergoing in vitro fertilization (IVF) have a • Methotrexate is a folic acid antagonist that inhibits
two to three times increased risk of both ectopic and DNA synthesis and cell reproduction, primarily in
heterotopic pregnancies. actively proliferating cells such as malignant cells,
trophoblasts, and fetal cells.
• Tubal surgery increases the incidence of a tubal
ectopic pregnancy. • The optimal candidates for MTX treatment of an
ectopic pregnancy should be hemodynamically stable,
• Any sexually active woman presenting with abdominal
willing, and compliant with follow-up, and have serum
pain and vaginal bleeding after an interval of amenor-
J%)NGXGNŭO+7O.PQHGVCNECTFKCECEVKXKV[
rhea should be considered to have an ectopic preg-
and an ectopic mass size <3–4 cm.
nancy until proved otherwise.
• Two regimens have been described: single-dose and
• The aim of good clinical practice is to diagnose an
multidose. Both have a success rate of 90%, although
ectopic pregnancy before it ruptures. An unruptured
the multidose results in more side effects.
ectopic pregnancy can be treated conservatively,
whereas a ruptured ectopic pregnancy will require • Surgical therapy is indicated in the following situations:
surgical intervention. When an ectopic pregnancy hemodynamic instability, suspected rupture, contrain-
ruptures, it becomes a life-threatening emergency. dications to MTX, or failed medical therapy.
• A combination of serum human chorionic gonadotro- • The two surgical options for the management of an
pin (hCG) and transvaginal ultrasonography (TVUS) is unruptured tubal ectopic pregnancy are UCNRKPIQUVQO[
the best method for diagnosing an ectopic pregnancy. and UCNRKPIGEVQO[. Both procedures can be done
either by laparoscopy or by laparotomy.
• With a serum hCG level of 1500 or 2000 mIU/mL, an
intrauterine pregnancy should be demonstrated using
CH 30_p428-446_v3.indd 445 17-07-2015 22:32:55

Self-Assessment
is done for adnexal mass, tenderness, and fullness
Case-based questions in the pouch of Douglas. Ultrasonography is per-
formed to look for free fluid and adnexal mass with
Case 1 gestational sac.
3. IV access should be established, blood transfusion
Mrs. HG, 29, had been attempting to conceive for the started, and TVUS performed. She should be taken
past 3 years. She had a missed miscarriage 2 years ago for laparotomy and salpingectomy.
and underwent surgical evacuation. She presented at 6
4. Women with gestational sac >4 cm and hCG >5000
YGGMUŏCOGPQTTJGCYKVJKPVGTOKVVGPVETCORKPICDFQOKPCN
mIU/mL, with a live embryo, and who are hemo-
pain on the left side. She also had some vaginal spotting.
dynamically stable need surgical intervention with
The pain worsened and she fainted once when she tried
laparoscopy. Other indications for laparoscopy are
to stand up.
failed medical therapy and contraindications to
1. What is the diagnosis and why? methotrexate.
3. If she is pale, BP is 100/70 at admission, and TVUS
revealed 1000 mL of blood in the peritoneal cavity,
Case 2
what is the management? 1. Medical therapy with methotrexate would be the ideal
4. What are the indications for surgical management treatment for an unruptured tubal ectopic pregnancy.
with laparoscopy? 2. Methotrexate is a folic acid antagonist that inhibits
DNA synthesis and cell reproduction, primarily in
actively proliferating cells such as trophoblasts and
Case 2 fetal cells.
Mrs. DS, 24, gravida 1, para 0, presented with acute ab- 3. Single-dose therapy: 50 mg/m2 of methotrexate is
dominal pain. Her last period was scanty. She had done a given IM. The serum hCG level is checked on Days
home pregnancy test that was positive. A TVUS showed 4 and 7. There should be a drop of 15% from Day 4
an unruptured left tubal pregnancy. The serum hCG level to 7 or 25% from Day 1 to 7. The dose is repeated if
was 1200 mIU/mL. needed. The serum hCG levels are monitored weekly
till undetected.
1. What would be the optimal treatment for this woman? 4. The two surgical options for the management of an
2. How does methotrexate act? unruptured tubal ectopic pregnancy are UCNRKPIQUVQ-
3. Describe the single-dose regimen for methotrexate O[ and UCNRKPIGEVQO[. Both procedures can be done
therapy. either by laparoscopy or by laparotomy.
4. What are the surgical options for treatment of a tubal
ectopic pregnancy?
Sample questions
Answers
1. Discuss the etiology, clinical features, and manage-
Case 1 ment of unruptured tubal pregnancy.
1. Ruptured ectopic pregnancy: the history of amenor-
rhea, with worsening abdominal pain, vaginal bleed-
ing, and fainting episode indicate that the pregnancy Short-answer questions
is probably ectopic and there is intra-abdominal
bleeding. 1. Pelvic hematocele
2. The diagnosis is confirmed by clinical examination 2. Medical management of ectopic pregnancy
to check pulse, blood pressure, abdominal tender- 3. Laparoscopic surgery in ectopic pregnancy
ness, rigidity, and guarding. A vaginal examination 4. Decidual cast
CH 30_p428-446_v3.indd 446 17-07-2015 22:32:55

Intrauterine Fetal
31 Death
Case scenario
Mrs. RT, 25, a pregestational insulin-dependent diabetic, presented at

37 weeks’ gestation with loss of fetal movement for 2 days. She and her
husband were extremely anxious and wanted to know if there was a
problem.
Introduction Early fetal deaths refer to death of fetuses

between 20 and 27 weeks’ gestation (>500 g). Late
Intrauterine fetal death (IUFD), like miscarriage, fetal deaths refer to fetal deaths after 28 weeks,
is a traumatic and devastating event for the cou- birth weight of 1000 g or more, or crown–heel
ple, their families, and the obstetrician. An empa- length of 35 cm. Although some countries define
thetic approach to the couple and their families, stillbirth as fetal death occurring as early as 16
counseling, emotional support, and a system- weeks’ gestation, developing countries such as
atic approach to finding the cause are essential. India classify deaths after 28 weeks as stillbirth.
The neonatologist and geneticist must also be
involved in counseling. The cause of death must
be identified and explained, and further manage-
ment must be discussed. Causes of I FD
Though all cases of IUFD should be investigated,
often the cause is unknown.
&GſPKVKQP
Intrauterine fetal death refers to a fetus with
nexplained I FD
no signs of life in utero. The terms fetal death, A significant percentage of stillbirths (25%–60%)
fetal demise, stillbirth, and stillborn are used may not have a defined etiology. The closer IUFD
interchangeably. occurs to term, the more likely it is to have no
CH 31_p447-454_v2.indd 447 17-07-2015 22:37:26

identifiable fetal, placental, maternal, or obstet- Immune or nonimmune

ric etiology.
hydrops
Fetal growth restriction Hydrops fetalis, of both immune and nonimmune
etiologies, may lead to IUFD.
Fetal growth restriction (FGR) is the second most
common cause of IUFD. When growth restriction
goes unrecognized, it is the single largest risk fac- Cord complications (cord
tor for stillbirth. Fetal growth restriction increases accident )
the risk of stillbirth five-fold to seven-fold.
Complications involving the cord (entangle-
ment, tight nuchal cord, true knots) are often
Placental dysfunction blamed for an unexplained fetal death. Nuchal
Placental dysfunction may result from various eti- cord occurs in one out of three pregnancies, but
ologies such as hypertensive disorders, antiphos- very rarely causes fetal death. Postnatal exam-
pholipid antibody syndrome, or pregestational ination of the umbilical cord around the neck
insulin-dependent diabetes. It can result in fetal will allow assessment of how tight it was and if
demise. it could have been the cause of death. True knots
are sometimes seen. Nuchal cord or knots in the
cord must be considered the cause of fetal death
Congenital anomalies only after thorough assessment and elimination
Stillborn fetuses have a high rate of major struc- of other etiologies.
tural congenital anomalies. Routine second tri- Causes of IUFD are listed in Box 31.1.
mester targeted scan with termination of lethal
anomalies will lower this rate.
Box 31.1 Causes of I FD

Chromosomal abnormalities
• Unexplained IUFD
Lethal chromosomal abnormalities will result in • Unrecognized fetal growth restriction
early pregnancy loss. However, trisomies involving Ŧ Single largest risk factor
chromosomes 13, 18, and 21 and aneuploidies of • Placental dysfunction
the sex chromosomes commonly result in late fetal Ŧ Hypertensive disorders
death. A stillborn fetus with a congenital anomaly Ŧ Antiphospholipid antibody syndrome
is more likely to have a chromosomal abnormality. Ŧ Pregestational insulin-dependent diabetes
• Congenital anomalies
Ŧ Major structural anomalies
Infections Ŧ Lethal anomalies
Infections play an important role in the etiology • Chromosomal abnormalities
Ŧ Trisomies 21, 13, 18
of IUFD, accounting for almost 50% of stillbirths
Ŧ Aneuploidy of sex chromosomes
in developing countries. Parvovirus, cytomegalo-
Ŧ Strong association with congenital anomalies
virus (CMV), toxoplasmosis, Listeria, and herpes • Infections
simplex virus are established causes of intrauter- Ŧ Parvovirus, CMV, toxoplasmosis, isteria, and her-
ine fetal demise. Maternal malaria and hepatitis pes simplex
are more commonly implicated in developing Ŧ Maternal malaria and hepatitis
countries. • Placental abruption
• Immune or nonimmune hydrops
• Cord complications
Placental abruption Ŧ Entanglement
Ŧ True knot
Though uncommon, placental abruption results
Ŧ Tight nuchal cord
in 10%–20% of all stillbirths. The larger the area
After eliminating other causes
of placental separation, the greater is the risk of
fetal demise. C cytomegalovirus; D intrauterine fetal death.
CH 31_p447-454_v2.indd 448 17-07-2015 22:37:26

Intrauterine Fetal Death 449
isk factors for I FD

Certain factors in pregnancy can increase the risk
of stillbirth. These are enumerated in Box 31.2.
Diagnosis of I FD
When the pregnant woman presents with absence
of previously perceived fetal movements, it
should raise suspicion of IUFD. Intrauterine fetal
death may also be suspected when fetal heart
sounds are not audible on auscultation at a rou-
tine antenatal checkup. Occasionally the woman
may present with vaginal bleeding, with or with-
out uterine contractions. Auscultation of the fetal
heart by stethoscope or Doppler is insufficient to
confirm IUFD.
An ultrasound examination is essential to
Figure 31.1 Spalding’s sign in intrauterine fetal death.
confirm fetal death by noting the absence of fetal
Collapse and overlapping of the skull bones (arrow) are
cardiac activity.
seen on ultrasound imaging. (Photo courtesy: Mediscan
Other ultrasound features of IUFD have also
Systems, Chennai.)
been described. The ultrasound features that may
help confirm the diagnosis are given in Box 31.3.
Box 31.2 isk factors for intrauterine fetal death Breaking the news to the
• Prolonged pregnancy (>42 weeks) couple
• Multiple gestation
• Diabetes (poorly controlled) Intrauterine fetal death is a devastating event
• Antiphospholipid syndrome for the couple and their family. The obstetrician
• Hypertensive disorders must display great sensitivity and empathy. The
• Advanced maternal age woman and her husband should be informed
• Obesity about the problem in privacy. It is common for
• Uterine rupture the couple and the family to feel that the obste-
trician has been negligent. However, it is import-
ant to not take on a defensive tone. There should
be no attempt to place the blame on the woman,
Box 31.3 7
NVTCUQWPFHGCVWTGUVQEQPſTO even by insinuation.
diagnosis of intrauterine fetal death
All the proceedings should aim to support the
• Absence of fetal cardiac activity couple’s choices. The following points must be
• Spalding’s sign discussed:
Ŧ Collapse of fetal skull with overlapping bones
(Fig. 31.1) • Establishing cause of death by evaluation
• Hydrops • Expectant management and its complications
• Robert’s sign • Mode of delivery
Ŧ Intrafetal gas (within the heart, great vessels, joints) • Timing of delivery
• *[RGTƀGZKQPQHVJGURKPG • Importance of autopsy and other postnatal
• Crowding of the rib shadow tests on the fetus
• Retroplacental clots in the presence of a massive
• Timing and management of subsequent
abruption
pregnancy
CH 31_p447-454_v2.indd 449 17-07-2015 22:37:26

Evaluation of cause of I FD Laboratory investigations

An identifiable etiology for fetal demise may not Women who have had a late IUFD should have
be found in up to 60% of stillbirths, even after laboratory investigations to
complete evaluation. However, every attempt • identify the cause of the fetal death,
must be made to determine the cause of fetal • rule out disseminated intravascular coagula-
death because it will assist in deciding on recur- tion (DIC) that may result from fetal demise.
rence risk, preconceptional counseling, future However, DIC occurs only in 10%–25% of
pregnancy management, the need for prenatal IUFDs and usually occurs 3–4 weeks after the
diagnostic procedures with the next pregnancy, event or later. Coagulation workup is there-
and future neonatal management. fore not required immediately after IUFD
When clinical findings strongly suggest a (see Chapter 45, Nonhemorrhagic shock in
cause for the fetal demise, further testing may not pregnancy).
be required or may be limited to a fewer number
of tests. For example, an obvious cause could Tests can be divided into those that should
include cord prolapse, a true knot, or anenceph- be done generally for all women with IUFD and
aly. In that case, no further evaluation would be specific tests that are indicated by a suspected
required. cause of IUFD.
Complete evaluation consists of a thorough
history of current and past illnesses, a clinical Tests for all women with I FD
evaluation, laboratory tests if indicated, and a
The tests that should be done for all women with
fetal autopsy that should include examination of
IUFD are listed in Box 31.5.
the placenta.
5RGEKſEVGUVUHQTUWURGEVGFECWUG
Clinical evaluation of I FD
Clinical evaluation is the first step in coming to
In certain women with IUFD, a cause could be
a conclusion about the cause for the IUFD. The
suspected from the clinical evaluation. These
components of clinical evaluation are listed in
women should undergo specific tests for the sus-
Box 31.4.
pected cause of IUFD.
Box 31.4 Clinical evaluation of intrauterine fetal • Anticardiolipin antibodies and lupus
death anticoagulant should be tested to rule out
antiphospholipid antibody (APA) syndrome
• History
since unrecognized APA syndrome is associ-
Ŧ Hypertension
Ŧ Diabetes
ated with late fetal demise.
Ŧ Bleeding with or without pain • If the maternal clinical picture, ultrasound
Ŧ Rupture of membranes findings, or histopathologic findings of the
Ŧ Fever with or without rashes fetus or placenta suggest a specific infection,
• Past obstetric history serologic testing for cytomegalovirus titer,
Ŧ Previous stillbirths toxoplasmosis titer, parvovirus B19 titer, and
Ŧ Previous macrosomic/small babies Listeria culture are obtained.
• Family history of diabetes
• Examination
Ŧ Blood pressure Box 31.5 Tests for all women with intrauterine
Ŧ Proteinuria
fetal death
Ŧ Uterine size • Complete blood count
Ŧ Bleeding • Screening for diabetes (if not done during pregnancy)
• Ultrasonography • Kleihauer test to rule out massive fetal–maternal hem-
Ŧ Evaluation for fetal growth restriction orrhage
Ŧ Fetal structural anomalies • Indirect Coombs test to rule out Rh alloimmunization
CH 31_p447-454_v2.indd 450 17-07-2015 22:37:26

• Tests for inherited thrombophilia are not be handled with respect. Following the autopsy,
indicated. some parents may want to follow rituals spe-
• To identify chromosomal abnormalities leading cific to their culture or religion. If it is explained
to fetal demise, an amniocentesis or chorionic to the parents that the autopsy may contribute
villus sampling may be indicated. An amnio- information that will help in calculating the
centesis done immediately after fetal death recurrence risk, most parents will agree to the
allows successful cytogenetic studies, whereas examination.
the culture of fetal tissues after delivery is not as A specialized perinatal pathologist should ide-
successful. Polymerase chain reaction (PCR) for ally perform the postmortem. If facilities are not
viral infection and amniotic fluid culture may available, then the fetus or organs can be sent to
also be carried out in suspected cases of intrau- a center where these facilities are available. The
terine infection. fetus and placenta should be examined as soon
• If ultrasonography reveals hydrops and the as possible after delivery.
woman is not Rh negative or alloimmunized,
causes of nonimmune hydrops and minor blood
group incompatibilities must be looked for.
Fetal examination
A detailed external examination of the fetus is
Specific tests for suspected cause of IUFD are
essential. Fetal weight, length, head, and abdomi-
given in Box 31.6.
nal circumference and measurement of the limbs
should be recorded. Abnormalities, dysmorphic
Box 31.6 5
RGEKſEVGUVUHQTUWURGEVGFECWUGQH features, and relevant negative findings must be
intrauterine fetal death documented. Detailed photographs of the entire
• Anticardiolipin antibodies (IgG, IgM) fetus and a facial photograph will be useful for
• Lupus anticoagulant future reference (Box 31.7).
• 6GUVUHQTURGEKſEKPHGEVKQP
Ŧ Cytomegalovirus titer
Ŧ Toxoplasmosis titer
Gross and histological
Ŧ Parvovirus B19 titer examination of the placenta
Ŧ isteria culture
Ŧ PCR for viral infection Gross and histological examination of the pla-
Ŧ #OPKQVKEƀWKFEWNVWTG centa is an essential part of the autopsy. Any
• Fetal karyotyping relevant gross findings should be documented.
Ŧ Amniocentesis immediately after diagnosis Histological examination of the placenta may
Ŧ Chorionic villus sampling yield findings of clinical relevance. Diffuse pla-
• Minor blood group incompatibilities cental infarction may explain FGR leading to
Ŧ In the presence of fetal hydrops fetal demise and may also point to the possi-
g immunoglobulin G; g immunoglobulin M; PC polymerase bility of antiphospholipid antibody syndrome.
chain reaction.
Box 31.7 (
GVCNſPFKPIUVQDGFQEWOGPVGF
during postmortem
Postmortem and placental • Weight
examination • Length
• Head circumference
A postmortem examination is a very important • Abdominal circumference
part of the investigation for the etiology of still- • Measurement of limbs
birth. The need for it must be discussed with the • Abnormalities
parents with great sensitivity and compassion. • Dysmorphic features
• 4GNGXCPVPGICVKXGſPFKPIU
Cultural values must be kept in mind. Many fam-
• Detailed photographs of entire fetus including face
ilies may hesitate to proceed with a postmortem
• Gross and histological examination of the placenta
examination if they feel that the fetus will not
CH 31_p447-454_v2.indd 451 17-07-2015 22:37:26

Leukocyte infiltration may be present with Induction of labor

chorioamnionitis.
If the parents do not permit an autopsy, the Most women with IUFD opt for delivery within
following may be performed, although they are 24–48 hours. The majority of women (90%)
not substitutes for a complete postmortem: deliver within 24 hours of induction and com-
plications are minimal. The two advantages of
• Photographs of the fetus immediate induction are as follows:
• Whole-body radiography
• Ultrasonography • Postmortem examination will be more inform-
• Needle biopsies ative since autolysis or maceration of the baby
• Magnetic resonance imaging (MRI) is less.
• The risk of DIC is low.
Delivery issues Methods of induction

At term, and with a favorable cervix, labor can
An extremely difficult diagnosis to accept, par-
be induced with oxytocin. If the cervix is not
ents usually struggle to come to terms with fetal
favorable, cervical ripening can be achieved with
demise. If there is no immediate medical com-
prostaglandins or mechanically with a Foley
plication putting the mother’s health at risk, the
catheter (Box 31.3).
couple should be allowed to make an informed
Misoprostol and prostaglandin E2 (PGE2)
decision about the timing of the delivery. At
are equally effective, but misoprostol is cheaper
the same time, the couple should be reassured
and safe. Vaginal misoprostol is given at the
that the fetal demise would not place the moth-
dose of 100 μg 6 hourly, for a maximum of four
er’s health at risk. However, in the presence of
doses, before 26 weeks. After 27 weeks, the dose
obstetric complications, pregnancy must be ter-
is reduced to 25–50 μg 4 hourly. Misoprostol
minated immediately.
usage may be associated with uterine rupture
• The majority of women (85%–90%) will in a previous uterine scar. It should therefore be
deliver spontaneously within 3 weeks of IUFD. avoided.
However, expectant management may lead to In women at 24–28 weeks’ gestation, the addi-
severe maternal anxiety. tion of mifepristone shortens expulsion time. A
• A small number of women (25%–30%) may dose of 200 mg of oral mifepristone is followed
develop DIC if undelivered 4 weeks after IUFD. by misoprostol 48 hours later.
• Vaginal delivery is the preferred route of deliv- The methods for induction in the presence of
ery unless there are definite indications for a IUFD are listed in Box 31.9.
cesarean section.
Box 31.9 Induction for intrauterine fetal death
Indications for immediate • Oxytocin
Ŧ At term with favorable cervix
delivery Ŧ Preceded by cervical ripening if needed
Immediate delivery, as soon as the diagnosis is • Misoprostol
made, is indicated in conditions which jeopar- Ŧ <26 weeks
100 μg 6 hourly
dize maternal well-being (Box 31.8).
Maximum of 4 doses
Ŧ >27 weeks
25–50 μg 4 hourly
Maximum of 6 doses
Box 31.8 Indications for immediate delivery
Ŧ Avoid in case of previous cesarean section
• Severe preeclampsia/eclampsia • Mifepristone + misoprostol
• Placental abruption Ŧ 24–28 weeks
• Chorioamnionitis Ŧ 200 mg of mifepristone
• Ruptured membranes Ŧ Followed by misoprostol 48 hours later
CH 31_p447-454_v2.indd 452 17-07-2015 22:37:26

Indications for cesarean • It is very important to talk to the couple and

the family and discuss with them the possible
section cause for the fetal demise. Emotional support
In the presence of IUFD, it is best for the woman and psychological counseling should be pro-
to have a vaginal delivery. However, a cesarean vided for whatever extent possible.
section may be indicated for specific obstetric • Lactation should be suppressed with cabergo-
indications (Box 31.10). line. Cabergoline 0.25 mg bid × 2 days will sup-
press lactation.
• Women who are Rh negative should receive
the full dose (300 μg) of anti-D immunoglobu-
Determining time of fetal lin because it might not always be possible to
demise ascertain if the fetus is Rh positive or not.
• At the follow-up visit, the couple should be coun-
When a fetal demise occurs remote from labor, it seled regarding risks of recurrence and plans
is not always easy to determine when the event for future pregnancy. Preventive measures, if
happened. Soon after fetal demise, the fetus starts any, should be discussed. Contraceptive advice
undergoing changes, including desquamation and should be given.
maceration. Table 31.1 gives guidelines for estimat-
The essential components of postnatal man-
ing an approximate time of death prior to delivery.
agement are summarized in Box 31.11.
Postnatal management Box 31.11 Postnatal management

Postnatal management is an important part of • Counseling for couple and family
handling IUFD. Ŧ Possible cause for the fetal demise
Ŧ Risk in next pregnancy
• Suppression of lactation
Ŧ Cabergoline 0.25 mg bid × 2 days
Box 31.10 Indications for cesarean section in
• Rh negative women
intrauterine fetal death
Ŧ 300 μg of anti-D immunoglobulin
• Major degree of placenta previa • Follow-up visit
• Transverse lie Ŧ Plans for future pregnancy
• 2 or more previous scars on the uterus Ŧ Preventive measures, if any
• 5KIPKſECPVOCETQUQOKC Ŧ Contraceptive advice
Table 31.1 Guidelines for estimating approximate time of death prior to delivery
Finding Estimated time of fetal demise prior to delivery

Brown or red discoloration of the umbilical cord or desquamation At least 6 hours
ŮEO
Desquamation of the face, back, abdomen At least 12 hours
&GUSWCOCVKQPŮQHVJGDQF[QTŮDQF[\QPGU At least 18 hours
Skin color brown or tan At least 24 hours
/WOOKſECVKQP
KGTGFWEGFUQHVVKUUWGXQNWOGNGCVJGT[UMKP At least 2 weeks
deeply brown-stained tissues)

Body zones: Scalp, face, neck, chest, back, arms, hand, leg, foot, and scrotum.
CH 31_p447-454_v2.indd 453 17-07-2015 22:37:26

Key points
• Intrauterine fetal death (IUFD) refers to a fetus death because it will assist in deciding on recurrence
with no signs of life in utero. The terms fetal death, risk, preconceptional counseling, future pregnancy
fetal demise, stillbirth, and stillborn are used inter- management, the need for prenatal diagnostic proce-
changeably. dures with the next pregnancy, and future neonatal
management.
• #UKIPKſECPVRGTEGPVCIGQHUVKNNDKTVJU
ŌOC[
PQVJCXGCFGſPGFGVKQNQI[6JGENQUGT+7(&QEEWTUVQ • A postmortem examination is a very important part of
VGTOVJGOQTGNKMGN[KVKUVQJCXGPQKFGPVKſCDNGHGVCN the investigation for the etiology of stillbirth.
placental, maternal, or obstetric etiology.
• 6JGOCLQTKV[
ŌQHYQOGPYKNNFGNKXGT
• The causes implicated in stillbirths include unrecog- spontaneously within 3 weeks of IUFD. However,
nized fetal growth restriction, placental dysfunction, expectant management may lead to severe maternal
congenital anomalies, chromosomal abnormalities, anxiety.
infections, placental abruption, hydrops (immune and
• #UOCNNPWODGT
ŌQHYQOGPFGXGNQR
nonimmune), and cord complications.
disseminated intravascular coagulation (DIC) if unde-
• #PWNVTCUQWPFGZCOKPCVKQPKUGUUGPVKCNVQEQPſTOHGVCN livered 3-4 weeks after IUFD. Vaginal delivery is the
death by noting the absence of fetal cardiac activity. RTGHGTTGFTQWVGQHFGNKXGT[WPNGUUVJGTGCTGFGſPKVG
• Intrauterine fetal death is a devastating event for the indications for cesarean section.
couple and their family. The obstetrician must display • Most women with IUFD opt for delivery within 24–48
great sensitivity and empathy. The woman and her JQWTU6JGOCLQTKV[QHYQOGP
FGNKXGTYKVJKP
husband should be informed about the problem in hours of induction and complications are minimal.
privacy.
• At the follow-up visit, the couple should be counseled
• #PKFGPVKſCDNGGVKQNQI[HQTHGVCNFGOKUGOC[PQVDG regarding risks of recurrence and plans for future
HQWPFKPWRVQQHUVKNNDKTVJU*QYGXGTGXGT[CV- pregnancy. Preventive measures, if any, should be
tempt must be made to determine the cause of fetal discussed. Contraceptive advice should be given.
Self-Assessment
2. In addition to checking her blood sugar levels, a baseline
Case-based question EQCIWNCVKQPRTQſNGUJQWNFDGQTFGTGFVQTWNGQWV&+%
Mrs. RT, 25, a pregestational insulin-dependent diabetic, 3. Vaginal delivery is the preferred route of delivery unless
presented at 37 weeks’ gestation with loss of fetal move- VJGTGCTGFGſPKVGKPFKECVKQPUHQTCEGUCTGCPUGEVKQP
ment for 2 days. 4. A postmortem fetal examination is advised.
1. *QYKU+7(&EQPſTOGF!
2. 9JCVNCDQTCVQT[KPXGUVKICVKQPUUJQWNFDGQTFGTGF!
3. What would be the best method of delivering the
Sample questions
RCVKGPV!
4. 9JCVRQUVPCVCNKPXGUVKICVKQPUCTGGUUGPVKCN!
1. What are the causes of intrauterine fetal death!*QY
do you evaluate a patient after a intrauterine fetal
Answers deathCVYGGMU!
1. Intrauterine fetal deathKUEQPſTOGFD[VJGCDUGPEGQH

fetal heart motion on ultrasound. Other signs of IUFD Short-answer questions
on ultrasound include collapse of the fetal skull with
QXGTNCRRKPIDQPGUJ[FTQRUKPVTCHGVCNICUJ[RGTƀGZ- 1. Intrauterine fetal death
ion of the spine, and crowding of the rib shadow. 2. 7NVTCUQPQITCRJKEſPFKPIUKPKPVTCWVGTKPGFGCVJQH
fetus
CH 31_p447-454_v2.indd 454 17-07-2015 22:37:26

Multifetal
32 Pregnancy
Case scenario
Mrs. RN, 30, was referred at 32 weeks’ gestation from a primary health
center since the uterine size was larger than the gestational age. She
hailed from a local village and had antenatal care by the village health
worker who had prescribed iron tablets. She was referred to the doctor
since the health care worker felt her abdomen was too big. She also had
swelling of both feet.
Introduction Currently the global incidence is 32/1000 (3.2%),

but it is thought to be less in the developing
Multifetal pregnancies are on the increase glob- world. Triplet and higher-order pregnancies
ally due to several factors, the most important increased till the year 1998 but have decreased to
being the use of assisted reproductive tech- 1.43/1000 since then. This is due in part to strin-
niques (ART). Early diagnosis is important for gent guidelines restricting transfer of multiple
proper counseling and management so as to embryos into the uterus during IVF.
optimize maternal and perinatal outcome.
ygosity
Twin pregnancy Twin pregnancies can be monozygotic (MZ) or
Twin pregnancy is the most common form of dizygotic (DZ). Dizygotic twins result from fer-
multifetal pregnancy. tilization of two ova by two sperms, whereas
MZ twins arise from a single fertilized ovum
which subsequently divides into two embryos.
Incidence 70% of twin pregnancies are DZ. Incidence of
The incidence of twin pregnancy rose sharply MZ twins has remained stable globally, but the
from 1980 to 2004 but has stabilized after that. incidence of DZ twins has increased in recent
CH 32_p455-473_v3.indd 455 17-07-2015 22:52:01

years and varies among different ethnic groups. past decade. ART can also increase cleavage of
Assisted reproductive techniques have markedly the embryo, thereby increasing the incidence of
increased the incidence of DZ twins but have MZ to some extent.
had only a marginal effect on the incidence of
MZ twins. Differences between MZ and DZ twins
are given in Table 32.1.
Placentation
Dizygotic twins are always dichorionic (DC) and
Etiology diamniotic (DA) with either two separate pla-
centas or one fused placenta.
Monozygotic twins occur in 1 in 250 (0.4%) preg-
In MZ twins, placentation depends on the
nancies, whereas DZ twins are more common.
timing of division of the embryo. If the division
The etiology of MZ twins is not well understood.
occurs early, the amnion and chorion develop
Dizygotic twins occur due to multiple ovulation
later and individually cover the fetuses result-
resulting from an increase in follicle-stimulating
ing in DC/DA pregnancies. If the division occurs
hormone (FSH) levels. The etiological factors caus-
late, the fetuses may be partially fused resulting
ing DZ twins are listed in Box 32.1. The increased
in conjoint twins. Four types of MZ twin preg-
FSH level that is usually found in older women,
nancies are described, depending on the placen-
multiparas, certain races, and obese women is
tation (Table 32.2) (Fig. 32.1).
thought to be the causative factor.
Assisted reproductive techniques give rise to
multifetal pregnancies depending on the num- Box 32.1 isk factors for di ygotic twin
pregnancy
ber of embryos transferred. Ovulation induction
and ART account for the increase in incidence • Increase in FSH levels
of DZ twins in recent years. Guidelines have Ŧ Maternal age
emerged regarding the number of embryos that Ŧ Multiparity
can be transferred, and this has led to the reduc- Ŧ Race
tion in and stabilization of the incidence in the Ŧ Maternal obesity
• Past h/o dizygotic twins
• Maternal family h/o twins
Table 32.1 Differences between mono ygotic and • Ovulation induction
di ygotic twins Ŧ Clomiphene
Ŧ Gonadotropins
Mono ygotic Di ygotic • ART
Ŧ IVF
Phenotype Identical Nonidentical
Genotype Identical Nonidentical A , assisted reproductive technique; S , follicle-stimulating
hormone; , in vitro fertilization.
Gender Same Same or different
Incidence
Ethnic variation Absent Present Determination of chorionicity
Increase with ART Minimal Marked
Adverse perinatal High Low Perinatal mortality in twins varies with chorio-
outcomes nicity. Determination of chorionicity is, there-
A assisted reproductive techniques. fore, essential for risk assessment and planning
Table 32.2 Types of placentation in mono ygotic twins
Type of placentation Timing of cleavage Frequency

after fertili ation
Diamniotic dichorionic (DA/DC) <72 hours 25%–30%
Diamniotic monochorionic (DA/MC) 4–7 days 70%–75%
Monoamniotic monochorionic (MA/MC) 8–12 days 1%–2%
Conjoint twins >12 days Rare
CH 32_p455-473_v3.indd 456 17-07-2015 22:52:01

Multifetal Pregnancy 457
ichorionic Monochorionic Monochorionic Monochorionic

iamniotic iamniotic monoamniotic monoamniotic ith
conjoint t ins
Figure 32. 1 Placentation of monozygotic twins. Four types of monozygotic pregnancies can occur, depending on the
time of cleavage.
management. Chorionicity is determined by and two chorions (four layers) or two amnions
ultrasonography and is most reliable in the first and one fused chorion (three layers). In MC
trimester (Table 32.3). Transvaginal ultrasonog- twins, only two layers are seen.
raphy (TVUS) in the first trimester is 95%–100%
sensitive in determining the chorionicity and
amnionicity.
Between 6 and 10 weeks’ gestation, the pres-
ence of two gestational sacs indicates DC twins.
(Fig. 32.2). The dividing membrane is also thick
in DC twins. A single sac with a single yolk sac
but two fetuses indicates monoamniotic (MA)
twins. (Fig. 32.3). In late first or early second tri-
mester, the number of placentas should be iden-
tified and documented. A single placenta may be
seen in DC or monochorionic (MC) twins, but
two placentas definitely indicate dichorionicity.
Similarly, fetuses of different genders indicate
dichorionicity. The number of layers in the divid-
ing membrane can be counted near the insertion Figure 32.2 Dichorionic twins. Ultrasonography shows
into the placenta. two fetuses with a thick membrane in between. (Photo
In DC twins, examination of the placental courtesy: Mediscan Systems, Chennai.)
membranes at delivery will reveal two amnions
Table 32.3 Determination of chorionicity
Dichorionic Monochorionic
First trimester
Gestational sacs Two One
Dividing membrane Thick (>2 mm) Thin (<2 mm)
Second trimester
Placenta Two One
Fetal gender Discordant Concordant or
discordant
Twin peak sign Present Absent Figure 32.3 Monoamniotic twins. Ultrasonography
T sign Absent Present shows two fetuses in the same gestational sac with no
Dividing membrane Three or four Two layers dividing membrane. (Photo courtesy: Mediscan Systems,
layers Chennai.)
CH 32_p455-473_v3.indd 457 17-07-2015 22:52:02

Between 11 and 14 weeks’ gestation, a trian- Clinical features of twin

gular projection of placenta can be seen between
the two layers of the dividing membrane near pregnancy
the placental surface. This is called the twin peak Twin pregnancy may be suspected on the basis
sign or lambda sign and is seen only in DC twins of history and physical examination, and con-
(Fig. 32.4). In MC twins, there is no extension of firmation of diagnosis is by ultrasonography.
tissue between the layers of the dividing mem- Diagnosis in the first trimester is essential for
brane, and the membrane joins the placenta at appropriate management so that optimal peri-
right angles, giving rise to the T sign (Fig. 32.5). natal and maternal outcome can be achieved.
istory
Particular details in history that indicate a pos-
sibility of twin pregnancy are listed in Box 32.2.
Box 32.2 istory

• Advanced maternal age
• High parity
• History of ovulation induction
Ŧ Clomiphene citrate
Ŧ Gonadotropins
• Assisted reproduction therapy
• Family history of twins
• Parents one of twins
• Past history of twins
Figure 32.4 Lambda sign or twin peak sign. A triangular • Symptoms
projection of the placenta is seen between the layers Ŧ First trimester
of the membrane in dichorionic twins. (Photo courtesy: Hyperemesis
Mediscan Systems, Chennai.) Ŧ Second and third trimester
Overdistended uterus
Pressure symptoms
- Breathlessness
- Backache
- Gastrointestinal symptoms
Physical examination
Physical examination in early and late preg-
nancy usually reveals a uterus larger than what
is appropriate for gestational age and appears
overdistended in third trimester (Fig. 32.6). Other
findings include anemia, signs of preeclampsia,
polyhydramnios, and pedal edema (Box 32.3).
Obstetric examination reveals fundal height
at least 4–5 cm more than what corresponds to
the gestational age. Multiple fetal parts can be
felt. Though four poles (two cephalic and two
podalic) may be felt, palpation of three poles
Figure 32.5 T sign. There is no extension of placental or two heads is considered adequate for clini-
tissue between the layers of the dividing membrane in cal diagnosis of twins. Polyhydramnios may be
monochorionic twins. (Photo courtesy: Mediscan Systems, present. Malpresentations of the first and sec-
Chennai.) ond twin are common. Auscultation of two fetal
CH 32_p455-473_v3.indd 458 17-07-2015 22:52:02

Box 32.4 ltrasonography in twin pregnancy

• Diagnosis of twins
• Determination of chorionicity and amnionicity
• Detection of fetal anomalies
• Evaluation of fetal growth
• Evaluation of fetal well-being
• Measurement of cervical length
• Guiding procedures
Ŧ Selective termination
Ŧ Selective fetoreduction
Ŧ Amniocentesis
Ŧ Septostomy
Ŧ Amnioreduction
Ŧ Diagnosis of malpresentation
Figure 32.6 Overdistended uterus. In third trimester, the Ŧ Assistance in labor
abdomen is overdistended due to the presence of twin
fetuses and polyhydramnios.
This will help in the determination of ges-
Box 32.3 Physical examination in twin tational age, chorionicity, and amnionicity.
pregnancy The membrane is visualized best in early preg-
nancy. Accurate assignment of gestational age is
important for decisions regarding the timing of
Ŧ Anemia
Ŧ Pedal edema
delivery.
Ŧ High blood pressure
• Obstetric examination
Ŧ 7VGTKPGUK\GNCTIGTVJCPFCVGUKPſTUVVTKOGUVGT Maternal adaptation to twin
Ŧ Fundal height more than expected (by 4–5 cm)
Ŧ Multiple fetal parts pregnancy
Ŧ Three or four fetal poles
All the physiological changes of pregnancy are
Ŧ Polyhydramnios
Ŧ Two fetal hearts magnified and multiplied in twin pregnancy.
Ŧ Malpresentations The uterus is larger, levels of human chorionic
gonadotropin (hCG) and human placental lac-
togen (hPL) are higher, and there is a greater
hearts, with a minimum difference of 10 bpm, increase in blood volume and cardiac output.
heard simultaneously (by two examiners) is con- These physiological changes give rise to prob-
sidered diagnostic of twins. lems in the mother as discussed later in the
chapter.
ltrasonography in Maternal complications

twin pregnancy Maternal complications should be anticipated
Ultrasonography is an essential tool in the manage- antenatally, intrapartum and postpartum.
ment of twin pregnancy. It is useful for diagnosis
in early and late pregnancy and subsequently for Antenatal complications
monitoring the pregnancy and for guiding pro-
Complications that are seen in singleton preg-
cedures (Box 32.4).
nancy occur more frequently in twin pregnancy,
When the scan is performed in early first tri-
and they are more severe. The antenatal mater-
mester, the following should be noted:
nal complications are listed in Box 32.5.
• Number of fetuses, gestational sacs, and yolk Spontaneous miscarriage is more common
sacs in MZ twins. Hyperemesis is considered to be
• Presence of membrane between fetuses due to higher than usual levels of E hCG.
CH 32_p455-473_v3.indd 459 17-07-2015 22:52:02

pedal edema due to pressure on the iliac veins/

Box 32.5 Antenatal maternal complications
in twin pregnancy vena cava, gastrointestinal symptoms such as
dyspepsia, early satiety due to displacement and
Antenatal pressure caused by the expanding uterus, and
• First trimester
respiratory difficulty due to upward displace-
Ŧ Hyperemesis
ment and splinting of the diaphragm are seen
Ŧ Spontaneous miscarriage
often in twin pregnancies.
Ŧ Hypertensive disorders
Ŧ Gestational diabetes reterm labor
Ŧ Anemia Twin pregnancy is a well-known cause of
• Third trimester preterm labor and accounts for 10% of all
Ŧ Preterm labor preterm labors. The mean gestational age at
Ŧ Polyhydramnios delivery of twins is 36 weeks. Preterm labor
Ŧ Antepartum hemorrhage
occurs in 50% of twin pregnancies. The risk
Placental abruption
is higher in MC pregnancies. This is the most
Placenta previa
Ŧ Pressure symptoms
important cause of perinatal mortality in mul-
Respiratory difficulty tifetal pregnancy.
Gastrointestinal symptoms Prediction of preterm labor
Edema
Identification and management of women at
high risk for preterm labor improves perinatal
mortality. Dilatation of the internal os can be
Anemia is common in twin pregnancies, assessed by digital examination and has been
especially in developing countries. Increase in found to be useful as a predictor of preterm
plasma volume is responsible for the exagger- labor. The two tests useful in the prediction
ated physiological anemia, but the increased of preterm labor are measurement of cervical
demands of the growing fetuses cause iron and length by TVUS and fetal fibronectin (fFN) levels
folic acid deficiency. The resultant anemia is usu- in maternal serum (Box 32.6). When the results
ally dimorphic (see Chapter 49, Hematological of the two tests are combined, the predictive
disorders). value is higher. In a woman who has a cervical
Polyhydramnios occurs in 5%–8% of twin length >25 mm at 24 weeks with negative fFN,
pregnancies and is more common in MZ twins the risk of preterm delivery prior to 32 weeks
with complications such as twin-to-twin trans- would be low. The monitoring of cervical length
fusion syndrome (TTTS). Acute polyhydram- of by TVUS should begin by 16–18 weeks in mul-
nios can occur at or after 28 weeks’ gestation. tifetal pregnancies.
Increased levels of hPL lead to a higher incidence
of gestational diabetes.
Gestational hypertension is much more com- Box 32.6 Prediction of preterm labor in twin
mon in multifetal pregnancies. Preeclampsia is pregnancy
three to four times more common, occurs ear-
• Digital examination
lier in gestation, and tends to be more severe.
Ŧ Dilatation of internal os
The relative risk of eclampsia is also three times • Cervical length by TVUS
higher. Ŧ At 24–28 weeks
The incidence of placental abruption is <25 mm: High risk
higher and is probably due to the higher inci- >25 mm: Low risk
dence of hypertension. One of the placentas • (GVCNſDTQPGEVKP
may be implanted in the lower segment or part Ŧ At 28 and 32 weeks
of a large fused placenta may extend to the lower Positive: High risk
uterine segment, giving rise to placenta previa. Negative: Low risk
The overdistended uterus gives rise to dis- • Combination of both
Ŧ Higher predictive value
comfort and pressure symptoms. Vague aches
and pains, backache due to exaggerated lordosis, S transvaginal ultrasonography
CH 32_p455-473_v3.indd 460 17-07-2015 22:52:02

Prevention of preterm labor

Box 32.7 Intrapartum and postpartum
Several interventions have been tried but none complications
have been found useful in randomized con-
• First stage
trolled trials in the prevention of preterm labor Ŧ Prolonged labor
in twin pregnancies. The interventions are listed Ŧ Malpresentations
in Table 32.4. Bed rest and hospitalization are Ŧ Need for augmentation
recommended only if there is hypertension, Ŧ Prelabor rupture of membranes
preeclampsia, or other complications. Cervical Ŧ Cord prolapse
cerclage was not found to be useful even when • Second stage
the cervical length was <25 mm and may actu- Ŧ Operative vaginal deliveries
ally lead to preterm labor. Tocolytics are useful Forceps
in established preterm labor to prolong preg- Vacuum extraction
Assisted breech delivery
nancy by a few days but not recommended for
Internal podalic version
prophylaxis. The physiological changes in car-
Ŧ Cesarean section
diovascular system are exaggerated in multifetal Ŧ Abruption of placenta of second twin
pregnancy, and this predisposes to pulmonary • Third stage
edema. This risk increases particularly with Ŧ Atonic postpartum hemorrhage
betamimetics which, therefore, are not recom- Ŧ Retained placenta
mended. Progestins have also not been found • Postpartum
to be beneficial. Corticosteroid for acceleration Ŧ Secondary postpartum hemorrhage
of pulmonary maturity is indicated in women Ŧ Thromboembolism
diagnosed to be in preterm labor. Ŧ .CEVCVKQPCNFKHſEWNVKGU
Measures that may reduce the risk of preterm
labor are limited to physical activity with rest common, either in the first or the second twin.
for 1–2 hours in the afternoon and 6–8 hours at The second twin may present by vertex to begin
night, light work, frequent and regular antenatal with but change to breech or transverse lie after
visits, and serial ultrasonographic evaluation for the delivery of the first twin. Operative vagi-
cervical length and other complications. nal delivery with forceps or vacuum extraction,
assisted breech delivery (especially of the sec-
Intrapartum and postpartum ond twin), internal podalic version, and breech
extraction may be required. Incidence of cesar-
complications
ean section is much higher than in singleton
Intrapartum and postpartum complications are pregnancies. The inadequate uterine contrac-
also higher in twin pregnancy (Box 32.7). tions due to overdistension lead to atonic post-
The overdistended uterus does not contract partum hemorrhage and retained placenta.
adequately; therefore, labor may be prolonged Secondary postpartum hemorrhage due to
and require augmentation. Malpresentations are endometritis or retained placental tissue is more
Table 32.4 Measures for prevention of preterm labor
Preventive measure 'HſECE[

Bed rest and hospitalization If there is hypertension/preeclampsia
Cervical cerclage Not effective even in short cervix
Tocolytics In established preterm labor
To prolong pregnancy for few days
Progestins Not been found effective
Limited physical activity
Light work
Found to be effective; recommended
Regular antenatal visits
Serial TVUS for cervical length
S, transvaginal ultrasonography.
CH 32_p455-473_v3.indd 461 17-07-2015 22:52:02

likely. Thromboembolism also occurs more fre- abdominal circumference of >20 mm between
quently than in singleton pregnancy. the two fetuses is also diagnostic of discordant
growth. The percentage of discordancy is calcu-
lated as follows:
Fetal complications
Weight of Weight of
Fetal complications are much higher in twin _
Percentage of larger twin smaller twin
pregnancy and account for the high perinatal discordancy = Weight of larger twin
mortality and morbidity. They occur in both DZ
and MZ twins, but there are certain complica-
tions unique to MZ twins. Discordancy can be due to difference in
growth potential of the two fetuses, placen-
Fetal complications common to tal insufficiency, or fetal malformation. Dis-
both mono- and di ygotic twins cordancy of more than 25%–30% is associated
with higher perinatal mortality. Discordancy
Fetal complications common to both MZ and DZ usually becomes manifest after 24 weeks' ges-
twins are listed in Box 32.8. tation. Ultrasonography is the only tool avail-
able for diagnosis of discordancy. In discordant
Congenital anomalies are much more common
twins, the growth-restricted twin has a poorer
in multifetal pregnancy compared to singleton
perinatal outcome and should be monitored
pregnancy. There is a two-fold increase in con-
closely.
genital anomalies in twins compared to single-
tons (2% vs. 4%). Congenital anomalies are more Prematurity is the most important cause of
common in MZ twins. There can be discordance perinatal mortality in multifetal pregnancy.
in anomalies, with one fetus being normal, even Prematurity may be due to spontaneous preterm
in MZ twins. labor or iatrogenic prematurity due to early
induction for obstetric indications. Preterm neo-
Fetal growth restriction (FGR) is another cause
nates are prone to hypothermia, intracranial
of perinatal mortality in twins. Twin fetuses grow
hemorrhage, respiratory distress syndrome, nec-
normally till 30–32 weeks’ gestation, but the
rotizing enterocolitis, and sepsis (see Chapter 24,
growth rate beyond this slows even in an uncom-
Common problems of the newborn).
plicated twin pregnancy. The slowing down of
the growth trajectory may be due to crowding,
uteroplacental insufficiency, or abnormal pla-
cental implantation. Complications unique to M twins
50% of twin fetuses weigh <2500 g at birth and
10% weigh <1500 g. Fetal growth restriction in Dichorionic diamniotic MZ twins behave very
twins cannot be suspected or evaluated by clini- similar to DZ twins. Due to the sharing of the
cal examination. Serial ultrasonography from 28 placenta, MC/DA and MC/MA twins are prone
weeks’ gestation is essential for identifying FGR. to some unique complications. These arise due
to vascular communications in the placenta. In
Discordant growth leading to a difference in addition, MA twins tend to have other specific
birth weight is another cause of mortality and problems. Perinatal mortality is, therefore, sig-
morbidity. (Discordancy is defined as >20% nificantly higher in MZ twins. Complications
difference in birth weight.) A difference in unique to MZ twins are listed in Box 32.9.
Box 32.9 Complications unique to mono ygotic

Box 32.8 Fetal complications in mono ygotic twins
and di ygotic twin pregnancies
• Monoamniotic twins
• Congenital anomalies • Twin-to-twin transfusion syndrome (TTTS)
• Fetal growth restriction • Twin reversed arterial perfusion sequence (TRAP)
• Gowth discordancy • Twin anemia-polycythemia sequence (TAPS)
• Prematurity • Conjoint twins
CH 32_p455-473_v3.indd 462 17-07-2015 22:52:02

onoamniotic t ins are usually artery-to-artery or vein-to-vein.

Of all MZ twins, 1% are MA, and the perina- Since the pressure is equal on both sides with no
tal mortality in this situation is 20%. Diagnosis gradient, the blood supply to the fetuses is not
of MA twins can be made if ultrasonography in compromised.
early pregnancy shows a single gestational sac Occasionally, the artery of one fetus commu-
with a single yolk sac and two fetuses. Perinatal nicates with the vein of the other fetus, giving
mortality is higher than in diamniotic twins due rise to a pressure gradient and hence twin-to-
to cord entanglement. twin transfusion syndrome (TTTS) occurs (Fig.
Close monitoring by ultrasonography and 32.7). This occurs in 15% of MC twins. Blood
cardiotocography is mandatory from the time from one fetus flows to the other unidirection-
of viability. Elective delivery by cesarean section ally, leading to hyperperfusion of the recipient
at 32–34 weeks is recommended for MA twins. twin and hypoperfusion of the donor twin (Box
Betamethasone should be administered prior 32.11). Polyhydramnios leads to uterine overdis-
to delivery to accelerate pulmonary maturity tension and preterm labor.
(Box 32.10). With severe oligohydramnios, the dividing
membrane appears attached to the fetal body, a
in to t in trans usion syn rome condition called stuck twin. When one twin dies,
the sudden hypotension in the surviving twin
Vascular communications exist between the two
placentas in all MC twins. These communications
Box 32.11 Changes in the donor and recipient
twins in twin-to-twin transfusion
Box 32.10 Monoamniotic twins syndrome
• 1% of all monozygotic twins • Donor twin

• Associated with several complications Ŧ Oligohydramnios
• High (20%) perinatal mortality rate Ŧ Fetal growth restriction
• Cord entanglement is the most important cause of Ŧ Pulmonary hypoplasia
perinatal mortality Ŧ Contractures
• Close monitoring by • Recipient twin
Ŧ Ultrasonography Ŧ Polyhydramnios
Ŧ Cardiotocography Ŧ Cardiac failure
• Deliver by cesarean section • If one fetus dies, the surviving twin may have
• Deliver at 32–34 weeks Ŧ Multiorgan failure
• Betamethasone prior to delivery Ŧ Neurological damage
Vein
rtery
onor t in
ecipient
t in
a. b.
Figure 32. 7 Twin-to-twin transfusion syndrome. a. Anastomosis between the arteries of the donor twin and veins
of the recipient twin. Perfusion from the donor to the recipient occurs due to pressure gradient. b. The donor fetus
is hypoperfused with fetal growth restriction, and the recipient twin is hyperperfused and plethoric. (Photo courtesy:
Dr Rajnish Samal, Bangalore.)
CH 32_p455-473_v3.indd 463 17-07-2015 22:52:02

leads to neurological damage. This may also Expectant management is usually resorted to
result from thromboplastins released from the in Stage I disease, but close monitoring is man-
dead fetus. datory. Serial amnioreduction involves remov-
Diagnosis of TTTS is by sonography and the ing amniotic fluid by amniocentesis repeatedly
criteria are listed in Box 32.12. None of the find- from the recipient twin under ultrasonic guid-
ings are pathognomonic. The most reliable find- ance. Laser ablation of communicating vessels
ing is the discrepancy in amniotic fluid volume. is performed using fetoscope and requires tech-
The Quintero staging system is useful in cat- nical expertise. This procedure is performed for
egorizing severity of disease (Box 32.13). In addi- TTTS occurring early in gestation and has the
tion, evaluation of the cardiovascular function of highest survival rate. Septostomy refers to the
the fetuses using fetal echocardiography is use- puncture of the septum between the two sacs
ful in management. to create an iatrogenic monoamniotic sac. The
fluid volume equalizes between the two sacs.
Management of TTTS Selective feticide is not used often except in TTTS
Management depends on the gestational age and that occurs before 20 weeks’ gestation. The pro-
the severity (stage) of the disease. The therapeutic cedure is associated with high risk of death for
options currently available are listed in Box 32.14. the other twin since vascular communications
Best results are obtained when treated at Stage II. exist.
If left untreated, the mortality rate is 80%–100%.
Laser ablation has the best survival rate compared
Box 32.12 Sonographic criteria for diagnosis of
twin-to-twin transfusion syndrome to other modalities of therapy and is currently rec-
ommended for all except TTTS Stage I.
• Monochorionicity
• Same gender
• 5KIPKſECPVITQYVJFKUEQTFCPEG in reverse arterial per usion
• Discrepancy in se uence
Ŧ Size of umbilical cord Twin reversed arterial perfusion (TRAP) se-
Ŧ #OPKQVKEƀWKFXQNWOG quence is a rare condition (1/36,000 deliveries)
Polyhydramnios (single deepest pocket >8 cm)
in which large placental arteries of both twins
in one
Oligohydramnios (single deepest pocket <2 cm)
communicate. Often a large vein-to-vein shunt
in other is also present.
• Cardiac dysfunction in recipient twin The donor twin pumps deoxygenated blood
into the umbilical vessels of the second twin and
supplies mainly to the lower half of the body. The
Box 32.13 uintero staging system for TTTS heart and other structures of the upper half of
the body do not develop in the recipient (acar-
• Stage I: Donor twin bladder visible
diac) twin (Fig. 32.8). The donor twin develops
• Stage II: Donor twin bladder not visible, normal Doppler
cardiac failure since it has to pump blood into
• 5VCIG +++ &KUEQTFCPV COPKQVKE ƀWKF XQNWOGU FQPQT
twin bladder not visible, and abnormal Doppler stud- both fetuses. Mortality rate is high for the donor
ies of the umbilical artery, ductus venosus, or umbil- twin. Management is expectant or by laser abla-
ical vein tion of communicating vessel (Box 32.15).
• Stage IV: Ascites or frank hydrops in either twin
• Stage V: Demise of either fetus in anemia polycythemia se uence
Twin anemia–polycythemia sequence (TAPS)
is an uncommon condition that affects 5%
Box 32.14 Therapeutic options for twin-to-twin
of MC twins. It occurs due to a few arteriove-
transfusion syndrome
nous anastomoses of small vessels in the pla-
• Expectant management centa. It can be considered a variant of TTTS
• Serial amnioreduction with a significant difference in hemoglobin
• Laser ablation of vascular anastomosis levels between the fetuses but no major differ-
• Septostomy
ence in amniotic fluid volume. One twin will
• Selective feticide
be pale due to severe anemia and the other will
CH 32_p455-473_v3.indd 464 17-07-2015 22:52:02

Box 32.16 Twin anemia polycythemia sequence
Placenta • Occurs in 5% of monochorionic twins

• Minor variant of TTTS
• Arteriovenous anastomoses of small vessels
• 5KIPKſECPVFKHHGTGPEGKPJGOQINQDKPNGXGNU
• One twin anemic, other twin polycythemic
onor t in
• 0QFKHHGTGPEGKPCOPKQVKEƀWKFXQNWOG
• Most cases undiagnosed
• Diagnosis
Ŧ 2GCMU[UVQNKEƀQYKP/%#
• Management
car ia t in
Ŧ Expectant
Ŧ Laser occlusion of communicating vessels
CA, middle cerebral artery; S, twin-to-twin transfusion
syndrome.
Figure 32.8 Twin reverse arterial perfusion. The donor

twin pumps deoxygenated blood into the umbilical vessels
of the second twin and supplies mainly to the lower half
of the body. The upper half of the second twin does not
develop, giving rise to an acardiac twin.
Box 32.15 Twin reversed arterial perfusion

• Rare condition
• Large placental arterial communication
• Recipient (acardiac) twin
Ŧ Receives deoxygenated blood
Ŧ $NQQFƀQYOCKPN[VQNQYGTJCNHQHDQF[
Ŧ Lacks heart and other structures Figure 32.9 Conjoint twins. The conjoint twins are joined
• Donor twin at the lower thorax and abdomen. Photo courtesy:
Ŧ Cardiac failure Dr Rajnish Samal, Bangalore.)
Ŧ High mortality
• Treatment The twins may be connected at any level and
Ŧ Expectant may share varying number of organs (Fig. 32.9).
Ŧ Laser ablation of communicating vessel Diagnosis is by ultrasonography. When diag-
nosed early, termination of pregnancy is advised.
have a suffused appearance due to polycythe- If diagnosed in the third trimester, delivery is
mia. It can also occur following laser therapy in by cesarean section. Surgical separation may
TTTS. Antenatally, TAPS may go undiagnosed. be possible depending on the number and the
Ultrasonographic measurement of peak systolic nature of organs shared (Box 32.17).
blood flow in the middle cerebral arteries (MCA)
will detect anemia in one twin and can be used Box 32.17 Con oint twins
for diagnosis. When severe, intrauterine death • Extremely rare
of one or both fetuses can occur. Management • High mortality rate
is expectant; severe cases may need laser abla- • Can be connected at any level
tion of communicating vessels (Box 32.16). • May share vital organs
• Diagnosis
Conjoint t ins Ŧ Ultrasonography
Conjoint twins are the result of incomplete divi- • Management
Ŧ Termination of pregnancy
sion of the embryo, taking place between 13 and
Ŧ If late in pregnancy, cesarean section
15 days after fertilization. These are very rare
Ŧ Surgical separation if possible
(1/50,000 deliveries), and mortality is very high.
CH 32_p455-473_v3.indd 465 17-07-2015 22:52:03

Management of twin Management First trimester

pregnancy Once twin pregnancy is suspected clinically,
confirmation of diagnosis is by ultrasonogra-
Antenatal care phy. At 11–13 weeks, chorionicity should be
determined, nuchal translucency measured,
Diet and congenital anomalies looked for. Basic
investigations including hemoglobin and blood
Appropriate maternal nutrition and weight
grouping should be ordered. The mother should
gain are crucial to achieve optimal perina-
be counseled regarding risks, outcomes, nutri-
tal and maternal outcome. Since the dietary
tional needs, and weight gain. Recommended
requirements are increased in twin pregnancy,
cumulative weight gain is almost twice that rec-
dietary advice is mandatory. Calories should
ommended for singletons. Prenatal supplemen-
be increased by 300 kcal/day over and above
tation of folic acid must be given, as shown in
that recommended for a singleton pregnancy.
Box 32.19.
Carbohydrates, protein, fat, and micronutrient
requirements are also higher. Iron and folic acid
deficiency are common and supplementation of
Management Second trimester
these along with calcium is essential.
ee s
Weight gain Routine antenatal visits are scheduled every
2–3 weeks, which is more frequently than for sin-
Recommended weight gain in twin pregnancy is gletons. Iron, calcium, and micronutrient supple-
almost twice that recommended for singletons. mentation should be started. Ultrasonography
For women with normal body mass index (19–25 should be performed at 18 weeks for fetal mor-
kg/m2), recommended weight gain is 16.8–24.5 kg. phology and cervical length.
ee s
Goals of management The blood pressure should be monitored closely
Management of twin pregnancy is aimed at early since early onset preeclampsia can occur. Oral
diagnosis of twins, early identification of com- glucose tolerance test must be performed at 24
plications, and timely intervention for optimal weeks. Hemoglobin level must be rechecked.
maternal and perinatal outcome (Box 32.18). Ultrasonography must be repeated at 24 and
Box 32.19 Management of twin pregnancy

Box 32.18 Goals of management in twin First trimester
pregnancy
• Ultrasonography
• Early diagnosis of twins Ŧ 6–8 weeks
• Determination of chorionicity Number of fetuses
• Detection of congenital anomalies Number of gestational sacs
• Monitoring fetal growth Number of yolk sacs
• +FGPVKſECVKQPQHFKUEQTFCPE[ Gestational age
• Prevention of preterm labor Ŧ 11–13 weeks
• Early diagnosis of maternal complications Chorionicity
Ŧ Preeclampsia Nuchal translucency
Ŧ Anemia Congenital anomalies
• Decision regarding • Counseling
Ŧ Timing of delivery Ŧ Diet
Ŧ Mode of delivery Ŧ Weight gain
• Advise regarding Ŧ Pregnancy outcome
Ŧ Breastfeeding • Supplementation
Ŧ Contraception Ŧ Folic acid
CH 32_p455-473_v3.indd 466 17-07-2015 22:52:03

Box 32.20 Management in twin pregnancy Box 32.21 Management of twin pregnancy
Second trimester Third trimester
• 14–20 weeks • Uncomplicated twin pregnancy
Ŧ Iron, calcium, zinc, magnesium supplementation Ŧ Antenatal check
Ŧ Antenatal visits 2–3 weekly 2 weekly till 36 weeks
Ŧ Ultrasonography at 18 weeks Weekly till delivery
Morphology Ŧ Monitor blood pressure
Cervical length Ŧ Restrict physical activity
• 20–28 weeks Ŧ Watch for
Ŧ Monitor blood pressure Polyhydramnios
Ŧ Oral GTT at 24 weeks Pressure symptoms
Ŧ Repeat hemoglobin Ŧ Ascertain presentation of both fetuses
Ŧ Ultrasonography 24 and 28 weeks Ŧ Ultrasonography 2 weekly
Fetal growth • Complicated twin pregnancy
Discordancy Ŧ Weekly antenatal check
TTTS Ŧ Weekly ultrasonography
Cervical length Fetal growth
Ŧ fFN if cervical length <25 mm Biophysical profile
Doppler velocimetry
f HGVCNſDTQPGEVKP , glucose tolerance test; S,
twin-to-twin transfusion syndrome. Ŧ 2TGUGPVCVKQPQHſTUVCPFUGEQPFVYKP
Confirmed by ultrasonography
28 weeks for fetal growth, early detection of dis-

cordancy, TTTS, and cervical length. If available, Timing of delivery
fFN levels, may be checked if cervical length is Most twin pregnancies go into spontaneous
<25 mm. (Box 32.20). labor by 37–38 weeks. Studies have shown that
fetuses in twin pregnancy mature faster; the
Management Third trimester stillbirth rate at 39 weeks is equivalent to the
stillbirth rates for singletons at 42 weeks. It is
The mother must be seen every 2 weeks till 36 recommended, therefore, that uncomplicated
weeks and every week thereafter (Box 32.21). DC twins should be delivered by 38 weeks.
A rise in blood pressure, polyhydramnios, and Monochorionic diamniotic twins have a higher
pressure symptoms are watched for. Physical late pregnancy death rate and should be deliv-
activity must be restricted. Serial ultrasonogra- ered by 36 weeks. Complicated twin pregnancies
phy must be performed to check fetal growth. should be delivered earlier, depending on the
In uncomplicated twin pregnancies (DA fetal and maternal status.
twins, normal fetal growth, no discordancy, no
poly/oligohydramnios, and no maternal compli-
Mode of delivery
cations), routine antenatal testing has no proven
benefit. In complicated twin pregnancies, fetal In uncomplicated twins, the mode of delivery is
surveillance must begin by 32 weeks. Weekly determined by the presentation of the fetuses,
testing is recommended. Assessment of amni- especially the first twin. If the first twin is in vertex
otic volume is important in the evaluation of presentation, the twins could be vertex–vertex
fetal well-being. The deepest vertical pocket can (42%) or vertex–nonvertex (38%). If the first twin
be measured in each sac. This may be difficult is not a vertex presentation, it is referred to as
in some women; therefore, amniotic fluid index nonvertex–vertex (20%) (Box 32.22).
can be calculated by measuring four quadrants,
disregarding the membrane. Doppler velocime- Box 32.22 Mode of delivery
try of the umbilical vessels is useful in FGR.
Presentation of both twins should be ascer- Fetal presentation Mode of delivery
Vertex–vertex (42%) Vaginal
tained clinically and confirmed by ultrasonogra-
Vertex–nonvertex (38%) Vaginal
phy, if necessary, so that mode of delivery can be
Nonvertex–vertex (20%) Cesarean section
planned.
CH 32_p455-473_v3.indd 467 17-07-2015 22:52:03

lective cesarean section &GNKXGT[QHſTUVVYKP

Elective cesarean section is indicated in some Delivery of the first twin is completed as in sin-
situations as listed in Box 32.23. gleton fetus. The cord should be clamped with a
single clamp to indicate the first twin.
Management of labor
Complications can occur at any stage of labor as
Delivery o secon t in
already discussed. In anticipation of problems,
preparations should be made for twin delivery as Twenty to thirty minutes was considered to
listed in Box 32.24. be the optimal interval between the delivery
The mother should be kept on oral fluids of the first and second twin. Later studies
because the need for administration of anes- have shown that, as long as the fetal heart
thesia may arise. Intravenous fluid with a large rate of the second twin remains normal on
bore needle must be started when the woman is electronic monitoring, this interval can be
in active labor. Intravenous access is essential to longer.
administer oxytocin for augmentation of labor • As soon as the first twin is delivered, the
and prevention of postpartum hemorrhage, and maternal abdomen should be palpated to
to transfuse blood if required. Electronic fetal ascertain the lie and presentation of the sec-
monitoring of both fetuses is recommended. ond twin.
Uterine contractions and cervical dilatation • Fetal heart rate should be monitored.
should be monitored and plotted on a parto- • If the presentation is vertex and the uterine
gram. If uterine contractions are inadequate, contractions are adequate, artificial rupture of
labor should be augmented with oxytocin. membranes should be performed and the sec-
ond twin delivered.
• If uterine contractions are not adequate, aug-
Box 32.23 Indications for elective cesarean mentation of labor is done by adding oxytocin
section in twin pregnancy to the infusion.
• Absolute indications • If the presentation of the second twin is
Ŧ First twin in transverse lie breech, when adequate uterine contractions
Ŧ Monoamniotic twins are present, membranes may be ruptured
Ŧ FGR with abnormal Doppler velocimetry artificially and the second twin delivered by
Ŧ Conjoint twins assisted breech delivery.
• Relative indications • If the lie is transverse, external version should
Ŧ First twin in breech/ other non-vertex presentations be performed to convert to longitudinal lie
and delivery proceeded with.
, fetal growth restriction. • If external version is unsuccessful, internal
podalic version and breech extraction should
be performed (Fig. 32.10).
Box 32.24 Preparations for twin delivery • Ultrasonography may be used to assist in
• -GGRVJGRCVKGPVQPQTCNƀWKFU external and internal version.
• Start intravenous infusion with large bore needle • If there is vaginal bleeding indicating placen-
• Delivery team should consist of tal abruption of the second twin or fetal dis-
Ŧ Obstetrician tress, delivery should be expedited.
Ŧ Assistant • Occasionally, cesarean section may be
Ŧ Pediatrician
required for these indications or if the cervix
Ŧ Anesthetist
clamps down after delivery of first twin.
• Ensure availability of
Ŧ Cross-matched blood
• Two clamps should be applied to the cord of
Ŧ Electronic fetal monitoring the second twin to identify it as belonging to
Ŧ Two delivery sets the second twin.
Ŧ Oxytocin and methyl ergometrine
Procedure to be followed for vaginal delivery
Ŧ Ultrasonography
of the twins is given in Figure 32.11.
CH 32_p455-473_v3.indd 468 17-07-2015 22:52:03

Management of third stage

As soon as the second twin is delivered, 10 units
of oxytocin should be added to the infusion to
prevent postpartum hemorrhage. The placen-
tas should be delivered when signs of placental
separation are visible. Once delivered, the pla-
centas should be examined. If it is a fused single
placenta, the number of layers in the inter-twin
membrane must be counted. Presence of three
or four layers indicates DC/DA twins; presence
of two layers indicates MC/DA twins (Box 32.25;
Fig. 32.12).
Puerperium
Breastfeeding should be encouraged. Mothers
must be counseled to breastfeed both babies
Figure 32.10 Internal podalic version and breech since milk secretion is usually adequate for
extraction. The right hand is introduced into the uterus and both. Since feeding two babies is tiring and
the feet of the fetus are grasped and pulled down and the challenging, help, guidance, and support are
baby is delivered by breech extraction. essential.
eli ery of first t in
Monitor fetal heart

scertain lie presentation
of secon t in
econ t in erte econ t in breech econ t in trans erse
ssiste breech
eli er as erte ternal ersion
eli ery
uccessful Unsuccessful
eli er as nternal po alic ersion

erte or breech an breech e traction
Figure 32.11 Vaginal delivery of twins.
CH 32_p455-473_v3.indd 469 17-07-2015 22:52:03

gestations diagnosed in the first trimester. The

Box 32.25 Management of third stage in twin
pregnancy frequency is more before fetal cardiac activity
is identified. If this happens later in pregnancy,
• Add 10 units of oxytocin to infusion the dead fetus may get absorbed or be seen as
• Deliver placenta(s)
a flattened structure attached to the placenta or
• Examine placenta(s)
membranes, and is known as fetus papyraceus.
• Examine inter-twin membrane
Ŧ Three or four layers—dichorionic diamniotic
Ŧ Two layers—monochorionic diamniotic Death of one fetus
Single fetal demise in the second or third tri-
mester occurs in 5% of twin pregnancies and is
more often seen in MC twins. Due to placental
vascular communications in MC twins, demise
of one twin can cause sudden hypotension, ane-
mia, and ischemia in the second twin, resulting
in multicystic encephalomalacia in the surviving
twin. In DC twins, the condition that led to the
death of one fetus may also affect the second
twin, but the overall risk is not very high. Preterm
labor can occur. Coagulation defect due to the
release of thromboplastin from the dead fetus is
possible, but is rare (Box 32.26).
Management depends on the chorionicity.
Monochorionic twins must be monitored by
ultrasonography for fetal well-being and detec-
tion of multicystic lesion in the brain. Steroids
must be administered if delivery is required
before 34 weeks. Monochorionic twins may have
to be delivered when the gestational age crosses
34 weeks. Dichorionic twins may be monitored
and delivered at term (Box 32.27).
Figure 32.12 Dichorionic diamniotic placenta. Box 32.26 Death of one fetus in twin pregnancy
Examination of the membrane between the two fetuses
• Fetal death in second or third trimester
reveals four layers, two amnions and two chorions.
Ŧ Occurs in 5% of twin pregnancies
Ŧ More common in monochorionic twins
• Etiology
Ŧ Anomalies
Special situations Ŧ 2NCEGPVCNKPUWHſEKGPE[
Ŧ Infections
During the course of the pregnancy or delivery, Ŧ Maternal conditions
situations may arise that are uncommon and Ŧ Cord abnormalities
need expertise in management. Ŧ Twin-to-twin transfusion syndrome
• Problems in the surviving twin
Ŧ Monochorionic twins
anishing twin Multicystic encephalomalacia
Vanishing twin is the term used when twin preg- Multiorgan damage
• Complications
nancy is identified early in gestation but one sac
Ŧ Preterm labor
disappears. The cause of death of the fetus is
Ŧ Coagulopathy
not known. It occurs in about 20%–30% of twin
CH 32_p455-473_v3.indd 470 17-07-2015 22:52:03

performed in MC twins since there are vascular

Box 32.27 Management of surviving twin
communications. Ultrasonography is manda-
• Monochorionic twins tory to detect anomalies and to guide the proce-
Ŧ Close monitoring dure (Box 32.28).
Nonstress test
Ultrasonography
- Biophysical profile
- Multicystic lesions in brain Selective termination
Ŧ Steroids if <34 weeks
Ŧ Deliver after 34 weeks When one or more anomalous fetuses are termi-
• Dichorionic twins nated, the term selective termination is used. This
Ŧ /QPKVQTD[DKQRJ[UKECNRTQſNG procedure is performed at a later gestational age
Ŧ Deliver at term than fetal reduction (Box 32.29).
Box 32.29 Selective termination in multifetal

Interlocking of twins pregnancy
This is an extremely rare complication that • Congenital/chromosomal anomalous fetus

• %QPſTOGFD[
occurs in labor. One pole or body of the second
Ŧ ultrasonography
fetus obstructs the delivery of the first twin. The
Ŧ chorion villous sampling
most common situation is where the after com- Ŧ amniocentesis
ing head of the first twin during breech delivery • Performed in second trimester
interlocks with the leading head of the second • Transabdominal procedure
twin. The head of the second twin may be pushed • Potassium chloride into selected fetus
up, but it is difficult. Survival of the first twin may
be compromised. Delivery by cesarean section is
recommended when interlocking occurs. Triplets and higher-order
multiple pregnancies
Multifetal pregnancy
Incidence of triplets is 14–15/1000; higher-order
reduction births are less common (Fig. 32.13). The inci-
dence of triplets rose with the increase in use
Pregnancies with more than two fetuses are of assisted reproductive technologies but has
associated with several risks to the fetuses and reduced after guidelines regarding the number
the mother. Selective reduction of higher-order
multifetal pregnancy is performed to improve
perinatal outcome. The procedure may be per-
formed transabdominally, between 10 and 13
weeks. Two to three mL of potassium chloride is
injected into the fetal thorax. The transvaginal
or transcervical approach is used when abdom-
inal approach is not feasible. It should not be
Box 32.28 Multifetal pregnancy reduction

• Done in higher order multiple pregnancies
• Transabdominal approach
• At 10–13 weeks
• Should not be done in monochorionic twins
• Ultrasonography to detect anomalies mandatory
• Select the fetus most easily accessible
Figure 32.13 The triplets. The fetuses are preterm and
• 2–3 mL of potassium chloride into fetal thorax
growth restricted. (Photo courtesy: Dr. Rajnish Samal,
• Fetal death due to cardiac asystole
Bangalore.)
CH 32_p455-473_v3.indd 471 17-07-2015 22:52:04

of embryos that can be transferred have been

Box 32.30 igher order multifetal pregnancies
enforced. All maternal complications seen
in twins occur more frequently and are more • Incidence
severe. Prematurity is the most important cause Ŧ Triplets: 14–15/1000
Ŧ Higher order: Less frequent
of perinatal mortality (Box 32.30).
• Maternal complications
The woman must have more frequent check-
Ŧ More severe
ups; the mother and fetus should be monitored • Perinatal mortality and morbidity
closely. Serial weekly ultrasonography is recom- Ŧ Preterm labor and prematurity
mended from 28 weeks. Prophylactic cortico- Ŧ Congenital anomalies
steroids must be administered between 28 and Ŧ PROM
34 weeks. Delivery by cesarean section at 32–34 Ŧ FGR
weeks is recommended for triplets. Ŧ Vascular communications
, fetal growth restriction; P , prelabor rupture
of membranes.
Key points
• The incidence of multifetal pregnancies, especially • Ultrasonography is an extremely useful tool in the
dizygotic (DZ) twin pregnancy, has increased globally FKCIPQUKUQHOWNVKHGVCNRTGIPCPE[KFGPVKſECVKQPQH
due to the increased use of assisted reproductive complications, and management.
techniques (ARTs).
• Monozygotic twins are prone to unique complications
• According to placentation, four types of twin pregnan- such as monoamniotic twins, twin-to-twin transfusion
cies are described. Dizygotic twins are always dichori- syndrome, twin reverse arterial perfusion, twin ane-
onic and diamniotic (DC/DA). Placentation depends on mia–polycythemia sequence, and conjoint twins.
the timing of division of the embryo.
• Monoamniotic twins have a high perinatal mortal-
• Determination of chorionicity is essential for risk as- ity rate due to cord complications, preterm labor,
sessment and planning management. Chorionicity can congenital anomalies, and FGR. They should be
DGFGVGTOKPGFKPVJGſTUVCPFQTUGEQPFVTKOGUVGTD[ closely monitored by ultrasonography and delivered by
ultrasonography. cesarean section at 32–34 weeks.
• &KCIPQUKUQHVYKPUKUD[ENKPKECNUWURKEKQPCPFEQPſT- • Twin-to-twin transfusion syndrome occurs due to
mation is by ultrasonography. communication between the artery of one fetus and
• All the physiological changes of pregnancy in the the vein of the other fetus in the placenta. It can give
mother are exaggerated in multifetal pregnancies. rise to oligohydramnios and FGR in the donor twin and
polyhydramnios and cardiac failure in the recipient.
• Maternal complications seen in singleton pregnancies
occur more frequently and in a more severe form in • The goals of management are to diagnose the multife-
twin pregnancies. The most important complications tal pregnancy early, determine chorionicity, diagnose
are anemia, preeclampsia, preterm labor, antepartum fetal complications, prevent preterm labor, diagnose
hemorrhage, and polyhydramnios. and treat maternal complications, decide timing and
mode of delivery, and provide contraceptive advise.
• Intrapartum complications include malpresentations,
increase in operative vaginal and abdominal delivery, • Supplementation of iron and calcium, frequent ante-
and postpartum hemorrhage. natal visits, and timely and judicious use of ultra-
sonography to monitor fetal growth and well-being are
• Perinatal mortality is higher in twin pregnancy due to essential components of antenatal management.
fetal complications such as prematurity, fetal growth
restriction (FGR), congenital anomalies, and growth • Uncomplicated twins must be delivered by 37–38
discordancy. weeks.
• Prematurity is the most important cause of perinatal • +HVJGſTUVVYKPRTGUGPVUD[XGTVGZXCIKPCNFGNKXGT[

mortality. Preterm labor can be predicted by cervical is recommended; if nonvertex, cesarean section is
length measurement using ultrasonography at 24–28 advisable.
YGGMUCPFOCVGTPCNNGXGNUQHHGVCNſDTQPGEVKP
H(0 • When the woman is in labor, everything must be kept
• Clinical features of multifetal pregnancies include ready for twin delivery.
history of ART and maternal symptoms. Examina- • If the second twin presents in transverse lie, external
tion reveals overdistended uterus and multiple fetal version should be performed and if unsuccessful,
parts. Three fetal poles must be palpated to clinically internal podalic version and breech extraction are
diagnose twins. recommended.
(Continued)
CH 32_p455-473_v3.indd 472 17-07-2015 22:52:04


• Active management of the third stage is recommended. • Selective termination is performed when one or more
6JGRNCEGPVCUJQWNFDGGZCOKPGFVQEQPſTOEJQTKQPKEKV[ fetuses are anomalous.
• Intrauterine death of one fetus can cause problems in • Triplets and higher-order multiple births are rare
the other twin in MC twin pregnancies. The surviving and are associated with high perinatal mortality and
twin should be monitored and delivered at term if DC maternal complications. Triplets should be monitored
or earlier if monochorionic. by ultrasonography and delivered by cesarean section
• Multifetal pregnancy reduction is the selective reduc- at 32–34 weeks.
tion of higher-order pregnancy to twins, to improve
perinatal outcome.
Self-Assessment
Case-based questions 4. a. Investigations: Hemoglobin, other routine tests if
not already done, oral glucose tolerance test if not
already done.
Case 1
b. Ultrasonography: For fetal size, biometry, discor-
Mrs. RN, 30, is referred at 32 weeks from a primary health FCPE[COPKQVKEƀWKFXQNWOGPWODGTQHRNCEGP-
center since examination revealed a uterus larger than tas, inter-twin membrane if visible, fetal anomalies.
the gestational age and has been diagnosed to have twin c. If uncomplicated, two placentas visible or fetuses
pregnancy. of different gender: 2 weekly antenatal checkup till
36 weeks, weekly thereafter.
1. What details will you ask for in the history?
2. What will you look for on clinical examination?
3. What other complications do you anticipate?
Case 2
4. How will you monitor the mother and the fetus? 1. a. General examination: Pallor, blood pressure.
b. 1
DUVGVTKEGZCOKPCVKQP2TGUGPVCVKQPQHſTUVVYKP
polyhydramnios.
Case 2 c. 7
NVTCUQPQITCRJ[2TGUGPVCVKQPQHſTUVCPFUGEQPF
Mrs. SM, 28, is referred in labor with twin pregnancy. twins, fetal weights.
2. Vaginal delivery, if no severe FGR or discordancy.
1. How will you decide on the mode of delivery? 3. Placental abruption of second twin.
2. +HVJGſTUVVYKPRTGUGPVUD[XGTVGZJQYYKNN[QW 4. Atonic postpartum hemorrhage, retained placenta,
deliver? traumatic postpartum hemorrhage if operative vaginal
3. #HVGTVJGFGNKXGT[QHVJGſTUVVYKPVJGTGKUCIWUJQH delivery.
fresh bleeding and fetal heart deceleration of the
second twin. What is your diagnosis?
4. What complications do you anticipate after the deliv- Sample questions
ery of twins?
Answers 1. Discuss the diagnosis and antenatal complications of
multifetal pregnancy.
Case 1 2. Discuss the management of second stage in delivery
of twins.
1. a. History of infertility, use of ovulation-inducing 3. What are the maternal and fetal complications of twin
drugs, family history of twins. pregnancy?
b. History of pressure symptoms, acute abdominal
distension.
2. a. General examination: Pallor, blood pressure, Short-answer questions
pedal edema.
1. Conjoint twins
b. Obstetric examination: Fundal height, multiple
fetal parts, three fetal poles, two fetal hearts, 2. Maternal complications of twin pregnancy
polyhydramnios. 3. Twin-to-twin transfusion syndrome
3. Preeclampsia, preterm labor, anemia, gestational 4. Delivery of second twin
diabetes, polyhydramnios, antepartum hemorrhage. 5. Vanishing twin
CH 32_p455-473_v3.indd 473 17-07-2015 22:52:04

Fetal Growth
Disorders:
33 Growth Restriction
and Macrosomia
Case scenarios
Mrs. HJ, 26, gravida 2, para 1, live 1, weighed 43 kg and had gained
only 4 kg during her pregnancy. She was 34 weeks by dates. Clinical
examination showed the uterine size to be smaller than expected for the
gestational period. She was suspected to have fetal growth restriction.
She had been referred for further evaluation and management.
Mrs. KL, 29, gravida 2, para 1, live 1, weighed 103 kg and had ges-
tational diabetes. She was 36 weeks by dates. Estimated fetal weight
at 36 weeks was 3900 g. She and her husband were concerned that the
baby was big and so they had come for a discussion of mode of delivery
and possible complications.
Introduction
Fetal growth restriction (FGR) and macrosomia
are two extremes of fetal growth disorders. In
FGR, the fetus fails to reach its full growth poten-
tial. In macrosomia, the fetus exhibits inappro-
priate and excessive growth, especially dispro-
portionate fat deposition (Fig. 33.1).
Fetal growth restriction is linked to an increased
risk of perinatal morbidity and mortality. Growth-
restricted fetuses are more prone to intrauterine
hypoxia/asphyxia. Stillbirth and hypoxic-isch-
emic encephalopathy (HIE) are more likely to
occur in growth-restricted fetuses. Figure 33.1 #ITQYVJTGUVTKEVGFKPHCPV
5)#KUƀCPMGFQP
Macrosomia, on the other hand, is associated its right by an infant of normal growth and on its left by a
with both maternal and fetal morbidity. It is large-for-gestational-age (LGA) infant.
CH 33_p474-494_v3.indd 474 18-07-2015 11:08:40

Growth Restriction and Macrosomia 475
associated with fetal complications such as peri- 14–15 weeks’ gestation to 10 g/day at 20 weeks,
natal asphyxia, death, and shoulder dystocia. and to 30–35 g/day at 32–34 weeks. Between 32
Maternal risks of macrosomia are cesarean sec- and 34 weeks the fetus gains approximately
tion, prolonged labor, postpartum hemorrhage, 230–285 g/week. The rate of weight gain
and perineal trauma. decreases after that. After 41 weeks, there may
even be a slight loss of weight.
Fetal growth and

determinants of birth weight Fetal growth restriction
The natural growth potential of the fetus is
dictated, on one hand, by the fetal genome and, &GſPKVKQP
on the other, by the intrauterine environment
(Fig. 33.2). The intrauterine environment is under A fetus with an estimated weight below the 10th
the influence of both maternal and placental fac- percentile for a given gestational age is consid-
tors. Fetal growth is dependent on satisfactory ered to have fetal growth restriction (FGR), also
transport of essential nutrients and oxygen across called intrauterine growth restriction (IUGR),
the placenta. Both maternal nutrition and pla- caused by a pathologic process that inhibits intrin-
cental perfusion play a major role in the ability of sic growth potential. The World Health
the placenta to transfer substrates across to the Organization (WHO) defines FGR as birth weight
fetus. Fetal hormones also play a role in promot- <2500 g for developing countries, but this defini-
ing normal growth. In the third trimester, insulin- tion is not universally accepted.
like growth factors (IGFs) coordinate a precise The term small for gestational age (SGA) is
and orderly increase in growth. Insulin and thy- sometimes used for a fetus exhibiting less than
roxine (T4) are required through late gestation to expected growth (<10th percentile), but this
regulate appropriate growth in both normal and includes both constitutionally small but healthy
abnormal nutritional circumstances. fetuses (50%–70%) and fetuses that are actually
The total substrate needs of the fetus are rela- growth restricted (20%).
tively small in the first half of pregnancy. The rate To avoid confusion, the term FGR should be
of fetal growth is much more in the late third used with regard to the fetus, whereas SGA
trimester as compared with that in early preg- should be used only in reference to the newborn
nancy. Fetal weight increases from 5 g/day at (Box 33.1).
s Maternal factors
etal ntrauterine
etus
genome en ironment
nsulin
Placental factors
hyro ine
Maternal Placental
nutrition perfusion
Figure 33.2 Determinants of birth weight and fetal growth. KPUWNKPNKMGITQYVJHCEVQT
CH 33_p474-494_v3.indd 475 18-07-2015 11:08:40

happens in the late second trimester or in the

Box 33.1 &
GſPKVKQPUHQTITQYVJTGUVTKEVGF
fetuses and SGA infants early third trimester, it results in asymmetric
FGR. The fetal head size stays normal but the
• Fetal growth restriction abdominal circumference (AC) decreases. The
Ŧ Estimated weight <10th percentile
decrease in abdominal size is due to the decrease
Ŧ Not achieved growth potential
in liver volume (caused by reduced glycogen
Ŧ Pathologic process involved
• SGA
storage in the liver) and subcutaneous fat. Faced
Ŧ 50%–70% small but healthy by a hostile environment, the fetus compensates
Ŧ 20% growth restricted by redistributing blood flow to vital organs such
as the brain, heart, and placenta, and decreases
S A small for gestational age.
flow to nonvital fetal organs such as abdominal
viscera, lungs, skin, and kidneys.
The key differences between symmetric and
Constitutionally small fetus asymmetric FGR are listed in Table 33.1.
Constitutionally small fetuses are SGA babies that
weigh >10th percentile for the gestational age but Table 33.1 Comparison between symmetric and
are small due to constitutional factors such as asymmetric growth restriction
maternal ethnicity, body mass index (BMI), or Symmetric Asymmetric
female gender. The perinatal outcome is normal. FG FG
Distribution 20%–30% 70%–80%
Late-onset FG Insult Early Late
Growth pattern Proportionate Disproportionate
Fetuses with late-onset FGR weigh >10th percen- Head circumference Decreased Normal
tile but have not achieved their growth potential
since the growth restriction sets in after 34 weeks.
This may account for perinatal deaths that occur
in fetuses of ‘normal’ weight. The condition is Incidence
difficult to diagnose except by Doppler studies of
the middle cerebral artery (MCA) and umbilical FGR is a major health concern in developing
artery. Routine screening for this condition is not countries such as India. The incidence of FGR
warranted. is 23%, or approximately 30 million term new-
borns per year in developing countries. Nearly
75% of all affected newborns are born in Asia,
%NCUUKſECVKQPQH()4 mainly in South-Central Asia.
On the other hand, the prevalence of FGR is
approximately 10% of the general population in
Symmetric FG
developed countries.
Symmetric FGR comprises 20%–30% of growth-
restricted fetuses. This is a growth pattern in
which there is a proportionate decrease in isk factors for FG
growth of all fetal organs. The head size and
A single risk factor or a combination of risk fac-
abdominal size are proportionately small. This is
tors can result in FGR. Maternal, placental, and
due to the universal impairment of early fetal
fetal causes have been implicated in the patho-
cellular hyperplasia, caused by infection,
physiology of FGR.
teratogens, or chromosomal abnormality. This
insult usually happens early in fetal develop-
ment and therefore affects the fetus uniformly. Maternal factors
Maternal factors that can result in poor fetal
Asymmetric FG growth can act by
Asymmetric FGR occurs in 70%–80% of • reducing uteroplacental perfusion,
growth-restricted fetuses. When the insult (usu- • inducing hypoxemia, and
ally placental insufficiency) to the fetus • providing decreased nutritional substrates.
CH 33_p474-494_v3.indd 476 18-07-2015 11:08:40

Reduced uteroplacental perfusion can occur more to the final fetal weight, paternal genes
in maternal medical conditions associated with also have an effect. Chromosomal abnormali-
vascular disease. Placental microthrombi, occlu- ties contribute to 20% of all FGR. This usually
sion of vessels and infarcts may decrease placen- affects fetal growth early in gestation, rather
tal perfusion. Placental underperfusion is the than late.
most common cause of FGR in the fetus with no The common chromosomal abnormalities
congenital anomalies. associated with FGR are as follows:
Chronic maternal hypoxemia can lead to fetal
• Aneuploidy (e.g., trisomy 18 or 13, Turner 45 X,
hypoxemia and FGR.
triploidy)
If the mother is undernourished, there is
• Partial deletions, duplications, and mutations
decreased nutrition for the fetus.
• Ring chromosomes
The maternal factors that can result in FGR
• Confined placental mosaicism
are enumerated in Box 33.2.
Box 33.2 Maternal factors leading to FG Congenital anomalies

educed uteroplacental perfusion In the presence of major or multiple structural
• Pregnancy-related hypertensive diseases congenital anomalies, the fetus is unable to keep
Ŧ Chronic hypertension up normal growth velocity. Many congenital
Ŧ Gestational hypertension anomalies associated with FGR result from chro-
Ŧ Preeclampsia mosomal abnormalities.
• Pregestational diabetes mellitus
• 4GPCNKPUWHſEKGPE[
• Autoimmune disease Multiple pregnancy
Ŧ Systemic lupus erythematosus (SLE)
• Antiphospholipid antibody (APA) syndrome In multiple pregnancy, FGR is usually seen in the
ypo emia third trimester, when fetal nutritional require-
ments are not met. Fetal growth in multiple
• Cyanotic cardiac disease
• Pulmonary disease (including severe, uncontrolled
pregnancy depends on the following:
asthma) • Number of fetuses present
• Severe anemia
• Type of placentation (monochorionic vs.
• Living at a high altitude
dichorionic)
• 5OQMKPI
• Presence of complications such as
Decreased nutritional substrates
– Twin–twin transfusion
• Low prepregnancy weight – Congenital anomalies
• Poor weight gain in pregnancy
• Pregnancy at the extremes of reproductive age
• Short interpregnancy interval Congenital infection
fetal growth restriction. Transplacental transmission of maternal infec-
tion early in pregnancy may result in FGR. This
Fetal factors accounts for 5% of all cases of FGR. Congenital
infections associated with FGR are rubella,
Fetal factors usually result in early and sym- toxoplasmosis, cytomegalovirus, varicella-zos-
metric IUGR. This means that the growth ter, malaria, syphilis, and herpes simplex.
restriction may be identified in the first and
second trimesters. Since fetal factors cause
global decrease in fetal growth, all fetal mea- Placental factors (including
surements are below expected, resulting in
symmetric growth restriction. umbilical cord abnormalities)
Abnormal placentation
Genetic factors Abnormal placentation resulting in poor placental
Fetal weight is influenced greatly by the fetal perfusion and placental insufficiency is the most
genome. Although maternal genes contribute common pathophysiology associated with FGR.
CH 33_p474-494_v3.indd 477 18-07-2015 11:08:40

Table 33.2 isk factors for fetal growth restriction
Maternal factors Placental factors Fetal factors

Decrease placental per usion enetic isor ers
• Hypertensive disorders • Abnormal placentation • Aneuploidy
• Diabetes • Structural abnormalities • Deletions, duplications
• Antiphospholipid antibody syndrome • Abnormalities of the cord • Ring chromosomes
• Systemic lupus erythematosus • Mosaicism
• Renal disorders
Congenital mal ormations
ulti etal pregnancy
aternal hypo emia In ections
• Cyanotic heart disease oxoplasma
• Anemia • Rubella
• Pulmonary disease • Cytomegalovirus
• High altitude • Syphilis
Decrease nutrition • Herpes simplex
• Varicella–zoster
• Low prepregnancy weight
• Poor weight gain
• Short interpregnancy interval
Structural placental abnormalities Box 33.3 Perinatal risks for infants with FG
Placental abnormalities such as abruption, • Increase in perinatal mortality
infarction, circumvallate placenta, hemangioma, • Increase in perinatal morbidity
and chorioangioma have also been associated Ŧ Nonreassuring fetal status
with FGR. Ŧ Operative vaginal delivery
Ŧ Cesarean section
Ŧ Prematurity
mbilical cord abnormalities Ŧ Hypoxic-ischemic encephalopathy
Cord abnormalities such as velamentous or Ŧ Meconium aspiration
marginal cord insertion and single umbilical Ŧ Neonatal hypothermia
Ŧ Hypoglycemia
artery have been associated with FGR.
Ŧ Necrotizing enterocolitis
Risk factors for FGR are listed in Table 33.2.
Ŧ Bronchopulmonary dysplasia
• Long-term consequences
Ŧ Metabolic syndrome
Impact of FG fetal growth restriction.
A growth-restricted fetus faces an increased risk

of perinatal mortality and morbidity. As the fetal Perinatal complications of growth-restricted
weight decreases, perinatal mortality and mor- neonates are listed in Box 33.3.
bidity increase exponentially. Almost 50% of
stillbirths are associated with FGR. When growth
restriction goes unrecognized, it accounts for
10% of perinatal mortality. However, the mor- Screening for FG
bidity and mortality are more significant if the
fetal weight is <5th percentile.
There are also long-term health consequences
In low-risk pregnancies
for survivors. Long-term consequences for Clinical assessment is enough for screening for
growth-restricted infants in adulthood include growth restriction in low-risk pregnancies. In a
hypertension, type 2 diabetes, heart disease, low-risk pregnancy, further diagnostic tests are
stroke, and osteoporosis, (discussed in detail required only when there is clinical suspicion of
later in this chapter). FGR on routine clinical examination.
CH 33_p474-494_v3.indd 478 18-07-2015 11:08:40

Symphysio-fundal height Diagnosis of FG

Abdominal palpation alone is not a reliable
The diagnosis of FGR depends on history of risk
clinical tool to assess FGR. Measuring the sym-
factors mentioned earlier and clinical suspi-
physio-fundal height (see Chapter 8, History tak-
cion arising during physical examination,
ing and examination of the obstetric patient) may
which is then confirmed or excluded by an
raise a suspicion of FGR when the fundal height
ultrasound examination.
in centimeters is at least 3 cm below the gesta-
tional age in weeks. For example, if at 36 weeks’
gestation, the symphysio-fundal height is only
32 cm, FGR is suspected.
ltrasound imaging in FG
Ultrasound is the best tool for the diagnosis and
terine artery Doppler evaluation of FGR as it is highly reliable and
reproducible. The role of ultrasound in FGR is
Notching or increased pulsatility index in uter-
fourfold (Box 33.5).
ine artery Doppler in the first or second trimes-
ter has been studied as a screening test. A posi-
tive test is associated with a threefold increase ltrasound diagnosis of FG
in the risk for FGR, but the sensitivity of the test
Ultrasound diagnosis of FGR depends on the
is higher for predicting FGR with preeclampsia.
following:
The test is not recommended for routine screen-
ing (see Chapter 10, Obstetric ultrasound and • Establishment of accurate gestational age
other imaging). • Assessment of fetal size and rate of growth
• Growth charts
In high-risk pregnancies
Establishment of accurate
Certain pregnancies are at increased risk for the
occurrence of FGR, based on factors in the past
gestational age
or present history. These pregnancies should be Gestational age is best established in the first
screened for FGR by both clinical assessment trimester using crown–rump length (CRL) mea-
and serial ultrasonography. surement. Once established in the first trimester,
The factors that place a pregnancy at high risk the estimated date of delivery should not be
for FGR are summarized in Box 33.4. changed. This is particularly important in high-
risk pregnancies where follow-up is required to
identify FGR. Accurate gestational age helps in
plotting an accurate growth chart.
Box 33.4 igh-risk factors for FG
• 2TGUGPEGQHENKPKECNTKUMHCEVQTU
Ŧ Preeclampsia Box 33.5 ole of ultrasound in FG
Ŧ Maternal hypertension
Ŧ Systemic lupus erythematosus • +FGPVKſECVKQPQH()4
Ŧ Insulin-dependent diabetes with vascular disease Ŧ By using growth charts
Ŧ Cyanotic heart disease • +FGPVKſECVKQPQHV[RGQH()4
• Previous birth of a growth-restricted infant Ŧ Symmetric
• First trimester screening for Down syndrome with Ŧ Asymmetric
Ŧ Low PAPP-A • +FGPVKſECVKQPQHECWUG
• Triple or quadruple screening for Down syndrome Ŧ Infections
with Ŧ Structural abnormalities
Ŧ Elevated levels of hCG, inhibin, or AFP Ŧ Aneuploidy
Ŧ #UUQEKCVGFYKVJſXGHQNFKPETGCUGKP()4 • Antenatal surveillance
Ŧ #OPKQVKEƀWKFCUUGUUOGPV
A P alpha fetoprotein; fetal growth restriction; hC human Ŧ $KQRJ[UKECNRTQſNG
chorionic gonadotropin; PAPP-A pregnancy-associated plasma
protein A. fetal growth restriction.
CH 33_p474-494_v3.indd 479 18-07-2015 11:08:41

Assessment of fetal si e stimate etal eight

and rate of growth Fetal weight estimation has become one of the
reliable methods of identifying the growth-
The four biometric measurements of the fetus
restricted fetus. Most commonly, the formula for
include the following:
estimating EFW uses a combination of BPD,
• Biparietal diameter (BPD) HC, AC, and FL. These formulas are usually
• Head circumference (HC) included in the software package in the ultra-
• Fetal abdominal circumference (AC) sound machine. Fetal weight distribution by ges-
• Femur length (FL) tational age is also provided in standardized
tables, and the percentile can be calculated.
The serial measurements of these parameters,
especially of the AC, help in identifying the ea to ab omen ratio
growth-restricted fetus (see Chapter 10, Obstetric
In early pregnancy the HC is larger than the AC.
ultrasound and other imaging). FGR cannot be
As the pregnancy progresses, this proportion
diagnosed by ultrasound unless the AC is
changes and at term the AC is larger than the HC.
measured.
In growth-restricted fetuses with asymmetric
The ultrasound methods used for diagnosing
FGR, the HC will be equal to or greater than the
FGR include the following:
AC. Therefore, an elevated HC/AC ratio helps in
• Measurement of the AC the diagnosis of FGR.
• Calculation of the estimated fetal weight
(EFW) Serial observation o biometric
• Head-to-abdomen ratio (HC/AC ratio) gro th patterns (gro th velocity)
• Serial observation of biometric growth pat- Growth charts are available using ultrasound
terns (growth velocity) biometric parameters. Preferably, the growth
curves should be based on a homogeneous fetal
Ab ominal circum erence population. Customized growth charts take into
Of the four biometric parameters, decreased AC consideration factors that normally influence
is the most sensitive single indicator of FGR. If fetal growth. They make adjustments for mater-
previous ultrasound scans are done at 11–13+6 nal height, weight, parity, ethnic origin, and fetal
and 18–22 weeks, the optimal time to screen for sex, giving an individual growth chart for every
FGR is at 32 weeks’ gestation. If clinical suspicion patient. These are more accurate than popula-
arises before that, an ultrasound examination tion-based growth charts in the diagnosis of
should be done to confirm or rule out FGR. FGR and exclusion of the constitutionally small
The fetal growth curve can be extrapolated fetus.
from the previous readings. If the curve main- Figure 33.4 shows the growth chart for sym-
tains the expected growth velocity, then FGR can metric FGR where the growth restriction has
be ruled out. A fetus that is constitutionally started early and has affected both the head size
small but otherwise healthy will maintain the (BPD and HC) and the AC.
growth velocity. This is also called a fetus with a Figure 33.5 shows the growth chart for asym-
low growth profile (Fig. 33.3). If the AC falls metric FGR where the growth restriction has
below the expected curve, then FGR can be diag- started later and affects the AC, with sparing of
nosed. If the FGR has to be confirmed, an ultra- the head size.
sound should be repeated after an interval of
2 weeks.
When the AC and EFW are less than the 10th
percentile, FGR can be diagnosed accurately. Antenatal interventions
Conversely, an AC within the normal range reli- in I G
ably excludes growth restriction. Although FGR
is considered to exist when the AC is <10th per- Very few prenatal interventions have shown to
centile, fetal morbidity increases when the AC is reduce the perinatal outcome in the presence
<5th percentile. of FGR. Treatment of infections such as malaria
CH 33_p474-494_v3.indd 480 18-07-2015 11:08:41

Figure 33.3 (GVCNITQYVJEJCTVQHCHGVWUYKVJNQYITQYVJRTQſNG6JGHGVCNDKQOGVTKERCTCOGVGTU

$2&*%#%CPF
FL) are all at the low normal percentile but are maintaining the growth velocity. The fetus is constitutionally small but
otherwise healthy. AC abdominal circumference; BPD biparietal diameter; femur length; A gestational age;
C head circumference.
in endemic areas has been shown to be of some Management of pregnancy

benefit. Discontinuation of smoking may be
effective in preventing FGR. Low-dose aspirin complicated by FG
has been extensively studied and has been
found to reduce FGR associated with pre- Initial evaluation
eclampsia when started before 16 weeks.
Initial evaluation aims at differentiating the
healthy SGA fetus from the growth-restricted
fetus (Box 33.6).
+PVGTXGPVKQPUYKVJPQDGPGſV
Bed rest, protein supplementation, IV fluids, Subsequent management
Fructodex, L-arginine, zinc supplementation,
Once the diagnosis of FGR is made, subsequent
calcium supplementation, plasma volume
management of the pregnancy involves a two-
expansion, maternal oxygen therapy, heparin,
pronged approach:
and low-dose aspirin are not beneficial and may
be potentially harmful in the prevention and • Evaluation of fetal health
treatment of FGR. • Decision about timing of delivery
CH 33_p474-494_v3.indd 481 18-07-2015 11:08:41

Figure 33.4 Fetal growth chart showing symmetric fetal growth restriction. All fetal biometric parameters are below
VJGVJEGPVKNGCVYGGMUŏIGUVCVKQPAC abdominal circumference; BPD biparietal diameter; femur length; A
gestational age; C head circumference.
Evaluation of fetal health helps determine

Box 33.6 Initial evaluation in FG
whether the fetus is tolerating or not tolerating
• Healthy SGA fetus (constitutionally small) the hostile intrauterine environment. The
Ŧ Normal detailed ultrasound decision on the timing of the delivery depends
Ŧ Normal umbilical artery Doppler
on both the fetal status and the maternal
Ŧ Normal AFV
condition.
Ŧ Follow with
Routine antenatal care
• Growth-restricted fetus Evaluation of fetal health
Ŧ Abnormal umbilical artery Doppler
Ŧ Decreased AFV #OPKQVKEƀWKFXQNWOG
Ŧ Follow with
Enhanced fetal surveillance Amniotic fluid volume is important both in diag-
Ŧ May require nosis and in prognostication in fetuses with FGR.
Preterm delivery Oligohydramnios is highly suggestive of FGR and
A , Amniotic fluid vloume; fetal growth restriction; S A is associated with an increased risk of perinatal
small for gestational age. mortality.
CH 33_p474-494_v3.indd 482 18-07-2015 11:08:41

Figure 33.5 (GVCNITQYVJEJCTVUJQYKPICU[OOGVTKEHGVCNITQYVJTGUVTKEVKQP6JG#%JCUPQVMGRVWRVJGITQYVJXGNQEKV[

CPFJCUHCNNGPDGNQYVJGVJEGPVKNGCVŌYGGMUŏIGUVCVKQP
TGFCTTQYAC abdominal circumference; BPD biparietal
diameter; femur length; A gestational age; C head circumference.
$KQRJ[UKECNRTQſNG umbilical artery and MCA is initiated when FGR

is suspected.
BPP is useful in determining the timing of deliv- Umbilical artery Doppler waveform rep-
ery in the presence of FGR (see Chapter 11, resents increased placental resistance. Pulsatility
Antepartum fetal surveillance). Index values increase as peripheral resistance
increases. Umbilical artery Doppler is considered
Doppler velocimetry abnormal if diastolic flow is reduced, absent, or
Doppler studies of the umbilical artery, the mid- reversed after 20 weeks’ gestation (see Chapter 11,
dle cerebral artery and the ductus venosus help in Antepartum fetal surveillance).
making a decision about the timing of delivery. Reduced end-diastolic flow in the fetal umbil-
ical artery indicates that
mbilical artery
• 30% of the villus vasculature has ceased to
Doppler velocimetry of the umbilical artery is
function,
the primary surveillance tool for monitoring
• perinatal morbidity is still low, and
pregnancies where growth restriction is caused
• it is safe to manage pregnancy expectantly.
by placental dysfunction (asymmetric FGR).
Antepartum surveillance with Doppler of the Absent or reversed flow in the umbilical artery
CH 33_p474-494_v3.indd 483 18-07-2015 11:08:42

• indicates 60%–70% obliteration of placental Temporal sequence of events

arteries, and
• is associated with The sequence of events that occur in fetal deteri-
– fetal hypoxia and oration is given in Figure 33.6.
– significant increase in perinatal morbidity
and mortality. e uction in umbilical enous flo
Prompt delivery is indicated in the presence
of absent or reversed flow in the umbilical
e uction in li er si e
artery
ecrease in ab ominal circumference
i le cerebral artery e uce umbilical artery

As the FGR leads to progressive hypoxia, the iastolic flo increase in in ices
fetus compensates by cerebral vasodilatation
(brain-sparing effect). The MCA Doppler demon- ncrease mi le cerebral artery
strates high diastolic flow. iastolic flo ecrease in in ices
Ductus venosus bsent follo e by re erse

umbilical artery iastolic flo
An absent or reversed ductus venosus A-wave
indicates cardiovascular damage and may be a
sign of impending fetal acidemia and death. bsent or re erse iastolic
Fetal evaluation in a growth-restricted fetus is flo in uctus enosus
onreacti e nonstress test
Box 33.7 Further evaluation in FG late ecelerations abnormal biophysical profile
• AFV Figure 33.6 Sequence of events in fetal deterioration.

Ŧ Oligohydramnios
Highly suggestive of FGR
+PETGCUGFTKUMQHRGTKPCVCNOQTVCNKV[ Timing of delivery
• BPP
Ŧ Helps in timing of delivery Symmetric FG
• UA Doppler
Ŧ 4GFWEGFGPFFKCUVQNKEƀQY The fetus with symmetric FGR is frequently asso-
30% of villus vasculature has ceased to function ciated with structural and/or chromosomal
Perinatal morbidity still low abnormality. The outcome is usually poor. The
Safe to manage pregnancy expectantly pregnancy is commonly terminated after evalu-
Ŧ #DUGPVQTTGXGTUGFƀQY ating the fetus for cause of the FGR.
60%–70% obliteration of placental arteries
Fetal hypoxia
Significant increase in perinatal morbidity and Asymmetric FG
mortality
Should be delivered The timing of delivery of the fetus with asym-
• MCA Doppler metric FGR depends on the underlying etiology
Ŧ *KIJFKCUVQNKEƀQY
DTCKPURCTKPIGHHGEV of the growth restriction and the gestational age.
Fetal hypoxia The fetus should be delivered when the chance
• Ductus venosus Doppler of intrauterine death exceeds that of neonatal
Ŧ Absent or reversed ductus venous a-wave death.
Impending acidemia and death Fetuses with growth restriction are hypox-
A COPKQVKEƀWKFXQNWOGBPP DKQRJ[UKECNRTQſNG CA middle emic, leading to metabolic deterioration.
cerebral artery; A umbilical artery. Therefore, the timing of delivery becomes
CH 33_p474-494_v3.indd 484 18-07-2015 11:08:42

• Antenatal steroids should be administered (see

ecision for eli ery Chapter 36, Prelabor rupture of membranes).
• Magnesium sulfate is also recommended for
neuroprotection (see Chapter 36, Prelabor rup-
ture of membranes).
ymmetric symmetric • BPP and Doppler studies should be performed
weekly and fetal growth evaluation once in
2 weeks.
ssociate ith
eli ery base on • Normal umbilical artery flow by Doppler
estational age velocimetry is reassuring and allows for con-
structural an or
Maternal health
chromosomal tinuation of pregnancy, with close surveillance.
e erity of
abnormality • Although pregnant women with absent umbili-
etal ell being
cal artery diastolic flow can be watched closely
especially if <32 weeks, reversal of diastolic flow
bnormalities on warrants termination. When diastolic flow is
eli er absent, it is likely to progress to reversal in a few
fetal sur eillance
days; therefore, daily monitoring is essential.
eli er Gestational age 34 weeks

Beyond 34 weeks, since survival is better, the
Figure 33.7 Schematic representation of decision for threshold for delivery is lower.
delivery in fetal growth restriction (FGR).
• BPP and Doppler studies should be performed
critical. A fine balance needs to be achieved twice weekly and fetal growth assessed once in
between premature delivery and an increasingly 2 weeks.
hostile intrauterine environment.
Decision for delivery is individualized Box 33.8 Gestational age and timing of delivery
(Fig. 33.7) and is based on the following: ee s
• Gestational age of the fetus • Secondary to maternal disease

• Maternal health • Prognosis poor
• Delivery based on maternal condition
• Severity of FGR
• Fetal well-being ee s
• Prognosis remains poor
• Steroids for pulmonary maturation
Gestational age 28 weeks • Magnesium for neuroprotection
The prognosis is very poor in fetuses that have • $22YGGMN[
developed growth restriction in the second tri- • &QRRNGTUVWFKGUYGGMN[
• Delivery based on fetal compromise
mester. It is usually secondary to severe maternal
disease, for example, early onset severe pre- ee s
eclampsia. In this situation, delivery is dictated • $22YGGMN[
by the maternal condition. • &QRRNGTYGGMN[
• Delivery if
Ŧ 7#CDUGPVFKCUVQNKEƀQY
Gestational age 28 34 weeks Ŧ BPP abnormal
Ŧ No interval growth
Morbidity and mortality remain relatively high
• &GNC[FGNKXGT[VQYGGMUKH
in growth-restricted fetuses under 32–34 weeks’
Ŧ FGR mild
gestation. Ŧ Doppler studies stay normal
• Decision to deliver must be based on firm evi- BPP DKQRJ[UKECNRTQſNG()4HGVCNITQYVJTGUVTKEVKQP A
dence of fetal compromise. umbilical artery.
CH 33_p474-494_v3.indd 485 18-07-2015 11:08:42

• Delivery is recommended if umbilical artery

Box 33.9 Mode of delivery in the growth-
diastolic flow is absent, BPP is abnormal, or restricted fetus
there is no interval growth.
• If all parameters are normal and FGR is mild, • Vaginal delivery
Ŧ In mild to moderate FGR
deliver at 38 weeks.
Ŧ #VŌYGGMUŏIGUVCVKQP
Decision making regarding timing of delivery is Ŧ Careful monitoring of the fetal heart rate
summarized in Box 33.8. Growth-restricted fetus chronically hypoxemic
During labor, oxygenation may be compromised
Mode of delivery Ŧ FGR associated with
absent or reversed UA diastolic flow
The mode of delivery depends on the fetal con- oligohydramnios
decelerations on NST
dition (Box 33.9).
The suggested management of the pregnancy fetal growth restriction; S nonstress test; A umbilical
with FGR is given in Figure 33.8. artery.
eonatal care for the

Intrapartum management
growth-restricted infant
In the presence of FGR, intrapartum fetal distress
should be anticipated. Electronic fetal monitor- At birth, the growth-restricted infant has a typi-
ing is mandatory. A cesarean section is recom- cal appearance (Box 33.10; Fig. 33.9).
mended if there is thick meconium in early labor Infants with FGR have a higher risk of neona-
or a nonreassuring fetal heart pattern. tal morbidity and mortality, particularly among
Clinical iagnosis
of
Constitutionally outine
U oppler ormal antenatal
small fetus care
ymmetiric aluate eli er

bnormal for cause
ee s
bnormal oppler
ssociate maternal
con ition
ee s ee s
minister steroi s
PP an U oppler PP ee ly
eli er monitore ee ly U oppler ee ly
ro th by U e ery
ro th by U e ery t o ee s
ee s
ormal
bsent re erse
e erse U
U
bnormal PP Continue sur eillance
Poor gro th bnormal PP
Poor gro th
ormal
eli er eli er
eli er at ee s
Figure 33.8 Suggested management of pregnancy with FGR. A COPKQVKEƀWKFKPFGZBPP DKQRJ[UKECNRTQſNG D

end-diastolic waveform; fetal growth restriction; A umbilical artery; S ultrasound.
CH 33_p474-494_v3.indd 486 18-07-2015 11:08:42

those born very preterm, as discussed earlier in

Box 33.10 Appearance of the growth-restricted
infant at birth this chapter. A neonatologist should be available
for skilled resuscitation and careful evaluation of
• Thin the fetus for fetal infections/abnormality. The
• .QQUGRGGNKPIUMKP
neonate needs to be stabilized and screened for
• &GETGCUGFUMGNGVCNOWUENGOCUU
the following:
• Depleted subcutaneous fat tissue
• (CEGUJTWPMGP • Hypothermia
Ŧ .CEMUEJWDDKPGUUQHVJGPQTOCNPGYDQTP • Hypoglycemia
• Umbilical cord often thin • Hypocalcemia
• Meconium staining may be present
• Coagulation defects
• *GCFNCTIGTKPTGNCVKQPVQUK\GQHVJGVTWPM
CU[OOGV-
ric fetal growth restriction)
Long-term sequelae
More than 30 years ago, Barker hypothesized
that growth-restricted infants with low birth
weight exhibit an increased risk of obesity,
hypertension, dyslipidemia, insulin resistance
(leading to type 2 diabetes mellitus), and cardio-
vascular morbidity in adult life (Box 33.11). These
diseases are collectively called the metabolic
syndrome and are associated with an increased
risk of premature death. Small body size at birth
and during infancy, followed by accelerated
weight gain in childhood, has a significant
impact on these chronic diseases. This has been
termed the fetal origin of adult disease. The
adverse intrauterine environment at critical
periods of growth causes permanent program-
ming of fetal tissues (known as thrifty pheno-
type). This results in fixed functional capacity of
the tissues and when exposed to better nutrition
a. later in life, leads to obesity and metabolic
syndrome.
In addition, short stature in children and
adults, premature adrenarche, and the polycys-
tic ovarian syndrome (PCOS) are endocrine
Box 33.11 Barker s hypothesis Fetal origin

of adult disease
• Growth-restricted, low-birth-weight infants
Ŧ As adults develop metabolic syndrome
Obesity
Hypertension
Dyslipidemia
b. Insulin resistance (type 2 diabetes mellitus and
Figure 33.9 A growth-restricted infant at birth. a. It shows PCOS)
FGETGCUGFUMGNGVCNOWUENGOCUUFGRNGVGFUWDEWVCPGQWU Cardiovascular morbidity
• Metabolic syndrome leads to
HCVVKUUWGCPFCUJTWPMGPHCEGb. The head is larger in
Ŧ KPETGCUGFTKUMQHRTGOCVWTGFGCVJ
TGNCVKQPVQVJGVTWPM
Photo courtesy: Dr. Padmapriya
Dore, Vellore.) PC S polycystic ovarian syndrome.
CH 33_p474-494_v3.indd 487 18-07-2015 11:08:43

sequelae of FGR. The combination of early onset isk factors for macrosomia
growth delay and prematurity significantly
increases the risk for neurological sequelae and The two strongest factors for macrosomia are
motor and cognitive delay. high BMI and maternal diabetes. As these two
The worst outcomes are observed in the more problems increase in developing countries, more
severely growth-restricted infants who are pre- cases of obstetric complications resulting from
term, and who exhibit the most overt evidence of macrosomia are seen. The other risk factors are
impaired umbilical flow. However, neurological excessive weight gain in pregnancy, maternal
sequelae can be minimized in the fetus with impaired glucose tolerance, multiparity, paren-
FGR by tal height, previous macrosomic baby, male
• Carefully selecting timing of delivery. fetus, and postdated pregnancy (Box 33.12).
• Keeping the fetus well oxygenated during Macrosomia can occur in all diabetic preg-
labor. nancies, but the incidence appears to be greater
• Providing skilled neonatal care at birth. in infants born to mothers with pregestational
diabetes. The macrosomic infant of a diabetic
mother has a significant increase in fat mass and
Macrosomia a different body morphology as compared with
other macrosomic infants (Box 33.13; Fig. 33.10).
DGſPKVKQP Box 33.12 isk factors for macrosomia

A macrosomic or large-for-gestational-age • High BMI (tMIO2)
(LGA) infant is one whose birth weight is equal • Maternal diabetes
to or greater than the 90th percentile for a given • Excessive weight gain in pregnancy
gestational age. This definition is based on the • Maternal impaired glucose tolerance
average birth weight at each gestational age, and • Parental height
is country specific. • Previous macrosomic baby
For example, an infant born at term and weigh- • Male fetus
• Postdated pregnancy
ing t4500 g is considered to have macrosomia in
the United States. However, a WHO study has B body mass index.
shown that in India, an infant weighing t3250 g at
term would be greater than the 90th percentile Box 33.13 Macrosomic infant of diabetic mother
and therefore, by definition, has macrosomia. • Growth is disproportionate
The definition of macrosomia differs in coun- • Chest much larger than the head
tries, and, within the country, it may differ • 5KIPKſECPVN[NCTIGUJQWNFGTU
between the urban and the rural population. In • +PETGCUGFUMKPHQNFUKPVJGWRRGTGZVTGOKVKGU
developing countries, as the prevalence of obe- • Typical appearance
sity and diabetes increases, the prevalence of Ŧ Barrel-chested infant
fetal macrosomia will also rise. Ŧ 5JQTVPGEM
Ŧ Broad shoulders
Ŧ #VJKIJTKUMHQTUJQWNFGTF[UVQEKC
Incidence
The incidence of macrosomia varies with the inci-
dence of risk factors. The incidence of birth of
babies weighing >4000 g is approximately 9%.
Globally there is a 15%–20% increase in macroso-
mia due to the increase in obesity and diabetes.
The incidence in India is difficult to estimate since
the definition and birth weight cutoff vary. Diabetes
is a common problem in India, and the incidence
of obesity is on the increase; hence, there is a 15% Figure 33.10 Macrosomic infant. Note barrel chest, short
increase in macrosomia in India as well. PGEMCPFDTQCFUJQWNFGTU
CH 33_p474-494_v3.indd 488 18-07-2015 11:08:43

Pathophysiology macrosomia is usually not accurate, the diagno-

sis of macrosomia may be overlooked, resulting
of macrosomia in potentially serious consequences for the
infant and the mother.
Macrosomia is caused by the increased supply of
nutritional substrate resulting from certain asso-
ciated maternal conditions such as poorly con- Fetal consequences
trolled diabetes or maternal obesity (Fig. 33.11).
Difficulty and delay in delivery may result in
Hyperglycemia in the fetus results in the produc-
perinatal asphyxia and rarely death. Shoulder
tion of insulin, insulin-like growth factors (IGFs),
dystocia is a feared complication of macrosomia.
growth hormone, and other growth factors. These,
Up to 25% of infants with shoulder dystocia
in turn, stimulate fetal growth and excessive
experience brachial plexus or facial nerve inju-
deposition of fat and glycogen. In postdated preg-
ries, and fractures of the humerus or clavicle.
nancy, the growth process continues in utero,
Brachial plexus injuries, such as Erb–Duchenne
resulting in a larger birth weight at delivery.
palsy, are ordinarily attributed to delivery com-
plicated by shoulder dystocia.
1DUVGVTKEUKIPKſECPEG Neonatal hypoglycemia, hypoxic encephal-
opathy, respiratory distress, hyperbilirubinemia,
of macrosomia and other complications associated with mater-
nal diabetes are also common in a macrosomic
Macrosomia can be a more significant obstetric infant.
risk in developing countries, where poor nutri-
tion in adolescence can inhibit complete pelvic
growth, early marriages lead to pregnancy before Long-term consequences
the pelvis is fully developed, and facilities for
operative delivery of women with obstructed
for macrosomic infants
labor are not reliably available (Box 33.14). There are long-term consequences for the infant
born with macrosomia. These infants are at
Box 33.14 1DUVGVTKEUKIPKſECPEGQHOCETQUQOKC increased risk of developing impaired glucose
tolerance and obesity as adults. They are also at
• $KIIGTQDUVGVTKETKUMKPFGXGNQRKPIEQWPVTKGU risk for developing metabolic syndrome (includ-
Ŧ Poor nutrition leading to poor pelvic growth
ing an abnormal lipid profile).
Ŧ Pregnancy before full pelvic development
The consequences for the macrosomic infant
Ŧ Unreliable facilities for operative delivery
Consequences of Maternal consequences

fetal macrosomia
Pregnancies complicated by macrosomia are
The delivery of a macrosomic infant is an obstet- at an increased risk for cesarean section. The
ric challenge. Since clinical diagnosis of incidence of prolonged labor and postpartum
nsulin
Maternal iabetes
s
ncrease fetal gro th
ntermittent fetal
Maternal obesity cessi e eposition
hyperglycemia
of fat an glycogen
ro th hormone
cessi e eight
gain ther gro th factors
Figure 33.11 Pathophysiology of macrosomia in maternal diabetes and obesity. KPUWNKPNKMGITQYVJHCEVQT
CH 33_p474-494_v3.indd 489 18-07-2015 11:08:44

Box 33.15 Fetal, neonatal, and long-term Clinical assessment

consequences in macrosomia
The prediction of fetal weight by clinical assess-
• Fetal consequences ment is notoriously difficult. The quantity of
Ŧ Perinatal asphyxia amniotic fluid, uterine size, and maternal body
Ŧ Death fat make it difficult to accurately assess fetal size
Ŧ Shoulder dystocia by palpation through the abdominal wall.
*WOGTWUENCXKEWNCTHTCEVWTG
Brachial plexus injury
Facial nerve injury
• Neonatal consequences ltrasound prediction
Ŧ Hypoglycemia
Ŧ Hypoxic-ischemic encephalopathy of macrosomia
Ŧ Respiratory distress
Although ultrasonography enables the direct
Ŧ Hyperbilirubinemia
measurement of various fetal body parts, its accu-
• Long-term consequences in adulthood
Ŧ Impaired glucose tolerance and obesity racy in predicting macrosomia is poor. Estimated
Ŧ Metabolic syndrome fetal weigh is calculated using different formulas.
Ŧ #DPQTOCNNKRKFRTQſNG The larger the fetus, the less accurate is the ultra-
sound estimation of fetal weight. It is also poor in
predicting fetal weight in multiple gestation and
hemorrhage increases with macrosomia. Vaginal
diabetic pregnancies. Measurement of the AC and
delivery of a macrosomic infant increases the
calculation of the EFW using fetal biometry are
risk of third- or fourth-degree lacerations
the common ultrasonographic methods to assess
fivefold.
macrosomia.
Maternal consequences of macrosomia are
given in Box 33.16.
Abdominal circumference
Box 33.16 Maternal consequences AC is the most common single parameter used to
of macrosomia
assess risk of macrosomia.
• Prolonged labor
• Postpartum hemorrhage Estimated fetal weight
• Perineal trauma
The formula for calculating EFW commonly
includes a combination of BPD, HC, AC, and FL.
Diagnosis of macrosomia
Soft tissue measurements
Macrosomia can be accurately diagnosed only
by weighing the newborn after delivery. The pre- Measurement of subcutaneous fat at mid-hu-
natal diagnosis of fetal macrosomia continues to merus, abdominal wall, thigh, and other areas
remain inaccurate. Methods that have been con- has been evaluated but has not been found
ventionally used to predict birth weight are to be any more accurate than estimated body
weight.
• Assessment of maternal risk factors
• Clinical examination
• Ultrasound measurement of the fetus Magnetic resonance imaging
Magnetic resonance imaging (MRI) is superior
Assessment of maternal to ultrasonography in the diagnosis of macro-
somia and prediction of shoulder dystocia, but
risk factors it is expensive and not recommended for rou-
The presence of risk factors for macrosomia tine use.
should alert the clinician to the possibility of Prenatal prediction of macrosomia is summa-
macrosomia. rized in Box 33.17.
CH 33_p474-494_v3.indd 490 18-07-2015 11:08:44

accurately predict serious complications such as

Box 33.17 Prenatal prediction of macrosomia
shoulder dystocia and its attendant sequelae.
• #UUGUUOGPVQHOCVGTPCNTKUMHCEVQTU Such complications, however, do not depend on
• Clinical examination fetal weight alone, but on multiple factors
Ŧ &KHſEWNV
including maternal and fetal anatomy. The
Ŧ Complicated by
majority of macrosomic infants do well with vag-
amniotic fluid volume
maternal body fat
inal delivery, even if there is shoulder dystocia.
• Ultrasound measurement of the fetus Vaginal delivery can be offered for women with
Ŧ Abdominal circumference suspected macrosomia. The woman’s obstetric
Ŧ Estimated fetal weight history, her progress during labor, the adequacy
Formulae using biometric parameters of her pelvis, and other evidence suggestive of
• Soft tissue measurements fetopelvic disproportion should be used to
Ŧ Measurement of subcutaneous fat determine whether a cesarean section would be
Midhumerus required (Fig. 33.12).
Abdominal wall
Thigh
• MRI
Ŧ Expensive
Ŧ Not recommended for routine use
ole of elective induction
magnetic resonance imaging.
of labor
The fetus gains approximately 200 g/week after
37 weeks. It has been suggested that early induc-
Management of suspected tion of labor before or at term will prevent fur-
fetal macrosomia ther growth of the fetus and therefore avoid the
complications of macrosomia. Unfortunately,
In the presence of suspected macrosomia (by induction of labor has not shown to be beneficial
history of risk factors, clinical assessment, or and actually increases the rate of cesarean
ultrasound estimation), clinicians would like to section.
Clinical suspicion of macrosomia

History of ris factors
Clinical assessment
Ultrasoun estimation
Pre ious poor obstetric history

Prolonge labor
Possibility of shoul er ystocia
na e uate pel is
etopel ic isproportion
Vaginal eli ery Cesarean section

Careful monitoring of labor
Figure 33.12 Delivery options in suspected macrosomia.
CH 33_p474-494_v3.indd 491 18-07-2015 11:08:44

ole of elective cesarean offered with great caution or an elective cesarean

section may be offered directly.
section
Prophylactic cesarean delivery for suspected Maternal diabetes
fetal macrosomia <4000 g (in Indian women)
may not be effective for pregnancies without Vaginal delivery can be offered to a woman with
diabetes. Even in pregnancies complicated by gestational diabetes. When macrosomia is sus-
diabetes, elective cesarean section to reduce the pected in a mother with gestational diabetes, a
risks of birth trauma is not cost-effective and is cesarean section may be offered electively if the
not routinely recommended. EFW is >4000 g. The risk of shoulder dystocia is
higher in infants of diabetic mothers because of
the abnormal fat distribution. The labor should
Fetal macrosomia in special be monitored carefully for signs of fetopelvic
situations disproportion.
Previous cesarean section Previous shoulder dystocia

In a woman with a previous cesarean section, Since the recurrence of shoulder dystocia in the
macrosomia has to be taken into consideration subsequent pregnancy is low, a woman with a
when discussing vaginal birth after cesarean previous history of shoulder dystocia may be
(VBAC) with the patient. If the fetus is consid- allowed to deliver vaginally.
ered to have macrosomia, especially in the pres-
ence of maternal diabetes, VBAC should be
Key points
• Fetal growth restriction (FGR) and macrosomia are • Maternal factors that can result in poor fetal growth
two extremes of fetal growth disorders. can act by reducing uteroplacental perfusion, induc-
• The natural growth potential of the fetus is dic- ing hypoxemia and providing decreased nutritional
tated by the fetal genome and by the intrauterine substrates.
environment. • Fetal factors that can result in FGR include chromo-
somal abnormalities, congenital anomalies, congenital
• Maternal nutrition, placental perfusion, and fetal
infections, and multiple pregnancy.
hormones play a role in promoting normal growth.
• Placental factors causing FGR include abnormal
Fetal growth restriction placentation, structural placental abnormalities, and
umbilical cord abnormalities.
• A fetus with an estimated weight below the 10th
percentile for a given gestational age is considered to • Screening for FGR is only by clinical assessment in
have FGR. NQYTKUMRTGIPCPEKGU
• The term small for gestational age (SGA) includes • %GTVCKPRTGIPCPEKGUCTGCVKPETGCUGFTKUMHQTVJG
both constitutionally small but healthy fetuses (50%– occurrence of FGR, based on factors in the past
70%) and fetuses that are actually growth restricted or present history. These pregnancies should be
(20%). screened for FGR by both clinical assessment and
serial ultrasonography.
• The term FGR should be used with regard to the fetus,
whereas SGA should be used only in reference to the • Ultrasound is the best tool for the diagnosis and
newborn. evaluation of FGR as it is highly reliable and
reproducible.
• #HGVWUYKVJITQYVJTGUVTKEVKQPHCEGUCPKPETGCUGFTKUM
of perinatal mortality and morbidity.
(Continued)
CH 33_p474-494_v3.indd 492 18-07-2015 11:08:44


• ()4KUENCUUKſGFKPVQU[OOGVTKECPFCU[OOGVTKE given gestational age. This is based on the average
growth restriction. birth weight at each gestational age, and is country
URGEKſE
• In symmetric , the insult usually happens early
in fetal development and therefore affects the fetus • /CETQUQOKCKUCPKORQTVCPVTKUMHCEVQTHQTHGVCN
uniformly. complications such as perinatal asphyxia, death, and
UJQWNFGTF[UVQEKC/CVGTPCNTKUMUQHOCETQUQOKCCTG
• 9JGPVJGKPUWNV
WUWCNN[RNCEGPVCNKPUWHſEKGPE[VQ
cesarean section, prolonged labor, postpartum hemor-
the fetus happens in the late second trimester or
rhage, and perineal trauma.
in the early third trimester, it results in asymmetric
. • The two strongest factors for macrosomia are mater-
nal obesity and maternal diabetes.
• FGR is diagnosed and followed up with ultrasound ex-
aminations. Abdominal circumference and estimated • Methods that are used for the prenatal diagnosis of
fetal weight are the two important measurements for HGVCNOCETQUQOKCCTGCUUGUUOGPVQHOCVGTPCNTKUM
diagnosis. factors, clinical examination, and ultrasound measure-
ment of the fetus.
• The decision on timing of delivery are based on the
ſPFKPIUQP&QRRNGTXGNQEKOGVT[ • Abdominal circumference and estimated fetal weight
are the two important ultrasound measurements for
• The decision to deliver also depends on the gesta-
diagnosis of macrosomia.
tional age and the fetal and maternal condition.
• The majority of macrosomic infants do well with vagi-
• There are short-term and long-term consequences
nal delivery, even if there is shoulder dystocia.
of FGR. Low-birth-weight, growth-restricted fetuses
JCXGCPKPETGCUGFTKUMQHFGXGNQRKPIVJGOGVCDQNKE • 6JGYQOCPŏUQDUVGVTKEJKUVQT[RTQITGUUFWTKPINCDQT
syndrome as adults. adequacy of the pelvis, and other evidence suggestive
of fetopelvic disproportion should be used to deter-
mine whether a cesarean section would be required.
Macrosomia
• Elective preterm induction of labor and elective cesar-
• A macrosomic or large-for-gestational-age infant is ean section have not been shown to be effective in
QPGYJQUGDKTVJYGKIJVKU VJRGTEGPVKNGHQTC reducing complications of macrosomia.
Self-Assessment
3. What are the fetal complications of macrosomia?
Case-based questions 4. How will you manage this pregnancy?
Case 1
/TU*,ITCXKFCRCTCNKXGYGKIJGFMICPF Answers
JCFICKPGFQPN[MIKPVJKURTGIPCPE[5JGYCUYGGMU
by dates. Clinical examination showed the uterine size to Case 1
be smaller than expected for the gestational period.
1. History of previous baby with growth restriction,
1. *QYYKNN[QWOCMGCENKPKECNFKCIPQUKUQHITQYVJ OCVGTPCNTKUMHCEVQTUUWEJCUJ[RGTVGPUKQPFKCDGVGU
restriction? renal disorder, or APA syndrome must be considered.
2. What is symmetric and asymmetric growth restriction? Examination may reveal uterine size less than the
3. *QYYKNN[QWEQPſTOVJGFKCIPQUKU! period of gestation and symphysio-fundal height less
4. How will you manage this pregnancy? by 3 cm or more for appropriate gestational age.
2. In symmetric FGR, the insult usually happens early in
fetal development and therefore affects the fetus uni-
Case 2 HQTON[9JGPVJGKPUWNV
WUWCNN[RNCEGPVCNKPUWHſEKGPE[
/TU-.ITCXKFCRCTCNKXGYGKIJGFMICPF to the fetus happens in the late second trimester or in
JCF IGUVCVKQPCN FKCDGVGU 5JG YCU YGGMU D[ FCVGU the early third trimester, it results in asymmetric FGR.
'UVKOCVGFHGVCNYGKIJVCVYGGMUYCUI The abdominal size is smaller than the head size.
3. &KCIPQUKUKUEQPſTOGFD[WNVTCUQWPFUECPWUKPI
1. What is macrosomia? CDFQOKPCNEKTEWOHGTGPEGGUVKOCVGFHGVCNYGKIJV*%
2. 9JCVCTGVJGTKUMHCEVQTUHQTOCETQUQOKC! AC ratio, and serial growth charts.
CH 33_p474-494_v3.indd 493 18-07-2015 11:08:44

4. +H()4KUEQPſTOGFHGVCNYGNNDGKPICUUGUUOGPVKU due to delayed delivery. Neonatal hypoglycemia, HIE,

by BPP, Doppler study of the umbilical and middle respiratory distress, and hyperbilirubinemia are the
cerebral arteries, and serial growth chart. Since other complications.
UJGKUYGGMURTGIPCPVKHVJG$22&QRRNGT 4. 6JGOQVJGTŏUDNQQFUWICTUUJQWNFDGOQPKVQTGFCPF
UVWF[CPFITQYVJCTGPQTOCNFGNKXGTCVYGGMU controlled. She should be delivered at term. Elective
If BPP is abnormal or umbilical artery Doppler cesarean section is not indicated. Watch for shoulder
UJQYUCDUGPVQTTGXGTUGFFKCUVQNKEƀQYFGNKXGT dystocia.
immediately.
Case 2
Sample questions
1. A macrosomic infant is one whose birth weight is Long-answer question
VJRGTEGPVKNGHQTCIKXGPIGUVCVKQPCNCIG+VKU
1. &GſPGHGVCNITQYVJTGUVTKEVKQP&GUETKDGVJG
EQWPVT[URGEKſE
etiology, diagnosis, and management of fetal
2. The two strongest factors for macrosomia are mater- growth restriction.
PCNQDGUKV[CPFOCVGTPCNFKCDGVGU1VJGTTKUMHCEVQTU
are excessive weight gain in pregnancy, previous
macrosomic baby, ethnicity, postdated pregnancy, Short-answer questions
and male fetus.
3. Shoulder dystocia is a major complication of mac- 1. Symmetric and asymmetric growth restriction
rosomia and can lead to brachial plexus or facial 2. Doppler velocimetry in FGR
nerve injuries, and fractures of the humerus or clavi- 3. $CTMGTŏUJ[RQVJGUKU
cle. Perinatal asphyxia and rarely death can occur 4. Fetal macrosomia
CH 33_p474-494_v3.indd 494 18-07-2015 11:08:44

Disorders of
34 Amniotic Fluid
Case scenario
Mrs. DA, 30, multigravida, was referred from a primary health center.
She was 31 weeks’ pregnant and complained of difficulty in breathing.
Her abdomen looked tense and overdistended. On further questioning,
Mrs. DA said that her primary care doctor had informed her that she had
excessive fluid in the uterine cavity. The baby could be at risk and there
was a possibility of complicated delivery. She was asked to go to a tertiary
care center.
Introduction #OPKQVKEƀWKFRTQFWEVKQP
Amniotic fluid volume (AFV) may be higher or and clearance
lesser than normal in some pregnancies. Women
with a decrease in fluid may not be symptomatic Amniotic fluid is produced and reabsorbed con-
but when there is gross excess of fluid, distension tinuously. The entire volume of fluid is replaced
of abdomen is obvious and other symptoms due several times a day. The major sources of amni-
to overdistension of the abdomen are also evident. otic fluid are fetal urine and fetal lung fluid,
In addition, the underlying cause of gross increase and clearance is by fetal swallowing and by
or decrease in fluid can be detrimental to the fetus. intramembranous transfer to fetal blood. These
are discussed in detail in Chapter 5, Placenta,
fetal membranes, and amniotic fluid. The vol-
0QTOCNCOPKQVKEƀWKF ume of inflow and clearance at term are given
in Box 34.1. It is evident from the data given in
Box 34.1 that the fluid is in dynamic equilibrium
Amniotic fluid surrounds the fetus from early
because net inflow and net clearance are equal.
pregnancy. It has several functions as high-
Changes that affect fetal urine production,
lighted in Chapter 5, Placenta, fetal membranes,
lung fluid secretion, and fetal swallowing or an
and amniotic fluid.
CH 34_p495-507_v3.indd 495 18-07-2015 11:26:35

Box 34.1 8
QNWOGQHCOPKQVKEƀWKFKPƀQY Polyhydramnios
and clearance day at term
Polyhydramnios or hydramnios is defined as
Production
excessive volume of amniotic fluid. Diagnosis
• Fetal urine: 800–1200 mL of polyhydramnios is made when the AFI is
• Fetal lung secretion: 170 mL
>25 cm or LVP (SDP) is >8 cm. Polyhydramnios
• Oral–nasal secretions: 25 mL
is classified into mild, moderate, and severe as
Clearance given in Box 34.2. Mild hydramnios is the most
• Fetal swallowing: 500–1000 mL common and occurs in 80% of cases.
• Intramembranous transfer: 200–400 mL
• Transmembranous transfer: 10 mL
Incidence
The incidence of polyhydramnios is 1%–2%.
alteration in intramembranous flow can affect 'VKQNQI[CPFRCVJQIGPGUKU

the AFV drastically.
Most cases of polyhydramnios are considered
idiopathic (no known cause). Undetected con-
genital and/or chromosomal anomaly may be
0QTOCNCOPKQVKEƀWKF present in these cases and perinatal mortality is
increased two- to five-fold.
volume Polyhydramnios may be caused by fetal
anomalies that interfere with fetal swallowing,
The volume of amniotic fluid increases with ges-
absorption of fluid, or an increase in fetal urine
tational age and reaches a peak at 34–36 weeks.
production. Maternal diabetes is also a common
Thereafter, it reduces and the rate of reduction is
cause.
more rapid after 40 weeks.
An etiological factor can be identified in most
Amniotic fluid volume increases at high alti-
cases of severe polyhydramnios but only in 15%
tudes and with maternal hydration; it decreases
of mild polyhydramnios. The possibility of chro-
with fluid restriction and dehydration.
mosomal anomaly and perinatal mortality is
higher as the severity of hydramnios increases.
Conditions associated with polyhydramnios
Evaluation of amniotic and the pathogenesis in each condition are listed
in Table 34.1.
ƀWKFXQNWOG
Gross increase or decrease in AFV can be sus- Clinical features
pected on clinical examination. Accurate Mild hydramnios may be detected only by ultraso-
methods of measurement such as dye dilution nography. Moderate and severe polyhydramnios
techniques are not used in routine practice. are associated with overdistension of the abdo-
The most practical method of assessment is men (Fig. 34.1). Uterine overdistension causes
by ultrasonography. Two techniques are com- dyspnea by pushing the diaphragm upward.
monly used:
• Single deepest pocket (SDP)
• Amniotic fluid index (AFI)
Box 34.2 %NCUUKſECVKQPQHRQN[J[FTCOPKQU
Amniotic fluid index is more commonly used and • Mild (80%): Vertical pockets of 8–11 cm or AFI of 25–30
is more sensitive. The values can be affected by • Moderate (15%): Vertical pockets of 12–15 cm or AFI
differences in ultrasound techniques and pres- of 30–35
sure of transducer on the abdomen. Techniques • Severe (5%): Vertical pockets of >15 cm or AFI of >35;
for evaluation of AFV are described in Chapter 11, HTGGƀQCVKPIHGVWU
Antepartum fetal surveillance. A COPKQVKEƀWKFKPFGZ
CH 34_p495-507_v3.indd 496 18-07-2015 11:26:35

Disorders of Amniotic Fluid 497
Table 34.1 'VKQNQI[CPFRCVJQIGPGUKUQHRQN[J[FTCOPKQU
Etiology Pathogenesis
etal con itions
astrointestinal obstruction
• Esophageal atresia, duodenal atresia Inhibition of fetal swallowing
eurological anomalies
• Anencephaly • Inhibition of swallowing
• 6TCPUWFCVKQPHTQOGZRQUGFOGPKPIGU
• Lack of ADH from pituitary gland
• 5RKPCDKſFC • 6TCPUWFCVKQPHTQOGZRQUGFOGPKPIGU
• Myotonic dystrophy • Inhibition of swallowing
etal aneuploidy
• Trisomy 18, 21 • Inhibition of swallowing
• Intestinal abnormalities
onimmune hydrops
• win-to-twin transfusion syndrome
• Rh isoimmunization Increased urine output due to fetal anemia
• Parvovirus infection and cardiac failure
Alpha thalassemia Fetal anemia and cardiac failure
Bartter syndrome Polyuria due to renal hypokalemic alkalosis
aternal con itions
• Diabetes mellitus Polyuria due to fetal hyperglycemia
• diopathic No cause can be found
AD antidiuretic hormone.
Polyhydramnios usually develops gradually

but can be acute and very symptomatic.
Differential diagnosis
Differential diagnosis for polyhydramnios
includes multiple pregnancy, ovarian cyst with
pregnancy, and maternal ascites, all conditions
where the abdomen is overdistended. Acute
hydramnios must be differentiated from placen-
tal abruption with concealed hemorrhage.
%QORNKECVKQPU
Overdistension of the uterus leads to premature
uterine contractions and preterm labor. Sudden
release of fluid due to rupture of membranes
can cause placental abruption. In the presence
of overdistension, uterine contractions are poor,
Figure 34.1 Overdistended abdomen due to
leading to dysfunctional labor and postpartum
polyhydramnios. hemorrhage. Malpresentations and malpositions
are common. There is a considerably increased
Pedal, vulval, and abdominal wall edema result risk of operative vaginal delivery and cesarean
from uterine pressure on the inferior vena cava. sections due to malpresentations, malpositions,
Rarely, pressure on the ureter leads to oliguria. and hypotonic uterine action.
CH 34_p495-507_v3.indd 497 18-07-2015 11:26:35

Box 34.3 %
QORNKECVKQPUCUUQEKCVGFYKVJ Box 34.4 *
KUVQT[CPFRJ[UKECNGZCOKPCVKQP
RQN[J[FTCOPKQU KPRQN[J[FTCOPKQU
• Maternal • History
Ŧ Dyspnea, respiratory distress Ŧ Gradual or sudden abdominal distension
Ŧ Prelabor rupture of membranes Ŧ Dyspnea
Ŧ Preterm labor Ŧ Pedal/vulval edema
Ŧ Placental abruption Ŧ Tight feeling in the uterus
Ŧ Dysfunctional labor • 2J[UKECNGZCOKPCVKQP
Ŧ Operative vaginal delivery Ŧ Inspection
Ŧ Cesarean section Overdistended uterus
Ŧ Atonic postpartum hemorrhage Ŧ Palpation
• Fetal Uterine size larger than gestational age
Ŧ Macrosomia Uterus tense
Ŧ Chromosomal anomalies Fluid thrill
Ŧ Malpresentations Difficulty in palpation of fetal parts
Ŧ Malpositions Malpresentations
Ŧ Cord prolapse Ŧ Auscultation
Ŧ High perinatal mortality Muffled fetal heart sounds
Cord prolapse occurs because malpresenta- A comprehensive ultrasonographic evaluation

tions and malpositions prevent proper apposition is then performed to look for fetal gastrointestinal
of the presenting part in the lower uterine seg-
ment; with membrane rupture and sudden gush
of amniotic fluid, the cord slips past the present-
ing part.
Fetal macrosomia may be present due to asso-
ciated diabetes. Perinatal mortality is increased
two- to fivefold due to fetal congenital and chro-
mosomal anomalies, abruption, prematurity,
and operative delivery (Box 34.3).
Diagnosis
Diagnosis begins with history and physical
examination (Box 34.4). In acute hydramnios, a.
the woman complains of sudden abdominal dis-
tension. Pedal and vulval edema is usually pres-
ent. The uterus is overdistended, tense, and filled
with fluid. Fetal parts are difficult to palpate and
the fetus may be in transverse lie or other mal-
presentation. Fetal heart sounds are muffled and
fluid thrill can be elicited.
Investigations
The single most diagnostic evaluation is ultra-
sonography (Fig. 34.2). As discussed earlier, SDP
b.
(LVP) of >8 cm or AFI of >25 cm is used for confir- Figure 34.2 Polyhydramnios on ultrasonography.
mation of diagnosis (Fig. 34.2a). Once the diagno- a..CTIGRQEMGVUQHCOPKQVKEƀWKFYKVJHGVCNNKODUƀQCVKPI
sis is confirmed, classification into mild, moderate, KPƀWKFb. Polyhydramnios with an anencephalic fetus.
or severe polyhydramnios should be done. Photo courtesy: Mediscans Systems, Chennai.)
CH 34_p495-507_v3.indd 498 18-07-2015 11:26:35

anomalies, anencephaly (Fig. 34.2b), spina bifida, 0QPURGEKſEVTGCVOGPV

hydrops, signs of chromosomal anomalies, mul-
tifetal pregnancy, and twin-to-twin transfusion Idiopathic polyhydramnios is the most common
syndrome (TTTS). Amniocentesis or cordocen- and is managed with measures to relieve symp-
tesis for fetal karyotyping should be performed toms and prevent complications. Treatment
in the presence of structural abnormalities or if depends on the following:
chromosomal anomalies are suspected. • Severity of polyhydramnios
If hydrops is detected, it is important to • Gestational age
evaluate for immune or nonimmune causes. • Symptoms
Parvovirus infection and thalassemia can be
diagnosed from a fetal blood sample. il to mo erate polyhy ramnios
Glucose tolerance test should be ordered to These patients may be followed by serial ultra-
exclude maternal diabetes. sonography. The AFI stabilizes or normalizes in
Evaluation of polyhydramnios is shown in many women. In women with symptomatic mod-
Figure 34.3. erate polyhydramnios, hospitalization and indo-
methacin may occasionally be required (refer to
section Medical management on the next page).
Management
In most women with polyhydramnios, no cause 5GXGTGRQN[J[FTCOPKQU
is found; therefore management is directed at
relieving symptoms and optimizing timing of In women with severe polyhydramnios, man-
delivery. agement depends on gestational age.
)GUVCVKQPCNCIGYGGMU
5RGEKſEVTGCVOGPV • Decompression amniocentesis (amnioreduc-

tion) to reduce AFV to normal
If an etiological factor is identified, management • Indomethacin for maintenance of normal AFV
should address the specific cause. Maternal • Betamethasone 12 mg intramuscular every
diabetes should be well controlled. If the fetal 12 hours × 2 doses to accelerate pulmonary
anomaly is incompatible with life, for example, maturity
anencephaly, pregnancy should be terminated. • Serial monitoring of AFV by ultrasonography
If aneuploidies or other congenital anomalies • Deliver as close to term as possible
are diagnosed, the parents should be counseled
and neonatologists and pediatric surgeons )GUVCVKQPCNCIG YGGMU
consulted. • Deliver
Ultrasonography
LVP
nomalies
e ere hy ramnios Hy rops Multiple pregnancy ormal
Cor ocentesis
aryotyping ests for immune
clu e
est for par o irus infection nonimmune hy rops
halassemia
Figure 34.3 Evaluation of clinical polyhydramnios. A COPKQVKEƀWKFKPFGZ , glucose tolerance test; P, largest
vertical pocket; S, twin-to-twin transfusion syndrome.
CH 34_p495-507_v3.indd 499 18-07-2015 11:26:36

Amnioreduction Medical management

In moderate-to-severe polyhydramnios, removal Mild idiopathic polyhydramnios may respond to
of amniotic fluid (amnioreduction) may be medical therapy. In moderate-to-severe polyhy-
performed for decompression. This is bene- dramnios, amnioreduction is performed before
ficial when the woman is symptomatic, the starting medical therapy.
hydramnios is severe or in TTTS. Medical ther-
apy with indomethacin is more effective after In omethacin
amnioreduction. Indomethacin is a prostaglandin synthetase
inhibitor (Box 34.6). When administered to
roce ure mothers, it crosses the placenta and reduces
• Ultrasonography is performed to locate the fetal renal blood flow and urine output and also
placenta and to choose the site of amniocen- stimulates fetal vasopressin secretion. This in
tesis, avoiding the placenta. turn reduces the AFV since fetal urine produc-
• The selected area of the abdomen is painted tion is an important source of amniotic fluid.
and draped. Dosage and side effects of indomethacin are
• Local anesthetic is infiltrated. listed in Box 34.6.
• An 18-gauge spinal needle is inserted into Amniotic fluid volume should be monitored
the amniotic fluid in the lower quadrants to closely since oligohydramnios may develop.
allow for decrease in uterine size as the fluid Closure of fetal ductus arteriosus and fetal
is removed. renal compromise are major side effects. As the
• A sterile tubing with a three-way stopcock is risk of these problems increases dramatically
attached to the hub of the needle and the other after 32–34 weeks, the drug should not be used
end of the tube to a vacuum suction bottle or beyond 34 weeks’ gestation. Indomethacin is
other suction device. It should not be allowed also used as a tocolytic.
to drain by gravity alone.
• Fluid can be removed as rapidly as possible. Sulin ac
Enough fluid is removed to achieve an SDP of Sulindac is a nonsteroidal anti-inflammatory
8 cm or AFI of 15 cm. However, not more than agent. It also reduces the AFV and has less
5 L is removed at one sitting. effect on fetal ductus arteriosus. Its usefulness
• If the fluid stops draining, the needle tip is in polyhydramnios has not been adequately
adjusted. evaluated.
• The fetal heart beat is documented at the end
of the procedure.
• Antibiotics and tocolytics are not required.
Amniotic fluid volume should be monitored Box 34.6 +PFQOGVJCEKPKPRQN[J[FTCOPKQU
weekly following amniocentesis. If fluid accu- • Prostaglandin synthetase inhibitor
mulates again, the procedure may have to be • Mechanism of action
repeated. Ŧ Stimulates fetal vasopressin production
Ŧ Reduces fetal urine production
Complications o amniocentesis • Dosage
Complications of amniocentesis are listed in Ŧ 25 mg four times daily, oral
Ŧ Can increase to 2–3 mg/kg/day
Box 34.5.
• Maternal side effects
Ŧ Nausea, gastritis, vomiting
Ŧ Oligohydramnios
• Fetal complications
Box 34.5 %QORNKECVKQPUQHCOPKQEGPVGUKU
Ŧ Closure of ductus arteriosus
• Preterm labor If used for >48 hours
• Prelabor rupture of membranes Worsens with advancing gestation
• Placental abruption Ŧ Renal damage and renal failure
• Intra-amniotic infection (rare) • Should not be used after 32–34 weeks’ gestation
CH 34_p495-507_v3.indd 500 18-07-2015 11:26:36

Timing of delivery must be performed as soon as membranes rup-

ture. Hypotonic uterine dysfunction is common
Women with mild or moderate polyhydramnios and oxytocin augmentation may be required.
can be delivered at term. If hydramnios is severe, Prophylactic uterotonics must be used in
planned delivery with abdominal decompres- the third stage to prevent atonic postpartum
sion at 37 weeks is safer. Preinduction cervical hemorrhage.
ripening with prostaglandins (PG) and labor Management of polyhydramnios is summa-
induction with oxytocin can be used if needed rized in Figure 34.4.
and are certainly not contraindicated.
Management of labor ligohydramnios

Fetal lie and presentation must be checked to
ensure vertex presentation. Sudden decompres-
sion due to spontaneous rupture of membranes
&GſPKVKQP
can cause placental abruption or cord prolapse. Oligohydramnios is defined as reduced amni-
Therefore, gradual decompression by amnio- otic fluid as evidenced by an AFI of <5 cm or
centesis or controlled amniotomy by needle SDP <2 cm. An AFI between 5 and 8 cm is con-
puncture is recommended. Pelvic examination sidered borderline/low normal AFV.
Mil to mo erate
e ere polyhy ramnios
polyhy ramnios
Monitor PP
Me ical management ee s ee s
as re uire
Me ical mangement Confirm pulmonary

eli er at term ecompression by maturity
amniocentesis
Monitor PP
eli er
eli er at ee s
Confirm erte
presentation
mniocentesis or
controlle
amniotomy
ugment ith o ytocin if re uire

Prophylactic o ytocin units V infusion
in thir stage
Figure 34.4 Management of polyhydramnios. BPPDKQRJ[UKECNRTQſNG S nonstress test.
CH 34_p495-507_v3.indd 501 18-07-2015 11:26:36

Incidence In the first trimester, oligohydramnios or

reduced gestational sac fluid may occur but the
The incidence of idiopathic oligohydramnios at etiology is usually unknown. The criterion for
term is 11%–12%. Beyond 41 weeks, AFI decreases diagnosis is a difference of <5 mm between the
by 25% per week. In conditions causing placental mean gestational sac size and the crown-rump
insufficiency, the incidence is much higher. length. Reduced fluid prior to 10 weeks is gener-
ally associated with a poor outcome.
In the second trimester, the common causes
'VKQNQI[CPFRCVJQIGPGUKU of oligohydramnios are chromosomal and con-
Conditions that reduce fetal urine production genital anomalies, rupture of membranes, pla-
result in oligohydramnios. This may occur due cental abruption, and fetal growth restriction.
to renal agenesis or outflow obstruction in the Oligohydramnios can also be idiopathic. An
fetal urinary tract. Chromosomal anomalies elevated maternal serum alpha fetoprotein in
and polycystic kidneys are also associated with association with oligohydramnios carries a poor
oligohydramnios. Decreased renal blood flow prognosis.
in fetal growth restriction and placental insuffi- In the third trimester, oligohydramnios is
ciency result in decreased urine output and oli- usually due to fetal growth restriction, placental
gohydramnios. Postterm pregnancy and rupture insufficiency, prelabor rupture of membranes, or
of membranes are common causes. Maternal postmaturity.
dehydration also results in reduced AFV as seen
in hot summer months. Maternal ingestion of %QORNKECVKQPUCPFQWVEQOG
prostaglandin synthetase inhibitors (ibuprofen,
indomethacin, nimesulide) can result in oligohy- Perinatal mortality is increased in the presence
dramnios. Causes of oligohydramnios are listed of oligohydramnios. This can be due to the caus-
in Box 34.7. ative factors or the effects of reduced AFV. All the
maternal and fetal conditions that cause oligohy-
dramnios such as congenital anomalies, chromo-
somal defects, fetal growth restriction, placental
Box 34.7 Causes of oligohydramnios insufficiency, and postmaturity are associated
with an increase in perinatal mortality.
• Maternal
In addition, the reduction in AFV in the second
Ŧ Prelabor rupture of membranes
Ŧ Postterm pregnancy
trimester leads to skeletal deformities, contrac-
Ŧ 2NCEGPVCNKPUWHſEKGPE[ tures, and amniotic bands. Pulmonary hypopla-
Preeclampsia sia is a common problem when oligohydramnios
Pregestational diabetes occurs in the second trimester. The pathogenesis
Ŧ Placental abruption has been postulated to be thoracic compression,
Ŧ Dehydration lack of fetal breathing movements, and failure to
• Fetal retain intrapulmonary amniotic fluid. The prog-
Ŧ Fetal growth restriction nosis is poor with pulmonary hypoplasia.
Ŧ Twin-to-twin transfusion In the third trimester, adverse outcome is
Ŧ Congenital anomalies due to cord compression, meconium aspiration,
Renal agenesis
fetal heart rate abnormalities, or fetal hypoxia.
Outflow obstruction to urinary tract
Maternal complications include chorioamnioni-
Polycystic kidneys
Ŧ Chromosomal anomalies tis due to prelabor rupture of membranes, higher
Triploidy risk of labor induction, instrumental delivery,
Trisomy 18 and cesarean section. Maternal and fetal com-
Turner syndrome plications are listed in Box 34.8.
• Drugs Outcome is poorer when oligohydramnios
Ŧ Prostaglandin synthetase inhibitors occurs earlier in pregnancy. First trimester
Ŧ ACE inhibitors reduction in fluid volume results in sponta-
• Idiopathic neous miscarriage in 95% of women. Severe sec-
AC , angiotensin-converting enzyme. ond trimester oligohydramnios results in fetal
CH 34_p495-507_v3.indd 502 18-07-2015 11:26:36

Box 34.8 /
CVGTPCNCPFHGVCNEQORNKECVKQPU Diagnosis
in oligohydramnios
istory
• Maternal
Ŧ Chorioamnionitis When reduced AFV is suspected clinically, his-
Ŧ Induction of labor tory of rupture of membranes, watery discharge,
Ŧ Instrumental delivery uterine contractions, hypertension, and history
Ŧ Cesarean section suggestive of antiphospholipid antibody syn-
• Fetal drome should be asked for.
Ŧ Due to etiological factors
Congenital anomalies
Chromosomal abnormalities Physical examination
Fetal growth restriction
Blood pressure should be checked to exclude
Intrauterine death
hypertension/preeclampsia. Obstetric examina-
Intrauterine infection following ROM
Prematurity
tion reveals uterine size less than what is appro-
Ŧ Due to reduced AFV priate for gestational age. The uterus may be
Skeletal deformities felt hugging the fetus with very little amni-
Contractures otic fluid surrounding the fetus. (Box 34.9).
Amniotic bands and autoamputation Speculum examination may reveal watery or
Pulmonary hypoplasia blood-stained discharge in the presence of rup-
Umbilical cord compression tured membranes.
Meconium aspiration
Fetal heart rate abnormalities
Low Apgar scores Box 34.9 *
KUVQT[CPFRJ[UKECNGZCOKPCVKQP
Intrapartum death in oligohydramnios
A COPKQVKEƀWKFXQNWOG rupture of membranes. • History
Ŧ Watery/blood-stained vaginal discharge
Ŧ Hypertension
Ŧ Preeclampsia
or neonatal death in 80%. Oligohydramnios in Ŧ Pregestational hypertension
the third trimester is associated with higher Ŧ Antiphospholipid antibody syndrome
cesarean section rates, low Apgar scores, and Ŧ Family history
hypoxic ischemic encephalopathy. Perinatal Congenital anomalies
mortality is 15%. Chromosomal abnormalities
Ŧ Medications
ACE inhibitors
Prostaglandin synthetase inhibitors
Clinical features • 2J[UKECNGZCOKPCVKQP
Oligohydramnios is usually suspected when Ŧ Blood pressure
the uterine size is less than what is appropri- Ŧ Uterine size less than gestational age
ate for the gestational age. Women with prela- Ŧ 4GFWEGFCOPKQVKEƀWKFQPRCNRCVKQP
bor rupture of membranes may present with • 5RGEWNWOGZCOKPCVKQP
Ŧ Watery/blood-stained discharge
history of vaginal discharge. In women pre-
Ŧ 2QQNKPIQHƀWKFKPVJGRQUVGTKQTHQTPKZ
senting with hypertension, preeclampsia, ges-
tational age >40 weeks, and other maternal AC , angiotensin-converting enzyme.
risk factors for placental insufficiency, ultra-

sonography should be performed to look for
oligohydramnios.
Investigations
Ultrasonography should be performed to
Differential diagnosis confirm the diagnosis and to estimate AFI
Differential diagnosis includes wrong dates and (Fig. 34.5). If oligohydramnios is confirmed,
fetal growth restriction. targeted ultrasonography is recommended to
CH 34_p495-507_v3.indd 503 18-07-2015 11:26:36

watery discharge, microscopic examination of

vaginal swab for ferning or detection of vaginal
pH of >7.5 by nitrazine test will confirm rupture
of membranes (see Chapter 36, Prelabor rup-
ture of the membranes). Management is as for
preterm prelabor rupture of membranes.
Management
Management depends on the gestational age at
diagnosis, the cause of oligohydramnios, and
fetal prognosis.
Figure 34.5 Oligohydramnios on ultrasonography. Only
VYQUOCNNRQEMGVUQHCOPKQVKEƀWKF
YJKVGCTTQYUCTGUGGP First trimester
(Photo courtesy: Mediscan Systems, Chennai.)
If reduced gestational sac fluid is found in the first
trimester, the woman should be counseled regard-
detect fetal anomalies such as renal agenesis, ing the risk of spontaneous miscarriage. Follow-up
polycystic kidneys, outflow obstruction, mark- with serial ultrasonography is recommended.
ers of chromosomal abnormalities, and fetal
growth restriction. Doppler ultrasonography of
Second trimester
renal arteries may confirm renal agenesis. Fetal
MRI can also be used to confirm diagnosis. If Since prognosis is poor in second trimester oligo-
structural anomalies are detected, fetal blood hydramnios, counseling is important. The under-
sampling and karyotyping are recommended. lying cause should be determined. Amnioinfusion
The placenta should be localized and abruption may be required to visualize the fetus on ultra-
should be ruled out (Fig. 34.6). sonography and perform proper evaluation.
If there is history of watery vaginal discharge, Termination of pregnancy is recommended if
rupture of membranes must first be excluded the fetal anomaly is lethal. Follow-up with serial
by speculum examination. If there is no obvious ultrasonography is recommended for others.
Clinical iagnosis
of oligohy ramnios
Ultrasonography
Chromosomal etal gro th Placental History of aginal

Congenital anomalies
anomalies restriction abnormalities ischarge
peculum
urther e aluation by Cor ocentesis Maternal e aluation ollo up
e amination
M renal artery oppler aryotyping etal sur eillance an eli er
clu e M
Figure 34.6 Evaluation of oligohydramnios. A COPKQVKEƀWKFKPFGZ , rupture of membranes.
CH 34_p495-507_v3.indd 504 18-07-2015 11:26:36

Third trimester • Rarely, in preterm prelabor rupture of mem-

branes, after the leak is sealed
Management depends on the cause of
oligohydramnios. Procedure
• Ultrasonography is performed to localize the
• Postterm pregnancy with reduced AFI should
placenta and identify a pocket of amniotic fluid.
be delivered.
• The abdomen is painted and draped.
• If the fetus is growth restricted, manage-
• A 20-g needle is inserted, taking care to avoid
ment should be directed toward the underly-
fetal parts.
ing maternal condition. The fetus should be
• The needle is connected to sterile tubing, a
monitored by serial ultrasonography com-
three-way stopcock, and a 50-mL syringe.
bined with umbilical and middle cerebral
• Normal saline is injected under ultrasound
artery Doppler. Delivery should be dictated
guidance till normal AFV is achieved.
by fetal condition.
• Antibiotics are not recommended. Anti-D
• Women with preterm prelabor rupture of
globulin must be administered to Rh-negative
membranes should be managed conserva-
women.
tively till 34 weeks with close monitoring
and delivered if leakage of fluid persists (see In women with preterm prelabor rupture of
Chapter 36, Prelabor rupture of membranes). membranes, if the leakage stops spontaneously,
pulmonary hypoplasia can be prevented and
Women with idiopathic oligohydramnios should
outcome improved with amnioinfusion.
be observed and monitored by nonstress test,
serial ultrasonography, and biophysical profile.
Timing of delivery
5RGEKſEOGCUWTGUVQKPETGCUG When an etiological factor is detected, timing
AF of delivery is guided by the specific condition
such as preeclampsia, growth restriction, or fetal
aternal hy ration anomaly. Pregnancies with idiopathic oligo-
Review of randomized trials has shown that hydramnios are delivered at 38 weeks or when
oral hydration with 1500–2000 mL of fluid per there is nonreassuring fetal status.
day increases AFV. This is particularly useful in
women with dehydration and in hot summer
months. Intravenous infusion of hypotonic fluid Management of labor
has also been found to be useful but the effect is
similar to oral hydration. Close monitoring is essential in labor. Electronic
fetal monitoring is recommended. Membranes
Amnioin usion should be ruptured when the woman enters active
Amnioinfusion refers to the instillation of fluid phase of labor, to look for meconium. If meco-
into the amniotic cavity, either abdominally or nium staining and/or fetal heart decelerations
transcervically. Transcervical amnioinfusion are present, transcervical amnioinfusion should
is usually performed in labor and is discussed be considered (see Chapter 17, Intrapartum fetal
in Chapter 17, Intrapartum fetal surveillance. surveillance). If fetal heart rate abnormalities
Abdominal amnioinfusion is performed in the persist, immediate cesarean section is indicated.
second trimester: Management of oligohydramnios is outlined in
Figure 34.7.
• To facilitate visualization of anomalies on
ultrasonography
CH 34_p495-507_v3.indd 505 18-07-2015 11:26:36

Management of oligohy ramnios
irst trimester econ trimester hir trimester
Counsel Counsel
erial scans clu e anomalies ro th
Postterm P M iopathic
clu e PP M restriction
erial scans
Consi er amnioinfusion
Maternal hy ration
erial PP
Lea age persists etal

ee s
or ee s compromise
eli er
Figure 34.7 Management of oligohydramnios. BPPDKQRJ[UKECNRTQſNG S nonstress test; PP , preterm prelabor

rupture of membranes.
-G[RQKPVU
• #OPKQVKEƀWKFUWTTQWPFUVJGHGVWUHTQOGCTN[RTGIPCP- • Polyhydramnios may be suspected clinically and is
cy. Changes that affect the production or clearance EQPſTOGFD[WNVTCUQPQITCRJ[YJKEJKUVJGUKPINGOQUV
QHCOPKQVKEƀWKFECPCHHGEVVJGCOPKQVKEƀWKFXQNWOG important diagnostic evaluation. Congenital and chro-
(AFV) drastically. mosomal anomalies of the fetus and other causative
factors should also be evaluated on ultrasonography.
• Evaluation of AFV is by ultrasonography. Single deepest
RQEMGVCPFCOPKQVKEƀWKFKPFGZCTGVJGVGEJPKSWGUWUGF • Management consists of amnioreduction in acute and
• 'ZEGUUKXG#(8KUMPQYPCUpolyhydramnios. It may be severe cases and indomethacin in moderate hydram-
mild, moderate, or severe. nios <34 weeks.
• Polyhydramnios is caused by conditions that inhibit • Mild-to-moderate polyhydramnios should be deliv-

fetal swallowing and conditions that increase fetal GTGFCVVGTODWVUGXGTGJ[FTCOPKQUTGSWKTGURNCPPGF
urine production. delivery at 37 weeks. Amniocentesis or controlled am-
PKQVQO[KUTGSWKTGFVQRTGXGPVEQORNKECVKQPUKPNCDQT
• Polyhydramnios is most often idiopathic. The com-
mon causes are fetal gastrointestinal tract obstruc- • 4GFWEGFCOPKQVKEƀWKFKUMPQYPCUoligohydramnios.
tion, neurological anomalies such as anencephaly, • Oligohydramnios is caused by conditions that reduce
chromosomal anomalies, and maternal diabetes. urine output such as renal agenesis, placental insuf-
• Women with polyhydramnios present with overdisten- ſEKGPE[RQUVOCVWTKV[RTGVGTORTGNCDQTTWRVWTGQH
sion of abdomen. It may be chronic or acute. membranes, and chromosomal anomalies.
• Polyhydramnios is associated with maternal and fetal • Oligohydramnios in the second trimester has
complications. poor prognosis due to the high risk of pulmonary
(Continued)
CH 34_p495-507_v3.indd 506 18-07-2015 11:26:37

-G[RQKPVU Continued
hypoplasia, skeletal malformations, and fetal • Oligohydramnios in the second trimester should be
anomalies. followed up with serial scans after counseling.
• Cord compression, meconium aspiration, and fetal • Oligohydramnios in the third trimester should be
J[RQZKCCTGVJGRTQDNGOUGPEQWPVGTGFKPVJGVJKTF initially treated by maternal oral hydration. Fetal
trimester. suveillance includes nonstress test and biophysical
• When oligohydramnios is clinically suspected, ultra- RTQſNG6JGYQOCPUJQWNFDGFGNKXGTGFFGRGPFKPI
UQPQITCRJ[UJQWNFDGRGTHQTOGFVQEQPſTOFKCIPQUKU on the level of fetal jeopardy (when the tests become
and determine the cause. abnormal).
• Management depends on gestational age and cause
of oligohydramnios.
Self-Assessment
4. a. 7NVTCUQPQITCRJ[VQGZENWFGNGVJCNCPQOCNKGU
Case-based questions such as anencephaly, other anomalies such as
esophageal atresia, placental localization; GTT for
Case 1 diabetes.
Mrs. DA, 30, multigravida, was referred from a primary b. Amnioreduction to relieve respiratory distress.
health center. She was 31 weeks’ pregnant and com- c. Close follow-up and planned delivery at 37 weeks.
RNCKPGF QH FKHſEWNV[ KP DTGCVJKPI *GT CDFQOGP NQQMGF
tense and overdistended.
Case 2
2. How will you evaluate this woman? 1. Wrong dates, fetal growth restriction, oligohydram-
3. 9JCVEQORNKECVKQPUFQ[QWGZRGEV! nios.
4. How will you manage her condition? 2. *KUVQT[CPFTGXKGYQHRTGXKQWUUECPUVQEQPſTO
FCVGUDNQQFRTGUUWTGCPFWTKPGRTQVGKPVQGZENWFG
preeclampsia; ultrasonography to look for fetal
Case 2 growth restriction and oligohydramnios. If oligo-
hydramnios is diagnosed, targeted scan for fetal
Mrs. PM, 28, primigravida, came for routine antenatal anomalies.
EJGEMWRCVYGGMUŏIGUVCVKQP#DFQOKPCNGZCOKPCVKQP 3. If no fetal anomaly is detected and there is no growth
revealed uterus corresponding to 28 weeks’ gestation. restriction, mother should be given oral hydration. Fe-
1. What is the provisional diagnosis? tus should be monitored with weekly NST and BPP.
Deliver at 38 weeks if there is no complication. If not,
2. How will you evaluate her?
deliver when the tests become abnormal.
4. Electronic fetal monitoring, early amniotomy to look
4. How will you manage her in labor?
for meconium, cesarean section if fetal status is
nonreassuring.
#PUYGTU
Case 1
5CORNGSWGUVKQPU
1. Acute polyhydramnios. Placental abruption must be .QPICPUYGTSWGUVKQP
GZENWFGF
1. Discuss the etiology, clinical features, and
2. a. History of bleeding, abdominal pain, and reduced management of polyhydramnios.
fetal movements—for placental abruption.
b. %
NKPKECNGZCOKPCVKQPōƀWKFVJTKNNFKHſEWNV[KPRCNRCVKQP
QHHGVCNRCTVUOCNRTGUGPVCVKQPOWHƀGFJGCTVUQWPFU 5JQTVCPUYGTSWGUVKQPU
3. a. Maternal complications—preterm labor, prelabor
rupture of membranes, dysfunctional labor, atonic 1. Acute polyhydramnios
postpartum hemorrhage, cesarean section, instru- 2. Oligohydramnios in second trimester
mental delivery, placental abruption. 3. #OPKQVKEƀWKFKPFGZ
b. Fetal complications—anomalies, malpresenta- 4. Amnioreduction for polyhydramnios
tions, cord prolapse. 5. Amnioinfusion
CH 34_p495-507_v3.indd 507 18-07-2015 11:26:37

Preterm Labor
35 and Birth
Case scenario
Mrs. VC, 29, gravida 3, para 2, had two preterm births and her previ-
ous babies were delivered at 36 and 34 weeks. The second one needed
admission to the newborn nursery due to complications of prematurity.
At 33 weeks, she was admitted with mild uterine contractions.
Preterm labor leading to preterm birth (PTB) is a Preterm labor is defined as the presence of
major clinical problem, especially in developing uterine contractions of sufficient frequency
countries that have limited resources to handle and intensity to result in progressive efface-
the problems of the premature neonate. Globally, ment and dilatation of the cervix, between fetal
every year, an estimated 15 million babies are born viability and 37 weeks.
preterm and more than 1 million deaths are directly Fetal viability may be defined as gestational
attributable to preterm birth (before 37 completed age between 20 and 28 weeks’ gestation, depend-
weeks of gestation). This number is rising. ing on the facilities available and the prevailing
Preterm birth is a major contributor to neona- neonatal survival rate. In developed countries,
tal mortality and morbidity and has long-term 20 weeks is considered to be a viable gestational
adverse consequences for health. In comparison age, whereas in India, 28 weeks would be accept-
to children born at term, children who are born able. Those between 24 and 28 weeks may be
prematurely have a higher risk of cerebral palsy, described as being at the threshold of viability,
sensory deficits, learning disabilities, and respi- but survival depends on institutional neonatal
ratory illnesses. Complications related to pre- care facilities.
term birth are the leading cause of death among The classification of preterm birth can be by
children younger than 5 years of age. gestational age at birth or birth weight (Box 35.1).
CH 35_p508-521_v3.indd 508 18-07-2015 11:43:19

Preterm Labor 509
Box 35.1 %NCUUKſECVKQPQHRTGVGTODKTVJ Previous miscarriages

• By gestational age at birth Previous spontaneous miscarriages, especially if
Ŧ Extremely preterm: <28 weeks recurrent and in the second trimester, are associ-
Ŧ Very preterm: 28 to <32 weeks ated with an increased risk of preterm labor.
Ŧ Moderate to late preterm: 32 to <36+6 weeks There is a small but significant increase in risk
• By birth weight with prior induced abortion as well.
Ŧ Low birth weight (LBW): <2500 g
Ŧ Very low birth weight (VLBW): <1500 g
Ŧ Extremely low birth weight (ELBW): <1000 g Demographic factors
Demographic factors for preterm labor include
extremes of maternal age (<17 or >35 years), low
Incidence socioeconomic status, and low prepregnancy
weight.
The rate of preterm births ranges from 5% to
18% globally. Currently the rate of preterm
births in India is approximately 20%. According
Lifestyle issues
to the World Health Organization (WHO), India Inadequate maternal weight gain, obesity, smok-
has the greatest number of preterm births in the ing, stress, excessive physical activity, and psy-
world (approximately 3.6 million). This includes chological factors have also been implicated.
spontaneous and iatrogenic (induced) preterm
births. The incidence has been rising, largely terine overdistension
due to
Multiple pregnancy or polyhydramnios causing
• increase in assisted reproductive technology; uterine overdistension may precipitate preterm
• increase in multiple pregnancies; and birth. Excessive uterine stretch due to overdis-
• increase in preterm labor inductions. tension causes activation of the endocrine cas-
cade responsible for initiation of labor. Multiple
Prematurity is one of the leading causes of gestation accounts for almost 25% of preterm
perinatal mortality and morbidity in India, as in births under 32 weeks. A prior preterm twin birth
other countries. is associated with an increased risk of preterm
birth in a subsequent singleton pregnancy.
isk factors for aginal bleeding

preterm labor Vaginal bleeding in the first and second trimes-
ters, especially recurrent episodes, is associated
Many preterm births occur among women with
with an increased risk of preterm birth. Placenta
no risk factors. This makes it difficult to specifi-
previa and placental abruption in the late third
cally prove the cause of preterm labor. However,
trimester are associated with vaginal bleeding
the following are known risk factors and may
and frequently lead to preterm birth.
predict PTB.
Infections
Prior preterm labor Malaria is associated with preterm birth, low
Prior preterm labor is the strongest risk factor for birth weight, and neonatal morbidities. Treatment
future preterm birth. The risk of preterm birth of maternal malaria decreases the risk.
increases two-fold with every subsequent pre- Genital tract infections by Mycoplasma hom-
term delivery. Preterm births tend to occur at the inis, Ureaplasma urealyticum, and bacterial
same gestational age as the previous birth. A vaginosis have been implicated, but treatment
spontaneous preterm birth before 34 weeks is for any of these potential risk factors has not
the best predictor for recurrence of early spon- been shown to result in a decreased risk of pre-
taneous preterm birth. term birth.
CH 35_p508-521_v3.indd 509 18-07-2015 11:43:19

Chorioamnionitis is an important cause of Fetal factors

preterm labor. The infection is often subclinical
and amniotic fluid cultures may be negative. It is Fetal growth restriction and congenital anoma-
possible that the bacteria have invaded the lies of the fetus are associated with increased risk
maternal tissues but not entered the amniotic of preterm labor.
fluid. The endotoxins stimulate uterine contrac-
tions through release of cytokines. Periodontal disease
Asymptomatic bacteriuria and urinary tract
infections (UTIs), especially pyelonephritis, Although a causative relationship between peri-
have been implicated in the causation of preterm odontal disease and preterm labor has not been
birth. established, treatment of periodontal disease
has been shown to reduce the risk of preterm
labor.
Cervical and uterine factors
Short cervi Maternal medical disorders
A short cervix on ultrasound examination at Planned preterm birth may occur in situations
16–28 weeks’ gestation is predictive of preterm where maternal medical disorders such as anti-
birth. Since cervical shortening (effacement) phospholipid antibody syndrome, hypertensive
precedes labor, a high Bishop score on digital disorders, or diabetes necessitate the early deliv-
examination is also indicative of risk for preterm ery of a fetus that is unable to tolerate the intra-
birth. Cervical length screening is discussed later uterine environment. Other medical conditions
in this chapter. such as asthma and seizure disorder have also
been implicated in the increased risk of preterm
Cervical surgery labor.
Ablative and excisional procedures on the cervix The risk factors for preterm birth are listed in
can lead to late miscarriage and preterm birth. Box 35.2.
When planning cervical surgery on women in
the childbearing age group, the consequences
of extensive surgery should be kept in mind and
the least amount of intervention should be
Complications of
undertaken. prematurity in the neonate
terine abnormalities Complications resulting from prematurity con-
Preterm labor is associated with unicornuate tribute to the higher rate of infant mortality
uterus and uterine duplication abnormalities and morbidity in preterm infants, compared
(uterus didelphys, bicornuate uterus, septate with that in infants born at term. The greater
uterus). A large fibroid distorting the cavity may the immaturity, the greater is the risk of
also result in preterm birth. Women who have complications.
preterm birth due to uterine septum, bicornuate Complications of the premature infant are
uterus, or large fibroids will have a good response divided into the following:
to surgical correction of the abnormality.
• Short-term complications in the neonatal
period
Pregnancies following assisted • Long-term sequelae in neonates who survive
reproductive techniques and are discharged from the neonatal inten-
sive care unit (NICU; Box 35.3).
Preterm labor is more common in pregnan-
cies conceived after induction of ovulation, in The neonatal complications of prematurity
vitro fertilization, and donor or frozen embryo are discussed in Chapter 24, Common problems
transfer. of the newborn.
CH 35_p508-521_v3.indd 510 18-07-2015 11:43:20

Preterm Labor 511
Box 35.2 isk factors for preterm birth Box 35.3 eonatal complications of prematurity
• Prior preterm labor • Immediate or short-term complications in the neona-
Ŧ Strongest predictor tal period
<34 weeks Ŧ Hypothermia
Ŧ Risk increased twofold Ŧ Respiratory abnormalities
Ŧ Usually occurs at the same gestational age Ŧ Cardiovascular abnormalities
Ŧ Risk increased with increasing number of preterm Ŧ Intracranial hemorrhage
births Ŧ Hypoglycemia
• Prior miscarriage Ŧ Necrotizing enterocolitis
Ŧ Spontaneous Ŧ Infection
Recurrent, second trimester Ŧ Retinopathy of prematurity
Ŧ Induced • Long-term sequelae in neonates who survive and are
discharged from the NICU
• Demographic factors
Ŧ Neurodevelopmental disabilities such as cerebral
Ŧ Maternal age <17 or >35 years
palsy
Ŧ Low socioeconomic status
Ŧ Increase in infant mortality
Ŧ Low prepregnancy weight
• Uterine overdistension C neonatal intensive care unit.
Ŧ Multiple pregnancy
Ŧ Polyhydramnios
• Vaginal bleeding
Ŧ Recurrent episodes
Ŧ Placenta previa
Assessment of risk
Ŧ Placental abruption of preterm birth during
• Infections
Ŧ Malaria pregnancy
Ŧ Genital tract infections
Ŧ Asymptomatic bacteriuria/UTI (pyelonephritis) Since most women who have preterm birth do
• Cervical factors not have any risk factors, it is difficult to antici-
Ŧ Short cervix pate them. However, certain factors may be
Ŧ Previous cervical surgery assessed in women who are at risk for preterm
• Uterine abnormalities birth (Box 35.4).
Ŧ Unicornuate uterus
Ŧ Uterine duplication abnormalities
Uterus didelphys
Bicornuate uterus Box 35.4 Assessment of the risk of preterm
Ŧ Septate uterus
birth during pregnancy
Ŧ .CTIGſDTQKFFKUVQTVKPIVJGECXKV[ • History
• Pregnancies following assisted reproductive tech- Ŧ Prior preterm birth
niques Ŧ Gestational age at which it occurred
• Fetal factors Ŧ Prior cervical surgery
Ŧ Fetal growth restriction Ŧ Known uterine abnormalities
Ŧ Congenital anomalies Ŧ Other risk factors listed in Box 35.1
• Periodontal disease • Physical examination
• Maternal medical disorders Ŧ General examination
Ŧ Antiphospholipid antibody syndrome Ŧ Estimation of body mass index
Ŧ Hypertensive disorders Ŧ Vaginal examination
Ŧ Diabetes Ŧ Cervical tears
Ŧ Obesity Ŧ Scarred cervix
Ŧ Chronic bronchitis and asthma Ŧ Short cervix
Ŧ Seizure disorder • Cervical length screening
Ŧ Ultrasonography
urinary tract infection.
CH 35_p508-521_v3.indd 511 18-07-2015 11:43:20

Cervical length screening >25 mm at 24–28 weeks, the risk of preterm birth
is extremely low.
The risk of spontaneous preterm birth increases
as cervical length decreases. The risk is highest
when a short cervix is detected before 24 weeks’
Measuring cervical length
gestation. by ultrasound
Routine assessment of cervical length by ultra- Transvaginal ultrasound examination is per-
sound is not recommended in singleton pregnan- formed to measure cervical length (Fig. 35.1).
cies in low risk women, that is, women who have Transvaginal ultrasound is reproducible,
not had a prior preterm birth. It is only indicated dependable, and a very sensitive approach to
in the presence of certain risk factors (Box 35.5). measuring cervical length. The woman’s bladder
In women who have had a previous preterm should be empty for the TVUS. Transabdominal
birth, cervical length assessment may be done ultrasound (TAUS) examination is not reliable
serially from the 16th to 28th week of gestation to for the detection of a short cervix.
decide whether there is risk of recurrence of The cervix is measured from the internal os to
preterm birth in the current pregnancy. Cervical the external os (Fig. 35.1a and 35.1b). If the inter-
length assessment may also be done when a nal os is open (Fig. 35.2), cervical length is mea-
woman is admitted with suspected preterm labor. sured from the tip of the funnel to the external os
(Box 35.6).
&GſPKVKQPQHUJQTVEGTXKZ
The diagnosis of a short cervix is made when
cervical length on transvaginal ultrasound
(TVUS) at 16–28 weeks’ gestation is
• d20 mm in women with no prior preterm
delivery
• <25 mm in women with a prior preterm
delivery
Cervical length <25 mm between 16 and 28
weeks’ gestation by TVUS examination is reliably
associated with an increased risk of spontaneous
preterm birth. On the other hand, if the cervix is
a.
Box 35.5 Indications for cervical length

assessment
• Previous preterm labor
• History of cervical surgery
Ŧ LEEP
Ŧ Amputation/Fothergill’s surgery
Ŧ Conization
• 4GEWTTGPVDNGGFKPIKPſTUVQTUGEQPFVTKOGUVGT
• Uterine overdistension
Ŧ Multifetal pregnancy
Ŧ Polyhydramnios
• Uterine anomalies
Ŧ Unicornuate uterus b.
Ŧ Septate uterus Figure 35.1 Measurement of the cervix with transvaginal
Ŧ Bicornuate uterus ultrasonography. a. The length of the cervix measured from
• Pregnancies following ART the internal os to the external os is 34.3 mm at 19 weeks
A assisted reproductive technique; P loop electrosurgical (normal). b. A short cervix measuring 20.3 mm at 24
excision procedure. weeks. (Photo courtesy: Mediscan Systems, Chennai.)
CH 35_p508-521_v3.indd 512 18-07-2015 11:43:20

Preterm Labor 513
Interventions with no proven

DGPGſV
Several strategies have been tried without evi-
dence of success in the prevention of preterm
labor (Box 35.7).
+PVGTXGPVKQPUYKVJRTQXGPDGPGſV
Some interventions that have proved to be
effective in preventing preterm birth are listed
in Box 35.8.
Figure 35.2 Transvaginal ultrasonography of a cervix Diagnosis an treatment
demonstrating funneling of the amniotic membrane
protruding into the internal os and shortened cervical
o asymptomatic bacteriuria
length of 21.5 mm. (Photo courtesy: Mediscan Systems, Pregnant women with asymptomatic bacteriuria
Chennai.). should be treated with antibiotics to reduce the
risk of preterm birth. Women with recurrent
UTIs, diabetes mellitus, or underlying renal dis-
Box 35.6 Measurement of cervical length ease are at high risk for asymptomatic bacteri-
• TVUS used uria and should be screened regularly during
Ŧ Reproducible pregnancy.
Ŧ Dependable
Ŧ Sensitive Cervical cerclage
• TAUS not reliable
Cervical cerclage has proved useful in women
• Bladder emptied
• Cervix measured
with known cervical insufficiency (see Chapter 29,
Ŧ From internal os to external os Miscarriage and recurrent pregnancy loss).
Ŧ Tip of funnel to external os
A S transabdominal ultrasound; S transvaginal ultrasound. Box 35.7 +PVGTXGPVKQPUYKVJPQRTQXGPDGPGſV
• Enhanced antenatal care
• /QFKſECVKQPQHOCVGTPCNCEVKXKV[
DGFTGUV
ther ultrasound signs • Supplementation with various nutrients and vitamins
of preterm labor • Screening for genital tract infections
• Empirical use of antibiotics
Other signs seen on ultrasound that are associ- • Cervical cerclage in
ated with preterm birth are as follows: Ŧ women with prior preterm labor with normal cervical
length
• Funneling: Protrusion of amniotic membranes Ŧ women with a short cervix with no history of preterm
into the cervical canal (Fig. 35.2) labor
• Debris/sludge (hyperechoic matter in the Ŧ multiple pregnancy
amniotic fluid close to the internal cervical os) may actually precipitate preterm labor
Prevention of preterm Box 35.8 +PVGTXGPVKQPUYKVJRTQXGPDGPGſV
labor •
•
Diagnosis and treatment of asymptomatic bacteriuria
Cervical cerclage
Due to the morbidity and mortality associated • Progesterone therapy
with preterm labor, strategies have been tried to • Periodontal care
• Cessation of smoking
prevent preterm birth. Some of these have been
• Increasing interpregnancy interval
clearly shown to be of no use. Other strategies
• Avoidance or treatment of malaria
are of proven benefit.
CH 35_p508-521_v3.indd 513 18-07-2015 11:43:20

In women with a previous preterm birth who is the most important clinical criterion for the
have an ultrasound-proved short cervix between diagnosis of preterm labor. The diagnosis can be
18 and 24 weeks, cervical cerclage is effective in made with greater confidence if in addition there
the prevention of preterm birth. is vaginal bleeding and/or ruptured membranes.
Overdiagnosis of preterm labor is common.
rogesterone therapy Not all preterm labors will end with preterm
Progesterone therapy administered in the second birth. Approximately 30% of preterm labor
trimester may reduce the risk of preterm birth. resolve spontaneously. Of the women who are
The effect of progesterone is dependent on the hospitalized for preterm labor, 50% continue
preparation, dosage, and route of administration. their pregnancy till term.
The indications for and the effects of proges-
terone therapy in preterm birth are enumerated Diagnostic criteria
in Box 35.9.
Adherence to certain clinical criteria can help
Dosage classify and diagnose preterm labor with cer-
Progesterone is started at 16–20 weeks’ gestation tainty (Box 35.11). With threatened preterm
and continued through 36 weeks’ gestation or labor, contractions are monitored and cervical
until delivery. The dosage for the different indi- changes reassessed 30–60 minutes later. If there
cations are summarized in Box 35.10. is progressive effacement and dilatation, it must
be treated as preterm labor. Women who have
Other interventions had threatened preterm labor have a greater
Periodontal care, cessation of smoking, weight incidence of late preterm labor (34 to <37 weeks).
optimization, spacing of pregnancies, and treat-
ment of infections such as malaria in endemic (GVCNſDTQPGEVKP
areas can reduce the risk of preterm labor. Testing for fetal fibronectin (fFN) may be done to
determine whether preterm labor will lead to
preterm birth.
Diagnosis of preterm labor Fetal fibronectin is a fibronectin protein pro-
Suspected preterm labor is a common reason for duced by fetal cells. It is found at the interface
hospitalization of pregnant women. Cervical of the chorion and the decidua. It is thought to
change (dilatation and/or effacement) in the be a ‘trophoblast glue’ that acts as an adhesive
presence of regular painful uterine contractions between the fetal membranes and the uterine
decidua. It is released into cervicovaginal secre-
tions when there is disruption of the chorion/
Box 35.9 Progesterone therapy in preterm birth decidual interface that may occur at the time of
• Indicated in
Ŧ asymptomatic women with previous preterm birth
Ŧ CU[ORVQOCVKEYQOGPYKVJCUJQTVEGTXKZ
ŭOO
Box 35.11 Diagnostic criteria for preterm labor
• Progesterone therapy reduces hreatened preterm labor
Ŧ preterm births • Irregular or regular uterine activity
Ŧ perinatal/neonatal deaths • Associated with
Ŧ respiratory distress syndrome in the neonate Ŧ cervical length >10 mm
Ŧ cervical dilatation 1–2 cm
Preterm labor
Box 35.10 Dosage of progesterone for • Regular uterine activity
prevention of preterm labor
Ŧ Contraction frequency of
• Asymptomatic women with previous preterm birth at least 1 every 10 minutes or
Ŧ 17-D-hydroxyprogesterone caproate 250 mg IM 6 per hour
weekly or • Associated with
Ŧ Micronized progesterone 100 mg daily vaginally Ŧ cervical length <10 mm
• #U[ORVQOCVKEYQOGPYKVJCUJQTVEGTXKZ
ŭOO Ŧ cervical dilatation >2 cm
Ŧ Micronized progesterone 200 mg daily vaginally Ŧ vaginal bleeding or rupture of membranes
CH 35_p508-521_v3.indd 514 18-07-2015 11:43:20

Preterm Labor 515
preterm labor. The presence or absence of fFN is

Box 35.12 Interpretation of fF levels
used to predict preterm birth. Testing for fFN is
expensive and not done routinely in India. • Cervical length between 20 and 30 mm
Testing for fFN, if done, should be used as an Ŧ fFN positive
Increased risk of preterm birth in the next 7 days
additional test only in women who have preterm
Ŧ fFN negative
contractions and whose cervical length falls
Low risk of preterm birth
between 20 and 30 mm. In this situation it is diffi-
cult to predict preterm labor with cervical length f HGVCNſDTQPGEVKP
alone.
The test is done by obtaining a swab from the
posterior vaginal fornix. No digital examination
should be done prior to obtaining the swab. cells and may leak into cervical secretions during
Interpretation of results of fFN testing is sum- detachment of the fetal membrane.
marized in Box 35.12. A bedside dipstick method is now commer-
cially available for this test. It seems to be more
Insulin-like growth useful for its negative predictive value, that is,
the absence of IGFBP-1 is a reassuring sign that
factor-binding protein-1
the likelihood of preterm birth is low.
Phosphorylated insulin-like growth factor-bind- The management of preterm uterine contrac-
ing protein-1 (IGFBP-1) is secreted by decidual tions is given in Figure 35.3.
Preterm uterine contractions
hreatene preterm labor Preterm labor
Contractions or in minutes
Contractions or in minutes Cer ical length mm
Cer ical length mm Cer ical ilatation cm
Cer ical ilatation cm Vaginal blee ing M
Hospitali e Hospitali e
epeat pel ic e amination Cer ical length cm Corticosteroi s
after minutes ocolysis
Mg for neuroprotection
reat U if present
Prepare for eli ery
f or P nform neonatologist
o further contractions
o cer ical changes
Home egati e Positi e
ischarge
o return if pains recur
Figure 35.3 The evaluation and management of preterm uterine contractions at <34 weeks’ gestation. f HGVCNſDTQPGEVKP
BP- insulin-like growth factor-binding protein-1; gS magnesium sulphate; S spontaneous rupture of membrane;
, urinary tract infection.
CH 35_p508-521_v3.indd 515 18-07-2015 11:43:20

Management of echanism o action

The mechanisms of action of antenatal steroids
preterm labor are summarized in Box 35.14.
A woman in preterm labor at <34 weeks’ gesta- estational age o a ministration
tion should be hospitalized to initiate certain
Corticosteroids may be administered between 24
interventions (Fig. 35.3).
and 34 weeks' gestation to a woman in whom
The management of preterm labor is summa-
preterm birth is anticipated. In places where neo-
rized in Box 35.13.
natal salvage is poor prior to 28 weeks, it might be
prudent to administer the dose after 28 weeks’
Administration gestation.
The risk of severe respiratory morbidity after
of corticosteroids 34 weeks’ gestation is low and the efficacy of
Liggin and Howie, in 1972, demonstrated that a corticosteroid therapy after this age is doubtful.
single course of antenatal corticosteroid therapy The American College of Obstetricians and
administered between 24 and 34 weeks’ gesta- Gynecologists (ACOG) has not recommended
tion to women at risk for preterm birth reduced antenatal corticosteroids for gestations >34
the incidence and severity of respiratory distress weeks. However, the Royal College of
syndrome (RDS) and mortality in the neonate by Obstetricians and Gynaecologists (RCOG) guide-
50%. Since then, this therapy has saved count- lines recommend routine administration of
less preterm neonates globally. antenatal glucocorticoids for all women at risk
Other benefits of corticosteroid therapy that of preterm birth <35 weeks’ gestation and all
have been demonstrated more recently are the women undergoing elective cesarean delivery
reduction in risk for up to and including 38+6 weeks’ gestation.
• intraventricular hemorrhage; Drugs an osage

• necrotizing enterocolitis; and Both betamethasone and dexamethasone may be
• systemic infection in the first 48 hours of life. used. Betamethasone is preferred because of the
lesser number of doses required. Dexamethasone
is less expensive.
Box 35.13 Management of preterm labor
The course of therapy is listed in Table 35.1.
• Corticosteroids for fetal lung maturity
• Tocolysis to delay delivery
Box 35.14 Action of antenatal steroids
Ŧ Facilitates in utero transfer to tertiary center
Ŧ Gives time for corticosteroids and magnesium sul- • Accelerating development of type 1 and type 2
fate to act pneumocytes
• Magnesium sulfate for fetal neuroprotection Ŧ Improved maximal lung volume
• Antibiotic therapy for women with UTI Ŧ Improved compliance
• +PVGTXGPVKQPUYKVJPQDGPGſV Ŧ Improved gas exchange
Ŧ Complete bed rest • Induction of type 2 pneumocytes
Ŧ Hydration Ŧ Increased surfactant production
Ŧ Maintenance therapy with tocolytics Ŧ Enhanced neonatal response to postnatal surfactant
Ŧ Antibiotics treatment
To prolong gestation • Induction of pulmonary E-receptors
To decrease neonatal morbidity Ŧ Release of surfactant
Ŧ #DUQTRVKQPQHCNXGQNCTƀWKF
, urinary tract infection.
Table 35.1 Course of therapy for antenatal corticosteroids
Drug umber of doses Dosage Interval

Betamethasone 2 12 mg IM 24 hours apart
Dexamethasone 4 6 mg IM 12 hours apart
CH 35_p508-521_v3.indd 516 18-07-2015 11:43:20

Preterm Labor 517
escue salvage or booster ose Box 35.16 Characteristics of tocolytics

Evidence suggests that multiple courses of ste-
• Effective in
roids can have deleterious effects on the fetus, Ŧ reducing or abolishing contractions
most importantly growth restriction. Repeated Ŧ for an average of 48 hours
courses are therefore not recommended. Ŧ may prolong pregnancy up to 7 days
However, if the last dose of steroids was given • Most useful in women with
more than 2 weeks prior to expected delivery, Ŧ preterm labor at gestational age 28–34 weeks
and the gestational age at administration of
the initial course was <28 weeks’ gestation, a
single repeat dose of 12 mg of betamethasone The mechanism of action, dose, and maternal
may have some benefit. and fetal side effects of tocolytic agents are enu-
The recommendations for corticosteroid merated in Table 35.2.
therapy are summarized in Box 35.15.
Calcium channel bloc ers i e ipine
Nifedipine is the first-line therapy for tocoly-
Tocolysis sis since it performs best for the following
It is often difficult to differentiate true preterm outcomes:
labor from false or threatened preterm labor. Of
• Delivery delayed by 48 hours
the total number of women thought to be in
• Decreased neonatal mortality
preterm labor, only 50% go on to deliver at term.
• Decreased neonatal RDS
In women with true preterm labor (in whom
progressive cervical changes are documented), Nifedipine is more effective than E-agonists
tocolytic therapy helps by inhibiting and stop- and has fewer side effects. Currently, this is the
ping contractions temporarily. However, the drug of choice in most centers.
underlying stimulus that initiated the process
of labor is not affected. Therefore, tocolytic Cycloo ygenase inhibitors
therapy may only provide short-term prolonga- In omethacin
tion of pregnancy. This is particularly useful
when corticosteroids are administered for fetal Indomethacin is the second line of treatment for
lung maturity. Tocolysis provides time for the tocolysis. If given for not more than 48 hours, it
steroids to act. is most effective in abolishing preterm con-
Women with preterm contractions without tractions, with the least maternal side effects.
cervical change, especially those with a cervical However, it does not perform as well in decreas-
dilatation of <2 cm, should not be treated with ing neonatal mortality and RDS as compared
tocolytics. with nifedipine.
The characteristics of tocolytics are enumer- Indomethacin is not recommended beyond
ated in Box 35.16. 32 weeks’ gestation. When used for more than 48
hours, it can cause fetal renal failure and oligohy-
dramnios. Premature closure of ductus arterio-
Box 35.15 Administration of antenatal
sus is also a known complication.
corticosteroids
• In women at risk for preterm labor
E Agonists ito rine an terbutaline
• Between 24 and 34 weeks The E-mimetic drugs, ritodrine and terbu-
Ŧ Preferably after 28 weeks taline, can cause severe maternal hypotension
• Effective for 7 days and tachycardia. In multiple gestation, mater-
• Repeat courses not recommended nal pulmonary edema and maternal mortality
Ŧ Associated with fetal growth restriction have been reported with the use of these drugs.
• Rescue or salvage dose, if indicated They were introduced as the first line of toco-
Ŧ 2 weeks elapsed since last dose
lytics, but now their use is not recommended
Ŧ )GUVCVKQPCNCIGCVſTUVFQUGYGGMU
because of the unacceptably high maternal
Single 12-mg dose of betamethasone
side effects.
CH 35_p508-521_v3.indd 517 18-07-2015 11:43:20

CH 35_p508-521_v3.indd 518
Table 35.2 Mechanism of action, dose, and maternal and fetal side effects of tocolytic agents
Drug Class of drug Mechanism of action Dose Maternal side effects Fetal side effects
Nifedipine Calcium channel • Decreases intracellular • 30 mg loading dose &K\\KPGUUƀWUJKPI No known adverse effects

ſTUVNKPGVTGCVOGPV blocker free calcium • Then 10–20 mg and hypotension
for tocolysis) • Results in myometrial every 4–6 hours
relaxation
Indomethacin Cyclooxygenase • Inhibits cyclooxygenase • 50–100 mg loading Nausea, esophageal In utero constriction of
(should not be given inhibitor production dose (oral or per TGƀWZICUVTKVKUCPF ductus arteriosus, renal
for >48 hours due to • Decreases prostaglandin rectum) emesis; platelet dysfunction, oligohy-
fetal side effects) production • Followed by 25 mg dysfunction dramnios, necrotizing
orally every enterocolitis in preterm
4–6 hours newborns, and PDA in
neonate
Ritodrine E-Mimetic • Inhibits interaction • IV infusion Tachycardia, Fetal tachycardia
(currently not (E-adrenergic between actin 0.05–0.1 mg/min hypotension,
recommended due receptor agonist) and myosin • Increased at tremor, palpitations,
to maternal side • Diminishes myometrial 15-minute intervals shortness of breath,
effects) contractility to 0.35 mg/min chest discomfort,
pulmonary edema,
hypokalemia,
hyperglycemia
Terbutaline E-Mimetic • Inhibits interaction • 0.25 mg SC every Same as ritodrine Same as ritodrine
(E-adrenergic between actin 20–30 minutes for
receptor agonist) and myosin 4 doses
• Diminishes myometrial • Then 0.25 mg SC
contractility every 3–4 hours for
24 hours
Atosiban Oxytocin receptor • Selective oxytocin– • IV bolus 6.75 mg Hypersensitivity, Minimal
antagonist vasopressin receptor • Then 300 μg/min injection site reactions
antagonist infusion for 3 hours
• Then 100 μg/min for
up to 45 hours
PDA, patent ductus arteriosus; SC, subcutaneous.
18-07-2015 11:43:20
Preterm Labor 519
Terbutaline is used when immediate short- Magnesium sulfate

term tocolysis is needed as in uterine hyperstim-
ulation or prior to external cephalic version. for fetal neuroprotection
Cerebral palsy refers to a heterogeneous group of
itric o i e onors lyceryl trinitrate disorders of movement and/or posture. It is the
Transdermal glyceryl trinitrate has been used as most common cause of severe motor disability
a tocolytic as well. Its efficacy in preventing pre- in childhood. Compared with term infants, the
term labor is limited. incidence of cerebral palsy, sensory deficits, and
learning disabilities is very high in children born
agnesium sul ate before 34 weeks, and even higher in children
Magnesium sulfate has been extensively studied born before 32 weeks.
as a tocolytic due to its inhibition of myometrial For women at risk of preterm birth, antenatal
contractility. However, it has not been found to administration of magnesium sulfate provides
be effective in preterm labor. good neuroprotection. Maternal administration
of magnesium sulfate in women expected to have
O ytocin antagonists Atosiban a preterm delivery within 24 hours has consis-
Atosiban is as effective as E-mimetics for prevent- tently demonstrated a decreased risk of cerebral
ing preterm birth within 48 hours of initiating palsy and severe motor dysfunction in offspring.
treatment. Use of atosiban is associated with a sig-
nificantly lower risk of maternal side effects than estational age o a ministration
E-mimetics. However, this drug is available only in Magnesium sulfate for neuroprotection is
Europe and not in other countries, including India. administered when delivery is expected in the
Contraindications to tocolysis are listed in next 24 hours
Box 35.17.
• due to preterm labor;
• due to preterm prelabor rupture of membranes;
aintenance therapy ith tocolytics
• before an elective preterm delivery (induc-
There is not enough evidence to continue toco- tion or cesarean delivery for maternal or fetal
lytics after 48 hours. Maintenance therapy with indications).
tocolytics is ineffective for preventing preterm
birth and improving neonatal outcomes, and is Magnesium sulfate for neuroprotection is
not recommended for this purpose. most effective in pregnancies between 24 and
32 weeks’ gestation.
ocolysis in omen
ith multiple pregnancy Dose o magnesium sul ate
The use of tocolytics to inhibit preterm labor in or neuroprotection
multiple pregnancy has been associated with a Dose of magnesium sulfate for neuroprotection
greater risk of maternal complications, such as is given as follows:
pulmonary edema, especially with the use of
• Magnesium sulfate is given as
E-mimetics. Nifedipine is considered safe in
– 4 g intravenous loading dose followed by
multiple pregnancy.
– 1 g/hour infusion
• The therapy is discontinued 24 hours after ini-
Box 35.17 Contraindications to tocolysis tiation if delivery has not occurred
• The dose may be repeated if labor does not
• Intrauterine fetal demise
progress and the woman returns later in pre-
• Lethal fetal anomaly
• Nonreassuring fetal status
term labor
• Severe preeclampsia or eclampsia Magnesium sulfate by itself provides a certain
• Maternal bleeding with hemodynamic instability degree of tocolysis. However, if the pain is not
• Chorioamnionitis
subsiding with magnesium sulfate alone, tocoly-
• Preterm prelabor rupture of membranes
sis may be initiated to allow the magnesium sul-
• /CVGTPCNEQPVTCKPFKECVKQPUVQVQEQN[UKU
CIGPVURGEKſE
fate enough time to provide neuroprotection.
CH 35_p508-521_v3.indd 519 18-07-2015 11:43:21

Indomethacin is the tocolytic of choice when

Box 35.18 Magnesium sulfate for
magnesium sulfate is being used. It is better to neuroprotection
avoid nifedipine and E-mimetics in conjunc-
tion with magnesium sulfate because of the • When preterm delivery expected in next 24 hours
• Decreases risk of cerebral palsy
potential for serious maternal complications.
• Most effective between 24 and 32 weeks’ gestation
The use of magnesium sulfate for fetal neuro-
• Dosage
protection is summarized in Box 35.18. Ŧ 4 g intravenous loading dose followed by
Ŧ 1 g/hour infusion
• Discontinued 24 hours after initiation
ole of antibiotics in • Tocolysis with indomethacin, if required
prolonging pregnancy or
improving neonatal outcome
Box 35.19 Management of preterm delivery
Antibiotics have no role in prolonging gestation
or improving neonatal outcome in women with • Cephalic presentations may be delivered vaginally
preterm labor with membranes intact. • Vaginal delivery
Ŧ Carefully controlled
Ŧ Nontraumatic
• Breech presentations at <34 weeks’ gestation
Management of preterm Ŧ Cesarean section
• Early AROM should be avoided
delivery • EFM is recommended during labor
• A neonatologist and team should be available at the
If labor progresses in spite of tocolysis, all pre- time of birth
cautions should be taken for safely delivering the A CTVKſEKCNTWRVWTGQHOGODTCPGU electronic fetal
baby (Box 35.19). monitoring.
Key points
• Preterm birth is a major contributor to neonatal • Certain interventions help in preventing preterm labor:
mortality and morbidity and has long-term adverse Treatment of asymptomatic bacteriuria, cervical cer-
consequences for health. clage, cessation of smoking, and progesterone therapy.
• 2TGVGTONCDQTKUFGſPGFCUVJGRTGUGPEGQHWVGTKPG • Progesterone therapy administered in the second
EQPVTCEVKQPUQHUWHſEKGPVHTGSWGPE[CPFKPVGPUKV[VQ trimester may reduce the risk of preterm birth.
result in progressive effacement and dilatation of 17-D-Hydroxyprogesterone caproate 250 mg IM is
the cervix, between fetal viability and 37 weeks. started at 20 weeks and given weekly till 36 weeks.
Vaginal micronized progesterone can also be given.
• Prior preterm labor is the strongest risk factor for
future preterm birth. • (GVCNſDTQPGEVKPCPFKPUWNKPNKMGITQYVJHCEVQTDKPFKPI
• Cervical length screening by ultrasound is useful in protein-1 can be used to predict if preterm birth will
assessing risk in women with previous preterm birth. occur in a woman with preterm labor.
• Management of preterm labor includes administration
• The risk of spontaneous preterm birth increases
of corticosteroids, tocolysis, and magnesium sulfate
as cervical length decreases. The risk is highest
for neuroprotection.
when a short cervix is detected before 24 weeks’
gestation. • If labor progresses in spite of tocolysis, all
• The diagnosis of a short cervix is made when cervical precautions should be taken to safely deliver the baby.
length on transvaginal ultrasound (TVUS) at 16–28 • Complications of the premature infant are divided into
YGGMUŏIGUVCVKQPKUŭOOKPYQOGPYKVJPQRTKQT short-term complications in the neonatal period and
preterm delivery and <25 mm in women with a prior long-term sequelae.
preterm delivery.
CH 35_p508-521_v3.indd 520 18-07-2015 11:43:21

Preterm Labor 521
Self-Assessment
2. Because she has had previous preterm birth, cervical
Case-based questions length assessment should have been done from 16
weeks. A short cervix <25 mm can be treated with
Case 1 17-alpha hydroxyprogesterone caproate or micro-
Mrs. VC, 29, gravida 3, para 2, had two preterm births and nized progesterone.
her previous babies were delivered at 36 and 34 weeks. 3. Hospitalize the patient; start on corticosteroids and
The second one needed admission to the newborn tocolytics. Perform urine culture and treat if positive.
nursery due to complications of prematurity. At 33 weeks The neonatologist should be informed.
she was admitted with mild uterine contractions. 4. The complications her premature neonate can face
are respiratory distress, intraventricular hemorrhage,
1. After two prior preterm births, what is the risk of this sepsis, hypothermia, hypoglycemia, necrotizing
woman having another preterm birth? enterocolitis, and retinopathy.
2. How could she have been screened for recurrence of
preterm birth in this pregnancy?
3. What are the steps you will take to manage her at Case 2
33 weeks?
1. Diagnosis is preterm labor since the cervix is <1-cm
4. What are the complications that her infant can face?
long and 2-cm dilatated, and contractions are 1 in
10 minutes. She also appears to be having a urinary
Case 2 tract infection which could be precipitating the pre-
term labor.
Mrs. WE, 22, gravida 2, para 1, live 1, at 32 weeks’ ges- 2. Urine should be sent for culture and sensitivity;
tation, presented to the hospital with complaints of in- empirical antibiotic therapy should be started;
creased low back pain and pelvic pressure. She stated corticosteroids should be administered and tocolysis
that she had painful and frequent micturition and had given for 48 hours.
‘menstrual-type cramping. On examination, there was 3. 1TCNPKHGFKRKPGYQWNFDGVJGſTUVEJQKEGHQTVQEQN[UKU
scant blood from the cervix, which appeared old. The cer- 4. Since it is a breech presentation at 32 weeks, a
vix was 2-cm dilatated, <1-cm long, and soft in consist- cesarean section would be the choice for mode of
ency. She was having contractions every 10 minutes. The delivery.
fetus was in breech presentation and appropriately grown
for the gestation.
1. What is the diagnosis and what could be the cause? Sample questions
2. How would you manage this patient?
3. What would be your choice for tocolytic agent? Long-answer question
4. If the contractions do not subside and she goes into 1. &GſPGRTGVGTONCDQT'ZRNCKPGVKQNQI[CPFOCPCIGOGPV
labor, what would be the best mode of delivery? of preterm labor.
Answers Short-answer questions

1. Causes of preterm labor
Case 1 2. Neonatal complications of prematurity
1. The risk of recurrent preterm birth after two consecutive 3. Prevention of preterm labor
preterm births is approximately 30%. 4. Tocolytic therapy
CH 35_p508-521_v3.indd 521 18-07-2015 11:43:21

Prelabor Rupture
36 of the Membranes
Case scenario
Mrs. HK, 30, a primigravida at 30 weeks of pregnancy, was referred from

a peripheral hospital with history of watery discharge. The discharge
had begun 12 hours ago but Mrs. HK and her husband had not realized
that it was a problem. On arrival at the local hospital, they were told
that the membranes had ruptured spontaneously and since she was
preterm, she had to be in a tertiary center.
Introduction • Midtrimester or previable PROM is defined as

PROM between 16 and 24 weeks’ gestation.
Rupture of membranes before the onset of labor,
whether it occurs at term or preterm, is a cause for
worry because it is associated with perinatal and Incidence
maternal complications. The important goals of
management are optimizing timing of delivery and Prelabor rupture of membranes occurs in
minimizing perinatal mortality and morbidity. 10% of all pregnancies, of which 7%–8% occur
after 37 weeks. The incidence of PPROM is 2%.
Midtrimester PROM occurs in 0.3%–0.7% of
&GſPKVKQP pregnancies.
Prelabor rupture of membranes (PROM) is

defined as rupture of membranes before the Pathophysiology
onset of regular uterine contractions.
The fetal membranes consist of an inner amnion
• When PROM occurs at or after 37 weeks’ gesta- and outer chorion. The amnion surrounds the
tion, it is referred to as term PROM. amniotic cavity and is lined by a single layer of
• Preterm PROM (PPROM) is defined as PROM cuboidal epithelium. The chorion is thicker,
between 24 and 37 weeks. adherent to the maternal decidua, and consists
CH 36_p522-533_v3.indd 522 18-07-2015 12:08:46

Prelabor Rupture of the Membranes 523
of reticular and trophoblastic layers. There is

Box 36.2 isk factors of prelabor rupture
compact spongy connective tissue between the of membranes (P M)
amnion and chorion.
With advancing gestational age, remodel- • Urogenital infections
Ŧ Chlamydia trachomatis
ing of membranes occurs through changes in
Ŧ richomonas vaginalis
collagen and intercellular matrix. This results
Ŧ Bacterial vaginosis
in weakening of the membranes and suscepti- Ŧ Group B beta-hemolytic streptococcus
bility to rupture. These changes are mediated Ŧ eisseria gonorrhoeae
through matrix metalloproteinases (MMP). Any • Uterine overdistension
condition that causes increase in MMP levels or Ŧ Polyhydramnios
decrease in tissue inhibitors of MMP (TIMP) can Ŧ Multifetal pregnancy
give rise to membrane weakening and PROM. • Connective tissue disorders
Increase in local cytokines and collagenase also Ŧ Ehlers–Danlos syndrome
causes membrane weakening. Increase in intra- • Others
uterine pressure due to polyhydramnios and/or Ŧ Prepregnancy
multiple pregnancy acts as a mechanical factor Low socioeconomic status
Low BMI
leading to membrane rupture (Box 36.1).
Previous PROM/preterm birth
Cervical conization
Ŧ During pregnancy
isk factors Bleeding in first or second trimester
Maternal smoking
In most cases of PROM, no etiological factor is Nutritional deficiencies (copper, vitamin C)
identified. Risk factors for PROM are listed in Preterm labor
Box 36.2. Urogenital infection and microbial Cervical cerclage
colonization lead to preterm labor by causing Invasive procedures
an increase in local cytokine or an imbalance - Amniocentesis
- Cordocentesis
between MMPs and TIMPs. The organisms impli-
- Fetoscopy
cated are Chlamydia trachomatis, Trichomonas
vaginalis, group B beta-hemolytic streptococci
(GBS), and Neisseria gonorrhoeae. Bacterial vag-
inosis also predisposes to PROM and preterm PROM. Risk factors may be present prior to preg-
labor. Amniotic fluid cultures are positive in nancy or may be identified during pregnancy.
25%–35% of women with PROM. Several risk Previous preterm birth with or without PROM is
factors have been known to be associated with an important risk factor. Cervical cerclage as well
as invasive procedures such as amniocentesis,
cordocentesis, and fetoscopy are well-recognized
risk factors for midtrimester PROM.
Box 36.1 Pathophysiology of rupture
of membranes
• Physiological remodeling
Ŧ Changes in collagen
Complications
Ŧ Changes in intercellular matrix Maternal and fetal complications increase with
• Mediated by
duration of rupture of membranes and fetal
Ŧ increase in
prematurity.
cytokines
MMP
collagenase Maternal complications
Ŧ decrease in TIMP
Ŧ increase in intrauterine pressure Ascending infection resulting in maternal chorio-
polyhydramnios amnionitis is the most common complication.
multiple pregnancy This occurs in 25% of women with PROM. The risk
P, matrix metalloproteinase; P, tissue inhibitors of matrix increases as the duration of rupture of membranes
metalloproteinases. increases. The risk is higher in preterm PROM than
CH 36_p522-533_v3.indd 523 18-07-2015 12:08:46

Box 36.3 Maternal complications of prelabor Box 36.4 Fetal and neonatal complications
rupture of membranes of prelabor rupture of membranes
(P M)
• Placental abruption • Fetal infection
• Retained placenta Ŧ Pneumonia
• Puerperal endometritis Ŧ Septicemia
• Maternal sepsis Ŧ Perinatal death
• Cesarean section • Cord prolapse
• Preterm PROM
Ŧ Prematurity
in term PROM. The risk of infection decreases with Ŧ Respiratory distress syndrome
increasing gestational age. Fever, malodorous vag- Ŧ Necrotizing enterocolitis
inal discharge, uterine tenderness, and fetal tachy- Ŧ Intraventricular hemorrhage
• Second trimester PROM
cardia are the signs of clinical chorioamnionitis.
Ŧ Pulmonary hypoplasia
Placental abruption, retained placenta, puerperal
Ŧ Limb deformities
endometritis, and maternal sepsis are other known • Long-term sequelae
complications (Box 36.3). Ŧ Periventricular leukomalacia
Ŧ Cerebral palsy
Fetal complications Ŧ Hearing and visual defects
Ŧ Mental retardation
Chorioamnionitis leads to fetal pneumonia, sep- Ŧ Chronic lung diseases
ticemia, and perinatal death.
Prelabor rupture of membranes can be asso-
ciated with cord prolapse. Oligohydramnios can
cause cord compression, meconium passage Clinical features
and aspiration, fetal distress, and fetal hypoxia.
Prematurity, respiratory distress syndrome, necro- Most women with PROM present with history
tizing enterocolitis, and intraventricular hemor- of watery discharge per vaginum. This usually
rhage are common following PPROM. Perinatal occurs in a gush and continues as a trickle. It
mortality is higher in preterm birth associated can also occur as intermittent discharge of small
with PROM compared to preterm birth with amounts of fluid which may be mistaken for
intact membranes. Prelabor rupture of mem- urinary incontinence. Occasionally, the woman
branes in the second trimester, leading to oligo- may be unaware of any discharge. Uterine con-
hydramnios, can result in pulmonary hypoplasia tractions may begin a few hours later, especially
and limb deformities. Long-term sequelae such in women at term. In women with prolonged
as cerebral palsy, mental retardation, periventric- rupture of membranes, fever, uterine tender-
ular leukomalacia, visual and hearing disabili- ness, and/or malodorous discharge are indica-
ties, and chronic lung disease also result from this tive of chorioamnionitis. The uterus may be felt
condition (Box 36.4). hugging the fetus if the volume of amniotic fluid
is remarkably reduced.
Amniotic fluid may be seen draining through
Prediction and prevention the introitus, especially when the woman is
asked to cough. Speculum examination reveals
Previous PROM is a strong risk factor for PROM in clear fluid flowing through the cervical os or fluid
the current pregnancy. However, prediction is dif- collected in the posterior fornix (Box 36.5).
ficult. Cervical length <25 mm on ultrasound and
positive fetal fibronectin test in maternal plasma
at 22–24 weeks’ gestation indicate higher risk. Clinical course
Since it is not possible to predict or pre-
vent PROM in most women, routine screening • Prelabor rupture of membranes is usually fol-
tests and preventive measures are not currently lowed by the onset of labor. The latent period
recommended. between rupture of membrane and onset of
CH 36_p522-533_v3.indd 524 18-07-2015 12:08:46

gush of watery discharge through the introitus

Box 36.5 Clinical features of prelabor rupture of
membranes spontaneously or on coughing. Speculum exam-
ination usually reveals draining of fluid through
• Watery discharge per vaginum the cervical os or fluid in the posterior fornix. If
Ŧ )WUJQHƀWKF
leakage of amniotic fluid is not seen, a vulval pad
Ŧ Continuous trickle
may be applied and the pad examined after a few
Ŧ Intermittent discharge
• Uterine contractions few hours later
hours (Box 36.6).
• Chorioamnionitis Digital vaginal examination should be avoided
Ŧ Fever for the following reasons:
• It shortens the latency period between mem-
Ŧ /CNQFQTQWUCOPKQVKEƀWKF
brane rupture and delivery.
• Fluid draining through introitus
• Speculum examination
• It increases the risk of infection.
Ŧ Fluid draining through cervical os Digital vaginal examination should not
Ŧ Fluid collected in posterior fornix be performed in PROM unless delivery is
imminent.
labor increases as gestational age decreases.

When membranes rupture at term, 50% deliver %QPſTOCVQT[VGUVUHQT
within 5 hours, 85% within 48 hours, and 95% diagnosis of P M
within 72 hours. However, in PROM before 34
weeks, 50%–60% deliver within 1 week. • Nitrazine test: The normal vaginal pH is between
• Occasionally, the leakage may stop due to seal- 4.5 and 5.5. When the vaginal fluid shows a pH
ing of the rent in the membranes, fluid may >6–6.5 on testing with nitrazine paper (color
reaccumulate, and pregnancy may continue. changes to blue), it confirms the presence of
This occurs in 2–3% of women. It is commonly alkaline amniotic fluid. The test has a sensitivity
seen in PROM associated with amniocentesis of 90%. False positive test may be obtained if the
in the second trimester. fluid is contaminated by urine or blood.
Box 36.6 Clinical evaluation

Clinical evaluation • History
Ŧ Watery discharge per vaginum
This consists of history, physical examination, Ŧ Duration of discharge
confirmatory tests, assessment of gestational Ŧ Gestational age
age, and maternal/fetal complications. Ŧ Uterine contractions
Ŧ Symptoms of chorioamnionitis
Ŧ Fetal movements
istory • Physical examination
Ŧ Fever, tachycardia
As already discussed, history of sudden gush of
Ŧ Uterine height
watery discharge per vaginum, continuous trickle,
Ŧ Presentation
or intermittent discharge is the most common Ŧ Fetal heart rate
presentation. Gestational age should be assessed Ŧ Uterine tenderness
and history of uterine contractions or symptoms • Examination of the vulva
of chorioamnionitis should be obtained. Ŧ )WUJQHCOPKQVKEƀWKF
• Speculum examination
Ŧ &TCKPKPIQHƀWKFVJTQWIJVJGEGTXKECNQU
Physical examination Ŧ Fluid collected in posterior fornix
On physical examination, height of uterine fun- Color of amniotic fluid
dus, presence of uterine contractions, presenta- Malodorous discharge
Ŧ Cervical effacement
tion of the fetus, signs of chorioamnionitis, and
Ŧ Cervical dilatation
fetal heart rate abnormalities should be noted.
Ŧ Cord/fetal limb prolapse
Vulva should be examined for visualization of
CH 36_p522-533_v3.indd 525 18-07-2015 12:08:46

• Fern test: Fluid from the posterior fornix is Management

smeared on a glass slide using a swab and
allowed to dry. When examined under the Management consists of initial evaluation, con-
microscope, fern pattern is seen due to inter- firmation of diagnosis, and decision regarding
action between proteins and salts in the amni- delivery.
otic fluid. This test also has a sensitivity of 90%.
Contamination by cervical mucus can yield a
false positive result. Initial evaluation
• Ultrasonography: This may reveal oligo-
hydramnios. When the history is suggestive When the woman is admitted with a history sug-
of ruptured membranes and other tests are gestive of PROM, history and physical examina-
equivocal, this may be used as an aid to diag- tion should proceed as given in Box 36.6. If obvi-
nosing PROM. ous discharge of fluid is not seen, a speculum
• Indigo carmine test: After intra-amniotic examination should be performed.
injection of indigo carmine, the vulval pad is The crucial decision to be made is whether
stained blue if there is PROM. This test is now to deliver immediately or opt for expectant
obsolete and not in use. management. This decision is based on poten-
• Other tests: When membranes rupture, there tial risks and benefits of waiting as opposed
is an increase in fetal fibronectin (fFN) and to immediate delivery. Management depends
insulin-like growth factor binding protein 1 on gestational age, duration of rupture of
(IGF BP1) in cervicovaginal secretions. Tests membranes, fetal well-being, and presence of
to detect fFN and IGF BP1 have been found to infection.
have high sensitivity and specificity. A rapid
• Establish gestational age using last menstrual
immunoassay to identify placental alpha-I
period and early ultrasonography.
microglobulin in the vaginal fluid is an accu-
• Ascertain duration of rupture of membranes
rate test with a sensitivity and specificity of
by history.
nearly 99%–100%. This test is not routinely
• Avoid digital vaginal examination.
available for clinical use in India.
• Perform a speculum examination if needed to
Confirmatory tests are listed in Box 36.7. confirm PROM.
• Document history of digital vaginal examina-
tion, if performed elsewhere before admission
Box 36.7 %
QPſTOCVQT[VGUVUHQTRTGNCDQT
to hospital.
rupture of membranes
• Look for presence of chorioamnionitis.
• Nitrazine test – Clinical evaluation should be performed
Ŧ R* QH COPKQVKE ƀWKF Ō
PKVTC\KPG RCRGT VWTPU daily.
blue)
– Signs of infection (fever, uterine tenderness)
• Fern test
should be looked for.
Ŧ Arborization on glass slide
Ŧ Interaction between proteins and salts
– Leukocytosis and elevated C-reactive pro-
• Ultrasonography tein levels have low sensitivity and therefore
Ŧ Oligohydramnios are not of much use.
• Indigo carmine test – Routine vaginal swab cultures are not rec-
Ŧ +PLGEVKQPQHF[GKPVQCOPKQVKEƀWKF ommended as they have not been proved to
Ŧ Obsolete be useful.
• Other tests – Amniocentesis and culture of amniotic fluid
Ŧ Examination of cervicovaginal secretions has been used for diagnosis of infection but
Increase in fFN there is insufficient evidence of benefit to
Increase in IGF BP1 recommend its routine use.
Placental alpha-I microglobulin
• Perform ultrasonography to
- Sensitivity and specificity 99%–100%
– confirm gestational age
f HGVCNſDTQPGEVKP BP insulin-like growth factor binding – evaluate fetal well-being
protein 1.
CH 36_p522-533_v3.indd 526 18-07-2015 12:08:47

– estimate fetal weight

Box 36.8 Indications for immediate delivery
– exclude
multiple pregnancy • Woman in active labor
polyhydramnios • Nonreassuring fetal status
fetal anomalies.
• Fetal death
• Perform nonstress test to assess fetal
• 5KIPKſECPVXCIKPCNDNGGFKPI
well-being.
• Ascertain carrier status for group B strepto-
coccus (GBS) by prior vaginal swab/urine
culture. Immediate delivery
• Ascertain fetal presentation and position.
• Ascertain if woman is in labor. Indications for immediate delivery irrespective
of gestational age are listed in Box 36.8.
Subsequent management Gestational age-based management

Subsequent management may be immediate If there is no indication for immediate delivery,
delivery based on obstetric indications or based management depends on gestational age.
on gestational age. Initial evaluation is outlined in Figure 36.1.
oman ith atery

aginal ischarge
estational age
History uration of membrane rupture
Physical
physical e amination Chorioamnionitis
etal presentation
Cer ical effacement

peculum e amination Cer ical ilatation
atery ischarge
ern test itra ine test Confirm membrane rupture
etal ell being

Ultrasonography
estational age
etal eight
cti e labor
es Chorioamnionitis o Management base
mme iate eli ery
onreassuring fetal status on gestational age
etal eath
Figure 36.1 Initial evaluation of prelabor rupture of membranes. S , nonstress test.
CH 36_p522-533_v3.indd 527 18-07-2015 12:08:47

anagement o O at or a ter • There should be no clinical evidence of

ee s (at or near term) chorioamnionitis.
• There should be no colonization by GBS.
Two options are available for women who pres-
ent with PROM after 36 weeks’ gestation: anagement guidelines
1. Immediate induction of labor • The woman should be hospitalized.
2. Expectant management • Prophylactic broad-spectrum antibiotics
should be administered if duration of mem-
mmediate induction of labor
brane rupture exceeds 18 hours.
Current recommendation for management of • Fetal surveillance is mandatory. Daily fetal
women in this group is immediate induction of movement count, nonstress test, and biophys-
labor with oxytocin. ical profile are recommended.
• Amniotic fluid volume should be assessed by
• Earlier observational studies had shown an
ultrasonography every 24 hours.
increase in cesarean section rates with induc-
• Clinical signs of chorioamnionitis should be
tion, especially in women with an unfavora-
watched for.
ble cervix. However, subsequent studies and
• Duration of expectant management varies
meta-analysis have shown that immediate
with the center but the risk of chorioamnioni-
delivery, compared to expectant management,
tis increases after 24 hours. Hence, most cent-
has the following advantages:
ers induce labor after 24 hours.
– Reduced incidence of chorioamnionitis and
endometritis Management of PROM at/or after 36 weeks is
– Reduced rates of neonatal ICU admissions summarized in Figure 36.2.
– Reduced cost of treatment
– No increase in cesarean section rates
relabor rupture o membranes
• In randomized controlled trials, preinduc-
tion cervical ripening with prostaglandins has at ee s
no advantage over oxytocin induction alone. The management of PROM at this gestational
However, if vaginal misoprostol 25/50 μg age is based on the following observations:
6 hourly or prostaglandin E2 is used in women
• Acute and severe neonatal complications are
with an unfavorable cervix, a significant pro-
uncommon after 34 weeks’ gestation.
portion of women in this category deliver
• The specific gestational age beyond which
within 24 hours, without additional oxytocin
neonatal morbidity is definitely reduced is
• Women who deliver within 12 hours of rup-
34 weeks.
ture of membranes do not develop maternal
• The risk of chorioamnionitis increases by
or neonatal sepsis and therefore do not need
waiting.
prophylactic antibiotics as a routine.
• Expectant management prolongs pregnancy
• Prophylactic antibiotics (Inj. ampicillin 1 g
by only a few days.
and Inj. gentamicin 140 mg IV) are used only if
duration of rupture of membranes is t18 hours. Management
Expectant management • Immediate delivery is recommended at this
gestational age.
Expectant management may be acceptable in
• Preinduction cervical ripening by prostaglan-
women who refuse induction because 75%–80%
dins followed by induction with oxytocin is the
will deliver within 24 hours and the incidence of
recommended management.
cesarean section, operative vaginal delivery, and
• Cesarean section is performed only if there are
neonatal infection is not significantly increased.
specific indications.
Criteria to be satisfied before deciding on
• Corticosteroids are not recommended after
expectant management are as follows:
34 weeks.
• There should be no fetal distress. • Broad-spectrum antibiotics are administered
• The liquor should not be meconium stained. if the duration of rupture exceeds 18 hours.
CH 36_p522-533_v3.indd 528 18-07-2015 12:08:47

Confirm iagnosis
o igital aginal e amination
ot illing to un ergo in uction

o meconium
mme iate in uction recommen e
o fetal istress
o antibiotics unless uration of rupture hours
o chorioamnionitis
o coloni ation ith
pectant management
Monitor mother an fetus

ntibiotics if uration hours
eli er after hours
Figure 36.2 Management of prelabor rupture of membranes at/or after 36 weeks. BS, Group B streptococcus.
relabor rupture o membranes betamethasone for enhancing fetal lung matu-

at ee s rity are administered.
• If facilities for the care of preterm neonates are
Management at this gestational age is based on
inadequate, the woman should be transferred
the following facts:
to a higher center.
• Delivery before 32 weeks is associated with • On admission,
high risk of perinatal mortality and long-term – cord compression should be excluded and
sequelae due to prematurity. fetal well-being evaluated by continuous
• Prolongation of pregnancy can reduce these fetal heart rate monitoring and biophysical
risks. profile.
• Latency period is shorter in women with – occult uterine contractions should be
– low amniotic fluid index (<5 cm) excluded by external tocography.
– shorter cervix (length <3 cm) • Subsequent monitoring:
• Pregnancy has been prolonged for a mean – Clinical signs of sepsis: Fever, uterine ten-
duration of 7 days by expectant management derness, foul smelling discharge.
in different clinical trials. – Fetal well-being: Ultrasonography and bio-
• The woman should be transferred to a center physical profile on alternate days.
with facility for management of preterm Corticosteroids
babies.
Two doses of betamethasone (12 mg IM at 24
Management hour interval) should be administered. This
does not increase the risk of maternal or neona-
• Expectant management is recommended for
tal infection. Use of corticosteroids is discussed
women without maternal or fetal complications.
in detail in Chapter 35, Preterm labor.
• Immediate induction is undertaken if there are
Corticosteroids reduce the neonatal risk of
signs of fetal compromise, chorioamnionitis,
the following:
placental abruption, or established labor.
• The woman should be hospitalized and • Respiratory distress syndrome
advised bed rest with minimal activity. Broad- • Intraventricular hemorrhage
spectrum antibiotics for chorioamnionitis and • Necrotizing enterocolitis
CH 36_p522-533_v3.indd 529 18-07-2015 12:08:47

Antibiotics effects on the brain cells. It should be given when

Prophylactic antibiotics are recommended in preterm delivery is anticipated in the next 12
PROM before 34 weeks and should be adminis- hours and the fetus is viable. Benefit is seen even
tered as soon as rupture of membranes is con- when administered for 2 hours prior to delivery.
firmed. Antibiotics have the following beneficial Magnesium sulfate is safe, inexpensive, and eas-
effects: ily available. Dosage and administration are dis-
cussed in Chapter 35, Preterm labor.
• Increase the latency period
ocolytics
• Reduce the incidence of maternal and neona-
tal sepsis and intraventricular hemorrhage Tocolysis has not been found to be beneficial
in PPROM. It can increase the risk of sepsis by
According to a review of randomized trials,
delaying delivery in women with subclinical
the use of antibiotics has the following benefits:
infection.
• Reduction in chorioamnionitis Timing and mode of delivery
• Reduction in neonatal infection
• Reduced need for oxygen therapy to the newborn • Labor should be induced at 34 weeks.
• Reduced need to use surfactant for improving • Continuation of pregnancy beyond 34 weeks
fetal pulmonary maturity may be considered only if the drainage of
• Delivery between 3 and 7 days of the intervention amniotic fluid stops and amniotic fluid vol-
ume returns to normal.
ecommended drugs and dosage • Cesarean section is performed only for obstet-
Recommendations of the National Institute ric indications.
of Child Health and Human Development- • Cervical ripening with prostaglandins and
Maternal and Fetal Medicine Units (NICHD- labor induction with oxytocin is the recom-
MFMU) are given in Box 36.9. Ampicillin is effec- mended mode of delivery.
tive against group B streptococcus and aerobic
Management of PROM at 28–34 weeks is sum-
gram-negative bacilli, and erythromycin targets
marized in Figure 36.3.
Mycoplasma. Amoxicillin with clavulinic acid
should not be used since it increases the risk O be ore ee s
of necrotizing enterocolitis. A single dose of
azithromycin (1 g oral at admission or 250 mg Management at this gestational age is based on
oral once daily for 5 days) may be used instead the following facts:
of erythromycin. • Pregnancies before 24 weeks are considered
agnesium sulfate for neuroprotection previable even in developed countries. In
India, pregnancies up to 28 weeks have a poor
According to randomised trials, administra- prognosis in most centers and may be consid-
tion of magnesium sulfate to mothers at risk for ered previable.
preterm delivery at <34 weeks, gestation reduces • Associated abnormal placentation is found in
the risk of cerebral palsy and gross motor dys- many women and has a poor prognosis.
function. Magnesium sulfate is said to act • Prolongation of pregnancy may range from 1
through its vasodilator and anti-inflammatory to 5 weeks with conservative management.
• Risk of intrauterine death, neonatal complica-
tions such as pulmonary hypoplasia, respiratory
Box 36.9 IC D-MFM recommendaion
for antibiotics
distress, sepsis, intraventricular hemorrhage,
necrotizing enterocolitis, and long-term com-
• Inj. ampicillin 2 g IV 6 hourly and plications including bronchopulmonary dys-
for 48 hours
• Inj. erythromycin 250 mg IV 6 hourly plasia, limb deformities, and retinopathy are
Followed by increased.
• T. amoxicillin 250 mg oral 8 hourly and • Maternal and fetal complications correlate
for 5 days
• T. erythromycin 333 mg oral 8 hourly with oligohydramnios.
C D- National Institute of Child Health and Human • Risks and benefits vary with gestational age
Development-Maternal and Fetal Medicine Units. and risks are higher before 24 weeks.
CH 36_p522-533_v3.indd 530 18-07-2015 12:08:47

P M ee s
Hospitali e
History
Physical e amination
PP
Chorioamnionitis
Placental abruption es
eli er
etal compromise
cti e labour
o
pectant management

Mo ifie be rest
Corticosteroi s
ntibiotics
o es Magnesium sulfate
eli er at ee s Preterm labor
eli er
Figure 36.3 2TGNCDQTTWRVWTGQHOGODTCPGUCVŌYGGMU$22DKQRJ[UKECNRTQſNG056PQPUVTGUUVGUV
• Midtrimester PROM can occur following inva- – Antibiotics

sive procedures such as amniocentesis, fetos- – Corticosteroids
copy, and cordocentesis. The site of puncture – Deliver when labor sets in or if complica-
is small and most often closes spontaneously. tions occur
• Risks and benefits should be discussed with
the couple and management decided upon
accordingly. ther therapeutic
Management
modalities in P M
• Termination of pregnancy may be consid- Other modalities of treatment have been tried
ered in women with previable (<24–26 weeks) in the management of PROM. These include the
PROM. This option should be discussed with following:
the couple
• Amnioinfusion to increase the amniotic fluid
• In women who opt for continuation of preg-
volume
nancy and those >26 weeks' gestation, expect-
• Tissue sealants to close the defect in the
ant management is on the same lines as in
membranes
28–32 weeks. This includes the following:
– Fibrin patch
– Hospitalization and bed rest with toilet
– Platelets
privileges
– Cryoprecipitate
– Initial assessment of fetal status and uterine
– Gelfoam
contractions
– Subsequent serial monitoring of mother These methods of management are considered
and fetus experimental and need not always successful.
CH 36_p522-533_v3.indd 531 18-07-2015 12:08:47

Key points
• 2TGNCDQTTWRVWTGQHOGODTCPGU
241/KUFGſPGFCU estimate fetal weight, exclude multiple pregnancy, and
rupture of membranes before onset of regular uterine ascertain fetal presentation and position. Subsequent
contractions. management depends on gestational age.
• Physiological remodeling of collagen in the fetal mem- • Diagnosis of chorioamnionitis is usually clinical. The
branes, alteration in cytokines, matrix metalloproteinases signs are uterine tenderness, malodorous discharge,
and collagenase, and increase in intrauterine pressure fever, and tachycardia. Leukocyte count, C-reactive
can lead to PROM. RTQVGKPCOPKQVKEƀWKFEWNVWTGCPFXCIKPCNUYCDEWN-
• Risk factors for PROM are urogenital infections, tures are not sensitive and not used.
uterine overdistension, connective tissue disorders, • The recommended management of PROM at or after
KPXCUKXGRTQEGFWTGUCPFPWVTKVKQPCNFGſEKGPEKGU 36 weeks is immediate induction of labor since this
• The most important maternal complication of PROM reduces the risk of chorioamnionitis, endometritis,
is chorioamnionitis. Placental abruption, retained and neonatal intensive care admissions. Expectant
placenta, puerperal endometritis, and maternal sepsis management is reserved for those who are not willing
can also occur. for labor induction.
• Fetal/neonatal complications are fetal infection, cord • For women with PROM between 34 and 36 weeks,
prolapse, and prematurity and its complications. immediate delivery is recommended since acute and
Second trimester PROM can lead to pulmonary hypo- severe neonatal complications are rare after 34 weeks
plasia and limb deformities and long-term sequelae. and waiting increases the risk of chorioamnionitis.
• Women with PROM present with watery vaginal • Prelabor rupture of membranes at 28–34 weeks is
managed expectantly since delivery before 32 weeks
discharge. Uterine contractions may follow.
is associated with prematurity and its complications.
• Fluid can be seen discharging through the vulva, and
through the cervix on speculum examination. • Expectant management of PROM at 28–32 weeks
EQPUKUVUQHOQFKſGFDGFTGUVENQUGOQPKVQTKPIQH
• Digital vaginal examination should be avoided in mother and fetus, and administration of corticosteroids
PROM since it increases the risk of infection. and antibiotics. Tocolytics are not recommended.
• 5GXGTCNVGUVUCTGWUGFVQEQPſTO241/6JGUGCTG • Prelabor rupture of membranes before 28 weeks’
nitrazine test, fern test, ultrasonography, and indigo gestation is associated with poor fetal survival. Fetal
carmine test. complications, long-term sequelae, and perinatal
• Management consists of initial evaluation to establish OQTVCNKV[CTGJKIJGT4KUMUCPFDGPGſVUUJQWNFDGFKU-
gestational age and ascertain duration of membrane cussed with the couple before management decisions
rupture and ultrasonography to evaluate fetal well-being, are made.
Self-Assessment
Mrs. AN, 28, third gravida, was admitted to the labor room
Case 1 at 39 weeks’ gestation with history of watery discharge for
Mrs. HK, 30, primigravida at 30 weeks’ pregnancy, was 3 hours. There were no uterine contractions.
referred from a peripheral hospital with history of watery 1. 9JCVYQWNF[QWNKMGVQMPQYD[JKUVQT[!
discharge for 12 hours. On arrival at the local hospital,
2. Describe the physical examination.
she was told that the membranes had ruptured and, since
3. 9JCVKUVJGOCPCIGOGPV!9J[!
she was preterm, she had to be in a tertiary center.
4. +UVJGTGCPCNVGTPCVKXGOGVJQFQHOCPCIGOGPV!
2. *QYYKNN[QWGXCNWCVGVJGYQOCPCVCFOKUUKQP!
3. Why should the woman be shifted to a tertiary level
EGPVGT!
4. 9JCVKUVJGOCPCIGOGPVCPFYJ[!
CH 36_p522-533_v3.indd 532 18-07-2015 12:08:47

2. a. Maternal temperature, pulse, uterine tenderness,

Answers contractions, and fetal presentation and
position.
Case 1 b. Speculum examination—cervical effacement,
1. Diagnosis is by history of watery vaginal discharge. Vis- FKNCVCVKQPEQNQTQHCOPKQVKEƀWKFRTGUGPEGQH
ualization of discharge at the vulval outlet and through foul-smelling discharge, and cord prolapse. AVOID
VJGEGTXKECNQUQPURGEWNWOGZCOKPCVKQPYKNNEQPſTOVJG digital vaginal examination.
diagnosis. If in doubt, nitrazine test can be performed. c. Nonstress test for fetal heart pattern.
A drop of discharge may be collected from the posterior 3. Immediate delivery is the recommended
fornix and smeared on a glass slide to look for ferning. management. This reduces the risk of chorioam-
Ultrasonography may reveal oligohydramnios. nionitis, endometritis, and neonatal intensive care
2. Assess gestational age, fetal presentation and admission. Labor should be induced with oxytocin.
position. At admission, perform cardiotocography Antibiotics should be given if duration exceeds
to exclude cord compression. Look for uterine 18 hours.
contractions. Check maternal pulse and temperature 4. Expectant management is an alternative if the woman
and look for uterine tenderness and malodorous is not willing for labor induction.
discharge to exclude chorioamnionitis.
3. Since the gestational age is 30 weeks, facilities for
neonatal care of preterm should be available. Sample questions
4. Expectant management is the treatment of choice
since delivery at 30 weeks has high perinatal mortal- Long-answer questions
ity due to prematurity.
1. &GſPGRTGNCDQTTWRVWTGQHOGODTCPGU
241/
'ZRGEVCPV OCPCIGOGPV KU D[ OQFKſGF DGF TGUV Discuss the etiology and management of PPROM at
maternal and fetal monitoring, corticosteroids for 29 weeks, gestation.
accelerating fetal pulmonary maturity, and prophy- 2. *QYYKNN[QWGXCNWCVGCPFOCPCIG241/CVVGTO!
lactic antibiotics. Administer of magnesium sulfate for
fetal neuroprotection if labor begins before 34 weeks.
Case 2 1. Risk factors for PROM
2. Complications of PROM
1. Duration of watery discharge, any digital vaginal
3. Tests for diagnosis of rupture of membranes
examination performed elsewhere, fever, malodorous
discharge, fetal movements.
CH 36_p522-533_v3.indd 533 18-07-2015 12:08:48

Postterm
37 Pregnancy
Case scenario
Mrs. DS, 26, a primigravida, had regular menstrual cycles. According to

her LMP, she was 41 weeks. She and her husband were anxious that she
had not delivered even a week after the expected date of confinement.
Introduction The concern with late-term and postterm

pregnancies is the association with perinatal
A pregnancy that is prolonged beyond the morbidity and mortality. It is essential that the
expected date of delivery causes great anxiety gestational age be accurately confirmed in early
for the pregnant couple. Although the gestation pregnancy to help in the correct diagnosis and
at which the mother should be delivered after appropriate management of late-term and post-
the due date varies in different guidelines, it is term pregnancies.
accepted that postterm pregnancies should be Although 42 weeks is used as a cutoff for the
closely monitored and delivered before compli- definition of postterm pregnancy, it does not rep-
cations arise. resent an absolute threshold. The risk of meco-
nium and perinatal complications increases
&GſPKVKQP beyond 41 weeks’ gestation in all countries. The
South Asian fetus (including Indian) is known to
The term late-term pregnancy is used to define mature 1 week earlier, and the rates of antepar-
a pregnancy between 41 weeks and 41+6 weeks, tum stillbirth begin to rise 1 week earlier than in
while pregnancies at 42 weeks (294 days) and the Western population. Therefore, management
beyond are defined as postterm, postdated, or of postterm pregnancies must be tailored to suit
prolonged. the population.
Based on this evidence, it is prudent, in the
• Late term: 41 weeks to 41+6 weeks Indian context, to apply the term postterm or
• Postterm: 42 weeks and beyond postdated to pregnancies at 41 weeks or beyond.
CH 37_p534-541_v3.indd 534 18-07-2015 12:18:54

Postterm Pregnancy 535
Incidence parturition (see Chapter 6, Physiology of labor).

The absence of the fetal brain causing dysfunc-
The incidence of postterm pregnancy varies tion of the HPA axis is considered responsible
with the approach to management, criteria for prolonged pregnancy in anencephalic preg-
for dating of pregnancy, and the population. nancies. Placental sulfatase converts dehydroe-
Approximately 2% of pregnancies go beyond piandrosterone sulfate (DHEAS) to estrogen,
42 weeks in India and 10% beyond 41 weeks. The which is involved in triggering parturition.
incidence of postterm pregnancy (>42 weeks) is Deficiency of placental sulfatase has also been
approximately 6%–7% in Western countries. implicated in prolonged pregnancy.
isk factors for postterm Consequences of postterm

pregnancy pregnancy
There is no identifiable etiological cause for the Late-term and postterm pregnancies are asso-
majority of postterm pregnancies. The most ciated with fetal, neonatal, and maternal risks.
consistent risk factor for postterm pregnancy is Placental dysfunction and insufficiency occurs
a previous postterm pregnancy. There is a two with placental aging and is the cause of perinatal
to threefold increase in the risk of another post- mortality and morbidity. Placental infarcts, cal-
term pregnancy following a previous postterm cification, fibrin deposits around the villi, and
pregnancy. This risk of recurrence becomes intervillous and arterial thrombosis are seen in
fourfold after two postterm pregnancies. The the placentae of postterm pregnancies. Placental
risk factors for postterm pregnancy are listed in apoptosis or programmed cell death increases
Box 37.1. significantly. These changes lead to placental
Other risk factors for postterm pregnancy are insufficiency, which in turn results in oligohy-
obesity, nulliparity, and male fetus. Genetic dramnios and cord compression.
predisposition has been found in some ethnic Meconium passage may be a function of fetal
groups, and the risk is higher if the mothers of maturity but also occurs due to cord compres-
women have had postterm pregnancies. sion and hypoxia. The changes of postmaturity
The fetal hypothalamic–pituitary–adrenal syndrome (described later) are also attributed to
(HPA) axis plays a major role in the initiation of placental senescence.
On the other hand, the placenta may con-
tinue to function and the fetus continues to
grow, though at a lower rate. Postterm pregnancy
is associated with a twofold increased risk of
Box 37.1 isk factors for postterm pregnancy
macrosomia.
• History of postterm birth Postterm pregnancies are also known to be
Ŧ 1 previous postterm birth associated with an increased risk of neonatal
Twofold to threefold increase in risk convulsions, meconium aspiration syndrome,
Ŧ 2 previous postterm births and low Apgar scores.
Fourfold increase in risk
The pathophysiology of fetal complications
• Nulliparity
in postterm pregnancies is summarized in
• Male fetus
• $/+ŮMIO2 Figure 37.1.
• Older maternal age
• Fetal disorders
Ŧ Anencephaly Perinatal mortality
Ŧ 2NCEGPVCNUWNHCVCUGFGſEKGPE[
Birth at t41 weeks’ gestation is associated with
• Genetic predisposition
30% greater neonatal mortality than at 38–40
B body mass index. weeks’ gestation.
CH 37_p534-541_v3.indd 535 18-07-2015 12:18:54

Postterm pregnancy
Continue
Placental aging
placental function
Placental apoptosis
etal macrosomia
nter illous ascular thrombosis
ibrin eposits
Calcification
nfarction
Prolonge labor
houl er ystocia
nstrumental eli ery
Cesarean section
Placental insufficiency
irth injury
etal hypo ia ro th restriction ligohy ramnios
Cor compression
Meconium passage
Meconium aspiration
syn rome
Figure 37.1 Pathophysiology of fetal complications in postterm pregnancy.
Fetal risks due to placental aging is often associated with postterm pregnancy.
Oligohydramnios is associated with an increased
As the placenta ages, its function decreases, risk of the following:
resulting in several risks to the fetus (Box 37.2).
• Umbilical cord compression
2NCEGPVCNKPUWHſEKGPE[ • Fetal heart rate abnormalities
• Lower Apgar scores
The placental changes described earlier give
rise to placental insufficiency and fetal hypoxia.
Placental dysfunction leads to decreased fetal
Meconium passage
renal blood flow and reduced urine production. Meconium staining of the amniotic fluid, skin,
This results in oligohydramnios. membranes, and umbilical cord is commonly
seen with the postmature newborn. Meconium
ligohydramnios passage may be a sign of the following:
Decreased amniotic fluid or oligohydram- • Physiological maturation of the gut
nios is a sign of placental insufficiency and • Fetal hypoxia which may result from
CH 37_p534-541_v3.indd 536 18-07-2015 12:18:54

Box 37.2 Fetal risks due to placental aging

• 2NCEGPVCNKPUWHſEKGPE[
Ŧ Oligohydramnios
• Oligohydramnios
Ŧ Umbilical cord compression
Ŧ Fetal heart rate abnormalities
Ŧ Lower Apgar scores
• Meconium passage
Ŧ Maturation of gut
Ŧ Fetal hypoxia Figure 37.2 The postterm infant. There is very little
Cord compression subcutaneous tissue. The skin is dry and peeling and has
Placental insufficiency prominent creases.
• Meconium aspiration syndrome
Ŧ Chemical pneumonitis
• Fetal distress Box 37.3 Appearance of the postterm infant
Ŧ Nonreassuring fetal heart tracings • Small for gestational age
• Increased risk of cesarean section • Long, thin body with long nails
• Postmaturity syndrome Ŧ Minimal subcutaneous tissue
• Skin
Ŧ Dry
Ŧ Meconium stained
– cord compression
Ŧ Parchment-like and peeling
– placental insufficiency
Ŧ Loose over the thighs and buttocks
In the presence of oligohydramnios, the Ŧ Prominent creases
meconium is thick since it is not diluted by the • Sparse or absent lanugo
amniotic fluid. • Increased scalp hair
Meconium aspiration syndrome Fetal risks due to continued

The fetus may aspirate meconium before, during, placental function
or after birth. In some newborns, the aspirated
meconium causes chemical pneumonitis, air- As described earlier, some fetuses continue to grow
way obstruction, and pulmonary hypertension, postterm due to continued placental function.
a syndrome known as meconium aspiration syn- This can result in macrosomia (see Chapter 33,
drome. This is associated with a high risk of peri- Fetal growth disorders: Growth restriction and
natal death. macrosomia).
Fetal distress Macrosomia

Macrosomia is associated with an increased
Intrapartum fetal distress is common in post-
incidence of the following:
term fetuses. Variable decelerations and pro-
longed decelerations occur in labor due to cord • Prolonged labor
compression. This increases the risk of a cesar- • Operative vaginal delivery
ean section. • Cesarean section
Postmaturity syndrome • Birth injury
Placental insufficiency can lead to the postma-

turity (or dysmaturity) syndrome. This occurs in
Maternal risks
10%–20% of postterm pregnancies. These infants Maternal risks are a consequence of macrosomia
exhibit characteristics of chronic intrauterine mal- and other fetal complications. Late-term and
nutrition (Fig. 37.2). The distinctive appearance of postterm pregnancies are associated with sev-
the postmature fetus is summarized in Box 37.3. eral maternal risks (Box 37.4).
CH 37_p534-541_v3.indd 537 18-07-2015 12:18:55

alone. When ultrasonography is used to confirm

Box 37.4 Maternal risks in the postterm
pregnancy LMP dating, the rate of postterm pregnancies
drops (see Chapter 10, Obstetric ultrasound and
• Severe perineal lacerations other imaging).
• Infection
• Postpartum hemorrhage • Accuracy of estimation of gestational age
• Instrumental delivery by ultrasonography in the first trimester is
• Cesarean section ±5–7 days.
• Parental anxiety • The first trimester gestational age assignment
significantly reduces the incidence of induc-
tion for pregnancy of >41 weeks.
Management of the
Membrane sweeping
late-term and postterm Membrane sweeping (or stripping) is associ-
pregnancy ated with a significant reduction in the num-
ber of pregnancies that go beyond 41 weeks’
As gestational age advances, the perinatal gestation (see Chapter 16, Induction of labor).
mortality increases. As discussed earlier, the Sweeping the membrane from the uterine wall
gestational age at which the increase in mor- causes increased local production and release
tality occurs varies with ethnicity. The mortal- of prostaglandin F2D from the decidua and
ity is lowest at 40 weeks in Caucasian popula- adjacent membrane, thereby leading to onset
tions and at 39 weeks in South Asian countries of labor. It should be offered to women com-
(including India). The rate of antepartum mencing at 40 weeks.
stillbirths increases significantly after 41 The steps taken to prevent postterm preg-
weeks. Hence, it is recommended that women nancy are listed in Box 37.5.
should be induced by 41 completed weeks
of gestation and be delivered not later than
41+3 weeks. Antenatal surveillance
The management of the late-term and post-
term pregnancies involves a three-pronged for fetal well-being
approach: Since there is an increased risk of oligohydram-
• Prevention of postterm pregnancy nios and fetal hypoxia/asphyxia in the late-
• Antenatal surveillance for fetal well-being term and postterm pregnancy, it is advisable
• Cervical ripening and induction of labor to start the fetal surveillance (see Chapter 11,
Antepartum fetal surveillance) from 40 weeks,
although Western guidelines recommend start-
Prevention of postterm ing from 41 weeks. The recommended tests are
listed in Box 37.6.
pregnancy
Accurate determination
Box 37.5 Prevention of postterm pregnancy
of gestational age
• Accurate determination of gestational age
Using the woman’s recall of the last menstrual Ŧ $GUVFQPGKPVJGſTUVVTKOGUVGT
period (LMP) alone to assign gestational age and Ŧ Accuracy ±5–7 days.
the estimated date of delivery has been proved Ŧ Reduces incidence of induction for postterm
to be unreliable. Often a pregnancy is incorrectly • Membrane sweeping or stripping
classified as late term or postterm because of Ŧ Should be offered to women from 40 weeks
wrong dates. Some women may conceive later in Ŧ Increases local production and release of prosta-
glandin F2D
the cycle because of delayed ovulation, and this
Ŧ Leads to onset of labor
may also alter the due date calculated by LMP
CH 37_p534-541_v3.indd 538 18-07-2015 12:18:55

may actually decrease the risk of a cesarean sec-

Box 37.6 Fetal surveillance in the late-term
and postterm pregnancy tion with postterm pregnancy.
• Daily fetal movement count

• #UUGUUOGPVQHCOPKQVKEƀWKFXQNWOG Intrapartum management
• NST Due to the increased risk of perinatal morbidity
• Frequency of NST and AFI
and mortality, the fetus must be monitored care-
Ŧ Twice weekly till delivery
fully during labor.
A COPKQVKEƀWKFKPFGZ056PQPUVTGUUVGUV
• In labor, early artificial rupture of membranes
is suggested to check for meconium.
• Early amniotomy helps in identifying thick
Cervical ripening and meconium. If meconium is present in very early
induction of labor labor in a nullipara, a cesarean section is rec-
ommended. In multiparas and those in active
Induction of labor at 41 completed weeks is
labor, the treatment must be individualized.
recommended over expectant management.
• Electronic fetal monitoring is recommended
Women in this situation also prefer induction
for all postterm pregnancies in labor.
over waiting for spontaneous labor. It has been
• In case of nonreassuring fetal heart patterns
shown that induction of labor
(prolonged or variable decelerations), delivery
• does not increase cesarean section rate and should be expedited depending on the stage of
• lowers perinatal mortality. labor.
• If the fetus is macrosomic, prolonged labor
If the cervix is not ripe, cervical ripening is
and shoulder dystocia should be anticipated.
indicated prior to induction (see Chapter 16,
Induction of labor). Induction has not been Management of late-term and postterm preg-
shown to increase the cesarean section rate and nancies is summarized in Figure 37.3.
Late term an postterm

pregnancy
echec gestational age from

first trimester ultrasoun
ee s
ee s
ssessment of cer i
eeping of egin fetal Cer i unfa orable

Cer i fa orable
membranes sur eillance Cer ical ripening
aily fetal mo ement count arly artificial rupture hic meconium in arly artificial rupture
onstress test of membranes early labor of membranes
mniotic flui in e
ytocin ytocin
Cesarean section
etal monitoring etal monitoring
Figure 37.3 Management of late-term and postterm pregnancies.
CH 37_p534-541_v3.indd 539 18-07-2015 12:18:55

Key points
• The term late term RTGIPCPE[KUWUGFVQFGſPGC • &GETGCUGFCOPKQVKEƀWKFQTQNKIQJ[FTCOPKQUKUCUKIP
pregnancy between 41 weeks and 41+6 weeks. QHRNCEGPVCNKPUWHſEKGPE[CPFKUQHVGPCUUQEKCVGFYKVJ
• Pregnancies at 42 weeks (294 days) and beyond are postterm pregnancy.
FGſPGFCUpostterm, post ate , or prolonge . • Oligohydramnios leads to cord compression and
• Late-term and postterm pregnancies are associated meconium passage.
with perinatal morbidity and mortality. • $KTVJCVŮYGGMUŏIGUVCVKQPKUCUUQEKCVGFYKVJ
• The risk of meconium and perinatal complications greater neonatal mortality than at 38–40 weeks’
increases beyond 41 weeks’ gestation in all coun- gestation.
tries. Based on evidence, it is prudent, in the Indian • Postterm pregnancy can be prevented by accurate
context, to apply the term postterm or postdated to determination of gestational age and by sweeping of
pregnancies at 41 weeks or beyond. membranes.
• The most consistent risk factor for postterm pregnancy • #PVGPCVCNUWTXGKNNCPEGKPENWFKPICPVGPCVCNƀWKFKPFGZ
is a previous postterm pregnancy. and nonstress test is recommended after 40 weeks.
• Postterm pregnancy is associated with a twofold • It is recommended that women should be induced by
increased risk of macrosomia. 41 completed weeks of gestation and be delivered not
• 2NCEGPVCNKPUWHſEKGPE[NGCFUVQVJGRQUVOCVWTKV[
QT later than 41+3 weeks.
dysmaturity) syndrome, which occurs in 10%–20% of • +PNCDQTGCTN[CTVKſEKCNTWRVWTGQHOGODTCPGUKUUWI-
postterm pregnancies. gested to check for meconium.
• /GEQPKWOUVCKPKPIQHVJGCOPKQVKEƀWKFUMKPOGO- • Electronic fetal monitoring is recommended for all
branes, and umbilical cord is commonly seen with a postterm pregnancies in labor.
postmature newborn.
Self-Assessment
Case-based questions Answers
Case 1 Case 1
Mrs. DS, 26, is a primigravida. Her menstrual cycles were 1. 6JGIGUVCVKQPCNCIGQHYGGMUKUEQPſTOGFD[
regular and according to her LMP, she is now 41 weeks. rechecking the LMP and the gestational age assigned
D[VJGſTUVVTKOGUVGTWNVTCUQWPFUECPKHCXCKNCDNG+H
1. *QYYKNN[QWEQPſTOJGTIGUVCVKQPCNCIG! not, gestational age assigned by the second trimester
2. 9JGPYKNN[QWFGNKXGTJGT! scan is used.
3. *QYYKNN[QWFGNKXGTJGT! 2. Since she is 41 weeks, she can be induced immedi-
4. *QYYKNN[QWOCPCIGJGTKPVTCRCTVWO! ately and delivered.
3. Pelvic examination should be performed to assess
Bishop score. If unfavorable, preinduction ripening
Case 2 should be followed by rupture of membranes and
Mrs. GH, 31, is a gravida 2, para 1, live 1. Labor was oxytocin infusion.
induced at 41 weeks in her last pregnancy. She is now 4. Intrapartum electronic fetal monitoring is essential.
41+3 weeks and has been referred from a primary center. If there is thick meconium in early labor with an
unfavorable cervix, a cesarean section should be
1. 9JCVCTGVJGTKUMUVQVJGHGVWU! done. Watch for prolonged labor and fetal heart
2. 9JCVCTGVJGHGCVWTGUQHRQUVOCVWTKV[U[PFTQOG! decelerations. If the fetus is macrosomic, watch for
3. Does postterm pregnancy pose any increased risk to shoulder dystocia.
VJGOQVJGT!
4. What would be the appropriate management plan
HQTJGT!
CH 37_p534-541_v3.indd 540 18-07-2015 12:18:55

Case 2 Sample questions

1. Postterm pregnancies are known to be associated
with an increased risk of perinatal morbidity and mor- Long-answer question
tality. The common risks are macrosomia, postma- 1. 9JCVKURQUVVGTO
RQUVFCVGFRTGIPCPE[!*QYKUKV
VWTKV[U[PFTQOGQNKIQJ[FTCOPKQUCPFHGVCNJ[RQZKC OCPCIGF!
asphyxia.
2. The postmaturity syndrome results in loss of
UWDEWVCPGQWUHCVTGUWNVKPIKPCNQPIVJKPDQF[NQPI Short-answer questions
ſPIGTPCKNUFT[RGGNKPICPFYTKPMNGFUMKPCPF
increased scalp hair. 1. Postmaturity syndrome
3. Maternal risks are severe perineal laceration, 2. Antenatal surveillance in postterm pregnancy
infection, postpartum hemorrhage, cesarean section,
and parental anxiety.
4. Immediate induction of labor with cervical ripening,
rupture of membranes, and oxytocin. A cesarean
section is recommended if the liquor is meconium
stained and cervix is unfavorable.
CH 37_p534-541_v3.indd 541 18-07-2015 12:18:55

Red Cell
38 Alloimmunization
Case scenario
Mrs. MN, 26, gravida 2, para 0, had a miscarriage a year ago. Her blood
group and Rh typing were not done. She did not receive anti-D after the
miscarriage. In the current pregnancy, she was found to be Rh negative
and her husband was Rh positive. An indirect Coombs test showed a titer
of 1: 32. The couple did not know the implications of the test and were
worried about its effect on the current pregnancy. They came to the clinic
for counseling and antenatal care.
Hemolytic disease of the newborn (HDN) or A mother mounts an immune response when
erythroblastosis fetalis used to be a major cause exposed to a blood group factor (red cell antigen)
of fetal loss and infant mortality. A major cause that is not present in her blood. The immune
of HDN is an incompatibility of the rhesus (Rh) response results in the production of immuno-
blood group factor between the mother and the globulin G (IgG) antibodies. This is called red cell
fetus, also known as red cell alloimmunization. alloimmunization.
Most commonly, hemolytic disease is triggered by The transplacental passage of these antibod-
the D antigen. The discovery of anti-D immuno- ies attacks the fetal red blood cells (RBCs) that
globulin to prevent alloimmunization, along are positive for these surface antigens, resulting
with early and accurate diagnosis of fetal red cell in hemolytic disease of the fetus and newborn
hemolysis using amniocentesis and ultrasonog- (HDFN).
raphy has reduced mortality remarkably.
CH 38_p542-559_v3.indd 542 18-07-2015 13:58:32

Red Cell Alloimmunization 543
Red cell alloimmunization may occur as a conse- Incidence of h-negative

quence of either of the following:
• Fetomaternal hemorrhage (FMH) in a preg-
individuals
nancy where the fetus has inherited a blood The incidence of Rh-negative individuals varies
group factor from the father that the mother by race. It is the lowest in Asians, with an inci-
does not have dence of 0.3% in the Chinese and Japanese. It
• Maternal transfusion with blood or blood is the highest in the Basques of Spain with an
products containing blood group factors that incidence of 30%–35%. In Caucasians, the inci-
the mother does not have dence of Rh-negative genotype is 15%. In India,
the incidence is approximately 8%–10% of the
population.
The h blood group system
h factor
There are 50 different red cell surface antigens
capable of causing maternal alloimmuniza- The Rh blood system is collectively called the Rh
tion and fetal hemolytic disease. Of these, the factor and includes the D, c, C, e, and E antigens.
Rh blood group system is the most common. It should be remembered that no d (little d) anti-
The Rh system was named after rhesus mon- gen exists and therefore d denotes the absence
keys whose blood was used in making the of the D antigen. The D (big D) antigen of the Rh
discovery. blood group system (Rh D) causes most cases of
The Rh system was discovered in 1940 when severe hemolytic disease.
Landsteiner and Weiner injected rhesus monkey The chronology of discovery of the Rh factor
erythrocytes into rabbits and guinea pigs. The and HDN is summarized in Box 38.1.
antisera that resulted from this caused aggluti-
nation in 85% of blood samples of white indi- Inheritance of the h factor
viduals. Agglutination denotes the presence of
Rh antigens, and the individual is Rh positive The Rh antigens are encoded by three sets of
(Fig. 38.1). Absence of agglutination denotes that allelomorphic genes—D(d), Cc, and Ee—in all
the individual is Rh negative. Subsequently, a humans. Every individual inherits one of each
causal relationship was found between the pres- set (three each) from each parent. However, Rh
ence of these antibodies in Rh-negative women positivity is determined only by the presence of
and the development of hemolytic disease in the the D antigen. If D is inherited from only one
neonate. parent, the individual is Rh-positive heterozy-
gous (e.g.,Cde/cDe). On the other hand, if D is
h
antigen
Box 38.1 Timeline of discovery of h factor
and D
1939: HDN (erythroblastosis fetalis) described by
Levine and Stetson; cause not known
1940: Rh factor discovered by Landsteiner and Weiner
1941: HDN linked to Rh factor by Levine, Ketrin, and
Burnham
8GTKſECVKQP D[ %JQYP VJCV VTCPURNCEGPVCN RCU-
sage of Rh D–positive erythrocytes into the ma-
ternal circulation caused Rh immunization
1960: The administration of Rh D IgG (anti-D immuno-
globulin) demonstrated to prevent Rh D alloim-
Figure 38.1 Diagrammatic representation of Rh surface munization
antigens. Individuals with the surface antigens are Rh
positive and those without the antigens are Rh negative. D , hemolytic disease of the newborn
CH 38_p542-559_v3.indd 543 18-07-2015 13:58:33

inherited from both parents, the individual is ather h positi e homo ygous
Rh-positive homozygous (e.g., cDe/CDe). Those
who are homozygous recessive (dd) are Rh nega- Mother
tive (lacking Rh antigens). h negati e
Despite the genetic complexity, a simple homo ygous
model using the two alleles D and d usually can
a.
predict the inheritance of this trait (Box 38.2).
ather h positi e hetero ygous
Chance of having h-positive
Mother
fetus for h-positive father h negati e
homo ygous
and h-negative mother
b.
If the father is Rh positive and the mother is Rh
negative, the fetus will be affected by Rh allo-im- Figure 38.2 Inheritance of Rh factor. a. A homozygous
munization only if it is Rh positive. The risk of Rh-positive father will have 100% Rh-positive babies with
an Rh-negative mother. b. A heterozygous Rh-positive
the fetus being Rh positive depends on whether
father will have 50% Rh-positive babies with an
the father is homozygous (DD) or heterozygous
Rh-negative mother. The other 50% will be Rh negative.
(Dd). The homozygous father will have 100%
chance of having an Rh-positive baby with an
Rh-negative mother (Fig. 38.2a), whereas a het-
erozygous father has a 50% chance of having an caused by prior transfusion if Kell compatibility
Rh-positive baby (Fig. 38.2b). was not checked for when the blood was cross-
Regardless of the father’s genotype, if he is matched. Anti-c and anti-E antibodies can also
Rh positive and the mother is Rh negative, it is cause hemolytic disease. Women with sensiti-
assumed that there will be an incompatibility zation to antigens other than D that are known
issue, and the pregnancy is managed accordingly. to cause hemolytic disease are uncommon and
After birth, the Rh factor of the infant is checked. are managed in the same way as women with D
alloimmunization.
ther minor antibodies

h alloimmuni ation in
Other than D, the most frequently encountered
antibodies are Lewis antibodies (Lea and Leb) pregnancy
and I antibodies, but they are not implicated
Rh alloimmunization in pregnancy is a conse-
in HDN. Kell antibodies (anti-K) can produce
quence of Rh-positive fetal blood leaking into
HDN. Kell alloimmunization is frequently
the circulation of an Rh-negative mother.
Box 38.2 Inheritance of the h factor Pathophysiology

• Three sets of allelomorphic genes If an Rh-positive mother is pregnant with an
Ŧ D d), Cc, and e Rh-negative fetus, then there is opportunity
• One of each set inherited for the Rh-positive fetal blood to mix with the
Ŧ Three each (e.g.,cDe/CDe) maternal blood (Fig. 38.3).
• If D present The conditions in which transplacental leak-
Ŧ Rh positive
age of fetal blood can occur are listed in Box 38.3.
DD present
When the maternal immune system is
- Homozygous Rh positive (35% of individuals)
presented with a foreign protein (Rh antigen),
D(d) present
- Heterozygous Rh positive (65% of individuals) it mounts a response by producing immu-
noglobulin M (IgM) and later IgG antibodies
h rhesus. (Fig. 38.4). IgG antibodies cross the placenta. The
CH 38_p542-559_v3.indd 544 18-07-2015 13:58:33

In the first affected pregnancy, the fetal

Box 38.3 Conditions in which transplacental
leakage of fetal blood can occur effects of alloimmunization either are nonexis-
tent or tend to be less severe. The exception is a
• FMH woman who has developed antibodies following
Ŧ Antepartum
a blood transfusion and is pregnant for the first
Ŧ Intrapartum
time. The fetal effects worsen with each subse-
• Abortion
Ŧ Therapeutic
quent affected pregnancy.
Ŧ Spontaneous In the subsequent pregnancy (if the fetus is
Ŧ Molar pregnancy Rh-positive), the antibodies cross into the fetus,
• Ectopic pregnancy attack them and cause hemolysis (Fig. 38.5).
• Placental abruption
• Abdominal trauma
• Obstetric procedures
Fetomaternal hemorrhage
Ŧ Amniocentesis Fetomaternal hemorrhage (FMH) or leaking of
Ŧ Chorionic villus sampling (CVS) fetal blood into the maternal circulation occurs in
Ŧ Fetal blood sampling (FBS)
as many as 75% of women during delivery. The fre-
Ŧ External cephalic version
quency and volume of spontaneous FMH increase
Ŧ Manual removal of the placenta
with advancing gestational age and are highest at
fetomaternal hemorrhage. delivery. The quantity of FMH is the same whether
it is a vaginal delivery or a cesarean section. The
majority will have a leak of <3 mL. The risk of sensiti-
zation depends on the volume of FMH (Table 38.1).
woman will carry these antibodies throughout her Hemorrhage volumes sufficient to cause
life. This may happen even before a pregnancy if alloimmunization are produced in 15%–50% of
an Rh-negative woman receives a transfusion of births. However, only <1% of women will have
an Rh-positive blood product (RBCs or platelets). FMH of >15 mL.
etal re bloo cells ith Maternal re bloo cells

h surface antigens ith absent h surface
antigens
a. b.
Figure 38.3 Transplacental transmission of fetal blood cells. a.The Rh-positive fetus in the Rh-negative mother. b. Blood
cells with the Rh surface antigen can cross the placenta into the maternal circulation in certain clinical situations.
CH 38_p542-559_v3.indd 545 18-07-2015 13:58:33

nti h
antibo y
Table 38.1 The risk of sensiti ation in relation to
the volume of FM
olume of FM (mL) isk of sensiti ation ( )

0.1 3
0.2–1 25
>5 65
, fetomaternal hemorrhage.
of the mother. ABO incompatibility confers

substantial protection against the primary Rh
immune response. In spite of the FMH, there are
factors that prevent alloimmunization in some
Rh-negative women (Box 38.4). ABO incompati-
bility protects against Rh alloimmunization.
The risk of FMH can be reduced in the ante-
natal period as well as during delivery (Box 38.5).
Figure 38.4 Maternal production of Rh antibodies (IgG).

atural history of red cell
g immunoglobulin G. alloimmuni ation
The first pregnancy is referred to as the primary
sensitizing pregnancy. The maternal primary
immune response to the D antigen takes an
average of 12–16 weeks but may take up to 12
months. The response is usually weak, consist-
ing predominantly of IgM that does not cross
the placenta. The weak response, combined with
the fact that most of the significant FMH occurs
during delivery, protects most first pregnancies
from severe disease.
Box 38.4 Fetomaternal hemorrhage and allo-

immuni ation
• FMH
Ŧ Increases with gestational age
30% in third trimester
Ŧ Occurs in 75% of women at delivery
Ŧ Majority <3 mL
Ŧ 5WHſEKGPVVQECWUGCNNQKOOWPK\CVKQP
Figure 38.5 Maternal antibodies identify fetal red cells as 15%–50% of women
foreign protein and destroy them, causing hemolysis. Factors affecting alloimmunization
Ŧ Frequency and volume of FMH
Ŧ ABO incompatibility
Protects against primary Rh immune response
Antibody response to FMH varies consid- Ŧ Immunogenicity of fetal RBCs
erably in individuals and depends on gesta- Ŧ Maternal capacity for immunogenic response
tional age, volume of hemorrhage, antigenicity
of RBCs, and immunogenic response capacity fetomaternal hemorrhage; BC red blood cell; h, rhesus.
CH 38_p542-559_v3.indd 546 18-07-2015 13:58:33

Box 38.5 educing the risk of FM in the Box 38.6 atural history of h alloimmuni ation
h-negative mother
• First pregnancy
• Antenatal period Ŧ Primary sensitizing pregnancy
Ŧ Invasive tests only if absolutely indicated Ŧ Immune response takes
Ŧ Extrauterine/intrauterine manipulations only if 12–16 weeks
absolutely indicated Up to 12 months
Ŧ Force avoided during all extrauterine/intrauterine Ŧ Immune response weak
manipulations Ŧ Mostly IgM antibodies
Ŧ Abdominal palpation minimized in placental • Subsequent pregnancies
abruption Ŧ Amnestic response
• Vaginal delivery Ŧ Rapid response
Ŧ Immediate cord clamping Ŧ IgG antibodies
Ŧ Methylergometrine avoided Cross placenta
Ŧ Manual removal of placenta avoided Destroy fetal red cells
Ŧ Blood spill into the peritoneal cavity minimized/ g immunoglobulin G; g immunoglobulin M; h rhesus.
avoided
Ŧ Manual removal of placenta avoided
Ŧ Uterus to be handled gently small amount of bilirubin produced by hemoly-
sis and no intervention is needed.
fetomaternal hemorrhage; h rhesus.
In moderate HDFN, the placenta metabo-
lizes the bilirubin but hyperbilirubinemia can be
accelerated after birth and may lead to kernic-
The exceptions to this are as follows: terus with neurological damage unless treated
promptly.
• A woman who has developed antibodies follo- In severe cases, there can be fetal anemia
wing a blood transfusion and is pregnant for and ultimately fetal hydrops (Box 38.7). Fetal
the first time hydrops is due to cardiac failure resulting from
• An Rh-negative woman whose mother was Rh the anemia.
positive and was exposed to maternal Rh anti-
gens in utero—known as the grandmother theory
Box 38.7 emolytic disease of the fetus and
Subsequent pregnancies are considered sen- the newborn
sitized pregnancies. In the subsequent preg-
Mild cases
nancy with an Rh-positive fetus, when fetal • Hemolysis tolerated by fetus
blood leaks into the maternal circulation, an • Mild anemia and jaundice at birth
amnestic response is generated from the previ- • Usually resolves without treatment
ously primed RBCs. This is a rapid response and
Moderate cases
consists almost exclusively of IgG. IgG antibod- • Increased circulating bilirubin cleared by placenta
ies cross the placenta, destroy the Rh D–positive • After birth bilirubin not cleared by immature liver
fetal red cells, and cause the following: Ŧ Hyperbilirubinemia
Bilirubin encephalopathy (kernicterus)
• Fetal anemia
Ŧ Moderate anemia
• Fetal hydrops Postnatal treatment required
• Hyperbilirubinemia in the newborn
Severe cases
The natural history of Rh alloimmunization is • Severe fetal anemia
summarized in Box 38.6. • Hepatosplenomegaly
• Erythroblasts (immature RBCs) in circulation
• Liver dysfunction
atural history of DF • Fetal cardiac failure
• Fetal hydrops
The old term for this condition is erythroblas-
Ŧ Stillbirth
tosis fetalis. HDFN can be mild, moderate, or Ŧ Neonatal death
severe depending on the rate of hemolysis. In
mild HDFN, the fetus is able to metabolize the BC, red blood cell.
CH 38_p542-559_v3.indd 547 18-07-2015 13:58:34

Effects of h alloimmuni ation • detects the presence of antibodies in the

maternal serum and
on the mother • indicates the degree of alloimmunization by
Rh alloimmunization is associated with a large quantitative titer.
placenta. This hyperplacentosis can cause pre-
eclampsia. A syndrome (Ballantyne syndrome), Procedure
in which the mother has edema, mild albumin-
uria, and elevated blood pressure, mirroring the ICT is performed in the following manner:
features of hydrops, has been described. Other • Maternal plasma is incubated with known
maternal problems are related to invasive pro- Rh-positive RBCs. The antibody in maternal
cedures such as cordocentesis and amniocen- plasma coats the RBCs.
tesis, done as part of fetal therapy. Maternal • Antihuman globulin serum is added to the red
effects of Rh alloimmunization are given in cells.
Box 38.8. • The red cells coated with antibodies are agglu-
tinated by the antihuman globulin.
• This is considered a positive ICT.
Box 38.8 Maternal effects of h alloimmuni ation
• A positive test indicates that the fetus is at risk
• Hyperperplacentosis of developing hemolytic disease, but it is not a
Ŧ Preeclampsia diagnostic test.
• Ballantyne syndrome
Ŧ Edema Titration is done for the quantity of the anti-
Ŧ Mild albuminuria body present in the serum. Using doubling dilu-
Ŧ Elevated blood pressure tions of the serum, the maximum dilution of the
• Problems related to test serum that is able to produce agglutination
Ŧ Cordocentesis is calculated. The Rh antibody titer is expressed
Ŧ Amniocentesis as 1:8, 1:16, 1:32, etc.
h, Rhesus. It is important to remember that there is no
direct relationship between the antibody titer
and the severity of the disease.
Screening for Critical titer

A critical titer is defined as the titer that indicates
alloimmuni ation in women a significant risk for fetal hydrops. This value
On the first prenatal visit, all pregnant women varies between laboratories as does the critical
should be tested for ABO blood group and titer level associated with hydrops. Therefore,
Rh-D type. If the mother is Rh negative, and her the same laboratory should be used when repeat
husband/partner is Rh positive she should be titers are done. For most centers, critical titer val-
screened for the presence of Rh antibodies. This ues vary between 1:8 and 1:32.
is done even if the woman is a multigravida who The frequency of testing is listed in Box 38.9.
has received anti-D immunoglobulin in her pre-
vious pregnancies, since postpartum adminis-
tration of anti-D does not guarantee prevention
Determining fetal h factor
of Rh alloimmunization. If the fetal Rh factor is known, then management
of an alloimmunized pregnancy is easier. If the
fetus is Rh negative, then no investigation or
Indirect Coombs test intervention would be required. Though not cur-
rently available on a routine basis, two tests are
The test most commonly test used to detect
possible to identify the fetal Rh factor:
unbound Rh antibodies in the maternal serum
is the indirect Coombs test (ICT). This blood test • Noninvasive fetal testing for the Rh D gene:
most accurately Sorting of maternal blood for fetal cells using
CH 38_p542-559_v3.indd 548 18-07-2015 13:58:34

Box 38.9 Frequency of screening Box 38.10 Anti-D immunoglobulin

+PVJGſTUVRTGIPCPE[ • Anti-D immunoglobulin
• #VſTUVDQQMKPI Ŧ Polyclonal or monoclonal
• At 20 weeks Ŧ Polyclonal antibodies used currently
• At 28 weeks (before antenatal administration of anti-D) • Dose
In subsequent pregnancies Ŧ 300 μg (1 μg = 5 IU)
• Previous pregnancy with no or mild hemolytic disease Will neutralize 15 mL of Rh-positive RBCs
Ŧ #VſTUVDQQMKPI Ŧ 50 μg
Ŧ Every 4–6 weeks subsequently Will neutralize 2.5 mL of Rh-positive RBCs
• Previous pregnancy with severe hemolytic disease • Half-life of 16–24 days.
Ŧ Titer not required • Administered deep IM
Ŧ Testing for fetal anemia beginning from 16–18 Ŧ Deltoid muscle
weeks Ŧ Anterolateral aspect of the thigh
• Given within 72 hours of delivery or incidence of FMH
• Can be omitted if husband/partner is Rh negative
flow cytometry has been reported to be suc- fetomaternal hemorrhage; RBCs, red blood cells;
h rhesus.
cessful in identifying an Rh D–positive fetus.
• Cell-free fetal DNA (cfDNA) in the maternal
plasma or serum has been used to detect Rh D
sequences in the case of an Rh D–positive fetus. Antenatal anti-D prophylaxis
Initially, anti-D prophylaxis was administered
only postnatally. However, a small number of
Management of pregnancy women have been found to develop alloimmuni-
zation due to FMH that occurs antenatally. When
in a nonimmuni ed mother anti-D immunoglobulin is administered early in
the third trimester, it is possible to reduce the
If the ICT is reported as being negative, then the
incidence of antenatal alloimmunization from
mother is not alloimmunized. The aim of man-
1% to 0.1%.
agement would be to prevent alloimmunization
by ensuring the following: • It is, therefore, recommended that all Rh-negative
women with no evidence of alloimmunization
• Minimizing the chances of FMH as already
(ICT negative) should be administered 300 μg of
discussed (Box 38.5)
anti-D immunoglobulin at 28 weeks’ pregnancy.
• Preventing alloimmunization by administra-
However, the cost and supply of antenatal anti-
tion of anti-D immunoglobulin
D is a major consideration in some developing
countries.
Anti-D immunoglobulin • A second dose at 34 weeks is used in some
countries, but is not recommended by all and
for prophylaxis against is not used in centers in India.
alloimmuni ation • Postnatal anti-D prophylaxis is mandatory
unless antenatal prophyaxis was administered
Anti-D immunoglobulin or Rho(D) immuno-
within 3 weeks of delivery.
globulin is a derivative of human plasma. It is
extracted by cold alcohol fractionation from
the sera of individuals with high titers. Anti-D
immunoglobulin binds to D antigen sites on
Postnatal and other indications
fetal erythrocytes present in the maternal circu- for anti-D prophylaxis
lation; thus, the maternal immune system does
Postnatal and other indications for anti-D pro-
not recognize the foreign antigen. This prevents
phylaxis are given as follows:
the formation of antibodies. The important
features of anti-D immunoglobulin are listed in • Administration of anti-D postnatally is man-
Box 38.10. datory to all Rh-negative women who are
CH 38_p542-559_v3.indd 549 18-07-2015 13:58:34

nonalloimmunized. A dose of 300 μg should

Box 38.11 isk factors for large FM
be administered within 72 hours of delivery.
This provides protection against 15–20 mL of • Operative vaginal delivery
FMH. • Cesarean section
• Manual removal of placenta
• If the dose is omitted after delivery, it may be
• Postterm pregnancies
given as late as within 13 days postpartum
since it provides partial protection. fetomaternal hemorrhage.
• If delivery occurs within 3 weeks of antenatal
prophylaxis, postnatal dose is not required.
• In addition to postpartum prophylaxis, there
are several obstetric indications for anti-D Kleihauer–Betke test identifies the percentage
prophylaxis. These indications for and dosage of fetal cells in the maternal circulation and
of anti-D prophylaxis are listed in Table 38.2. helps in assessing the volume of FMH so that
an appropriate dose of anti-D may be adminis-
In a multigravida undergoing sterilization tered. In places where a Kleihauer–Betke test is
after a pregnancy, anti-D is considered nei- not available, it is suggested that higher doses be
ther necessary nor cost-effective and therefore administered in order to protect the majority of
the woman should be given the option of an women in highrisk situations.
informed choice for anti-D prophylaxis.
In certain situations, >15 mL of fetal blood
may enter the maternal circulation. Risk factors
for large FMH are enumerated in Box 38.11. Management of pregnancy
When large FMH is suspected, quantitative
assessment is done by in an alloimmuni ed mother
• Rosette test Management of pregnancy in an alloimmunized
• Kleihauer–Betke acid elution test mother includes the following steps:
A positive rosette test indicates a larger • A positive anti-D titer at the booking visit only
volume of hemorrhage but does not quan- indicates that the fetus is at risk for hemolytic
tify it accurately. Hence, when this test is pos- disease. It does not indicate that hemolytic
itive, Kleihauer–Betke test is essential. The disease has occurred or will develop.
Table 38.2 bstetric indications for and dosage of anti-D prophylaxis
Sensiti ing event Dosage of anti-D ( g)

6JGTCRGWVKEVGTOKPCVKQPQHRTGIPCPE[
ſTUVVTKOGUVGT 50–100
Spontaneous miscarriage with instrumentation 50–100
Ectopic pregnancy 50–100
Vaginal or cesarean delivery 300
Before 12 weeks After 12 weeks
gestation gestation
Invasive prenatal diagnosis (amniocentesis, chorionic 100 300
villus sampling, fetal blood sampling)
Intrauterine procedures (e.g., insertion of shunts, 100 300
embryo reduction)
Antepartum hemorrhage – 300
External cephalic version – 300
Closed abdominal injury 100 300
CH 38_p542-559_v3.indd 550 18-07-2015 13:58:34

• A detailed history regarding the severity of positive). Such women are monitored for evi-
disease in the previous fetuses is important. dence of fetal anemia starting at 16–18 weeks’
Gestational age at which the fetus was deliv- gestation.
ered, treatment given, and the fetal outcome
should be noted.
• The zygosity of paternal blood may be tested. Serial amniocentesis and Liley curve
If the father is heterozygous, there is a 50% In the past, if the mother had a critical titer (1:16
chance of the fetus being Rh negative. This is or higher), serial amniocentesis was done to plot
not performed as a routine in most centers. the Liley curve. Since fetuses affected by hemo-
lytic disease secrete abnormally high levels of
bilirubin into the amniotic fluid, amniocentesis
Determining fetal h factor is done to obtain the amniotic fluid. The amount
Currently, fetal Rh factor testing is not done. of bilirubin is quantitated by spectrophotomet-
rically measuring delta optical density (DOD)
at 450 nm wavelength in the specimen of amni-
Determining the severity of otic fluid. This value is then plotted on the Liley
fetal anemia curve. Depending on whether the value falls in
zone 1, 2, or 3 (Fig. 38.6), a decision is made to
Once the titers are documented, further fol- watch expectantly, deliver the baby, or proceed
low-up includes screening for fetal anemia using with intrauterine fetal transfusion.
serial amniocentesis, ultrasound, and Doppler. This test can be used only after 27 weeks’ ges-
• In women with a history of mild or moder- tation since the original data included only preg-
ate hemolytic disease of the fetus, monitor- nancies after this period of gestation. This method
ing for fetal anemia should begin by 20 weeks’ of evaluation was routinely used until recently.
gestation. However, Doppler velocimetry of the middle cere-
• In a woman who has had severe HDFN in a bral artery (MCA) is a more sensitive, specific, and
previous pregnancy, a severe degree of fetal noninvasive method of determining fetal anemia.
anemia is expected (if this fetus is also Rh Liley curve, therefore, is no longer used.
one
e ere
one
one
Mo erate
one
one
M Unaffecte
Figure 38.6 Liley curve. The optical density (DOD) at 450 nm wavelength is plotted against gestation in weeks.
CH 38_p542-559_v3.indd 551 18-07-2015 13:58:34

Fetal middle cerebral artery peak compared with a subsequent one. Generally, the
systolic velocity fetal effects are milder with the first alloimmu-
nized pregnancy and worsen with each subse-
Currently, the severity of fetal anemia is assessed quent one.
by Doppler velocimetry of the fetal middle cere-
bral artery peak systolic velocity (MCA-PSV; • ICT should be repeated once a month till 28
Fig. 38.7). This has become the standard of care weeks and every 2–3 weeks thereafter.
in the management of Rh alloimmunization. • If the titer remains below the critical level (1:16
Measurement of MCA-PSV is usually initiated or 1:32), the mother may be delivered at term.
at 20 weeks’ gestation since intravascular trans- • If the titer rises above the critical level, sur-
fusions (IVTs) are difficult to perform before veillance with MCA-PSV Doppler should be
20 weeks. However, if there is a past history of initiated.
severe hemolytic disease, measurements can be • If the MCA-PSV is <1.5 MoM, the woman may
started at 16 weeks. be monitored and delivered at 37–38 weeks.
The sensitivity of increased MCA-PSV [above • If the MCA-PSV is >1.5 MoM, fetal blood trans-
1.5 multiples of the median (MoMs)] for the pre- fusion will be required.
diction of moderate or severe anemia is 100%. The management of the first affected Rh
Conversion calculators are available to convert alloimmunized pregnancy is summarized in
the actual MCA-PSV (in cm/second) to MoMs, Figure 38.8.
to correct for gestational age. The technique of
performing MCA Doppler is important and the
guidelines must be followed. Management of pregnancy
with previously affected fetus
ther ultrasonographic signs of In pregnancies with a previously affected fetus,
fetal anemia Coombs test will be positive in high titers.
Management is based on MCA-PSV and not on
Other signs of fetal anemia are listed in Box 38.12.
the ICT titers.
/CPCIGOGPVQHVJGſTUV • In women with a history of mild or moderate

hemolytic disease of the fetus, monitoring for
affected pregnancy fetal anemia should begin by 20 weeks’ gesta-
tion or 2 weeks prior to the onset of fetal dis-
The approach to an alloimmunized pregnancy
ease in the previous pregnancy.
differs for the first alloimmunized pregnancy as
• In a woman who has had severe HDFN in a
previous pregnancy, a severe degree of fetal
anemia is expected (if the present fetus is
also Rh-positive). Such women are moni-
tored by ultrasound starting at 16–18 weeks’
gestation.
Box 38.12 ther signs of fetal anemia

• Polyhydramnios
• Hepatosplenomegaly
• Increased placental thickness
• Increased right atrial size
• Fetal hydrops (due to severe anemia and cardiac failure)
Ŧ Ascites
Ŧ Pleural effusion
Figure 38.7 Doppler waveform of increased middle
Ŧ Pericardial effusion
cerebral artery peak systolic velocity (MCA-PSV). (Photo
Ŧ Subcutaneous edema
CH 38_p542-559_v3.indd 552 18-07-2015 13:58:34

irst affecte pregnancy
Monthly C till ee s
hen C e ery ee s
iter
iter
critical le el
eli er at term oppler MC P V
MoM MoM
eli er at
ee s
ee s ee s
eli er
Figure 38.8 6JGOCPCIGOGPVQHVJGſTUVCHHGEVGF4JCNNQKOOWPK\GFRTGIPCPE[ BS fetal blood sampling; C indirect

Coombs test; CA-PS middle cerebral artery peak systolic velocity; o multiples of median.
• Monitoring should be done once in 2 weeks. Intrauterine blood

If the MCA-PSV remains <1.5 MoM, moni-
toring can continue and delivery may be transfusion
planned between 34 and 36 weeks. Antenatal
corticosteroids should be administered if <34 Severe fetal anemia is defined as a hematocrit
weeks. below 30% or 2 standard deviations below the
• If MCA-PSV is >1.5 MoM, FBS should be done mean hematocrit for the gestational age.
by cordocentesis. Once fetal anemia is confirmed, a decision
• If cord blood hematocrit is >30%, FBS should is made to either deliver the baby or proceed
be repeated once a week. Delivery should be with an IUT. Intrauterine transfusion is gen-
planned between 34 and 36 weeks. erally done between 18 and 35 weeks’ gesta-
• If fetal hematocrit is <30%, intrauterine trans- tion. It is technically difficult to perform an
fusion (IUT) is indicated. IUT before 18 weeks. After 34 weeks, it is safer
to deliver the baby and treat with postnatal
Management of Rh alloimmunized pregnancy transfusion.
with a previously affected fetus is summarized
in Figure 38.9.
CH 38_p542-559_v3.indd 553 18-07-2015 13:58:34

Pregnancy ith
pre iously affecte fetus
oppler MC P V e ery
ee s from ee s
MoM MoM
Continue MC P V
eli er after
ee s etal hematocrit etal hematocrit
ntrauterine transfusion epeat epen ing

on ee ly MC P V
f hematocrit stays
eli er at ee s
Figure 38.9 The management of Rh alloimmunized pregnancy with a previously affected fetus. BS fetal blood sampling;
CA-PS middle cerebral artery peak systolic velocity; o multiples of the median.
Fetal blood sampling There are prescribed formulas and charts to

calculate the volume for infusion. The volume of
When the MCA-PSV is increased and the deci- blood is calculated based on the following:
sion has been made to proceed with an IUT, FBS
is done to document the severity of anemia and • Initial fetal hematocrit
plan the volume of IUT. This is usually done at • Size of the fetus
the time of IUT. • Hematocrit of the donor blood
• Target hematocrit
Preparation for intrauterine

transfusion Sites of transfusion
The following are the sites of transfusion:
Blood for transfusion
• Intraperitoneal transfusion (IPT): The trans-
Blood for transfusion should be fused blood cells are absorbed through the
• type O Rh(D) negative blood, diaphragmatic lymphatics. Transfusion into
• cross-matched to the mother’s blood, and the peritoneal cavity is not effective in fetuses
• tightly packed to achieve a final hematocrit of with severe anemia and hydrops.
75%–85%. • Intravascular transfusion (IVT): This is much
more effective than IPT, particularly in
hydropic fetuses, and is the preferred route of
olume of blood for I T transfusion. The two sites used for direct vas-
The hematocrit obtained with the FBS at the cular access are as follows:
initiation of the procedure helps calculate the vol- – The intrahepatic portion of the umbilical
ume of blood to be transfused into the fetus. vein (ductus venosus)
CH 38_p542-559_v3.indd 554 18-07-2015 13:58:35

– The umbilical vein at the site of cord inser- • A 20-gauge needle is inserted through the
tion into the placenta maternal and fetal abdominal wall, and a blood
• Combined IPT and IVT: The combined direct sample is obtained from the fetal umbilical
intravascular/intraperitoneal approach pro- vessel. The blood is immediately processed to
duces a stable hematocrit between procedures check for fetal hematocrit. Using a standard
and offers the possibility of performing IUT at formula, the volume of blood to be transfused
less frequent intervals. is calculated.
• Using the same needle, blood is pushed into
The prerequisites and the sites of transfusion are
the fetal circulation (Figs 38.10–38.12).
• The transfusion is continued till the target
hematocrit is obtained. After 24 weeks’ gesta-
Procedure of intrauterine tion, the target fetal hematocrit is 40%–50%.
transfusion
The procedure of IUT consists of the following
steps:
• The procedure is done under sterile condi- ransfusion
Ultrasoun
tions, preferably in the operation theater, with probe
nee le
everything set up for an emergency cesarean
section in case it is needed.
• Maternal sedation is usually administered to Umbilical
alleviate anxiety. ein
• The procedure is done under ultrasound
guidance.
• Fetal movement is minimized with an injec-
tion of a paralyzing agent (such asvecuronium
bromide or pancuronium bromide) into the Figure 38.10. Graphic representation of intrauterine
fetal thigh. transfusion of blood. Under ultrasound guidance, a long
20-gauge needle is placed in the umbilical vein and blood
transfused into the fetal circulation.
Box 38.13 Prerequisites and sites of intrauterine
transfusion
• Initial fetal blood sampling
Ŧ Severity of anemia
Ŧ Plan volume of IUT
• Blood for transfusion
Ŧ O Rh(D) negative blood
Ŧ Cross-matched to maternal blood
Ŧ Hematocrit of 75%–85%
• Volume of blood to be transfused
Ŧ Depends on
Initial fetal hematocrit
Size of the fetus
Hematocrit of donor blood
Target hematocrit
• Sites of transfusion
Ŧ Intraperitoneal
Ŧ Intravascular
Ductus venosus
Cord insertion
Ŧ Mixed (intraperitoneal +IVT) Figure 38.11 Ultrasound of intravascular intrauterine
transfusion. The needle tip is seen in the intrahepatic
intrauterine transfusion; intravascular transfusion. portion of the umbilical vein (ductus venosus). (Photo
courtesy: Mediscan Systems, Chennai.).
CH 38_p542-559_v3.indd 555 18-07-2015 13:58:35

Box 38.14 Posttransfusion follow-up and

subsequent transfusions
• Ultrasonography
Ŧ To assess hydrops
Ŧ MCA Doppler to assess anemia
• Subsequent transfusions
Ŧ Hematocrit decreases 1% per day
Ŧ Second IUT after 10–14 days
Ŧ After 2–3 transfusions
Every 3–4 weeks
CA middle cerebral artery.
This helps in deciding if the mother requires

anti-D immunoglobulin or not (Box 38.15).
Figure 38.12 Intrauterine transfusion being performed Box 38.15 Follow up with neonatal h type
under ultrasound guidance. The needle can be seen and DCT
entering the abdomen and into the uterus (yellow arrow).
• Baby Rh positive and DCT negative
The blood is being pushed in with a syringe (white arrow).
Ŧ Postnatal dose of anti-D immunoglobulin for
(Photo courtesy: Mediscan Systems, Chennai.). mother
Posttransfusion follow-up and • Baby Rh positive and DCT positive
Ŧ Mother alloimmunized
subsequent transfusions Ŧ 0QDGPGſVHTQOCPVK&KOOWPQINQDWNKP
• Baby Rh positive and weak positive DCT
Posttransfusion, the fetus is followed up with Ŧ Evaluate further to exclude
ultrasound imaging to document the decrease Other minor group
in hydrops. Doppler velocimetry of the MCA is ABO incompatibility
done to note the improvement in fetal anemia.
A repeat transfusion is planned based on the DC direct Coombs test.
following:
• The final hematocrit achieved during the last emolytic disease of the fetus
transfusion
• The rate of drop of hematocrit and newborn
After the first IUT, the fetal hematocrit will Clinical presentation
decrease approximately at the rate of 1% per day.
As discussed earlier in this chapter, HDFN may
This can be more rapid in a hydropic fetus. The
be mild, moderate, or severe.
second IUT is usually planned 10–14 days after the
At delivery, if HDFN is anticipated, cord blood
first IUT. After two or three transfusions, fetal eryth-
should be collected and sent for the following tests:
ropoiesis is suppressed and the drop in hematocrit
slows down. The interval between transfusions • Hematocrit
can be extended to 3–4 weeks (Box 38.14). • Reticulocyte count
• DCT
• Bilirubin
Management of the neonate
Clinically, the neonates have one or more of
All newborns of Rh-negative, nonisoimmunized the following:
mothers should undergo the following:
• Hyperbilirubinemia
• Blood grouping, Rh typing • Hydrops fetalis
• Direct Coombs test (DCT) • Anemia
CH 38_p542-559_v3.indd 556 18-07-2015 13:58:35

yperbilirubinemia Box 38.16. Features of hydrops fetalis

Hyperbilirubinemia was formerly known as
• Severe anemia
icterus gravis neonatorum. It occurs within the • Congestive cardiac failure
first 24 hours after birth. Hemolysis of the fetal Ŧ Ascites
red blood cells continues after birth and the Ŧ Pleural and pericardial effusions
unconjugated bilirubin level increases. If the Ŧ Subcutaneous and scalp edema
level rises above 20 mg/dL, it crosses the blood– • Placental enlargement
brain barrier and gives rise to bilirubin enceph- • Hepatosplenomegaly
alopathy (kernicterus). This is more common in • Stillbirth
preterm babies since the liver is immature. • Ultrasonography
Treatment of hyperbilirubinemia involves the Ŧ Fluid in pleural, peritoneal, and pericardial cavities
following: Ŧ ‘Halo’ around the head due to scalp edema
Ŧ Large placenta
• Phototherapy Ŧ Hepatosplenomegaly
• Exchange transfusion
Treatment of hyperbilirubinemia is discussed
in detail in Chapter 23, The newborn. may cause respiratory distress. Treatment is by
transfusion if anemia is moderate or by exchange
y rops etalis transfusion if there is accompanying hydrops or
Hydrops fetalis is also known as erythroblastosis cardiac failure.
fetalis or immune hydrops. This is the most severe Indications for exchange transfusion are
form of HDFN where hemolysis sets in in-utero. listed in Box 38.17.
There is severe anemia with congestive cardiac The process of exchange transfusion is sum-
failure, ascites, and pleural and pericardial effu- marized in Box 38.18.
sions. The diagnosis of hydrops is made when Following exchange transfusion, the baby
fluid is present in two cavities (e.g., peritoneal, should be monitored for immediate and late
pericardial, or pleural). There is subcutaneous and complications such as congestive cardiac failure,
scalp edema and marked enlargement of the pla- hyperkalemia, hypocalcemia, and necrotizing
centa. Extramedullary hematopoiesis causes hep- enterocolitis.
atosplenomegaly. Prognosis is poor and fetuses
with severe hydrops are stillborn, if left untreated.
Antenatal ultrasonography demonstrates fluid Box 38.17 Indications for exchange transfusion
in pleural, peritoneal, and pericardial cavities, • Cord blood bilirubin >5 mg/dL
‘halo’ around the head due to scalp edema, a large • Hemoglobin <10 g/dL
placenta, and hepatosplenomegaly. Due to early • Hydrops fetalis
diagnosis using ultrasonography and treatment • Rise in bilirubin by >1 mg/dL/hour
with IUT, this condition is seen less often now. • Total bilirubin >20 mg/dL
Features of hydrops fetalis are listed in Box
38.16. Treatment postnatally is by exchange
transfusion.
Box 38.18 Process of exchange transfusion
Anemia • Usually double-volume transfusion
Anemia is usually referred to as congenital • 160 mL of ‘O’ negative blood
Ŧ Cross-matched with mother’s and baby’s serum
anemia of the newborn. It is usually seen at birth
Ŧ Packed cells suspended in maternal fresh frozen
(early onset anemia). There is pallor, tachycar- plasma
dia, and tachypnea at birth. Associated hydrops Ŧ For every 15 mL blood removed, 10 mL transfused
CH 38_p542-559_v3.indd 557 18-07-2015 13:58:35

Key points
• There are 50 different red cell surface antigens ca- • Hemolytic disease of the fetus and newborn (HDFN)
pable of causing maternal alloimmunization and fetal can be mild, moderate, or severe depending on the
hemolytic disease. Of these, the rhesus (Rh) blood rate of hemolysis.
group system is the most common.
• 1PVJGſTUVRTGPCVCNXKUKVCNNRTGIPCPVYQOGPUJQWNF
• In Caucasians, the incidence of Rh-negative geno- be tested for ABO blood group and Rh-D type. If the
type is 15%. In India, the incidence is approximately mother is Rh negative, and her husband/partner is Rh
8%–10% of the population. positive, she should be screened for the presence of
• The Rh blood system is collectively called the Rh Rh antibodies.
factor and includes the D, c, C, e, and E antigens. • The test most commonly used to detect unbound an-
It should be remembered that no d (little d) antigen tibodies in the maternal serum is the indirect Coombs
exists and therefore d denotes the absence of the D test (ICT).
antigen.
• Anti-D immunoglobulin is mandatory in a nonsensi-
• The risk of the fetus being Rh positive depends on tized woman who undergoes a sensitizing event. The
whether the father is homozygous (DD) or heterozy- dosage depends on the gestational age at the time of
gous (Dd). The homozygous father will have 100% the event.
chance of an Rh-positive baby with an Rh-negative
• Routine antenatal prophylactic dose is recommended
mother, whereas a heterozygous father has a 50%
at 28 weeks.
chance of having an Rh-positive baby.
• 6JGſTUVCHHGEVGFRTGIPCPE[KPCPCNNQKOOWPK\GF
• Anti-Kell, anti-c, and anti-E antibodies can also cause
woman is managed by serial ICT titers monthly till 28
hemolytic disease.
weeks and once in 2–3 weeks thereafter. If the titer
• If an Rh-positive mother is pregnant with an Rh- is more than the critical level, middle cerebral artery
negative fetus, then there is opportunity for the Rh- peak systolic velocity (MCA-PSV) is required. Most of
positive fetal blood to mix with the maternal blood. these women can be delivered at 37–38 weeks.
• When the maternal immune system is presented with • In pregnancies with a previously affected fetus, man-
a foreign protein (Rh antigen), it mounts a response by agement is based on MCA-PSV. If <1.5 MoM, serial
producing immunoglobulin M (IgM) and later immuno- monitoring and delivery at 34–36 weeks are recom-
globulin G (IgG) antibodies. mended.
• +PVJGſTUVCHHGEVGFRTGIPCPE[VJGHGVCNGHHGEVUQH • Fetal anemia (hematocrit <30%) is treated with intrau-
alloimmunization either are nonexistent or tend to be terine transfusion.
less severe. • HDFN may present as hyperbilirubinemia, anemia, or
• In the subsequent pregnancy (if the fetus is Rh posi- hydrops fetalis. Severe disease may require exchange
tive), the antibodies cross into the fetus, attack them, transfusion.
and cause hemolysis, fetal anemia, and hydrops.
Self-Assessment
4. If the ICT titer begins to rise and reaches 1:32, how
Case-based questions will you manage her?
Case 1
Mrs. MN, 26, gravida 2, para 0, at 20 weeks’ gestation, Case 2
had a miscarriage a year ago. Her blood group and Rh Mrs. VC, 28, gravida 1, para 0, was Rh negative. Her hus-
typing were not done. She did not receive anti-D after band was Rh positive. She was 24 weeks’ pregnant.
the miscarriage. In the current pregnancy, she was found
to be Rh negative and her husband was Rh positive. An 1. What is antenatal prophylaxis?
indirect Coombs test showed a titer of 1:8.
2. When should postnatal prophylaxis be given? What
1. How is the Rh factor inherited? dosage should be given?
2. What is the indirect Coombs test and critical titer? 3. What is a Kleihauer–Betke test?
3. How will you manage this patient? 4. What are the risk factors for a large fetomaternal
hemorrhage?
CH 38_p542-559_v3.indd 558 18-07-2015 13:58:35

immunization. Antenatal anti-D immune globulin can

Answers be administered early in the third trimester to reduce
the incidence of antenatal alloimmunization from 1%
Case 1 to 0.1%.
2. Postnatal anti-D prophylaxis is given within 72 hours
1. Every individual inherits one of each set (three each) of delivery. The dosage given is 300 μg, although a
from each parent. If at least one D antigen is present, larger dose may be required with a greater amount of
the individual will be Rh positive. fetomaternal hemorrhage.
2. ICT is used to detect unbound Rh antibodies in the 3. #-NGKJCWGTŌ$GVMGCEKFGNWVKQPVGUVKFGPVKſGUHGVCN
OCVGTPCNUGTWO+VKURGTHQTOGFD[ſTUVOKZKPIVJG cells in the maternal circulation and will allow assess-
maternal plasma with Rh-positive cells, and later ment of the volume of fetomaternal hemorrhage that
exposing the red cells to antihuman globulin serum has occurred.
and looking for agglutination of cells. 4. Operative vaginal delivery, cesarean section, manual
#ETKVKECNVKVGTKUFGſPGFCUVJGVKVGTVJCVKPFKECVGUC removal of placenta, and postterm delivery.
UKIPKſECPVTKUMHQTHGVCNJ[FTQRU
3. 6JKUKUVJGſTUVCHHGEVGFRTGIPCPE[5JGECPDGOCP-
aged by serial ICT monthly till 28 weeks and once in Sample questions
2–3 weeks thereafter. If the titer does not rise above
the critical level, she can be delivered at 37–38 Long-answer question
weeks. 1. Outline the management of the red cell alloimmun-
4. If the level rises above 1:32 (critical level), she should ized woman in pregnancy.
be monitored by Doppler assessment of middle cer-
ebral artery peak systolic velocity (MCA-PSV). If it is
<1.5 MoM, she can be monitored and delivered after Short-answer questions
34–36 weeks. If the level is>1.5 MoM, fetal blood
sampling is required to assess fetal anemia. 1. Rh alloimmunization prophylaxis
2. Fetal complications of Rh alloimmunization
3. Intrauterine transfusion for hemolytic diseases of the
Case 2 fetus
1. In spite of giving postnatal anti-D prophylaxis, a small
number of women have been found to develop allo-
CH 38_p542-559_v3.indd 559 18-07-2015 13:58:35

Antepartum
39 Hemorrhage
Case scenario
Mrs. AN, 22, primigravida, was admitted to the labor room at 32 weeks’
pregnancy with sudden onset of profuse vaginal bleeding. There was no
associated abdominal pain. On examination, she had tachycardia, pulse
was 110/min and blood pressure was 100/70 mm Hg. The uterus was 32
weeks size, not tense or tender, and the fetus was in breech presentation.
She had gone to the primary health center and was referred to a tertiary
center for management. Her parents and husband, who accompanied
her, were extremely worried about the condition of the mother and baby.
Obstetric hemorrhage can occur in the first, Antepartum hemorrhage (APH) is defined as
second, or third trimester. It is one of the lead- bleeding from or into the genital tract after 24
ing causes of maternal mortality and accounts weeks’ gestation (period of fetal viability) and
for 25% of maternal deaths. It is also the most prior to delivery of the baby. Some guidelines
preventable cause of maternal mortality. Prompt define APH as bleeding occurring after 20 weeks’
diagnosis, resuscitation, and management are pregnancy. It is also referred to as bleeding in the sec-
essential to save the mother and fetus. ond half of pregnancy or late pregnancy bleeding.
CH 39_p560-581_v3.indd 560 18-07-2015 13:07:05

Antepartum Hemorrhage 561
3WCPVKſECVKQP • Physical examination should assess maternal

pulse, blood pressure, pallor, and signs of shock
• Minor hemorrhage: Blood loss <50 mL that has such as sweating, tachypnea, and restlessness.
settled (includes spotting) Abdominal examination should include uterine
• Major hemorrhage: Blood loss of 50–1000 mL size, tenderness, contractions, lie and presenta-
• Massive hemorrhage: Blood loss of >1000 mL tion of fetus, station, and fetal heart sounds.
• Vaginal examination should not be performed
unless placenta previa is excluded or consid-
Incidence ered extremely unlikely by clinical examination.
Antepartum hemorrhage occurs in 3%–5% of all

pregnancies.
Immediate management
• An intravenous line should be inserted with
a wide bore needle and infusion of normal
Causes of antepartum saline or colloids should be started.
• Blood sample should be drawn for hematocrit,
hemorrhage cross-matching, and other tests depending on
The two most common conditions causing APH initial diagnosis (discussed later in this chapter).
are placenta previa and placental abruption. • The bladder should be catheterized and hourly
Causes of APH are listed in Box 39.1. urine output monitored.
• Blood should be transfused as required.
• Once the patient is stabilized hemodynami-
cally, ultrasonography should be performed to
Initial management of diagnose the cause of bleeding and assess fetal
antepartum hemorrhage status.
Initial assessment and immediate manage-
Women who present with APH must be evaluated ment of APH are summarized in (Fig. 39.1).
initially to assess the condition of the mother • Subsequent management depends on the
and fetus and supportive measures should be cause of bleeding.
initiated. Measures to establish the diagnosis of
cause of hemorrhage and specific management
should follow.
History
Initial assessment
Physical e amination
• When a pregnant woman presents with bleed-
ing after 20 weeks’ gestation, she should be
admitted to labor and delivery unit. Maternal fetal e aluation
• History should include gestational age, amount ntra enous crystalloi s
loo transfusion
of bleeding, preexisting obstetric problems
such as hypertension, presence of risk factors
for APH, uterine contractions, rupture of mem- Ultrasonography
branes, trauma, and other relevant details.
Placenta Placental Unclassifie

Box 39.1 Causes of antepartum hemorrhage
pre ia abruption
• Placenta previa
• Vasa previa Manage
• Rupture of marginal sinus accor ingly
• Local lesions in the vulva, vagina, or cervix
Figure 39.1 Antepartum hemorrhage: Immediate
• 7PENCUUKſGF
management.
CH 39_p560-581_v3.indd 561 18-07-2015 13:07:05

Placenta previa Box 39.2 isk factors for placenta previa

• Increasing maternal age
A placenta that is implanted low down in the
• Multiparity
uterine cavity in such a manner that it lies ‘in
• Nonwhite race
the way’ of the fetus during delivery is referred to • Male fetus
as placenta previa. Since the placenta lies in the • Multifetal gestation
lower segment, it can separate before or in early • Previous cesarean section
labor and cause significant hemorrhage. • Previous placenta previa
• Prior curettage/intrauterine surgery
• Maternal smoking/cocaine use
&GſPKVKQP
Placenta previa is defined as a placenta that is
implanted over or adjacent to the internal os.
The placenta, therefore, is entirely or partially scarring. This also accounts for the increased
implanted in the lower uterine segment. risk in women with a previous cesarean sec-
tion. The incidence of previa increases with
Incidence the number of cesarean sections: 1% with one
cesarean section, 1.7% with two cesarean sec-
Incidence varies from 3–5/1000 at term. The inci- tions, and 3% with three or more cesarean sec-
dence is much higher in the second trimester. tions. The reason for the increased incidence
in women with previous placenta previa is not
Pathogenesis clear.
The placenta normally implants in an area of

good blood supply and decidualization, which %NCUUKſECVKQP
is the uterine fundus. Suboptimal decidualiza-
6JGQTKIKPCNENCUUKſECVKQP
tion or blood supply in the upper segment can
be responsible for implantation in the lower seg- The original classification of placenta previa is
ment, leading to placenta previa. The placenta as given below:
may also extend to the lower segment when • Type I: Placenta just dips into the lower segment.
the surface area is large, such as in multifetal • Type II: Placenta reaches the edge of the inter-
pregnancy. nal os but does not cover it.
• Type III: Placenta covers the internal os com-
pletely when the cervix is not dilated but only
isk factors partially when the cervix is dilated.
Risk factors for placenta previa are listed in • Type IV: Placenta covers the internal os com-
Box 39.2. pletely even when the cervix is fully dilated.
Increasing maternal age, parity, male fetus,
The above classification is not relevant in
and nonwhite race are associated with an
modern obstetrics for the following reasons:
increased risk. Smoking and cocaine use cause
reduced uteroplacental oxygenation, thereby • The classification is based on pelvic examina-
increasing the placental surface area. The larger tion, which is dangerous and not performed in
the placenta, the more likely it is to extend into women with placenta previa.
the lower segment. Multifetal pregnancy is • The diagnosis of placenta previa is now made
associated with larger placentae or more than by ultrasonography and exact localization is
one placenta. Part of a large placenta or one possible.
of the placentas may be in the lower segment. • Type II placenta can become type III when
Previous curettage and prior intrauterine sur- the cervix is 8 cm dilated; similarly, type IV
gery can cause endometrial scarring leading placenta previa can become type III when the
to implantation of the placenta at the site of cervix is dilated.
CH 39_p560-581_v3.indd 562 18-07-2015 13:07:05

%WTTGPVENCUUKſECVKQP • Extent covering the os: Placentae covering

the os are less likely to migrate; 25% persist as
On the basis of ultrasonographic findings, placenta previa. Marginal placenta previa diagnosed in
previa is classified into four types (Fig. 39.2): early gestation are more likely to migrate and
• Total placenta previa: Internal os is completely only 2.5% persist as previa.
covered by the placenta. • Location: Placentae in the anterior wall are less
• Partial placenta previa: Internal os is partially likely to migrate than those in the posterior wall.
covered by the placenta.
• Marginal placenta previa: The placental edge Clinical features
comes up to the internal os but does not cover it.
• Low-lying placenta: The placenta is in the Clinical features of placenta previa are listed in
lower segment but the placental edge is </= 2 Box 39.3.
cm from the internal os. The most common clinical presentation of
placenta previa is painless vaginal bleeding.
Bleeding is usually spontaneous but can be pro-
Placental migration voked by digital examination or coitus.
The majority (90%) of placenta previa diagnosed
in the second trimester resolves by term. This is Timing of initial episode of bleeding
known as placental migration. This occurs due
to (a) differential growth of upper and lower seg- • One-third of affected pregnant mothers have
ment of the uterus and (b) growth of the placenta their first bleed prior to 30 weeks’ gestation.
implanted in the lower segment toward the more These women are
vascular upper segment, along with atrophy of the – more likely to require blood transfusions,
distal part. Migration depends on the following: – at greater risk of preterm delivery and
perinatal mortality.
• Gestational age at diagnosis: Earlier the ges- • One-third of patients bleed between 30 and 36
tational age at diagnosis, more the chances of weeks.
migration. • The remaining have the initial episode after 36
weeks.
• 10% of women bleed at onset of labor at term.
Bleeding is due to uterine contractions, for-
mation of the lower uterine segment leading
to detachment of the placental tissue from the
otal Partial
Box 39.3 Clinical features of placenta previa
• Painless vaginal bleeding
• May occur in
Ŧ second trimester
Ŧ third trimester
Ŧ at the onset of labor
• Bleeding may be
Ŧ small amounts
Ŧ recurrent
Marginal Lo lying Ŧ profuse
• May be associated with
Figure 39.2 %NCUUKſECVKQPQHRNCEGPVCRTGXKC1PVJGDCUKU
Ŧ premature uterine contractions
QHWNVTCUQPQITCRJKENQECNK\CVKQPRNCEGPVCRTGXKCKUENCUUKſGF
Ŧ malpresentations
into four types—total, partial, marginal, and low lying.
CH 39_p560-581_v3.indd 563 18-07-2015 13:07:05

myometrium, and shearing of maternal blood associated with a significant risk of placenta
vessels. The bleeding, therefore, is maternal. accreta.
When bleeding is profuse, the lower uterine seg- Cesarean section is the recommended route
ment cannot contract to occlude the vessels. of delivery in most cases. Malpresentations also
Massive hemorrhage, which causes reduced contribute to the high cesarean section rates.
uteroplacental flow and separation of placental In cases of marginal or low-lying placenta,
cotyledons, results in fetal compromise. especially associated with malpresentations,
Uterine contractions occur along with bleed- operative vaginal delivery may be required.
ing in 20% of women. Malpresentations, espe- Amniotic fluid embolism may occur because
cially breech or transverse lie, are common since the maternal venous sinuses are open once the
the lower segment is occupied by the placenta. hemorrhage occurs and uterine contractions
For the same reason, the presenting part is high favor entry of amniotic fluid into the maternal
and deviated to one iliac fossa or the other. venous circulation.
Postpartum hemorrhage is common since
the lower uterine segment does not contract
Complications and retract to close the placental bed vessels.
The complications of placenta previa are listed Placenta accreta aggravates the situation.
in Box 39.4.
Fetal complications
Maternal complications Prematurity was the most common cause of
Profuse hemorrhage can lead to maternal hypo- perinatal mortality before the introduction of
volemic shock. expectant management. Bleeding occurs in
Preterm labor is a common complication of two-thirds of women before 34 weeks and when
placenta previa. Thrombin produced at the site the bleeding persists, delivery may be the only
of placental separation stimulates uterine con- option. As already mentioned, preterm labor and
tractions. Prelabor rupture of membranes may prelabor rupture of membranes can also occur.
also occur. Fetal growth restriction is seen in 15% of
Due to poor decidualization in the lower uter- women with placenta previa. This may be due
ine segment, placenta accrete occurs in 1%–5% to recurrent episodes of bleeding and associated
of cases of placenta previa. Placenta previa in placental insufficiency.
a woman with a previous cesarean section is The incidence of congenital anomalies of the
central nervous system, cardiovascular, gastro-
intestinal, and respiratory systems is increased
in placenta previa.
Box 39.4 Complications of placenta previa
Malpresentations are common. Bleeding
• Maternal during labor and operative delivery can lead to
Ŧ Hemorrhagic shock perinatal hypoxia and asphyxia. Perinatal mor-
Ŧ Preterm labor tality is increased due to all the causes men-
Ŧ Prelabor rupture of membranes tioned before.
Ŧ Postpartum hemorrhage
Ŧ Operative vaginal delivery
Ŧ Cesarean section Diagnosis
Ŧ Placenta accreta
Ŧ #OPKQVKEƀWKFGODQNKUO Traditionally, the diagnosis is by history, phys-
Ŧ Maternal mortality ical examination, and ultrasound evaluation.
• Fetal However, since second trimester ultrasonogra-
Ŧ Prematurity phy has become a routine in most centers, pla-
Ŧ Fetal growth restriction centa previa may be identified in many women.
Ŧ Congenital anomalies The majority of previa diagnosed in the 18–20
Ŧ Malpresentations weeks scan will migrate upwards. In a woman
Ŧ Hypoxia in whom a previa is diagnosed in the second tri-
Ŧ Perinatal death
mester, ultrasound should be repeated at 28–32
CH 39_p560-581_v3.indd 564 18-07-2015 13:07:05

weeks and 36 weeks to confirm or rule out the

Box 39.6 ltrasonography in placenta previa
persistence of previa.
• Transabdominal
Ŧ Used for quick screening
istory Ŧ Fundal placenta excludes placenta previa
Painless vaginal bleeding is the most important Ŧ 95% accuracy
presenting symptom. As already mentioned, Ŧ False positive
Full bladder
bleeding may be mild or moderate and recur-
Ŧ False negative
rent. Placenta previa should be suspected in any
Fetal head low in the pelvis
woman who presents with painless bleeding • Transvaginal
after 20 weeks’ gestation, unless proved other- Ŧ 7UGFHQTEQPſTOCVKQP
wise. History of pain due to uterine contractions Ŧ 100% accuracy
may be present in some cases. Ŧ Does not provoke bleeding
Ŧ Tip of transducer placed 2–3 cm below cervix
Physical examination • Translabial (transperineal)
Ŧ Alternative to transvaginal
Presence of pallor and signs of shock should be
looked for. Uterine size, presence of uterine con-
tractions, and fetal presentation should be noted
Transabdominal ultrasonography
(Box 39.5).
Pelvic examination should not be performed This is used for quick initial screening (Fig. 39.3).
in women presenting with bleeding after 20 If the placenta is in the upper segment, placenta
weeks’ pregnancy. previa can be excluded. Accuracy for diagnosis
of placenta previa by ultrasonography is 95%. If
the maternal bladder is full, a false positive result
Investigations is common because the anterior and posterior
ltrasonography uterine walls are compressed together by the
bladder. The patient should be asked to empty
Ultrasonography is the simplest, safest, and
the bladder before confirming the diagnosis.
most accurate method of diagnosis of placenta
previa. Transabdominal and transvaginal ultra- Transvaginal ultrasonography
sonography are used. Occasionally, translabial Transvaginal ultrasonography (TVUS) is the
imaging is used (Box 39.6). most accurate (100%) modality of imaging for
previa (Fig. 39.4). It does not provoke bleeding,
Box 39.5 istory and physical examination
• History
Ŧ Gestational age
Ŧ Painless bleeding
Ŧ Amount of bleeding
Mild/moderate/profuse
Previous episodes
Ŧ Uterine contractions
• Physical examination
Ŧ General examination
Pallor
Pulse/BP/respiratory rate
Ŧ Obstetric examination
Uterine size
Contractions
Fetal lie
Figure 39.3 Abdominal ultrasonography of total
Fetal presentation
placenta previa. The placenta (PL) is seen covering the
Station of presenting part
cervical os (cx). (Photo courtesy: Mediscan Systems,
Fetal heart rate
Chennai.)
CH 39_p560-581_v3.indd 565 18-07-2015 13:07:05

Figure 39.4 Transvaginal ultrasonography of placenta Figure 39.5 Distance of placental edge from the cervical
previa. The placenta (PLA) is seen covering the cervical os. Ultrasonographic image shows the cervical os (cx),
os (OS). (Photo courtesy: Mediscan Systems, Chennai.) fetal head (HD), and placenta extending to the margin
of the os. The distance from the cervical os is marked
(1.61 cm). (Photo courtesy: Mediscan Systems, Chennai.)
if performed carefully. To prevent slippage of
probe into the cervix, the tip of the probe should
be placed at an angle to the cervix and 2–3 cm In women with previous cesarean section
below the cervix. Cervical dilatation and placen- and anterior placenta previa, evaluation with
tal location can also be determined. color-flow Doppler is essential to exclude
placenta accreta. The ultrasonographic appear-
Translabial ultrasonography
ance of placenta accreta is given in detail in
Translabial (transperineal) ultrasound is also an Chapter 43, Complications of the third stage of
accurate method and is used as an alternative to labor).
TVUS.
agnetic resonance imaging
• Transabdominal scan should be performed
first and if placenta previa is suspected, TVUS Magnetic resonance imaging (MRI) has been
should be proceeded with. studied and found to be useful but since TVUS
• If placenta previa is diagnosed in the second tri- is safe, accurate, and easily accessible, MRI is not
mester, ultrasonography should be repeated at recommended for this purpose.
28–32 weeks with a final evaluation at 36 weeks.
Two measurements should be made during Management
ultrasonography: With accurate diagnosis of placenta previa by
1. The actual distance between the placental ultrasonography and practice of expectant man-
edge and internal os (Fig. 39.5): agement, the perinatal mortality in placenta pre-
via has been reduced considerably.
When the placental edge is touching the inter-
nal os, the distance is 0 mm. When the placen-
Initial management
taledge stops at a distance of 2 cm from the
internal os, it is considered to be a low-lying pla- Initial management is as described earlier in this
centa. In this condition, vaginal delivery may be chapter.
offered, in the absence of torrential bleeding.
• Maternal condition should be assessed, mater-
2. If the placenta is covering the os, the extent nal shock should be corrected, and the mother
that the placenta covers the internal os should must be stabilized.
be documented. If it reaches across the inter- • Ultrasonography should be performed for pla-
nal os, it is a partial previa. If it crosses the cental localization.
internal os and goes to the other side of the • Fetal status should be assessed by biophysical
cervix, it is a total previa. profile and nonstress test.
CH 39_p560-581_v3.indd 566 18-07-2015 13:07:06

Subsequent management – Serial ultrasound scans and nonstress tests

for fetal growth and surveillance
Subsequent management (Fig. 39.6) depends on – Hemoglobin and/or hematocrit
gestational age and severity of hemorrhage as – Iron supplementation
given below: • Counseling
• Placenta previa diagnosed in second trimester – To avoid sexual intercourse
• Placenta previa diagnosed in early third tri- – To report if there is bleeding
mester with spontaneous cessation of bleeding
• Placenta previa with profuse hemorrhage in lacenta previa ith pro use hemor
second or third trimester rhage in secon or thir trimester
• When initial bleeding is profuse and uncon-
lacenta previa iagnose in the sec
trolled, immediate resuscitation of the mother
on trimester and cesarean section is indicated irrespective
• Diagnosis is usually by routine ultrasonogra- of gestational age. If during expectant man-
phy at 18–20 weeks agement, bleeding recurs or is profuse, admit,
• Counseling is important evaluate, transfuse blood if needed, and assess
– Reassure that most placentae will migrate fetal well-being. Continue monitoring and
– To report immediately if there is bleeding follow-up. If bleeding increases progressively
– Repeat ultrasonography is essential and gestational age is >34 weeks, deliver.
– No restriction of activity or sexual intercourse
• Repeat ultrasonography at 28 weeks; if still in Timing of delivery
lower segment, rescan at 4-weekly intervals till If there is no recurrent episode of bleeding
36 weeks and fetal growth is normal, delivery should be
• If persistent at 36 weeks, decide on mode of planned at 37 weeks.
delivery
Mode of delivery
lacenta previa iagnose in early
ndications for cesarean section
thir trimester ith spontaneous
cessation o blee ing • Complete placenta previa, even if the fetus is
dead or malformed
• Expectant management is the choice of treat- • Marginal placenta previa
ment. This is based on the following facts: • Internal os to placental margin distance of <2 cm
– Perinatal mortality is due to prematurity. • Malpresentations with any type of placenta
Prolongation of pregnancy reduces perina- previa
tal mortality • Fetal compromise—growth restriction, fetal
– Initial bleeds are usually minor and self- heart decelerations
limiting, and not fatal for the mother or • Profuse bleeding at any gestational age irre-
fetus spective of type of placenta previa
• If gestational age is <34 weeks, administer two
doses of betamethasone 12 mg IM 24 hours aginal delivery
apart Vaginal delivery is attempted only when the
• If Rh negative, administer anti-D immuno- placental margin is >2 cm from the internal
globulin os. There is controversy regarding the mode of
• Tocolytics are not recommended as a routine delivery when the placental edge is between
• Cervical cerclage is not recommended 0 and 2 cm but since the incidence of cesarean
• Patient can be discharged if there is no bleed- section is almost 90% in these cases, elective
ing for 1 week and cesarean section is recommended.
– the patient understands the risks associated
with outpatient management
– has emergency transport to hospital • In women with low-lying placenta, labor
– lives within 20–30 minutes from hospital should be induced at 38–39 weeks by cervical
• Follow-up visits ripening with prostaglandins.
CH 39_p560-581_v3.indd 567 18-07-2015 13:07:06

Painless blee ing
History an physical e amination
ransfuse stabili e
hemo ynamic status
VU
b ominal ultrasonography
ssess gestational age

fetal ell being
lee ing stoppe lee ing profuse fetal

no fetal compromise compromise
mme iate eli ery

econ trimester hir trimester by cesarean section
erial scans
egular follo up
an ee s
Maternal fetal
Placenta migrates Placenta persists
monitoring
teroi s if ee s
eli er at ee s
Central marginal
placenta pre ia Placental e ge
Placental e ge cm from os
cm from os
Cesarean section Vaginal eli ery
Figure 39.6 Management of placenta previa. S transvaginal ultrasonography.
• Pelvic examination should be performed gen- • Intrapartum electronic fetal monitoring is

tly. Fornices should be palpated for bogginess, recommended.
indicating presence of placenta. If no boggi- • Prophylactic uterotonics must be adminis-
ness is felt, fingers are introduced into the os tered in the third stage.
and amniotomy is performed. • Postpartum hemorrhage should be watched for.
CH 39_p560-581_v3.indd 568 18-07-2015 13:07:06

Cesarean section in placenta previa Both approaches may be associated with profuse
bleeding.
Cesarean section in placenta previa is associ-
ated with difficulties and complications as given • The fetus should be delivered as cephalic or
below: breech, depending on the presentation. If the
fetus is in transverse lie, the feet should be
• Fetal malpresentation may make extraction of identified first. Traction may be applied to the
the fetus difficult. feet and the fetus delivered as breech.
• Poorly developed and vascular lower uterine • If there is profuse bleeding from the lower
segment may lead to an extension of the inci- segment, hemostatic mattress sutures can
sion and hemorrhage. be used to control hemorrhage. If bleeding
• Difficulty may be encountered in uterine entry continues, internal iliac artery ligation or
with an anterior placenta. There may be a a B-Lynch procedure may be required (see
need to cut through the placenta or separate Chapter 43, Complications of the third stage of
it partially. labor).
• Excessive blood loss may occur that further
compromises the condition of the fetus and
mother.
• Placenta accreta and percreta (encountered in
about 5% of cases with no previous scar in the Placental abruption
uterus, and in up to 67% of cases with multiple
Approximately one-third of all antepartum hem-
cesarean sections) may necessitate peripar-
orrhages are due to placental abruption. The risk
tum hysterectomy.
of maternal complications and fetal compromise
• Postpartum hemorrhage may occur due to
is high; therefore, prompt delivery is indicated in
inability of the lower uterine segment to con-
most cases.
tract efficiently.
roce ure &GſPKVKQP

• Cesarean section for placenta previa should be
Placental abruption, also known as abruptio
performed by a senior obstetrician.
placenta, is defined as premature separation of
• Preoperative ultrasonography should be per-
normally implanted placentae, after 24 weeks’
formed to determine the exact location of the
gestation. The bleeding occurs between the
placenta and to exclude placenta accreta.
decidua and maternal surface of placenta.
• Adequate blood (two to four units) should be
cross-matched and kept available.
• Fetal lie, presentation, and position of the fetal
back and limbs (if breech or transverse lie)
Incidence
should be determined prior to surgery. The incidence of placental abruption ranges
• Regional or general anesthesia may be used. from 1/100 to 1/230 deliveries. Milder degrees
• A transverse incision on the lower segment are more common but severe abruption associ-
should be used if the lower segment is formed. ated with fetal and/or maternal complications
A vertical lower-segment incision may be occur less frequently. The incidence peaks at
required if the lower segment is not formed or 24–26 weeks’ gestation. Placental abruption
is vascular. accounts for one-third of all APH.
• If the placenta is anterior, one of two
approaches is used:
– Cut through the placenta
%NCUUKſECVKQP
– Find the plane between the placenta and Traditionally, placental abruption is classified
the uterine wall, separate the placenta into four grades according to the severity of
and push it upward, and enter below the abruption and associated maternal and fetal
placenta complications (Box 39.7). Abdominal pain and
CH 39_p560-581_v3.indd 569 18-07-2015 13:07:06

vaginal bleeding are the predominant symp-

toms, but external bleeding may be absent in
concealed hemorrhage.
Placenta
Pathogenesis
In placental abruption, hemorrhage occurs at
the placental–decidual interphase. The blood
seeps between the membranes and uterine e eale
wall and finally escapes through the cervix into hemorrhage
the vagina in revealed abruption (Fig. 39.7a). In
some cases, blood may be trapped behind the
placenta or membranes even after total sepa- a.
ration of placenta occurs. There is no external
bleeding and the condition is known as con-
cealed abruption (Fig. 39.7b). This can occur due
to the following:
• Placental margin remains attached though the Co ceale
hemorrha e
rest of the placenta is separated
• Placental membranes remains attached
• Blood enters the amniotic cavity through a
rent in the membranes.
• The outflow of bleeding is obstructed by the
fetal head.
Most often the revealed abruption and con-
cealed abruption coexist and this is referred to as b.
mixed abruption. Figure 39.7 Placental abruption. a. Revealed
hemorrhage. The blood enters the space between the
membranes and the uterine wall and escapes through the
cervix. b. Concealed hemorrhage. The blood is trapped
Box 39.7 %
NCUUKſECVKQP
ITCFKPIQHRNCEGPVCN behind the placenta.
abruption
Grade 0 Asymptomatic, small retroplacental clot
Grade 1 Vaginal bleeding
Abdominal pain—mild In abruption, the bleeding is from the mater-
Uterine tenderness or tetany nal vessels in the decidua; therefore, the blood
loss is maternal. A retroplacental hematoma
No fetal distress
is formed initially that enlarges and expands,
No maternal complications
resulting in total or near total separation of the
Grade 2 Vaginal bleeding present/absent placenta (Fig. 39.8). Occasionally, bleeding is
Abdominal pain—moderate from feto-placental vessels.
Uterine tenderness and tetany The pathological process leading to hem-
Fetal distress
orrhage is vasospasm of abnormal arterioles.
This results in thrombosis and decidual necro-
No maternal complications
sis. There is also poor trophoblastic invasion.
Grade 3 Vaginal bleeding present/absent This leads to inadequate uteroplacental circu-
Abdominal pain—severe and persistent lation demonstrated by abnormal uterine artery
Marked uterine tenderness and tetany Doppler flow. These pathological changes in the
Fetal death placenta occur in hypertension, preeclampsia,
and thrombophilias. Shearing forces resulting
Maternal shock/coagulopathy/renal failure
from trauma can also cause hemorrhage.
CH 39_p560-581_v3.indd 570 18-07-2015 13:07:06

Figure 39.8 Specimen of placenta shows retroplacental Figure 39.9 Couvelaire uterus. Blood has seeped into the
clots formed in concealed hemorrhage. (Photo courtesy: myometrium and the uterus appears bluish black. (Photo
Dr Rajnish Samal, Bangalore.) courtesy: Dr Rajnish Samal, Bangalore.)
Retroplacental hemorrhage and separation isk factors

of cotyledons interfere with nutrient and oxygen
supply to the fetus, resulting in fetal hypoxia and Risk factors for placental abruption are listed
ultimately fetal death. in Box 39.8. The exact etiology is not known but
Profuse bleeding, concealed or revealed, presence of risk factors is associated with an
causes maternal hypotension and hypovolemic increased incidence of abruption.
shock. Reduced renal perfusion causes acute Advanced maternal age and multiparity
renal cortical necrosis and/or tubular necrosis increase the risk due to damaged endometrium
and renal failure (see Chapter 55, Renal and uri- and poor decidualization.
nary tract disorders). Smoking and cocaine abuse cause placental
The coagulation cascade is activated due hypoperfusion due to vasospasm of decidual
to the release of thromboplastin resulting in vessels.
disseminated intravascular coagulation (DIC) Risk of abruption increases five-fold with
(see Chapter 45, Nonhemorrhagic shock in chronic hypertension and eight-fold with pre-
pregnancy). eclampsia. Poor secondary trophoblastic inva-
Thrombin, produced during the process of sion, poor placental perfusion, decidual necrosis,
coagulation, is auterotonic agent and causes uter- and hemorrhage which are common in these con-
ine hypertonus and tetany, preterm labor, and ditions increase the risk of abruption. Acquired
prelabor rupture of membranes. Blood seeps into thrombophilias (antiphospholipid antibody syn-
the uterine myometrium resulting in Couvelaire drome) and some hereditary thrombophilias
uterus (Fig. 39.9). The Couvelaire uterus appears (hyperhomocysteinemia, factor C deficiency) also
purplish due to the effusion of blood through the increase the risk by reducing placental perfusion.
myometrium and under the uterine serosa. Uterine anomalies and myoma are associated
In some women, abruption occurs in the first, with inadequate decidualization.
second, or early third trimester. There is a small Abdominal trauma causes shearing of placenta
amount of retroplacental hemorrhage but the and tearing of vessels, leading to abruption.
bleeding is arrested and pregnancy continues. External cephalic version, if not performed
This is referred to as chronic abruption. Maternal carefully, can cause traction on the cord and pre-
serum alpha fetoprotein is elevated in these mature separation of placenta.
cases and fetal growth restriction is common. Previous abruption is an important risk fac-
Pathogenesis of placental abruption is given tor and the recurrence rate is about 5%. Grade
in Figure 39.10. 3 abruption has a higher recurrence rate (12%).
CH 39_p560-581_v3.indd 571 18-07-2015 13:07:07

a Vasospasm of arterioles
Hypertension hrombosis
Preeclampsia eci ual necrosis
hrombophilias Poor trophoblastic in asion
Placental abruption
e eale Conceale
ehin placenta behin
membranes behin fetal
hea into amniotic ca ity
eparation of placenta
etus
e uce supply of Mother
nutrients an o ygen
Hypo ia eath Hypo olemic shoc C enal failure
Figure 39.10 Pathogenesis of placental abruption. D C, disseminated intravascular coagulation; fetal growth
restriction.
Rapid uterine decompression by sudden

Box 39.8 isk factors for placental abruption
release of amniotic fluid can lead to placental
separation. This usually happens in polyhydram- • Inadequate decidualization
nios and multifetal pregnancy, both of which are Ŧ Maternal age
Ŧ Increasing parity
risk factors as well.
Ŧ 7VGTKPGCPQOCNKGUſDTQKFU
Abruption in preterm prelabor rupture of
• Vasospasm and placental hypoperfusion
membranes may be due to release of thrombin, Ŧ Hypertension
which is a uterotonic. Membrane rupture may Ŧ Preeclampsia
also be the consequence of abruption. Ŧ Thrombophilias—acquired and inherited
Ŧ Smoking/cocaine use
• Rapid decompression of the uterus
Clinical features Ŧ Polyhydramnios
Ŧ Multifetal gestation
Clinical features vary with the following: Ŧ Preterm prelabor rupture of membranes
• Acute abruption • Shearing of placental vessels
Ŧ Abdominal trauma
– Revealed hemorrhage
Ŧ External cephalic version
– Concealed hemorrhage
• Other causes
• Chronic abruption Ŧ Previous abruption
CH 39_p560-581_v3.indd 572 18-07-2015 13:07:07

Acute placental abruption Box 39.9 Clinical features of acute placental

Revealed abruption is more common and abruption
occurs in 90% of cases. The most important • Vaginal bleeding
symptom is vaginal bleeding with abdominal Ŧ Mild/profuse
pain. When the placenta is located on the pos- • Abdominal pain
terior uterine wall, back pain may be predom- Ŧ Mild/severe/persistent
inant. The uterus is tense and tender. Uterine • Backache
• Uterine tenderness
contractions may be present.
• Uterine tetany
Bleeding may be mild or profuse. There is
maternal tachycardia and hypotension. The • Overdistended uterus
severity of pain and uterine tenderness may pro- • Maternal
gressively worsen. Ŧ Hypotension
As more and more cotyledons separate, Ŧ Tachycardia
fetal heart decelerations occur. When >50% Ŧ Decreased urine output
of the placenta separates, fetal death results. Ŧ Signs of disseminated intravascular coagulation
Fetal heart trace may reveal variable or late • Fetal heart rate abnormalities
decelerations, prolonged bradycardia, poor Ŧ Variable/late decelerations
variability, or a sinusoidal pattern prior to Ŧ Poor variability
fetal death. Ŧ Prolonged bradycardia
Ŧ Sinusoidal pattern
Maternal urine output drops as renal failure
sets in. Disseminated intravascular coagulation
ensues and worsens the renal failure and hemor-
rhage (Box 39.9). Box 39.10 Complications of placental abruption
Concealed hemorrhage occurs in 10% of • Maternal
cases. The degree of hypotension is out of Ŧ Hypovolemic shock
proportion to the amount of bleeding seen Ŧ Renal failure
externally. Bleeding may be mild, moderate, Ŧ Disseminated intravascular coagulation
or absent. The uterus is overdistended when Ŧ Preterm labor
the blood collects behind the placenta and Ŧ Prelabor rupture of membranes
membranes, or enters the amniotic cavity. Ŧ Instrumental delivery
This makes palpation of fetal parts difficult. Ŧ Cesarean section
The uterus may become woody hard when Ŧ Postpartum hemorrhage
Ŧ Rh sensitization
blood infiltrates the myometrium (Couvelaire
Ŧ Sheehan syndrome
uterus).
Ŧ Maternal death
• Fetal
Ŧ Fetal hypoxia
Chronic placental abruption Ŧ Prematurity
Chronic placental abruption is usually due Ŧ Fetal growth restriction
Ŧ Fetal death
to chronic placental ischemia and presents
with recurrent episodes of bleeding. It results
in growth restriction and oligohydramnios.
Coagulation abnormalities do not occur. Maternal complications
Since the bleeding is from the decidual vessels,
hypotension, hypovolemia, and shock are com-
Complications of placental mon complications. Preexisting hypertension
may mask the effects of blood loss but eventually
abruption hypotension becomes evident. Acute renal failure
Maternal and fetal complications of abruption may result from hypotension and underperfu-
are listed in Box 39.10. sion and/or DIC. Acute tubular necrosis is more
CH 39_p560-581_v3.indd 573 18-07-2015 13:07:07

common and manifests as oliguria. Acute bilat-

Box 39.11 Screening tests for placental
eral cortical necrosis can also occur but is rare. abruption
Disseminated intravascular coagulation is
due to release of thromboplastin from the pla- • First trimester
Ŧ Decreased PAPP-A levels
cental bed, activating the coagulation cascade
(see Chapter 45, Nonhemorrhagic shock in preg-
Ŧ Uterine artery Doppler at 11–14 weeks
nancy). Fibrinogen is consumed during this pro- High pulsatility index
cess, resulting in fall in plasma fibrinogen levels. Diastolic notch
Increase in fibrinolysis leads to elevated levels of Ŧ Elevated hCG
fibrin degradation products and/or D-dimers. Ŧ Elevated serum alpha fetoprotein
Nonreassuring fetal heart status often neces-
hC human chorionic gonadotropin; PAPP-A, pregnancy-
sitates delivery by forceps, vacuum extraction, or associated plasma protein A.
cesarean section.
Postpartum hemorrhage may be a conse-
quence of a Couvelaire uterus that does not Diagnosis
contract adequately or DIC. Excessive bleeding,
either antepartum or postpartum and the atten- The diagnosis of placental abruption is clinical
dant severe hypotension can cause necrosis of since investigations may be noncontributory.
the physiologically enlarged pituitary (Sheehan
syndrome). istory
Preterm prelabor rupture of membranes is
A history should be obtained of bleeding, asso-
commonly associated with placental abruption.
ciated pain, uterine contractions, rupture of
As already mentioned, release of thrombin and
membranes, hypertension or preeclampsia, and
the resultant uterine contractions probably play
reduced fetal movements. Symptoms such as
a role.
restlessness, anxiety, tachypnea, thirst and faint-
Maternal mortality in abruption may be
ing, are indicative of hypovolemia (Box 39.12).
due to irreversible shock, respiratory distress
syndrome, renal failure, or multiorgan failure.
Mortality is higher in women with preeclampsia Box 39.12 istory in placental abruption
and preexisting anemia.
• Gestational age
• Presenting symptoms
Fetal complications Ŧ Vaginal bleeding
Mild/profuse
As discussed earlier in the chapter, placental Ŧ Pain
separation leads to fetal hypoxia and fetal death. Abdominal pain
Prematurity is another cause of perinatal mor- Backache
tality. The incidence of congenital anomalies has Pain of uterine contractions
been found to be higher in placental abruption Ŧ Vaginal discharge
(4.4%). Chronic abruption causes fetal growth Ŧ Symptoms of blood loss and hypovolemia
restriction. Fainting
Restlessness
Palpitation
Prediction of placental Tachypnea
abruption Thirst
Sweating
Attempts have been made to use the tests for Ŧ Decreased fetal movements
Down syndrome screening and prediction of • Past history
preeclampsia, to identify women at high risk Ŧ Hypertension
for placental abruption (Box 39.11).The tests Obstetric history
lack adequate sensitivity and positive predictive Ŧ Preeclampsia
Ŧ Previous abruption
value for abruption, and therefore are not rec-
Ŧ Recurrent episodes of bleeding
ommended routinely for this purpose.
CH 39_p560-581_v3.indd 574 18-07-2015 13:07:07

Physical examination Box 39.13 Physical examination in placental

Severity of bleeding, uterine size, and condition abruption
of the mother and fetus should be assessed on • General examination
physical examination (Box 39.13). Vaginal exam- Ŧ Pulse
ination should not be performed until placenta Ŧ Blood pressure
previa is excluded by ultrasonography. However, Ŧ Amount of bleeding
if rupture of membranes is evident, the present- • Abdominal examination
Ŧ Uterine size
ing part is engaged or well-fixed, and definite
Ŧ Consistency
clinical signs of abruption are present, careful
Ŧ Tenderness
pelvic examination may be undertaken. The Ŧ Contractions
presence of clots in the vagina, dilatation and Ŧ Palpation of fetal parts
effacement of cervix, the presence or absence of Ŧ Presentation
membranes, presentation, station of presenting Ŧ Fetal heart sounds
part, and draining of blood-stained amniotic • Local examination
fluid should be documented. Ŧ Vaginal bleeding
Ŧ .GCMKPIQHCOPKQVKEƀWKF
• Vaginal examination (if performed)
Placenta previa versus placental Ŧ Clots in the vagina
abruption Ŧ Cervical effacement
The most important differential diagnosis for
Ŧ Presence or absence of membranes
placental abruption is placenta previa, since Ŧ Presentation/station
these two conditions are the most common Ŧ $NQQFUVCKPGFCOPKQVKEƀWKF
causes of APH. The differentiating features are
given in Table 39.1. However, confirmation of the
diagnosis is finally by ultrasonography.
The two may coexist in 10% of cases. Findings on
ultrasonography are variable (Fig. 39.11).
Investigations
• A retroplacental hematoma is not always seen.
ltrasonography Early retroplacental clot is isoechoic or hyper-
Ultrasonography is the most important step in echoic and may be interpreted as thickened
evaluation. This is more useful in excluding pla- placental tissue. The clot becomes hypoechoic
centa previa rather than confirming abruption. and sonolucent after 1–2 weeks.
Table 39.1 Differences between placenta previa and placental abruption
Placenta previa Placental abruption
Bleeding • Painless • Associated with pain

• Recurrent, small bouts • Usually single bout
Shock Proportionate to blood loss Out of proportion to blood loss (if concealed)
Uterine size Corresponds to gestation Larger than gestation
Uterus Relaxed Tense and tender
Malpresentations Common Not common
Presenting part High and mobile Fixed or engaged
Fetal parts Well felt &KHſEWNVVQRCNRCVG
Fetal heart rate and trace Normal Abnormal
Renal failure and DIC Not common Common
Placenta accreta Common Not common
D C, disseminated intravascular coagulation.
CH 39_p560-581_v3.indd 575 18-07-2015 13:07:07

• Stabilize the patient with crystalloids and col-

loids as required.
• Send blood for coagulation profile—platelet
count, prothrombin time, partial thrombo-
plastin time, plasma fibrinogen levels, and
fibrinogen and fibrin degradation products.
• Perform ultrasonography to exclude placenta
previa and, if possible, to confirm abruption.
• Assess fetal status by biophysical profile and
nonstress test.
• Perform a bedside clotting test if facilities for
DIC workup are not available.
• If hourly urine output is <30 mL/hour, insert a
Figure 39.11 Abdominal ultrasonography of placental central venous line.
abruption. Preplacental hematoma seen on the fetal
surface of the placenta.
Subse uent management
• If a retroplacental hematoma can be identi- This depends on fetal condition, gestational
fied, it indicates massive bleeding and the age, presence of uterine contractions, and rup-
woman will be in shock. ture of membranes. Management options are as
• Subchorionic and preplacental hematomas follows:
may be seen located between membranes and • Immediate delivery
the uterine wall or on the fetal surface of the – Vaginal delivery
placenta. – Cesarean section
• Intrauterine clots may be seen floating in amni- • Expectant management
otic fluid which ‘jiggle’ on maternal movement
or on bouncing with the transducer (‘Jello’ Immediate delivery
sign).
• The sensitivity of ultrasonography in identify- Most women with placental abruption require
ing placental abruption is 25%–50%. immediate delivery since the bleeding is moder-
ate to severe and maternal complications and/or
agnetic resonance imaging fetal distress are usually present.
Indications for immediate delivery are listed
Magnetic resonance imaging can be used to
in Box 39.14.
diagnose abruption when in doubt but is not
recommended routinely. Mode of delivery
After the initial treatment to stabilize the moth-
Management er’s condition, the fetal heart rate pattern is
Management depends on the following: evaluated by electronic fetal monitoring and
• Severity of abruption a decision is taken regarding mode of delivery
• Gestational age (Box 39.15).
• Maternal condition
• Condition of the fetus
Box 39.14 Indications for immediate delivery in
placental abruption
Initial management
• Irrespective of gestational age
Initial management is as described earlier in this Ŧ Moderate-to-severe bleeding
chapter. Ŧ Maternal complications
• Evaluate mother for amount of blood loss and Ŧ Fetal distress
Ŧ Fetal death
correct maternal shock.
• Gestational age >34 weeks
• Catheterize the bladder and monitor hourly
Ŧ Mild bleeding
urine output.
CH 39_p560-581_v3.indd 576 18-07-2015 13:07:07

When the fetus is alive, a close watch should

Box 39.15 Mode of delivery in placental
abruption be kept on the fetal status. Partial abruption can
progress rapidly to complete separation of the
• Cesarean section, if placenta and fetal death; therefore, continuous
Ŧ the abruption is severe and bleeding persistent
fetal heart rate monitoring is essential.Immediate
Ŧ nonreassuring fetal status
cesarean section is warranted in the presence of
Ŧ maternal renal failure or DIC
• Vaginal delivery, if
fetal heart rate abnormalities.
Ŧ the fetus is alive, fetal heart rate pattern is normal When the fetal heart pattern becomes abnor-
Ŧ bleeding is mild to moderate mal, and a decision for a cesarean section has
Ŧ fetus is dead but maternal condition is stable been made, the decision-to-delivery time should
not exceed 20 minutes, to avoid fetal asphyxia.
D C disseminated intravascular coagulation.
ostpartum management
Cesarean section • Maternal pulse, blood pressure, and urine out-
Immediate cesarean section is indicated if the put should be monitored.
bleeding is profuse and persistent indicating • 20 units of oxytocin should be administered in
severe abruption, if the fetal heart trace is abnor- 500 mL of normal saline.
mal, or if maternal complications such as DIC • If the uterus is atonic, ergometrine and pros-
or renal failure are present. Correction of DIC taglandin F2-a should be administered (see
with blood and blood products must proceed Chapter 43, Complications of the third stage of
simultaneously with preparations for cesarean labor).
section.
A Couvelaire uterus may be found at cesarean pectant management
section. A Couvelaire uterus does not contract There is only a limited role for expectant man-
adequately because of extravasation of blood agement in placental abruption since fetal
into the myometrium, and atonic postpartum growth restriction, oligohydramnios, preterm
hemorrhage is common. Prophylactic uteroton- labor, or progresses of abruption are common.
ics must be administered and bleeding must be The indications are listed in Box 39.16.
managed aggressively. Expectant management consists of the
aginal delivery following:
Vaginal delivery may be an option in certain • Discharge after 48 hours
situations (given in Box 39.15). The steps are as • Counseling regarding immediate return to
follows: hospital if
– fetal movements decrease
• Vaginal examination to assess the cervical – bleeding recurs
effacement and dilatation – uterine contractions begin
• Amniotomy • Weekly biophysical profile and estimation of
• Continuous electronic fetal monitoring fetal growth and weight
mandatory • Betamethasone two doses 24 hours apart to
• Oxytocin augmentation, if required accelerate pulmonary maturity
• If fetal heart trace shows abnormality, imme- • Role of tocolysis in the event of preterm labor
diate cesarean section controversial; not recommended as routine
• If delay in second stage, instrumental delivery • Kleihauer-Betke test and administration of
undertaken anti-D immunoglobulin, if Rh negative
• Prophylactic uterotonics (oxytocin) manda-
tory after delivery of the placenta
Box 39.16 Indications for expectant management
With a dead fetus, delivery is achieved fol- in placental abruption
lowing amniotomy in most cases, as long as the
• Nonsevere abruption at <34 weeks
maternal condition is stable. Oxytocin augmen-
• No maternal complications
tation may be required in a few but hyperstimu-
• Fetal surveillance tests are normal
lation should be watched for.
CH 39_p560-581_v3.indd 577 18-07-2015 13:07:07

• Deliver if fetal growth restriction, oligohy- &GſPKVKQP

dramnios or recurrent bleeding
• Induction of labor 37–38 weeks by cervical rip- Vasa previa is defined as the presence of umbil-
ening with prostaglandinE2, amniotomy, and ical vessels running through the membranes
oxytocin across the internal os below the presenting part,
• Management of placental abruption is given in before reaching the placenta.
Figure 39.12 Since the vessels are not protected by
Wharton’s jelly, they are prone to rupture and com-
pression and torrential bleeding during labor.
This can be of two types:
asa previa 1. Velamentous insertion of cord (Fig. 39.13)
2. Vessels running between placenta and its suc-
Vasa previa is rare cause of antepartum
centuriate lobe
hemorrhage. Bleeding occurs intrapartum
and can be profuse; therefore, fetal hypoxia is Clinical features and management of vasa
common. previa are summarized in Box 39.17.
lee ing an pain

ense ten er uterus
tabili e mother
C or up an other tests
Monitor urine output
clu e placenta pre ia

Ultrasonography ssess gestational age
aluate fetal ell being
Mo erate to se ere blee ing etus ea Mil blee ing

Maternal complications
onreassuring fetal status
estation ee s estation ee s
mme iate cesarean section
mme iate eli ery pectant management

mniotomy an o ytocin etal sur eillance
estation ee s ecurrent blee ing
eli er
mniotomy o ytocin
Figure 39.12 Management of placental abruption. D C, disseminated intravascular coagulation;

CH 39_p560-581_v3.indd 578 18-07-2015 13:07:07

7PENCUUKſGFJGOQTTJCIG
Unclassified hemorrhage is APH with no
evidence of placental abruption or placenta
Placenta previa. Clinical course and management are
Umbilical cor Box 39.18 7PENCUUKſGFJGOQTTJCIG

• No evidence of placenta previa or abruption
• Most commonly due to
Vasa pre ia Ŧ marginal sinus rupture
umbilical essels Ŧ tumors of the cervix/infections
Ŧ exaggerated show
• Diagnosis
Figure 39.13 Vasa previa. Velamentous insertion of the Ŧ Exclude placenta previa and abruption
cord with umbilical vessels running along the membranes Ŧ Speculum examination after bleeding stops
across the internal os before entering the placenta. • Management
Ŧ Evaluate fetal status
Ŧ If gestation >37 weeks—deliver
Box 39.17 Clinical features and management of
Ŧ If gestation <37 weeks
vasa previa
Fetal surveillance
• The condition is rare Deliver at 38 weeks/term
• Bleeding is from fetal vessels
• Occurs when membranes rupture
• High perinatal mortality (75%)
• &KHſEWNVVQFKCIPQUGCPVGPCVCNN[
• If diagnosed antenatally
Ŧ Elective cesarean section
• If diagnosed intrapartum
Ŧ Expedite delivery
Ŧ Resuscitate neonate
Key points
• Antepartum hemorrhage (APH) is bleeding from the • Transvaginal and translabial ultrasonography have
genital tract after 24 weeks’ gestation prior to delivery close to 100% accuracy in the diagnosis of placenta
of the baby. previa.
• The important causes are placenta previa and placen- • The typical presentation is painless vaginal bleeding.
tal abruption. The uterus is relaxed, malpresentations are common,
and the presenting part is high up.
• Initial assessment consists of history and physical
examination to assess maternal status, amount of • Vaginal examination should not be performed in
bleeding, gestational age, and fetal status. women presenting with bleeding in the third trimester,
• After the mother is stabilized, ultrasonography should until placenta previa is excluded.
be performed to determine the cause of bleeding and • Initial bleeding is usually mild and occurs before 32
evaluate fetal status. weeks’ gestation.
• 2NCEGPVCRTGXKCKUFGſPGFCUCRNCEGPVCVJCVKUKO- • Expectant management is the option if placenta previa
planted over or adjacent to the internal os. It is classi- is diagnosed in early third trimester and there is spon-
ſGFKPVQVQVCNRCTVKCNOCTIKPCNCPFNQYN[KPIRNCEGPVC taneous cessation of bleeding.
previa. • If bleeding is profuse, immediate delivery is indicated.
(Continued)
CH 39_p560-581_v3.indd 579 18-07-2015 13:07:08


• If the placenta is total or marginal or the placental • Shock is out of proportion to amount of blood loss in
edge is <2 cm from the os, cesarean section is indi- concealed hemorrhage. Maternal renal failure and dis-
cated. If the placental edge is >2 cm from os, vaginal seminated intravascular coagulation are other major
delivery may be attempted. complications.
• Placenta accreta and postpartum hemorrhage are • Fetal distress and fetal death are common in severe
common complications. abruption.
• Placental abruption is the premature separation of a • Ultrasonography is not a sensitive method to diagnose
PQTOCNN[KORNCPVGFRNCEGPVC+VKUENCUUKſGFCUITCFG abruption. It is used mainly to exclude placenta previa
1, 2, and 3. It may be concealed, revealed, or mixed. TCVJGTVJCPEQPſTOCDTWRVKQP
• The usual presentation of placental abruption is • If bleeding is moderate to severe, maternal complications
bleeding and pain. Uterine contractions and rupture of are present, or there is nonreassuring fetal status, im-
membranes may be present. The uterus is tense and mediate cesarean section is indicated. If bleeding is mild
tender, uterine size is larger than gestational age, and and gestation is >34 weeks, or if the fetus is dead and
HGVCNRCTVUCTGFKHſEWNVVQRCNRCVG maternal status is stable, vaginal delivery can be tried.
Self-Assessment
Case 1 Case 1
Mrs. AN, 22, primigravida, was admitted to the labor room 1. Placenta previa and placental abruption. Other condi-
at 32 weeks’ pregnancy with sudden onset of vaginal VKQPUUWEJCUXCUCRTGXKCCPFWPENCUUKſGFDNGGFKPI
bleeding. There was no associated abdominal pain. On CTGWPNKMGN[CPFUJQWNFDGEQPUKFGTGFQPN[KHVJGſTUV
examination, she had tachycardia, pulse rate was 110/ two are excluded.
min, and blood pressure was 100/70 mm Hg. The uterus 2. a. History: Painless bleeding.
was 32 weeks size, not tense or tender, and the fetus was b. Physical examination: Tachycardia and drop in
in cephalic presentation. blood pressure.
• What is the differential diagnosis? c. Abdominal examination: Relaxed uterus, size cor-
• *QYYKNN[QWEQPſTOVJGFKCIPQUKU! TGURQPFKPIVQIGUVCVKQPOCNRTGUGPVCVKQPƀQCVKPI
• How will you manage? head.
• What complications do you anticipate? d. Abdominal ultrasonography followed by transvagi-
nal ultrasonography (TVUS).
3. Initial management: Start IV line, send blood for
Case 2 hematocrit and cross-match, transfuse if hematocrit
is low.
Mrs. SK, 30, multigravida, was admitted to the labor room
If the bleeding stops and fetal evaluation is normal,
at 36 weeks’ gestation with vaginal bleeding, abdomi-
expectant management. Regular fetal surveillance
nal pain, and absent fetal movements since the onset
and delivery at 37 weeks. If total or marginal placenta
of bleeding. She was pale, restless and sweating, had
previa or if placental edge is <2 cm from the os, ce-
tachycardia, and the blood pressure was 80/60 mm Hg.
sarean section. If placental edge is >2 cm from the os,
Fetal heart tones were not recordable.
vaginal delivery.
• What is the likely diagnosis?
4. Maternal complications: Preterm labor, placenta
• What are the maternal complications? What compli-
accreta, postpartum hemorrhage, cesarean section,
cation does this woman have?
instrumental delivery.
• What would be the management?
Fetal complications: Prematurity, malpresentations,
• If the fetus was alive and bleeding was moderate,
fetal hypoxia, fetal death.
how would you manage the case?
CH 39_p560-581_v3.indd 580 18-07-2015 13:07:08


1. Placental abruption with fetal demise. Long-answer questions
1. &KUEWUUVJGGVKQNQI[CPFENCUUKſECVKQPQHRNCEGPVC
2. Hypovolemic shock, DIC, renal failure, cesarean sec- previa. How would you manage a third gravida with
tion, maternal mortality. painless vaginal bleeding at 32 weeks’ gestation?
This patient has hypovolemic shock.
2. Discuss the clinical features, diagnosis, and manage-
3. Initial management: IV line, blood transfusion, mater- ment of placenta previa.
nal stabilization. Monitor urine output, perform DIC 3. &GſPG#2* What are its causes? How do we
workup. manage a case of placental abruption at 32 weeks’
Since the fetus is dead, immediate delivery is indicat- gestation?
ed. If the patient stabilizes after resuscitation, amni-
otomy with oxytocin may result in vaginal delivery. If
profuse bleeding persists, cesarean section should be Short-answer questions
performed. 1. Expectant management in placenta previa
4. With moderate bleeding and a live fetus, stabilize the 2. Cesarean section in placenta previa
patient, perform amniotomy and administer oxytocin 3. Complication of abruptio placenta
with electronic fetal monitoring. If nonreassuring fetal 4. Couvelaire uterus
status, immediate cesarean section. If trace normal 5. Differential diagnosis of bleeding at 32 weeks’
throughout, vaginal delivery. gestation
CH 39_p560-581_v3.indd 581 18-07-2015 13:07:08

Section 6
Obstetric
Complications:
Intrapartum
CH 40_p582_598_v3.indd 582 18-07-2015 13:24:40

Abnormal Labor:
Abnormalities in
40 Passage and
Powers
Case scenario
Mrs. BN, 28, primigravida, at 40+3 weeks’ gestation, was admitted to the
labor room with pains. On examination, she had regular uterine contrac-
tions once every 5 minutes, lasting for 40 seconds. The vertex was three-fifth
palpable abdominally, and fetal heart sounds were normal. She was diag-
nosed to be in labor; on pelvic examination, the cervix was fully effaced
and 4-cm dilated. The vertex was at –2 station. She was expected to deliver
in the next 6 hours. But, on examination after 4 hours, the contractions
were once every 8–10 minutes, lasting for 30 seconds. The vertex was still
three-fifth palpable, cervix was 5-cm dilated, and vertex was at –2 station.
The mother and her relatives were worried about the lack of progress in
labor.
Introduction the labor curve falls outside the normal. The

abnormality may be in the latent or active
The process of labor proceeds normally in most phase of the first stage or in the second stage
women. However, abnormalities of labor do occur. of labor.
These may be due to abnormalities of the pelvis,
uterine contractions, malpresentations or large size
of the fetus. A thorough knowledge of the condi-
tions leading to labor abnormalities, is essential for Causes of abnormal labor
optimal maternal and perinatal outcome.
Causes of abnormal labor may be in the pas-
sage, powers, or passenger (Box 40.1). Most
&GſPKVKQP often, they occur in combination and one
abnormality can lead to another. This chapter
Labor is considered abnormal when it is pro- deals with abnormalities of the passage and
longed or does not progress as expected and powers.
CH 40_p582_598_v3.indd 583 18-07-2015 13:24:40

Box 40.1 Causes of abnormal labor Box 40.2 Pelvic diameters in contracted pelvis
• Abnormalities in passage • Inlet contraction
Ŧ Bony pelvis Ŧ Anteroposterior diameter <10 cm
Contracted pelvis Ŧ Transverse diameter <12 cm
Pelvic configuration Ŧ Diagonal conjugate <11.5 cm
Ŧ Soft tissues • Midpelvic contraction
Noncompliant cervix (cervical dystocia) Ŧ 6TCPUXGTUG RQUVGTKQTUCIKVVCNFKCOGVGTŭEO
Congenital anomalies of uterus, cervix, and vagina Ŧ Transverse (interischial spinous) diameter <8 cm
Myoma, ovarian mass • Outlet contraction
• Abnormalities in powers Ŧ Interischial tuberous diameter =/<8 cm
Ŧ Abnormal uterine action
Hypotonic uterine action
Diagnosis of contracted pelvis is made when
Hypertonic uterine action
Precipitate labor
the pelvic diameters are as given in Box 40.2.
Ŧ Inadequate maternal powers When there is inlet contraction, the head does
• Abnormalities in passenger (fetus) not descend until onset of labor or may not enter
Ŧ Large size the pelvis at all. This can result in floating head at
Ŧ Abnormal presentation term, deflexion or extension of fetal head (leading
Face, brow to face or brow presentation) or transverse lie.
Breech Midpelvic contraction is more common than
Shoulder inlet contraction. Interischial spinous (trans-
Compound verse) diameter at midpelvis is the narrowest
Ŧ Abnormal position diameter of the pelvis and is normally 10 cm;
Occipitoposterior
when this is less than 8 cm, the head cannot pass
Asynclitism
through and results in obstructed labor.
• Fetal anomalies
Hydrocephalus
Interischial tuberous diameter of <8 cm is
Meningocele/meningomyelocele diagnostic of outlet contraction and is associ-
Fetal abdominal distension ated with a narrow subpubic arch. This pushes
the head posteriorly and results in third- and
fourth-degree perineal tears. Isolated outlet con-
traction is rare; it is usually associated with mid-
Abnormalities of passage pelvic contraction (Box 40.3).
As already mentioned, abnormalities of pas-

Box 40.3 Contracted pelvis
sage include those of the bony pelvis or soft
tissues. • &GſPKVKQP
Ŧ One or more diameters < normal
Ŧ At one or more levels
• Occur in
Abnormalities of bony pelvis Ŧ Short women (height <146 cm)
Contracted pelvis and abnormal pelvic config- Ŧ Rickets/osteomalacia
uration are the usual abnormalities of the bony Ŧ Pelvic trauma
pelvis. These abnormalities of the bony pelvis Ŧ Abnormalities of vertebral column
lead to cephalopelvic disproportion. Ŧ Lower limb deformities
• Inlet contraction
Ŧ Nonengagement of head
Ŧ Face/brow/shoulder presentation
Contracted pelvis
Ŧ Floating head at term
The pelvis is said to be contracted if one or • Midpelvic contraction
more diameters of the pelvis at one or more Ŧ Prolonged labor
planes is less than normal. Contraction may be Ŧ Obstructed labor
at the inlet, midpelvis, or outlet. Combinations • Outlet contraction
Ŧ Isolated outlet contraction is rare
of contraction at various levels may be present.
Ŧ Usually associated with midpelvic contraction
Contraction in one diameter may be compen-
Ŧ Causes third- or fourth-degree perineal tears
sated by slight increase in another diameter.
CH 40_p582_598_v3.indd 584 18-07-2015 13:24:40

Abnormal Labor: Abnormalities in Passage and Powers 585
A pelvis that is of normal configuration but The anthropoid pelvis is anteroposteriorly

has smaller diameters is often seen in short, oval and has increased anteroposterior (AP)
small-built women (height <146 cm). The fetus diameter at all levels. Occipitoposterior positions
is also smaller in these women; therefore, labor and face-to-pubis delivery are more common.
proceeds normally. But, if the baby is large, labor The platypelloid or flat pelvis is transversely
is prolonged or may even be obstructed. oval and has increased transverse diameters and
Contracted pelvis is also seen in the following narrow AP diameters. Asynclitic engagement,
conditions: deflexion and extension of head, and arrest in the
transverse diameter are the problems encoun-
• Rickets/osteomalacia
tered (Table 40.1).
• Pelvic fractures
• Abnormalities of vertebral column such as
kyphosis, scoliosis, and spina bifida Cephalopelvic disproportion
• Lower limb deformities, for example, poliomy-
elitis Anatomical disproportion between the fetal
head and maternal pelvis, known as cephalopel-
2GNXKEEQPſIWTCVKQP vic disproportion (CPD), can lead to abnormal
labor. Cephalopelvic disproportion may be due
Four major types of pelvis have been described— to the following:
gynecoid, android, anthropoid, and platypel-
loid (see Chapter 2, Anatomy of the bony pelvis • Contracted pelvis
and fetal skull). The gynecoid pelvis is the nor- • Pelvic configuration
mal female type and all normal pelvic diameters • Large size of the fetus
are described with reference to this. The normal • Fetal malposition
pelvic configuration is such that the fetal presen-
tation is usually vertex in left occipitotransverse abor in omen ith C D
(OT) or occipito anterior (OA) position and car-
Normal labor and delivery are possible in women
dinal movements of labor proceed normally.
with mild to moderate CPD because of the fol-
The android pelvis has converging sidewalls,
lowing reasons:
contraction at the midpelvis, a narrow interi-
schial spinous diameter, and beaked forepelvis. • Contraction in one diameter may be compen-
Obstructed labor, persistent occipitoposterior sated by increase in another diameter.
(OP) position, and deep transverse arrest are • Good uterine contractions assist in overcom-
common. ing obstruction.
Table 40.1 'HHGEVUQHRGNXKEEQPſIWTCVKQPQPNCDQT
Type of pelvis Shape and diameters Effects on labor

Gynecoid Normal female • Vertex presentation
• OA/OT position
• Normal labor
Android Converging side walls Prolonged labor
Midpelvic contraction Obstructed labor
Beaked forepelvis • Persistent OP position
• Deep transverse arrest
Anthropoid Anteroposteriorly oval OP position
Smaller transverse diameters Face-to-pubis delivery
Platypelloid Transversely oval Asynclitism
Smaller AP diameters • Extended head (face)
• Transverse arrest
AP, anteroposterior; A, occipitoanterior; P, occipitoposterior; , occipitotransverse.
CH 40_p582_598_v3.indd 585 18-07-2015 13:24:40

• The pelvic diameters increase slightly in labor

Box 40.5 istory
due to uterine contractions and pressure of the
presenting part (‘give’ of the pelvis). • Past history
• The fetal head molds and the fetal diameters Ŧ Poliomyelitis
Ŧ Rickets/osteomalacia
reduce, facilitating descent of the head.
Ŧ Pelvic trauma
Ŧ Tuberculosis of the spine
Complications o C D
• Obstetric history
The fetal head does not fit well in the lower Ŧ Prolonged labor
uterine segment and cervix. The intrauterine Ŧ &KHſEWNVQRGTCVKXGXCIKPCNFGNKXGT[
pressure is transmitted to the forewaters, lead- Ŧ Cesarean section
ing to prelabor rupture of membranes. Cord Ŧ Fetal asphyxia
prolapse is also common for the same reason. Ŧ Intrapartum fetal death
Cervical dilatation may not occur since the ver- Ŧ History of large baby, weight >3.5 kg
tex does not press against it during contraction.
Malpresentations are common. Labor may be
prolonged with associated increase in risk of Physical e amination
fetal asphyxia, intrauterine infection (mater- Women with a small pelvis are generally short.
nal and fetal), operative vaginal delivery, and The abdomen may be pendulous. Obstetric
cesarean section. Obstructed labor and uterine examination may reveal a mobile head at term,
rupture can occur where facilities for cesarean deflexed head, occiput posterior position, or
section are not available (Box 40.4). malpresentations such as face or breech. The
mother’s gait, vertebral column, and lower limbs
Diagnosis o C D should be examined (Box 40.6).
Diagnosis of contracted pelvis is by history, phys-
Clinical pelvimetry
ical examination, and pelvimetry. Tests have been
evolved to assess the disproportion between the Clinical internal pelvimetry by pelvic exam-
fetal head and the pelvis. However, monitoring ination is the only method commonly used to
the progress in labor is the best way to assess CPD. assess the type and dimensions of the pelvis.
Predictive values of clinical pelvimetry are poor.
Clinical evaluation An idea about the pelvic configuration and
istory
Multiparous women with pelvic abnormalities
have a history of previous difficult labor, difficult Box 40.6 Physical examination
operative vaginal delivery, cesarean section, fetal • General examination
asphyxia, or intrapartum death. Nulliparous Ŧ Height <146 cm
women may give a history of rickets or poliomy- Ŧ Gait
elitis in childhood (Box 40.5). Ŧ Spine
Kyphosis
Scoliosis
Box 40.4 Complications of cephalopelvic
Spina bifida
disproportion
Ŧ Lower limbs
• Prelabor rupture of membranes Poliomyelitis
• Cord prolapse • Obstetric examination
• Lack of cervical dilatation Ŧ Pendulous abdomen
• Malpresentations Ŧ Mobile head
• Prolonged labor Ŧ &GƀGZGFJGCF
Ŧ Fetal asphyxia Ŧ Occipitoposterior position
Ŧ Maternal and fetal infection Ŧ Malpresentations
• Operative vaginal delivery Face
• Cesarean section Brow
• Obstructed labor Breech
• Uterine rupture Shoulder
CH 40_p582_598_v3.indd 586 18-07-2015 13:24:40

obvious reduction in diameters can be obtained for a narrow subpubic angle in which the head
by estimation of diagonal conjugate, interischial emerges more posteriorly (android pelvis).
spinous diameter, intertuberous diameter, sub-
pubic arch, and subpubic angle (see Chapter 2, Assessment of CPD
Anatomy of the bony pelvis and fetal skull). Clinical assessment of the pelvis and diagnosis
Procedure of contracted pelvis or abnormal pelvic config-
uration is possible, to some extent, with clinical
The bladder and bowel should be empty for
pelvimetry. An assessment of CPD resulting from
proper assessment of the pelvis. An enema is not
pelvic abnormalities or the size of the fetal head
necessary but a mild laxative may be adminis-
is difficult. Disproportion is best diagnosed in
tered the previous night. The mother should be
labor by poor progress or failure to progress.
asked to void before the procedure. Pelvic exam-
The head fitting test and the Munro-Kerr–
ination is performed under aseptic precautions,
Muller test have been described and used in the
with the mother in dorsal position. The index
past, but the sensitivity and predictive value of
and middle fingers of the right hand are intro-
these tests are low, they are not reproducible,
duced into the vagina and the pelvis assessed
and they are difficult to perform in a woman who
systematically as described in Box 40.7.
is not in labor. Moreover, they assess dispropor-
The diagonal conjugate is measured as
tion only at the inlet. These tests are, therefore,
described in Chapter 2, Anatomy of the bony pel-
not used in modern obstetric practice.
vis and fetal skull. The sacral promontory is not
easily reached (‘tipped’) in the normal gynecoid *GCFſVVKPIVGUV
pelvis. Hence, the diagonal conjugate cannot be
measured. The AP diameter of the inlet (the true The woman is placed in the semirecumbent
conjugate or obstetric conjugate) is estimated by position with a 45 degree tilt. The legs are
subtracting 1.5–2 cm from the diagonal conjugate semiflexed at the thigh and knee. Standing on
since this cannot be measured directly. The pos- the woman’s right, the obstetrician grasps the
terior sagittal diameter can be measured directly fetal head with the fingers of the left hand and
as the distance from the tip of coccyx to the mid- pushes it downward and backward into the pelvis
point of the line joining the two ischial tuberosi- (Fig. 40.1). The right hand is placed on the lower
ties. This diameter, if adequate, can compensate abdomen, flush with the pubic bone. If the fetal
head is felt to enter the pelvis, there is no CPD; if
the head comes flush with or overrides the pubic
bone, CPD is diagnosed.
Box 40.7 Clinical pelvimetry ormal gynecoid
pelvis
Assessment of inlet
• Diagonal conjugate: 12.5 cm
• Sacral promontory: Not easily tipped
Assessment of midcavity
• Sacral curvature
Ŧ Above downward: Well curved
Ŧ Side to side: Well curved
• 5CETQUEKCVKEPQVEJ#FOKVUſPIGTU
• Pelvic side walls: Parallel
• Ischial spines: Not prominent
• Interischial spinous diameter: >10 cm
• Forepelvis: Rounded
Assessment of the outlet
• Subpubic arch: Rounded
Figure 40.1 *GCFſVVKPIVGUV9QOCPKUKPUGOKTGEWODGPV
• Subpubic angle: Admits 2ſPIGTU
0)
position. The fetal head is pushed down into the pelvis
• Interischial tuberous diameter: Admits 4 knuckles
YKVJNGHVJCPFCPFVJGTKIJVJCPFKUMGRVƀWUJYKVJVJG
• Posterior sagittal diameter: >7.5 cm
pubic symphysis.
CH 40_p582_598_v3.indd 587 18-07-2015 13:24:40

unro- err uller test -ray pelvimetry

The Munro-Kerr–Muller test is an abdominovag- X-Ray pelvimetry was used to measure the pel-
inal examination (Fig. 40.2). The steps of the vic diameters and evaluate the type of pelvis in
examination are as follows: the past, but it has not been found to be more
useful than clinical pelvimetry. Anteroposterior,
• The bladder and rectum should be empty.
superior, lateral, and inferior views were used to
• The woman is placed in the dorsal position.
assess the shape of inlet and outlet and measure
• Aseptic precautions to be followed.
AP and transverse diameters at inlet, cavity, and
• The index and middle fingers of the gloved
outlet. However, X-ray pelvimetry is not useful
right hand are introduced into the vagina
for diagnosis or prediction of CPD. It may be
and clinical pelvimetry, if not already done, is
used in women with a history of pelvic fractures
performed.
to assess the extent of deformity.
• The fingers are placed at the level of ischial
spines. Computerised tomographic pelvimetry
• The left hand is placed on the mother’s Computed tomographic (CT) pelvimetry is asso-
abdomen. ciated with far less radiation to the fetus and is
• The fetal head is pushed into the pelvis (down- easier to perform. The ability to predict CPD is
ward and backward) with the left hand. similar to that of X-ray pelvimetry.
• If the leading part of the vertex can be pushed
down to the level of ischial spines (touches the Magnetic resonance imaging
fingers of the right hand), CPD is ruled out. There is no risk of radiation exposure with mag-
• If the vertex does not come down to the level of netic resonance imaging (MRI) and the measure-
ischial spines, the right thumb is placed on the ments are more accurate. However, prediction of
pubic symphysis: dystocia and CPD is not superior to that in other
– Fetal head is flush with the symphysis— methods.
minor degree of disproportion. Pelvimetry by imaging techniques is listed in
– Fetal head overrides the symphysis—major Box 40.8.
degree of disproportion.
anagement o labor in omen
ith C D
In the past, when the clinical diagnosis of CPD
was considered reliable, all women with a major
Box 40.8 Pelvimetry by imaging techniques

• X-ray pelvimetry
Ŧ Risk of radiation to fetus
Ŧ Can measure AP and transverse diameters
Ŧ Can evaluate pelvic shapes
Ŧ Not a good predictor of CPD
• CT pelvimetry
Ŧ Less radiation risk to fetus
Ŧ Easier to perform
Ŧ More accurate measurement of pelvic diameters
Ŧ Not a good predictor of CPD
• MRI pelvimetry
Ŧ No risk of radiation to fetus
Figure 40.2 Munro-Kerr–Muller test. Index and middle Ŧ Accurate measurement of pelvic diameters
ſPIGTUQHVJGTKIJVJCPFCTGKPVTQFWEGFKPVQVJGXCIKPC Ŧ Not a good predictor of CPD/dystocia
and placed at the level of ischial spines; thumb is placed Ŧ Expensive
ƀWUJYKVJVJGRWDKEU[ORJ[UKU*GCFKURWUJGFFQYPKPVQ AP, anteroposterior; CPD, cephalopelvic disproportion; C com-
the pelvis with the left hand. puted tomography , magnetic resonance imaging.
CH 40_p582_598_v3.indd 588 18-07-2015 13:24:40

degree of disproportion were delivered by cesar-

Box 40.9 Causes of nondilatation of the cervix
ean section. Those with minor degree of CPD
were subjected to ‘trial of labor.’ Good uterine • Poor uterine contractions
contractions were ensured and oxytocin admin- • Cervix not well applied to presenting part
Ŧ Malpresentations
istered, if required. With the ‘give’ of the pelvis
Ŧ Malposition
and adequate uterine contractions, deflexion
• Previous surgery
and malposition were corrected and vaginal Ŧ Conization
delivery achieved. Cesarean section was under- Ŧ Fothergill’s operation
taken when there was no progress in labor. Ŧ Amputation
In current obstetrics, no special test is done to • Lack of preparatory changes in cervix
diagnose or predict CPD prior to onset of labor.
A short primigravida or a macrosomic fetus
may alert the obstetrician about the possibil-
the fetus. Uterine anomalies such as septate or
ity of CPD in labor. Women with obvious pelvic
bicornuate uterus may be associated with poor
abnormalities following trauma or spinal or limb
uterine contractions and lead to dysfunctional
deformities are delivered by cesarean section.
labor.
All other women are managed as described in
Chapter 15, Management of normal labor and
delivery. If labor does not progress normally, a Myoma and ovarian mass
decision regarding augmentation with oxytocin,
A myoma in the lower uterine segment, below
instrumental vaginal delivery, or cesarean sec-
the presenting part or an ovarian mass that lies
tion is taken as described later in this chapter.
in the pouch of Douglas or below the level of the
fetal head, can also cause obstruction to the pas-
Abnormalities of soft tissues sage of the fetus.
Dystocia due to abnormalities of soft tissues is
uncommon. Most often, nondilatation of the
cervix is due to CPD or poor uterine contractions.
Abnormalities in
oncompliant cervix (cervical passenger
dystocia) Labor abnormalities due to fetal malposition,
Good uterine contractions and pressure by the deflexion, malpresentations, and fetal size are
bag of membranes and/or presenting part are common. These can be overcome to some extent
important for cervical dilatation. In the absence by good uterine contractions and a roomy pelvis.
of these, the cervix may not dilate. The cervix However, fetuses in abnormal presentations are
undergoes changes in preparation for dilatation commonly delivered by cesarean section.
during labor (see Chapter 6, Physiology of labor). Abnormalities of the passenger are dealt with
Failure of these changes to occur can result in in Chapter 41, Abnormal labor: Malpositions and
nondilatation of the cervix despite good uterine malpresentations and Chapter 42, Abnormal
contractions. Scarring of the cervix due to prior labor: Breech presentation and shoulder dystocia.
surgeries such as conization, amputation, or
Fothergill’s surgery can also interfere with cervi-
cal dilatation (Box 40.9).
Malposition
Occipitoposterior position is a common cause
Congenital anomalies in the vagina, of abnormal labor. Prolongation of first and
second stages of labor can occur and opera-
cervix, and uterus tive vaginal delivery or cesarean section rates
Vertical septum in the vagina and cervix and are higher in this position. Spontaneous rota-
vaginal reconstructive surgery with resultant tion to occipitoanterior (OA) position occurs in
scarring can cause obstruction to the passage of majority of women, and a smaller proportion
CH 40_p582_598_v3.indd 589 18-07-2015 13:24:40

rotate posteriorly and deliver as face to pubis. contractions is, therefore, important in the man-
Persistent occipitoposterior or arrest in the agement of labor.
transverse diameter occurs in 5% of women (see
Chapter 41, Abnormal labor: Malpositions and
malpresentations).
Deflexion is another important cause of
&GſPKVKQPUCPFVGTOKPQNQI[
abnormal labor. Head is deflexed in occipitopos- Standardization of terminology regarding uter-
terior position and the engaging diameter is ine activity is essential for proper documenta-
occipitofrontal, which is larger than suboccipi- tion and communication. The terminology used
tobregmatic diameter. With further extension of and their definitions are given in Box 40.10.
the head, brow or face may present (see Chapter Strength of uterine contractions is expressed
41, Abnormal labor: Malpositions and malpre- in Montevideo units (MVU). Montevideo units
sentations). With good uterine contractions, in are calculated by the average strength of con-
a proportion of women, the head flexes, bring- traction (increase in uterine pressure above
ing the smaller diameter to engage. This pro- baseline) in mm Hg × number of contractions in
cess takes longer and leads to prolonged labor. 10 minutes.
When flexion does not occur, cesarean section is In normal labor, frequency of contractions,
required. duration, and intensity increase progressively
Other malpresentations such as breech during labor.
and transverse lie are discussed in Chapter 41, During the active phase, the variables are as
Abnormal labor: Malpositions and malpresen- follows:
tations and Chapter 42, Abnormal labor: Breech
presentation and shoulder dystocia. • Basal tone: 10–12 mm Hg
• Intensity: 40–50 mm Hg
• Frequency: 3–5/10 min
• Duration: 60–90 seconds
Abnormalities in powers
Uterine action is the main force responsible for
cervical effacement, dilatation, and flexion of Box 40.10 &
GſPKVKQPUCPFVGTOKPQNQI[WUGF
for uterine activity
the fetal head, descent, and rotation in the first
and second stages of labor. Maternal voluntary • Frequency
expulsive efforts come into play in the second Ŧ Time in minutes
stage. Ŧ From beginning of one contraction to the beginning
of next contraction
Ŧ Evaluated over 10 minutes
Ŧ 0QTOCNKHŭEQPVTCEVKQPUOKP
• Duration
ormal uterine contractions Ŧ Time in seconds
Normal uterine contractions begin at the cornu Ŧ From the beginning of one contraction to the end
of contraction
and move down in waves through the upper and
• Relaxation time
lower segment of uterus. There is fundal domi-
Ŧ Time in seconds or minutes
nance or a gradient of activity which is more at Ŧ From end of one contraction to the beginning of
the fundus and less in the lower segment. During next contraction
uterine contractions, the blood flow to the inter- • Baseline tone
villous space diminishes. The temporary hypox- Ŧ Intrauterine pressure during relaxation, in mm Hg
emia is well tolerated by normal healthy fetuses. Ŧ 'ZRTGUUGFCUUQHVQTſTOQPRCNRCVKQP
However, if the interruption to the blood flow • Intensity/strength
is prolonged as in excessive or prolonged uter- Ŧ Intrauterine pressure during peak contraction, in
mm Hg
ine contractions, it can result in fetal hypoxia,
Ŧ Also expressed in Montevideo units
acidosis, and asphyxia. The fetal heart rate pat-
Ŧ Expressed as mild, moderate, or severe on palpation
terns become abnormal. Assessment of uterine
CH 40_p582_598_v3.indd 590 18-07-2015 13:24:41

Assessment of uterine
activity
Uterine activity is assessed by the following
methods:
• Abdominal palpation
• External tocodynamometry
• Intrauterine pressure catheters (IUPC)
Abdominal palpation
Uterine contractions can be palpated by hands
placed on the maternal abdomen, over the uter-
ine fundus. The hands should be placed on the
abdomen for a duration of three to four contrac-
Figure 40.3 External tocodynamometer. The
tions. Estimation of duration of contraction may
tocodynamometer is placed on the abdomen at the level
be inaccurate since the beginning and end of
of the uterine fundus. The contraction is seen on the
contraction are difficult to palpate. Contractions
monitor and recorded on the trace.
are palpable only after they reach 10 mm Hg.
Assessment of the intensity of contractions is
also arbitrary. If the contraction is of adequate
intensity, the uterus cannot be indented by the
examining fingers.
External tocodynamometry
The tocodynamometer is placed on the abdom-
inal wall at the level of the uterine fundus.
When the uterine muscle contracts, it raises the
abdominal wall, causing pressure on the trans-
ducer. An electronic signal is sent to the fetal
monitor and a uterine contraction wave form
is displayed. The beginning of the contraction,
its frequency, and its end can be made out
Figure 40.4 Intrauterine pressure catheter. The catheter
with the help of external tocodynamometry
is introduced into the uterine cavity and connected to a
(Fig. 40.3). The assessment of frequency and pressure sensor.
interval between contractions is more accurate
than abdominal palpation. However, the precise
strength of the contractions cannot be made out after contraction recorded. Recording of intra-
from the wave form. The measurement of inten- uterine pressure is accurate with IUPC and a
sity varies depending on the tightness of the quantitative assessment is possible. However, it
elastic belt holding the transducer in place and is not recommended as a routine practice in the
the thickness of the abdominal wall. management of labor since it does not improve
outcome. An IUPC is currently used only in some
specific circumstances as given below:
Intrauterine pressure catheters
• Obese women in whom palpation is difficult
A fluid-filled or transducer-tipped catheter is
• To titrate dose of oxytocin during augmentation
placed inside the uterine cavity after amniotomy
• Research purposes
and is connected to a pressure sensor. The pres-
sure is recorded in mm Hg (Fig. 40.4). The basal Techniques to assess uterine activity are sum-
tone should be noted and pressure during and marized in Box 40.11.
CH 40_p582_598_v3.indd 591 18-07-2015 13:24:41

Box 40.11 Assessment of uterine activity

• Abdominal palpation
Ŧ Most commonly used
Ŧ Hands placed on uterine fundus
Ŧ 3–4 contractions palpated
Ŧ Cannot accurately delineate beginning/end of con-
traction
Ŧ Cannot accurately assess intensity
• External tocodynamometer
Ŧ Used with external fetal monitoring
Ŧ Placed at uterine fundus
Ŧ More accurate assessment of frequency and du-
ration Figure 40.5 Hypotonic uterine action. Tracing from the
Ŧ Assessment of intensity can be inaccurate external tocodynamometer shows uterine contractions
• Intrauterine pressure catheter which are infrequent and of short duration and low
Ŧ Possible only after amniotomy intensity.
Ŧ Assessment of intensity accurate
Ŧ Basal tone can be assessed
Ŧ Can be associated with complications Box 40.12 ypotonic uterine dysfunction
Abruption, perforation, and infection
• Characteristics
Ŧ Not recommended as a routine practice
Ŧ Frequency <3 in 10 minutes
Ŧ Intensity <25 mm Hg
Ŧ Duration <40 seconds
Ŧ Low or absent basal tone
Abnormal uterine action Ŧ Normal gradient of contraction
Abnormal uterine action is classified as • Causes
Ŧ Cephalopelvic disproportion
• Hypotonic dysfunction Ŧ Nulligravida
• Hypertonic dysfunction Ŧ Chorioamnionitis
– Tachysystole Ŧ Overdistension of uterus
– Incoordinate uterine action Multifetal pregnancy
– Precipitate labor Polyhydramnios
Ŧ Epidural analgesia
• Management
ypotonic dysfunction Ŧ Rule out cephalopelvic disproportion/malposition
Hypotonic dysfunction is the most common Ŧ If no cephalopelvic disproportion
abnormality of uterine action encountered in Amniotomy
Augmentation with oxytocin
labor. The uterine contractions are infrequent
and of short duration and low intensity, and do
not result in cervical dilatation (Fig. 40.5). The
there is no disproportion and the woman is in
basal tone is low or absent but the gradient of
active phase of labor, it is prudent to wait for
contraction is normal. The contractions are not
4 hours. If reassessment after 4 hours reveals
very painful.
no progress or poor progress, amniotomy and
The most common cause of hypotonic
augmentation of labor with oxytocin are rec-
uterine dysfunction is CPD. This should be
ommended. Low- or high-dose regimens of
excluded in all women with inadequate uterine
oxytocin may be used as described in Chapter
contractions.
16, Induction of labor. High-dose regimens are
Causes and characteristics of hypotonic uter-
associated with lower cesarean section rates,
ine dysfunction are listed in Box 40.12.
reduction in the duration of labor, and higher
rate of vaginal delivery. However, frequency of
anagement tachysystole is higher.
Cephalopelvic disproportion and malposition Chorioamnionitis can interfere with cer-
should be ruled out by a pelvic examination. If vical dilatation in spite of adequate uterine
CH 40_p582_598_v3.indd 592 18-07-2015 13:24:41

contractions with oxytocin. Cesarean section

Box 40.13 Clinical features and management
may be required in this situation. of tachysystole
Clinical features
ypertonic dysfunction • >5 contractions/10 min
The most common hypertonic dysfunction is • Decrease in fetal oxygenation
tachysystole and is caused by injudicious use of • Fetal heart rate abnormalities
• Usually due to oxytocin/misoprostol
oxytocin. Fetal hypoxia is more common with
• 20% occur in spontaneous labor
hypertonic dysfunction.
/CPCIGOGPV
achysystole • Change maternal position
Tachysystole is defined as >5 contractions in 10 • Stop oxytocin
• Remove vaginal misoprostol
minutes (Fig. 40.6). The term hyperstimulation
• IV bolus Ringer lactate 500 mL
is not currently used. Fetal oxygenation suffers
• Inj. terbutaline 0.25 mg SC
and fetal heart rate abnormalities and decelera-
tions occur. The most common cause is oxyto- SC subcutaneous.
cin infusion, in high doses. Misoprostol can also
cause tachysystole, if used in high doses (50 μg). Incoor inate uterine action
Approximately 20% of tachysystoles occur in
spontaneous labor. Incoordinate uterine action is a hypertonic
dysfunction in which basal tone is elevated and
Management the gradient of uterine contraction is distorted.
Oxytocin infusion should be stopped. Vaginal The frequency, duration, and intensity of con-
misoprostol should be removed. Changing mater- tractions are incoordinate (Fig. 40.7). The cervix
nal position and administration of a bolus of intra- does not dilate though the woman experiences
venous Ringer lactate 500 mL are also effective. Inj. painful contractions.
terbutaline 0.25 mg administered subcutaneously
relaxes the uterus. If fetal heart abnormalities per- anagement
sist, cesarean section may be required. Maternal sedation with 100 mg of intramuscu-
Clinical features and management of tachysy- lar morphine 8 mg pethidine reduces the uter-
stole are summarized in Box 40.13. ine contractions and basal tone. After a period
of rest, the uterus may start contracting nor-
mally and can be augmented with oxytocin.
Amniotomy should be performed to exclude
meconium staining of amniotic fluid.
Clinical features and management of incoor-
dinate uterine action are given in Box 40.14.
Figure 40.6 Tachysystole. Tracing shows >5 contractions Figure 40.7 Incoordinate uterine action. The frequency,
in 10 minutes, characteristic of tachysystole. duration, and intensity of contractions are incoordinate.
CH 40_p582_598_v3.indd 593 18-07-2015 13:24:42

Box 40.14 Clinical features and management Abnormal labor patterns

of coordinate uterine action
Labor does not progress normally in all women.
Clinical features
Obstetricians tend to use terms like ‘failure to
• Elevated basal tone
• Distorted gradient of contractions
progress,’ ‘abnormal labor,’ or ‘dystocia’ in these
• No cervical dilatation situations. In fact many cesarean sections are
• Contractions painful done for these indications. However, these terms
/CPCIGOGPV
are inexact and unclear. A labor pattern that does
• Maternal sedation not follow the usual pattern of a normal labor are
• Wait for 4–6 hours best described as protraction disorders, where
• Amniotomy labor progresses slowly, or arrest disorders, where
• Oxytocin if required labor comes to a stop. Abnormal labor patterns are
classified as shown in Table 40.2.
recipitate labor
Precipitate labor is defined as an extremely short
&KUQTFGTUQHVJGſTUVUVCIG
labor where the total duration of labor is <3 Several factors contribute to abnormal labor pat-
hours. This can occur due to low resistance of the terns in the first stage. It is important to under-
soft tissues of the pelvis, hypertonic uterine con- stand that usually a combination of factors are
tractions, or lack of pain sensation in the mother. present and one factor can lead to the other.
Precipitate labor may recur in subsequent Management depends on a full understanding of
pregnancies; therefore, it is important to antic- the cause(s) in a given patient and the benefits and
ipate and be prepared for it. risks of various interventions must be balanced.
Complications
Vigorous uterine contractions can lead to lac-
Prolonged latent phase
erations of the cervix, vagina, and perineum. Prolonged latent phase is defined as that which
Placental abruption and meconium passage are exceeds 20 hours in a nullipara and 14 hours in
also associated with precipitate labor. a multipara, which is more than the 95th cen-
Fetal oxygenation is impaired during tumul- tile. Latent phase begins with onset of regular
tuous uterine contractions, leading to asphyxia uterine contractions. However, the onset and
and low Apgar scores. Brachial plexus injuries end of latent phase cannot be established with
and injuries due to unexpected fall on the floor accuracy. It is also difficult to differentiate latent
can also occur. phase of labor from false labor pains.
Table 40.2 Abnormal labor patterns
Abnormal pattern ullipara Multipara

&KUQTFGTUQHſTUVUVCIG
Prolongation disorder
Prolonged latent phase >20 hours >14 hours
Protraction disorders
Protracted active phase <1.2 cm/hour <1.5 cm/hour
Protracted descent <1 cm/hour <2 cm/hour
Arrest disorders
Prolonged deceleration phase >3 hours >1 hour
Arrest of dilatation >2 hours >2 hours
Arrest of descent >1 hour >1 hour
Disor ers o the secon stage
Protracted descent <1 cm/hour <2 cm/hour
Arrest of descent >2 hours >1 hour
CH 40_p582_598_v3.indd 594 18-07-2015 13:24:42

Management
on
t cti
Expectant management is recommended. ler
Sedation with intramuscular injection of 8–10 Cer i cm

mg of morphine or 100 mg pethidine alleviates Plot
escent
pain. False labor pains normally reduce and dis- of hea
Plot
appear after 6–8 hours. In 85% of women, regu-
lar contractions begin and active labor sets in.
If mild contractions persist, augmentation with
oxytocin is recommended. Increased risk of ime Hours
cesarean section, low Apgar scores, and meco-
nium passage can occur in this group of women. Figure 40.8 Protracted active phase. Partograph shows
cervical dilatation of 2 cm in 4 hours.
Protraction disorders
In protraction disorders, dilatation and descent t cti
o
ler
occur but at a much slower pace.
Cer ix cm
Plot
Protracted active phase esce t

o hea
Plot
The normal rate of cervical dilatation in the
active phase is 1.2 cm/hour for nulliparas and 1.5
cm/hour for multiparas according to Friedman
(see Chapter 15, Management of normal labor ime ours
and delivery). A rate of dilatation that is less

Figure 40.9 Protracted descent. Partograph shows
than the minimum rate of cervical dilatation is
descent of fetal head by 1 cm in 4 hours.
called protracted active phase (Fig. 40.8).
Protracted descent Arrest disorders

Protracted descent of fetal head is descent at a Arrest of dilatation is diagnosed when the cer-
rate less than 1 cm/hour in nulliparas and 2 cm/ vix ceases to dilate in the active phase of labor,
hour in multiparas (Fig. 40.9). after rupture of membranes, despite adequate
Causes of protracted active phase and pro- uterine contractions (>200 MVU) for >2 hours.
tracted descent are hypotonic uterine dys- The American College of Obstetricians and
function, malposition of the presenting part Gynecologists defines it as no cervical dilatation
especially OP and CPD, maternal obesity, and after 6 cm for >4 hours (Fig. 40.10). Similarly,
epidural analgesia. when descent of the fetal head does not occur
for >1 hour despite good uterine contractions,
Management arrest of descent is diagnosed (Fig. 40.11).
Abdominal and pelvic examination should be

performed to assess uterine contractions, descent
of the presenting part, its position, and flexion/ ler
t cti
o
deflexion. Abnormalities of the bony pelvis must

Cer ix cm
be excluded. Maternal hydration must be main- Plot
tained by infusion of Ringer lactate solution. esce t

o hea
If uterine contractions are inadequate, aug- Plot
mentation with oxytocin usually promotes flexion

and rotation of the fetal head. Amniotomy, before
oxytocin, shortens the duration of labor by 1–2
ime ours
hours and helps to detect meconium. With good
uterine contractions and ‘give’of the pelvis, labor Figure 40.10 Arrest of dilatation. Cervical dilatation has
progresses normally. arrested at 6 cm for 6 hours.
CH 40_p582_598_v3.indd 595 18-07-2015 13:24:43

of the descent of the fetus takes place in the second

t cti
on stage. The normal duration of the second stage
ler
in nulliparas is 2 hours if no regional anesthesia
Cer i cm
Plot
is used and 3 hours with regional anesthesia. In
escent multiparas, it is 1 hour and 2 hours, respectively
of hea
Plot (Fig. 40.12).
Disorders of second stage may be due to the
following:
ime Hours • Protracted descent: <1 cm/hour in nullipara;

<2 cm/hour in multipara
Figure 40.11 Arrest of descent. The descent of the fetal • Arrest of descent: No progress in descent >2
head is arrested at the same station for 4 hours.
hours in nullipara; >1 hour in multipara
Disorders of the second stage are usually due

Arrest of dilatation and descent are usu- to large size of the baby, malposition, or CPD.
ally due to a large baby, malposition, and CPD. As in arrest disorders in active phase, hypotonic
Hypotonic uterine dysfunction may be the result uterine dysfunction may be secondary. Poor
of obstruction; therefore, caution should be
exercised before augmenting labor.
Management
o
ler
t cti
Abdominal and vaginal examination to exclude
malposition, large fetus, and CPD are manda- Cer ix cm
Plot
tory. Augmentation with oxytocin achieves vag- esce t
inal delivery in the absence of these factors. o hea
Plot
Disorders of the first stage, their causes, and
management are summarized in Table 40.3.
Disorders of second stage ime ours
Figure 40.12 Arrest of descent in second stage. After full

The second stage starts with full dilatation of the dilatation of the cervix, the descent of the fetal head has
cervix and ends with the delivery of the fetus. Most not progressed for 2 hours.
Table 40.3 %
CWUGUCPFOCPCIGOGPVQHFKUQTFGTUQHſTUVUVCIGQHNCDQT
Disorder Causes Management

Prolonged latent phase • Delayed cervical ripening • Sedation
• Asynchrony of contractions and • Amniotomy
cervical changes
• Oxytocin augmentation
Protracted active phase and • Hypotonic uterine dysfunction • Exclude CPD
protracted descent
• Large baby • Amniotomy
• Malposition, CPD • Oxytocin augmentation
• Obesity
• Epidural analgesia
Arrest of dilatation and descent • Large baby, malposition • Exclude CPD
• CPD • Oxytocin augmentation
• Hypotonic uterine dysfunction
CPD, cephalopelvicdisproportion.
CH 40_p582_598_v3.indd 596 18-07-2015 13:24:43

maternal expulsive force is also a contributing

Box 40.15 Disorders of second stage of labor
factor.
• &GſPKVKQP
Ŧ Protracted descent
Complications <1 cm/hour in nullipara
Prolongation of the second stage is associated <2 cm/hour in multipara
with maternal and perinatal morbidity. Risk of low Ŧ Arrest of descent
5-minute Apgar scores, asphyxia, and admission No descent after full dilatation of cervix
to the neonatal intensive care unit is increased. >2 hours in nullipara
>1 hour in multipara
Chorioamnionitis, instrumental delivery, cesar-
• Causes
ean section, postpartum hemorrhage, perineal
Ŧ Large baby
trauma, and pelvic relaxation leading to prolapse Ŧ Malposition
are the maternal complications. Ŧ CPD
Ŧ Hypotonic uterine dysfunction
Management Ŧ Poor maternal expulsive efforts
• Complications—fetal
Excluding disproportion and malposition is, there- Ŧ Low 5-minute Apgar scores
fore, the most important first step in the man- Ŧ Asphyxia
agement. Treatment should be individualized. Ŧ Admission to neonatal ICU
Fetal heart rate should be closely monitored and • Complications—maternal
delivery expedited if there is abnormality. If CPD Ŧ Chorioamnionitis
is excluded with reasonable certainty, in a nulli- Ŧ Instrumental delivery
para, judicious use of oxytocin and encouraging Ŧ Cesarean section
maternal expulsive efforts may achieve vaginal Ŧ Postpartum hemorrhage
Ŧ Perineal trauma
delivery. In a multipara, one needs to be careful
Ŧ Pelvic relaxation
about oxytocin augmentation, especially in case
• Management
of undiagnosed CPD, due to the increased risk of Ŧ Exclude CPD, malposition
uterine rupture. Instrumental delivery should be Ŧ Augment with oxytocin if no CPD
considered if the head is below the level of ischial Ŧ Encourage maternal expulsive powers
spines. Cesarean section may be required if there Ŧ Monitor fetal heart rate
is evidence of CPD or no response to oxytocin. Ŧ Instrumental delivery
Disorders of second stage and their management Ŧ Cesarean section
are summarized in Box 40.15. CPD, cephalopelvic disproportion.
Key points
• Labor is said to be abnormal if it is prolonged or does not • Contracted pelvis is diagnosed by history, physical
RTQITGUU#DPQTOCNKV[ECPQEEWTKPſTUVQTUGEQPFUVCIG examination, and clinical pelvimetry. X-ray, CT, and
MRI pelvimetry are not used routinely.
• Causes of abnormal labor may be in the passage,
passenger, or powers. • /CNRQUKVKQPCPFFGƀGZKQPQHVJGJGCFCPFOCNRTGUGP-
tations are important causes of abnormal labor.
• Cephalopelvic disproportion results from contracted
RGNXKUCDPQTOCNRGNXKEEQPſIWTCVKQPNCTIGHGVWUQT • Normal uterine action is essential for normal labor.
fetal malposition. 6GTOKPQNQI[WUGFKPFGſPKPIPQTOCNCPFCDPQTOCN
uterine contractions are frequency, duration, intensity,
• The pelvis is said to be contracted if one or more relaxation time, and baseline tone.
diameters of the pelvis at one or more planes is less
than normal. • Uterine contractions are assessed by palpation and
external tocodynamometry. Intrauterine pressure cath-
• Midpelvic contraction is more common than inlet or eter is not recommended in routine practice.
outlet contraction.
• Abnormal uterine action may be hypotonic dysfunc-
• Four types of pelvis have been described—gynecoid, tion or hypertonic dysfunction. Hypotonic dysfunction
android, anthropoid, and platypelloid. Gynecoid pelvis is the most common abnormality and is managed by
is the most favorable. augmentation with oxytocin.
(Continued)
CH 40_p582_598_v3.indd 597 18-07-2015 13:24:43


• #DPQTOCNNCDQTRCVVGTPUECPQEEWTKPſTUVCPF • Disorders of active phase are managed by exclusion
second stage and may be protraction or arrest of CPD and augmentation with oxytocin.
disorders.
• Disorders of second stage are usually due to CPD.
• Disorders of active phase are mostly due to malposi- This has to be excluded before labor is augmented.
tion, large size of the baby, cephalopelvic dispro- Management must be individualized and instrumental
portion (CPD), hypotonic uterine dysfunction, or a delivery or cesarean section may be required when
combination of these. there is no response to oxytocin.
Self-Assessment
1. #FKHſEWNVHQTEGRUFGNKXGT[EQWNFDGFWGVQCNCTIG
Case 1 baby or contracted pelvis. Weight of the baby was
Mrs. BN, 28, primigravida, at 40+3 weeks’ gestation, was 3.8 kg, which could have been the reason for the
admitted to the labor room with pains. On examination, FKHſEWNVFGNKXGT[
she had regular uterine contractions once every 5 minutes, 2. Clinical pelvimetry to exclude contracted pelvis and
NCUVKPIHQTUGEQPFU6JGXGTVGZYCUVJTGGſHVJRCNRCDNG FGVGTOKPGRGNXKEEQPſIWTCVKQP
abdominally, and fetal heart sounds were normal. On pelvic 3. +HVJGRGNXKEEQPſIWTCVKQPCPFFKOGPUKQPUCTGPQTOCN
examination, the cervix was fully effaced and 4-cm dilated. since the estimated fetal weight is 200 g less than the
The vertex was at –2 station. She was expected to deliver previous one, labor may be allowed to progress with
in the next 6 hours. But, on examination after 4 hours, the close monitoring of uterine contractions, descent of
contractions were once every 8–10 minutes, lasting for 30 XGTVGZFKNCVCVKQPQHEGTXKZCPFHGVCNJGCTVTCVG#NNſPF-
UGEQPFU6JGXGTVGZYCUUVKNNVJTGGſHVJRCNRCDNGVJGEGTXKZ ings should be marked on a partograph. If the parto-
was 5-cm dilated, and the vertex was at –2 station. graph is normal and the curve is to the left of alert line,
spontaneous delivery can be awaited. If there is poor
1. Mark this course of labor on a partograph. What is
progress, despite good uterine contractions, assisted
the diagnosis?
vaginal delivery or cesarean section will be required.
2. What is the next step in evaluation?
Sample questions
Case 2
/TU%0CUGEQPFITCXKFCYKVJRTGXKQWUFKHſEWNVHQTEGRU
delivery of a 3.8 kg baby, was admitted to labor room with 1. A primigravida at term is admitted in active labor.
pains. Her contractions were every 3 minutes, lasting for Uterine contractions became gradually less frequent,
ŌUGEQPFUXGTVGZHQWTſHVJRCNRCDNGGUVKOCVGFHGVCN cervical dilatation progressed by only 2 cm in 4 hours,
weight 3.6 kg, cervix 4-cm dilated, and vertex at –3 station. and there was no descent of vertex. How will you
manage her labor?
1. 9JCVKUVJGUKIPKſECPEGQHVJGJKUVQT[!
2. 9JCVCTGVJGFKUQTFGTUQHNCDQTKPſTUVCPFUGEQPF
2. What evaluation will you do?
stage? Discuss their etiolgy, diagnosis and
3. How will you manage her labor?
management.
Answers Short-answer questions

Case 1 1. Incoordinate uterine action
2. Trial labor
1. On the partograph, the curve has crossed the alert
line, and there is poor progress in labor. Uterine con- 3. Precipitate labor
tractions have decreased in frequency and intensity; 4. Secondary arrest of labor
the diagnosis is hypotonic uterine dysfunction. 5. Monitoring uterine activity during labor
2. Abdominal examination to estimate the weight of the 6. Assessment of CPD
baby. Pelvic examination to exclude CPD, OP posi- 7. Causes of mobile head at term
VKQPFGƀGZKQPECRWVOQNFKPICPFOGEQPKWO 8. Munro-Kerr–Muller method of assessment of CPD
3. If there is no clinical evidence of CPD, labor should be 9. Hypotonic uterine dysfunction
augmented with oxytocin. Pelvic examination should be
repeated 4 hours later. Uterine contractions, descent of
the head, and fetal heart rate should be monitored.
CH 40_p582_598_v3.indd 598 18-07-2015 13:24:43

Abnormal Labor:
41 Malpositions and
Malpresentations
%CUGUEGPCTKQ
Mrs. DN, 29, a third gravida with previous normal deliveries, was admitted
to the labor room with pains for 6 hours and ruptured membranes for 2
hours. She had gone to a nursing home for delivery but was told that the
baby was lying across the abdomen and advised to go to a bigger center.
Mrs. DN and her husband were frightened and confused and wanted to
know what was wrong and what had to be done.
Introduction fetus may also present as breech or with the shoul-

der as the leading part. These constitute malposi-
Malpositions and malpresentations are common tions and malpresentations.
causes of abnormal labor. Malpresentations of the
fetus complicate labor in about 5% of pregnancies
and malpositions, especially the occipitoposterior /CNRQUKVKQPU
position, complicates another 20%. Malpositions The fetal presentation is usually vertex and the
and malpresentations are associated with an occiput may be anterior, transverse, or posterior.
increase in maternal and fetal complications, and The vertex in the occipitotransverse positions will
perinatal and maternal morbidity and mortal- usually rotate to the anterior or posterior positions.
ity. Anticipation, early identification, and prompt When the vertex presents with the occiput in
intervention can reduce the rate of complications the right or left posterior quadrant of the pelvis
and improve outcome. (LOP or ROP), it is referred to as malposition.
&GſPKVKQPU /CNRTGUGPVCVKQPU
The presentation of the fetus may be cephalic but Presentations other than vertex are called mal-
the head may be flexed, deflexed, or extended. The presentations. These include face, brow, breech,
CH 41_p599_620_v3.indd 599 18-07-2015 17:56:07

is usually transient and changes to longitudinal or

$QZ /CNRQUKVKQPUCPFOCNRTGUGPVCVKQPU
transverse lie at the onset of labor.
• Malpositions
Ŧ Right and left occipitoposterior
• Malpresentations
7PUVCDNGNKG
Ŧ Presentation other than vertex When the fetal lie and presentation change
Face repeatedly, after 37 weeks’ gestation, it is called
Brow
unstable lie. The lie may be oblique, transverse,
Breech
or longitudinal and presentation may be shoulder,
Shoulder
Compound
breech, or cephalic.
• Abnormal axial lie
Ŧ Transverse lie
Ŧ Oblique lie Etiology
Ŧ Unstable lie
Malpresentations, abnormal lie, and malpositions
have some common etiological factors.
shoulder, and compound presentations. These are
listed in Box 41.1. /CVGTPCNHCEVQTU
Multiparity is associated with a lax abdomi-
#DPQTOCNCZKCNNKG nal wall with loss of muscle tone. This results
Fetal lie is normally longitudinal; however, in failure to brace and maintain the fetal lie
in certain conditions, the fetus may lie in the and presentation. The fetus moves freely and
oblique or transverse axis, referred to as abnor- changes the lie and attitude in polyhydram-
mal axial lie. nios. In placenta previa (Fig. 41.1a), the pla-
centa occupies the lower uterine segment and
prevents the head or breech from entering the
6TCPUXGTUGNKG pelvis, resulting in transverse lie. It can also lead
The fetus is said to be in transverse lie when to breech presentation because the bulky head
the long axis of the fetus is perpendicular to the does not have adequate space in the lower pole
long axis of the uterus. of the uterus. Abnormal pelvic configuration
and cephalopelvic disproportion can prevent
the head or breech from entering the pelvis
1DNKSWGNKG and cause extension of the head or malposi-
When the long axis of the fetus is at an angle to tion. Therefore transverse or oblique lie, face
the long axis of the uterus, the lie is oblique. This or brow presentations, and occipitoposterior
a. b. .
(KIWTG Uterine causes of malpresentations. C Placenta previa reduces the space available in the lower segment for
the bulky head, leading to breech presentation. D Subseptate uterus causes transverse lie. E#ſDTQKFKPVJGNQYGTWVGTKPG
segment reduces the space available for the bulky head and leads to breech presentation.
CH 41_p599_620_v3.indd 600 18-07-2015 17:56:07

Abnormal Labor: Malpositions and Malpresentations 601
positions are common. Uterine malformations

$QZ '
VKQNQI[QHOCNRTGUGPVCVKQPU
such as subseptate uterus are associated with OCNRQUKVKQPUCPFCDPQTOCNNKG
transverse lie (Fig. 41.1b). Tumors in the pelvis
such as fibroids or ovarian tumors (Fig. 41.1c) • Maternal factors
Ŧ Multiparity
also prevent entry of head or breech into the
Ŧ Polyhydramnios
pelvis (Box 41.2).
Ŧ Placenta previa
Ŧ #DPQTOCNRGNXKEEQPſIWTCVKQP
(GVCNHCEVQTU Ŧ Cephalopelvic disproportion
Ŧ Uterine anomalies
Prematurity is the most common cause of Ŧ Tumors in the pelvis
abnormal lie and malpresentation. The amount • Fetal factors
of amniotic fluid is more relative to the size of Ŧ Prematurity
the fetus and the fetus takes up any position or Ŧ Multifetal pregnancy
presentation till 37 weeks. In multifetal preg- Ŧ Macrosomia
nancy, the first or second twin may be in an Ŧ Anomalies
abnormal lie or malpresentation. There may be
associated polyhydramnios which is an addi-
tional factor. Fetal macrosomia causes ceph- (>35 years), increasing fetal weight, and obesity.
alopelvic disproportion. Fetal anomalies such Abnormal pelvic configuration is also known to
as hydrocephalus, anencephaly, fetal hydrops, be associated with occipitoposterior position.
tumors in the fetal neck, and sacrococcygeal When the anteroposterior diameter of pelvic
tumors also cause malpresentations. inlet is equal to or more than the transverse
diameter, as in android and anthropoid pelvis,
occipitoposterior position results. In addition, in
/CNRQUKVKQPU android pelvis, the forepelvis is beaked and nar-
row and the posterior half of the pelvis is room-
ier; therefore, the bulky occiput occupies the
1EEKRKVQRQUVGTKQTRQUKVKQP posterior half of pelvis. High assimilation pelvis,
Occipitoposterior positions occur usually as in which the last lumbar vertebra is included in
a variation of the normal but can also be due the sacrum, has a high angle of inclination at the
to abnormal pelvic configuration. When the inlet and favors the occipitoposterior position.
occiput occupies one of the posterior quad- Causes of occipitoposterior position are listed in
rants of the pelvis, the position is referred to as Box 41.3.
occipitoposterior.
/GEJCPKUOQHNCDQT
Incidence Mechanism of labor may proceed normally and
Approximately 20% of fetuses are in the occip- the fetus may deliver in the occipitoanterior
itoposterior position at the onset of labor. Of
these, 75% rotate during labor and 25% deliver
$QZ 'VKQNQI[QHQEEKRKVQRQUVGTKQTRQUKVKQP
as occipitoposterior. About 75% of occipitopos-
terior deliveries occur in fetuses that were in the • Nulliparity
occipitoanterior position at the onset of labor. • Older age
This is the result of malrotation. Overall, 5% of • Obesity
all deliveries occur as occipitoposterior. • Birth weight of fetus >4 kg
• #PVGTQRQUVGTKQTFKCOGVGTCVKPNGVŮVTCPUXGTUGFKCOGVGT
Ŧ Android pelvis
Etiology Ŧ Anthropoid pelvis
• High angle of inclination
The most common causes of occipitoposte-
Ŧ High assimilation pelvis
rior position are nulliparity, obesity, older age
CH 41_p599_620_v3.indd 601 18-07-2015 17:56:07

The mechanism of labor is similar to occipitoan-

$QZ -
G[RCTCOGVGTUKPQEEKRKVQRQUVGTKQT
RQUKVKQP terior positions with some differences:
• Denominator: The occiput • The most common position is ROP. The sagit-
• #VVKVWFG&GƀGZKQP tal suture occupies the same (right) oblique
• Engaging diameter: Occipitofrontal (11 cm) diameter of the pelvic inlet as in left occip-
• Possible positions: Right occipitoposterior (ROP) itoanterior, since the left oblique diameter is
Left occipitoposterior (LOP) occupied by the sigmoid colon.
• The head is deflexed; hence, the engaging
diameter is occipitofrontal (11 cm) (Fig. 41.3).
position or the mechanism may be abnormal With good uterine contractions and increasing
and cause problems during labor. flexion, this changes to suboccipitobregmatic
Denominator, attitude, engaging diameter, (9.5 cm).
and positions are given in Box 41.4. • Internal rotation of the occiput is through 135
degrees (3/8th of a circle).
0QTOCNOGEJCPKUOQHNCDQT
KPQEEKRKVQRQUVGTKQTRQUKVKQP #DPQTOCNOGEJCPKUOQHNCDQT
There are two occipitoposterior positions, ROP KPQEEKRKVQRQUVGTKQTRQUKVKQP
and LOP, where the occiput is in the right or left
When anterior rotation of the head fails to occur,
posterior quadrant of the pelvis, respectively
labor becomes abnormal. One of the following
(Fig. 41.2). As already mentioned, the majority
can happen (Fig. 41.4):
of fetuses in the occipitoposterior position at the
onset of labor will deliver as occipitoanterior. • Posterior rotation (malrotation)
• Short anterior rotation (transverse arrest)
• Nonrotation (persistent occipitoposterior)
osterior rotation (malrotation)

The vertex rotates posteriorly through 45 degrees
(1/8th of a circle) and the occiput is in the sacral
hollow. The sagittal suture is in the anteroposte-
rior diameter of the pelvis and delivery occurs
a.
b. ccipitofrontal
iameter
(KIWTG Right and left occipitoposterior positions. C
Right occipitoposterior position with the back of the fetus
to the right and posterior and occiput in the right posterior
quadrant of the pelvis. D Left occipitoposterior position (KIWTG Occipitofrontal diameter. In occipitoposterior
with the back of the fetus to the left and posterior and RQUKVKQPUVJGJGCFKUFGƀGZGFCPFVJGQEEKRKVQHTQPVCN
occiput in the left posterior quadrant of the pelvis. diameter enters the pelvis.
CH 41_p599_620_v3.indd 602 18-07-2015 17:56:07

Abnormal Labor: Malpositions and Malpresentations
ight occipitoposterior
Posterior rotation hort anterior rotation onrotation

irect eep trans erse arrest Persistent occipitoposterior
(KIWTG Abnormal mechanisms of labor in occipitoposterior position. The occiput, from right occipitoposterior position,
can undergo posterior rotation, short anterior rotation, or remain as persistent ocipitoposterior by nonrotation.
as occipitoposterior or face to pubis. This usually as occipitoposterior can cause anal sphincter
happens in anthropoid pelvis. injuries and third or fourth degree perineal tears
because the bulky occiput emerges posteriorly
Short anterior rotation and stretches the perineum. The anteroposterior
The vertex rotates anteriorly by 45 degrees (1/8th diameter of the OP fetal vertex that presents in
of a circle). But further anterior rotation does not the pelvic outlet is greater than the anteroposte-
occur due to smaller interischial spinous diam- rior diameter that presents when the fetus is in
eter and converging sidewalls in android pelvis the OA position. The head delivers by extension
and anthropoid pelvis. Moreover, in android pel- and this results in an even greater presenting
vis, the flat sacrum and reduced sacral hollow anteroposterior diameter. This disproportion
do not permit posterior rotation. The labor is increases the risk of vaginal and perineal lacera-
arrested with the sagittal suture in the transverse tions and operative birth.
diameter of the pelvis, resulting in transverse Maternal and fetal complications are listed in
arrest or deep transverse arrest. Box 41.5.
onrotation
The vertex does not rotate but persists in occip- $QZ /
CVGTPCNCPFHGVCNEQORNKECVKQPU
QHQEEKRKVQRQUVGTKQTRQUKVKQP
itoposterior position with the sagittal suture in
the oblique diameter of the pelvis, that is, per- • Maternal complications
sistent occipitoposterior. Posterior rotation and Ŧ Prolonged labor
vaginal delivery may occur in some but opera- Ŧ Prelabor rupture of membranes
tive intervention is required in most. Ŧ Prolapse of the cord
Ŧ Anal sphincter injuries
Ŧ Oxytocin augmentation
/CVGTPCNCPFHGVCN Ŧ Instrumental delivery
Ŧ Cesarean section
EQORNKECVKQPU • Fetal complications
Maternal and fetal complications are due to pro- Ŧ Low 5-minute Apgar score
longed labor and operative interventions. Since Ŧ Meconium aspiration
Ŧ Hypoxic ischemic encephalopathy
the deflexed vertex does not fit well in the lower
Ŧ Birth trauma
segment, prelabor rupture of membranes and,
Ŧ Admission to neonatal intensive care unit
occasionally, cord prolapse may occur. Delivery
CH 41_p599_620_v3.indd 603 18-07-2015 17:56:07

&KCIPQUKU Management
Diagnosis of occipitoposterior position is done • When occipitoposterior position is diagnosed,
by physical examination. assess
– uterine contractions
– descent and flexion of the presenting part
#DFQOKPCNGZCOKPCVKQP – cervical dilatation
There may be a depression between the head – station of the vertex
and the trunk, referred to as suprapubic flat- – pelvic configuration
tening. Since the limbs are anterior, fetal move- – fetal weight
ments are seen more clearly. On umbilical grip, – fetal heart rate
the fetal back is posterior and difficult to palpate. • Administer epidural or parenteral analgesia
On the second pelvic grip, the head is deflexed, since labor is likely to be prolonged
with the occiput and sinciput at the same level. • Maintain hydration
The fetal heart is heard at the flank, on the same • If contractions are inadequate, augment labor
side as the fetal back. with oxytocin
• If prelabor rupture of membranes occurs,
exclude
2GNXKEGZCOKPCVKQP – cord prolapse
– meconium staining of amniotic fluid
The anterior fontanel is felt easily since the head • Maintain partograph
is deflexed. The sagittal suture is in the oblique • If labor progresses normally, deliver vaginally
diameter and the posterior fontanel is in the
posterior quadrant of the pelvis. The position
is ROP if the posterior fontanel is in the right anagement in the case o posterior
posterior quadrant and LOP if the posterior rotation
fontanel is in the left posterior quadrant of the
pelvis. • When the vertex rotates posteriorly, delivery
Diagnostic features of occipitoposterior posi- takes place as face to pubis (Fig. 41.5).
tion are listed in Box 41.6. • The sagittal suture is in the anteroposterior
diameter of the pelvis and the occiput is felt in
the hollow of the sacrum.
• The mother tends to push prematurely due
to pressure on the rectum by the occiput. The
anal opening dilates and appears stretched.
$QZ &
KCIPQUKUQHQEEKRKVQRQUVGTKQT • With further uterine contractions, the sinciput
RQUKVKQP hitches under the pubic symphysis and the fore-
head, vertex, and occiput are born by flexion.
Ŧ Inspection
Suprapubic flattening
Fetal movements clearly seen
Ŧ Palpation
Umbilical grip
- Fetal back posterior
- Limbs anterior
Second pelvic grip
- Sinciput and occiput at same level
Ŧ Auscultation
Fetal heart at the flank
Ŧ Sagittal suture in oblique diameter
Ŧ Anterior fontanel easily felt, in anterior quadrant
(KIWTG Face-to-pubis delivery. When the occiput
Ŧ Posterior fontanel in posterior quadrant
rotates posteriorly, the fetus is delivered as face to pubis.
CH 41_p599_620_v3.indd 604 18-07-2015 17:56:08

• The sinciput, nose, mouth, and chin are then

born by extension.
• Since the bulky occiput is delivered posteriorly,
a liberal episiotomy should be given to prevent
perineal laceration and anal sphincter injury.
• Most cases require assisted delivery with for-
ceps. The application of forceps and direc-
tion of traction are described in Chapter 19,
Operative vaginal delivery.
anagement in the case o short

anterior rotation
• The vertex may rotate anteriorly by 45 degrees
(KIWTG Vacuum extraction in occipitoposterior
with the sagittal suture in the transverse diam-
position. The cup should be applied close to the posterior
eter of the pelvis and the occiput on the left or HQPVCPGNVQRTQOQVGƀGZKQPCPFCRRN[VTCEVKQP
right side.
• Assess uterine contractions, weight of the
baby, flexion and descent of the vertex, and
fetal heart rate. • Epidural analgesia facilitates the procedure
• Perform pelvic examination to but pudendal block may also be used.
– exclude cephalopelvic disproportion • The bladder should be emptied.
– look for signs of obstruction such as caput • The left hand is used for ROP and the right
and molding. hand for LOP position.
• Augment labor with oxytocin if there is (a) • The hand is held with the palm facing upward.
no cephalopelvic disproportion or sign of Four fingers are inserted behind the head into
obstruction,(b) no fetal distress, and (c) uter- the hollow of the sacrum. The posterior ear
ine contractions are inadequate. should be felt.
• Vertex may rotate anteriorly or posteriorly
with good uterine contractions, and normal • Method 1
delivery may occur. – The head is grasped with the fingers over the
• If (a) the vertex descends below +2 station in posterior parietal bone and the thumb on
traverse position, (b) the fetus is of average size, the anterior parietal bone (Fig. 41.7).
(c) there is no fetal distress, (d) the cervix is fully – The head is dislodged slightly and flexed by
dilated, and (e) the pelvic configuration is nor- upward pressure close to the sinciput and
mal, vaginal delivery may be attempted by rotated to bring the occiput anteriorly.
– vacuum extraction • Method 2
– manual rotation and forceps delivery – The rotation may be performed using fin-
– forceps rotation and delivery. gers. The tips of the index and middle fin-
8CEWWOGZVTCEVKQP gers are placed on the lambdoid suture close
to the posterior fontanel (Fig. 41.8).
Vacuum extraction can be used to deliver the – The vertex is rotated by a movement of
fetus. The cup should be applied close to the the forearm and simultaneously
posterior fontanel to promote flexion during applying gentle pressure on the suture with
traction (Fig. 41.6). the finger tips. The vertex flexes, moves
With traction, the head flexes, rotates, and slightly upward, and rotates.
descends. Posterior cups for delivery of occipi- • Once rotation is achieved, delivery is com-
toposterior/transverse are also available. pleted by forceps.
/CPWCNTQVCVKQPCPFHQTEGRUFGNKXGT[
• This procedure requires expertise and should (QTEGRUTQVCVKQPCPFFGNKXGT[
be undertaken only if the head is below +2 Forceps that are designed for rotation such as
station. Kielland’s forceps or Barton’s forceps should
CH 41_p599_620_v3.indd 605 18-07-2015 17:56:08

&GGRVTCPUXGTUGCTTGUV
This usually occurs in women with android or
anthropoid pelvis, where the transverse diame-
ter is less or when there is cephalopelvic dispro-
portion. A diagnosis of deep transverse arrest is
made only when uterine contractions are ade-
quate and the cervix is fully dilated. The dura-
tion of the arrest of descent should be1 hour or
more (Box 41.7).
/CPCIGOGPVQHFGGR
(KIWTG Manual rotation of the fetal head. The hand
VTCPUXGTUGCTTGUV
KUJGNFYKVJVJGRCNOHCEKPIWRYCTFUVJGHQWTſPIGTU Due to obstruction at the level of the ischial
are inserted into the hollow of the sacrum and head is spines, there is usually molding and caput forma-
ITCURGFD[VJGſPIGTUQPVJGRQUVGTKQTRCTKGVCNDQPGCPF tion. Since the pelvic configuration is abnormal
the thumb on the anterior parietal bone. and the arrest of descent occurs above +2 station,
vaginal delivery is usually not attempted. Delivery
is by cesarean section.
+PFKECVKQPUHQTEGUCTGCPUGEVKQP
KPQEEKRKVQRQUVGTKQTRQUKVKQP
These are listed in Box 41.8.
$QZ &GGRVTCPUXGTUGCTTGUV
• Etiology
Ŧ Android pelvis
Ŧ Anthropoid pelvis
(KIWTG Digital rotation of the fetal head. The tips of • Diagnosis
VJGOKFFNGCPFKPFGZſPIGTUCTGRNCEGFQPVJGNCODFQKF Ŧ Cervix fully dilated
suture close to the posterior fontanel and with gentle Ŧ Vertex at the level of ischial spines
pressure the head is rotated. Ŧ Sagittal suture in the transverse diameter of
pelvis
Ŧ Good uterine contractions
Ŧ Arrest of descent for 1 hour
be used. Forceps rotation requires training and • Management
expertise and is not used in modern obstetrics Ŧ Cesarean section
(see Chapter 19, Operative vaginal delivery).
• Cesarean section is indicated if (a) attempts at
vaginal delivery are not successful, (b) there is
$QZ +PFKECVKQPUHQTEGUCTGCPUGEVKQP
fetal distress, (c) vertex is above +2 station, or
(d) the pelvis is inadequate. • Persistent occipitoposterior position
• If the vertex does not rotate or descend below • Deep transverse arrest
the level of the ischial spines, in spite of good • Failed vaginal delivery with vacuum/forceps/manual
rotation
uterine contractions, after full dilatation of the
• Fetal distress
cervix for 1 hour, a diagnosis of deep transverse
• )TQUUN[CDPQTOCNRGNXKEEQPſIWTCVKQP
arrest is made.
CH 41_p599_620_v3.indd 606 18-07-2015 17:56:08

/CNRTGUGPVCVKQPU $QZ 'VKQNQI[QHHCEGRTGUGPVCVKQP

• Primary face presentation
Malpresentations are associated with higher Ŧ Multiparity
maternal and fetal risks; therefore, they should Ŧ Fetal anomalies
be diagnosed early and progress in labor should Anencephaly
be monitored carefully. Meningocele
Dolichocephaly
Tumors in the neck
(CEGRTGUGPVCVKQP - Thyroid enlargement
- Other tumors
Face presentation results when the head is Loops of cord around the neck
hyperextended with the occiput touches the fetal Ŧ Polyhydramnios
back. In face presentation, all parts of the face, Ŧ Prematurity
from the chin to the glabella (the smooth area • Secondary face presentation
between the eyebrows just above the root of the Ŧ #DPQTOCNRGNXKEEQPſIWTCVKQP
nose), present in the pelvis. Ŧ Large baby/contracted pelvis
Incidence
Face presentation occurs in 1/200–1/500 $QZ -
G[RCTCOGVGTUCPFRQUKVKQPU
KPHCEGRTGUGPVCVKQP
deliveries.
• Denominator: The mentum (chin)
• Attitude: Complete extension
• Engaging diameter: Suboccipitomental (9.5 cm)
Etiology • Possible positions: Right mentoanterior (RMA)
Left mentoanterior (LMA)
Face presentation can be primary or secondary. Right mentoposterior (RMP)
Primary face presentation occurs in fetal malfor- Left mentoposterior (LMP)
mations such as anencephaly, meningocele, or
dolichocephaly. Tumors in the anterior aspect of
the neck, spasm of extensor muscles of neck, and
loops of cord around the neck cause extension of %CTFKPCNOQXGOGPVU
the fetal head. Polyhydramnios and prematurity, ngagement
by increasing the space available and allowing
the extended head to descend, can also cause The submentobregmatic diameter engages in
face presentation (Box 41.9). the left or right oblique diameter. The vertical
Secondary face presentation occurs in labor. distance between the face and biparietal diame-
Extension of the head usually results when there ter is 7 cm. This is more than the vertical distance
is abnormal pelvic configuration with a narrow between the pelvic brim and ischial spines.
anteroposterior diameter, as in platypelloid Therefore, when the biparietal diameter crosses
pelvis. The biparietal diameter is caught in the the brim, the face is well below the ischial spines.
anteroposterior diameter of the inlet and acts as Hence, the head is palpable per abdomen even
a fulcrum with the occiput and sinciput on either after the face has descended below the level of
side. With uterine contractions, when the fetal ischial spines.
trunk and occiput are pushed into the pelvis, the
sinciput moves upward, the head extends gradu- Descent
ally, and face presentation results. The fetus descends with good uterine
contractions.
/GEJCPKUOQHNCDQT
The denominator, attitude, engaging diameter, Increasing e tension
and positions are given in Box 41.10. The four As the fetal trunk descends, extension of the
positions are shown in Figure 41.9. head increases.
CH 41_p599_620_v3.indd 607 18-07-2015 17:56:08

a. b.
(KIWTG The four positions in face presentation. C Left mentoanterior and right mentoanterior positions. D Left
mentoposterior and right mentoposterior positions.
Internal rotation $QZ %QORNKECVKQPUQHHCEGRTGUGPVCVKQP

The mentum rotates anteriorly toward the pubic
• Maternal
symphysis through 45 degrees (1/8th of a cir- Ŧ Prelabor rupture of membranes
cle) in mentoanterior positions and through Ŧ Prolapse of the cord
135 degrees (3/8th of a circle) in mentoposterior Ŧ Prolonged labor
positions. The rotation takes place at a lower Ŧ Operative vaginal delivery
level than in vertex presentation. Ŧ Cesarean section
• Fetal
Ŧ Congenital anomalies
le ion Ŧ Fetal heart rate abnormalities
The chin hitches under the pubic symphysis and Ŧ Facial edema
the mouth, nose, glabella, forehead, and occiput Ŧ Laryngeal/tracheal edema
are born, in that order, by flexion. Ŧ Admission to neonatal intensive care unit
estitution Ab ominal e amination

The neck untwists toward the opposite side. The back is anterior in mentoanterior positions
but is felt posteriorly at the flank in mentopos-
ternal rotation terior positions (Box 41.12). The sinciput is at
a higher level than the occiput. The cephalic
External rotation of the head follows restitu- prominence (the most prominent part of the
tion as the shoulders rotate toward the pubic fetal head) is the occiput and is felt on the same
symphysis. side as the fetal back (Fig. 41.10). A groove may
be felt between the occiput and the back.
%QORNKECVKQPU
aginal e amination
Maternal and fetal complications in face presen- On vaginal examination, all structures between
tation are listed in Box 41.11. the chin and glabella—mentum, mouth, nose,
glabella, and malar eminences—are felt. The
mentum occupies one of the four quadrants of
&KCIPQUKU
the pelvis. On vaginal examination, the face may
Diagnosis of face presentation is by physical be mistaken for breech and is differentiated by
examination. the features listed in Table 41.1.
CH 41_p599_620_v3.indd 608 18-07-2015 17:56:08

$QZ &KCIPQUKUQHHCEGRTGUGPVCVKQP 2TQITGUUKPNCDQT

• Abdominal examination The mentum is anterior in >60% of cases of face
Ŧ Umbilical grip presentation, transverse in 10–15% of cases, and
Back anterior in mentoanterior positions posterior in only 20–25% of cases. Labor pro-
Back posterior, at the flank in mentoposterior gresses normally in mentoanterior positions
positions since the engaging diameter is similar to that in
Ŧ Second pelvic grip vertex presentation. It is important to remember
Sinciput at higher level than occiput
that internal rotation of the mentum takes place
Groove felt between occiput and back
at a much lower level than in vertex.
Cephalic prominence on same side as back
Ŧ Auscultation The majority of mentoposterior positions
Fetal heart heard clearly in mentoanterior posi- also rotate anteriorly and deliver normally.
tion However, 25% may remain as mentoposterior
Toward the flank in mentoposterior position or rotate to direct posterior. A persistent men-
• Vaginal examination toposterior position cannot deliver vaginally.
Ŧ Chin, mouth, malar eminences, nose, glabella felt This is because, with uterine contractions, the
Ŧ Mentum in anterior or posterior quadrant fetal chest also enters the pelvis and results in
an impacted mentoposterior position, causing
obstructed labor (Fig. 41.11).
Management
Management of the first stage is the same as
in vertex presentation. Uterine contractions,
descent of the presenting part, fetal heart rate,
Cephalic
cervical dilatation, station, and rotation of men-
prominence tum should be monitored and marked on a par-
tograph. If the mentum rotates anteriorly, the
baby is delivered normally. If there is a delay in
the second stage, forceps can be used, provided
the mentum has rotated anteriorly. However,
vacuum extraction cannot be used.
(KIWTG Cephalic prominence. In face presentation,
the cephalic prominence which is the most prominent part
of the fetal head is the occiput and is felt on the same side
as the back.
6CDNG &KHHGTGPVKCVKPIHCEGHTQODTGGEJ
RTGUGPVCVKQP
Face Breech
Mouth and malar Anus and ischial tuberosi-
eminences not in ties in same line
same line
+HſPIGTKPVTQFWEGF +HſPIGTKPVTQFWEGF
sucking movements gripping by anal sphincter
felt felt
0QOGEQPKWOQPſPIGT Meconium present on
ſPIGT (KIWTG Impacted mentoposterior. If mentoposterior
does not rotate anteriorly, with uterine contractions, the
External genitalia not felt External genitalia felt
chest also enters the pelvis.
CH 41_p599_620_v3.indd 609 18-07-2015 17:56:09

If the position is mentoposterior and rotates fontanel present in the pelvis. Incidence is 1 in
to mentoanterior, normal delivery ensues. If 1500 deliveries.
uterine contractions are not adequate, oxytocin
augmentation may be considered, provided the
baby is of average weight and pelvic configura-
tion is normal. Etiology
Cesarean section is required if
Prematurity, multiparity, and cephalopelvic
• the fetus is large; disproportion are the most common causes of
• the mentum does not rotate anteriorly 1 hour brow presentation. Other conditions that give
after full dilatation; rise to face presentation such as tumors in the
• fetal heart rate abnormalities occur. neck, spasm of the extensor muscles, and poly-
hydramnios can also cause brow presentation.
The incidence of cesarean section is 60% in
face presentation. In mentoposterior position, at
cesarean section, the head should be flexed with %QWTUGKPNCDQT
the hand to facilitate delivery.
Management of face presentation is summa- The denominator, engaging diameter, and posi-
rized in Box 41.13. tions are given in Box 41.14. Frontal bone or ‘fron-
tum’ is the denominator. The four positions are left
and right frontum anterior and frontum posterior.
The engaging diameter is verticomental (13.5
$TQYRTGUGPVCVKQP cm) which is the largest diameter of the fetal
head. Vaginal delivery, therefore, is not possible
Brow presentation is a position of partial exten- unless the fetus is very small or premature or
sion, halfway between complete flexion and the pelvis is very roomy.
complete extension. In brow presentation, all Brow presentation is usually found early in
structures from the orbital ridges to the anterior labor. With good uterine contractions, it usually
flexes to vertex or extends further to face pre-
sentation. If brow presentation persists in estab-
lished labor, there is no mechanism of labor and
$QZ /CPCIGOGPVQHHCEGRTGUGPVCVKQP delivery. If undiagnosed, it can result in uterine
• Estimate weight of baby rupture, especially in multigravida.
• Perform internal pelvimetry
• Monitor
Ŧ Uterine contractions %QORNKECVKQPU
Ŧ Descent of presenting part
Prelabor rupture of membranes and prolapse
Ŧ Fetal heart rate
of the cord can occur. If undiagnosed, uterine
Ŧ Station of presenting part rupture is a known complication. Fetal compli-
Ŧ Rotation cations are related to the associated anomalies,
• Mentoanterior operative delivery, and obstructed labor.
Ŧ If rotation is complete
Normal delivery
Forceps delivery
$QZ -
Ŧ If no rotation
KPDTQYRTGUGPVCVKQP
Cesarean section
• Mentoposterior Denominator: The frontum
Ŧ If rotates anteriorly: Deliver Attitude: Partial extension
Ŧ If no rotation: Cesarean section Engaging diameter: Verticomental (13.5 cm)
• Oxytocin augmentation Left frontoanterior (LFA)
Ŧ Only if Left frontoposterior (LFP)
Positions:
baby weight average Right frontoanterior (RFA)
pelvic configuration normal Right frontoposterior (RFP)
CH 41_p599_620_v3.indd 610 18-07-2015 17:56:09

Abnormal Labor: Malpositions and Malpresentations 611
&KCIPQUKU 6TCPUXGTUGNKG
On abdominal examination, the head feels
When the longitudinal axis of the fetus is per-
broader. The sinciput is higher than the occiput
pendicular to the long axis of the uterus, the
but not as high as in face presentation (Fig. 41.12).
lie is said to be transverse. If the long axis of the
Diagnosis can be made with certainty only on
fetus is at an angle to the long axis of the uterus,
vaginal examination. The anterior fontanel, fore-
it is known as oblique lie. This usually becomes
head, and orbital ridges are felt (Fig. 41.13).
transverse lie or longitudinal lie once uterine
contractions begin. The presenting part is the
Management shoulder in transverse lie.
If brow presentation is diagnosed in early labor,
the mother may be monitored closely and vagi- Incidence
nal examination repeated after 4–6 hours to see
if flexion to vertex or extension to face presen- Transverse lie is seen in 1/300 deliveries at term.
tation has occurred. Oxytocin augmentation is
not recommended. Once the woman is in active Etiology
labor, if brow presentation persists, cesarean
section is indicated. A summary of brow presen- Conditions that prevent the fetal head or breech
tation is given in Box 41.15. from entering the pelvis predispose to transverse
lie. These may be placenta previa, contracted
pelvis, cephalopelvic disproportion, or tumors
in the lower uterine segment such as myomas.
Prematurity, polyhydramnios, multifetal preg-
nancy, uterine anomalies such as subseptate
$QZ $TQYRTGUGPVCVKQP
• Incidence
Ŧ 1/1500 deliveries
nterior • Etiology
fontanel Ŧ Prematurity
Ŧ Multiparity
Ŧ Polyhydramnios
Ŧ Fetal anomalies
Ŧ Tumors in the neck
(KIWTG Brow presentation. On abdominal
Ŧ Spasm of the extensor muscles
examination, the sinciput is higher than occiput.
• Complications
Ŧ Cord prolapse
Ŧ Uterine rupture
Ŧ Fetal anomalies
Ŧ Asphyxia
• Diagnosis
Ŧ Abdominal examination
Fetal head feels large
Sinciput at higher level than occiput
Ŧ Vaginal examination
Orbital ridges, forehead, anterior fontanel felt
• Management
(KIWTG Brow presentation, vaginal examination. Ŧ Early labor: Monitor and wait
The orbital ridges, forehead, and anterior fontanel are felt. Ŧ Late in labor: Cesarean section
CH 41_p599_620_v3.indd 611 18-07-2015 17:56:09

uterus, and multiparity are also etiological fac- • Dorsosuperior

tors (Box 41.16). • Dorsoinferior
Spontaneous resolution to longitudinal lie
%QWTUGKPNCDQT can occur as gestation advances. When the lie
The fetal back may face upward, downward, persists toward term, conversion to vertex or
anteriorly, or posteriorly; therefore, there are breech is less likely.
four positions (Fig. 41.14): There is no mechanism of labor in trans-
The denominator and positions are given in verse lie and vaginal delivery is not possible.
Box 41.17. With uterine contractions, the shoulder enters
In addition, depending on the direction of the pelvis and labor does not progress. When
the fetal back, four positions are described as membranes rupture, the cord or an arm may
follows: prolapse. As the uterus contracts further,
obstructed labor results and a retraction ring
• Dorsoanterior or Bandl’s ring is formed. In nulliparas, con-
• Dorsoposterior tractions may cease and result in hypotonic
dysfunction. In multiparas, however, contrac-
tions continue and the uterus ruptures.
$QZ 'VKQNQI[QHVTCPUXGTUGNKG
• Maternal factors
Ŧ Multiparity
Ŧ Contracted pelvis
$QZ -
KPVTCPUXGTUGNKG
Ŧ Placenta previa
Ŧ Subseptate uterus Denominator: Acromion
Ŧ Polyhydramnios Lie: Transverse
Ŧ Pelvic tumors Possible positions: Left acromioanterior
• Fetal factors Right acromioanterior
Ŧ Prematurity Left acromioposterior
Ŧ Multifetal pregnancy Right acromioposterior
orsoanterior orsoposterior
orsoinferior orsosuperior
(KIWTG The four positions in transverse lie: Dorsoanterior, dorsoposterior, dorsosuperior, and dorsoinferior.
CH 41_p599_620_v3.indd 612 18-07-2015 17:56:09

%QORNKECVKQPU $QZ &KCIPQUKUQHVTCPUXGTUGNKG

Transverse lie is associated with maternal and • Abdominal examination
fetal complications (Box 41.18). Ŧ Inspection: Uterine ovoid is transverse
Ŧ Palpation
Fundal grip: No fetal pole felt
&KCIPQUKU
Umbilical grip
Diagnosis of transverse lie can be made clinically - Fetal back felt in dorsoanterior position
in most cases. - Limbs felt in dorsoposterior position
- Head in one flank, back on the other
Ab ominal e amination Pelvic grip: Lower pole empty
Ŧ Auscultation
On abdominal examination, the uterine ovoid Fetal heart below umbilicus
is transverse. There is no pole palpable on fun- Easily heard in dorsoanterior position
dal grip. On umbilical grip, the fetal back is felt Not easily heard in dorsoposterior position
easily in the dorsoanterior position and the limbs • Vaginal examination
are felt in the dorsoposterior position. The fetal Ŧ Bag of membranes felt
head is felt on one flank and the breech on the Ŧ Presenting part high up
opposite flank. On pelvic grip, the lower pole is Ŧ Shoulder, elbow, arm, ribs, acromion, scapula
empty except late in labor when the shoulder
occupies it. The fetal heart is easily heard below
the umbilicus in the dorsoanterior position and
heard with difficulty in the dorsoposterior posi-
tion (Box 41.19).
aginal e amination
If transverse lie is diagnosed or suspected on
abdominal examination, vaginal examination
should be performed only after ruling out pla-
centa previa by ultrasound scan. On vaginal
examination, a conical bag of membranes is felt
if the cervix is dilated. The shoulder is high up
and felt with difficulty in early labor. After rupture
of membranes, the scapula, acromion, shoulder
or elbow, and ribs can be felt. When membranes
rupture, cord prolapse is common. One arm may
also prolapse into the vagina or outside the introi-
tus. In case of arm prolapse, shaking hands with
(KIWTG Transverse lie with arm and cord prolapse.
the prolapsed hand helps in identifying whether
The left hand and forearm of the fetus and cord are seen
it is the right or left arm (Fig. 41.15).
lying outside the introitus. (Photo courtesy: Dr Rajnish
Samal, Bangalore.)
$QZ %QORNKECVKQPUKPVTCPUXGTUGNKG
Management
• Complications in transverse lie
Ŧ Maternal Management depends on the following:
• Gestational age
Ŧ Cord prolapse
Ŧ Arm prolapse • Presence of placenta previa
Ŧ Obstructed labor • Stage of labor
Ŧ Uterine rupture • Rupture of membranes
Ŧ Cesarean section
• Fetal Vaginal delivery is possible only if the tranverse
Ŧ Asphyxia lie can be converted into longitudinal lie with
Ŧ Fetal death cephalic presentation. This can be attempted only
CH 41_p599_620_v3.indd 613 18-07-2015 17:56:09

if placenta previa is excluded. In most cases, cesar- • If the mother is seen late in labor with or
ean section is the mode of delivery. without arm prolapse, deliver is by cesarean
section.
• If transverse lie is diagnosed in midtrimester or
early third trimester, only follow-up is required. Management of transverse lie is outlined in
• If it is diagnosed at or after 36 weeks’ gestation, Figure 41.16.
ultrasonography is performed to exclude pla-
centa previa and polyhydramnios. Cesarean section in transverse lie
• If there is no placenta previa, external cephalic
Cesarean section in a woman with transverse lie
version is attempted at 37 weeks.
is not a simple procedure.
• If successful, onset of labor is awaited with
weekly review to ensure that fetus has not • The lower segment may be narrow and space
reverted to transverse lie. may be insufficient for delivery of the fetus.
• If unsuccessful, delivery is by cesarean section • With rupture of membranes and reduced
after 38 weeks. amount of amniotic fluid, the uterus may be
• If diagnosed early in labor and the membranes hugging the fetus and delivery may become
are not ruptured, external cephalic version difficult.
is attempted after placenta previa has been • There may be obstructed labor with the forma-
excluded. If external cephalic version is unsuc- tion of Bandl’s ring.
cessful, delivery is by cesarean section. • If fetus is delivered through a traditional
• If diagnosed early in labor after membranes lower segment incision, the lateral ends of
rupture, cord prolapse should be ruled out. the incision can extend to involve the uter-
Delivery is by cesarean section. ine vessels.
rans erse lie
Mi trimester or
t or after ee s n labor n obstructe labor
early thir trimester
ollo up Membranes
ot rupture upture
Ultrasonography Vaginal e amination

Longitu inal lie rans erse lie
e clu e placenta pre ia e clu e cor prolapse
ternal cephalic
ersion
uccessful ot successful
Vaginal eli ery Cesarean section
(KIWTG Management of transverse lie.
CH 41_p599_620_v3.indd 614 18-07-2015 17:56:10

• The incision should be ‘U’ shaped, inverted T • Oxytocin infusion is started with 5 units of
shaped, lower segment vertical, or an upper oxytocin in normal saline (see Chapter 16,
segment classical. Induction of labor).
• Halothane anesthesia may be required to relax • When contractions occur once every 10 min-
the uterus and deliver the fetus in obstructed utes, vaginal examination is performed to
labor. ensure that presentation is cephalic and to
• The fetal head and back must be located before exclude cord presentation.
uterine incision is made. • Artificial rupture of membranes is done, taking
• The fetus should be delivered by traction on care to avoid cord prolapse.
the feet and legs and not on the arm. • When amniotic fluid escapes, the head usually
• Delivery may be difficult in the dorsoanterior enters the pelvis.
and dorsoinferior positions. • Oxytocin infusion is continued and labor man-
• If there is placenta previa, the placenta should aged accordingly.
be cut through or partially separated and
pushed away from the field of incision before %QORQWPFRTGUGPVCVKQP
delivery of the fetus.
When one of the extremities present along with
one of the fetal poles, it is known as compound
7PUVCDNGNKG presentation (Fig. 41.17). A foot or lower limb
When the fetal lie and/or presentation changes presenting with breech is not included in this
repeatedly after 37 weeks’ gestation, it is known definition.
as an unstable lie. Polyhydramnios and placenta
previa are the usual causes. Ultrasonography Incidence
should be performed to exclude these condi- Compound presentation occurs in 1/1000–
tions. As term approaches, the lie may stabilize 1/1200 deliveries. The combination of vertex and
as longitudinal. hand is the most common presentation.
5VCDKNK\KPIKPFWEVKQP Etiology
• If unstable lie persists after 38–39 weeks’ ges- Prematurity is the most common cause since the
tation, stabilizing induction is undertaken. small preterm head allows enough room for a
Woman is admitted to the labor room. limb to descend by the side of the head or breech.
• If the lie is transverse, external cephalic ver- Other causes are maternal age, multiparity, con-
sion is performed. tracted pelvis, and external cephalic version.
a. b.
(KIWTG Compound presentation. C Hand and head. D Hand, foot, and head.
CH 41_p599_620_v3.indd 615 18-07-2015 17:56:10

/GEJCPKUOQHNCDQT Management
The possible combinations are as follows: Labor may be allowed to progress normally
especially if the limb is at the same level or
• Vertex and hand/upper limb
above the level of vertex. If the limb is below
• Vertex and foot
the level of vertex, it may not retract sponta-
• Vertex, hand, and foot
neously. An attempt may be made to gently
• Breech and hand/upper limb
push the limb up, past the presenting part. The
When labor begins, the limb usually moves up fetal heart should be monitored closely, pref-
and normal delivery occurs in most cases. Labor erably using electronic fetal heart rate mon-
may be prolonged but once the limb retracts, itoring. Cesarean section is indicated if (a)
labor progresses normally. If the limb does not repeat vaginal examination reveals persistent
retract, labor may not progress and delivery by compound presentation, (b) cord prolapse
cesarean section is indicated. occurs, (c) progress of labor does not occur, or
(d) there is fetal heart rate abnormality.
%QORNKECVKQPU
Since the presenting part does not fit well in the 7ODKNKECNEQTFRTGUGPVCVKQP
lower uterine segment, cord prolapse is com-
mon. Fetal heart rate abnormalities and asphyxia CPFRTQNCRUG
are also common complications. Maternal and Umbilical cord presentation is one where the
fetal complications are listed in Box 41.20. cord is felt alongside the presenting part or
below it and the membranes have not ruptured.
&KCIPQUKU When membranes rupture and the cord is
Diagnosis of compound presentation is usually felt alongside the presenting part, it is called
made in labor by vaginal examination. The hand occult cord prolapse. When it is felt below the
or the foot may be felt through the membranes presenting part, it is called overtcord prolapse.
or, if the membranes have ruptured, can be felt The cord may prolapse into the vagina or outside
more readily. Presence of cord should always be the introitus (Fig. 41.18).
looked for.
Incidence
$QZ %QORQWPFRTGUGPVCVKQP The incidence of cord prolapse is 0.6% of all
• &GſPKVKQP deliveries.
Ŧ One or other extremities with vertex or breech
Ŧ Vertex with hand/foot or both Etiology
Ŧ Breech with hand
• Incidence When the presenting part does not fit well in the
Ŧ 1 in 1000–1200 lower uterine segment, cord prolapse can occur.
• Etiology
Ŧ Prematurity, multiparity
Ŧ Contracted pelvis, external cephalic version
• Complications
Ŧ Maternal
Prolonged labor
Cesarean section
Ŧ Fetal
Cord prolapse
Fetal heart rate abnormalities
Asphyxia
• Diagnosis a. b.
Ŧ Vaginal examination
(KIWTG Cord presentation and prolapse. C Cord
• Management
prolapse with the membranes not ruptured. Cord is felt
Ŧ In early labor: Wait and watch
alongside the head. D Cord prolapse with the membranes
Ŧ If no progress: Cesarean section
ruptured. The cord lies below the head.
CH 41_p599_620_v3.indd 616 18-07-2015 17:56:10

The conditions include (a) malpresentations and handling of the cord also cause spasm.
such as face, brow, breech, transverse lie, and Spasm leads to hypoxia.
compound presentation, (b) conditions where
the presenting part is small as happens in pre- &KCIPQUKU
maturity and multifetal pregnancy, and (c) con-
ditions where there is excessive amniotic fluid It is not possible to diagnose cord presentation
(polyhydramnios), cephalopelvic disproportion, or prolapse by clinical examination antena-
multiparity, and long umbilical cord (Box 41.21). tally. On ultrasonography, loops of cord may be
Iatrogenic causes are artificial rupture of visible below the presenting part, especially in
membranes, internal podalic version, external malpresentations.
cephalic version, amnioinfusion, and application Cord prolapse should be suspected when
of scalp electrode, manual rotation of fetal head, there is sudden bradycardia or moderate to
and insertion of intrauterine pressure catheter. severe variable decelerations. Diagnosis is by
vaginal examination. Occult cord may be diffi-
%QPUGSWGPEGUQHEQTFRTQNCRUG cult to palpate but must be looked for.
Cord presentation should be anticipated in
The cord which prolapses may be compressed
the following situations:
between the bony pelvis and the presenting
part leading to fetal hypoxia, asphyxia, and fetal • Malpresentations
death. Exposure of the cord to atmospheric tem- • Preterm labor
perature leads to spasm of the umbilical vessels. • Polyhydramnios
Manipulation to replace the cord into the uterus • Mobile head
• Artificial rupture of membranes
• External cephalic version
$QZ %QTFRTQNCRUG • Internal podalic version
• When fetal heart abnormalities occur immedi-
• &GſPKVKQP
Ŧ Cord alongside or below presenting part
ately after rupture of membranes
Ŧ Membranes ruptured
• Types
Management
Ŧ Occult
Cord alongside the presenting part As soon as cord prolapse is diagnosed, it is
Ŧ Overt important to determine if the cord pulsations
Cord below the presenting part are present or not. If the cord has prolapsed
• Incidence some time earlier and the pulsations are
Ŧ 0.6% of deliveries
absent, there is no urgency for delivery. Usually
• Etiology
vaginal delivery is recommended, except in
Ŧ Spontaneous
Malpresentations
situations such as transverse lie where it is not
Prematurity feasible.
Polyhydramnios If cord pulsations are present, in order to avert
Multifetal pregnancy death or hypoxic injury, the fetus must be deliv-
Multiparity ered as soon as possible. Diagnosis-to-delivery
Long cord interval is crucial. Vaginal delivery is feasible
Cephalopelvic disproportion only in a few, where the cervix is fully dilated
Ŧ Iatrogenic and delivery is imminent. Most women need a
Artificial rupture of membranes cesarean section. Measures should be taken to
Amnioinfusion prevent compression of the cord while waiting
Insertion of intrauterine pressure catheter, scalp
for cesarean section.
electrode
External cephalic version
Management depends on the stage of labor.
Internal podalic version
• Consequences %QTFRTQNCRUGKPVJGſTUVUVCIGQHNCDQT
Ŧ Cord compression/spasm • Delivery should be by immediate cesarean
Ŧ Fetal hypoxia
section. Alert operating room staff, anesthe-
Ŧ Fetal death
tists, and neonatologist.
CH 41_p599_620_v3.indd 617 18-07-2015 17:56:10

• While waiting for cesarean section, manipula- • If the fetus is in transverse lie or the presenting
tions of the cord must be avoided. part is high (above 0 station), deliver by cesar-
• Loops of cord may be replaced into the vagina ean section.
if they are outside the introitus. • If the vertex is below the level of the ischial
• Wrapping in towels soaked in warm saline has spine, vacuum extractor or forceps may be
not been found useful. used to deliver vaginally.
• To reduce compression of the cord by the • If presentation is breech, breech extraction
presenting part, various techniques may be is an option but cesarean section is usually
followed: resorted to in this situation.
– Elevate the foot end of bed (steep • If the fetus is in transverse lie and the mem-
Trendelenburg position) branes have just ruptured, internal podalic
– Alternatively, use knee–chest position version and breech extraction is an option in
– Fill maternal bladder using Foley’s catheter the following situations:
– Push up the presenting part with a hand in – The fetal weight is average.
the vagina – The fetus is the second of twins.
– Administer 0.25 mg of terbutaline subcuta-
neously for tocolysis Internal podalic version and breech
– Monitor fetal heart rate continuously extraction in a singleton fetus is associated
with high perinatal mortality and should be
Cor prolapse in the secon performed only by an experienced obstetri-
stage o labor cian and only if facilities for immediate cesar-
ean section are not available.
• If cord prolapse occurs in the second stage of Management of cord prolapse is outlined in
labor, vaginal delivery may be feasible. Figure 41.19.
• Assess presentation and station of the present-
ing part.
Cor prolapse
eel for pulsations
Cor pulsations Cor pulsations

present absent
Cer i not fully Cer i fully ait aginal

ilate ilate eli ery
elie e rans erse lie Verte belo reech belo

compression erte high spines spines
Cesarean section Cesarean section Vacuum forceps reech e tration
(KIWTG Management of cord prolapse.
CH 41_p599_620_v3.indd 618 18-07-2015 17:56:10

2TGXGPVKQP • Take precautions during amnioinfusion or

inserting a fetal scalp electrode.
• Anticipate cord prolapse when membranes
rupture in malpresentations, preterm labor, %QTFRTGUGPVCVKQP
and polyhydramnios.
• Monitor fetal heart rate and perform a vagi- Cord presentation may be an incidental finding
nal examination immediately if there are on ultrasonography. This can be confirmed by
abnormalities. color flow Doppler studies. If cord presentation
• Take precautions when performing artificial rup- is found remote from term, follow-up with ultra-
ture of membranes especially when the present- sonography is required. If it persists or is found
ing part is high or when there is polyhydramnios. after 38 weeks, elective cesarean section is usu-
Use a needle rather than Kocher’s forceps and ally performed.
perform ‘controlled’ rupture of membranes.
-G[RQKPVU
• Malpresentations and malpositions are important negotiate the pelvic diameters. Normal delivery is
causes of abnormal labor. not possible unless the head extends further to face
• Vertex presentations other than left occipitoanterior RTGUGPVCVKQPQTƀGZGUVQXGTVGZRTGUGPVCVKQP
are referred to as malpositions. The most common is • When the longitudinal axis of the fetus is perpendicu-
occipitoposterior position. lar to the uterine ovoid, it is referred to as transverse
• Malpresentations are presentations other than vertex lie. When membranes rupture, cord or arm prolapse
such as face, brow, breech, shoulder, and compound can result.
presentations. • There is no mechanism of labor in transverse lie.
• Abnormal axial lie can be transverse, oblique, or It has to be converted to cephalic presentation by
unstable lie. external cephalic version after 37 weeks or early in
labor. Placenta previa must be excluded in all cases of
• Malpresentations have some common etiological transverse lie.
factors such as multiparity, polyhydramnios, placenta
RTGXKCCDPQTOCNRGNXKEEQPſIWTCVKQPEGRJCNQRGNXKE • Neglected shoulder presentation can result in
disproportion, uterine malformations, prematurity, obstructed labor and uterine rupture. If external
multiple pregnancy, or fetal anomalies. cephalic version is not successful, cesarean section
is required.
• Most fetuses in occipitoposterior position deliver nor-
mally. Abnormal mechanisms are posterior rotation, • When one of the extremities present along with one
short anterior rotation, or nonrotation. of the fetal poles (except a combination of breech and
foot), it is known as a compound presentation. If the
• Posterior rotation results in face-to-pubis delivery. limb is at the same level or above the level of the ver-
Short anterior rotation can cause deep transverse ar- tex, it usually retracts in labor. If there is no progress
rest. If the vertex is below +2 station, instrumental de- in labor, cesarean section is indicated.
livery is possible. If not, cesarean section is required.
• When a loop of cord is felt alongside the presenting
• Face presentation results when the head is hyperextend- part and the membranes are intact, it is known as cord
ed. The engaging diameter is submentobregmatic. presentation. If the membranes are ruptured, the cord
• Normal delivery occurs in mentoanterior presentations enters the vagina ahead of the presenting part. This is
and most mentoposterior presentations that undergo known as cord prolapse.
rotation. • As soon as the cord is felt, it is important to determine
• A persistent mentoposterior position cannot deliver if cord pulsations are present. If pulsations are present
vaginally. If anterior rotation does not occur in men- and delivery is not imminent, immediate cesarean sec-
toposterior position, cesarean section is required. tion is mandatory.
• Brow presentation is the result of partial extension of • Cord should be replaced into the vagina and head
the head. The engaging diameter (verticomental) is elevated to relieve compression while preparing for
the largest diameter of fetal head; therefore, it cannot cesarean section.
CH 41_p599_620_v3.indd 619 18-07-2015 17:56:10

5GNH#UUGUUOGPV
%CUGDCUGF3WGUVKQPU attempted. If unsuccessful, cesarean section should
be performed.
%CUG
Mrs. CN, 31, third gravida with previous normal deliver- %CUG
ies, was admitted to the labor room with pains for 6 hours. Check for cord pulsation. If pulsations are present,
The doctor who examined her in a primary center had call for help. Replace the prolapse loops of cord into
diagnosed transverse lie and had referred her for further the vagina and push them up as high as possible.
care. Push the presenting part up to prevent compression
How will you clinically diagnose transverse lie? of the cord.
What is the next step in the evaluation? Pelvic examination should be done to assess cervical
dilatation, fetal presentation, and station. If the cervix
What complications do you anticipate if labor is al-
is fully dilated and the presenting part is below the
lowed to progress?
ischial spines, vaginal delivery may be attempted us-
How will you manage the case?
ing vacuum extraction or breech extraction depending
on the presentation. If the cervix is not fully dilated,
%CUG cesarean section should be performed.
Malpresentations such as breech, transverse lie,
Mrs. AD, multigravida at term, was admitted in labor. The DTQYCPFHCEGCTVKſEKCNTWRVWTGQHOGODTCPGUYJGP
membranes ruptured at the time of admission and along presenting part is high, polyhydramnios, multifetal
YKVJVJGIWUJQHCOPKQVKEƀWKFCNQQRQHEQTFUNKRRGFQWV pregnancy, external cephalic version, and internal
podalic version.
What is the immediate management?
How will you decide on mode of delivery?
What are the causes of cord prolapse? 5CORNGSWGUVKQPU
.QPICPUYGTSWGUVKQPU
#PUYGTU
Discuss the diagnosis and management of deep
%CUG transverse arrest.
How will you diagnose right occipitoposterior position
Abdominal examination—fundal grip does not reveal clinically? Discuss the management of labor in this
CP[HGVCNRQNG7ODKNKECNITKRōJGCFKUHGNVKPQPGƀCPM situation.
and breech in the other. Back or limbs may be felt
Discuss the etiology, diagnosis, and management of
anteriorly. First pelvic grip reveals an empty lower
a case of transverse lie in labor.
pole. Fetal heart sounds are heard at or below the
level of the umbilicus.
Ultrasonography to exclude placenta previa. If 5JQTVCPUYGTSWGUVKQPU
excluded, pelvic examination to assess dilatation and
effacement of cervix, presence of bag of membranes. Face-to-pubis delivery
The shoulder, elbow or arm, acromion, and ribs will Mentoposterior position
be felt high up. Cord prolapse
Early rupture of membranes, cord prolapse, arm Shoulder presentation with arm prolapse
prolapse, fetal distress, fetal hypoxia, and fetal death. Compound presentation
Obstructed labor and uterine rupture. Etiology of malpresentations
Since she is in early labor and membranes are Brow presentation
not ruptured, external cephalic version may be
CH 41_p599_620_v3.indd 620 18-07-2015 17:56:10

Abnormal Labor:
Breech Presentation
42 and Shoulder
Dystocia
Case scenario
Mrs. RN, 29, multigravida at 40 weeks, was admitted with labor pains. On
examination, the contractions were every 10 minutes, lasting for 20 sec-
onds, and the presentation was breech. Fetal and maternal risks of both
vaginal breech delivery and cesarean section were explained to Mrs. RN
and her husband. They were worried and confused about which mode of
delivery to opt for.
Introduction and the conduct of vaginal breech delivery are

very different from cephalic presentation.
Breech presentation is the most common malpre-
sentation and is an important cause of abnormal
labor. The perinatal mortality and morbidity are
higher than in vertex presentation at all gestational &GſPKVKQP
ages. Mode of delivery in breech has also been a When the podalic pole or the buttocks present
subject of controversy that has been influenced by with the legs extended or flexed, it is termed
the results of several randomized trials. breech presentation.
Shoulder dystocia is an obstetric emergency.
Perinatal mortality is high when dystocia is
severe or is inappropriately managed.
Incidence
The incidence is 3%–4% at term although it is 7%
Breech presentation at 32 weeks. Most fetuses that present as breech
before term turn spontaneously to cephalic pre-
Though the lie is longitudinal, the mechanism sentation. The incidence decreases as the gesta-
of labor, complications to the mother and fetus, tional age increases.
CH 42_p621_640_v3.indd 621 18-07-2015 18:02:14

Etiology septate uterus, myoma in the lower uterine seg-

ment, multiparity, and multiple pregnancy are
The causes of breech presentation are listed in other etiological factors. Previous breech pre-
Box 42.1. sentation also increases the risk. Congenital
Prematurity is the most common cause and anomalies of the fetus such as anencephaly,
breech presentation in prematurity is due to the hydrocephalus, and neuromuscular disorders
relative increase in the volume of amniotic fluid. such as myotonic dystrophy, trisomy 13, 18, and
Polyhydramnios is also an etiological factor, due 21 are also associated with increased risk.
to the increase in liquor volume. Placenta previa
and cornuofundal insertion of placenta, uter-
ine anomalies, especially bicornuate uterus and
%NCUUKſECVKQP
The three types of breech presentation are as
Box 42.1 Etiology of breech presentation follows (Fig. 42.1):
• 4GNCVKXGCDUQNWVGKPETGCUGKPVJGCOPKQVKEƀWKF • Frank (extended) breech
Ŧ Prematurity
• Complete (flexed) breech
Ŧ Polyhydramnios
• Incomplete breech
• Multiparity
• Multifetal pregnancy
• Abnormal placentation
Ŧ Placenta previa
Frank breech
Ŧ Cornuofundal placenta • The fetus is flexed at the hips and extended at
• Uterine anomalies the knees.
Ŧ Septate uterus • This constitutes 60%–70% of all breech
Ŧ Bicornuate uterus
presentations.
• Myoma in the lower segment
• Frank breech fits snugly in the lower uterine
• Fetal anomalies
Ŧ Neural tube defects
segment.
Hydrocephalus • The breech is compact and may be mistaken
Anencephaly for the head on abdominal examination.
• Fetal neuromuscular disorders • The extended legs splint the body, making
Ŧ Myotonic dystrophy external version difficult.
Ŧ Trisomy 13, 18, 21 • The head is less ballotable.
a. b. .
Figure 42.1 Types of breech presentation. a.(TCPMDTGGEJōƀGZGFCVVJGJKRUCPFGZVGPFGFCVVJGMPGGUb. Complete

DTGGEJōƀGZGFCVVJGJKRUCPFMPGGUc.+PEQORNGVGDTGGEJōGZVGPFGFCVVJGJKRUCPFMPGGU
CH 42_p621_640_v3.indd 622 18-07-2015 18:02:15

Abnormal Labor: Breech Presentation and Shoulder Dystocia 623
• Prognosis for vaginal delivery is better than for Complications of breech

other types of breech.
• Cord prolapse is less common since the cervix presentation
is usually well applied to the compact breech.
Breech presentation and delivery are associated
with higher perinatal morbidity and mortality.
Complete breech Some maternal complications can also occur.
• The fetus is flexed at the hip and knees.

• It constitutes 5%–10% of breech presentations.
Fetal complications
• The irregular breech does not fit well in the The increase in perinatal mortality and morbid-
lower uterine segment. ity in breech presentations is due to the follow-
• Cord prolapse is more common. ing reasons:
• There is lesser chance of vaginal delivery than
• Inherent problems in the fetus in breech
in the frank breech.
presentation: These include complications of
prematurity, congenital anomalies, chromo-
Incomplete breech somal anomalies, and neuromuscular disor-
ders. These may also be the cause of breech
• One or both hips are extended and the knee or presentation.
foot presents below the breech. • Complications of breech presentation/deliv-
• When one or both feet are below the breech, it ery: These occur during labor or delivery and
is known as footling breech. are due to the malpresentation.
• It constitutes 20%–25% of breech presenta- Fetal complications are listed in Box 42.2.
tions. Prematurity is the most common cause of
• This has the highest risk of cord prolapse. breech presentation and is associated with
• There is a high risk of head entrapment. increase in perinatal mortality and morbidity.
• There is less chance of cervical dilatation. When the gestational age is >32 weeks and the
• There is a high risk of cesarean section. fetal weight is >1500 g, mortality is low irrespec-
Breech presentation is also classified as com- tive of the mode of delivery. However, when
plicated and uncomplicated depending on the fetal weight is between 1000 and 1500 g, vaginal
presence of associated maternal complications delivery is associated with a higher rate of com-
that can affect perinatal outcome. plications. There is increased risk of intracranial
hemorrhage, birth injuries, and entrapment
of the aftercoming head. Therefore, cesarean
Complicated breech section is recommended in these cases. These
When a breech presentation is associated with
maternal factors which adversely influence the
prognosis, such as gestational hypertension, Box 42.2 Fetal Complications of breech
preeclampsia, pregestational or gestational dia- presentation
betes, or maternal cardiac disease are present, it • Inherent problems in the fetus
is referred to as complicated breech presentation. Ŧ Prematurity
These maternal complications can potentially Ŧ Congenital anomalies
increase perinatal and maternal morbidity asso- Ŧ Chromosomal anomalies
ciated with the maneuvers involved in vaginal Ŧ Neuromuscular disorders
breech delivery. • Complications due to breech presentation/delivery
Ŧ Cord accidents
Cord prolapse
ncomplicated breech Cord entanglement
Ŧ $KTVJCURJ[ZKC
Breech presentation with no associated mater-
Ŧ Entrapment of aftercoming head
nal complications is referred to as uncompli-
Ŧ Birth trauma
cated breech presentation.
CH 42_p621_640_v3.indd 623 18-07-2015 18:02:15

complications can occur during breech delivery

Box 42.4 Denominator, engaging diameter, and
by cesarean section as well. positions in breech presentation
When the breech does not fit well in the lower
uterine segment, cord prolapse is common. The • Denominator: Sacrum
• Engaging diameter: Bitrochanteric (9.5 cm)
cord may get entangled during assisted breech
Left sacroanterior (LSA)
delivery. Birth asphyxia is related to the inter-
Right sacroanterior (RSA)
val between delivery of breech and delivery of • Positions:
Left sacroposterior (LSP)
the aftercoming head. Head entrapment occurs Right sacroposterior (RSP)
when the breech escapes through an incom-
pletely dilated cervix as in preterm breech or
in extended head. Birth injuries that can occur
during breech delivery are listed in Box 42.3. Delivery of breech
Tentorial tears and intracranial hemorrhage The cardinal movements are as follows:
occur during delivery of the head due to sudden
decompression. Brachial plexus injuries, spinal • Engagement
cord injuries, and epiphyseal separation of bone • Descent with compaction
may occur due to undue traction. • Internal rotation of anterior buttock
• Delivery by lateroflexion
ngagement
Perineal tears and vaginal and cervical lacera-
The bitrochanteric diameter engages in the left
tions can occur during assisted breech delivery.
oblique diameter of pelvis in RSA position.
The risk of cesarean section is high.
Descent ith compaction

With each uterine contraction, the fetus flexes
Mechanism of labor and the fetal limbs and trunk come closer to each
other and become compact, a process referred to
The mechanism of labor with breech presenta-
as compaction.
tion is described in three stages:
1. Delivery of the breech
2. Delivery of the shoulders Internal rotation
3. Delivery of the head Irrespective of the position, there is always one
anterior buttock. This rotates through 45 degrees
The denominator, engaging diameters, and posi-
or 1/8th of a circle and comes to lie under the
tions in breech presentation are given in Box 42.4.
pubic symphysis.
There are four positions depending on the
quadrant of the pelvis which the sacrum occu-
pies (Fig. 42.2). Right sacroanterior is the most .CVGTQƀGZKQP
common position. The anterior buttock hitches under the symphy-
sis pubis, fetal trunk flexes laterally, and the pos-
terior buttock is born first followed by the ante-
rior buttock.
Box 42.3 Birth in uries in breech delivery
• Tentorial tears
Delivery of the shoulders
• Intracranial hemorrhage
• $TCEJKCNRNGZWUKPLWT[ • The bisacromial diameter engages in the
• 5RKPCNEQTFKPLWTKGU same oblique diameter as the bitrochanteric
• Separation of epiphysis of femur or humerus diameter.
• Fracture femur or humerus • Internal rotation of the anterior shoulder
• Depressed fracture skull
occurs by 45 degrees.
• +PLWT[VQGZVGTPCNIGPKVCNKC
• The anterior shoulder hitches under the pubic
• +PLWT[VQCDFQOKPCNXKUEGTC
symphysis.
CH 42_p621_640_v3.indd 624 18-07-2015 18:02:15

Left sacroanterior Left sacroposterior

L L P
ight sacroanterior ight sacroposterior

P
Figure 42.2 Fetal positions in breech presentation. Left and right sacroanterior and sacroposterior.
• The posterior shoulder sweeps the perineum Diagnosis

and is born first followed by the anterior
shoulder. The diagnosis of breech presentation is usually
by clinical examination.
Delivery of the head
• The suboccipitofrontal diameter engages in the Abdominal examination
opposite (right) oblique diameter of the pelvis.
On fundal grip, the hard, compact, globular head
• The occiput rotates internally through
is felt at the uterine fundus and is ballotable inde-
45 degrees and hitches under the pubic
pendent of the fetal body (Fig. 42.4). In extended
symphysis.
(frank) breech, the head may be mistaken for a
• The head is born by flexion. The face sweeps
breech since the head is not freely ballotable due
the perineum and is born first, followed by the
to the splinting by the extended legs. On pelvic
occiput.
grip, the firm, irregular, broad breech is felt in the
Mechanism of labor is shown in Figure 42.3. lower pole. This is not independently ballotable.
CH 42_p621_640_v3.indd 625 18-07-2015 18:02:15

a. b. . .
. . .
Figure 42.3 Mechanism of labor in breech presentation showing different movements (a g)CUFGUETKDGFKPVJGVGZV
Frank breech is also compact and may be mis- feet are felt below the buttocks in footling
taken for the head. The second pelvic grip helps presentation.
in assessing the descent of the bitrochanteric The breech may be mistaken for a face
diameter. The fetal heart sounds are heard above on vaginal examination in early labor. The
the umbilicus on the side of the back. differentiating features are described in
Chapter 41, Abnormal labor: Malpositions and
malpresentations.
aginal examination
On vaginal examination, the sacrum, ischial
ltrasonography
tuberosities, anus, feet or knee, and external
genitalia are felt (Box 42.5). The feet are not If breech presentation persists after 34 weeks,
felt in frank breech, felt by the side of the but- ultrasonography should be performed. It helps
tocks in complete breech, and one or both to ascertain the cause of breech presentation,
a. b.
Figure 42.4 #DFQOKPCNGZCOKPCVKQPKPDTGGEJRTGUGPVCVKQPa. The ballotable head is felt at the fundus. b. The soft
nonballotable breech is felt in the lower pole.
CH 42_p621_640_v3.indd 626 18-07-2015 18:02:15

Box 42.5 Diagnosis of breech External cephalic version

• #DFQOKPCNGZCOKPCVKQP Conversion of noncephalic presentation to
Ŧ Fundal grip cephalic presentation by abdominal manip-
Hard, globular, compact head ulation is known as external cephalic version.
Ballotable Ultrasonography is mandatory before ECV is
Ŧ Umbilical grip attempted. Several factors influence the success of
Back to one side the procedure, as listed in Box 42.7. Success rate is
Limbs on the other side higher with multipara, complete breech with ade-
Ŧ First pelvic grip
quate liquor and placenta in the upper segment.
Firm, broad, irregular breech
Not ballotable
• 8CIKPCNGZCOKPCVKQP Complications o C
Ŧ Sacrum Fetal bradycardia can occur during or following
Ŧ Ischial tuberosities ECV but is usually transient. Placental abruption
Ŧ Feet/knee
and uterine rupture have been reported.
Ŧ Anus
Ŧ 'ZVGTPCNIGPKVCNKC
Contrain ications
There are absolute and relative contraindica-
locate the placenta, diagnose fetal anoma- tions to ECV as listed in Box 42.8.
lies, and estimate fetal weight (Box 42.6). Other
imaging such as computerized tomography and
radiopelvimetry are not recommended. roce ure ( ig )
• Ultrasonography is mandatory before ECV.
• Cardiotocography is performed to ensure nor-
Management mal fetal heart rate.
• Sedation/epidural analgesia is not recom-
mended.
Antenatal management • Tocolysis (0.25 mg terbutaline SC) should be
Breech presentation is common before 34 weeks’ given 30 minutes before the procedure.
gestation and most of the cases convert sponta- • The mother is placed in supine position.
neously to cephalic presentation. If it persists • The breech is disengaged from the pelvis.
as breech after 34 weeks, the mother should be • The fetal head is manipulated toward the pel-
reviewed 2 weeks later. Perinatal mortality and vis. This may be in the direction that the fetus
morbidity are higher in vaginal breech delivery; faces (forward roll) or backward (backward
therefore, external cephalic version (ECV) should flip). Forward roll is easier and is normally
be performed at 36 weeks in nullipara and at preferred.
37 weeks in multipara. Spontaneous version is • Ultrasonography may be used during the pro-
unlikely after this period of gestation and there is cedure to guide the manipulation and monitor
less chance of reversion to breech after version. fetal heart rate.
Box 42.6 Information obtainable from Box 42.7 External cephalic version
ultrasonography
• Performed at
• Type of breech Ŧ 36 weeks in nullipara
• Fetal weight Ŧ 37 weeks in multipara
• Location of placenta • Higher success rate in
• 8QNWOGQHCOPKQVKEƀWKF Ŧ Multiparous women
• %QPſTOCVKQPQHIGUVCVKQPCNCIG Ŧ Complete breech
• (NGZKQPGZVGPUKQPQHJGCF Ŧ Adequate liquor volume
• Fetal anomalies Ŧ Average fetal weight
• Uterine anomalies Ŧ Placenta in upper segment
CH 42_p621_640_v3.indd 627 18-07-2015 18:02:16

Box 42.8 External cephalic version

• The fetal head is held in position in the pelvis
complications and contraindications for a few minutes.
• Cardiotocography is performed to ensure nor-
• Complications
mal fetal heart rate.
Ŧ Fetal bradycardia
• The procedure can be repeated if presentation
Ŧ Placental abruption
Ŧ Fetomaternal hemorrhage
reverts to breech, even in early labor.
Ŧ Uterine rupture
• Contraindications Mode of delivery in term breech
Ŧ Absolute
Multifetal pregnancy
Until the mid 1990s, vaginal breech delivery was
Gestational hypertension/preeclampsia the norm, unless there was a clear indication for
Placenta previa cesarean section. However, the perinatal mortal-
/CLQTWVGTKPGCPQOCNKGU ity and morbidity associated with vaginal breech
Oligohydramnios delivery was found to be higher compared to deliv-
Rupture of membranes ery by cesarean section, in several studies. Other
Ŧ Relative observational studies revealed no difference. To
Previous cesarean section resolve this controversy, a randomized multi-
Fetal growth restriction center trial known as the Term Breech Trial was
/CLQTHGVCNCPQOCN[ undertaken and the results were published in the
Fetal macrosomia
year 2000. The perinatal mortality and morbidity
Abnormal cardiotocography
were significantly higher in the vaginal delivery
a. b.
. .
Figure 42.5 'ZVGTPCNEGRJCNKEXGTUKQPa d. The fetus in breech presentation is turned in the direction in which the
fetus faces and converted into cephalic presentation.
CH 42_p621_640_v3.indd 628 18-07-2015 18:02:16

group in this study. Following this, cesarean sec-

Box 42.10 Criteria for patient selection for
tion rate for breech presentation has increased vaginal breech delivery
dramatically. However, subsequent trials did not
confirm this observation. The American College • Complete breech
• Estimated fetal weight between 2–3.5 kg
of Obstetricians and Gynecologists (ACOG) has
• (NGZGFJGCF
recommended that planned vaginal delivery of
• Uncomplicated breech
a term singleton breech fetus is reasonable and
safe in experienced hands, if hospital-specific
guidelines are followed.
labor are the same as for cephalic presentation.
Epidural analgesia is very useful.
Elective cesarean section
Indications for elective cesarean section are General guidelines for
given in Box 42.9. Elective cesarean section
should be a planned procedure, performed at
intrapartum management
38–39 weeks’ gestation. • Induction of labor is not recommended.
• Membranes should not be ruptured early.
aginal breech delivery • Electronic fetal monitoring is recommended.
• Oxytocin augmentation is usually not rec-
Vaginal breech delivery can be one of the ommended. If used, it must be under close
following: supervision.
• Assisted breech delivery • Partogram must be maintained.
• Total breech extraction • Intravenous line should be started when the
• Spontaneous breech delivery woman enters the second stage of labor so that
oxytocin may be added if required.
Spontaneous breech delivery occurs only in
very preterm fetuses. Most breech presentations
are delivered by assisted breech delivery. Rarely, Assisted breech delivery
total breech extraction is performed.
Assisted breech delivery is one where the fetus
is delivered spontaneously up to the umbilicus
Patient selection and the rest of the body is delivered by various
The criteria for patient selection for vaginal maneuvers.
breech delivery are listed in Box 42.10. The following personnel and equipment
should be available:
Management of labor • Skilled obstetrician

• Able assistant
Breech delivery should be undertaken in cen-
• Neonatologist
ters where facilities for immediate cesarean sec-
• Facilities for lithotomy position
tion are available. Informed consent should be
• Forceps for aftercoming head
obtained. General principles of management of
roce ure
• When in the second stage, the mother should
Box 42.9 Indications for elective cesarean
be placed in lithotomy position with the but-
section in breech presentation
tocks just over the edge of the couch.
• Estimated fetal weight >3.5 kg • When the fetal anus is seen at the introitus
• Incomplete (footling) breech between contractions, a generous episiotomy
• *[RGTGZVGPFGFHGVCNJGCF should be made (Fig. 42.6a)
• Complicated breech
• The fetus should be allowed to deliver spon-
• Placenta previa
taneously till the umbilicus. The feet may be
• Contracted pelvis
hooked out if required.
CH 42_p621_640_v3.indd 629 18-07-2015 18:02:16

a. b. .
Figure 42.6 Assisted breech delivery. a. Episiotomy is given when the anus is visible at the introitus and does not recede
between contractions. b. The fetus is held by femoropelvic grip. c. When the scapula is visible, the anterior arm may be
helped out by hooking it out over the face.
• The fetus is wrapped in a towel to avoid cuta-

neous stimulation. This also makes it easier to
hold the baby.
• The fetus should be held by placing the
thumbs on the sacrum and the index fingers
on the iliac crests—known as the femoropelvic
grip (Fig. 42.6b).
• The back of the fetus should face the obstetri-
cian throughout the procedure.
• At this point, a loop of the umbilical cord is
gently pulled down and kept to one side to pre-
vent compression and traction.
• When the inferior angle of the scapula is vis-
ible, the anterior arm may be helped out by
bringing it down over the chest (Fig. 42.6c) a. b.
• The aftercoming head is delivered by forceps. Figure 42.7 Burns–Marshall technique Step 1. a. and
One of the manual methods may be tried b. Illustration and image showing fetus hanging by its
before applying forceps but forceps can be weight.
applied electively as well.
• The duration between delivery of the fetus up
to the umbilicus and delivery of the mouth is
crucial to avoid asphyxia. This usually takes • When the hairline is visible under the pubic
2–3 minutes but should not exceed 5 minutes. arch, the assistant should apply suprapubic
pressure to flex the head.
• The baby should be held with thumb and ring
Delivery o the a tercoming hea finger on either side of the feet and the index
This is usually performed by one of the maneu- and middle finger between the heels (Fig.
vers or using forceps. No attempt should be 42.8a and b).
made to deliver the head till the nape of the neck • The baby is swung in an arc over the mother’s
(hairline) is visible. Undue traction can cause abdomen while the assistant provides perineal
extension of the head and prevent delivery. support.
aneuvers Mauriceau Smellie eit Technique

Burns Marshall Technique • Once the shoulders are delivered, the baby is
• After the shoulders are delivered, the baby is held astride the obstetrician’s left forearm
allowed to hang by its weight (Fig. 42.7a and b) (Fig. 42.9).
CH 42_p621_640_v3.indd 630 18-07-2015 18:02:16

Delivery by orceps
• The Piper’s forceps has been designed with a
good perineal curve for delivery of the aftercom-
ing head. However, any low forceps can be used.
• Forceps delivery may be used as the method
of choice. Most obstetricians try one manual
technique and, if unsuccessful, use forceps.
• Since the forceps flexes the head and the trac-
tion is directly on the head rather than through
the spinal column, the risk of injury to the spi-
nal cord is less.
a. b. • Once the nape of the neck is visible, the baby is
wrapped in a sterile towel (including the arms)
Figure 42.8 Burns–Marshall technique Step 2. a and and lifted up to the horizontal plane by the
b. Illustration and image showing the fetus is held by its assistant (Fig. 42.10).
HGGVYKVJVJWODCPFTKPIſPIGTQPGKVJGTUKFGCPFKPFGZ • The blades of the forceps are applied from below.
CPFOKFFNGſPIGTDGVYGGPVJGNGIUCPFUYWPIKPCPCTE
over the mother’s abdomen.
&KHſEWNVKGUGPEQWPVGTGFFWTKPI
assiste breech elivery
• The index and middle fingers of the left hand Difficulties may be encountered during the
of the obstetrician should be placed on each delivery of the breech, shoulders/arms, or after-
maxilla. coming head (Table 42.1).
• The index finger of the right hand is placed
on one shoulder and the middle and ring fin-
gers on the other shoulder and gentle down- Extended legs
ward traction is applied till nape of the neck is There may be difficulty in delivering the legs
visible. when they are extended at the knee as in frank
• The assistant should apply suprapubic pressure. breech presentation. The obstetrician’s hand
• The fetus is lifted toward the mother’s abdo- should be passed along the thigh to the popliteal
men; the mouth, nose, and forehead are fossa, gentle pressure applied to flex the legs, the
delivered in that order. foot grasped, and traction applied to deliver the
a. b.
Figure 42.9 Mariceau–Smellie–Viet Technique. a and b. Illustration and image showing delivery of the aftercoming
head by Mauriceau–Smellie–Viet technique.
CH 42_p621_640_v3.indd 631 18-07-2015 18:02:17

a. b.
Figure 42.10 Delivery of the aftercoming head by forceps. a. and b. Illustration and image showing the fetus help
up by wrapping in a towel and forceps applied from below.
Table 42.1 &

KHſEWNVKGUKPCUUKUVGFDTGGEJ
delivery
Problem Management
'ZVGPFGFNGIU Gentle pressure on popliteal
fossa
'ZVGPFGFCTOU • Lovset’s maneuver
• Bringing down the
posterior arm
Nuchal arm Rotate in the direction of the
nuchal arm
Entrapment of Duhrssen’s incisions
aftercoming head
Posterior rotation • Rotate trunk and head
of head anteriorly Figure 42.11 &GNKXGT[QHVJGGZVGPFGFNGIU6JGJCPF
• Prague maneuver is passed along the thigh to the popliteal fossa, the
MPGGKUHNGZGFCPFVJGNGIKUDTQWIJVFQYP
leg. The other leg usually slips out or the same Hence, the posterior arm that is brought anteri-
procedure can be repeated (Fig. 42.11). orly usually slips out or can be helped out. The
Extended arms other arm can be delivered directly or the same
If the arms are extended at the shoulders and procedure repeated (Fig. 42.12).
elbow, one of the following two techniques may The fetus is held by the hips and turned half a
be used. circle, keeping the back uppermost. Downward
traction is applied at the same time, so that the
ovset s maneuver arm that was posterior becomes anterior and can
The fetus is rotated through 90 degrees and then in be delivered under the pubic arch. The delivery
the opposite direction through 90 degrees to bring of the arm is accomplished by placing one or two
the other posterior arm anteriorly to lie under the fingers on the upper part of the arm. The arm is
pubic arch. The posterior arm is at a lower level drawn down over the chest as the elbow is flexed,
than the anterior arm due to the pelvic inclination. with the hand sweeping over the face.
CH 42_p621_640_v3.indd 632 18-07-2015 18:02:17

Figure 42.13 &GNKXGT[QHVJGGZVGPFGFCTOUD[

bringing down the posterior arm. The fetus is pulled
toward the mother’s thigh and the hand introduced into
VJGUCETCNJQNNQYVQHNGZVJGRQUVGTKQTCTOCPFDTKPIKV
down.
same procedure may be repeated to deliver the

other arm.
uchal arms
When the arm is flexed at the elbow with the
forearm behind the occiput, it is referred to as
a nuchal arm. To relieve a nuchal arm when it
is encountered, the infant is rotated so that the
fetal face turns towards the pelvis side wall. The
fetus should be rotated in the direction in which
the nuchal arm points (Fig. 42.14). This maneu-
ver causes friction to be exerted by the vaginal
walls, allowing the elbow to be drawn toward the
face, thus freeing the arm.
Figure 42.12 Lovset’s maneuver. The fetus is rotated
through 90 degree in one direction and then in the
other direction to bring the arms down.
To deliver the second arm, the baby is turned

half a circle in the opposite direction, keeping
the back uppermost and applying downward
traction, and the second arm is delivered in the
same way under the pubic arch.
Bringing down the posterior arm

The fetus is grasped by the legs and pulled toward
the mother’s right thigh. The obstetrician’s left
hand is introduced into the sacral hollow along
the left arm of the fetus, to the elbow (Fig. 42.13).
The arm is flexed by gentle pressure at the cubi- Figure 42.14 Delivery of nuchal arms. The fetus is
tal fossa, swept over the face, and delivered. The rotated in the direction in which the arm points.
CH 42_p621_640_v3.indd 633 18-07-2015 18:02:17

Entrapment of the head gestational age <32 weeks; therefore, cesarean

When the breech and fetal body slip out through section is recommended in these cases. The
an incompletely dilated cervix, the head may be mode of delivery should be individualized for
entrapped. This is common in preterm breech preterm breeches >32 weeks’ gestational age
where the head is larger than the body or with and weight >1.5 kg. Difficulties may be encoun-
premature bearing-down efforts. The cervix tered even during cesarean section in preterm
clamps down on the neck. Every effort should breech.
be made to prevent this complication since the
fetal mortality is high. Incisions may be made
at 4 o’clock and 8 o’clock positions on the cer- Shoulder dystocia
vix (Duhrssen’s incisions) and head delivered.
These incisions are rarely used in contemporary Shoulder dystocia is defined as failure of the
obstetric practice. shoulders to deliver after the head has deliv-
ered. There is a need for additional maneu-
Posterior rotation of the head vers, after the head is delivered and gentle
traction has failed to deliver the shoulders.
Rarely, the back of the fetus may rotate posteri-
The delivery of the shoulders is prevented
orly. Every effort should be made during assisted
by impaction of the shoulders in the pelvis.
breech delivery to prevent this complication.
Prolongation of head-to-body delivery time
When this happens, the trunk and fetal head
beyond 60 seconds is also used to define the
should be rotated anteriorly. If this fails, Prague
condition, but since the duration is not often
maneuver where fetus is delivered as occipi-
measured or documented, this definition is
toposterior may be required to deliver the head.
not widely accepted.
all these maneuvers are performed under gen-
eral or regional anesthesia.
Incidence
Total breech extraction
Shoulder dystocia occurs in 0.6%–1.4% of deliv-
When the fetus is delivered entirely by the obste- eries. The reported incidence varies depending
trician, it is known as breech extraction. In mod- on the criteria used for diagnosis.
ern obstetrics, it is performed only in case of sec-
ond of twins, following internal podalic version.
The procedure is usually performed under gen- Pathophysiology
eral anesthesia (Box 42.11).
In vertex presentation, the head enters the pelvis
in one of the oblique diameters and the shoul-
Delivery of preterm breech ders engage with the bisacromial diameter in the
opposite oblique diameter.
Since the head is larger relative to the body, the
When external rotation of the head occurs
risk of entrapment of the head is more with vag-
after delivery, the anterior shoulder rotates
inal delivery in preterm breech. Vaginal deliv-
internally, bringing the bisacromial diameter in
ery is associated with high perinatal mortality
the anteroposterior diameter of the pelvis. The
and morbidity if the fetal weight is <1.5 kg or
posterior shoulder is at a lower level in the sacral
hollow and is delivered first, followed by the
anterior shoulder.
If the shoulders fail to rotate, both shoulders
Box 42.11 Total breech extraction
enter the pelvis together or if the bisacromial
• Entire delivery by obstetrician diameter is more than average, the anterior or
• General anesthesia required the posterior shoulder, or both shoulders get
• Indication impacted. Impaction of the anterior shoulder
Ŧ Second of twins, after internal podalic version
is more frequent. Brachial plexus injury results
CH 42_p621_640_v3.indd 634 18-07-2015 18:02:17

due to stretching of the nerves, especially during Combination of factors such as diabetes, mac-
traction or manipulation. rosomia, and instrumental delivery increases
the risk more than a single risk factor. Similarly,
a combination of obesity, diabetes, and previous
isk factors shoulder dystocia increases the risk significantly.
Maternal diabetes and fetal macrosomia are the

strongest risk factors for shoulder dystocia.
Fetal macrosomia is an important risk factor,
Diagnosis
especially when the fetal weight is >4.5 kg. Risk In women with risk factors, shoulder dystocia
of shoulder dystocia increases as the fetal weight should be anticipated and the obstetrician and
increases beyond 4000 g. However, the majority nurses must be prepared. Signs of shoulder dys-
of fetuses weighing >4 kg do not have shoulder tocia are as follows:
dystocia.
Diabetes, pregestational or gestational, is a risk • Difficulty in delivering the face after delivery of
factor since it brings about certain morphologi- the occiput
cal changes in the fetus. Fetal growth is dispro- • Retraction of the neck and face against the
portionate with the chest being much larger than vulva (turtle sign)
the head and with significantly large shoulders. • Failure of restitution
Maternal obesity or excessive weight gain in
pregnancy and postmaturity are also risk factors.
The fetal weight increases in all these conditions Consequences
and the fetal chest and trunk grow larger relative
to the head. Perinatal morbidity and mortality increase sig-
Labor abnormalities such as protracted active nificantly in shoulder dystocia. Brachial plexus
phase and prolonged second stage may be indic- injury is the most important fetal complication;
ative of large fetus and after the head is delivered, it is seen in 21% of cases of shoulder dystocia. It
shoulders may be impacted. Instrumental deliv- resolves spontaneously in most cases, but per-
eries, especially the use of rotational forceps, manent disability can occur in 10%. Fracture
also increase the risk. Oxytocin augmentation is of the clavicle and humerus can occur during
also a risk factor. Oxytocin is most often used in manipulations. Cord compression, hypoxia,
hypotonic uterine dysfunction which could be asphyxia, and fetal death are known complica-
due to large fetal size. Advanced maternal age tions (Box 42.13).
and male fetal gender have also been found to Third and fourth degree perineal tears, vag-
increase the risk (Box 42.12). Previous shoulder inal lacerations, postpartum hemorrhage, and
dystocia is a major risk factor as well; the recur- uterine rupture are the maternal complications
rence rate is 10%. associated with shoulder dystocia.
Box 42.12 isk factors for shoulder dystocia Box 42.13 Consequences of shoulder dystocia
• Fetal macrosomia • Fetal
• Pregestational or gestational diabetes Ŧ $TCEJKCNRNGZWUKPLWTKGU
• /CVGTPCNQDGUKV[GZEGUUKXGYGKIJVICKP Ŧ Fracture clavicle
• Postmaturity Ŧ Fracture humerus
• Labor abnormalities Ŧ *[RQZKC
Ŧ Protracted active phase Ŧ #URJ[ZKC
Ŧ Prolonged second stage Ŧ Fetal death
Ŧ 1Z[VQEKPCWIOGPVCVKQP • Maternal
Ŧ Instrumental delivery Ŧ Third and fourth degree perineal tears
• Previous shoulder dystocia Ŧ Cervical and vaginal lacerations
• Advanced maternal age Ŧ Postpartum hemorrhage
• Male fetus Ŧ Ruptured uterus
CH 42_p621_640_v3.indd 635 18-07-2015 18:02:18

Prediction using models and mannequins. A stepwise man-

agement algorithm should be displayed in the
Although there are known risk factors, in 50% of labor room.
cases of shoulder dystocia none of the risk fac- There are several maneuvers to be used when
tors is present and the dystocia is an unantic- shoulder dystocia occurs; some are less invasive
ipated event. It is, therefore, difficult to predict and easier to perform than the others. Generally,
shoulder dystocia. It is also difficult to accurately the easier and effective maneuvers should be
estimate fetal weight even with ultrasonography. used first.
Estimation of birth weight, measurement of
fetal biparietal, abdominal, and chest diameters, Immediate steps
and chest and abdominal circumference, and cal-
culation of various ratios have been used to pre- • Call for help.
dict shoulder dystocia but they lack sensitivity and • Bring the woman to the edge of the bed to
specificity. Abdominal circumference of 35 cm or facilitate vaginal maneuvers.
more and difference between abdominal and bipa- • Ask the woman to stop pushing.
rietal diameters, in combination with fetal weight, • Do not apply undue traction on the head.
have been found to be useful by small studies, but • Do not apply fundal pressure.
large randomized controlled trials have failed to • Perform a generous episiotomy.
prove the usefulness of these measurements. The HELPERR mnemonic summarizes the
steps required to deliver a mother with shoulder
dystocia.
Prevention H. Call for help
E. Evaluate the need for an episiotomy
Since it is not possible to predict shoulder dysto-
L. Elevate and hyperflex the legs (McRobert’s
cia, prevention is also difficult.
maneuver)
• Induction of labor is not recommended for P. Suprapubic pressure
prevention of shoulder dystocia. E. Enter maneuvers (internal rotation)
• Elective instrumental delivery is not R. Remove the posterior arm
recommended. R. Roll the woman
• Elective cesarean section to prevent shoulder
dystocia is not recommended as a routine
First-line maneuvers
intervention.
• Cesarean section is recommended in selected These maneuvers have a high rate of success and
situations: should be attempted first.
– According to ACOG guidelines, when esti-
mated fetal weight is >5 kg in nondiabetics c oberts maneuver
and >4.5 kg in diabetics, cesarean should be McRoberts’ maneuver is the first step. Remove
considered. For developing countries, the the legs from stirrups and hyperflex the legs
cut off weights are lower (4 kg), but there is onto the mother’s abdomen. This straightens the
no definite guideline. sacrum, rotates the pubic symphysis anteriorly,
– In women with previous shoulder dystocia and reduces the angle of inclination. It may also
and brachial plexus injury with suspected increase the anteroposterior diameter margin-
macrosomia in current pregnancy, cesarean ally. The impacted anterior shoulder slips under
section may be considered. the pubic symphysis (Fig. 42.15).
• Prophylactic McRoberts’ maneuver is not
recommended.
Suprapubic pressure
McRoberts’ maneuver should be combined
Management with suprapubic pressure. The pressure should
be applied from the side of the fetal back and
All members of the labor room team should have directed downward into the pelvis and laterally
training in management of shoulder dystocia toward the opposite side in order to adduct the
CH 42_p621_640_v3.indd 636 18-07-2015 18:02:18

a.
b.
Figure 42.15 McRoberts’ maneuver. a./QVJGTŏUNGIUCTGJ[RGTHNGZGFCVVJGJKRUCPFMPGGUb. The sacrum

straightens and the pubic symphysis tilts anteriorly, reducing the angle of inclination.
shoulders, reduce the bisacromial diameter, and and vice versa. The posterior shoulder should be
bring the shoulders to the oblique diameter of rotated by 180 degrees and brought under the
the pelvis (Fig. 42.16). pubic symphysis, simultaneously adducting the
If these two simple maneuvers do not suc- shoulders (Fig. 42.17).
ceed, the more complicated maneuvers must be
attempted. ubin s maneuver
The fingers of one hand are inserted anteriorly
Second-line maneuvers or posteriorly (whichever is the most accessible)
on to the back of the fetal shoulder and rotated
Second-line maneuvers should be attempted to bring the shoulders in the oblique diameter of
without delay when the first-line maneuvers fail. the pelvis. Adduction of the shoulder also occurs
Skilled obstetricians should perform the sec- with this maneuver. The bisacromial diameter
ond-line maneuvers as they are difficult to per- decreases and is also brought to the large (oblique)
form and may be associated with fetal injuries. diameter of the pelvis, facilitating delivery.
oo s cor scre maneuver (rotation Delivery o the posterior arm

o posterior shoul er) ( ac uemier maneuver)
The physician places at least two fingers on the The hand is passed into the sacral hollow and the
anterior aspect of the fetal posterior shoulder, posterior arm is identified and flexed by gentle
applying gentle upward pressure around the cir- pressure on the cubital fossa. The arm slips over
cumference of the arc and rotating the shoulder the fetal face and chest. The forearm is grasped
toward the fetal chest. If the back of the fetus is to and the arm and posterior shoulder pulled down
the mother’s left, the right hand should be used into the pelvis. The posterior shoulder may have
CH 42_p621_640_v3.indd 637 18-07-2015 18:02:18

Figure 42.16 Suprapubic pressure. This is combined with McRoberts’ maneuver and directed into the pelvis and
laterally to adduct the shoulders.
Figure 42.17 Wood’s maneuever. The entire hand is passed into the sacral hollow and the posterior shoulder
rotated by 180 degree to bring it under the pubic symphysis.
to be rotated using the arm to achieve delivery. Middle fingers of both hands may be used, one
The anterior shoulder can then be delivered from the anterior aspect and another from the pos-
or rotated posteriorly and the same procedure terior aspect, to get better traction. Alternatively, a
repeated. This procedure is associated with an soft rubber catheter or tube can be used to hook
increased risk of fracture humerus and brachial the axilla and apply traction. This has the advan-
plexus injury. tage of better hold and availability of more space
since the hands are not inside the vagina/pelvis.
2QUVGTKQTCZKNNCſPIGTQTUNKPIVTCEVKQP
If the elbow cannot be reached by the hand in he all ours or as in techni ue
the sacral hollow, the middle finger can be used The mother is rolled onto the ‘all fours’ position,
to hook the posterior axilla and apply traction. on her hands and knees. The Gaskin maneuver
CH 42_p621_640_v3.indd 638 18-07-2015 18:02:18

is a safe, rapid, and effective technique for the The third-line maneuvers are used as a last
reduction of shoulder dystocia. The change resort and usually result in high maternal and
in position disimpacts the shoulders because fetal morbidity.
of an increase in pelvic diameters by as much Cleidotomy: One or both clavicles are
as 10 to 20 mm. The delivery is completed by fractured.
downward traction on the posterior shoulder Symphysiotomy: The pubic symphysis is
without any further maneuvers in a large num- incised and separated to increase the anteropos-
ber of cases. terior diameter of the pelvis.
Zavanelli maneuver: The fetal head is
replaced into the uterine cavity and the fetus
delivered by cesarean section. In. terbutaline is
Third-line maneuvers used to relax the uterus; the head is rotated to the
The perinatal mortality increases as the first- occipitoanterior position, flexed, and replaced
and second-line maneuvers fail. The head-to- into the uterus. This maneuver is most often
shoulder delivery time increases and the risk of associated with fetal demise and is done only to
asphyxia and fetal death is high. safeguard the mother’s life.
Key points
• Breech presentation occurs in 3%–4% of all labors • Mode of delivery in breech may be by elective cesar-
at term. ean section or vaginal breech delivery.
• Prematurity is the most common cause of breech • Elective cesarean section should be performed at
presentation. Other etiological factors are the same as 38–39 weeks when indications are present.
for other malpresentations. • Vaginal breech delivery should be undertaken only in
• Types of breech presentations are complete, incom- centers with facilities for immediate cesarean section
plete, and frank breech. and guidelines must be followed.
• (TCPMQTGZVGPFGFDTGGEJJCUVJGDGUVEJCPEGQH • Selection of patients for vaginal delivery should be
vaginal delivery and the least risk of cord prolapse. DCUGFQPURGEKſGFUGNGEVKQPETKVGTKC
• Assisted breech delivery should be performed by
• Breech presentations may be complicated or uncom-
skilled obstetrician.
plicated depending on the presence or absence of
maternal risk factors. • Mode of delivery of preterm breech should be individu-
alized.
• Perinatal mortality and morbidity are high in breech
presentation. These may be due to inherent problems • 5JQWNFGTF[UVQEKCKUFGſPGFCUHCKNWTGQHVJGUJQWN-
in the fetus or the result of breech presentation and ders to deliver after the head has delivered. There
delivery. is a need for additional maneuvers, after the head
is delivered and gentle traction has failed to deliver
• Mechanism of labor in breech is described in three the shoulders. It is associated with high risk of fetal
stages—delivery of the breech, shoulders, and after- CURJ[ZKCCPFHGVCNFGCVJ
coming head. The engaging diameter is bitrochanteric
and the denominator is sacrum. • Risk factors for shoulder dystocia are fetal macroso-
mia due to diabetes, postmaturity, and maternal
• &KCIPQUKUKUWUWCNN[D[ENKPKECNGZCOKPCVKQP#DFQOK-
obesity; labor abnormalities such as protracted active
PCNGZCOKPCVKQPTGXGCNUVJGJGCFCVVJGHWPFWUCPF
phase and prolonged second stage; instrumental
breech in the lower pole.
FGNKXGTKGUCPFQZ[VQEKPCWIOGPVCVKQP
• 1PXCIKPCNGZCOKPCVKQPVJGDTGGEJOC[DGOKUVCMGP
for the face. • +VKUFKHſEWNVVQRTGFKEVQTRTGXGPVUJQWNFGTF[UVQEKC
• If the breech presentation persists after 34 weeks, • Shoulder dystocia is an obstetric emergency. Manage-
WNVTCUQPQITCRJ[KUOCPFCVQT[VQGZENWFGHGVCNWVGTKPG OGPVEQPUKUVUQHXCTKQWUſTUVUGEQPFCPFVJKTFNKPG
anomalies, locate the placenta, estimate fetal weight, maneuvers. McRoberts’ maneuver with suprapubic
CPFCUUGUUCOPKQVKEƀWKFXQNWOG RTGUUWTGKUVJGKOOGFKCVGſTUVUVGRCPFJCUCJKIJ
success rate.
• 'ZVGTPCNEGRJCNKEXGTUKQPUJQWNFDGRGTHQTOGFCV
weeks in a nullipara and 37 weeks in a multipara.
CH 42_p621_640_v3.indd 639 18-07-2015 18:02:18

Self-Assessment
3. Vaginal delivery is to be considered if frank or com-
Case-based questions RNGVGDTGGEJHGVCNYGKIJVMIƀGZGFJGCFCPF
placenta in the upper segment.
Case 1 4. Forceps can be applied electively. Alternatively,
Mrs. RN, 29, multigravida with two previous normal deliv- either Burns–Marshall or Mauriceau–Smellie–Veit
eries, at 40 weeks of gestation, was admitted with labor technique can be tried and, if unsuccessful, forceps
RCKPU 1P GZCOKPCVKQP VJG EQPVTCEVKQPU YGTG GXGT[ can be applied.
minutes, lasting for 20 seconds, and the presentation was
breech.
1. How will you proceed to evaluate her?
Case 2
2. 9JCVKUVJGſTUVUVGRKPVJGOCPCIGOGPV! 1. Pregestational diabetes, fetal weight of 3.8 kg,
3. What are the factors you will take into consideration RTQNQPIGFſTUVUVCIGRTQNQPIGFUGEQPFUVCIG
for decision regarding vaginal delivery? QZ[VQEKPCWIOGPVCVKQPCPFKPUVTWOGPVCN
4. How will you deliver the aftercoming head? delivery.
2. Call for help, ask the patient to stop pushing, stop
applying traction, bring the patient to the edge of the
Case 2 bed, and perform a liberal episiotomy.
Mrs. JR, second gravida, with previous normal delivery, 3. McRoberts’ maneuver with suprapubic pressure
pregestational diabetic on insulin, presented in active la- OWUVDGVTKGFſTUV6JGNGIUUJQWNFDGVCMGPQHHVJG
bor at term. The estimated fetal weight was 3.8 kg. The UVKTTWRUCPFƀGZGFVQYCTFVJGCDFQOGPJ[RGTƀGZ-
ſTUVUVCIGQHNCDQTYCURTQNQPIGFCPFQZ[VQEKPYCUWUGF ing the knee and hip. Suprapubic pressure should
to augment labor. Forceps was applied since the second be directed into the pelvis and toward the front of the
stage was prolonged (1 hour and 15 minutes). After de- fetus in order to adduct the shoulders. If this fails,
livery of the head, the shoulders could not be delivered. Woods corkscrew maneuver or Rubin’s maneuver
should be tried.
1. What are the risk factors in this lady for occurrence of 4. Third- and fourth-degree perineal tears, vaginal and
shoulder dystocia? cervical lacerations, postpartum hemorrhage, and
2. What are the immediate steps in the management uterine rupture are the possible maternal complica-
CUUQQPCUFKHſEWNV[KUGPEQWPVGTGFKPFGNKXGTKPIVJG VKQPU$TCEJKCNRNGZWUKPLWTKGUHTCEVWTGENCXKENGQT
shoulders? JWOGTWUCURJ[ZKCCPFHGVCNFGCVJCTGVJGHGVCN
3. How will you deliver the shoulders? complications.
4. What are the maternal and fetal complications?
Sample questions
Answers
Case 1 1. Discuss the etiology, diagnosis, and
1. a. #DFQOKPCNGZCOKPCVKQP%JGEMV[RGQHDTGGEJ management of breech presentation at
descent of breech, fetal heart rate. 36 weeks’ gestation.
b. 8CIKPCNGZCOKPCVKQP%JGEMEGTXKECNGHHCEGOGPV
dilatation, type of breech, station, presence of
OGODTCPGURGNXKEEQPſIWTCVKQP
c. 7NVTCUQPQITCRJ['ZENWFGHGVCNCPQOCNKGU 1. 'ZVGTPCNEGRJCNKEXGTUKQP
placenta previa, and uterine anomalies; assess 2. Mechanism of labor in breech presentation
ƀGZKQPQHJGCFNKSWQTXQNWOGV[RGQHDTGGEJCPF 3. Assisted breech delivery
fetal weight. 4. Burns–Marshall technique
2. 'ZVGTPCNEGRJCNKEXGTUKQPKUVQDGRGTHQTOGFKH 5. Shoulder dystocia
membranes are intact, liquor volume is adequate,
6. McRoberts’ maneuver
fetal weight is <3.5 kg, and placenta is in the upper
segment.
CH 42_p621_640_v3.indd 640 18-07-2015 18:02:18

Complications
43 of the Third
Stage of Labor
Case scenario
Mrs. GN, 29, third gravida, had a vaginal delivery of a baby boy weighing
2.9 kg. Following delivery of the placenta, there was continuous, profuse
bleeding. She received parenteral uterotonics, the uterus was massaged,
and blood transfusion was started. The bleeding however did not reduce.
She looked pale and anxious, and her blood pressure dropped further.
Her family was informed that she needed an emergency surgical proce-
dure, and there was the possibility of a hysterectomy.
Introduction world. Other complications such as adherent

placenta and uterine inversion, are also asso-
The third stage of labor is the time of placental ciated with a high risk of maternal mortality
separation and subsequent arrest of bleeding by and morbidity. Most of these complications
contraction and retraction of the uterus. In most and deaths are preventable if the third stage of
women, this stage proceeds normally. However, labor is managed in a timely and appropriate
complications can occur before and after the manner.
delivery of the placenta. Complications of the Complications of the third stage of labor are
third stage are usually associated with blood listed in Box 43.1.
loss, hypotension, and shock, which may be life Amniotic fluid embolism is discussed in
threatening. Chapter 45, Nonhemorrhagic shock in pregnancy.
Postpartum hemorrhage (PPH), which is The majority of third stage complications are
the most common complication encountered associated with hemorrhage. Clinical manifes-
in the third stage, accounts for 25% of mater- tations of blood loss in pregnancy are different
nal deaths in India and in the developing from those in the nonpregnant state.
CH 43_p641_661_v3.indd 641 18-07-2015 18:05:50

Box 43.1 Complications of third stage labor Box 43.2 Causes of primary postpartum
hemorrhage
Ŧ Primary • Uterine atony
Atonic • Retained placenta or membranes
Traumatic • Trauma to the reproductive tract
Ŧ Secondary • Disseminated intravascular coagulation
• Retained placenta
• Adherent placenta
Ŧ Accreta
Ŧ Percreta
Ŧ Increta Atonic postpartum hemorrhage
• Uterine inversion
• #OPKQVKEƀWKFGODQNKUO Uterine atony or failure of the uterus to contract
and retract effectively enough to occlude the spi-
ral arterioles is the most common cause of PPH.
This accounts for 80% of PPH and is seen in 1 in 20
deliveries. Risk factors are listed in Box 43.3.
Postpartum hemorrhage
revention
&GſPKVKQP Active management of the third stage of labor as
discussed in Chapter 15, Management of normal
Postpartum hemorrhage is defined as blood labor and delivery is the most important preven-
loss of >500 mL following vaginal delivery tive step. Active management consists of con-
and >1000 mL following a cesarean section. trolled cord traction, administration of utero-
Postpartum haemorrhage can also be defined tonics, and assessment of uterine tone and size.
as blood loss that results in hemodynamic In randomized controlled trials, this has been
instability. A fall in hematocrit of >10% between proven to reduce PPH and need for additional
admission and the postpartum period and uterotonics. During a cesarean section, sponta-
excessive bleeding requiring blood transfusion neous separation of the placenta reduces risk of
are the other definitions used. Blood loss of bleeding.
500–1000 mL after vaginal delivery is classified
as minor PPH and >1000 mL as PPH. The inci-
dence of PPH is 2.5%–3%.
PPH is divided into the following:
Box 43.3 isk factors for atonic postpartum
• Primary PPH: Bleeding occurring within 24 hemorrhage
hours of delivery
• Secondary PPH: Bleeding occurring after 24 • Antepartum
Ŧ Advanced maternal age
hours but before 12 weeks of delivery
Ŧ Multiparity
Ŧ Previous atonic postpartum hemorrhage
Ŧ Uterine overdistension
Primary postpartum Multifetal pregnancy
hemorrhage Polyhydramnios
Primary PPH is more common than secondary Placental abruption
PPH. Incidence varies, depending on the man- Placenta previa
agement of the third stage and administration of • Intrapartum
prophylactic uterotonics. The causes of primary Ŧ Prolonged labor
PPH are listed in Box 43.2. Ŧ Induced labor
Disseminated intravascular coagulation is Ŧ Instrumental delivery
Ŧ Precipitate labor
dealt with in Chapter 45, Nonhemorrhagic shock
Ŧ General anesthesia
in pregnancy.
CH 43_p641_661_v3.indd 642 18-07-2015 18:05:50

Complications of the Third Stage of Labor 643
Clinical eatures symptoms associated with the amount of blood

Since the myometrium fails to contract, the loss so that early treatment can be instituted.
uterus feels flabby and is filled with blood. The
uterine fundus is palpable above the umbilicus.
The bleeding is torrential and leads to hypoten-
anagement o
sion and tachycardia. Depending on the amount postpartum hemorrhage
of bleeding, tachycardia, tachypnea, and hypo- Profuse bleeding and a relaxed uterus indicate
tension occur (Box 43.4). atonic hemorrhage; however, bleeding due to
retained placental tissue and cervical or vagi-
Clinical mani estations nal lacerations should always be excluded. As
soon as the placenta is delivered, it should be
o hemorrhage in pregnancy
inspected for missing cotyledons.
The increase in blood volume, along with other When blood loss is estimated to be 500–1000
hemodynamic adaptations in pregnancy, allow mL, the patient must be monitored closely. Blood
pregnant and parturient women to withstand loss at delivery is often underestimated.
moderate blood loss without manifesting the Once blood loss is estimated to be >1000 mL,
classic symptoms and signs of shock. This can management has to be prompt and appropri-
lead to underestimation of blood loss and late ate. It is important to ensure that the uterus is
recognition of shock. well contracted. Uterotonics are the first line of
Early symptoms of blood loss such as dizzi- management of atonic PPH. Oxytocin infusion,
ness or palpitation are experienced only when (20 units in normal saline) may be started if the
the blood loss exceeds 1000 mL. As the blood loss uterus is not well contracted. Injection methyl
increases, symptoms and signs appear rapidly ergometrine 0.25 mg can be administered IV if
(Table 43.1). It is important to be aware of the there are no contraindications.
The first step in the management is to establish
good IV access, infuse IV normal saline rapidly, send
a sample for blood tests and cross-match, and get
Box 43.4 Atonic postpartum hemorrhage
additional assistance. A senior obstetrician, senior
• Most common cause of postpartum hemorrhage midwives, and nurses should be called in for help;
(80%) the anesthetist and blood bank should be alerted.
• Prevention Evaluation, resuscitation, communication
Ŧ Active management of third stage
with the patient’s relatives and the medical team,
Ŧ Await spontaneous placental separation during ce-
sarean section
and procedures to arrest bleeding should pro-
• Clinical features ceed simultaneously as described below.
Ŧ Profuse bleeding The management of PPH includes the follow-
Ŧ 7VGTWUƀCDD[ſNNGFYKVJDNQQF ing steps:
Ŧ Fundus palpable above the umbilicus
• Insert a large-bore intravenous line. If neces-
Ŧ 5KIPUCPFU[ORVQOUQHDNQQFNQUUUJQEM
sary, two lines can be started.
Table 43.1 Physiological response to hemorrhage in pregnancy
Class Blood loss (mL) Percentage of Clinical features

blood volume
Class 1 1000 15 &K\\KPGUURCNRKVCVKQP
Class 2 1500 20–25 6CEJ[ECTFKCVCEJ[RPGCUYGCVKPI
narrow pulse pressure
Class 3 2000 30–35 5KIPKſECPVVCEJ[ECTFKCCPFVCEJ[RPGC
RCNNQTEQNFCPFENCOO[GZVTGOKVKGU
hypotension
Class 4 Ů 40 5JQEMCKTJWPIGTTGPCNHCKNWTG
CH 43_p641_661_v3.indd 643 18-07-2015 18:05:50

Table 43.2 terotonics used in the management of postpartum hemorrhage
Drug Dose oute Frequency Comment

1Z[VQEKP IV: 20–40 units in 500 mL Continuous #XQKFWPFKNWVGFTCRKF+8KPHWUKQPYJKEJ
normal saline or lactated causes hypotension
Ringer's solution
Methyl ergometrine IV: 0.25 mg Every 2–4 hours Avoid if patient is hypertensive
PGF2D IM: 0.25 mg 'XGT[ŌOKP Avoid in asthmatic patients; relative
FQUGUOCZKOWO EQPVTCKPFKECVKQPKHJGRCVKETGPCNCPF
ECTFKCEFKUGCUG&KCTTJGCHGXGT
tachycardia can occur
Misoprostol ŌzITGEVCNN[ Used only if injectable uterotonics not
(PGE1) available
KPVTCOWUEWNCTN[ KPVTCXGPQWUN[P RTQUVCINCPFKP
• Obtain blood sample for hematocrit and

cross-match.
• Start normal saline infusion with 20 units of
oxytocin.
• Monitor pulse, blood pressure, and respiratory
rate.
• Insert Foley catheter and monitor urine
output.
• Other uterotonics are used as second line
(Table 43.2).
• Place a hand on the uterus to check for con-
traction and provide uterine massage.
• Continue volume resuscitation with normal
saline/lactated Ringer’s and colloids while
awaiting blood.
• Transfuse blood and blood products as Figure 43.1 Bimanual uterine compression. The right
required. If specific group not available or in JCPFKUOCFGKPVQCſUVCPFRNCEGFKPVJGXCIKPCCPFNGHV
case of emergency, 'O' negative blood can be hand is placed on the abdomen on the posterior surface of
used. the uterus and the uterus should be compressed between
• If bleeding continues, inspect the cervix and the two hands.
vagina for lacerations and explore the uterine
cavity for retained placental tissue. control bleeding. This may be difficult in obese
women. The aorta is compressed against the
lumbosacral vertebrae. The obstetrician stands
Mechanical interventions
by the side of the woman and compresses the
• Bimanual compression This should be aorta against the spine with a fist placed on the
attempted next. The uterus should be com- abdomen, using sufficient pressure (Fig. 43.2).
pressed between the hand placed on the
abdomen on the posterior surface of the uter- If the above measures fail, other methods
ine fundus while the fist of the other hand is must be resorted to.
placed in the vagina pushing against the ante-
rior aspect of the uterus (Fig. 43.1). terine tamponade
• Aortic compression Aortic compression can The uterine cavity may be tightly packed with
be used as an alternative to bimanual uterine gauze or a fluid-filled balloon to compress the
compression or if uterine compression fails to blood vessels and thereby stop the bleeding.
CH 43_p641_661_v3.indd 644 18-07-2015 18:05:50

alloon filling the

uterine ca ity
a. b.
Figure 43.3 The ebb balloon tamponade. a. The Ebb
Figure 43.2 Aortic compression. The obstetrician should balloon tamponade system. b. The double balloon is
UVCPFQPVJGNGHVUKFGQHVJGOQVJGTOCMGVJGJCPFKPVQ RNCEGFKPVJGWVGTKPGECXKV[CPFXCIKPCCPFKPƀCVGF
CſUVCPFEQORTGUUVJGCQTVCCICKPUVVJGNWODQUCETCN
vertebrae.
• The tube is inserted into a condom and
terine packing
securely tied with a sterile string.
• The tube with the condom is inserted into the
Packing the uterine cavity is an effective way to uterine cavity.
control bleeding. This can be used while trans- • The condom is inflated by attaching a syringe
porting the patient to a tertiary center. or an IV infusion set to the catheter.
• Use a gauze long enough to packthe entire • 500–600 mL of saline is usually required.
cavity. • A portion of the catheter extends into the
• Begin at the fundus and proceed downward, vagina and a vaginal pack is inserted to keep
making sure that there is no dead space. it in place.
• Remove pack after 24 hours. • The condom is deflated and removed after
• Insert a Foleby catheter in the bladder to pre- 8–12 hours.
vent urinary retention.
Surgical intervention
Balloon tamponade Surgical intervention is the next step when initial
Intrauterine balloon tamponade is an effective measures and uterine balloon tamponade fails.
method to stop bleeding. The catheter with the The patient is shifted to the operating room.
attached balloon is inserted into the uterine cav- Adequate blood and blood products must be
ity and inflated with 500–600 mL of saline. The kept available. The surgical options are listed in
balloon adapts to the shape of the uterus and Box 43.5.
occludes the venous sinuses. It is removed after Arterial ligation
8–12 hours.
Ligation of the arteries supplying the uterus
Several types of balloons are available com-
reduces pulse pressure and perfusion. Since the
mercially (Bakri balloon, BT-Cath balloon). The
collaterals are abundant, the uterus does not
Glenveigh Ebb Complete Tamponade System
undergo avascular necrosis.
has two balloons and provides uterine and
Uterine artery ligation The uterine artery is
vaginal tamponades (Fig. 43.3). A Sengstaken–
ligated as it turns upward in the broad ligament,
Blakemore tube (used for esophageal variceal
at the level of the uterovesical peritoneal reflec-
bleeding) can be used depending on availability.
tion (O’Leary’s technique). Care should be taken
Condom tamponade is simple, effective, easy to
to avoid the ureter. The suture (polyglactin 910)
use, and ideally suited for resource-poor settings
should initially include part of the uterine myo-
(Fig. 43.4). The procedure is described below.
metrium and then go round the uterine vessel.
• Foley catheter, Ryle’s tube, or a simple rubber Bilateral uterine artery ligation controls bleeding
catheter can be used. in 75% of cases (Fig. 43.5).
CH 43_p641_661_v3.indd 645 18-07-2015 18:05:50

Box 43.5 Surgical procedures for atonic

• Arterial ligation
Ŧ Uterine artery ligation
Ŧ Stepwise devascularization
Ŧ Internal iliac artery ligation
• Uterine compression sutures
Ŧ B-Lynch suture
Ŧ Pereira technique
a. Ŧ Hayman technique
• Hysterectomy
should be ligated as well (Fig. 43.6). Ligating the

ovarian artery in the infundibulopelvic ligament
can reduce the blood flow to the ovary, and it
should be undertaken with caution.
Internal iliac artery ligation Internal iliac
artery ligation is more difficult than uterine
artery ligation and stepwise devascularisation:
this is undertaken only if bleeding is not con-
trolled by the other two procedures. The pos-
terior peritoneum is opened and the common
iliac vessel identified. The internal iliac artery
is located and the anterior division is ligated.
Bilateral internal iliac artery ligation stops hem-
orrhage in 80% of cases.
terine compression sutures

Uterine compression sutures are easier to per-
form than arterial ligation and very effective in
arresting hemorrhage. The sutures compress the
anterior and posterior atonic walls of the uterus,
achieving hemostasis.
b. They are used as first line surgical procedures
by many obstetricians. Several techniques are
Figure 43.4 Condom tamponade. a. A Foley’s catheter
available, but the method most popular is the
is inserted into the condom and securely tied. b. The
condom is inserted into the uterine cavity (not shown in
B-Lynch suture. Chromic catgut or polyglactin
VJGKOCIGKPƀCVGFD[CVVCEJKPICP+8KPHWUKQPUGVYKVJ 910 sutures are used. The suture passes through
500–600 mL of saline. the lower segment, passes over the fundus and
returns again through the lower segment (as
shown in Fig. 43.7). It is tied firmly to compress
the uterus. Transverse and vertical sutures are
placed in the Pereira technique (Fig. 43.8) and
Stepwise devascularization If the bleeding multiple vertical sutures are used in the Hayman
continues, the ascending uterine artery is ligated technique
at intervals as it ascends in the broad ligament.
This reduces the blood flow through the branches
that supply the uterus. Each suture should ysterectomy
include the myometrium and the uterine vessel. Hysterectomy is the last resort when bleeding is
The utero-ovarian vessel, which is the anasto- not controlled by other measures. If blood loss is
mosing branch of the uterine and ovarian vessels, severe and the woman is not hemodynamically
CH 43_p641_661_v3.indd 646 18-07-2015 18:05:50

Poi t o li atio
teri e artery
Figure 43.5 Uterine artery ligation. The uterine artery is ligated as it turns upward in the broad ligament. A part of the
myometrium should be included in the stitch.
Utero o arian
anastomosis
arion artery
tep ise ligation
Uterine artery
Figure 43.6 Stepwise devascularization. The uterine artery is ligated at intervals as it ascends in the broad ligament. The
utero-ovarian vessels should also be ligated.
a. b.
Figure 43.7 B-Lynch suture. a.6JGUWVWTGRCUUGUVJTQWIJVJGNQYGTUGIOGPVIQGUQXGTVJGHWPFWUCPFCICKPVJTQWIJ
the lower segment. b. The uterus is well compressed when the suture is tied.
CH 43_p641_661_v3.indd 647 18-07-2015 18:05:51

Box 43.6 In uries of the genital tract

• Lower genital tract
Ŧ Perineal lacerations
Ŧ Vaginal lacerations
Ŧ Cervical tears
Ŧ Vulvar hematoma
• Upper genital tract
Ŧ Uterine rupture
Ŧ Broad ligament/retroperitoneal hematoma
Box 43.7 isk factors for lower genital tract

in uries
• Episiotomy
Figure 43.8 Pereira sutures. Multiple vertical and • Malpresentations
horizontal sutures placed on the uterus with multiple bites Ŧ Assisted breech delivery
through the subserosa of the uterus. Ŧ Face to pubis delivery
• Fetal macrosomia
• 2TKQTUWTIGT[QPVJGEGTXKZ
stable, a subtotal supracervical hysterectomy Ŧ Conization
may be performed to save time. Ŧ Cerclage
Ŧ Amputation
Selective arterial emboli ation
Occlusion of the uterine vessels with gelatin
particles is effective in 90%–95% of cases. The extension of vaginal or cervical tears or they may
patient must be hemodynamically stable; the follow uterine rupture.
procedure is expensive, needs expertise, and is Risk factors for lower genital tract injuries
available only in tertiary centers. The uterine causing hemorrhage are listed in Box 43.7.
artery is cannulated through the transfemoral
approach and the gelatin particles are injected Clinical eatures o lo er
into the vessel. genital tract injuries
Management of atonic PPH is summarized in
Figure 43.9. Unlike atonic PPH, the bleeding is a continuous
trickle of fresh blood with the uterus well con-
tracted. In case of broad ligament hematoma,
Traumatic postpartum hemorrhage retroperitoneal hemorrhage or vulvar hema-
Bleeding from genital tract injuries is referred toma, the bleeding may not be obvious but the
to as traumatic PPH. This is the second most patient shows signs of hemorrhagic shock. The
common cause of PPH. clinical features of lower genital tract injuries are
The common injuries that give rise to hemor- listed in Box 43.8.
rhage are listed in Box 43.6.
is actors Box 43.8 Clinical features of lower genital tract

in uries
Rupture of an unscarred uterus may result from
obstructed labor, high forceps, or rotational for- • %QPVKPWQWUUVGCF[VTKEMNGQHDNQQF
ceps deliveries. Rupture of a scarred uterus can • Uterus well contracted
occur in normal labor. Uterine rupture is dis- • 5JQEMYKVJQWVGZVGTPCNJGOQTTJCIG
Ŧ Broad ligament hematoma
cussed in Chapter 44, Obstructed labor and uter-
Ŧ Retroperitoneal hemorrhage
ine rupture. Hematomas of the broad ligament
Ŧ Vulvar hematoma
or retroperitoneum can occur due to upward
CH 43_p641_661_v3.indd 648 18-07-2015 18:05:51

tonic PPH
loo loss mL loo loss mL
ytocin infusion units Call for help

njection ergometrine mg V
Monitor pulse P
atch for further blee ing
Promote uterine contraction

esuscitate
Monitor ytocin infusion units
Large bore V line
pulse P njection ergometrine mg V
V flui s
Uterine output njection P α
loo transfusion
minutes oses
lee ing continues
ortic bimanual compression

Uterine balloon tampona e
lee ing continues
urgical inter ention
Uterine artery ligation Uterine compression

tep ise e asculari ation utures
nternal iliac artery ligation
lee ing continues
Hysterectomy
Figure 43.9 Management of atonic postpartum hemorrhage (PPH).
CH 43_p641_661_v3.indd 649 18-07-2015 18:05:51

Diagnosis o lo er aginal lacerations

genital tract injuries Vaginal lacerations usually occur in association
The steps in the diagnosis of lower genital tract with perineal lacerations but can also occur as
injuries are summarized in Box 43.9. isolated tears in the middle or upper vagina,
or in the paraurethral area. Rotational forceps,
anagement o lo er assisted breech delivery, and vacuum extraction
genital tract injuries are common causes.
Vaginal lacerations extending to the fornix
Evaluation of the patient and supportive care
must be examined carefully to ensure that there
should proceed simultaneously as in the case of
is no intraperitoneal extension or broad liga-
atonic PPH. The patient’s pulse, blood pressure,
ment/retroperitoneal hematoma.
and respiration should be monitored; intrave-
nous access should be obtained, and a blood Diagnosis and management
sample should be collected for hematocrit and The vaginal wall must be retracted with a Sims
cross-matching. speculum, and the vagina should be inspected
Once the site of laceration is established, all around. The vaginal fornices should be visu-
volume resuscitation, transfusion, and surgical alized for extension of tears. Bimanual pel-
management of the laceration should proceed vic examination and ultrasonography may be
together. required to exclude broad ligament or retroperi-
Diagnosis and management of individual toneal hematoma.
lower genital tract injuries are described below. Small lacerations that do not bleed can be left
Perineal lacerations alone. Others must be sutured in layers. If intra-
peritoneal or retroperitoneal extension is sus-
Perineal lacerations can result in a significant
pected, laparotomy is indicated. In the absence
amount of blood loss unless prompt repair is
of these, tears involving the fornix can also be
undertaken.
sutured from below.
Diagnosis and management Cervical tear
Diagnosis is by inspection of the lower genital Cervical tears commonly occur at the 3 o’clock
tract under good light. Perineal lacerations can and 9 o’clock positions on the cervix, though
be easily visualized, but the extent of involve- they can occur anywhere on the cervix.
ment of the anal sphincters and anal mucosa Diagnosis and management
must be ascertained. Repair of perineal lacera-
tions is dealt with in Chapter 15, Management of Inspection of the cervix Careful inspection of
normal labor and delivery. the cervix is most crucial for diagnosis of cervical
tears. This is difficult since it is soft and thrown
into folds after delivery. For best visualization
of the cervix, the following procedure must be
Box 43.9 Steps in the diagnosis of lower
followed:
genital tract in uries
• Lithotomy position • The patient should be in the lithotomy
• Adequate light position.
• Inspection of perineum • Adequate light is mandatory.
• Inspection of the vulva • Two Sims speculums are used to retract the
• Inspection of vagina anterior and posterior vaginal walls.
Ŧ Sims speculum • Two sponge holding forceps must be applied
• +PURGEVKQPQHEGTXKZ on the lips of the cervix, beginning anteriorly
Ŧ Sims speculum or posteriorly, at a distance of approximately 2
Ŧ Two sponge holding forceps cm from each other (Fig. 43.10).
• $KOCPWCNRGNXKEGZCOKPCVKQP
• The part of the cervix between the two sponge
• Ultrasonography
holding forceps should be inspected for tears.
CH 43_p641_661_v3.indd 650 18-07-2015 18:05:52

Colporrhexis
Avulsion of the cervix from the vagina is known
as colporrhexis (Fig. 43.12). This can cause intra-
peritoneal bleeding.
Diagnosis and management
Diagnosis is by speculum examination and
bimanual pelvic examination. Laparotomy is
indicated, and the rent can be repaired if small.
If it involves a large area of the cervix and vagina,
hysterectomy may be required.
Laparotomy and repair of the tear is the treat-
ment of choice.
Figure 43.10 Visualization of cervical tear. Two Sims ulvar hematoma
speculums are used to retract the anterior and posterior Vulvar hematoma can occur following normal or
walls of the vagina and two sponge holding forceps are instrumental delivery or episiotomy. Laceration
CRRNKGFVQVJGEGTXKZCDQWVEOCRCTVCPFVJGRQTVKQPQH of an underlying vessel is responsible for the
VJGEGTXKZDGVYGGPVJGHQTEGRUKUXKUWCNK\GF
hematoma (Fig. 43.13).
• The forceps should be moved in a circle around Vulvar hematoma is associated with excruciating
the edges of the cervix, and the entire cervix pain, urinary retention, rectal pain or tenesmus
should be inspected. and sometimes hypovolemia (Box 43.10). A
swelling that is fluctuant and covered with dis-
Small cervical tears <2 cm can be left alone
colored skin may be visible. When the hematoma
if there is no bleeding since they heal rapidly.
Larger ones must be sutured. It is important to
include the apex of the tear; therefore, suturing
should begin above the apex. Absorbable sutures
(chromic catgut/polyglactin 910) should be
used; sutures may be interrupted or continuous
(Fig. 43.11). If the tear extends to the lower seg-
ment, laparotomy is necessary.
Cer ix
pe
ing
forceps rea o a ulsio tear
eo a i al ault
Figure 43.11 Repair of cervical tear. Suturing should Figure 43.12 %QNRQTTJGZKU%GTXKZKUCXWNUGFHTQOVJG
DGIKPCVVJGCRGZQHVJGVGCTCPFRTQEGGFFQYPYCTF vagina.
CH 43_p641_661_v3.indd 651 18-07-2015 18:05:52

Hematoma
Le ator ani
Hematoma
a. b.
Figure 43.13 Vulvar hematoma. a. The hematoma can be visualized as a swelling on the labium majus. b. The
JGOCVQOCKUUWRGTſEKCNVQVJGNGXCVQTCPKOWUENG

Box 43.10 ulvar hematoma
Pelvic examination may reveal a mass in the
• Caused by
broad ligament.
Ŧ laceration of underlying blood vessel
When there is no external bleeding but the
• Occurs following
Ŧ normal delivery
patient is in shock, emergency ultrasound may
Ŧ instrumental delivery be performed to look for broad ligament or ret-
• Clinical features roperitoneal hematoma.
Ŧ 'ZETWEKCVKPIRCKP Immediate laparotomy and repair of the rent
Ŧ Urinary retention is the recommended treatment.
Ŧ Swelling Management of lower genital tract injuries is
Fluctuant summarized in Box 43.11.
%QXGTGFD[FKUEQNQTGFUMKP
Ŧ Hypovolemia
Box 43.11 Management of lower genital tract

is above the pelvic diaphragm, it may be diag- in uries
nosed only by vaginal examination. In women
• Perineal lacerations
who complain of severe pain or inability to
Ŧ Ascertain the degree of tear
void, vulvar hematoma should be thought of Ŧ Suture in layers
and a prompt examination is indicated. • Vaginal tears
Management is by incision and drainage. The Ŧ +PVTCRGTKVQPGCNGZVGPUKQP
clots must be evacuated and bleeding point, if Ŧ Broad ligament hematoma Laparotomy
any, ligated. Often, there is no definite bleeder Ŧ Retroperitoneal hematoma and repair
that is identified. The cavity of the hematoma Ŧ 0QGZVGPUKQP5WVWTGKPNC[GTU
is closed with mattress sutures. Selective angio- • Cervical tear
graphic embolization of the blood vessel has Ŧ 'ZVGPUKQPVQNQYGTUGIOGPV.CRCTQVQO[CPFTGRCKT
been used in cases of intractable hematoma. Ŧ 6GCTUEOPQDNGGFKPI.GCXGCNQPG
Ŧ Tears >2 cm: Suture
Broad ligament hematoma 5JQWNFKPENWFGCRGZ
or retroperitoneal hemorrhage Absorbable suture
These are upper genital tract injuries but may Interrupted/continuous
result from upward extension of vaginal or cer- • %QNRQTTJGZKU.CRCTQVQO[CPFTGRCKTJ[UVGTGEVQO[
• Vulvar hematoma
vical tears or following colporrhexis. As already
Ŧ Incision and drainage
mentioned, external hemorrhage may not be
Ŧ Selective arterial embolization
profuse but the woman may be in shock.
CH 43_p641_661_v3.indd 652 18-07-2015 18:05:52

Secondary postpartum Retained placenta occurs in 2%–3% of deliveries.

There are three clinical situations:
hemorrhage • The placenta is detached but not expelled
Secondary PPH is defined as excessive bleed- (trapped placenta).
ing that occurs between 24 hours and 12 weeks • The placenta has not separated from the uter-
postpartum. It most often occurs in the first 3–4 ine wall but does not invade the myometrium
weeks. It is discussed in Chapter 22, The abnor- (placenta adherens).
mal puerperium. • The placenta is attached to or invades the
myometrium (adherent placenta).
Complications of Adherent placenta is discussed later in this
chapter. The first two conditions are discussed
postpartum hemorrhage here.
As already discussed, PPH is a major cause of
maternal mortality. The complications of PPH isk factors
The risk factors for retained placenta are listed
in Box 43.13.
Sheehan s syndrome
Catastrophic PPH can result in Sheehan’s syn-
drome (pituitary infarction). Severe hypoten- Prevention
sion can cause poor perfusion in the hypo- Active management of the third stage, and avoid-
thalamo-hypophyseal portal system and ing ergometrine before placental expulsion, can
consequent infarction of the anterior pituitary reduce the risk of retained placenta.
gland leading to moderate to severe hypopi-
tuitarism. The most common presentation is
failure of lactation and secondary amenorrhea Trapped placenta
in a woman with a history of PPH (see Chapter
Diagnosis
52, Endocrine disorders).
Trapped placenta usually occurs due to adminis-
tration of injection ergometrine before placental
etained placenta expulsion or mismanagement of the third stage
such as cord traction before signs of placental sep-
The placenta is said to be retained if it is not aration. The uterus may be well contracted and the
expelled within 30 minutes of delivery of the os closed. The lower pole of the placenta may be felt
fetus. When the placenta is retained for lon- through the os, on pelvic examination.
ger than normal, risk of hemorrhage increases.
Management
Box 43.12 Complications of postpartum The management of trapped placenta consists
hemorrhage of measures to aid spontaneous expulsion failing
• *[RQXQNGOKEUJQEM which, manual removal is proceeded with.
Ŧ Renal failure
Ŧ Multiorgan failure
Box 43.13 isk factors for retained placenta
• Transfusion-related complications
• Acute respiratory distress syndrome • Preterm birth
• Infection and septicemia • Previous retained placenta
• Venous thrombosis and embolism • Induced/Augmented labor
• Postpartum pituitary necrosis (Sheehan’s syndrome) • IV ergometrine
• Anemia • Mismanagement of third stage of labor
• Maternal death • Uterine anomalies
CH 43_p641_661_v3.indd 653 18-07-2015 18:05:52

• The first step in the management is to empty If these methods fail and/or if there is profuse
the bladder. bleeding, manual removal of the placenta should
• If the uterus is relaxed, stimulating uterine be resorted to.
contractions with oxytocin may result in pla-
cental expulsion.
• If the uterus is contracted and os is closed,
uterine relaxation is achieved with glyceryl
anual removal o placenta
trinitrate (400 Pg sublingual or 50 Pg intrave- Indications
nous). Close monitoring of blood pressure is
The indications for manual removal of the pla-
mandatory since glyceryl trinitrate can cause
centa are as follows:
hypotension. The placenta can be removed by
controlled cord traction or manually. • Placenta adherens with profuse bleeding and/
• If these measures fail, manual removal of the or not responding to other methods
placenta is required. • Trapped placenta not responding to other
methods
Placenta adherens
Diagnosis Procedure
Failure of placental separation is usually due to • Shift the patient to the operating theater.
defective myometrial contractions in the area • Administer prophylactic antibiotics (1 g of
underlying the placenta. It may also be due to ampicillin +500 mg metronidazole IV, just
generalized uterine atony. The placenta may before the procedure, followed by oral amoxi-
separate partially, giving rise to profuse bleed- cillin 500 mg 6 hours later).
ing. The uterus may be relaxed on palpation. • The procedure should be performed under
Ultrasonography can also be used to differ- general anesthesia, preferably with halothane
entiate between trapped placenta and placenta for uterine relaxation.
adherens. In trapped placenta, the myometrium • The patient should be in the lithotomy
is thick all around and a clear demarcation is position.
seen between the placenta and myometrium. • Hold the umbilical cord with the left hand and
keep it taut. This helps in guiding the right
Management hand up to the placenta (Fig. 43.14).
• Under aseptic precautions, insert the
The management of placenta adherens consists right hand with fingers kept close together
of the following steps: (accoucher’s hand) and proceed along the
stretched cord into the uterine cavity to the
• Oxytocin promotes uterine contractions and
placenta.
separation of the placenta. It is administered
• Once the placenta is located, place the left
as IV infusion (20 units in 500 mL of saline) or
hand on the uterine fundus.
intramuscular injection (10 units IM),
• Insert the margin of the right hand into the
• The umbilical vein is catheterized with size
plane between the placenta and the uterine
10 nasogastric tube and one of the following
wall. Proceed to separate the placenta from
injected:
the uterine wall along this plane of cleavage.
– Normal saline
• Once the placenta is fully separated, remove
– PGF2D (20 mg in 20 mL of saline)
it by grasping it with the hand as the hand is
– Oxytocin (50 units in 30 mL of saline)
withdrawn, keeping the left hand on the uter-
– Misoprostol (800 Pg dissolved in 30 mL of
ine fundus to ensure that the uterus is well
saline)
contracted.
Prostaglandin F2D and misoprostol have been • Start oxytocin infusion (20 units in 500 mL of
shown to be more effective than oxytocin when normal saline) to promote uterine contrac-
injected intraumbilically. tions and prevent PPH or uterine inversion.
CH 43_p641_661_v3.indd 654 18-07-2015 18:05:52

a. b.
Figure 43.14 Manual removal of placenta. a. 6JGEQTFKUJGNFVCWVD[VJGNGHVJCPFVJGſPIGTUQHVJGTKIJVJCPFCTGMGRV
close together (accoucher’s hand) and inserted into the uterine cavity. b. The margin of the hand is inserted into the plane
between the placenta and uterine wall.
Adherent placenta • Placenta increta: The villi invade into the

myometrium.
Adherent placenta is an uncommon but dreaded • Placenta percreta: The villi invade the entire
complication. Morbidity and mortality are high, depth of the myometrium and extend to the
especially with placenta accreta. serosa.
Clinical differentiation between the three
&GſPKVKQP grades of adherent placenta is not possible and
the management is essentially the same. Hence
Adherent placenta is an abnormality of placental
all grades of adherent placenta will be discussed
implantation wherein part or all of the placenta
together as placenta accreta.
is attached to or infiltrates the myometrium. This
is due to the partial or total absence of decidua
basalis and the fibrinoid (Nitabuch) layer. There
are three grades of adherent placenta (Fig. 43.15): Incidence
• Placenta accreta: Anchoring villi attach to the The incidence of placenta accreta is increasing
myometrium. due to the increase in cesarean section rates. It
eci ua
Myomectomy
a. b. . .
Figure 43.15 Adherent placenta. a.0QTOCNRNCEGPVCVJGXKNNKFQPQVKPXCFGVJGO[QOGVTKWOb.2NCEGPVCCEETGVGVJGXKNNK
attach to the myometrium. c.2NCEGPVCKPETGVCVJGXKNNKKPXCFGVJGO[QOGVTKWOd.2NCEGPVCRGTETGVCVJGXKNNKKPXCFGVJG
GPVKTGFGRVJQHVJGO[QOGVTKWOCPFGZVGPFVQVJGUGTQUC
CH 43_p641_661_v3.indd 655 18-07-2015 18:05:53

was 1 in 2500 earlier but has now increased to

Box 43.14 isk factors for adherent placenta
1 in 250 deliveries in the West. The incidence in
India is also on the increase. Placenta accreta • Placenta previa
is most common and occurs in 80%, placenta • Prior uterine surgery
Ŧ Cesarean section
increta in 14%, and placenta percreta in 6% of
Ŧ Myomectomy
cases of adherent placenta.
Ŧ Curettage
• Multiparity
• 5WDOWEQWUſDTQKFU
Etiology and risk factors • Endometrial ablation
Defective decidualization is considered to be the • Uterine irradiation
most important causative factor. This may be
primary but most often is secondary to a previ-
ous cesarean section or uterine curettage. In the Occasionally, placenta percreta may infiltrate
absence of well-formed decidua, the anchoring into the bladder, giving rise to hematuria ante-
villi attach to the myometrium or penetrate it natally. During surgery, separation of the bladder
to varying extents. When the placenta implants from the lower uterine segment is extremely dif-
in the lower uterine segment (placenta pre- ficult in these cases.
via), the risk of placenta accreta is increased.
Combination of a previous cesarean section
and an anterior placenta previa increases the Diagnosis
risk manifold. The risk increases further as the
number of cesarean sections increases. Antenatal
The risk factors for adherent placenta are
Ultrasonography with color Doppler is a sen-
sitive method of antenatal diagnosis of pla-
centa accreta. Three-dimensional sonography
Clinical features improves the sensitivity further (Fig. 43.16).
The sonographic findings of placenta accrete
Placenta accreta is usually diagnosed when the
placenta fails to separate and there is profuse
Magnetic resonance imaging is also useful
bleeding when manual removal is attempted.
The plane of cleavage is not obtained and the • when ultrasonography is inconclusive,
placenta cannot be separated. This is one of • when the placenta is located posteriorly, and
the causes of massive PPH, shock, and mater- • to determine the extent of invasion into the
nal death. bladder and adjacent structures.
a. b.
Figure 43.16 Placenta accreta. a. Ultrasonography shows loss of continuous white line at serosal–bladder interface
(arrow). b.%QNQT&QRRNGTUJQYUKPETGCUGKPVJGXCUEWNCTNCMGUKPVJGRNCEGPVC
CTTQY
Photo courtesy: Mediscan
5[UVGOU%JGPPCK
CH 43_p641_661_v3.indd 656 18-07-2015 18:05:53

When inflated immediately after delivery of

Box 43.15 5
QPQITCRJKEſPFKPIUQHRNCEGPVC
accreta the baby, bleeding reduces.
• The baby is delivered by a classical cesarean
• /[QOGVTKCN VJKEMPGUU
HTQO UGTQUC VQ TGVTQRNCEGPVCN section, avoiding the placental site.
vessels) <1 mm
• No attempt should be made to separate or
• .CTIGKPVTCRNCEGPVCNDNQQFNCMGU
• Loss or thinning of the normal hypoechoic area
deliver the placenta.
behind the placenta (clear space) • The uterine incision should be closed and hys-
• Loss of normal continuous white line at serosal–blad- terectomy proceeded with.
der interface (bladder line) • Pelvic arterial embolization or bilateral inter-
• Focal nodular projections into the bladder nal iliac artery ligation may be performed to
• Color Doppler control hemorrhage, before proceeding with
Ŧ +PETGCUGKPXCUEWNCTNCMGUYKVJVWTDWNGPVƀQY hysterectomy.
Ŧ Hypervascularity of serosal–bladder interface
Placenta accreta diagnosed during

manual removal
This situation is associated with profuse bleed-
Management ing and shock. Prompt resuscitation is essential.
There are two clinical situations: Most women require hysterectomy to control
bleeding. Pelvic arterial embolization, if avail-
• Placenta accreta diagnosed antenatally
able, is a useful adjunct.
• Placenta accreta diagnosed during manual
removal of placenta
Conservation of uterus
Placenta accreta diagnosed
Conservation of the uterus is indicated
antenatally
• when future fertility is desired and
When diagnosed antenatally, maternal out-
• when maternal condition does not permit
come is better. The management should be a
hysterectomy.
well-planned team approach. A senior obstetri-
cian, an anesthetist, and a urologist should work The measures that can be tried for uterine con-
together. servation are as follows:
roce ure • Removal of the placenta piecemeal and mat-

tress sutures over the placental site
If placenta accreta has been diagnosed antena- • Removal of placenta and tamponade by packing
tally, an elective cesraean section is scheduled. • Selective arterial embolization
• The patient and relatives should be counseled • Leaving the placenta in situ and administra-
regarding complications such as massive hem- tion of methotrexate
orrhage, need for blood transfusion, hysterec- • Leaving the placenta in situ and follow-up
tomy, and admission to intensive care unit. All uterine conservative techniques are asso-
• Blood and blood products must be kept ready. ciated with complications as listed in Box 43.16.
• General anesthesia is usually preferred.
• The placenta should be localized and the
extent of penetration of the myometrium and
adjacent structures determined.
• The operative procedure, decision regarding terine inversion
the conservation of the uterus versus hysterec-
tomy, site of incision, and measures to reduce
bleeding should be planned.
&GſPKVKQP
• Preoperative placement of balloon catheters Uterine inversion is the collapse of the uter-
into the internal iliac arteries is controversial. ine fundus into the uterine cavity. This is a rare
CH 43_p641_661_v3.indd 657 18-07-2015 18:05:53

• Fourth-degree inversion: There is complete

Box 43.16 Complications of uterine conserva-
tive techniques inversion of the uterus and vagina.
• Hemorrhage %NCUUKſECVKQPCEEQTFKPI
• Sepsis
• Fistula formation to the time of occurrence
• Uterine necrosis
• Acute: Occurs within 24 hours of delivery
• Need for hysterectomy later
• Subacute: Occurs between 24 hours and 4 weeks
• Maternal death
after delivery
• Chronic: Occurs 4 weeks after delivery
complication that occurs before or after placen-
tal separation and expulsion. Inversion causes
profuse, life-threatening hemorrhage, shock,
Etiology and risk factors
and maternal death. The most common etiological factors are umbil-
ical cord traction and fundal pressure when the
uterus is relaxed especially when the placenta is
Incidence attached at the fundus. The risk factors are listed
Incidence varies from 1 in 2,000 to 1 in 20,000 in Box 43.17.
deliveries.
Clinical features
%NCUUKſECVKQP The usual clinical presentation is sudden profuse
bleeding, hypotension, and shock, before or after
Uterine inversion is classified depending on the
placental delivery. The uterine fundus is either
following:
not palpable abdominally or an obvious dimple is
• The extent of inversion felt over the fundus. Vaginal examination reveals
• Time of occurrence the prolapsed inverted uterine fundus inside the
%NCUUKſECVKQPDCUGFQPGZVGPV Box 43.17 isk factors for uterine inversion

of inversion (Fig. 43.17)
• Fundal attachment of the placenta
• First-degree (complete) inversion: The uterine • Fetal macrosomia
fundus descends into the cavity but does not • Short umbilical cord
protrude through the os. • Uterine overdistension
• Second-degree (complete) inversion: The fun- • Nulliparity
• Rapid labor
dus protrudes through the os.
• Third-degree inversion: The fundus protrudes
• Placenta accreta
through the introitus.
egree egree egree V egree
Uterine
fun us
Cer i
Cer i
Uterine
fun us
ntroitus
Uterine fun us
Figure 43.17 %NCUUſECVKQPQHWVGTKPGKPXGTUKQP6JGHQWTFGITGGUQHWVGTKPGKPXGTUKQPCTGUJQYP
CH 43_p641_661_v3.indd 658 18-07-2015 18:05:53

uterine cavity, in the vagina or outside the introi- • If the placenta is attached to the uterus, ensure
tus. The placenta may be attached to the uterine the following:
wall. The shock is often out of proportion to the – It should not be separated till uterine relax-
blood loss and is considered to be neurogenic, ant is administered and replacement is
due to stretching of the parasympathetic nerves. about to begin.
Ultrasonography reveals an abnormal uterine – The placenta can also be removed manually
contour and the uterine fundus is seen within the after replacing the uterus. This reduces bleed-
cavity. Often there is no time to perform imaging ing but makes replacement more difficult.
since the patient bleeds profusely and is in shock.
Manual replacement
Management
Immediate manual replacement should be
The definitive treatment consists of replac- attempted by placing a hand in the vagina with
ing the uterus to its original position by man- fingers around the inverted fundus and pushing
ual or hydrostatic manipulation. This controls the fundus toward the umbilicus along the axis
the hemorrhage and restores hemodynamic of the vagina (Fig. 43.18).
instability. If the cervix is felt as a constricting ring, one of
the following uterine relaxants is administered:
General measures – Glyceryl trinitrate 50–200 Pg IV
General measures to resuscitate the patient and – Terbutaline 0.25 mg subcutaneous or IV
prepare for manual replacement must be insti- – Magnesium sulfate 4–6 g IV
tuted immediately. – Inhalational anesthetic such as halothane
or enflurane
• Call for help. A senior obstetrician, nurse, and Once the uterus relaxes, manual replacement
anesthetist must be summoned. is performed.
• Stop oxytocin infusion.
• Insert a large-bore intravenous cannula and
begin fluid resuscitation. ydrostatic method
• Draw blood for hematocrit, coagulation ( Sullivan s method)
workup, and cross-matching.
The vagina is filled with warm saline from a bag that
• Start blood transfusion as soon as possible.
is placed at a height above the patient. The obste-
trician’s hand or a ventouse cup is used to close the
eplacement of the uterus introitus and retain the saline in the vagina. The
hydrostatic pressure of saline distends the vagina,
Replacement of the uterus by manual or hydro-
increases the circumference at the vaginal vault,
static method should be attempted first. Surgical
and pushes the uterine fundus up. After the uterus
procedures are warranted only if these fail.
is replaced, oxytocin (20 units in 500 mL of saline) is
• The part that came down last should be replaced given as an infusion to promote uterine contraction
first. The uterine fundus should go in last. and prevent recurrence of inversion.
Figure 43.18 /CPWCNTGRNCEGOGPVQHKPXGTUKQP*CPFKUKPVTQFWEGFKPVQVJGXCIKPCYKVJVJGſPIGTUCTQWPFVJGKPXGTVGF

uterine fundus and the fundus is pushed toward the umbilicus.
CH 43_p641_661_v3.indd 659 18-07-2015 18:05:53

Surgical methods Box 43.18 Surgical interventions for uterine

If manual and hydrostatic methods fail, the inversion
patient must be shifted to the operating the- • Abdominal approach
ater and one of the surgical methods must be Ŧ Huntington procedure: Traction on round ligaments
resorted to. These are listed in Box 43.18. Ŧ Haultain procedure: Incision on the posterior uter-
ine surface to cut the ring
• Vaginal approach
Ab ominal approach Ŧ Spinelli procedure: Incision of constricting cervical
If manual and hydrostatic methods fail, imme- ring anteriorly
diate laparotomy is warranted. The inverted Ŧ Cascarides procedure: Incision of constricting cer-
vical ring posteriorly
uterus appears like a depression or cup within
the constriction ring. The tubes, round liga-
ments and ovaries are pulled into the cup. In
the Huntington procedure, the round ligament
is held with a Babcock or Allis clamp and gen- aginal approach
tle traction applied to pull the fundus up. In the The constriction ring formed by the cervix is incised
Haultain procedure, a vertical incision is made anteriorly (Spinelli) or posteriorly (Cascarides) to
on the posterior uterine surface, the constriction enable the uterus to be replaced. Vaginal surgical
ring is cut, and the uterine fundus is pulled up. procedures are used in chronic inversion.
Key points
• Postpartum hemorrhage (PPH) is a major complication of • +HVJGVGCTGZVGPFUTGVTQRGTKVQPGCNN[QTKPVTCRGTKVQ-
the third stage of labor. It is a leading cause of maternal PGCNN[NCRCTQVQO[KUKPFKECVGF
mortality and accounts for 25% of maternal deaths in
• Secondary PPH is usually due to endometritis or
India.
retained placental tissue. Antibiotics are usually ad-
• Other complications of the third stage include retained ministered for all women with secondary PPH.
RNCEGPVCCFJGTGPVRNCEGPVCWVGTKPGKPXGTUKQPCPF
• 4GVCKPGFRNCEGPVCECPDGFWGVQVTCRRGFRNCEGPVC
COPKQVKEƀWKFGODQNKUO6JGUGCTGNGUUEQOOQPVJCP
RNCEGPVCCFJGTGPUQTRNCEGPVCCEETGVC
RQUVRCTVWOJGOQTTJCIG
22*DWVCNUQECWUGJGOQT-
TJCIGJ[RQVGPUKQPUJQEMCPFOCVGTPCNFGCVJ • Trapped placenta can be removed by controlled
cord traction after administration of glyceryl
• 2QUVRCTVWOJGOQTTJCIGKUFGſPGFCUDNQQFNQUU
trinitrate.
mL following vaginal delivery and >1000 mL following
cesarean delivery. It may be primary or secondary. • 2NCEGPVCCFJGTGPUOC[DGOCPCIGFYKVJQZ[VQEKP
+HPQVUWEEGUUHWNOCPWCNTGOQXCNKUKPFKECVGF
• Primary PPH may be atonic or traumatic. Atonic PPH
KUVJGOQUVEQOOQPECWUGQH22*5GXGTCNTKUMHCE- • Adherent placenta is a rare complication associated
VQTUJCXGDGGPKFGPVKſGF with life-threatening massive hemorrhage. The pla-
centa invades the myometrium and there is no plane
• Prevention of atonic PPH is by active management of
of separation. Adherent placenta is of three types:
the third stage and prophylactic uterotonics.
CEETGVCKPETGVCCPFRGTETGVC
• 1PEGCVQPKE22*QEEWTUOCPCIGOGPVUJQWNFDG
• The most common causes of adherent placenta area
RTQORV'XCNWCVKQPTGUWUEKVCVKQPCPFEQOOWPKECVKQP
previous cesarean section and placenta previa.
should proceed simultaneously.
• +HFKCIPQUGFCPVGPCVCNN[D[WNVTCUQPQITCRJ[RNCPPGF
• Administration of uterotonics should be followed by
management is possible and mortality is less.
bimanual compression of the uterus and aortic com-
RTGUUKQP+HVJGTGKUPQTGURQPUGWVGTKPGVCORQPCFG • +HFKCIPQUGFFWTKPIOCPWCNTGOQXCNDNGGFKPIUJQEM
must be attempted before surgical intervention. and mortality are high.
• $.[PEJUWVWTGUVGRYKUGFGXCUEWNCTK\CVKQPKPVGTPCN • Uterine inversion is a rare complication associated
KNKCECTVGT[NKICVKQPCPFJ[UVGTGEVQO[CTGVJGUWTIKECN YKVJRTQHWUGDNGGFKPICPFUJQEM6JGUJQEMKUJ[RQX-
interventions available for PPH. olemic and neurogenic.
• Traumatic PPH is due to trauma to the upper or • Inversion is managed by replacement of the uterus
lower genital tract. The lower genital tract should be OCPWCNN[J[FTQUVCVKECNN[QTUWTIKECNN[
GZRNQTGFCPFVJGNCEGTCVKQPKFGPVKſGFCPFUWVWTGF
CH 43_p641_661_v3.indd 660 18-07-2015 18:05:53

Self-Assessment
3. %QPFQODCNNQQPVCORQPCFGDNQQFVTCPUHWUKQPCPF
Case-based questions ƀWKFTGRNCEGOGPV
4. Surgical intervention. Laparotomy and B-Lynch
Case 1 UWVWTG+HDNGGFKPIKUPQVEQPVTQNNGFWVGTKPGCTVGT[NK-
/TU)0VJKTFITCXKFCFGNKXGTGFPQTOCNN[CVCNQECN gation and stepwise devascularization. Hysterectomy
JQURKVCN C DCD[ YGKIJKPI MI (QNNQYKPI FGNKXGT[ QH if bleeding continues.
VJGRNCEGPVCVJGTGYCUEQPVKPWQWURTQHWUGDNGGFKPI#V
CFOKUUKQPUJGYCURCNGRWNUGYCUOKPCPFDNQQF
pressure was 90/70 mm of Hg. Case 2
1. 9JCVKUVJGECWUGQHDNGGFKPINKMGN[VQDG! 1. 4GVCKPGFRNCEGPVCRTQDCDN[RCTVKCNN[UGRCTCVGF
2. 9JCVKUVJGKPKVKCNOCPCIGOGPV! 2. #DFQOKPCNGZCOKPCVKQPVQNQQMHQTEQPUKUVGPE[QH
3. 9JCVOGCUWTGUUJQWNFDGVCMGPDGHQTGUJKHVKPIVJG VJGWVGTWU8CIKPCNGZCOKPCVKQPVQNQQMHQTVTCRRGF
RCVKGPVVQCVGTVKCT[EGPVGT! RNCEGPVC1Z[VQEKPKPHWUKQPYKVJWPKVUKPO.
4. 9JCVKUVJGHWTVJGTOCPCIGOGPV! QHUCNKPG+HWPUWEEGUUHWNKPVTCWODKNKECNQZ[VQEKP
injection.
3. 8QNWOGTGUWUEKVCVKQPDNQQFVTCPUHWUKQPCPFOCPWCN
Case 2 removal of the placenta under general anesthesia.
/TU 2& UGEQPF ITCXKFC FGNKXGTGF C NKXG DCD[ IKTN 4. *[RQVGPUKQPUJQEMTGPCNHCKNWTGUGRUKURKVWKVCT[
XCIKPCNN[(QNNQYKPIVJKUVJGRNCEGPVCYCUPQVFGNKXGTGF PGETQUKUCPF5JGGJCPŏUU[PFTQOGCPGOKCXGPQWU
She was shifted to a higher center after waiting for 45 VJTQODQGODQNKUOCPFCEWVGTGURKTCVQT[FKUVTGUU
OKPWVGU6JGRCVKGPVYCUDNGGFKPIJCFJ[RQVGPUKQPCPF syndrome.
YCUNQQMKPIRCNG
1. 9JCVKUVJGFKCIPQUKU! Sample questions
2. 9JCVKUVJGKPKVKCNOCPCIGOGPVQHTGVCKPGFRNCEGPVC!
3. 9JCVKUVJGOCPCIGOGPVPQY! Long-answer questions
4. What are the complications of hemorrhage and
J[RQVGPUKQP! 1. Describe the causes of postpartum hemorrhage.
&KUEWUUKPFGVCKNVJGRTGFKURQUKPIECWUGUFKCIPQUKU
and management of atonic PPH.
Answers 2. Enumerate the important complication of the third
stage of labor. Describe the causes and management
Case 1 of retained placenta.
1. /QUVNKMGN[VQDGCVQPKERQUVRCTVWOJGOQTTJCIGDWV
VTCWOCVQVJGIGPKVCNVTCEVUJQWNFDGGZENWFGFD[ Short-answer questions
GZCOKPCVKQP
1. Traumatic PPH
2. Catheterize the bladder. Insert a large-bore intrave-
2. Predisposing factor for atonic PPH
PQWUNKPGCPFDGIKPQZ[VQEKPKPHWUKQPYKVJWPKVU
3. Inversion of uterus
in 500 mL of normal saline. Obtain blood sample
HQTJGOCVQETKVCPFETQUUOCVEJKPICPFEQPVKPWG 4. Internal iliac ligation
with volume replacement and blood transfusion. 5. Manual removal of placenta
Perform bimanual uterine compression and aortic 6. Vulval hematoma
compression. 7. Placenta accreta
CH 43_p641_661_v3.indd 661 18-07-2015 18:05:53

Obstructed Labor
44 and Uterine Rupture
Case scenario
Mrs. AP, 20, primigravida, was brought from a village with labor pains
for the past 28 hours. She had not undergone regular antenatal checkup
and after the onset of labor had been at home for 24 hours, under the
care of an untrained local dai, who was her neighbor. Since she did not
deliver after all attempts by the dai, she was taken to the local primary
health center. She was told that the baby was big and could not be deliv-
ered vaginally. She was referred to a tertiary center. She looked exhausted
and dehydrated, the lower uterine segment was stretched, the bladder
edematous, and fetal heart sounds could not be heard.
Introduction bstructed labor

Undiagnosed cephalopelvic disproportion, &GſPKVKQP
malpresentations, and fetal anomalies caus-
ing obstructed labor are not uncommon in Obstructed labor results when mechanical causes
developing countries, particularly in resource- prevent the fetus from descending through the
poor rural settings. They are, however, rare pelvis, in spite of good uterine contractions. It
in the developed world. Obstructed labor is contributes to approximately 8% of maternal mor-
associated with high perinatal mortality and tality globally. Obstruction may occur at any level
maternal morbidity and mortality. When left in the pelvis.
undiagnosed or when access to a health care
facility is unavailable, uterine rupture results. Etiology
This is a preventable obstetric catastrophe and Any condition that interferes with the normal
must be avoided. descent of the fetus can give rise to obstruction.
CH 44_p662-669_v3.indd 662 18-07-2015 17:27:49

Obstructed Labor and Uterine Rupture 663
Box 44.1 Causes of obstructed labor Box 44.2 isk factors for obstructed labor
• Cephalopelvic disproportion • Short stature
Ŧ #DPQTOCNRGNXKEEQPſIWTCVKQP • Teenage pregnancy
Ŧ Small pelvis • Uncontrolled diabetes
Ŧ Fetal macrosomia • Lack of transport facilities
• Malpresentations • Lack of access to health facilities
Ŧ Transverse lie
Ŧ Brow
Ŧ Face include short stature that is associated with small
Ŧ Breech
pelvis, teenage pregnancies, and uncontrolled
Ŧ Compound
diabetes with fetal macrosomia (Box 44.2).
• Soft tissue dystocia
Ŧ Cervical stenosis
Ŧ Fibroid in the lower uterine segment Course in labor
Ŧ Ovarian tumors
When there is obstruction to the passage of the
• Fetal anomalies fetus, the uterus continues to contract in an
Ŧ Hydrocephalus attempt to overcome the obstruction. As the uterus
Ŧ Fetal ascites/hydrops contracts, the muscle fibers of the upper segment
Ŧ Fetal tumors become shorter and thicker with each contraction
and those of the lower segment become longer
The most common cause is cephalopelvic dis- and thinner. Ultimately, a demarcation develops
proportion (CPD). This could be due to an between the contracted upper segment and the
abnormal pelvic configuration or a large fetus. stretched lower segment. This is the physiologi-
Malpresentations and fetal anomalies are also cal retraction ring (see Chapter 14, Normal labor:
important causes (Box 44.1). Mechanics, mechanism, and stages).
When there is obstruction to the passage of the
fetus, the process continues; the contracted upper
isk factors segment pushes the fetus further into the lower
Women living in rural areas in developing coun- segment; the demarcation becomes more distinct
tries may be managed by untrained personnel, and is now known as the Bandl’s ring. This ring
due to poor transport facilities preventing access can be palpated abdominally, running transversely
to better care. Malpresentations and CPD, com- or obliquely across the uterus (Fig. 44.1).
plicated by prolonged and obstructed labor, may The lower uterine segment is stretched and
not be diagnosed or may be diagnosed late. This extends higher into the abdomen. The stretched
is the most important risk factor for obstructed lower segment is friable and thin. This condition
labor and uterine rupture. Other risk factors is described as threatened rupture.
hic upper
segment
Upper
segment
an l s raing
Physiological
retraction ring
hin stretche
Lo er segment lo er segment
Figure 44.1 Bandl’s ring. a. Nonpregnant uterus. b. Normal labor. c. Obstructed labor. Bandl's ring. The demarcation
between upper segment and lower segment is not visible in the nonpregnant uterus, becomes obvious in labor and
Bandl's ring forms at the demarcation in obstructed labor.
CH 44_p662-669_v3.indd 663 18-07-2015 17:27:49

The fetal head is jammed in the pelvis, and the

Box 44.3 Clinical features of obstructed labor
urinary bladder is compressed between the pubic
bone and the fetal head. The bladder becomes • History
edematous and is pulled up. Ultimately, this leads Ŧ Prolonged labor
Ŧ Prolonged rupture of membranes
to pressure necrosis of the bladder. This area
sloughs off after 10–14 days, forming a vesicovag-
Ŧ Patient anxious and exhausted
inal fistula. Ŧ Signs of dehydration
As the process continues unrelentingly, the Ŧ Tachycardia
fetus becomes hypoxic and ultimately intrauter- Ŧ Tachypnea
ine death results. Ŧ Fever
With further uterine contractions, the lower Ŧ Evidence of acidosis
segment ruptures (uterine rupture), extruding • Abdominal examination
the fetus and placenta into the peritoneal cavity. Ŧ Uterus tonically contracted
A primigravid uterus contracts vigorously Ŧ Bandl’s ring
initially and may subsequently develop uterine Ŧ Malpresentation or transverse lie
inertia. A multigravid uterus, on the other hand, Ŧ Bladder edematous and pulled up
continues to contract and is more likely to rupture.
Ŧ Cervix not well applied to presenting part
Ŧ Large caput
Clinical features Ŧ Irreducible molding
Ŧ Arm prolapse in transverse lie
The mother has usually gone through prolonged Ŧ /GEQPKWOUVCKPGFHQWNUOGNNKPICOPKQVKEƀWKF
labor before obstructed labor develops. With the
rupture of membranes, amniotic fluid volume
reduces drastically and the uterus hugs the fetus. Box 44.4 istory in obstructed labor
Intra-amniotic infection can occur, especially if • Maternal age
multiple vaginal examinations are performed. • Parity
The woman is dehydrated; there may be acidosis. • Antenatal care
Fetal heart sounds may be irregular or absent. • Time of onset of pains
On pelvic examination, it is usually found that • Time of rupture of membranes
• Multiple vaginal examinations
the cervix is not well applied to the presenting
• Fetal movements
part and hangs loose. There is a large caput and
• Fever
irreducible molding. In transverse lie, the arm
may have prolapsed (Box 44.3).
are important findings for deciding the mode of
delivery (Box 44.5).
Diagnosis
The diagnosis of obstructed labor is by history Management
and clinical examination.
Correction of dehydration, prevention of sepsis,
Patients with obstructed labor are usually
and prompt delivery of the fetus are the key steps
referred from a smaller facility or have been in
in management.
labor at home. On arrival at hospital, a detailed
history should be obtained as given in Box 44.4. • Correct dehydration and acidosis with intrave-
nous dextrose saline and Ringer lactate.
• Send blood for routine investigations such as
Physical examination hematocrit, plasma glucose, creatinine, and
The clinical findings described earlier should be electrolytes.
looked for. The pulse, blood pressure, and tem- • Catheterize and record urine output.
perature should be recorded. The bladder should • If membranes have been ruptured for >18 hours,
be catheterized and urine output recorded. start an antibiotic. Injection ampicillin 2 g IV stat
Uterine contractions, the presence of Bandl’s followed by 1 g IV 6 hourly till delivery is recom-
ring, fetal presentation, station and position, the mended. If the mother has fever or foul-smelling
presence of fetal heart sounds, fetal abnormali- amniotic fluid (suspected chorioamnioni-
ties, cervical dilatation, and foul-smelling liquor tis), in addition, a single daily dose of injection
CH 44_p662-669_v3.indd 664 18-07-2015 17:27:49

Box 44.5 Physical examination in obstructed &GſPKVKQPU

labor
Uterine rupture is the nonsurgical, full-thickness
• Maternal height tear through all layers of the uterine wall with or
• Pulse without expulsion of the fetus.
• Blood pressure In incomplete rupture or dehiscence, all
• Temperature layers of the uterine wall are not separated and
• Urine output
the peritoneum is intact.
• Presentation/position/station
• Fetal heart rate/abnormal EFM trace Incidence
• Cervical dilatation
• /GEQPKWOUVCKPGFHQWNUOGNNKPICOPKQVKEƀWKF Uterine rupture, including incomplete rup-
ture or dehiscence, occurs in 1 in 2000 deliver-
, electronic fetal monitoring. ies in developed countries. In India and other
developing countries, the incidence is 10-fold
higher. The overall incidence varies from 1/100
gentamicin is recommended. It is adminis- to 1/1000. Of these, 50%–60% occur in a scarred
tered in a dose of 3–5 mg/kg (180–300 mg for a uterus.
60 kg woman) in 100 mL of normal saline over Maternal mortality due to uterine rupture in
30 minutes. Discontinue antibiotics when the India is 6%–9%. Perinatal deaths occur in 80% of
mother is afebrile for 48 hours. uterine rupture.
• Exclude uterine rupture by clinical examina-
tion and if necessary, by ultrasonography.
• Immediate cesarean section is recommended
for all women in obstructed labor, irrespective
Etiology
of the presentation, cervical dilatation, or con- upture of unscarred uterus
dition of the fetus.
• If the cervix is fully dilated, the vertex is at or Most ruptures in an unscarred uterus occur due
below the level of the ischial spines, and the fetus to obstructed labor. Intrauterine manipulations
is dead, craniotomy followed by vaginal delivery such as internal podalic version, trauma, injudi-
is an option. This must be performed in the oper- cious use of oxytocin and other uterotonic agents,
ating theatre by an experienced obstetrician. grandmultiparity, and overdistended uterus are
• During cesarean section, the following precau- other causes (Box 44.6).
tions should be taken:
– Incise the uterovesical peritoneum at a
higher level to avoid damage to the bladder. Box 44.6 Causes of rupture of unscarred uterus
– Make the uterine incision large enough to
• Obstructed labor
avoid lateral extension. Ŧ Cephalopelvic disproportion
– Have an assistant ready to disengage the Ŧ Malpresentations
presenting part through the vagina. Ŧ Soft tissue dystocia
– Anticipate malpresentations and deliver Ŧ Fetal anomalies
appropriately. • Injudicious use of uterotonics
– Explore the uterine incision for downward or Ŧ Oxytocin
lateral extensions after delivering the fetus. Ŧ Prostaglandins
• Intrauterine manipulations
Ŧ Internal podalic version
terine rupture Ŧ Midforceps
Ŧ Destructive operations
Uterine rupture is a life-threatening compli- • Overdistended uterus
cation in obstetrics. Rupture of a uterus with a • Grandmultiparity
previous cesarean section scar is most common. • Congenital uterine anomalies
Ŧ Bicornuate uterus
Rupture of an unscarred uterus is rare in modern
• Placenta accreta
obstetrics. Maternal and perinatal mortality and
• Trauma
morbidity are high in uterine rupture.
CH 44_p662-669_v3.indd 665 18-07-2015 17:27:49

upture of scarred uterus Box 44.8 Clinical features of uterine rupture

• Rupture of unscarred uterus
The majority of uterine ruptures are scar ruptures.
Ŧ Cessation of uterine contractions
This is usually less catastrophic than the rupture
Ŧ Persistent abdominal pain
of an unscarred uterus. These may be incomplete Ŧ Feeling of something giving way
ruptures (scar dehiscence) or complete ruptures. Ŧ Tachycardia
Scar rupture can occur in the conditions listed Ŧ Hypotension
in Box 44.7. The risk is much higher in previous Ŧ Loss of fetal movements
classical cesarean sections and hysterotomies. Ŧ Hematuria
In previous lower segment cesarean sections, use Ŧ Loss of uterine contour
of prostaglandins and oxytocin increases the risk. Ŧ Firm, contracted uterus felt separately
Previous vigorous curettage and uterine perfora- Ŧ Loss of fetal station
tion have also been implicated. Ŧ Fetal parts felt easily
Ŧ Fetal heart rate changes
Ŧ (TGGƀWKFKPVJGCDFQOGP
Clinical features Ŧ Vaginal examination
Vaginal bleeding
upture of unscarred uterus Receding of the presenting part
• Rupture of scarred uterus
When the uterus ruptures, the strong and tonic Ŧ Fetal bradycardia
uterine contractions of obstructed labor subside Ŧ Variable and late decelerations
and there is cessation of pain. The mother com- Ŧ Vaginal bleeding
plains of a feeling of something giving way. Ŧ Persistent abdominal pain
Soon there are signs of intraperitoneal hemor- Ŧ Hematuria
rhage and shock. There is tachycardia, hypoten- Ŧ Signs of intra-abdominal hemorrhage
sion, and persistent abdominal pain. Free fluid may Ŧ All other features as described above
be present in the abdomen. Hematuria indicates
extension of the uterine rupture to the bladder. Antepartum rupture occurs in previous classi-
The fetal movements may be excessive initially cal cesarean section, hysterotomy, and previous
but become less, and the movements may disap- upper segment rent repair. The risk is high in the
pear as fetal hypoxia sets in. Fetal bradycardia is third trimester, after 34 weeks.
followed by disappearance of fetal heart sounds. As
the fetus gets extruded into the peritoneal cavity, Intrapartum rupture
the uterus contracts and is felt as a globular struc-
Intrapartum ruptures are the most common.
ture; fetal parts are easily palpable superficially.
Fetal heart abnormalities such as bradycardia
There is loss of station of the presenting part as the
and variable and late decelerations are the ear-
fetus moves up into the peritoneal cavity (Box 44.8).
liest sign of lower segment scar rupture in labor.
Maternal tachycardia and hypotension indicate
upture of scarred uterus rupture and intra-abdominal bleeding. Vaginal
bleeding and persistent abdominal pain that
Antepartum rupture
is present even between contractions are other
Rupture during the antenatal period may be silent clinical features. Other signs are similar to those
and present only after fetal compromise occurs. seen in the rupture of an unscarred uterus.
Occult rupture that occurred intrapartum may
Box 44.7 Causes of rupture of a scarred uterus present as persistent abdominal pain and vaginal
bleeding or hematuria.
• Previous cesarean section
Ŧ Classical
Ŧ Lower segment Sites of rupture
• Previous hysterotomy
• Previous myomectomy The site of rupture depends on the etiology.
• Previously repaired uterine rupture
• Rupture due to obstructed labor is in the lower
• Previous vigorous curettage or perforation of uterus
segment, may be a transverse or oblique tear,
CH 44_p662-669_v3.indd 666 18-07-2015 17:27:49

and may extend upwards to the upper segment Intra-abdominal bleeding can give rise to hem-
or downwards to the cervix and vagina. orrhagic shock with all its associated compli-
• Nonobstructive ruptures are usually in the cations such as renal failure and disseminated
upper segment, at the fundus (Fig. 44.2). intravascular coagulation.
• If the uterus is scarred, the rupture happens at Rents in the lower segment can extend to the
the site of the scar. vagina, cervix, or bladder. Rupture of the vaginal
vault is known as colporrhexis. This may be dif-
ficult to repair. Rupture close to the broad liga-
Timing of rupture ments can extend to involve uterine vessels and
Uterine rupture can occur antenatally or in labor. form broad ligament hematomas. Fetal hypoxia
leading to hypoxic ischemic encephalopathy
• Rupture of an unscarred uterus occurs and fetal death are common (Box 44.9).
after prolonged labor or with intrauterine
manipulations.
• Rupture of an upper segment scar can occur Prediction of scar rupture
in the third trimester of pregnancy since the
Prediction of scar rupture has been discussed in
upper segment stretches during pregnancy.
Chapter 20, Cesarean section and management of
This is usually seen in previous classical cesar-
pregnancy with previous cesarean.
ean section, previous uterine rupture, and
myomectomy.
• Scars of previous lower segment cesarean sec-
tion usually rupture in labor. Box 44.9 Complications of uterine rupture
• Maternal
Ŧ Hemorrhage
Differential diagnosis Ŧ Shock
Ŧ Disseminated intravascular coagulation
Other conditions that present with pain, signs of Ŧ Renal failure
hemorrhage, and fetal heart rate changes are pla- Ŧ Extension to adjacent structures
cental abruption, other causes of intra-abdominal Bladder
hemorrhage such as rupture of liver in severe pre- Uterine vessels
eclampsia, and chorioamnionitis. Cervix
Vagina
Ŧ Maternal mortality
Complications • Fetal
Ŧ Hypoxic ischemic encephalopathy
Maternal morbidity and mortality and peri-
Ŧ Perinatal mortality
natal mortality are high in uterine rupture.
a. b. .
Figure 44.2 Uterine rupture. a. Figure shows a vertical uterine rupture extending into the upper segment. b. Image
shows uterine rupture (as depicted in a.) extending into upper segment. c. Fetus is seen in the peritoneal cavity. (Photo
courtesy: Dr Rajnish Samal, Bangalore).
CH 44_p662-669_v3.indd 667 18-07-2015 17:27:49

Diagnosis • Catheterize the bladder; document and moni-

tor urine output.
istory • Perform laparotomy at the earliest. General
anesthesia is preferable.
Diagnosis of uterine rupture is by history and
• The abdominal incision may be transverse,
physical examination. History should focus on
but a vertical incision may give better access
risk factors and symptoms suggestive of rup-
and may be required in some cases.
ture. Physical examination, including general,
• Deliver the fetus that is lying partially or com-
abdominal, and pelvic examination, reveals
pletely in the peritoneal cavity.
signs described earlier. Intrapartum dehiscence
• Identify the site of rupture. The surgical
or rupture is suspected when there are changes
options are as follows:
in fetal heart rate patterns along with maternal
– Repair of rent: This is recommended if the
hypotension and shock, in a woman with pre-
rent is clean and easily repairable and/or the
vious uterine surgery. Ultrasonography may be
mother is desirous of further childbearing.
required when diagnosis is in doubt. The fetus is
The mother should be counseled regarding
seen lying in the peritoneal cavity with the con-
the risk of scar rupture during subsequent
tracted uterus seen separately. Free fluid is pres-
pregnancy. Elective cesarean section should
ent in the peritoneal cavity.
be performed in the next pregnancy at or
before 36 weeks.
Management – Rent repair with sterilization is recommended
Immediate laparotomy is indicated in all women in women who have completed their family.
with uterine rupture. – Total hysterectomy is recommended when
there is fundal rupture, the rent is difficult
• In case of suspected scar dehiscence or rup- to repair, and/or there is profuse uncontrol-
ture, laparotomy should be performed imme- lable bleeding.
diately to save the fetus. – Subtotal hysterectomy may be required in
• If the woman is admitted with clinical find- rare situations when the woman is bleeding
ings of rupture, stabilize her by correction profusely and is hemodynamically unstable.
of hypotension and shock. Start intravenous This procedure is associated with decreased
saline or Ringer lactate through a wide-bore operating time, morbidity and mortality,
cannula or central venous line, pending and duration of hospital stay.
arrival of blood. • Identify injury to other organs such as bladder
• Begin blood transfusion as soon as possible. and ureter and repair accordingly.
Key points
• Obstructed labor is rare in developed countries but • Once a woman is admitted with obstructed labor, she
is still encountered in developing countries. It is an should be hydrated, antibiotics should be adminis-
important cause of perinatal and maternal mortality. tered, and she should be taken for an immediate
cesarean section.
• The most common cause is cephalopelvic dispropor-
tion. Malpresentations, fetal anomalies, and soft tissue • Uterine rupture is a life-threatening complication in
dystocia are other causes. obstetrics. This can occur in an unscarred or scarred
• When there is obstruction to the passage of the uterus.
fetus, the upper segment contracts and the lower • Rupture of an unscarred uterus follows obstructed
segment stretches.The Bandl’s retraction ring forms labor, intrauterine manipulations, or injudicious use of
at the junction of the two segments. This goes on uterotonics or trauma.
to threatened rupture and ultimately rupture of the
• Rupture of a scarred uterus occurs in women with pre-
uterus.
vious cesarean section, myomectomy, hysterotomy, or
• The diagnosis of obstructed labor is by history and rent repair.
physical examination.
(Continued)
CH 44_p662-669_v3.indd 668 18-07-2015 17:27:49


• The clinical presentation in uterine rupture is with signs • If the woman is desirous of further childbearing and
of intra-abdominal hemorrhage, the contracted uterus the rent is clean and repairable, rent repair without
felt separately, and fetal parts easily palpated with loss tubectomy may be an option. Rent repair and steriliza-
of station of the presenting part. tion should be performed if it is technically feasible
• Fetal heart rate abnormalities are the earliest signs of and bleeding is not profuse.
rupture of a scarred uterus. • Hysterectomy is the treatment of choice if there is
• Once rupture is diagnosed, laparotomy should be profuse bleeding and the rent is not repairable.
performed immediately, after stabilizing the mother.
Self-Assessment
4. Rapidly hydrate the patient with normal saline and
Case-based question Ringer lactate, cross-match blood, ask for hematocrit
Mrs. AP, 20, primigravida, was brought from a village with and routine investigations, and start on injection am-
labor pains for the past 28 hours. She had been at home picillin 2 g IV stat and then 6 hourly and single daily
for 24 hours, being taken care of by an untrained dai. Since dose of gentamicin (3–5 mg/kg) in 100 mL of saline
she did not deliver after all her attempts, she was taken to as infusion. Take for a cesarean section as soon as
the local primary health center. She was told that the baby she is stabilized.
was big and could not be delivered vaginally. She was re- 5. Bladder injury while opening uterovesical peritoneum,
ferred to a tertiary center. She looked exhausted and dehy- FKHſEWNV[KPFGNKXGTKPIVJGJGCFUKPEGKVKULCOOGFKP
drated, the lower segment was stretched, the bladder was the pelvis, extension of uterine incision to the uterine
GFGOCVQWUCPFVJGXGTVGZVYQſHVJRCNRCDNG vessels or bladder, and hemorrhage due to friable
lower segment.
2. What history would you ask for?
3. What will you look for on physical examination? Sample questions
4. How will you manage this case?
5. What complications do you expect during cesarean Long-answer question
section?
What are the causes and clinical features of uterine rup-
ture? How will you manage a multigravida with uterine
Answers rupture due to obstructed labor?
1. Obstructed labor with probably threatened rupture.

2. Duration of ruptured membranes, pelvic examinations Short-answer questions
performed by dai, fever, and fetal movements.
3. General examination—pulse, BP, and temperature 1. Bandl’s ring
Abdominal examination—uterine tenderness, Bandl’s 2. Threatened rupture of uterus
ring, and fetal heart rate and abnormalities 3. Causes of obstructed labor
Pelvic examination—foul-smelling or meconium- 4. Complications of ruptured uterus
UVCKPGFCOPKQVKEƀWKFECRWVOQNFKPICPFEGTXKECN
dilatation
CH 44_p662-669_v3.indd 669 18-07-2015 17:27:50

Nonhemorrhagic
45 Shock in Pregnancy
Case scenario
Mrs. AN, 32, was brought to the emergency room with shock, circulatory
collapse, and altered sensorium. She had delivered at a local hospital
2 hours earlier after labor induction with vaginal misoprostol supple-
mented by oxytocin. After delivery, she needed suturing of a cervical tear
but did not have significant postpartum hemorrhage. On examination,
she had cold and clammy extremities; her pulse was 120/min, BP 90/60
mm Hg, and respiratory rate 40/min. She had been referred to a tertiary
care center for management.
Introduction #OPKQVKEƀWKFGODQNKUO
Hypotension with associated shock during
pregnancy and puerperium is an emergency.
&GſPKVKQP
It is most often due to hemorrhage, but there Sudden cardiovascular collapse, altered men-
are other conditions that lead to hypotension tal status, and DIC due to the entry of amni-
as well. Amniotic fluid embolism may go undi- otic fluid, fetal debris, and fetal antigens into
agnosed since the condition is rare and clinical the maternal circulation through maternal
diagnosis is difficult. Sepsis leading to hypo- venous channels in the uterus or cervix is
tension and septic shock can occur follow- known as amniotic fluid embolism syndrome
ing chorioamnionitis and intrapartum sepsis. (AFES). This is believed to be an anaphylactoid
This is not uncommon in developing coun- reaction.
tries. Disseminated intravascular coagulation The following four criteria should be present
(DIC) is a condition that can occur in women to diagnose a case of AFES:
with obstetric complications such as placental
abruption, intrauterine fetal death, and massive 1. Acute hypotension or cardiac arrest
hemorrhage due to any cause. 2. Acute hypoxia
CH 45_p670-682_v3.indd 670 18-07-2015 16:19:12

Nonhemorrhagic Shock in Pregnancy 671
3. Coagulopathy or severe hemorrhage in the Pathogenesis

absence of other explanations
4. All of these should occur during labor, cesar- Amniotic fluid embolism syndrome is a sud-
ean delivery, dilation and evacuation, or den serious event that occurs usually in the few
within 4 hours postpartum with no other hours before or after delivery. The exact patho-
explanation of findings genesis of this syndrome has not been worked
out. Even though amniotic fluid in variable
quantities enters the maternal circulation in a
Incidence good proportion of women during labor, only a
Amniotic fluid embolism syndrome is a rare small number develop hypoxic shock and circu-
condition, and the incidence is 1–12 cases per latory failure. Therefore, it is thought that it is an
100,000 deliveries. unpredictable idiosyncratic reaction. The shock
is due to an anaphylactoid reaction to fetal anti-
gens in the amniotic fluid. The physical presence
isk factors of amniotic fluid debris in the pulmonary capil-
There are two basic events that result in this lary bed and maternal immunologic and inflam-
complication: matory reactions to fetal antigens in the amni-
otic fluid are implicated in the pathogenesis of
• A breach in the physical barrier between the syndrome.
mother and fetus at the endocervical veins,
maternal venous sinuses in the placental bed,
or other sites of uterine trauma, such as lower Phases of AFES
segment incision for cesarean section.
The following phases are described in mothers
• Increase in intrauterine pressure over and
who have AFES:
above the pressure inside these venous chan-
nels. Amniotic fluid enters the maternal • Phase 1: A nondescript prodromal phase of
venous channels through veins that drain the nausea, vomiting, mild tachypnea, mental
uterus or cervix. confusion or agitation, chills, and paresthesiae
in the extremities in some women.
The risk factors can be classified as follows:
• Phase 2: A phase of acute hypoxia and acute
• Conditions that cause opening up of venous pulmonary hypertension that lasts for about
channels in the uterus 15–30 minutes. Several hours may elapse
• Situations that lead to a pressure gradient between the entry of amniotic fluid and the
between the uterus and cervix on the one hand occurrence of hypoxia. Vasospasm in the
and maternal venous channels on the other pulmonary vasculature, acute pulmonary
hand (Box 45.1) hypertension, and features of acute right ven-
tricular failure have been demonstrated by
transesophageal echocardiography during
Box 45.1 4
KUMHCEVQTUHQTCOPKQVKEƀWKF this early phase of AFES. A gross–ventilation
GODQNKUOU[PFTQOG perfusion mismatch ensues. Large areas of
• Opening up of venous channels in the uterus
the alveolar surface are ventilated but not per-
Ŧ Placenta previa fused. Unoxygenated blood is shunted into the
Ŧ Abruption of placenta pulmonary veins and into the left heart. This
Ŧ Cervical lacerations leads to acute hypoxia and the PaO2 and oxy-
Ŧ Uterine atony gen saturation decrease.
Ŧ Cesarean section • Phase 3: A phase of acute left ventricular (LV)
Ŧ Instrumental delivery failure sets in after 3–4 hours. The contributing
• Situations causing undue increase in intrauterine factors for LV dysfunction are
pressure – hypoxic injury to the left ventricle;
Ŧ Labor induction
– cardiodepressant immunologic and inflam-
Ŧ Precipitate labor
matory mediators released by the mother’s
Ŧ Eclampsia
immune system;
CH 45_p670-682_v3.indd 671 18-07-2015 16:19:12

– direct depressant effect of amniotic fluid on levels are elevated in some women with AFES.
the left ventricle. These observations support an immunologi-
Left ventricular failure decreases cardiac cally mediated inflammatory response leading
output and leads to tachycardia and hypoten- to damaged alveolocapillary membrane and
sion. Further, LV failure also causes an increase leakage of fluid into the pulmonary interstitium
in the hydrostatic pressure at the venous end which damages the alveolar capillary membrane
of pulmonary capillaries and contributes and causes a leak of fluid.
to pulmonary edema. This in turn worsens In women who survive the first few hours
hypoxia. With supportive therapy, this acute after the hypoxic hypotensive episode, recovery
LV dysfunction is reversible. is usually rapid. This is in sharp contrast to non-
• Phase 4: A few hours after the early pulmonary cardiogenic pulmonary edema in women with
edema, leakage of fluid into the alveoli occurs adult respiratory distress syndrome where recov-
due to damaged alveolar–capillary membrane. ery may take several days.
This is presumably due to local inflammatory The sequence of events is depicted in
mediators. Figure 45.1.
• Phase 5: Disseminated intravascular coagula-
tion and consumption coagulopathy ensue.
The fetal material in maternal circulation %QORNKECVKQPU
probably triggers DIC.
With the decline in maternal mortality due to
Serum complement is low, serum inflamma- sepsis and hemorrhage in developed countries,
tory markers are elevated, and serum tryptase AFES has emerged as an important cause for
pen enous channels in uterus

ncrease intrauterine pressure
isseminate intra ascular mniotic flui fetal ebris an

coagulation antigens enter circulation
ausea omiting
Pro romal phase
tachypnea chills
Ventilation perfusion
cute hypo ia
mismatch
Pulmonary hypertension
cute right heart failure
Hypo ic injury to the left entricle
Car io epressant effect of
amniotic flui
cute left entricular failure achycar ia

Hypotension
amage to al eolar capillary

membrane
Pulmonary e ema
Figure 45.1 2CVJQIGPGUKUCPFRJCUGUQHCOPKQVKEƀWKFGODQNKUOU[PFTQOG

#('5
CH 45_p670-682_v3.indd 672 18-07-2015 16:19:12

maternal mortality accounting for 10%–20% of

Box 45.3 %
NKPKECNHGCVWTGUQHCOPKQVKEƀWKF
maternal deaths. In developing countries, the GODQNKUOU[PFTQOG
actual figures for the incidence of AFES and
maternal mortality due to this complication are • Onset
Ŧ Sudden onset
not available.
Ŧ Just before or in labor
Maternal mortality in AFES used to be
Ŧ Within 4 hours of delivery
approximately 80% earlier. With current man- • Symptoms
agement strategies this has now declined to Ŧ Tachypnea
approximately 20% in developed countries. In Ŧ Restlessness
underresourced areas, the prognosis continues Ŧ Nausea, vomiting
to be dismal. Ŧ Paresthesia
There is considerable morbidity in surviving Ŧ Altered sensorium
mothers. Of the survivors, 60%–80% suffer sig- Ŧ Convulsions
nificant neurologic damage. Neonatal mortality Ŧ Coma
is 20%–60% and approximately 50% have neuro- • Signs
logic sequelae. Ŧ Cold extremities
Ŧ Hypotension
The complications of AFES are listed in
Ŧ Crepitations and rhonchi
Box 45.2.
Ŧ Bleeding from venipuncture sites
Ŧ Vaginal bleeding
%NKPKECNHGCVWTGU
The majority of women with AFES present just • Hematocrit may be low; peripheral smear
before or during labor or in the first 4 hours after may show thrombocytopenia and fragmented
delivery. Rarely, they may present with shock up red blood cells schistocytes if the woman has
to 48 hours after normal or instrumental delivery DIC.
or after a cesarean section. Amniotic fluid embo- • Serum creatinine may be elevated and serum
lism syndrome has also been reported after first electrolytes show metabolic acidosis with an
or second trimester abortion, amniocentesis, or anion gap >20, indicating lactic acidosis.
abdominal trauma. Clinical features are given in • Chest X-ray shows pulmonary infiltrates and
Box 45.3. loss of lung volume.
• Electrocardiography (ECG) shows sinus tachy-
cardia, acute right ventricular strain pattern,
Investigations or ventricular arrhythmia. The cardiac rhythm
Since AFES is an emergency, investigations and may be irregular.
resuscitative measures must proceed simulta-
neously. Investigations are aimed at evaluat-
ing the woman’s condition rather than aid in
&KHHGTGPVKCNFKCIPQUKU
diagnosis. As evident from the above description, the clin-
ical features overlap widely with a number of
• At admission to the emergency room, pulse
conditions that cause hypotension and acute ill-
oximetry shows severe hypoxia (saturation
ness in a woman in labor or postpartum. These
<60%). Blood gas studies show hypoxia, meta-
bolic acidosis, and hypocapnea (PCO2 <30).
• Obstetric conditions such as placental abruption,
uterine rupture, uterine atony, and eclampsia
• Medical conditions such as septic shock, pul-
Box 45.2 %
QORNKECVKQPUQHCOPKQVKEƀWKF
GODQNKUOU[PFTQOG monary embolism, air embolism, anaphylaxis,
massive aspiration, transfusion reaction, and
• Maternal mortality peripartum cardiomyopathy
• Neurologic sequelae in mothers
• Anesthetic problems such as high spinal anes-
• Neonatal mortality
thesia or anaphylactic reaction to local anes-
• Neurologic sequelae in neonates
thetic agent
CH 45_p670-682_v3.indd 673 18-07-2015 16:19:12

Diagnosis Management
A high index of suspicion, quick diagnosis, and There is no specific drug or antidote to counter
immediate resuscitative measures are the key to the chain of events that occur in AFES.
successful outcome in AFES. The aim of treatment is to correct the phys-
iological abnormalities such as hypoxia, hypo-
• Diagnosis is mainly clinical. Most often the tension, and consumption coagulopathy so that
diagnosis is arrived at by an analysis of the maternal cerebral hypoxia, acute renal failure,
sequence of events and by a process of exclu- and fetal hypoxic ischemic encephalopathy
sion of other obstetric emergencies that pre- are prevented. All women with suspected AFES
sent in similar fashion. Amniotic fluid embo- should be managed in a well-equipped ICU in a
lism must be considered when a woman tertiary care institution.
without significant blood loss during or fol-
lowing delivery presents with respiratory dis- • Admit the woman in the ICU.
tress, hypotension, and shock (Box 45.4). • Administer oxygen through venturi mask
• There are no confirmatory laboratory tests. (high-flow oxygen therapy).
• If the patient has a pulmonary artery catheter • Connect to ECG monitor.
inserted, samples drawn may show amniotic • Insert bladder catheter and record urine output.
fluid debris, but this is only supportive evi- • Place a central venous pressure (CVP) line.
dence and not confirmatory evidence. • Send blood sample for Hb, peripheral smear
• Serological tests for TKH2 (a fetal antigen blood culture, electrolytes, serum creatinine,
present in maternal lung) and insulin-like liver function tests (LFT), prothrombin time,
growth factor–binding protein 1 (IGF–BP1) and partial thromboplastin time. If the woman
are research tools and not available for routine has oozing from venipuncture sites, send for
clinical use. a full DIC workup. Send a sample for blood
grouping and cross-matching.
• Place an intra-arterial line and send for blood
gases.
• Monitor ECG, blood pressure, hourly urine
Box 45.4 &
KCIPQUKUQHCOPKQVKEƀWKFGODQNKUO output, oxygen saturation, and blood gases.
U[PFTQOG • Use IV fluids very carefully to maintain an
• History hourly urine output of >30 mL and a CVP of
Ŧ Risk factors approximately 10 cm.
• Clinical features • If PaO2 is <65%, intubate and ventilate to main-
Ŧ Sudden onset tain optimal oxygen saturation. If hypotension
Ŧ During or after labor is not corrected, start norepinephrine or dopa-
Ŧ Symptoms and signs mine infusion. If woman has DIC and is bleed-
Tachycardia, tachypnea ing, use packed cells, platelet concentrates,
Hypotension
and fresh frozen plasma to correct coagulation
Acute right ventricular failure
abnormality and to maintain an Hb of 10 g/dL.
Left heart failure
Pulmonary edema
Hypoxia 1DUVGVTKEOCPCIGOGPV
DIC
Ŧ Investigations
If AFES occurs intrapartum, a decision must be
Pulse oximetry made regarding immediate delivery and mode
Blood gas analysis of delivery. Urgent delivery is indicated if there
- Hypoxia is nonreassuring fetal status on electronic fetal
- Metabolic acidosis monitoring, if there is rapid progressive deteri-
Chest X-ray oration of the mother’s clinical status, or if deliv-
- Pulmonary infiltrates ery would save the mother’s life. Vaginal delivery
Platelet count is reasonable if the cervix is fully dilated and the
DIC workup fetal head has descended to at least +2 or +3 sta-
D C, disseminated intravascular coagulation. tion. Otherwise an emergency cesarean section
CH 45_p670-682_v3.indd 674 18-07-2015 16:19:12

is indicated. If there is significant coagulopa- • Tachypnea

thy, this should be concurrently controlled with • Leukocytosis (WBC count >12,000/μL) or leu-
blood products. Adequate packed cells, fresh fro- kopenia (WBC count <4000/μL)
zen plasma, and cryoprecipitate should be avail- • Thrombocytopenia
able in the operation room. • Hypoxemia
• Oliguria
• Increased serum creatinine
Septicemia and Septic As the sepsis worsens, severe sepsis is diagnosed
shock by the appearance of the following signs:
• Hypotension
The sepsis syndrome is a continuum. It consists of
• Worsening oliguria
an initial phase of bacteremia followed by a sys-
– Urine output, 30 mL/hour for 2 hours
temic inflammatory response syndrome (SIRS)
• Worsening renal failure
in the host. If treatment is delayed, septic shock
– Serum creatinine >2 mg/dL
ensues followed by multiorgan dysfunction and
• Acute lung injury
death. Progression of symptoms is rapid and delay
• Serum bilirubin >2 mg/dL
in initiating treatment can lead to a fatal outcome.
• Platelets <100,000 mm3
The systemic inflammatory response syn-
• Prothrombin time >1.5 (INR)
drome is a constellation of features that represent
the host response to different stimuli, including In the presence of gram-negative organisms
trauma, ischemia, inflammation, and infection. and, occasionally, with gram-positive organisms
The clinical features are alteration in body tem- endotoxins are released, leading to septic shock
perature (hyperthermia or hypothermia), chills (described in detail later in the chapter).
and rigors, tachycardia or bradycardia, hypoten-
sion, tachypnea, and metabolic acidosis.
Incidence
&GſPKVKQPU Sepsis in pregnant women is less common (inci-
dence 0.3%) than in the general population (inci-
The definitions of the terminology used in sepsis dence 0.6%). The incidence of septic shock is
syndrome are given below. estimated to be 1 in 8000. However, septic shock
is a common cause of maternal and neonatal
• Bacteremia occurs when bacteria enter the
mortality particularly in developing countries
bloodstream from a site of infection. Blood
such as India. Maternal mortality can reach 13%
cultures are usually positive for the concerned
in severe sepsis and up to 30% in septic shock.
pathogen.
Neonatal mortality can be as high as 40%.
• Sepsis is proven or probable infection with
systemic manifestations.
• Septic shock refers to sepsis-related hypoten- Predisposing factors
sion that persists in spite of adequate fluid
replacement. Septicemia and septic shock usually occur
following maternal infection at one of the fol-
lowing sites:
%NKPKECNETKVGTKCHQTVJG • Pyelonephritis due to anatomic alterations in
diagnosis of sepsis the renal tract in pregnancy
• Endometritis in the puerperium due to a large
Infection and bacteremia may lead to sepsis,
area of denuded maternal tissues exposed to
which is diagnosed by the presence of the fol-
bacteria
lowing signs:
• Septic abortion where inadequate evacuation
• Fever (temperature >38.3°C or 101°F) or hypo- of the products provides a nidus for bacterial
thermia (temperature <36°C or 97 °F) proliferation
• Tachycardia • Perforation of the uterus with peritonitis
CH 45_p670-682_v3.indd 675 18-07-2015 16:19:13

• Infection of surgical wounds (cesarean sec- • There is concomitant myocardial depression

tion, episiotomy) where a breach in the skin is and this further aggravates the situation.
liable for bacterial contamination • The alveolar capillary membrane is damaged
and there is exudation of fluid into the lungs
$CEVGTKQNQI[ leading to adult respiratory distress syndrome
(ARDS).
Pelvic infection leading to septicemia is usually
• A similar cascade is initiated by gram-positive
caused by gram-negative aerobes and anaer-
organisms and their exotoxins.
obes. Gram-positive organisms are more com-
• The pathogenesis of septic shock is summa-
mon in wound infections. The causative organ-
rized in Figure 45.2.
isms and the toxins involved vary depending on
the site and are listed in Table 45.1.
Pathogenesis of septic shock ram negati e bacteria

enter bloo stream
The pathogenesis of septic shock due to gram-
negative infections has been worked out in detail.
The concept has been extended to gram-positive
infections. elease of lipopolysacchari e en oto in
• Gram-negative organisms release a bacterial

lipopolysaccharide (LPS) called ‘endotoxin.’
• The endotoxin activates an inflammatory cas-
cti ation of inflammatory casca e
cade in the host resulting in release of inflam-
matory mediators. This is responsible for the
hemodynamic changes.
• Systemic inflammatory response results in ystemic inflammatory response syn rome
ncrease capillary permeability
release of cytokines. The cytokines cause
Vaso ilatation
increased capillary permeability and activate
the coagulation system.
• The first event is increased capillary perme-
ability and consequent massive leak of fluid Lea age of flui into the interstitium
into the interstitium. hypotension tachycar ia
• Concurrently, there is vasodilatation leading to
tachycardia and hypotension. The extremities
feel warm—‘warm shock.’ If this phase is not ecrease renal perfusion
aggressively treated with IV fluids and broad- isseminate intra ascular coagulation
Multiorgan failure
spectrum antibiotics, renal perfusion declines,
ult respiratory istress syn rome
urine output drops, the coagulation cascade
is activated, and DIC and multiorgan failure Figure 45.2 Pathogenesis of septic shock.
ensue.
6CDNG Causative organisms and toxins
Location of infection Causative organism Toxin

Pyelonephritis coli lebsiella Pseudomonas 'PFQVQZKP
.25
Endometritis Same as above
Pelvic infection Same as above and anaerobes 'PFQVQZKP
.25
Septic abortion Same as above and anaerobes 'PFQVQZKP
.25
Wound infection Group A hemolytic streptococci Toxic shock like exotoxin
Staphylococcus aureus TSST1
Methicillin-resistant SA Superantigen
Clostridium perfringens Exotoxin
PS, lipopolysaccharide; SA, Staphylococcus aureus; SS , toxic shock syndrome toxin1.
CH 45_p670-682_v3.indd 676 18-07-2015 16:19:13

%NKPKECNHGCVWTGUQHUGRVKEUJQEM Box 45.5 Diagnosis of septic shock

There is abrupt onset of fever, chills, and tachy- • History
cardia during bacteremia. Ŧ Risk factors
Septic shock has the following phases: Septic abortion
Puerperal endometritis
• Warm phase—phase of peripheral vasodilata- Pyelonephritis
tion Wound infection
– Tachycardia • Symptoms and signs
– Hypotension Ŧ (GXGTEJKNNU
– Warm extremities due to vasodilatation Ŧ Hypotension
– Low CVP due to marked decrease in intra- Ŧ Tachycardia
vascular fluid volume Ŧ Tachypnea
• Evidence of multiorgan failure
• Cold phase—phase of peripheral vasoconstric-
Ŧ Oliguria/anuria
tion
Ŧ Respiratory distress
– Elevated CVP due to cardiac failure Ŧ Disseminated intravascular coagulation
– Poor tissue perfusion and lactic acidosis Ŧ Cardiac failure
– Tachypnea Ŧ Altered sensorium
– Adult respiratory distress syndrome
– Altered sensorium
– DIC
• Multiorgan failure due to hypotension and • Treatment is directed toward correcting the
DIC hemodynamic derangements caused by the
– Acute renal failure endotoxin.
– Altered LFT • The woman is admitted to the ICU.
– Respiratory failure • IV access is established through a central vein;
– Cardiac failure blood samples are collected for hemogram,
culture, creatinine, electrolytes, LFTs, pro-
Diagnosis thrombin time, and aPTT.
• The bladder is catheterized and urine sent for
A high index of suspicion is necessary to rec-
culture.
ognize sepsis early. Unexplained tachycardia, a
• Rapid infusion of IV normal saline 2–4 L to get
spike of fever, and chills with concurrent drop
the CVP up to 8–12 cm and to maintain a urine
in blood pressure should prompt early interven-
output of 30–50 mL/hour is mandatory.
tion. As outcome is critically dependent on early
• Oxygen is administered through venturi mask
initiation of treatment, early recognition is of
to achieve a saturation of >95% and PaO2 of
paramount importance. Diagnostic features are
>65%. If this is unsuccessful, the patient may
listed in Box 45.5.
need to be intubated and ventilated.
• In patients in whom hypotension persists
Management even after rapid IV fluid administration, pres-
When sepsis is suspected, a three-pronged strat- sor agents (dopamine, norepinephrine, dobu-
egy is instituted. All the steps are undertaken tamine) may have to be considered.
concurrently to • In patients with established acute renal failure,
dialysis may be necessary till renal function
• initiate emergency goal-directed treatment; improves.
• identify the organism and antibiotic therapy;
and +FGPVKſECVKQPQHQTICPKUOU
• find the source of infection.
CPFCPVKDKQVKEVJGTCR[
'OGTIGPE[IQCNFKTGEVGFVTGCVOGPV Appropriate antibiotic therapy is the mainstay of
treatment of sepsis.
Goal-directed treatment consists of initial resus-
citative measures to achieve hemodynamic • Blood, urine, and pus are sent for culture.
stability. Pending culture reports, antibiotics are started
CH 45_p670-682_v3.indd 677 18-07-2015 16:19:13

6CDNG #PVKDKQVKEVJGTCR[KPUGRVKEUJQEM
In ection #PVKDKQVKETGEQOOGPFGF
Initial therapy
Secondary level hospital
Gram negative infections Ampicillin or augmentin & gentamicin IV
Anaerobes suspected Add metronidazole or clindamycin
ertiary level hospital
ESBL gram-negative infections Meropenem or aztreonam
A itional therapy
Surgical wound infections
Suspected staphylococcal infection Cloxacillin
Suspected MRSA Vancomycin/linezolid
Suspected Group A E-hemolytic High dose Benzyl penicillin 20,00,000
streptococci units 24 hourly
ecroti ing fasciitis Add clindamycin
Suspected clostridial myositis High dose benzyl penicillin and
clindamycin/metronidazole
SB , extended spectrum beta lactamase; SA, methicillin-resistant Staphylococcus aureus.
against gram-negative, gram-positive, and activation of the intrinsic pathway of coagula-

anaerobic bacteriae. tion and consumption of coagulation factors
• The choice of antibiotics is given in Table 45.2. with a resultant bleeding diathesis.
+FGPVKſECVKQPQHUKVGQHKPHGEVKQP 0QTOCNEQCIWNCVKQPRCVJYC[
Unless the site of infection is identified and the An outline of the normal coagulation and fibri-
pus or infected tissue removed, it is not possible nolysis cascades is shown in Figure 45.3.
to eradicate the infection.
• Site of infection is identified by clinical %JCPIGUKPPQTOCNRTGIPCPE[
examination, ultrasonography, computer-
ized tomography, and/or magnetic resonance Pregnancy is considered to be a compensated
imaging when required. hypercoagulable state due to the changes that
• If the uterus is found to be gangrenous, an occur in the coagulation pathways. This explains
emergency hysterectomy may be lifesaving. the tendency for DIC in the face of additional
Pelvic abscess should be drained by colpot- insults in pregnancy. The physiological changes
omy. Laparotomy is indicated when there is in pregnancy are as follows:
intra-abdominal collection of pus. • Platelet counts marginally decrease, but plate-
let aggregation increases.
• There is an increase in fibrinogen and factors
Disseminated VII, VIII, IX, and X.
KPVTCXCUEWNCTEQCIWNCVKQP • Thrombin activation is enhanced.
• The fibrinolytic pathway as represented by
plasmin activity is partly suppressed.
&GſPKVKQP
Disseminated intravascular coagulation (DIC)
is defined as activation of coagulation in the
%CWUGUQH&+%KPRTGIPCPE[
microcirculation by (a) entry of large amounts The most serious forms of DIC are still encoun-
of tissue thromboplastin into the circulation tered in obstetric practice. It was in fact first rec-
or (b) widespread endothelial injury leading to ognized in placental abruption. The obstetric
CH 45_p670-682_v3.indd 678 18-07-2015 16:19:13

a a a a
Collagen rauma
n othelial amage issue factor
a V V a
a
V a Prothrombin
a a a a
Va
Ca ibrinogen
b a a nhibits
hrombin a
ibrin
Plasminogen
Plasminogen acti ator a
Plasmin ibrin clot
ibrinogen fibrin split pro ucts imers

Figure 45.3 0QTOCNEQCIWNCVKQPCPFſDTKPQN[VKERCVJYC[U
conditions where DIC is encountered and the

Box 45.6 %
CWUGUQHFKUUGOKPCVGFKPVTCXCUEWNCT
pathogenesis are given in Box 45.6. EQCIWNCVKQPCPFRCVJQIGPGUKU
%QORNKECVKQPU Ŧ Large amounts of thromboplastin at the site of
abruption
Disseminated intravascular coagulation ad- • #OPKQVKEƀWKFGODQNKUO
versely affects maternal and fetal outcome. With Ŧ (GVCNUSWCOGUHGVCNCPVKIGPU
severe DIC there is a significant increase in ma- Ŧ Anaphylactoid reaction
ternal mortality. Perinatal mortality is 30% in the • Sepsis syndrome
presence of severe DIC. Ŧ Endotoxins and exotoxins
Ŧ 5[UVGOKEKPƀCOOCVQT[TGURQPUGU[PFTQOG
Ŧ Cytokine storm
%NKPKECNHGCVWTGU Ŧ Endothelial injury
Clinical features include bleeding from various • Eclampsia and HELLP syndrome
Ŧ Endothelial injury
sites, symptoms due to clotting in microcircu-
• Intrauterine death of the fetus
lation and end-organ failure, and CNS hypoxia.
Ŧ Release of thromboplastin from placenta
The clinical features of DIC are listed in Box 45.7. • Acute fatty liver of pregnancy
Ŧ Endothelial injury
Diagnosis Ŧ Decreased production of coagulation factors from
liver
A diagnosis of DIC may be suspected clinically P, hemolysis, elevated liver enzyme levels, and low platelet
but must be confirmed by laboratory tests. levels.
CH 45_p670-682_v3.indd 679 18-07-2015 16:19:13

can be performed by collecting a blood sample

Box 45.7 %
NKPKECNHGCVWTGUQHFKUUGOKPCVGF
KPVTCXCUEWNCTEQCIWNCVKQP in a plain tube and observing the time taken
for the formation of a clot. In established DIC,
• Bleeding from venipuncture sites the clot may not form for several hours and
• Ecchymoses
even if a clot is formed, it is soft and friable and
• Oozing/bleeding from incisions/ lacerations/ placental site
does not retract.
Ŧ Episiotomy
Ŧ Cesarean section incisions
• All bleeding parameters such as bleeding
Ŧ Profuse vaginal bleeding time, clotting time, prothrombin time, partial
• Hypotension and shock thromboplastin time, and thrombin time are
• Symptoms due to clotting in microvasculature prolonged.
Ŧ Tissue hypoxia and lactic acidosis • The peripheral smear shows thrombocytope-
Ŧ Decreased urine output nia and schistocytes (fragmented RBCs with
Ŧ Metabolic acidosis abnormal shapes).
Ŧ Acidotic breathing • Plasma fibrinogen is markedly decreased
Ŧ Hypoxia and tachypnea (hypofibrinigenemia). High levels of fibrino-
Ŧ Altered sensorium gen and fibrin split products (D-dimers) are
present in the peripheral blood. These are due
to secondary hyperfibrinolysis by the plasmin
• A history of predisposing obstetric events such system. The fibrinogen/fibrin split products
as abruption, sepsis, or amniotic fluid embo- in turn inhibit formation of fibrin and cause a
lism is usually present. vicious cycle.
• Clinical features of bleeding, ecchymoses, or
end-organ failure are sufficient to make a clin-
ical diagnosis. Management
• Further evaluation by laboratory tests is aimed
at confirming the diagnosis and assessing the Management of DIC consists of control of hem-
severity of DIC (Box 45.8). orrhage, replacement of blood and blood prod-
• Whole blood clotting time is markedly pro- ucts, and treatment of the underlying cause.
longed. A bedside test (‘clot retraction test’) • Supportive treatment with the appropriate
blood products is crucial in controlling hem-
orrhage. Packed cells are used for correction
Box 45.8 .
CDQTCVQT[VGUVUKPFKUUGOKPCVGF
KPVTCXCUEWNCTEQCIWNCVKQP of anemia, platelet concentrates for treating
thrombocytopenia, and fresh frozen plasma or
• Negative bedside clotting test cryoprecipitate to replenish deficient factors.
• Prolongation of
• Recombinant factor VIIa can be used in uncon-
Ŧ bleeding time
trollable bleeding, but its use may be associ-
Ŧ clotting time
Ŧ prothrombin time
ated with increased risk of stroke or pulmonary
Ŧ partial thromboplastin time embolism. Therefore, it should be used with
• Peripheral smear caution.
Ŧ Thrombocytopenia • Heparin (to prevent clotting) and epsilon-
Ŧ (TCIOGPVGF4$%U aminocaproic acid (to inhibit fibrinolysis) are
• Decrease in not useful in the management of DIC.
Ŧ ſDTKPQIGP • Concurrently, the underlying obstetric con-
• Increase in dition such as placental abruption, sepsis, or
Ŧ ſDTKPURNKVRTQFWEVU
&FKOGTU amniotic fluid embolism should be promptly
BCs, red blood cells. managed.
CH 45_p670-682_v3.indd 680 18-07-2015 16:19:13

-G[RQKPVU
• Apart from hemorrhage, the common emergencies in • There is increased capillary permeability, exudation
QDUVGVTKEUVJCVOC[NGCFVQUJQEMCTGCOPKQVKEƀWKF QHƀWKFKPVQNWPIUECWUKPICFWNVTGURKTCVQT[FKUVTGUU
embolism, sepsis, and disseminated intravascular syndrome, hypotension, and hypoxia.
EQCIWNCVKQP
&+%6JGUGCTGCUUQEKCVGFYKVJJKIJ
• Clinical diagnosis is by history of predisposing factors,
maternal mortality.
fever, and chills followed by hypotension, tachycardia,
• #OPKQVKEƀWKFGODQNKUOKUCTCTGEQPFKVKQPVJCVQEEWTU tachypnea, oliguria or anuria, respiratory distress, and
in labor or within 4 hours of delivery. bleeding tendency due to DIC.
• It occurs in conditions that cause opening up of the • Emergency supportive treatment should be initiated to
venous channels in the uterus and increase in intrau- correct hypotension, hypoxia, and metabolic problems.
terine pressure. The risk factors are labor induction, Antibiotic therapy should be started pending culture
precipitate labor, cervical lacerations, cesarean sec- TGRQTV1TICPKUOECWUKPIUGRUKUOWUVDGKFGPVKſGF
tion, and instrumental delivery. by culture of blood, urine, or pus. The site of infection
• The exact pathogenesis is not known. It is considered UJQWNFDGKFGPVKſGFCPFRWUKPHGEVGFVKUUWGTGOQXGF
to be an idiosyncratic anaphylactoid reaction to the surgically.
COPKQVKEƀWKFVJCVGPVGTUVJGEKTEWNCVKQP • Pregnancy is considered to be a hypercoagulable
• The woman presents with sudden onset of respiratory state due to the changes that take place in the
symptoms, hypotension, hypoxia, pulmonary edema, coagulation system in normal pregnancy. DIC is a
left heart failure, and DIC. pathological disruption of the clotting mechanisms in
pregnancy.
• The diagnosis is mainly clinical. Chest X-ray may
UJQYRWNOQPCT[KPſNVTCVGU • Disseminated intravascular coagulation can occur
whenever there is a risk factor such as placental
• The management is supportive. The woman should CDTWRVKQPCOPKQVKEƀWKFGODQNKUOU[PFTQOGUGRUKU
be admitted to the ICU, hemodynamically stabilized preeclampsia, or acute fatty liver of pregnancy.
YKVJ+8ƀWKFUQZ[IGPCFOKPKUVGTGFKPVWDCVGFCPF
ventilated if necessary, and DIC managed with blood • The woman presents with bleeding and ecchymoses.
and blood products. Soon there is hypotension and shock. Reduced urine
output, acidosis, and hypoxia ensue.
• Septicemia and septic shock can occur following cho-
rioamnionitis, puerperal sepsis and endometritis, post- • The diagnosis of DIC is by a history of bleeding, hypo-
abortal infection, pyelonephritis, or wound infection. tension, and end-organ failure. Bleeding parameters
are deranged, platelet count is low, peripheral smear
• The organisms are usually gram-negative bacilli and shows fragmented red blood cells. There is a marked
anaerobes. Infections by gram-positive organisms also FGETGCUGKPUGTWOſDTKPQIGPNGXGNUCPFKPETGCUGKP
occur. ſDTKPURNKVRTQFWEVU
&FKOGTU
• (QNNQYKPIDCEVGTGOKCGPFQVQZKPUCTGTGNGCUGFKPVQ • Management is by replacement of blood and blood
VJGEKTEWNCVKQP6JGUGCEVKXCVGJQUVEGNNKPƀCOOCVQT[ products and treatment of the cause. Recombinant
TGCEVKQPTGNGCUGQHE[VQMKPGUCPFU[UVGOKEKPƀCOOC- factor VIIa should be used with caution.
tory response syndrome.
5GNH#UUGUUOGPV
%CUGDCUGFSWGUVKQPU 1.
2.
What is the likely diagnosis? Why?
What differential diagnosis would you consider?
Case 1 3. *QYYKNN[QWEQPſTOVJGFKCIPQUKU!
4. How will you manage this case?
Mrs. AN, 32, was brought to the emergency room with
shock, circulatory collapse, and altered sensorium. She
had delivered 2 hours earlier after labor induction with Case 2
vaginal misoprostol, supplemented by oxytocin, at a local
hospital. After delivery she needed suturing of a cervical Mrs. PM, 28, who delivered vaginally at a primary center,
VGCTDWVFKFPQVJCXGUKIPKſECPVRQUVRCTVWOJGOQTTJCIG was brought with high fever and altered sensorium. She
On examination, she had cold and clammy extremities; was in labor for 26 hours, ruptured membranes 20 hours
her pulse was 120/min, BP 90/60 mm Hg, and respiratory prior to delivery, and was examined internally by the local
rate 40/min. dai several times. Her pulse was 160/min on admission,
CH 45_p670-682_v3.indd 681 18-07-2015 16:19:13

$2 YCU OO *I VGORGTCVWTG YCU u( CPF Case 2
lochia malodorous.
1. Septicemia with septic shock.
1. What is the diagnosis? 2. Prolonged labor, prolonged rupture of membranes,
2. What do you think caused this? multiple pelvic examinations, and failure to start
3. What is the initial management? antibiotics after membrane rupture for 18 hours.
4. If a collection is found in the pouch of Douglas, how 3. Shift to ICU. General supportive therapy to correct
will you manage? J[RQVGPUKQPQZ[IGPCPFKPVTCXGPQWUƀWKFU
Antibiotics to cover gram-negative, anaerobic, and
gram-positive organisms. Culture blood and urine.
#PUYGTU Change antibiotics if necessary later. Correct DIC.
Identify the site of infection.
4. 6JKUUJQWNFDGEQPſTOGFD[WNVTCUQPQITCRJ[+HVJGTG
Case 1 is no collection at any other intra-abdominal site,
1. #OPKQVKEƀWKFGODQNKUO
C5JGJCFNCDQTKPFWEGF drainage of pus by colpotomy.
with misoprostol and augmented with oxytocin, both
of which could have caused strong uterine contrac-
VKQPU
D5JQEMQEEWTTGFJQWTUCHVGTFGNKXGT[
E 5CORNGSWGUVKQPU
There is no hemorrhage.
2. Cardiomyopathy, undiagnosed valvular disease, and .QPICPUYGTSWGUVKQP
uterine inversion.
1. Discuss the etiology, pathogenesis, and manage-
3. Diagnosis is clinical, by history and clinical examination.
ment of gram-negative septicemia and septic shock
%JGUV:TC[OC[TGXGCNRWNOQPCT[KPſNVTCVGU
in pregnancy.
Demonstration of fetal cells, debris, and hair in blood
obtained by pulmonary catheterization is diagnostic
but seldom performed. 5JQTVCPUYGTSWGUVKQPU
4. Shift the patient to the ICU, start general supportive
therapy to correct hypotension, administer oxygen, and 1. #OPKQVKEƀWKFGODQNKUO
intubate and ventilate if required. Correct DIC. Monitor 2. 5[UVGOKEKPƀCOOCVQT[TGURQPUGU[PFTQOG
5+45
BP, oxygen saturation, urine output, and ECG. 3. Causes of DIC in pregnancy
CH 45_p670-682_v3.indd 682 18-07-2015 16:19:13

Abnormalities of the
Placenta, Umbilical
46 Cord, and Fetal
Membranes
Case scenario
Mrs. DS, 23, had an uncomplicated vaginal delivery. Six hours later, she
started bleeding profusely in the postpartum ward. The bleeding was
accompanied by painful uterine cramping. She was rushed back to the
operating theater to investigate the cause for bleeding. Exploration of
the uterus revealed the presence of a retained cotyledon of placenta.
Introduction placentas and the majority of abnormal pla-

centas can be accomplished within a minute or
The placental unit is made up of the parenchyma, so. It is essential that the obstetrician performs
umbilical cord, and membranes (chorion and a thorough, accurate examination of the pla-
amnion). Primary placental abnormalities can centa. Universal examination of the placenta in
have an impact on both maternal and fetal health. the delivery room, with documentation of find-
Conversely, maternal or fetal disorders may have ings, is good clinical practice. In the presence of
an effect on the placenta, since this is the crucial abnormal appearance or certain clinical condi-
maternal–fetal interface. tions, the placenta can be sent for pathological
Examination of the placenta directly after evaluation.
birth can yield invaluable information for Placental implantation, development, and
the immediate and later management of anatomy are presented in Chapter 5, Placenta,
mother and infant. The examination of normal fetal membranes, and amniotic fluid.
CH 46_p683-692_v3.indd 683 18-07-2015 16:31:22

Advantages of examining Box 46.2 0

QTOCNſPFKPIUVQDGU[UVGOCVKECNN[
noted and documented in the term
the placenta placenta
Examination of the placenta may yield informa- • Shape of the placenta

tion in several conditions (Box 46.1). Ŧ Round or oval
• Size of the term placenta
Ŧ Diameter: 15–25 cm
Box 46.1 Conditions in which placental Ŧ Weight: 500–600 g
examination is important
Ŧ Thickness: 3 cm
• Maternal disorders with an impact on the fetus • Maternal surface
• Preterm birth Ŧ Color: Dark maroon
• Fetal growth restriction Ŧ Appearance: Distinct cotyledons
• Stillbirth or neonatal death Ŧ Structure: Complete, with no missing cotyledons
• Neonatal neurodevelopmental impairment • Fetal surface
• Zygosity and pathology (e.g., twin-to-twin transfusion) Ŧ Shiny and gray
in multifetal gestation Ŧ Membranes translucent
• Potentially recurrent disorders Color of the underlying maroon villous tissue
seen
Clinical characteristics
of the normal placenta Box 46.3 7ODKNKECNEQTF0QTOCNſPFKPIU
at term • Length: 55–60 cm
Ŧ Best assessed at delivery
The normal placenta can be rapidly examined • Diameter: 2.0–2.5 cm
and assessed at delivery (Fig. 46.1). The placenta • Wharton’s jelly: Abundant
must be kept on a flat surface and examined. The • No true knots or thromboses
findings to be systematically noted and docu- • 2 arteries and 1 vein
mented are listed in Box 46.2. Ŧ Best assessed in the middle third or the fetal third
The umbilical cord is examined along with the of the cord
placenta. The findings should be documented
(Box 46.3).
placenta
Placental abnormalities may be anatomical
or the result of maternal or fetal pathology.
Abnormalities of the placenta could include
variations in the following:
• Size/weight
• Shape
• Implantation
• Maternal surface and substance
• Mass lesions
Abnormalities of si e weight
The placental weight is usually one-sixth or
Figure 46.1 The normal placenta. The fetal surface one-seventh of the infant’s weight and is 500–600 g
is seen, with the umbilical cord and the shiny fetal at term. Maternal and fetal conditions have an
membranes. effect on the placental weight (Box 46.4).
CH 46_p683-692_v3.indd 684 18-07-2015 16:31:23

Abnormalities of the Placenta, Cord, and Fetal Membranes 685
Box 46.4 Effect of maternal and fetal factors enestrate placenta

on placenta A rare variant is fenestrate placenta, which is
arge placenta the absence of the central portion of a discoidal
placenta.
• High placental weight or >4 cm thick
• Associated with
Succenturiate placenta
Ŧ maternal diabetes mellitus
Ŧ fetal or maternal anemia Succenturiate placenta (Fig. 46.3) is a smaller
Ŧ fetal hydrops version of the bilobed placenta. An additional
Ŧ congenital syphilis lobe (or lobes) of placental tissue is located on
Small placenta the fetal membranes, a few centimeters away
• Low placental weight or <2.5 cm thick)
from the main disc of the placenta. A placen-
• Associated with tal artery and vein extend from and within the
Ŧ preeclampsia membrane of the main placental mass to each
Ŧ fetal growth restriction lobe and then divide into smaller vessels sup-
Ŧ some aneuploidies (not trisomy 21) plying individual cotyledons. The ancillary lobes
Ŧ infection function normally.
The lobe (or lobes) may be expelled in the
third stage along with the main placental mass
or may be retained. When the succenturiate lobe
Abnormalities of shape is retained in the uterus, examination of the pla-
centa may reveal a circular defect in the mem-
ilobe or uple placenta branes. Torn ends of the vessels are seen leading
Bilobed or duplex placenta (Fig. 46.2) refers to up to the defect. Retention of the succenturiate
complete separation of the placenta into two lobe may go unnoticed and leads to secondary
lobes with separate umbilical arteries and veins postpartum hemorrhage and sepsis.
that unite in a single umbilical cord. The complications associated with a succen-
turiate lobe are listed in Box 46.5.
i iscoi al an tri iscoi al placentas
Other variants are bidiscoidal and tridiscoidal
placentas, which do not have as complete a sep-
aration between lobes as the bilobed placenta.
The incomplete parenchymal separation typi-
cally occurs in the area of the cord insertion site.
Figure 46.3 Placenta succenturiata. An additional lobe

of placental tissue is located a few centimeters away from
the main disc of the placenta (arrow). (Photo courtesy:
Box 46.5 Complications of succenturiate lobe

• Placenta previa or vasa previa
Figure 46.2 Bilobed placenta. Complete separation of
• Retained succenturiate lobe resulting in
the placenta into two lobes is seen with separate umbilical
Ŧ delayed postpartum hemorrhage
arteries and veins that unite in a single umbilical cord
Ŧ delayed infection
(arrow). (Photo courtesy: Mediscan Systems, Chennai.)
CH 46_p683-692_v3.indd 685 18-07-2015 16:31:24

lacenta membranacea Abnormalities of the maternal

Placenta membranacea is a rare type of placenta placental surface and
in which all or part of the fetal membranes is
covered by functional placental tissue. These substance
placentas are often deeply implanted and asso-
In arcts
ciated with placenta previa or accreta. They may
require manual removal. They are associated Fresh infarcts are dark red, while older infarcts
with a slightly increased risk of are gray. Infarcts occupying <5% of the placen-
tal mass are not clinically important. Larger
• second trimester miscarriage infarcted areas are associated with the following:
• preterm birth
• antepartum and postpartum bleeding
• Stillbirth
• Neurological sequelae
Circumvallate placenta
Circumvallate placenta refers to a placenta ibrin eposition
where the fetal surface presents a central Firm gray areas may represent fibrin deposition
depression surrounded by a thickened whit- that has no clinical significance unless extensive.
ish-gray ring. The ring is formed by a double Extensive fibrin deposition is seen in pregnan-
layer of amnion and chorion. This ring may cies complicated by antiphospholipid antibody
be at a variable distance from the umbilical syndrome. It may be associated with placental
cord insertion site and the fetal vessels do not insufficiency leading to
extend beyond this ring. These placentas are
• fetal growth restriction and
associated with the complications listed in
• poor fetal outcome.
Box 46.6.
A deep yellow band of fibrin deposition along
the maternal floor is suspicious for a maternal
Circummarginate placenta
floor infarction, a lesion that carries significant
The ring of membranes is flat and near the edge morbidity and recurrence risk.
of the placenta with no central depression. It is
not associated with adverse outcomes. %CNEKſECVKQP
Calcification may be seen as whitish speckling
over the maternal surface of the placenta. It can
Abnormalities of implantation be palpated as diffuse particulate roughness or
lacenta accreta increta discrete hard patches over the basal surface of
the cotyledons. It is a normal part of placental
an percreta
maturation in the third trimester and is known to
In these serious abnormalities, trophoblas- occur earlier in smokers. Placental calcification
tic tissues invade the myometrium to varying in the second trimester is an abnormal finding
depths. They can cause torrential bleeding. and is associated with fetal growth restriction or
This is discussed in greater detail in Chapter 43, fetal distress.
Complications of the third stage of labor. The significance of placental calcification is
listed in Box 46.7.
Box 46.6 Complications associated with Box 46.7 5KIPKſECPEGQHRNCEGPVCNECNEKſECVKQP

circumvallate placenta
• Normal part of placental maturation
• Second trimester bleeding • Occurs earlier in smokers
• Abruption • #DPQTOCNſPFKPIKPUGEQPFVTKOGUVGT
• Preterm delivery Ŧ Associated with
• Congenital malformations fetal growth restriction
• Perinatal mortality fetal distress in labor
CH 46_p683-692_v3.indd 686 18-07-2015 16:31:25

ass lesions Box 46.8 Complications associated with long

Mass lesions may consist of infarcts, thrombi, umbilical cord
cysts, tumors, or abscesses. These are abnormal • Cord accidents
and should be examined histologically. Ŧ Entanglement
Chorioangiomas are focal fleshy, dark red Ŧ Knotting
areas in the placental parenchyma. These benign Ŧ Cord prolapse
hemangiomas occur in 1% of placentas. Small • Fetal growth restriction
chorioangiomas are usually of no clinical signif- • Fetal death
icance. However, large chorioangiomas are asso- • Long-term adverse neurological outcome
ciated with fetal anemia, thrombocytopenia,
hydrops, hydramnios, fetal growth restriction,
prematurity, and stillbirth. Box 46.9 Complications associated with short
umbilical cord
ale appearing placenta
• Associated with fetal inactivity related to
Severe fetal anemia may cause the placenta to Ŧ fetal malformations
appear pale. There may be associated hydrops of Ŧ myopathic and neuropathic diseases
the placenta. Ŧ oligohydramnios
umbilical cord
Abnormalities of the umbilical cord may be
benign, with no associated fetal complications.
However, when umbilical vessels are involved,
adverse fetal effects could result. Abnormalities of
the cord could include variations in the following:
• Length
• Coiling
• Edema
• Cord insertion
• Knots
• Vessels
Abnormal length
The length of the umbilical cord reflects the ten- Figure 46.4 Umbilical cord. The coiling of the blood
sion placed on the cord by fetal movements. More vessels in the umbilical cord is seen.
active the fetus, the longer is the cord. Conversely,
an inactive fetus will have a short cord. The nor-
(Fig. 46.4). The normal umbilical cord coil index
mal cord is between 50 cm and 60 cm long.
is one coil per 3–5 cm. Coiling of the umbilical
A long umbilical cord is diagnosed when the
cord is thought to protect it from compression,
length is >70 cm.
kinking, and torsion, thus preventing disruption
The complications associated with a long
of the blood supply to the fetus.
umbilical cord are enumerated in Box 46.8.
The umbilical coiling index (UCI) is the num-
A short umbilical cord (<40 cm) results from
ber of coils divided by the total cord length.
fetal inactivity (Box 46.9).
Hypocoiling is defined as UCI values less than the
10th percentile. Hypercoiling is defined as UCI
Coiling values greater than the 90th percentile. Both hypo-
The blood vessels in the umbilical cord charac- coiling and hypercoiling of the umbilical cord are
teristically twist or coil around the central axis associated with abnormalities (Box 46.10).
CH 46_p683-692_v3.indd 687 18-07-2015 16:31:25

Box 46.10 Abnormalities associated with

J[RQEQKNKPICPFJ[RGTEQKNKPI
of the umbilical cord
ypocoiling
• Growth restriction
• Fetal heart rate abnormalities
• Preterm birth
• Hypertensive disorders
• Abruptio placentae
• Oligohydramnios
• Intrauterine death
ypercoiling
• Diabetes mellitus
• Polyhydramnios
• Respiratory distress of the newborn
Figure 46.5 Battledore placenta. The umbilical cord is

Edema of the cord inserted into the margin of the placenta.
Mild edema of the cord can be present but is of no

clinical significance. Massive edema (resulting in placenta resembles the bat used in the game).
regional or diffuse cord diameters of >3 cm) can Marginal insertions are benign.
cause vascular compromise and is often associated
with acute changes in the fetal heart rate pattern.
elamentous cor insertion
Areas of massive edema can be seen in trisomy 18 A velamentous cord inserts into the membranes
and omphalocele. Diffuse edema can be associated rather than the placental disc. Since the vela-
with hemolytic disease of the newborn, maternal mentous vessels are surrounded only by fetal
hypertensive disorders, or diabetes. membranes, with no Wharton’s jelly, they are
prone to compression or tearing. Velamentous
Stricture vessels can also occur between lobes of a
bilobed placenta. When the vessels lie over the
A stricture may be an artifact or the result of internal os, they are called vasa previa and can
torsion or amniotic bands. Strictures have been be associated with torrential bleeding in labor.
implicated in the etiology of fetal compromise Velamentous umbilical cord has been asso-
or demise. ciated with several obstetric complications,
including fetal growth restriction, prematurity,
Placental insertion congenital anomalies, and low Apgar score.
The umbilical cord normally inserts centrally or
slightly eccentrically and directly into the placen- Cord knots
tal disc. Approximately 90% of cord insertions are
central or eccentric. Abnormalities of umbilical alse nots
cord insertion are more common in pregnancies False knots are tortuosities of the umbilical
resulting from in vitro fertilization and in multi- vessels that bulge out from the side of the cord
ple gestations. (Fig. 46.6). They are not associated with any
adverse outcome.
attle ore placenta
In the battledore placenta, the insertion occurs at rue nots
the margin of the placenta (Fig. 46.5) (Battledore True knots occur in 1% of births (Fig. 46.7). They
is an older form of shuttlecock and the battledore are associated with a 10% perinatal mortality
CH 46_p683-692_v3.indd 688 18-07-2015 16:31:25

Figure 46.6 False knot in cord. Tortuosities of the

umbilical vessels are seen bulging from the cord.
Figure 46.8 Cut section of the umbilical cord. One large,

thin-walled umbilical vein (white arrow) and two smaller,
thick-walled umbilical arteries (yellow arrows) are seen.
Box 46.11 5
KIPKſECPEGQHUKPINGWODKNKECN
CTVGT[
57#
• May result from one of the following
Ŧ Primary agenesis of one of the umbilical arteries
Ŧ Secondary atresia or atrophy of a previously nor-
mal umbilical artery
Figure 46.7 True knot in cord.
Ŧ Persistence of the original single allantoic artery of
the body stalk
• Associated with anomalies, particularly
Ŧ genitourinary
Ŧ cardiac
Ŧ gastrointestinal
rate. A true cord knot occurs when the fetus
• When not associated with anomalies
passes through a loop of umbilical cord, usually
Ŧ Good outcome
early in pregnancy. In most cases, a knot does • The outcome of SUA with associated anomalies or
not cause fetal compromise. However, when aneuploidy depends on the underlying chromosomal
tension is placed on the cord before or during and structural abnormalities
labor and delivery, blood flow may be compro- Ŧ Fetal karyotype analysis should be offered when
mised and result in fetal asphyxia and intrauter- fetal anomalies are detected
ine fetal demise.
Cord vessels
As soon as the cord is cut, the blood vessels in
the cord must be examined and the number Thrombosis
should be documented. The normal cord con- Thrombosis of cord vessels is abnormal and
tains one large, thin-walled umbilical vein and should be investigated. Possible causes include
two smaller, thick-walled umbilical arteries the following:
(Fig. 46.8).
• Cord compression from a true knot
• Cord prolapse, or head compression
5KIPKſECPEGQHUKPINGWODKNKECNCTVGT[
• Marginal or membranous cord insertion
The presence of a single umbilical artery • Fetal hypercoagulable state (e.g., sepsis, heredi-
(SUA) carries significant clinical connotations tary thrombophilia)
(Box 46.11). • Maternal diabetes mellitus
CH 46_p683-692_v3.indd 689 18-07-2015 16:31:27

7ODKNKECNEQTFE[UVU
Umbilical cord cysts may occur anywhere along
the length of the cord. They arise from embryonic
remnants of the vitelline duct and urachus. First
trimester umbilical cord cysts noted on ultra-
sound are often transient and have no clinical
significance. Persistent cysts have been associ-
ated with a variety of fetal anomalies (particularly
patent urachus and omphalocele), but the preva-
lence rate of these cysts is not documented.
Abnormalities of the fetal

membranes Figure 46.10 Meconium-stained placenta and umbilical
cord. This can be seen in postterm babies and after
Healthy fetal membranes are translucent (Fig. intrauterine fetal hypoxia.
46.9), slightly gray, and glistening. They do not
contain blood vessels or nerves. The elastic prop-
erties and built-in tensile strength of fetal mem-
branes allow them to stretch and accommodate Opa ue ull membranes
the growing fetus and amniotic fluid. Mild chorioamnionitis turns the membranes
opaque and dull. In more severe infections, there
may be a yellow discoloration of the membranes
econium staining
accompanied by a foul odor.
The fetus passes meconium in many situations.
In postterm fetuses, meconium passage may
be normal. However, meconium is also passed Amnion no osum
in the presence of fetal hypoxia and acidosis. Multiple tiny white, gray, or yellow nodules may
Meconium stains the fetal membranes green be seen on the amnion overlying the placenta.
(Fig. 46.10). These are called amnion nodosum. They are
associated with prolonged oligohydramnios.
Amniotic ban s
When there is disruption of the amnion, deli-
cate or robust bands of amnion form between
the amnion and the fetus. These may entrap
fetal parts and may lead to amputation and
deformities.
ltrasound examination
of the placenta
Ultrasound examination of the placenta is just
as important as the examination of the fetus.
Examining the placenta presents a unique
opportunity to detect problems that will sig-
Figure 46.9 A healthy fetal membrane. nificantly affect perinatal outcome. Most of the
CH 46_p683-692_v3.indd 690 18-07-2015 16:31:29

abnormalities described above can be identified Storing the fresh placenta

by ultrasound. 2D imaging provides excellent
information about the location and architec- In some clinical situations examination of the
ture of the placenta. 3D Doppler imaging of the fresh placenta will yield valuable information.
placenta is promising to be a detailed method The indications include the following:
for examining uteroplacental structure and • Evaluation of placental surface changes
function. • Palpation for solid lesions
• Cultures
• Cytogenetic studies
Pathological examination • Injection of twin placentas to detect
of the placenta anastomoses
Fresh placentas should be refrigerated (not
Pathological examination of the placenta is frozen) at 4°C and may be stored this way for
indicated when any abnormality of potential 3–7 days.
clinical significance is identified. Indications
for pathological examination are listed in
Box 46.12. Fixing the placenta
When the placenta and umbilical cord need to
undergo histopathological examination, they
Box 46.12 Indications for pathological should be fixed in 10% formalin. A plastic con-
examination of placenta tainer with a lid is ideal to hold the placenta. The
• Poor pregnancy outcome formalin should completely cover the placenta
Ŧ Prematurity and cord.
Ŧ Fetal growth restriction The pathologist should be given a clear picture
Ŧ Perinatal death and asphyxia of the clinical situation for which the placenta is
• Maternal disorders being examined.
Ŧ Third trimester bleeding In the case of a poor obstetric outcome, hav-
Ŧ Evidence of fetal or maternal infection ing a routine standard gross and histological
• Multiple pregnancy
evaluation of the placenta is extremely helpful
Ŧ Zygosity
to the clinician in counseling the family for a
Ŧ Vascular anastomoses
future pregnancy.
-G[RQKPVU
• The placental unit is made up of the parenchyma, • In a succenturiate placenta, an additional lobe
umbilical cord, and fetal membranes (chorion and (or lobes) of placental tissue is located a few
amnion). centimeters away. It may be associated with vasa
previa or postpartum hemorrhage and infection.
• Universal examination of the placenta in the delivery
TQQOYKVJFQEWOGPVCVKQPQHſPFKPIUKUIQQFENKPKECN • Circumvallate placenta is associated with second
practice. trimester bleeding, abruption, preterm delivery, and
• Placental examination is an essential component of perinatal mortality.
the autopsy in cases of stillbirth or neonatal death. • Placenta accreta, increta, and percreta are abnormali-
• The placental weight is usually one-sixth or one- ties of implantation.
seventh of the infant’s weight. Heavier placentas will • Examination of the surface of the placenta may reveal
be thicker and lighter placentas will be thinner due to ſDTKPFGRQUKVKQPECNEKſECVKQPCPFOCUUNGUKQPU
the effects on placental development. • The umbilical cord is usually 50–60 cm in length. Both
• Bilobed or duplex placenta refers to complete separation long and short cords are associated with perinatal
of the placenta into two lobes with separate umbilical morbidity and mortality.
arteries and veins that unite in a single umbilical cord.
(Continued)
CH 46_p683-692_v3.indd 691 18-07-2015 16:31:29

-G[RQKPVU Continued
• Abnormalities of umbilical cord insertion include • Abnormalities of the fetal membranes may include
battledore placenta and velamentous cord insertion. meconium staining, opacity due to infection, amnion
• True knots occur in 1% of births and are associated nodosum, and amniotic bands.
with a 10% perinatal mortality rate. • Pathological examination of the placenta is indicated
• A single umbilical artery may be associated with other YJGPCP[CDPQTOCNKV[QHRQVGPVKCNENKPKECNUKIPKſECPEG
KUKFGPVKſGF
anomalies and/or aneuploidy.
Self-Assessment
2. A succenturiate cotyledon left behind in the uterus
Case-based questions may also be associated with delayed infection.
3. A velamentous cord inserts into the membranes
Case rather than the placental disc. When the vessels lie
Mrs. DS, 23, had an uncomplicated vaginal delivery. Six over the internal os, they are called vasa previa and
hours later, she started bleeding profusely in the post- can be associated with torrential bleeding in labor.
partum ward. The bleeding was accompanied by painful 4. A single umbilical artery may be associated with
uterine cramping. She was rushed back to the operating gastrointestinal, genitourinary, and cardiac anomalies
theater to investigate the cause for bleeding. Exploration and/or aneuploidy.
of the uterus revealed the presence of a retained cotyledon
of placenta.
1. What would be the commonest cause for the retained
Sample questions
cotyledon of placenta?
2. What other complication can arise in this situation?
3. What is velamentous insertion of the cord? What 1. Describe the examination of the placenta at birth.
complication is it associated with? What are the common indications for a pathological
4. 9JCVKUVJGUKIPKſECPEGQHUKPINGWODKNKECNCTVGT[! examination of the placenta?
Answers
1. Succenturiate placenta
1. In a succenturiate placenta, an additional lobe (or
2. False and true knots of the umbilical cord
lobes) of placental tissue is located a few centimeters
3. Velamentous cord insertion
away from the placental disc. In this case, the suc-
centuriate lobe would have been left behind. 4. Battledore placenta
CH 46_p683-692_v3.indd 692 18-07-2015 16:31:29

Section 7
Maternal Diseases
Complicating
Pregnancy
CH 47_p693-723_v3.indd 693 19-07-2015 11:09:43

Hypertensive
47 Disorders
Case scenario
Mrs. MN, 23, primigravida, presented at 34 weeks’ pregnancy with

elevated blood pressure. She had regular antenatal care at the local
primary health center from the third month of pregnancy. She was
told that her blood pressure was high at 29 weeks’ pregnancy and was
started on medication; however, during her subsequent checkup at 31
and 33 weeks, her blood pressure continued to be high and the baby was
not growing as expected. She was referred for further management to a
tertiary center.
Hypertensive disorders of pregnancy are com- Hypertension in pregnancy is defined as a sys-
monly encountered and are major causes of tolic blood pressure (BP) t 140 mm Hg and/or
perinatal mortality, morbidity, and maternal diastolic BP t 90mm Hg (Korotkoff 5), the mea-
complications. Preeclampsia/eclampsia is one of surements confirmed by two or more readings
the leading causes of maternal death. In the past 4–6 hours apart. If Korotkoff 5 is absent, muffling
decade, there have been major advances in the or Korotkoff 4 may be accepted.
understanding of pathophysiology of these disor- A rise in systolic BP of 30 mm Hg or diastolic
ders and based on these, new guidelines for man- BP of 15 mm Hg above the midpregnancy BP
agement have evolved. A thorough knowledge of is no longer used as a criterion for diagnosis of
the guidelines is essential for early diagnosis and hypertension in pregnancy.
appropriate treatment of the condition.
CH 47_p693-723_v3.indd 694 19-07-2015 11:09:43

Hypertensive Disorders 695
%NCUUKſECVKQP Box 47.2 Gestational hypertension

• Features
The American College of Obstetricians and
Ŧ $2ŮOO*IEJGEMGFJQWTUCRCTV
Gynecologists (ACOG) has classified hypertension
Ŧ &GXGNQRUCHVGTYGGMU
in pregnancy as given in Box 47.1. Ŧ No proteinuria
Ŧ 4GUQNXGUD[YGGMURQUVRCTVWO
• Can be
Ŧ 0QPUGXGTG
$2ŌOO*I
Gestational hypertension Ŧ 5GXGTG
$2ŮOO*I
• %NKPKECNEQWTUG
When hypertension (BP: 140/90 mm Hg or Ŧ 2TGGENCORUKCKPŌ
more) develops for the first time after 20 weeks’ Ŧ 'ENCORUKCKP
gestation, documented on two occasions at least Ŧ %JTQPKEJ[RGTVGPUKQPKPCUOCNNPWODGT
4 hours apart in a previously normotensive Ŧ 4GVWTP VQ PQTOCN D[ YGGMU RQUVRCTVWO KP VJG
woman, and there is no proteinuria, it is called rest
gestational hypertension. The clinical course • 2TQIPQUKU
may be any of the following: Ŧ Good
9JGPJ[RGTVGPUKQPFGXGNQRUCHVGTYGGMU
• 15%–25% of women develop proteinuria and 0QPUGXGTGJ[RGTVGPUKQP
preeclampsia syndrome.
• 5% of women develop eclampsia even before
The risk factors, pathogenesis, and patho-
proteinuria sets in.
physiology of gestational hypertension are not
• In others, preeclampsia does not develop, and
clearly defined and are poorly understood. The
the hypertension resolves within 12 weeks after
pathologic changes in the organ systems that
delivery—reclassified as transient hypertension.
occur with preeclampsia are not seen in gesta-
• Hypertension may persist 12 weeks after deliv-
tional hypertension and the maternal and fetal
ery in a small group of women—reclassified as
complications are also uncommon.
chronic hypertension.
When gestational hypertension develops late
in the third trimester (after 36 weeks), the prog-
nosis is good and progression to preeclampsia is Preeclampsia syndrome
uncommon. When it develops early, progression
Preeclampsia syndrome is a new-onset hyper-
to preeclampsia is more likely.
tension (t 140/90 mm Hg) that develops after 20
Gestational hypertension may be nonsevere (BP
weeks’ gestation with proteinuria with or with-
140/90–160/110 mm Hg) or severe (BP t 160/110
out evidence of multiorgan involvement.
mm Hg). Severe gestational hypertension is associ-
Proteinuria is defined as
ated with higher perinatal morbidity and mortality
(Box 47.2). • 300 mg or more in 24-hour urine sample (or)
• spot urinary protein : creatinine ratio of t 0.3
(or)
• 30 mg/dL protein or 1+ dipstick in single ran-
Box 47.1 #
%1)ENCUUKſECVKQPQHJ[RGTVGPUKQP dom urine sample if the other two are not
in pregnancy available.
• )GUVCVKQPCNJ[RGTVGPUKQP Estimation of proteinuria by dipstick is not
• 2TGGENCORUKCCPFGENCORUKCU[PFTQOG a sensitive method and has high false-positives
• %JTQPKEJ[RGTVGPUKQP
and false-negatives but is often used when rapid
• 2TGGENCORUKCUWRGTKORQUGFQPEJTQPKEJ[RGTVGPUKQP
detection is required. A 24-hour urine collection
AC #OGTKECP%QNNGIGQH1DUVGVTKEKCPUCPF)[PGEQNQIKUVU is cumbersome. Urine protein : creatinine ratio
CH 47_p693-723_v3.indd 695 19-07-2015 11:09:43

696 'UUGPVKCNUQH1DUVGVTKEU
is currently preferred and correlates well with • The signs and symptoms of severe preeclamp-
24-hour urine protein. sia are manifestations of multiorgan involve-
Even in the absence of proteinuria, evidence ment. These are listed in Table 47.1.
of multiorgan involvement such as headache, • Serum creatinine of t1.1 mg/dL or a doubling of
visual disturbances, epigastric pain, thrombo- serum creatinine in the absence of preexisting
cytopenia, or elevated liver enzymes along with renal disease is used as a sign of renal involve-
gestational hypertension is considered preec- ment instead of oliguria that was used earlier.
lampsia (Box 47.3). • Nonsevere preeclampsia can progress rapidly
to severe preeclampsia.
%NCUUKſECVKQPQHRTGGENCORUKC Criteria or iagnosis o severe
Preeclampsia is classified into nonsevere and se- preeclampsia
vere based on the criteria listed in Box 47.4 (ACOG The clinical and laboratory features listed in
Task Force on Hypertension in Pregnancy, 2013). Table 47.1 are usually present in most women
with severe preeclampsia. However, some fea-
onsevere preeclampsia tures are characteristic of the disease and are
considered as criteria for diagnosis of severe
The nonsevere category includes what was preeclampsia (Box 47.4).
earlier called mild and moderate. The BP is
>140/90 mm Hg but <160/110 mm Hg, con- • Proteinuria of >5 g/24 hours (3+ or more in
firmed by repeated examination 4 hours apart. random sample) was considered an important
Proteinuria is usually present. indicator in the past but has been excluded now
since there is minimal relationship between
severity of proteinuria and perinatal outcome.
Severe preeclampsia • Similarly, fetal growth restriction has also
When BP is t160/110 mm Hg, it is categorized as been eliminated since management of growth
severe preeclampsia. restriction does not depend on the severity of
preeclampsia.
• It is recommended that BP t 160/110 mm Hg be
confirmed by repeat examination 4 hours later
but can be confirmed within a shorter interval to Imminent eclampsia
facilitate initiation of treatment. In women with persistent symptoms of severe pre-
eclampsia such as headache, visual disturbances,
Box 47.3 Preeclampsia syndrome
Box 47.4 %TKVGTKCHQTUGXGTGRTGGENCORUKC
• 0GYQPUGVJ[RGTVGPUKQP
• &GXGNQRUCHVGTYGGMU • $NQQFRTGUUWTGŮOO*I
• 9KVJRTQVGKPWTKC • *GCFCEJGCPFXKUWCNFKUVWTDCPEGU
• +PVJGCDUGPEGQHRTQVGKPWTKC • 7RRGTCDFQOKPCN
GRKICUVTKERCKP
Ŧ 'XKFGPEGQHOWNVKQTICPKPXQNXGOGPV • 6JTQODQE[VQRGPKC
z.
• %NCUUKſGFKPVQ • 'NGXCVGFNKXGTGP\[OGU
Ŧ Nonsevere • 5GTWOETGCVKPKPG OIF.
Ŧ Severe • 2WNOQPCT[GFGOC
Table 47.1 %CWUCVKQPQHENKPKECNNCDQTCVQT[HGCVWTGUQHUGXGTGRTGGENCORUKC
Causation %NKPKECNNCDQTCVQT[HGCVWTGU
%GTGDTCNGFGOC *GCFCEJG
%JCPIGUKPVJGQRVKEHWPFWU 8KUWCNFKUVWTDCPEGU
.KXGTKUEJGOKC 'RKICUVTKERCKPGNGXCVGFNKXGTGP\[OGU
4GPCNKPXQNXGOGPV 2TQVGKPWTKCGNGXCVGFUGTWOETGCVKPKPG
.GHVXGPVTKEWNCTHCKNWTG 2WNOQPCT[GFGOC
2NCVGNGVCIITGICVKQPCPFCEVKXCVKQP/KETQCPIKQRCVJKEJGOQN[UKU 6JTQODQE[VQRGPKC
7VGTQRNCEGPVCNKPUWHſEKGPE[ (GVCNITQYVJTGUVTKEVKQP
CH 47_p693-723_v3.indd 696 19-07-2015 11:09:43

epigastric pain, and high BP, the term imminent of proteinuria in a woman with chronic hyper-
eclampsia was formerly used. However, eclamp- tension, it is termed superimposed preeclamp-
sia can occur without such symptoms or acute sia. Other signs and symptoms of multiorgan
rise in BP; hence, currently it is classified as severe involvement may also be present. Superimposed
preeclampsia and the term “imminent eclamp- preeclampsia develops at an earlier gestational
sia” is not used any more. age, is more severe, and is associated with higher
perinatal loss and fetal growth restriction than
Eclampsia preeclampsia that develops in a previously nor-
motensive woman (Box 47.6).
Occurrence of convulsions in a woman with
preeclampsia is termed eclampsia. Seizures in
the second half of pregnancy and up to 48 hours
postpartum, not attributable to any other cause, ther hypertensive
are always considered to be eclampsia. Seizures
may occur antepartum, intrapartum, or within
disorders
48 hours after delivery. Rarely, they may occur Other uncommon types of hypertensive disor-
beyond 48 hours postpartum. Eclampsia is dis- ders are described in the following subsections.
cussed in detail later in this chapter.
Atypical preeclampsia
Chronic hypertension Preeclampsia or eclampsia that develops in a
Chronic hypertension is defined as hyperten- woman in the absence of either hypertension
sion (t 140/90mm Hg) detected before 20 weeks’ or proteinuria is termed atypical preeclampsia.
pregnancy or that continues beyond 12 weeks Gestational hypertension or proteinuria may be
postpartum. Hypertension may be primary or present with evidence of multiorgan involve-
secondary to renal or vascular disease (Box 47.5). ment such as headache, epigastric pain, throm-
BP usually decreases during the second tri- bocytopeniaor elevated liver enzymes.
mester. A woman with chronic hypertension
may have normal BP during this period and the Delta hypertension
BP may rise to prepregnant levels in the third tri-
mester. This can be misdiagnosed as new-onset Rise in BP in the third trimester but not equal
hypertension if the woman has not been seen to or beyond the cutoff value of 140/90 mm Hg
early in pregnancy. Preexisting end-organ dam- is called delta hypertension. These women may
age and other systemic signs may, sometimes, develop eclampsia or hemolysis, elevated liver
help to differentiate between the two. enzyme levels, and low platelet levels (HELLP)
syndrome and need close monitoring.
Preeclampsia superimposed Capillary leak syndrome

on chronic hypertension Gross pedal edema, ascites, pulmonary edema,
and proteinuria may develop without associated
When there is worsening of preexisting hyper-
tension, new-onset proteinuria, or worsening
Box 47.6 Preeclampsia superimposed on
chronic hypertension
Box 47.5 Chronic hypertension
• 9QTUGPKPIQHJ[RGTVGPUKQP
• *[RGTVGPUKQPDGHQTGYGGMUŏRTGIPCPE[ • New-onset proteinuria
• %QPVKPWGUDG[QPFYGGMURQUVRCTVWO • 9QTUGPKPIQHRTQVGKPWTKC
• /C[DG • (GCVWTGUQHOWNVKQTICPKPXQNXGOGPV
Ŧ 2TKOCT[ • %QORCTGFYKVJRTGGENCORUKC
Ŧ 5GEQPFCT[ Ŧ 1EEWTUGCTNKGTKPIGUVCVKQP
YGGMU
• %JTQPKEXGTUWUIGUVCVKQPCNJ[RGTVGPUKQP Ŧ *[RGTVGPUKQPOQTGUGXGTG
Ŧ 6KOGQHQPUGV Ŧ *KIJGTRGTKPCVCNOQTDKFKV[CPFOQTVCNKV[
Ŧ 'XKFGPEGQHGPFQTICPFCOCIG Ŧ )TGCVGTHGVCNITQYVJTGUVTKEVKQP
CH 47_p693-723_v3.indd 697 19-07-2015 11:09:43

hypertension. This is called capillary leak syndrome.

Box 47.7 4KUMHCEVQTUHQTRTGGENCORUKC
Thrombocytopenia, abnormal liver enzymes, clini-
cal symptoms, and eclampsia may develop later. • 2TKOKRCTKV[
• #IG[GCTU
• #FXCPEGFOCVGTPCNCIG
[GCTU
• *KIJDQF[OCUUKPFGZ
MIO2
+PEKFGPEGQHJ[RGTVGPUKXG • /WNVKRNGRTGIPCPE[
• *[FCVKFKHQTOOQNG
disorders • 4JKUQKOOWPK\CVKQP
• /CVGTPCNOGFKECNRTQDNGOU
Incidence of hypertensive disorders varies widely Ŧ Diabetes
with population and ethnicity. Hypertensive dis- Ŧ Hypertension
orders occur in approximately 2%–5% of all preg- Ŧ Renal disease
nancies in the developed world and inapproxi- Ŧ %QPPGEVKXGVKUUWGFKUQTFGTU
mately 10% of pregnancies in India. Incidence of Ŧ #PVKRJQURJQNKRKFCPVKDQF[U[PFTQOG
eclampsia is 1% of all pregnancies in India, but the • 2CUVJKUVQT[QHRTGGENCORUKC
incidence is much lower in developed countries. • (COKN[JKUVQT[QHRTGGENCORUKC
• 4CEG
• .QYUQEKQGEQPQOKEUVCVWU
4KUMHCEVQTUHQT • 'PXKTQPOGPVCNHCEVQTU
preeclampsia Abnormal trophoblastic invasion

Risk factors for gestational hypertension are Delivery of placenta leads to rapid resolution of
not clearly defined; however, several risk factors all the features of preeclampsia. This observa-
have been identified for preeclampsia. tion indicates that placenta plays a critical role
Age is an important risk factor for preeclamp- in the development of preeclampsia.
sia andis most common in primiparous, young In normal pregnancy, the endovascularcy-
women. Chronic hypertension is seen more often totrophoblasts penetrate the endothelium and
in older women (>35 years). Obesity, diabetes, muscle layer of the walls of spiral arterioles and
multiple pregnancy, preexisting medical condi- convert them into low-resistance vascular chan-
tions, and past history of preeclampsia are other nels (see Chapter 5, Placenta, fetal membranes,
risk factors as listed in Box 47.7. and amniotic fluid). This trophoblastic invasion
takes place in the following two stages:
• Stage 1: Invasion of the decidual segment of
2CVJQRJ[UKQNQI[QH the spiral arterioles at 10–12 weeks
• Stage 2: Invasion of the myometrial segment of
preeclampsia the spiral arterioles at 16–18 weeks
The pathophysiology of gestational hypertension Although the first stage proceeds normally,
is unknown. Several theories have been proposed the second stage of invasion (penetration of the
for the pathogenesis of preeclampsia syndrome. myometrial segment) does not occur in preec-
It involves maternal and fetoplacental factors. lampsia (Fig. 47.1). This failure of trophoblastic
The currently accepted plausible mechanisms invasion is due to defective differentiation of
include the following: trophoblast. The arterioles continue toremain as
narrow vessels.
• Abnormal trophoblastic invasion
• Placental underperfusion/hypoxia
• Release of placental factors into maternal 2NCEGPVCNJ[RQRGTHWUKQPCPF
circulation
• Maternal vascular endothelial dysfunction
hypoxia
and inflammation Failure of trophoblastic invasion and vasodilata-
• Immunological factors tion result in placental hypoperfusion. Similarly,
• Genetic factors other medical conditions associated with reduced
%*ARAXKPFF 19-07-2015 11:09:43

nchoring illi
Cytotrophoblast
tra illous trophoblast

n o ascular trophoblast
eci ua
piral arteriole
Myometrium
Figure 47. 1 #DPQTOCNVTQRJQDNCUVKEKPXCUKQPa. 0QTOCNRTGIPCPE[6JGGPFQXCUEWNCTE[VQVTQRJQDNCUVURGPGVTCVGVJGYCNNU

QHVJGURKTCNCTVGTKQNGUKPVJGFGEKFWCCPFO[QOGVTKWOCPFEQPXGTVVJGOKPVQNQYTGUKUVCPEGEJCPPGNUb.2TGGENCORUKC
6JGRGPGVTCVKQPQHVJGYCNNQHVJGO[QOGVTKCNUGIOGPVQHVJGURKTCNCTVGTKQNGUKUPQVUGGP
uteroplacental flow such as hypertension, dia- linked to HELLP syndrome. Placental changes
betes, and connective tissue disorders also lead develop in women with susceptible genes.
to placental hypoperfusion. Placental perfusion
declines progressively as pregnancy advances.
The resultant is chemia and hypoxia lead to the Maternal vascular endothelial
release of substances into the maternal circula- F[UHWPEVKQP
tion that cause endothelial dysfunction.
Several pro-angiogenic and anti-angiogenic fac-
torsare produced by the placenta, and the bal-
+OOWPQNQIKECNHCEVQTU ance between these determines normal endo-
In normal pregnancy there is an immunological thelial function
tolerance to paternal and fetal antigens, thus facil- The proangiogenic and antiangiogenic fac-
itating placental implantation and continuation tors are listed below.
of pregnancy. The natural killer cells (NK cells) in – Proangiogenic factors: VEGF, PIGF
the decidua and the human leukocyte antigens – Antiangiogenic factor: Soluble fms-like
(HLAs) of the cytotrophoblasts come in contact tyrosine kinase-1 (sFlt-1).
but do not react adversely and the fetus is immu-
nologically tolerated. In preeclampsia, this immu- In normal pregnancy, there is a balance
nological tolerance is believed to be lost leading to between production of pro-angiogenic factors
abnormal trophoblastic invasion. In nulliparous and anti-angiogenic factors. In preeclampsia,
women who have not previously been exposed to the placental hypoperfusion and the resul-
paternal antigens or when paternal antigenic load tant hypoxia lead to increase in production of
is high, as in multifetal or molar pregnancies, this anti-angiogenic factors and decrease in pro-an-
immune maladaptation is probably more fre- giogenic factors. This results in reduced produc-
quent and this may explain the greater predisposition of vasodilator prostaglandin [prostaglandin
tion to preeclampsia in these conditions. I2(PGI2)] and nitric oxide (NO) by the endothe-
lium, endothelial damage and dysfunction.
In addition, placental hypoxia causes release
)GPGVKEHCEVQTU of syncytiotrophoblast debris and microparticles
leading to production of cytokines, interleukins, and
Risk of preeclampsia is higher in a woman with tumor necrosis factor-alpha (TNF-D), which in turn
a family history and a history of preeclampsia. induce oxidative stress. This oxidative stress leads
There is, therefore, a hereditary predisposition. to increase in free radicals that cause endothelial
Several genes have been implicated. Genes for inflammation, damage, and dysfunction (Fig. 47.2).
antiangiogenic factors are present on chromo- The damaged endothelium serves as a nidus
some 13, and genes on chromosome 12q are for platelet aggregation and microvascular
CH 47_p693-723_v3.indd 699 19-07-2015 11:09:43

mmune mala aptation efecti e trophoblastic

genetic factors in asion of spiral arterioles
Placental hypoperfusion
yncytiotrophoblast ebris
Placental ischemia hypo ia
microparticles from placenta
ncrease in antiangiogenic factors s lt

Cyto ines interleu ins
ecrease in angiogenic factors
α
V P
i ati e stress
n othelial amage an
ysfunction
ncrease ascular permeability

Micro ascular coagulation
platelet aggregation asospasm
Preeclampsia
Figure 47.2 2CVJQRJ[UKQNQI[QHRTGGENCORUKCPl RNCEGPVCNITQYVJHCEVQTs lt- UQNWDNGHOUNKMGV[TQUKPGMKPCUG

TNF-DVWOQTPGETQUKUHCEVQTCNRJC XCUEWNCTGPFQVJGNKCNITQYVJHCEVQT
coagulation, and this leads to thrombocytopenia, • As already mentioned, there is platelet aggre-
increased vascular permeability, and vasospasm. gation and microvascular coagulation.
• Endothelins are released by the endothelium.
2CVJQIGPGUKUQH They are vasoconstrictors.
• The balance between the productionof vasodi-
preeclampsia lator prostaglandin (PGI2 and vasoconstrictor
prostaglandin (thrombaxane A2) is altered.
The endothelial damage and dysfunction lead to
• The endothelins, reduced levels of NO and
the following events:
increase in thromboxane A2 together lead to
• There is increased response to pressor agents vasospasm in the small blood vessels in the
such as angiotensin II and norepinephrine. end-organs.
• The increased capillary permeability leads to • This causes ischemia of the surrounding
leakage of platelets and fibrinogen through the tissues, necrosis and hemorrhage, which are
damaged endothelium and increase in extravas- characteristic changes in preeclampsia (Fig.
cular fluid. 47.3).
CH 47_p693-723_v3.indd 700 19-07-2015 11:09:44

n othelial amage
an ysfunction
ncrease pressor mbalance in ncrease en othelins ncrease platelet

ncrease
response to prostacyclin ecrease pro uction aggregation an
capillary permeability
angiotensin thromba ane ratio of nitric o i e coagulation
ema Hypertension Vasospasm hrombocytopenia
pasm of essels
at en organs
schemia
ecrosis
Hemorrhage
Figure 47.3 2CVJQIGPGUKUQHRTGGENCORUKC PKVTKEQZKFG
Pathology hemoconcentration. Due to these changes,

women with preeclampsia are very sensi-
The placental changes that predispose to preeclamp- tive to vigorous fluid therapy and acute blood
sia begin early in pregnancy, but the pathological loss and are at risk for pulmonary edema and
changes progress gradually. Ultimately, the individ- hypotension.
ual end-organs are affected to varying degrees and • Proteinuria and the resultant hypoalbumine-
manifest varying degrees of pathological changes. mia lead to reduction in plasma oncotic pres-
sure. This, along with extravasation of fluid,
can give rise to edema.
Cardiovascular changes
Increased vascular permeability, increased ematological changes
peripheral resistance and hypertension lead to
Significant hematological changes are also observed
significant changes in the cardiovascular system
• Thrombocytopenia occurs in all the different
• Due to hypertension and increased peripheral
types of hypertensive disorders in pregnancy.
resistance, there is increased load on the left
This may become severe in severe preeclamp-
ventricle. If hypertension is severe, this can
sia and HELLP syndrome.
lead to left ventricular dysfunction.
• Microangiopathic hemolysis occurs due to
• Increased capillary permeability causes extrava-
endothelial damage, platelet adherence, and
sation of fluid into the extravascular space,
fibrin deposition. This results in elevated lactic
especially lungs, causing pulmonary edema.
dehydrogenase(LDH) levels and appearance
• Due to vasospasm and shrinkage of intravascular
of schistocytes and spherocytes in the periph-
compartment, the blood volume expansion that
eral smear.
is expected in normal pregnancy does not occur.
• Intravascular coagulation leads to reduction in
• Contracted intravascular compartment and
levels of factor VIII, antithrombin III, and pro-
expanded extravascular compartment is an
teins C and S and increase in D-dimers.
important feature of preeclampsia.
• Extravasation of plasma into intersti- Cardiovascular and hematological changes in
tial space and vasoconstriction lead to preeclampsia are summarized in Table 47.2.
CH 47_p693-723_v3.indd 701 19-07-2015 11:09:44

Table 47.2 Cardiovascular and hematological changes in preeclampsia
Pathogenesis %NKPKECNOCPKHGUVCVKQPU
8CUQEQPUVTKEVKQP +PETGCUGFNQCFQPNGHVXGPVTKENG
+PETGCUGKPRGTKRJGTCNTGUKUVCPEG .GHVXGPVTKEWNCTF[UHWPEVKQP
&GETGCUGKPECRKNNCT[XQNWOGGZRCPUKQP
+PETGCUGFECRKNNCT[RGTOGCDKNKV[ *GOQEQPEGPVTCVKQP
'ZVTCXCUCVKQPQHƀWKFKPVQKPVGTUVKVKCNURCEG 2WNOQPCT[GFGOC
4GFWEGFRNCUOCQPEQVKERTGUUWTG 2GFCNCPFIGPGTCNK\GFGFGOC
/KETQCPIKQRCVJKEJGOQN[UKU • Elevated LDH
• 5EJKUVQE[VQUKUURJGTQE[VQUKU
• 'NGXCVGF&FKOGTU
• 4GFWEGFNGXGNUQHHCEVQT8+++CPVKVJTQODKP+++RTQVGKPU%CPF5
2NCVGNGVCFJGUKQPCPFCIITGICVKQP 6JTQODQE[VQRGPKC
D NCEVKEFGJ[FTQIGPCUG
enal changes • Liver changes in preeclampsia consist of (a)

periportal hemorrhages and (b) vasospasm
Histological and functional changes occur in the and infarction around the sinusoids.
renal system. • Serum glutamic oxaloacetic transaminase
• Swelling of the endothelial cells of the renal glo- (SGOT) and serum glutamic pyruvic transam-
meruli, obstructing the lumen of the capillaries, inase (SGPT) levels increase, indicating
known as glomerular capillary endotheliosis, severe disease.
is a characteristic histological renal lesion in • Hemorrhagic infarctions can form hematoma,
preeclampsia. The glomeruli are enlarged and which may extend to become subcapsular
have markedly reduced blood flow. hematoma. Rarely, this can rupture causing
• Glomerular filtration is reduced due to (a) life-threatening hemorrhage.
reduced plasma volume, (b) reduction in renal • Stretching of the liver capsule (Glisson capsule)
blood flow because of high resistance, and (c) due to edema and hematoma causes epigastric
glomerular capillary endotheliosis. pain. Liver involvement also causes nausea
• Proteinuria occurs due to increased perme- and vomiting.
ability of the glomeruli to proteins. Most of the
protein excreted is albumin.
• Serum creatinine levels increase. Central nervous system
• Uric acid levels are elevated due to decreased
clearance of uric acid by the kidney.
changes
• Activation of renin–angiotensin system leads Changes in the central nervous system are sig-
to reduced excretion of sodium and chloride, nificant and may lead to convulsions
causing sodium retention.
• Cortical and sub-cortical hemorrhages are the
• Acute tubular necrosis can occur when there
most common lesions in the brain. Softening,
is profuse hemorrhage, hypotension, and
necrosis, perivascular infarcts, and hemor-
hypovolemia.
rhages are also seen.
• For the same reasons, acute cortical necrosis,
• Endothelial damage leads to leakage of fluid
which is rare, can also occur.
into the interstitial tissue, causing perivascu-
Changes in renal function are listed in Box 47.8. lar edema and convulsions. Autoregulation
of cerebral blood flow is lost, and there is cer-
ebral hyperperfusion, causing headache,
epatic changes papilledema, and scotomata.
The pathological process of preeclampsia leads • The changes in the brain are termed posterior
to changes in the liver as well. reversible encephalopathy syndrome (PRES)
CH 47_p693-723_v3.indd 702 19-07-2015 11:09:44

Changes in the liver, central nervous system,

Box 47.8 enal changes in preeclampsia
and retina are summarized in Table 47.3.
• )NQOGTWNCTECRKNNCT[GPFQVJGNKQUKU
• 4GFWEGFINQOGTWNCTDNQQFƀQY
• 4GFWEVKQPKP)(4
Ŧ 4GFWEVKQPKPRNCUOCXQNWOG
Placental changes
Ŧ 4GFWEVKQPKPTGPCNDNQQFƀQY Placental changes play a major role in pathogen-
Ŧ )NQOGTWNCTGPFQVJGNKQUKU esis of preeclampsia.
• Proteinuria
• +PETGCUGKPUGTWOETGCVKPKPG • Due to the failure of the second stage of troph-
• &GETGCUGFENGCTCPEGQHWTKECEKF oblastic invasion, the diameter of the spiral
Ŧ 'NGXCVGFNGXGNUQHWTKECEKF arteries in the myometrium is reduced. The
• &GETGCUGFGZETGVKQPQHUQFKWOCPFEJNQTKFG vessel wall undergoes necrosis and the cell wall
Ŧ 5QFKWOTGVGPVKQP is replaced by amorphous material. This pro-
• #EWVGVWDWNCTPGETQUKU gresses to obliteration of the vessels and areas
• #EWVGEQTVKECNPGETQUKU of placental infarction (Box 47.9). Fetalgrowth
INQOGTWNCTſNVTCVKQPTCVG restriction, placental abruption, and preterm
labor are probably due to these changes.
when they involve predominantly the occipi- Box 47.9 Placental changes in preeclampsia
tal lobes. This causes blurred vision, diplopia, Spiral arteries in the myometrium
and, rarely, blindness. • .CEMQHVTQRJQDNCUVKEKPXCUKQP
• Widespread cerebral edema can occur and • 0CTTQYKPIQHVJGCTVGTKGU (GVCNITQYVJTGUVTKEVKQP
manifest as confusion and coma. • 0GETQUKUQHXGUUGNYCNN 2NCEGPVCNCDTWRVKQP
• 1DUVTWEVKQPQHVJGNWOGP 2TGVGTONCDQT
• 2NCEGPVCNKPHCTEVKQP
etinal changes rophoblast
Release of
Vasospasm is the most common finding in the • Apoptosis U[PE[VKQVTQRJQDNCUV
fundus. Hemorrhages and exudates are seen debris
in severe preeclampsia. Papilledema can also Release of
• 0GETQUKU
OKETQRCTVKENGU
occur. Rarely, retinal detachment can occur,
'PFQVJGNKCN
especially following a convulsion. This can cause • &GIGPGTCVKQP
KPƀCOOCVKQP
temporary blindness.
Table 47.3 epatic, central nervous system, and retinal changes in preeclampsia
Pathology %NKPKECNOCPKHGUVCVKQPU
*GRCVKEEJCPIGU
}
2GTKRQTVCNJGOQTTJCIGU 'NGXCVGF5)165)26
8CUQURCUOCPFKPHCTEVKQPCTQWPFUKPWUQKFU 0CWUGCXQOKVKPI
*GOCVQOCU Spontaneous rupture
5VTGVEJKPIQHNKXGTECRUWNG 'RKICUVTKERCKP
%GPVTCNPGTXQWUU[UVGOEJCPIGU
%QTVKECNCPFUWDEQTVKECNJGOQTTJCIG
5QHVGPKPIKPHTCEVKQPPGETQUKU %QPXWNUKQPUEQPHWUKQPEQOC
(QECNCPFIGPGTCNK\GFGFGOC *GCFCEJGXKUWCNFKUVWTDCPEGU
2QUVGTKQTTGXGTUKDNGGPEGRJCNQRCVJ[
4GVKPCNEJCPIGU
}
8CUQURCUO
*GOQTTJCIGUCPFGZWFCVGU 8KUWCNFKUVWTDCPEGU
2CRKNNGFGOC
4GVKPCNFGVCEJOGPV Blindness
S UGTWOINWVCOKEQZCNQCEGVKEVTCPUCOKPCUGS P UGTWOINWVCOKER[TWXKEVTCPUCOKPCUG
CH 47_p693-723_v3.indd 703 19-07-2015 11:09:44

• There is increased apoptosis, necrosis, and supplementation in high doses (2g/day) was
degeneration of the trophoblast especially found useful in calcium-deficient and high-risk
syncytiotrophoblast. More syncytiotropho- women.
blast debris and microparticles are released into Identification of pregnancies that are at high
the maternal circulation, resulting in inflam- risk for preeclampsia, appropriate preconcep-
mation of the endothelium and endothelial tional education, close monitoring during preg-
dysfunction. nancy, and early intervention if BP rises are the
most effective methods of prevention of severe
disease and eclampsia.
2TGFKEVKQPQHRTGGENCORUKC
Several tests to identify placental hypoperfusion,
Low-dose aspirin
endothelial dysfunction, and other pathological Platelet aggregation and increase in platelet-
changes of preeclampsia have been developed. derived thromboxane are implicated in the
Most tests lack adequate sensitivity and predic- pathogenesis of preeclampsia. Aspirin, admin-
tive value and are therefore not used. Provocative istered in low doses (60–80 mg/day), reduces
biophysical tests such as rollover test and angio- thromboxane synthesis by the platelets with-
tensin II challenge test based on increased sen- out decreasing the production of prostacyclin.
sitivity and response to pressor agents were also ACOG and National Institute for Health and
used in the past. They are also unreliable and Care Excellence (NICE) guidelines have recom-
time consuming; therefore, they are currently mended the use of aspirin in doses of 75 mg/day,
not used. started at 12 weeks and continued till delivery.
The indications are as follows:
• Women at high risk for preeclampsia

terine artery Doppler velocimetry – Hypertensive disease during a previous
Decreased flow in the uterine artery early in ges- pregnancy
tation is used as predictive test for preeclamp- – Chronic kidney disease
sia. Uterine artery Doppler study is more useful – Autoimmune disease such as systemic lupus
in the second trimester. Impaired blood flow is erythematosus
diagnosed by the following: – Antiphospholipid antibody syndrome
– Type 1 or type 2 diabetes
• Presence of diastolic notching (Fig. 47.4) – Chronic hypertension
• High resistance or pulsatility index or systolic/
diastolic ratio • Women with two or more of the following
The tests are more useful for prediction of moderate risk factors for preeclampsia:
fetal growth restriction than for prediction of – First pregnancy
preeclampsia and are not recommended for rou- – Age t40 years
tine screening. – Pregnancy interval of >10 years
– Body mass index (BMI) of 35 kg/m2 or more
at first visit
– Family history of preeclampsia
2TGXGPVKQPQHRTGGENCORUKC – Multiple pregnancy
Since the pathogenesis of preeclampsia is com-

plex, preventive strategies have not been very
effective. Several approaches and interventions
%QORNKECVKQPUQH
(low-salt diet, fish oil, diuretics, antihyperten- preeclampsia
sives, heparin, and antioxidants) have been
studied, but none of them has been proven to Maternal and perinatal complications are min-
be useful in preventing preeclampsia. Calcium imal with gestational hypertension; however,
CH 47_p693-723_v3.indd 704 19-07-2015 11:09:44

Figure 47.4 7VGTKPGCTVGT[&QRRNGTXGNQEKOGVT[a.0QTOCNRTGIPCPE[0QTOCNU[UVQNKECPFFKCUVQNKEƀQYKPWVGTKPGCTVGT[

b.&KCUVQNKEPQVEJKPICPFJKIJTGUKUVCPEGƀQY6JGYJKVGCTTQYUKPFKECVGFKCUVQNKEPQVEJKPI2WNUCVKNKV[KPFGZKUCNUQJKIJ

Photo courtesy: /GFKUECP5[UVGOU%JGPPCK
preeclampsia is associated with maternal and cesarean section. Long-term maternal compli-
perinatal morbidity and mortality. cations that are associated with preeclampsia
arehypertension, cardiovascular disease, and
metabolic syndrome.
Maternal complications include placental abrup-
tion, pulmonary edema, rupture of liver due
Fetal complications
to hematoma, renal failure, HELLP syndrome, Fetal growth restriction due to placental insuffi-
disseminated intravascular coagulation (DIC), ciency is common in preeclampsia. Increase in
and convulsions (Box 47.10). There is increased perinatal mortalityand morbidity in severe pre-
risk of labor induction, operative delivery, and eclampsia is due to fetalgrowth restriction and
prematurity. Prematurity may be due to sponta-
neous preterm labor or induced labor for severe
Box 47.10 Maternal complications in preeclampsia
preeclampsia or fetal compromise. Intrauterine
• 5JQTVVGTO hypoxia and death, intrapartum asphyxia, and
Ŧ 2NCEGPVCNCDTWRVKQP hypoxic ischemic encephalopathy are the other
Ŧ 2TGVGTONCDQT complications (Box 47.11).
Spontaneous
+PFWEGF
Ŧ PulOQPCT[GFGOC
Ŧ 4WRVWTGQHNKXGTFWGVQJGOCVQOC
Ŧ *'..2U[PFTQOG
Ŧ DIC Box 47.11 Fetal complicationsin preeclampsia
Ŧ #EWVGTGPCNHCKNWTG
Ŧ 'ENCORUKC • 5JQTVVGTO
Ŧ 1RGTCVKXGXCIKPCNFGNKXGT[ Ŧ (GVCNITQYVJTGUVTKEVKQP
Ŧ CGUCTGCPUGEVKQP Ŧ 2TGOCVWTKV[
• .QPIVGTO Ŧ +PVTCWVGTKPGFGCVJ
Ŧ 4GEWTTGPVRTGGENCORUKC Ŧ +PVTCRCTVWOCURJ[ZKC
Ŧ %JTQPKEJ[RGTVGPUKQP Ŧ *[RQZKEKUEJGOKEGPEGRJCNQRCVJ[
Ŧ %CTFKQXCUEWNCTFKUGCUG Ŧ 2GTKPCVCNOQTVCNKV[
Ŧ /GVCDQNKEU[PFTQOG • .QPIVGTO
Ŧ Cerebral palsy
D C disseminated intravascular coagulation P JGOQN[UKU Ŧ 1VJGTPGWTQNQIKECNFKUQTFGTU
GNGXCVGFNKXGTGP\[OGNGXGNUCPFNQYRNCVGNGVNGXGNU
CH 47_p693-723_v3.indd 705 19-07-2015 11:09:44

%NKPKECNHGCVWTGUQH istory
hypertensive disorders Gestational age at which hypertension is first
detected, whether it is before or after 20 weeks,
Most women with gestational hypertension and is crucial. BP at the booking visit, especially in
nonseverepreeclampsia are asymptomatic. An the first trimester, should be noted. Past history
increase in diastolic BP during a routine antena- of gestational hypertension, gestational age at
tal visit is the first sign. This usually occurs after which it occurred, family history of hypertension,
32 weeks. There may be a rapid weight gain of history of diabetes, renal disease, autoimmune
>1kg/week. disorders, or other medical disorders should
Women with severe preeclampsia can pres- alsobe enquired into. Symptoms and signs of
ent with nausea, vomiting, headache, blurring severe preeclampsia should be evaluated.
of vision, and/or epigastric (upper abdominal)
pain. Pedal edema extending to legs and vulval
edema/ascites can occur with severe protein- Physical examination
uria. Breathlessness may be present when there
BP readings should be taken in the sitting posi-
is pulmonary edema. Decreased fetal move-
tion with an appropriate cuff. The diastolic
ments are indicative of intrauterine hypoxia
BP is recorded when the sound disappears
(Box 47.12).
(Korotkoff 5), or muffles (Korotkoff 4) as men-
tioned earlier. Mild elevations of BP should
Box 47.12 %
NKPKECNHGCVWTGUQHJ[RGTVGPUKXG be reconfirmed by repeat examination after 4
disorders hours. Cardiovascular and respiratory systems
and abdomen should be examined. History
• )GUVCVKQPCNJ[RGTVGPUKQPCPFPQPUGXGTGRTGGENCOR-
sia and physical examination are summarized in
Ŧ #U[ORVQOCVKE Box 47.13.
Ŧ 4KUGKPFKCUVQNKE$2FWTKPICPVGPCVCNXKUKV
Ŧ 9GKIJVICKP MIYGGM
• 5GXGTGRTGGENCORUKC Investigations
Ŧ 0CWUGCXQOKVKPI
Ŧ *GCFCEJG Investigations are ordered for the following rea-
Ŧ 8KUWCNFKUVWTDCPEGU sons(Box 47.14):
Ŧ 'RKICUVTKEWRRGTCDFQOKPCNRCKP
• Determine if it is gestational hypertension,
Ŧ 'FGOC
preeclampsia, or chronic hypertension.
2GFCNGZVGPFKPIVQNGIU
Vulval Urinalysis for proteinuria is the first step in
Ŧ #UEKVGU further evaluation. The dipstick method is usu-
Ŧ 1NKIWTKC ally used at initial evaluation. If this is 1+ or more,
Ŧ 4GFWEGFHGVCNOQXGOGPVU
a spot urine protein : creatinine ratio or 24-hour
urinary protein may be performed.
Microscopic examination of a centrifuged
urine sediment for red blood cell (RBC) casts,
&KCIPQUKUQHJ[RGTVGPUKXG granular casts, or microscopic hematuriamay
give clues to underlying parenchymal renal
disorders disease.
Diagnosis of hypertensive disorders in preg- • Assess the severity of the disease.
nancy is clinical, by identification of rise in BP.
Tests to assess severity of preeclampsia
Once hypertension is documented, further eval-
include serum creatinine to assess renal function,
uation is aimed at
platelet count for thrombocytopenia, LDH, and
• Making a diagnosis of gestational hyperten- peripheral smear for schistocytes as evidence of
sion, preeclampsia, or chronic hypertension microangiopathic hemolysis and liver enzymes
• Determination of severity of the disease to evaluate liver involvement.
CH 47_p693-723_v3.indd 706 19-07-2015 11:09:44

Box 47.13 istory and physical examination Box 47.14 Investigations

• History • 6QFGVGTOKPGPCVWTGQHJ[RGTVGPUKXGFKUGCUG
Ŧ )GUVCVKQPCN CIG CV FGVGEVKQP QH PGYQPUGV J[RGT- Ŧ 7TKPGCNDWOKP
tension Ŧ 7TKPGOKETQUEQR[
Ŧ &QEWOGPVGFDNQQFRTGUUWTGCVſTUVXKUKV 4$%ECUVU
Ŧ 5[ORVQOUQHUGXGTGRTGGENCORUKC )TCPWNCTECUVU
Ŧ 'ZEGUUKXGXQOKVKPI • 6QFGVGTOKPGUGXGTKV[
Ŧ 2CUVJKUVQT[ Ŧ 2NCVGNGVEQWPV
*[RGTVGPUKQPKPRTGXKQWURTGIPCPE[ Ŧ .KXGTGP\[OGU
)GUVCVKQPCN CIG CV YJKEJ J[RGTVGPUKQP YCU 5)165)26
FGVGEVGF Ŧ LDH
Ŧ (COKN[JKUVQT[ Ŧ 2GTKRJGTCNUOGCTHQTUEJKUVQE[VGU
*KUVQT[QHRTGGENCORUKCGUUGPVKCNJ[RGTVGPUKQP Ŧ 5GTWOETGCVKPKPG
Ŧ /GFKECNJKUVQT[ • 6QCUUGUUHGVCNYGNNDGKPI
Diabetes Ŧ Nonstress test
Hypertension Ŧ 7NVTCUQPQITCRJ[
#WVQKOOWPGFKUGCUG 'UVKOCVGFYGKIJV
#PVKJ[RGTVGPUKXGOGFKECVKQPU (GVCNITQYVJ
4GPCNFKUGCUGEQPPGEVKXGVKUUWGFKUQTFGTU $KQRJ[UKECNRTQHKNG
#PVKRJQURJQNKRKFCPVKDQF[U[PFTQOG
• 2J[UKECNGZCOKPCVKQP D NCEVKEFGJ[FTQIGPCUG BC TGFDNQQFEGNNS UGTWO
INWVCOKEQZCNQCEGVKEVTCPUCOKPCUGS P UGTWOINWVCOKER[TWXKE
Ŧ )GPGTCNGZCOKPCVKQP
VTCPUCOKPCUG
$QF[OCUUKPFGZ
Blood pressure
• Close monitoring
- 5KVVKPIRQUKVKQP
• Appropriate timing of delivery
- #RRTQRTKCVGEWHH
- -QTQVMQHHQT
• Appropriate mode of delivery
'FGOC
Ŧ %CTFKQXCUEWNCTU[UVGO
Ŧ 4GURKTCVQT[U[UVGO
2WNOQPCT[GFGOC
/CPCIGOGPVQHPQPUGXGTG
Ŧ #DFQOKPCNGZCOKPCVKQP gestational hypertension
#DFQOKPCNYCNNGFGOC
#UEKVGU Nonsevere gestational hypertension is associ-
7VGTKPGJGKIJV ated with low maternal and perinatal mortality
5KIPUQHOWNVKHGVCNOQNCTRTGIPCPE[ and morbidity.
'XKFGPEGQHHGVCNITQYVJTGUVTKEVKQP However, severe hypertension, preeclamp-
sia, or even eclampsia can develop in 15%–25%
of these women; therefore, close monitoring is
• Evaluate fetal well-being.
essential.
Fetal well-being is evaluated by nonstress test
(NST). Ultrasound evaluation yields very useful
information about the status of the fetus such as Maternal monitoring
estimated fetal weight, fetal growth as assessed
by biometric parameters, and fetal well-being as Worsening of hypertension or development of
assessed by liquor volume and biophysical profile. preeclampsia should be recognised immediately
and treatment instituted.
• Women with nonsevere new-onset hyperten-
/CPCIGOGPVQH sion can be managed on an outpatient basis.
• They should be seen twice weekly in the out-
hypertensive disorders patient clinic. BP, urine protein, and signs and
symptoms of severe disease should be moni-
The goals of management are as follows:
tored. Platelet count and liver enzymes should
• Early identification of worsening of the disease be checked once a week.
CH 47_p693-723_v3.indd 707 19-07-2015 11:09:45

• Patients should be educated regarding signs Antenatal glucocorticoids

and symptoms of severe hypertension/
preeclampsia. Gestational hypertension develops after 34
• Salt restriction is not recommended. weeks in most women. Glucocorticoids for
• Bed rest is not recommended for nonsevere accelerating pulmonary maturity are recom-
hypertension. Bed rest increases the risk of mended only in the rare cases needing delivery
venous thromboembolism and does not pre- before 34 weeks.
vent progression to severe preeclampsia.
However, depending on the nature of work and 6KOKPIQHFGNKXGT[
level of BP, restriction of activity and rest for var-
Women with hypertension should be delivered
ying periods of time may be required in moder-
no later than 40 weeks because there is a poten-
ate hypertension (150/100–160/109 mm Hg).
tial increase in risk of complications beyond
term.
Fetal surveillance
• Women with mild elevation of BP (approxi-
Serial evaluation of fetal well-being is essential mately 140/90 mm Hg) may be delivered by
for successful outcome. 39–40 weeks’ gestation.
• If BP is higher (150/100–160/109 mm Hg),
• Daily fetal movement count is recommended.
delivery between 37 and 38 weeks is recom-
• There are no definite guidelines regarding
mended.
the necessity for or frequency of perform-
ing NSTs, biophysical profile, or fetal growth
assessment. /QFGQHFGNKXGT[
• NSTs and biophysical profile are usually per- Ripening of the cervix with prostaglandins and
formed once in 2 weeks till 36 weeks and weekly induction of labor with amniotomy followed by
thereafter. Fetal growth assessment should be oxytocin is safe. A cesarean section is performed
performed once in 2 weeks after 34 weeks. only for obstetric indications.
Since hypertension can worsen in the intra-
Antihypertensive therapy partum period, close monitoring of BP, protein-
uria, and other clinical signs and symptoms of
The purpose of antihypertensive therapy is to severe preeclampsiais mandatory during labor.
reduce the BP to a level that will reduce mater-
nal complications such as severe hypertension,
abruption, liver, brain, and renal involvement /CPCIGOGPVQHUGXGTG
without reducing placental perfusion.
gestational hypertension
• According to randomized trials, antihyperten-
sive therapy for nonsevere (mild to moderate) Women who develop severe gestational hyper-
hypertension does not improve maternal or tension (>160/110 mm Hg) even in the absence
perinatal outcome. of proteinuria are at a high risk of developing
• It reduces the risk of severe hypertension maternal or fetal complications. They should be
but not the risk of preeclampsia, fetal growth managed like severe preeclampsia.
restriction, prematurity, or placental abrup- Management of gestational hypertension is
tion. Antihypertensives are, therefore, not rec- given in Figure 47.5.
ommended in nonsevere hypertension.
• However, the guidelines are not very definite for
women with moderate hypertension (150/100– /CPCIGOGPVQHPQPUGXGTG
160/109 mm Hg). Antihypertensives reduce the
risk of development of severe hypertension by
preeclampsia
40%–50%. Therefore, in women with moderate Progression to severe preeclampsia occurs in a
hypertension in developing countries (where higher percentage of women with nonsevere pre-
intensive monitoring may not be available), eclampsia. If progression to severe preeclamp-
oral antihypertensives may be used. sia does not occur, management is similar to
%*ARAXKPFF 19-07-2015 11:09:45

estational
hypertension
e ere onse ere
Manage as in se ere ee ly t ice

preeclampsia antenatal isits
Maternal monitoring bloo

etal monitoring aily fetal
pressure proteinuria signs
mo ement count ee ly
an symptoms of
an P fetal gro th
preeclampsia platelet count
once in ee s
li er en ymes
o be rest
o corticosteroi s
ntihypertensi es
if P
f P is bet een
f P is eli er at
an
ee s
eli er at ee s
Figure 47.5 /CPCIGOGPVQHIGUVCVKQPCNJ[RGTVGPUKQPBPP DKQRJ[UKECNRTQſNG S nonstress test.
nonseveregestational hypertension with some 6KOKPIQHFGNKXGT[

differences.
Waiting beyond gestational age of 37 weeks
• Women with proteinuria should be hospital- increases risk of progression to severe pre-
ized. BP, proteinuria, and signs and symptoms eclampsia and is also associated with other
of severe preeclampsia should be monitored adverse maternal outcomes. Therefore, women
daily. with nonsevere preclampsia should be delivered
• Fetal surveillance is by daily fetal movement by 37 weeks, in the absence of complications
count, NST and biophysical profile (BPP) (Fig. 47.6).
weekly, and fetal growth monitoring once in
2–3 weeks.
• Complete bed rest is not recommended, but
reduced level of physical activity and rest for
/QFGQHFGNKXGT[
4–6 hours/day are usually advised. This reduces
risk of progression to severe preeclampsia. Mode of delivery is the same as for nonsevere
• Recommendations for antihypertensive ther- gestational hypertension. Intrapartum elec-
apy and corticosteroids are same as for nonse- tronic fetal monitoring is recommended. Close
vere gestational hypertension. monitoring of the mother is essential.
CH 47_p693-723_v3.indd 709 19-07-2015 11:09:45

onse ere preeclampsia
Hospitali e
Maternal monitoring aily etal monitoring

bloo pressure proteinuria aily fetal mo ement count
igns an symptoms of se ere PP ee ly
preeclampsia etal gro th monitoring
ee ly platelet count an li er en ymes once in ee s
estricte acti ity

ntihypertensi e of P
o corticosteroi s
o maternal Maternal
fetal compromise fetal compromise
eli er ee s eli er at ee s
Figure 47.6 /CPCIGOGPVQHPQPUGXGTGRTGGENCORUKC
/CPCIGOGPVQHUGXGTG Box 47.15 Maternal evaluation in severe

preeclampsia
preeclampsia
• )GUVCVKQPCNCIG
Definitive management of preeclampsia is deliv- • /QPKVQT
ery of the fetus and placenta. Prompt delivery Ŧ $NQQFRTGUUWTGJCNHJQWTN[
prevents maternal and perinatal complications. Ŧ 7TKPGQWVRWVJQWTN[
However, preterm delivery is not desirable for Ŧ 7TKPGRTQVGKPD[FKRUVKEMJQWTN[
the fetus. Hence, the benefits (to the mother) of • 'XCNWCVGU[ORVQOUCPFUKIPU
immediate delivery must be weighed against the Ŧ *GCFCEJG
advantages (to the fetus) of waiting. Ŧ 8KUWCNFKUVWTDCPEGU
Ŧ 'RKICUVTKEWRRGTCDFQOKPCNRCKP
• Once severe preeclampsia is diagnosed, the Ŧ #NVGTGFUGPUQTKWOEQPHWUKQP
woman should be admitted to the delivery Ŧ $TGCVJNGUUPGUU
room. Maternal condition should be evalu- Ŧ 8CIKPCNDNGGFKPI
ated (Box 47.15), and the mother should be Ŧ 7VGTKPGEQPVTCEVKQPU
stabilized before further management is
planned. • Antihypertensives: Antihypertensives must be
started immediately to reduce the systolic BP
to 140–150 mm Hg and diastolic BP to 90–100
Immediate management
mm Hg. Antihypertensives of choice are nifedi-
Antihypertensives, corticosteroids and seizure pine, labetalol, or hydralazine (discussed later
prophylaxis should be started as soon as possible. in this chapter).
CH 47_p693-723_v3.indd 710 19-07-2015 11:09:45

• Seizure prophylaxis: Magnesium sulfate • In developed countries, the gestational age cut-
should be administered for seizure prophy- off for viability is 24 weeks. In under-resourced
laxis. Dosage and administration are discussed countries, perinatal survival is low before
later in this chapter. 26 weeks; hence, 26 weeks or the institutional
• Corticosteroids: Administer betamethasone to cutoff (28 weeks) may be used as limit of viability.
accelerate pulmonary maturity if gestational • Perinatal complications in the surviving
age is between 26 and 34 weeks. fetuses include respiratory distress syndrome,
• Maternal/fetal evaluation This consists of chronic lung disease, and neurodevelopmen-
investigations to look for multiorgan involve- tal problems and in the mother, HELLP syn-
ment and evaluation of fetal status (Box 47.16). drome, renal failure, and pulmonary edema.
• Parents should be counseled regarding these,
Box 47.16 /
CVGTPCNHGVCNGXCNWCVKQPKPUGXGTG and pregnancy should be terminated after sta-
preeclampsia bilizing the mother.
• +PXGUVKICVKQPU
Ŧ Urine protein : Creatinine ratio anagement o severe preeclampsia at
Ŧ 2GTKRJGTCNUOGCTHQTUEJKUVQE[VGU ee s gestation
Ŧ 5)165)26
Betamethasone should be administered to women
Ŧ 2NCVGNGVEQWPV
at this gestational age, as already mentioned.
Ŧ 5GTWO.&*
Ŧ 5GTWOETGCVKPKPG
Management at 26/28–34 weeks may be any
• Fetal evaluation of the following:
Ŧ Nonstress test • Delivery 24 hours after administration of steroids
Ŧ 7NVTCUQPQITCRJ[
• Immediate delivery within 24 hours of admin-
)GUVCVKQPCNCIG
istration of steroids
$KQRJ[UKECNRTQHKNG
'UVKOCVGFYGKIJV
• Expectant management.
7ODKNKECNCTVGT[&QRRNGT &GNKXGT[JQWTUCHVGTUVGTQKFU
D NCEVKEFGJ[FTQIGPCUGS UGTWOINWVCOKEQZCNQCEGVKE At gestational age 26–34 weeks, if maternal condi-
VTCPUCOKPCUGS P UGTWOINWVCOKER[TWXKEVTCPUCOKPCUG tion is not satisfactory or there is fetal compromise,
delivery is warranted. However, we can to wait for
Subsequent management 24 hours for the steroids to take effect. Indications
After observation for 24–48 hours, decision for delivery are summarized in Box 47.17.
regarding further management is taken. This
depends on the following: Box 47.17 +PFKECVKQPUHQTFGNKXGT[CVŌ
• Maternal and fetal condition weeks in severe preeclampsia
• Gestational age • 2GTUKUVGPVJKIJ$2FGURKVGCPVKJ[RGTVGPUKXGU
• %GTGDTCNU[ORVQOUFGURKVGOCIPGUKWOUWNHCVG
Gestation >34 and <26 weeks are indications • /CVGTPCNTGPCNHCKNWTG
ETGCVKPKPG OIF.
for delivery. • &+%*'..2U[PFTQOG
Ŧ 6JTQODQE[VQRGPKC
anagement o severe preeclampsia Ŧ 'NGXCVGFNKXGTGP\[OGU
ŮYGGMUŏIGUVCVKQP Ŧ Elevated LDH
In severe preeclampsia t34 weeks’ gestation Ŧ 5EJKUVQE[VGUKPDNQQFUOGCT
prognosis for fetal survival is good and waiting • #DPQTOCNWODKNKECNCTVGT[&QRRNGT
will jeopardize the mother and the child. Hence, Ŧ #DUGPVTGXGTUCNQHFKCUVQNKEƀQY
• #OPKQVKEƀWKFXQNWOG
#(+EO/82EO
immediate delivery is recommended.
• 0QPTGCUUWTKPIHGVCNJGCTVVTCEKPI
anagement o severe preeclampsia • 5GXGTG()4
VJEGPVKNGHQTIGUVCVKQP
• 2TGVGTONCDQTRTGNCDQTTWRVWTGQHOGODTCPGU
241/
ee s gestation (previable preeclampsia)
Both maternal and perinatal outcomes are poor A COPKQVKEƀWKFKPFGZBP DNQQFRTGUUWTGD C FKUUGOKPCVGF
KPVTCXCUEWNCTEQCIWNCVKQP HGVCNITQYVJTGUVTKEVKQP P
in early onset preeclampsia and waiting will JGOQN[UKUGNGXCVGFNKXGTGP\[OGNGXGNUCPFNQYRNCVGNGVNGXGNU
jeopardize the mother. D NCEVCVGFGJ[FTQIGPCUG P OCZKOWOXGTVKECNRQEMGV
CH 47_p693-723_v3.indd 711 19-07-2015 11:09:45

+OOGFKCVGFGNKXGT[YKVJKPJQWTUQHUVGTQKFU
Box 47.19 /
CVGTPCNCPFHGVCNOQPKVQTKPIKP
However, delivery should be proceeded with severe preeclampsia
immediately (within 24 hours of steroid adminis-
• $2JQWTN[JQWTN[
tration) if maternal condition is rapidly deteriorat- • +PVCMGQWVRWVEJCTV
ing as indicated by rising BP or persistent cerebral • 7TKPGRTQVGKPD[FKRUVKEMFCKN[
symptoms. Immediate delivery is also warranted • 5KIPUCPFU[ORVQOUGXCNWCVGFFCKN[
in placental abruption, intrauterine fetal death, or • 6GUVVYKEGYGGMN[
grossly preterm fetus (<26 weeks; Box 47.18). Ŧ 5GTWOETGCVKPKPG
Ŧ .KXGTGP\[OGU
Ŧ 2NCVGNGVEQWPV
Box 47.18 +PFKECVKQPUHQTKOOGFKCVGFGNKXGT[CV
• (GVCNYGNNDGKPICUUGUUGF
ŌYGGMUKPUGXGTGRTGGENCORUKC
Ŧ &(/%
• 4KUKPIDNQQFRTGUUWTGFGURKVGCPVKJ[RGTVGPUKXGU Ŧ 6YKEGYGGMN[
Ŧ %GTGDTCNU[ORVQOUKPFKECVKPIKORGPFKPIUGK\WTGU NST
Ŧ 2NCEGPVCNCDTWRVKQP BPP
Ŧ 2WNOQPCT[GFGOC 7ODKNKECNCTVGT[&QRRNGT
Ŧ +PVTCWVGTKPGFGCVJQHVJGHGVWU
BP DNQQFRTGUUWTGBPP DKQRJ[UKECNRTQſNGD C daily fetal
OQXGOGPVEQWPV S nonstress test.
Expectant management • Multiparous women with a favorable cervix

Expectant management is of no benefit to the and normal fetal test results can be delivered
mother but improves fetal survival and achieves by labor induction following cervical ripening.
prolongation of pregnancy. Randomized tri- • When the cervix is unfavorable, gestational age
als and systematic reviews have concluded that is approximately 34 weeks, if there is associated
expectant management achieves pregnancy pro- fetal growth restriction with abnormal fetal test-
longation of 7–14 days with maternal complica- ing, a cesarean section is usually the preferred
tion rate of <5%. mode of delivery.
• Regional anesthesia is recommended for a
• Expectant managementshould be undertaken cesarean section.
only in a tertiary-level center with neonatal • Worsening of hypertension, convulsions, and
intensive care facilities. pulmonary edema can occur in labor. Close
• The mother must be hospitalized till delivery. monitoring of BP (half-hourly) and other mater-
• Discontinue magnesium sulfate after 24–48 hours. nal parameters is mandatory.
• Continue oral antihypertensives. • The second stage may be cut short with outlet
• Close maternal and fetal monitoring is man- forceps.
datory (Box 47.19). • Injection oxytocin 10 units IM should be
given after delivery of placenta since excessive
iming of delivery
blood loss is tolerated poorly by these women.
Women managed expectantly should be delivered Methergine should be avoided.
at 34 weeks. Any abnormal maternal or fetal test
result or maternal complication during expectant Management of severe preeclampsia is sum-
management (listed in Box 47.19) is an indication marized in Figure 47.7.
for immediate delivery (after administration of
betamethasone.)
Antihypertensives in
ode of delivery preeclampsia
Decision regarding mode of delivery must take
Severe hypertension can lead to maternal com-
into account the gestational age and favourabil-
plications such as left ventricular failure, cere-
ity of the cervix.
brovascular hemorrhage, and convulsions in
• Severe preeclampsia is not an indication for an severe preeclampsia. Antihypertensives reduce
elective cesarean section. A cesarean section is these maternal risks by lowering the BP. They
performed only for obstetric indications. also improve the perinatal survival indirectly,
CH 47_p693-723_v3.indd 712 19-07-2015 11:09:45

e ere preeclampsia
Hospitalise
Chec tart
P ntihypertensi es
Urine output urine protein aluate
Magnesium sulfate
igns an symptoms of teroi s if ee s
preeclampsia
Mother
Urine protein creatinine etus
Li er en ymes onstress test
Peripheral smear Ultrasonography
Platelet count U oppler
Creatine
ubse uent management
Persistent high P
Persistent cerebral symptoms es
Placental abruption mme iate eli ery
Pulmonary e ema
estation or ee s
e ere es
bnormal P oppler Corticosteroi s
H LLP Preterm labor P M eil ery after hours
pectant management
iscontinue magnesium sulfate
Continue antihypertensi es
es
Maternal fetal complications
eil er
P M preterm labor
eli er at ee s
Figure 47.7 /CPCIGOGPVQHUGXGTGRTGGENCORUKCBP DNQQFRTGUUWTGBPP DKQRJ[UKECNRTQſNG HGVCNITQYVJ

TGUVTKEVKQP P JGOQN[UKUGNGXCVGFNKXGTGP\[OGNGXGNUCPFNQYRNCVGNGVNGXGNU056PQPUVTGUUVGUV A WODKNKECN
artery.
CH 47_p693-723_v3.indd 713 19-07-2015 11:09:45

by prolongation of pregnancy. Lowering of BP i e ipine

beyond a threshold level can cause decrease in Nifedipine is a calcium channel blocker and is
placental perfusion and fetal growth restriction. useful for rapid lowering of BP. It is the drug of
choice in severe hypertension, as an alterna-
Target blood pressure tive to labetalol. Side effects include tachycar-
dia, hypotension, and headache. Nifedipine can
Target BP in severe hypertension is 140–150 potentiate the action of magnesium sulfate, but
mm Hg systolic and 90–100 mm Hg diastolic. this drug interaction is rare.
In women with chronic hypertension and end-
organ damage, the target BP should be 140/90
mm Hg.
y rala ine
Hydralazine is a peripheral vasodilator and low-
ers the BP rapidly. The side effects may mimic
Antihypertensive drugs impending eclampsia and include tachycardia,
The antihypertensive drugs commonly used palpitation, headache, nausea, vomiting, and epi-
in preeclampsia and their dosage are listed in gastric pain. This drug has been largely replaced
Table 47.4. by labetalol and nifedipine.
D ethyl opa ther drugs

D-Methyldopa is not useful in severe preeclamp- Diuretics have been used in management of mild to
sia for rapid lowering of BP. The drug is safe in moderate hypertension but are currently not recom-
pregnancy and has no major side effects. It is mended. Clonidine has unacceptable side effects
useful in chronic hypertension and moderate and rebound hypertension. Sodium nitroprusside
gestational hypertension. It can be used as out- may be used as an infusion in refractory hyperten-
patient therapy. sion. Diazoxide and D-adrenergic blockers such as
prazosin have also been used in refractory hyperten-
abetalol sion but are not recommended for routine use.
Labetalol can be used for rapid reduction of BP.
Reduction in placental perfusion is not a con-
cern when used for short periods of time as in ELLP syndrome
severe preeclampsia. Intravenous labetalol is
HELLP is a syndrome characterized by hemo-
often used as the drug of choice in severe hyper-
lysis, elevated liver enzymes, and low platelet
tension. Oral labetalol may be used in expectant
count. It is probably a form of severe preeclamp-
management of severe preeclampsia or moder-
sia. However, 15%–20% of women with HELLP
ate hypertension.
Table 47.4 Antihypertensives used in preeclampsia drugs and dosage
Drug Mechanism Dosage

DOGVJ[NFQRC %GPVTCNN[CEVKPI ŌOIJQWTN[QTCNOCZKOWOIFC[
4GFWEGUU[ORCVJGVKEQWVƀQY
&GNC[GFQPUGVQHCEVKQP
ŌJQWTU
Labetalol #NRJCDGVCCFTGPGTIKEDNQEMGT ŌOI+8'XGT[ŌOKP
4CRKFQPUGVQHCEVKQP
ŌOKP OIVYKEGFCKN[QTCNOIOCZKOWO
E[ENG
0KſFKRKPG %CNEKWOEJCPPGNDNQEMGT OIGXGT[OKPQTCN
4CRKFQPUGVQHCEVKQP
ŌOKP (QNNQYGFD[ŌOIŌJQWTN[
*[FTCNC\KPG 2GTKRJGTCNXCUQFKNCVQT ŌOI+8
4CRKFQPUGVQHCEVKQP
ŌOKP 'XGT[ŌOKPOCZKOWOOI
CH 47_p693-723_v3.indd 714 19-07-2015 11:09:45

syndrome do not have hypertension or protein- &KHHGTGPVKCNFKCIPQUKU

uria. HELLP syndrome is also more common in
multiparous women. HELLP syndrome may be misdiagnosed as AFLP.
Idiopathic thrombocytopenia, acute appendici-
tis and cholecystitis, and thrombotic thrombocy-
Pathogenesis and pathology topenic purpura are other differential diagnoses.
The hepatic involvement and hemolysis are
more severe than in preeclampsia. Infarction
and hemorrhage are more pronounced, and rup- Management
ture of liver hematoma is more common.
Progressive and sudden deterioration of mater-
nal condition can occur with HELLP syndrome.
%NKPKECNHGCVWTGUCPFFKCIPQUKU Therefore, expectant management is not rec-
ommended irrespective of gestational age. Once
HELLP syndrome usually develops between 28
HELLP syndrome is diagnosed, patient must be
and 36 weeks’ gestation. Hypertension and pro-
delivered.
teinuria are present in 80% of women, but either or
both may be absent. The common symptoms are • Corticosteroids should be administered for pul-
nausea, vomiting, epigastric pain, and occasion- monary maturity if gestational age is <34 weeks.
ally headache. Abruptio placenta, DIC, pulmonary • Antihypertensives and magnesium sulfate
edema, or rupture of liver hematoma may occur. should be used if indicated.
Diagnosis of HELLP syndromeis made when • High-dose dexamethasone has not been found
all of the following criteria are present: to be beneficial and is not recommended.
• Labor may be induced following cervical rip-
• Microangiopathic hemolysis characterized by
ening with prostaglandins.
– Schistocytes/burr cells on blood smear
• Intramuscular injections, pudendal block, and
– Low serum haptoglobin (<25 mg/dL)
spinal/epidural anesthesia must be avoided
– Serum bilirubin t1.2 mg/dL
because of risk of bleeding.
• Platelet count <100,000/mm3
• Platelet transfusions are indicated if there is
• Serum SGOT/SGPT—twice the upper limit of
significant bleeding or when platelet count is
normal
<20,000/mm3.
If all of the criteria are not present, it is referred
to as partial HELLP syndrome. Elevated LDH
(>600 units/L) is nonspecific and is not included
2QUVRCTVWOOCPCIGOGPVQH
in the criteria. preeclampsia
Pathogenesis and clinical features of HELLP
After delivery, BP normalizes gradually and
syndrome are summarized in Box 47.20.
dose of antihypertensives should be adjusted
accordingly. Patient should be followed up till BP
returns to normal. If BP is persistently elevated
Box 47.20 ELLP syndrome after 12 weeks, the diagnosis may be changed
• &GXGNQRUDGVYGGPCPFYGGMU to chronic hypertension and further evaluation
• JCXGJ[RGTVGPUKQPCPFRTQVGKPWTKC is required.
• 5[ORVQOU
Ŧ 0CWUGCXQOKVKPI
Ŧ 'RKICUVTKERCKP
Ŧ *GCFCEJG Chronic hypertension
• %QORNKECVKQPU
Ŧ 2NCEGPVCNCDTWRVKQP Pregnancy in women with chronic hyperten-
Ŧ DIC sion is associated with suboptimal maternal and
Ŧ 2WNOQPCT[GFGOC perinatal outcome. Chronic hypertension is usu-
Ŧ 4WRVWTGQHNKXGTJGOCVQOC ally seen in older women. Even in the absence of
D C FKUUGOKPCVGFKPVTCXCUEWNCTEQCIWNCVKQP P JGOQN[UKU
superadded preeclampsia, maternal complica-
GNGXCVGFNKXGTGP\[OGNGXGNUCPFNQYRNCVGNGVNGXGNU tions and fetalgrowth restriction are common.
CH 47_p693-723_v3.indd 715 19-07-2015 11:09:46

When there is superadded preeclampsia, the

Box 47.22 ltrasonography in chronic
maternal and perinatal morbidity and mortality hypertension
are much higher compared with preeclampsia
arising de novo. The maternal and fetal complica- • (KTUVVTKOGUVGT
Ŧ )GUVCVKQPCNCIGGUVKOCVGF
tions are listed in Box 47.21.
• 5GEQPFVTKOGUVGT
Ŧ ŌYGGMU/QTRJQNQI[
Box 47.21 %QORNKECVKQPUQHEJTQPKEJ[RGTVGPUKQP • 6JKTFVTKOGUVGT
• 5WRGTKORQUGFRTGGENCORUKC Ŧ 5GTKCNDKQOGVT[$22KHWVGTKPGJGKIJVIGUVCVKQPCNCIG
• (GVCNITQYVJTGUVTKEVKQP Ŧ 5GTKCNWODKNKECNCTVGT[&QRRNGTKH()4FKCIPQUGF
• 2TGVGTODKTVJ BPP DKQRJ[UKECNRTQſNG HGVCNITQYVJTGUVTKEVKQP
• 2NCEGPVCNCDTWRVKQP
• %GTGDTCNJGOQTTJCIG
• Ultrasonography must be performed as indi-
cated in Box 47.22.
Diagnosis
Diagnosis of chronic hypertension is by history
Eclampsia
and BP recording in the first trimester. Since BP Eclampsia is the occurrence of convulsions in
falls in the second trimester of pregnancy, if the a woman with preeclampsia in the absence of
patient is seen for the first time in the second tri- other neurological conditions. Hypertension
mester, the diagnosis may be missed. The sub- and proteinuria precede the onset of eclamp-
sequent rise in BP may be interpreted as gesta- sia in most cases, but occasionally they may
tional hypertension. Most women have essential be absent.
hypertension, but renal, endocrine, and other
causes of hypertension must be excluded.
Incidence
Management Incidence is variable. In developed countries it
is 1.6–10/10,000 births. It occurs in 2%–3% of
• Preconceptional counseling is essential.
women with severe preeclampsia, not receiving
Patient should be evaluated for causes and
seizure prophylaxis. In developing countries, the
complications of hypertension.
incidence is much higher andoccurs in 1%–3.5%
• Most antihypertensives are safe in pregnancy
of all births.
except angiotensin receptor blockers and
angiotensin-converting enzyme inhibitors.
These drugs should be discontinued and sub- 4KUMHCEVQTU
stituted with safer drugs (described above).
Risk factors are the same as for preeclampsia
• Preconceptionally or if first seen during preg-
(Box 47.7). Young primigravid women from low
nancy, investigations should be performed to
socioeconomic status are at the highest risk.
screen for underlying renal disease, diabetes,
Eclampsia is rare before 20 weeks’ gestation.
and other comorbidities.
It usually occurs in the third trimester, labor, or
• Low-dose aspirin should be started at
postpartum. The timing of eclampsia is as follows:
12 weeks as prophylaxis against superimposed
preeclampsia. • Antepartum—55%
• If the BP rises, dose of antihypertensives must be • Intrapartum—30%
increased. Alternatively, change over to or addi- • Postpartum <48 hours after delivery—10%
tion of nifedipine or labetalol may reduce the BP. • Late postpartum >48 hours to <4 weeks after
• If superimposed preeclampsia develops, delivery—5%
patient must be managed accordingly
• Regular antenatal care, close monitoring of BP
and proteinuria, clinical monitoring of fetal
Pathology
growth, and delivery at term is the recom- Loss of autoregulation of cerebral circulation
mended management. causes segmental constriction and dilatation,
CH 47_p693-723_v3.indd 716 19-07-2015 11:09:46

ischemia, hemorrhage and necrosis. In addi-

Box 47.23 6
TCPUKGPVEJCPIGUCHVGTGENCORVKE
tion, there is exudation of fluid causing cerebral convulsions
edema. Features of hypertensive encephalopa-
thy are also seen. • *[RGTECRPGC
• *[RQZKC
• .CEVKECEKFQUKU
• Proteinuria
%NKPKECNHGCVWTGU • 1NKIWTKC
Typical eclamptic convulsions last for 3–4 min- • *GOQINQDKPGOKC
utes and havefour stages. • *GOQINQDKPWTKC
• (GVCNDTCF[ECTFKC
Premonitory stage
eclampticus, can result in prolonged coma and
The premonitory symptoms occur before the death.
onset of convulsions. These are:
• Headache—frontal or occipital
• Scotomata, blurred vision, diplopia, and Complications
photophobia Complications of eclampsia occur in 70% of
• Epigastric or right upper quadrant pain women (Box 47.24). Maternal death occurs in
• Mental confusion approximately 2% of women and perinatal mor-
tality may be as high as 25%–30% in developing
Tonic phase countries.
Tonic phase lasts for 15–20 seconds. There is

Box 47.24 %QORNKECVKQPUQHGENCORUKC
tonic spasm of the muscles and the body is rigid.
Twitching of the muscles of the face is seen. • /CVGTPCN
There may be frothing in the mouth. Ŧ +PVTCETCPKCNJGOQTTJCIG
Ŧ #URKTCVKQPRPGWOQPKC
Ŧ #EWVGRWNOQPCT[GFGOC
Clonic phase Ŧ Injuries
Ŧ 2NCEGPVCNCDTWRVKQP
Clonic phase lasts for 60–70 seconds and the Ŧ Renal failure
muscles contract and relax. The muscles of the Ŧ Blindness
face including the jaw and eyelids are involved Ŧ *GRCVQEGNNWNCTFCOCIG
initially, but soon the contractions spread to the Ŧ DIC
limbs and the entire body. The contractions are Ŧ 2U[EJQUKU
forceful; the woman may bite her tongue or may Ŧ /CVGTPCNOQTVCNKV[
• Fetal
fall off the bed.
Ŧ (GVCNJGCTVTCVGCDPQTOCNKVKGU
Ŧ #URJ[ZKC
Ŧ 2TGOCVWTKV[
2JCUGQHEQOC Ŧ +PVTCWVGTKPGFGCVJ
The convulsions slowly cease and coma usually
&+%FKUUGOKPCVGFKPVTCXCUEWNCTEQCIWNCVKQP
follows. This lasts for variable length of time. As
she wakes up, the woman may be agitated and
confused.
Following convulsions, there may be tran-
&KHHGTGPVKCNFKCIPQUKU
sient metabolic and other changes as listed in When convulsions occur in a pregnant woman
Box 47.23. They revert to normal with treatment in the third trimester or within 48 hours post-
during the next few hours; urine output improves partum, in the absence of previous known
and fetal heart rate becomes normal. Labor may seizure disorders, the diagnosis is eclampsia
begin after convulsions. unless proved otherwise.
Another convulsion may follow soon. The differential diagnosis to be consid-
Repeated convulsions, known as status ered is listed in Box 47.25. The most important
CH 47_p693-723_v3.indd 717 19-07-2015 11:09:46

Box 47.25 &KHHGTGPVKCNFKCIPQUKUKPGENCORUKC Box 47.26 Initial management in eclampsia

• Epilepsy • Patient in lateral position
• %GTGDTCNXGPQWUVJTQODQUKU • $GFUYKVJRTQVGEVKXGUKFGTCKNU
• *[RGTVGPUKXGGPEGRJCNQRCVJ[ • /QWVJICIMGRVTGCFKN[CXCKNCDNG
• 2QUVGTKQTTGXGTUKDNGGPEGRJCNQRCVJ[U[PFTQOG • /QWVJUWEVKQPVQTGOQXGUGETGVKQPUCPFXQOKVWU
• +PVTCETCPKCNVWOQTU • 8KVCNUKIPUOQPKVQTGF
• /GPKPIKVKUGPEGRJCNKVKU Ŧ Pulse
Ŧ Blood pressure
Ŧ Respiratory rate
Ŧ 1Z[IGPUCVWTCVKQPYKVJRWNUGQZKOGVT[
differential diagnosis is epilepsy. If there is sig- • 1Z[IGPCFOKPKUVGTGFD[OCUM
nificant papilledema, brain tumors must be con- • +8ƀWKFU
sidered. In women with postpartum eclampsia, • CVP line if required
cerebral venous thrombosis must be excluded.
Hypertensive encephalopathy and infections are C P EGPVTCNXGPQWURTGUUWTG intravenous.
other conditions that cause convulsions with-

out focal neurological signs. Posterior revers-
use if convulsions recur. Vomitus and secre-
ible encephalopathy syndrome (PRES) closely
tions must be aspirated. Initial management
resembles eclampsia and presents with head-
should continue as given in Box 47.26.
ache, visual disturbances, confusion, seizures,
• Intravenous fluids should be administered
and, occasionally, hypertension.
with caution. Due to maldistribution of fluid
/CPCIGOGPVQHGENCORUKC between the extravascular and intravascular
compartments, pulmonary edema can occur
6TCPUHGTVQVGTVKCT[EGPVGT easily. Ringer lactate 100–125 mL/hour is
recommended.
Patients with eclampsia should be transferred • The bladder should be catheterized after the
to a tertiary center for management after initi- first dose of magnesium sulfate is adminis-
ating antihypertensive and anticonvulsant treat- tered. Urine output must be monitored hourly.
ment. Intravenous magnesium sulfate 4 g and
oral nifedipine 20 mg should be administered.
Anticonvulsant therapy
Padded mouth gag should be placed to prevent
injury to the tongue. Intravenous line should /CIPGUKWOUWNHCVG
be in place with infusion of dextrose saline, and
Drug of choice for management and prevention
patient should be accompanied by a physician
of eclamptic convulsions is magnesium sulfate.
during transport.
• Several randomized trials and meta-analyses
Management have proved the superiority of magnesium
Management of a woman with eclampsia con- sulfate over phenytoin, diazepam, and lytic
sists of the following: cocktail for control of convulsions. Further
respiratory depression is much less frequent
• Initial supportive management
with magnesium sulfate.
• Anticonvulsant therapy
• Lytic cocktail, once popular in India, is not
• Antihypertensive therapy
used any more. Phenytoin and diazepam may
• Obstetric management
be used when convulsions continue despite
Initial management adequate dose of magnesium sulfate.
• Pharmacology of magnesium sulfate is given
Patient must be kept comfortable, steps to pre-
in Box 47.27. It is excreted by the kidney and
vent aspiration and injury and other supportive
blood levels increase in renal dysfunction;
measures initiated.
hence, dosage must be adjusted, if there is
• Patient should be kept in left lateral position in renal impairment. Urine output should be
a bed with protective side rails to prevent fall. monitored and maintained at >100 mL/4
Padded mouth gag should be kept ready for hours for continuation of treatment.
%*ARAXKPFF 19-07-2015 11:09:46

Box 47.27 2JCTOCEQNQI[QHOCIPGUKWOUWNHCVG Box 47. 28 &

QUCIGQHOCIPGUKWOUWNHCVGKP
eclampsia
• 'SWCNN[GHHGEVKXGD[+8CPF+/TQWVGU
• /GEJCPKUOQHCEVKQP • +PVTCXGPQWUTGIKOGP
Ŧ %GPVTCNCPVKEQPXWNUCPVCEVKQP Ŧ .QCFKPIFQUG
Ŧ 2GTKRJGTCNEWTCTGNKMGCEVKQP IFKNWVGFKPO.QH+8HNWKF
Ŧ 2TGXGPVKQPQHECNEKWOKPƀWZCVO[QPGWTCNLWPEVKQP #FOKPKUVGTGFQXGTŌOKPWVGU
• 'ZETGVGFD[MKFPG[ Ŧ /CKPVGPCPEGVJGTCR[
• 'ZEGUUFQUCIGECWUGU IJQWTYKVJKPHWUKQPRWOR
Ŧ Respiratory depression • +PVTCOWUEWNCTTGIKOGP
Ŧ Renal failure Ŧ .QCFKPIFQUG
• 6JGTCRGWVKEDNQQFNGXGNU 4 IQHUQNWVKQP+8QXGTOKPWVGU
Ŧ ŌO'S. IOKP PQVVQDGGZEGGFGF
• 'HHGEVUQPHGVWU (QNNQYGFD[IQHUQNWVKQP
Ŧ .QUUQHXCTKCDKNKV[QHHGVCNJGCTVTCVG IKPGCEJDWVVQEMFGGR+/
/C[DGOKZGFYKVJO.QHNKFQECKPG
Ŧ /CKPVGPCPEGVJGTCR[
IQHUQNWVKQPJQWTN[CNVGTPCVGDWVVQEMU
• Respiratory depression can occur with high Ŧ /QPKVQTGFDGHQTGGCEJFQUG
blood levels. Patellar tendon reflexes disap- RGURKTCVQT[TCVGUJQWNFDG OKP
pear when levels rise and can be used to moni- 2CVGNNCTTGHNGZUJQWNFDGRTGUGPV
tor toxicity. Respiratory rate and patellar ten- UrKPGQWVRWVUJQWNFDG O.JQWTU
don reflexes should be monitored every hour Ŧ +HEQPXWNUKQPUTGEWTCHVGTNQCFKPIFQUG
to rule out magnesium toxicity. #FFKVKQPCNIQHUQNWVKQP+8QXGTŌOKPWVGU
• Routine estimation of plasma levels is not
recommended. diastolic to 90–100 mm Hg. Antihypertensives
• Calcium gluconate is the antidote for magne- used are listed as follows:
sium. Calcium gluconate 1g should be admin-
istered intravenously if respiratory depression • Tab. nifedipine oral
occurs. • Injection labetalol IV
• Although magnesium is a uterine relaxant, • Injection hydralazine IV
it does not affect uterine contractions at the The dosage and administration have been dis-
usual therapeutic levels. cussed earlier in this chapter.
• Fetal heart rate trace may reveal loss of vari-
ability when the mother is on magnesium sul- Obstetric management
fate, but this is clinically insignificant. Once the patient is settled, convulsions are con-
trolled, and antihypertensives are administered,
Dosage and administration steps must be taken to deliver the fetus.
Magnesium sulfate can be administered intrave-
• The woman may already be in labor. Fetal heart
nously or intramuscularly. Intramuscular admin-
rate changes such as bradycardia, tachycardia,
istration is painful and has been abandoned in
and decelerations can occur during convulsions,
most centers. The dosage is given in Box 47.28.
but they recover after the seizure. Delivery should
It is the same for prophylaxis and treatment of
be expedited by artificial rupture of membranes
convulsions. The loading dose can be given
and oxytocin augmentation as required.
regardless of urine output. The drug should be
• If not in labor, decision regarding mode of
discontinued 24 hours after deliveryor24 hours
delivery should take into account the following:
after the last seizure, whichever occurs later.
– Gestational age
– Cervical Bishop score
– Estimated fetal weight
Antihypertensive management – Fetal compromise
– Maternal complications
BP must be controlled immediately. The systolic • If the gestational age is closer to term, the
BP should be maintained at 140–160 mm Hg and cervix is favorable, and there is no fetal
CH 47_p693-723_v3.indd 719 19-07-2015 11:09:46

compromise or maternal complication, vagi-

Box 47.29 +PFKECVKQPUHQTEGUCTGCPUGEVKQP
nal delivery is the option. Prostaglandins may
be used to ripen the cervix further and labor • 2TGOCVWTKV[YGGMU
induced with oxytocin. • 8GT[WPHCXQTCDNGEGTXKZ
• 5GXGTGHGVCNITQYVJTGUVTKEVKQP
• Prolonged second stage should be avoided. It
• #DPQTOCNHGVCNVGUVU
is advisable to shorten the second stage with
• /CVGTPCNEQORNKECVKQPU
outlet forceps. Ŧ 2WNOQPCT[GFGOC
• Methergine should not be used. Oxytocin 10 Ŧ Renal failure
units IM is administeredafter delivery of pla- Ŧ 2NCEGPVCNCDTWRVKQP
centa to minimize third stage hemorrhage. • 1DUVGVTKEKPFKECVKQPU
Ŧ /CNRTGUGPVCVKQPU
+PFKECVKQPUHQTEGUCTGCPUGEVKQP Ŧ (GVCNOCETQUQOKC
A cesarean section is indicated in situations where Ŧ +PVTCRCTVWOPQPTGCUUWTKPIHGVCNUVCVWU
labor may be prolonged or for obstetric reasons
(Box 47.29). General anesthesia is associated with risk of
difficult intubation and acute rise in BP during
• Epidural analgesia/anesthesia is recom-
intubation.
mended during labor and for cesarean sec-
tion. Spinal anesthesia or combined epidural Management of eclampsia is outlined in
and spinal techniques may also be used. Figure 47.8.
clampsia
Hospitali e
nitial supporti e treatment

e ith protecti e rails
nticon ulsant management ntihypertensi e management
Mouth gag
Magnesium sulfate nifi ipine mg hourly or
uction bstetric management
loa ing ose njection labetalol mg V
V flui s
Maintenance therapy Continue as re uire
ygen
Monitor ital signs
n labor
ot in labor
M o ytocin
ee s
ee s
Lo ishop score
High ishop score
etal compromise
o fetal compromise
o maternal complications
bstetric in ications
Prostaglan ins Cesarean

M o ytocin section
Figure 47.8 /CPCIGOGPVQHGENCORUKCA CTVKſEKCNTWRVWTGQHOGODTCPGU
CH 47_p693-723_v3.indd 720 19-07-2015 11:09:46

Postpartum management Contraception

BP may remain elevated for a few days postpar- Intrauterine devices, progesterone-only pill,
tum. Oral nifedipine or labetalol can be con- and injectable pregestational agents are safe in
tinued. Close attention should be paid to fluid women with hypertensive disorders. Combined
management and monitoring of BP. Follow-up oral contraceptives can be started after BP
with BP monitoring should continue till it returns to normal.
returns to normal. If BP remains elevated after 6
weeks postpartum, patient should be evaluated
for chronichypertension.
Key points
• *[RGTVGPUKQPKPRTGIPCPE[KUFGſPGFCUU[UVQNKEDNQQF • 6JGTGCTGPQTGNKCDNGUGPUKVKXGVGUVUVQRTGFKEV
RTGUUWTGQHOO*ICPFQTFKCUVQNKEDNQQFRTGU- RTGGENCORUKC7VGTKPGCTVGT[&QRRNGTKUOQTGWUGHWNKP
UWTGQHOO*IVJGOGCUWTGOGPVUEQPſTOGFD[ RTGFKEVKQPQHHGVCNITQYVJTGUVTKEVKQP
TGRGCVGFTGCFKPIUŌJQWTUCRCTV • .QYFQUGCURKTKPOIFC[KUTGEQOOGPFGFHQT
• 6JG#OGTKECP%QNNGIGQH1DUVGVTKEKCPUCPF RTGXGPVKQPQHRTGGENCORUKCKPJKIJTKUMYQOGP
)[PGEQNQIKUVU
#%1)ENCUUKſGUJ[RGTVGPUKQP • /CVGTPCNCPFRGTKPCVCNEQORNKECVKQPUCTGOKPKOCNYKVJ
KPRTGIPCPE[KPVQHQWTECVGIQTKGUIGUVCVKQPCN IGUVCVKQPCNJ[RGTVGPUKQP/CVGTPCNEQORNKECVKQPUQH
J[RGTVGPUKQPRTGGENCORUKCCPFGENCORUKCU[PFTQOG RTGGENCORUKCCTGRNCEGPVCNCDTWRVKQPRTGVGTONCDQT
EJTQPKEJ[RGTVGPUKQPCPFRTGGENCORUKCUWRGTKO- JGOQN[UKUGNGXCVGFNKXGTGP\[OGNGXGNUCPFNQY
RQUGFQPEJTQPKEJ[RGTVGPUKQP RNCVGNGVNGXGNU
*'..2U[PFTQOGCEWVGTGPCNHCKNWTG
• )GUVCVKQPCNJ[RGTVGPUKQPFGXGNQRUCHVGTYGGMUŏ CPFGENCORUKC
IGUVCVKQPCPFVJGTGKUPQRTQVGKPWTKC • 2GTKPCVCNEQORNKECVKQPUQHRTGGENCORUKCCTGITQYVJ
• 2TGGENCORUKCKUPGYQPUGVJ[RGTVGPUKQPYKVJRTQ- TGUVTKEVKQPRTGOCVWTKV[CURJ[ZKCCPFTKUMQH
VGKPWTKCVJCVFGXGNQRUCHVGTYGGMUŏIGUVCVKQP6JKU RGTKPCVCNOQTVCNKV[
OC[DGPQPUGXGTGQTUGXGTGDCUGFQPEGTVCKPETKVGTKC • 9QOGPYKVJPQPUGXGTGIGUVCVKQPCNJ[RGTVGPUKQPCPF
• %JTQPKEJ[RGTVGPUKQPKURTGUGPVDGHQTGYGGMUŏIGU- RTGGENCORUKCCTGCU[ORVQOCVKE
VCVKQPCPFEQPVKPWGUDG[QPFYGGMURQUVRCTVWO • 5GXGTGRTGGENCORUKCKUCUUQEKCVGFYKVJU[ORVQOU
• 9JGPVJGTGKUYQTUGPKPIQHJ[RGTVGPUKQPRTQVGKPWTKC CPFUKIPUUWEJCUPCWUGCXQOKVKPIGRKICUVTKERCKP
QTPGYQPUGVRTQVGKPWTKCKPCYQOCPYKVJEJTQPKE GFGOCCUEKVGUCPFTGFWEGFHGVCNOQXGOGPVU
J[RGTVGPUKQPKVKURTGGENCORUKCUWRGTKORQUGFQP • &KCIPQUKUQHJ[RGTVGPUKQPKPRTGIPCPE[KUENKPKECN
EJTQPKEJ[RGTVGPUKQP 1PEGJKIJDNQQFRTGUUWTGKUKFGPVKſGFKVKUKORQTVCPV
• 4KUMHCEVQTUHQTJ[RGTVGPUKQPCTGRTKOKRCTKV[[QWPIGT VQFKHHGTGPVKCVGCOQPIIGUVCVKQPCNJ[RGTVGPUKQPRTGGE-
CIGITQWRQTCIG OWNVKHGVCNRTGIPCPE[OQNCT NCORUKCCPFEJTQPKEJ[RGTVGPUKQP
RTGIPCPE[OCVGTPCNOGFKECNRTQDNGOURCUVCPF • 6JKUFKHHGTGPVKCVKQPKUD[JKUVQT[RJ[UKECNGZCOKPCVKQP
HCOKN[JKUVQT[QHRTGGENCORUKCNQYUQEKQGEQPQOKE CPFKPXGUVKICVKQPU6JGUGXGTKV[QHRTGGENCORUKCCNUQ
UVCVWUCPFGPXKTQPOGPVCNHCEVQTU JCUVQDGFGVGTOKPGF
• 2CVJQIGPGUKUQHRTGGENCORUKCDGIKPUYKVJCDPQTOCN • 0QPUGXGTGIGUVCVKQPCNJ[RGTVGPUKQPECPDGOCPCIGF
VTQRJQDNCUVKEKPXCUKQPNGCFKPIVQRNCEGPVCNJ[RQRGTHW- CUQWVRCVKGPVD[OQPKVQTKPIDNQQFRTGUUWTGWTKPG
UKQPKUEJGOKCCPFJ[RQZKC.GXGNUQHCPVKCPIKQIGPKE RTQVGKPCPFVGUVUVQGZENWFGRTQITGUUKQPQHFKUGCUG
HCEVQTUKPETGCUGCPFCPIKQIGPKEHCEVQTUFGETGCUG (GVWUKUOQPKVQTGFD[FCKN[OQXGOGPVEQWPVCPFPQP-
ECWUKPIGPFQVJGNKCNFCOCIGCPFF[UHWPEVKQPNGCFKPI UVTGUUVGUVDKQRJ[UKECNRTQſNGQPEGKPYGGMU
VQKPETGCUGFXCUEWNCTRGTOGCDKNKV[CPFOKETQXCUEWNCT
EQCIWNCVKQPXCUQURCUOCPFRNCVGNGVCIITGICVKQP • 9QOGPYKVJPQPUGXGTGJ[RGTVGPUKQPUJQWNFDGFG-
NKXGTGFD[ŌYGGMUŏIGUVCVKQPFGRGPFKPIQPVJG
• 'PFQVJGNKCNFCOCIGCPFF[UHWPEVKQPKUVJGDCUKE blood pressure.
RCVJQNQI[KPCNNQTICPUECWUKPIKUEJGOKCPGETQUKU
CPFJGOQTTJCIG • 9QOGPYKVJPQPUGXGTGRTGGENCORUKCUJQWNFDG
JQURKVCNK\GFCPFOQPKVQTGFOQTGENQUGN[CPFFGNKXGTGF
• 2CVJQNQIKECNEJCPIGUCTGUGGPKPOWNVKRNGQTICP D[ŌYGGMU
U[UVGOUKPVJGDQF[UWEJCUVJGJGCTVMKFPG[UDTCKP
NKXGTTGVKPCCPFRNCEGPVC • 9QOGPYKVJUGXGTGIGUVCVKQPCNJ[RGTVGPUKQPUJQWNF
DGJQURKVCNK\GFCPFUVCTVGFQPCPVKJ[RGTVGPUKXGUCPF
(Continued)
CH 47_p693-723_v3.indd 721 19-07-2015 11:09:46


OCIPGUKWOUWNHCVG%QTVKEQUVGTQKFUUJQWNFDGIKXGPKH • 'ZRGEVCPVOCPCIGOGPVRTQNQPIURTGIPCPE[D[Ō
IGUVCVKQPCNCIGKUŌYGGMU$NQQFRTGUUWTGWTKPG FC[UCPFKORTQXGURGTKPCVCNUWTXKXCN
QWVRWVCPFRTQVGKPWTKCUJQWNFDGEJGEMGFJQWTN[ • #PVKJ[RGTVGPUKXGUWUGFKPRTGGENCORUKCCTG
• +PXGUVKICVKQPUKPENWFGNKXGTGP\[OGURNCVGNGVEQWPV DOGVJ[NFQRCNCDGVCNQNPKHGFKRKPGCPFJ[FTCNC\KPG
RGTKRJGTCNUOGCTCPFUGTWOETGCVKPKPG(GVCNYGNN • *'..2U[PFTQOGEQPUKUVUQHJGOQN[UKUGNGXCVGFNKXGT
DGKPIUJQWNFDGCUUGUUGFD[DKQRJ[UKECNRTQſNGCPF GP\[OGUCPFVJTQODQE[VQRGPKC9QOGPYKVJ*'..2
WODKNKECNCTVGT[&QRRNGT U[PFTQOGUJQWNFDGFGNKXGTGFCUUQQPCURQUUKDNG
• +OOGFKCVGFGNKXGT[KUKPFKECVGFKPYQOGPCV CHVGTCFOKPKUVTCVKQPQHCPVKJ[RGTVGPUKXGUOCIPGUKWO
QTYGGMUŏIGUVCVKQPRGTUKUVGPVRTQVGKPWTKCCPF UWNHCVGCPFDGVCOGVJCUQPG
EGTGDTCNU[ORVQOURWNOQPCT[GFGOCTGPCNHCKNWTG • 'ENCORUKCKUVJGQEEWTTGPEGQHEQPXWNUKQPUKPC
*'..2U[PFTQOGCDTWRVKQPQTHGVCNEQORTQOKUG YQOCPYKVJUGXGTGRTGGENCORUKC
• 'ZRGEVCPVOCPCIGOGPVKUCPQRVKQPHQTYQOGP • 'ENCORUKCKUCUUQEKCVGFYKVJOCVGTPCNCPFHGVCNEQO-
DGVYGGPCPFYGGMUŏIGUVCVKQP6JKUEQPUKUVUQH RNKECVKQPUOQTVCNKV[CPFOQTDKFKV[
ENQUGOQPKVQTKPIQHOCVGTPCNCPFHGVCNYGNNDGKPICPF
FGNKXGT[CVYGGMUQTGCTNKGTKHVJGTGKUOCVGTPCNQT • /CPCIGOGPVQHGENCORUKCKUD[IGPGTCNUWRRQTVKXG
HGVCNEQORTQOKUG VJGTCR[OCIPGUKWOUWNHCVGHQTEQPVTQNQHUGK\WTGU
CPVKJ[RGTVGPUKXGUCPFKOOGFKCVGFGNKXGT[
5GNH#UUGUUOGPV
Case-based questions 1. 9JCVKUVJGFKCIPQUKU!
2. 9JCVKUVJGKOOGFKCVGOCPCIGOGPV!
Case 1 3. 9JCVKUVJGQDUVGVTKEOCPCIGOGPV!
4. 9JCVEQORNKECVKQPUFQ[QWCPVKEKRCVG!
rs RTKOKITCXKFCRTGUGPVGFCVYGGMUŏRTGI-
PCPE[YKVJGNGXCVGFDNQQFRTGUUWTGUKPEGYGGMUJGCF-
CEJG CPF GRKICUVTKE RCKP 'ZCOKPCVKQP TGXGCNGF DNQQF Answers
RTGUUWTGQHOO*ICPFWTKPGRTQVGKPQPFKRUVKEM
QH 6JG WVGTWU EQTTGURQPFGF VQ VJG IGUVCVKQPCN CIG
CPFVJGHGVCNJGCTVTCVGYCUPQTOCN
Case 1
1. 5GXGTGRTGGENCORUKCōDNQQFRTGUUWTGOO
1. 9JCVKUVJGFKCIPQUKU!
*ICPF RTQVGKPWTKC
2. *QYYKNN[QWGXCNWCVGVJKURCVKGPV!
2. $NQQFRTGUUWTGWTKPGRTQVGKPWTKPGQWVRWVCPFUKIPU
3. 9JCVEQORNKECVKQPUFQ[QWCPVKEKRCVG! CPFU[ORVQOUUWEJCUJGCFCEJGXKUWCNFKUVWTDCPE-
4. 9JCVKUVJGOCPCIGOGPV! GUGRKICUVTKERCKPDTGCVJNGUUPGUUXCIKPCNDNGGFKPI
CPFHGVCNOQXGOGPVU
Case 2
+PXGUVKICVKQPUōWTKPGRTQVGKPETGCVKPKPGTCVKQNKXGTHWPE-
/TU ,% RTKOKITCXKFC ECOG HQT TGIWNCT CPVGPCVCN VKQPVGUVUUGTWOETGCVKPKPGRGTKRJGTCNUOGCTRNCVGNGVU
EJGEMWRCVYGGMU*GTDNQQFRTGUUWTGYCUHQWPFVQDG and LDH.
OO*ICPFWTKPGRTQVGKPYCUPGICVKXG (GVCNGXCNWCVKQPō056DKQRJ[UKECNRTQſNGCPFWODKNKECN
1. 9JCVKUVJGFKCIPQUKU! artery Doppler.
2. *QYYKNN[QWFKHHGTGPVKCVGVJKUHTQOEJTQPKEJ[RGTVGPUKQP! 3. #DTWRVKQPRWNOQPCT[GFGOCGENCORUKCTGPCNHCKN-
3. *QYYKNN[QWGXCNWCVGVJKUYQOCP! WTG&+%*'..2CDPQTOCNDKQRJ[UKECNRTQſNGCPF
4. 9JCVKUVJGOCPCIGOGPV! Doppler study.
4. #PVKJ[RGTVGPUKXGō6PKHGFKRKPGOIJQWTN[QT+8
NCDGVCNQNŌOIGXGT[ŌOKPWVGUVKNN$2TG-
Case 3 FWEGUVQOO*I/CIPGUKWOUWNHCVGNQCFKPI
FQUGI+8KPHWUKQPHQNNQYGFD[IJQWTN[
# [GCTQNF UGEQPF ITCXKFC YCU DTQWIJV VQ VJG NCDQT
TQQOCVYGGMUŏIGUVCVKQPYKVJEQPXWNUKQPUQPVJGYC[ $GVCOGVJCUQPGOI+/3JQWTU
VQJQURKVCN6JGTGYCUCJKUVQT[QHJKIJDNQQFRTGUUWTGHQT +H DNQQF RTGUUWTG CPF QVJGT U[ORVQOU CTG WPFGT EQP-
YGGMUCPFJGCFCEJGHQTFC[1PGZCOKPCVKQPRCVKGPV VTQNPQHGVCNEQORTQOKUGōGZRGEVCPVOCPCIGOGPVVKNN
YCU PQV HWNN[ EQPUEKQWU YCU TGUVNGUU CPF JCF C DNQQF YGGMUCPFFGNKXGT+HPQVKOOGFKCVGFGNKXGT[
RTGUUWTGQHOO*I
CH 47_p693-723_v3.indd 722 19-07-2015 11:09:46

Case 2 3. 5KPEGIGUVCVKQPCNCIGYGGMUVJGEGTXKZNKMGN[VQ
DGWPHCXQTCDNG%GUCTGCPUGEVKQPWPFGTGRKFWTCN
1. 0QPUGXGTGIGUVCVKQPCNJ[RGTVGPUKQP CPGUVJGUKCCHVGTVJGOQVJGTKUUVCDKNK\GF
2. 0QHCOKN[JKUVQT[QHRTGGENCORUKCJKUVQT[QHJKIJ 4. 2WNOQPCT[GFGOCTGPCNHCKNWTGEGTGDTCNJGOQTTJCIG
DNQQFRTGUUWTGRTKQTVQRTGIPCPE[QTKPVJGſTUV TGEWTTGPEGQHEQPXWNUKQPUCDTWRVKQP&+%DNKPFPGUU
VTKOGUVGTWTKPGOKETQUEQR[HQTITCPWNCTECUVUCPF RU[EJQUKUCPFHGVCNJGCTVTCVGCDPQTOCNKVKGU
TGFEGNNURQUKVKXGōGUUGPVKCNQTTGPCNJ[RGTVGPUKQP
+H HCOKN[ JKUVQT[ QH RTGGENCORUKC RTGUGPV PQTOCN DNQQF Sample questions
RTGUUWTGRTKQTVQRTGIPCPE[CPFKPVJGſTUVVTKOGUVGTCPF
WTKPGOKETQUEQR[PQTOCNIGUVCVKQPCNJ[RGTVGPUKQP Long-answer questions
3. /QVJGTNKXGTHWPEVKQPVGUVURNCVGNGVEQWPVCPFUKIPU 1. &KUEWUUVJGENKPKECNHGCVWTGUCPFOCPCIGOGPVQH
CPFU[ORVQOUQHRTGGENCORUKCōYGGMN[ GENCORUKC
(GVCN OQXGOGPV EQWPV 056 CPF DKQRJ[UKECN RTQſNGō 2. %NCUUKH[J[RGTVGPUKXGFKUQTFGTUQHRTGIPCPE[*QY
QPEGKPYGGMU YKNN[QWOCPCIGPQPUGXGTGRTGGENCORUKC!
3. 9JCVCTGVJGUKIPUCPFU[ORVQOUQHUGXGTGRTGGE-
4. /CPCIGCUQWVRCVKGPV%JGEMWRYGGMN[/QPKVQTVJG NCORUKC!*QYYKNN[QWOCPCIGUGXGTGRTGGENCORUKC
OQVJGTCPFVJGHGVWU+HDNQQFRTGUUWTGOO*I CVYGGMUŏIGUVCVKQP!
FGNKXGTCVŌYGGMU+HDNQQFRTGUUWTGŌOO
*IFGNKXGTCVŌYGGMU
Case 3 1. %QORNKECVKQPUQHRTGGENCORUKC
2. %QORNKECVKQPUQHGENCORUKC
1. #PVGRCTVWOGENCORUKC 3. *'..2U[PFTQOG
2. )GPGTCNUWRRQTVKXGOCPCIGOGPVōNGHVNCVGTCNRQUK- 4. 2CVJQIGPGUKUQHRTGGENCORUKC
VKQPDGFYKVJUKFGTCKNUCPFUWEVKQPVQTGOQXGUGETG-
5. 5KIPUCPFU[ORVQOUQHUGXGTGRTGGENCORUKC
VKQPU%JGEMDNQQFRTGUUWTGRWNUGCPFTGURKTCVKQP
6. &KHHGTGPVKCNFKCIPQUKUQHGENCORUKC
/CIPGUKWOUWNHCVGNQCFKPIFQUG 7. /CIPGUKWOUWNHCVGKPGENCORUKC
+PLGEVKQPNCDGVCNQN ŌOI +8 GXGT[ Ō OKPWVGU VKNN 8. #PVKJ[RGTVGPUKXGUKPRTGGENCORUKCGENCORUKC
DNQQFRTGUUWTGEQOGUFQYPVQOO*I U[PFTQOG
+PXGUVKICVKQPUōNKXGT GP\[OGU RNCVGNGV EQWPV UGTWO
ETGCVKPKPG056DKQRJ[UKECNRTQſNGCPFWODKNKECNCTVGT[
Doppler.
CH 47_p693-723_v3.indd 723 19-07-2015 11:09:46

Pregestational
48 and Gestational
Diabetes
Case scenario
Mrs. PN, 28, second gravida, was referred to the antenatal clinic by a
village midwife at 30 weeks as she felt that the baby was big. Oral glu-
cose tolerance test revealed high fasting and postglucose plasma glucose
values. She was admitted to the hospital for control of diabetes and evalu-
ation of fetus.
Introduction Incidence
Diabetes is a common medical disorder in India The prevalence and incidence of diabetes are
and so it is not uncommon to encounter it in increasing globally. In urban India diabetes preva-
pregnant women. Diabetes in pregnancy is asso- lence is 9% and in rural India the prevalence is 4%.
ciated with high perinatal mortality and morbid- Further, diabetes mellitus (DM) occurs at a younger
ity if hyperglycemia is not well controlled. With age in the Indian population. This is related to life-
better understanding of the pathophysiology of style changes with increasing prevalence of obe-
diabetes in pregnancy, and better glycemic con- sity, metabolic syndrome, and polycystic ovary
trol with insulin, perinatal outcome has improved syndrome (PCOS). These conditions predispose to
dramatically. Early diagnosis, preconceptional type 2 diabetes occurring at a younger age. This has
advice, good glycemic control, and appropriate led to an increase in gestational diabetes mellitus
monitoring of fetal well-being are all essential to (GDM), a forerunner of type 2 diabetes and preges-
achieve this. tational diabetes in Indian women.
CH 48_p724-739_v3.indd 724 19-07-2015 01:15:51

Pregestational and Gestational Diabetes 725
Box 48.1 %
NCUUKſECVKQPQHFKCDGVGU Box 48.2 Pregestational (overt) diabetes
in pregnancy
• Type 1 diabetes
• Pregestational or overt diabetes Ŧ Younger age group
Ŧ Type 1 Ŧ #DUQNWVGKPUWNKPFGſEKGPE[
Ŧ Type 2 Immune mediated
• Gestational diabetes +FKQRCVJKE
Ŧ Nonobese
Ŧ 'WIN[EGOKCFKHſEWNVVQCEJKGXG
Ŧ More prone to
MGVQCEKFQUKU
%NCUUKſECVKQP J[RQIN[EGOKC
• Type 2 diabetes
Diabetes in pregnancy is classified as in Box 48.1. Ŧ Older age group
A classification by Priscilla White that had Ŧ +PETGCUGFKPUWNKPTGUKUVCPEG
been in use since 1978 has been now replaced by Ŧ EEGNNF[UHWPEVKQP
Ŧ Usually obese
the above classification.
Ŧ *CXGCUUQEKCVGFOGVCDQNKEU[PFTQOG2%15
Ŧ /C[DGQPQTCNJ[RQIN[EGOKECIGPVU
Ŧ Less prone to
MGVQCEKFQUKU
Pregestational or overt J[RQIN[EGOKC
diabetes mellitus PC S RQN[E[UVKEQXCT[U[PFTQOG
The two major types of diabetes that can predate

pregnancy are type 1 diabetes (formerly known
as insulin-dependent diabetes) and type 2 dia- pancreatic E-cell dysfunction. Women with type
betes (formerly known as non-insulin-depen- 2 diabetes are usually obese and have a history
dent diabetes). suggestive of PCOS or other components of the
metabolic syndrome. They may be on oral hypo-
Type 1 diabetes glycemic agents (OHAs) before pregnancy, and
this has to be reviewed in the preconceptional
Type 1 diabetes may occur at any age but occurs period.
more commonly in younger subjects. It is char-
acterized by absolute insulin deficiency. This is
mostly immunologically mediated. Weight loss
at presentation, very high and fluctuating plasma Gestational diabetes
glucose levels, high risk for diabetic ketoacidosis
(DKA), and difficulty in achieving and maintain- mellitus
ing euglycemia are hallmarks of this condition.
Further, individuals with type 1 diabetes are &GſPKVKQP
prone to hypoglycemic episodes when they are
on insulin (Box 48.2). Gestational diabetes mellitus is defined as any
degree of glucose intolerance with onset in or
first recognition in pregnancy, irrespective of
whether insulin is used for treatment or not.
Type 2 diabetes Because of the increasing number of women
who probably have pregestational diabetes that
Most women with overt diabetes in pregnancy has been first discovered in pregnancy, other ter-
have type 2 diabetes. This disorder usually minology has been introduced.
occurs in the older age group. It is associated Gestational diabetes: Diabetes diagnosed
with increased peripheral insulin resistance and during the second half of pregnancy.
CH 48_p724-739_v3.indd 725 19-07-2015 01:15:51

Box 48.3 Gestational diabetes Box 48.5 Substances causing increase

in insulin resistance
• )GUVCVKQPCN FKCDGVGU KU FKCIPQUGF HQT VJG ſTUV VKOG KP
RTGIPCPE[ • *WOCPRNCEGPVCNNCEVQIGP
• +VKUFWGVQWPOCUMKPIQHUWUEGRVKDKNKV[VQV[RGFKCDGVGU • Estrogen and progesterone
• +VUJCTGUEQOOQPHGCVWTGUYKVJV[RGFKCDGVGU • %QTVKUQNRTQNCEVKP
• /QUVUWDLGEVUPGGFQPN[NKHGUV[NGEJCPIGHQTEQPVTQN • 6WOQTPGETQUKUHCEVQTD
• 1EECUKQPCNN[KPUWNKPKUPGGFGFVQCEJKGXGGWIN[EGOKC • %TGCEVKXGRTQVGKP
• QHRCVKGPVUFGXGNQRQXGTVFKCDGVGUNCVGTKPNKHG • Interleukin-6
Overt diabetes or diabetes mellitus in pregnancy: are not adequate for the fetus, maternal amino
Diabetes diagnosed by standard nonpregnant cri- acids and free fatty acids are utilized as substrate
teria early in pregnancy. for energy. This leads to mild ketosis and is referred
Women with GDM have metabolic charac- to as accelerated starvation of pregnancy.
teristics similar to women with type 2 diabetes,
and 50% of them develop type 2 diabetes later in
life. Gestational diabetes mellitus may therefore Increased insulin resistance
be considered to be due to pregnancy induced Peripheral resistance to insulin increases gradu-
unmasking of susceptibility to type 2 diabetes ally as pregnancy advances. It is due to increasing
(Box 48.3). levels of diabetogenic placental hormones (the
most important being human placental lactogen)
(Box 48.5) and other diabetogenic substances, in
particular, tumor necrosis factor-D(TNF-D).
Glucose metabolism in
pregnancy Postprandial hyperglycemia
To understand the maternal and fetal complica- Insulin resistance leads to decreased uptake of
tions in pregnant diabetics, it is important to be glucose by cells and consequent postprandial
aware of the changes in glucose metabolism in hyperglycemia. Both increase in insulin resis-
pregnancy. The characteristic changes in glucose tance and placental insulin destruction necessi-
homeostasis are listed in Box 48.4. tate increased insulin secretion by E-cells. Despite
this increase in insulin, hepatic glucose output
Fasting hypoglycemia continues unabated due to a lack of inhibition
of glucagon and an increase in human placental
The fasting hypoglycemia is due to continuous lactogen. Overall, the changes in glucose metab-
fetal utilization of glucose irrespective of mater- olism in pregnancy lead to a diabetogenic state.
nal glucose levels, that is, the fetus continues to be The progressive increase in insulin resistance
fed even if the mother starves. The hemodilution of culminates in overt abnormality of glucose tol-
pregnancy and decreased caloric intake in the first erance, at approximately 24–28 weeks’ gestation.
trimester due to nausea and vomiting contribute This is the reason for performing the screening
to the hypoglycemia. When blood levels of glucose test for GDM at this period of gestation, even if
first trimester tests are normal.
Box 48.4 Changes in glucose metabolism

in pregnancy
• 6GPFGPE[HQTHCUVKPIJ[RQIN[EGOKC 5ETGGPKPIHQTFKCDGVGU
• +PETGCUGKPRQUVRTCPFKCNINWEQUG
• +PETGCUGFKPUWNKPTGUKUVCPEG
in pregnancy
• 'ZCIIGTCVGFKPUWNKPUGETGVKQPKPTGURQPUGVQINWEQUG
It is well known that overt diabetes in pregnancy
• &GUVTWEVKQPQHKPUWNKPD[RNCEGPVCNKPUWNKPCUG
is associated with maternal and fetal com-
• +PETGCUGKPJGRCVKEINWEQUGQWVRWV
plications. However, there was no consensus
CH 48_p724-739_v3.indd 726 19-07-2015 01:15:51

regarding need for routine screening since

Box 48.6 9
QOGPCVJKIJTKUMHQTFGXGNQRKPI
the effect of treating minor abnormalities of gestational diabetes
blood glucose were not clear. The recently pub-
lished Hyperglycemia and Adverse Pregnancy • 2GTUQPCNJKUVQT[QH
Ŧ )&/KPCRTGXKQWURTGIPCPE[
Outcome (HAPO) study has clearly established
Ŧ KORCKTGFINWEQUGVQNGTCPEG
that there is a linear association between ris-
Ŧ INWEQUWTKC
ing blood glucose levels and adverse pregnancy • /GODGT QH CP GVJPKE ITQWR YKVJ C JKIJ RTGXCNGPEG QH
outcome, even with minor degrees of glucose type 2 diabetes mellitus
intolerance not amounting to diabetes melli- • 5VTQPIHCOKN[JKUVQT[QHV[RGFKCDGVGU
tus. A large interventional study showed that Ŧ First degree relatives
diagnosis and appropriate treatment of glucose • Maternal age >25 years
intolerance significantly reduced these com- • /CVGTPCNDKTVJYGKIJV MIQTMI
plications, particularly fetal macrosomia and • /GFKECNEQPFKVKQPU
perinatal mortality. The important issues that Ŧ /GVCDQNKEU[PFTQOG
confront the clinician are (a) whom to screen, Ŧ 2QN[E[UVKEQXCT[U[PFTQOG
2%15
Ŧ %WTTGPVWUGQHINWEQEQTVKEQKFU
(b) how to screen, and (c) when to screen for
Ŧ Hypertension
gestational diabetes.
• Obesity
Ŧ 2TGRTGIPCPE[$/+ MIO2
Whom to screen Ŧ 5KIPKſECPV YGKIJV ICKP KP GCTN[ CFWNVJQQF CPF
DGVYGGPRTGIPCPEKGU
Screening for diabetes may be as follows: Ŧ 'ZEGUUKXGIGUVCVKQPCNYGKIJVICKP
• Universal: Offered to every pregnant woman. • 2TGXKQWURQQTQDUVGVTKEQWVEQOGUWIIGUVKXGQH)&/
Ŧ &GNKXGT[QHCDCD[ MI
• Selective: Offered only to women with risk
Ŧ Unexplained perinatal loss
factors.
Ŧ *[RGTVGPUKQPRQN[J[FTCOPKQU
The decision on whether to perform universal Ŧ $KTVJQHCOCNHQTOGFKPHCPV
or selective screening in a given ethnic group Ŧ 0GQPCVCNJ[RQIN[EGOKC
would depend on risk categorization, as shown • )N[EQUWTKCCVVJGſTUVRTGPCVCNXKUKV
in Box 48.6. Women with none of the listed risk B body mass index; D gestational diabetes mellitus; PC S
RQN[E[UVKEQXCT[U[PFTQOG
factors are considered low risk for developing
GDM. Since Indians belong to an ethnic group
that is at high risk for developing type 2 DM, all
Indian women belong to the high risk category.
It is, therefore, recommended that all Indian
women be offered screening for GDM.
Two-step approach
The increase in prevalence of obesity in The two-step approach consists of screening
Western countries has resulted in most Western with glucose challenge test (GCT) followed by
women being placed in the high risk category. glucose tolerance test (GTT) for those who are
Current recommendation by the International positive.
Association of Diabetes and Pregnancy Study
Group (IADPSG) is to screen all pregnant women
lucose challenge test
at the first antenatal visit. If the screening is
negative at this time, it should be repeated at Fifty grams of oral glucose is administered irre-
24–28 weeks. spective of the time of last meal. Plasma glu-
Selective screening is practiced in some coun- cose is measured 1 hour later. A value of 130 or
tries with low prevalence of diabetes. 140 mg% is used as a cutoff. Those with values
above the cutoff should undergo diagnostic test-
ing with oral GTT (OGTT). A cutoff of 130 mg%
ow to screen has a higher pickup rate, but either cutoff may
Screening of asymptomatic women with no his- be used. With the simplification of screening
tory of prior glucose abnormality may be by a as detailed below, the two-step approach is not
two-step approach or a one-step approach. commonly used at present.
CH 48_p724-739_v3.indd 727 19-07-2015 01:15:51

Box 48.7 1
PGUVGRCRRTQCEJHQTFKCIPQUKU Box 48.8 75-g, 2-hour oral glucose tolerance
QH)&/CPFQXGTV&/ test
• 2GTHQTOGFKP • 1XGTPKIJVHCUVKPI
Ŧ CNNRTGIPCPVYQOGP • (CUVKPIRNCUOCINWEQUG
• 2GTHQTOGFCVſTUVRTGPCVCNXKUKV • IINWEQUGOKZGFKPO.QHNKOGLWKEGYCVGT
• )&/KUFKCIPQUGFKH • 2NCUOCINWEQUGCVCPFJQWTU
Ŧ HCUVKPIRNCUOCINWEQUG OIDWVOI • %WVQHHXCNWGU
• 1XGTVFKCDGVGUKUFKCIPQUGFKH Ŧ Fasting: 92 mg%
Ŧ HCUVKPIRNCUOCINWEQUGŮOI Ŧ 1 hour: 180 mg%
Ŧ *D#%ŮWUKPICUVCPFCTFK\GFCUUC[ Ŧ 2 hours: 153 mg%
Ŧ TCPFQORNCUOCINWEQUGŮOI • )&/FKCIPQUGFKH
• 1TCN)66CVŌYGGMUTGEQOOGPFGFKH Ŧ CP[QPGXCNWGGSWCNVQQTOQTGVJCPEWVQHHXCNWG
Ŧ HCUVKPIRNCUOCINWEQUGOI D gestational diabetes mellitus.
D diabetes mellitus; D gestational diabetes mellitus;
INWEQUGVQNGTCPEGVGUV
Box 48.9 9
JGPVQUETGGPHQTFKCDGVGU
in pregnancy
ne-step approach
• *KIJTKUMYQOGP
The IADPSG, along with the American Diabetes Ŧ (KTUVXKUKV(CUVKPIRNCUOCINWEQUG
Association (ADA), has recently recommended Ŧ +HPGICVKXGIJQWT)66CVŌYGGMU
the one-step approach. This approach is recom- • .QYTKUM
mended for all pregnant women. Screening is Ŧ IJQWT)66CVŌYGGMU
performed at the first antenatal visit, using fasting INWEQUGVQNGTCPEGVGUV
plasma glucose (FPG) for the diagnosis of GDM.
This also allows for the identification of women Health Organization (WHO) also recommends
with undiagnosed type 2 diabetes. Fasting plasma the 75-g, 2-hour GTT, but the cutoff values are
glucose, random plasma glucose, or HbA1c is marginally different. The IADPSG values are cur-
used for diagnosis of overt diabetes (Box 48.7). rently accepted (Box 48.8).
ral glucose tolerance test

When to screen
Oral glucose tolerance test has been used as a
As already mentioned, all women in the high-
diagnostic test for diabetes. In pregnancy, there
risk category must be screened at the first visit by
is a delayed absorption of glucose and delayed
the one-step procedure and if negative, screened
insulin peak with slow return of blood glucose to
again at 24–28 weeks. Oral glucose challenge test
normal. Therefore, a modified, prolonged GTT,
for low risk women is performed first at 24–28
proposed by Carpenter and Coustan, had been
weeks (Box 48.9).
in vogue for several years. A glucose load of 100 g
is used and plasma glucose levels are measured
hourly for 3 hours. This 3-hour, 100-g glucose Diabetes in Pregnancy Study
OGTT is recommended by the American College
of Obstetricians and Gynecologists (ACOG) and
Group India Guidelines
has been in use globally until recently. However, Because of the high prevalence of diabetes in
this test has been simplified to a 75-g, 2-hour India, the Diabetes in Pregnancy Study Group
GTT by the IADPSG and is currently recom- India (DIPSI) recommends screening of all preg-
mended for use in pregnancy. nant Indian women at the first visit. Irrespective
of the time of the last meal, 75-g oral glucose
75-g, 2-hour oral glucose should be administered and plasma glucose
tested 2 hours later. The advantage of this is that
tolerance test
women need not be fasting and the test can be
The 2-hour test is convenient to perform and the performed at the first visit. The compliance,
75-g glucose load is better tolerated. The World therefore, is good.
CH 48_p724-739_v3.indd 728 19-07-2015 01:15:51

• Plasma glucose t140 mg%: Gestational diabe- delivery and cesarean section result from fetal
tes mellitus macrosomia.
• Plasma glucose t120 mg%: Impaired gesta-
tional glucose tolerance
Fetal complications
Maternal hyperglycemia is the most important
+ORCEVQHFKCDGVGU cause of fetal and neonatal complications. The
three major fetal complications resulting from
on pregnancy uncontrolled hyperglycemia are
Pregestational and gestational diabetes are asso- • spontaneous miscarriage,

ciated with several complications in the mother • congenital anomalies, and
and fetus. • macrosomia.
Pregestational diabetes with uncontrolled hyper-
/CVGTPCNEQORNKECVKQPU glycemia is associated with spontaneous miscar-
riage and congenital anomalies. In gestational
Pregestational diabetes is associated with a diabetes, where the hyperglycemia occurs for
higher rate of maternal complications than ges- the first time in the late second trimester, there
tational diabetes (Box 48.10). Poor glycemic con- is increased risk of macrosomia. Fetal complica-
trol is the most important factor responsible for tions are listed in Box 48.11.
maternal complications. Spontaneous miscarriage is associated with
Gestational hypertension occurs in 25%–30% pregestational diabetes due to poor control of
of diabetic pregnancies. Preeclampsia is more diabetes in the first trimester.
common in women with diabetic nephropathy Congenital anomalies are associated with
and vasculopathy. Hypertension may predate poor control of diabetes in the first trimester
pregnancy in many type 2 diabetics, and this during organogenesis. They occur in 5%–7% of
may worsen in pregnancy. women with overt diabetes and are due to ele-
Polyhydramnios is the result of maternal vated blood sugar before the seventh week of
hyperglycemia leading to fetal hyperglycemia gestation. Ketonemia, hypoglycemia, and an
and fetal polyuria. Increased amniotic fluid glu- excess of oxygen free radicals also play a role.
cose may also be responsible. Infections such as The common congenital anomalies are listed in
vaginal candidiasis, urinary tract infections, and Box 48.12). Caudal regression, though specific to
puerperal sepsis are related to poor glycemic diabetes, is not a common anomaly.
control. Polyhydramnios and ascending infec- Fetal growth restriction occurs in women with
tion (with resultant chorioamnionitis) are two pregestational diabetes and associated vascu-
risk factors for preterm labor. Operative vaginal lopathy, hypertension, and preeclampsia.
Macrosomia is defined as birth weight >90th
Box 48.10 /CVGTPCNEQORNKECVKQPUKPFKCDGVGU percentile for gestational age for the population
or birth weight >4000–4500 g. DIPSI has sug-
• GDM and overt DM gested that a birthweight of >3500 g should be
Ŧ )GUVCVKQPCNJ[RGTVGPUKQPCPFRTGGENCORUKC
Ŧ Polyhydramnios
Ŧ Preterm labor
Box 48.11 Fetal complications
Ŧ +PHGEVKQPU
7TKPCT[VTCEVKPHGEVKQP • 1XGTVWPEQPVTQNNGF&/
8CIKPCNECPFKFKCUKU Ŧ 5RQPVCPGQWUOKUECTTKCIG
Puerperal sepsis Ŧ Congenital anomalies
• +PETGCUGFTKUMQH Ŧ (GVCNITQYVJTGUVTKEVKQP
EGUCTGCPUGEVKQP • GDM and overt DM
operative vaginal delivery Ŧ /CETQUQOKC
• +PWPEQPVTQNNGFQXGTV&/ Ŧ Prematurity
Ŧ -GVQCEKFQUKU Ŧ Late intrauterine death
D diabetes mellitus; D gestational diabetes mellitus. D diabetes mellitus; D , gestational diabetes mellitus.
CH 48_p724-739_v3.indd 729 19-07-2015 01:15:51

Box 48.12 Congenital anomalies in diabetic Box 48.13 eonatal complications

pregnancy
• Respiratory distress syndrome
• Central nervous system • Prematurity
Ŧ #PGPEGRJCN[ • *[RQIN[EGOKC
Ŧ 5RKPCDKſFC • *[RQECNEGOKC
Ŧ *QNQRTQUGPEGRJCN[ • Hyperbilirubinemia
• %CTFKCE • 2QN[E[VJGOKC
Ŧ 8GPVTKEWNCTUGRVCNFGHGEV • Cardiomyopathy
Ŧ 6TCPURQUKVKQPQHITGCVXGUUGNU
Ŧ 6GVTCNQI[QH(CNNQV
• Renal throughout the pregnancy reduces the risk of
Ŧ Agenesis macrosomia.
Ŧ %[UVKEMKFPG[ Premature labor may be spontaneous, due
• Caudal regression syndrome to polyhydramnios, or induced. Preterm induc-
tion of labor is indicated in preeclampsia, fetal
growth restriction, macrosomia, or worsening
considered as macrosomic in the Indian context. nephropathy. Intrauterine death and stillbirths
It is the most common complication of diabetic occur due to poor glycemic control, preeclamp-
pregnancy, and occurs in 50% of women with sia, or DKA. Hyperglycemia is the most import-
GDM and DM. Maternal hyperglycemia causes ant factor leading to fetal hypoxia.
fetal hyperglycemia and fetal hyperinsulin-
emia, leading to fetal macrosomia. Insulin-like eonatal complications
growth factors, leptin, and maternal obesity are
also contributing factors. Macrosomic infants Neonatal mortality and morbidity are increased
have relatively broader shoulders, which leads due to the problems listed in Box 48.13.
to increased risk of shoulder dystocia and cesar- Most complications are due to fetal hypergly-
ean section (Fig. 48.1). Tight control of glycemia cemia and hyperinsulinemia and resultant E-cell
hyperplasia. Complications such as prematurity
and respiratory distress syndrome are now less
often seen because strict control of glucose lev-
els allows for delivery at or close to term. Risk
of neonatal hypoglycemia increases if glycemic
control is not achieved at term and intrapartum.
Hyperglycemia stimulates fetal erythropoie-
tin production and results in polycythemia and
hyperbilirubinemia.
.CVGEQORNKECVKQPUKPVJGKPHCPV
QHVJGFKCDGVKEOQVJGT
There is a 1%–3% risk of developing diabetes
later in life. The risk increases if the father is also
a diabetic. There is also increased occurence of
obesity in adult life.
/CPCIGOGPV
Gestational diabetes
Diagnosis and treatment of GDM reduces
Figure 48. 1 (GVCNOCETQUQOKC
Photo courtesy: maternal and fetal morbidity, especially fetal
&T4CLPKUJ5COCN$CPICNQTG macrosomia.
CH 48_p724-739_v3.indd 730 19-07-2015 01:15:51

Preconceptional management Box 48.14 /GFKECNPWVTKVKQPCNVJGTCR[

Women at risk for development of GDM should • Daily requirements
be given preconceptional advice. Obese women, Ŧ Calorie intake
including those with PCOS, should be advised 0QTOCNYGKIJVMECNMI
to lose weight prior to pregnancy and counseled 1XGTYGKIJVCPFQDGUGŌMECNMI
about acceptable weight gain during pregnancy. /QTDKFN[QDGUGMECNMI
Ŧ Carbohydrates: 40%–50%
Ŧ Fats: 30%–40%
Antenatal management
Ŧ Proteins: 20%
Appropriate antenatal management with • Distribution
repeated counseling, attention to measures to Ŧ OGCNUCPFUPCEMU
optimise plasma glucose levels, and close mon-
itoring of the mother and fetus are important to
ensure optimal outcome. Exercise
Moderate exercise, for example, walking briskly
e ical management for 45–60 min/day, is recommended. This
Hyperglycemia is the single most important factor reduces the need for insulin and achieves better
responsible for maternal and fetal complications glycemic control.
in GDM, especially fetal macrosomia. The goal of
Pharmacotherapy
medical management is to reduce blood glucose
levels to normal and at the same time avoid hypo- Treatment with medications is required when
glycemia. This is achieved by diet, exercise, and optimal plasma glucose levels are not achieved
pharmacotherapy with insulin or OHAs. after 1–2 weeks of initiating MNT (3 days, if in the
The target plasma glucose levels in pregnancy third trimester).
are as follows: nsulin
• Fasting: d95 mg% Human insulin is recommended in pregnancy
• 1-hour postprandial: d140 mg% since it is least antigenic. Rapid-acting insulin
• 2-hour postprandial: d120 mg% analogs (lispro, aspart) have been found to be
Diet safe but are expensive. Long-acting analogs such
as glargine have not been studied sufficiently
Diet and lifestyle modification remain the cor- and, therefore, not recommended in pregnancy.
nerstones of therapy in gestational and preges- A combination of short-acting and interme-
tational diabetes. With these two modalities of diate-acting insulin in the proportion of 30:70,
therapy, optimal glycemic control can be achieved twice daily, before breakfast and before dinner is
in 85% of subjects with GDM. Dietary counsel- usually sufficient to achieve good control of glu-
ing is referred to as medical nutritional ther- cose in GDM. If fasting glucose and postdinner
apy (MNT; Box 48.14). Caloric restriction should glucose values are high, the night dose of inter-
be recommended for all overweight and obese mediate-acting insulin should be increased. If
women regardless of the presence of hyperglyce- postdinner glucose remains elevated, a third dose
mia. The permitted weight gain during pregnancy of short-acting insulin may be given at bedtime. A
in Western women is as follows: fourth dose of short-acting insulin may occasion-
Body mass index Permitted weight ally be required before lunch, if the predinner or
(BMI-kg/m2) gain (kg) postlunch glucose levels are high (Box 48.15).
18–24.9 (normal) 11–16 lucose monitoring
25–29.9 (overweight) 7–11 Women should be educated regarding self-
t30 (obese) 5–7 kg monitoring of glucose. Frequency of monitoring
is given in Box 48.16.
The BMI for the definition of overweight and
obesity in Asian women is lower (23 and 25 kg/m2 ral hypoglycemic agents
respectively); therefore, the recommended weight Oral hypoglycemic agents are used as an alterna-
gain in pregnancy is also lower. tive to insulin. The two drugs used are glyburide
CH 48_p724-739_v3.indd 731 19-07-2015 01:15:51

anomalies, miscarriages, and ketoacidosis is

Box 48.15 +PUWNKPVJGTCR[KP)&/
not increased in these women. Target glucose
• 5JQTV+PVGTOGFKCVGCEVKPIKPUWNKP levels can be achieved and maintained by MNT
• 6YKEGFCKN[FQUGU alone or MNT and pharmacotherapy. If euglyce-
• %CNQTKEEQPVGPVQHOGCNUCFLWUVGFVQſPGVWPGEQPVTQN
mia is maintained, macrosomia and fetal death
• 5JQTVCEVKPIKPUWNKPCFFGF
are uncommon. Antepartum surveillance is
Ŧ #VDGFVKOGKHRQUVFKPPGTINWEQUGJKIJ
Ŧ 2TGNWPEJKHRQUVNWPEJINWEQUGJKIJ
not routinely required in women with uncom-
• Human insulin used plicated GDM with no previous complications.
• Insulin analogs A cesarean section should be performed for
Ŧ 4CRKFCEVKPI5CHG obstetric indications only. Women with com-
Ŧ .QPICEVKPI0QVTGEQOOGPFGF plicated GDM or those requiring insulin may
be delivered at 38 weeks since waiting beyond
that can increase the risk of macrosomia and
Box 48.16 Glucose monitoring shoulder dystocia. Management is outlined in
Figure 48.2.
• 5GNHINWEQUGOQPKVQTKPI
• Timing
Ŧ Fasting
Ŧ 2QUVRTCPFKCNQTJQWTUCHVGTOGCN
• (TGSWGPE[
U for gestational age in first trimester
Ŧ &CKN[VKNNGWIN[EGOKCKUCEJKGXGFCPFVYKEGYGGMN[
VJGTGCHVGT
U for fetal morphology at ee s

Box 48. 17 ral hypoglycemic agents
• )N[DWTKFG
INKDGPENCOKFG
Ŧ Dose: 2.5 mg to initially M an e ercises
Ŧ %CPDGKPETGCUGFVQOIFC[
Ŧ 0GGFHQTCFFKVKQPCNKPUWNKPKUNGUU
Ŧ (CKNWTGQHVJGTCR[JKIJKHHCUVKPIINWEQUG OI aluate for macrosomia at
• /GVHQTOKP ee s by ultrasoun
Monitor bloo pressure
Ŧ 7UGHWNKPQDGUGYQOGP
Ŧ &QUGŌOIFC[
Ŧ 0GGFHQTCFFKVKQPCNKPUWNKPKUOQTG
Macrosomia
o macrosomia
(glibenclamide) and metformin. They have been hypertension
hypertension
prior stillbirth
found to be safe in pregnancy. Compliance is prior stillbirth
Controlle
better, administration is easier, and maternal/ Controlle on iet
ith insulin H
fetal complications are not increased. For these
reasons, OHAs are being used as primary treat-
ment in many centers currently (Box 48.17).
outine fetal
C PP t ice ee ly
sur eillance
Obstetric management not re uire
from ee s
The risk of antepartum and intrapartum compli-
cations is increased in gestational and pregesta-
tional diabetes. Close monitoring of mother and
fetus and early diagnosis of complications are eli er at ee s eli er at ee s
the primary focus of obstetric management.
Figure 48. 2 /CPCIGOGPVQHIGUVCVKQPCNFKCDGVGUOGNNKVWU
Antepartum
FKCIPQUGFKPVJGſTUVVTKOGUVGTBPP DKQRJ[UKECNRTQſNG
The diagnosis of GDM is usually made in the C ECTFKQVQEQITCRJ[ OGFKECNPWVTKVKQPCNVJGTCR[
first or second trimester. The risk of congenital AQTCNJ[RQIN[EGOKECIGPVU S ultrasonography.
CH 48_p724-739_v3.indd 732 19-07-2015 01:15:51

Box 48.18 +PVTCRCTVWOOCPCIGOGPVQH)&/ Box 48.19 /

CVGTPCNEQORNKECVKQPU
in pregestational diabetics
• 1DUVGVTKEOCPCIGOGPV
Ŧ /QPKVQTFKNCVCVKQPCPFFGUEGPV • Nephropathy
Ŧ Maintain a partogram Ŧ +PETGCUGFTKUMQHRTGGENCORUKC
Ŧ 9CVEJHQTCTTGUVQHFKNCVCVKQPFGUEGPV Ŧ 9QTUGPKPIQHRTQVGKPWTKC
Ŧ /QPKVQTHGVCNJGCTVGNGEVTQPKECNN[ Ŧ 9QTUGPKPIQHJ[RGTVGPUKQP
Ŧ #PVKEKRCVGUJQWNFGTF[UVQEKC • Retinopathy
• )N[EGOKEEQPVTQN Ŧ 9QTUGPKPIQHRTQNKHGTCVKXGTGVKPQRCVJ[
Ŧ 6CTIGVINWEQUGNGXGNOI Ŧ Vitreous hemorrhage
Ŧ GDM on diet 6TGCVOGPV .CUGT VJGTCR[ CPF IQQF IN[EGOKE
/QPKVQTINWEQUGŌJQWTN[ EQPVTQN
#FOKPKUVGTKPUWNKPQPN[KHTGSWKTGF • Coronary heart disease
Ŧ GDM on insulin Ŧ +PETGCUGKPOCVGTPCNOQTVCNKV[
%QPVKPWGWUWCNDGFVKOGFQUGQHKPUWNKP AC CPIKQVGPUKPEQPXGTVKPIGP\[OG
9KVJJQNFOQTPKPIFQUGQHKPUWNKPCPFRTQXKFGKP-
VTCXGPQWU KPHWUKQP FGZVTQUG KP VJG OQTPKPI
KHWPFGTIQKPI
- KPFWEVKQP
Pregestational (overt) diabetes
- GNGEVKXGEGUCTGCPUGEVKQP Pregestational diabetics are prone to fetal com-
/QPKVQTECRKNNCT[INWEQUGJQWTN[ plications such as spontaneous miscarriage
#FFUQNWDNGKPUWNKPVQKPHWUKQP and congenital anomalies that are not seen in
6KVTCVGFQUGVQOCKPVCKPVCTIGVINWEQUGNGXGN gestational diabetics. In addition, preexisting
D IGUVCVKQPCNFKCDGVKEOGNNKVWU maternal complications such as nephropathy
and retinopathy may worsen during pregnancy
(Box 48.19).
Obstetric management consists of electronic fetal ephropathy
heart monitoring, monitoring cervical dilatation
Proteinuria worsens during pregnancy in women
and descent, and preparing for management of
with diabetic nephropathy. Most women with dia-
shoulder dystocia. Uncomplicated GDM on diet
betic nephropathy have associated hypertension
will not require insulin during labor but those on
and are on antihypertensives. Antihypertensives
insulin in pregnancy will require intrapartum insu-
such as angiotensin-converting enzyme (ACE)
lin. Plasma glucose may be monitored 4–6 hourly.
inhibitors are contraindicated in pregnancy.
The target value for intrapartum glucose
These women should be switched to a safer
level is <140 mg%. Higher values lead to neona-
medication preconceptionally. Hypertension
tal hypoglycemia. The target levels are achieved
may worsen in pregnancy and these women
by insulin infusion titrated according to capil-
may develop superimposed preeclampsia with
lary glucose levels monitored by glucometer
its associated fetal and maternal complications.
hourly (Box 48.18).
This, in turn, may worsen renal function.
Postpartum management
etinopathy
Insulin requirement falls immediately after
delivery. Most women with GDM will not require Longstanding pregestational diabetes may be
insulin in the postnatal period. Glucose levels associated with nonproliferative and proliferative
should be tested 24 hours after delivery. Women retinopathy. Proliferative retinopathy can worsen
with GDM should be advised about postpartum in pregnancy and vitreous hemorrhage can occur.
diet, exercise, and lifestyle modification. Laser photocoagulation should be performed
A 75-g GTT should be performed 6–12 weeks before the hemorrhage occurs. Good glycemic
after delivery and repeated 3 yearly since women control is mandatory to reduce the risk of these
with GDM are at a high risk for development of complications. Most retinal changes regress
type 2 diabetes. after delivery, but a few may persist or progress;
CH 48_p724-739_v3.indd 733 19-07-2015 01:15:51

therefore, ophthalmic evaluation, treatment, avoid complications, plasma glucose and HbA1c
and follow-up are mandatory during and after should be at optimal levels. Periconceptional
pregnancy. folic acid supplementation is recommended to
reduce the risk of neural tube defects. Commonly
Preconceptional management used antihypertensives such as D-methyldopa,
nifedipine, and labetalol are safe in pregnancy.
Preconceptional management is an important If the patient is on ACE inhibitors or angioten-
aspect of management of women with preges- sin II receptor blockers (ARB), these should be
tational diabetes. The degree of glycemic control changed to one of the previously mentioned
should be assessed and complications should be antihypertensives and control optimized.
looked for. Medications must be evaluated and
changed if required. Oral hypoglycemic agents
Antenatal management
are not recommended in pregestational diabetes
and should be changed to insulin. The patient Maternal and perinatal morbidity and mor-
should be counseled regarding potential com- tality are higher in pregestational diabetes.
plications to the mother and fetus and the need Management should be in consultation with an
for tight control of blood sugar levels should be endocrinologist/diabetologist and neonatologist.
emphasized (Box 48.20). The risk of congenital
anomalies increases when the HbA1c is >10% at e ical management
conception and in the first trimester. In order to Medical management is aimed at maintaining
plasma glucose values within target levels. This is
the key factor in reducing perinatal mortality and
Box 48.20 Preconceptional management morbidity in diabetic pregnancies. Hypoglycemia
QHFKCDGVGUOGNNKVWU should also be avoided. Nocturnal drop in glu-
• 'XCNWCVGIN[EGOKEEQPVTQN cose values should be looked for between 2 and 4
am and should be maintained at >60mg%.
Test Target value (mg dL)
(CUVKPIINWEQUG &KGV
/GFKECNPWVTKVKQPCNVJGTCR[
JQWTRQUVRTCPFKCNINWEQUG Overall, the dietary requirements are the same
JQWTRQUVRTCPFKCNINWEQUG as in GDM. It is important to achieve tight gly-
0QEVWTPCN
ŌCOINWEQUG cemic control without causing hypoglycemia
and ketosis. Total calories are divided into three
*D#E
meals and three snacks as discussed earlier and
• 1RVKOK\GYGKIJVVQ$/+MIO2 distributed as follows:
• #UUGUUEQORNKECVKQPU
Ŧ 5GTWOETGCVKPKPG • Breakfast: 10%–20%
Ŧ 7TKPGRTQVGKPCPFOKETQCNDWOKP • Lunch: 20%–30%
Ŧ 1RJVJCNOKEGZCOKPCVKQP • Dinner: 30%–40%
Ŧ '%)'EJQECTFKQITCO • Snacks: 30% (each snack–10%)
Ŧ 65*
• 4GXKGYOGFKECVKQPU Supplementation of folic acid, calcium, mag-
Ŧ 1TCNJ[RQIN[EGOKE%JCPIGVQKPUWNKP nesium, and zinc is required.
Ŧ #%'KPJKDKVQTU#4$U%JCPIGVQUCHGTFTWIU
• Counsel about Exercise
Ŧ /CVGTPCNEQORNKECVKQPU Moderate exercise is advisable to assist in glyce-
Ŧ (GVCNEQORNKECVKQPU mic control and to avoid excessive weight gain.
Ŧ 0GGFHQTVKIJVIN[EGOKEEQPVTQN
Diet Pharmacotherapy
/QFGTCVGGZGTEKUG ral hypoglycemic agents
/GFKECVKQPU
• 2TGUETKDGHQNKECEKFOIFCKN[ Metformin and glyburide (glibenclamide) have
not been adequately studied in pregestational
AC CPIKQVGPUKPEQPXGTVKPIGP\[OGA BCPIKQVGPUKPTGEGRVQT
DNQEMGTB , body mass index; C GNGEVTQECTFKQITCRJ[ diabetes; therefore, they are not recommended
S , thyroid-stimulating hormone. routinely. However, metformin is currently
CH 48_p724-739_v3.indd 734 19-07-2015 01:15:51

recommended as an adjunct to insulin or as Antepartum management

primary therapy in obese, mild diabetics. First trimester
nsulin If the woman has not been seen preconception-
Insulin therapy is started prepregnancy and ally, she should be evaluated for glycemic con-
continued through pregnancy. Intensive insu- trol, renal functions, and retinopathy at the first
lin therapy is required to achieve euglycemia visit. Counseling regarding permitted weight
throughout the day. The requirement of insulin gain, diet, exercises, pharmacotherapy, need for
declines in the first trimester due to nausea and tight glycemic control, target glucose values, and
vomiting. Ketosis is common at this time and potential fetal and maternal complications is
should be watched for and treated early. Insulin mandatory. An ultrasound scan should be per-
requirement increases in the second half of preg- formed in the first trimester for accurate estima-
nancy and should be adequately replaced. tion of gestational age. This is important since
Short-acting insulin, four times a day, admin- many women may require induction of labor.
istered before breakfast, lunch, and dinner and Measurement of nuchal translucency and first
at bedtime is usually recommended in preges- trimester screening for Down syndrome should
tational diabetes. Occasionally, a combination be done, if available, since second trimester
of intermediate-acting (NPH) and short-act- screening cannot be done in diabetics. Folic acid
ing insulin, given twice daily, may be sufficient. supplementation should be continued.
Rapid-acting insulin analogs (lispro, aspart) may Second trimester
be used, but glargine insulin has not been ade-
Maternal serum alpha fetoprotein is estimated
quately evaluated. Self-glucose monitoring is
at 16–18 weeks’ pregnancy to detect neural tube
convenient and practical. Glucose levels should
defects. The levels are lower in diabetic preg-
be monitored fasting and postmeal (breakfast,
nancy, and this should be kept in mind when
lunch, and dinner) and dose of insulin adjusted
interpreting the results. Detailed assessment of
accordingly.
fetal anatomy including a four-chamber view of
Medical management in pregestational dia-
the heart should be performed at 18–20 weeks.
betics is outlined in Box 48.21.
Fetal echocardiography is recommended in all
diabetic pregnancies (Box 48.22).
bstetric management
Third trimester
The clinician should be aware of the special
obstetric issues in a pregnancy complicated by Clinical examination includes close monitoring
pregestational diabetes and should have exper- of blood pressure and obstetric examination
tise to manage them. to identify polyhydramnios, macrosomia, or
growth restriction. Urine examination for pro-
teinuria is mandatory at every visit.
Box 48.21 /
GFKECNOCPCIGOGPVQHRTGIGUVC-
tional diabetes during pregnancy
Beginning at 28 weeks, fetal growth should
be evaluated. Interval between scans depends
• Diet on severity of diabetes, glycemic control, and
• /QFGTCVGGZGTEKUG fetal growth abnormality including macroso-
• 2JCTOCEQVJGTCR[
mia or growth restriction and associated com-
Ŧ 1TCN J[RQIN[EGOKE CIGPVU $GKPI GXCNWCVGF /GV-
HQTOKPKPOKNFQDGUGFKCDGVKEU plications such as preeclampsia. Nonstress test
Ŧ Insulin (NST) should begin at 32 weeks. Biophysical
Human insulin used profile and fetal umbilical and middle cerebral
5JQTVCEVKPI
FQUGURGTFC[QTKPVGTOGFKCVG artery Doppler velocimetry are also useful if
CEVKPI UJQTVCEVKPI
FQUGURGTFC[ there is growth restriction. These tests may be
Ŧ Insulin analogs performed 2- to 4-weekly if glycemic control is
/C[WUGTCRKFCEVKPICPCNQIU good and fetal growth is normal. In poorly con-
.QPICEVKPICPCNQIPQVTGEQOOGPFGF trolled diabetes, preeclampsia, macrosomia,
• )NWEQUGOQPKVQTKPI
or fetal growth restriction, more frequent test-
Ŧ Fasting and postmeal
ing, such as weekly or twice a week, is required
Ŧ +PUWNKPCFLWUVGFCEEQTFKPIN[
(Box 48.23). Estimation of fetal weight at term
CH 48_p724-739_v3.indd 735 19-07-2015 01:15:51

Box 48.22 #
PVGRCTVWOOCPCIGOGPVQH iming o elivery
RTGIGUVCVKQPCNFKCDGVKEUKPVJGſTUV The timing of delivery has to be balanced
and second trimesters between prematurity and complications arising
• First trimester from delay. Early delivery is associated with an
Ŧ Evaluation increase in risk of respiratory distress syndrome.
)N[EGOKEUVCVWU Prolonging the pregnancy in the presence of
Retinopathy maternal or fetal compromise increases perina-
Nephropathy tal mortality and morbidity.
Ŧ Counseling In women with good glycemic control and no
&KGVCPFGZGTEKUG fetal compromise, preeclampsia, or hyperten-
Insulin therapy sion, delivery is recommended at 39–40 weeks.
5GNHINWEQUGOQPKVQTKPI
Those with poor glycemic control should be
6CTIGVINWEQUGXCNWGU
delivered by 37 weeks. In women with maternal
%QORNKECVKQPU
- Maternal
or fetal compromise, delivery should be planned
- Fetal when the fetal testing becomes abnormal or
Ŧ Ultrasonography when preeclampsia worsens (Fig. 48.3).
#EEWTCVGGUVKOCVKQPQHIGUVCVKQPCNCIG
0WEJCNVTCPUNWEGPE[ o eo elivery
• 5GEQPFVTKOGUVGT Vaginal delivery of a macrosomic baby can give
Ŧ /CVGTPCNUGTWOCNRJCHGVQRTQVGKP rise to shoulder dystocia and brachial plexus
Ŧ Ultrasonography
injury. Although abdominal circumference and
Fetal morphology
fetal weight have been used to predict shoulder
(GVCNGEJQECTFKQITCO
Ŧ %NQUGOQPKVQTKPIQHDNQQFRTGUUWTG
dystocia, they have poor predictive value. The
risk of cephalopelvic disproportion and shoul-
der dystocia increases when fetal weight is >4000
g. A cesarean section is usually performed in this
Box 48.23 /
CPCIGOGPVQHRTGIGUVCVKQPCN situation. Pregestational diabetes with associ-
diabetics in the third trimester
ated preeclampsia or severe fetal compromise is
• %NKPKECNGZCOKPCVKQP also an indication for an elective cesarean sec-
Ŧ $NQQFRTGUUWTG tion (Box 48.24).
Ŧ 5[ORJ[UKQHWPFCNJGKIJV
(GVCNOCETQUQOKC Intrapartum management
(GVCNITQYVJTGUVTKEVKQP
Ŧ Polyhydramnios
Maintenance of glucose levels below 140 mg%
Ŧ 8WNXQXCIKPCNECPFKFKCUKU during labor is essential to avoid neonatal hypo-
• 'XCNWCVKQPQHHGVCNYGNNDGKPI glycemia. This is achieved by infusion of glucose
Ŧ Ultrasonography and insulin and hourly monitoring of plasma
5VCTVGFCVYGGMU glucose levels.
1PEGKPQTYGGMUQTVYKEGCYGGM Prolonged labor and arrest of dilatation or
.QQMHQT descent are indicative of cephalopelvic dispro-
- DKQRJ[UKECNRTQHKNG portion. Prolonged second stage is a forerunner
- WODKNKECNCPFOKFFNGEGTGDTCNCTVGT[&QRRNGT of shoulder dystocia. Progress of labor should
- HGVCNITQYVJCPFYGKIJV be closely monitored and plotted on a parto-
Ŧ Nonstress test
gram. Electronic fetal monitoring is essential.
5VCTVGFCVYGGMU
Weekly as primary test
6YKEGYGGMN[KHKPFKECVGF Box 48.24 +PFKECVKQPUHQTGNGEVKXGEGUCTGCP
section
• 'UVKOCVGFYGKIJV MI
is useful to some extent in deciding on mode of
• 5GXGTGRTGGENCORUKC
delivery, although it is not a sensitive predictor of
• 5GXGTGHGVCNEQORTQOKUG
shoulder dystocia.
CH 48_p724-739_v3.indd 736 19-07-2015 01:15:52

Pregestational iabetes
Monitor glycemic control

associate maternal complications
an fetal ell being
oo glycemic control
o fetal compromise Poor glycemic control orsening
o preeclampsia bnormal PP oppler preeclampsia
hypertension
eli er at ee s eli er at ee s eli er hen re uire
Figure 48.3 6KOKPICPFOQFGQHFGNKXGT[KPRTGIGUVCVKQPCNFKCDGVKEUBPPDKQRJ[UKECNRTQſNG
Intrapartum management is the same as for intrauterine devices are safe in gestational dia-
GDM on insulin, as summarized in Box 48.18. betics. In pregestational diabetics with vascu-
lopathy, oral contraceptive pills can increase the
ostpartum management risk of thrombosis and worsen insulin resistance.
Insulin requirement falls immediately after Intrauterine contraceptive devices can be used in
delivery. The dose of insulin should be adjusted these women and, contrary to popular belief, the
accordingly. Breastfeeding should be encour- risk of infection does not increase. Long-acting
aged as it helps in calorie consumption and gly- progestins have not been adequately evaluated
cemic control (Box 48.25). (Box 48.26).
Contraception
Box 48.26 Contraceptive options in diabetes
Low-dose oral contraceptive pills, progester-
one-only pills, injectable progestogens, and • Gestational diabetes
Ŧ .QYFQUGQTCNEQPVTCEGRVKXGRKNNU
Ŧ Progestins
Ŧ +PVTCWVGTKPGEQPVTCEGRVKXGFGXKEGU
Box 48.25 Postpartum management
Ŧ $CTTKGTEQPVTCEGRVKQP
in pregestational diabetics
Ŧ 6WDGEVQO[
• &GETGCUGKPUWNKPFQUGVQQPGVJKTFQTQPGJCNH • Pregestational diabetes
• /QPKVQTINWEQUGNGXGNUFCKN[ Ŧ $CTTKGTEQPVTCEGRVKQP
• %JCPIGVQQTCNJ[RQIN[EGOKEFTWIUCHVGTJQWTU Ŧ +PVTCWVGTKPGEQPVTCEGRVKXGFGXKEGU
• 'PEQWTCIGDTGCUVHGGFKPI Ŧ 6WDGEVQO[
KHHCOKN[EQORNGVG
CH 48_p724-739_v3.indd 737 19-07-2015 01:15:52

Key points
• &KCDGVGUKPRTGIPCPE[KUCUUQEKCVGFYKVJJKIJRGTKPC- • &KCDGVGUKUCUUQEKCVGFYKVJUGXGTCNOCVGTPCNCPFHGVCN
VCNOQTVCNKV[CPFOQTDKFKV[KHDNQQFINWEQUGNGXGNUCTG EQORNKECVKQPU-GVQCEKFQUKUOKUECTTKCIGCPFEQPIGP-
PQVYGNNEQPVTQNNGF KVCNCPQOCNKGUQEEWTQPN[KPRTGIGUVCVKQPCNFKCDGVGU
• 6JGRTGXCNGPEGCPFKPEKFGPEGCTGKPETGCUKPIINQD- • 5GXGTCNPGQPCVCNRTQDNGOUCPFNCVGEQORNKECVKQPUECP
CNN[FWGVQEJCPIGUKPNKHGUV[NGCPFKPETGCUGKP CNUQQEEWTKPFKCDGVGU
QDGUKV[OGVCDQNKEU[PFTQOGCPFRQN[E[UVKEQXCT[
• /CPCIGOGPVQHRTGIGUVCVKQPCNFKCDGVGUUVCTVUYKVJ
syndrome.
RTGEQPEGRVKQPCNYGKIJVTGFWEVKQPCPFEQWPUGNKPIQH
• &KCDGVGUKPRTGIPCPE[KUENCUUKſGFCUIGUVCVKQPCNCPF JKIJTKUMYQOGP
RTGIGUVCVKQPCNFKCDGVGU2TGIGUVCVKQPCNFKCDGVGUECP
• 2TGIGUVCVKQPCNFKCDGVKEUUJQWNFDGGXCNWCVGFHQT
be type 1 or type 2.
PGRJTQRCVJ[CPFTGVKPQRCVJ[RTKQTVQRTGIPCPE[
• 6[RGFKCDGVGUQEEWTUCVC[QWPIGTCIGCPFKUFWGVQ 6JQUGQPQTCNJ[RQIN[EGOKECIGPVU
1*#UUJQWNF
CDUQNWVGKPUWNKPFGſEKGPE[9QOGPYKVJV[RGFKCDG- DGUYKVEJGFVQKPUWNKP#PVKJ[RGTVGPUKXGUUWEJCU
VGUCTGPQVQDGUGCPFCTGRTQPGVQMGVQCEKFQUKU CPIKQVGPUKPEQPXGTVKPIGP\[OG
#%'KPJKDKVQTUCPF
• 6[RGFKCDGVGUQEEWTUKPQNFGTYQOGPCPFKUFWG CPIKQVGPUKP++TGEGRVQTDNQEMGTU
#4$UUJQWNFDG
VQRGTKRJGTCNKPUWNKPTGUKUVCPEGQTEEGNNF[UHWPE- EJCPIGFVQD-methyldopa or labetalol.
VKQP6JGUGYQOGPCTGQDGUGCPFMGVQCEKFQUKUKU • )N[EGOKEEQPVTQNKUD[OGFKECNPWVTKVKQPCNVJGTCR[
WPEQOOQP
/06GZGTEKUGUCPFKPUWNKPKPCNNFKCDGVKEU1TCN
• )GUVCVKQPCNFKCDGVGUKUFGſPGFCUINWEQUGKPVQNGTCPEG J[RQIN[EGOKEFTWIUOC[DGWUGFCUCPCNVGTPCVKXGKP
YKVJQPUGVQTſTUVTGEQIPKVKQPKPRTGIPCPE[KTTGURGEVKXG gestational diabetes.
QHYJGVJGTKPUWNKPKUWUGFHQTEQPVTQN+VUJCTGUOCP[ • 6KIJVIN[EGOKEEQPVTQNKUVJGMG[VQRTGXGPVKQPQHCNN
EQOOQPHGCVWTGUYKVJV[RGFKCDGVGU EQORNKECVKQPU
• 2J[UKQNQIKECNEJCPIGUKPECTDQJ[FTCVGOGVCDQNKUOKP • Ultrasonography should be used to estimate gestational
RTGIPCPE[KPENWFGHCUVKPIJ[RQIN[EGOKCKPETGCUGKP CIGCPFGXCNWCVGPWEJCNVTCPUNWEGPE[KPVJGſTUVVTKOGU-
RGTKRJGTCNTGUKUVCPEGVQKPUWNKPRQUVRTCPFKCNJ[RGT- VGTGZENWFGEQPIGPKVCNCPQOCNKGUCVŌYGGMUCPF
IN[EGOKCCPFCPQXGTCNNFKCDGVQIGPKEUVCVGKPFWEGF GXCNWCVGHGVCNYGNNDGKPICPFITQYVJKPVJGVJKTFVTKOGUVGT
D[FKCDGVQIGPKEJQTOQPGUCPFQVJGTFKCDGVQIGPKE
• +PEQORNKECVGFRTGIPCPEKGUHGVCNYGNNDGKPIKUGXCNW-
UWDUVCPEGURTQFWEGFKPRTGIPCPE[
CVGFD[PQPUVTGUUVGUV
056DKQRJ[UKECNRTQſNG
• 5ETGGPKPIHQTFKCDGVGUECPDGD[CVYQUVGRCRRTQCEJ
$22WODKNKECNCTVGT[CPFOKFFNGEGTGDTCNCTVGT[
VJCVEQPUKUVUQHCINWEQUGEJCNNGPIGVGUVHQNNQYGFD[ &QRRNGTXGNQEKOGVT[6GUVKPIUJQWNFDGIKPCV
FKCIPQUVKEVGUVKPIYKVJINWEQUGVQNGTCPEGVGUV
)66 YGGMU(TGSWGPE[QHVGUVKPIFGRGPFUQPUGXGTKV[QH
QTD[CQPGUVGRCRRTQCEJRGTHQTOGFCVVJGſTUVXKUKV FKCDGVGUIN[EGOKEEQPVTQNCUUQEKCVGFOCVGTPCNEQO-
VJCVEQPUKUVUQHHCUVKPIQTTCPFQORNCUOCINWEQUGQT RNKECVKQPUCPFHGVCNYGNNDGKPI
*D#E
• 7PEQORNKECVGFIGUVCVKQPCNCPFRTGIGUVCVKQPCNFKCDG-
• 1TCNINWEQUGVQNGTCPEGVGUV
1)66YKVJIINWEQUG VGUOC[DGFGNKXGTGFCVŌYGGMU'CTN[FGNKXGT[KU
KUVJGFKCIPQUVKEVGUVEWTTGPVN[TGEQOOGPFGF2NCUOC KPFKECVGFHQTRQQTIN[EGOKEEQPVTQNHGVCNEQORTQOKUG
INWEQUGKUOGCUWTGFHCUVKPICPFCPFJQWTUCHVGT QTRTGGENCORUKC
INWEQUGCFOKPKUVTCVKQP
• #PGNGEVKXGEGUCTGCPUGEVKQPKUTGEQOOGPFGFKHHGVCN
• 4KUMECVGIQTK\CVKQPKUWUGFVQFGEKFGQPQPGUVGR YGKIJVKU MI
CRRTQCEJQT)66CVŌYGGMU+PVGTOGFKCVGCPF
• +PVTCRCTVWOIN[EGOKEEQPVTQNKUD[KPHWUKQPQHINWEQUG
JKIJTKUMYQOGPWPFGTIQVJGQPGUVGROQPKVQTKPICV
CPFKPUWNKPCPFJQWTN[INWEQUGOQPKVQTKPIVQVKVTCVG
VJGſTUVCPVGPCVCNXKUKVCPFKHPQTOCN)66KUTGRGCVGF
KPUWNKPFQUGKPQTFGTVQCXQKFPGQPCVCNJ[RQIN[EGOKC
CVŌYGGMU
5GNH#UUGUUOGPV
XCNWGQHOIF.CPFJQWTXCNWGQHOIF.*GT
Case-based questions DNQQFUWICTUYGTGPQVVGUVGFKPVJGRTGXKQWURTGIPCPE[
Case 1 1. 9JCVKUVJGFKCIPQUKUKPVJKUECUG!
2. 9JCVOCVGTPCNEQORNKECVKQPUFQ[QWCPVKEKRCVG!
/TU20UGEQPFITCXKFCCVYGGMUYCUTGHGTTGFVQ
VJGCPVGPCVCNENKPKED[CXKNNCIGOKFYKHGUKPEGUJGHGNVVJCV 3. 9JCVHGVCNCPFPGQPCVCNEQORNKECVKQPUFQ[QW
VJGDCD[YCUDKI1TCNINWEQUGVQNGTCPEGVGUVYKVJIINW- CPVKEKRCVG!
EQUGTGXGCNGFHCUVKPIINWEQUGXCNWGQHOIF.JQWT 4. *QYYKNN[QWEQPVTQNDNQQFUWICT!
CH 48_p724-739_v3.indd 738 19-07-2015 01:15:52

Case 2 CPCIGFCUCIGUVCVKQPCNFKCDGVKE+HOIF.CP
O
QTCN)66UJQWNFDGRGTHQTOGFCVYGGMU
/TU ,% UGEQPF ITCXKFC YKVJ C RTGXKQWU PQTOCN 3. #VYGGMUŏRTGIPCPE[CXCNWGQHOIF.
FGNKXGT[JCFEQOGHQTTQWVKPGCPVGPCVCNECTGCVYGGMUŏ KPFKECVGURTGIGUVCVKQPCNFKCDGVGU5RQPVCPG-
RTGIPCPE[ QWUOKUECTTKCIGEQPIGPKVCNOCNHQTOCVKQPUCPF
MGVQCEKFQUKUCTGVQDGCPVKEKRCVGF
1. 9KNN[QWUETGGPHQTFKCDGVGU!9J[!
4. /CVGTPCNUGTWOCNRJCHGVQRTQVGKPCVYGGMU
2. *QYYKNN[QWUETGGP!
WNVTCUQPQITCRJ[CVYGGMUVQGZENWFGEQPIGPKVCN
3. +HVJGUETGGPKPIVGUVTGXGCNUCTCPFQORNCUOC
CPQOCNKGUCPFHGVCNGEJQECTFKQITCOHQTECTFKCE
INWEQUGXCNWGQHOIYJCVEQORNKECVKQPUFQ
anomaly.
[QWCPVKEKRCVG!
4. 9JCVCFFKVKQPCNGXCNWCVKQPYKNN[QWFQKPVJGſTUVCPF
UGEQPFVTKOGUVGTU! Case 3
6JGUVGRUKPVJGOCPCIGOGPVCTGCUHQNNQYU
Case 3 1. #FOKPKUVGTVJGWUWCNFQUGQHKPUWNKPVJGPKIJVDGHQTG
/TU0%RTKOKITCXKFCRTGIGUVCVKQPCNFKCDGVKEQP KPFWEVKQP
CPFWPKVUQHUQNWDNGKPUWNKPYKVJDTGCMHCUVNWPEJ 2. %JGEMHCUVKPIDNQQFINWEQUGQPVJGFC[QHKPFWEVKQP
CPFFKPPGTCPFCVDGFVKOGYCUCFOKVVGFHQTNCDQTKPFWE- 3. 5VCTVQPFGZVTQUGKPHWUKQP
VKQP1WVNKPGVJGUVGRUQHOCPCIGOGPV 4. #FFUQNWDNGKPUWNKPVQVJGKPHWUKQPVQOCKPVCKPINWEQUG
NGXGNCVOI
5. /QPKVQTRNCUOCINWEQUGJQWTN[/QPKVQTRTQITGUUQH
Answers labor; maintain a partogram.
6. /QPKVQTVJGHGVCNJGCTVGNGEVTQPKECNN[
Case 1 7. #PVKEKRCVGUJQWNFGTF[UVQEKCCPFDGRTGRCTGF
1. )NWEQUGKPVQNGTCPEGJCUDGGPFKCIPQUGFHQTVJGſTUV 8. 2GTHQTOCEGUCTGCPUGEVKQPKHVJGTGKUCTTGUVQH
VKOGJGPEGVJGFKCIPQUKUKUIGUVCVKQPCNFKCDGVGU FGUEGPVFKNCVCVKQP
2. 5JGKUKPVJGVJKTFVTKOGUVGTōRQN[J[FTCOPKQU
IGUVCVKQPCNJ[RGTVGPUKQPRTGGENCORUKCCPFRTGVGTO
NCDQTUJQWNFDGCPVKEKRCVGF+PVTCRCTVWOōRTQNQPIGF Sample questions
NCDQTKPUVTWOGPVCNFGNKXGT[UJQWNFGTF[UVQEKCCPF
EGUCTGCPUGEVKQP Long-answers questions
3. /CETQUQOKCPGQPCVCNJ[RQIN[EGOKCJ[RQECNEGOKC
and hyperbilirubinemia. 1. #[GCTQNFUGEQPFITCXKFCYKVJRTGIGUVCVKQPCN
FKCDGVGUEQOGUHQTCPVGPCVCNEJGEMWRCVYGGMUŏ
4. 5VCTVQP/06CPFOQFGTCVGGZGTEKUGUCPFTGEJGEM
IGUVCVKQP&KUEWUUVJGOCPCIGOGPV
DNQQFINWEQUGCHVGTFC[U5VCTVQPINKDGPENCOKFG
OIFCKN[KHHCUVKPIINWEQUGKU OIDWV 2. &KUEWUUVJGFKCIPQUKUCPFOCPCIGOGPVQHIGUVC-
OI6JGFQUGECPDGKPETGCUGFD[OIVQC tional diabetes.
OCZKOWOQHOIDGHQTGFKPPGT+HHCUVKPIINWEQUG
KU OIUVCTVQPKPUWNKPōEQODKPCVKQPQHKPVGT-
OGFKCVGCPFUJQTVCEVKPIVYKEGFCKN[ōCPFCFLWUVVJG
FQUGVQCEJKGXGVCTIGVINWEQUGXCNWGU 1. 5ETGGPKPIHQTIGUVCVKQPCNFKCDGVGU
2. 2TGEQPEGRVKQPCNOCPCIGOGPVQHCPQXGTVFKCDGVKE
3. /GFKECNPWVTKVKQPVJGTCR[
Case 2 4. (GVCNOCETQUQOKC
1. ;GU5JGKUHTQOCPGVJPKEITQWRYKVJJKIJTKUMHQT 5. 1TCNINWEQUGVQNGTCPEGVGUVKPRTGIPCPE[
diabetes and is >25 years old. 6. /CVGTPCNEQORNKECVKQPUKPCRTGIPCPVFKCDGVKE
2. $[VJGQPGUVGRCRRTQCEJCVVJGſTUVXKUKVD[CHCUV- 7. (GVCNEQORNKECVKQPUQHFKCDGVGUKPRTGIPCPE[
KPIRNCUOCINWEQUG+H OIF.UJGUJQWNFDG
CH 48_p724-739_v3.indd 739 19-07-2015 01:15:52

Hematological
49 Disorders
Case scenario
Mrs. CP, 21, gravida 2, para 1, was in the 16th week of gestation. Her
first child was 1 year old. She felt tired and breathless when she climbed
stairs. She appeared pale on her routine antenatal checkup.
Introduction Anemia in pregnancy

Anemia is the most common hematological dis- Anemia is one of the most prevalent problems
order in pregnancy. It is a major public health involving nutritional deficiency in pregnant
concern in developing countries. women. Maternal anemia results in significant
The majority of anemia in pregnancy is due perinatal morbidity and mortality.
to iron, folate, or vitamin B12 deficiency. Less
commonly, it could be a consequence of hemo-
globinopathies such as thalassemia and sickle Prevalence
cell anemia. It could also be due to autoimmune
Anemia affects nearly 50% of pregnant women
hemolytic anemia or aplastic anemia. Sometimes,
globally. As compared with 25% in developed
anemia can be associated with systemic diseases
countries, the prevalence of anemia in Indian
such as chronic infections, rheumatoid arthritis,
mothers is between 80% and 90%.
human immunodeficiency virus (HIV), and renal
failure.
Another hematological disorder encountered
in pregnancy is thrombocytopenia. It can be ges-
&GſPKVKQP
tational thrombocytopenia, immune thrombo- Anemia is defined by the World Health
cytopenia (ITP), or a result of complications of Organization (WHO) as hemoglobin levels of
pregnancy. d11 g/dL or hematocrit of <33%. It can also be
CH 49_p740-757_v3.indd 740 19-07-2015 11:21:16

Hematological Disorders 741
defined as a value less than the fifth percentile CNCUUKſECVKQPQHCPGOKC

of the distribution of hemoglobin or hemato-
crit in a healthy reference population based on Anemias can be classified according to their eti-
the trimester of pregnancy. The Federation of ology. Nutritional deficiency is the commonest
Obstetric and Gynecological Societies of India cause. Anemia can also occur due to decreased
(FOGSI) has suggested a cutoff of 10 g/dL for production of red blood cells, increased destruc-
India. tion of RBCs, or blood loss (Box 49.2)
Physiological anemia Box 49.2 %

NCUUKſECVKQPQHCPGOKCDCUGF
of pregnancy on etiology
In normal pregnancy, there is an increase in #PGOKCUCUUQEKCVGFYKVJPWVTKVKQPCNFGſEKGPE[

blood volume, which results in an associated • +TQPFGſEKGPE[
hemodilution. Although red blood cell (RBC) • (QNKECEKFFGſEKGPE[
mass increases during pregnancy, plasma vol- • Vitamin B12FGſEKGPE[
ume increases more, resulting in a relative • %QODKPGFFGſEKGPEKGU
anemia (see Chapter 3, Maternal physiology Anemias associated with decreased production of
in pregnancy). This results in a physiologically blood cells
lowered hemoglobin level, hematocrit value, • $QPGOCTTQYFKUQTFGTU
and RBC count. It has no effect on the mean cor- • $QPGOCTTQYUWRRTGUUKQP
puscular volume (MCV). Since these changes • %JTQPKETGPCNFKUQTFGTU
are trimester dependent, anemia is defined as Ŧ .QYNGXGNUQHGT[VJTQRQKGVKP
• *[RQVJ[TQKFKUO
given in Box 49.1.
Anemias associated with increased red blood cell
destruction
Categori ation of anemia • +PJGTKVGFJGOQN[VKECPGOKCU

Ŧ 5KEMNGEGNNCPGOKC
according to severity Ŧ 6JCNCUUGOKCOCLQT
Ŧ *GTGFKVCT[URJGTQE[VQUKU
Anemia is categorized by the WHO and the
• #ESWKTGFJGOQN[VKECPGOKCU
Indian Council of Medical Research (ICMR) as Ŧ #WVQKOOWPGJGOQN[VKECPGOKC
given in Table 49.1. Ŧ *GOQN[VKECPGOKCCUUQEKCVGFYKVJ
VJTQODQVKEVJTQODQE[VQRGPKERWTRWTC
JGOQN[VKEWTGOKEU[PFTQOG
Box 49.1 &GſPKVKQPQHCPGOKC malaria
• ŭIF.KPVJGſTUVVTKOGUVGT Anemia due to blood loss
• ŭIF.KPVJGUGEQPFVTKOGUVGT • *GOQTTJCIKECPGOKC
• ŭIF.KPVJGVJKTFVTKOGUVGT • *GCX[OGPUVTWCNDNGGFKPI
• IF.CVYGGMRQUVRCTVWO • Gastrointestinal bleeding
• IF.CVYGGMURQUVRCTVWO • 1DUVGVTKEJGOQTTJCIG
6CDNG Categori ation of anemia
Category W ICM

JGOQINQDKPKPIF.
JGOQINQDKPKPIF.
Mild anemia 9 –10.9 10 –11
Moderate anemia 7 –10.9 7 –10
Severe anemia <7 4 –7
8GT[UGXGTG <4, decompensated <4
C +PFKCP%QWPEKNQH/GFKECN4GUGCTEJ 9QTNF*GCNVJ1TICPK\CVKQP
CH 49_p740-757_v3.indd 741 19-07-2015 11:21:16

+TQPOGVCDQNKUO Most of the increased iron requirement occurs

in the second half of pregnancy. The requirement
Iron requirements vary in the nonpregnant and the becomes 6 mg/day after midpregnancy as com-
pregnant woman. There is an increased demand pared with 1–2 mg/day in the nonpregnant state.
for iron in pregnancy to supply the fetus and pla- Since only 10% of ingested iron is absorbed, the
centa, in addition to supporting the increase in daily intake should be at least 60 mg, especially
the mother’s blood volume. The body’s iron stores after 20 weeks’ gestation.
also have to be supplemented in anticipation of The iron requirement for the entire dura-
blood loss during delivery and the postpartum tion of pregnancy is approximately 1000 mg.
period. Pregnancy causes important changes in Another 200 mg of iron is saved due to preg-
iron metabolism to meet these demands. nancy amenorrhea.
This iron is distributed among various preg-
+TQPOGVCDQNKUOKPVJGPQPRTGIPCPV nancy demands as described in Box 49.3.
woman
Box 49.3 &
KUVTKDWVKQPQHVQVCNKTQPTGSWKTGOGPV
The normal daily diet contains 10–20 mg of iron. in pregnancy
Absorption of iron takes place in the duodenum.
• (GVWUCPFRNCEGPVCOI
Ferric iron is converted to ferrous iron before
• /CVGTPCNJGOQINQDKPGZRCPUKQPOI
absorption, and only approximately 10%–15% • $NQQFNQUUCVFGNKXGT[OI
(1–2 mg) of ingested iron is absorbed. Once it • 4GRNCEGOGPV QH NQUU VJTQWIJ WTKPG UYGCV CPF HGEGU
enters the blood, it is transported by transferrin. 200 mg
The transferrin–iron complex is stored as follows:
• Bone marrow for formation of hemoglobin
(75%) ITQPFGſEKGPE[CPGOKC
• Liver and spleen for storage as hemosiderin
Iron deficiency anemia is the commonest nutri-
and ferritin (10%–20%)
tional anemia in pregnancy. A pregnant woman
• Muscles for formation of myoglobin (10%)
often has insufficient iron stores to meet the
• Other tissues for formation of iron-containing
demands of pregnancy. All pregnant women
enzymes (5%)
should be screened for anemia during preg-
The body draws on these stores during peri- nancy. Those with iron deficiency anemia should
ods of increased iron requirement. be treated with supplemental iron, in addition
Daily loss of iron is approximately 1–1.5 mg, to prenatal vitamins. Indian women are at high
usually through sweat, urine, and menstrual risk for iron deficiency anemia, and supplemen-
blood. If the loss exceeds the amount absorbed tal iron should be prescribed routinely. Patients
from the diet, there is iron deficiency anemia. with anemia other than iron deficiency anemia
Regulation of iron content of the body is by regu- should be further evaluated.
lation of absorption. Iron supplementation is not
routinely required in the nonpregnant woman
who is not anemic, because she can meet the %CWUGUQHKTQPFGſEKGPE[KPRTGIPCPE[
requirements through diet. This is in contrast to a in developing countries
pregnant woman who requires iron supplementa-
tion to meet the increased demands of pregnancy. Pregnant women in developing countries are
more prone to iron deficiency due to the causes
listed in Box 49.4.
+TQPOGVCDQNKUOKPRTGIPCPVYQOGP
In pregnancy, iron is mobilized from maternal 'HHGEVUQHKTQPFGſEKGPE[
iron stores due to increased demands. However, anemia on pregnancy
iron stores are low in women from developing
countries. Therefore, in addition to dietary iron, Iron deficiency anemia during pregnancy can
supplemental iron is mandatory in pregnant have several adverse effects on the mother.
women. There is increased susceptibility to infection,
CH 49_p740-757_v3.indd 742 19-07-2015 11:21:16

Box 49.4 %
CWUGUQHKTQPFGſEKGPE[ %NKPKECNHGCVWTGUQHKTQPFGſEKGPE[
in developing countries anemia
• +PCFGSWCVGKPVCMG The clinical features of iron deficiency anemia
Ŧ .QYDKQCXCKNCDKNKV[KPFKGV are listed in Box 49.6.
Ŧ &KGVUYKVJNQYKTQPEQPVGPV
• Iron loss
Box 49.6 Clinical features of anemia
Ŧ *QQMYQTOKPHGUVCVKQP
Ŧ Malaria • Mild-to-moderate anemia
• .QYKTQPUVQTGU Ŧ (CVKIWG
Ŧ 5JQTVKPVGTRTGIPCPE[KPVGTXCN Ŧ *GCFCEJG
Ŧ /WNVKRCTKV[ Ŧ 'ZGTEKUGKPVQNGTCPEG
• &GHGEVKXGCDUQTRVKQP Ŧ Giddiness
Ŧ 2JQURJCVGUCPFRJ[VCVGUKPFKGV Ŧ Palpitation
Ŧ &GſEKGPE[QHXKVCOKP%CPFXKVCOKP# Ŧ Edema
• Severe anemia
Ŧ %QPIGUVKXGECTFKCEHCKNWTG
thromboembolism, and a high risk of preterm
labor. Blood loss during delivery or antepartum
hemorrhage is tolerated poorly.
Effects on the fetus are not manifest unless the
Physical examination
anemia is moderate to severe. Moderate anemia The following may be seen in a woman with
has been associated with an increased risk of low severe or chronic anemia:
birth weight, prematurity, and perinatal mortal-
• Pallor of the mucus membranes (nonspecific
ity. Severe anemia with maternal hemoglobin
finding)
levels <6 g/dL has been associated with abnor-
• Spoon-shaped nails (koilonychia)
mal fetal oxygenation resulting in nonreassuring
• A glossy tongue, with atrophy of the lingual
fetal heart rate patterns, reduced amniotic fluid
papillae
volume, fetal cerebral vasodilatation, and fetal
• Fissures at the corners of the mouth (angular
death. Thus, maternal blood transfusion should
stomatitis)
be considered for fetal indications. Obstetric
• Splenomegaly (in severe, persistent, untreated
consequences of iron deficiency anemia in preg-
cases)
nancy are listed in Box 49.5.
• Systolic murmur at the aortic area (hemic
murmur)
Box 49.5 1
DUVGVTKEEQPUGSWGPEGUQHKTQP • Signs of cardiac failure
FGſEKGPE[CPGOKC – Pedal or generalized edema
aternal – Tachycardia and hepatomegaly
• 2TGVGTOFGNKXGT[
– Crepitations at lung bases
• 2WGTRGTCNUGRUKU
• 2WGTRGTCNVJTQODQGODQNKUO Diagnosis
• Poor tolerance to blood loss
• 2QUVRCTVWOFGRTGUUKQP emoglobin complete bloo count
etal and neonatal conse uences an peripheral smear
• 2TGOCVWTKV[ The diagnosis of iron deficiency anemia is
• 2GTKPCVCNOQTVCNKV[ commonly made with a complete blood count
• .QYDKTVJYGKIJV (which includes hemoglobin, hematocrit, and
• 2QQTOGPVCNCPFRU[EJQOQVQTRGTHQTOCPEG the red cell indices) and peripheral smear. In
• .QYKTQPUVQTGU some women, iron studies may be required
• 9KVJOCVGTPCNJGOQINQDKPIF. to establish the etiology. A peripheral smear
Ŧ 0QPTGCUUWTKPIHGVCNJGCTVTCVGRCVVGTPU helps to differentiate between iron deficiency
Ŧ 4GFWEGFCOPKQVKEƀWKFXQNWOG
and vitamin B12/folic acid deficiency anemia.
Ŧ Fetal cerebral vasodilatation
Classically, iron deficiency anemia will exhibit
Ŧ (GVCNFGCVJ
smaller RBCs and is called microcytic anemia.
CH 49_p740-757_v3.indd 743 19-07-2015 11:21:16

With vitamin B12 or folate deficiency, the RBCs Prophylactic measures against iron
are much larger and so it is called macrocytic FGſEKGPE[CPGOKCKPRTGIPCPE[
anemia.
Red cell indices should also be determined. In developing countries, the prevalence of
Anemias can be differentiated by the MCV. Iron low iron stores and iron deficiency anemia in
deficiency anemia will have an MCV of <80 fL, women of fertile age and in pregnant women is
whereas vitamin B12 or folic acid deficiency considerable.
anemia will have an MCV >100 fL. Mean cor- Iron supplementation is essential in all preg-
puscular hemoglobin concentration (MCHC) is nant women due to the following reasons:
a sensitive index of iron deficiency anemia.
• During pregnancy maternal requirement for
iron increases.
Serum erritin • The demand for absorbed iron increases
Measurement of serum ferritin is considered steadily during pregnancy:
to be a sensitive test for the diagnosis of iron – 0.8 mg/day in the initial 10 weeks’ gestation
deficiency anemia. The levels do not change – 6 mg after midpregnancy
with recent iron intake. Ferritin levels <15 μg/L – 7.5 mg/day in the last 10 weeks’ gestation
are diagnostic of iron deficiency, but treatment • During the entire gestational period, the aver-
should be initiated when levels are <30 μg/L. age demand for absorbed iron is 4–6 mg/day.
• Only 10% of elemental iron will be absorbed
Serum iron an total iron bin ing (e.g., 6 mg will be absorbed when 60 mg of ele-
capacity mental iron is taken).
• Dietary iron intake is inadequate to fulfill the
Serum iron (<30 μg/dL) and total iron-binding body iron demands in the second and third tri-
capacity (TIBC >400 μg/dL) are indicative of iron mesters of pregnancy.
deficiency but are not as sensitive or specific as
ferritin levels. Increase in ietary iron
Diagnostic tests for iron deficiency anemia
Pregnant women should be advised to take a
diet rich in iron, such as green leafy vegetables,
sprouts, jaggery, meats, and liver. Overcooking of
food should be avoided. Cooking in iron vessels
Box 49.7 &
KCIPQUVKEVGUVUHQTKTQPFGſEKGPE[
should be encouraged.
anemia
• *GOQINQDKPJGOCVQETKV Supplemental iron
Ŧ .QYJGOQINQDKPCPFJGOCVQETKV
WHO guidelines have recommended the
• %QORNGVGDNQQFEQWPV
Ŧ .QY4$%EQWPV
following:
Ŧ 0QTOCNQTGNGXCVGFYJKVGDNQQFEGNNEQWPV • Iron should be provided to pregnant women
Ŧ 'NGXCVGFRNCVGNGVEQWPV during antenatal visits.
• 4GFEGNNKPFKEGU
• Iron should be started with the first antenatal
Ŧ .QY/%8
H.
visit.
Ŧ .QY/%*%

• 2GTKRJGTCNDNQQFUOGCT
• For countries such as India, where prevalence
Ŧ 4$%UOKETQE[VKECPFJ[RQEJTQOKE of anemia is 80%–90% in pregnancy, WHO rec-
Ŧ #PKUQE[VQUKUCPFRQKMKNQE[VQUKU ommends daily supplementation of 60 mg ele-
• +TQPUVWFKGU mental iron, in the form of ferrous salts, along
Ŧ .QYUGTWOHGTTKVKPNGXGNU with 400 μg of folic acid for a duration of
Ŧ .QYUGTWOKTQPNGXGNU – At least 6 months during pregnancy
Ŧ 'NGXCVGFVQVCNKTQPDKPFKPIECRCEKV[ – 3 months postpartum
• 6GUVUVQFGVGTOKPGGVKQNQI[
Ŧ 5VQQNGZCOKPCVKQPHQTJQQMYQTOKPHGUVCVKQP The Government of India (Ministry of Health)
Ŧ 2GTKRJGTCNUOGCTHQTOCNCTKCNRCTCUKVGU recommends 100 mg of elemental iron (335 mg
Ŧ 7TKPGOKETQUEQR[HQTEJTQPKETGPCNFKUGCUG of ferrous sulfate) and 500 μg of folic acid for
C C OGCPEQTRWUEWNCTJGOQINQDKPEQPEGPVTCVKQP C mean
100 days from 14 weeks’ gestation for all preg-
EQTRWUEWNCTXQNWOG BC red blood cell. nant women. The tablets of ferrous sulfate
CH 49_p740-757_v3.indd 744 19-07-2015 11:21:16

and folic acid are supplied free of cost by the • Ferrous sulfate: 150 mg/200 mg (45 mg/60 mg
Government of India. elemental iron) per tablet/capsule
• Ferrous gluconate: 300 mg (30 mg elemental
arasite control measures iron) per tablet/capsule
Since the prevalence of hookworm infestation The tablets supplied by the Government of
is >20% in India, a single dose of albendazole India can be used two times a day. The efficacy of
400 mg or mebendazole 500 mg in the second all iron salts mentioned above is similar, and no
trimester is recommended by WHO for all preg- one preparation is superior to the other.
nant women in endemic areas. A large number of other oral iron-containing
Prophylactic measures for iron deficiency preparations and nutritional supplements are
anemia are summarized in Box 49.8. available. Some enteric-coated, sustained-re-
lease preparations such as carbonyl iron, iron
Box 49.8 Prophylactic measures against iron polymaltose complex, and ferrous glycine sul-
FGſEKGPE[CPGOKC fate are also available. These are more expensive
• +PETGCUGKPFKGVCT[KTQP but poorly absorbed because they do not release
Ŧ )TGGPNGCH[XGIGVCDNGU the drug in the duodenum where iron is best
Ŧ 5RTQWVU absorbed. These preparations are not superior
Ŧ Meat to the ferrous salts mentioned above and are not
Ŧ .KXGT recommended.
• +TQPUWRRNGOGPVCVKQP Recommendations for the administration of
Ŧ 60–100 mg elemental iron oral iron are enumerated in Box 49.9.
Ŧ 9KVJzIHQNKECEKF
Ŧ (QTCVNGCUVFC[UHTQOYGGMU Side effects
• 2CTCUKVG EQPVTQN OGCUWTGU
VQ DG IKXGP KP UGEQPF Approximately 30% or more of women will have
VTKOGUVGT
gastrointestinal symptoms:
Ŧ #NDGPFC\QNGOIUKPINGFQUGQT
Ŧ /GDGPFC\QNGOIUKPINGFQUG • Nausea
• Constipation or diarrhea
• Epigastric distress and/or vomiting
6TGCVOGPVQHKTQPFGſEKGPE[CPGOKC Women should be reassured that the side
The treatment of iron deficiency anemia is by effects will usually subside after 10–14 days of
iron therapy. Route of iron therapy depends on continuous usage.
severity of anemia, gestational age, patient com-
pliance, and other factors.
Oral iron therapy Box 49.9 ecommendations for the administra-

Oral iron is considered as first-line therapy tion of oral iron
since it is inexpensive and effective when taken • $GUVVCMGPQPCPGORV[UVQOCEJ
properly. Ŧ 'CTN[KPVJGOQTPKPIQT
The recommended oral daily dose for the Ŧ JQWTUCHVGTHQQF
treatment of iron deficiency anemia in preg- • +TQPUCNVUPQVVQDGIKXGPYKVJHQQF
nant women is in the range of 120–200 mg/day Ŧ #DUQTRVKQP KORCKTGF YKVJ RJQURJCVGU RJ[VCVGU
and tannates
of elemental iron, depending on the severity of
• (CEVQTUVJCVKPJKDKVVJGCDUQTRVKQPQHKTQPUCNVU
anemia. This may require iron tablets/capsules Ŧ Antacids
to be taken two to three times daily. Ŧ H2TGEGRVQTDNQEMGTU
Choice of preparation Ŧ 2TQVQPRWORKPJKDKVQTU
Ŧ /KNMCPFFCKT[RTQFWEVUGIIUEGTGCN
The most appropriate and effective oral iron Ŧ %CNEKWOUWRRNGOGPVU
therapy is the use of a tablet/capsule containing Ŧ %GTVCKPCPVKDKQVKEU
GISWKPQNQPGU
ferrous salts. • (CEVQTUVJCVCKFKPCDUQTRVKQPQHKTQP
Ŧ 1TCPIGNGOQPLWKEG
• Ferrous fumarate: 300 mg (100 mg elemental
Ŧ Vitamin C
iron) per tablet/capsule
CH 49_p740-757_v3.indd 745 19-07-2015 11:21:16

esponse to therapy sorbitol citrate is given as 100 mg/day, deep

An increase in the reticulocyte count is used as intramuscular in the gluteal region, using the ‘Z’
an indicator of response to iron therapy. technique to avoid staining of skin.
Reticulocyte count increases 7–10 days after However, the intravenous route is now pre-
start of therapy. Hemoglobin level increases by ferred for the following reasons:
0.3–1 g/dL per week with adequate replacement. • Mobilization of iron from intramuscular sites
If hematological improvement does not occur in is slow
3 weeks, the following steps are recommended: • Rise in the hemoglobin concentration is
• Reassess compliance not appreciably faster with intramuscular
• Exclude and treat hookworm infestation or administration
bleeding hemorrhoids • Intramuscular iron injection
• Exclude concomitant folate deficiency – Is poorly absorbed
• Exclude thalassemia and chronic illness – Is painful
– Stains the buttocks
– Is associated with the development of glu-
arenteral iron therapy
teal sarcomas
The rise in hemoglobin with parenteral iron ther-
apy is the same as with oral therapy. Ensuring Intravenous iron therapy
compliance is the most important advantage.
There are a number of intravenous iron formu-
Indications for parenteral iron therapy are
lations approved for use. In selecting the dose of
parenteral iron required, the iron deficit is cal-
culated based on the fact that 1 g of hemoglobin
Box 49.10 Indications for parenteral iron contains 3.3 mg of elemental iron, along with
therapy other variables such as blood volume, desired
hemoglobin level, and whether or not one wishes
• Unresponsiveness to oral iron
• Noncompliance to provide additional iron for body stores.
• Intolerance to oral iron Iron dextran
• 0GGFHQTCSWKEMTGEQXGT[HTQOCPGOKC
Ŧ %NQUGVQFGNKXGT[ • Contains 50 mg of elemental iron/mL
• +H JGOQINQDKP KU Ō IF. CHVGT YGGMUŏ IGUVCVKQP • Approved for intramuscular/intravenous route

)QXGTPOGPVQH+PFKCTGEQOOGPFCVKQP • The low-molecular-weight preparation preferred
– Lesser adverse effects than high-molecular-
weight dextran
Calculation of dosage • May be given as repeated doses of 100 mg IV/
In calculating the dose of parenteral iron day (or)
required, the hemoglobin deficit is calculated by • As total dose infusion
subtracting the woman’s hemoglobin from the – Test dose of 25 mg given as slow intravenous
normal level (14 g/dL). The total dose is calcu- push
lated and 1000 mg is added to replenish the iron – Observed for 15 minutes for reaction
stores. The formula for calculating total dose of – Total dose in 500 mL of normal saline over
iron required is given as follows: 4 hours
• Safe in pregnancy
Total dose of iron 2.2 u prepregnant weight(kg)
Ferric gluconate compound
u hemoglobin deficit (g/dL) 1000 mg
or • Only for intravenous route
• 125 mg of ferric gluconate complex diluted in
Total dose of iron 0.3 u prepregnant weight (lb) 100 mL of isotonic saline
u hemoglobin deficit (%) 1000 mg • Infused over 30–60 minutes
Intramuscular iron therapy Iron sucrose
For many years, parenteral iron was given only • Only for intravenous route
by the intramuscular route. Iron dextran or iron • Contains 20 mg iron/mL
CH 49_p740-757_v3.indd 746 19-07-2015 11:21:16

• 200 mg infused over 60 minutes Exchange transfusion

• Total dose administered in divided doses of Exchange transfusion is rarely used now. It may
200 mg/day as daily infusions be indicated in women with severe anemia in
Iron isomaltoside
congestive cardiac failure who are prone to fluid
overload and worsening of cardiac failure with
• 20 mg/kg infused over 15 minutes blood transfusion.
(GTTKEECTDQZ[OCNVQUG
• Ferric hydroxide carbohydrate complex
Intrapartum management of iron
• Less anaphylactic reactions compared with FGſEKGPE[CPGOKC
other preparations Intrapartum management of iron deficiency
• Well tolerated in pregnancy anemia consists of the following steps:
• 20 mg/kg infused over 15 minutes
• Maximum dose of 1000 mg • Close monitoring for signs of fluid overload
and congestive cardiac failure is mandatory.
The intravenous iron preparations are listed • Oxygen by mask should be provided if the ane-
in Table 49.2. mia is severe.
• Prolonged second stage should be avoided.
loo trans usion • Active management of third stage should be
performed to prevent excessive blood loss.
Blood transfusion may be required in certain sit- • Oxytocics should be administered to prevent
uations in iron deficiency anemia. Severe anemia third-stage hemorrhage.
in any trimester is an indication for transfusion.
Blood transfusion is also required in situations Postnatal hemoglobin should be estimated
where rapid improvement in hemoglobin is before discharge in the following situations:
essential as in women in labor or close to term. • Women delivered by cesarean section
Packed cells are used to avoid fluid overload. • Postpartum bleeding >500 mL
Transfusion should be given slowly at the rate of • Uncorrected antenatal anemia
80–100 mL/hour. If mild anemia is diagnosed in the postpar-
The indications for blood transfusion in preg- tum period, oral iron therapy is the treatment of
nant women are given in Box 49.11. choice. If anemia is moderate or severe, intrave-
nous iron is recommended.
Box 49.11 +PFKECVKQPUHQTDNQQFVTCPUHWUKQP
• *GOQINQDKPIF.CVCP[IGUVCVKQPCNCIG Contraception
• *GOQINQDKPIF.KPNCVGVJKTFVTKOGUVGT
Contraception is important in women with ane-
• 9QOGPYKVJUGXGTGCPGOKCKPNCDQT
mia. Adequate spacing of pregnancies allows
6CDNG Intravenous iron preparations
Drug Maximum approved Test dose Elemental iron

dose per day (mg of concentration
GNGOGPVCNKTQP
OIO.
+TQPFGZVTCP
NQY 100 4GSWKTGF 50
OQNGEWNCTYGKIJV
(GTTKEINWEQPCVG 125 4GEQOOGPFGFKHFTWI 12.5
allergies present
+TQPUWETQUG 200–300 4GEQOOGPFGFKHFTWI 20
allergies present
Iron isomaltoside OIMI No 100
Ferric OIMI
OCZKOWO No 50
ECTDQZ[OCNVQUG OI
CH 49_p740-757_v3.indd 747 19-07-2015 11:21:16

time for replenishing iron stores and reduces

Box 49.12 %CWUGUQHHQNKECEKFFGſEKGPE[
risk of anemia in subsequent pregnancy.
Progesterone-only pill, injection medroxypro- • &KGVCT[KPUWHſEKGPE[
gesterone, or combined oral contraceptive pills • /WNVKHGVCNRTGIPCPE[
• &TWIU
may be used. Intrauterine devices are not con-
Ŧ Dilantin
traindicated, but menorrhagia may be a prob-
• /CNCDUQTRVKQPU[PFTQOGU
lem. Multiparous women must be encouraged to • *GOQN[UKU
undergo tubal ligation. Ŧ Malaria
Ŧ 5KEMNGEGNNFKUGCUG
MGICNQDNCUVKECPGOKC
in pregnancy Box 49.13 /
CPCIGOGPVQHHQNKECEKFFGſEKGPE[
anemia
Folic acid deficiency and vitamin B12 deficiency • Diagnosis
can give rise to anemia with large cells (mega- Ŧ /CETQE[VKECPGOKC
loblasts) in blood and the bone marrow. Due Ŧ /%8 H.
to abnormalities in DNA synthesis, nuclear Ŧ .QYUGTWOHQNKECEKFNGXGN
maturation is incomplete and the red cells Ŧ 'NGXCVGFUGTWO.&*NGXGNU
are large (macrocytes) and neutrophils are Ŧ 'NGXCVGFUGTWOJQOQE[UVGKPGNGXGNU
hypersegmented. • 2TQRJ[NCZKU
Ŧ zIQHHQNKECEKFFC[FWTKPIRTGIPCPE[
Ŧ &KGVTKEJKPHQNKECEKF
FQNKECEKFFGſEKGPE[CPGOKC (TGUJNGCH[XGIGVCDNGU
.GIWOGU
Folate deficiency is much less common than iron Animal proteins
deficiency. Most iron supplements contain folic • Treatment
acid. Folic acid is anyway recommended to all Ŧ 1TCNHQNKECEKFVCDNGVUzIFC[
CNQPIYKVJKTQP
women contemplating pregnancy to reduce the Ŧ &KGVCT[CFXKEG
risk of neural tube defects. Ŧ %QTTGEVEQPEWTTGPVKTQPFGſEKGPE[
Folic acid deficiency coexists with iron defi- D NCEVCVGFGJ[FTQIGPCUG C OGCPEQTRWUEWNCTXQNWOG
ciency or vitamin B12 deficiency.
An increased MCV (typically >100 fL) can be
Box 49.14 Causes of vitamin B12FGſEKGPE[
suggestive of folic acid and/or vitamin B12 defi-
ciency. Determining serum levels of vitamin • +PCFGSWCVGFKGVCT[KPVCMG
XGIGVCTKCPUCPFXGICPU
B12 and folic acid will differentiate between the • 2GTPKEKQWUCPGOKCECWUGFD[NCEMQHKPVTKPUKEHCEVQT
• )CUVTGEVQO[CPFICUVTKVKU
two. If the folic acid level is low, the mother is
• +PUWHſEKGPV RCPETGCVKE RTQVGCUG
GI EJTQPKE RCPETG-
treated with oral folic acid at a dose of 1 mg three CVKVKU<QNNKPIGTŌ'NNKUQPU[PFTQOG
times daily. • /CNCDUQTRVKQPU[PFTQOGU
• *+8KPHGEVKQP
Etiology • *GTGFKVCT[FKUQTFGTU
JWOCPKOOWPQFGſEKGPE[XKTWU
The most common cause of folate deficiency is
dietary insufficiency. Causes of folic acid defi-
ciency are listed in Box 49.12. The causes for vitamin B12 deficiency are listed
The diagnosis and treatment of folic acid defi- in Box 49.14.
ciency anemia are summarized in Box 49.13.
Clinical symptoms of vitamin B12
itamin B12 FGſEKGPE[CPGOKC FGſEKGPE[CPGOKC
In severe vitamin B12 (cobalamin) deficiency, Vitamin B12 stores are very large in the body, and
the woman presents with profound anemia and it takes years to deplete them. Symptoms there-
macrocytic red cells (MCV >100 fL) with or with- fore take a long time to manifest. If there is iron
out varying neurological disturbances. deficiency anemia concomitantly, vitamin B12
%*ARAXKPFF 19-07-2015 11:21:16

Box 49.15 Signs and symptoms of severe 'HHGEVUQHOGICNQDNCUVKE

vitamin B12FGſEKGPE[
anemia on pregnancy
• 5OQQVJDGGH[TGFVQPIWGYKVJNQUUQHRCRKNNCG
• )CUVTQKPVGUVKPCNU[ORVQOU
Association between folic acid/vitamin B12 defi-
Ŧ $WTPKPIQTUQTGPGUUQHVQPIWG ciency anemia and preeclampsia-like syndrome,
Ŧ #PQTGZKC fetal growth restriction, and placental abruption
Ŧ 0CWUGCCPFXQOKVKPI has been reported but not proven.
Ŧ *GCTVDWTP
Ŧ (NCVWNGPEG
• 0GWTQNQIKECNU[ORVQOU
Treatment of vitamin B12
Ŧ 2CTGUVJGUKCU FGſEKGPE[CPGOKC
Ŧ 0WODPGUU
Ŧ 9GCMPGUU 2CTGPVGTCNEQDCNCOKP
Ŧ .QUUQHFGZVGTKV[
Ŧ +ORCKTGFOGOQT[ Intramuscular or deep subcutaneous cobalamin
Ŧ 2GTUQPCNKV[EJCPIGU is administered:
• 5MGNGVCNEJCPIGU
• 1000 μg (1 mg) every day for 1 week
Ŧ Osteoporosis
• Followed by 1 mg every week for 4 weeks
deficiency anemia may get masked. The clinical Dimorphic anemia

signs and symptoms of severe vitamin B12 defi-
ciency are listed in Box 49.15. Dimorphic anemia refers to anemia that has
two different causes acting together, for exam-
ple, iron deficiency as well as a vitamin B12 defi-
Diagnosis ciency, or iron deficiency and folate deficiency.
The diagnosis of vitamin B12 deficiency anemia is Dimorphic anemia can occur in pregnancy and
commonly made with a complete blood count and is not uncommon in women with chronic mal-
peripheral smear. Serum levels of folic acid and nutrition, multifetal pregnancy, or malabsorp-
vitamin B12 may be required to differentiate the two tion. The peripheral smear shows macrocytic
anemias since both result in megaloblastic (mac- and microcytic, hypochromic red cells with
rocytic) anemia. Diagnostic tests for vitamin B12 anisocytosis. Treatment is by correction of iron
deficiency anemia are enumerated in Box 49.16. and vitamin B12/folic acid deficiency.
Box 49.16 Diagnostic tests for vitamin B12 Sickle cell disease
FGſEKGPE[CPGOKC
in pregnancy
• %QORNGVGDNQQFEQWPV
Ŧ .QYJGOQINQDKPCPFJGOCVQETKV Sickle cell disease (SCD) is an inherited disorder
Ŧ .QY4$%EQWPV due to homozygosity for the abnormal hemoglo-
Ŧ *KIJ/%8
H. bin—hemoglobin S (HbS). The two classic fea-
Ŧ .QY/%*% tures are as follows:
Ŧ 0QTOCNQTNQYTGVKEWNQE[VGEQWPV
Ŧ 0QTOCNQTNQYYJKVGDNQQFEGNNEQWPV • Hemolysis
Ŧ .QYRNCVGNGVEQWPVU – Results in anemia (‘sickle cell anemia’)
• 2GTKRJGTCNDNQQFUOGCT • Vaso-occlusive phenomena
Ŧ /CETQE[VKE4$%U – Lead to recurrent painful episodes (‘sickle
Ŧ *[RGTUGIOGPVGFPGWVTQRJKNU cell crisis’)
• 5GTWONGXGNU
Ŧ .QYXKVCOKP$12 levels Most pregnancies complicated by SCD
Ŧ *KIJJQOQE[UVGKPGNGXGNU will result in live birth. However, there is an
C OGCPEQTRWUEWNCTXQNWOG C C OGCPEQTRWUEWNCTJGOQ- increased risk of obstetric, fetal, and medical
INQDKPEQPEGPVTCVKQP BC red blood cell. complications.
CH 49_p740-757_v3.indd 749 19-07-2015 11:21:17

Pathophysiology of sickle The pathophysiology of SCD is encapsulated

in Figure 49.1.
cell disease
Anemia occurs as a result of the sickle hemo-
globinopathies. Deoxygenation of the abnor- Prepregnancy evaluation,
mal RBCs results in sickling. These permanently counseling, and immuni ation
damaged RBCs are then removed by the reticu-
loendothelial system, with the average RBC life A woman with SCD who is contemplating preg-
span reduced to 17 days. The result is a chronic nancy should undergo prepregnancy counseling
compensated anemia, with hemoglobin level and evaluation (Box 49.17).
typically between 6.5 and 9.5 g/dL.
The stiff, inflexible sickle cells obstruct Box 49.17 Prepregnancy evaluation,
the microvasculature. This can result in vas- counseling, and immuni ation
cular stasis, hypoxia, acidosis, and increased in sickle cell disease
2,3-diphosphoglycerate leading to further deox- • %QPſTOCVKQPQHUWDV[RGQHFKUGCUG
KHPQVCNTGCF[FQPG
ygenation, and, thus, more sickling. The micro- • $CUGNKPGDNQQFRTGUUWTG
vascular injury can result in ischemic necrosis Ŧ 4KUMHCEVQTHQT
and end-organ infarction. Organs affected by UWRGTKORQUGFRTGGENCORUKC
chronic sickling include the spleen, lungs, kid- UVTQMG
neys, heart, and brain. • *GOQINQDKPJGOCVQETKVCPFHGTTKVKPNGXGN
Ŧ 9QOGP YKVJ JKIJ KTQP UVQTGU UJQWNF PQV TGEGKXG
KTQPUWRRNGOGPVU
ic le cell • *GRCVKVKU$CPF%UETGGPKPIVQCUUGUUVJGTKUMQHRGTK-
hemoglobinopathies natal transmission
• &KUEQPVKPWKPI VJG HQNNQYKPI OGFKECVKQPU EQPVTCKPFK-
ECVGFKPRTGIPCPE[
Ŧ *[FTQZ[WTGC
eo ygenation
Ŧ %JGNCVKPICIGPVU
of abnormal
Cs Ŧ #PIKQVGPUKPEQPXGTVKPIGP\[OGKPJKDKVQTU
Ŧ #PIKQVGPUKP++TGEGRVQTDNQEMGTU
• )GPGVKEEQWPUGNKPI
Ŧ %JGEMJWUDCPFHQTJGOQINQDKPQRCVJ[
ic ling of
Cs Ŧ &KUEWUUTKUMQHVTCPUOKVVKPI5%&VQHGVWU
Ŧ &KUEWUURTGPCVCNFKCIPQUKUYKVJRQUUKDNGVGTOKPC-
VKQPQHCPCHHGEVGFRTGIPCPE[
Ŧ &KUEWUU RTGKORNCPVCVKQP IGPGVKE FKCIPQUKU HQT UG-
NGEVKQPQHGODT[QUYKVJQWV5%&
emo e by tiff infle ible sic le cells
• +OOWPK\CVKQPYKVJHQNNQYKPIXCEEKPGU
reticuloen othelial obstruct an injure
system micro asculature Ŧ 2PGWOQEQEECN
Ŧ *CGOQRJKNWUKPƀWGP\CV[RG$
Ŧ Meningococcal
SCD UKEMNGEGNNFKUGCUG
erage C Vascular stasis
life span Hypo ia
re uce to ci osis
ays iphosphoglycerate Course of SCD during
pregnancy
Chronic Maternal morbidity from SCD is the same during
compensate schemic necrosis pregnancy as during the nonpregnant state. The
anemia n organ infarction most common maternal SCD complications that
Hb g L occur in over 50% of pregnant women are as
follows:
Figure 49.1 2CVJQRJ[UKQNQI[QHUKEMNGEGNNFKUGCUG b,
JGOQINQDKP BC, red blood cell. • Anemia
CH 49_p740-757_v3.indd 750 19-07-2015 11:21:17

• Acute painful episodes (‘sickle cell crisis’) .CDQTCPFFGNKXGT[

– Pain involving the abdomen, chest, verte-
brae, or extremities There are no medical contraindications to
– More common in later pregnancy and vaginal delivery. Cesarean section can be
postpartum done when indicated for obstetric reasons.
– Associated with thrombophlebitis or Thromboprophylaxis, adequate hydration, and
preeclampsia blood transfusion are recommended in the case
– More common in sickle cell anemia of a cesarean delivery.
%QTFDNQQF
Effect of SCD on maternal
The cord blood is collected for the following:
and fetal outcomes
• Testing the newborn for hemoglobinopathy
Pregnancy complicated with SCD has an • Storing the stem cells (if negative for hemo-
increased risk of the following: globinopathy) for future transplantation to a
• Gestational hypertension and preeclampsia family member affected with SCD
• Eclampsia
• Preterm labor
• Postpartum infection Thalassemias
• Abruption
• Fetal growth restriction in pregnancy
Women with sickle cell trait do not have an Healthy adults have >95% hemoglobin A
increased risk for pregnancy complications. (HbA), which consists of two E-globin and two
However, they may have increased risk for ane- E-globin chains. Thalassemias are character-
mia and bacteriuria. ized by impaired production of one or more of
In spite of improved maternal and fetal the normal globin chains found in hemoglobin.
survival, pregnant women with the sickle hemo- The clinical consequences can be ineffective
globinopathies remain at risk for renal insuffi- erythropoiesis, hemolysis, and anemia of vary-
ciency, cerebrovascular accident, cardiac dys- ing degrees.
function, leg ulcers, and sepsis, particularly from
encapsulated organisms.
Types of thalassemias
Prenatal care in SCD The characteristics of the different types of thal-
assemias are listed in Box 49.18.
A pregnant woman who has SCD requires close
observation. Other than routine prenatal care,
Box 49.18 Characteristics of different types
women with SCD also specifically require the of thalassemias
following:
x D- or EVJCNCUUGOKCminor or trait
• Folic acid supplementation (iron cannot be Ŧ /CLQTKV[QHCHHGEVGFCFWNVUCTGCU[ORVQOCVKE
administered) /KETQE[VKEJ[RQEJTQOKETGFEGNNU
• Frequent blood tests for anemia 9KVJQTYKVJQWVOKPQTFGITGGQHCPGOKC
• Urine culture for bacteriuria every trimester • 6JCNCUUGOKCKPVGTOGFKC
• Serial ultrasound monitoring for fetal growth Ŧ %QOOQPVJTQWIJQWVVJGYQTNF
• Fetal surveillance from 34 weeks Ŧ /QTG VJCP QPG JGOQINQDKP OWVCVKQP KP VJG UCOG
patient
• Checking for red blood alloimmunization
(QTGZCORNGUKEMNGEGNNVJCNCUUGOKCJGOQINQDKP
because of previous frequent blood transfusions '
*D'EVJCNCUUGOKC
Prophylactic blood transfusions have been x E6JCNCUUGOKCmajor
Ŧ .KHGNQPIVTCPUHWUKQPFGRGPFGPVCPGOKC
recommended for women with previous perina-
x D6JCNCUUGOKCmajor
tal mortality, severe anemia, to treat acute com-
Ŧ +PEQORCVKDNGYKVJGZVTCWVGTKPGNKHG
plications or in preparation for surgery.
CH 49_p740-757_v3.indd 751 19-07-2015 11:21:17

Genetics of thalassemias are infertile. E-Thalassemia is a lifelong trans-

fusion-dependent anemia. It is characterized by
Inheritance is autosomal recessive. The gene the following:
loci for the D-globin chains are located on the
short arm of chromosome 16. The E-chain gene • Erythropoiesis and hemolysis are ineffective.
is located on the short arm of chromosome 11. • During fetal life, high levels of HbF are
Thalassemias are prevalent in many ethnic protective.
groups in India. • After birth, as HbF levels fall, the infant devel-
If both parents have thalassemia minor (or ops anemia.
trait), the offspring have a 50% chance of inher- • Blood tests
iting the trait; 25% will have thalassemia major – Profound hypochromic, microcytic anemia
and 25% will be unaffected (Fig. 49.2). – Bizarre red cell morphology
– Increased indirect bilirubin and lactate
dehydrogenase
– Reduced or absent haptoglobin
E-Thalassemia minor or trait

E-Thalassemia minor occurs in individuals who
are heterozygous for the gene mutation and
therefore have variable production of the E-
globin chain. It has variable clinical effects,
depending on the rate of E-chain production. It
may be unmasked during pregnancy or uncov-
Mother trait ather trait ered after a mother has delivered a homozygous
infant.
Hemoglobin electrophoresis in thalassemia
minor characteristically shows the adult hemo-
globin, HbA2, to be increased to >3.5%.
Obstetric implications
The following are the obstetric implications:
• Fertility not impaired
• Pregnancy outcomes good
halassemia rait Unaffecte • May become disproportionately anemic
major no thalassemia trait – Require iron or folate supplementation dur-
Figure 49.2 +PJGTKVCPEGRCVVGTPQHVJCNCUUGOKCUYJGP ing pregnancy
DQVJRCTGPVUJCXGVJCNCUUGOKCVTCKV • Important to offer prenatal diagnosis to assess
fetal hemoglobinopathy (see Chapter 12,
E-Thalassemia Prenatal screening, prenatal diagnosis, and
fetal therapy)
In the E-thalassemias, point mutations cause – Amniocentesis or chorion villus sampling
absence of or reduction in E-chain production. – Noninvasive prenatal testing
Elevated levels of hemoglobin F (HbF) can often Polymerase chain reaction (PCR) of fetal
be found and HbA is usually absent in these DNA
individuals.
D-Thalassemia
E-Thalassemia ma or (Cooley
D-Thalassemia disorders involve loss of one of
CPGOKC the four D-globin genes. The characteristics of
E-Thalassemia major occurs when both E-genes different types of D-thalassemia are summarized
are missing. The majority of affected women in Box 49.19.
CH 49_p740-757_v3.indd 752 19-07-2015 11:21:17

Box 49.19 Types of D-thalassemia depending TJTQODQE[VQRGPKCU

QPPWODGTQHIGPGUFGNGVGF
• &GNGVKQPQHQPGD-globin gene
in pregnancy
Ŧ D6JCNCUUGOKCminima Thrombocytopenia or low platelet count is often
Ŧ Silent carrier encountered in pregnancy. It is typically defined
Ŧ .CDQTCVQT[XCNWGUKPVJGPQTOCNTCPIG
as a platelet count lower than 150,000/μL. The
• &GNGVKQPQHVYQDEJCKPIGPGU
obstetrician may encounter thrombocytopenia
Ŧ D6JCNCUUGOKCminor or trait
Ŧ /KNFVQOQFGTCVGJ[RQEJTQOKEOKETQE[VKECPGOKC
in one of the following three clinical situations:
Ŧ #HHGEVGFYQOCPVQNGTCVGURTGIPCPE[YGNN • Preexisting thrombocytopenia
• &GNGVKQPQHVJTGGQHVJGHQWTD-globin genes – Immune thrombocytopenia
Ŧ D6JCNCUUGOKCinterme ia or b isease • Decreasing platelet count or newly discovered
Ŧ *D*CPF*D$CTVUKP4$%U
thrombocytopenia in pregnancy
Ŧ *GOQN[VKECPGOKCUQQPCHVGTDKTVJ
– Gestational thrombocytopenia
Ŧ #PGOKCQHXCT[KPIUGXGTKV[
Ŧ 9QTUGPKPIQHCPGOKCFWTKPIRTGIPCPE[KPCHHGEVGF
– Immune thrombocytopenia
YQOCP • Acute onset of thrombocytopenia in the set-
• &GNGVKQPQHCNNHQWTD-globin genes ting of
Ŧ D6JCNCUUGOKCmajor – severe preeclampsia
Ŧ 4$%UEQPVCKP*D$CTVU – hemolysis, elevated liver enzymes, and low
Ŧ (GVCNJ[FTQRUKPVTCWVGTKPGHGVCNFGCVJQTGCTN[PGQ- platelet count (HELLP) syndrome
PCVCNFGCVJ – acute fatty liver of pregnancy (AFLP)
Ŧ 2QUUKDKNKV[QHFGXGNQROGPVQHRTGGENCORUKCKPYQOCP – disseminated intravascular coagulation
ECTT[KPICHHGEVGFHGVWU
Management of thrombocytopenia in preg-
b JGOQINQDKP* BC red blood cell.
nancy depends on its cause.
ormal platelet count

1DUVGVTKEKORNKECVKQPU
in pregnancy
repregnancy
The majority of women have platelet counts
• Prepregnancy counseling should be offered within the normal range of 150,000–450,000/μL
to identify the couple at risk for an affected during normal pregnancies. However, the plate-
fetus. let counts may be slightly lower than in healthy,
• Partner should be screened for thalassemia. nonpregnant women.
• Prenatal diagnosis can be discussed.
• Women with hemoglobin H (HbH) disease
should be advised to start folic acid 5 mg daily. )GUVCVKQPCNVJTQODQE[VQRGPKC
renatal Diagnosis
• Prenatal diagnosis should be offered (cho- The diagnosis of gestational thrombocytopenia
rionic villus sampling or amniocentesis; see is based on the following criteria:
Chapter 12, Prenatal screening, prenatal diag-
• Mild thrombocytopenia (mostly >100,000/μL,
nosis, and fetal therapy).
rarely <70,000/μL)
• Women with HbH disease will require folate
• No thrombocytopenia outside of pregnancy
supplementation.
• Occurs late in gestation
• Blood should be transfused for severe symp-
• No fetal/neonatal thrombocytopenia
tomatic anemia.
• Spontaneous resolution after delivery
abor elivery an postpartum It is suggested that gestational thrombocyto-
• These can be managed as in a normal preg- penia may be a mild and transient manifestation
nancy with focus on managing anemia. of immune thrombocytopenia.
CH 49_p740-757_v3.indd 753 19-07-2015 11:21:17

anagement anagement
The management of gestational thrombocyto- The management of ITP involves the following:
penia involves
• Measures to improve maternal platelet counts
• Follow-up of platelet counts during pregnancy • Appropriate obstetric management
and in the postpartum period • Management of neonatal thrombocytopenia
• Obstetric management
Measures to improve maternal platelet counts
latelet counts • If the counts stay >70,000/μL, it is difficult to
After the initial diagnosis, platelet counts can distinguish the condition from gestational
be repeated at each antenatal checkup. If the thrombocytopenia. No treatment is required.
counts drop below 70,000/μL, the counts should
be repeated weekly. In the antenatal period:
• Women with no bleeding manifestations and
Obstetric management platelet counts t30,000/μL
Routine obstetric management is appropriate. – No treatment until 36 weeks’ gestation (or
sooner if delivery is imminent)
• Epidural and spinal analgesia may be given in • If platelet counts are <30,000/μL or clinically
women with a platelet count between 50,000 relevant bleeding is present, first-line therapy is
and 80,000/μL. – Oral corticosteroids (prednisone 1 mg/kg/
• The neonate must be checked for thrombo- day) or
cytopenia, although it is rare following gesta- – Intravenous immunoglobulin (IVIg 1 g/kg)
tional thrombocytopenia. • Medications are adjusted to maintain a safe
• Postpartum follow-up of platelet counts is platelet count
needed to rule out ITP.
At the time of delivery:
+OOWPGVJTQODQE[VQRGPKC • Although worsening of the disease is not

typical during pregnancy, when it occurs, the
Immune thrombocytopenia occurs in approxi- mother is at risk for bleeding complications at
mately 1 in 1000 to 1 in 10,000 pregnant women. the time of delivery.
The characteristics of ITP are summarized in • For a woman whose platelet count is <80,000/
Box 49.20. μL but who has not required therapy during
pregnancy
– Oral prednisone can be started 10 days prior
Box 49.20 Characteristics of ITP to anticipated delivery (10–20 mg/kg/day
and titrated as necessary).
• +OOWPQNQIKECNN[OGFKCVGFRNCVGNGVFGUVTWEVKQP
Ŧ 2NCVGNGVOGODTCPGIN[EQRTQVGKPUCVVCEMGFD[CPVK-
• A platelet count of t50,000/μL is recom-
RNCVGNGVCPVKDQFKGU
KOOWPQINQDWNKP) mended prior to labor and delivery.
Ŧ 2NCVGNGVUFGUVTQ[GFTCRKFN[ • A combination of platelet transfusion and IVIg
Ŧ 0QVEQORGPUCVGFD[DQPGOCTTQY may be used to achieve these levels.
• 2GTUKUVGPVVJTQODQE[VQRGPKC
z.
• 0QTOCN QT KPETGCUGF OGICMCT[QE[VGU QP DQPG OCT-
Measures to manage ITP in pregnancy are
TQYCURKTCVG summarized in Figure 49.3.
• #DUGPEGQHURNGPQOGICN[
• *KUVQT[QH
Ŧ GCU[DTWKUKPI 1DUVGVTKEOCPCIGOGPV
Ŧ RGVGEJKCG Management of labor and delivery is based
Ŧ GRKUVCZKU on obstetric indications. Platelet counts
Ŧ gingival bleeding must be monitored and maintained as out-
P KOOWPGVJTQODQE[VQRGPKC lined above. A platelet count >50,000/μL is
CH 49_p740-757_v3.indd 754 19-07-2015 11:21:17

Management of
P in pregnancy
ntenatal perio Labor an eli ery
Platelet counts Platelet counts

L L a
Platelet counts
o blee ing ignificant Platelet count
to be maintaine
manifestations blee ing L
at L
but no therapy
or regional anesthesia
as re uire
platelet counts shoul
in antenatal perio
o treatment till Pre nisone be L
ee s pre nisolone
mg g aily
eli ery ral pre nisone Platelet
imminent Vg g g starte ays transfusion
prior to anticipate an
eli ery Vg g g
Figure 49.3 /CPCIGOGPVQH+62KPRTGIPCPE[ P KOOWPGVJTQODQE[VQRGPKC g KPVTCXGPQWUKOOWPQINQDWNKP
generally considered safe for delivery (vaginal reported to range from 10% to 15% in pregnan-
or cesarean). cies complicated by ITP. Platelet counts <20,000/
To protect the fetus, which might have throm- μL occur in approximately 5% of patients.
bocytopenia, forceps and vacuum-assisted deliv- The incidence of neonatal intracerebral hem-
ery are avoided. orrhage is <1%. There are no differences in the
rate of fetal complications with cesarean deliv-
/CPCIGOGPVQHPGQPCVCNVJTQODQE[VQRGPKC ery compared with those with vaginal delivery.
The risk of severe neonatal thrombocytope-
nia (e.g., platelet count <50,000/μL) has been
Key points
• #PGOKCKUCOCLQTRWDNKEJGCNVJEQPEGTPKPFGXGNQRKPI • +TQPFGſEKGPE[CPGOKCFWTKPIRTGIPCPE[JCUDGGP
EQWPVTKGU+VKUFGſPGFD[VJG9QTNF*GCNVJ1TICPK\C- CUUQEKCVGFYKVJCPKPETGCUGFTKUMQHNQYDKTVJYGKIJV
VKQPCUJGOQINQDKPNGXGNUQHŭIF. RTGVGTOFGNKXGT[CPFRGTKPCVCNOQTVCNKV[
• 6JGOCLQTKV[QHCPGOKCKPRTGIPCPE[KUFWGVQKTQP • 6JGFKCIPQUKUQHKTQPFGſEKGPE[CPGOKCKUEQOOQPN[
HQNCVGQTXKVCOKP$12FGſEKGPE[.GUUEQOOQPN[KV OCFGYKVJCEQORNGVGDNQQFEQWPVCPFRGTKRJGTCN
EQWNFDGCEQPUGSWGPEGQHJGOQINQDKPQRCVJKGUUWEJ UOGCT+PUQOGYQOGPKTQPUVWFKGUOC[DGTGSWKTGF
CUVJCNCUUGOKCCPFUKEMNGEGNNCPGOKC VQGUVCDNKUJVJGGVKQNQI[
• +TQPFGſEKGPE[CPGOKCYKNNGZJKDKVUOCNNGTTGFDNQQF • 1TCNKTQPKUEQPUKFGTGFſTUVNKPGVJGTCR[HQTKTQP
EGNNU
4$%U=OGCPEQTRWUEWNCTXQNWOG
/%8 FGſEKGPE[CPGOKCUKPEGKVKUKPGZRGPUKXGCPFGHHGEVKXG
H.?CPFKUECNNGFOKETQE[VKECPGOKC9KVJXKVCOKP$12 or YJGPVCMGPRTQRGTN[
HQNKECEKFFGſEKGPE[VJG4$%UCTGOWEJNCTIGT
/%8
H.CPFUQKVKUECNNGFOCETQE[VKECPGOKC
(Continued)
CH 49_p740-757_v3.indd 755 19-07-2015 11:21:17


• +PVTCXGPQWUKTQPVJGTCR[KUKPFKECVGFKPVJGRTGUGPEG • +PVJGEVJCNCUUGOKCURQKPVOWVCVKQPUECWUGCDUGPEG
QHWPTGURQPUKXGPGUUVQQTKPVQNGTCPEGQHQTCNKTQPCPF QHQTTGFWEVKQPKPEEJCKPRTQFWEVKQP
YJGPVJGTGKUPGGFHQTCSWKEMTGEQXGT[HTQOCPGOKC x E6JCNCUUGOKCOCLQTQEEWTUYJGPDQVJE-genes are

GIENQUGVQFGNKXGT[ OKUUKPI6JGOCLQTKV[QHCHHGEVGFYQOGPCTGKPHGTVKNG
• (QNCVGFGſEKGPE[KUOWEJNGUUEQOOQPVJCPKTQP
x E6JCNCUUGOKCOKPQTQEEWTUKPKPFKXKFWCNUYJQCTG
FGſEKGPE[+VKUCOCETQE[VKECPGOKC
JGVGTQ\[IQWUHQTVJGIGPGOWVCVKQPCPFVJGTGHQTGJCXG
• In severe vitamin B12
EQDCNCOKPFGſEKGPE[VJG XCTKCDNGRTQFWEVKQPQHVJGEINQDKPEJCKP2TGIPCPE[
YQOCPRTGUGPVUYKVJRTQHQWPFCPGOKCCPFOCETQE[VKE QWVEQOGUCTGIQQFCNVJQWIJCPGOKCOC[YQTUGP
TGFEGNNU
/%8 H.YKVJQTYKVJQWVXCT[KPIPGWTQ-
x D6JCNCUUGOKCFKUQTFGTUKPXQNXGCNQUUQHQPGQH
NQIKECNFKUVWTDCPEGU
VJGHQWTDINQDKPIGPGU2TGIPCPE[KPYQOGPYKVJ
• 5KEMNGEGNNFKUGCUG
5%&KUCPKPJGTKVGFFKUQTFGT DVJCNCUUGOKCOKPQTKUVQNGTCVGFYGNN9QOGPYKVJ
FWGVQJQOQ\[IQUKV[HQTVJGCDPQTOCNJGOQINQDKP *D*FKUGCUGOC[JCXGYQTUGPKPIQHCPGOKCKP
JGOQINQDKP5
*D56JGVYQENCUUKEHGCVWTGUCTG RTGIPCPE[
JGOQN[UKUTGUWNVKPIKPCPGOKC
ŎUKEMNGEGNNCPGOKCŏ
• 6JTQODQE[VQRGPKCQTNQYRNCVGNGVEQWPVKUQHVGP
CPFXCUQQEENWUKXGRJGPQOGPC
GPEQWPVGTGFKPRTGIPCPE[+VKUV[RKECNN[FGſPGFCUC
• /QUVRTGIPCPEKGUEQORNKECVGFD[5%&YKNNTGUWNV RNCVGNGVEQWPVNQYGTVJCPz.
KPNKXGDKTVJ*QYGXGTVJGTGKUCPKPETGCUGFTKUMQH • 6JTQODQE[VQRGPKCOC[DGGPEQWPVGTGFKPRTGI-
QDUVGVTKEHGVCNCPFOGFKECNEQORNKECVKQPURCTVKEWNCTN[ PCPE[CUCRTGGZKUVKPIEQPFKVKQP=KOOWPGVJTQODQ-
KPUKEMNGEGNNCPGOKC
*D55 E[VQRGPKC
+62?CUPGYN[FKUEQXGTGF
IGUVCVKQPCNQT
• 9QOGPYKVJUKEMNGEGNNVTCKVFQPQVJCXGCPKPETGCUGF +62QTCURCTVQHCRTGIPCPE[EQORNKECVKQP=UGXGTG
TKUMHQTRTGIPCPE[EQORNKECVKQPU RTGGENCORUKCJGOQN[UKUGNGXCVGFNKXGTGP\[OGU
CPFNQYRNCVGNGVEQWPV
*'..2U[PFTQOGCEWVG
• 6JCNCUUGOKCUCTGEJCTCEVGTK\GFD[KORCKTGFRTQFWE-
VKQPQHQPGQTOQTGQHVJGPQTOCNINQDKPEJCKPUHQWPF HCVV[NKXGTQHRTGIPCPE[QTFKUUGOKPCVGFKPVTCXCUEW-
KPJGOQINQDKP6JGENKPKECNEQPUGSWGPEGUECPDG NCTEQCIWNCVKQP
&+%?
KPGHHGEVKXGGT[VJTQRQKGUKUJGOQN[UKUCPFCPGOKCQH • 6TGCVOGPVQHUKIPKſECPVVJTQODQE[VQRGPKC
z.
XCT[KPIFGITGGU KUYKVJRTGFPKUQPGQTKPVTCXGPQWUKOOWPQINQDWNKP
Self-Assessment
%CUGDCUGFSWGUVKQPU 2. *QYECPYGRTGFKEVKHVJGDCD[KUCHHGEVGFQTPQV!
3. 9JCVCTGVJGGHHGEVUQHRTGIPCPE[QPCYQOCPYKVJ
EVJCNCUUGOKCVTCKV!
Case 1
4. 9JCVCTGVJGEJCTCEVGTKUVKEUQHEVJCNCUUGOKCOCLQT!
/TU%2KUCITCXKFCRCTCCPFKUKPVJGVJYGGM
QHIGUVCVKQP*GTſTUVEJKNFKU[GCTQNF5JGHGGNUVKTGF
CPF DTGCVJNGUU YJGP UJG ENKODU UVCKTU 5JG CRRGCTGF Answers
RCNGQPJGTTQWVKPGCPVGPCVCNEJGEMWR
1. &GſPGCPGOKCKPRTGIPCPE[ Case 1
2. *QYYKNN[QWKPXGUVKICVGJGT! 1. #PGOKCKUFGſPGFCUJGOQINQDKPNGXGNQHŭIF.
3. *QYYKNN[QWOCPCIGKTQPFGſEKGPE[CPGOKC! KPVJGſTUVVTKOGUVGTŭIF.KPVJGUGEQPFVTKOGU-
4. 9JCVCTGVJGENKPKECNEQPUGSWGPEGUQHKTQPFGſEKGPE[ VGTCPFŭIF.KPVJGVJKTFVTKOGUVGT
CPGOKCKPRTGIPCPE[! 2. %QORNGVGDNQQFEQWPVYKNNUJQYNQYJGOQINQDKPCPF
JGOCVQETKVNQY4$%EQWPVCPF/%8H.2GTKRJ-
GTCNUOGCTYKNNUJQYOKETQE[VKEJ[RQEJTQOKE4$%U
Case 2 6JGTGYKNNDGNQYUGTWOKTQPCPFHGTTKVKPNGXGNUCPF
GNGXCVGFVQVCNKTQPDKPFKPIECRCEKV[
/TU;*KUCITCXKFCRCTC5JGKUYGGMURTGI-
PCPV 5JG KU MPQYP VQ JCXG EVJCNCUUGOKC VTCKV 5JG JCU 3. 1TCNKTQPKUſTUVNKPGVJGTCR[UKPEGUJGKUQPN[YGGMU
OCTTKGFCFKUVCPVTGNCVKXG5JGCPFJGTJWUDCPFCTGCPZ- RTGIPCPV5JGUJQWNFDGRNCEGFQPCHGTTQWUUCNV
KQWUVQMPQYKHVJGEVJCNCUUGOKCVTCKVYKNNJCXGCP[GHHGEV RTGRCTCVKQPEQPVCKPKPIOIGNGOGPVCNKTQPVYKEG
QPVJGRTGIPCPE[QTVJGDCD[ FCKN[5JGUJQWNFDGIKXGPCRRTQRTKCVGKPUVTWEVKQPU
HQTVCMKPIVJGKTQP+HUJGKUWPCDNGVQVQNGTCVGKTQPQT
1. 9JCVKUVJGKPJGTKVCPEGRCVVGTPQHVJCNCUUGOKCU! KUPQPEQORNKCPVQTKHVJGJGOQINQDKPKUIF.CHVGT
CH 49_p740-757_v3.indd 756 19-07-2015 11:21:17

YGGMUŏIGUVCVKQPKPVTCXGPQWUKTQPVJGTCR[OC[DG
considered.
5CORNGSWGUVKQPU
4. /QFGTCVGVQUGXGTGKTQPFGſEKGPE[CPGOKCFWTKPI
RTGIPCPE[JCUDGGPCUUQEKCVGFYKVJCPKPETGCUGF
.QPICPUYGTSWGUVKQPU
TKUMQHNQYDKTVJYGKIJVRTGVGTOFGNKXGT[CPFRGTKPC- 1. 9JCVCTGVJGECWUGUQHCPGOKC!*QYYKNN[QW
VCNOQTVCNKV[ OCPCIGCRTGIPCPVYQOCPCVVGTOYKVJJGOQINQDKP
QHIF.!
2. &KUEWUUVJGGVKQNQI[FKCIPQUKUCPFOCPCIGOGPVQH
Case 2 KTQPFGſEKGPE[CPGOKCKPRTGIPCPE[
1. +PJGTKVCPEGKUCWVQUQOCNTGEGUUKXG6JGJWUDCPF
JCUVQDGVGUVGFHQTVJGVTCKV+HDQVJRCTGPVUJCXG
VJCNCUUGOKCOKPQT
QTVTCKVVJGQHHURTKPIJCXGC
5JQTVCPUYGTSWGUVKQPU
EJCPEGQHKPJGTKVKPIVJGVTCKVYKNNJCXGVJCNCU- 1. 2TGXGPVKQPQHCPGOKCKPRTGIPCPE[
UGOKCOCLQTCPFYKNNDGWPCHHGEVGF 2. 2TQRJ[NCEVKEKTQPVJGTCR[
2. 6JGRCTGPVUOWUVDGEQWPUGNGFHQTRTGPCVCNFKCI- 3. %NCUUKſECVKQPQHCPGOKCKPRTGIPCPE[
PQUKU#EJQTKQPKEXKNNWUUCORNKPIQTCOPKQEGPVG- 4. 5KEMNGEGNNFKUGCUGEQORNKECVKPIRTGIPCPE[
UKUOC[DGQHHGTGFUQVJCVVJGHGVCNUVCVWUECPDG
5. E6JCNCUUGOKCVTCKVKPRTGIPCPE[
FGſPGF
3. 2TGIPCPE[QWVEQOGUCTGIQQF6JGYQOCPOC[
DGEQOGFKURTQRQTVKQPCVGN[CPGOKECPFYKNN
TGSWKTGKTQPQTHQNCVGUWRRNGOGPVCVKQPFWTKPI
RTGIPCPE[
4. E6JCNCUUGOKCOCLQTKUCNKHGNQPIVTCPUHWUKQP
FGRGPFGPVCPGOKC6JGTGKURTQHQWPFJ[RQEJTQOKE
OKETQE[VKECPGOKCDK\CTTGTGFEGNNOQTRJQNQI[
KPETGCUGFKPFKTGEVDKNKTWDKPCPFNCEVCVGFGJ[FTQIG-
PCUGCPFTGFWEGFQTCDUGPVJCRVQINQDKP
CH 49_p740-757_v3.indd 757 19-07-2015 11:21:17

Cardiovascular
50 Diseases
Case scenario
Mrs. VN, 22, primigravida, at 26 weeks’ pregnancy, was referred from the
local primary health center with difficulty in breathing, which was more
on lying down. She also had cough with frothy expectoration. She had been
told by her local doctor that she had some problem with the heart and had
to be managed in a bigger hospital. She had shortness of breath and palpi-
tations on and off prior to pregnancy but had never consulted a doctor.
Introduction India, rheumatic valvular diseases are common

and among these, rheumatic mitral stenosis
Cardiac disease can be a cause of maternal mor- accounts for 90% of cases. In developed coun-
tality and morbidity. Rheumatic valvular disease tries, congenital heart disease, especially atrial
is still seen frequently in developing countries. septal defect (ASD), is the most common cardiac
Congenital heart diseases and pregnancy after disease in pregnancy.
valve replacement are also encountered often.
The cardiovascular changes in pregnancy may
not be well tolerated by women with cardiac dis- Cardiovascular changes
ease, and the situation needs specialized care.
Management has to be multidisciplinary, involv- in pregnancy
ing the obstetrician, cardiologist, neonatologist
and intensivist, to optimize outcome. Important anatomical and functional changes
occur in the cardiovascular system in preg-
nancy. These have been discussed in Chapter
Incidence 3, Maternal physiology in pregnancy. These
changes begin by 6–8 weeks’ pregnancy, reach
The overall incidence of heart disease in preg- a peak by 25–30 weeks, and plateau till deliv-
nancy is 1%. In developing countries including ery. The important changes in cardiovascular
CH 50_p758-773_v3.indd 758 19-07-2015 01:17:16

Cardiovascular Diseases 759
Table 50.1 Cardiovascular changes that may cause maternal cardiac

decompensation
Changes due to pregnancy Effect on cardiovascular system

regnancy
Increase in blood volume
Increase in cardiac output Increase in preload
Increase in stroke volume
Supine hypotension 2QQTXGPVTKEWNCTſNNKPI
Increase in heart rate 2WNOQPCT[EQPIGUVKQPGFGOC
abor
6CEJ[ECTFKCFWGVQRCKPCPZKGV[ • 4GFWEGFNGHVXGPVTKEWNCTſNNKPI
• 4GFWEGFEQTQPCT[DNQQFƀQY
2WORKPIQHDNQQFHTQOWVGTWU
2WNOQPCT[EQPIGUVKQPGFGOC
+PETGCUGKP%1$2YKVJEQPVTCEVKQPU
ostpartum
5JWPVKPIQHDNQQFHTQOWVGTWU 2WNOQPCT[EQPIGUVKQPGFGOC
uerperium
/QDKNK\CVKQPQHGZVTCXCUEWNCTƀWKF 2WNOQPCT[EQPIGUVKQP
Increase in vascular resistance Increase in afterload
BP blood pressure; C cardiac output.
system that may compromise cardiac func-

Box 50.1 0
;*#ENCUUKſECVKQPQHECTFKCEFKUGCUG
tion in women with heart disease are as in pregnancy
follows:
• Class I: ncompromise no limitation o physical
activity
• Increase in cardiac output Ŧ 0QU[ORVQOUQHECTFKCEKPUWHſEKGPE[
QPYCNMKPI
• Decrease in peripheral resistance ENKODKPIUVCKTUGVE
• Increase in heart rate • Class II: Slight limitation o physical activity
• Increase in blood volume Ŧ Comfortable at rest
Ŧ Mild symptoms caused by ordinary activity
Changes in the cardiovascular system in • Class III: ar e limitation o physical activity
pregnancy that may cause maternal decom- Ŧ Comfortable at rest
pensation are given in Table 50.1. Ŧ Symptoms caused by less than ordinary activity

YCNMKPICUJQTVFKUVCPEG
• Class IV: Severely compromise
Ŧ Symptoms at rest
(WPEVKQPCNENCUUKſECVKQP Ŧ Discomfort increased by any activity

A 0GY;QTM*GCTV#UUQEKCVKQP
of cardiac disease
Clinical classification by the New York Heart
Association (NYHA) is used for functional classi- Predictors of cardiac
fication of the degree of heart failure in preg-
nancy. This classification is based primarily on complications
symptoms of fatigue, palpitation, dyspnea, and
Certain factors are predictive of maternal dec-
anginal pain (Box 50.1).
ompensation during pregnancy. These are as
Women with NYHA class I and class II disease
follows:
go through pregnancy uneventfully, but those in
class III and class IV disease are prone to • NYHA classification III or IV
complications. • Cyanosis
CH 50_p758-773_v3.indd 759 19-07-2015 01:17:16

• Left atrial/ventricular obstruction as indi-

Box 50.2 Maternal complications of cardiac
cated by disease in pregnancy
– mitral valve area <2 cm2
– aortic valve area <1.5 cm2 • #EWVGRWNOQPCT[GFGOC
• Cardiac failure
– peak left ventricular outflow gradient >30
• 9QTUGPKPIQH0;*#ENCUU
mmHg
• #TTJ[VJOKCU
• Myocardial dysfunction Ŧ #VTKCNſDTKNNCVKQP
– Ejection fraction <40% Ŧ Supraventricular tachycardia
• History of Ŧ Ventricular arrhythmia
– heart failure • Infective endocarditis
– arrhythmia • Maternal death
– stroke A 0GY;QTM*GCTV#UUQEKCVKQP
– transient ischemic attack
isk categori ation III and IV disease. The complications are listed
in Box 50.2.
of cardiac disease
in pregnancy Acute pulmonary edema
Maternal mortality in cardiac disease varies with Acute pulmonary edema is common in women
the type of lesion. Risk categorization helps in with left atrial/ventricular outflow obstruction
prepregnancy counseling and management as seen in moderate-to-severe mitral stenosis
(Table 50.2). and aortic stenosis. It is precipitated by tachycar-
dia and increased venous return that occurs in
labor and postpartum. Increase in left atrial
Complications pressure leads to pulmonary congestion and
pulmonary edema. Risk of pulmonary edema
Although most women with uncomplicated increases during late second trimester, labor,
mild cardiac disease have an uneventful preg- and immediate and late postpartum. Pulmonary
nancy and labor, complications do occur. The edema can also be precipitated by certain inter-
risk is much higher in women with NYHA class current events as listed in Box 50.3.
Table 50.2 isk categori ation of cardiac disease in pregnancy
isk category Cardiac disease

.QYTKUM
OCVGTPCNOQTVCNKV[ • Septal defects
• /KVTCNUVGPQUKU0;*#ENCUU+CPFENCUU++
• Patent ductus arteriosus
• 2WNOQPCT[VTKEWURKFNGUKQPU
/QFGTCVGTKUM
OCVGTPCNOQTVCNKV[Ō • /KVTCNUVGPQUKU0;*#ENCUU+++CPFENCUU+8
• /CTHCPU[PFTQOGYKVJPQTOCNCQTVC
• Uncomplicated coarctation of aorta
• Uncorrected TOF
• Prosthetic valves
*KIJTKUM
OCVGTPCNOQTVCNKV[Ō • 'KUGPOGPIGTU[PFTQOG
• /CTHCPU[PFTQOGYKVJCDPQTOCNCQTVC
• Dilated cardiomyopathy
A 0GY;QTM*GCTV#UUQEKCVKQP VGVTCNQI[QH(CNNQV
CH 50_p758-773_v3.indd 760 19-07-2015 01:17:16

Treatment is by salt and fluid restriction, and

Box 50.3 Factors increasing risk of pulmonary
edema administration of digoxin and diuretics till symp-
toms and signs regress.
• 0QTOCNRTGIPCPE[
Ŧ 2TGIPCPE[ CV Ō YGGMU YJGP DNQQF XQNWOG
peaks Worsening of A class
Ŧ Labor
&WGVQRWORKPIQHDNQQFHTQOWVGTWU Insidious worsening of NYHA class occurs as
Ŧ Immediate postpartum pregnancy progresses. It can precipitate pulmo-
&WGVQUJWPVKPIQHDNQQFHTQORNCEGPVCNDGF nary edema or congestive cardiac failure.
Ŧ Puerperium
&WGVQOQDKNK\CVKQPQHGZVTCXCUEWNCTHNWKF
• Intercurrent events
Arrhythmias
Ŧ Hypertension Atrial fibrillation is the most common arrhyth-
Ŧ #PGOKC mia encountered. Inadequate left atrial filling
Ŧ /WNVKHGVCNRTGIPCPE[
and consequent increase in left atrial pressure
Ŧ 6J[TQVQZKEQUKU
can lead to pulmonary edema. Atrial fibrillation
Ŧ #EWVGHGDTKNGKNNPGUU
Ŧ #VTKCNſDTKNNCVKQP
can occur anytime in pregnancy.

Diagnosis and management Atrial fibrillation can be associated with acute
The mother usually presents with sudden onset pulmonary edema or congestive cardiac failure.
of dyspnea, cough with pink, frothy expectora- The pulse is irregular and the rate is usually
tion, hemoptysis, and orthopnea. Examination >110/min. An ECG showing irregular ventricular
reveals tachycardia and coarse crepitations in rate and absent P waves is diagnostic.
both lungs. If not treated promptly, the condition Digoxin reduces the heart rate and controls
can be fatal. the fibrillation. E-Blockers such as propranolol
Management consists of oxygen by mask, or calcium channel blockers such as verapamil
semirecumbent position, digitalization espe- can be used. Anticoagulation should be consid-
cially if there is atrial fibrillation, and intrave- ered to prevent thromboembolism.
nous diuretic (furosemide). Parenteral morphine
is required to reduce the anxiety. Rotating cuff or Infective endocarditis
tourniquet applied to all four limbs and released
in succession reduces venous return. Emergency Infective endocarditis can occur in valvular
valvotomy or balloon valvuloplasty may be and congenital heart disease (except ASD),
required in women with tight mitral stenosis and in women with prosthetic valves and
with intractable or recurrent pulmonary edema. shunts. Bacteremia occurs during vaginal
delivery and cesarean section. Antibiotic pro-
phylaxis was administered in labor to all
Cardiac failure women with cardiac disease earlier, but it is
Cardiac failure can occur in the late second tri- now known that (a) delivery is associated with
mester with worsening of NYHA class II to III or very low risk of bacteremia, (b) there is con-
IV, chronic left heart failure, or right heart failure vincing evidence that antibiotic prophylaxis
as in pulmonary stenosis. prevents endocarditis, and (c) the risk of
adverse reaction to antibiotics outweighs
benefits in most situations.
Diagnosis and management Therefore, the American Heart Association
Cardiac failure presents with gradually worsening (AHA) and American College of Obstetricians
dyspnea, orthopnea, edema, and fatigue. Jugular and Gynecologists (ACOG) recommend it only
venous pressure is elevated, and there is tachycar- for high-risk patients (Box 50.4). However, sev-
dia, pedal edema, and tender hepatomegaly. Basal eral institutions use antibiotics in moderate-risk
crepitations are usually present. patients as well (Box 50.5).
CH 50_p758-773_v3.indd 761 19-07-2015 01:17:16

Box 50.4 Antibiotic prophylaxis for infective Maternal mortality

endocarditis (A A and AC G)
Maternal deaths can occur in cyanotic congeni-
• 4GEQOOGPFGFQPN[HQTJKIJTKUMYQOGP tal heart diseases, rheumatic valvular disease,
Ŧ 9QOGPYKVJRTQUVJGVKEXCNXGU and cardiomyopathy. Lesions that are associated
Ŧ Prior endocarditis with pulmonary hypertension have high risk of
Ŧ %[CPQVKEJGCTVFKUGCUGWPTGRCKTGFTGRCKTGFYKVJKP maternal mortality. Pregnancy is contraindi-
6 months
cated in those with high risk conditions (Box
Ŧ 2CVKGPVUYKVJECTFKCEVTCPURNCPVCVKQP
• #PVKDKQVKETGIKOGP 50.1). Women with moderate risk should have
Ŧ In active labor corrective surgery before pregnancy. Causes of
+PLGEVKQPCORKEKNNKPI+8+/UKPINGFQUG KPLGE- mortality are listed in Box 50.6.
VKQPIGPVCOKEKPOIMI+8
(QNNQYGFJQWTUNCVGTD[
- KPLGEVKQPCORKEKNNKPI+/+8
Fetal risks
- or COQZKEKNNKPIQTCN In uncomplicated rheumatic valvular disease,
+HCNNGTIKEVQRGPKEKNNKP fetal complications are uncommon. Spon-
- +PLGEVKQPXCPEQO[EKPI+8QXGTŌJQWTU
taneous miscarriage, preterm labor, and fetal
KPLGEVKQPIGPVCOKEKPOIMI+8
- r cefazoline or EGHVTKCZQPGI+8
growth restriction can occur in tight mitral ste-
- r ENCTKVJTQO[EKPC\KVJTQO[EKPOIQTCN nosis, complex cyanotic heart disease, right to
- r ENKPFCO[EKPOIQTCN left shunt, tetralogy of Fallot (TOF), and
Eisenmenger syndrome.
AC #OGTKECP%QNNGIGQH1DUVGVTKEKCPUCPF)[PGEQNQIKUVU
A A #OGTKECP*GCTV#UUQEKCVKQP Risk of congenital heart disease is increased
in infants of parents with congenital cardiac dis-
ease. The risk varies with the type of lesion, but
the overall risk is approximately 1%–6% when
Box 50.5 Antibiotic prophylaxis in moderate- the mother has a congenital cardiac disease.
risk patients Marfan syndrome and some hypertrophic car-
diomyopathies that are inherited as autosomal
• Moderate-risk patients
dominant carry a 50% risk.
Ŧ %QPIGPKVCNJGCTVFKUGCUG
QVJGTVJCPJKIJTKUM
Ŧ Mitral and aortic stenosis
Ŧ /KVTCNXCNXGRTQNCRUGYKVJTGIWTIKVCVKQP Clinical features
Ŧ Hypertrophic cardiomyopathy
• #PVKDKQVKETGIKOGP Diagnosis of cardiac
Ŧ In active labor
+PLCORKEKNNKPI+/+8or
disease in pregnancy
#OQZKEKNNKPIQTCN Anatomical and physiological changes in preg-
+HCNNGTIKEVQRGPKEKNNKP nancy can mimic cardiac disease, making diagno-
- +PLXCPEQO[EKPI+8QXGTŌJQWTU sis of cardiac disease difficult. These are described
in detail in Chapter 3, Maternal physiology in
pregnancy. The changes that mimic cardiac dis-
ease are summarized in Box 50.7.
Infective endocarditis presents with fever; pete-
Box 50.6 Causes of maternal death
chiae over the skin, conjunctiva, and retina;
changing murmurs or appearance of new mur- • #EWVGRWNOQPCT[GFGOC
murs; and splenomegaly. Blood cultures usually • Infective endocarditis
reveal Streptococcus fecalis or D-hemolytic • %QPIGUVKXGECTFKCEHCKNWTG
Streptococcus. Vegetations are seen on the valves • Pulmonary hypertension
• #QTVKEFKUUGEVKQP
on echocardiography. Treatment is with a high
• #TTJ[VJOKCU
doses of appropriate antibiotics.
CH 50_p758-773_v3.indd 762 19-07-2015 01:17:16

indicative of valvular and congenital heart dis-

Box 50.7 Cardiovascular changes that mimic
heart disease ease, respectively. Findings on physical exam-
ination as listed above or signs of congestive car-
• 5[ORVQOUCPFUKIPU diac failure necessitate further evaluation.
Ŧ $TGCVJNGUUPGUURCNRKVCVKQPHCVKIWG
Electrocardiography and chest X-ray can be used
Ŧ Prominent neck veins
for diagnosis of cardiac disease in pregnancy.
Ŧ Pedal edema
• #PCVQOKECNEJCPIGU
The abdomen must be shielded for chest radiog-
Ŧ Displacement of the heart to the left raphy. However, echocardiography is used exten-
Ŧ #RGZDGCVUJKHVGFWRYCTFUCPFNCVGTCNN[ sively for accurate diagnosis of cardiac disease
Ŧ 2J[UKQNQIKECNVJKTFJGCTVUQWPF since both anatomical and functional evaluation
Ŧ Functional systolic murmurs is feasible. Rarely, cardiac catheterization may be
Ŧ Internal mammary venous hum required for diagnosis of the exact valvular or
• '%)EJCPIGU congenital lesion (Box 50.9).
Ŧ .GHVCZKUFGXKCVKQP
Ŧ 56FGRTGUUKQPPQPURGEKſE566EJCPIGU
• Chest X-ray Management
Ŧ #RRCTGPVKPETGCUGKPECTFKCEUK\G
Ŧ 5VTCKIJVGPKPIQHNGHVJGCTVDQTFGT Preconceptional management
Preconceptional counseling and management
A diagnosis of cardiac disease should be are important to achieve optimal outcome in
made only if the symptoms and signs described women with cardiac disease. This consists of his-
in Box 50.8 are present. History of rheumatic tory, accurate identification of cardiac lesion,
fever in childhood is significant. Dyspnea, cya- evaluation of cardiac status by ECG and echocar-
nosis, and recurrent respiratory infections from diography, NYHA classification, and assessment
birth or childhood suggest congenital heart of potential for maternal morbidity and mortal-
disease. ity associated with the lesion.
Diagnostic evaluation
Box 50.9 Diagnostic evaluation of cardiac
As already mentioned, history of rheumatic fever disease
and cardiac symptoms from childhood are • History
Ŧ Symptoms of heart disease from childhood
Ŧ History of rheumatic fever
Box 50.8 Symptoms and signs suggestive
• 5[ORVQOUCPFUKIPU
of cardiac disease
Ŧ &[URPGCCVTGUVQTVJQRPGCJGOQRV[UKU
• Symptoms Ŧ Murmurs
Ŧ Dyspnea on mild activity )TCFG+++U[UVQNKE
Ŧ &[URPGCCVTGUVQTVJQRPGC #UUQEKCVGFYKVJVJTKNN
Ŧ 2CTQZ[UOCNPQEVWTPCNF[URPGC Diastolic murmurs
Ŧ Hemoptysis Ŧ 5KIPUQHEQPIGUVKXGECTFKCEHCKNWTG
Ŧ Chest pain Ŧ #TTJ[VJOKCU
Ŧ Pedal edema up to the knees • Further evaluation
• 5KIPU Ŧ '%)
Ŧ Cyanosis Ŧ %JGUV:TC[ōCHVGTUJKGNFKPICDFQOGP
Ŧ 'FGOCPQVUWDUKFKPIYKVJQXGTPKIJVTGUV Ŧ 'EJQECTFKQITCRJ[
Ŧ )TCFG+++QT+8U[UVQNKEOWTOWTU Valvular disease
Ŧ /WTOWTUCUUQEKCVGFYKVJVJTKNN %QPIGPKVCNJGCTVFKUGCUG
Ŧ Diastolic murmurs Cardiomyopathy
Ŧ 5KIPUQHEQPIGUVKXGECTFKCEHCKNWTG Ŧ Cardiac catheterization
Ŧ 5KIPUQHRWNOQPCT[GFGOC #EEWTCVGFKCIPQUKUQHNGUKQP
Ŧ #TTJ[VJOKC #EWVGEQTQPCT[FKUGCUG
CH 50_p758-773_v3.indd 763 19-07-2015 01:17:16

Surgical correction should be advised for cor-

Box 50.11 Conditions in which surgical
rectable congenital heart diseases and moder- intervention prior to pregnancy
ate-to-severe mitral and aortic stenosis. If the is recommended
woman is on anticoagulants, changing over from
• 5GXGTG/5/4
warfarin to heparin should be discussed. Drugs
• 5GXGTG#5#4
that are teratogenic should be discontinued and
• .CTIG#5&85&
safer drugs should be substituted. If pregnancy is • 2&#YKVJOQFGTCVGRWNOQPCT[J[RGTVGPUKQP
contraindicated (as in Eisenmenger syndrome), • Severe coarctation of aorta
the couple should be counseled regarding this • 6GVTCNQI[QH(CNNQV
and contraception advised (Box 50.10). A CQTVKETGIWTIKVCVKQPAS aortic stenosis; ASD atrial septal
defect; OKVTCNTGIWTIKVCVKQP S mitral stenosis; PDA patent
ductus arteriosus; SD ventricular septal defect.
Contraindications
to pregnancy Surgical intervention prior to pregnancy
Pregnancy is contraindicated in the following should be advised in women with cardiac
conditions where the maternal mortality is lesions that carry significant risk in pregnancy
>25%. (Box 50.11).
• Eisenmenger syndrome
• Pulmonary hypertension Termination of pregnancy
• Marfan syndrome with abnormal aorta
Often, valvular and congenital heart disease in
• Dilated cardiomyopathy
woman present for the first time in pregnancy. If
Pulmonary hypertension is the main cause of maternal risk is estimated to be high (conditions
mortality. Aortic dissection may occur in Marfan listed in the section Contraindications to preg-
syndrome. nancy), termination of pregnancy is advisable.
The decision should be individualized and made
after discussion with the couple.
Box 50.10 Preconceptional management
of women with cardiac disease
• History Antepartum management
Ŧ Effort tolerance
Women with cardiac disease should be managed
Ŧ %CTFKCEUWTIGT[
in a tertiary center by a team consisting of cardi-
Ŧ Medications
%CTFKCEFTWIU
ologist, obstetrician, anesthetist, and neonatolo-
#PVKEQCIWNCPVU gist. Thorough clinical evaluation must be per-
#PVKJ[RGTVGPUKXGU formed at the first visit to establish the nature of
Ŧ %QORNKECVKQPUKPRTGXKQWURTGIPCPE[ lesion, functional NYHA class, and maternal and
9QTUGPKPIQHHWPEVKQPCNENCUU fetal risks. Medication should be reviewed to
2WNOQPCT[GFGOC%%( make sure that they are safe in pregnancy. The
Infective endocarditis mother should be counseled regarding lifestyle
• Evaluation and warning signs, depending on the nature of
Ŧ Type of lesion lesion. The need for elective cardiac surgery dur-
Ŧ Severity ing pregnancy should be discussed. A close
Ŧ (WPEVKQPCNENCUUKſECVKQP
watch should be kept on maternal hemoglobin
Ŧ 4KUMUVTCVKſECVKQP
and blood pressure. Anemia and hypertension
Ŧ Presence of pulmonary hypertension
• %QWPUGNKPI
should be managed appropriately. Fetal growth
Ŧ Maternal risks should be monitored (Box 50.12).
Ŧ Fetal complications
Ŧ 4KUMQHEQPIGPKVCNJGCTVFKUGCUGKPVJGHGVWU anagement o A class I an II
Ŧ 5WTIKECNKPVGTXGPVKQPRTKQTVQRTGIPCPE[ Women in NYHA class I and II usually have an
Ŧ %QPVTCKPFKECVKQPUVQRTGIPCPE[ uncomplicated pregnancy and can be managed
CC EQPIGUVKXGECTFKCEHCKNWTG on an outpatient basis.
CH 50_p758-773_v3.indd 764 19-07-2015 01:17:16

be the same throughout pregnancy and need

Box 50.12 Antepartum management in women
with cardiac disease hospitalization.
• 6JQTQWIJGXCNWCVKQPCVſTUVXKUKV
In uction o labor
• Establish
Ŧ #EEWTCVGFKCIPQUKU Most women with cardiac disease have sponta-
Ŧ 0;*#ENCUUKſECVKQP neous onset of labor at or near term. Induction
Ŧ 4KUMUVTCVKſECVKQP of labor is not indicated for cardiac disease. It
Ŧ /CVGTPCNHGVCNTKUMU may be required for other obstetric indications.
• /GFKECVKQPUTGXKGYGF If induction is required, prostaglandins may be
Ŧ 5VQRVGTCVQIGPKEFTWIU used for cervical ripening. Oxytocin infusion
Ŧ %JCPIGVQUCHGTFTWIU should be given in a higher concentration in
• %QWPUGNTGICTFKPI
lower volume in order to avoid fluid overload.
Ŧ 6GTOKPCVKQPQHRTGIPCPE[
The dosage regimen is as follows:
Ŧ %CTFKCEUWTIGT[FWTKPIRTGIPCPE[
Ŧ Lifestyle
• Administer 10 units oxytocin in 100 mL of nor-
Physical activity as tolerated
mal saline by infusion pump.
#XQKFUVTGUU
Ŧ 2TQORVTGRQTVKPIQHTGURKTCVQT[KPHGEVKQPU
• Start with 0.6–1.2 mL/hour (1–2 mIU/min).
Ŧ 5[ORVQOUQHRWNOQPCT[GFGOC%%( • Increase every 30 minutes by 1.2 mL/hour
• Monitor (2 mIU/min).
Ŧ *GOQINQDKP • Maximum dose is 20 mL/hour (32 mIU/min).
Ŧ $NQQFRTGUUWTG
Ŧ (GVCNITQYVJ
Ŧ Maternal complications
%QPIGUVKXGECTFKCEHCKNWTG Vaginal delivery is preferred. Cardiac disease
- JVP is not an indication for a cesarean section.
- *GRCVQOGICN[ Cesarean section may be performed for obstetric
Pulmonary edema indications.
#TTJ[VJOKCU
Labor is considered to be equivalent to mod-
• Prompt treatment of
erate exercise. The hemodynamic changes
Ŧ anemia
Ŧ hypertension
during labor such as tachycardia, increase in car-
Ŧ respiratory infection diac output, and increase in venous return can
Ŧ asymptomatic bacteriuria precipitate acute pulmonary edema or cardiac
failure.
CC EQPIGUVKXGECTFKCEHCKNWTG P LWIWNCTXGPQWURTGUUWTG
A 0GY;QTM*GCTV#UUQEKCVKQP Tachycardia is aggravated by the pain of uter-
ine contractions, anxiety, and apprehension.
Therefore, adequate analgesia is mandatory.
• The blood volume and cardiac output gradu- Epidural analgesia is recommended, but hypo-
ally increase and peak at 28–30 weeks, and the tension must be avoided. Parenteral morphine
functional classification may worsen. Hence, or pethidine given in adequate doses may also
this must be reevaluated at every visit and at be sufficient.
28–30 weeks. The second stage should be cut short with
• If women remain in class I/II, they can be outlet forceps in order to avoid bearing-down
admitted at term for delivery. efforts and additional strain on the heart.
Ergometrine should be avoided since it
results in forceful uterine contraction and
anagement o A class III I shunting of blood into the heart. It can also
Women in class III/IV have to be hospitalized. cause an acute rise in blood pressure. Injection
Once treatment is initiated for cardiac failure or furosemide 40 mg IV after delivery of the
pulmonary edema, the condition may improve placenta reduces the preload and the risk of
and it may be possible to discharge and manage pulmonary edema.
as an outpatient. However, most women who are Management of labor is summarized in
in class III or IV in early pregnancy continue to Box 50.13.
CH 50_p758-773_v3.indd 765 19-07-2015 01:17:16

Box 50.13 Management of labor in cardiac Box 50.14 Contraception in women with cardiac
disease disease
• 5GOKTGEWODGPVRQUKVKQPYKVJNCVGTCNVKNV • 2TQIGUVGTQPGQPN[RTGRCTCVKQPU
• #PCNIGUKC Ŧ Minipill
Ŧ 'RKFWTCNCPCNIGUKC
or Ŧ &GRQOGFTQZ[RTQIGUVGTQPGCEGVCVG
Ŧ +PLGEVKQPOQTRJKPGOIJQWTN[
or Ŧ .0I+75
Ŧ +PLGEVKQPRGVJKFKPGOIJQWTN[ • 5WTIKECNOGVJQFU
• Monitor half hourly Ŧ Tubectomy
Ŧ Pulse Ŧ Vasectomy
Ŧ $NQQFRTGUUWTG g- SNGXQPQTIGUVTGNKPVTCWVGTKPGU[UVGO
Ŧ #WUEWNVCVGNWPIDCUGU
• ,WFKEKQWUWUGQHKPVTCXGPQWUƀWKFU
• +PHGEVKXGGPFQECTFKVKURTQRJ[NCZKUCUTGSWKTGF
• 5GEQPFUVCIG
Ŧ %WVUJQTVYKVJHQTEGRUXCEWWO
Cardiac procedures
• 'TIQOGVTKPGCXQKFGF
• +PLGEVKQP HWTQUGOKFG OI +8 CFOKPKUVGTGF CHVGT
in pregnancy
placental delivery Cardiac surgery may be required during preg-
nancy in women with life-threatening complica-
tions. The most commonly performed procedure
Postpartum management is balloon mitral valvotomy. Indications are as
follows:
Postpartum monitoring and management of
complications are crucial. • Mitral stenosis with
– recurrent or intractable pulmonary edema;
• Close monitoring should continue for 24 hours – congestive cardiac failure not responding to
after delivery since cardiac decompensation medical management;
can occur during this period. – NYHA class III or IV in early pregnancy.
• Complications that can occur in the puerperium
are sepsis, thromboembolism, and postpartum The procedure is usually performed in the
hemorrhage. Mobilization of extravascular fluid second trimester, but if pulmonary edema is
can lead to cardiac decompensation and pul- intractable, the procedure can be undertaken at
monary edema. any gestational age. Following valvotomy, the
• Cardiac status should be reassessed 6 weeks mitral valve area increases, and functional class
postpartum. Decision regarding cardiac sur- improves to class I or II.
gery should be made at this time. Valve replacement in pregnancy is associ-
ated with increased maternal morbidity and
high fetal mortality especially if cardiopulmo-
Contraception nary bypass is used.
Contraceptive methods that are safe in women
with cardiac disease are listed in Box 50.14.
Estrogen-containing pills increase the risk alvular heart disease
of thromboembolism and should be avoided.
Intrauterine copper-containing devices may
give rise to bleeding or infection and should be
Mitral stenosis
used with caution. In women with NYHA class Rheumatic mitral stenosis is the most common
III or IV disease, husbands should be advised valvular heart disease encountered in pregnancy
to undergo vasectomy. Tubal sterilization can and accounts for 90% of cardiac lesions encoun-
be performed in women with class I and II dis- tered during pregnancy in the developing world.
ease, and 6 weeks postpartum in women with The stenosis is said to be severe if the valve area
class III and IV disease, when the cardiac sta- is d1.5 cm2, moderate if 1.5–2.5 cm2, and mild if
tus has improved. 2.5–4 cm2. Symptoms usually develop when
CH 50_p758-773_v3.indd 766 19-07-2015 01:17:16

there is moderate stenosis (Box 50.15). Women Mitral regurgitation

with valve area <1 cm2 are more prone to pulmo-
nary edema and require hemodynamic monitor- Mitral regurgitation may be due to rheumatic
ing in labor. fever or mitral valve prolapse. Blood regurgitates
When the venous return increases in preg- into the left atrium, the left atrium dilates, and
nancy, the cardiac output does not increase as pulmonary congestion and edema result. Atrial
expected due to the narrow mitral valve. This fibrillation is also common. Eventually, the left
results in pulmonary venous congestion, pul- ventricle dilates and ejection fraction falls.
monary edema, and congestive cardiac failure. Mitral regurgitation may be asymptomatic
Tachycardia that occurs in pregnancy reduces when mild. Severe regurgitation can cause pulmo-
left ventricular filling and further compro- nary edema, right heart failure, atrial fibrillation,
mises cardiac output and increases pulmonary pulmonary systolic hypertension, and congestive
congestion. cardiac failure.
Maternal complications in mitral stenosis are Valve replacement prior to pregnancy is
pulmonary edema, congestive cardiac failure, recommended in symptomatic women, with atrial
atrial fibrillation, and embolization. fibrillation, ejection fraction <50%, and pulmo-
Women with moderate or severe mitral steno- nary systolic hypertension. Management of preg-
sis should be advised valvotomy or valve replace- nancy is by avoiding fluid overload, use of diuret-
ment prior to pregnancy. Management of uncor- ics, and treatment of atrial fibrillation.
rected mitral stenosis in pregnancy consists of
reducing the heart rate with digoxin to reduce Mitral valve prolapse
ventricular rate (particularly in atrial fibrilla-
tion), diuretics to relieve fluid overload and pul- Mitral valve prolapse occurs due to myxomatous
monary congestion, small doses of E-blockers if degeneration of the valve or chordae tendineae.
heart rate is suboptimally controlled with digoxin Mitral insufficiency may develop later. Most
and penicillin prophylaxis against rheumatic women are asymptomatic. They withstand preg-
fever. Surgical intervention may be required in nancy well. Occasionally chest pain, palpitations,
intractable or recurrent pulmonary edema. and arrhythmias develop. They are managed with
Labor and delivery should be carefully managed E-blockers. Infective endocarditis prophylaxis is
as outlined earlier in this chapter. indicated when mitral prolapse is complicated by
mitral regurgitation.
Box 50.15 Mitral stenosis
• Severity
Aortic stenosis
Ŧ /KNFXCNXGCTGCŌEO2 Aortic stenosis may be congenital or rheumatic
Ŧ /QFGTCVGXCNXGCTGCŌEO2 in etiology. Mild-to-moderate stenosis is well
Ŧ 5GXGTGXCNXGCTGCEO2
tolerated in pregnancy, but severe stenosis with
• 2CVJQRJ[UKQNQI[KPRTGIPCPE[
a valve area of <1 cm2 is associated with high
Ŧ Inability to increase cardiac output
Ŧ 2WNOQPCT[EQPIGUVKQPCPFGFGOCFWGVQ
maternal mortality.
increased venous return Obstruction at the aortic valve leads to left
tachycardia ventricular overload, increase in left ventricular
• Complications end-diastolic pressure, and fall in ejection frac-
Ŧ Pulmonary edema tion. There is reduced cardiac output and
Ŧ %QPIGUVKXGECTFKCEHCKNWTG decrease in cerebral, cardiac, and uterine perfu-
Ŧ #VTKCNſDTKNNCVKQP sion. Pulmonary edema, exertional angina, syn-
Ŧ Thromboembolism cope, arrhythmias, stroke, aortic rupture, and
• /CPCIGOGPV death are known complications.
Ŧ &KIQZKP Severe aortic stenosis should be corrected by
Ŧ Diuretics
surgery before pregnancy. Mild-to-moderate ste-
Ŧ E-blockers
nosis can be managed with close observation, but
Ŧ 2GPKEKNNKPRTQRJ[NCZKU
severe stenosis requires bed rest and vigilant
CH 50_p758-773_v3.indd 767 19-07-2015 01:17:16

Table 50.3 Features of valvular lesions
Lesion Pathophysiology Complications

/KVTCNTGIWTIKVCVKQP • 4GIWTIKVCVKQPQHDNQQFKPVQNGHVCVTKWO • Pulmonary edema
• Left atrial dilatation • #VTKCNſDTKNNCVKQP
• 2WNOQPCT[EQPIGUVKQP • Pulmonary hypertension
• Left ventricular dilatation • Cardiac failure
• Fall in ejection fraction
Mitral valve prolapse /KVTCNTGIWTIKVCVKQP • %JGUVRCKPRCNRKVCVKQPU
• #TTJ[VJOKCU
#QTVKEUVGPQUKU • Left ventricular overload • Pulmonary edema
• Increase in end-diastolic pressure • #TTJ[VJOKCUUVTQMG
• Fall in ejection fraction • #QTVKETWRVWTGCPIKPCU[PEQRGFGCVJ
• Decreased cardiac output
#QTVKEKPUWHſEKGPE[ 0QOCLQTEJCPIGU
Pulmonary stenosis • 4KIJVXGPVTKEWNCTQXGTNQCF • 4KIJVJGCTVHCKNWTG
• 4KIJVCVTKCNFKNCVCVKQP • #TTJ[VJOKCU
management. Hypovolemia, fluid overload, and

Box 50.16 Complications of pregnancy
hypotension should be avoided. Severe stenosis in women with prosthetic valves
may require balloon valvotomy during pregnancy.
Aortic insufficiency is well tolerated in preg- • Structural failure of the valve
• Infective endocarditis
nancy. Pulmonary stenosis is usually congenital
• Thromboembolism
and should be corrected before pregnancy. In
• Cardiac failure
women with uncorrected stenosis, right heart • *GOQTTJCIGFWGVQCPVKEQCIWNCVKQP
failure and arrhythmias can occur. • /KUECTTKCIG
The features of various valvular lesions are • Stillbirth
summarized in Table 50.3. (Features of mitral • Warfarin embryopathy
stenosis are already summarized in Box 50.15.)
Pregnancy in women Anticoagulants in pregnancy

with prosthetic valves Most young women with valve replacement have
mechanical prosthetic valves, and anticoagula-
Pregnancy in women with prosthetic mitral or tion is mandatory. Warfarin is the drug of choice
aortic valves is common now. Most women with in the nonpregnant state, but choice of anticoag-
prosthetic valves have an uncomplicated preg- ulants in pregnancy is complicated. The effects
nancy. There are two types of valves: of warfarin, unfractionated heparin and low-
• Bioprosthetic molecular-weight heparin (LMWH) are listed in
– Do not require anticoagulants Table 50.4.
– Have higher failure rate
• Mechanical
ar arin
– Increased risk of thromboembolism Warfarin has the lowest risk of maternal throm-
– Anticoagulants required boembolism in pregnancy. However, warfarin
– Lower failure rate crosses the placenta and when used in the first
trimester of pregnancy, there is a 5%–10% risk of
Complications of pregnancy congenital anomalies. The risk is highest between
6 and 12 weeks’ gestation.
with prosthetic valves
Warfarin embryopathy affects cartilage and
The complications are listed in Box 50.16. bone, giving rise to epiphyseal stippling,
CH 50_p758-773_v3.indd 768 19-07-2015 01:17:16

Table 50.4 Anticoagulants in pregnancy
Warfarin nfractionated heparin Low-molecular-weight heparin

Risk of thromboembolism Least More More
Crosses placenta ;GU No No
6GTCVQIGPKEGHHGEVU ;GU No No
Late fetal deaths ;GU No No
Loss of bone mineral density No ;GU Less
Thrombocytopenia No ;GU Less
/QPKVQTGFYKVJ PT PTT #PVK:C
Secreted in breast milk ;GU No No
P prothrombin time; P partial thromboplastin time.
hypoplasia of nasal bone and limbs, and chon- reverses the anticoagulant action only partially;
dromalacia. Exposure in the second trimester therefore, most clinicians prefer to switch to
can cause central nervous system defects and heparin before labor and delivery.
late fetal loss. The fetal complications are dose
dependent and are higher when the dose is ecommended
>5 mg/day.
If warfarin is administered prior to or during
anticoagulant regimen
labor, the anticoagulant effect is difficult to The American College of Cardiology (ACC) and
reverse and risk of maternal and fetal hemor- AHA recommend the following:
rhage is high. Therefore, it is prudent to switch
to unfractionated heparin before planned • Stop warfarin between 6 and 12 weeks and
delivery. start on dose-adjusted unfractionated hepa-
rin/LMWH 12 hourly.
• Switch to warfarin at 12 weeks and continue
n ractionate heparin till 36 weeks.
The molecule of unfractionated heparin is large • Add aspirin 80–100 mg daily.
and does not cross the placenta; therefore, • Discontinue warfarin and aspirin and restart
there are no teratogenic effects. Valve thrombo- heparin/LMWH at 36 weeks.
sis is higher with unfractionated heparin com- • Switch from LMWH to heparin 36 hours prior
pared with that with warfarin. Loss of bone to planned delivery.
mineral density (10% if used for >6 months) is • Stop heparin 6 hours prior to planned delivery.
also associated with the use of heparin. This Resume 6 hours after vaginal delivery or 12
usually recovers after discontinuation of ther- hours after a cesarean section.
apy. Heparin-induced thrombocytopenia (HIT) • Restart warfarin and overlap with heparin till
occurs in 2%–3% of women. Protamine sulfate adequate blood levels are achieved.
reverses the effect of heparin. Therefore, hepa-
rin is the drug of choice before labor and
delivery. Congenital heart
o molecular eight heparin
disease
Low-molecular-weight heparin does not cross Long-term survival after surgery for congenital
the placenta. Thromboembolic events are rare heart disease has improved dramatically in the
when therapeutic levels are used with monitor- past few decades due to improved techniques.
ing of anti-Xa levels. Risk of thrombocytopenia Pregnancy in women with corrected congenital
and osteoporosis is low. Therapeutic dosage heart disease is now commonly encountered. In
requires 12-hourly administration. Protamine developed countries, where the incidence of
CH 50_p758-773_v3.indd 769 19-07-2015 01:17:16

rheumatic fever has reduced markedly, congeni- Fetal complications

tal heart disease is more common than rheu-
matic valvular disease. Fetal complications of congenital heart diseases
Hemodynamic changes of pregnancy can are spontaneous abortion, preterm birth, fetal
affect women with congenital heart disease. The growth restriction, and fetal death. All fetal com-
maternal cardiovascular complications are listed plications are more common in cyanotic and
as follows: uncorrected congenital heart diseases.
• Fall in systemic vascular resistance increases

the magnitude of right to left shunts. Septal defects and
• Increase in cardiac output and blood volume patent ductus arteriosus
leads to congestive cardiac failure in women with
myocardial dysfunction or valvular disease. Atrial septal defect and ventricular septal defect
• Risk of thromboembolism increases due to (VSD) are the most common congenital cardiac
hypercoagulability of pregnancy. diseases seen in pregnancy. Pregnancy is well tol-
• Risk of infective endocarditis is high in women erated if the defect is small and there is no reversal
with uncorrected complex cyanotic congeni- of shunt. Most women with large VSD become
tal heart disease and those within 6 months of symptomatic early and would have had surgery
surgery. before pregnancy. Similarly, most cases of patent
• Arrhythmias worsen in pregnancy and can ductus are identified in childhood and corrected.
cause cardiac decompensation. In women with uncorrected septal defects and
patent ductus arteriosus (PDA), fall in systemic
resistance in pregnancy can cause reversal of flow
through the defect. Pulmonary hypertension, car-
isk factors for maternal diac failure, and arrhythmias are common com-
and fetal complications plications. Ventricular septal defect and PDA are
associated with high risk of infective endocarditis.
The major risk factors that increase maternal
Symptoms and maternal complications of septal
and fetal complications in women with congeni-
defects and PDA are summarized in Table 50.5.
tal heart disease are as follows:
• Maternal cyanosis Cyanotic congenital
• NYHA class III and IV
• Left ventricular outflow obstruction
heart diseases
• Right heart dilatation Tetralogy of Fallot (TOF), transposition of great
• Anticoagulant therapy vessels (TGV), and Eisenmenger syndrome may
• Arrhythmias be encountered in pregnancy.
Table 50.5 Symptoms and maternal complications of septal defects and patent ductus arteriosus
Atrial septal defect entricular septal defect Patent ductus arteriosus

Symptoms Mostly asymptomatic #U[ORVQOCVKEKHEO 2
Symptomatic
2TGIPCPE[ Well tolerated Tolerated in small defects Tolerated if no reversal
Complications • Pulmonary hypertension • Pulmonary hypertension • Pulmonary hypertension
• Cardiac failure • Left ventricular failure • Cardiac failure
• #TTJ[VJOKCU • Infective endocarditis • 2WNOQPCT[J[RGTVGPUKQP
cardiac failure
• 2CTCFQZKECNGODQNKUO • Reversal of shunt • $CEVGTKCNGPFQCQTVKVKU

'KUGPOGPIGTU[PFTQOG
CH 50_p758-773_v3.indd 770 19-07-2015 01:17:17

Tetralogy of Fallot and/or left ventricle is dilated and systolic func-

tion is reduced.
Tetralogy of Fallot is the most common cyanotic
heart disease. Since patients become symptom-
atic very early in life, surgical correction is under- Peripartum cardiomyopathy
taken usually in childhood. Women with cor- Peripartum cardiomyopathy (PPCM) is a left
rected TOF tolerate pregnancy well so long as ventricular dilatation and systolic dysfunction
there is no residual lesion. In uncorrected TOF, characterized by the following:
cyanosis worsens due to increase of shunt. Risk
of fetal complications such as fetal growth • Absence of prior cardiac disease or identifiable
restriction, spontaneous abortion, and fetal cause of cardiac failure
death is high. Postoperative pulmonary insuffi- • Development in the last trimester, usually
ciency and right ventricular dysfunction are after 34 weeks’ gestation or postpartum up to
associated with high risk of complications such 5 months
as heart failure, arrhythmias, and pulmonary The incidence varies from 1/1000 to 1/4000
hypertension. Hypotension and epidural anal- births. The etiology is unknown although viral
gesia should be avoided. infection, autoimmune response, and hyperten-
sion have been postulated. Other features are
Transposition of great vessels listed in Box 50.17.
Uncorrected TGV is associated with high neona- Management

tal mortality. Hence, all women who conceive
have surgically corrected TGV. Postsurgical car- Once diagnosed, cardiac failure should be treated
diac dysfunction in TGV is also associated with with bed rest, diuretics, and digoxin. Prophylactic
cardiac failure and mortality. anticoagulation may be required. Combined oral
contraceptive pills must be avoided and subse-
quent pregnancies strongly discouraged.
Eisenmenger syndrome
When pulmonary vascular resistance is higher
than the systemic resistance, causing right to Box 50.17 Peripartum cardiomyopathy
left shunting of blood, it is called Eisenmenger • Dilated cardiomyopathy
syndrome. This develops in ASD, VSD, and • Left ventricular systolic dysfunction
PDA. Cardiac failure, arrhythmia, cerebrovascu- • Occurs
lar accident, thromboembolism, hyperviscosity Ŧ #HVGTYGGMUŏIGUVCVKQP
syndrome, and sudden death can occur. Risk of Ŧ Up to 5 months postpartum
maternal death is as high as 40%. Pregnancy • +PEKFGPEGŌ
is, therefore, contraindicated and should be • 4GEWTTGPEGKPUWDUGSWGPVRTGIPCPE[
terminated in Eisenmenger syndrome. • 2TQITGUUGUYKVJUWDUGSWGPVRTGIPCPE[
• &KCIPQUKU
Ŧ 5WFFGPQPUGVQHECTFKCEHCKNWTGCHVGTYGGMU
Cardiomyopathy Ŧ 'ZENWUKQPQHRTKQTECTFKCEFKUGCUG
Ŧ 0QKFGPVKſCDNGECWUG
Cardiomyopathy may be associated with ven- Ŧ 'EJQECTFKQITCRJ[
tricular hypertrophy (hypertrophic cardiomyop- 'LGEVKQPHTCEVKQP
athy) or dilatation (dilated cardiomyopathy). Left ventricular end-diastolic dimension
Hypertrophic cardiomyopathy is an autosomal EOO2
dominant disorder. Women may be asymptom- • Complications
atic but dyspnea, angina pain, and arrhythmias Ŧ Thromboembolism
Ŧ Cardiac failure
can occur. Pregnancy is well tolerated in a few,
• /QTVCNKV[Ō
but complications are common. Dilated cardio-
• %QORNGVGTGEQXGT[RQUVRCTVWOō
myopathy may be inherited or acquired. Right
CH 50_p758-773_v3.indd 771 19-07-2015 01:17:17

Key points
• Cardiac disease is an important cause of maternal • 2TGEQPEGRVKQPCNOCPCIGOGPVEQPUKUVUQHTKUMUVTCVKſ-
mortality and morbidity. ECVKQPCPFCFXKEGTGICTFKPICXQKFCPEGQHRTGIPCPE[
• 6JGJGOQF[PCOKEEJCPIGUKPRTGIPCPE[CPFNCDQT 5WTIKECNEQTTGEVKQPUJQWNFDGFQPGKHRQUUKDNG
EQORTQOKUGECTFKCEHWPEVKQPKPYQOGPYKVJJGCTV • 4KUMUQHOCVGTPCNCPFHGVCNEQORNKECVKQPUKPENWFKPI
disease. TKUMQHEQPIGPKVCNJGCTVFKUGCUGKPVJGQHHURTKPIUJQWNF
• (WPEVKQPCNENCUUKſECVKQPD[VJG0GY;QTM*GCTV DGFKUEWUUGFYKVJVJGOQVJGT
#UUQEKCVKQP
0;*#KUWUGFHQTTKUMUVTCVKſECVKQPCPF • /QVJGTUYKVJECTFKCEFKUGCUGUJQWNFDGOQPKVQTGF
OCPCIGOGPV ENQUGN[HQTCPGOKCJ[RGTVGPUKQPCPFKPHGEVKQPCPF
prompt treatment of these conditions is mandatory.
• Factors that predict maternal decompensation are
0;*#ENCUU+++CPF+8NGHVXGPVTKEWNCTQDUVTWEVKQP • #PVGRCTVWOOCPCIGOGPVKUDCUGFQP0;*#
O[QECTFKCNF[UHWPEVKQPCPFRTGXKQWUJGCTVHCKNWTG ENCUUKſECVKQP9QOGPYKVJENCUU+CPF++FKUGCUG
CTTJ[VJOKCUQTUVTQMG WUWCNN[JCXGCPWPEQORNKECVGFRTGIPCPE[
• Maternal complications in heart disease are acute • 9QOGPYKVJENCUU+++CPF+8FKUGCUGOC[JCXGVQ
RWNOQPCT[GFGOCECTFKCEHCKNWTGCTTJ[VJOKCU DGOCPCIGFCUKPRCVKGPVU
KPHGEVKXGGPFQECTFKVKUCPFOCVGTPCNFGCVJ
• Cardiac disease is not an indication for cesarean
• #EWVGRWNOQPCT[GFGOCKUVJGOQUVEQOOQP UGEVKQP.CDQTUJQWNFDGOCPCIGFECTGHWNN[UGEQPF
EQORNKECVKQPCPFECPQEEWTFWTKPIRTGIPCPE[ UVCIGEWVUJQTVCPFGTIQOGVTKPGCXQKFGF
NCDQTQTRWGTRGTKWO6JGTKUMKUKPETGCUGFD[KP-
• Mitral stenosis is the most common cardiac disease
VGTEWTTGPVGXGPVUUWEJCUCPGOKCJ[RGTVGPUKQPQT
KPFGXGNQRKPIEQWPVTKGU8CNXGCTGCQHEO2 is
KPHGEVKQP+VKUOCPCIGFD[RCTGPVGTCNFKWTGVKEUCPF considered severe stenosis.
FKIKVCNK\CVKQPKHTGSWKTGF+PVTCEVCDNGCPFTGEWTTGPV
RWNOQPCT[GFGOCKUCPKPFKECVKQPHQTUWTIKECN • 2TGIPCPE[KPYQOGPYKVJRTQUVJGVKEXCNXGUOWUVDG
correction. OCPCIGFYKVJECTGHWNEJQKEGQHCPVKEQCIWNCPVUCEEQTF-
KPIVQEWTTGPVIWKFGNKPGU
• Recommendations for infective endocarditis prophy-
NCZKUJCXGEJCPIGFKPTGEGPV[GCTU%WTTGPVN[KVKU • %QPIGPKVCNJGCTVFKUGCUGUGPEQWPVGTGFKPRTGIPCPE[
TGEQOOGPFGFQPN[HQTYQOGPYKVJJKIJTKUMFKUGCUG CTGUGRVCNFGHGEVURCVGPVFWEVWUCTVGTKQUWU
2&#
and in some moderate-risk diseases. E[CPQVKEJGCTVFKUGCUGUCPF'KUGPOGPIGTU[PFTQOG
• Fetal risks in cardiac disease include spontaneous • /QUVYQOGPYKVJEQPIGPKVCNJGCTVFKUGCUGYQWNF
OKUECTTKCIGRTGVGTONCDQTCPFHGVCNITQYVJTGUVTKE- JCXGJCFEQTTGEVKXGUWTIGT[DGHQTGGODCTMKPIQP
VKQPKPVKIJVOKVTCNUVGPQUKUCPFEQPIGPKVCNJGCTV RTGIPCPE[(CNNKPU[UVGOKETGUKUVCPEGKPETGCUGKP
disease. ECTFKCEQWVRWVJ[RGTEQCIWNCDKNKV[QHRTGIPCPE[CPF
risk of infective endocarditis pose special problems in
• /CP[QHVJGU[ORVQOUCPFUKIPUQHPQTOCN
WPEQTTGEVGFEQPIGPKVCNJGCTVFKUGCUG
RTGIPCPE[ECPOKOKEECTFKQXCUEWNCTFKUGCUG
&KCIPQUKUQHECTFKCEFKUGCUGKPRTGIPCPE[UJQWNF • Peripartum cardiomyopathy is an uncommon problem
DGDCUGFQPURGEKſEU[ORVQOUCPFUKIPUCPF VJCVTGEWTUKPUWDUGSWGPVRTGIPCPEKGUCPFJCUCJKIJ
GEJQECTFKQITCRJ[ maternal mortality risk.
Self-Assessment
3. *QYYKNN[QWOCPCIGVJGECUG!
Case-based questions 4. 9JGPYKNN[QWTGEQOOGPFUWTIKECNKPVGTXGPVKQP!
Case 1
Case 2
/TU80RTKOKITCXKFCCVYGGMUŏRTGIPCPE[KUTG-
HGTTGFHTQOVJGNQECNRTKOCT[JGCNVJEGPVGTYKVJFKHſEWNV[ /TU0%UGEQPFITCXKFCRTGUGPVUCVYGGMUŏIGUVC-
KP DTGCVJKPI YJKEJ KU OQTG QP N[KPI FQYP CPF EQWIJ VKQP5JGYCUFKCIPQUGFCUJCXKPIOKVTCNUVGPQUKUFWTKPI
YKVJ HTQVJ[ GZRGEVQTCVKQP 5JG JCF UJQTVPGUU QH DTGCVJ JGTRTGXKQWURTGIPCPE[
CPFRCNRKVCVKQPUQPCPFQHHRTGRTGIPCPE[CPFCJKUVQT[QH 1. *QYYKNN[QWGXCNWCVGJGT!
HGXGTYKVJLQKPVRCKPUKPEJKNFJQQF 2. *QYYKNN[QWOCPCIGJGT!
1. 9JCVKUVJGFKCIPQUKU! 3. 9JCVEQPVTCEGRVKQPYKNN[QWCFXKUG!
2. 9JCVEQWNFJCXGRTGEKRKVCVGFVJKU! 4. 9JCVUJQWNFJCXGDGGPCFXKUGFRTKQTVQVJKURTGIPCPE[!
CH 50_p758-773_v3.indd 772 19-07-2015 01:17:17

#NNQYURQPVCPGQWUQPUGVQHNCDQT#XQKFƀWKFQXGT-
Answers NQCFCPFGTIQOGVTKPG/QPKVQTRWNUGDNQQFRTGUUWTG
TGURKTCVKQP CPF NWPI DCUGU %WV UJQTV UGEQPF UVCIG
Case 1 YKVJHQTEGRU
1. 4JGWOCVKEXCNXWNCTFKUGCUGRTQDCDN[OKVTCNUVGPQUKU Monitor for pulmonary edema after delivery
YKVJCEWVGRWNOQPCT[GFGOC +H ENCUU +++ QT +8 JQURKVCNK\G EQPUKFGT VGTOKPC-
2. *GOQF[PCOKEEJCPIGUGURGEKCNN[KPETGCUGKP VKQP QH RTGIPCPE[ UKPEG UJG KU KP GCTN[ RTGIPCPE[
ECTFKCEQWVRWVDNQQFXQNWOGCPFJGCTVTCVG %NQUGOQPKVQTKPIHQTEQORNKECVKQPUVJTQWIJQWVRTGI-
KPRTGIPCPE[#NUQCPGOKCJ[RGTVGPUKQPQT PCPE[ .CDQT CPF FGNKXGT[ CU KP ENCUU ++ DWV YKVJ
intercurrent infection. ENQUGOQPKVQTKPI
3. *QURKVCNK\CVKQPUGOKTGEWODGPVRQUKVKQPQZ[IGP 3. 5KPEGVJKUKUJGTUGEQPFRTGIPCPE[UVGTKNK\CVKQP
D[OCUMKPLGEVKQPOQTRJKPGOI+/KPVTCXGPQWU UJQWNFDGTGEQOOGPFGF+HWPYKNNKPIRTQIGUVGT-
HWTQUGOKFGOICPFFKIKVCNKUKHVJGTGKUCUUQEKCVGF QPGQPN[RKNNKPLGEVKQPFGRQOGFTQZ[RTQIGUVGTQPG
CVTKCNſDTKNNCVKQP CEGVCVGQTNGXQPQTIGUVTGNKPVTCWVGTKPGU[UVGO

.0I+75
4. If acute pulmonary edema does not respond to treat-
ment or if it is recurrent. 4. $CNNQQPXCNXQVQO[DGHQTGVJGUGEQPFRTGIPCPE[

1. *KUVQT[ō0;*#ENCUUCPFEQORNKECVKQPUFWTKPIRTGXK- Long-answer questions
QWURTGIPCPE[
'ZCOKPCVKQPōU[ORVQOU CPF UKIPU KPFKECVKXG QH 1. &KUEWUUVJGOCPCIGOGPVQHNCDQTKPCYQOCPYKVJ
FGEQORGPUCVKQPUWEJCUF[URPGCQTVJQRPGCEQWIJ JGCTVFKUGCUGEQORNKECVKPIRTGIPCPE[
JGOQRV[UKUCPFRGFCNGFGOC 2. 9JCVKU0;*#ENCUUKſECVKQPQHECTFKCEFKUGCUG!
5KIPUQHCPGOKCCTTJ[VJOKC
RWNUGTCVGCPFTJ[VJO *QYYKNN[QWOCPCIGCYQOCPYKVJOKVTCNUVGPQUKU
'%)CPFGEJQECTFKQITCRJ[VQFGVGTOKPGVJGCTGCQH ENCUU++YJQRTGUGPVUCVYGGMUŏIGUVCVKQP!
mitral valve.
2. (WPEVKQPCNENCUUKſECVKQPCEEQTFKPIVQUGXGTKV[QH
symptoms. Short-answer questions
+H ENCUU + QT ++ TGIWNCT HQNNQYWR GCTN[ TGEQIPKVKQP 1. #EWVGRWNOQPCT[GFGOCKPRTGIPCPE[
CPF EQTTGEVKQP QH CPGOKC J[RGTVGPUKQP CPF KPHGE-
2. &KCIPQUKUQHJGCTVFKUGCUGKPRTGIPCPE[
VKQPU CPF OQPKVQTKPI QH HGVCN ITQYVJ CPF OCVGTPCN
3. /CPCIGOGPVQHNCDQTKPYQOGPYKVJECTFKCEFKUGCUG
EQPFKVKQP 9CVEJ HQT YQTUGPKPI QH HWPEVKQPCN ENCUU
RWNOQPCT[GFGOCECTFKCEHCKNWTGQTCTTJ[VJOKCU 4. 0;*#ENCUUKſECVKQPQHECTFKCEFKUGCUGKPRTGIPCPE[
CH 50_p758-773_v3.indd 773 19-07-2015 01:17:17

Hepatobiliary and
51 Gastrointestinal
Disorders
Case scenario
Mrs. MP, 31, gravida 2, para 1, live 1, presented at 32 weeks with severe
pruritus that was worse at night. There were scratch marks over her
abdomen and extremities. She was extremely distressed and her family
was very concerned.
Introduction epatobiliary disorders

Hepatobiliary disorders that occur during preg-
nancy can be a clinical challenge. Some hepatic Pregnancy is associated with many normal phys-
disorders are unique to pregnancy, whereas iological and anatomical changes that must be
some new or chronic hepatic diseases unre- taken into consideration when dealing with hepa-
lated to pregnancy may result in adverse out- tobiliary diseases and their correct diagnoses.
comes. Physiological changes in biliary function Some classic signs of chronic liver disease,
increase the risk of gallstones, which can be a for example, spider angiomas and palmar ery-
clinical challenge in the pregnant woman. thema, are also common during a normal preg-
Gastrointestinal (GI) disorders are some of nancy and usually disappear after delivery. The
the most frequent complaints during preg- hyperestrogenemia of pregnancy is responsible
nancy. Some women have GI disorders that are for these changes, just as it is in nonpregnant
unique to pregnancy, for example, hyperemesis women with cirrhosis.
gravidarum (see Chapter 28, Hyperemesis grav- In late pregnancy, the liver is difficult to pal-
idarum). Pregnant women may have chronic pate because of the expanding uterus. A palpa-
GI disorders that evoke special concern during ble liver is always an abnormal finding in late
pregnancy. To optimize care for these pregnant pregnancy.
women requires understanding of the presenta- In normal pregnancy, most biochemical tests
tion and prevalence of various GI disorders. of liver function remain within the normal range,
CH 51_p774-789_v3.indd 774 19-07-2015 01:17:56

Hepatobiliary and Gastrointestinal Disorders 775
even if slightly increased or decreased from base- infiltration of hepatocytes without inflammation
line levels. or necrosis. An excessive fetal fatty acid accumu-
lation is released into the maternal circulation.
The resulting increased load of long-chain fatty
epatic disorders acids is deposited in maternal liver tissue and
in pregnancy leads to impaired hepatic function.
The condition often develops in the second
If a woman is found to have hepatic disease in half of pregnancy, usually closer to term, with a
pregnancy, it could be a liver disease unique to mean gestational age reported at 36 weeks, but
pregnancy, a new liver disease presenting during may only be diagnosed after delivery.
pregnancy, or preexisting chronic liver disease. Acute fatty liver of pregnancy is caused by an
autosomal recessive genetic error. It is associ-
epatic isor ers uni ue ated with a maternal genetic predilection or with
to pregnancy a fetal deficiency of a genetically determined
enzyme:
Certain liver diseases are associated exclusively
with pregnancy. The liver diseases unique to • Maternal genetic mutation that affects mito-
pregnancy include the following: chondrial fatty acid oxidation pathway
• Fetal deficiency of long-chain 3-hydroxyacyl-
• Hyperemesis gravidarum (see Chapter 28,
coenzyme A dehydrogenase (LCHAD)
Hyperemesis gravidarum)
• Acute fatty liver of pregnancy (AFLP)
• Intrahepatic cholestasis of pregnancy (ICP) Symptoms of AFLP
• Hemolysis, elevated liver enzymes, and low Symptoms usually develop over several days to
platelet count (HELLP) syndrome (see Chapter weeks and include the following:
47, Hypertensive disorders)
• Subcapsular hematoma/hepatic rupture
• Anorexia
epatic iseases that can occur • Lethargy
in pregnancy • Abdominal pain
• Ascites
Hepatic diseases that can occur both in the • Progressive jaundice
nonpregnant and pregnant state include the • Transient polyuria and polydipsia due to tran-
following: sient diabetes insipidus
• Acute viral hepatitis
Acute fatty liver of pregnancy is associated
• Biliary disease
with acute renal failure in up to 60% of cases.
ree isting chronic liver isease There is decreased renal perfusion or acute tubu-
in pregnancy lar necrosis. Hepatic encephalopathy occurs in
60% of patients. Approximately 50% of patients
Preexisting chronic liver diseases that can have also have hypertension, proteinuria, and edema
an impact on pregnancy include the following: suggestive of preeclampsia. In the early stages, it
• Chronic viral hepatitis may be difficult to differentiate AFLP from severe
• Cirrhosis and portal hypertension preeclampsia and/or HELLP syndrome. Even the
• Wilson’s disease most severely affected women will have complete
recovery of liver and kidney function after deliv-
ery. However, AFLP is associated with substantial
epatic disorders unique maternal and perinatal morbidity and mortality.
to pregnancy Associated maternal complications include post-
partum hemorrhage, renal failure, hypoglycemia,
disseminated intravascular coagulation (DIC),
Acute fatty liver of pregnancy pancreatitis, and pulmonary edema.
Although a rare complication of pregnancy, AFLP The clinical features of AFLP are summarized
is an obstetric emergency that can lead to fulmi- in Box 51.1.
nant hepatic failure. It is associated with fatty
CH 51_p774-789_v3.indd 775 19-07-2015 01:17:56

Management requires a multidisciplinary

Box 51.1 Clinical features of AFLP
approach involving hepatologists, nephrolo-
• Obstetric emergency with high mortality gists, anesthetists, and intensivists. Prompt ini-
• /KETQXGUKEWNCTHCVV[KPſNVTCVKQPQHJGRCVQE[VGU tiation of supportive therapy including correc-
• Occurs closer to term
tion of hypoglycemia and transfusion of blood
Ŧ May be diagnosed after delivery
products to correct coagulopathy may be life-
• Risk factors associated with AFLP
Ŧ Older maternal age
saving. Delivery is the definitive treatment and
Ŧ Primiparity should be undertaken as early as possible. The
Ŧ Multiple gestation management of AFLP is outlined in Box 51.2.
Ŧ Preeclampsia
Ŧ Male fetus Prognosis
Ŧ Being underweight Maternal mortality
Ŧ Previous history of AFLP
• Associated with Maternal mortality is due to hepatic failure lead-
Ŧ maternal genetic mutation ing to hepatic encephalopathy, renal failure, and
Ŧ HGVCN.%*#&FGſEKGPE[ coagulopathy. Mortality rate can be up to 10% in
Ŧ recurrence, though rare rural India and centers where facilities for man-
• Symptoms include agement of complications are not available. The
Ŧ nausea and vomiting with progressive jaundice mortality rate can be very low in tertiary centers.
• Complications Liver function usually returns to normal within a
Ŧ Acute renal failure 60%
week but may be delayed for months. Complete
Ŧ Fulminant hepatic failure
recovery is generally anticipated.
Hepatic encephalopathy 60%
Ŧ Hypertension, proteinuria, edema 50% Perinatal mortality
Ŧ Other maternal complications include
Perinatal mortality rates can be as high as 85%.
hypoglycemia
The major cause of perinatal mortality is preterm
DIC birth due to urgent need for delivery.
pancreatitis
pulmonary edema Intrahepatic cholestasis
A P, acute fatty liver of pregnancy; D C, disseminated intravas-
cular coagulation; C AD, long-chain 3-hydroxyacyl-coenzyme A
of pregnancy
dehydrogenase. Intrahepatic cholestasis of pregnancy is the
most common liver disorder unique to preg-
Diagnosis nancy. It usually manifests in the third trimester
The typical clinical presentation is supported by
the following laboratory findings: Box 51.2 Management of AFLP
• Serum aminotransferase moderately elevated • +PVTCXGPQWUƀWKFUHQTEQTTGEVKQPQH

(300–500 U/L) Ŧ hypovolemia
• Bilirubin elevated (5 mg/dL or higher; Table 51.1) Ŧ hypoglycemia
• Blood products as needed
• Leukocytosis
• &GNKXGT[
FGſPKVKXGVTGCVOGPV
• Hypoglycemia
Ŧ Stops overload of fatty acids on mother’s liver
• Elevated ammonia levels Ŧ Induction of labor, although cesarean section is
• Thrombocytopenia common
• Neutrophilia General anesthesia preferred
• Coagulopathy Regional anesthesia not recommended
• Renal dysfunction - Risk of hematoma due to coagulopathy
• Recovery within 48–72 hours after delivery
• Severe disease associated with high mortality
Management Ŧ Management of
When AFLP is suspected, it is an indication for renal failure
hospitalization since the disease is associated hepatic failure
with progressive and sudden deterioration. A P, acute fatty liver of pregnancy.
CH 51_p774-789_v3.indd 776 19-07-2015 01:17:56

(mean onset at 30 weeks’ gestation) and is at night and the lack of sleep can cause emo-
characterized by severe pruritus along with an tional disturbance. There are no skin lesions, but
increase in direct bilirubin. There is little mater- it is common to see excoriations on the extremi-
nal risk, but ICP is associated with an increased ties and abdomen due to scratching.
risk of preterm delivery and sudden intrauter- Jaundice is not common but mild jaundice
ine fetal death. Symptoms resolve after delivery. occurs in 10%–15% of cases, typically within 4
weeks of the onset of itching. Abdominal pain
Prevalence is uncommon. Encephalopathy or other fea-
tures of liver failure do not occur, and their
The incidence of ICP in India has been reported presence should alert one for other causes of
to be 0.8%–1.2%. liver disease.
Cholestasis reduces the absorption of fat-solu-
Etiology and pathogenesis ble vitamins that can lead to vitamin K deficiency,
possibly resulting in an increased incidence
The etiology of ICP is multifactorial, involving of intrapartum and postpartum hemorrhage.
hormonal and genetic factors. Vitamin K should be administered to the mother.
Estrogen and progesterone
The risk of recurrence of ICP during subse-
quent pregnancies is 45%–70%.
The high levels of these two hormones in preg-
nancy are implicated in the etiology of ICP. This .CDQTCVQT[ſPFKPIU
is indicated by the fact that ICP occurs mainly
Urine bile salts are positive. An increase in
during the third trimester, when serum concen-
serum total bile acid (TBA) concentrations to
trations of estrogens and progesterone reach their
>10 μmol/L may be the first or only laboratory
peak. Intrahepatic cholestasis of pregnancy is also
abnormality, but this test is not usually available
more commonly associated with multiple preg-
in most centers.
nancies, where higher levels of estrogens and pro-
Serum aminotransferases are normal. Bilirubin
gesterone are seen, as compared with singleton
levels are elevated but <5 mg/dL.
pregnancies. These high levels have a cholestatic
The clinical features of ICP are listed in
on the hepatic transport system.
Box 51.3.
Genetic factors
There is evidence that genetic factors have an Box 51.3 Clinical features of intrahepatic
impact on familial cases and increase the inci- cholestasis of pregnancy
dence in certain ethnic groups. The combina- • Physical presentations
tion of genetic factors and high levels of sex hor- Ŧ Pruritus
mones produced in pregnancy can predispose Starts in second or third trimester
to the development of ICP. This may also lead to Generalized
ICP occurring with the use of estrogen–proges- Worse on palms and soles
terone combination oral contraceptive pills. Worse at night
- Sleep disruption
Environmental factors - Emotional disturbance
Although environmental factors have been sus- Scratch marks on extremities and abdomen
Ŧ Jaundice
pected because of seasonal variation in certain
10%–15% of women
countries, they have not been proven to have an
Starts 1–4 weeks after itching
effect on ICP. Ŧ 8KVCOKP-FGſEKGPE[
• Recurrence risk in next pregnancy
Clinical features Ŧ 45%–70%
• Laboratory values
The characteristic symptom of ICP is pruritus Ŧ Total bile acids >10 μmol/L
that starts in the second or third trimester of Ŧ #.6CPF#56PQTOCN
6CDNG
pregnancy, and disappears after delivery. It is Ŧ Bilirubin elevated but <5 mg/dL
often generalized but is worse on the palms and A , alanine aminotransferase; AS , aspartate
the soles of the feet. The itching is usually worse aminotransferase.
CH 51_p774-789_v3.indd 777 19-07-2015 01:17:56

Management of ICP Box 51.5 Maternal outcome in ICP

Management includes • Maternal prognosis good
• Following delivery
• symptomatic treatment of the patient
Ŧ Pruritus disappears rapidly
• close monitoring and decision for early deliv- Ŧ Liver function tests normalize
ery of the fetus. • No hepatic sequelae
• Increased risk for gallstones
reatment o pruritus • Estrogen-containing OCPs
The treatment of pruritus in ICP is summarized Ŧ Can result in cholestatic hepatitis
Ŧ Preferred OCPs
in Box 51.4.
Low-dose estrogen OCPs
Progesterone-only OCPs
onitoring o etus
CP, intrahepatic cholestasis of pregnancy; CP, oral
Fetal mortality can be as high as 10%, but the contraceptive pill.
cause of fetal death in ICP is unknown. It seems
to be the result of acute anoxic injury rather than
chronic placental insufficiency. No test reliably
Fetal outcome
predicts the risk of fetal demise. In contrast to the good prognosis for the
mother, fetal morbidity and mortality are high.
arly elivery Intrahepatic cholestasis of pregnancy is associ-
The majority of intrauterine fetal deaths in sin- ated with the following:
gleton pregnancies complicated by ICP occur • Prematurity
after 37 weeks’ gestation. Therefore, delivery • Meconium-stained amniotic fluid
is recommended no later than 37–38 weeks’ • Intrauterine demise
gestation. • Increased risk for respiratory distress syn-
Since the mother may have vitamin K defi- drome (regardless of fetal maturity)
ciency, the newborn should receive an injection
of vitamin K on delivery (which is a routine part
of newborn care). epatic hematoma and rupture
Hepatic hematoma and rupture are rare com-
Maternal outcome plications of pregnancy. The incidence of hema-
toma is 1 in 40,000 deliveries and that of liver
Maternal outcome in ICP is summarized in capsular rupture is 1 in 250,000 deliveries.
Box 51.5.
• Subcapsular hematoma formation and liver
capsular rupture carry a very high maternal
and perinatal mortality.
Box 51.4 Treatment of pruritus in intrahepatic • They are complications of preeclampsia/
cholestasis of pregnancy eclampsia and HELLP syndrome.
• 7TUQFGQZ[EJQNKECEKF
7&%# • The exact cause of the hematoma is not known,
Ŧ 500 mg twice daily but hepatic blood flow obstruction due to fibrin
Ŧ Relieves pruritus deposits in the hepatic sinusoids may occa-
Ŧ +PETGCUGUDKNGƀQY sionally lead to formation of subcapsular liver
Ŧ Reduces bilirubin levels hematoma.
• Cholestyramine • When the hematoma continues to grow, it
Ŧ 8–16 g/day bursts through the Glisson’s capsule and
Ŧ Decreases ileal absorption of bile salts results in catastrophic liver rupture.
Ŧ Much less effective than UDCA • Subcapsular hematoma and liver rupture usu-
• Dexamethasone
ally present in the second or third trimester. In
Ŧ Occasionally prescribed
30% of cases they occur postpartum, within 48
Ŧ When response to UDCA unsatisfactory
hours of delivery.
CH 51_p774-789_v3.indd 778 19-07-2015 01:17:56

Clinical features and management women who remain at risk for developing viral
hepatitis in pregnancy. Governmental and non-
Women with subcapsular hematoma and rup- governmental programs are under way to achieve
ture present with acute abdominal and shoulder universal immunization against hepatitis A and B
pain, signs of intraperitoneal hemorrhage, and in India.
shock. The diagnosis is made by the presence of
the following:
epatitis A
• Elevated liver enzymes
• Anemia Hepatitis A virus (HAV) behaves the same way in
• Evidence of DIC pregnancy as in nonpregnant women. Hepatitis
• Intra-abdominal hemorrhage or liver hematoma A virus infection occurs due to person-to-person
– On ultrasonography/CT scan transmission through fecal–oral contamination.
Volume resuscitation, transfusion of blood Clinical eatures

and blood products, and immediate laparot- The clinical features of hepatitis A are enumer-
omy are recommended. The fetus is delivered by ated in Box 51.6.
cesarean section, and the bleeding from the liver
is controlled by packing/ligation of the hepatic Diagnosis
vessel or partial resection of the necrotic seg-
The diagnosis is made by a combination of clini-
ments of liver.
cal features, laboratory investigations, and sero-
logical testing.
.CDQTCVQT[ſPFKPIU
epatic diseases that can Laboratory findings include the following:
occur in pregnancy • Serum aminotransferases
Hepatic diseases that occur in pregnancy can run – Elevated >1000–2000 U/L
a more severe course in contrast to the nonpreg- Alanine aminotransferase (ALT) > aspar-
nant state. Maternal mortality and morbidity, and tate aminotransferase (AST)
fetal survival may also be affected due to the dis- • Serum total and direct bilirubin
ease, and, therefore, the need for early delivery. – Peak after elevation in ALT and AST
– Usually elevated to >10 mg/dL
iral hepatitis in pregnancy

Viral hepatitis is one of the most commonly occur- Box 51.6 Clinical features of hepatitis A
ring infections in pregnant women. It has a poten-
• Symptoms
tial for serious adverse effects. The incidence of
Ŧ Malaise
viral hepatitis A, B, and C is the same in pregnancy
Ŧ Fever
as it is for the general population, but the inci- Ŧ Fatigue
dence of hepatitis E is much higher in pregnancy. Ŧ Anorexia
The types of viral hepatitis include the Ŧ Nausea
following: Ŧ Right upper quadrant or epigastric pain
• Signs
• Hepatitis A
Ŧ Jaundice of varying degrees
• Hepatitis B Ŧ Tender hepatomegaly
• Hepatitis C Ŧ Hepatomegaly
• Hepatitis D Ŧ High colored urine
• Hepatitis E Ŧ Stool chalky white or acholic
• Fulminant hepatitis
Hepatitis A and B can be prevented effectively
Ŧ Coagulopathy
through vaccination. However, globally there are Ŧ Encephalopathy
a large number of unvaccinated, nonimmune
CH 51_p774-789_v3.indd 779 19-07-2015 01:17:57

Serology he hepatitis virus

Serum immunoglobulin M (IgM) for anti-hepa- Antigen
titis A virus (HAV) is the gold standard for detec- The hepatitis B virus (HBV) contains three prin-
tion of acute illness and remains positive for 4–6 cipal antigens:
months.
• Hepatitis B surface antigen (HBsAg)
Course in pregnancy – Present on the surface of the virus
– Circulates freely in the serum
The disease tends to be more severe with
increasing gestational age. Severe illness during • Hepatitis B core antigen (HBcAg)
the third trimester may be associated with an – Present only in hepatocytes
increased risk for preterm labor. – Does not circulate in the serum
Pregnancy complications include the following:
• Hepatitis B e antigen (HBeAg)
• Preterm labor – Presence indicative of active viral replication
• Placental abruption – Indicative of high infectivity
• Prelabor rupture of the membranes
Chronic hepatitis or carrier state
Perinatal transmission of the virus does not If the HBsAg persists for more than 6 months after
occur. There are no neonatal consequences. the acute infection, the woman is considered to
have a chronic carrier state. Hepatitis B surface IgG
anagement in pregnancy antibody (anti-HBs) is absent in the carrier state.
The disease is usually self-limited. Treatment in Antibody
pregnancy consists of rest and a balanced diet.
Patients with fulminant infection require aggres- Anti-HBs is formed after the HBsAg is cleared
sive supportive therapy and should be trans- from the body after an acute infection. It also
ferred to a tertiary care center. forms after vaccination against HBV. Its presence
Infected women should avoid handling food confirms immunity to HBV.
that will be eaten by others in the family.
Breastfeeding is permissible with appropriate is actors or hepatitis in ection
hygienic precautions. Although HBsAg has been detected in a variety of
body fluids, only serum, semen, and saliva have
oste posure prophyla is been proved to be infectious.
A woman with close personal contact with some- All pregnant women should be screened for
one known to have an acute hepatitis A infection hepatitis B by testing for HBsAg in the first tri-
should receive mester. Their immunization status for hepatitis
B should also be checked.
• single 0.02 mL/kg IM dose of immunoglobulin
– should be given within 2 weeks’ exposure Clinical eatures
– provides protection for up to 3 months Clinical presentation is similar to hepatitis A
– is 80%–90% effective infection.
If the patient is infected in the third trimester,
the newborn should be given passive immuno- Diagnosis
prophylaxis with hepatitis A immunoglobulin As in hepatitis A infection, the transaminase lev-
within 48 hours of delivery. els are increased and are usually >1000 U/L. The
serum bilirubin is raised to >10 mg/dL. It is not
epatitis B possible to differentiate between HAV and HBV
infection without a serum test for the presence
The hepatitis B virus (HBV) is acquired through of HBsAg. Diagnosis of acute hepatitis B infec-
multiple routes, including mucosal, paren- tion is made with detection of
teral, sexual, and mother-to-child transmission.
Hepatitis B in pregnancy has an impact on both • HBsAg and
maternal and fetal health. • IgM antibodies to HBcAg.
CH 51_p774-789_v3.indd 780 19-07-2015 01:17:57

ransmission to husban the infant’s mucosal membranes. Postexposure

If a woman is found to be HBsAg positive, her immunoprophylaxis with hepatitis B immuno-
husband/partner should be tested for HBsAg. If globulin and HBV vaccine can help prevent 85%–
he is negative, he should receive the rapid immu- 95% of cases of perinatal transmission.
nization course with hepatitis B vaccine (0, 1, and The risk of perinatal transmission of HBV to
2 months). Until the husband’s/partner’s immu- the newborn from mothers who are HbsAg posi-
nity is confirmed, they should be advised to use a tive is summarized in Box 51.7.
condom since HBV can be sexually transmitted. HBeAg should be tested at 34–36 weeks. If
positive, the risk of perinatal transmission can
ransmission to me ical an be very high if prophylaxis is not given.
parame ical sta Prevention of transmission of HBV from an
HBsAg-positive woman during pregnancy and at
A woman infected with HBV is highly infectious
delivery is outlined in Figure 51.1.
to anyone handling her bodily fluids. Standard
universal precautions should be taken to prevent Intrapartum care
contamination.
The route of delivery depends on obstetric indi-
he e ects o in ection cations. Caregivers must use standard universal
on pregnancy outcomes precautions to avoid acquiring the infection.
The following are the effects of HBV infection on reast ee ing

pregnancy outcomes:
Breastfeeding is not contraindicated for women
• Acute HBV infection during pregnancy is usu- who are HBsAg-positive at the time of delivery
ally not severe. since the benefits of breastfeeding outweigh the
• It is not associated with increased mortality or risks.
teratogenicity.
• Hepatitis B infection during gestation is not an epatitis C
indication for termination of pregnancy.
• There is an increased risk of The incidence of hepatitis C virus (HCV) in preg-
– low birth weight nant women is the same as in the general popu-
– preterm birth lation (0.5%–1.4%). The routes of transmission,
clinical features, and management of hepatitis C
anagement in pregnancy are summarized in Box 51.8.
Management of HBV in pregnancy focuses on
epatitis D
• treatment of HBV during pregnancy and
• prevention of perinatal transmission. Hepatitis D virus (HDV) is an incomplete viral
particle that depends on the presence of HBV
Treatment of B during pregnancy for survival. It can occur as a coinfection along
Treatment of acute infection during pregnancy is with HBV infection or may follow HBV infection
mainly supportive. Monitoring of liver function (superinfection). It is transmitted through per-
tests and prothrombin time (PT) indicates the cutaneous or mucosal contact with blood.
severity of disease. Antiviral therapy is unneces-
sary, except in women who have acute liver fail-
ure or protracted severe hepatitis. Box 51.7 isk of perinatal transmission
of hepatitis B virus
Prevention of perinatal transmission
• +PHGEVKQPKPVJGſTUVVTKOGUVGT
Vertical transmission from mother to child • Infection in the second trimester: 10%
accounts for half of the cases of HBV in the • Infection in the third trimester: 60%
world. Maternal–infant transmission can occur • Without neonatal prophylaxis: 10%–20%
in utero, at birth, or after birth. The commonest • Presence of HBeAg
route of transmission is at birth when maternal Ŧ Without neonatal prophylaxis, risk of infection: 90%
secretions in the birth canal come in contact with BeAg, hepatitis B e antigen.
CH 51_p774-789_v3.indd 781 19-07-2015 01:17:57

creening at
first boo ing
H s g positive
Husban nfant
creene for H s g an anti H s Pre ention of perinatal transmission
Hepatitis immunoglobulin Hepatitis accine

H s g negative anti H s positive
H at birth ithin hours of birth
epeat at an
mmuni ation ith hepatitis
months
accine at an months
Husban immune
Use of con oms till
to H V
immunity confirme
H s g an anti H s
teste at an
months to confirm
immunity
Figure 51.1 2TGXGPVKQPQHVTCPUOKUUKQPQHJGRCVKVKU$XKTWU

*$8HTQOCP*$U#IRQUKVKXGYQOCPKPRTGIPCPE[CPFCV
delivery. Anti- Bs JGRCVKVKU$UWTHCEGKOOWPQINQDWNKP)
+I)CPVKDQF[ BsAg hepatitis B surface antigen.
Chronic infection with hepatitis D produces chronic hepatitis D develop cirrhosis and portal
more severe disease than the other forms of hep- hypertension. The progress of disease can be
atitis. Approximately 70%–80% of patients with very rapid and result in cirrhosis within 2 years.
Perinatal transmission can occur at the time of
delivery, but neonatal prophylaxis against hepati-
Box 51.8 epatitis C virus outes of
tis B is effective at decreasing transmission rates.
transmission, clinical features,
and management
• Routes of transmission
epatitis E
Ŧ Needle stick injuries Hepatitis E virus (HEV) is more easily acquired
Ŧ Intravenous drug use and has more adverse effects in pregnancy than
Ŧ Transfusion of unscreened blood products
in the nonpregnant state. It is also associated
Ŧ Sexual contact
with a greater mortality rate in pregnancy. It is
Ŧ 2GTKPCVCNVTCPUOKUUKQP

• Clinical features
not associated with chronic hepatitis or cirrhosis.
Ŧ 70% asymptomatic It is endemic in developing countries. It is pri-
Ŧ Only 30% symptomatic marily transmitted through
Present with symptoms similar to hepatitis A or B
• fecal–oral contamination and
• Routine screening of pregnant women
• contaminated water supplies.
Ŧ Not recommended
• Management
Ŧ General supportive measures
Clinical presentation
Ŧ Route of delivery does not affect transmission The clinical presentation of hepatitis E is listed
Ŧ No neonatal vaccination in Box 51.9.
CH 51_p774-789_v3.indd 782 19-07-2015 01:17:57

mimic AFLP, and the disease is differentiated by

Box 51.9 Clinical presentation of hepatitis E
the markedly elevated liver enzymes. Maternal
• #U[ORVQOCVKEKPHGEVKQP
mortality is high due to hepatic encephalopa-
• (WNOKPCPVJGRCVKVKUYKVJJGRCVKEGPEGRJCNQRCVJ[
thy, renal failure, coagulopathy, metabolic acido-
Ŧ Can be confused with acute fatty liver of pregnancy
sis, and sepsis. Patients with fulminant infection
Ŧ 25%–100% mortality
require aggressive supportive therapy and should
• Self-limited disease lasting 1–4 weeks
• Associated with increased rates of
be transferred to a tertiary care center. Liver trans-
Ŧ abortion plantation may be required.
Ŧ stillbirth
Ŧ neonatal deaths Clinical and laboratory
ſPFKPIUKPCEWVGJGRCVKE
Intrapartum care
diseases in pregnancy
In the absence of signs of acute maternal dis-
ease, transmission does not depend on the The different presentations and laboratory find-
route of delivery. A vaginal delivery or a cesarean ings in various acute hepatic diseases in preg-
section may be undertaken based on obstetric nancy are summarized in Table 51.1.
indications.
reast ee ing
Breastfeeding is not contraindicated.
Preexisting chronic liver
disease in pregnancy
Fulminant hepatitis in pregnancy
Fulminant hepatitis in pregnancy can occur fol-
Chronic autoimmune hepatitis
lowing infection with HBV, HAV, or HEV. The dis- Chronic autoimmune hepatitis is a disorder of
ease starts with the usual mild symptoms of hep- unknown etiology in which progressive destruc-
atitis but progresses rapidly. Clinical features may tion of liver parenchyma ultimately leads to
Table 51.1 %QORCTKUQPQHENKPKECNCPFNCDQTCVQT[ſPFKPIUKPCEWVGJGRCVKEFKUGCUGUQHRTGIPCPE[
nset in enal
pregnancy Clinical Liver function function ematological
Disorder (trimester) ſPFKPIU tests test and coagulation tests
AST ALT Bilirubin Creatinine Plat Fib PT emolysis

( L) (mg dL) (mg dL)
Hyperemesis First Severe N&V N N n N N N N
Pruritus,
Cholestasis Third N 1–5 N N N N N
jaundice
N&V, ±HTN,
Acute fatty
Third hepatic/ 300–500 = or >5 nnn pp ppp n nnn
liver
renal failure
HTN, head-
Second
HELLP ache, blurred 200–700 2–4 n pp p N nnn
– third
vision
1000–
Hepatitis Variable Jaundice 5–20 N p N n N
>2000
n, increased levels; p, decreased levels; A , alanine aminotransferase; AS CURCTVCVGCOKPQVTCPUHGTCUG%TGCVETGCVKPKPG(KDſDTKPQIGP
P, hemolysis, elevated liver enzymes, and low platelet count; , hypertension; , normal; , nausea and vomiting; Plat, platelets;
P , prothrombin time.
CH 51_p774-789_v3.indd 783 19-07-2015 01:17:57

cirrhosis. The disease is usually treated with Clinical features

immunosuppressive drugs. The drugs used are
corticosteroids and azathioprine. The disease Symptoms related to gallstones develop when the
can relapse in pregnancy. Risk of spontaneous gallbladder contracts in response to a fatty meal.
miscarriage and fetal demise is high. Gallstones can manifest with the following:
• Right upper quadrant pain
Cirrhosis and portal • Nausea and vomiting
• Acute cholecystitis
hypertension – Low-grade fever
Women with decompensated cirrhosis are often – Mild leukocytosis
anovulatory and rarely conceive. Women who
do conceive face increased maternal mortality. Diagnosis
Fetal and neonatal outcomes are also poor, with Ultrasound examination is the gold standard for
increased rates of preterm deliveries, spontaneous diagnosis of biliary sludge and gallstones.
abortions, stillbirths, and neonatal mortality.
resentation
The four presentations of gallstone disease are
Gallstones in pregnancy summarized in Box 51.10.
Gallstones (cholelithiasis) occur more com-
monly during pregnancy due to decreased gall- Differential diagnosis
bladder motility and increased cholesterol sat-
uration of bile. Up to 10% of pregnant women Gallstone disease presents in pregnancy with the
may develop stones or bile sludge during preg- same symptoms as in the nonpregnant patient.
nancy or in the immediate postpartum period. However, right upper quadrant pain can occur in
However, only 1% will develop symptoms related other conditions specific to pregnancy. The dif-
to sludge and/or gallstones and the rest will ferential diagnosis for right upper quadrant pain
remain asymptomatic. in pregnancy and the differences from gallblad-
Increasing age, obesity, and genetic factors der disease are enumerated in Box 51.11.
contribute to the development of gallstones in
pregnancy. Management of gallstone disease
in pregnancy
Physiological biliary changes Uncomplicated biliary colic and acute chole-
in pregnancy cystitis can often be treated with conservative
A variety of physiological changes in the biliary therapy. If surgical intervention is required, it
system occur in pregnancy that promote gall-
stone formation. The two important changes are Box 51.10 Presentations of gallstone disease
as follows:
• Acute cholecystitis
• Facilitation of cholesterol stone formation Ŧ &WGVQKPƀCOOCVKQPQHOWEQUCNNKPKPI
– Estrogen increases cholesterol secretion Ŧ Right hypochondrial or epigastric pain
– Progesterone reduces bile acid secretion Ŧ Positive Murphy’s sign
Concentration of cholesterol increases Tenderness in subcostal region on deep palpa-
in bile tion during a deep breath
• Biliary colic
– Ability to dissolve cholesterol reduces.
Ŧ Due to stone blocking cystic duct opening
• Stasis
Ŧ Pain may be generalized, not always localized
– Progesterone slows gallbladder emptying • Gallstone pancreatitis
– Bile stasis promotes the formation of stones Ŧ Elevated levels of serum amylase and lipase
The above changes lead to formation of sludge • Choledocholithiasis
Ŧ Gallstones in the common bile duct
and gallstones in pregnant women. These phys-
Ŧ %QPſTOGFD[WNVTCUQWPFQTGPFQUEQRKETGVTQITCFG
iological alterations return to normal within EJQNCPIKQRCPETGCVQITCRJ[
'4%2
2 months following delivery.
CH 51_p774-789_v3.indd 784 19-07-2015 01:17:57

pathophysiology of the alteration in bowel pat-

Box 51.11 Differential diagnosis for right upper
quadrant pain in pregnancy tern may be specific to hormonal and struc-
tural changes that occur during pregnancy (see
• Severe preeclampsia Chapter 3, Maternal physiology in pregnancy).
Ŧ Differentiated by
Surgical conditions such as appendicitis may
hypertension
also present in pregnancy and may present a
thrombocytopenia
• Acute fatty liver of pregnancy
diagnostic challenge.
Ŧ Differentiated by
higher AST and ALT
hypoglycemia
acute renal failure
Constipation and diarrhea
DIC
After nausea and vomiting, the two common GI
A , alanine aminotransferase; AS , aspartate aminotransferase; problems that occur in pregnancy are constipa-
D C, disseminated intravascular coagulation.
tion and diarrhea.
is preferably done laparoscopically in the sec-
ond trimester since it may be associated with Constipation
the risk of abortion in the first trimester and
the risk of preterm labor in the third trimester. Constipation is more common in the first tri-
Management is summarized in Figure 51.2. mester (due to decreased intake of both solids
and liquids) but may occur in any trimester.
Constipation is defined as
Gastrointestinal disorders • straining at defecation at more than 25% of
bowel movements;
Pregnant women are susceptible to a host • hard stool at more than 25% of bowel
of bowel disturbances at rates similar to movements;
those in the nonpregnant state. However, the • two or fewer movements a week.
iliary colic or acute cholecystitis
aile conser ati e treatment

Uncomplicate bstructi e jaun ice
allstone pancreatitis e ists
Peritonitis suspecte
Conser ati e therapy
in first an thir
trimester
Laparoscopic CP for impacte
cholecystectomy common bile
ntra enous flui in secon trimester uct stone
o el rest
Pain control
ntibiotics if nee e
May recur in
uccessful in
uring pregnancy
Figure 51.2 Management of gallstone disease in pregnancy. CP, endoscopic retrograde cholangiopancreatography.
CH 51_p774-789_v3.indd 785 19-07-2015 01:17:57

• Antidiarrheals
Box 51.12 Management of constipation
– Loperamide—safe in pregnancy
• Dietary changes • Specific treatment for the cause of diarrhea
Ŧ >8 glasses of water/day
Ŧ (KDGTKPVCMG
ŌIFC[
• Increasing physical activity
• Using bulking agents
emorrhoids
Ŧ Isphaghula husk Hemorrhoids are varicosities in the anal canal
Ŧ Methyl cellulose caused by pressure from the gravid uterus. They
• Laxatives are a common complaint during pregnancy in
Ŧ .KSWKFRCTCHſP
up to 30% of women. They are more frequent in
Ŧ Milk of magnesia
the last trimester of pregnancy and immediately
Ŧ Lactulose
Ŧ Castor oil should not be used
postpartum.
The precipitating causes for hemorrhoids in
pregnancy are listed in Box 51.13.
Causes of constipation Symptoms and management
Constipation may occur in 30% of pregnant
Hemorrhoids may present with pruritus, pain,
women. The etiology is multifactorial, and is a
and bleeding. The pregnant woman may feel the
combination of the following:
hemorrhoids as a bulge at the anal verge.
• Decreased small bowel motility Management includes the following:
• Decreased colonic motility
• Relief of symptoms
• Increased absorption of water
– Local antipruritic and anesthetic preparations
• Mechanical interference by gravid uterus
– Sitz baths
– Late in pregnancy
– Treatment of constipation
• Iron and calcium supplements
• Recurrent and severe hemorrhoids
– Surgical treatment (hemorrhoidectomy)
Management
Constipation is managed primarily by dietary
and behavioral modification. )CUVTQGUQRJCIGCNTGƀWZ
The measures for the management of consti- Gastroesophageal reflux disease (GERD or
pation are listed in Box 51.12. heartburn) is common during pregnancy. The
symptoms worsen from the first to the third
Diarrhea trimester and usually disappear after delivery.
Gastroesophageal reflux tends to recur in subse-
The causes for diarrhea are the same as for a quent pregnancies, and can affect both multipa-
nonpregnant woman and may have infectious rous and nulliparous women.
and noninfectious causes.
Diarrhea is evaluated with stool exam- Pathophysiology of GE D
ination for ova, parasites, bacteria, and fecal
leukocytes. The causes leading to GERD in pregnancy are
enumerated in Box 51.14.
Management
The treatment of acute diarrhea includes con- Box 51.13 Precipitating factors for hemorrhoids
in pregnancy
servative measures:
• Enlarging gravid uterus
• Oral rehydration Ŧ Increased abdominal pressure
– Fluids containing salt and sugar Ŧ Vascular engorgement and venous stasis
• Correction of potential electrolyte abnormalities • Constipation
– Bananas (K+ replacement) • Postpartum period
– Orange juice Ŧ Pushing efforts during delivery
CH 51_p774-789_v3.indd 786 19-07-2015 01:17:57

anorexia, and raised white blood cell (WBC)

Box 51.14 Pathogenesis of GE D in pregnancy
count may be considered to be due to pregnancy.
• Intrinsic factors The location of the appendix also changes due
Ŧ Abnormal esophageal motility to displacement of the colon by the enlarging
Decreased LES pressure
uterus, and the pain is a typical. Therefore, the
Ŧ Increased gastric pressure
risk of perforation is higher.
• Mechanical factors
Ŧ Enlarging gravid uterus
Increased intra-abdominal pressure
Displacement of the LES Diagnosis
)'4&ICUVTQGUQRJCIGCNTGƀWZFKUGCUG.'5, lower esophageal
sphincter.
Physical signs
The physical signs of acute appendicitis in preg-
Management nancy depend on the trimester when it occurs.
Management consists of the following: • Abdominal pain

– First trimester: Right lower quadrant
• Lifestyle modifications – Second trimester: At the level of the umbilicus
– Elevate head end of bed – Third trimester: Diffuse or in the right upper
– Eat small, frequent meals quadrant
– Avoid eating for 2 hours before bedtime • Nausea, vomiting, and anorexia
• Medications
– Antacids ltrasound
– Sucralfate
– Histamine 2 (H2) blockers Ultrasound imaging may be useful in locating
Cimetidine, ranitidine, and famotidine the appendix and confirming the diagnosis of
– Proton pump inhibitors appendicitis.
Treatment
Appendicitis
The treatment of appendicitis is surgical.
Acute appendicitis is the most common non- Laparoscopy or laparotomy is used, depending
obstetric cause of acute abdomen in pregnancy. on the trimester of pregnancy and accessibility
The diagnosis may be delayed because many of the appendix.
of the symptoms such as nausea and vomiting,
Key points
• Some hepatic disorders are unique to pregnancy, • Acute fatty liver of pregnancy results in substan-
whereas some new or chronic hepatic diseases may tial maternal and perinatal morbidity and mortality.
result in adverse outcomes. Associated maternal complications include postpartum
hemorrhage, renal failure, hypoglycemia, dissemi-
• Gastrointestinal disorders are some of the most fre-
nated intravascular coagulopathy, pancreatitis, and
quent complaints during pregnancy.
pulmonary edema.
• Although a rare complication of pregnancy, acute
• #URCTVCVGCOKPQVTCPUHGTCUG
#56CNCPKPGCOK-
HCVV[NKXGTQHRTGIPCPE[
#(.2KUCPQDUVGVTKEGOGT-
PQVTCPUHGTCUG
#.6CPFDKNKTWDKPNGXGNUOC[UJQYC
gency that can lead to fulminant hepatic failure. It is
modest increase in AFLP.
EJCTCEVGTK\GFD[OKETQXGUKEWNCTHCVV[KPſNVTCVKQPQH
hepatocytes. • +PVTCJGRCVKEEJQNGUVCUKUQHRTGIPCPE[
+%2KUVJG
most common liver disorder unique to pregnancy.
• Acute fatty liver of pregnancy is associated with
acute renal failure or hepatic encephalopathy in • The characteristic symptom of ICP is pruritus that
up to 60% of cases. starts in the second or third trimester of pregnancy,
(Continued)
CH 51_p774-789_v3.indd 787 19-07-2015 01:17:57

Key points
%QPVKPWGF
and disappears after delivery. Mild jaundice occurs • Vertical transmission from mother to child accounts for
in 10%–15% of cases. Liver enzymes stay normal in half of the cases of HBV in the world. The commonest
ICP. route of transmission is at birth when maternal secre-
tions in the birth canal come in contact with the infant’s
• Treatment of pruritus is with ursodeoxycholic acid
mucosal membranes.

7&%#EJQNGUV[TCOKPGQTQEECUKQPCNN[FGZCOGVJC-
UQPG'CTN[FGNKXGT[KUVJGFGſPKVKXGVTGCVOGPV • Neonates of mothers who are positive for HBsAg
should receive passive and active immunization.
• Subcapsular hematoma formation and liver capsular
rupture are rare complications of pregnancy but carry • )CNNUVQPGU
EJQNGNKVJKCUKUQEEWTOQTGEQOOQPN[FWT-
a very high maternal and perinatal mortality. ing pregnancy due to decreased gallbladder motility
and increased cholesterol saturation of bile.
• Viral hepatitis is one of the most commonly occurring
infections in pregnant women with a potential for seri- • Gallstone disease can present in pregnancy as acute
ous adverse effects. cholecystitis, biliary colic, gallstone pancreatitis, or
choledocholithiasis.
• In viral hepatitis, serum aminotransferases are
elevated to 1000–2000 U/L and the serum bilirubin is • Pregnant women are susceptible to a host of bowel
raised to >10 mg/dL. disturbances at rates similar to that in the nonpregnant
state.
• *GRCVKVKU$XKTWU
*$8JCUCPKORCEVQPDQVJOC-
ternal and fetal health. All pregnant women should • Surgical conditions such as appendicitis may also
be screened for hepatitis B by testing for hepatitis B present in pregnancy and may present a diagnostic
UWTHCEGCPVKIGP
*$U#IKPVJGſTUVVTKOGUVGT challenge.
Self-Assessment
Case 1 Case 1
Mrs. MP, 31, gravida 2, para 1, live 1, presented at 24 weeks 1. 5JGJCU+%26JGFKCIPQUKUKUEQPſTOGFYKVJ
with severe pruritus that was worse at night. There were elevated levels of total bile acids, normal levels
scratch marks over her abdomen and extremities. She was of AST and ALT, and mild elevation of bilirubin
extremely distressed and her family was very concerned.
OIF.
2. High levels of estrogen and progesterone in
1. 9JCVKUVJGFKCIPQUKUCPFJQYYKNN[QWEQPſTOKV!
pregnancy are implicated in the etiology of ICP.
2. 9JCVKUVJGGVKQNQI[! Genetic factors may also contribute.
3. *QYYKNN[QWOCPCIGVJKUEQPFKVKQP! 3. Management includes symptomatic treatment of
4. 9JCVKUVJGHGVCNQWVEQOG! the patient with ursodeoxycholic acid and close
monitoring and decision for early delivery of the
fetus.
Case 2 4. Fetal morbidity and mortality are high. ICP is associ-
/TU 52 YCU C ITCXKFC RCTC NKXG 1P JGT ſTUV ated with prematurity, meconium-stained amniotic
prenatal visit she tested positive for HBsAg. ƀWKFKPVTCWVGTKPGFGOKUGCPFKPETGCUGFTKUMHQT
respiratory distress syndrome.
1. What is the course of hepatitis B in pregnancy
2. *QYFQ[QWCUUGUUVJGTKUMQHVTCPUOKUUKQPVQVJGDCD[!
3. How do you counsel health care workers who are Case 2
OCPCIKPIVJGRCVKGPV!
1. Acute HBV infection during pregnancy is usually not
4. How will you prevent mother to child transmission of
severe. It is not associated with increased mortality
JGRCVKVKU$!
CH 51_p774-789_v3.indd 788 19-07-2015 01:17:57

or teratogenicity. It is not an indication for termination

of pregnancy.
Sample questions
2. HBeAg should be tested at 34–36 weeks. If
positive, the woman is extremely infective.
Perinatal transmission can be very high if prophy- 1. 9JCVECWUGUKPVTCJGRCVKEEJQNGUVCUKUQHRTGIPCPE[!
laxis is not given. Discuss its management.
3. A woman infected with HBV is very infectious to 2. Describe the clinical features, diagnosis, and
CP[QPGJCPFNKPIJGTDQFKN[ƀWKFU5VCPFCTFWPKXGTUCN management of acute fatty liver of pregnancy.
precautions such as double gloving should be taken
to prevent contamination.
4. Postexposure immunoprophylaxis with hepatitis Short-answer questions
B immunoglobulin and hepatitis B virus vaccine
1. Gallstone disease in pregnancy
can help prevent 85%–95% of cases of perinatal
transmission. 2. Constipation in pregnancy
CH 51_p774-789_v3.indd 789 19-07-2015 01:17:57

Endocrine Disorders
52 and Obesity
Case scenario
Mrs. LM, 27, had been on thyroxine for hypothyroidism for the past sev-
eral years. She was planning a pregnancy. She and her husband were
concerned about hypothyroidism and its effect on the baby. Her recent
blood tests showed a thyroid-stimulating hormone (TSH) value of 6.3
mIU/mL and free T4 of 1.0 ng/dL. They wanted to know whether it was
safe to go ahead with a pregnancy.
Introduction associated with medical problems that increase

maternal mortality and morbidity as well as
The fetoplacental unit can be likened to a new leading to several obstetric complications.
endocrine organ that is unique to pregnancy. As
a result, considerable endocrine changes occur
in pregnancy. The pregnant woman and the fetus Endocrine disorders
adapt by alterations in the endocrine metabo-
lism. Manifestations of endocrine diseases can This chapter presents an overview of different
be masked by the physiological changes of preg- endocrine disorders that affect pregnancy and
nancy. More importantly, therapy for the mother perinatal outcomes. Optimal diagnostic and man-
has to take into consideration its effects on the agement strategies are discussed. Major endocrine
fetus. disorders that women faces during pregnancy
The growing incidence of obesity is a global include gestational diabetes mellitus, preexisting
problem. The incidence is on the rise in India type 1 diabetes mellitus (see Chapter 48, Diabetes),
as well, due to caloric abundance and changing and thyroid, parathyroid, adrenal, and pituitary
lifestyle in both urban and rural areas. Obesity is disorders.
CH 52_p790-806-v3.indd 790 19-07-2015 01:18:48

Endocrine Disorders 791
Thyroid disorders in Effect of estrogen on thyroid-

binding globulin
pregnancy
Estrogen has the following effects on thyroid-
There are several important issues that must binding globulin:
be considered when thyroid disorders occur
during pregnancy or when women with preex- • Estrogen increases thyroid-binding globulin
isting treated dysfunction become pregnant. level.
Both hypothyroidism and hyperthyroidism • Total T3 and T4 levels are elevated.
during pregnancy may result in complications • Free hormone levels are usually normal or at
for both the mother and the baby. Even sub- the upper limits of normal. Therefore, it is
clinical hypothyroidism and thyroid autoim- advisable to check free T3 and T4, along with
munity have been linked to adverse maternal TSH, to evaluate thyroid function during
and fetal outcomes. pregnancy.
The accurate diagnosis and appropriate See Chapter 3, Maternal physiology in preg-
treatment of thyroid disease during pregnancy nancy for details.
entails a complete understanding of the changes
in thyroid physiology and thyroid function tests
that accompany normal pregnancy. ypothyroidism in pregnancy
The clinical manifestations, diagnosis, and treat-
Physiological adaptation ment of hypothyroidism during pregnancy are
discussed next.
during pregnancy
The thyroid gland undergoes significant changes vert hypothyroidism
in size and function during pregnancy. Several
Overt hypothyroidism is hypothyroidism with
physiological adaptive changes occur.
clinical symptoms, which has been confirmed
with blood tests of thyroid function. Typically
Effect of human chorionic the TSH will be elevated to >10 mIU/mL with
gonadotropin decreased free T4.
Overt hypothyroidism complicating preg-
Human chorionic gonadotropin (hCG) has the nancy is uncommon. Its incidence in preg-
following effects on thyroid function: nancy is low because women with untreated
• Placental hCG is structurally similar to thyroid- hypothyroidism may be anovulatory and have
stimulating hormone (TSH). an increased rate of first trimester spontaneous
• It stimulates TSH receptors resulting in abortion.
– increased thyroxine production;
– suppression of TSH during the first tri- Impact on pregnancy
mester; In women with overt hypothyroidism and a con-
– slight increase in TSH levels by the second tinuing pregnancy, there are both maternal and
trimester. fetal adverse effects as enumerated in Box 52.2.
These changes necessitate the use of
trimester-specific cutoffs while interpreting TSH Subclinical hypothyroidism
values (Box 52.1).
Subclinical hypothyroidism has no clinical
symptoms but is diagnosed because of abnor-
Box 52.1 6
TKOGUVGTURGEKſEPQTOCNTCPIGUHQT malities in thyroid function tests. The TSH will
thyroid-stimulating hormone be elevated with a normal free T4.
It is more common than overt hypothyroid-
• First trimester: 0.1–2.5 mIU/mL
ism, occurring in 2.5% of screened women. The
• Second trimester: 0.2–3.0 mIU/mL
incidence is reported to be as high as 5% in India,
• Third trimester: 0.3–3.0 mIU/mL
which is not an iodine-sufficient country.
CH 52_p790-806-v3.indd 791 19-07-2015 01:18:48

Box 52.2 Adverse effects of overt Box 52.3 Indications for screening for
hypothyroidism on pregnancy hypothyroidism in pregnancy
Maternal • Family or personal history of thyroid disease
• Preeclampsia and gestational hypertension • Positive thyroid peroxidase antibodies in the past
• Anemia • Past thyroid surgery or past radioactive iodine treatment
• Preterm delivery • History of head and neck radiation
• Placental abruption • Type 1 diabetes
• Increased rate of cesarean section • (TQOCPCTGCQHOQFGTCVGVQUGXGTGKQFKPGKPUWHſEKGPE[
• Symptoms of hypothyroidism
Fetal • Infertility
• Prematurity
• Respiratory distress syndrome
• Perinatal mortality
Diagnosis of hypothyroidism
• Neuropsychological and cognitive impairment The classic symptoms of hypothyroidism such as
tiredness and lethargy may be difficult to assess
in the presence of pregnancy, which itself might
Impact on pregnancy give rise to these symptoms.
Although subclinical hypothyroidism has a lower
rate of pregnancy complications, it is also impli- hyroi unction tests
cated in an increased risk for severe preeclamp-
Tests to evaluate thyroid function include the
sia, preterm delivery, placental abruption, and/
following:
or pregnancy loss. This association seems to be
higher in women with elevated thyroid peroxi- • TSH: This is the test commonly used for diag-
dase (TPO) antibody levels. nosis. Trimester-specific cutoffs should be
used.
Cognitive impairment
• Free T4: Pregnancy and trimester-specific
There is insufficient evidence to indicate that cutoffs should be used.
subclinical hypothyroidism impairs neuropsy- • Total T3 and T4 values can be elevated in preg-
chological and cognitive development of the nancy due to elevated thyroxine-binding globu-
fetus or the newborn. However, since there is lin (TBG) levels. If reliable free T3 and T4 assays
potential for impairment, treatment of preg- are not available, total T3 and T4 levels 1.5-fold
nant women with subclinical hypothyroidism is the nonpregnant cutoff may be used.
recommended.
Diagnostic criteria for hypothyroidism in
pregnancy are summarized in Box 52.4.
Causes of hypothyroidism
The following are the causes of hypothyroidism:
Box 52.4 Diagnostic criteria for hypothyroidism
• Iodine deficiency in pregnancy
• Autoimmune thyroiditis (Hashimoto’s thyroid-
itis) • Overt hypothyroidism
Ŧ 'NGXCVGFVTKOGUVGTURGEKſE65*EQPEGPVTCVKQP
– Most common cause of hypothyroidism
>2.5 mIU/mL in the first trimester
– Diagnosed by elevated titers of TPO antibody
>3 mIU/mL in the second and third trimesters
(also called thyroid microsomal antibody) Ŧ Decreased free T4 concentration
<0.7 ng/dL in the first trimester
Screening for hypothyroidism <0.5 ng/dL in the second and third trimesters
• Subclinical hypothyroidism
Universal screening for hypothyroidism is not Ŧ 'NGXCVGF VTKOGUVGTURGEKſE UGTWO 65* EQPEGP-
recommended in pregnancy. Targeted screen- tration
ing can be offered to women who have one or Ŧ Normal free T4 concentration
more of the risk factors listed in Box 52.3. S thyroid-stimulating hormone.
CH 52_p790-806-v3.indd 792 19-07-2015 01:18:48

Treatment of hypothyroidism in • In women with hypothyroidism predating

pregnancy pregnancy, the dose should be reduced to the
prepregnancy dose.
Both overt hypothyroidism and subclinical • In women with subclinical hypothyroidism
hypothyroidism should be treated in pregnancy. diagnosed in pregnancy:
– If TPO antibody is negative, treatment can
omen ith hypothyroi ism prior to be discontinued.
pregnancy – If TPO antibody is positive, treatment may
In women who are on treatment prior to preg- be continued for 6 months.
nancy, it is recommended that TSH levels be • TSH and free T4 should be repeated 4–6 weeks
brought to below 2.5 mIU/mL prior to conception. after stopping medication and further treat-
Requirement of thyroxine increases as early as ment decided upon.
4 weeks’ gestation; therefore, the dose of levothy-
roxine should be increased by 25% (25–50 μg) as
soon as pregnancy is confirmed in a woman with yperthyroidism and
overt hypothyroidism. pregnancy
omen iagnose to have The clinical manifestations, diagnosis, and treat-
ment of hyperthyroidism during pregnancy are
hypothyroi ism in pregnancy
discussed here.
Levothyroxine (synthetic T4) is the treatment
of choice for hypothyroidism in pregnancy. The
goal of T4 replacement therapy is to restore nor- vert hyperthyroidism
mal thyroid function (euthyroidism) as soon
Overt hyperthyroidism is symptomatic hyper-
as possible. It is recommended that TSH value
thyroidism that has been confirmed by low/
should be kept at or below 2.5 mIU/L, especially
undetectable TSH and elevated free T4 and/or
during the first trimester.
free T3 levels. It is a relatively uncommon condi-
TSH levels should be monitored every 4 weeks in
tion in pregnancy, occurring in only 0.1%–0.4%
the first half of pregnancy and later every 8 weeks.
of all pregnancies.
The treatment and monitoring of hypothyroid-
High serum hCG concentrations during early
ism in pregnancy are summarized in Box 52.5.
pregnancy may result in transient subclinical or,
ostpartum osage rarely, overt hyperthyroidism.
The criteria for TSH levels differ in nonpregnant
women as compared with those in pregnant Subclinical hyperthyroidism
women.
Subclinical hyperthyroidism (low TSH, normal
free T4) may be followed up in pregnancy with
Box 52.5 Treatment and monitoring of no treatment. In these women, TSH, free T4,
hypothyroidism in pregnancy and/or total T4 or total T3 are monitored every
• Women on treatment prior to pregnancy 4–6 weeks.
Ŧ TSH should be <2.5 mIU/mL before conception.
Ŧ Dose should be increased by 25% (25–50 μg) on
diagnosis of pregnancy. Clinical presentation
Ŧ Dose should be titrated with TSH levels.
Many of the symptoms of overt hyperthyroidism
• Newly diagnosed overt and subclinical hypothyroidism
Ŧ Levothyroxine (synthetic T4)
may be confused with symptoms of pregnancy.
Ŧ Euthyroid state to be achieved rapidly (TSH These are as follows:
ŭO+7O. • Tremors
• TSH monitored • Sweating
Ŧ 'XGT[YGGMUKPſTUVJCNHQHRTGIPCPE[
• Heat intolerance
Ŧ Every 8 weeks in latter half of pregnancy
• Palpitation
S thyroid-stimulating hormone. • Weakness
CH 52_p790-806-v3.indd 793 19-07-2015 01:18:48

Signs and symptoms that strongly suggest hyperthyroidism in pregnancy and occurs in
Graves’ disease (autoimmune hyperthyroidism) 0.1%–1% of pregnancies.
are as follows: • hCG-mediated hyperthyroidism occurs in
1%–3% of all pregnancies. It is due to the fact
• Onset of symptoms prior to pregnancy
that there is significant similarity between the
• Symptoms persisting beyond the first trimester
E-subunits of hCG and TSH. As a result, hCG
• Diffuse goiter
has weak thyroid-stimulating activity and may
• Significant infiltrative ophthalmopathy (exoph-
cause hyperthyroidism during the period of
thalmos) or dermopathy
highest serum hCG concentrations (the first
• Prior history of autoimmune problems
trimester).
• Conditions that are associated with high hCG
Screening for hyperthyroidism levels may also present with thyrotoxicosis:
Although a positive association exists between – Hyperemesis gravidarum
the presence of thyroid antibodies and preg- – Multiple pregnancy
nancy loss, currently universal screening for – Gestational trophoblastic neoplasm
antithyroid antibodies and possible treatment is • Toxic multinodular goiter and toxic adenoma
not recommended. may present with hyperthyroidism.
• Other uncommon causes include drug-
Diagnosis of hyperthyroidism induced thyrotoxicosis, subacute thyroiditis,
and thyroid carcinoma.
The diagnosis of hyperthyroidism during preg-
nancy is based on thyroid function tests and is
listed in Box 52.6.
Impact on pregnancy
aternal a verse e ects
Causes of hyperthyroidism Before planning pregnancy, it is recommended
in pregnancy that a woman with thyrotoxicosis undergoes
treatment till she is euthyroid.
The following are the causes of hyperthyroidism:
The effect of thyrotoxicosis on pregnancy
• Autoimmune hyperthyroidism (Graves’ might be due to the disease itself or the antithy-
disease) is the most common cause of roid medications used. Inadequately controlled
thyrotoxicosis is associated with
Box 52.6 Diagnostic criteria for overt • miscarriage
and subclinical hyperthyroidism • placental abruption
vert hyperthyroidism • preterm labor
• TSH • preeclampsia
Ŧ Suppressed (<0.1 mIU/L) or • increase in perinatal mortality
Ŧ Undetectable (<0.01)
• Serum free T4 and/or free T3 etal a verse e ects
Ŧ Elevated Fetal adverse effects include the following:
• Serum total T4 and/or total T3
Ŧ Elevated • Fetal hypothyroidism and goiter may result
• TRAb from over treatment of the mother.
Ŧ Present only in Graves’ disease • Transplacental transfer of TSH antibodies may
Subclinical hyperthyroidism also lead to fetal hyperthyroidism and goiter.
This may result in the fetal complications
• TSH
Ŧ Low
listed as follows:
• Serum free T4 and/or free T3 – Fetal growth restriction
Ŧ Normal – Fetal tachycardia
Ab TSH receptor antibody; S thyroid-stimulating hormone. – Advanced bone age
CH 52_p790-806-v3.indd 794 19-07-2015 01:18:48

– Fetal hydrops
Box 52.7 Antithyroid drugs, their side
– Fetal death effects, and monitoring of dosage
in pregnancy
Treatment of hyperthyroidism • Propylthiouracil
in pregnancy Ŧ 50 mg bid or tid
Ŧ 4GEQOOGPFGFKPſTUVVTKOGUVGT
Similar to all autoimmune disorders, Graves’ Ŧ Crosses placenta less readily than carbimazole
disease may go into remission in pregnancy. Ŧ Can cause agranulocytosis and rarely hepatic
Medication may not be required in the second failure
and third trimesters, but the disorder may recur • Carbimazole
3 months after delivery. Ŧ 5–15 mg daily
Therapy for hyperthyroid women in pregnancy Ŧ Recommended in second and third trimesters
is limited by the fact that all available medications Ŧ Crosses placenta readily
have the potential for fetal adverse effects. Ŧ Can be teratogenic (choanal atresia and aplasia
cutis)
Ŧ Can cause agranulocytosis
Aims o treatment • Monitoring of dosage
Ŧ TSH and free T4 concentrations
The following are the aims of treatment:
Every 4 weeks
• Optimize good fetal and maternal outcome. More frequently immediately after switching
• Maintain the mother’s serum free T4 concen- antithyroid drugs
Maintained within the trimester-specific range
tration at or just above the trimester-specific
Ŧ Free T4 concentration
normal range for pregnancy.
Maintained at or just above upper limit of normal
• Use the lowest possible dose of antithyroid drugs. Ŧ Monitoring throughout pregnancy essential
Maternal hyperthyroidism in the third trimester
Drug therapy may increase risk of low birth weight
Thioamides are recommended for treatment of TSH, Thyroid-stimulating Hormone.
moderate-to-severe hyperthyroidism compli-

anagement o symptoms
cating pregnancy. Available thioamides include
propylthiouracil (PTU), methimazole (MMI), and
o thyroto icosis
carbimazole (CBZ) that is completely metabo- E-blockers, such as atenolol or propranolol, may be
lized to MMI. required for the management of tachycardia and
In the past, PTU was considered the drug of tremor. However, E-blockers cannot be used for
choice throughout pregnancy for women with longer than 2–6 weeks because of concerns regard-
hyperthyroidism, because of concerns about ing fetal growth restriction and hypoglycemia.
the possible teratogenic effects of CBZ. However,
there have been reports of severe PTU-related Surgery
liver failure, though rare. This has led to a change Surgery is rarely required in pregnancy. If it is
in the recommendations. Currently, PTU is used required, surgery may be offered in the second
only in the first trimester and CBZ in the second trimester. Indications are as follows:
and third trimesters.
• Patient with a very large goiter
• Poor response to antithyroid medications and
Drugs o choice significant fetal effects
The following are the drugs of choice:
a ioio ine ablation
• Propylthiouracil
Radioiodine for ablating the thyroid gland is
• Methimazole
used on the nonpregnant woman. However, it
• Carbimazole
may cause ablation of the fetal thyroid tissue
The dosage and side effects of antithyroid that is present by 10–12 weeks. It is therefore
drugs in pregnancy are summarized in Box 52.7. absolutely contraindicated during pregnancy.
CH 52_p790-806-v3.indd 795 19-07-2015 01:18:48

Antithyroid medications and Box 52.8 Management of thyroid cancer

breastfeeding in pregnancy
Antithyroid medications may be used safely • Well-differentiated thyroid cancers (papillary and follicular
carcinoma)
during lactation. The recommended drugs and
Ŧ Slow growing
their dosage are as follows:
Ŧ Surgery may be deferred till the postpartum period if
• Carbimazole size remains stable
– Up to a dose of 30 mg/day • Monitoring with ultrasound during pregnancy
• Propylthiouracil Ŧ Surgery in second trimester if
50% increase in cancer volume
– Up to a dose of 300 mg/day
• Rare cases of aggressive tumors with metastases
• Should be given after a feed
Ŧ Surgery in second trimester
• Suppressive thyroxine therapy indicated
Ŧ when surgery postponed
Thyroid nodules and thyroid Ŧ after second trimester surgery
cancer in pregnancy • Radioiodine therapy and scans
Ŧ Absolutely contraindicated in pregnancy and
It is not uncommon to find thyroid nodules in lactation
pregnancy, especially with the routine use of
ultrasonogram. Thyroid nodules should be inves-
tigated the same way as in a nonpregnant woman.
year after pregnancy loss (miscarriage, abortion,
Management of thyroid nodules ectopic pregnancy) or delivery. The diagnosis of
postpartum thyroiditis is based on clinical man-
in pregnancy ifestations and thyroid function tests. The two
Management of thyroid nodules in pregnancy main types of thyroiditis are as follows:
proceeds as follows:
• Postpartum thyrotoxicosis
• Nodules >1 cm should be subjected to fine- • Postpartum exacerbation of chronic lympho-
needle aspiration cytology (FNAC). cytic (Hashimoto’s) thyroiditis
• Nodules <1 cm may also need to be aspirated
if they sonologically show suspicious features The typical sequence of clinical events is as
such as follows:
– hypoechogenicity,
• Hyperthyroidism
– microcalcifications,
– Usually begins 1–4 months after delivery
– increased vascularity.
– Lasts 2–8 weeks
If the nodule is confirmed to be malignant, • Followed by hypothyroidism
the management is as discussed below. – Lasts from about 2 weeks to 6 months
• Followed by recovery
Thyroid cancer in pregnancy
Thyroid cancer discovered during pregnancy reatment
does not have a negative impact on the progno- The hyperthyroid phase is usually mild and may
sis. The management of thyroid cancer in preg- not require treatment. During the hypothyroid
nancy is summarized in Box 52.8. phase of postpartum thyroiditis, symptomatic
women require treatment with thyroxine.
Postpartum thyroid
dysfunction Graves disease
Graves’ disease may develop postpartum or there
Postpartum thyroiditis
may be an exacerbation. Women whose disease is
Postpartum thyroiditis is a destructive thyroiditis under control with antithyroid drug therapy may
induced by an autoimmune mechanism within 1 have a relapse in the postpartum period.
CH 52_p790-806-v3.indd 796 19-07-2015 01:18:48

Parathyroid dysfunction Impact o hyperparathyroi ism on

pregnancy
in pregnancy
Hyperparathyroidism is associated with
Parathyroid glands secretes parathyroid hormone
(PTH) that, along with 1,25-dihydroxyvitamin D, • preeclampsia
is responsible for maintaining calcium and phos- • preterm birth
phate homeostasis. PTH (also known as parathor- • high perinatal mortality—25% of cases
mone) is a small protein that controls calcium • high incidence of neonatal hypocalcemia
and phosphate homeostasis, as well as bone
reatment
physiology. PTH has effects antagonistic to those
of calcitonin (produced by the thyroid). Surgical excision of the adenoma is the only effective
Calcium and PTH metabolism in pregnancy is treatment of hyperparathyroidism. Complications
summarized in Box 52.9. due to surgery, particularly in the presence of a
single lesion, are low, and the cure rates are high.
yperparathyroidism ypoparathyroidism
Hyperparathyroidism is rare in pregnancy. Causes Damage to or removal of the parathyroid glands
of hyperparathyroidism in pregnancy are as during surgery for thyroid gland pathology is the
follows: most common etiology of hypoparathyroidism.
• Single parathyroid adenoma—80% of cases resenting symptoms

• Primary hyperplasia of the parathyroid glands Hypoparathyroidism should be suspected in a
• Multiple adenomas woman who has a history of thyroid surgery and
• Parathyroid carcinoma—rare presents with symptoms of hypocalcemia. The
symptoms and signs of hypocalcemia are the
Hyperparathyroid crisis is a serious compli- same in pregnancy as in the nonpregnant women
cation that may occur in pregnancy or the post- and include carpopedal spasm and tetany.
partum period. If not recognized and treated
promptly, hyperparathyroid crisis may progress Diagnosis o hypocalcemia
to uremia, coma, and death. The diagnosis of hypoparathyroidism is con-
firmed by the presence of persistent low serum
Diagnosis calcium and high serum phosphate levels in the
The diagnosis of hyperparathyroidism is based presence of normal renal function.
on persistent hypercalcemia (>9.5 mg/dL) in
Impact on pregnancy
the presence of increased serum PTH levels.
Ultrasound imaging may identify the parathyroid Hypoparathyroidism in pregnancy is associated
adenoma. with the following:
• Perinatal loss
– Spontaneous abortions
– Stillbirths
Box 52.9 PT metabolism and calcium in – Neonatal deaths
pregnancy • Fetal hyperparathyroidism
• PTH
– Generalized skeletal demineralization
Ŧ 5NKIJVN[FGETGCUGFKPVJGſTUVJCNHQHRTGIPCPE[ – Subperiosteal bone resorption
Ŧ Returns to normal by midgestation – Bowing of the long bones
• Calcium – Osteitis fibrosa cystica
Ŧ 50% protein bound (mostly to albumin) – Rib and limb deformities
Ŧ 10% in the form of anion complexes
Ŧ 40% circulates free as ionized calcium reatment o hypoparathyroi ism
Ŧ Active transfer of maternal calcium to the fetus Treatment of hypoparathyroidism in pregnancy
P parathyroid hormone. does not differ from that in the nonpregnant state.
CH 52_p790-806-v3.indd 797 19-07-2015 01:18:48

The woman is prescribed a normal high-calcium adverse outcomes. However, current recommen-
diet and vitamin D supplementation. dation is to administer 1000 IU of vitamin D daily
to all pregnant women. Vitamin D may also be
8KVCOKP&FGſEKGPE[ given as 60,000 IU every 2 months.
Studies have found an association between low

calcium and vitamin D levels and adverse health
outcomes in mother and child. However, there is
Adrenal disorders and
no definite evidence whether the low levels cause pregnancy
the adverse effects or are a marker of poor health,
which by itself may result in adverse effects. Adrenal disease, including disorders such as con-
genital adrenal hyperplasia (CAH), Addison dis-
• Normal values of vitamin D3: >20 ng/mL
ease, Cushing syndrome, pheochromocytoma,
• Vitamin D insufficiency: 10–20 ng/mL
and primary hyperaldosteronism, can cause
• Vitamin D deficiency: <10 ng/mL
female subfertility or infertility and have a nega-
These values are relevant when they occur tive impact on maternal and fetal health during
despite the availability of adequate sunlight. pregnancy.
There are several observational studies that
suggest an association between low maternal
vitamin D levels and a higher risk of developing Congenital adrenal hyperplasia
• Gestational diabetes Congenital adrenal hyperplasia is an inherited
• Preeclampsia endocrine disorder that affects the adrenal gland.
• Small for gestational age infants It occurs due to the deficiency of 21-hydroxylase
enzyme (>90% of all cases of CAH), deficiency
'HHGEVUQHXKVCOKP&FGſEKGPE[ of 11-E-hydroxylase enzyme (5%–8% of cases of
CAH), or deficiency of 17-D-hydroxylase (very
on pregnancy rare). It can be broadly divided into the following:
There are several observational studies that sug-
• Classical forms of CAH
gest an association between low maternal vita-
• Late-onset CAH
min D levels and adverse pregnancy outcome as
outlined in Box 52.10. Adrenal androgens are produced in excess
Although vitamin D insufficiency and defi- since they are intermediate metabolites that
ciency are common in India, very low levels are accumulate due to enzyme deficiency. This can
not seen frequently. Routine screening for vita- give rise to androgenization, anovulation, and
min D levels is not currently recommended in infertility. Treatment with glucocorticoids and
pregnancy. assisted reproductive techniques has improved
successful pregnancy rates.
Treatment
There are no studies that conclusively show that Effect on pregnancy
administration of vitamin D decreases the risk of Congenital adrenal hyperplasia is an autosomal
recessive disorder. If the fetus is affected, the
Box 52.10 Effects of low levels of vitamin D on excessive androgens produced can cause viril-
pregnancy ization of the female fetus.
• Low levels of vitamin D are associated with
Ŧ gestational diabetes Management during pregnancy
Ŧ preeclampsia
Ŧ small for gestational age infants
Management during pregnancy has to take into
Ŧ primary cesarean section consideration the glucocorticoid requirements
Ŧ postpartum depression of the mother as well as monitoring of the fetus.
• Very low levels of vitamin D in the mother can lead to
• Glucocorticoids
Ŧ low vitamin D and calcium levels in the neonate and
– Hydrocortisone,cortisoneacetate,prednisone,
Ŧ neonatal convulsions
and methylprednisolone may be used.
CH 52_p790-806-v3.indd 798 19-07-2015 01:18:48

• Clinical status, serum electrolyte levels, and

Box 52.11 Management of suspected fetal
serum androgen levels are checked regularly. congenital adrenal hyperplasia
• Fetal sex determination is important since
a male fetus will not be affected by maternal • Diagnosis
Ŧ Chorionic villus sampling (12 weeks)
androgens.
To determine genotype or
Ŧ Amniocentesis (16 weeks) to determine
abor an elivery 17-hydroxyprogesterone levels in the amniotic
Congenital adrenal hyperplasia is managed fluid
during labor and delivery as follows: - High levels confirm presence of 21-hydroxy-
lase deficiency
• Stress-dose glucocorticoid therapy with hydro- Sex determination
cortisone ester - Male or female
– 50–100 mg IV 8 hourly • Treatment
– At the initiation of active labor/or at induc- Ŧ Oral dexamethasone is given to mother
tion of anesthesia 20 μg/kg of maternal body weight/day in divided
– Continued until after delivery doses beginning at 4–6 weeks’ gestation
Crosses the placenta and suppresses the fetal
– Followed by a rapid taper to previous main-
adrenal gland
tenance doses Ŧ Oral dexamethasone is discontinued in case of
• Cesarean section for male fetus
– previous surgery for virilization normal genotype on chorionic villus sampling
– android pelvis (unaffected female fetus)
normal 17-hydroxyprogesterone levels in the
valuation o the in ant amniotic fluid
Ŧ Oral dexamethasone is continued throughout preg-
A female infant should be examined for ambigu- nancy in case of
ous genitalia. Virilization of the female genitalia affected female
may occur due to
• maternal hyperandrogenism or
• inherited 21-hydroxylase deficiency (if father infancy and early childhood. However, dexa-
is a carrier) methasone therapy can result in weight gain,
If the external genitalia are ambiguous, appro- striae, and glucose intolerance in mothers.
priate laboratory studies should be performed on
the infant to exclude 21-hydroxylase deficiency, #FTGPCNKPUWHſEKGPE[
which can be a life-threatening emergency.
or Addison disease
Prenatal diagnosis and treatment Addison disease is a very rare disorder.
Adrenocortical insufficiency occurs due to the
of CA
destruction or dysfunction of the entire adrenal
In the past two decades it has become possible to cortex. It affects glucocorticoid and mineralo-
diagnose a fetus with 21-hydroxylase deficiency corticoid function. The onset of disease usually
prenatally. In a pregnant woman with a history of occurs when 90% or more of both adrenal cor-
an affected child, oral dexamethasone is started tices are dysfunctional or destroyed. It is com-
at 4–6 weeks’ gestation. Prenatal diagnosis is monly an autoimmune disorder. In developing
done using chorionic villus sampling or amnio- countries, it could be caused by infections such
centesis. Further treatment with dexamethasone as tuberculosis.
depends on the findings. Management of women Maternal exhaustion and low blood pressure
with a previous history of an affected child or in may be present. The symptoms of vomiting and
female fetuses with ambiguous genitalia is sum- hyperpigmentation, which occur in Addison
marized in Box 52.11. disease, may be mistaken for symptoms of
Prenatal treatment with dexamethasone is pregnancy. The diagnosis can be confirmed
safe for the mother and the fetus. An increase in based on results of adrenal function tests.
morbidity or mortality has not been reported in Addison disease has been associated with
fetuses treated to term and monitored through fetal growth restriction.
CH 52_p790-806-v3.indd 799 19-07-2015 01:18:48

Box 52.12 Management of Addison disease in Box 52.13 The impact of Cushing syndrome
pregnancy, labor, and delivery on pregnancy
• Glucocorticoid and mineralocorticoid replacement dos- • 5KIPKſECPVTKUMQHOCVGTPCNOQTDKFKV[
ages are continued throughout pregnancy Ŧ Hypertension and preeclampsia
• Increased glucocorticoid dosage may be required in the Ŧ Gestational diabetes
third trimester Ŧ Congestive heart failure due to severe hyperten-
• During labor sion
Ŧ Adequate saline hydration Ŧ Wound breakdown after surgery
Ŧ 25 mg of intravenous hydrocortisone sodium suc- Ŧ Profound proximal myopathy
cinate Ŧ Emotional lability/psychosis
Every 6 hours • Fetal morbidity and mortality
• At the time of delivery Ŧ Premature delivery
Ŧ High-dose parenteral hydrocortisone Ŧ High perinatal mortality including stillbirths
Ŧ 100 mg 6 hourly or as a continuous infusion Ŧ 0GQPCVCNEQTVKUQNFGſEKGPE[
• After delivery
Ŧ Dosage can be rapidly tapered to maintenance
dose in 3 days of catecholamines, mostly norepinephrine and
epinephrine to a lesser extent. The main sign of
the disease is severe hypertension.
Management in pregnancy, labor, When associated with pregnancy, it can be
catastrophic for the mother and fetus. The mor-
and delivery tality rates can be as high as 50% for both mother
Management of Addison disease is summarized and fetus. An unrecognized pheochromocytoma
in Box 52.12. can be fatal because an uncontrollable hyper-
tensive crisis may be precipitated by anesthesia
or even normal delivery.
Cushing syndrome in
pregnancy Diagnosis in pregnancy
Cushing syndrome is a collection of signs and There should be a high index of suspicion in
symptoms due to prolonged exposure to corti- pregnant women who develop severe uncontrol-
sol. Signs and symptom may include abdominal lable hypertension in pregnancy associated with
obesity along with thin arms and legs, a round unusual features such as the following:
red face (‘moon face’), fat deposition between
• Headache
the shoulders, weak muscles and bones, acne,
• Palpitation
reddish striae, and fragile skin that heals poorly.
• Excessive sweating
Women may have hirsutism and anovulation
• Family history of pheochromocytoma
leading to irregular menstruation. Occasionally
there may be changes in mood, headaches, and Screening of 24-hour urinary catecholamine
a chronic feeling of tiredness. levels in a sample collected during or immedi-
ately after a hypertensive crisis will confirm the
Impact on pregnancy diagnosis.
Cushing syndrome is extremely rare in preg-

Management in pregnancy
nancy. The impact of Cushing syndrome on
pregnancy is summarized in Box 52.13. Management in pregnancy includes the following:
x D-Adrenergic blockade with phenoxy-
Pheochromocytoma in benzamine
x E-Blockade with propranolol after successful
pregnancy D-adrenergic blockade
A pheochromocytoma is a rare neuroendocrine • Surgical removal of tumor before 24 weeks
tumor of the medulla of the adrenal glands (orig- – Surgical approach difficult after 24 weeks
inating in the chromaffin cells), or extra-adrenal • Vaginal delivery associated with higher mor-
chromaffin tissue that secretes high amounts tality than cesarean delivery
CH 52_p790-806-v3.indd 800 19-07-2015 01:18:48

Primary hyperaldosteronism or cabergoline. Currently cabergoline is the drug of

choice. Ovulatory cycles are restored in 80%–90%
Primary hyperaldosteronism is an extremely rare of women and pregnancy is possible.
cause of hypertension in pregnancy. A total of 18
cases of pregnancies complicated by hyperaldo- ect o pregnancy on prolactinoma
steronism have been reported in the literature. Prolactinomas may undergo enlargement in
The classic symptoms of hyperaldosteronism pregnancy, but the majority will not become
are as follows: symptomatic.
• Hypertension
• Hypokalemia ollo up o prolactinoma in preg
• Elevated urine potassium levels nancy
The commonest cause of hyperaldosteronism Follow-up of prolactinoma in pregnancy is as
is an adrenal adenoma. Excision of the adenoma follows:
may be done in the second trimester. • Dopamine agonist is discontinued on diagno-
sis of pregnancy
• Macroadenomas
– Monthly screening for symptoms
Pituitary disorders Headache
in pregnancy Visual field changes
Diabetes insipidus
In pregnancy there is a gradual increase in mater- – Visual fields tested each trimester
nal pituitary volume over the course of gestation,
Enlargement requiring intervention is
with an increased final weight of 660–760 mg, as
well as a volume increase of 30% above the pre- • rare in microadenomas;
gestational volume. Prolactin levels begin to rise • more common in macroadenomas that have
at 5–8 weeks’ gestation and peak in the third tri- been treated surgically or with radiotherapy
mester (100–400 ng/mL). For details, see Chapter earlier;
3, Maternal physiology in pregnancy. • 30% in macroadenomas that have not been
treated surgically or with radiotherapy earlier.
Anterior pituitary disorders anagement o symptomatic prolacti
Prolactinoma and pregnancy noma in pregnancy
Management of symptomatic prolactinoma in
Prolactinomas are the most common hormone-
pregnancy includes the following:
secreting pituitary tumors. Based on its size, a pro-
lactinoma can be classified as • Restarting dopamine agonist
• Delivery if pregnancy is sufficiently advanced
• Microprolactinoma (<10 mm diameter)
• Surgical decompression is rarely required
• Macroprolactinoma (>10 mm diameter)
Lactotrophs in the anterior pituitary undergo Sheehan syndrome (pituitary
neoplastic transformation and result in a tumor.
This leads to excess synthesis and secretion of
infarction)
prolactin (hyperprolactinemia). Prolactinomas Sheehan syndrome is infarction of the pituitary
can cause symptoms due to gland after postpartum hemorrhage (PPH) and
results in hypopituitarism. The pituitary gland
• hyperprolactinemia
enlarges in pregnancy. Due to the increase in size,
• space-occupying effects of the tumor itself
the pituitary gland is more susceptible to isch-
Hyperprolactinemia causes symptoms of emia when systemic blood pressure falls in PPH
galactorrhea, amenorrhea, and infertility. Both (see Chapter 3, Maternal physiology in pregnancy).
microprolactinomas and macroprolactinomas are In developing countries, postpartum pituitary
treated with the dopamine agonists bromocriptine infarction continues to be a common cause of
CH 52_p790-806-v3.indd 801 19-07-2015 01:18:48

Maternal obesity also has an impact on the

Box 52.14 Clinical presentation of Sheehan
syndrome fetus, resulting in an increased risk of prema-
turity, stillbirth, congenital anomalies, macro-
• History of postpartum hemorrhage severe enough somia with possible birth injury, and childhood
Ŧ to cause hypotension
obesity.
Ŧ to require transfusion of multiple units of blood
• Severe hypopituitarism
Ŧ 5KIPKſECPVU[ORVQO
Failure of lactation during the first days after
delivery 9*1ENCUUKſECVKQP
Ŧ Development of profound lethargy, anorexia, and
weight loss
of obesity
• Moderate hypopituitarism
The cutoff BMI for definition of normal and
Ŧ Failure of postpartum lactation
Ŧ Failure to resume menses in the weeks and
obese women in developed countries is based
months after delivery on mortality outcomes in the Caucasian popu-
Ŧ Gradual loss of sexual hair lation. However, Asian women are smaller and
Ŧ Milder degrees of fatigue, anorexia, and weight complications of obesity occur at a lower BMI.
loss Hence, the World Health Organization (WHO)
• Mild hypopituitarism has developed a classification for the Asian pop-
Ŧ Delay in recognition—may take years ulation as given in Box 52.15.
• &GſEKGPE[QHCNNCPVGTKQTRKVWKVCT[JQTOQPGU
The commonest cause for obesity is overeat-
Ŧ GH, prolactin, gonadotropin (FSH and LH), TSH,
CPFCFTGPQEQTVKEQVTQRKEJQTOQPG
#%6*FGſEKGPE[
ing and inadequate physical activity, that is, an
• Shrinkage of pituitary size resulting in an ‘empty sella’ imbalance between calories consumed and calo-
on MRI ries spent. Other causes such as hypothyroidism,
S follicle-stimulating hormone; growth hormone;
hypothalamic problems, Cushing syndrome,
luteinizing hormone; magnetic resonance imaging; and drug-induced obesity are rare and should
S thyroid-stimulating hormone. be excluded by history and clinical examina-
tion. Polycystic ovarian syndrome is commonly
hypopituitarism because of the persisting high associated with obesity in young women, but
rate of profound PPH. the condition is grossly overdiagnosed. Many
Much less commonly, infarction may occur women with this diagnosis may be just obese
immediately postpartum, even in the absence with associated menstrual irregularity.
of obvious hemorrhage. The clinical features
of Sheehan syndrome are enumerated in
Box 52.14. Complications of obesity
reatment Metabolic syndrome is the most common prob-
Treatment of hypopituitarism in Sheehan syn- lem associated with obesity (Box 52.16). This
drome requires lifelong replacement of all the consists of increased waist–hip ratio, abdominal
deficient hormones. obesity, impaired glucose tolerance or diabetes,
besity in pregnancy Box 52.15 9

*1ENCUUKſECVKQPQHQDGUKV[KP
Asian women
Obesity is not the result of a simple imbalance Category BMI (kg m2)
between calorie intake and energy expenditure. Normal weight 18.5–23
It is a complex multifactorial disorder involving Overweight 23–27.5
genetic, environmental, and endocrine factors. Obese >27.5
Overweight and obese women are not only Class I 27.5–31
at increased risk of several pregnancy complica- Class II 31–35
%NCUU+++ Ů
tions, they also face the problem of postpartum
weight retention. B body mass index; World Health Organization.
CH 52_p790-806-v3.indd 802 19-07-2015 01:18:48

Box 52.16 Metabolic syndrome and its Box 52.17 Complications of obesity
complications in pregnancy
• Increased waist–hip ratio • Preconceptional
• Abdominal obesity Ŧ Pregestational diabetes
• Impaired glucose tolerance or diabetes Ŧ Hypertension
• Hypertension • Antepartum
• Dyslipidemia Ŧ Gestational diabetes
• Complications Ŧ Hypertension/preeclampsia
Ŧ Menstrual disorders and infertility Ŧ Fetal macrosomia
Ŧ Long-term complications Ŧ Venous thromboembolism
Atherosclerosis Ŧ Inaccurate ultrasonographic measurements
Coronary heart disease • Intrapartum
Stroke Ŧ Postterm pregnancy
Ŧ Labor induction
Ŧ Prolonged labor
hypertension, dyslipidemia, and the complica- Ŧ Operative vaginal delivery
tions of these. Menstrual disorders and infertility Ŧ Cesarean section
are quite common. Other long-term complications Ŧ Shoulder dystocia
include atherosclerosis, coronary heart disease, Ŧ &KHſEWNV[KPGNGEVTQPKEHGVCNOQPKVQTKPI
stroke, osteoarthritis of the knees, cholecystitis, • Intraoperative
and cholelithiasis. The risk of endometrial and Ŧ &KHſEWNVKPVWDCVKQP
breast cancer is also increased in obese women. Ŧ Aspiration
Diagnosis of obesity in pregnancy is based on • Postpartum
prepregnancy BMI. It is encountered in 6%–10% of
Ŧ Venous thromboembolism
pregnancies and so is a very important and com-
Ŧ Wound infection
mon medical disorder complicating pregnancy.
Box 52.18 Fetal complications due to maternal

Complications in obesity
pregnancy • Prematurity
• Macrosomia
Pregestational diabetes is present in 15% and • Low Apgar scores
hypertension in 30% of obese pregnant women. • Increase in neonatal intensive care unit admissions
Many others develop gestational diabetes, • Perinatal mortality
hypertension, preeclampsia, or venous throm- • Childhood/adolescent/adult obesity
• Metabolic syndrome in adulthood
boembolism. Obstetric palpation and ultraso-
nographic evaluation are difficult. Labor may
be prolonged, and the risk of operative deliv-
eries, cesarean section, and shoulder dystocia and risks of obesity should be discussed with
is increased. The complications that can occur the patient. Diabetes and hypertension should
during pregnancy are listed in Box 52.17. be evaluated and controlled, and medications
In addition, the risk of fetal complications is reviewed.
also increased (Box 52.18).
Antepartum management
Management Pregnant woman with obesity should be coun-
seled regarding recommended weight gain
during pregnancy, based on prepregnancy BMI
Preconceptional management (Table 52.1). Dietary modification and lifestyle
Preconceptional counseling regarding weight changes should be explained and reinforced
optimization is mandatory. The complications repeatedly.
CH 52_p790-806-v3.indd 803 19-07-2015 01:18:48

performed in the first trimester for dating of preg-

Table 52.1 ecommended weight gain based on
nancy, in the second trimester for morphology,
prepregnancy BMI
and in the third trimester to exclude macrosomia.
ecommended Close monitoring of blood pressure is essential.
Prepregnancy BMI weight gain (kg)
Normal 11–16
Overweight and 7–11
class I obese Consultation with an anesthetist should be sought
Class II and III obese 5–7 for women with morbid obesity. Shoulder dysto-
B body mass inde cia should be anticipated. An experienced obste-
trician should be present at cesarean section.
Thromboprophylaxis is required postpartum.
Screening for gestational diabetes at the first The infant should be followed up for child-
visit is mandatory. If negative, the test should be hood obesity and other metabolic problems that
repeated at 24 weeks. Ultrasonography should be may occur later.
Key points
• Thyroid dysfunction during pregnancy may result in • Thioamides are recommended for treatment of
complications for both the mother and the baby. moderate-to-severe hyperthyroidism complicating
• Overt hypothyroidism complicating pregnancy is pregnancy. Available thioamides include propylthioura-
uncommon. Its incidence in pregnancy is low because EKN
TGEQOOGPFGFKPVJGſTUVVTKOGUVGTCPFECTDKOC\QNG
untreated hypothyroid women may be anovulatory and (recommended in the second and third trimesters).
JCXGCPKPETGCUGFTCVGQHſTUVVTKOGUVGTURQPVCPGQWU • Thyroid cancer discovered during pregnancy does not
abortion. have a negative impact on the prognosis.
• Subclinical hypothyroidism has no clinical symptoms • Postpartum thyroiditis is a destructive thyroiditis
but is diagnosed because of abnormalities in thyroid induced by an autoimmune mechanism within 1 year
function tests. The thyroid-stimulating hormone (TSH) after pregnancy loss (miscarriage, abortion, ectopic
will be elevated with a normal free T4. pregnancy) or delivery.
• Subclinical hypothyroidism has a lower rate of • Hyperparathyroidism is rare in pregnancy. The com-
pregnancy complications but is also implicated in an monest cause of hyperparathyroidism in pregnancy is
increased risk for severe preeclampsia, preterm deliv- a single parathyroid adenoma. It is treated by surgical
ery, placental abruption, and/or pregnancy loss. excision.
• Universal screening for hypothyroidism is not recom- • Damage to or removal of the parathyroid glands
mended in pregnancy. Targeted screening can be during surgery for thyroid gland pathology is the most
offered to women who have one or more risk factors. common etiology of hypoparathyroidism.
• Both overt hypothyroidism and subclinical hypothyroid- • Hypoparathyroidism may result in perinatal morbid-
ism should be treated in pregnancy. ity and mortality. Fetal hyperparathyroidism can be a
• In women who are on treatment prior to pregnancy, problem. Treatment is with a normal high-calcium diet
it is recommended that TSH levels be brought below and vitamin D supplementation.
2.5 mIU/mL prior to conception. • Adrenal disease, including disorders such as con-
• Overt hyperthyroidism is symptomatic hyperthyroidism genital adrenal hyperplasia (CAH), Addison disease,
VJCVJCUDGGPEQPſTOGFD[NQYWPFGVGEVCDNG65*CPF Cushing syndrome, pheochromocytoma, and primary
elevated free T4 and/or free T3 levels. It is a relatively hyperaldosteronism, can cause female subfertility or
uncommon condition in pregnancy, occurring in only infertility and have a negative impact on maternal and
0.1%–0.4% of all pregnancies. fetal health during pregnancy.
• High serum hCG concentrations during early preg- • Although CAH has a low rate of pregnancies, suc-
nancy may result in transient subclinical or, rarely, cessful births have been reported in a small number
overt hyperthyroidism. of women who became pregnant.
• Management of women with a previous history of an
• Graves’ disease is the commonest cause of hyper-
thyroidism in pregnancy. The other cause is hCG- affected child or in female fetuses with ambiguous genita-
lia includes prenatal diagnosis to rule out CAH in the fetus.
mediated hyperthyroidism.
(Continued)
CH 52_p790-806-v3.indd 804 19-07-2015 01:18:48


• Addison disease is a very rare disorder. Adrenocorti- • Sheehan syndrome is infarction of the pituitary gland
ECNKPUWHſEKGPE[QEEWTUFWGVQVJGFGUVTWEVKQPQT after postpartum hemorrhage (PPH) and results
dysfunction of the entire adrenal cortex. It can result in in hypopituitarism. Failure of lactation during the
fetal growth restriction. ſTUVFC[UCHVGTFGNKXGT[KUCUKIPKſECPVU[ORVQOKP
• Cushing syndrome is a collection of signs and pregnancies complicated by profound PPH.
symptoms due to prolonged exposure to cortisol. It is • Treatment of hypopituitarism requires replacement
very rare in pregnancy and has been associated with QHCNNVJGFGſEKGPVJQTOQPGU
UKIPKſECPVOCVGTPCNCPFHGVCNOQTDKFKV[CPFOQTVCNKV[
• Obesity is a common problem encountered in the
• A pheochromocytoma is a rare neuroendocrine tumor obstetric population. It is associated with several
of the medulla of the adrenal glands. When associated obstetric complications such as diabetes, hyperten-
with pregnancy, it can be catastrophic for the mother sion, fetal macrosomia, shoulder dystocia, cesarean
and fetus. delivery, PPH, and deep vein thrombosis (DVT).
• Prolactinomas are the most common hormone- • Preconceptional counseling and weight optimization
secreting pituitary tumors. They may undergo enlarge- are mandatory in obese women. During pregnancy,
ment in pregnancy, but the majority will not become close monitoring of blood sugar levels and blood
symptomatic. Symptomatic prolactinomas will require pressure is mandatory.
restarting of dopamine agonist.
Self-Assessment
Case-based scenarios Case 3
Mrs. AC, 22, has come for prepregnancy counseling. Her
Case 1 BMI is 31 and her mother is diabetic.
Mrs. LM, 27, has been on thyroxine for the past several 1. What evaluation would you do?
years for hypothyroidism. She is now planning a preg-
2. What complications are likely if she conceives?
nancy. She and her husband are concerned about hy-
3. How will you counsel her?
pothyroidism and its effect on the baby. Her recent blood
tests showed a TSH value of 6.3 mIU/mL and free T4
of 1.0 ng/dL. They want to know whether it is safe to go
ahead with a pregnancy. Answers
1. What is the recommended level of TSH preconcep- Case 1
tionally?
2. What are the diagnostic criteria for hypothyroidism in 1. In women who are on treatment prior to pregnancy, it
pregnancy? is recommended that TSH levels be brought below
3. What is the impact of hypothyroidism on pregnancy? 2.5 mIU/mL prior to conception.
4. What are the goals of treatment of hypothyroidism in 2. 1XGTVJ[RQVJ[TQKFKUO'NGXCVGFVTKOGUVGTURGEKſE
pregnancy? TSH with decreased free T4. Subclinical hypothyroid-
KUO'NGXCVGFVTKOGUVGTURGEKſEUGTWO65*EQPEGP-
tration with normal free T4 concentration.
Case 2 3. Hypothyroidism is associated with an increased risk
for severe preeclampsia, preterm delivery, placental
Mrs. GH, 29, delivered vaginally 7 days ago. She had abruption, and/or pregnancy loss. There may also be
profuse PPH due to atonic uterus and had hypovolemic cognitive impairment in the offspring.
shock. She required 6 units of packed cells. She has
4. The goal of T4 replacement therapy is to restore
not been able to establish lactation. She feels tired and
normal thyroid function (euthyroidism) as soon as
exhausted.
possible. It is recommended that TSH value should
1. What is the diagnosis and the pathophysiology? be kept at or below 2.5 mIU/L, especially during the
2. *QYKUVJGFKCIPQUKUEQPſTOGF! ſTUVVTKOGUVGT
3. What are the effects of hypopituitarism?
4. What is the treatment in this case?
CH 52_p790-806-v3.indd 805 19-07-2015 01:18:49

Case 2 2. Antenatal—gestational diabetes, hyperten-

sion, preeclampsia, fetal macrosomia, prolonged
1. She has Sheehan syndrome. The pituitary gland pregnancy, induction of labor, prolonged labor,
enlarges in pregnancy. Due to the increase in size, instrumental delivery, cesarean section, DVT,
the pituitary gland is more susceptible to ischemia shoulder dystocia, and anesthetic complications.
when systemic blood pressure falls in postpartum 3. Weight optimization before pregnancy by diet and
hemorrhage. regular exercises. Keep the weight gain in pregnancy
2. Failure to establish lactation is a strong indication of appropriate to the prepregnancy BMI. Screening for
Sheehan syndrome. Tiredness and exhaustion could diabetes during pregnancy, and close watch on the
DGCUKIPQHCFTGPCNKPUWHſEKGPE[5JGPGGFUVQDG blood pressure and fetal growth.
GXCNWCVGFKOOGFKCVGN[HQTCFTGPCNFGſEKGPE[CPF
in 4–6 weeks the pituitary hormone levels should be
measured. Sample questions
3. Hypopituitarism may result in failure to establish lacta-
tion, profound fatigue, anorexia, and weight loss. There Long-answer question
will be loss of sexual hair and failure to resume menses.
4. She will require long-term replacement of pituitary 1. Discuss thyroid disorders in pregnancy.
hormones. 2. Sheehan syndrome: Pathophysiology and
management.
Case 3
1. History of irregular cycles and family history of hyper-
tension. Examination to look for acanthosis nigricans, 1. Postpartum thyroiditis
hypertension, and hirsutism. Fasting and postprandial 2. Prenatal diagnosis of CAH
glucose estimation. 3. Complications of obesity in pregnancy
CH 52_p790-806-v3.indd 806 19-07-2015 01:18:49

Respiratory,
Dermatological, and
53 Connective Tissue
Disorders
Case scenario
Mrs. BN, 24, primigravida, at 32 weeks of pregnancy, presented with

skin lesions over the abdomen and thighs that were severely pruritic.
She was worried that the condition could be serious and affect the baby
as well.
Introduction resting minute ventilation increase, and func-

tional residual capacity is decreased. Oxygen
Disorders of various organ systems are fre- consumption increases by 20%–30%. Dyspnea
quently encountered in pregnancy. Pregnancy is, therefore, common in pregnancy and is partly
predisposes to some of these disorders; some due to the central effect of progesterone.
are aggravated by pregnancy and some affect the Diseases of the respiratory tract are very com-
mother and fetus adversely. mon in pregnancy. Diseases of the cardiovascu-
lar system such as valvular and congenital heart
diseases, cardiomyopathy, and preeclampsia can
cause pulmonary edema and dyspnea. This should
Disorders of the be distinguished from primary respiratory condi-
tions. Respiratory infections may be self-limiting
respiratory tract but can progress to bronchitis or pneumonia.
Preexisting asthma may complicate pregnancy.
Changes in the respiratory system in pregnancy
are described in Chapter 3, Maternal physiol-
ogy in pregnancy. Hormonal changes affect the hinitis
mucous membrane producing edema, conges-
Rhinitis is common in pregnancy. The causes are
tion, and increase in secretions. As the uterus
as follows:
enlarges, the diaphragm is displaced upwards,
causing changes in pulmonary function. The • Pregnancy rhinitis
vital capacity is maintained, tidal volume and • Allergic rhinitis
CH 53_p807-814_v3.indd 807 19-07-2015 01:19:34

• Rhinitis medicamentosa
Box 53.1 espiratory infections in pregnancy
• Sinusitis
• Acute bronchitis
Pregnancy rhinitis is due to the hyperemia Ŧ Community acquired
and edema of the nasal mucosa. Preexisting aller- Ŧ Viral infection
gic rhinitis can worsen during pregnancy. Nasal Influenza/adenovirus/rhinovirus
drops and sprays can give rise to rhinitis medica- Ŧ Symptomatic therapy
mentosa. Sinusitis is usually bacterial. • Pneumonia
Treatment is symptomatic, usually with saline Ŧ Community acquired
nasal drops and steam inhalation. Allergic rhini- Ŧ Present with fever, chills, cough, and dyspnea
tis responds to cromolyn sodium, nasal sprays, Ŧ Bacterial or viral
Ŧ Requires hospitalization
and leukotriene modulators such as montelu-
Ŧ Antibiotics if bacterial
kast. Bacterial sinusitis requires antibiotics.
Amoxicillin with clavulanic acid
Azithromycin
Acute bronchitis Cephalosporins
Levofloxacin/ofloxacin
Viral upper respiratory infections may progress
to bronchitis. The infections are community
acquired and caused by influenza virus, adenovi-
ruses, and rhinoviruses. Treatment is symptom- depends on the preexisting severity of asthma.
atic, and antibiotics are required only if there is Exacerbations are associated with respiratory
secondary bacterial superinfection with puru- infections and poor compliance with inhaled
lent sputum. Amoxicillin can be used and is safe steroids. Symptoms can worsen during labor.
in pregnancy.
Effect of asthma on pregnancy
Pneumonia Women with asthma have a higher risk of
Pneumonia is usually community acquired. It developing complications such as preeclamp-
may be viral or bacterial. Bacterial pneumo- sia and preterm labor, fetal growth restriction,
nia is caused by Streptococcus pneumoniae, and perinatal mortality. Severe asthma causes
Haemophilus influenzae, or Mycoplasma pneu- respiratory alkalosis, hypoxia, and decreased
moniae. Clinical features are the same as in maternal oxygenation. This leads to decreased
nonpregnant patients. Fever, chills cough, puru- placental blood flow and fetal growth restric-
lent or rusty sputum, and dyspnea are the usual tion. Therefore, good control of asthma with
symptoms. Viral pneumonia is often compli- appropriate inhaled steroids used with an
cated by super added bacterial infection. inhalation device or nebulizer reduces the risk
Pregnant women with pneumonia should be of complications.
admitted and symptomatic treatment should
be given. Antibiotics are required for treatment
Clinical features
of bacterial pneumonia. Amoxicillin with clavu-
lanic acid, azithromycin, cephalosporins, levo- Symptoms of asthma in pregnancy are the same
floxacin, or ofloxacin may be used (Box 53.1). as in nonpregnant patients and include cough,
dyspnea, and wheezing on auscultation. The trig-
gers for asthma are also the same. According to
Asthma the severity of symptoms, asthma in pregnancy
Asthma is a common medical condition that is classified into intermittent, mild persistent,
complicates pregnancy. moderate persistent, and severe persistent dis-
ease. Severity is assessed by measurement of
forced expiratory volume (FEV1) and peak expi-
Effect of pregnancy on asthma ratory flow rate (PEFR). Arterial blood gas analy-
The symptoms may worsen, improve, or remain sis is required during an acute severe attack or in
stable during pregnancy. Risk of exacerbation status asthmaticus.
CH 53_p807-814_v3.indd 808 19-07-2015 01:19:34

Respiratory, Dermatological, and Connective Tissue Disorders 809
Management of chronic asthma E-agonists and inhaled corticosteroids are

safe in pregnancy. Oral steroids may be used
Management of chronic asthma is by the when indicated, although there are some con-
following: cerns about their effect on the mother and fetus.
• Assessment of severity by measurement of Leukotriene modifiers are not as effective as
FEV and PEFR E-agonists or corticosteroids, although they are
• Patient education safe in pregnancy. Theophylline has been used
• Avoidance of triggers as oral maintenance therapy and has no adverse
• Pharmacotherapy effects on pregnancy.
Respiratory infection is often the precipitat-
Assessment of severity is essential for plan-
ing factor for an acute episode of asthma. This
ning therapy. It also helps to differentiate
must be treated with appropriate antibiotics.
asthma from the progesterone-induced dys-
pnea of pregnancy. Patient education should
focus on precipitating factors, lifestyle changes, Management of acute asthma
breathing exercises, early recognition of symp-
toms, and prompt initiation of treatment. Early hospitalization is recommended for acute
Identification and avoidance of triggers is asthma in pregnancy. Management is outlined
mandatory in all asthmatics. in Box 53.3.
harmacotherapy
Pharmacotherapy depends on severity. Drugs
used are inhaled corticosteroids such as Asthma may worsen during labor. PEFR and
budesonide and fluticasone; long-acting E-ag- FEV1 should be measured and serially moni-
onists (LABA) such as salmeterol and formo- tored in labor in symptomatic women. If the
terol; short-acting E-agonists (SABA) such as woman has received oral or parenteral steroid
salbutamol; oral corticosteroids; leukotriene therapy in the preceding 4 weeks, hydrocorti-
modifiers such as montelukast and zafirlukast; sone 100 mg should be administered 8 hourly
and oral corticosteroids such as prednisolone. as stress dose and continued for 24 hours
A stepwise approach is used as given in Box 53.2. after delivery. Oxytocin and prostaglandin
E1 and E2 may be used, but prostaglandin F2D
and methergine are contraindicated. Regional
Box 53.2 Stepwise approach for management anesthesia is recommended for a cesarean
of chronic asthma
section.
• Intermittent
Ŧ SABA as required
• Mild persistent
Ŧ SABA as required Box 53.3 Management of acute asthma
Ŧ Low-dose inhaled corticosteroids in pregnancy
• Moderate persistent
Ŧ SABA as required • Acute asthma
Ŧ Low-dose inhaled corticosteroids Ŧ Hospitalization
Ŧ LABA Ŧ Oxygen by mask
• Severe persistent Ŧ Pulse oximetry
Ŧ SABA as required Ŧ E-adrenergic agonist
Ŧ High-dose inhaled corticosteroids oral/SC/inhaled
Ŧ LABA Ŧ Corticosteroids oral/IV
• Very severe persistent • Status asthmaticus
Ŧ LABA Ŧ Admission to ICU
Ŧ High-dose inhaled corticosteroids using nebulizer Ŧ E-agonists
Ŧ Oral/parenteral corticosteroids Ŧ Corticosteroids IV
Ŧ Intubation and mechanical ventilation
ABA long-acting E-agonists; SABA short-acting E-agonists.
CH 53_p807-814_v3.indd 809 19-07-2015 01:19:34

ascular changes
Dermatological disorders
Vascular changes such as palmar erythema and
in pregnancy spider nevi do not require any treatment and
resolve spontaneously after delivery. Pyogenic
Several dermatological changes occur in normal granulomas are red, nodular, and pedunculated
pregnancy. Most of these are self-limiting and lesions. The term pyogenic granuloma is a mis-
resolve after delivery. Treatment is not required nomer because the lesion is neither pyogenic
unless the symptoms are troublesome. nor is it a granuloma. The lesions often ulcerate
and are usually seen on the gums, scalp, trunk,
fingers, and toes. Treatment should be delayed
Dermatological changes until delivery and troublesome persistent lesions
in pregnancy can be cauterized.
Dermatological changes in pregnancy include
pigmentary and vascular changes in the skin, Connective tissue changes
changes in the connective tissue, hair, and nails. Striae are seen in most pregnant women but are
These changes are listed in Box 53.4. more severe in obese women. They occur on the
abdomen, thighs, buttocks, and breasts. They
Pigmentary changes usually fade after delivery and do not respond to
or warrant any treatment.
Pigmentary changes are common in pregnancy.
Fibroepithelial polyps persist after delivery
Most pigmentary changes regress after delivery.
and should be cauterized.
Melasma or chloasma typically affects the face
and involves the forehead, cheeks, and bridge of
the nose. This may worsen with exposure to sun- air and nail changes
light. Persistent melasma can be treated with top- Changes in the hair and nail are due to the hor-
ical retinoic acid, salicylic acid, hydroquinone, or monal changes of pregnancy. Hirsutism, if obvi-
tretinoin. ous, can be treated with waxing or electrolysis.
Box 53.4 Dermatological changes in pregnancy

2TGIPCPE[URGEKſE
• Pigmentary changes dermatoses
Ŧ Hyperpigmentation There are some skin conditions that occur in
Areola, genital skin, neck, and axillae
pregnancy, present with pruritus with or without
Linea nigra
rashes, and resolve after delivery. Some of these
Melasma
Melanocytic nevi
may be associated with fetal complications as
• Vascular changes well.
Ŧ Spider nevi
Ŧ Palmar erythema Intrahepatic cholestasis
Ŧ Pyogenic granuloma
Ŧ Vulvar varicosities and hemorrhoids In cholestasis of pregnancy that occurs in the
Ŧ Varicose veins and venous stars in the lower limbs third trimester, the primary symptom is pru-
• Connective tissue changes ritus associated with mild elevation of direct
Ŧ Striae gravidarum bilirubin and liver enzymes to a lesser extent.
Ŧ Fibroepithelial polyps Pruritus is generalized, and may be intense and
• Hair and nail changes worse at night. There is no skin rash. The condi-
Ŧ Puerperal hair loss tion was formerly termed pruritus of pregnancy.
Ŧ Hirsutism
Intrahepatic cholestasis is discussed in greater
Ŧ Brittle nails
detail in Chapter 51, Hepatic and gastrointestinal
Ŧ Distal onycholysis
disorders.
CH 53_p807-814_v3.indd 810 19-07-2015 01:19:34

Pruritic urticarial papules and Box 53.6 Atopic eruption of pregnancy

plaques of pregnancy • Three types of lesions
Pruritic urticarial papules and plaques of preg- Ŧ Eczematous patches (eczema of pregnancy)
nancy (PUPPP) is the most common dermatosis Ŧ Erythematous papules (prurigo of pregnancy)
Ŧ Follicular lesions (pruritic folliculitis of pregnancy)
in pregnancy. The condition is characterized by
• Associated with pruritus
erythematous papules and plaques that occur
• Appears in second trimester
in the third trimester, associated with itching • No fetal complications
(Box 53.5). The lesions begin as papules within • Resolves after delivery
the abdominal striae and spread to the thighs, • Treatment
buttocks, and arms. Individual lesions coalesce Ŧ Antihistamines
to form plaques. PUPPP is more common with Ŧ Topical corticosteroids
stretching of the abdominal wall as in multiple
pregnancy. Lesions resolve after delivery. The
Treatment is with antihistamines and topical
disorder does not cause any maternal or fetal
corticosteroids. Rarely, oral corticosteroids or
complications.
cyclosporine may be required.
reatment
Initial treatment is with antihistamines. Topical Pemphigoid gestationis
corticosteroids are effective and are used to Pemphigoid gestationis is also known as herpes
relieve symptoms. Oral prednisolone may be gestationis. This is a rare form of dermatosis and
required with severe itching. is an autoimmune disorder. The lesions appear in
the second trimester and consist of vesicles, bul-
Atopic eruption of pregnancy lae, or erythematous plaques (Box 53.7). They are
Atopic eruption of pregnancy (AEP) includes seen over the trunk, buttocks, and limbs. There is
three types of lesions (Box 53.6): associated pruritus. The condition can become
worse after delivery and last for several months.
• Eczematous patches that are dry, scaly, and thick- The lesions can recur in subsequent pregnancies,
ened and are usually seen on the flexures, nipples, during menstruation, and with oral contracep-
neck, and face. The lesions appear in the second tive use. Risk of fetal mortality is increased due to
trimester and are associated with pruritus. prematurity and low birth weight.
• Erythematous papules or nodules usually Treatment of mild-to-moderate cases is
appear on the trunk or extensor surfaces and with topical corticosteroids, but most women
are also known as prurigo of pregnancy. require oral prednisolone 20–40 mg/day. Once
• Follicular lesions and sterile pustules, referred new lesions stop appearing, the dose may be
to as pruritic folliculitis of pregnancy. All
lesions resolve after delivery and do not recur
in subsequent pregnancies.
Box 53.7 Pemphigoid gestationis
• Uncommon disorder
Box 53.5 Pruritic urticarial papules and plaques
• Autoimmune etiology
of pregnancy
• Occurs in second trimester
• Most common pregnancy dermatosis • Vesicles, bullae, and plaques
• Occurs in third trimester • Associated with pruritus
• Begin as papules within striae • May worsen postpartum
• Coalesce to form plaques • May persist for several months
• Associated with pruritus • Can recur in subsequent pregnancies
• Resolve after delivery • Fetal complications
• No maternal/fetal complications Ŧ Prematurity
• Treatment Ŧ Low birth weight
Ŧ Antihistamines • Treatment
Ŧ Topical steroids Ŧ Mild to moderate: Topical steroids
Ŧ Occasionally oral prednisolone Ŧ Severe: Oral prednisolone
CH 53_p807-814_v3.indd 811 19-07-2015 01:19:34

reduced. Long-term treatment may be required. Systemic lupus erythematosus

Intravenous immunoglobulin and plasmaphere-
sis have been used in severe cases. Antepartum Systemic lupus erythematosus occurs pre-
fetal surveillance is essential. dominantly in women. Clinical manifestations
include fever, malaise, symmetric small joint
polyarthritis, photosensitivity, rash, and anemia.
Pustular psoriasis of pregnancy Involvement of renal, vascular, neurological, and
(impetigo herpetiformis) musculoskeletal systems may occur. Diagnosis is
made using the clinical criteria as laid down by
Pustular psoriasis of pregnancy (impetigo her- American Rheumatology Association, along with
petiformis) manifests as white, sterile pustules on the identification of antinuclear antibodies and
erythematous papules or plaques. The pustules other autoantibodies.
are seen in inframammary areas, axillae, groin, During pregnancy, SLE improves in one-third
and gluteal areas. The pustules rupture, leaving of women, worsens in one-third of women, and
raw areas. Onset is usually in the third trimester. remains unchanged in one-third of women.
Associated symptoms are fever, nausea, vomiting, Good outcome can be expected in the following
diarrhea, and chills. The condition resolves after cases:
delivery but can recur in subsequent pregnancy.
Fetal growth restriction and stillbirths can occur. • Disease has been under remission for 6 months
Treatment is with oral prednisolone 60–80 prior to pregnancy.
mg/day. The dose can be tapered when lesions • There is no lupus nephritis.
subside. • APAs are negative.
• There is no superimposed preeclampsia.
Complications
Connective tissue The multiorgan involvement of the disease with
resultant hypertension, thrombophilia, renal
disorders in pregnancy failure due to lupus nephritis, and pulmonary
hypertension as well as steroid-induced diabe-
Connective tissue disorders are autoimmune
tes mellitus can lead to several complications in
and, like other autoimmune disorders, they
pregnancy as listed in Box 53.8. Lupus nephritis
often tend to go into remission in pregnancy.
• The common connective tissue disorders
complicating pregnancy are systemic lupus Box 53.8 Complications of systemic lupus
erythematosus (SLE) and antiphospholipid erythematosus in pregnancy
antibody (APA) syndrome. Rheumatoid arthri- • Maternal
tis, scleroderma, and vasculitis are uncommon Ŧ Preeclampsia
in pregnancy. Ŧ Preterm labor
• Pregnancy-related changes in autoimmun- Ŧ Eclampsia
ity can alter the course of these diseases, and Ŧ HELLP syndrome
Ŧ Anemia
amelioration of symptoms or exacerbations
Ŧ Thrombocytopenia
can occur. Placental insufficiency and fetal
Ŧ Deep vein thrombosis
loss can occur in SLE and APA syndrome. Ŧ Stroke/pulmonary embolism
• Pregnancy must be planned when the disease Ŧ Maternal infections
is in remission. Medications must be reviewed. Ŧ Maternal mortality
Nonsteroidal anti-inflammatory agents should • Fetal
be discontinued. Prednisolone and azathio- Ŧ Prematurity
prine are safe in pregnancy, but cyclophos- Ŧ Fetal growth restriction
phamide, methotrexate, and leflunomide are Ŧ Perinatal mortality
contraindicated. Evaluation for and treatment Ŧ Neonatal lupus syndrome
of APA syndrome with anticoagulants is manda- Ŧ Congenital complete heart block
tory (Chapter 54, Thromboembolic disorders). P hemolysis, elevated liver enzymes, low platelets.
CH 53_p807-814_v3.indd 812 19-07-2015 01:19:35

significantly worsens the outcome of pregnancy Neonatal lupus syndrome manifests as skin
and is associated with a high risk of preeclamp- lesions, hematological abnormalities, and hepatic
sia, eclampsia, and fetal growth restriction. involvement. These are transient and resolve after
a few days. Congenital heart block occurs in the
Management fetus of women with high titers of SS-A and SS-B
antibodies. Diagnosis can be made by 18–26
Disease activity should be monitored by clin- weeks. The heart block is permanent and the
ical and laboratory parameters. A close watch prognosis is guarded.
should be kept on the blood pressure, maternal
hemoglobin, platelet count, and proteinuria.
Contraception
Antepartum fetal surveillance is mandatory.
Low-dose aspirin (75 mg/day) should be started Combined oral contraceptives should not be
as soon as pregnancy is confirmed. Oral pred- used in women with nephritis, APA syndrome,
nisolone is the mainstay of treatment; the dose and vascular involvement. Progestin-only pills
should be adjusted according to disease severity. or injectables and intrauterine devices may be
Azathioprine and hydroxychloroquine may be used.
used if required.
Key points
• Diseases of the respiratory tract such as rhinitis and • 2TGIPCPE[URGEKſEFGTOCVQUGURTGUGPVYKVJRTWTKVWU
acute bronchitis are common in pregnancy. with or without rashes and resolve after delivery.
• Rhinitis could be due to mucosal congestion of • Intrahepatic cholestasis presents with pruritus and
pregnancy, allergy, or sinusitis. Treatment is mild elevation of liver enzymes. There is no skin rash.
symptomatic and with antihistamines. Treatment is with antihistamines. Ursodeoxycholic
• Acute bronchitis is usually viral and treated sympto- acid relieves symptoms.
matically. Pneumonia may be viral or bacterial. Antibi- • Pruritic urticarial papules and plaques of pregnancy
otics are required for bacterial infections. is the most common dermatosis in pregnancy. Atopic
• Asthma may worsen, improve, or remain stable in dermatoses are less common. All dermatoses in preg-
pregnancy. Severe asthma causes hypoxia and respir- nancy are treated symptomatically with antihistamines
atory alkalosis. Assessment of severity is with forced and topical steroids.
GZRKTCVQT[XQNWOGCPFRGCMGZRKTCVQT[ƀQYTCVG • Systemic lupus erythematosus improves in one-
• Management of asthma consists of assessment of third of women, worsens in one-third of women, and
severity, patient education, avoidance of triggers, and remains unchanged in one-third of women during
pharmacotherapy. Drugs used are inhaled steroids, pregnancy.
long-acting E-agonists, short-acting E-agonists, leukot- • Systemic lupus erythematosus is associated with
TKGPGOQFKſGTUCPFQTCNUVGTQKFU5VGRYKUGCRRTQCEJ complications such as preeclampsia, preterm labor,
with these drugs is recommended. HELLP syndrome, deep vein thrombosis, maternal
• Dermatological disorders are common in pregnancy. mortality, fetal growth restriction, and high perinatal
Most are self-limiting and resolve after delivery. mortality.
Self-Assessment
1. What are the common conditions that present with
Case-based questions pruritus?
2. If the lesions are erythematous papules on the
Case 1 striae over the abdomen and thighs, what is your
Mrs. BN, 24, primigravida, at 32 weeks’ pregnancy, pre- diagnosis?
sented with skin lesions over the abdomen and thighs 3. What is the treatment?
that were severely pruritic.
CH 53_p807-814_v3.indd 813 19-07-2015 01:19:35

Case 2 2. Acute asthma should be managed with hospitaliza-

tion; administration of oxygen; oral or intravenous
Mrs. SM, 28, primigravida, presented at 24 weeks’ gesta- corticosteroids; and oral, subcutaneous, or inhaled
tion with acute asthma. She was a known asthmatic from short-acting E- agonists. Oxygen saturation should be
childhood, on inhaled bronchodilators. monitored by pulse oximetry.
3. Chronic asthma is managed by assessment of
1. What complications do you expect in an asthmatic in
severity by measurement of forced expiratory volume
pregnancy?

('8CPFRGCMGZRKTCVQT[ƀQYTCVG
2'(4RCVKGPV
2. How will you manage this acute asthmatic attack?
education, and avoidance of triggers. Medications
3. How will you manage chronic asthma in pregnancy? include inhaled corticosteroids, long-acting
4. How will you manage her in labor? Eagonists and short-acting E-agonists. Pharmaco-
therapy depends on the severity of symptoms.
4. FEV1 and PEFR should be monitored. If she had
Answers received oral or parenteral steroids in the past 4
weeks, hydrocortisone 100 mg is administered IV
Case 1 8t hourly for 24 hours or till delivery. Methergine and
prostaglandin F2D should be avoided. Cesarean sec-
1. Intrahepatic cholestasis, pruritic urticarial papules and
tion should be under regional anaesthesia.
plaques, atopic eruptions, and pemphigoid gesta-
tionis are the common conditions associated with
pruritus. Pustular psoriasis also occurs in pregnancy.
2. The most likely diagnosis is pruritic urticarial papules Sample questions
and plaques of pregnancy (PUPPP) since it is the
most common condition and is seen over the striae. Long-answer question
3. Local emollient creams, antihistamines, and topical 1. Discuss the management of asthma in pregnancy.
steroids.
Case 2 1. Pruritic urticarial papules and plaques of pregnancy
1. Worsening of symptoms can occur. Preeclampsia, 2. 2TGIPCPE[URGEKſEFGTOCVQUGU
preterm labor, fetal growth restriction, and increase in 3. Pregnancy in a woman with systemic lupus
perinatal mortality are other complications. erythematosus
CH 53_p807-814_v3.indd 814 19-07-2015 01:19:35

Thromboembolic
54 Disorders
Case scenario
Mrs. GN, 26, came with her husband for a consultation to the clinic.
She had been married for 6 years, had three miscarriages—two in the
first trimester and one in the second—and one stillbirth in a preg-
nancy complicated by high blood pressure. She had been investigated
elsewhere and was told that she had an abnormal blood test that pre-
disposes to clot formation. She did not understand the significance of
this and wanted to know what should be done during her next preg-
nancy and whether any treatment was necessary before she attempted
pregnancy.
Introduction Thrombophilias
Pregnancy is a hypercoagulable state. Any addi- Normal coagulation is inhibited by several reg-
tional risk factor that predisposes to coagulation ulatory proteins. Deficiency of these proteins
can give rise to thromboembolism. Some of can lead to a hypercoagulable state, resulting in
these risk factors, such as thrombophilias, are venous or arterial thrombosis and embolism.
associated with poor obstetric outcome due to This condition is known as thrombophilia,
the involvement of placental vessels. Deep vein which may be acquired or inherited. The
thrombosis (DVT) and pulmonary embolism are commonest presenting manifestation in throm-
also common in pregnancy and the puerperium. bophilia is venous thromboembolism. However,
Diagnosis and management of these conditions the process may involve the placental vascula-
require a thorough understanding of the patho- ture and therefore may also cause obstetric
physiology, clinical judgment, and expertise. problems.
CH 54_p815-826_v3.indd 815 19-07-2015 01:20:19

Acquired thrombophilias syndrome. This requires a second hit or a precip-

itating factor in the form of pregnancy, oral con-
in pregnancy traceptive pills, smoking, malignancy, hyperten-
The most common acquired thrombophilia in sion, dyslipidemia, or prolonged immobilization.
pregnancy is antiphospholipid antibody (APA) Therefore, the mere presence of antibodies is
syndrome. Others are heparin-induced throm- only a predisposing factor and not the same as
bocytopenia and thrombophilias associated with having APA syndrome.
cancers, which are not of obstetric significance.
Criteria for diagnosis of APA
Antiphospholipid syndrome
antibody syndrome The international consensus revised (Sapporo)
criteria, 2006, for the diagnosis of APA syndrome
Antiphospholipid antibody syndrome is defined are given in Box 54.1.
as the presence of antiphospholipid antibodies
along with thrombotic or obstetric events. It is • One clinical criterion and one lab criterion
of two types: must be present for the diagnosis of APA
syndrome
• Primary APA syndrome: There is no underlying • The significance of the presence of antibod-
connective tissue disorder. ies to prothrombin, annexin V, phosphatidyl
• Secondary APA syndrome: Occurs in associa- serine, and phosphatidyl inositol is unclear,
tion with a connective tissue disorder such as hence these antibodies are not included in the
systemic lupus erythematosus (SLE). definition.
Antiphospholipid antibodies
Antiphospholipid antibodies are antibodies Box 54.1 Antiphospholipid antibodies
syndrome Sapporo criteria (2006)
against the cell membrane phospholipids or their
binding proteins. These phospholipids are • Clinical criteria
expressed on the cell membrane of the endothe- Ŧ Occurrence of arterial/venous/small vessel thrombo-
lial cells and have antithrombotic and anticoagu- sis, with unequivocal imaging or histologic evidence
of thrombosis
lant action, serving to prevent coagulation within
In any tissue or organ, excluding superficial
blood vessels. Antibodies against these cause venous thrombosis
slow and progressive thrombosis. These antibod- Ŧ Pregnancy morbidity
ies are present most often in women with SLE or 1PG QT OQTG WPGZRNCKPGF HGVCN FGCVJU Ů
other connective tissue disorders but can also be weeks’ gestation with normal fetal morphology
present in 2%–5% of normal women. The anti- by prenatal ultrasound examination or direct
bodies may be immunoglobulin G (IgG), immu- postnatal examination
Ů WPGZRNCKPGF EQPUGEWVKXG URQPVCPGQWU
noglobulin M (IgM), or immunoglobulin A (IgA).
pregnancy losses of <10 weeks’ gestation, after
The antiphospolipid antibodies are as follows: exclusion of maternal anatomic and hormonal
abnormalities and paternal and maternal chro-
• Anti-E-2 glycoprotein1 antibody
mosomal abnormalities
• Lupus anticoagulant (LA) ŮRTGVGTOFGNKXGTKGUQHCOQTRJQNQIKECNN[PQTOCN
• Anti-cardiolipin antibody (ACA) infant before 34 weeks’ gestation due to severe
• Antibodies to phosphatidyl serine and phos- preeclampsia, eclampsia, or features consistent
phatidyl inositol with placental insufficiency
• Antibody to prothrombin • Laboratory criteria– should be present on 2 occasions
at least 12 weeks apart
• Antibody to annexin V
Ŧ Lupus anticoagulant
All antiphospholipid antibodies are not incrim- Ŧ Anticardiolipin antibody IgG or IgM, medium or high
inated in the causation of APA syndrome. titer
These antibodies are present in a small pro- Ŧ Anti-E-2 glycoprotein1 antibody IgG or IgM, medium
or high titer
portion of normal women, but all women with
such circulating antibodies do not develop APA g immunoglobin G, g immunoglobin M.
CH 54_p815-826_v3.indd 816 19-07-2015 01:20:19

Thromboembolic Disorders 817
• Generally accepted features of placental insuf-

Box 54.2 bstetric complications of antiphos-
ficiency include pholipid antibody syndrome
– abnormal or nonreassuring fetal surveil-
lance test • Recurrent pregnancy loss (3 or more) <10 weeks
• Pregnancy loss >10 weeks
– abnormal umbilical Doppler flow velocime-
• Pregnancy loss before 34 weeks due to
try waveform analysis
Ŧ early onset preeclampsia
– oligohydramnios Ŧ placental abruption
– birth weight less than the 10th percentile for Ŧ fetal growth restriction
the gestational age Ŧ intrauterine fetal death
Pathogenesis
The antiphospholipid antibodies act by be repeated 12 weeks later. If the second test is
positive, the diagnosis is confirmed. When the
• procoagulant action on protein C, annexin V, second test is negative and the index of suspi-
platelets, proteases, tissue factor, and impaired cion is high, a third test may be done after a few
fibrinolysis, increasing the risk of vascular weeks.
thrombosis; In women with APA syndrome, both anti-car-
• increasing vascular tone with resultant diolipin antibody (ACA) and lupus anticoagulant
increased risk of atherosclerosis, fetal neuro- (LA) may be positive in 85%; only one antibody
logical damage, and fetal loss due to involve- may be present in 15%. In 11% of women, only
ment of placental vessels; and anti-E-2 glycoprotein antibody is positive.
• increasing trophoblastic apoptosis and decreas- Hence, all three antibodies should be tested. The
ing trophoblastic fusion and invasion, leading tests are listed in Box 54.3.
to poor placentation. Anticardiolipin antibodies are detected using
enzyme-linked immunosorbent assay (ELISA)
Pathology and reported as GPL or MPL units for IgG and
IgM, respectively.
The pathological changes include thrombosis of
placental vessels with perivascular inflammation,
placental infarcts, and hypovascular villi. These
changes lead to poor placental perfusion, resulting Box 54.3 Diagnostic tests for antiphospholipid
in preeclampsia, pregnancy loss and placental antibody syndrome
abruption. • Anticardiolipin antibody
Ŧ Tested using ELISA
bstetric complications in APA Ŧ Positive if
IgM and IgG antibodies >40 units MPL or GPL
syndrome • Lupus anticoagulant
Obstetric complications in antiphospholipid APA Ŧ /QTGURGEKſEDWVNGUUUGPUKVKXG
syndrome are listed in Box 54.2. In addition, Ŧ Coagulation tests used
aPTT
women with APA syndrome are also prone to
dRVVT
development of thromboembolism during preg-
Kaolin clotting time
nancy and puerperium. • Anti-E-2 glycoprotein 1
Ŧ Most common antiphospholipid antibody
Diagnosis Ŧ Tested using ELISA
Ŧ Positive if
Antiphospholipid antibody syndrome is IgM and IgG antibodies
suspected when there is a history of thrombo- >99th percentile for the lab
embolism, known obstetric complications of • If any test is positive, the test should be repeated 12
APA syndrome, a history of systemic lupus ery- weeks later
thematosus (SLE), or other connective tissue dis-
aP activated partial thromboplastin time; d dilute Russell
orders. In women with a suggestive history, labo- viper venom time; SA enzyme-linked immunosorbent assay;
ratory tests are indicated. A positive test should g immunoglobulin G; g immunoglobulin M.
CH 54_p815-826_v3.indd 817 19-07-2015 01:20:19

Lupus anticoagulant is a misnomer; it is a pro- administered in prophylactic dose, as UFH or

coagulant and not an anticoagulant. It is measured LMWH. The advantages of LMWH are discussed
indirectly using activated partial thromboplastin later in the section Therapeutic anticoagulation.
time (aPTT). Dilute Russell viper venom time
(dRVVT) and kaolin clotting time (KCT) can also be nfractionated heparin
used, but aPTT is the primary test. A significantly Unfractionated heparin is administered as sub-
prolonged aPTT that is not corrected by the addi- cutaneous injection, 5000 units twice daily, to
tion of normal plasma indicates the presence of prevent thrombosis. It does not cross the pla-
LA. centa. Monitoring of aPTT and platelet count is
Anti-E-2 glycoprotein1 is also detected using not required when administered in this prophy-
ELISA and reported as SGU and SMU for IgG and lactic dose.
IgM antibodies, respectively.
Low-molecular-weight heparin
Management Low-molecular-weight heparin is given as a

once-daily dose (dalteparin 5000 units or enoxa-
oals o management parin 40 mg). It is more expensive but more
The goals of management are as follows: convenient.
In women who have had a history of venous
• To minimize maternal and perinatal risks and thromboembolism, heparin or warfarin must be
improve pregnancy outcome continued till 6 weeks postpartum. In women
• To prevent another thrombotic episode in a who have received anticoagulation for miscar-
woman with a history of thrombosis riage or pregnancy loss, the anticoagulation may
Preconceptional counseling is essential. Low- be stopped after delivery.
dose aspirin should be started in the preconcep-
tional period along with folic acid.
Obstetric management
e ical management Obstetric management consists of monitoring
the mother and fetus for complications and
Medical management includes
deciding the appropriate timing of delivery.
• low-dose aspirin
• Early ultrasonography is performed to estab-
• heparin
lish gestational age.
– unfractionated heparin (UFH)
• Blood pressure and urine protein are closely
– low-molecular-weight heparin (LMWH)
monitored.
Low-dose aspirin
• Ultrasonography should be performed at
18–20 weeks for morphology. Serial scans are
Low-dose aspirin has an antiplatelet effect and repeated once in 2–4 weeks from 28 gesta-
stimulates normal growth of trophoblasts. It is tional weeks to monitor fetal growth.
usually started as soon as pregnancy is confirmed. • Biophysical profile and Doppler flow veloci-
Currently, most investigators recommend start- metry of the umbilical artery and middle cer-
ing it preconceptionally since it has beneficial ebral artery are performed in the presence of
effects on implantation as well. Low-dose aspirin fetal growth restriction.
alone, at the dose of 75 mg daily, improves preg- • Planned delivery is recommended. In pregnan-
nancy outcome in 42%–80% of women. Aspirin cies with fetal or maternal compromise, deliv-
should be discontinued at 36 weeks. ery is planned at or after 34 weeks, ensuring
fetal maturity. If there is no maternal or fetal
eparin compromise, delivery is usually at 38 weeks.
A combination of heparin and aspirin improves • Heparin should be stopped 12 hours prior to
pregnancy outcome by 80%. The medications planned delivery and restarted 6 hours after
should be started as soon as fetal cardiac activity delivery. Low dose aspirin is stopped at 36
is confirmed on ultrasound scan. Heparin is weeks or 1 week prior to planned delivery.
CH 54_p815-826_v3.indd 818 19-07-2015 01:20:19

• Postpartum, if anticoagulation is indicated,

Box 54.5 isk grouping of inherited
changeover to warfarin is more conveni- thrombophilias
ent because of the oral route of administra-
tion. This should be continued for 6 weeks in • High risk group
Ŧ FVL/PGM homozygous
women with a history of thrombosis in the pre-
Ŧ #PVKVJTQODKP+++FGſEKGPE[
sent pregnancy, and for 6 months in women
Ŧ Compound heterozygous
with past and family history of thrombosis. • Low risk group
Ŧ FVL/PGM heterozygous
Ŧ 2TQVGKP%RTQVGKP5FGſEKGPE[
Ŧ Hyper-homocysteinemia
Inherited thrombophilias
factor V Leiden; P prothrombin gene (G20210A)
in pregnancy mutation.
Inherited thrombophilias are a group of disor-

ders that are genetically inherited and associated Box 54.6 Adverse pregnancy outcomes
with a risk of arterial or venous thrombosis. In in inherited thrombophilias
addition, they have been implicated in adverse • Recurrent miscarriage
pregnancy outcomes. They are uncommon in the • Stillbirth
Asian population. • Preeclampsia
%NCUUKſECVKQP
Inherited thrombophilias are broadly classified
evidence, testing for thrombophilias is not rec-
into two groups as given in Box 54.4.
ommended in women with these outcomes.
The mere presence of a carrier state of throm-
bophilia does not increase the risk of thrombo-
sis. Thrombosis generally occurs when other Screening for thrombophilias
associated risk factors (second hit) such as The recommendations regarding screening for
immobilization, obesity, and infection are thrombophilias include the following:
present.
Based on the risk of thromboembolism, inher- • Routine screening for all pregnant women is
ited thrombophilias are also classified into high not indicated due to the low prevalence of the
risk and low risk groups as given in Box 54.5. condition.
• There is insufficient evidence to support
screening for thrombophilias in women with
Adverse pregnancy outcomes recurrent pregnancy loss, preeclampsia, or any
Inherited thrombophilias have been implicated other adverse pregnancy outcome.
in the poor pregnancy outcomes outlined in • Indication for screening includes women with
Box 54.6. a first-degree relative with high risk throm-
However, the association between adverse bophilia or women with a history of venous
pregnancy outcomes and inherited throm- thromboembolism in the nonpregnant state.
bophilias is not consistent. Since there is no clear
Diagnosis
Box 54.4 Inherited thrombophilias The tests recommended for diagnosis are as
• &GſEKGPE[QHCPVKEQCIWNCPVU
follows:
Ŧ #PVKVJTQODKPFGſEKGPE[ • Genotyping for factor V Leiden
Ŧ 2TQVGKP%CPFRTQVGKP5FGſEKGPE[ • Antithrombin–heparin cofactor assay
Ŧ Hyperhomocysteinemia • Functional assay for protein C and protein S
• Gene mutations of procoagulant factors
• Polymerase chain reaction (PCR) for pro-
Ŧ Factor V Leiden (FVL) mutations
thrombin gene mutation
Ŧ Prothrombin gene (G20210A) mutation (PGM)
• Fasting plasma homocysteine levels
CH 54_p815-826_v3.indd 819 19-07-2015 01:20:20

Management Box 54.7 isk factors for thromboembolism

in pregnancy
Women with a diagnosis of thrombophilia
should have preconception counseling regard- • 5RGEKſEVQRTGIPCPE[
ing the risk of thrombosis. If there is a history Ŧ Hypercoagulable state
of thromboembolism in association with high- Ŧ Venous stasis
risk thrombophilia, antepartum and intrapar- Ŧ Endothelial injury
tum prophylactic anticoagulation is required.
Ŧ Cesarean delivery
The presence of additional risk factors for
• 0QVURGEKſEVQRTGIPCPE[
thromboembolism (given later in this chapter) Ŧ Obesity (BMI >30 kg/m2)
and the severity of thrombophilia should be Ŧ Maternal age >35 years
taken into account before anticoagulation is Ŧ Severe proteinuria
decided upon. Dosage of prophylactic UFH Ŧ Prolonged bed rest
and LMWH is as described earlier for APA Ŧ Antiphospholipid syndrome
syndrome. Ŧ Inherited thrombophilias
Ŧ Anemia
Ŧ Hemorrhage
Ŧ Genetic factors
Thromboembolic B body mass index.
disorders in pregnancy
Clinical features
Deep vein thrombosis
Deep vein thrombosis usually occurs in the lower
Venous thrombosis and pulmonary embolism limbs and ileofemoral veins. It involves the left
occur in 1/1000 pregnancies. Venous thrombosis leg in 90% of cases. The woman usually presents
is more common antepartum, and pulmonary with a sudden onset of unilateral painful pale
embolism is more frequent in the postpartum swelling of the entire lower limb (phlegmasia
period. alba dolens). Reflex arterial spasm leads to a cold
lower limb with reduced arterial pulsations. Calf
muscle tenderness and Homan’s sign (patient
isk factors
winces due to calf muscle pain when the foot is
4KUMHCEVQTUURGEKſEVQRTGIPCPE[ dorsiflexed) can be elicited.
Risk factors specific to pregnancy (Box 54.7) are The major complication of DVT is the occur-
as follows: rence of pulmonary embolism, which may be a
life-threatening event.
• Hypercoagulability or prothrombotic state of
pregnancy which is due to Diagnosis
– increase in fibrinogen and factors VI, VIII,
IX, X, and XII Clinical diagnosis is difficult; therefore, further
– decrease in anticoagulant factors protein C evaluation is essential. The tests used for the
and protein S diagnosis of DVT are listed in Box 54.8.
– increase in plasminogen activator inhibitors Duplex ultrasound is considered to be the
• Venous stasis in the lower limbs due to the primary noninvasive diagnostic method for DVT.
pressure on the pelvic vessels and vena cava It combines compression ultrasonography with
by gravid uterus
• Endothelial injury Box 54.8 Tests used for the diagnosis of deep
vein thrombosis
4KUMHCEVQTUPQVURGEKſE • Duplex ultrasonography/compression ultrasonography
VQRTGIPCPE[ • Magnetic resonance venography
• Ascending contrast venography
Risk factors not specific to pregnancy are listed
• D-dimer assay
in Box 54.7.
CH 54_p815-826_v3.indd 820 19-07-2015 01:20:20

Doppler waveform analysis. It is most often used sensitive since D-dimer levels are elevated in
for calf and iliac veins. normal pregnancy, preeclampsia, multifetal
Compression ultrasonography (CUS) is a pregnancy, and placental abruption. High levels
good screening test for DVT. It is highly sensitive of >500 ng/mL may be indicative of thrombosis.
and specific for femoral vein thrombosis. The The algorithm used for the diagnosis of DVT is
ultrasound transducer is placed over the femoral given in Figure 54.1.
vein, beginning at the inguinal ligament and
moving down the leg to the superficial and deep Management
veins. Noncompressibility of the venous lumen
and echogenic material in the lumen are diag- Management consists of bed rest and therapeutic
nostic of thrombus. anticoagulation, which is discussed later in this
MR venography is not used during pregnancy chapter. Once the symptoms are better, the patient
but is useful in the puerperium. Pelvic veins can may be ambulated. Elastic compression stockings
be assessed better with this. should be used and continued for 1–2 years. Edema
D-dimer assays are useful in nonpregnant of the affected leg, venous ulcers, and persistent
women, but during pregnancy, the test is not pain are common postthrombotic complications.
Clinical suspicion
of thrombosis
uple ultrasoun
or compression
ultrasonography
Positi e egati e
High in e of Lo in e of
nticoagulation suspicion of pel ic suspicion of pel ic
ein thrombosis ein thrombosis
mpiric o empiric
anticoagulation anticoagulation
M enography
erial uple
scans
Positi e egati e
reatment o treatment
Figure 54.1 Diagnosis of deep vein thrombosis in pregnancy.
CH 54_p815-826_v3.indd 821 19-07-2015 01:20:20

Pulmonary embolism Box 54.9 Diagnosis of pulmonary embolism

Pulmonary embolism can occur during preg- • 0QPURGEKſEVGUVU
nancy or the puerperium but is uncommon in Ŧ Chest X-ray
the absence of DVT. However, 30%–60% of Ŧ ECG
women with DVT can have silent pulmonary Ŧ Arterial blood gases
embolism. Ŧ Echocardiography
• 5RGEKſEFKCIPQUVKEVGUVU
Ŧ Ventilation–perfusion scans
Clinical features Ŧ Computerized tomographic pulmonary angiography
Ŧ Magnetic resonance pulmonary angiography
The usual presentation is unexplained tachycar- Ŧ Pulmonary angiography
dia, dyspnea, and hypoxemia. Pleuritic pain and • Evaluation of lower limbs for deep vein thrombosis
hemoptysis may ensue, and when pulmonary Ŧ Duplex/Compression ultrasonography
embolism is massive, there is sudden severe
hypotension.
plasminogen activators has been used in severe

Diagnosis
massive pulmonary embolism but not recom-
Readily available tests such as chest X-ray and mended as a routine.
ECG are not sensitive tests for the diagnosis of
pulmonary embolism. There are no radio-
graphic findings specific for this condition, Anticoagulation
although wedge-shaped pleural-base opacities,
blunting of the costophrenic angle due to pleu- in pregnancy
ral reaction, and elevated hemidiaphragm due
to the loss of lung volume may be suggestive. Anticoagulation in pregnancy may be (a) pro-
Similarly, ECG changes characteristic of acute phylactic, to prevent thromboembolism in high-
cor pulmonale are seen in only 25% of patients. risk women and those on prosthetic valves and
Moreover, pregnancy-associated changes in also for the management of APA or (b) therapeu-
ECG may increase false-positive results. tic, for treatment of DVT or pulmonary
However, these tests can be used to exclude other embolism.
conditions that can present with similar symp-
toms such as acute pulmonary edema.
Furthermore, they may aid decision making
Therapeutic anticoagulation
regarding the need and urgency of other more Therapeutic anticoagulation is required in
sensitive and specific secondary diagnostic tests women with established DVT or pulmonary
to diagnose pulmonary embolism (Box 54.9). embolism. Unfractionated heparin or LMWH
Ventilation–perfusion scan and computer- may be used in weight-adjusted doses.
ized tomographic pulmonary angiography are
the specific tests used for the diagnosis of pul-
monary embolism. The evaluation of the lower
Low-molecular-weight heparin
limbs by Duplex scan/ CUS for evidence of DVT Low-molecular-weight heparin is preferred to
is mandatory whenever pulmonary embolism is UFH because it has several advantages as listed
suspected. in Box 54.10. However, the cost of therapy is
higher with LMWH and so UFH is still used in
resource-poor settings. Low-molecular-weight
Management
heparin is administered without laboratory
Therapeutic anticoagulation should be started monitoring, since no laboratory assessment of
immediately when the diagnosis is confirmed. the anticoagulant effect is consistent with clini-
Venacaval filters are used in cases of recurrent cal endpoints. Anti–factor Xa levels must main-
pulmonary embolism arising from the pelvis or tained at 0.5-1 IU/mL. However, routine moni-
lower limbs. Thrombolytic therapy with tissue toring of Anti Xa levels is not recommended.
CH 54_p815-826_v3.indd 822 19-07-2015 01:20:20

Box 54.10 Therapeutic use of low- Intrapartum management

molecular-weight heparin Delivery should be a planned event in a woman
• Indications on therapeutic anticoagulation. Anticoagulants
Ŧ Established DVT/pulmonary embolism should be stopped 24–36 hours before planned
• Drug of choice because of delivery or cesarean section. This reduces the
Ŧ better bioavailability risk of maternal bleeding and hematoma forma-
Ŧ longer plasma half-life tion with epidural or spinal anesthesia. Regional
Ŧ predictable dose response
anesthesia should not be administered within 24
Ŧ more reduction in thrombus size
hours of the last therapeutic dose of either UFH
Ŧ lower risk of major bleeding
Ŧ lower incidence of recurrent thromboembolism
or LMWH.
Ŧ low risk of osteoporosis
Ŧ low risk of thrombocytopenia Postpartum anticoagulation
Ŧ less frequent dosing
Therepeutic anticoagulation should be contin-
• No laboratory monitoring
• Must be switched to UFH at 36 weeks
ued for 6 months postpartum. Low-molecular-
weight heparin is started 6 hours after vaginal
D deep vein thrombosis; , unfractionated heparin.
delivery or 12 hours after a cesarean section along
The effect of LMWH cannot be completely with warfarin 5 mg daily. Dosage of LMWH is grad-
reversed with protamine sulfate; hence, it is pru- ually reduced and replaced by warfarin to main-
dent to switch to UFH at 36 weeks. tain international normalized ratio (INR) at 2–3.
nfractionated heparin
Thromboprophylaxis
Unfractionated heparin is indicated for imme-
diate treatment of pulmonary embolism or
in pregnancy and the
when anticoagulation is required when imme- postpartum period
diate delivery or a cesarean section is antici-
Thromboembolism in pregnancy and the
pated. Initial administration is by intravenous
puerperium can be minimized by prophylactic
route, monitored by aPTT levels. aPTT should
anticoagulation and nonpharmacological meth-
be maintained at 1.5–2.5 times the control val-
ods like compression stocking. However, use of
ues. After 7–10 days, subcutaneous 12-hourly
anticoagulants has complications. Hence, it
doses should be used. The effects of UFH can be
should be administered only when there are
reversed with protamine sulfate when required
indications and adherence to guidelines is
(Box 54.11).
Dosage of LMW and F Box 54.12 Therapeutic doses of LMW

and F
Therapeutic, weight-adjusted doses of LMWH
and UFH are given in Box 54.12. Drug Dosage oute
Box 54.11 Therapeutic use of unfractionated • Enoxaparin 1 mg/kg, 12 hourly SC

heparin • Dalteparin 200 units/kg once daily SC
(or) 100 units/kg 12 hourly SC
• Indications
Ŧ Immediate treatment of pulmonary embolism • Tinzaparin 175 units/kg once daily SC
Ŧ When delivery/cesarean section anticipated 70–100 units/kg
Ŧ After 36 weeks in all women on therapeutic anti- (5000–10,000 units) IV bolus
coagulation 15–20 units/kg
• Initially administered as IV (1000 units)/hour Infusion
• Switch to subcutaneous 12 hourly after 7–10 days Followed 7–10 days later
• Monitored with aPTT by 10,000 units 12 hourly SC
Ŧ 1.5–2.5 times control values
• Can be reversed with protamine sulfate low-molecular-weight heparin; , unfractionated
heparin.
CH 54_p815-826_v3.indd 823 19-07-2015 01:20:20

essential. Women are categorized into high, • Antenatal anticoagulation, continued post-
intermediate, and low risk based on factors listed natally for 6 weeks to 6 months, is recom-
in Box 54.13. mended for all high risk, intermediate risk,
and low risk women with >4 risk factors.
• All pregnant women should undergo risk
Those with 3 or less risk factors may be given
assessment prepregnancy or early in preg-
postnatal thromboprophylaxis.
nancy, when they are hospitalized and
• Cesarean section alone in the absence of
postpartum.
associated risk factors is not an indication for
thromboprophylaxis. It should be given only if
Box 54.13 isk categori ation for an associated risk factor is present.
thromboembolism in pregnancy
High risk • Any previous VTE except a
single event related to major
Dosage of anticoagulants
surgery for thromboprophylaxis
• High risk thrombophilia + VTE
Low-molecular-weight heparin is preferred to
Intermediate • Hospital admission UFH. The dosage has been described earlier.
risk • Single previous VTE related to
major surgery
• High risk thrombophilia + no VTE
• Medical comorbidities like sickle Cerebral venous
cell disease, nephrotic
syndrome, SLE or heart failure thrombosis
Low risk • Obesity (BMI >30 kg/m2) Cerebral venous thrombosis sometimes occurs
• Age >35 in the puerperium. There is thrombosis of the
Ŗ 2CTKV[Ů superior sagittal sinus due to thrombophilia.
• Gross varicose veins The patient complains of severe headache and
• Immobilization may have seizures. The condition must be dif-
• Family history of unprovoked or ferentiated from postpartum eclampsia. Fundus
estrogen-provoked VTE in
examination shows papilledema due to raised
ſTUVFGITGGTGNCVKXG
intracranial pressure, and physical examination
• Low risk thrombophilia
may reveal mild weakness of the lower limbs
• Multiple pregnancy
(paraparesis) or weakness of one half of the
• Preeclampsia
body (hemiparesis). There may be urinary reten-
Transient risk • Dehydration/hyperemesis
tion. The diagnosis is confirmed by MR venogra-
factors • Current systemic infection
phy, and treatment is with anticonvulsants and
• Long-distance travel anticoagulation.
B , body mass index; VTE, venous thromboembolism.
Key points
• &GſEKGPE[QHVJGRTQVGKPUVJCVKPJKDKVEQCIWNCVKQPKU • The three important antiphospholipid antibodies are
known as thrombophilia. This may be acquired or lupus anticoagulant, anticardiolipin antibody, and
congenital. anti-E-2 glycoprotein antibodies. Antiphospholipid
• The most common acquired thrombophilia is antiphos- antibody syndrome is the presence of these antibodies
pholipid antibody (APA) syndrome. This is associated along with thrombotic events or pregnancy morbidity.
with several obstetric complications, including miscar- • Diagnosis of APA is by history of thromboembolism or
riage, placental abruption, preeclampsia, and fetal a characteristic obstetric event and presence of one of
growth restriction. the antibodies on two occasions, 12 weeks apart.
(Continued)
CH 54_p815-826_v3.indd 824 19-07-2015 01:20:20


• Medical management is with low-dose aspirin and endothelial injury, and other risk factors such as
heparin, either unfractionated or low-molecular-weight obesity, prolonged bed rest, APA syndrome, cesarean
heparin. Aspirin should be discontinued at 36 weeks section, and genetic factors.
and heparin 12 hours before delivery. • Deep vein thrombosis in pregnancy involves the left
• Obstetric management consists of close monitoring leg in 90% of cases. Pain, tenderness in calf muscles,
of blood pressure, fetal growth, and fetal well-being and positive Homan’s sign are the typical clinical fea-
by serial ultrasonography and planned delivery at 38 tures. Screening is by compression ultrasonography
weeks. Maternal or fetal complications may indicate
%75CPFEQPſTOCVKQPKUD[&WRNGZWNVTCUQPQITCRJ[
earlier delivery. although other tests are available.
• Women on prophylactic anticoagulation for recur- • Management is with bed rest, therapeutic anticoagula-
rent pregnancy loss or pregnancy loss do not require tion, and gradual ambulation.
postpartum anticoagulation. • Pulmonary embolism usually occurs following DVT.
• Postpartum anticoagulation with warfarin should be Clinical symptoms are dyspnea, hypoxemia, and
continued for 6 weeks in those without thrombotic tachycardia.
event and for 6 months in those with thrombotic event.
• Diagnosis is by computerized tomographic pulmonary
• +PJGTKVGFVJTQODQRJKNKCUCTGENCUUKſGFCUJKIJTKUM angiography, although other tests are available. Treat-
group and low risk group, based on the risk of throm- ment is by therapeutic anticoagulation.
boembolism. • Low-molecular-weight heparin is the drug of choice for
• Pregnancy complications in inherited thrombophilias therapeutic and prophylactic anticoagulation in preg-
are recurrent miscarriage, stillbirth, preeclampsia, fetal nancy. It has the advantages that it does not cross the
growth restriction, and placental abruption. placenta and has a longer half-life, better bioavail-
ability, low risk of thrombocytopenia and osteoporosis,
• Routine screening for inherited thrombophilia or
and predictable dose response.
screening in women with obstetric problems is not
recommended except in those with a positive family • Unfractionated heparin is used only for immediate
history of high risk thrombophilia or a thrombotic event treatment of pulmonary embolism and when delivery
in the nonpregnant state. or a cesarean section is imminent.
• Management is with anticoagulation during the antepar- • Thromboprophylaxis is indicated in women with pro-
tum and postpartum periods depending on the history of longed immobilization, APA syndrome, and inherited
thromboembolism and associated risk factors. thrombophilias. It is also indicated in women undergo-
ing a cesarean section when additional risk factors are
• Deep vein thrombosis (DVT) occurs in pregnancy
present.
due to the hypercoagulability of blood, venous stasis,
Self-Assessment
Mrs. KT, 30, was 24 weeks’ pregnant. Her body mass
Case 1 index was 38 and her hemoglobin was 8 g/dL. She com-
Mrs. GN, 26, came for a consultation with her husband plained of acute pain in the left lower limb with swelling
to the clinic. She had been married for 6 years, had three over the calf muscles. She was brought to the hospital.
OKUECTTKCIGUōVYQ KP VJG ſTUV VTKOGUVGT CPF QPG KP VJG 1. What is the diagnosis likely to be?
second—and one stillbirth in a pregnancy complicated by
2. What are the risk factors for this condition?
high blood pressure.
1. What conditions can give rise to the obstetric compli- 4. How will you manage the complication?
cations in this woman?
2. What important details would you like to know in
history?
3. What investigations will you do?
4. How will you manage her next pregnancy?
CH 54_p815-826_v3.indd 825 19-07-2015 01:20:20

inherited thrombophilias, cesarean section, and

Answers maternal age >35 years.
3. History of calf muscle pain, tenderness, edema,
Case 1 and Homan’s sign.
1. Acquired and inherited thrombophilias. Compression ultrasonography and Duplex scan.
2. Past and family history of thromboembolism, fetal 4. Bed rest till swelling subsides and therapeutic
weight, history of the live abortus or dead fetus, anticoagulation with LMWH (enoxaparin) 1 mg/kg
severity of hypertension, and proteinuria. 12-hourly SC throughout pregnancy. Ambulation
3. If there is no past or family history of thromboembo- after symptoms subside and elastic bandage or
lism, LA, ACA, and anti-E-2 glycoprotein 1. pressure stockings. Planned delivery at 38 weeks,
If a family history of thrombophilia, or past history and discontinue LMWH 24 hours prior to induction.
or family history of thromboembolism is present, Restart warfarin and LMWH postpartum and gradu-
thrombophilia workup should be done. ally switch to warfarin.
4. If she is positive for APA, aspirin 75 mg when preg-
PCPE[KUEQPſTOGF7(*QT./9*
GPQZCRCTKP
OI5%FCKN[YJGPECTFKCECEVKXKV[KUEQPſTOGF Sample questions
The following is recommended:
• Close monitoring of blood pressure and fetal Long-answer question
growth.
1. What is antiphospholipid antibody syndrome?
• Serial ultrasound scans for fetal growth and Discuss the clinical presentation, diagnosis, and
well-being. management of pregnancy in a third gravida with
If pregnancy progresses with no complications, two previous miscarriages and antiphospholipid
deliver at 38 weeks. Stop aspirin at 36 weeks and syndrome.
LMWH 12 hours prior to delivery.
Case 2 1. Inherited thrombophilias
1. Deep vein thrombosis. 2. Prophylactic anticoagulation
2. Pregnancy, obesity, prolonged immobilization, ane- 3. Pulmonary embolism in pregnancy
mia, multifetal pregnancy, antiphospholipid positive, 4. Deep vein thrombosis in pregnancy
CH 54_p815-826_v3.indd 826 19-07-2015 01:20:20

Urinary Tract and
55 Renal Disorders
Case scenarios
Mrs. JP, 29, was in her sixth month of pregnancy. She gave a history of
dysuria for 2 days. She presented with fever, chills, and severe flank pain.
Mrs. BN, 24, was pregnant with her first pregnancy. She developed
hypertension at 32 weeks, and this progressed rapidly to preeclamp-
sia. She had abruption at 35 weeks. She developed severe hypovolemic
shock. In spite of adequate volume replacement, she developed oliguria.
She was transferred to a tertiary center for further care.
Introduction In the presence of preexisting kidney disease,

the effect of the kidney disease on the pregnancy
Pregnant women commonly face renal and as well as the effect of pregnancy on the kidney
urinary tract disorders. Anatomical and physio- disease has to be taken into consideration to
logical changes that occur in pregnancy predis- properly manage the pregnancy.
pose women to development of these problems Certain complications of pregnancy can result
and sometimes to rapid worsening of disease. in acute renal injury and lead to renal failure. Being
Some conditions (e.g., nephrolithiasis) may be aware of these complications and taking early pre-
preexisting and may be uncovered in pregnancy. ventive steps can help avert acute renal injury.
Some renal conditions (e.g., preeclampsia) are
unique to pregnancy.
Understanding the physiological changes that
rinary tract changes
occur in a normal pregnancy helps in the proper due to pregnancy
interpretation of common laboratory and diag-
nostic studies when evaluating renal disease in Pregnancy affects both the kidney and the rest
women during pregnancy. of the urinary tract. Increase in renal blood flow
CH 55_p827-841_v3.indd 827 19-07-2015 01:21:05

and glomerular filtration rate (GFR) and dil-

atation of the renal pelvis and ureters are the
&GſPKVKQPU
most significant changes. These changes have Asymptomatic bacteriuria
been discussed in greater detail in Chapter
3, Maternal physiology in pregnancy. These Asymptomatic bacteriuria is commonly defined
changes have an impact on renal and urinary as the presence of more than 100,000 organ-
tract disorders. isms/mL in two consecutive urine samples in an
asymptomatic woman. Untreated ASB is a risk
factor for acute cystitis (40%) and pyelonephritis
(25%–30%) in pregnancy (Box 55.2). Its associa-
tion with maternal complications such as preterm
rinary tract disorders birth or low birth weight is unproven.
The most common urinary tract disorder in Acute cystitis

pregnancy is urinary tract infection (UTI).
Acute cystitis is symptomatic infection of the
lower urinary tract. There is inflammation of
the bladder mucosa as a result of bacterial infec-
rinary tract infection tion. Acute cystitis develops in approximately
1% of pregnant patients. It may progress to
in pregnancy pyelonephritis in 15%–50% of cases.
Urinary tract infections are among the most Acute pyelonephritis

common bacterial infections occurring in
Acute pyelonephritis is an infection of the upper
pregnancy.
urinary tract and kidneys. Pyelonephritis is the
Hormonal and mechanical changes of preg-
most common serious medical complication in
nancy increase urinary stasis and vesicoureteral
pregnant women, occurring in approximately 2%
reflux, thus predisposing to the occurrence of
of all pregnancies. Acute pyelonephritis is char-
UTI. The other important contributing factor is
acterized by fever, flank pain, and tenderness
the short urethra in women, making it easier for
in addition to significant bacteriuria. It occurs
bacteria to gain access (Box 55.1).
most often in the second trimester and is more
Vaginal infections can cause or mimic UTIs.
common in young primigravidas (Box 55.3).
Differentiating between the two depends on
a good history, physical examination, and the
Box 55.2 Asymptomatic bacteriuria
results of vaginal and urinary cultures.
UTIs in pregnancy may be one of the • >100,000 colonies/mL in two consecutive samples
following: • Implies persistent actively multiplying bacteria in the
urinary tract
• Asymptomatic bacteriuria (ASB) • Usually single organism
• Symptomatic lower UTI (cystitis) • Found in 2%–7% of pregnancies
• Pyelonephritis • 1HVGPFGXGNQRUKPſTUVVTKOGUVGT
• Risk of progression
Ŧ Cystitis: 40%
Ŧ Pyelonephritis: 25%–30%
Box 55.1 isk factors for TI in pregnancy
• Changes in pregnancy Box 55.3 Characteristics of pyelonephritis
Ŧ Hormonal changes
Ŧ Mechanical changes • 5KIPKſECPVDCEVGTKWTKC
• Lead to • Fever
Ŧ increased urinary stasis • Flank pain
Ŧ KPETGCUGFXGUKEQWTGVGTCNTGƀWZ • Flank tenderness
• Other factors • More common in
Ŧ Short urethra in women Ŧ second trimester
Ŧ young primigravidas
CH 55_p827-841_v3.indd 828 19-07-2015 01:21:05

Urinary Tract and Renal Disorders 829
Pathophysiology of TIs Box 55.6 rganisms causing TI in pregnancy

Infections result from ascending colonization of • scherichia coli
the urinary tract, mainly by existing vaginal, per- • lebsiella pneumoniae
ineal, and fecal flora. • Proteus mirabilis
Maternal physiological and anatomical fac- • nterobacter species
tors predisposing to ascending infection are • Staphylococcus saprophyticus
• Group B E-hemolytic Streptococcus
• Proteus species
atural course of TI
Untreated asymptomatic bacteriuria may lead to Other organisms may also be responsible for
UTI and pyelonephritis. In developed countries, infection, as listed in Box 55.6.
all women are screened for asymptomatic bac- Drug resistance is an alarming problem glob-
teriuria with a urine culture at the first antenatal ally. Infections caused by extended-spectrum
visit. Urine culture may not be cost-effective E-lactamase (ESBL)–producing strains are increas-
in underresourced areas. Therefore, testing for ingly implicated even in uncomplicated UTIs. In
nitrites in urine with a dipstick is an alterna- India, ESBL-producing bacteria are a growing
tive (discussed later in this chapter). All preg- problem, even in pregnant women.
nant women should be screened by one of the
methods.
In most cases of UTI in pregnancy, the prog-
Clinical manifestations of TI
nosis is good and most women will recover with Cystitis
appropriate antibiotic coverage. Untreated UTIs
The symptoms of cystitis (Box 55.7) may be mis-
are associated with risks to both the fetus and
leading in pregnant women who may experience
the mother, as listed in Box 55.5.
frequency, urgency, and suprapubic pressure as
a result of pregnancy itself.
Microbiology of TI
yelonephritis
Escherichia coli is the predominant organism
implicated in 80% of both asymptomatic bacte- In addition to symptoms of cystitis, women with
riuria and UTI in pregnant women. pyelonephritis also present with the symptoms
listed in Box 55.8.
Box 55.4 Physiological and anatomical factors Box 55.7 Symptoms of cystitis
predisposing to ascending infection
• Burning with urination (dysuria)
• Urinary retention caused by Ŧ /QUVUKIPKſECPVU[ORVQO
Ŧ weight of the enlarging uterus • Hematuria
Ŧ urinary stasis due to • Frequency
progesterone-induced ureteral smooth muscle • Urgency
TGNCZCVKQP • Suprapubic pain
• 8GUKEQWTGVGTCNTGƀWZ
• Glycosuria
Box 55.8 Symptoms of pyelonephritis
• Symptoms of cystitis
Box 55.5 Complications of untreated TI • Fever (>38°C)
in pregnancy • Rigors
• Pyelonephritis • %QUVQXGTVGDTCNCPINGƀCPMVGPFGTPGUU
QPCHHGEVGFUKFG
• Preterm birth Ŧ 4KIJVUKFGƀCPMRCKPOQTGEQOOQPVJCPNGHVUKFG
• Fetal growth restriction and low birth weight ƀCPMRCKP
• Increased perinatal mortality • #PQTGZKC
CH 55_p827-841_v3.indd 829 19-07-2015 01:21:05

Of the women with severe pyelonephritis,

Box 55.10 Diagnostic tests for TI
20% will develop complications that include sep- in pregnancy
tic shock syndrome or acute respiratory distress
syndrome (ARDS). It is therefore very important • Urinalysis
Ŧ Macroscopic appearance
to recognize this condition and institute imme-
Ŧ Microscopic analysis
diate treatment. Complications of acute pyelo-
Leukocytes
nephritis are listed in Box 55.9. Red blood cells
Bacteria
Diagnosis of TI • Urine protein
• Dipstick test
Urinalysis and urine culture (with antibiotic sen- Ŧ Leukocyte esterase
sitivity) are important in confirming the diagnosis Ŧ Nitrites
of UTI and pyelonephritis. Although a first morn- • Urine culture and sensitivity
ing specimen of urine is preferred because there urinary tract infection.
is a greater concentration of bacteria, the urine
sample can be collected at any time of the day.
Collecting the urine specimen rinalysis

An optimal clean-catch, midstream urine is col- Appearance
lected by instructing the woman to follow the The urine may appear turbid because of pyuria
following steps (to minimize the degree of con- (presence of leukocytes/pus cells in the urine).
tamination with bacteria from the urethra and
Pyuria or leukocyturia
surrounding area):
The centrifuged specimen is examined for the
• With one hand, spread the labia. presence of leukocytes (pus cells) and the pus
• With the other hand, wash the urethral meatus cells are counted per high-power field (hpf).
with water. True UTI is unusual without pyuria. However,
• Void the initial portion of the bladder contents pyuria can occur without UTI in the following
into the toilet. conditions:
• Catch the middle portion of the bladder con-
tents in the sterile collection container, while • Patients who have already taken antibiotics
keeping the labia spread with the first hand. • Contamination from vaginal secretions
• Other causes of urinary tract inflammation
A catheterized specimen is collected only if
the patient is
est or nitrites
• unable to void,
• too ill or bedridden, Biochemical reagent strips are available to test
• extremely obese. for leukocyte esterase and nitrites in urine. Griess
reagent may also be used for testing for nitrites.
Diagnostic tests for UTI in pregnancy are The presence of leukocytes does not always indi-
listed in Box 55.10. cate bacteriuria; hence, nitrite dipstick test is
more reliable and is used as a rapid test for the
diagnosis of urinary infection. All uropathogens
Box 55.9 Complications of acute pyelonephritis do not reduce nitrates to nitrite. The sensitivity is
30%–40%, but the test has high specificity.
• Bacteremia
Findings that raise suspicion for the presence
• Septic shock syndrome
of UTI are summarized in Table 55.1.
• 'PFQVQZKEUJQEM
• Adult respiratory distress syndrome
• Hemolytic anemia rine culture an antibiotic sensitivity
• Thrombocytopenia
It is mandatory to send the urine for culture and
antibiotic sensitivity prior to starting antibiotic
Ŧ Preterm labor
therapy.
CH 55_p827-841_v3.indd 830 19-07-2015 01:21:05

Symptomatic women with pyuria

Table 55.1 Findings on urinalysis that may
indicate the presence of TI t105 (100,000) cfu/mL is considered significant
and indicative of an infection. Some clinically
Test Finding suggestive of TI symptomatic women with significant pyuria
Clarity Turbid in the presence of pyuria show a lower colony count on urine culture. In
Odor Ammonia odor in infections these women, t104 cfu/mL may also be taken as
with urea-splitting organism significant infection.
(Proteus, lebsiella)
Leukocytes >10/hpf indicates possible UTI Antibiotic sensitivity
(pus cells)/hpf The determination of antibiotic sensitivity and
Leukocyte esterase Positive results indicate resistance is very important. The effect of an
(dipstick test for presence of neutrophils; antibiotic against bacterial growth can be mea-
enzyme present >4 WBCs/hpf, an indicator sured with broth dilution tests or agar diffusion
in WBCs) of UTI
tests. The final result of the test is the minimum
Nitrites (dipstick Positive test indicates that bacte- inhibitory concentration (MIC) of commonly
test—surrogate TKCOC[DGRTGUGPVKPUKIPKſECPV
marker for numbers
used antibiotics. This indicates which antibiotic
bacteriuria) may be used to treat the UTI successfully.
Red blood cells Microscopic hematuria (>5/
hpf) common with urinary tract Management
infection but not in urethritis or
vaginitis Asymptomatic bacteria and cystitis can be treated
Protein/albumin In UTI, usually trace to 1+ as outpatient, while pyelonephritis requires
(dipstick test) hospitalization.
Bacteria Microscopic bacteriuria may
be seen. Five bacteria per hpf Management of asymptomatic
correspond to a colony count of bacteriuria and acute cystitis
105/mL
hpf JKIJRQYGTſGNF urinary tract infection; BCs white Women with UTI are advised to drink plenty of
blood cells. oral fluids.
Urine culture is essential in the evaluation of Asymptomatic bacteriuria

suspected UTI to Women who have been diagnosed as having
• confirm the presence of bacteriuria, asymptomatic bacteriuria can be treated with
• identify the organism, and nitrofurantoin 100 mg at bedtime for 10 days.
• detect the antibiotic sensitivity pattern. Antibiotic therapy for cystitis
Since most symptomatic women receive The following points should be noted about anti-
empirical antibiotic treatment while awaiting biotic therapy for cystitis:
the urine culture reports, the sensitivity pattern
• The majority of infections are by E. coli. Hence,
helps in deciding whether to continue the same
empirical antibiotic therapy is started to treat
antibiotic or switch to another one.
this organism since the culture results take
&GſPKVKQPQHUKIPKſECPVDCEVGTKCN 48 hours to be reported. A rapid dipstick test
may be performed before starting treatment.
count on culture
If required, antibiotics may be changed after
The colony count of the bacteria is important to culture results.
differentiate an actual infection from nonsignifi- • Oral antibiotics are the treatment of choice for
cant contamination of the urine sample. asymptomatic bacteriuria and cystitis.
Asymptomatic women • Treatment with a single dose of antibiotic is
not recommended in pregnancy.
105 colony-forming units per milliliter of urine
(cfu/mL) grown from a clean midstream speci- The common antibiotics used in cystitis are
men is a sign of a clinically significant UTI. listed in Box 55.11.
CH 55_p827-841_v3.indd 831 19-07-2015 01:21:05

– serum creatinine to monitor for acute renal

Box 55.11 Antibiotics used in the treatment
of cystitis in pregnancy injury
– serum electrolytes.
One of the following antibiotics, depending on sensitivity • Antibiotics should be administered.
• Nitrofurantoin monohydrate/macrocrystals
Ŧ 100 mg orally twice daily for 5–7 days Parenteral, broad-spectrum E-lactams are the
• #OQZKEKNNKP preferred antibiotics for initial empirical therapy
Ŧ 500 mg orally twice daily for 5–7 days of pyelonephritis. The commonly used antibi-
• #OQZKEKNNKPŌENCXWNCPCVG otics are third-generation cephalosporins such
Ŧ 500/125 mg orally twice daily for 3–7 days as cefoxitin or ceftriaxone, penicillins, extend-
• %GRJCNGZKP ed-spectrum penicillins, carbapenems, and
Ŧ 500 mg orally twice daily for 3–7 days aminoglycosides.
• %GHWTQZKOG
Most women will show definite improvement
Ŧ 250 mg orally twice daily for 3–7 days
within 24–48 hours of appropriate antibiotic
therapy. Once afebrile for 48 hours, pregnant
women can be switched to oral therapy depend-
Norfloxacin, ciprofloxacin, and co-trimoxazole ing on the culture and sensitivity results. They
should be avoided for the treatment of UTI in can then be treated on an outpatient basis for
pregnancy. 10–14 days. Culture should be repeated after 1
week.
• A follow-up culture is done to confirm sterili-
zation of the urine. A change of antibiotic or Supportive therapy
a longer course is warranted if the culture is Fever should be managed with antipyretics
positive. (preferably acetaminophen) and nausea and
• For women with persistent or recurrent bacte- vomiting with antiemetics.
riuria, prophylactic or suppressive antibiotics The management of pyelonephritis is sum-
may be warranted in addition to retreatment. marized in Box 55.12.
Treatment of dysuria in cystitis
Dysuria can be very distressing. For symptom- Box 55.12 Management of pyelonephritis
atic relief, the woman can be treated with flavox- • Hospitalization
ate or phenazopyridine for 48 hours. • Urine culture and antibiotic sensitivity
• Blood tests
• Flavoxate hydrochloride counteracts smooth
Ŧ Blood culture
muscle spasm of the urinary tract and exerts
Ŧ Hemogram, serum creatinine, electrolytes
its effect directly on the muscle. • Vital signs monitored
• Phenazopyridine exerts local analgesic and Ŧ Urine output
anesthetic effects on the urinary tract. Ŧ Tachypnea (early sign of respiratory distress)
Phenazopyridine causes the passage of orange Chest X-ray to rule out ARDS
colored urine, and the woman should be Ŧ Temperature
warned about it. Antipyretics
• +8ƀWKFU
Ŧ /CKPVCKPWTKPGQWVRWVQHŮO.JQWT
Management of pyelonephritis • IV antibiotics
Management of pyelonephritis consists of the Ŧ Third-generation cephalosporins
following: %GHQZKVKPQTEGHVTKCZQPG
Ŧ Penicillins
• Pyelonephritis should be treated with hospi- Ŧ 'ZVGPFGFURGEVTWORGPKEKNNKPU
talization and intravenous fluids. Ŧ Carbapenems
• Pregnant women should be evaluated with Ŧ Aminoglycosides
further tests. • Change to oral antibiotics when afebrile for 48 hours
• Blood should be drawn for Ŧ Continue for 10 days
– blood culture and sensitivity for bacteremia • 4GRGCVWTKPGEWNVWTGCHVGTYGGMVQEQPſTOEWTG
– hemogram to monitor anemia A DS acute respiratory distress syndrome.
CH 55_p827-841_v3.indd 832 19-07-2015 01:21:05

enal disorders The precipitating factor for ARF is renal isch-

emia. The degree of renal failure depends on the
severity of ischemia.
Acute renal failure (acute • Mild ischemia causes reversible ARF
renal in ury) in pregnancy • More prolonged ischemia leads to acute tubu-
lar necrosis (ATN)
Acute renal failure (ARF) or acute kidney injury • Severe ischemia gives rise to bilateral cortical
(AKI) in pregnancy is characterized by a rapid necrosis.
decrease in the glomerular filtration rate (GFR)
over a matter of minutes or days. It may result The four most common causes of intrare-
from many of the same causes that occur in nal ARF in late pregnancy and the postpartum
nonpregnant women. However, there are spe- period are discussed here.
cific conditions in pregnancy that may precip-
itate ARF.
ARF is suspected in the following conditions:
Severe preeclampsia
Pregnancy complications superimposed on se-
• Oliguria (urine output of <30 mL/hour or <400 vere preeclampsia may precipitate ARF. These
mL/24 hours) complications are as follows:
• Anuria (absent urination)
• Deteriorating renal function as demonstrated • Significant bleeding with hemodynamic
by rising serum creatinine instability
• Marked disseminated intravascular coagula-
Causes of A F unique to tion (DIC)
• HELLP syndrome (hemolysis, elevated liver
pregnancy enzymes, and low platelets)
Acute renal failure is associated with two dis- • Placental abruption that may occur with
tinct periods in pregnancy: the first trimester severe preeclampsia
and the third trimester. Postpartum ARF result-
ing from hemorrhage and sepsis are additional
important causes. Common causes are listed in syn rome
Box 55.13. HELLP is a syndrome characterized by hemo-
lysis, elevated liver enzymes, and low platelet
Box 55.13 Causes of A F in pregnancy count. Although it is associated with severe pre-
eclampsia, 15%–20% of women with HELLP syn-
%CWUGUKPVJGſTUVVTKOGUVGT
drome do not have hypertension or proteinuria.
• Prerenal causes Acute renal failure may occur in up to 40% of
Ŧ Hyperemesis gravidarum
women with the HELLP syndrome. As in severe
Ŧ Hemorrhage
preeclampsia, ARF may be a result of direct
Abortion
Ruptured ectopic pregnancy
renal injury or as a consequence of abruption.
Ŧ Sepsis Although the maternal mortality following ARF
Septic abortion in the HELLP syndrome is low (1%), perinatal
mortality rate is high.
Causes in the third trimester and postpartum period
• Prerenal causes
Ŧ Antepartum hemorrhage (placental abruption) Acute atty liver o pregnancy
Acute fatty liver of pregnancy (AFLP) is associ-
• Intrarenal causes
Ŧ Severe preeclampsia ated with fatty infiltration of hepatocytes without
Ŧ HELLP syndrome inflammation or necrosis. It is associated with
Ŧ Acute fatty liver of pregnancy ARF in up to 60% of cases. There is decreased
Ŧ Thrombotic microangiopathies renal perfusion or ATN. In the early stages, it may
A acute renal failure; P hemolysis, elevated liver en-
be difficult to differentiate AFLP from severe pre-
zymes, and low platelet count. eclampsia and/or HELLP syndrome.
CH 55_p827-841_v3.indd 833 19-07-2015 01:21:05

hrombotic microangiopathies thrombocytopenia (usually severe), microangio-

Thrombotic microangiopathies are a combina- pathic hemolytic anemia, mild renal failure (cre-
tion of thrombocytopenia and microangiopathic atinine <1.4 mg/dL), and neurological symptoms
anemia. They are rare and affect 1 in 25,000 preg- such as disorientation, ataxia, headache, focal
nancies. They are characterized by the presence neurological deficit, seizures, or aphasia. The eti-
of fibrin and/or platelet thrombi in the microcir- ology of TTP has been linked to abnormalities in
culation of multiple organs. It may be difficult to von Willebrand factor protease, otherwise known
differentiate severe preeclampsia from throm- as ADAMTS-13.
botic microangiopathies because of the similar Pregnancy-associated hemolytic uremic syn-
clinical and histological characteristics. A his- drome (HUS) occasionally develops as a compli-
tory of preceding hypertension and proteinuria cation of preeclampsia. The clinical features of
favors a diagnosis of preeclampsia. HUS are similar, but neurological involvement
Thrombotic microangiopathies can be is rare while renal involvement is profound.
divided into two distinct entities depending on Postpartum HUS has a high mortality rate.
which target organ is more affected and the tim- The differentiating features of severe pre-
ing of onset, as given in Box 55.14. eclampsia, HELLP syndrome, AFLP, TTP, and
In actual practice, the distinction may be dif- HUS are listed in Table 55.2.
ficult since the clinical manifestations of these
two conditions may overlap. terine hemorrhage and A F
Thrombotic thrombocytopenic purpura Acute renal failure is especially common in preg-
(TTP) is identified by the presence of fever, nancy complicated by massive hemorrhage and
hypotension/hypovolemia. The causes of massive
hemorrhage leading to ARF are listed in Box 55.15.
Box 55.14 Thrombotic microangiopathies
in pregnancy
Box 55.15 bstetric conditions causing hemo-
• hrombotic thrombocytopenic purpura P
rrhage and acute renal failure
Ŧ Neurological abnormalities dominant
Ŧ Kidney injury minimal • Placental abruption
Ŧ Diagnosed predominantly in the second and third • Disseminated intravascular coagulation
trimesters • Postpartum hemorrhage
• emolytic uremic syndrome S Ŧ Atonic/traumatic hemorrhage
Ŧ Renal failure profound Ŧ Adherent placenta
Ŧ Diagnosed primarily in the postpartum period. Ŧ Uterine rupture
Table 55.2 Differentiating features of severe preeclampsia, ELLP syndrome, AFLP, TTP, and S
Severe ELLP AFLP TTP S

preeclampsia
Onset of symptoms Third trimester Third trimester Third trimester Second or third Postpartum
trimester
Hypertension 100% 80% 25%–50% Occasionally +
Acute renal failure Mild Mild/moderate Moderate Mild/moderate Severe
Thrombocytopenia r + ++ ++
Hemolytic anemia Ŧ r ++ +
Increased PTT r r +
Increased liver transaminase r + ++
ADAMTS-13 activity <10% Ŧ Ŧ Ŧ ++ +
Renal outcome Good Good Good Poor Poor
A P acute fatty liver of pregnancy; P hemolysis, elevated liver enzymes, and low platelet count; S hemolytic uremic syndrome;
P partial thromboplastin time; P thrombotic thrombocytopenic purpura; +, positive; –, negative.
CH 55_p827-841_v3.indd 834 19-07-2015 01:21:05

If there is associated severe preeclampsia or

Box 55.17 Measures to prevent A F
HELLP syndrome, the renal consequences of
hemorrhage are worsened. Hemorrhage will • Prompt management of hypotension
exacerbate the hypovolemic state already asso- • 'CTN[KFGPVKſECVKQPQHQDUVGVTKEJGOQTTJCIG
Ŧ Adequate volume replacement
ciated with severe preeclampsia and precipitate
Ŧ Adequate blood component replacement
the development and progression of ATN.
• Appropriate management of severe preeclampsia
ATN is potentially reversible, and with sup- • Anticipation of and close monitoring for sepsis
portive therapy, the damage can be minimal. If syndrome in
the renal ischemia is mild and the renal failure Ŧ septic abortion
is reversible, the oliguric phase is followed by Ŧ pyelonephritis
the diuretic phase. Electrolyte disturbances are Ŧ chorioamnionitis
common during this phase.
Without immediate intervention, the ATN can The key issues in the management of ARF in
progress rapidly to bilateral renal cortical necro- pregnancy include the following:
sis (BRCN). This almost always leads to perma-
nent and irreversible renal damage. Of the cases • Correction of hypovolemia when present
of ARF, 20% will progress to BRCN. • Prevention of further injury
Diagnostic criteria for ATN and BRCN are • Initiation of renal replacement therapy (RRT
listed in Box 55.16. or dialysis) when indicated
• Treatment of underlying cause
• The delivery of baby and the placenta as
Management of A F promptly as possible
in pregnancy
Treatment of ARF in pregnancy poses special enal dialysis
challenges, as there are risks to both the mother The indications for dialysis are similar to other
and the fetus. Management is best provided by patients with ARF and are listed in Box 55.18.
a multidisciplinary team that involves obstetri-
cians, nephrologists, neonatologists, and other Options or ialysis
specialists, as needed. The options for RRT in ARF include the following:
revention o A • Intermittent hemodialysis
• Peritoneal dialysis (PD)
Prevention of ARF is summarized in Box 55.17.
• Continuous hemofiltration [continuous renal
replacement therapy (CRRT)]
Box 55.16 Diagnostic criteria for AT and • Slow low-efficiency dialysis (SLED)
B C
Peritoneal dialysis and intermittent hemodialy-
Diagnosis of A
sis still continue to be the more cost-effective and
• Urinary sodium >25 mEq/L affordable RRT modalities in developing countries.
• 7TKPGGZCOKPCVKQP The diagnostic and management algorithms
Ŧ Tubular cell debris for ARF occurring at different times during
Ŧ Brown granular (pigmented) casts
pregnancy are outlined in Figures 55.1 and 55.2.
Ŧ Oliguria (50% of cases)
Diagnosis of B C
• Anuria persisting for >1 week Box 55.18 Indications for T (dialysis)
• CT with contrast or selective renal angiography
(imaging not essential) • Electrolyte imbalance, especially hyperkalemia
Ŧ &GNC[GFſNNKPI • Metabolic acidosis
Ŧ Poor arborization of the interlobar arteries • Volume overload
Ŧ #DUGPV QT PQPJQOQIGPGQWU ſNNKPI CV VJG NGXGN QH • Symptomatic uremia
VJGEQTVGZ Ŧ Pericarditis
• Renal biopsy Ŧ Neuropathy
Ŧ Mental status changes
A acute tubular necrosis; B C bilateral renal cortical necrosis;
C computed tomography. renal replacement therapy.
CH 55_p827-841_v3.indd 835 19-07-2015 01:21:05

cute renal failure in first t o trimesters
Proteinuria hematuria ranular casts

ormal urinalysis Pyuria
C casts H Hypotension
Lo urinary so ium e er
e er ith rigors
Positi e urine culture
Vaginal blee ing
eptic abortion ith

Un erlying renal isease Prerenal a otemia
acute tubular necrosis or cute pyelonephritis
or acute glomerulonephritis hyperemesis gra i arum
cortical necrosis
Hemo ynamic support Hy ration

reat H Parenteral flui s
ntibiotics Hemo ynamic support
Consi er renal biopsy to treat hypo olemia
ialysis ntibiotics
Figure 55.1 Diagnostic and management algorithm for acute renal failure in the second trimester. hypertension; a
sodium.
cute re al ailure i thir trimester a postpartum
bstetric
yperte sio e er
hemorrha e
Protei uria ypo lycemia e ere

ri alysis
le ate ypo ibri o e emia thrombocytope ia
Protei uria irty bro
li er e ymes yperbilirubi emia emolytic a emia
ra ular casts
o platelets Prolo e P eurolo ical symptoms
e ere P cute atty li er o hromobotic cute

preeclampsia sy rome pre a cy microa iopathies tubular ecrosis
reat a lo
reat platelets emo y amic
eli ery
a esium sul ate upporti e therapy eli ery support
ialysis
eli ery or ialysis
eli ery
Figure 55.2 Diagnostic and management algorithm for acute renal failure occurring in the third trimester and postpartum
period. A , acute renal failure; P, hemolysis, elevated liver enzymes, and low platelet count; , hypertension;
a, sodium; P , partial thromboplastin time.
CH 55_p827-841_v3.indd 836 19-07-2015 01:21:06

Chronic renal diseases Box 55.21 Effect of chronic renal disease

on pregnancy
in pregnancy • Higher rates of adverse maternal outcomes
Chronic renal disorders can have adverse effects • Higher risk of poor fetal outcomes
on pregnancy and the disease itself may worsen • 2TGGENCORUKCOQTGFKHſEWNVVQFKCIPQUGKPVJGRTGUGPEG
QHRTGGZKUVKPIJ[RGTVGPUKQPCPFRTQVGKPWTKC
due to pregnancy.
• Greater risk of early onset preeclampsia
The common chronic renal disorders encoun-
tered in pregnancy are listed in Box 55.19.
Effect of kidney disease

Effect of pregnancy on pregnancy
on kidney disease Although the rate of live births is >90% in women
with normal renal function, women with chronic
Pregnancy can affect women with renal disease. kidney disease are at higher risk for adverse
Women who have hypertension and/or a pre- maternal and fetal outcomes as indicated in
pregnancy creatinine level of >1.5 mg/day are at Box 55.21.
risk for permanent exacerbation of the underly- A few common chronic renal disorders are
ing kidney disease. It is prudent for such women discussed in the following sections.
to avoid a pregnancy till these parameters are
improved.
The effects of pregnancy on kidney disease
ephrotic syndrome
are listed in Box 55.20. Nephrotic syndrome is a nonspecific kidney dis-
order due to glomerular injury. It is character-
ized by increased capillary wall permeability to
Box 55.19 Common chronic renal disorders serum proteins. The following clinical findings
in pregnancy are present:
• Chronic glomerulonephritis • Proteinuria (>3.5 g/24 hours)
• Nephrotic syndrome • Hypoalbuminemia (low levels of protein in the
• Renal failure due to nephrolithiasis blood)
• Lupus nephritis • Edema
• Diabetic nephropathy
• Hyperlipidemia
• Renal artery stenosis
Causes of nephrotic syndrome

Box 55.20 Effects of pregnancy on kidney
in pregnancy
disease The causes of nephrotic syndrome in pregnancy
• Proteinuria increases in 50% of cases are enumerated in Box 55.22.
• Hypertension develops in 25% of cases
Ŧ Severe hypertension
Box 55.22 Causes of nephrotic syndrome
Maternal adverse effects
in pregnancy
Premature delivery
Poor fetal outcome • Severe preeclampsia
• Worsening of edema Ŧ Most common cause
• Effect on renal function • 2TGGZKUVKPITGPCNFKUGCUGYKVJCOCTMGFKPETGCUGKP
Ŧ 4KUM QH RGTOCPGPV GZCEGTDCVKQP QH TGPCN FKUGCUG proteinuria during pregnancy
in women with Ŧ Lupus nephritis
prepregnancy creatinine level >1.5 mg/dL and or Ŧ Diabetic nephropathy
RTGGZKUVKPIJ[RGTVGPUKQP Ŧ Proliferative glomerulonephropathy
• Increased incidence of pyelonephritis Ŧ Other chronic renal disorders
CH 55_p827-841_v3.indd 837 19-07-2015 01:21:06

Management of nephrotic syndrome Box 55.23 Management of acute glomerulone-

in pregnancy phritis
Management involves the control of edema and • Control of hypertension

the prevention of deep vein thrombosis (DVT). • Electrolyte balance
• Management of edema
ema • Management of underlying cause
• Management of uremia
The following points should be noted about Ŧ Conservative measures
edema: Ŧ Possible renal dialysis
• Managed by limiting dietary sodium to 1.5 g
(approximately 60 mEq) of sodium per day
• proteinuria, which is common but normally
• Bed rest and leg elevation
less than 3.5 g/24 hours
• Diuretics occasionally indicated for severe,
intractable edema The condition may be difficult to differentiate
– Contraindicated in preeclampsia from preeclampsia.
• Record of daily weight to monitor edema
anagement
revention o eep venous thrombosis Management of acute glomerulonephritis is
Nephrotic syndrome is associated with an summarized in Box 55.23.
increased risk of DVT. Prophylactic antico- Chronic glomerulonephritis indicates pro-
agulation should be considered in pregnant gressive loss of renal function, proteinuria,
women with nephrotic syndrome and severe and diminishing renal size caused by primary
hypoalbuminemia. or secondary glomerular disease that has
failed to resolve or respond to treatment. End-
atural course in pregnancy stage renal failure eventually ensues, requiring
Prognosis depends on the cause of nephrotic hemodialysis.
syndrome. It is generally good if renal function Pregnancy does not adversely affect the
is adequate and there is no associated hyperten- course of renal disease in patients who have nor-
sion. When the syndrome is associated with high mal renal function before pregnancy.
levels of creatinine (azotemia), a successful preg-
nancy is unlikely.
Diabetic nephropathy
Glomerulonephritis Diabetic nephropathy may complicate up to
10% of pregnancies in women with pregesta-
Glomerulonephritis may be acute or chronic. tional diabetes. The characteristic pathology
Acute glomerulonephritis is uncommon in of diabetic nephropathy is diffuse or nodu-
pregnancy. Streptococcal infections usually occur lar glomerulosclerosis. The cause of diabetic
at a younger age. Acute glomerulonephritis may nephropathy is attributed to poor glycemic
be a presentation of the following renal conditions: control, hypertension, an increase in GFR, or
• Poststreptococcal glomerulonephritis an increase in protein intake and excretion, all
• Lupus glomerulonephritis of which are affected by pregnancy. Pregnancy
• Membranoproliferative glomerulonephritis has an adverse effect on diabetic nephropathy,
increasing proteinuria and creatinine clearance.
Acute glomerulonephritis is characterized by the
following:
Presenting signs
• Hematuria: Sudden appearance of red blood
cells and red blood cell casts in the urine Diabetic nephropathy usually presents with the
• Impaired renal function following:
• Sodium and water retention leading to • Significant proteinuria
– edema • Azotemia
– hypertension • Hypertension
CH 55_p827-841_v3.indd 838 19-07-2015 01:21:06

Prognosis Box 55.24 Clinical features of nephrolithiasis

Women with diabetic nephropathy are at Symptoms
increased risk for adverse maternal and fetal • Intense pain, abrupt in onset
outcome: • Flank pain
• Preterm delivery • Pain radiating to the groin or labia
• Dysuria
• Preeclampsia
• Gross or microscopic hematuria
• Hypertensive complications
Signs
Approximately 20% of women with diabetic • Costovertebral angle tenderness
nephropathy during pregnancy will progress to • )GPGTCNK\GFƀCPMVGPFGTPGUU
renal failure by 5 years postpartum. • Guarding
• Rigidity
ephrolithiasis
Nephrolithiasis is often a chronic renal disorder,
but symptoms may occur for the first time in
Box 55.25 +PXGUVKICVKQPUHQTVJGEQPſTOCVKQPQH
pregnancy.
nephrolithiasis
Nephrolithiasis (renal and ureteric calculi) is the
most common cause of nonobstetric abdominal • Urinalysis
pain needing hospitalization in pregnant women. Ŧ Presence of RBCs may suggest a calculus
The incidence and rate of recurrent calculi • Renal ultrasonography
Ŧ First-line screening tool for urolithiasis in pregnant
are similar in both pregnant and nonpregnant
women
patients. Nearly 80%–90% of patients are diag- Ŧ Ultrasound signs of ureteric calculus
nosed after the first trimester. Symptomatic stones *[FTQPGRJTQUKU ITGCVGT VJCP GZRGEVGF KP RTGI-
are found in the ureter twice as often as in the nancy
renal pelvis and affect both ureters with similar Identification of calculus
frequency. &KNCVGF WTGVGT GZVGPFKPI DGNQY VJG NGXGN QH VJG
The pregnant woman presents with abrupt iliac arteries
onset of intense pain, which radiates from the flank Asymmetry of ureteral jets suggesting obstruc-
tion of one of the ureters
to the groin or labia (typical ureteric colic). The pain
is usually intermittent and spasmodic, each epi- BCs red blood cells.
sode an hour or longer. The pain of ureteric colic

results from dilation, stretching, and spasm of the
ureter because of the acute ureteral obstruction.
The pain is often accompanied by nausea and Box 55.26 Management of urolithiasis
vomiting.
• Conservative management
Clinical presentation of nephrolithiasis is
Ŧ Bed rest
given in Box 55.24.
Ŧ +PVTCXGPQWUƀWKFUHQTJ[FTCVKQP
Ŧ 5VTCKPKPIWTKPGVJTQWIJCſNVGTVQEJGEMHQTRCUUCIG
Investigations of calculus
Ŧ Analgesics
The investigations for the confirmation of neph-
Ŧ Antiemetics
rolithiasis are listed in Box 55.25.
Ŧ Antibiotics indicated in the presence of a UTI
• Surgical interventions
Management Ŧ Ureteroscopy
Removal of stone with basket
Management of urolithiasis is summarized in
Contact lithotripsy (crushing of stone)
Box 55.26. The first line of management is con-
Ŧ Ureteral stent
servative. The goals are to facilitate the sponta- Placed after ureteroscopy
neous passage of the stone and pain relief. This Facilitates drainage of urine
will result in relief for 80% of patients. Surgical
intervention is resorted to only when there are
CH 55_p827-841_v3.indd 839 19-07-2015 01:21:06

indications that include intractable pain, ureteral

Box 55.27 Indications for surgical intervention
obstruction, and sepsis. in nephrolithiasis
Surgical management • Ureteral obstruction associated with worsening renal
A total of 20% of pregnant women with neph- function
rolithiasis will require surgical intervention. • +PVTCEVCDNGRCKPFGURKVGOCZKOCNEQPUGTXCVKXGOGCUWTGU
• Obstruction in a solitary kidney
Indications for surgical intervention are listed in
• Associated sepsis
Box 55.27.
Key points
• Anatomical and physiological changes that occur in • +PVJGſTUVVTKOGUVGT#4(WUWCNN[TGUWNVUHTQOJ[-
pregnancy predispose women to development of uri- peremesis gravidarum or septic abortion.
nary tract and renal problems and sometimes to rapid
• The four most common causes of ARF in late
worsening of disease.
pregnancy and the postpartum period are severe
• Women with chronic renal failure who have hyperten- preeclampsia, HELLP syndrome, acute fatty liver of
sion and/or a prepregnancy creatinine level of >1.5 mg/ pregnancy, and thrombotic microangiopathies.
FC[CTGCVTKUMHQTRGTOCPGPVGZCEGTDCVKQPQHVJGWP-
• Massive hemorrhage is also implicated as a cause of
derlying kidney disease. It is prudent for such women to
ARF in pregnancy.
avoid a pregnancy till these parameters are improved.
• *GOQTTJCIGYKNNGZCEGTDCVGVJGJ[RQXQNGOKEUVCVG
• Although the rate of live births is >90% in women with
already associated with severe preeclampsia and
normal renal function, women with chronic kidney
precipitate the development and progression of acute
disease are at higher risk for adverse maternal and
tubular necrosis.
fetal outcomes.
• Pregnancy in women with chronic renal failure is as-
• Urinary tract infections (UTIs) are among the most
sociated with an increase in the risk of complications.
common bacterial infections occurring in pregnancy.
The renal functions, proteinuria, and hypertension also
• Vaginal infections can cause or mimic UTIs. Differen- worsen in pregnancy.
tiating between the two depends on a good history,
• 0GRJTQVKEU[PFTQOGKUCPQPURGEKſEMKFPG[FKU-
RJ[UKECNGZCOKPCVKQPCPFVJGTGUWNVUQHXCIKPCNCPF
order due to glomerular injury. It is characterized
urinary cultures.
by increased capillary wall permeability to serum
• Untreated asymptomatic bacteriuria is a risk factor for proteins.
acute cystitis (40%) and pyelonephritis (25%–30%) in
• Acute glomerulonephritis may be a presentation of
pregnancy.
post streptococcal glomerulonephritis, lupus glomeru-
• #EWVGE[UVKVKUKUFWGVQVJGKPƀCOOCVKQPQHVJGDNCFFGT lonephritis, and membranoproliferative glomerulone-
mucosa as a result of bacterial infection. phritis.
• Acute pyelonephritis is an infection of the upper urinary • Chronic glomerulonephritis indicates progressive loss
VTCEVCPFMKFPG[U+VKUEJCTCEVGTK\GFD[HGXGTƀCPMRCKP of renal function, proteinuria, and diminishing renal
CPFVGPFGTPGUUKPCFFKVKQPVQUKIPKſECPVDCEVGTKWTKC size caused by primary or secondary glomerular
• Urinary tract infection is investigated with urinalysis disease that has failed to resolve or respond to treat-
and culture and antibiotic sensitivity of a clean-catch ment.
midstream urine specimen. • Diabetic nephropathy may complicate up to 10% of
• Pyelonephritis warrants hospitalization and treatment pregnancies in women with pregestational diabetes.
with parenteral antibiotics. The characteristic pathology of diabetic nephropathy is
diffuse or nodular glomerulosclerosis.
• Acute renal failure [ARF or acute kidney injury (AKI)]
in pregnancy is characterized by a rapid decrease in • Nephrolithiasis (renal and ureteric calculi) is the most
VJGINQOGTWNCTſNVTCVKQPTCVGQXGTCOCVVGTQHOKPWVGU common cause of nonobstetric abdominal pain need-
or days. ing hospitalization in pregnant women.
CH 55_p827-841_v3.indd 840 19-07-2015 01:21:06

Self-Assessment
been afebrile for 48 hours, she can be switched to
Case-based questions oral antibiotics.
3. Adverse effects can be preterm labor, and in severe
Case 1 cases, septic shock and acute respiratory distress
/TU ,2 YCU KP JGT UKZVJ OQPVJ QH RTGIPCPE[ 5JG syndrome.
gave a history of dysuria for 2 days. She presented with 4. Ů5
EHWO.KUEQPUKFGTGFUKIPKſECPVCPF
HGXGTEJKNNUCPFUGXGTGƀCPMRCKP indicative of a urinary infection.
2. How will you manage this patient? Case 2
3. What are the adverse effects of this condition?
1. Oliguria in spite of adequate volume replacement
4. &GſPGUKIPKſECPVDCEVGTKCNEQWPVQPWTKPGEWNVWTG
indicates acute renal failure. Renal function tests will
EQPſTOKPETGCUKPINGXGNUQHETGCVKPKPG
Case 2 2. HELLP is a syndrome characterized by hemolysis,
elevated liver enzymes, and low platelet count.
/TU$0YCURTGIPCPVYKVJJGTſTUVRTGIPCPE[5JG Although it is associated with severe preeclampsia,
developed hypertension at 32 weeks, and this progressed 15%–20% of women with HELLP syndrome do not
rapidly to preeclampsia. She had abruption at 35 weeks. have hypertension or proteinuria.
She developed severe hypovolemic shock. In spite of ad- 3. Along with the management of hypertension, magne-
equate volume replacement, she developed oliguria. She sium sulfate, and delivery, she might require dialysis.
was transferred to a tertiary center for further care. 4. The diagnosis of acute fatty liver should be suspected
1. What does oliguria signify? when preeclampsia is associated with hypoglyce-
2. What is HELLP syndrome? OKCJ[RQſDTKPQIGPGOKCJ[RGTDKNKTWDKPGOKCCPF
prolonged partial thromboplastin time in the absence
3. How will you manage this patient?
of abruptio placentae.
4. How will you differentiate acute fatty liver of
pregnancy?
Sample questions
Answers Long-answer question
Case 1 1. What are the causes and management of acute renal
failure in pregnancy?
1. Symptoms of lower urinary tract infection associated
YKVJHGXGTCPFƀCPMRCKPCTGUWIIGUVKXGQHCEWVG
pyelonephritis. Short-answer questions
2. She needs to be hospitalized; urinalysis and urine
culture with antibiotic sensitivity have to be done on a 1. UTI in pregnancy
clean-catch midstream urine specimen, and she has 2. Asymptomatic bacteriuria
to be started on parenteral antibiotics. After she has 3. Pregnancy in chronic renal disease
CH 55_p827-841_v3.indd 841 19-07-2015 01:21:06

56 Infections
Case scenario
Mrs. BG, 36, pregnant for the first time, presented at the antenatal
clinic with a few clear vesicles on her face and abdomen. Her 6-year-old
nephew was just recovering from chicken pox.
Introduction to have a high index of suspicion even for the

mildest symptom. Screening for some infections
Pregnant women are susceptible to infections is mandatory. Treatment for intrauterine infec-
just like other women. However, infections in tions is aimed at treating both the mother and
pregnancy are a complex issue because the the fetus.
embryo and fetus are vulnerable, right from the
time of the implantation of the fertilized ovum
through the time of delivery. Therapy is also Transmission of maternal
restricted because of the concern about terato-
genicity. In the peripartum period, the newborn infection
is susceptible to transmission of infection from
Transmission of maternal infection to the fetus
the mother.
and newborn can occur
Generally, infections that occur in the first tri-
mester (during the period of organogenesis) give • through the transplacental route
rise to congenital anomalies. However, some • as an ascending infection from the lower
infections are transmitted transplacentally even genital tract
at later periods of gestation. • through contact with genital lesions or secre-
Many of the infections in pregnancy may be tions during delivery
asymptomatic and therefore obstetricians have • through breastfeeding
CH 56_p842-862_v3.indd 842 19-07-2015 01:21:45

Infections 843
Immune response will confirm active fetal infection since maternal

IgM antibodies cannot cross the placenta. The
to infection presence of IgG antibodies in the amniotic fluid
or fetal blood is inconclusive since maternal IgG
Two types of antibodies may be produced in antibodies can cross the placenta.
response to an infection: immunoglobulin M
(IgM) and immunoglobulin G (IgG; Box 56.1).
They are specific for each different infection, for
example, rubella antibodies are different from
Types of infections
the antibodies for herpes. The infections in pregnancy that have an impact
on maternal/fetal health and discussed in this
Fetal status chapter are as follows:
When fetal infection is suspected, the presence • Viral
of IgM antibodies in amniotic fluid/fetal blood – Parvovirus B19
– Herpes simplex virus (HSV)
a – Cytomegalovirus (CMV)
Box 56.1 Antibodies produced in response
– Rubella
to infection
– Varicella
g antibodies – Human immunodeficiency virus (HIV)
• Indicate acute phase of infection • Protozoal
• First to be produced by the body in response to an – Toxoplasmosis
infection – Malaria
• Present within 1–2 weeks after the initial exposure • Bacterial
• Rise for a short time period and then decline
– Tuberculosis (TB)
• Eventually fall below detectable levels
• Do not cross the placenta
g antibodies
• Indicate lifelong immunity
iral infections
• Produced a few weeks after the initial infection
• Provide long-term protection Parvovirus B19 in pregnancy
• Rise in levels during active infection, stabilize later
Parvoviral B19 infection is a respiratory illness
• Persist lifelong
• Cross the placenta
that may be associated with a febrile illness,
rash, and arthralgia. Approximately 30%–50%
Antibody testing
of pregnant women are immune to the infec-
• Performed to determine immunity in pregnant women tion due to prior exposure to the infection. The
Ŧ Who have been exposed to someone with an in-
rate of parvoviral infection is highest in pregnant
fection or
Ŧ Who have symptoms suggestive of infection
school teachers who come in close contact with
• Distinction between current, recent, and old infections toddlers.
possible by comparing the absence or presence of
both IgG and IgM in the same sample Signs and symptoms
Ŧ IgM negative, IgG negative
No recent infection Parvoviral infection may vary from a mild asymp-
Susceptible to future infection tomatic illness to erythema infectiosum—a
Ŧ Only IgM positive febrile illness associated with a rash (‘slapped
Current infection cheek’ appearance, which is more common in
Ŧ IgM positive and IgG positive children than in adults), arthropathy, viral myo-
Recent infection
carditis, or rarely an aplastic crisis.
Ŧ Only IgG positive
By the time the rash develops at the end of the
Old infection (immune)
incubation period of 2 weeks, the woman is no
g immunoglobulin G; g immunoglobulin M. longer infective.
CH 56_p842-862_v3.indd 843 19-07-2015 01:21:45

• If fetal anemia is diagnosed

Box 56.2 Effect of parvovirus B19 on pregnancy
– Intrauterine transfusion or
• Risk of fetal loss if infection occurs – Delivery if fetus is term or near term
Ŧ KPſTUVVTKOGUVGT
Ŧ DGVYGGPCPFYGGMUŏIGUVCVKQP The long-term prognosis is good after intrauter-
Ŧ CHVGTYGGMU ine transfusion.
• Transient effusions
Ŧ Isolated fetal pleural or pericardial effusions
Due to pleural or myocardial inflammation
Genital herpes simplex
Ŧ Resolve spontaneously infection in pregnancy
• Fetal hydrops
Ŧ Severe anemia and nonimmune hydrops fetalis Genital HSV infection is common among women
Ŧ Higher incidence in women infected before of childbearing age. During pregnancy, the major
20 weeks concern is transmission of maternal HSV infec-
Ŧ Clinical course tion to the fetus, as neonatal infection can result
Rapid fetal death (within a few days to weeks) or in serious morbidity and mortality.
Resolves spontaneously with normal infant at Genital herpes is due to HSV-2 and HSV-1,
delivery
although HSV-2 infections are more common. It
is spread by sexual contact.
Effect on pregnancy Signs and symptoms

The effect of parvovirus B19 is summarized in The signs and symptoms of genital herpes sim-
Box 56.2. plex infection depend on whether it is a primary
or recurrent infection. The clinical presentation
is summarized in Box 56.3.
Diagnosis
If there is clinical suspicion or recent known Implications in pregnancy
exposure, a serum parvoviral test for IgM and
IgG is essential. ransmission to etus
Fetal infection is confirmed or ruled out by The risk of transmission to the fetus depends on
obtaining amniotic fluid (amniocentesis) or fetal the timing of infection and whether it is primary
blood (fetal blood sampling). Polymerase chain or recurrent.
reaction (PCR) is used to detect B19 DNA.
Primary infection in early pregnancy
Treatment • Rarely associated with miscarriage or congeni-

tal anomalies
There is no known antiviral treatment for this con- • Risk of transplacental infection of fetus low
dition. The clinical course is self-limiting. Fetal
surveillance should be instituted to diagnose fetal
anemia and nonimmune hydrops, which may Box 56.3 Clinical presentation of genital herpes
occur up to 12 weeks following a confirmed acute simplex
infection.
• Primary infection
Ŧ First occurrence of HSV infection
Diagnosis an management o etal Ŧ Symptoms
anemia hy rops Severe painful genital ulcers
Parvovirus B19 infection is usually suspected in Severe dysuria due to ulcerated vesicles
pregnancy in the presence of nonimmune fetal Tender inguinal lymphadenopathy
hydrops. If fetal infection has been diagnosed by • ecurrent infection
Ŧ Preexisting antibodies to HSV-1 or HSV-2
PCR on amniotic fluid or fetal blood, the follow-
Ŧ Disease milder
ing steps are followed:
Ŧ Low risk of maternal–fetal transmission at vaginal
• Periodic middle cerebral artery (MCA) Doppler delivery
to assess for the presence of fetal anemia S herpes simplex virus.
CH 56_p842-862_v3.indd 844 19-07-2015 01:21:45

Infections 845
Primary infection in the third trimester mother. Acyclovir, valacyclovir, and famciclo-
vir are used for treatment of maternal herpes.
• High risk of maternal–fetal transmission at
Acyclovir is safe in pregnancy and commonly
vaginal delivery (40%–50%)
used. Antiviral therapy may be used for treat-
Recurrent infection ment of primary infection or recurrent infec-
tion, or as suppressive therapy in women with
• Risk of transmission at delivery much lower
history of recurrent infections. The dosage is
than with primary genital infection (3%–5%)
given in Table 56.1.
Diagnosis of genital herpes simplex

Management of pregnancy
The diagnosis of HSV infection is summarized in
Box 56.4. Maternal HSV infection transmitted to the
infant during delivery can result in major neo-
natal morbidity and mortality. Neonatal infec-
Treatment of herpes simplex tion results from fetal contact with virus shed
in pregnancy from infected sites in the cervix, vagina, and the
vulva.
rimary in ection
Symptom control In ications or suppressive therapy
For symptom control, analgesia with parac- Suppressive therapy given from 36 weeks’ ges-
etamol or nonsteroidal anti-inflammatory drugs tation reduces the risk of HSV lesions at term
(NSAIDs) can be considered along with sitz baths. and the need for cesarean section. It is used in
An indwelling Foley catheter may be required women with
in women with severe dysuria.
• primary active infection in the first or second
Antiviral therapy trimester;
• recurrent infections in any trimester.
Antiviral therapy can decrease the symptoms
and consequences of primary infection in the
Cesarean section
Cesarean section is indicated in women with
Box 56.4 Diagnosis of herpes simplex virus active genital lesions in the 6 weeks leading up
infection to delivery.
• Clinical examination With spontaneous rupture of membranes in
Ŧ Painful vesicles (in primary infection) women with active lesions, a cesarean section
• 8KTCNEWNVWTGUQHƀWKFHTQOFGTQQHGFXGUKENGU must be performed within 4 hours. However,
Ŧ Sensitivity there is some benefit of doing cesarean section
KPRTKOCT[KPHGEVKQP even when the duration of rupture of membrane
KPTGEWTTGPVKPHGEVKQP is >4 hours.
• PCR
Ŧ More sensitive test than culture
Ŧ Preferred test in symptomatic patients aginal elivery
• Serology for IgG antibodies not used routinely Vaginal delivery is undertaken in women with no
g immunoglobulin G; PC polymerase chain reaction. active genital lesions.
Table 56.1 ecommended dosage of antiviral therapy in herpes simplex virus infection
Drug Primary infection ecurrent infection Suppressive therapy

Acyclovir 400 mg tid for 7–10 days 800 mg bid for 5 days 400 mg tid
Valacyclovir 1 g bid for 7–10 days 500 mg bid for 3 days 500–1000 mg od
CH 56_p842-862_v3.indd 845 19-07-2015 01:21:45

• To prevent neonatal transmission in asympto- variety of clinical manifestations. It is the most

matic women with a previous history of HSV common congenital viral infection, with a prev-
infection, avoid alence of approximately 0.5% in the newborn.
– fetal scalp electrode Congenital human CMV infection is the leading
– vacuum or forceps delivery infectious cause of mental disability and senso-
• If vaginal delivery is undertaken in the pres- rineural deafness.
ence of active lesions, the mother and the neo- In adults, CMV is transmitted by contact
nate should be given intravenous acyclovir. with infected nasopharyngeal secretions, urine,
saliva, semen, cervical and vaginal secretions,
eonatal S breast milk, tissue, or blood. After primary infec-
tion, the virus remains dormant and periodic
Neonatal HSV is a serious condition. It can be
reactivation occurs during which there is virus
due to the following:
shedding.
• Direct contact with virus during vaginal delivery Primary infection during pregnancy is associ-
• Postpartum HSV transmission to the neonate ated with 40% risk of fetal infection.
by not following proper hand washing Recurrent infection/reactivation is associated
• Very rarely, vertical transmission by trans- with a much lower risk of fetal infection (<1%).
placental or ascending transmembranous Maternal transmission to the fetus/infant is
infection through the following:
The clinical features of neonatal HSV are sum- • Transplacental infection
marized in Box 56.5. • Contact with maternal genital secretions dur-
ing delivery
Postpartum management • Ascending infection from the maternal genital
tract (not very common)
Thorough hand washing is recommended if the • Breast milk
mother or anyone who handles the newborn has
HSV lesions.
Breastfeeding is encouraged since it is quite Diagnosis of maternal
rare to have lesions on the chest. infection
Routine maternal testing for CMV is not recom-
Cytomegalovirus infection mended. Indications for diagnostic testing in
in pregnancy pregnancy are as follows:
Cytomegalovirus (CMV) is a commonly occur- • Mononucleosis-like illness in the mother
ring DNA herpes virus that presents with a wide • A fetal anomaly suggestive of congenital CMV
infection detected on prenatal ultrasound
examination (see Box 56.7)
Box 56.5 Clinical features of neonatal S
Diagnostic tests
• Mucocutaneous infection
Maternal IgG, IgM, and the IgG avidity testing
Ŧ 5MKPG[GCPFOQWVJ
5'/FKUGCUGQHECUGU
• HSV encephalitis with or without SEM should be done.
Ŧ +PQHPGQPCVCN*58FKUGCUG
Ŧ Presents with Diagnosis of recent infection
seizures (focal or generalized) Recent infection is diagnosed as follows:
lethargy
irritability • Detection of CMV IgM antibodies
tremors • Four-fold increase in CMV IgG antibodies
• Disseminated form
Ŧ Multiorgan dysfunction The anti-CM IgG avidity test
Ŧ HCVCN The anti-CMV IgG avidity test is currently the
S herpes simplex virus. most reliable procedure to identify primary
CH 56_p842-862_v3.indd 846 19-07-2015 01:21:45

Infections 847
infection in pregnant women. The IgG avid- Diagnosis of congenital

ity test is highly specific (100%) and sensi- CM infection
tive (94.3%). The avidity index helps to decide
whether the infection is recent or old. This is The steps to be followed for the diagnosis of
based on the fact that antibodies bind less avidly congenital CMV infection are delineated in
to antigens during the early stages (low avidity) Figure 56.1.
than in chronic stages of infection (high avidity). The first step in the prenatal diagnosis of con-
genital CMV infection is determination of mater-
nal primary and secondary infection by serolog-
Congenital CM infection ical testing. Following a diagnosis of maternal
infection, serial ultrasonography should be per-
Congenital human CMV infection is the leading
formed every 2 weeks to detect fetal abnormal-
infectious cause of mental disability and senso-
ities. Abnormal findings on ultrasound should
rineural deafness.
prompt further testing with amniocentesis.
The majority of women with primary CMV
Ultrasound findings suggestive of fetal CMV
diagnosed before 20 weeks’ gestation will deliver
infection are enumerated in Box 56.7.
an unaffected infant.
The clinical manifestations of congenital
renatal iagnosis o congenital
CMV are listed in Box 56.6.
C in ection
Amniocentesis is done to obtain amniotic fluid.
Fetal blood sampling for fetal IgM is not a reliable
test.
Box 56.6 The clinical manifestations
of congenital CM • Amniocentesis
– To obtain a sample of amniotic fluid
• QHKPHCPVU
– Done after 21 weeks’ gestation
Ŧ No manifestations at birth
– Time interval of 6 weeks between first diag-
• QHCHHGEVGFKPHCPVU
Ŧ Long-term neurological sequelae associated with nosis of maternal infection and prenatal
ventriculomegaly diagnosis
periventricular leukomalacia
microcephaly Box 56.7 7
NVTCUQWPFſPFKPIUUWIIGUVKXGQH
• Other clinical manifestations include fetal cytomegalovirus infection
Ŧ chorioretinitis
Ŧ sensorineural hearing loss • Symmetric fetal growth restriction
Ŧ hepatosplenomegaly • Cerebral ventriculomegaly
Ŧ purpuric skin eruption, petechiae • +PVTCETCPKCNECNEKſECVKQPU
Ŧ jaundice • Microcephaly
Ŧ fetal growth restriction • Oligohydramnios/polyhydramnios
• Blood tests reveal • Hyperechogenic bowel
Ŧ hemolytic anemia • *GRCVKEECNEKſECVKQPU
Ŧ thrombocytopenia • Hydrops fetalis/ascites
Ŧ hyperbilirubinemia • Pleural effusion
• Placental enlargement
C cytomegalovirus.
Ultrasoun
Pregnant oman
e amination for mniocentesis
ith serologically
structural an or for culture an
pro en CMV
gro th PC testing
infection
abnormalities
Figure 56.1 The steps for the diagnosis of congenital CMV infection. C cytomegalovirus; PC polymerase chain
reaction.
CH 56_p842-862_v3.indd 847 19-07-2015 01:21:45

• Diagnosis made by Maternal infection

– PCR for CMV DNA
Maternal rubella is a mild, self-limiting disease,
Although infection before 20 weeks’ gesta- which may go unnoticed. It is asymptomatic in
tion is associated with minimal risk of the fetus 25%–50% of cases.
being infected, women may choose to termi- The clinical manifestations in symptomatic
nate the pregnancy if they find that the fetus is patients include mild fever, malaise, rashes that
infected, because of the concern about long- spread from face to extremities, and lymphade-
term sequelae. nopathy.
Treatment of CM infection Fetal effects of rubella infection

in pregnancy congenital rubella syndrome
Rubella infection can have catastrophic effects
Use of antiviral drugs for treatment of CMV
on the developing fetus, resulting in sponta-
infections is rarely indicated in pregnant women
neous abortion, fetal infection, stillbirth, or fetal
since they do not decrease perinatal transmis-
growth restriction.
sion. Pregnant women must be counseled in
Congenital infection can affect almost all
depth about the extent of CMV infection and risk
organs of the fetus (Box 56.8). Severity of con-
of neurological sequelae.
genital rubella syndrome (CRS) is related to the
period of pregnancy at which infection occurs.
Management of congenital CM Earlier the gestational age of infection, more
infection in neonates severe are the effects (Table 56.2).
All neonates at risk of congenital CMV infection Diagnosis of rubella infection

should be assessed and investigated by a pedia-
trician after delivery. aternal in ection
Investigations to be done before 3 weeks of Acute rubella syndrome is best diagnosed by the
age are as follows: following:
• CMV culture or PCR: Urine or saliva and blood • Presence of rubella-specific IgM
for CMV IgM
• Complete blood examination and liver func- Box 56.8 Clinical features of congenital rubella
tion tests syndrome
• Central nervous system imaging
• Sensorineural hearing loss
• Ocular examination and newborn hearing Ŧ Most common defect
screen • Eye defects
Ŧ Cataract
Neonatal treatment with ganciclovir for 6 Ŧ Glaucoma
weeks has been proven to prevent late-onset Ŧ Retinitis
hearing loss. • Cardiac lesions
Ŧ Most common
Patent ductus arteriosus
ubella in pregnancy Branch pulmonary artery stenosis
Ŧ Other lesions
Rubella (German measles) is a childhood disease Pulmonary valvular stenosis
that has been eliminated to a large extent by rou- Aortic valve stenosis
Ventricular septal defect
tine childhood rubella vaccination. Rubella is
Tetralogy of Fallot
an RNA virus, transmitted through respiratory Coarctation of the aorta
droplets. Infection usually occurs in school-go- • Microphthalmia
ing children living in crowded areas. The incuba- • Microcephaly
tion period is 12–19 days. Although rubella is a • Cerebral palsy
mild infection in older children and adults, it can • Hepatosplenomegaly and jaundice
have potentially devastating effects on the devel-
• Mental disability
oping fetus.
CH 56_p842-862_v3.indd 848 19-07-2015 01:21:45

Infections 849
depending on gestational age. A good rule of

Table 56.2 isk of fetal infection and fetal defects
thumb to follow would be as follows:
based on gestational age
• Infection at <11 weeks’ gestation
Gestational isk of isk of
age (weeks) infection ( ) defect ( ) – Risk of multiple major defects high
– Termination offered
<11 80 100
• Infection at 13–16 weeks’ gestation
13–16 50 35 (deafness alone)
– Risk of sensorineural deafness high
After 16 25 0–1
– Counseling and termination of pregnancy
>36 100 Fetal growth restriction offered
only
• Infection after 16 weeks’ gestation
– Risk of defects very low
– May continue pregnancy
• IgG titer
– A four-fold rise in serum obtained 7–10 days
after onset of rash and repeated 2–3 weeks
later
aricella- oster infection
• Positive rubella culture in specimen from in pregnancy
– nasal swab, throat swab, blood, urine
Varicella-zoster virus (VZV) infection causes
Interpretation of maternal rubella IgM and IgG two clinically distinct forms of disease: varicella
antibodies is summarized in Table 56.3. (chicken pox) and herpes zoster (shingles). VZV
is a DNA virus from the herpes virus family.
etal in ection
Fetal infection is diagnosed by the following: Primary varicella infection
• Rubella-specific PCR in (chicken pox)
– chorionic villus sampling (CVS)
– fetal blood Varicella infection is not common in pregnancy.
• Ultrasound diagnosis difficult Primary VZV infection results in the diffuse
vesicular rash of chicken pox. Primary infec-
tion with VZV during pregnancy has significant
Counseling regarding risk implications for maternal and fetal health. The
severity of disease and complications are much
of fetal defects
more in adults. Varicella pneumonia is estimated
The possibility of severe defects in the infant can to complicate up to 10% of maternal infections
make the parents anxious. Counseling should and contributes to morbidity and mortality.
include risk of maternal–fetal transmission The characteristics of chicken pox are listed
in Box 56.9.
Table 56.3 Interpretation of maternal rubella IgM

and IgG antibodies
Box 56.9 Characteristics of chicken pox
IgM negative and IgG • Mother immune to rubella
positive • No recent infection • Transmitted as
• No risk of fetal infection Ŧ droplet infection
IgM negative and IgG • No recent infection Ŧ direct personal contact
negative • No immunity to rubella • Incubation period: 10–21 days
• Recommend rubella • Patient infectious
vaccine postpartum Ŧ 48 hours before rash appears
IgM positive and IgG • Indicates current infection Ŧ Until vesicles crust over
negative • Primary varicella infection
IgM positive and four-fold • Indicates recent infection Ŧ Provides immunity for life
increase in IgG 2–3 • VZV stays dormant in sensory nerve ganglia
weeks later Ŧ Herpes zoster (shingles) caused by reactivation
g immunoglobulin G; g immunoglobulin M. varicella-zoster virus.
CH 56_p842-862_v3.indd 849 19-07-2015 01:21:45

erpes oster Box 56.10 Clinical features of congenital

Herpes zoster results from reactivation of VZV varicella syndrome
virus that has been dormant in sensory nerve • Dermatomal skin scarring
ganglia. It presents as localized painful vesicles • Eye defects
along a sensory nerve dermatome. Maternal Ŧ Microphthalmia
herpes zoster infection is not associated with a Ŧ Chorioretinitis
significant risk of adverse effects on the fetus. Ŧ Cataracts
• Limb hypoplasia
• Neurological abnormalities
Maternal varicella Ŧ Microcephaly
Ŧ Cortical atrophy
Diagnosis Ŧ Mental disability
The diagnosis is clinical and is based on the Ŧ Dysfunction of bowel and bladder sphincters
classical appearance of the lesions. In cases of
doubt, varicella virus can be isolated from scrap-
ings from the lesions by culture or by fluorescent rate as high as 25%. Neonatal infection results
antibody testing. Serological testing for varicella from maternal infection that occurs
IgM is not necessary for the diagnosis of mater-
nal varicella. • Near or during the time of delivery
– Transplacental transmission
Fetal and neonatal risks – Ascending vaginal infection
• Immediately postpartum
The risk of spontaneous miscarriage does not – Direct contact
appear to be increased if chicken pox occurs in
the first trimester. The infant will develop passive immunity
when the maternal IgG antibodies cross the pla-
Congenital varicella syn rome centa. Severe chicken pox is most likely to occur
if the infant is born within 7 days of onset of the
Congenital varicella syndrome is an extremely
mother’s rash or if the mother develops the rash
rare disorder in which affected infants have dis-
up to 7 days after delivery when the infant has
tinctive abnormalities at birth due to maternal
not had the time to develop immunity.
infection up to 20 weeks’ gestation.
It is advised to avoid elective delivery until 5–7
• Affected newborns may have a low birth days after the onset of maternal rash to allow for
weight and characteristic abnormalities. The the passive transfer of antibodies from mother to
range and severity of associated symptoms child.
and physical findings may vary greatly from
case to case depending on when maternal
varicella-zoster infection occurred during fetal Management of varicella
development. in pregnancy
• Rates of congenital varicella syndrome
– Before 13 weeks: 0.4% aternal treatment
– Between 13 and 20 weeks: 2% Postexposure prophylaxis
• Since the risk of congenital varicella syndrome A pregnant woman who has never had chicken
is very low, termination of pregnancy is not pox but is exposed to an active case should be
warranted and need not be advised for women offered postexposure prophylaxis.
who develop chicken pox in pregnancy.
• Passive immunization with varicella-zoster
The clinical features of congenital varicella immune globulin (VZIG) reduces the risk of
syndrome are listed in Box 56.10. varicella infection and also reduces the sever-
ity of infection in those who develop chicken
eonatal in ection pox.
Neonatal varicella infection that is seen in the • VZIG is effective when given up to 10 days after
infant immediately after birth carries a mortality contact.
CH 56_p842-862_v3.indd 850 19-07-2015 01:21:45

Infections 851
ncomplicated varicella occurs by the transfer of blood, semen, vaginal

All pregnant women with uncomplicated vari- fluid, or breast milk. HIV is present both as free
cella should be treated with oral acyclovir virus particles and virus within infected immune
– 800 mg five times a day for 5–7 days cells in these bodily fluids.
– Within 24 hours of the onset of the rash India is home to the world’s third largest
Symptomatic treatment is essential for itching population suffering from HIV/AIDS. Women
and secondary infections. with heterosexually acquired HIV infection rep-
resent the most rapidly increasing group of HIV-
aricella pneumonia infected individuals in the world. They account
Varicella pneumonia during pregnancy is a med- for 1 in 4 new HIV diagnoses and deaths caused
ical emergency with a high mortality rate. by AIDS.
It is treated with intravenous acyclovir (10 mg/
kg every 8 hours). Screening for I
etal surveillance an
in pregnant women
prenatal iagnosis Screening for HIV in pregnant women consists of
Fetal surveillance and prenatal diagnosis con- the following:
sists of the following: • All pregnant women should be given pretest
• Detailed ultrasound can detect limb deform- counseling regarding screening for HIV.
ity, microcephaly, hydrocephalus, soft-tissue • All pregnant women (except those who opt
calcification, and fetal growth restriction. out) should undergo HIV screening early in
• Fetal sampling for the presence of varicella IgM each pregnancy.
is not a useful test to confirm fetal infection. • Repeat testing in the third trimester is
recommended for those who are at high risk
eonatal varicella in ection of infection.
• Women who present in labor without prior
Neonatal varicella infection is managed as HIV testing should undergo rapid HIV testing.
follows: • Rapid tests can be performed anywhere
• If delivery occurs within 7 days of onset of and do not require laboratory facilities or
maternal rash or if the mother develops a rash highly trained staff. Results come as fast as in
within 7 days of delivery, the neonate should 20 minutes.
be given VZIG. • A pregnant woman with a positive rapid HIV
test should be managed as if HIV-infected to
• Acyclovir should be administered to treat neo- prevent perinatal HIV transmission.
natal infection. • If no rapid testing is available, the untested
• Neonatal blood should be sent for VZV IgM woman should also be managed as if HIV-
antibody and later a follow-up sample should infected to prevent perinatal HIV transmission.
be tested for IgG antibody.
Effect of pregnancy on I infection

WOCPKOOWPQFGſEKGPE[
An HIV-positive woman may become pregnant
virus and pregnancy or a pregnant woman may be found to be HIV
The human immunodeficiency virus (HIV) is a positive when she is tested during the routine
lentivirus (a subgroup of retrovirus) that causes antenatal checkup.
the acquired immunodeficiency syndrome The disease does not worsen during preg-
(AIDS). In AIDS, there is a progressive failure of nancy and the rate of progression is not altered.
the immune system. Life-threatening oppor-
tunistic infections and cancers flourish in this
Sequelae of maternal I infection
immunosuppressed state. Without treatment,
life expectancy after infection with HIV is esti- An HIV-infected pregnancy is associated with
mated to be 9–11 years. Infection with HIV fetal sequelae. Sequelae can be minimized by the
CH 56_p842-862_v3.indd 851 19-07-2015 01:21:46

appropriate use of antiretroviral therapy (ART). apid tests

The most important and worrisome sequela Rapid tests are point-of-care tests, used when
is the vertical transmission of disease to the results are required within a short period of time,
fetus and infant. Mother-to-child transmission like a woman in labor. Positive tests should be
(MTCT) is responsible for 90% of HIV in children confirmed by Western blot tests.
worldwide.
Fetal sequelae of maternal HIV are summa- ucleic acid tests
rized in Box 56.11. Nucleic acid tests are used when the initial tests
are inconclusive, especially for determination of
Diagnosis HIV-1/HIV-2. They are expensive and not offered
routinely.
Tests used for screening and diagnosis of HIV
include antibody tests, antigen test, and nucleic
acid tests.
Factors that increase risk
of mother-to-child transmission
I antibo y tests
There are certain maternal and obstetric factors
HIV antibody tests are used most commonly for that increase the risk of MTCT (Box 56.12). These
screening and diagnosis. Antibody tests may be should be kept in mind during management of
as follows: HIV-positive women.
• Enzyme-linked immunosorbent assay (ELISA)
• Western blot Management of the pregnant
• Rapid tests woman with I
• Nucleic acid tests
The management of the pregnant woman with
ELISA test HIV infection has advanced significantly over
Enzyme-linked immunosorbent assay (ELISA) is the past three decades due to ART and a better
a sensitive test and is used as the primary screen- understanding of the prevention of perinatal
ing test. False positives can occur with ELISA. HIV transmission.
Hence, if the ELISA test is positive, Western blot Management of HIV successfully in preg-
test should be performed before the patient is nancy hinges on four main factors:
declared to be HIV positive. 1. Universal testing of pregnant women for
Western blot tests HIV infection
2. Use of ART to prevent vertical transmission
Western blot tests are more specific and are used
as confirmatory tests.
Box 56.12 Factors that increase risk of MTCT
Box 56.11 Fetal sequelae of I in pregnancy • Virus-related factors
• Spontaneous abortion, low birth weight, and stillbirth Ŧ Maternal viral load
• Increased risk of preterm delivery Ŧ Low CD4 count
• MTCT • Maternal disease-related factors
Ŧ Responsible for Ŧ Seroconversion during pregnancy
QH*+8KPHGEVKQPKPEJKNFTGPYQTNFYKFG Ŧ Advanced stage
• Route of transmission • Obstetric factors
+PVTCWVGTKPGVTCPUOKUUKQPŌ Ŧ Vaginal delivery
&WTKPIFGNKXGT[Ō Ŧ Prelabor rupture of membranes
2QUVFGNKXGT[VTCPUOKUUKQPŌ Ŧ Preterm labor
Ŧ Without antiretroviral therapy, rates of MTCT Ŧ Chorioamnionitis
ŌYKVJQWVDTGCUVHGGFKPI Ŧ Ventouse delivery
ŌYKVJRTQNQPIGFDTGCUVHGGFKPI Ŧ Antepartum invasive procedures
Ŧ With appropriate ART, rate of MTCT Ŧ Fetal scalp blood sampling
Ŧ Use of fetal scalp electrode
• Breastfeeding
A antiretroviral therapy; JWOCPKOOWPQFGſEKGPE[XKTWU
C mother-to-child transmission. C mother-to-child transmission.
CH 56_p842-862_v3.indd 852 19-07-2015 01:21:46

Infections 853
3. Use of cesarean section, when appropriate

Box 56.13 Management of pregnant women
4. Avoidance of breastfeeding, when feasible with I
A thorough history and physical examina- • History
tion should be performed in the HIV-infected Ŧ On antiretroviral therapy or not
pregnant woman. The history should include Ŧ Opportunistic infections
Candidiasis
details of opportunistic infections, sexually
TORCH infections
transmitted infections (STIs), medication use, Tuberculosis
immunization status, and substance abuse. Ŧ Medications used
Physical examination should specifically look Ŧ Immunization status
for signs of advanced HIV infection and con- Ŧ Substance abuse
comitant STIs. • Physical examination
Counseling should be provided to modify risk Ŧ Signs of advanced HIV infection
Ŧ Concomitant sexually transmitted infections
behavior regarding HIV transmission, smoking,
• Immunizations
and illicit drug use. In addition to routine immu- Ŧ DPT and other routine vaccines in pregnancy
nization, pregnant women with HIV should Ŧ *GRCVKVKU$KPƀWGP\CCPFRPGWOQEQEECNXCEEKPGU
receive hepatitis B, influenza, and pneumococ- • Chemoprophylaxis for pneumocystis pneumonia
cal vaccines. Inactivated influenza vaccine is • Antiretroviral therapy to be initiated by 14 weeks’
also strongly advised. gestation
Clinical screening for TB should be performed DP , diphtheria, pertussis, and tetanus; JWOCPKOOWPQFGſEKGP-
at each antenatal visit by asking for history cy virus; C , Toxoplasmosis, Other (syphilis, varicella-zoster,
ofcough, blood-stained sputum, fever, weight parvovirus B19), Rubella, Cytomegalovirus (CMV), and Herpes.
loss, and pleuritic pain. CD4 count should be
performed. ther laboratory evaluation
Because of the increased risk of pneumocystis in the pregnant patient with I
pneumonia, chemoprophylaxis with trimetho-
prim–sulfamethoxazole (one double-strength The pregnant patient with HIV should also be
tablet daily) is recommended for all pregnant evaluated with the following tests:
women with a CD4 count of <250 cells/mm3. • Hemoglobin and hematocrit (anemia is asso-
It is recommended that all pregnant HIV- ciated with increased risk of adverse preg-
infected women receive a combination antiret- nancy outcomes as well as increased MTCT)
roviral drug regimen, regardless of CD4 T-lym- • Viral load measurement (especially at 34–36
phocyte count or plasma HIV RNA copy number, weeks to decide on mode of delivery)
to prevent perinatal transmission. ART should be • Viral hepatitis markers [hepatitis B surface
initiated by 14 weeks’ gestation. antigen (HBsAg) and hepatitis C virus (HCV)
The management of pregnant women with antibodies]
HIV is summarized in Box 56.13. • Screening for gestational diabetes
• Screening for sexually transmitted infections
(STIs)
Monitoring of I • Testing for tuberculosis
HIV disease progression and response to anti- • Screening for genital infections
retroviral treatment are monitored using two
surrogate markers: General principles of antiretroviral
• CD4 T-lymphocyte (CD4) cell count therapy use during pregnancy
– Defines overall immune function of an HIV- The goals of ART are as follows:
infected patient
• Treatment of maternal HIV disease
– Determines the urgency to initiate ART
• Reduction of perinatal transmission
– Progression to AIDS signified by a count of
<200 cell/mm3
• HIV RNA (viral load)
Antiretroviral therapy in pregnancy
– Marker of response to ART The 2013 World Health Organization (WHO)
– Helps monitor effectiveness of therapy recommendations for ART in pregnancy have
CH 56_p842-862_v3.indd 853 19-07-2015 01:21:46

changed from the previous 2010 regimens. The

Box 56.14 Antiretroviral therapy regimen in
new recommendations are given in the next pregnant and breastfeeding women
subsections.
• Once-daily combination of
Ŧ Tenofovir (TDF) 300 mg
regnant an breast ee ing Ŧ Lamivudine (3TC) 300 mg (or)
omen ith I Ŧ Emtricitabine (FTC) 200 mg
Ŧ Efavirenz (EFV) 600 mg
Two options are available (Fig. 56.2):
Option 1. Pregnant and breastfeeding women
with HIV should be placed on lifelong ART • Women should be started on this regimen as
regardless of CD4 count or WHO clinical stage. soon as the diagnosis of HIV infection is made.
• ART should be initiated even if the woman
Option 2. Pregnant and breastfeeding women presents after 36 weeks’ gestation.
with HIV • Women who are HIV-infected, already receiv-
– With CD4 counts <500 or at clinical stage 3 ing ART and who become pregnant should
or 4 continue the same regimen throughout preg-
Lifelong therapy nancy, labor, and breastfeeding and lifelong
– With CD4 counts >500 thereafter.
ART should be initiated but stopped after • If the woman is diagnosed for the first time to
delivery and completion of breastfeeding be HIV positive during labor, the same ART
should be initiated immediately. Evaluation
Antiretroviral therapy regimen and CD4 assessment must be performed the
next day or as early as possible.
The recommended ART regimen for all preg-
nant women including those in the first trimes-
ter and women of childbearing age is given in
In ants
Box 56.14. Infant prophylaxis should begin at birth or when
HIV exposure is recognized postpartum (Fig. 56.3).
• Infants of mothers who are receiving ART and
are breastfeeding
– Should receive 6 weeks of infant prophylaxis
Pregnant an breastfee ing with daily nevirapine (NVP)
omen ith H V • Infants receiving replacement feeding
– Should receive 4–6 weeks of prophylaxis with
daily NVP or twice-daily zidovudine (AZT)
egar less of C counts
or clinical stage
C count
o eo elivery in I in ecte omen
C count
Although cesarean section should be the pre-
Clinical stage or ferred mode of delivery in HIV-infected women,
this is not practical in resource-limited regions.
Lifelong therapy ith

C or C V
C or C V I expose i a t
top after ee of
complete cessation of reast ee i eplaceme t ee i
breastfee ing aily P or ee s P or ee s or
t ice aily
Figure 56.2 ART for pregnant and breastfeeding women
with HIV. A antiretroviral therapy; efavirenz; Figure 56.3 Antiretroviral therapy for HIV-exposed
C emtricitabine; JWOCPKOOWPQFGſEKGPE[XKTWU infants. A zidovudine; JWOCPKOOWPQFGſEKGPE[
C lamivudine; D tenofovir. virus; P nevirapine.
CH 56_p842-862_v3.indd 854 19-07-2015 01:21:46

Infections 855
• Elective cesarean section is associated with Standard precautions should be implemented

reduced rates of MTCT among women universally. Although they are very important in
– Who have not received antiretroviral drugs known cases of HIV or hepatitis B, they should be
– Who have received AZT alone implemented in all cases, to avoid transmission
– Who have not achieved viral suppression from a patient whose infectious status is unknown.
(HIV viral load >1000 copies/mL)
• In resource-limited regions
Breastfeeding
– Vaginal delivery accepted
– Obstetric indications for cesarean Avoidance of breastfeeding is a definite way to
– Fetal scalp electrodes contraindicated prevent HIV transmission via breast milk during
– Amniotomy avoided unless delivery is the postnatal period. However, the 2010 WHO
imminent guidelines recommend exclusive breastfeeding
for 6 months, in combination with maternal or
To prevent transmission, it is mandatory that
infant antiretroviral prophylaxis, to minimize
universal precautions be used by all the staff
HIV transmission from the mother and, at the
dealing with the delivery of an HIV-infected
same time, optimize the benefits of breastfeed-
woman.
ing for the infant.
Replacement feeding is recommended for
niversal or standard precautions infants born to HIV-infected mothers in devel-
oped countries. However, in developing coun-
Universal (now referred to as standard) precau- tries, replacement feeding is associated with
tions ensure a high level of protection against greater infant morbidity and mortality from
transmission of infection including blood-borne diarrheal disease, pneumonia, and other infec-
viruses in the healthcare setting and are recom- tious diseases.
mended for the care and treatment of all patients Feeding should be either exclusive breastfeed-
and in the handling of the following: ing or exclusive replacement feeding for the first
• Blood, including dried blood 6 months. Mixed feeding is not recommended
• All other body substances, secretions, and excre- for infants of HIV-positive mothers.
tions (excluding sweat) regardless of whether
they contain visible blood The ational AIDS Control
• Nonintact skin
• Mucous membranes rgani ation guidelines
and PPTCT program
Universal or standard precautions are aimed at
preventing transmission of blood-borne viruses The National AIDS Control Organization (NACO),
(Box. 56.15). under the Ministry of Health, Government of
India, launched the Prevention of Parent to Child
Transmission (PPTCT) of HIV program in 2001–
Box 56.15 niversal or standard precautions 2002. In 2012, the policy of multidrug regimen,
for preventing transmission of blood- as recommended by the WHO, has also been
borne viruses
adopted by the PPTCT program (Box 56.16).
• Personal hygiene practices The PPTCT services are provided through
Ŧ Particularly hand washing the integrated counseling and testing centers
• Use of personal protective equipment (ICTCs). The ICTCs may be of the following types:
Ŧ Double gloving
Ŧ Gowns • Stand-alone ICTCs: These are located in medi-
Ŧ Protective eyewear cal colleges, district hospitals, Taluk hospitals,
• Aseptic technique and community health centers.
• Safe disposal systems for • Facility integrated ICTCs (F-ICTCs): These are
Ŧ sharps located in primary health centers. The staff is
Ŧ contaminated matter trained in counseling and testing for HIV with
• Adequate sterilization of reusable equipment
kits provided. If a woman tests positive, she is
• Environmental controls
referred to ICTCs.
CH 56_p842-862_v3.indd 855 19-07-2015 01:21:46

When the initial toxoplasmic infection occurs

Box 56.16 Goals of the PPTCT program
in pregnancy, transmission to the fetus results in
• Antenatal care congenital toxoplasmosis and associated neuro-
Ŧ Pretest and posttest counseling logical and ocular manifestations.
Ŧ Offering termination of pregnancy to HIV-positive
women
Ŧ Counseling regarding safe delivery, birth planning,
and infant feeding
Presentation in pregnancy
Ŧ Providing ART The clinical presentation of toxoplasmosis in
Ŧ Psychosocial support pregnancy is summarized in Box 56.17.
Ŧ Routine antenatal care
• Intrapartum care
• Postnatal care Effects on fetus
Ŧ Counseling regarding breastfeeding
Ŧ ART for mother and infant Most infected neonates have no clinical man-
Ŧ Family planning services ifestations. The characteristics of congenital
infection are summarized in Box 56.18.
• Screening centers: Health facilities where auxil-
iary nurse midwives are trained in counseling
and performing finger prick test. If a woman Box 56.17 Clinical presentation of toxoplasmosis
tests positive, she is referred to ICTCs. in pregnancy
With effect from January 1, 2014, pregnant • Brief febrile illness

• Usually asymptomatic
women who are found to be HIV positive are ini-
• Preconceptional disease not transmitted to fetus
tiated on lifelong ART, irrespective of CD4 count
Ŧ Except in women with AIDS
and WHO clinical staging. Their newborn (HIV- • Fetus affected with primary infection in pregnancy
exposed) babies are initiated on 6 weeks of syrup • Termination of pregnancy indicated with
NVP immediately after birth so as to prevent Ŧ Ultrasonographic evidence of fetal abnormalities
transmission of HIV from mother to child and Intracranial calcification
this is extended to 12 weeks of syrup NVP if the Hydrocephalus
duration of the ART of mother is <24 weeks. Intrahepatic calcifications
Hyperechoic bowel
• Risk of fetal infection increases with advancing gesta-
Proto oal infections tional age
Ŧ +PHGEVGFCVYGGMU(GVCNKPHGEVKQPKP
Ŧ +PHGEVGFCVYGGMU(GVCNKPHGEVKQPKP
Toxoplasmosis in pregnancy Ŧ +PHGEVGFCVYGGMU(GVCNKPHGEVKQPKP
Toxoplasma gondii is a common protozoan par- A DS CESWKTGFKOOWPQFGſEKGPE[U[PFTQOG
asite that infects humans and is mainly acquired
in childhood and adolescence. T. gondii infection
is acquired through
Box 56.18 Characteristics of congenital
• ingestion of cysts in infected, undercooked o oplasma infection
meat; • Classic tetrad of congenital o oplasma infection
• ingestion of oocysts that may contaminate cat includes
litter, soil, water, and food. Ŧ chorioretinitis
Ŧ hydrocephalus
Raising awareness of this infection is import-
Ŧ KPVTCETCPKCNECNEKſECVKQP
ant. Pregnant women are advised to Ŧ convulsions
• avoid handling cat litter; • Infected infants may also exhibit
• wash hands after handling uncooked meats; Ŧ jaundice
Ŧ hepatosplenomegaly
and
Ŧ anemia
• wash fruits and vegetables if consumed raw.
CH 56_p842-862_v3.indd 856 19-07-2015 01:21:46

Infections 857
Diagnosis Pyrimethamine (25 mg once per day orally)

and sulfadiazine (4 g/day orally divided into two
Due to the low prevalence of the disease, routine to four doses) are administered. Folic acid (10–25
screening of all pregnant women for toxoplas- mg/day orally) is added during pyrimethamine
mosis is not recommended. and sulfadiazine administration to prevent bone
The diagnosis of toxoplasmosis is usually marrow suppression.
made by detection of Toxoplasma-specific IgG,
IgM, or immunoglobulin A (IgA) antibodies. IgM
antibodies for Toxoplasma may persist for many Malaria in pregnancy
years. Therefore, IgM positivity alone may not Malaria is a major parasitic illness that has a del-
indicate a recent infection. All three antibodies eterious impact on maternal health. Pregnancy
should be tested for. reduces a woman’s immunity to malaria.
Repeat testing should be performed 2–3 Pregnant women therefore
weeks later if acute infection is suspected.
There are several tests available that detect • are more likely to get malaria than men or
these immunoglobulin antibodies within several nonpregnant women;
weeks of infection. • have more frequent episodes of malaria;
• suffer more serious forms of malaria; and
Prenatal diagnosis • have a higher risk of complications.
When toxoplasmosis is suspected in preg- Lack of immunity to malaria

nancy, due to either maternal disease or ultra-
sound features suggestive of toxoplasmosis, In India, the transmission of malaria follows a
prenatal diagnostic techniques may be uti- pattern of unstable transmission. Transmission
lized for confirming or ruling out fetal disease. is seasonal and the risk of getting malaria is
Prenatal confirmation allows decision making highest before the monsoon. This means that
for drug therapy. It also allows women to decide the majority of Indians do not develop acquired
whether they want to continue or terminate immunity and are susceptible to infection with
the pregnancy. malaria. Pregnant women with no previous
Amniotic fluid or fetal blood sampling is done immunity to malaria have a two-fold to three-
after 18 weeks’ gestation. PCR/DNA amplifica- fold likelihood of developing severe malarial
tion techniques are required for confirmation of infection as compared with nonpregnant adults
diagnosis of congenital infection. living in the same area. Primigravidas are more
susceptible than multigravidas.
Treatment
Microbiology
Spiramycin
Most infections are due to either Plasmodium
If a woman is diagnosed as having a primary
falciparum or Plasmodium vivax, but mixed
toxoplasmosis infection in pregnancy, treat-
infections with more than one malarial species
ment with spiramycin reduces the risk of fetal
also occur. The main burden of malarial infec-
infection. It is not effective if the fetus is already
tion during pregnancy results from infection
infected.
with P. falciparum. The majority of malaria-re-
Spiramycin is given as 1 g orally every 8 hours
lated deaths are due to P. falciparum.
on an empty stomach. Treatment is continued
till delivery.
Clinical features
yrimethamine sul a ia ine In endemic areas, where partial immunity is
an olic aci common, most malarial infections in preg-
If prenatal diagnosis confirms the presence of nant women are asymptomatic, but the mother
fetal infection, treatment with pyrimethamine, remains at risk for anemia and the fetus is at risk
sulfadiazine, and folic acid is recommended. The for low birth weight. Nearly 60% of pregnant
treatment is continued till delivery. women presenting with malaria are anemic.
CH 56_p842-862_v3.indd 857 19-07-2015 01:21:46

• Rapid detection tests may miss low para-

Box 56.19 Signs and symptoms of malaria
in pregnancy sitemia, which is more likely in pregnant
women, and rapid detection tests are relatively
• Fever associated with insensitive in P. vivax malaria.
Ŧ headache
• In a febrile patient, three negative malaria
Ŧ myalgia
smears 12–24 hours apart rule out the diagno-
Ŧ sweats and rigors
Ŧ nausea and vomiting
sis of malaria.
Ŧ diarrhea
• Examination may reveal Prevention and management
Ŧ pyrexia of malaria in pregnancy
Ŧ perspiration
Ŧ pallor/jaundice A simple approach to malaria prevention and
Ŧ splenomegaly treatment should follow four steps which are
Ŧ respiratory distress mentioned in Box 56.21.
• Falciparum malaria may be associated with
Ŧ confusion reatment
Ŧ coma
Ŧ neurological focal signs Malaria in pregnancy is an emergency and treat-
Ŧ severe anemia ment should be initiated immediately.
Ŧ TGURKTCVQT[FKHſEWNVKGU • Pregnant women with uncomplicated malaria
should be hospitalized.
If a pregnant woman presents with a flu-like • Pregnant women with severe and complicated
illness, a high index of suspicion for malaria is malaria may require admission to an intensive
important in an endemic area or with history care unit.
of recent travel to an endemic area. The signs • P. vivax, P. ovale, or P. malariae
and symptoms of malaria are summarized in – Chloroquine
Box 56.19. • Uncomplicated P. falciparum (or mixed, e.g.,
P. falciparum and P. vivax)
Effects of malaria on pregnancy – First trimester
Quinine
The effects of malaria on pregnancy are listed in
– Second and third trimesters
Box 56.20.
Artemisinin combination therapy
• Severe falciparum malaria
Diagnosis – Intravenous artesunate treatment of choice
Microscopic diagnosis allows species identifi- – Intravenous quinine if artesunate not
cation and estimation of parasitemia, so that available
appropriate antimalarials can be prescribed. • Primaquine should not be used in pregnancy.
• Fever
– Treated with antipyretics
Box 56.20 Adverse effects of severe malarial
infection • Screen women with malaria for anemia and
treat appropriately.
• Systemic infection may result in
Ŧ miscarriage The recommendations of the Government of
Ŧ premature birth India for the treatment of malaria in pregnancy
Ŧ stillbirth are listed in Table 56.4.
Ŧ maternal and fetal mortality
• Parasitemia may result in
Box 56.21 The ABCD approach to malaria
Ŧ severe maternal and fetal anemia
in pregnancy
Ŧ fetal growth restriction and low birth weight
Ŧ susceptibility of infant to malaria • Awareness of risk
• Placental malaria • ite prevention using insecticide-treated nets (ITNs)
Ŧ Occurs with P falciparum • Chemoprophylaxis
Ŧ Poor pregnancy outcome due to damage to villi • Diagnosis and treatment that must be prompt
CH 56_p842-862_v3.indd 858 19-07-2015 01:21:46

Infections 859
Table 56.4 ecommendations of Government of India for treatment of malaria in pregnancy
Type of infection Trimester Drug Day 1 Day 2 Day 3

Plasmodium viva All 10 mg/kg chloroquine 4 tablets 4 tablets 2 tablets
Plasmodium falciparum First 10 mg/kg quinine 3 times/day u 7 days
Second and third 50 mg artesunate orally or 4 tablets 4 tablets
500 mg sulfadoxine 3 tablets 0 4 tablets
+ 25 mg pyrimethamine
Severe P falciparum All 2.4 mg/kg artesunate IV or 0, 12, and 24 hours, and then daily
thereafter
20 mg/kg quinine On admission
Maintenance dose:
10 mg/kg 8-Hourly
Primaquine should not be prescribed in pregnancy.
Congenital malaria likelihood of progression from latent infection to

active disease. Fortunately pregnancy does not
Vertical transmission to the fetus can occur impact the response to treatment.
particularly when there is infection at the Pulmonary TB with respiratory symptoms is
time of birth and the placenta and cord are more common in pregnancy. Pregnant patients
blood film positive for malaria. Infection of with pulmonary TB
the newborn can occur despite appropriate
treatment in the mother during pregnancy. If • have the same clinical manifestations as non-
the placenta is positive for parasites, weekly pregnant patients and
screening of the newborn for 28 days is useful • may have delay in diagnosis because
to allow early detection and treatment of con- – malaise and fatigue may be attributed to
genital malaria. pregnancy and
– weight loss may be difficult to recognize.
Extrapulmonary TB may have vague symp-

Bacterial infections toms and diagnosis may be delayed in pregnancy.
Tuberculosis in pregnancy Diagnosis

In India tuberculosis (TB) continues to be a
The diagnosis and confirmation of infection may
major public health issue despite a global fall
require a combination of diagnostic tests.
in the incidence of TB. India accounts for one-
fifth of the global TB burden. Each year nearly • The tuberculin skin test (Mantoux) is con-
2 million people in India develop TB, of which sidered both valid and safe to use through-
approximately 0.87 million are infectious cases. out pregnancy but may not be useful in
It is estimated that approximately 330,000 countries like India where prior exposure
Indians die due to TB every year. rate is high.
Tuberculosis is a significant contributor • X-rays are useful in making a diagnosis and
to maternal mortality, with the disease being should not be avoided due to pregnancy.
among the three leading causes of death among • Sputum examination for acid-fast bacilli (AFB)
women aged 15–45 years. is useful.
• Although a culture may take 4–6 weeks to
obtain a result, it is still useful in the manage-
Signs and symptoms ment of multidrug-resistant TB.
Pregnancy does not negatively influence the • Lymph node biopsy may be required in women
pathogenesis of TB nor does it increase the with extrapulmonary TB.
CH 56_p842-862_v3.indd 859 19-07-2015 01:21:46

Effect of tuberculosis on pregnancy has been suggested in women undergoing treat-

ment for multidrug-resistant TB.
Maternal TB has been shown to have an increased Prophylactic pyridoxine in the dose of 10 mg/
association with the risk of the following: day is recommended along with antituberculosis
• Spontaneous abortion treatment (ATT).
• Perinatal mortality
• Small for gestational age and low birth weight Treatment of tuberculosis
in lactating women
Tuberculosis and the newborn Breastfeeding can be continued in women
Congenital TB is a rare complication of in utero receiving first-line ATT drugs. The drugs should
TB infection. It occurs by placental hematoge- be taken preferably after breastfeeding and the
nous transmission or by ingestion and aspiration next feed could be a bottlefeed.
of infected amniotic fluid. Supplemental pyridoxine should be admin-
The newborn infant is at a higher risk of post- istered to an infant on isoniazid (INH) or if the
natal infection due to exposure to the mother’s breastfeeding mother is taking INH because
aerosolized respiratory secretions. pyridoxine deficiency may cause seizures in the
newborn.
Treatment
Follow-up of the newborn infant
Antituberculous drugs should not be withheld
from a woman because of pregnancy. Untreated The follow-up of the newborn infant is summa-
TB disease is a greater threat to a pregnant rized in Box 56.23.
woman and the fetus than its treatment.
Pregnant women should be started on treat- Box 56.23 Follow-up of the newborn infant
ment as soon as TB is suspected. The preferred of a mother with tuberculosis
treatment regimen is summarized in Box 56.22. • Mother sputum positive
Multidrug-resistant TB poses a special prob- Ŧ Infant evaluated for active tuberculosis
lem since the safety of the second line of drugs is Chest X-ray
not established in pregnancy. Elective abortion Examination of gastric aspirate
Sputum for AFB
• Infant shows no evidence of active tuberculosis
Box 56.22 Treatment regimen for tuberculosis Ŧ INH prophylaxis for 3 months till
in pregnancy mother’s sputum becomes negative for AFB
• Isoniazid (INH) infant is tuberculin negative
• Rifampicin (RIF) • Infant tuberculin positive
For 2 months Ŧ INH prophylaxis for 6 months
• Ethambutol (EMB)
• Pyrazinamide (PZA) Ŧ Active tuberculosis ruled out
infant does not have active or latent infection
Followed by
Ŧ Routine BCG vaccination
• INH and RIF daily (or twice weekly) for 4 months
A B acid-fast bacilli; BC , Bacillus Calmette-Guérin; isoniazid.
Key points
• Infections in pregnancy are a complex issue be- • Two types of antibodies may be produced in response
cause the embryo and fetus are vulnerable, to an infection—immunoglobulin M (IgM) antibodies
right from conception through the time of indicate acute phase of infection. Immunoglobulin G
delivery. (IgG) antibodies indicate lifelong immunity.
• Transmission of maternal infection to the fetus or new- • Parvovirus B19 infection is a respiratory illness that
born can occur by hematogenous spread, through the may be associated with a febrile illness, rash, and
transplacental route, as an ascending infection from arthralgia in the mother. It can cause nonimmune
the lower genital tract or through breastfeeding. hydrops in the fetus.
(Continued)
CH 56_p842-862_v3.indd 860 19-07-2015 01:21:46

Infections 861

• Genital herpes simplex virus (HSV) infection is com- • All pregnant women should undergo HIV screening
mon among women of childbearing age. During preg- early in each pregnancy.
nancy, the major concern is transmission of maternal
• Repeat testing in the third trimester is recommended
HSV infection to the fetus, as neonatal infection can
for those who are at high risk of infection.
result in serious morbidity and mortality.
• Women who present in labor without prior HIV testing
• Neonatal HSV is a serious condition. It can be due
should undergo rapid HIV testing.
to direct contact with virus during vaginal delivery,
postpartum HSV transmission to the neonate by not • Management of HIV successfully in pregnancy
following proper hand washing, and very rarely due to hinges on universal testing of pregnant women for
vertical transmission by transplacental or ascending HIV infection; use of antiretroviral therapy to prevent
transmembranous infection. vertical transmission; use of cesarean section, when
appropriate; and avoidance of breastfeeding, when
• Cytomegalovirus is a commonly occurring DNA herpes
feasible.
virus that presents with a wide variety of clinical mani-
festations. Infection of the fetus is a common cause of • The goals of antiretroviral therapy in pregnancy are
sensorineural hearing loss and mental disability. treatment of maternal HIV disease and reduction of
perinatal transmission.
• Rubella is an RNA virus, transmitted through respira-
tory droplets. Although rubella is a mild infection • o oplasma gondii is a common protozoan parasite
in older children and adults, it can have potentially that infects humans.
devastating effects on the developing fetus. • When the initial toxoplasmic infection occurs in preg-
• Congenital infection with rubella can affect almost all nancy, transmission to the fetus results in congenital
organs of the fetus. Sensorineural hearing loss and toxoplasmosis and associated neurological and ocular
cataracts are the most common defects. Maternal manifestations.
infection after 16 weeks is associated with the least • Malaria is a major parasitic illness that has a deleteri-
number of congenital defects. ous impact on maternal health. Pregnancy reduces a
• Varicella-zoster virus (VZV) infection causes two clini- woman’s immunity to malaria.
cally distinct forms of disease: varicella (chicken pox) • Malaria in pregnancy is an emergency. Pregnant
and herpes zoster (shingles). women with uncomplicated malaria should be hospi-
• Primary VZV infection results in the diffuse vesicular talized. Pregnant women with severe and complicated
rash of chicken pox. Primary infection with VZV during malaria may require admission to an intensive care
RTGIPCPE[JCUUKIPKſECPVKORNKECVKQPUHQTOCVGTPCN unit.
and fetal health. • In India, tuberculosis continues to be a major public
• Congenital varicella syndrome is an extremely rare health issue despite a global fall in the incidence of
disorder in which affected infants have distinctive tuberculosis.
abnormalities at birth due to maternal infection up to • 6WDGTEWNQUKUKUCUKIPKſECPVEQPVTKDWVQTVQOCVGTPCN
20 weeks’ gestation. mortality, with the disease being among the three
• 6JGJWOCPKOOWPQFGſEKGPE[XKTWU
*+8KUCNGPVKXK- leading causes of death among women aged 15–45
rus (a subgroup of retrovirus) that causes the acquired years.
KOOWPQFGſEKGPE[U[PFTQOG
#+&5
Self-Assessment
Mrs. EL, 31, gravida 3, para 2, live 2, is in her 12th week
Case 1 QH RTGIPCPE[ CPF JCU EQOG HQT JGT ſTUV DQQMKPI XKUKV
/TU$)RTGIPCPVHQTVJGſTUVVKOGRTGUGPVUCVVJG One week later her HIV test is reported as positive. She
antenatal clinic with a few clear vesicles on her face and is devastated.
abdomen. Her 6-year-old nephew is just recovering from 1. How will you treat her to prevent MTCT?
chicken pox.
2. What infant prophylaxis should be administered
1. What is the treatment for chicken pox in pregnancy? at birth?
2. What is the major maternal complication of chicken pox? 3. What would be the optimal route of
3. What is the congenital varicella syndrome? delivery?
4. What is postexposure prophylaxis? 4. What is the recommendation for breastfeeding?
CH 56_p842-862_v3.indd 861 19-07-2015 01:21:47

should receive 4–6 weeks of prophylaxis with daily

Answers NVP (or twice-daily AZT).
3. Elective cesarean section is associated with reduced
Case 1 rates of MTCT.
1. All pregnant women with uncomplicated varicella 4. #XQKFCPEGQHDTGCUVHGGFKPIKUCFGſPKVGYC[VQ
UJQWNFDGVTGCVGFYKVJQTCNCE[ENQXKTOIſXG prevent HIV transmission via breast milk during the
times a day for 5–7 days, and treatment should be postnatal period. However, the 2010 WHO guidelines
started within 24 hours of the onset of the rash. recommend exclusive breastfeeding for 6 months,
2. Varicella pneumonia during pregnancy is a medical in combination with maternal or infant antiretroviral
emergency with a high mortality rate. It is treated with prophylaxis, to minimize HIV transmission from the
intravenous acyclovir 10 mg/kg every 8 hours. OQVJGTCPFCVVJGUCOGVKOGQRVKOK\GVJGDGPGſVU
3. Congenital varicella syndrome is an extremely rare of breastfeeding for the infant.
disorder in which affected infants have distinctive
abnormalities at birth. Affected newborns may have
a low birth weight and limb deformity, microcephaly, Sample questions
J[FTQEGRJCNWUCPFUQHVVKUUWGECNEKſECVKQP
4. A pregnant woman who has never had chicken Long-answer questions
pox but is exposed to an active case should be
1. Describe the effects of HIV on the fetus. How is
offered postexposure prophylaxis with VZIG. This
MTCT prevented?
reduces the risk of varicella infection and also
reduces the severity of infection in those who 2. Discuss the management of a pregnant woman who
develop chicken pox. has a positive screening test for HIV.

1. Blood tests for baseline CD4 and viral load and start 1. Universal precaution to be observed for HIV patient
QPQPEGFCKN[ſZGFFQUGEQODKPCVKQPQH6&( 6% at delivery
(or FTC) + EFV. 2. Management of malaria in pregnancy
2. Infant prophylaxis should begin at birth. Infants of 3. Fetal effects of maternal rubella
mothers who are receiving ART and are breastfeed- 4. PPTCT services
ing should receive 6 weeks of infant prophylaxis with 5. Varicella infection in pregnancy
daily NVP. Infants receiving replacement feeding 6. Tuberculosis in pregnancy
CH 56_p842-862_v3.indd 862 19-07-2015 01:21:47

Benign and
Malignant
57 Tumors of the
Reproductive Tract
Case scenario
Mrs. HN, 32, third gravida, wife of a construction worker, was referred
to the hospital at 11 weeks of gestation with a history of blood-stained
vaginal discharge and a friable growth on the cervix. She was suspected
to have cervical cancer and was referred for further management. She
had two living children aged 7 and 4 years, and the woman and her
husband were very worried and upset by the diagnosis of ‘cancer’
Introduction Benign neoplasms in

Benign and malignant tumors of the genital tract pregnancy
and also other malignancies can occur in preg-
nancy. Diagnosis of malignancy at any time in life The benign neoplasms of the genital tract that
is terrifying, more so during pregnancy. Pregnant may be encountered in pregnancy are listed in
women are usually young and may have other Box 57.1.
small children to take care of. Diagnosis and
management of any neoplasm and particularly Benign neoplasms of the cervix
cancer at this time should take into account
the mother and the unborn child. Management
Cervical polyp
decisions should be discussed with the woman Cervical polyps arise from the endocervix and
and her family and taken in consultation with a may be asymptomatic but usually present with
neonatologist, oncologist, and psychologist. irregular bleeding or spotting. They can be
CH 57_p863-875_v3.indd 863 19-07-2015 01:22:40

Box 57.1 Benign neoplasms of the genital tract Complications

in pregnancy Myomas in pregnancy can be associated with
• Cervix the complications listed in Box 57.2. The size of
Ŧ Polyp the myoma, location, and implantation of the
• Uterus placenta over the myoma are important con-
Ŧ Leiomyoma tributing factors. Large myomas that occupy
Ŧ Adenomyoma/adenomyosis the lower segment cause malpresentations
• Ovary and may also impede engagement of the fetal
Ŧ Functional cysts head. Placental implantation over the myoma
• Corpus luteum cysts can lead to miscarriage, placental abruption,
• Theca lutein cysts adherent placenta, and postpartum hemor-
Ŧ Luteomas
rhage. Submucous myomas may get infected
Ŧ Dermoid cyst
postpartum.
Ŧ Epithelial tumors
Diagnosis an management
Most myomas are diagnosed on routine ultraso-
nography. If the uterus appears larger than ges-
twisted off if the pedicle is slender. Thick pedi- tational age or irregular, ultrasonography should
cles must be ligated and the polyp excised. The be performed (Fig. 57.1).
procedure should be done cautiously because of Management is conservative. Even when
the increased risk of bleeding due to the vascu- myomas are encountered at a cesarean section,
larity of pregnancy. myomectomy is not indicated since trouble-
some bleeding can occur. Exceptions to this rule
are pedunculated subserous myomas and myo-
Benign neoplasm of the uterus mas located in the lower segment, in the line of
or close to the incision.
terine leiomyoma
The incidence of leiomyoma in pregnancy is Adenomyoma adenomyosis
approximately 2%. Myomas may be intramural,
subserous, submucous, cervical, or located in Although adenomyosis is usually seen in per-
the broad ligament. They can increase in size in imenopausal, multiparous women, adeno-
pregnancy due to high levels of estrogens. They myomas can occur in young women. They are
may outgrow their blood supply and undergo asymptomatic during pregnancy. Rarely, pla-
red degeneration, which is unique to pregnancy. centa previa, atonic hemorrhage, and uterine
rupture have been reported. Adenomyosis and
Symptoms adenomyoma are managed conservatively.
Small myomas are asymptomatic. The woman
may complain of a sensation of pelvic pressure
or may present with acute or chronic pain.
Box 57.2 Complications of myomas in preg-
e egeneration nancy
Red degeneration of myoma presents with acute • Spontaneous miscarriage
pain, low-grade fever, tenderness, and leucocy- • Preterm labor
tosis. The condition must be differentiated from • Malpresentations
appendicitis, pyelonephritis, and ureteric colic. • Placental abruption
The uterus is tender. The pain may last for 1 week • Obstructed labor
or more. Treatment is with analgesics. Surgery is • Cesarean section
• Adherent placenta
not indicated. Red degeneration is also known to
occur with the use of combined oral contracep-
• Puerperal sepsis
tive pills.
CH 57_p863-875_v3.indd 864 19-07-2015 01:22:40

Benign and Malignant Tumors of the Reproductive Tract 865
Benign neoplasms of the ovary Luteoma of pregnancy

In the preultrasonography era, the incidence of Luteomas of pregnancy are bilateral solid tumors
ovarian neoplasms in pregnancy was 1 in 2000. that occur rarely in pregnancy and secrete pro-
With routine ultrasonography and an increase in gesterone and testosterone. The tumors are 6–10
early detection, the incidence has increased to cm in size. They are usually asymptomatic, but
2.2%. The majority are benign tumors. 25% of tumors present with maternal virilization
and virilization of the female fetus. If diagnosed
antenatally and the fetus is female, removal of the
Functional cysts
tumor is recommended. Large tumors may also
Functional cysts are usually due to hormonal necessitate removal. Smaller luteomas normally
changes that occur with normal pregnancy or regress spontaneously after delivery (Box 57.5).
the high hCG levels in hydatidiform mole.
Cystic teratoma
Corpus luteum cysts
Corpus luteum cysts are multiloculated cysts that Cystic teratomas are the most common tumors
arise from the corpus luteum and often go unno- that present in pregnancy. They are cystic, con-
ticed. They are <10 cm in size, pink or hemorrhagic tain elements from all three germ cell layers, and
in appearance. They resolve spontaneously but are filled with fat. They are often found in the
may occasionally rupture. The features of corpus pouch of Douglas. They can undergo torsion or
luteum cysts are given in Box 57.3. rupture, or, rarely, obstruct labor.
heca lutein cysts Epithelial tumors

Theca lutein cysts are the result of stimulation by The common epithelial tumors such as serous
human chorionic gonadotropin (hCG) and occur and mucinous cystadenomas, endometrioid
in conditions with high levels of hCG. They are tumor, and Brenner tumor can occur in preg-
most common in molar pregnancy but may be nancy. The size may vary from small to very large
seen in multiple pregnancy, Rh isoimmuniza- tumors. Small tumors are asymptomatic, but
tion, and gestational diabetes. The characteris- large tumors present with mass or abdominal
tics of theca lutein cysts are given in Box 57.4. pain. They can undergo torsion or rupture and
occasionally obstruct labor. Malignancy has to
be excluded before conservative management is
Box 57.3 Corpus luteum cysts decided upon. Tumors of low malignant poten-
• <10 cm in size tial may also occur.
• Pink/hemorrhagic
• Asymptomatic Complications of benign ovarian
• Regress spontaneously
tumors in pregnancy
Most benign tumors are asymptomatic and
regress spontaneously. When the ovarian tumor
Box 57.4 Theca lutein cysts
is persistent, the enlarging uterus pushes it into
• Bilateral
• GrayiUJſNNGFYKVJUVTCYEQNQTGFƀWKF
• 1EEWTYKVJGNGXCVGFJ%)
Box 57.5 Luteoma of pregnancy
Ŧ Molar pregnancy
Ŧ Multiple pregnancy • Bilateral, solid tumors
Ŧ Rh isoimmunization • Secrete progesterone/testosterone
Ŧ Gestational diabetes • Regress spontaneously postpartum
• Asymptomatic • Usually asymptomatic
• Occasionally undergo torsion/rupture • Can cause virilization of mother/female fetus
• Regress spontaneously • Managed conservatively
• Managed conservatively • Surgical removal if large/complicated
CH 57_p863-875_v3.indd 865 19-07-2015 01:22:40

the abdomen after 12–14 weeks. They may occa- Malignancies in pregnancy
sionally be wedged posteriorly and obstruct
labor (Box 57.6). Rarely, malpresentations occur. Malignancy occurs in 1/1000 pregnancies. Delay
If there is torsion, it usually occurs in the second in diagnosis is common since many of the symp-
trimester or in the puerperium, when the tumors toms of malignancy overlap with symptoms
are freely mobile in the abdomen. of normal pregnancy and the large size of the
uterus makes physical examination difficult.
Cancers in pregnancy may be cancers of the
Diagnosis and management genital tract or other cancers. The common
Most benign tumors are diagnosed on routine nongenital tract cancers that occur in the repro-
ultrasonography in the first or second trimes- ductive age are thyroid cancer, leukemia, and
ter. Sonographic features of malignancy such as lymphoma.
solid areas, complex nature of the cyst, papillary
excrescences, and increased septal and cyst wall Special considerations
thickness should be looked for (Fig. 57.2).
Management is usually conservative since Diagnosis and management of cancer in preg-
most functional cysts regress by the second nancy has to take into account certain special
trimester. When masses are larger than 5–6 cm considerations which are as follows:
or persistent after 18 weeks, the risk of compli- • Clinical assessment is difficult.
cations is higher. When there is suspicion of • Staging is affected by the uterine size.
malignancy or a complication such as torsion, • Evaluation modalities such as computed
hemorrhage or rupture, immediate surgery is tomography (CT) scan and X-rays with con-
indicated irrespective of gestational age. trast studies can affect the fetus.
• Surgery and anesthesia may carry increased
• All other ovarian tumors should be followed
risk to the mother.
up till 18–20 weeks. Most cysts regress by this
• Pregnancy can affect the course of hormone-
gestational age, and if surgery is indicated, it is
sensitive cancers.
best performed in the second trimester.
• Treatment modalities such as chemotherapy
• Persistent cysts with benign features and <8
and radiotherapy can affect the fetus.
cm in size may be followed up or aspirated
• Termination of pregnancy has to be given due
under ultrasound guidance.
consideration.
• Dermoid cysts can be left alone and removed
• Deferring therapy till delivery may adversely
postpartum.
affect the prognosis.
• Complex masses, large tumors >8 cm, and
tumors that continue to increase in size should
be removed laparoscopically or by laparotomy. Gynecologic malignancies
Management of benign ovarian tumors in preg- Cervical and breast cancers are the most com-
nancy is shown in Figure 57.1. mon gynecologic cancers in pregnancy. Ovarian
cancers are less frequent (Box 57.7). Cancers of
the vulva and fallopian tube are rare.
Box 57.6 Complications of benign ovarian

Diagnosis of cancers
tumors in pregnancy
• Torsion
Ŧ Second trimester
Imaging
Ŧ Puerperium Ultrasonography is safe and is the preferred
• Hemorrhage mode of evaluation. Most radiological proce-
• Rupture dures such as chest or abdominal radiograph
• Malpresentations
result in exposure of <0.05 Gy, which is safe
• Obstruction to descent of fetal head
in pregnancy. Magnetic resonance imaging is
CH 57_p863-875_v3.indd 866 19-07-2015 01:22:40

enign o arian
tumors in pregnancy
a a
uspicion of o suspicion of
malignancy malignancy any si e
bser e till
mme iate surgery
ee s
pontaneous
Persistent tumors
regression
o further treatment
Comple cysts
imple cysts
ermoi cm or
cm
increase in si e
urgery
Conser ati e Conser ati e
laparoscopic
or aspiration surgery postpartum
laparotomy
Figure 57.1 Management of benign ovarian tumors in pregnancy.
found in higher than normal levels during fetal

Box 57.7 Incidence of gynecologic malignancies
in pregnancy development, differentiation, and maturation.
Their levels vary with gestational age. They can-
Cervical intraepithelial neoplasia 1.3/1000 not, therefore, be used for the diagnosis of ovar-
Invasive cervical cancer 1/1000 ian tumors in pregnancy (Box 57.8).
Ovarian cancer 0.1/1000
Breast cancer 0.33/1000
Box 57.8 Diagnostic tests for cancers in
pregnancy
preferred over CT scan, though CT scan may • Ultrasonography: Safe, recommended mode of imaging
be used if the benefits outweigh the risks in this • %6UECP$GPGſVUQWVYGKIJVJGTKUMU
situation. • MRI: Considered safe
• Radiography: Limited radiation, safe
• Tumor markers
Tumor markers Ŧ Levels elevated in pregnancy
Ŧ 8CT[YKVJIGUVCVKQP
Levels of tumor markers such as CA 125, serum
Ŧ Cannot be used
alpha fetoprotein, b hCG, and inhibin A are
CH 57_p863-875_v3.indd 867 19-07-2015 01:22:41

Management of cancers in Box 57.9 adiotherapy and chemotherapy in

pregnancy
pregnancy
• Radiotherapy
Management of malignancies in pregnancy has Ŧ First trimester—fetal death/congenital malforma-
to take into account the fetus as well. Termination tions
of pregnancy may be desirable in some situations Ŧ Second and third trimesters
to safeguard the mother. Treatment may have to Neurodevelopmental abnormalities
be modified and some treatments deferred till Carcinogenesis
delivery. All these issues have to be discussed (GVCNITQYVJFKUQTFGTU
with the woman and her partner and decisions Ŧ Contraindicated in pregnancy
must be made with their concurrence. • Chemotherapeutic drugs
Ŧ Teratogenic and mutagenic
Ŧ First trimester
Surgery Spontaneous miscarriage
Congenital malformations
The best time to perform surgery is the second
Mental retardation
trimester. The risk of miscarriage and preterm
Ŧ Second and third trimesters
labor is less. Lateral tilt is required to relieve the No adverse effects
pressure of the gravid uterus on the vena cava. Considered safe
Anesthesia is safe in pregnancy. Ŧ #HVGTYGGMUQTYKVJKPYGGMUQHGZRGEVGFFG-
livery
adiotherapy Neonatal myelosuppression
Maternal myelosuppression during delivery
Exposure to radiotherapy has several adverse ŦSepsis
effects on the fetus. Exposure in early pregnancy ŦHemorrhage
may result in fetal death or congenital malfor- ŦDeath
mations. Later in gestation, the effects include

carcinogenesis, neurodevelopmental abnor-
malities, mental retardation, growth restriction,
increases the risk of fatal sepsis, hemorrhage,
and skeletal and ophthalmic abnormalities.
and death.
Leukemia and other childhood tumors may
also occur later. The effects are dose related.
Radiotherapy is, therefore, contraindicated in Cervical intraepithelial
pregnancy. If considered mandatory, pregnancy
should be terminated.
neoplasia
Cervical intraepithelial neoplasia (CIN) is often
Chemotherapy encountered in pregnancy. When abnormal
cytological findings are reported, further evalu-
All chemotherapeutic drugs are theoretically ation is necessary for making a final diagnosis.
teratogenic and mutagenic, especially in the
first trimester. Congenital malformations, spon-
Abnormal cytology in pregnancy
taneous miscarriage, mental retardation, and
fetal growth restriction result from exposure to Cervical cytology if done during pregnancy may
chemotherapy. Hence, chemotherapy is con- reveal an abnormality. The abnormality may
traindicated in the first trimester of pregnancy. involve squamous or glandular cells. HPV test-
After the period of organogenesis, there may be ing must be performed, if available, in all women
no adverse effects; therefore, exposure to che- with atypical squamous cells of undetermined
motherapy in the second and third trimesters significance (ASC-US). Further evaluation of
is considered safe (Box 57.9). Administration ASC-US and low-grade squamous intraepithelial
within 3 weeks of expected delivery or after 35 lesion (LSIL) is by a repeat smear after delivery
weeks’ gestation can cause neonatal myelosup- or immediate colposcopy and biopsy depends
pression. Moreover, suppression of the mater- on the severity of abnormality and HPV positiv-
nal bone marrow during labor and delivery ity (Box 57.10).
CH 57_p863-875_v3.indd 868 19-07-2015 01:22:41

• A repeat colposcopy should be performed 6

Box 57.10 Evaluation of abnormal cytology in
pregnancy weeks postpartum before proceeding with
treatment since 70% of CIN may resolve.
• #5%75*28 PGICVKXGWPMPQYPōTGRGCV E[VQNQI[ • Cone biopsy and loop electrosurgical excision
YGGMURQUVRCTVWO
procedure (LEEP) should be avoided unless
• #5%75 *
28RQUKVKXGōEQNRQUEQR[YGGMU microinvasive or invasive cancer is suspected.
postpartum These procedures are associated with the
• LSIL risk of hemorrhage, infection, preterm labor,
• ASC-H/AGC and preterm prelabor rupture of membranes.
• HSIL If considered mandatory, they should be
• Squamous cell carcinoma Immediate colposcopy performed at 14–20 weeks. For a cone biopsy,
• Adenocarcinoma in situ and biopsy the cone should be shallow, away from the
• Adenocarcinoma internal os.
• Women with CIN can be delivered vaginally.
A C, atypical glandular cells; ASC- atypical squamous
cells that cannot exclude HSIL; ASC- S atypical squamous • Microinvasive carcinoma diagnosed by cone
EGNNUQHWPFGVGTOKPGFUKIPKſECPEG P human papilloma vi- biopsy, with cone margins free should be
rus; S high-grade squamous intraepithelial lesion; S delivered vaginally and definitive surgery per-
NQYITCFGUSWCOQWUGRKVJGNKCNNGUKQP
formed 6 weeks postpartum.
• Invasive cancer diagnosed on biopsy or coni-
Colposcopy an biopsy zation should be managed according to stage
and gestational age.
Colposcopy and biopsy are indicated when
Management of CIN in pregnancy is summa-
high-grade squamous intraepithelial lesions
rized in Figure 57.2.
(HSIL) or glandular lesions are reported on
cytology.
• Colposcopy is made easier in pregnancy due Invasive cervical cancer
to eversion of the cervix and visibility of the Cervical cancer is the most common malignancy
transformation zone. The eversion increases in pregnancy. Most cervical cancers in preg-
further as pregnancy advances. Directed nancy are early stage disease probably because
biopsy can be taken to confirm the diagnosis, advanced disease is symptomatic before preg-
from areas suspected to have cervical intraepi- nancy and also interferes with conception.
thelial neoplasia(CIN) II/III or invasive cancer.
Colposcopic interpretation in pregnancy is
difficult due to increased vascularity and preg-
Clinical features and diagnosis
nancy-related changes in the cervix. Most women with stage IA disease are asymp-
tomatic. When an obvious growth is present as in
• Endocervical curettage should not be per-
stage IB or greater, irregular bleeding or blood-
formed during pregnancy.
stained vaginal discharge can occur. Diagnosis
• Cervical biopsy may be associated with bleed-
is by clinical examination. Clinical features and
ing but can be controlled with packing.
diagnosis are listed in Box 57.11.
istological diagnosis of CI Management

Cervical biopsy may confirm CIN. When histo- Microinvasive cancer (stage IA1) with free cone
logical diagnosis of CIN has been made, most margins can be delivered vaginally at term
cases can be reevaluated after delivery and and total hysterectomy performed 6 weeks
treated. postpartum.
Management of invasive cancer depends on
• Many CIN lesions regress after delivery; there-
fore, it is acceptable to defer treatment of CIN • gestational age and
till 6 weeks postpartum. • stage of the disease.
CH 57_p863-875_v3.indd 869 19-07-2015 01:22:41

bnormal cytology
Colposcopy an biopsy
uspecte
C microin asi e in asi e
cancer
Vaginal eli ery Cone biopsy L P
Colposcopy ee s
postpartum
Microin asi e cancer n asi e cancer
efiniti e treatment
Vaginal eli ery Manage accor ingly
urgery postpartum
Figure 57.2 Management of cervical intraepithelial neoplasia in pregnancy. C , cervical intraepithelial neoplasia; P,
loop electrosurgical excision procedure.
arly stage isease (stages IA paclitaxel, deliver by cesarean section at 34

I an IIA) weeks, and proceed with radical surgery.
• If gestational age is >34 weeks, delivery by clas-
Management of early stage disease (stages IA2,
sical cesarean section and radical surgery are
IB, and IIA) depends on gestational age as dis-
recommended.
cussed below (Fig 57.3a).
• If gestational age is <20 weeks, radical hyster- ocally a vance isease (stages II
ectomy and pelvic lymphadenectomy should an III)
be performed. This may be performed with the
Management of locally advanced disease (stages
fetus in utero.
IIB and III) also depends on gestational age, as
• If gestational age is 20–34 weeks, the options
discussed below (Fig. 57.3b).
are as follows:
– Wait until 34 weeks, deliver by a cesarean • If gestational age is <20 weeks, external radia-
section, and proceed with radical surgery. tion should be administered first. Spontaneous
– Administer two to three cycles of neoad- abortion occurs within 2–5 weeks in most
juvant chemotherapy with cisplatin and women in the first trimester. Women in the
CH 57_p863-875_v3.indd 870 19-07-2015 01:22:41

Box 57.11 Clinical features and diagnosis of Mode of delivery

invasive cervical cancer Vaginal delivery does not worsen the prognosis
• Symptoms in stage IA1 or IA2 disease. However, progno-
Ŧ Asymptomatic sis may be altered in larger tumors of stage IB
Ŧ Irregular bleeding or more. In labor, cervical tears and spread of
Ŧ Vaginal discharge tumor and hemorrhage may occur. Episiotomy
• Diagnosis and staging must be avoided since tumor recurrence at this
Ŧ Speculum examination
site has been reported.
Ŧ Bimanual pelvic examination
Classical cesarean is recommended since an
Ŧ Rectal examination
• Further evaluation
incision on the lower segment may cut through
Ŧ Chest X-ray tumor and cause excessive bleeding.
Ŧ Ultrasonography
Liver varian cancer
Urinary tract
Ŧ MRI Ovarian cancers that occur in pregnancy are
In advanced disease usually early stage tumors. Germ cell tumors are
Size of the tumor more common than epithelial tumors.
Parametrial involvement
Liver metastasis
Hydronephrosis Clinical features and diagnosis
Most ovarian tumors are asymptomatic and diag-
nosed on routine ultrasound scan. Occasionally
they may present with torsion. Ultrasonographic
late first or second trimesters may need
features may suggest the diagnosis of malig-
evacuation of the uterus. This is followed by
nancy. Tumor markers may not be of use as dis-
brachytherapy.
cussed earlier.
• If gestational age is 20–34 weeks, the options
are Management
– Perform immediate hysterotomy/cesarean
section followed by a combination of radia- Immediate laparotomy is recommended in all
tion and chemotherapy (chemoradiation). women suspected to have malignant ovarian
– Administer neoadjuvant chemotherapy tumors, irrespective of gestational age.
with cisplatin and paclitaxel, and deliver by
a cesarean section at 34 weeks followed by Germ cell tumors
radiotherapy.
• If gestational age is >34 weeks, classical cesar- Most germ cell tumors in pregnancy are lim-
ean section followed by chemoradiation as per ited to one ovary. At laparotomy, unilateral or
protocol is recommended. bilateral oophorectomy should be performed.
Surgical exploration, lymphadenectomy, omen-
tectomy, and staging should be performed as
Metastatic disease
in the nonpregnant woman. In women with
Women with metastatic disease should be advanced disease in early pregnancy, termina-
treated as would the nonpregnant woman, since tion should be considered since chemotherapy
waiting is not an option. Delivery of the fetus by cannot be delayed till the second trimester.
hysterotomy or cesarean section, chemotherapy Adjuvant chemotherapy is required for all
for metastatic disease, and palliative radiation except stage IA dysgerminoma. A combination
for local disease control are the usual modalities of bleomycin, etoposide, and cisplatin is used.
of management. Chemotherapy can be administered in the sec-
Treatment of invasive cervical cancer in preg- ond and third trimester and the pregnancy may
nancy is summarized in Figure 57.3. be continued till term.
CH 57_p863-875_v3.indd 871 19-07-2015 01:22:41

n asi e cer ical cancer
arly in asi e cancer
ee s ee s ee s
a ical surgery Cesarean

ith fetus in utero ait till eoa ju ant section
ee s chemotherapy
eli er at a ical
eli er surgery
ee s
a ical a ical
surgery surgery
a.
I asi e cer ical ca cer
ocally a a ce isease etastatic esease
ysterotomy
ee s
ee s ee s ee s or cesarea
sectio
ysterotomy Cesarea
xtrer al
or cesarea sectio
ra iatio Chemotherapy
sectio
aluate uterus a iotherapy a iotherapy

a iotherapy
eoa u a t
rachytherapy
chemotherapy
eli er at ee s
a ical sur ery

b.
Figure 57.3 Treatment of invasive cervical cancer in pregnancy. a. Early b. Locally advanced and metastatic.
CH 57_p863-875_v3.indd 872 19-07-2015 01:22:41

Epithelial tumors Mammography is difficult to interpret

in pregnancy but is not contraindicated.
Management of malignant epithelial ovarian Ultrasonography and core/incisional or exci-
tumors in pregnancy depends on the stage of the sional biopsy are used for diagnosis. MRI may be
disease. useful in special situations.
• Tumors of low malignant potential and early Once the diagnosis is made, staging is man-
stage cancers predominate in pregnancy. A datory. Suspicious lymph nodes should be eval-
staging laparotomy should be performed as in uated by fine-needle aspiration biopsy. Further
the nonpregnant woman. Peritoneal washing, evaluation is given in Box 57.12.
bilateral oophorectomy, omentectomy, lym-
phadenectomy, and exploration of the abdo- Management
men are essential for staging. If the pregnancy
Treatment of breast cancer in pregnancy is along
continues, the woman may be delivered at
the same lines as in nonpregnant women with a
term.
few modifications.
• In women with early stage high risk disease,
three cycles of chemotherapy should be • Termination of pregnancy is not required.
administered after the first trimester. • Surgery may be mastectomy or breast-con-
• Management of advanced epithelial tumors serving surgery. Axillary node dissection is
depends on the gestational age. mandatory.
– First trimester: Hysterectomy and cytore- • Breast-conserving surgery should be followed
ductive surgery followed by adjuvant chem- by radiotherapy, which is contraindicated in
otherapy as in the nonpregnant woman. pregnancy. Hence, mastectomy may be an
– Second and third trimester: Removal of option even in early stage disease.
the bulky tumor, oophorectomy, and lim- • Breast-conserving surgery followed by chemo-
ited surgery followed by 3 cycles of chemotherapy during pregnancy and delayed radio-
therapy with cisplatin and paclitaxel is an therapy is also an option.
acceptable option. Completion of surgery • Chemotherapy should be administered with-
should be performed after delivery and out delay following surgery. However, it should
further courses of chemotherapy should be not be administered in the first trimester.
administered.
Breast cancer
Box 57.12 Clinical features, diagnosis, and
Gestational or pregnancy-associated breast can- evaluation of breast cancer in pregnancy
cer is one that is diagnosed in pregnancy, during
• Symptoms
lactation or anytime in the first year after deliv-
Ŧ Breast lump
ery. The majority of breast cancers associated
Ŧ Blood-stained nipple discharge
with pregnancy are infiltrating duct carcinoma. • Diagnosis
Breast cancers in pregnancy may be poorly Ŧ Clinical examination
differentiated and in more advanced stages. Ŧ Ultrasonography
Estrogen and progesterone receptor positivity is Ŧ Core/incisional/excisional biopsy
lower than in nonpregnant women with breast Ŧ Mammography
cancer. Pregnancy does not worsen the progno- Interpretation difficult
sis of the disease. Ŧ MRI
Liver and brain metastasis
Ŧ Chest X-ray
Clinical features and diagnosis Ŧ Bone scan
Most women with breast cancer present with a Only if bone metastasis suspected
lump that can be identified despite pregnancy- Ŧ Assessment of cardiac function and liver function
tests
related breast changes. Blood-stained nipple
for chemotherapy
discharge may be present occasionally.
CH 57_p863-875_v3.indd 873 19-07-2015 01:22:41

• The combination used for chemotherapy is pregnancy because of the associated risk of
doxorubicin and cyclophosphamide with or miscarriage, preterm birth, fetal renal failure,
without 5-fluorouracil. and oligohydramnios.
• Immunotherapy with monoclonal antibodies
such as trastuzumab is not recommended in
Key points
• Uterine leiomyomas, functional ovarian cysts, dermoid • Radiotherapy is contraindicated. Chemotherapy
cysts, and epithelial ovarian cysts are common benign UJQWNFPQVDGWUGFKPVJGſTUVVTKOGUVGT+VKUUCHGKP
neoplasms that occur in pregnancy. the second and third trimesters.
• Uterine leiomyomas are usually diagnosed on ultra- • Abnormal cytology other than atypical squamous cells
sound scan. QHWPFGVGTOKPGFUKIPKſECPEG
#5%75CPFNQYITCFG
• Myomas can give rise to complications in pregnancy. squamous intraepithelial lesions should be evaluated by
6JG[CNUQWPFGTIQTGFFGIGPGTCVKQPYJKEJKUCUUQEK- colposcopy. Biopsy must be performed if high-grade squa-
CVGFYKVJRCKPOKNFHGXGTCPFNGWEQE[VQUKU mous intraepithelial lesion or invasive cancer is suspected.
• Conization and loop electrosurgical excision proce-
• /CPCIGOGPVQHO[QOCUKUEQPUGTXCVKXG'XGPYJGP
dure (LEEP) should be performed only if microinva-
encountered at cesarean section, myomectomy
sive/invasive cancer is suspected.
should be avoided.
• Functional cysts of the ovary and luteoma regress • Treatment of cervical intraepithelial neoplasia (CIN)
URQPVCPGQWUN[CPFECPDGQDUGTXGFYKVJQWVKPVGT- should be deferred till the postpartum period.
vention. Luteoma can give rise to maternal and fetal • Treatment of invasive cervical cancer depends on
virilization. stage of the disease and gestational age.
• Cystic teratoma (dermoid cyst) and epithelial ovarian • Germ cell tumors are more common than epithelial
tumors can undergo torsion, especially in the second ovarian cancers.
trimester and the puerperium. Rupture and hemor-
• All ovarian cancers should be subjected to staging
rhage are other complications. laparotomy. Adjuvant chemotherapy can be adminis-
• When malignancy is suspected, the tumor should be VGTGFCHVGTVJGſTUVVTKOGUVGT
TGOQXGF#NNQVJGTVWOQTUECPDGHQNNQYGFWRVKNN
• )GUVCVKQPCNDTGCUVECPEGTKUWUWCNN[KPſNVTCVKPIFWEV
YGGMU+HVJG[FQPQVTGITGUUUKORNGE[UVUOC[DG
carcinoma. It tends to be more advanced and poorly
aspirated. Dermoid cysts and large cysts must be
differentiated in pregnancy.
removed.
• #HVGTEQPſTOCVKQPQHFKCIPQUKUQHDTGCUVECPEGTUVCI-
• Cervical and breast cancers are the most common
KPICPFOGVCUVCVKEYQTMWRUJQWNFDGFQPG
cancers in pregnancy.
• /CUVGEVQO[HQNNQYGFD[EJGOQVJGTCR[QTDTGCUV
• Ultrasonography is safe. CT scan and MRI can also
EQPUGTXKPIUWTIGT[HQNNQYGFD[EJGOQVJGTCR[CPF
be used in pregnancy.
delayed radiotherapy are treatment options.
Self-Assessment
3. 9JCVHCEVQTUYKNNFGVGTOKPGVJGVTGCVOGPV!
Case-based questions 4. +HVJGFKUGCUGKUKPUVCIG+$YJCVKUVJGVTGCVOGPV!
Case 1
/TU*0VJKTFITCXKFCYKHGQHCEQPUVTWEVKQPYQTMGT Case 2
YCUTGHGTTGFVQVJGJQURKVCNCVYGGMUŏIGUVCVKQPYKVJC
history of blood-stained vaginal discharge and a friable /TU06RTKOKITCXKFCYCUHQWPFVQJCXGCPQXCTKCP
ITQYVJQPVJGEGTXKZ5JGYCUUWURGEVGFVQJCXGEGTXKECN E[UVQHEOKPUK\GCVYGGMUŏIGUVCVKQPFWTKPITQWVKPG
ECPEGTCPFYCUTGHGTTGFHQTHWTVJGTOCPCIGOGPV ultrasonography.
1. What is the most likely diagnosis? 1. *QYYKNN[QWGXCNWCVGVJKURCVKGPV!
2. *QYYKNN[QWGXCNWCVGJGT! 2. What complications can occur?
CH 57_p863-875_v3.indd 874 19-07-2015 01:22:41

3. *QYYKNN[QWOCPCIG! 3. +HPQHGCVWTGUQHOCNKIPCPE[QDUGTXGVKNNŌYGGMU
4. +HVJGE[UVUJQYUHGCVWTGUQHOCNKIPCPE[YJCVKUVJG If it does not regress and is a simple cyst, aspirate.
management? If dermoid cyst, perform laparoscopic surgery at
ŌYGGMU+HUK\GKPETGCUGUQTHGCVWTGUUWIIGU-
tive of malignancy are present, perform laparoscopic
Answers surgery or laparotomy.
4. Laparotomy should be performed, irrespective of
Case 1 gestational age. Unilateral or bilateral oophorectomy
(depending on type of tumor) and staging should be
1. Invasive cervical cancer. done. Omentectomy, lymphadenectomy, and perito-
2. Speculum examination and bimanual pelvic and PGCNYCUJKPICTGGUUGPVKCN6JKUUJQWNFDGHQNNQYGF
rectal examination to stage the disease. Biopsy to D[EJGOQVJGTCR[CHVGTYGGMUŏRTGIPCPE[
EQPſTOFKCIPQUKU%JGUV:TC[CPFWNVTCUQPQITCRJ[
of the liver and urinary tract. MRI only if required and
the disease is in advanced stage. Sample questions
3. Stage of the disease and gestational age.
4. 4CFKECNUWTIGT[YKVJVJGHGVWUKPWVGTQKUVJGVTGCV- Long-answer question
ment of choice. This should be undertaken after
FKUEWUUKQPYKVJVJGRCVKGPV 1. Discuss the clinical features and management of
cervical cancer in pregnancy.
Case 2
1. Ultrasonographic features of malignancy should be
looked for—presence of solid areas, septal thickness, 1. Cervical intraepithelial neoplasia in pregnancy
VJKEMPGUUQHE[UVYCNNCPFRCRKNNCT[GZETGUEGPEGU 2. Evaluation and management of ovarian mass in
Features of cystic teratoma also should be noted. pregnancy
2. Torsion, hemorrhage, and rupture. 3. Management of gestational breast cancer
CH 57_p863-875_v3.indd 875 19-07-2015 01:22:41

Section 8
Social
Obstetrics
CH 58_p876-886_v3.indd 876 19-07-2015 01:23:46

58 Maternal Mortality
Case scenario
Mrs. VN, 28, a fourth gravida, was brought to the labor room in shock.
She had delivered normally 2 hours ago at a local hospital and had
started bleeding profusely after delivery of the placenta. She had been
given intravenous fluids and 1 unit of blood; some medications had been
administered, but the bleeding continued. Since there was no facility for
further management at the local center, she was referred to a tertiary-
level hospital. On the way, she lost consciousness. On examination, she
had acidotic breathing; peripheral pulse and blood pressure were not
recordable. She died 10 minutes after arrival at the tertiary center, while
resuscitative measures were underway.
Introduction &GſPKVKQPU
Maternal mortality is one of the indices of Maternal death is defined by the World Health
health care in every country. Maternal death Organization (WHO) as death of a woman occur-
is always a tragic event and most often avoid- ring during pregnancy, childbirth, or within 42
able. It is estimated that globally, every minute a days of delivery, irrespective of the duration and
mother dies due to complications of pregnancy site of pregnancy, from any cause related to or
or labor.Most maternal deaths occur in develop- aggravated by pregnancy or its management,
ing countries; 86% occur in sub-Saharan Africa but not from accidental or incidental causes.
and south Asia. Preventing maternal death Late maternal death is maternal death occur-
begins with preconceptional management; ring after 42 days but within 1 year of termina-
good antenatal, intrapartum, and postpartum tion of pregnancy.
care; early identification and management of Maternal mortality rate (MMR) is the number
anemia, hypertension, and hemorrhage and of maternal deaths in a given period per 100,000
health education.
CH 58_p876-886_v3.indd 877 19-07-2015 01:23:46

women of reproductive age during the same • Sub-Saharan Africa has the highest MMR
period. (510/100,000 live births), followed by South
Maternal mortality ratio (MMRatio) is de- Asia (190/100,000 live births). In contrast,
fined as the number of maternal deaths in a the MMR in the United States of America is
given period per 100,000 live births during the 21/100,000 live births.
same period. It is obtained by dividing the num- • Approximately 17% of maternal deaths occur
ber of maternal deaths in a population during in India. The MMR was 230/100,000 live birth-
some time interval by the number of live births sin 2008 and has decreased to 200/100,000 live
occurring in the same period. The MMRatio, births in 2010. Every 5 minutes, one woman
therefore, depicts the risk of maternal death rel- in India dies from complications of childbirth
ative to the frequency of childbearing. and 15% of women develop life-threatening
Direct maternal death is the death of a complications.
mother due to obstetric complications of preg- • The mortality ratio in India is not uniform but
nancy, labor, and puerperium or from interven- varies with the region and state (Fig. 58.1).
tions, omissions, incorrect treatment, or a chain The Empowered Action Group (EAG)
of events resulting from any of these factors, for states (Bihar, Jharkhand, Madhya Pradesh,
example, deaths due to eclampsia, postpartum Chattisgarh, Orissa, Rajasthan, Uttar Pradesh,
hemorrhage, or abortion. and Uttarakhand) have a much higher mor-
Indirect maternal death is the death of a tality ratio, and the southern states (Andhra
mother resulting from previous existing diseases Pradesh, Karnataka, Kerala, and Tamil Nadu)
or diseases that developed during pregnancy, have a lower ratio. The mortality ratios for
which were not due to obstetric causes but 2010–2012 are as follows:
aggravated by physiological adaptation to preg-
– EAG states and Assam: 257/100,000
nancy, for example, deaths due to mitral valve
– Southern states: 105/100,000
disease or renal failure.
– Other states: 208/100,000
Pregnancy-associated death is death of a
woman, from any cause, while pregnant or within This difference in mortality ratios is due to
one calendar year of termination of pregnancy, several factors, including availability of gov-
regardless of the duration or site of pregnancy. ernment health programs, accessibility, socio-
Pregnancy-related death is a pregnancy- economic status, culture and customs, literacy,
associated death that results from (a) complica- and awareness.
tions of pregnancy itself, (b) the chain of events • The majority (80%) of maternal deaths are
initiated by pregnancy that led to death, or (c) preventable.
aggravation of an unrelated condition by the
physiological or pharmacological effects of preg-
nancy and that subsequently caused death.
Causes of maternal
Maternal mortality Global mortality
and Indian scenario The causes of maternal mortality are shown in
Figure 58.2.
Maternal mortality in developing countries dif-
fers from that in developed countries. Even within
India maternal mortality varies from state to state. Direct causes
• The global number of maternal deaths has Direct causes are responsible for 75% of
declined from 523,000 in 1990 to 293,000 in 2013, maternal deaths. The major causes of mater-
as per data from UNICEF. The MMR declined by nal death are hemorrhage, sepsis, obstructed
45% with an annual reduction rate of 2.6%. labor and uterine rupture, and hypertensive
• At least 99% of maternal deaths occur in devel- disorders. The other direct causes are abortion,
oping countries; 800 women still die each day ectopic pregnancy, anesthetic accidents, and
due to direct or indirect causes. embolism.
CH 58_p876-886_v3.indd 878 19-07-2015 01:23:46

Maternal Mortality 879
Figure 58.1 Maternal mortality in various states of India, 2007–2009. (Source: Special Bulletin1HſEGQH4GIKUVTCT
General, India.)
Sepsis—puerperal and postoperative—is the

Hemorrhage is the leading cause and next leading direct cause, accounting for 19% of
accounts for almost 30% of deaths. This includes deaths.
antepartum and postpartum hemorrhage, ecto- Obstructed labor and resultant uterine rup-
pic pregnancy, and other causes of hemorrhage. ture and other complications occur in 10% of
CH 58_p876-886_v3.indd 879 19-07-2015 01:23:46

and other medical disorders of pregnancy.

Hypertensi e ther Anemia is the second most common cause and
isor ers
accounts for 19% of deaths. Malaria is common
Hemorrhage
in endemic areas. HIV infection is now emerging
bortion relate as an important cause since it can worsen during
causes pregnancy and also increase the risk of infection.
bstructe Cardiac diseases account for 5%–6% of
labor maternal deaths. Rheumatic valvular disease and
nemia congenital heart diseases are worsened by the
epsis physiological changes of pregnancy, anemia, and
hemorrhage. Hepatitis, transmitted by poor sani-
tary conditions, is also an indirect cause of death.
Co-incidental causes unrelated to pregnancy
Figure 58.2 Causes of maternal deaths, 2005. account for a small, variable percentage of all
deaths. Complications due to spontaneous and maternal mortalities. These are mainly due to
induced abortions such as bleeding and infection accidents or suicides.
account for 9% of deaths. Severe preeclampsia,
eclampsia, HELLP syndrome, and other hyper-
tensive disorders are the cause in 8% of deaths Timing of maternal deaths
(Box 58.1). Amniotic fluid embolism is now being
Most maternal deaths occur after delivery, in
recognized as one of the causes, although the
the immediate postpartum period. Postpartum
actual incidence is difficult to determine.
hemorrhage causes death in 2–3 hours. The time
to death in ruptured uterus, obstructed labor,
Indirect causes and eclampsia may vary from hours to 1–2 days.
Approximately one-fourth of the maternal deaths
The indirect causes of maternal death are ane-
occur in the antepartum period and are due to
mia, cardiovascular diseases, hepatitis, malaria,
antepartum hemorrhage, abortion, and ectopic
pregnancy. Intrapartum deaths are the least fre-
Box 58.1 Causes of maternal deaths quent. The proportion of deaths that occur in ante-
• Direct causes partum, intrapartum, and postpartum periods are
Ŧ *GOQTTJCIG as follows:
#PVGRCTVWOJGOQTTJCIG
• Antepartum: 25%
2QUVRCTVWOJGOQTTJCIG
• Intrapartum: 15%
'EVQRKERTGIPCPE[
Adherent placenta
• Postpartum: 65%
Injuries to the birth canal
Ŧ 5GRUKU
Puerperal endometritis Factors associated with
Postoperative infection
Ŧ 1DUVTWEVGFNCDQTWVGTKPGTWRVWTG high maternal mortality
Ŧ #DQTVKQP
Spontaneous Several factors are associated with higher mater-
Induced nal mortality rates. These are listed in Box 58.2.
Ŧ*GOQTTJCIG
ŦSepsis
Ŧ *[RGTVGPUKXGFKUQTFGTU
Age
• Indirect causes The mortality is higher in teenage pregnancies
Ŧ #PGOKC due to illegitimate pregnancies, induced abor-
Ŧ 1VJGTU tions, lack of antenatal care, higher risk of pre-
Coincidental causes
eclampsia, and obstructed labor. Similarly, mor-
Ŧ Accidents
tality is higher in older women (age >35 years)
Ŧ Suicides
due to multiparity, anemia, induced abortions,
CH 58_p876-886_v3.indd 880 19-07-2015 01:23:47

Box 58.2 Factors associated with high maternal Geographic location

mortality
The EAG states have a higher MMR. As already
• #IG mentioned, these states have low literacy rates,
Ŧ 13–19 years lower per capita income, early marriage, very lit-
Ŧ #IG [GCTU tle spacing between pregnancies, other customs
• Parity that place the mother at risk, poor utilization of
Ŧ 2TKOKITCXKFC
facilities, and higher prevalence of diseases such
Ŧ 2CTKV[
as malaria.
• Lack of antenatal care
• Place of delivery
• )GQITCRJKENQECVKQP rban and rural areas
• 4WTCNCTGCU
The mortality is more in rural areas due to lack
of availability or easy access to facilities, poverty,
illiteracy, and socioeconomic factors.
hypertensive disorders, and antepartum and
postpartum hemorrhage.
Parity The three delays

The second to the fourth pregnancies are con- Following are the three delays associated with a
sidered the safest. Complications are higher in high risk of mortality:
primigravidas but several times higher in mul-
tiparous women with four or more previous • Delay in deciding to seek care
deliveries. Age-related and parity-related com- • Delay in reaching the facility on time
plications account for the mortality. • Delay in receiving treatment
Delay in deciding to seek care is on the part
Socioeconomic status of the family and community. The reasons may
be financial, cultural, or social. Home care by
Health-seeking behavior, education, awareness, unskilled personnel and failure to recognize the
and nutrition are related to socioeconomic status. seriousness of the situation are also important
Maternal mortality is higher in women of low socio- factors.
economic strata. There is increased prevalence of Delay in reaching the facility is due to lack
anemia, malnutrition, unsafe abortion, and lack of of transportation, lack of good roads, and poor
antenatal care and immunization in this group. accessibility.
Delay in receiving treatment is a problem
Antenatal care faced at the healthcare facility. Lack of trained
personnel, lack of supplies, and incorrect treat-
Women who do not have regular antenatal care ment are the usual reasons.
are at a higher risk of anemia, infections, eclamp-
sia and severe preeclampsia, preterm labor
obstructed, and abnormal labor due to malpre-
sentations and cephalopelvic disproportion.
easons for decline in
Place of delivery maternal mortality
Home deliveries and those conducted by The MMR has shown a slow but steady decline
untrained personnel are associated with higher globally. Even in developing countries such as
risk. Approximately 65% of all deliveries in India India, the mortality has decreased. The reasons
still occur at home. for this are listed in Box 58.3.
CH 58_p876-886_v3.indd 881 19-07-2015 01:23:47

program, and National Rural Health Mission

Box 58.3 easons for decline in maternal
mortality (NRHM) are some of the important MCH
programs.
• Increase in deliveries by skilled attendants
• Increase in institutional deliveries
• Country-led health plans Child Survival and Safe
• Better antenatal care Motherhood program
• Increase in awareness
• Better availability of The CSSM program was launched in 1992 and
Ŧ blood banks continued till 1997. It consisted of a safe mother-
Ŧ antibiotics hood and child survival components. Provision
Ŧ cesarean section of aseptic delivery kits and strengthening of first
Ŧ safe abortions referral units for management of high-risk preg-
• 6TCKPKPIKPGOGTIGPE[QDUVGVTKEECTG nancies and obstetric emergencies resulted in a
modest reduction in maternal mortality.
This was subsequently incorporated in RCH
programs. CSSM program is discussed further
Strategies to reduce in Chapter 60, National health programs in
obstetrics.
maternal mortality
Although the mortality ratio has reduced, it has
eproductive and Child ealth
not reached the expected goals. Several strat- program
egies have been planned and implemented in The RCH programs, launched by the Ministry of
developing countries toward further reduction Health and Family Welfare, followed the CSSM
of maternal mortality. program. The first phase of the program was
launched in 1997.
Safe motherhood initiatives

eproductive and Child ealth-I
The safe motherhood initiative was launched
in 1987 to reduce maternal mortality by half by Phase 1 of the RCH program was between 1997
the year 2000 in developing countries. It was and 2004. The RCH-I interventions for reducing
later extended to 2010. Family planning, ante- maternal mortality are listed in Box 58.4.
natal, intrapartum, postpartum care, post- RCH-I is discussed further in Chapter 60,
abortion care, and control of sexually trans- National health programs in obstetrics.
mitted infections and HIV infection are the
goals of the program. This is discussed further Box 58.4 eproductive and child health
in Chapter 60, National health programs in interventions
obstetrics. • Antenatal care
• Intranatal care
• Postnatal care
Maternal and Child ealth • 'OGTIGPE[QDUVGVTKEECTG
• Institutional deliveries
services • (COKN[RNCPPKPI
Several national and international Maternal and • Safe abortion services
Child Health (MCH) services were introduced • +OOWPK\CVKQPCICKPUVVGVCPWU
to reduce maternal and child mortality, and to • 6TCKPKPI6$#UCPF#0/U
promote reproductive health along with physi- • 2TQXKFKPIVTCPURQTVCVKQP
• 7RITCFKPIQNF2*%UCPFUGVVKPIWRQH(47U
cal and psychological development of the child.
The Child Survival and Safe Motherhood (CSSM) A auxiliary nurse midwife; ſTUV TGHGTTCN WPKV P C
program, Reproductive and Child Health (RCH) primary health center; BA traditional birth attendant.
CH 58_p876-886_v3.indd 882 19-07-2015 01:23:47

epro uctive an Chil ealth II abortion care, SBA training, and maternal
The functions of RCH-I were enhanced and death review
strengthened by the RCH-II program launched • District health plan integrating village health
in 2005. The objectives are as follows: plans and state and national plans for health,
sanitation, and nutrition
• To establish healthcare services with improved • Indira Gandhi Matritva Sahyog Yojana
access and quality to respond to the needs of (IGMSY) to promote appropriate utilization of
the disadvantaged people services by providing cash incentives to mothers
• To ensure that no one is denied services • Pradhan Mantri Gram Sadak Yojana (PMGSY)
because of inability to pay to provide connectivity and improve transport
• To ensure better and equitable utilization of • Improving sanitation and hygiene
services • Promoting private–public partnership in
• To further reduce MMR, infant mortality rate, health services
and total fertility rate
The goals, objectives, and strategies of NRHM
The major strategies are as follows: are discussed in detail in Chapter 60, National
• Essential obstetric care, which includes insti- health programs in obstetrics.
tutional delivery and delivery in the presence
of skilled birth attendant (SBA) Millennium Development Goals
• Emergency obstetric care (EmOC) round the
clock at primary health centers (PHCs) and The Millennium Development Goals (MDGs)
community health centers were established by the United Nations in the
• Strengthening referral systems year 2000 and consist of eight international
• Safe abortion services development goals. Improving maternal health
• Newborn and child health services is one of the goals (goal 5):
• New initiatives such as training of doctors, • Target 5A: To reduce the MMR by 75% be-
Janani Suraksha Yojana, and the Vande Mat- tween 1990 and 2015
aram scheme • Target 5B: To achieve universal access to repro-
RCH-II is discussed in detail in Chapter 60, ductive health by 2015
National health programs in obstetrics. The targeted annual reduction in MMR is
5.5%. Implementation of this is by the steps and
strategies given in the following subsections.
ational ural ealth Mission
The NRHM was initiated in India in 2005 to Skilled birth attendants
provide affordable and quality health care
to the poorest households in the remotest Although deliveries in the presence of SBAs is an
regions of the country. Reduction in infant important strategy in MDGs, randomized trials
and maternal mortality is one of the goals of and meta-analysis have not shown a significant
NRHM. Under NRHM, the key strategies are as benefit. Moreover, in addition to SBAs being
follows: made available, their utilization by women must
be ensured.
• Creation of a cadre of accredited social health
activists (ASHA), who counsel women on ante-
natal care, delivery, breastfeeding, nutrition,
Emergency obstetric care
and sanitation and accompany the woman to The seven basic services for provision of EmOC
the health facility as outlined by the WHO are listed in Box 58.5.
• Strengthening of subcenters, PHCs, and com- In addition, if ability to perform a cesarean
munity health centers (CHCs) to provide section and facility for blood transfusion are
24-hour obstetric services available, it is considered comprehensive emer-
• Provision of guidelines for management of gency care. Blood transfusion is an important
obstetric emergencies, referrals, skills lab, component of obstetric care since hemorrhage
CH 58_p876-886_v3.indd 883 19-07-2015 01:23:47

Box 58.5 Basic services for emergency obstet- Policies and infrastructure
ric care Policies and protocols for management of vari-
• Administration of ous clinical situations and complications are an
Ŧ parenteral antibiotics essential and integral part of strategies to reduce
Ŧ uterotonics mortality. These include the following:
Ŧ OCIPGUKWO UWNHCVG KP UGXGTG RTGGENCORUKCGE-
lampsia • Protocols for antenatal and postnatal care
• #UUKUVGFXCIKPCNFGNKXGT[ • Management of complications
Ŧ Forceps • Timely referral systems
Ŧ Vacuum • Community services linked to a healthcare
• Manual removal of placenta facility to provide continuity of care
• 4GOQXCNQHTGVCKPGFRTQFWEVU • Steps to ensure that guidelines and protocols
Ŧ Manually
are available, accessible, and acceptable to the
Ŧ Vacuum aspiration
population
Ŧ &KNCVCVKQPCPFEWTGVVCIG
• 0GQPCVCNTGUWUEKVCVKQPYKVJDCICPFOCUM
• Empowerment of women and eradication of
gender inequality
• Practice of evidence-based medicine
• Regular monitoring and audit of outcomes
• Proper documentation
is the most common cause of maternal death. • Utilization of the data to further improve qual-
The time from onset of bleeding to death can ity of services
be 1–2 hours in antepartum and postpartum
hemorrhage, and this is due to hypovolemic
shock. Blood transfusion will help in buying
time while the patient is being shifted to a ongovernmental
higher center. organi ations
Several nongovernmental organizations (NGOs)
Availability of transport and also share the same goal and work toward reduc-
communication ing maternal deaths. A coordinated effort by the
Availability of transport and communication government, NGOs, and the private sector work-
reduces perinatal mortality significantly and ing together is a major strategy.
maternal mortality to some extent.
Availability of ultrasonography Maternal and Perinatal Death

Availability of ultrasonography helps in the Inquiry and esponse
early diagnosis of ectopic pregnancy, molar Maternal and Perinatal Death Inquiry and
pregnancy, and in the localization of placenta. Response (MAPEDIR) is an initiative by
Early referral for institutional care is made UNICEF, introduced in 2005. It is a collabo-
possible. rative initiative including the Government of
India, state governments, district administra-
Family planning tions, Panchayati Raj, NGOs, medical colleges,
WHO, and UNICEF. It consists of an inquiry to
Family planning reduces mortality in multiple
establish the cause of maternal deaths, sensi-
ways:
tize the health officials to the issues, and gal-
• Reduces the number of unwanted pregnancies vanize the community, organizations, and gov-
• Delays the first pregnancy ernment into taking action. If successful, this
• Reduces multiparity initiative could be extended to more states and
• Increases spacing between pregnancies could contribute significantly toward achieving
• Reduces unsafe abortion MDG 5.
CH 58_p876-886_v3.indd 884 19-07-2015 01:23:47

%QPſFGPVKCNKPSWKT[KPVQ +PVGTXGPVKQPUKPURGEKſE
maternal deaths clinical situations
Confidential inquiry into maternal deaths has
been initiated by a few state governments, and The major causes of maternal mortality have been
awareness is being created among the caregivers identified. Approaches for prevention and treat-
regarding the common causes of maternal death ment of these conditions have been developed
and appropriate action plans are being drawn up (Box 58.6). Educating both the skilled and unskilled
and implemented. birth attendants about the application of these is a
major step in the reduction of maternal mortality.
Box 58.6 +PVGTXGPVKQPUKPURGEKſEENKPKECNUKVWCVKQPU

• *GOQTTJCIG • Hypertensive disorders
Ŧ #EVKXGOCPCIGOGPVQHVJKTFUVCIGQHNCDQT Ŧ /QPKVQTKPIQHDNQQFRTGUUWTGFWTKPIRTGIPCPE[
Ŧ Use of misoprostol when skilled attendant is not avail- Ŧ .QYFQUGCURKTKPKPYQOGPCVJKIJTKUMQH
able preeclampsia
Ŧ Condom balloon tamponade Ŧ #FOKPKUVTCVKQPQHRTQRJ[NCEVKEOCIPGUKWOUWNHCVG
Ŧ 7UG QH WNVTCUQPQITCRJ[ KP CPVGRCTVWO JGOQTTJCIG Ŧ Administration of antihypertensives
CPFſTUVVTKOGUVGTDNGGFKPI • Obstructed labor
• Infection Ŧ 7UGQHRCTVQITCO
Ŧ $GVVGTUCPKVCVKQPCPFUCHGFTKPMKPIYCVGT Ŧ 'CTN[KFGPVKſECVKQPQHCDPQTOCNKV[CPFTGHGTTCN
Ŧ Distribution of clean delivery kits Ŧ Availability of facilities for cesarean section
Ŧ Promotion of si cleans at delivery—clean hands, • Anemia
clean perineum, clean delivery surface, clean cord, Ŧ Iron and folic acid supplementation
ENGCPV[KPIKPUVTWOGPVUCPFENGCPEWVVKPIUWTHCEGU Ŧ Treatment of worm infestations
Ŧ Use of antibiotics Ŧ Dietary advice
Ŧ #PVGPCVCNKOOWPK\CVKQPCICKPUVVGVCPWU • Abortion
Ŧ Anti-retroviral therapy for HIV-positive women Ŧ (COKN[RNCPPKPIUGTXKEGU
Ŧ %JGOQRTQRJ[NCZKU CICKPUV CPF RTQORV VTGCVOGPV QH • Safe abortion services
malaria
Ŧ Utilization of medical methods of abortion
Ŧ Use of antibiotics
Key points
• Maternal mortality is one of the indices of health. Most • /CVGTPCNOQTVCNKV[KP+PFKCXCTKGUYKVJVJGTGIKQPCPF
OCVGTPCNFGCVJUQEEWTKPFGXGNQRKPIEQWPVTKGU state. The Empowered Action Group states have a
• /CVGTPCNFGCVJKUFGſPGFCUFGCVJQHCYQOCPQE- JKIJGTOQTVCNKV[TCVKQ
EWTTKPIFWTKPIRTGIPCPE[FWTKPIEJKNFDKTVJQTYKVJKP • #VQVCNQHQHOCVGTPCNFGCVJUCTGRTGXGPVCDNG
42 days of delivery, irrespective of duration or site of • Causes of maternal mortality are divided into direct,
RTGIPCPE[HTQOCP[ECWUGTGNCVGFVQQTCIITCXCVGF indirect, and other causes.
D[RTGIPCPE[QTKVUOCPCIGOGPVDWVPQVHTQOCE-
cidental or incidental causes. • &KTGEVECWUGUCEEQWPVHQTQHFGCVJUCPFKPENWFG
JGOQTTJCIGUGRUKUQDUVTWEVGFNCDQTJ[RGTVGPUKXG
• aternal mortality rate ( ) is the number of FKUQTFGTUGEVQRKERTGIPCPE[CPGUVJGVKECEEKFGPVU
OCVGTPCNFGCVJUKPCIKXGPRGTKQFRGTYQOGP CPFGODQNKUO*GOQTTJCIGKUVJGNGCFKPIECWUGQH
QHTGRTQFWEVKXGCIGFWTKPIVJGUCOGRGTKQF
maternal mortality.
• /CVGTPCNOQTVCNKV[TCVKQ
//4CVKQKUVJGPWODGTQH
• Anemia is the most important indirect cause. Cardio-
maternal deaths per 100,000 live births, a measure of
vascular disease, hepatitis, malaria, and other medical
VJGTKUMQHFGCVJQPEGCYQOCPJCUDGEQOGRTGIPCPV
disorders are the other indirect causes.
• )NQDCN//4JCUFGENKPGFD[*QYGXGTQH
• /CLQTKV[QHFGCVJU
QEEWTKPVJGRQUVRCTVWO
OCVGTPCNFGCVJUQEEWTKPFGXGNQRKPIEQWPVTKGUQH
period.
maternal deaths occur in India.
(Continued)
CH 58_p876-886_v3.indd 885 19-07-2015 01:23:47


• #IGRCTKV[NQYUQEKQGEQPQOKEUVCVWUNCEMQHCPVGPC- • +ORTQXGOGPVKPOCVGTPCNJGCNVJKUQPGQHVJGIQCNUQH
VCNECTGRNCEGQHFGNKXGT[CPFIGQITCRJKENQECVKQPCTG Millennium Development Goals (MDGs). Implemen-
HCEVQTUVJCVKPƀWGPEGOCVGTPCNOQTVCNKV[ tation of this is by delivery by skilled birth attend-
• Maternal mortality has declined slowly and steadily CPVUVTCKPKPIKPGOGTIGPE[QDUVGVTKEECTG
'O1%
in the past few years. The reasons include increase improved transport and communication facilities,
in delivery by skilled attendants and hospital deliver- CXCKNCDKNKV[QHWNVTCUQPQITCRJ[HCOKN[RNCPPKPICPF
ies, country-led health plans, better antenatal and development of policies and infrastructure.
intrapartum care, better facilities for blood transfusion, • 5GXGTCNPQPIQXGTPOGPVCNQTICPK\CVKQPU
0)1UCNUQ
cesarean section, safe abortion, use of antibiotics, and work toward reduction of maternal deaths.
VTCKPKPIKPGOGTIGPE[QDUVGVTKEECTG
• %QPſFGPVKCNKPSWKT[KPVQOCVGTPCNFGCVJUCPF/CVGTPCN
• 6JGTGCTGUGXGTCNPCVKQPYKFGUVTCVGIKGUCPFRTQITCOU CPF2GTKPCVCN&GCVJ+PSWKT[CPF4GURQPUG
/#2'-
for reduction of maternal mortality. These include safe &+4CTGQVJGTKORQTVCPVUVTCVGIKGU
motherhood initiatives, Maternal and Child Health • +PVGTXGPVKQPUJCXGCNUQDGGPFGXGNQRGFVQOCPCIG

/%*UGTXKEGUKPENWFKPI%JKNF5WTXKXCNCPF5CHG URGEKſEENKPKECNUKVWCVKQPUVJCVCTGCUUQEKCVGFYKVJJKIJ
/QVJGTJQQF
%55/4GRTQFWEVKXGCPF%JKNF*GCNVJ maternal mortality.

4%*+CPF++CPF0CVKQPCN4WTCN*GCNVJ/KUUKQP

04*/
Self-Assessment
2. #EVKXGOCPCIGOGPVQHVJGVJKTFUVCIGQHNCDQT1Z[-
Case-based questions tocin immediately after placental delivery, and if not
available or if there is no skilled birth attendant, oral
Case or rectal misoprostol.
/TU 80 HQWTVJ ITCXKFC YCU DTQWIJV VQ VJG NCDQT
3. Administration of oxytocin, adequate blood transfu-
TQQOKPUJQEM5JGJCFFGNKXGTGFPQTOCNN[JQWTUCIQ
sion, intravenous crystalloids, and condom balloon
CVCNQECNJQURKVCNCPFJCFUVCTVGFDNGGFKPIRTQHWUGN[CH-
VCORQPCFGDGHQTGCPFFWTKPIVTCPUHGT'CTN[KFGPVKſ-
VGTFGNKXGT[QHRNCEGPVC5JGJCFDGGPIKXGPKPVTCXGPQWU
ECVKQPCPFKOOGFKCVGVTCPUHGTVQCJKIJGTEGPVGT
ƀWKFU CPF WPKV QH DNQQF UQOG OGFKECVKQPU JCF DGGP
CFOKPKUVGTGF DWV VJG DNGGFKPI EQPVKPWGF 5KPEG VJGTG
YCUPQHCEKNKV[HQTHWTVJGTOCPCIGOGPVCVVJGNQECNEGPVGT
she was referred to a tertiary-level hospital. On the way, Sample questions
she had lost consciousness. On examination, she had
CEKFQVKEDTGCVJKPIVJGRWNUGCPFDNQQFRTGUUWTGYGTGPQV Long-answer question
recordable. She died 10 minutes after arrival, while resus-
citative measures were underway. 1. &GſPGOCVGTPCNFGCVJCPFOCVGTPCNOQTVCNKV[TCVKQ
What are the causes and what are the steps taken to
1. What are the direct causes of maternal mortality? reduce maternal mortality ratio in India?
9JCVRGTEGPVCIGof maternal mortality occurs due to
JGOQTTJCIG!
2. How would you prevent this?

3. What could have been done at the local center by 1. Maternal mortality
way of treatment?
2. Causes of maternal mortality
3. 4%*KPVGTXGPVKQP
Answers
4. 5VTCVGIKGUVQTGFWEGOCVGTPCNOQTVCNKV[
1. &KTGEVECWUGUCTGJGOQTTJCIGUGRUKUQDUVTWEVGF
labor, hypertensive disorders, and abortion.
#RRTQZKOCVGN[QHFGCVJUQEEWTFWGVQ
JGOQTTJCIG
CH 58_p876-886_v3.indd 886 19-07-2015 01:23:47

59 Perinatal Mortality
Case scenario
Mrs. SG, 32, primigravida, at 38 weeks of gestation, was brought to the

hospital from a primary health center. She had been in labor for 18
hours. On examination, she was dehydrated and exhausted. The uterus
was term size, contracting every 5–6 minutes for 30–40 seconds. The
lower segment was stretched and there was a Bandl’s constriction ring.
On pelvic examination, the cervix was fully dilated, vertex at −2 station,
and molding was 3+; there was a large caput, membranes were absent,
and thick meconium stained fluid was draining. Fetal heart rate was
160–180/min; the electronic monitoring trace showed late decelerations.
A deeply asphyxiated baby weighing 3.8 kg was delivered by a cesarean
section. The baby died on the second neonatal day.
Introduction &GſPKVKQPU
Perinatal mortality is an index of antenatal
and intrapartum care and also of the socio-
Live birth
economic condition of the community. Like Live birth is defined as one in which the
maternal mortality, the perinatal mortality is newborn at or after birth shows any sign of
four to five times higher in developing coun- life such as breathing, presence of a heart-
tries than in the developed world. Although beat, movement of voluntary muscles or cord
institutional deliveries have increased under pulsations.
the national programs, this has not resulted in
the expected reduction in perinatal mortality.
CH 59_p887-894_v3.indd 887 19-07-2015 01:24:28

Stillbirth (fetal death) • The decline in mortality of fetuses after

28 weeks’ gestation has been steady, but
Stillbirth is one where the fetus shows no signs the decline between 20 and 27 weeks has
of life at or after birth. Stillbirths or fetal deaths remained static. The PNMR declined by 25%
are divided into early (20–27 weeks’ gestation or between 1990 and 2003 in the United States
fetus weighing >500 g) and late (>28 weeks’ ges- (from 9/1000 to 6.7/1000). Since then, the
tation or fetus weighing >1000 g). Developing PNMR has remained steady.
countries include under stillbirth only deaths • There are 5.9 million perinatal deaths world-
after 28 weeks, a fetus weighing >1000 g, or with wide annually and most of them are in devel-
a crown–heel length of >35 cm. oping countries.
Stillbirth rate is the number of stillbirths per • In the year 2010, the rates in India were as
1000 births, including live births and stillbirths. follows:
– Neonatal mortality rate: 33/1000 live births
eonatal death – Early neonatal mortality rate: 25/1000 live
births
Neonatal death is the death of an infant before – Stillbirth rate: 7/1000 births
28 days of age. Early neonatal death is one that – PNMR: 32/1000 births
occurs in the first 7 days after birth and late neo- • The stillbirth rates are unreliable since they are
natal death is one that occurs from 8 to 28 days grossly underreported.
after birth. • The majority (75%) of neonatal deaths occur in
Early neonatal mortality rate is the number the first week of life and 36% occur in the first
of neonatal deaths before 7 days after birth per 24 hours. Reducing early neonatal mortality
1000 live births. has been a major challenge.
Neonatal mortality rate is the number of • Neonatal deaths account for 40% of mortality
neonatal deaths before 28 days after birth per occurring in the under-5 age group in India.
1000 live births. Neonatal mortality rate dropped by 25% from
1980 to 1990, another 15% from 1990 to 2000,
Perinatal mortality and again by 15% from 2000 to 2009. It was 33
per 1000 live births in 2010.
Perinatal mortality or deaths, according to the
• The perinatal mortality varies in different
World Health Organization (WHO), include
states of India (Table 59.1).
fetal deaths after 28 weeks’ gestation and neo-
• The mortality rates also vary between rural
natal deaths within 7 days of birth. Where ges-
and urban areas (2010):
tational age is not known, fetal weight of 1000 g
or crown–heel length of 35 cm may be used. In Rural Urban Total
developed countries, deaths from 20 weeks’ ges- Overall PNMR/
tation are included under perinatal mortality. 1000 births 35 22 32
Perinatal mortality rate (PNMR) is the num-
Neonatal
ber of stillbirths plus neonatal deaths before
mortality rate 36 19 33
7 days per 1000 births, live and stillborn.
Early neonatal
mortality rate 28 15 25
Perinatal mortality global
and Indian scenario Causes of perinatal
Perinatal mortality rates vary in developing and mortality
developed countries. Even within India, the rates
Perinatal deaths, be they late fetal deaths or
differ between the states.
early neonatal deaths, are due to causes listed in
• PNMR has been declining steadily globally. Box 59.1.
CH 59_p887-894_v3.indd 888 19-07-2015 01:24:28

Perinatal Mortality 889
Table 59.1 Perinatal mortality rates (P M ) in different states of India (2010)
State P M Stillbirth rate eonatal mortality rate

( 1000 births) ( 1000 births) ( 1000 live births)
Madhya Pradesh 42 8 44
Orissa 41 8 42
Uttar Pradesh 35 5 42
Gujarat 32 8 31
Andhra Pradesh 31 7 30
Maharashtra 24 7 22
Tamil Nadu 23 10 16
Kerala 12 7 7
India 32 7 33
Box 59.1 Causes of perinatal mortality Sepsis

• Asphyxia An infection may be acquired antepartum through
Ŧ Antepartum transplacental transmission or intrapartum in
Ŧ Intrapartum prolonged labor, obstructed labor, and prelabor
• Infections rupture of membranes. Neonatal infections can
Ŧ Antepartum occur in prematurity or through infection of the
Ŧ Intrapartum
umbilical cord due to the lack of aseptic precau-
Ŧ Neonatal
tions at delivery. This can progress to septicemia
• Prematurity
and death.
• Pulmonary complications
Respiratory distress syndrome Prematurity
Meconium aspiration
Aspiration pneumonia Prematurity can be due to spontaneous preterm
Pulmonary hemorrhage birth or induced preterm delivery for maternal
• Congenital malformations or fetal compromise.
• Chromosomal anomalies Spontaneous preterm labor can occur in mul-
• Birth injuries tifetal pregnancy, cervical incompetence, prelabor
• Neonatal jaundice rupture of membranes, placental abruption, or
• Metabolic and other causes placenta previa.
Labor is induced preterm in conditions such
as severe preeclampsia/eclampsia, diabetes,
antiphospholipid antibody (APA) syndrome, and
Asphyxia rupture of membranes with maternal complica-
Asphyxia is the result of placental insufficiency tions or nonreassuring fetal status.
and can be due to maternal or fetal causes. It may The preterm neonate may develop respira-
be acute as in placental abruption, cord prolapse, tory distress syndrome, necrotizing enterocolitis,
obstructed labor, or uterine rupture. jaundice, pulmonary hemorrhage, or sepsis, and
Chronic asphyxia occurs in maternal medical all these conditions may contribute to perinatal
disorders and preeclampsia. mortality.
Intrapartum asphyxia occurs in prolonged
and difficult labors, instrumental delivery,
obstructed labor, and uterine rupture. Asphyxia
Low birth weight
can cause a stillbirth or neonatal death. Low birth weight occurs due to chronic placen-
tal insufficiency in maternal conditions such as
CH 59_p887-894_v3.indd 889 19-07-2015 01:24:28

preeclampsia, pregestational diabetes, chronic levels lead to kernicterus, brain damage, and
hypertension, APA syndrome, multifetal preg- death. Prematurity, Rh isoimmunization, ABO
nancy, and intrauterine infections. Fetal chro- and other incompatibilities, and septicemia are
mosomal or congenital anomalies may also be the common causes of neonatal jaundice.
the cause.
Low-birth-weight neonates are prone to
complications such as necrotizing enterocolitis, Metabolic and other causes
hypoxic ischemic encephalopathy (HIE), intra-
Hypoglycemia, hypokalemia, hypocalcemia,
cranial hemorrhage, sepsis, and jaundice.
and hypomagnesemia are metabolic abnor-
malities encountered in maternal diabetes,
Pulmonary complications sepsis, and prematurity. When severe and not
Respiratory distress syndrome is usually associ- treated promptly, they can cause neonatal death.
ated with prematurity and the resultant lack of Polycythemia, which is common in infants born
surfactant. Meconium aspiration occurs in post- to diabetic mothers, can also lead to cardiac fail-
maturity or in conditions in which intrauterine ure and death.
hypoxic episode has led to meconium passage.
This is aspirated when there is antepartum or intra-
partum hypoxia. Pulmonary hemorrhage occurs
in prematurity, sepsis, and low-birth-weight neo-
Predisposing factors
nates. Aspiration of the infected amniotic fluid in Several epidemiological factors and maternal
chorioamnionitis leads to aspiration pneumonia. and fetal conditions predispose to perinatal
mortality.
Congenital malformations
and chromosomal anomalies Epidemiological factors
Congenital malformations that are incompati-
The epidemiological factors are listed in
ble with life such as anencephaly, renal agenesis,
Box 59.2.
large diaphragmatic hernia, omphalocele, tra-
cheoesophageal fistula, and Potter’s syndrome
can cause perinatal deaths. Some anomalies
can be corrected by immediate surgery, but this
Maternal and fetal conditions
depends on the accuracy of antenatal diagnosis Maternal and fetal conditions that predispose
and neonatal surgical facilities available at the to stillbirth or neonatal death have been already
center where delivery takes place. Chromosomal discussed. These are listed in Box 59.3.
anomalies can also cause late fetal death or neo-
natal death.
Box 59.2 Epidemiological factors for perinatal
Birth in uries mortality
Birth injuries result from difficult or instrumen- • Maternal age
tal deliveries. Intracranial injuries can occur in Ŧ 13–19 years
assisted breech delivery and forceps delivery. Ŧ Age >35 years
Obstructed labor, malpresentations, and prema- • Parity
turity are the contributing factors. Ŧ 2CTKV[Ů
• Poor maternal nutrition
eonatal aundice • Rural areas
• Geographic location
Most cases of neonatal jaundice are mild and
• Female illiteracy
self-limiting. However, high indirect bilirubin
CH 59_p887-894_v3.indd 890 19-07-2015 01:24:28

pediatricians in community health centers.

Box 59.3 Maternal and fetal conditions
predisposing to perinatal mortality This leads to inadequate antenatal, intrapar-
tum, and neonatal care.
• Maternal conditions
Ŧ Hypertensive disorders
Ŧ Diabetes mellitus Female illiteracy
Female illiteracy is associated with poor utili-
Ŧ Maternal infections
zation of antenatal care, home deliveries, and
unsafe practices during delivery and in newborn
Ŧ Preterm labor care with an increase in the risk of maternal, ante-
Ŧ Antiphospholipid antibody syndrome natal, intrapartum, and neonatal complications.
Ŧ Obstructed labor/uterine rupture Lack of communication and
Ŧ Instrumental delivery
• Fetal conditions transportation services
Ŧ Congenital anomalies
Early referral and transfer to community or dis-
Ŧ Chromosomal anomalies
Ŧ Fetal growth restriction
trict healthcare services is made difficult due to
Ŧ Malpresentations poor communication and transport facilities.
This increases intrapartum asphyxia, stillbirths,
sepsis, and neonatal deaths.
Timing of perinatal deaths

The majority of perinatal deaths occur in the Strategies to reduce
neonatal period. One-third of stillbirths occur in
labor; two-thirds are late fetal deaths. Neonatal
perinatal mortality
deaths account for 40% of under-5 mortality. A large percentage of perinatal deaths are pre-
ventable. Several general and focused preventive
strategies have been initiated by the government
easons for high neonatal to reduce late fetal, intrapartum, and neonatal
deaths.
mortality in India
General measures
Low socioeconomic status
Prenatal nutrition
Low socioeconomic status predisposes to poor
nutrition, anemia, fetal growth restriction, Nutritional advice to pregnant mothers re-
preterm labor, and more home deliveries by garding the requirement for additional calo-
unskilled birth attendants. ries, carbohydrates, proteins, and minerals and
supplementation of folic acid and iron prevents
malnutrition and anemia in the mother and
ural health infrastructure decreases the risk of low birth weight.
A large percentage of the Indian population is
rural. Inadequate intrapartum and neonatal care Improving antenatal care
facilities in rural health centres is an important
Availability and utilization of antenatal care
contributing factor for high neonatal mortality.
in rural and semiurban areas helps in screen-
• Less than 20% of the rural community health ing and early identification of maternal com-
centers provide essential newborn care ser- plications such as preeclampsia and diabetes.
vices. Facilities for the care of low-birth-weight Ultrasonography aids the diagnosis of congeni-
babies are available in even fewer centers. tal malformations. Supplementation of folic acid
• Statistics in 2010 show that there is a 55% and iron reduces chances of anemia and helps
shortfall of obstetricians and 69% shortfall of prevent neural tube defects.
CH 59_p887-894_v3.indd 891 19-07-2015 01:24:28

Delivery by skilled birth attendants into Reproductive and Child Health (RCH)
programs.
Delivery by skilled birth attendants will ensure
early referrals when there are complications,
reduce the risk of obstructed labor, help in eproductive and Child ealth
appropriate management of malpresentations Programs I and II
and labor abnormalities, promote aseptic tech-
niques, and ensure early breastfeeding. RCH-I and II also focus on the following:
• Immunization
Training of midwives and traditional • Essential newborn care
birth attendants in newborn care – Resuscitation of the newborn
– Prevention of hypothermia
In areas where transportation to a good health – Prevention of infection
care facility is difficult, deliveries are conducted – Exclusive breastfeeding
by traditional birth attendants (TBAs) and mid- – Referral of sick newborn
wives. Training the midwives and TBAs in new-
born care is a strategy that has been successful Janani Suraksha Yojana (JSY), under RCH-II,
in many developing countries. encourages institutional delivery, thereby
improving newborn care. This is given in detail
in Chapter 60, National health programs in
Socioeconomic development
Obstetrics.
and education
Improving female literacy, socioeconomic con- ational ural ealth Mission
ditions, nutrition, sanitation, and supply of safe
water are essential basic steps to reduce perina- National Rural Health Mission (NRHM) has
tal mortality. been discussed in Chapter 60, National health
programs in obstetrics. Reducing perinatal and
infant mortality rates is one of the major objec-
tives of NRHM.
ational initiatives to Under NRHM, accredited social health activ-
ists (ASHAs) are selected for every 1000 popula-
improve perinatal mortality tion. The gaps in rural health care are bridged by
the ASHA. She counsels the mother regarding
Maternal and child care the place of delivery, breastfeeding, neonatal
services immunization, and prevention of infections.
With an aim to reducing maternal and infant

mortality, several programs have been intro-
Integrated Management of eonatal
duced under Maternal and Child Health (MCH) and Childhood Illness
services. Integrated Management of Neonatal and
Childhood Illness (IMNCI) is one of the main
Child Survival and Safe Motherhood interventions under NRHM. This is being set up
Program in subcenters and primary health centers. The
strategy encompasses a range of interventions to
Child Survival and Safe Motherhood Program is prevent and manage neonatal and childhood ill-
one of the MCH programs introduced in 1992 nesses such as asphyxia, sepsis, pneumonia, low
(refer to Chapter 60, National health programs birth weight, and other childhood illnesses.
in obstetrics). The program has undertaken
steps to reduce perinatal mortality by antena-
Special Care ewborn nits
tal care, identification of high risk pregnancies
and referral, provision of aseptic delivery kits, Special care newborn units (SCNUs) have been
and promotion of institutional deliveries. This established at district hospitals to educate med-
program has been subsequently incorporated ical officers and equip the facilities to care for
CH 59_p887-894_v3.indd 892 19-07-2015 01:24:28

newborns referred with problems. Newborn institution including transport to a facility, trans-
stabilization units (NBSUs) are set up at the first port between health facilities, cost of drugs and
referral units and community health centers to consumables, 3-day stay in hospital and 7-day
stabilize the neonate and offer initial care before stay in case of a cesarean section, and care of
transferring to district hospitals. sick neonate up to 30 days of age are taken care
of by the government. This program is discussed
Promotion of home-based further in Chapter 60, National health programs
in obstetrics.
newborn care
Promotion of home-based newborn care (HBNC) Comprehensive Emergency
initiative consists of empowering and training
bstetric and ewborn Care
village health workers and ASHAs in basic neo-
natal resuscitation, identification and manage- Comprehensive Emergency Obstetric and
ment of conditions such as neonatal infection Newborn Care (CEmONC) program has also
and hypothermia, and early referral. Easily com- been introduced at facilities at various levels.
prehensible standard management guidelines Round-the-clock emergency obstetric services;
are formulated and made available. infrastructure to manage emergencies such
Janani Shishu Suraksha Karyakram (JSSK) as eclampsia, antepartum/postpartum hem-
is aimed at eliminating out-of-pocket expenses orrhage, and other emergencies; blood bank
for the pregnant woman and sick neonate, facilities; availability of anesthetists; and new-
which are major deterrents to institutional born intensive care units are ensured under this
care. All expenses related to delivery in a public program.
Key points
• Perinatal mortality is an index of antenatal and intra- • Predisposing factors are environmental factors, mater-
partum care and the socioeconomic conditions of the nal age, parity, low socioeconomic status, poor maternal
EQOOWPKV[+VKUHQWTVQſXGVKOGUJKIJGTKPFGXGNQRKPI nutrition, geographic location, and female literacy.
countries than in developed countries.
• Maternal conditions that cause perinatal deaths are
• Perinatal mortality or deaths, according to the WHO, hypertensive disorders, antepartum hemorrhage,
include fetal deaths after 28 weeks’ gestation and neo- diabetes, preterm labor, maternal infections, multifetal
natal deaths within 7 days of birth. Where gestational pregnancy, and operative vaginal delivery.
age is not known, fetal weight of 1000 g or crown– • Fetal conditions are congenital and chromosomal anom-
heel length of 35 cm may be used. In the developed alies, fetal growth restriction, and malpresentations.
countries, deaths from 20 weeks are included under
perinatal mortality. • Strategies to reduce perinatal mortality consist of
prenatal nutrition, improving antenatal care, delivery
• Perinatal mortality rate (PNMR) is the number of
by skilled birth attendants, training of TBAs in newborn
stillbirths plus neonatal deaths before 7 days per 1000
care, and socioeconomic development and education.
births, live and stillborn.
• National programs under Maternal and Child Health
• Perinatal mortality rate has been decreasing globally. services have also incorporated strategies to reduce
Most deaths occur in the developing countries. The perinatal deaths. The programs include Child Survival
PNMR in India in 2010 was 32/1000 births. and Safe Motherhood Program, Reproductive and
• #VQVCNQHQHPGQPCVCNFGCVJUQEEWTKPVJGſTUV Child Health Programs I and II, and National Rural
week of life. Health Mission (NRHM).
• The PNMR varies in different states of India. • Under NRHM, Integrated Management of Neonatal
• Causes of perinatal deaths are asphyxia, infections, and Childhood Illness, special newborn care units,
prematurity, low birth weight, pulmonary complica- home-based newborn care, and Comprehensive
tions, congenital malformations, birth injuries, neonatal Emergency Obstetric and Newborn Care are initiatives
jaundice, and metabolic causes. to reduce perinatal mortality.
CH 59_p887-894_v3.indd 893 19-07-2015 01:24:28

Self-Assessment
weighing 3.8 kg was undertaken at a primary
Case-based question health center
Mrs. SG, 32, primigravida, at 38 weeks’ gestation, was c. Inappropriate intrapartum management and failure
brought to the hospital from a primary health center. She to identify delay in the progress of labor
had been in labor for 18 hours. On examination, she was d. Late referral from primary health center to a higher
dehydrated and exhausted. The uterus was term size, health care facility
contracting every 5–6 minutes for 30–40 seconds. The 3. The following could have been done to prevent this:
lower segment was stretched and there was Bandl’s con- a. Antenatal care, screening for diabetes, and
striction ring. On pelvic examination, the cervix was fully clinical/ultrasonographic estimation of fetal
FKNCVGFXGTVGZCVŦUVCVKQPCPFOQNFKPIYCU CVQE- weight
EKRKVQRCTKGVCN CPF CV RCTKGVQRCTKGVCN UWVWTGU # NCTIG
b. 'CTN[KFGPVKſECVKQPQHCDPQTOCNNCDQTCPFGCTN[
caput was present, membranes were absent, and thick
referral
meconium was draining. Fetal heart rate was 160–180/
c. Referral to a hospital with facilities for cesarean
min; electronic monitoring trace showed late decelera-
section for intrapartum care
tions. A deeply asphyxiated baby weighing 3.8 kg was
delivered by cesarean section. The baby died on the sec-
ond neonatal day.
Sample questions
1. What is the cause of death? Was it avoidable?
2. What are the predisposing factors? Long-answer question
3. What could have been done to prevent this?
1. &GſPGRGTKPCVCNOQTVCNKV[TCVG9JCVCTGVJGECWUGU
of perinatal mortality? How will you prevent perinatal
deaths?
Answers
1. The cause of death is asphyxia. It is avoidable.
2. The predisposing factors are given as follows: Short-answer questions
a. Lack of appropriate antenatal care and screening 1. Causes of perinatal deaths
for diabetes, and proper estimation of fetal weight 2. Strategies to reduce perinatal mortality
b. Lack of awareness and education due to which
delivery for a 32-year-old primigravida with a fetus
CH 59_p887-894_v3.indd 894 19-07-2015 01:24:28

National Health
60 Programs in
Obstetrics
Case scenario
Mrs. NT, 20, primigravida, from a village nearby, was brought to a pri-
vate hospital for delivery. She had antenatal care at a primary health
center elsewhere and was visiting her relatives when she started labor
pains. Her husband was a manual laborer and earned daily wages of
Rs. 250/day. The couple had saved only Rs. 2000 for anticipated expenses
during delivery. On arrival at the hospital, she was told that the delivery
would cost her Rs. 10,000. The couple was distraught and did not know
where to go.
Introduction Health care providers and the public must be

aware of these programs and utilize them appro-
Preventive medicine is an essential component of priately to achieve the goals of these programs.
obstetrics. The aim of obstetric care is to achieve
optical outcomes for the mother and child. This
is achieved through appropriate attention to Safe Motherhood Initiative
social and environmental factors in addition to
obstetric and neonatal care. There are several The Safe Motherhood Initiative (SMI) was
difficulties experienced by women in utilizing launched by the WHO in 1987, following a con-
health care facilities and this is one of the reasons ference in Nairobi, to reduce maternal mortality
for the high maternal and perinatal mortality in ratio in developing countries by half by the year
developing countries. To overcome these diffi- 2000; later it was extended to 2010. It is a world-
culties, which may be financial, social, cultural, wide effort that aims to increase attention to
or physical, the Government of India, the World and reduce the devastating numbers of women
Health Organization (WHO), and other organiza- who die during pregnancy or labor, or suffer
tions have introduced several health programs. life-threatening illness during pregnancy or
CH 60_p895-905_v3.indd 895 19-07-2015 01:27:03

The aims of Maternal and Child Health

Box 60.1 Pillars of safe motherhood
(MCH) services have been to reduce the mater-
• Family planning nal and childhood mortality and to promote
• Antenatal care reproductive health and optimize physical and
• Obstetric (intrapartum) care
psychological development of the child. Several
• Postnatal care
national and international programs have been
• Postabortion care
• STI/HIV control
instituted for this purpose. The current concepts
JWOCPKOOWPQFGſEKGPE[XKTWUS sexually transmitted
infection. • Integration of services by obstetricians, pedia-
tricians, community health workers, and social
workers to promote continuity of care
labor every year. The strategies and interven- • Risk-based approach—identification of
tions outlined by the WHO, referred to as the women and children at high risk, for better
‘pillars of safe motherhood’, are given in Box 60.1. utilization of resources
• Family planning services provide access to • Introduction and training of field workers such
contraception. Efforts are made to reduce as multipurpose workers, dais, traditional
maternal problems related to frequent preg- birth attendants (TBAs), anganwadi workers,
nancies at short intervals and offer safe medi- and accredited social health activists (ASHAs)
cal termination of pregnancy. • Utilizing primary health care to provide MCH
• Antenatal, intrapartum, and postnatal care care; provide education regarding nutrition,
are made available at primary health centers sanitation, and prevention of infections; and
(PHCs), first referral units (FRUs), and com- provide family-oriented care and support
munity health centers (CHCs). Round-the- The MCH programs in India are discussed in
clock availability of doctors and midwives is the subsequent sections.
ensured. Through the emergency obstetric
care (EmOC) program, health care providers
are trained in antenatal and intrapartum care.
• Institutional deliveries are encouraged and uti- Child Survival and Safe
lization of skilled birth attendants promoted. Motherhood program
• Referral system and transport facilities have
been strengthened. The Child Survival and Safe Motherhood (CSSM)
• Programs have been introduced to control sex- program was introduced in 1992, assisted by the
ually transmitted infections (STIs). Prevention, World Bank. The program integrated the services
early diagnosis, and treatment of STIs and of the Family Welfare Program, tetanus toxoid
human immunodeficiency virus (HIV) are immunization of pregnant women, and training
addressed. program for dais. The components of the CSSM
• Overall improvement of the status of women program are given in Box 60.2.
has been achieved through education, empow- The program made a significant impact in
erment, vocational training, and employment many parts of the country. CSSM has been sub-
opportunities. sequently incorporated into the Reproductive
and Child Health (RCH) program in 1996.
Maternal and Child ealth

services eproductive and Child
ealth Program I
Women in the reproductive age group and chil-
dren younger than 5 years are considered a vul-
nerable group with high mortality and morbidity.
&GſPKVKQP
They constitute one-third of the total population Reproductive health is defined as a state in which
of India. people have the ability to reproduce and regulate
CH 60_p895-905_v3.indd 896 19-07-2015 01:27:03

National Health Programs in Obstetrics 897
preterm and low-birth-weight babies, vitamin

Box 60.2 The components of CSSM program
A prophylaxis, and treatment of anemia
• Safe motherhood • Safe motherhood programs: Antenatal care,
Ŧ Early registration of pregnancy institutional deliveries, delivery in the pres-
Ŧ Provide minimum of three antenatal checkups
ence of skilled birth attendants, EmOC, and
Ŧ Tetanus immunization
safe abortion services
Ŧ +FGPVKſECVKQPQHJKIJTKUMRTGIPCPEKGUCPFTGHGTTCN
Ŧ Provision of aseptic delivery kits
• Prevention and management of STIs/RTIs/
Ŧ Strengthening FRUs for dealing with obstetric HIV: Specialist facilities for the diagnosis and
emergencies treatment of STIs/reproductive tract infections
Ŧ Training of TBAs (RTIs) in district hospitals and some subcenters
Ŧ Control of anemia in pregnant women • Adolescent health care: Prevention and treat-
Ŧ Promotion of institutional deliveries ment of anemia and awareness regarding
• Child survival component reproductive health issues
Ŧ Augmentation of oral rehydration therapy program • Integration of services for maternal and child
Ŧ Prevention of blindness care
Ŧ Prevention of acute respiratory infections
• Demand-driven services and programs
Ŧ Universal immunization
through decentralized participatory process
ſTUVTGHGTTCNWPKV BA traditional birth attendant. with a paradigm shift in programs
– From camp oriented to client oriented:
their fertility, women are able to go through Sterilization camps, IUD camps, and immu-
pregnancy and childbirth safely, the outcome of nization camps were replaced by a full range
pregnancies is successful in terms of maternal of RCH services that were need based.
and infant survival and well-being and couples – From target oriented to goal oriented:
are able to have sexual relations free of the fear of Targets for various programs and
pregnancies and of contracting diseases. camps were replaced by goals that were
Based on this concept, the first phase of the demand driven and involved community
program, RCH-I, was launched by the Ministry of participation.
Health and Family Welfare in the year 1997. The – From quantity oriented to quality oriented:
main aim was to reduce infant, child, and mater- The stress on quantity or numbers was
nal mortality rates. RCH-I incorporated the pro- replaced by well-planned health services of
grams listed in Box 60.3. high quality.
The program includes the following: • Upgradation of facilities in PHCs and setting
up of FRUs to provide comprehensive obstet-
• Family planning: Improved methods of con- ric and newborn care
traception, condom distribution, safe abor- • Improvement of outreach services for vulner-
tion services, and intrauterine contraceptive able groups such as urban slums, tribal popu-
device (IUD) insertion services lation, and adolescents
• Child health programs: Essential newborn care,
intensification of immunization, micronutrient
supply, exclusive breastfeeding, special care for eproductive and Child
ealth Program II
Box 60.3 Components of eproductive and
Child ealth Program I Phase II of RCH was launched on April 1, 2005.
• Family planning program The aim was to make a change in major critical
• Child Survival and Safe Motherhood program health indicators, that is, reduce maternal and
• Prevention and management of RTIs/STIs/HIV infant mortality rate and total fertility rate. The
• Adolescent health care and family life education program is a means to achieve outcomes envi-
• Client approach to health care sioned in the Millennium Development Goals,
JWOCPKOOWPQFGſEKGPE[XKTWU reproductive tract National Population Policy 2000, the Tenth Plan,
KPHGEVKQPS sexually transmitted infections. and National Health Policy 2002. RCH-I had
CH 60_p895-905_v3.indd 897 19-07-2015 01:27:03

several lacunae, and attempts have been made

Box 60.5 Ma or strategies of reproductive and
to rectify these in RCH-II. child health program II
• Essential obstetric care
b ectives Ŧ Institutional delivery
The overall objectives of RCH-II are as follows: Ŧ Skilled birth attendants at delivery
Ŧ Empower health workers by training them to use
• To establish health care services with improved emergency drugs
access and quality to respond to the needs of • Emergency obstetric care
the disadvantaged people Ŧ Operationalizing FRUs
• To ensure that no one is denied services Ŧ Round-the-clock services at PHCs and CHCs
because of the inability to pay Ŧ Blood storage facility
• To ensure better and equitable utilization of Ŧ Emergency obstetric and newborn care
• Strengthening referral system
services
Ŧ Communication facilities
Ŧ Transport services
Components of C -II Ŧ Linkage with self-help groups and NGOs
• Newborn and child health
Components of RCH-II are listed in Box 60.4.
Ŧ IMNCI services
Ŧ Skilled care at birth
Strategies of C -II Ŧ SNCUs
Ŧ Home-based newborn care
The essential strategies of RCH-II are listed in • Safe abortion services
Box 60.5. Ŧ Medical methods of abortion
Ŧ Manual vacuum aspiration
Essential obstetric care • New initiatives
Ŧ Training doctors in emergency obstetric care
Round-the-clock obstetric and newborn care
Ŧ Janani Suraksha Yojana
services are made available at PHCs and CHCs to Ŧ Vande Mataram scheme
ensure institutional delivery. Presence of a skilled
C CsEQOOWPKV[JGCNVJEGPVGTU C integrated management
attendant at delivery has been identified as an QHPGQPCVCNCPFEJKNFJQQF+NNPGUUP Cs RTKOCT[JGCNVJEGPVGTU
important strategy to reduce maternal mortal- S C sick newborn care unit.
ity, and this has been implemented in RCH-II.
Auxiliary nurse midwives (ANMs) and nurses are
now permitted to use drugs in emergency situa- room, operation theater, laboratory services,
tions to reduce maternal mortality. and blood storage facility so that they can per-
form cesarean sections.
Emergency obstetric care
Strengthening of referral system
EmOC and newborn care is made available at
FRUs. The FRUs have been equipped with labor First referral units are provided ambulances for
referral and quick transport of women and new-
born babies. Local self-help groups, nongov-
Box 60.4 Components of reproductive and child ernmental organizations (NGOs), and women
health program II groups have been involved in providing commu-
• Population stabilization nication and transport facilities.
• Maternal health
• Newborn care and child health Safe abortion services
• Adolescent health
• Control of RTIs/STDs Medical termination of early pregnancy with
• Urban and tribal health mifepristone and misoprostol and manual vac-
• New initiatives uum aspiration are safe methods of termination.
TGRTQFWEVKXGVTCEVKPHGEVKQPS D sexually transmitted Under RCH-II, facilities for these methods of ter-
disease. mination are provided.
CH 60_p895-905_v3.indd 898 19-07-2015 01:27:03

ewborn and child health • The program is 100% centrally sponsored.

components • The objective of the initiative is to reduce
maternal and infant mortality and promote
Integrate anagement o eonatal institutional deliveries.
an Chil hoo Illness • It integrates cash assistance with delivery and
postdelivery care.
Care of the newborn child and young children is
• The benefit is available to
a continuum. Therefore, it is desirable to have an
– Low-performing states: All pregnant women,
integrated approach to this vulnerable section.
delivering in government health centers
The Government has therefore introduced inte-
such as subcenters, PHC/CHC/FRU/gen-
grated management of neonatal and childhood
eral wards of district and state hospitals, or
illnesses (IMNCI).
accredited private institutions
• IMNCI is one of the main strategies under – High-performing states: Below-poverty-
RCH-II. It is an integrated approach to preven- line pregnant women, aged 19 years and
tion of diseases, promotion of child health and above
development, and provision of standard care – Low- and high-performing states: All women
for management of childhood illnesses. belonging to scheduled castes (SC) and
• Skilled personnel are trained to provide care scheduled tribes (ST), delivering in a gov-
from birth up to 2 months of age. ernment health center such as subcenters,
• Preservice IMNCI training is included in the PHC/CHC/FRU/general ward of district
medical curriculum. and state hospitals, or accredited private
• Facility-based IMNCI integrates IMNCI care institutions
with facility-based care and focuses on in- – In 2013, the age cutoff of 19 years has been
patient management of neonatal childhood removed for below-poverty-line women in
illnesses such as asphyxia, pneumonia, diar- all states.
rhea, malaria, respiratory infections, measles, • ASHAs serve as a link between the woman and
and malnutrition. the health care facility.
• The scale of cash assistance is different for
Stabilization care facilities for sick newborns rural and urban areas. Cash assistance con-
are provided at CHCs, FRUs, and district hospi- sists of a mother’s package and an ASHA’s
tals, and sick newborn care units (SNCUs) have package.
been set up at district hospitals. Home-based • The entitlements include drugs, consumables,
newborn care by the ASHAs has been developed transport from home to institution and back,
in some states. free food, free diagnostic tests, and treatment
of the newborn.
• Assistance covers normal delivery and cesar-
ew initiatives ean section at government hospitals or accred-
raining o octors ited private institutions.
• The scheme has resulted in a significant rise in
Training in EmOC for doctors working in FRUs,
institutional deliveries. The increase has been
PHCs, and CHCs is one of the important new
more in low-performing states.
initiatives of RCH-II. Training is also provided
in lifesaving anesthetic skills and performing a
cesarean section. an e ataram Scheme
Under the Vande Mataram scheme, any obstetric
anani Sura sha ojana or gynecology specialist can volunteer to provide
The Janani Suraksha Yojana (JSY) is a safe safe motherhood services. The enrolled doc-
motherhood intervention introduced by the tors have a Vande Mataram logo, and patients
Government of India under RCH-II and National are provided cards with the logo. Antenatal and
Rural Health Mission (NRHM) to encour- intrapartum care are provided by the doctor, and
age institutional delivery. It was launched on difficult cases may be referred to government
April 12, 2005. hospitals.
CH 60_p895-905_v3.indd 899 19-07-2015 01:27:03

ational ural ealth Box 60.7 Strategies of M
Mission •
•
Accredited social health activists (ASHAs)
Strengthening of subcenters, PHCs, and CHCs
The NRHM program was launched by the • District health plan
Government of India on April 12, 2005, for a • Sanitation and hygiene
• Strengthening of disease control programs
period of 7 years (2005–2012) to improve rural
• Public–private partnership
health care throughout the country. The objective
• Janani Shishu Suraksha Karyakram (JSSK)
of the program was to provide accessible, afford- • 0GYJGCNVJſPCPEKPIOGEJCPKUOU
able, accountable, effective, and reliable primary • Reorienting medical/health education
health care, especially to the poor and vulnerable
C Cs EQOOWPKV[JGCNVJEGPVGTUP Cs primary health centers.
sections of population. The program included
components of RCH-II, National Disease Control
Program, and strategies of NRHM.
volunteer, educated up to class 8, and receives
performance-based compensation for various
Goals of M activities.
The goals of the NRHM are listed in Box 60.6. • She is trained in public health with training
material developed at the national level.
• She performs the following functions:
Core strategies of M – She facilitates preparation and implementa-
Enhancing public health services at the village tion of village health plan along with angan-
level, PHCs, CHCs, and district level; integrat- wadi workers, ANMs, and self-help groups.
ing health and family welfare programs at the – She is given a drug kit containing essen-
national, state, block, and district levels; and col- tial allopathic drugs and Ayurveda, yoga
lection, assessment, and review are the important and naturopathy, Unani, Siddha, and
strategies of NRHM. To achieve these, the action Homeopathy (AYUSH) drugs and provides
plan consists of several components as listed in primary medical care for minor ailments.
Box 60.7. – She promotes immunization and provides
referral and escort services to pregnant
women and children.
Accredited social health activists – She serves as a link between pregnant
One accredited social health activist (ASHA) is women and the government or private insti-
selected for every 1000 population. tutions for facilitating assistance under JSY.
– She creates awareness in the community
• Every village has a female ASHA chosen by the regarding health, sanitation, and nutrition.
panchayat, to act as a link between the com- – She counsels women regarding safe deliv-
munity and public health system. She is a ery, breastfeeding, contraception, immuni-
zation, and STDs.
– She helps in the construction of household
Box 60.6 Goals of M toilets.
• Reduction in – She works closely with a Anganwadi workers
Ŧ infant mortality rate to 60/1000 live births and ANMs.
Ŧ maternal mortality ratio to 220/100,000 live births
• Universal access to public health services Strengthening of subcenters,
• Prevention and control of
Ŧ communicable diseases
P Cs, and C Cs
Ŧ noncommunicable diseases A variety of measures can be undertaken for
• Population stabilization strengthening of subcenters, PHCs, and CHCs,
• Promotion of healthy life style
such as follows:
• Revitalization of local health traditions and AYUSH
A S Ayurveda, yoga and naturopathy, Unani, Siddha, and • Strengthening of subcenters by (a) supplying
homeopathy. essential drugs, both allopathic and AYUSH,
CH 60_p895-905_v3.indd 900 19-07-2015 01:27:03

(b) commissioning of new subcenters and ther strategies

upgrading existing ones, and (c) providing
multipurpose health workers and additional Other strategies include the following:
ANMs whenever necessary • District Health Plan is an amalgamation of vil-
• Strengthening of PHCs by (a) providing round- lage health plans and state and national plans
the-clock service at PHCs, (b) supplying essen- for health, water supply, sanitation, and nutri-
tial drugs, and (c) upgrading existing PHCs tion. All health and family welfare programs at
and initiating new programs for the control of district levels merged together are called the
noncommunicable diseases District Health Mission, and all state-level plans
• Strengthening of CHCs for first referral care are together called the State Health Mission.
by (a) providing 24-hour service at CHCs, (b) • Sanitation and hygiene are guided by the
setting up standards for infrastructure, staff- District Health Mission and implemented
ing, and functioning of CHCs, and (c) hospital through village health and sanitation com-
management by the Rogi Kalyan Samiti or the mittee. ASHAs are involved in promoting con-
hospital management committee struction of household toilets.
• Disease control programs for malaria, TB,
anani Shishu Suraksha Karyakram filaria, blindness, and iodine deficiency are
integrated. New initiatives have been launched
Under JSY, institutional deliveries increased but for control of noncommunicable diseases.
out-of-pocket expenditure for women and their • Nearly 75% of health services are by the private
families was high. The Janani Shishu Suraksha sector; therefore, guidelines for private–public
Karyakram (JSSK) was launched in June 2011 partnership have been developed.
to assure free services to all pregnant women • Mobile medical units and ambulance services
and sick neonates accessing public health have been provided to remote areas.
institutions.
Expenses incurred are toward admission
charges, diagnostic tests, charges for a cesarean utcomes of M
section, diet, and transport. These factors are ational level
the cause for 25% of women not seeking institu-
tional delivery. Outcomes of NRHM at the national level are as
The scheme entitles pregnant women and follows:
sick newborn to a number of services listed in • Reduction in infant mortality rate, maternal
the following subsections. mortality ratio, and fertility rate
• Reduction in mortality rate of communica-
regnant omen
ble diseases such as kala-azar, dengue, and
Pregnant women are provided Japanese encephalitis
• free drugs, consumables, blood transfusion, • Reduction in the prevalence of leprosy
diagnostic tests, and diet; • Increase in the utilization of directly observed
• free transport from home to health care facil- therapy services (DOTS) for TB
ity and back and between facilities in case of • Increase in the utilization of FRUs
referral;
• free stay at the facility for >48 hours if required Community level
(3 days after normal delivery, 7 days after Outcomes of NRHM at the community level are
cesarean section); as follows:
• free cesarean section.
• Availability of generic drugs for common ail-
Sic ne born ments at subcenters, PHCs, and CHCs
• Good services at PHCs and CHCs
A sick newborn is provided
• Improved transport, referral, escort system,
• free treatment, drugs, consumables, and blood; and subsidized hospital care through JSY
• free transport; resulting in improved institutional delivery
• free stay at hospital up to 30 days. • Improved outreach services
CH 60_p895-905_v3.indd 901 19-07-2015 01:27:03

Key points
• The Government of India, the World Health Organiza- • The core strategies were essential obstetric care,
tion (WHO), and other organizations have launched emergency obstetric care, strengthening referral
several health programs for women from time to time. systems, newborn and child care, safe abortion
• The Safe Motherhood Initiative was launched by the services, and new initiatives.
WHO in 1987 to reduce the maternal mortality ratio in • Providing round-the-clock services at PHCs and
developing countries. community health centers (CHCs), improving trans-
• The pillars of the program were family planning, ante- port facilities, blood storage facility, and Integrated
natal care, intrapartum and postnatal care, postabor- Management of Neonatal and Childhood Illness
tion care, and control of sexually transmitted infection services were important components.

56+JWOCPKOOWPQFGſEKGPE[XKTWU
*+8/CVGTPCN • New initiatives included Janani Suraksha Yojana,
and Child Health (MCH) services were introduced Vande Mataram scheme, and training of doctors in
to reduce maternal and childhood mortality. Several emergency obstetric care.
programs have been introduced under MCH services.
• The National Rural Health Mission (NRHM)
• The Child Survival and Safe Motherhood (CSSM) was launched in 2005, for a period of 7 years.
program was introduced in 1992 and integrated The objective of NRHM is to provide affordable,
Family Welfare Program, TT immunization of pregnant accessible, and reliable health care to the poor
women, and Dais Training Program. The program had and vulnerable.
safe motherhood and child survival components. The
CSSM was incorporated into the Reproductive and • The goals of NRHM were reduction in infant and
Child Health (RCH) program later. maternal mortality rates, prevention and control of
communicable and noncommunicable diseases,
• Reproductive Health Program I was started in 1997
population stabilization, and revitalization of local
to reduce infant, child, and maternal mortality rates.
health traditions and Ayurveda, yoga and naturopathy,
The program includes family planning, child health
Unani, Siddha, and homeopathy (AYUSH).
programs, safe motherhood programs, prevention and
management of STIs/reproductive tract infections and • An accredited social health activist (ASHA) is an
HIV, adolescent health care, and integration of various integral and important part of NRHM. She is a
services for maternal and child care. volunteer who is trained in public health and serves
several functions.
• 5GVVKPIWRQHſTUVTGHGTTCNWPKVUCPFWRITCFCVKQPQHRTK-
mary health centers (PHCs) to provide comprehensive • Strengthening of subcenters, PHCs, and CHCs,
obstetric and newborn care were important strategies District Health Plan, sanitation and hygiene, and
of RCH-I. private–public partnership are core strategies.
• Reproductive Health Program II was launched in 2005 • The NRHM has achieved several positive outcomes at
to reduce maternal and infant mortality rates and total national and community levels.
fertility rate.
Self-Assessment
Case-based question Answers
Mrs. BN, 20, primigravida, from a village in Tamil Nadu, 1. Mrs. BN can make use of the Janani Suraksha Yojana,
was brought to an accredited private hospital for deliv- which is a new initiative under RCH-II/NRHM.
ery. She had antenatal care at a primary health center 2. In high-performing states, women below the poverty
elsewhere and was visiting her relatives when she line or belonging to SC/ST are eligible for the scheme
started labor pains. Her husband was a manual laborer for delivery at PHC/CHC/district hospital or accredited
and earned daily wages of Rs. 200/day. The couple had private hospitals.
saved only Rs. 2000 for anticipated expenses during 3. An accredited social health activist creates aware-
delivery. On arrival at the hospital, she was told that the ness regarding safe delivery, breastfeeding, and
delivery would cost her Rs. 10,000. The couple was dis- immunization and escorts pregnant women to PHCs
traught and did not know where to go. and to institutions to which they are referred.
1. What help is available to Mrs. BN? 4. An ASHA facilitates preparation and implementation
2. What are the criteria for eligibility? of the village health plan along with anganwadi work-
GTU#0/UCPFUGNHJGNRITQWRURTQXKFGURTKOCT[
3. Who normally accompanies pregnant women to the
OGFKECNECTGHQTOKPQTCKNOGPVURTQOQVGUKOOWPK\C-
hospital and advises them regarding the scheme?
VKQPETGCVGUCYCTGPGUUKPVJGEQOOWPKV[TGICTFKPI
4. What are the other functions of ASHA?
CH 60_p895-905_v3.indd 902 19-07-2015 01:27:03

JGCNVJUCPKVCVKQPCPFPWVTKVKQPEQWPUGNUYQOGP 2. What is NRHM? Discuss the goal, objectives, strate-

regarding safe delivery, breastfeeding, contracep- gies, and outcomes of NRHM.
VKQPKOOWPK\CVKQPCPF56&UJGNRUKPEQPUVTWEVKQP
of household toilets and works closely with angan-
wadi workers and ANMs. Short-answer questions
1. Safe Motherhood Initiative
2. Child Survival and Safe Motherhood Program
Sample questions 3. Reproductive and Child Health Programs
4. Janani Suraksha Yojana
1. Discuss the various health programs at the national
level to reduce maternal and infant mortality.
CH 60_p895-905_v3.indd 903 19-07-2015 01:27:03

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Essentials of Obstetrics

Front Matter.indd 1 19-07-2015 13:00:44

Dr Gita Arjun, facog

Front Matter.indd 3 19-07-2015 13:00:44

Copyright © 2015 by Wolters Kluwer Health (India)

10th Floor, Tower C

First Edition, 2015

Published by Wolters Kluwer (India) Pvt. Ltd., New Delhi

For product enquiry, please contact – Marketing Department (marketing@wolterskluwerindia.co.in) or log on

Front Matter.indd 4 19-07-2015 13:00:44

Front Matter.indd 5 19-07-2015 13:00:44

Front Matter.indd 7 19-07-2015 13:00:44

Section 1: Basic Science in Obstetrics 1

Section 2: Antenatal Management 98

Section 3: Intrapartum Management 190

Section 4: Postpartum Management 300

Front Matter.indd 9 19-07-2015 13:00:44

Section 6: Obstetric Complications: Intrapartum 582

Section 7: Maternal Diseases Complicating Pregnancy 693

Section 8: Social Obstetrics 876

Front Matter.indd 10 19-07-2015 13:00:44

CH 01_p001-023_v3.indd 1 17-07-2015 10:41:03

CH 01_p001-023_v3.indd 2 17-07-2015 10:41:03

Rectus sheath abdominis muscles lie on either side of midline.

Skin Anterior rectus

CH 01_p001-023_v3.indd 3 17-07-2015 10:41:04

muscle and may be entrapped or divided if the

Figure 1.2 Structures in the vulva.

CH 01_p001-023_v3.indd 4 17-07-2015 10:41:04

Labia majora Hymen

CH 01_p001-023_v3.indd 5 17-07-2015 10:41:04

The perineum Box 1.4 Muscles of the perineum

The urogenital triangle Muscles of the perineum

Box 1.3 Contents of the urogenital triangle Deep perineal muscles

CH 01_p001-023_v3.indd 6 17-07-2015 10:41:04

Box 1.5 5WRGTſEKCNCPFFGGRRGTKPGCNOWUENGU The anal triangle

The anal sphincters

CH 01_p001-023_v3.indd 7 17-07-2015 10:41:04

uper icial tra s erse

Figure 1.6 6JGCPCNVTKCPING6JGDQWPFCTKGUCTGUWRGTſEKCNVTCPUXGTUGRGTPGKOWUENGUCPVGTKQTN[EQEE[ZRQUVGTKQTN[

muscle and has three parts—subcutaneous,

Perineal body 2GNXKEƀQQT

ectum an Le ator ani

Figure 1.7 %QTQPCNUGEVKQPQHVJGKUEJKQTGEVCNHQUUCG6JGUGCTGYGFIGUJCRGFURCEGUQPGKVJGTUKFGQHVJGCPCNECPCN

CH 01_p001-023_v3.indd 8 17-07-2015 10:41:05

Figure 1.8 Muscles that form perineal body.

CH 01_p001-023_v3.indd 9 17-07-2015 10:41:05

Urethra Pubic bone

rcus ten ineus

Figure 1.9 %QORQPGPVUQHNGXCVQTCPKOWUENGōRWDQTGEVCNKURWDQXCIKPCNKUCPFKNKQEQEE[IGWU

Box 1.10 Internal genital organs

Pubis Internal genital organs

CH 01_p001-023_v3.indd 10 17-07-2015 10:41:06

CH 01_p001-023_v3.indd 11 17-07-2015 10:41:06

upra aginal cer i

CH 01_p001-023_v3.indd 12 17-07-2015 10:41:06

Structure of uterus Box 1.15 Histology of uterus

CH 01_p001-023_v3.indd 13 17-07-2015 10:41:06

which the peritoneum becomes loosely adher-

CH 01_p001-023_v3.indd 14 17-07-2015 10:41:07

Ligaments of the uterus

Changes in ovaries during pregnancy terosacral

CH 01_p001-023_v3.indd 15 17-07-2015 10:41:07

Figure 1.6 6JGCPCNVTKCPING6JGDQWPFCTKGUCTGUWRGTſEKCNVTCPUXGTUGRGTPGKOWUENGUCPVGTKQTN[EQEE[ZRQUVGTKQTN[

Figure 1.7 %QTQPCNUGEVKQPQHVJGKUEJKQTGEVCNHQUUCG6JGUGCTGYGFIGUJCRGFURCEGUQPGKVJGTUKFGQHVJGCPCNECPCN

Figure 1.9 %QORQPGPVUQHNGXCVQTCPKOWUENGōRWDQTGEVCNKURWDQXCIKPCNKUCPFKNKQEQEE[IGWU