Акушерство Фукс англ 2019

УДК 618.2(075.
8) 03-УЧБ-1785
ББК 56.16я73
А44
Reviewers:
I.B. Manukhin, MD, Professor, Head of Obstetrics and Gynecology Chair, General
Medicine Department, A.I. Yevdokimov Moscow State University of Medicine and Dentistry,
honored doctor of RF;
R.I. Shalina, MD, Professor, Obstetrics and Gynecology Chair, Department of Pediatrics,
Pirogov Russian National Research Medical University, honored doctor of RF
А44 Obstetrics / ed. by V.E. Radzinskiy, A.M. Fuks, Сh.G. Gagaev. — M.:
GEOTAR-Media, 2019.
ISBN 978-5-9704-4683-6
The present textbook was developed in accordance with the Federal Educational
Standard of the Russian Federation and syllabi for the course of Obstetrics in the USA
and Great Britain. This textbook differs from its counterparts by its integrated approach
to the contemporary knowledge system in obstetrics and perinatology. The textbook
can be of use to international students studying in Russia as well as Russian students
who plan to have their diplomas recognized abroad and to seek employment overseas.
The structure of the textbook, presentation of material, recourse to the international
classification of disease, the illustrative material, several stages of self-check tasks at the
end of each section — all these features provide for a better assimilation of the material,
give insight into the advantages of the training system in this country and, at the same
time, preparation for certification abroad.
The textbook is intended for medical students, resident medical practitioners,
obstetrician-gynecologists and general practitioners.
УДК 618.2(075.8)
ББК 56.16я73
Права на данное издание принадлежат ООО Издательская группа «ГЭОТАР-Медиа».

Воспроизведение и распространение в каком бы то ни было виде части или целого издания не
могут быть осуществлены без письменного разрешения ООО Издательская группа «ГЭОТАР-
Медиа».
© Коллектив авторов, 2018

© ООО Издательская группа «ГЭОТАР-Медиа», 2019
© ООО Издательская группа «ГЭОТАР-Медиа»,
ISBN 978-5-9704-4683-6 оформление, 2019
WRITING TEAM
Editors in Chief
Victor E. Radzinskiy,
MD, Professor, Head of Department of Obstetrics
and Gynecology with Perinatology Course, People’s
Friendship University of Russia (PFUR, Moscow,
Russia); corresponding member of RSA, Honored
Scientist of the Russian Federation
Aleksandr M. Fuks,
MD, Director, Department of Obstetrics and Gyneco-
logy, Queens Hospital Center (New York, USA);
Assistant Professor of Obstetrics, Gynecology and
Reproductive Science, Department of Obstetrics,
Gynecology and Reproductive Science, Icahn School
of Medicine at Mount Sinai (NY); Adjunct Assistant
Professor of Obstetrics and Gynecology, Department
of Obstetrics and Gynecology, New York Medical
College; Adjunct Assistant Professor of Obstetrics
and Gynecology, Department of Obstetrics and
Gynecology, St. George’s University School of
Medicine
Publishing editors
Cheleby G. Gagaev, Igor N. Kostin,

MD, Professor, Department of Obstetrics MD, Professor, Department of
and Gynecology with Perinatology Course, Obstetrics and Gynecology with
PFUR Perinatology Course, PFUR
4 Участники издания
Authors
Abramov Alexey, MD, Director of PFUR
Apresian Sergey, MD, Professor, Department of Obstetrics and Gynecology with
Perinatology Course, PFUR
Artymuk Natalia, MD, Professor, Head of Department of Obstetrics and
Gynecology at N2 Kemerovo State Medical Academy
Fatkullin Ildar, MD, Professor, Head of Department of Obstetrics and Gynecology,
Kazan State Medical University
Fuks Aleksandr, MD, Director, Department of Obstetrics and Gynecology,
Queens Hospital Center (New York, USA); Assistant Professor of Obstetrics,
Gynecology and Reproductive Science, Department of Obstetrics, Gynecology and
Reproductive Science, Icahn School of Medicine at Mount Sinai (NY); Adjunct
Assistant Professor of Obstetrics and Gynecology, Department of Obstetrics and
Gynecology, New York Medical College; Adjunct Assistant Professor of Obstetrics
and Gynecology, Department of Obstetrics and Gynecology, St. George’s University
School of Medicine
Gagaev Chelebi, MD, Professor, Department of Obstetrics and Gynecology with
Galina Tatiana, MD, Professor, Department of Obstetrics and Gynecology with
Golikova Tatiana, Candidate of Medical Sciences, Assistant Professor, Department
of Obstetrics and Gynecology with Perinatology Course, PFUR
Gordeev Alexander, Candidate of Medical Sciences, teaching assistant, Department
Khamoshina Marina, MD, Professor, Department of Obstetrics and Gynecology
with Perinatology Course, PFUR
Kostin Igor, MD, Professor, Department of Obstetrics and Gynecology with
Kuznetsova Olga, Candidate of Medical Sciences, Associate Professor, Department
Lebedeva Marina, Candidate of Medical Sciences, Associate Professor, Department
Orazmuradov Ogamurad, MD, Professor, Department of Obstetrics and
Gynecology with Perinatology Course, PFUR
Orazov Mekan, MD, Professor of Department of Obstetrics and Gynecology
with Perinatology Course, PFUR, Moscow, Russia
Ordiyants Irina, MD, Professor, Department of Obstetrics and Gynecology with
Penzhoyan Grigoryi, MD, Professor, Head Physician, Kasnodar Regional
Hospital 2, Head of Chair of Obstetrics and Gynecology, Department of Continuing
Medical Education, Kuban State Medical University, Krasnodar, Russia
Plaksina Nina, Candidate of Medical Sciences, Associate Professor, Department
Pogasov Alexander, Candidate of Medical Sciences, Associate Professor,
Department of Obstetrics and Gynecology with Perinatology Course, PFUR
Участники издания 5
Radzinskiy Victor, MD, Professor, Head of Department of Obstetrics and

Gynecology with Perinatology Course, PFUR, Moscow, Russia; Honored Scientist
of the Russian Federation, Сorresponding member of the RSA
Rudneva Olga, Obstetrician-Gynecologist, teaching assistant, Department of
Obstetrics and Gynecology with Perinatology Course, PFUR
Rymashevsky Alexander, MD, Professor, Head of Department of Obstetrics and
Gynecology, Rostov State Medical University
Semiatov Said, MD, Professor, Department of Obstetrics and Gynecology with
Smirnova Tatiana, Candidate of Medical Sciences, Associate Professor,
Department of Obstetrics and Gynecology with Perinatology Course, PFUR
Sokhova Zalina, Candidate of Medical Sciences, Associate Professor, Department
Solovyova Alina, MD, Professor, Department of Obstetrics and Gynecology and
Reproductive Medicine, Institute for Refresher Training, PFUR
Toktar Lilia, Candidate of Medical Sciences, Associate Professor, Department of
Obstetrics and Gynecology with Perinatology Course, PFUR
Totchiev Georgy, MD, Professor, Department of Obstetrics and Gynecology with
Yermolova Nina, Candidate of Medical Sciences, Associate Professor, Department
Yevtushenko Irina, MD, Professor, Professor, Head of Department of Obstetrics
and Gynecology, Siberian State Medical University
Zakharova Nina, MD, Professor, Department of Obstetrics and Gynecology with
СONTENTS
Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
Chapter 1. Fertilization, implantation and organogenesis . . . . . . . . . . . . . . . . . . . . . . . . . 22
1.1. Fertilization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
1.1.1. Germ cells . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
1.1.2. Fertilization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
1.2. Early pregnancy (first trimester) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
1.3. Second trimester . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
1.3.1. Changes in the fetus and extraembryonic structures . . . . . . . . . . . . . . . . . . 35
1.3.2. Development of placenta . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
1.4. Placental physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
1.5. Umbilical cord development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
1.6. Amniotic fluid composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
1.6.1. Development of amnion components . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
1.6.2. Composition of the amniotic fluid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
1.7. Critical periods of fetal development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
1.8. Fetal physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
1.8.1. Fetal circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
1.8.2. Organs and systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
1.8.3. Gestational programming . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56
Chapter 2. Physiological changes during pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
2.1. Metabolic changes during pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
2.1.1. Protein metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
2.1.2. Carbohydrate metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60
2.1.3. Lipid metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
2.1.4. Mineral and water metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
2.1.5. Acid-base balance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
2.2. Physiological changes in organs during pregnancy . . . . . . . . . . . . . . . . . . . . . . . 62
2.2.1. Central nervous system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
2.2.2. Endocrine system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
2.2.3. Cardiovascular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
2.2.4. Blood and hematopoiesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
2.2.5. Respiratory system. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
2.2.6. Digestive system. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68
2.2.7. Immune system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
2.2.8. Urinary system. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
2.2.9. Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
2.2.10. Reproductive system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
2.2.11. Musculo-skeletal system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72
2.3. Influence of harmful factors on fetus. Antenatal care . . . . . . . . . . . . . . . . . . . . . 73
2.4. Rational behavior of healthy pregnant woman . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
2.4.1. Lifestyle and daily regimen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
Contents 7
2.4.2. Daily recreation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
2.4.3. Diet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
2.4.4. Attitude to air and urban transport and driving a car . . . . . . . . . . . . . . . . . 79
2.4.5. Physical exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
2.4.6. Work and employment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
2.4.7. Housekeeping and renovation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
2.4.8. Visiting of public places . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
2.4.9. Clothes and shoes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
2.4.10. Hygiene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
2.4.11. Pharmaceuticals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84
Chapter 3. Antenatal and postpartum care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
3.1. Antenatal care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
3.1.1. Psychological features and behavior changes of pregnant woman . . . . . . . 86
3.1.2. Standards of antepartum care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
3.1.3. Examination of a pregnant woman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
3.1.4. Vitamins and microelements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
3.1.5. Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
3.2. Psychoprophylaxis and preparation for labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
3.3. Postpartum care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96
3.4. Breastfeeding. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
3.4.1. Facts about breastfeeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
3.4.2. Practical advice to lactating women . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98
3.4.3. Breastfeeding technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98
3.5. The newborn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
3.5.1. Anthropometric data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
3.5.2. Newborn care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
3.5.3. Postnatal diagnostics. Hereditary diseases. . . . . . . . . . . . . . . . . . . . . . . . . 104
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106
Chаpter 4. Diagnostics of pregnancy. Еstimation of gestational age and
expected date of delivery. Methods of examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108
4.1. History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108
4.2. Clinical signs of pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
4.3. Gold standard of pregnancy diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
4.3.1. Human chorionic gonadotropin (hCG) . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
4.3.2. Obstetric ultrasound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
4.4. Estimation of gestational age and date of delivery . . . . . . . . . . . . . . . . . . . . . . . 115
4.4.1. Last normal menstrual period (LMP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
4.4.2. Booking visit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
4.4.3. Date of quickening. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
4.4.4. Ultrasonic data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116
4.4.5. Objective findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117
4.5. Methods of examination. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117
4.5.1. Interview of pregnant and parturient woman . . . . . . . . . . . . . . . . . . . . . . 117
4.5.2. General objective examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
4.5.3. Laboratory and instrumental methods of investigation . . . . . . . . . . . . . . 129
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
8 Contents
Chapter 5. Female pelvis in obstetrics. Fetus in labor . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
5.1. Female pelvis in obstetrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
5.1.1. Planes and dimensions of true pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156
5.1.2. Pelvic axis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159
5.1.3. Pelvic inclination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160
5.2. Fetus as an object of labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168
Chapter 6. Origins of labor onset . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170
6.1. Mechanisms of uterine contractive activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170
6.2. Onset of labor and regulation of uterine activity . . . . . . . . . . . . . . . . . . . . . . . . 170
6.2.1. Regulation of uterine activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
6.2.2. Physiology of muscle contraction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
Chapter 7. Mechanism of labor in cephalic (vertex) presentations . . . . . . . . . . . . . . . . . 182
7.1. Factors determining the mechanism of labor . . . . . . . . . . . . . . . . . . . . . . . . . . . 182
7.2. Occipitoanterior variety of vertex presentation . . . . . . . . . . . . . . . . . . . . . . . . . . 186
7.3. Occipitoposterior variety оf vertex presentation . . . . . . . . . . . . . . . . . . . . . . . . . 190
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193
Chapter 8. Clinics and management of labor in vertex presentation . . . . . . . . . . . . . . . . 194
8.1. Basic concepts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 194
8.2. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196
8.3. Hospitalization for childbirth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196
8.4. Stages of labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196
8.4.1. The first stage of labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
8.4.2. The second stage of labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207
8.4.3. The third stage of labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222
Chapter 9. Obstetric anesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
9.1. Causes of pain in labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
9.2. Non-pharmaceutical methods of pain relief . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226
9.3. Pharmaceutical methods of pain relief . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227
9.3.1. Opioid analgesics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227
9.3.2. Ataralgesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 228
9.3.3. Inhalation analgesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 228
9.3.4. Regional anesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232
Chapter 10. Breech presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
10.1. Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
10.2. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
10.3. ICD-10 Code . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
10.4. Terminology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
10.5. Prevalence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
10.6. Complications of vaginal delivery in breech presentation . . . . . . . . . . . . . . . . 236
10.6.1. Complications of the first stage of labor . . . . . . . . . . . . . . . . . . . . . . . . . . 236
10.6.2. Complications of the second stage of labor . . . . . . . . . . . . . . . . . . . . . . . 236
Contents 9
10.7. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
10.8. Diagnostics of breech presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
10.9. Management of pregnancy in breech presentation . . . . . . . . . . . . . . . . . . . . . . 239
10.9.1. Mechanism of labor in frank breech presentation . . . . . . . . . . . . . . . . . . 241
10.9.2. Mechanism of labor with mixed footling and breech
presentations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 244
10.10. Maneuvers in breech presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250
10.10.1. Tsovyanov maneuver in frank breech presentation
(Tsovyanov I maneuver) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250
10.10.2. Tsovyanov maneuver in footling breech presentation
(Tsovyanov II maneuver). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251
10.10.3. Bracht maneuver. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251
10.10.4. Pinard maneuver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252
10.10.5. Løvset’s maneuver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
10.10.6. Mauriceau–Smellie–Veit (MSV) maneuver . . . . . . . . . . . . . . . . . . . . . 254
10.10.7. Martin–Wiegand maneuver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
10.10.8. Burns–Marshall maneuver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
10.10.9. Piper’s forceps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 256
10.11. Management of the third stage of labor and postpartum period . . . . . . . . . . 258
10.12. Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259
Chapter 11. Physiology of postpartum period . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263
11.1. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263
11.2. Anatomical and physiological changes in postpartum period . . . . . . . . . . . . . 263
11.2.1. Genitals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263
11.2.2. Lactation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267
11.2.3. Cardiovascular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270
11.2.4. Urinary system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
11.2.5. Digestive system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
11.2.6. Respiratory system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
11.2.7. Metabolism, fluid and electrolytes balance . . . . . . . . . . . . . . . . . . . . . . . 271
11.3. Clinical features of postpartum period . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
11.4. Management of postpartum period . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
11.5. Contraception in postpartum period . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
Chapter 12. Postpartum complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
12.1. Septic disorders in postpartum period . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
12.1.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
12.1.2. Historical background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
12.1.3. Etiology and pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282
12.1.4. Risk factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
12.1.5. Etiological structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 286
12.1.6. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 288
12.1.7. Nosological forms of postpartum infectious diseases . . . . . . . . . . . . . . . 290
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 313
12.2. Basic principles of diagnosing postpartum infectious disease. . . . . . . . . . . . . 313
12.3. Main components of postpartum infection management . . . . . . . . . . . . . . . . 314
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317
10 Contents
12.4. Non-infectious postpartum disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 318
12.4.1. Subinvolution of uterus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 318
12.4.2. Lochiometra . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 318
12.4.3. Retained fetal membranes in the uterus . . . . . . . . . . . . . . . . . . . . . . . . . . 319
12.4.4. Retained placental fragments in the uterus . . . . . . . . . . . . . . . . . . . . . . . 319
12.4.5. Cracked nipples . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319
12.4.6. Lactostasis (congestion of milk) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321
Chapter 13. Physiology of neonate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323
13.1. Introduction to neonatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323
13.2. Newborn characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323
13.3. Anatomical and functional features of the newborn’s organs
and systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
13.3.1. Respiratory system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
13.3.2. Cardiovascular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 328
13.3.3. Digestive system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 328
13.3.4. Urinary system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 329
13.3.5. Endocrine system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 329
13.3.6. Immune system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 329
13.4. Clinical examination of the newborn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 330
13.4.1. External inspection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331
13.4.2. Assessment of pose and position . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331
13.4.3. Evaluation of communicability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
13.4.4. Assessment of the infant’s cry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
13.4.5. Assessment of muscle tone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
13.4.6. Examination of the skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
13.4.7. Examination of organs and systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333
13.4.8. Neurological examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335
13.5. Newborn primary care in the delivery room. . . . . . . . . . . . . . . . . . . . . . . . . . . 336
13.6. Neonatal care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
13.6.1. Rooming-in and breastfeeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
13.6.2. Swaddling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 340
13.6.3. Sleeping of the newborn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 340
13.6.4. Care of umbilical cord remnant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342
13.7. Transient and adaptive dysfunctions in early neonatal period . . . . . . . . . . . . . 342
13.7.1. Physiological loss of body weight . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343
13.7.2. Body temperature fluctuations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343
13.7.3. Icterus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343
13.7.4. Erythema. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 344
13.7.5. Physiological skin peeling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 345
13.7.6. Caput succedaneum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346
13.7.7. Genital crisis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346
13.7.8. Milia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 347
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 348
Chapter 14. Diseases of newborns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 350
14.1. Newborns with intrauterine growth restriction . . . . . . . . . . . . . . . . . . . . . . . . . 350
14.1.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 350
14.1.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 350
14.1.3. Diagnosis of intrauterine growth restriction in newborns . . . . . . . . . . . . 350
Contents 11
14.2. Neonatal gastrointestinal disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351
14.2.1. Vomiting and regurgitations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 352
14.2.2. Intestinal dysbiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353
14.2.3. Nutritional dyspepsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 354
14.3. Premature infants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355
14.3.1. Definition and classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355
14.3.2. Care of preterm newborns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 356
14.4. Intrauterine infections of newborns. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357
14.4.1. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357
14.4.2. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357
14.4.3. Clinical features and diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358
14.5. Birth injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358
14.5.1. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359
14.5.2. Birth injury to nervous system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359
14.5.3. Spinal cord injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 360
14.5.4. Birth injury to peripheral nervous system . . . . . . . . . . . . . . . . . . . . . . . . 360
14.5.5. Birth injury to osteoarticular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . 361
14.5.6. Other birth injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 361
14.6. Newborn asphyxia. Resuscitation and intensive care. . . . . . . . . . . . . . . . . . . . 363
14.6.1. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363
14.6.3. Clinical presentations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 364
14.6.4. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 365
14.7. Respiratory distress syndrome in newborns . . . . . . . . . . . . . . . . . . . . . . . . . . . 367
14.7.1. Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 367
14.7.3. Clinical features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 368
14.7.4. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 368
14.8. Prevention of congenital malformations. Neonatal screening
for congenital and hereditary disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 369
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 370
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371
Chapter 15. Нemolytic disease of fetus and newborn . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373
15.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373
15.2. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373
15.2.1. Prevalence (U.S. data) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373
15.2.2. Morbidity and mortality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374
15.2.3. Racial features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374
15.2.4. Gender differences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374
15.3. Historical review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374
15.4. Isoimmunization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376
15.5. Fetal hemolytic disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377
15.5.1. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 378
15.5.2. Pathological anatomy and pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . 379
15.5.3. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380
15.6. Hemolytic disease of newborn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383
15.6.1. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383
15.6.2. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 384
15.6.3. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 387
12 Contents
15.7. Prevention of rhesus isoimmunization. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392
Chapter 16. Multiple pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395
16.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395
16.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395
16.3. Historical aspect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395
16.4. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399
16.5. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 401
16.6. Etiology and pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 402
16.7. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 405
16.8. Clinical features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 406
16.9. Management of pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407
16.9.1. Maternal and fetal complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407
16.9.2. Complications of multiple pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 408
16.9.3. The timing and mode of delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412
16.10. Management the delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413
16.11. Course and management of postpartum and neonatal periods . . . . . . . . . . . 416
16.12. Maternal and fetal outcomes of pregnancy and childbirth . . . . . . . . . . . . . . 417
16.13. Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419
Chapter 17. Abnormal labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421
17.1. Actuality, epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421
17.3. Etiology and pathogenesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 422
17.4. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 422
17.5. Uterine inertia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 424
17.5.1. Primary uterine inertia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 424
17.5.2. Secondary uterine inertia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 427
17.6. Excessive uterine activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 429
17.7. Uncoordinated uterine activity (hypertonic dysfunction) . . . . . . . . . . . . . . . . 431
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 432
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433
Chapter 18. Hemorrhage in obstetrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 435
18.1. General information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 435
18.1.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 435
18.1.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 436
18.2. Early pregnancy bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 437
18.2.1. Pregnancy and bleeding cervical ectopy. . . . . . . . . . . . . . . . . . . . . . . . . . 437
18.2.2. Pregnancy and bleeding cervical polyp . . . . . . . . . . . . . . . . . . . . . . . . . . 438
18.2.3. Pregnancy and cervical cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 438
18.2.4. Vaginal or vulvar injury, bleeding varices during pregnancy . . . . . . . . . 439
18.3. Hemorrhage in II–III trimesters and in I–II stages of labor . . . . . . . . . . . . . 439
18.3.1. Placenta previa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 440
18.3.2. Placental abruption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 450
18.4. Hemorrhage in III stage of labor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460
18.4.1. Prolonged III stage of labor due to abnormality of uterine
contractility . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460
18.4.2. Abnormalities of placenta attachment . . . . . . . . . . . . . . . . . . . . . . . . . . . 464
Contents 13
18.5. Postpartum hemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
18.5.1. Early postpartum hemorrhage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
18.5.2. Uterine hypotonia and atonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 469
18.5.3. Hemorrhage in late postpartum period . . . . . . . . . . . . . . . . . . . . . . . . . . 479
18.6. Hemorrhagic shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
18.6.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
18.6.2. Etiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 484
18.6.3. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 484
18.6.5. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 488
18.6.6. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 489
18.6.7. Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
18.7. Disseminated intravascular coagulation (DIС) . . . . . . . . . . . . . . . . . . . . . . . . 493
18.7.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
18.7.2. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
18.7.3. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 494
18.7.4. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495
18.7.6. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 496
18.7.7. Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497
18.8. Amniotic fluid embolization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497
18.8.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497
18.8.2. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497
18.8.3. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 498
18.8.5. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 500
18.8.6. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 501
18.8.7. Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 505
Chapter 19. Early toxicosis — hyperemesis gravidarum . . . . . . . . . . . . . . . . . . . . . . . . . 507
19.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 507
19.2. ICD-10 codes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 508
19.3. Historical review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 508
19.4. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 508
19.5. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
19.6. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
19.7. Common forms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
19.8. Rare forms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513
19.8.1. Dermatosis gravidarum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513
19.8.2. Tetаny gravidarum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513
19.8.3. Osteomalaсia gravidarum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513
19.8.4. Bronchial asthma gravidarum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 514
19.8.5. Acute yellow atrophy of the liver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 514
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 515
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 516
Chapter 20. Preeclampsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517
20.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517
20.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 518
20.3. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 519
14 Contents
20.4. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521
20.5. Clinical features and diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 522
20.6. HELLP syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
20.7. Acute fatty liver of pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
20.8. Differential diagnostics of preeclampsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 530
20.9. Therapy of preeclampsia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 531
20.9.1. Drug-free treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
20.9.2. Drug therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
20.10. Algorithm of labor management in pregnant women
with preeclampsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535
20.11. Postpartum period management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 536
20.12. Prevention of preeclampsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 538
Chapter 21. Miscarriage. Premature (preterm) birth . . . . . . . . . . . . . . . . . . . . . . . . . . . 540
21.1.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 540
21.1.2. Historical aspect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 541
21.1.3. Classification of miscarriage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 542
21.2. Spontaneous abortion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 549
21.2.1. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 549
21.2.2. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 549
21.2.3. Laboratory and instrumental methods of examination. . . . . . . . . . . . . . 551
21.2.4. Differential diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 552
21.2.5. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 553
21.2.6. Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 555
21.2.7. Prevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 555
21.3. Missed abortion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 556
21.3.2. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 556
21.3.3. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 557
21.4. Preterm birth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 559
21.4.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 559
21.4.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 560
21.4.3. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 560
21.4.4. Prediction of preterm birth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 561
21.4.5. Clinical features and diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 562
21.4.6. Treatment. Clinical management of preterm birth . . . . . . . . . . . . . . . . . 563
21.4.7. Prevention of premature birth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 571
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 571
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 572
Chapter 22. Pregnancy, labor and postpartum period in women
with extragenital diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 574
22.1. Blood disorders and pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 575
22.1.1. Anemia in pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 575
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 584
22.1.2. Idiopathic thrombocytopenic purpura . . . . . . . . . . . . . . . . . . . . . . . . . . . 584
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 589
Contents 15
22.2. Urinary truct disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 589
22.2.1. Asymptomatic bacteriuria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 590
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 593
22.2.2. Cystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 593
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 598
22.2.3. Pyelonephritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 598
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 605
22.2.4. Glomerulonephritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 605
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 612
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 613
22.3. Pregnancy and labor with diabetes mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . 615
22.3.1. General information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 616
22.3.2. Gestational diabetes mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 619
22.4. Arterial hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 628
22.4.1. Classification of hypertensive disorders during pregnancy . . . . . . . . . . . 629
22.4.2. Pathogenesis of gestational complications . . . . . . . . . . . . . . . . . . . . . . . . 631
22.4.4. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 633
22.4.5. Differential diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 634
22.4.6. Gestational complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 634
22.4.7. Treatment of hypertension. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 634
22.4.8. Treatment of complications in childbirth and puerperium . . . . . . . . . . 637
22.4.9. The timing and modе of delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 639
22.4.10. Antihypertensive therapy during lactation . . . . . . . . . . . . . . . . . . . . . . . 640
22.4.11. Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 641
22.4.12. Prevention. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 641
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 641
22.5. Arterial hypotension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 641
22.5.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 641
22.5.2. Screening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 641
22.5.3. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 642
22.5.4. Etiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 642
22.5.5. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 642
22.5.8. Gestational complications. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 643
22.5.9. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 643
22.5.10. Differential diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 644
22.5.11. Prevention of gestational complications . . . . . . . . . . . . . . . . . . . . . . . . . 644
22.5.12. Treatment of gestational complications in each trimester . . . . . . . . . . 644
22.5.14. The timing and modе of delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 645
22.5.15. Prevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 645
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 645
22.6. Heart defects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 646
22.6.1. Mitral valve prolapse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 646
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 652
22.6.2. Mitral valve stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 652
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 657
16 Contents
22.7. Gastrointestinal disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 658
22.7.1. Gastroesophageal reflux disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 658
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 661
22.7.2. Peptic ulcer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 661
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 666
22.7.3. Constipation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 666
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 671
22.7.4. Hemorrhoids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 671
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675
22.7.5. Liver disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 680
22.8. Thyroid diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 681
22.8.1. Diffuse toxic goiter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 681
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 689
22.8.2. Hypothyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 689
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 696
22.9. Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 697
22.9.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 697
22.9.2. Prevention. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 697
22.9.3. Screening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 698
22.9.4. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 698
22.9.5. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 698
22.9.6. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 699
22.9.9. Gestational complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 701
22.9.10. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 702
22.9.11. Differential diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 703
22.9.12. Prevention and prediction of pregnancy complications . . . . . . . . . . . . 704
22.9.13. Treatment of gestational complications in each trimester . . . . . . . . . . . 705
22.9.15. Timing and modе of delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 706
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 707
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 708
Chapter 23. Postterm pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 711
23.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 711
23.3. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 711
23.4. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 712
23.5. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 712
23.6. Clinical features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 712
23.7. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 713
23.8. Management of pregnancy and childbirth . . . . . . . . . . . . . . . . . . . . . . . . . . . . 714
23.9. Prevention of postterm pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 718
23.10. Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 718
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 718
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 719
Chapter 24. Abnormal fetal lie and presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 721
24.1. Abnormal fetal lie . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 721
24.1.1. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 722
Contents 17
24.1.2. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 723
24.1.3. Course and management of pregnancy and childbirth . . . . . . . . . . . . . . 723
24.1.4. Рregnancy and childbirth сomplications . . . . . . . . . . . . . . . . . . . . . . . . . 724
24.2. Malpresentation of head . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 725
24.2.1. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 725
24.2.2. Sinciput presentation (military position) . . . . . . . . . . . . . . . . . . . . . . . . . 726
24.2.3. Brow presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 728
24.2.4. Face presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 730
24.3. Asynclitic cephalic presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 734
24.3.1. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 734
24.3.2. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 734
24.3.3. Asynclitism variants. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 734
24.4. Persistent occiput position . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 736
24.4.1. Persistent occiput direct position . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 736
24.4.2. Persistent occiput transverse position. . . . . . . . . . . . . . . . . . . . . . . . . . . . 737
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 738
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 739
Chapter 25. Contracted pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 742
25.1.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 742
25.1.2. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743
25.1.3. Historical aspect. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743
25.2. Anatomically contracted pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 744
25.2.1. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 744
25.2.2. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 746
25.2.3. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 747
25.2.4. Transversely contracted pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 750
25.2.5. Flat pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 751
25.2.6. Generally contracted pelvis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 754
25.3. Management of labor in patients with anatomically contracted pelvis . . . . . . 756
25.3.1. Clinical course of the first stage of labor . . . . . . . . . . . . . . . . . . . . . . . . . 756
25.3.2. Clinical course of the second stage of labor . . . . . . . . . . . . . . . . . . . . . . . 757
25.3.3. Mоdе of delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 758
25.4. Functionally contracted pelvis (cephalopelvic disproportion) . . . . . . . . . . . . 758
25.5. Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 761
25.6. Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 761
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 761
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 762
Chapter 26. Maternal obstetric trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 765
26.1. Vulvar lacerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 765
26.2. Vaginal lacerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 766
26.3. Perineal tears. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 768
26.3.1. Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 768
26.3.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 768
26.3.3. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 770
26.3.5. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 771
26.3.6. Surgical treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 771
26.3.7. Prognosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 774
26.4. Hematoma of external genitals and vagina . . . . . . . . . . . . . . . . . . . . . . . . . . . . 774
18 Contents
26.4.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 775
26.4.4. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 775
26.4.5. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 776
26.5. Cervical tears . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 777
26.5.1. Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 777
26.5.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 777
26.5.4. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 778
26.6. Uterine rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 779
26.6.1. Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 779
26.6.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 780
26.6.4. Threatening uterine rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 783
26.6.5. Ongoing uterine rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 784
26.6.6. Accomplished uterine rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 784
26.6.7. Rupture in deficient uterine scar. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 785
26.6.8. Surgical techniques used in uterine rupture . . . . . . . . . . . . . . . . . . . . . . 788
26.7. Acute uterine inversion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 788
26.7.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 788
26.7.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 788
26.7.3. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 789
26.7.4. Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 789
26.7.6. Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 789
26.7.7. Differential diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 790
26.7.8. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 790
26.7.9. Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 790
26.7.10. Prevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 790
26.8. Overstrain and rupture of pelvic joints . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 791
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 791
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 793
Chapter 27. Operative obstetrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 796
27.1. Pregnancy-preserving surgical procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 796
27.1.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 796
27.1.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 796
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 800
27.2. Obstetric version . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 801
27.2.1. External cephalic version . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 801
27.2.2. Classical external & internal podalic version. . . . . . . . . . . . . . . . . . . . . . 803
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 806
27.3. Delivery operations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 807
27.3.1. Cesarean section . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 807
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 819
27.3.2. Operative vaginal delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 820
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 833
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 836
Contents 19
27.4. Minor obstetric operations (manipulations) . . . . . . . . . . . . . . . . . . . . . . . . . . . 838
27.4.1. Amniotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 838
27.4.2. Perineotomy and episiotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 840
27.4.3. Amnioinfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 841
27.4.4. Manual separation of the placenta and afterbirth . . . . . . . . . . . . . . . . . . 842
27.4.5. Control manual examination of the uterus walls . . . . . . . . . . . . . . . . . . . 843
27.4.6. Bimanual uterine compression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 844
27.4.7. Intrauterine balloon tamponade . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 844
27.4.8. Hysteroscopy in puerperium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 846
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 846
27.5. Fetus destroying operation (embryotomy) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 848
27.5.1. Craniotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 849
27.5.2. Craniotomy of aftercoming head . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 852
27.5.3. Cranioclasy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 853
27.5.4. Decapitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 854
27.5.5. Cleidotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 857
27.5.6. Evisceration, eventration and exenteration . . . . . . . . . . . . . . . . . . . . . . . 858
27.5.7. Spondylotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 859
27.5.8. Сomplications of fetus-destroying oрerations . . . . . . . . . . . . . . . . . . . . . 860
27.5.9. Postpartum management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 860
Remember . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 860
Check yourself . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 862
Answers to tests and clinical situations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 867
Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 872
ABBREVIATIONS
♠ — trade name of a drug
ACTH — adenocorticotropic hormone
AH — arterial hypertension
ALT — alanine aminotransferase
ALV — artificial lung ventilation
APPT — activated partial thromboplastin time
AST — aspartate aminotransferase
BCG — bacillus Calmette-Guerin vaccine
BFP — biophysical fetal profile
BP — arterial blood pressure
CNS — central nervous system
CRL — crown-rump length
CT — computed tomography
CTG — cardiotocography
DIC — disseminated intravascular coagulation
DM — diabetes mellitus
ECG — electrocardiography
EchoCG — echocardiography
ESR — erythrocyte sedimentation rate
FFP — fresh frozen plasma
FFTS — feto-fetal transfusion syndrome
FGR — fetal growth restriction
GI — gastrointestinal
hCG — human chorionic gonadotropine
HDN — hemolytic disease of newborn
HELLP — hemolysis, elevated liver enzymes, low platelet count
HIV — human immunodeficiency virus
ICD-10 — International Classification of Disease, 10th revision
Ig — immunoglobulin
IUGR — intrauterine growth restriction
IVF — in vitro fertilization
MRI — magnetic resonance imaging
PE — preeclampsia
PROM — preterm rupture of membranes
RDS — respiratory distress syndrome
T3 — triiodothyronine
T4 — thyroxin
TTH — thyrotropic hormone
US — ultrasound
UTI — urinary tract infection
WHO — World Health Organization
PREFACE
The present edition is the second part of a University textbook in Obstetrics and
Gynecology in accordance with State educational standards of the USA and the
Russian Federation and corresponding syllabi. The first part, Gynecology, published
in 20141 is now one of most popular textbooks; it is in demand among both medical
students and a broad spectrum of medical specialists in the system of continuing
medical education. The modern paradigm of educational innovations including the
interactive approach to learning that revolutionized the teaching of the twenty first
century has turned the tide on the old paternalist teaching method of ‘do as I do’
and required an active, independent search for sources and knowledge on the part
of the student in accordance with the obligatory requirements of the syllabi.
The present textbook was written in accordance with the Federal educational
standard of the Russian Federation and the syllabi for the course of Obstetrics in the
USA and Great Britain. It stands out among similar textbooks in that it offers an
integral approach to the system of modern knowledge in obstetrics and perinatology.
The textbook can be of use to international students studying in Russia as well
as Russian students who plan to have their diplomas recognized abroad and to
seek employment overseas. The structure of the textbook, presentation of material,
recourse to the international classification of disease, the illustrative material, several
stages of self-check tasks at the end of each section — all these features provide for
a better assimilation of the material, give insight into the advantages of the training
system in this country and, at the same time, preparation for certification abroad.
Following on from the preceding course in Obstetrics and Gynecology (abroad
and in certain Universities in Russia training proceeds in exactly this order2) the
present textbook does not recapitulate the basic material propounded in the first
part, Gynecology textbook: Chapter 1 Medical education in Russia, USA and
Europe; Chapter 2 A brief overview of development and present state of gynecology
and obstetrics; Chapter 3 Female reproductive system.
1 Gynecology: Textbook / Ed. By V.E. Radzinsky, A.M. Fuks.- M., GEOTAR-Media, 2014. — 1000
p. with ill. The textbook was awarded the Ministry of Health prize as a winner in the competition of 2014.
2 See Preface in the Gynecology textbook.
• Chapter 1
FERTILIZATION, IMPLANTATION AND
ORGANOGENESIS
Pregnancy is a long road to a new life; it begins at the moment when the
spermatozoon fertilizes the ovum, and ends with delivery. This period, which is
of paramount importance both for the mother and child, can be divided into the
following main stages of antenatal (pre-delivery) development.
• Embryonic stage starting at the moment of fertilization (at two weeks of
pregnancy)1 to full 10 weeks of pregnancy (full 8 weeks after fertilization) sees
the following events:
– 3–8 weeks: formation of rudiment organs in the fetus;
– 2–4 weeks: formation of the heart and vessels;
– 4–5 weeks: beginning of lung formation, early development of the nervous
system;
– 7–8 weeks: kidney formation.
• Fetal (syn.: antenatal) stage lasting from 11th-week of pregnancy until birth
(8–38 full weeks from fertilization or 10–40 weeks from the fi rst day of the last
menstrual period):
– 8–12 weeks: sex differentiation;
– 15–20 weeks: intensive growth and maturation of the cerebral cortex;
– 20–24 weeks: formation of major functional systems of the fetus.
Embryology (from Greek εμβρυον fetus, embryo, logos — study) developed as a
study of embryogenesis, intrauterine development from the moment of conception
until birth.
The first notions of the child’s intrauterine development emerged in ancient times;
they were propounded in the works of philosophers and doctors of Ancient India,
Egypt and Greece (Hippocratic Corpus). Some of them (like Anaxagoras in the 5th
cent. BC) thought that the paternal or maternal semen contains in miniature all the
parts of the future fetus (Fig. 1.1).
Thus there should exist a small human being not discernible by the eye; its de-
velopment means that it merely grows in size (the idea of premorphism from Lat.
praeformare, to form in advance).
Aristotle (384–322 BC) was the first to challenge these notions (Fig. 1.2). He
stated that the organs of the future fetus develop from the fertilized egg by way of
consecutive transformations (the idea of epigenesis from Lat. epi-, above and genesis,
origin). This thesis by Aristotle persisted in science without essential modifications
1 Henceforward the gestational age is determined starting from the fi rst day of the last menstrual
period, although conception takes place on day 10–18 of the menstrual cycle (2 weeks after the fi rst day
of the last menstrual period, on average).
Chapter 1. Fertilization, implantation and organogenesis 23
until the 17th century. For a long time, the ideas

of premorphism and epigenesis existed side by
side, with premorphism holding the predomi-
nant position, especially in the 17–18th cen-
turies.
The rise of embryology as a science is as-
sociated with the name of William Harvey
(1578–1657), English physician who made sem-
inal contributions to Anatomy and Physiology
(Fig. 1.3).
In 1651 he published his work Experiments
Concerning Animal Generation (Exercitationes
de generatione animalium) which saw count-
less later editions. Having studied the develop-
ment of chicken and some mammals, Harvey
contested the idea of self generation and put Fig. 1.1. Anaxagoras
forward closely reasoned arguments against the
premorphism doctrine. He generalized the no-
tion of the egg as a source of development for
all animals. However, due to the inadequacy of
microscopy equipment, Harvey had no oppor-
tunity of studying the egg of mammals.
Regnier de Graaf (1641–1673), Dutch anato-
mist and physiologist, came close to the discov-
ery of the ovum (Fig. 1.4).
De Graaf was the first to study testicular tu-
bules and defined them as ‘semen-producing
vessels’. In 1672 he described the follicles in
female sex glands which he mistakenly took for
eggs, ova, hence the word ‘ovarium’.
Only a hundred and fifty years later it be-
came possible to establish the truth: using more
Fig. 1.2. Aristotle
advanced microscopy equipment, K.M. Baer
showed that Graafian follicles are merely cavi-
ties where ova are formed and from where they
are released as a result of ovulation (from late
Latin ovulum, small egg, a diminutive word
for ovum).
Karl Ernst von Baer (1792–1876),
Academician of the St Petersburg Academy of
Sciences and its honorary member, holds a spe-
cial place among the founders of embryology
(Fig. 1.5).
He discovered the main laws of embryo-
genesis and made important theoretical gener-
alizations. K.M. Baer was the first to see and Fig. 1.3. William Harvey
24 Obstetrics
describe the ovum of mammals and humans

(1827); he discovered the blastula, explored and
described the development of all major organ
systems from the germinal layer in vertebrates.
Having established the law of similarity between
embryos of different calluses of vertebrates he
showed that during the intrauterine development
the first characteristics to become manifest are
the characteristics of the phyllum followed by
those of the class, order and so on; specific and
individual characteristics develop at later stages
of embryogenesis. He also noted that the human
embryo develops in a fashion similar to that of
all vertebrates.
Fig. 1.4. Regnier de Graaf
1.1. FERTILIZATION
1.1.1. Germ cells

The male germ cell (spermatozoon) (Fig. 1.6)
is a filamentous cell consisting of the head, neck
and tail. The nucleus contains 23 chromosomes,
a half of spermatozoa carry X-chromosome; their
mass is greater than that of the spermatozoa car-
rying Y-chromosome. The spermatozoa carrying
X-chromosome are less motile. The ejaculate is
a jelly-like mass containing a mixture of secret
from the testes, prostate, Kupffer cells and semi-
nal vesicles. Normally the volume of ejaculate is
Fig. 1.5. Karl Ernst von Baer 3–5 ml depending on the man’s age, nutrition
and the intensity of his sex life.
Ejaculate normally contains 200–500 million spermatozoa (no less than 150 mil-
lion); their concentration per 1 ml of sperm exceeds 6 million.
Spermatogenesis. Sperm is produced inside coiled seminiferous tubules that take
up over 97% of the volume of testes. Spermatozoa develop to become mature over
72 hours (Fig. 1.7).
The entire process of spermatogenesis can be broken up into four distinct stages:
reproduction, growth, maturation and formation.
Female germ cells (oocytes) (Fig. 1.8). Formation of the ovaries begins at 8 weeks
of intrauterine development. By the moment of birth, about 1 million of primary
follicles are contained in the cortical layer of the ovary, each of them carrying one
(seldom two) germ cell. Each primary follicle can achieve complete development and
produce an ovum ready to be fertilized. The store of follicles (oocyte pool, ovarian
reserve) cannot be replenished during the woman’s life; this is an individual amount
that reaches its peak values by 3–4 months of gestation (about seven million follicles).
Fig. 1.6. Spermatozoa

Ductus epididymidis
Ductulus aberrans
Ductus deferens
Ductuli efferentes
Ductus epididymidis
Rete testis
(mediastinum testis)
Ductulus aberrans
Ductuli seminiferi
contorti
Fig. 1.7. Structure of testis
As the ovary ages, the number of primordial follicles decreases due to the process
of apoptosis from 1 million at birth to 250,000–300,000 by the time of menarche.
Over the whole span of the woman’s sexual maturity only 400–500 follicles reach
maturation, other primary follicles die.
The mean lifespan of a spermatozoon after ejaculation is 48

NB! hours.
The development of follicles starts with mitosis of follicular cells and their trans-
formation from initially flat ones to cuboid-shaped and then to highly prismatic. The
reproducing cells now called granulosa fill the whole follicle. In the course of further
development the fluid secreted by granulosa cells begins to push the cells aside ousting
26 Obstetrics
a b
polar body
STRUCTURE
OF MATURE
OVUM corona radiata
zona
pellucida
yolk
membrane
ovoplasm
nucleus
c
Fig. 1.8. Ovum: a, b — photomicrography; c — ovum structure
them to the peripheral follicular layers. A cavity filled with follicular fluid is formed
inside the follicle. The follicle itself grows larger, distends; from compact it becomes
hollow, and now it is called a mature follicle (syn.: Graafian follicle, Graafian vesicle).
A developing follicle suppresses the maturation of other follicles. Other follicles that
have begun to mature undergo atresia.
The amount of follicles is not restored during a human lifetime; it

NB! is the pool of oocytes that emerged at the eighth week of intra-
uterine life that is spent.
Atresia of follicles means their destruction

NB!
In atresia the oocyte dies first, then follicular epithelium undergoes adipose trans-
formation and vacuolization; the fluid of the follicle is absorbed, its cavity becomes
hollow and gets obliterated by the ingrowing connective tissue.
A follicle is considered dominant once its diameter reaches 18 mm (Fig. 1.9).
On the outside it is surrounded with fibrous connective tissue consisting of two
layers: the external thin layer of dense connective tissue, and the internal layer rich
in vessels and consisting of large connective tissue cells.
The inner layer of the dominant follicle is represented by several layers of epithelial
cells forming the membrana granulosa. At one point of the mature follicle the cells
of membrana granulosa are collected into a mass which projects into the cavity of
the follicle; this formation is called cumulus oophorus, the ovum is contained inside
it. The ovum is surrounded by three coats:
• yolk membrane which is the superficial layer of the ovum cytoplasm;
• a thick luminous coat of the follicular epithelium, zona pellucida;
• radiate crown (corona radiata) — granulosa cells placed in a radial fashion in
2–3 layers; they adhere to the ovum immediately.
Granulosa cells are of great importance for the ovum nourishment. The follicular
fluid that is formed induces the Graafian vesicle to get larger leading to extreme
distention at its pole extending above the ovarian surface. The protein coat above it
gets overdistended, exsanguinated, thinned out.
The Graafian vesicle opens, under pressure the follicular fluid flows to the place
of rupture (stigma) and carries the ovum with it. The release of a mature ovum from
the follicle into the abdominal cavity is called ovulation.
Having left the follicle the ovum begins its extrafollicular life.
The lifespan of extrafollicular existence of an ovum is no longer

NB! than 24 hours
This premise is of fundamental importance in dealing with practical issues of

fertility and conception (for instance, when determining when to withdraw the
ovum in the procedure of in vitro fertilization and embryo transfer or in preven-
tion of unwanted pregnancy when determining the day most likely for conception
considering the lifespan of spermatozoa and the ovum, which is no more than
three days!)
The ovum released from the follicle finds itself in the abdominal cavity where it
has the opportunity to find its way into the lumen of the Fallopian tube and move
along into the uterine cavity.
After rupture of the Graafian vesicle its inner wall deflates forming folds, the cavity
gets filled with blood. At the same time, an intensive development and reproduction
of granulosa cells begins; now they are lutein cells producing progesterone. The lutein
cells appearing in the place of the ruptured follicle give rise to a temporary endocrine
structure, the corpus luteum. It grows in size fast; its fate depends on what happens
to the ovum. If the ovum is fertilized, the corpus luteum develops and is active until
28 Obstetrics
Dominant follicle
(ultrasound)
Dominant
follicle
Corpus luteum (ultrasound)
Fig. 1.9. Dominant follicle. Ultrasound (a) and laparoscopy (b) images
16 weeks gestation (corpus luteum of pregnancy). If fertilization does not occur, the
process ends in regression of the corpus luteum within 12–15 days. A connective tis-
sue adhesion, corpus albicans, remains in its place. It persists in the ovary for several
days and then resolves and disappears (Fig. 1.10).
a b
Corpus albicans
Corpus luteum
Fig. 1.10. Corpus luteum (a) and albicans (b) in the ovary
1.1.2. Fertilization
Fertilization (conception) is a process when the male and female

NB! sex cells unite and assimilate each other to produce a new organ-
ism with a unique genetic makeup
After the intercourse the ejaculate finds itself in the woman’s vagina, in the
posterior fornix predominantly; that is where the vaginal part of the uterine cervix
faces when the uterus is in anteflexio-anteversio position. After a normal ejaculation
100 million spermatozoa on average remain in the vagina.
A portion of the ejaculate may leak from the vagina, but even in the remaining
portion all the spermatozoa can hardly retain their vitality intact: under the impact
of the acidic medium most spermatozoa either die or lose their motility. Having
overcome the obstacle in the form of cervical plug the remaining sperm finds itself
in the uterine cavity within half an hour, in 1–2 hours — in the lumen of the uterine
tube. In this case the acidic vaginal medium, the cervix of uterus and the isthmus
of the uterine tube act as a selective filter and reservoir of spermatozoa: the popula-
tion of spermatozoa which reached the ampullar region of the uterine tube contains
healthier spermatozoa than the ejaculate (Fig. 1.11).
Up to the present day it has not been established where fertilization takes place.
Some researchers believe that the fusion occurs in the ampullar region of the uterine
tube, others state that this happens in the abdominal cavity followed by capture: the
fertilized ovum is captured by the fimbriae of the uterine tube. It was well established
that a woman with one ovary and one uterine tube on the opposite side can become
pregnant as in this case there is an opportunity for capture of the ovum from the
abdominal cavity.
30 Obstetrics
In uterine tubes the sperm become active under the impact of mucous secretion
of tubal epithelium, which leads to capacitation (binding) of spermatozoon to the
ovum surface. An acrosomal reaction follows: lysosome-like bodies contained in
the spermatozoon head dissolve the ovum coat and the spermatozoon can penetrate
inside (Fig. 1.12).
It is supposed that in fertilization lysosomes disintegrate releasing their own en-
zymes as well as a number of enzymes of other organelles that activate biochemical
reactions in the ovum. Once a spermatozoon (head, neck and the intermediate part)
penetrates the cytoplasm, the tail is discarded. Cortical granules form the fertiliza-
tion membrane — a new membrane resistant to such influence and preventing the
penetration of other spermatozoa.
The nuclei of the female and male germ cells transform into pronuclei. Upon their
contact the syncaryon stage (fusion of two nuclei) begins, thus a zygote (from Greek
zygote, joined together) appears — beginning of a new life.
Fig. 1.11. Spermatozoa attempting to penetrate the ovum (photomicrography)
Fig. 1.12. Spermatozoon penetrating the ovum (photo Lenart Nilsson)

Division of the zygote begins by the first day of its existence. Thus the fertilized
ovum begins to divide while it is in the uterine tube. During the period from ovula-
tion to implantation, which is within about one week, the fertilized ovum persists
in a free suspended state. Its transition along the whole length of the uterine tube
takes 3–4 days on average.
1.2. EARLY PREGNANCY (FIRST TRIMESTER)
Cleavage of the zygote into blastomeres (spheres of division) follows a strongly de-
fined genetic program starting 24 hours after fertilization spanning over the next three
days. Cleavage of a human zygote is complete, asymmetrical, and asynchronous. The
first cleavage takes place over 24 hours, others — every 12 hours.
The first two blastomeres differ from each other: one is dark, smaller in size; the
other one is larger and lighter. The light blastomeres cleave faster growing in one layer
over the dark ones. Within 40 hours the number of blastomeres becomes 4; on day 4
the embryo consists of 7–12 blastomeres; 50–60 hours after conception a morula is
formed (a diminutive word from Latin morum, mulberry) (Fig. 1.13).
For three days the morula persists in the uterine tube. Depending on the number
of blastomeres the stage of morula development can be defined as first or second.
For 4 days, as the outer layer of blstomeres grows thicker, an inner cavity, blasto-
coel, forms in the morula. This is the way the blastocyst, or the third presomite
stage, develops. The superficial light cells of the blastocyst give rise to an external
thin layer thus forming the primary trophoblast while the dark cells give rise to the
embryoblast.
The primary trophoblast is a stem cell for most placental cells

NB! and tissues; the embryoblast is a source of all fetal cells, tissues
and related membranes
Fig. 1.13. Morula 50–60 hours after fertilization

32 Obstetrics
The embryoblast presented as an aggregation of a number of cells (inner cell

mass) attaches itself to the trophoblast on the inside. As such the blastocyst enters
the uterus on day 4, and for another 24 hours it remains there in a free state (free
blastocyst stage) (Fig. 1.14).
From day 6–7, once the blastocyst hatches out of the partially dissolved zona pel-
lucida, its implantation (nidation, from Latin nidus, nest) takes place.
Implantation proceeds in two stages: adhesion and invasion. First the trophoblast
adheres to the endometrium and starts differentiating into cytotrophoblast still con-
nected to the embryo wall, and syncytiotrophoblast, a peripheral layer in the form of
cytoplasm mass with several nuclei without borders, that is, a typical symplast. They
are referred to as primitive, or prechoroid forms. During the invasion the lysosomes
of these primitive villi of syncytiotrophoblast release proteolytic, glycolytic and other
enzymes that ‘melt down’ the tissues of the uterine mucosa (Fig. 1.15).
Blastogenesis includes the stage of free blastocyst and implanta-

NB! tion process
The blastocyst invades energetically between epithelial cells of the endometrium

and finally positions itself inside the stroma. This process is accompanied by specific
morphological and metabolic changes promoting cell growth and differentiation.
It was established that the cytotrophoblast cells show the greatest enzymatic activ-
ity; the primary trophoblast produces proteolytic enzymes vigorously (proteolysis).
Fig. 1.14. Blastocyst in the uterine cavity 5–6 days after fertilization, free blastocyst stage
(photo Lenart Nilsson)
Fig. 1.15. Implantation complete: day 8 (photo Lenart Nilsson)
The depth and extent of invasion depend mostly on the lytic ability of the trophoblast.
Autolysis of the uterine epithelium itself is of no small importance in this process; it
proceeds under the control of progesterone (endometrial sensitivity). Blastocysts are
necessary in that they provide for a specific molecular environment.
Implantation is only possible when endometrium is ready for

NB! autolysis and the blastocyst is ready for proteolysis
If blastocysts start interacting with insensitive (unprepared) endometrium, they

do not get implanted. Based on this assertion, a theory of implantation window
was elaborated. In humans the implantation window is limited to day 19–22 of the
menstrual cycle, as a rule. This is the time when the uterine endometrium is ready
for implantation, which is manifested by production of a great number of biologically
active substances. The endometrial ability to receive the blastocyst ceases completely
on the 22nd day.
What factors determine the endometrial sensitivity to implantation?
• First, it is the physiological changes in the endometrium that take place in the
second phase of the menstrual cycle.
• Second, it is the rise of adhesion molecules on the endometrial surface; they
interact with ligands on the corresponding epithelium of the blastocyst (same as
in leukocyte adhesion to the vascular wall).
• Third, it is the rise of large cytoplasmatic formations (pinopodes) in endometrial
cells, which takes place exactly from the 19th to the 22nd day of the menstrual
cycle, that is, while the implantation window is open.
Implantation can only occur during the implantation window, a

NB! period of time limited to day 19-22 of the period when the endo-
metrium is sensitive to the blastocyst to the utmost
34 Obstetrics
Implantation occurs on the posterior wall in the superior uterine segment exactly
where a blood vessel runs close to the endometrial surface. This spot will later be-
come the uteroplacental area. The notion of uteroplacental area includes the zone of
immediate contact between the anchoring villi of the placenta with the endometrium
and the adjacent myometrial layers. Apart from this term, other names are used
depending on the gestational age. Thus, at the stage of implantation the zone of im-
mediate contact between the embryo and the endometrium and adjacent myometrial
layers is called implantation site or cytotrophoblast shield. Later, along with placenta
formation, the underlying endometrium is defined as decidua basalis as opposed
to decidua parietalis that is part of fetal membranes. When the placenta is born,
its rupture line passes roughly in the middle of d. basalis (from Latin decidere, fall
off) that is divided into two parts: the severed fragments on the maternal placental
surface called basal plate, and the remaining endometrial portions with the adjacent
myometrial layer — placental bed, or uterine bed.
During implantation the process of cleavage continues in the trophoblast: cyto-
plasmatic excrescences (primary villi) develop; the inner cell mass transforms into
embryonic disc (embryonic shield). The cleavage of cells in the trophoblast and in
the inner cell mass proceeds independently from each other. This stage is called
epiblastula. The embryonic shield has a compact structure; two types of cells are
distinguished in it: the ectoblast (ectoderm) and the endoblast (endoderm). The
embryonic disc and the cavities surrounding it take up only a smaller part of the
chorionic sac cavity; the greater part is taken up by loosely placed cells of the
extraembryonic mesenchyma (mesoderm) and the fluid contained in it; together
they form the extracoelomic cavity.
The embryo grows fast which is due to both cell division and the inflow of protein-
containing fluid coming through the trophoblast and accumulating inside. As a result,
the epiblastula transforms into the embryonic sac. Later a groove emerges circling
the embryonic sac; becoming deeper it forms a pedicle that connects the abdominal
part of the embryo with the rest of the embryonic sac. This portion of the embryonic
sac is called the yolk sac, the pedicle — the vitelline duct. As the nutrients supplied
by the yolk sac begin to run low, its walls deflate and get atrophied. Simultaneously
with the yolk sac formation the ectoderm and the parietal plate of the mesoderm
rise forming a fold around the protruding dorsal surface of the embryo. Growing in
all directions these folds meet over the embryo’s back; thus the embryo finds itself
enclosed in two sacs.
In the period between day 17 and 19 the chorionic sac continues to grow in
diameter later differentiating into two portions: the bald chorion (its thinning-out
segment protruding into the uterine cavity), and the bushy chorion where the mes-
enchyma continues to invade the distal segments of cellular columns forming typical
mesenchymal villi with a continuous coat of cyto- and syncytiotrophoblast. Lateral
branches emerge there thus expanding the intervillous space, whereas, in contrast,
there is no arborization of villi in the area of the bald chorion.
As the cytotrophoblast moves on in an alien antigen medium, muscular elements
and endothelium get lysed around the spiral artery wall, and the arterial lumen grows
considerably wider. The process that consists in lysis of muscular-elastic elements
and endothelium in the spiral arteries with their replacement by fibrinoid, drastic
enlargement of the lumen and formation of an ostium opening into the intervillous
placental space is called gestational modification of spiral arteries into uteroplacental
arteries. Gestational modification of spiral arteries, dissolution of their end portions
and formation of ostia opening into the intervillous space takes place 4–6 weeks
after fertilization, that is, at week 6–8 of obstetric gestational age thus giving rise to
uteroplacental blood circulation.
Towards the end of the FIRST trimester, after emergence of 20–30 uteroplacental
arteries, the cytotrophoblastic invasion runs low as most cells of the interstitial cyto-
trophoblast become gigantic multinuclear cells concentrating at the border between
the endometrium and myometrium. The initial extent of uteroplacental circulation
that developed due to the first wave of cytotrophoblastic invasion now becomes insuf-
ficient for further fetal development. That is why after a «rest period» lasting several
weeks there emerges a discrepancy between the inflow of arterial maternal blood
and the demands of the developing placenta and intensive organogenesis of the fetus
(another hypoxia stimulus). As a result, a second wave of cytotrophoblastic invasion
is launched at week 15 reaching its maximum degree at week 16–18. This wave ex-
pands to include mostly the arteries of the adjacent myometrium as well as those of
peripheral placenta affecting new spiral arteries of the nearby parietal endometrium.
In this way the placenta develops along with the uteroplacental bed enlarging both
their total area and the depth of penetration into the myometrium.
The waves of cytrophoblastic invasion into the endometrium, walls of arterioles
and arteries of the uteroplacental area are key processes that to a great extent
determine the blastocyst implantation, formation of uteroplacental circulation
and the rate of its growth depending on metabolic requirements of the embryo
and fetus.
1.3. SECOND TRIMESTER
1.3.1. Changes in the fetus and extraembryonic structures

The transition from first to second trimester is marked by an emergence of new
significant changes in the fetus and extraembryonic structures.
• First, the rudiments of major organs consistently build up their functions
requiring additional nourishment, more active metabolic processes, more
intensive placentofetal circulation.
– The development of blood circulation system outstrips other organs: there
emerges the fetal type of circulation with three bypasses (venous duct, foramen
ovale, arterial duct) where arterial blood from the umbilical vein mixes with
venous blood.
– The liver is active as the main organ of erythropoiesis.
– Lymphoid organs (the thymus, spleen, lymph nodes and others) gradually
begin their function.
• Second, the cytotrophoblastic invasion livens up after a period of certain
attenuation. It is aimed mainly at myometrial segments of uteroplacental arteries;
36 Obstetrics
this provides for the inflow of maternal arterial blood into the intervillous space
of placenta, which is necessary for fetal development.
• Third, a consistent transformation of extraembryonic organs takes place: the
allantois disappears having «fl ickered» for a brief period of time in the tenth
somite stage (its function was to help the embryo’s blood vessels move along and
connect with the capillaries in the wall of the chorionic sac, that is, to help the
formation of embryoplacental blood circulation). The yolk sac disappears too;
the amniotic cavity continues to grow as well; it closes ranks with the wall of the
chorionic sac and, together with decidua capsularis, gradually forms typical fetal
membranes. A second wave of cytotrophoblast invasion follows: the development
of the placenta, umbilical cord and formation of the amniotic space.
The second wave of cytotrophoblast invasion. At 16–18 weeks of gestation the
second wave of cytotrophoblast invasion begins due to a discrepancy between the
inflow of arterial maternal blood and the requirements of the developing placenta
and intensive organogenesis.
The main mechanism of the second wave consists in penetration of interstitial
cytotrophoblast through the walls of endometrial arterial segments, its egress through
the damaged endothelium into radial uterine arteries and further intravascular mi-
gration; from this moment on it is referred to as intravascular cytotrophoblast. The
way the intravascular proliferation and cytotrophoblast migration (the latter slowly
moves against the flow of maternal blood in proximal direction) are regulated on the
molecular level is not understood well enough.
The main physiological purpose of the second wave is to boost the inflow of
maternal blood into the intervillous space by way of gestational remodeling of walls
and enlarging the lumen of radial arteries, or rather, their myometrial segments. In
this way adequate hemodynamic conditions for a faster fetal growth in comparison
with less intensive accretion of placental mass are created.
Reaching its peak at 16-18 weeks, the second wave of cytotropho-

NB! blast invasion occurs due to an imbalance between the inflow of
maternal arterial blood, the demands of the developing placenta,
and intensive fetal organogenesis
As a result, the cytotrophoblast invasion, taken all round, is a unique short-term

tumor-like growth of specialized placental cells: first it is the growth of symplastic
complexes, and then — of invasive cytotrophoblast (both interstitial and intravas-
cular).
The wave-like and limited nature of the cytotrophoblastic invasion is regulated
by the hypoxia stimulus as well as by para- and autocrine molecular signals passing
between:
• the blastocyst and the adjacent endometrium;
• proliferate of villous cytotrophoblast from anchoring villi and components of the
surrounding matrix of spiral arterial walls within the endometrium (the fi rst wave
during the somite and postsomite stages of embryonic development);
• intravascular cytotrophoblast and the endothelium of myometrial segments in
uterine arteries (the second wave of cytotrophoblast invasion).
1.3.2. Development of placenta

By the end of the first trimester the anatomic formation of the placenta is roughly
complete; it is now ready to meet the growing requirements of the developing fetus.
Thus by the age of 12 weeks the placental mass amounts to 26 g while the embryo
weighs only 17 g (Fig. 1.16).
During weeks 13–16 the development of the placenta corresponds to the beginning
of fetalization. The villi are mostly of the intermediate immature type with character-
istic stromal channels and loose-lying Hofbauer cells (placental macrophages) in their
lumen. Another structural characteristic of the stroma of these villi is the immediate
adjacency of capillaries to the epithelial coat; due to this fact the distance between
the epithelium and capillaries is shortened. The villous epithelial coat is 2–12 μm
thick (9.6 μm on average), the area of capillaries and other fetal vessels amounts to
6% of the total villi area, and the total area of the villous tree amounts to 0.544 m2.
In regards to its structure, the placenta meets the demands of

NB! constantly increasing uteroplacental circulation and those of the
quickly increasing fetal weight
Thus during weeks 13–16 the placenta increases its mass from 30 to 65 g, the
fetus—from 23 to 80 g, which means that at the boundary between weeks 14–15 the
mass of the placenta and fetus level out, from now on the mass of the fetus always
exceeds that of the placenta. This is reciprocated by a considerable growth rate of
the main fetal organs.
During weeks 17–20, as the second wave of cytotrophoblast invasion unfolds;
the intermediate immature villi with an extensive network of stromal channels and
numerous Hofbauer cells retain their dominant role; stromal channels exercise the
function of collectors for placental macrophages. The first intermediate mature or
differentiated villi emerge; their main distinction is that stromal channels have disap-
peared as a result of fibroblast proliferation and strengthening of the collagen base
of the stroma. The average size of villi decreases to 150 μm while the total area of
the villous tree increases to 1.48 m2, and the average epithelium-capillary distance
amounts to 22.4 μm. The outcome of the second wave of cytotrophoblast invasion is
1000
100 620
290
80 250
100
Weight, g
180
30 115
17 65
23
10 Placental weight
10
Embryo weight
1
10 13 16 20 24 28
Gestational age (weeks)
Fig. 1.16. The mass of the placenta and embryo at different gestation ages
38 Obstetrics
that the fetus has almost doubled its mass (130 g at 17 weeks, and 250 g at 20 weeks)
while the gain in placental mass is rather small (80 g at 17 weeks, 115 g at 20 weeks).
Weeks 21–24 of gestation are marked by a rapid gain in fetal weight from 300 to
600 g while the placental weight gain is insignificant: from 150 to 180 g. Progressive
longitudinal growth of stem and intermediate differentiated villi is noted; the number
of small villi 50–80 μm in diameter is not great. However, the average epithelial-
capillary distance becomes 20 times shorter than at the previous gestational age
(from 0.6 to 0.89 μm). Besides, the total area of villi surface continues to grow and
amounts to 2.81 m2, which undeniably affects the diffusion ability of the placenta
and promotes the intensive increase in the size and weight of the main fetal organs.
During weeks 25–28 the placental weight increases from 110 to 250 g. Intermediate
differentiated branches predominate where small terminal villi appear. The size of in-
termediate villi is 80–100 μm; that of terminal villi — only 40–60 μm. The capillary
network is represented by wide sinusoids incorporated into the epithelial layer; in
small areas they adjoin the thinned-out denucleated syncytiotrophoblast. In this
way the first fragments of true placental barrier are formed. Thus, by the end of the
second trimester (28 weeks)
• weight of placenta is 250 g;
• fetal weight is four times greater than the placental weight (1100 g);
• the villous tree is represented by a ramified system of supporting and intermediate
differentiated villi and the fi rst generations of terminal branches;
• the high synthetic activity of syncytiotrophoblast persists;
• the aggregate area of villi is on the increase.
1.4. PLACENTAL PHYSIOLOGY
The placenta provides the fetus with the required nutrition, fluid and oxygen.
It also eliminates fetal waste; it produces a host of proteins and steroid hormones
needed in pregnancy. It is quite apparent that the placenta is not just a passive viaduct
for passage of various substances; it is an organ that plays the key role in providing
for fetal growth and development.
Placental blood flow. The placenta transports gases and solutions of many substanc-
es in both directions achieving the needed concentrations in the intervillous space
(maternal blood flow) and in fetal capillary blood. The blood flow velocity in these
two systems determines how well the fetus is supplied with oxygen and nutrients.
Uterine blood flow. Apart from the myometrium and endometrium, the uterine
artery supplies blood to the placenta in pregnancy, which takes up about 90% of the
total uterine blood flow in a term pregnancy. In uncomplicated singlet pregnancy the
maternal blood flow increases more than 50 times.
Placental metabolism. This very special role of the placenta is due to its intensive
metabolism. For instance, the placenta on the whole consumes as much oxygen as
the fetus does, and in terms of total weight it consumes much more [10 ml/(min
x kg)]. At the age of 22–36 weeks placental weight increases 4–5 times. Glucose
is the main component of oxidation processes occurring in placental tissues. The
placenta consumes up to 70% of total glucose coming from the mother. Besides, a
considerable portion of glucose comes to the placenta from the fetus. Despite the
fact that 1/3 of placental glucose can transform to free lactate, placental metabolism
is not of the anaerobic type. Most probably this lactate is fetal energy material. The
factors responsible for rapid changes in the consumption of oxygen and glucose by
the placenta have not been studied well enough; the same can be said about our
understanding of the mechanism regulating the placenta development. Lately there
was an important breakthrough in the study of gene influence on the processes of
development and differentiation of placental tissues. In late pregnancy there is an
increase in cellular mass of the trophoblast, which exceeds the increase in the mass
of endothelial cells in the capillaries of the villous tree. However it is not yet known
whether the proliferation of trophoblast cells is primary or it depends on proliferation
of endothelial cells. In term pregnancy the mass of the placenta amounts to 500 g
which accounts for 1/7 of the mass of a term fetus. In some clinical studies it was
noted that there is an association between decreased oxygen saturation of tissues and
increased placental weight. This means that a large placenta mostly occurs in preg-
nancy complicated with maternal anemia, in fetal hemolytic disease, in fetal hydrops
due to fetal α-thalassemia. A large placenta is also seen in diabetes mellitus, perhaps
resulting from insulin stimulating the mitotic activity or from enhanced angiogenesis.
Enlarged placenta is noted in cloned animals. It is believed that this is due to defec-
tive expression of specific imprinted genes. An association between a large placenta
and increased morbidity in the neonatal period and later life was noted in humans.
Receptors for many protein hormones responsible for insulin sensitivity were
found in placental tissues: insulin-like growth factors IGF-I, IGF-II, and epidermal
growth factor.
Alongside with long-term changes of maternal blood flow, the maternal cardiac
output volume doubles and the maternal circulating blood volume increases by 40%.
Such a considerable increase in maternal blood flow occurs on the account of two
factors: development of the placenta and expansion of maternal arterial bed. Alongside
the growth of the fetus and placenta, the volume of intervillous space almost triples
at 22–36 weeks gestation. Thus alongside increased placental diffusion capacity there
is a marked development of maternal placental vascular bed. Second, enhancement of
blood flow proceeds partially due to estrogen-driven direct induction of vasodilation
in the uterine blood flow system. This effect is induced by the action of nitric oxide.
As a result of these cumulative effects, uterine blood flow in term pregnancy amounts
to 750 ml/min, which amounts to 10–15% of maternal cardiac output.
The uterine artery is nearly always in the state of almost complete relaxation. However,
it is susceptible to some short-term regulatory influences, too. For instance, systemic
administration of vasodilator drugs can lead to a decrease in maternal blood flow.
1.5. UMBILICAL CORD DEVELOPMENT
The umbilical cord provides connection between the fetus and the placenta; the
umbilical cord develops side by side with the growth of the placenta. Early develop-
ment of the body stalk proceeds in close cooperation with the yolk sac, allantois and
their vessels, that is why at the end of the first trimester and at the beginning of the
40 Obstetrics
second trimester the fetus still retains partly reduced extraembryonic ducts — vitelline
and allantoic ducts, urachal remnants — in the proximal segment at the umbilical
ring. The allantoic duct is placed between two umbilical arteries; it is lined with a
layer of epithelial cells on a thin basal layer without the surrounding muscular coat.
Sometimes signs of epitheliocyte secretion are noted, but in most cases the allantoic
epithelium is at the stage of structural involution. Obliteration of the vitelline duct
is complete by 10 weeks of pregnancy as a rule, obliteration of the allantoic duct —
by the age of 5–6 months of pregnancy. Accessory vessels of a small size are noted
occasionally in the abdominal part of the umbilical cord; these vessels are of venous
or capillary type, they belong to the rudiments of the now-defunct vascular system
of the yolk sac. Starting at 9 weeks the umbilical cord becomes tortuous; it grows in
length quite rapidly (Fig. 1.17).
In the second trimester the umbilical cord shows the typical

NB! structure of a wire covered by simple epithelium and having a
stroma represented by Wharton’s jelly.
Two arteries and a vein run along the cord
One can measure the umbilical length as early as in the first trimester of pregnancy
when the size of the embryo is small compared with the amniotic cavity volume.
The umbilical length at this stage is comparable with the crown-rump length that
can be measured by ultrasound.
Surprisingly enough Leonardo da Vinci stated that «… the length of the umbilical
cord equals the fetus length at the given gestational age». This statement is true with
a minor adjustment: the umbilical cord is somewhat longer than the fetus (Table 1.1).
The diameter of umbilical vessels prior to 30–32 weeks of gestation grows in a
uniform, linear fashion, and then the growth practically stops. Starting at the age
of 34–35 weeks the umbilical diameter decreases progressively, and at 41–42 weeks
of gestation the average umbilical diameter is the same as at the gestational age of
27 weeks (15.5 and 15.0 mm, correspondingly). The progressive decrease in umbili-
Fig. 1.17. Twisting of umbilical vessels. Ultrasound color flow mapping

Table 1.1. Umbilical length at different gestational ages*
Gestational age, weeks M±SD, cm

20–21 32.4 ±8.6
22–23 36.4 ±9.0
24–25 40.1±10.1
26–27 42.5 ±11.3
28–29 45.0±9.7
30–31 47.6 ±11.3
32–33 50.2 ±12.1
34–35 52.5±11.2
36–37 55.5±12.6
38–39 57.4±12.6
40–41 59.6 ±12.6
42–43 60.3 ±12.7
44–45 60.4 ±12.7
46–47 60.5 ±13.0
* Naeye R.L. Umbilical cord length: Clinical significance // J. Pediatrics. — 1985. — Vol. 107,
N 2. — P. 278–281.
cal diameter in late pregnancy is due to physiologic reduction of Wharton’s jelly in

the umbilical cord.
The role and functional significance of the spin of umbilical vessels to the left
or to the right side are of special theoretical and practical interest. The ratio of
left (counterclockwise) spin incidence to right spin incidence is 6:1, while in 3–5%
of all pregnancies a nonhelical course of umbilical vessels is noted. It is believed
that the twisting index (the number of coils along the whole length of the cord)
completes its formation at the end of the first trimester and amounts to 13–15,
approximately.
The umbilical coiling index is the ratio of the total number of complete umbili-
cal vascular coils to the umbilical cord length; it amounts to 0.21+0.07 cm, that is,
0.2 coils per each centimeter of the cord length, or two complete coils per 10 cm.
Several hypotheses were put forward to explain why the cord more often twists in
the left direction (spin of the Earth, right- of left handedness), but there is no con-
vincing evidence supporting any of them. As for the role of the number of umbilical
coils, there is an opinion that hypocoiling, just like hypercoiling, is accompanied by
increased perinatal morbidity and mortality.
1.6. AMNIOTIC FLUID COMPOSITION

1.6.1. Development of amnion components
It appears sensible to distinguish two main stages in the development of amnion
components.
• Stage one: early interrelations between the membranes, conceptus and human
embryo during implantation, and placentation described above. It should be
42 Obstetrics
emphasized that the amniotic cavity grows in volume faster of all. However, in
the early stages the amount of amniotic fluid is not large: 5 ml at 8 weeks; 30 ml
at 12 weeks.
• Stage two: formation of the main components of fetal membranes, their fusion
with parietal endometrium and the uterine circulation.
During the second trimester, between weeks 15 and 17, the bald chorion together
with the thinned out decidua capsularis becomes closely contiguous with parietal
endometrium; by the end of week 20 they fuse completely.
By the end of week 20 the smooth chorion fuses with parietal

NB! endometrium completely
From the point of view of morphology, the complex process of interaction between
fetal and maternal tissues has not been studied well enough, although it is no less
interesting than formation of the uteroplacental area. As an environment for the fetus,
the amniotic fluid exercises several functions at the same time:
• providing a space for free movements of the growing fetus;
• cushioning against mechanical trauma, maintaining the temperature balance;
• preventing umbilical cord compression during delivery;
• the transport function and a part in the metabolism.
In early pregnancy the amniotic fluid is of yellowish color later becoming lighter
and clearer, in late pregnancy it is often turbid, opalescent with a pH of 6.98–7.23,
relative density of 1007–1080 g/L, protein content of 0.18–0.2%, glucose content of
22 mg%, urea — 23 mg%.
Studies of a centrifugate of amniotic fluid reveal hairs (Latin lanugo), epidermis
cells, cebaceous gland cells (Latin vernix caseosa). The amniotic fluid shows a char-
acteristically high metabolism rate: using radioactive Na24 isotopes it was established
that in the amniotic sac there is a complete turnover of the amniotic fluid every
2.9 hours, of sodium contained in it — every 14.5 hours.
The amniotic fluid volume depends on the gestational age, but it does not increase
evenly. At 8 weeks this volume increases at a rate of 10 ml per week, at 13 weeks —
25 ml per week, at 21 weeks — 60 ml per week; after that the rate goes down, and
at 33 weeks the volume stops increasing. The relative weekly gain in amniotic fluid
volume decreases from the 8th to 43rd week amounting to:
• +45% at 8 weeks;
• +25% at 15 weeks;
• +10% at 24 weeks;
• +0% at 33 weeks;
• -8% at 50 weeks.
The peak value of amniotic fluid volume occurs at the gestation age of 33.8 weeks;
it amounts to 931 ml on average. However, the amniotic fluid volume does not
change significantly in the interval between 22 weeks (630 ml) and 39 weeks (817 ml)
amounting to 777 ml on average (Fig. 1.18, 1.19).
Knowing these specific features, one can determine oligohydramnios or poly-
hydramnios at any gestational age. For instance, at 30 weeks gestation the average
volume of amniotic fluid is 817 ml (within 95% confidence interval — 318–2100 ml),
2500
2000
AMNIOTIC FLUID VOLUME (ml)
1500
99%
1000
95%
75%
500
50%
25%
5%
1%
0
8 12 16 20 24 28 32 36 40 44
GESTATIONAL AGE (weeks)
Fig. 1.18. The volume of amniotic fluid depending on gestational age

(Brace R.A., Wolf E.J., 1989)
80
60
40
20
0
8 12 16 20 24 28 32 36 40
-20
-40
-60
Fig. 1.19. Weekly gain in amniotic fluid volume: unbroken line — in ml; broken line —
in percentage of existing volume (Brace R.A., Wolf E.J., 1989)
thus we are dealing with oligohydramnios when the amniotic fluid volume is under
318 ml, and with polyhydramnios when it exceeds 2100 ml.
The origin of amniotic fluid in the first trimester is not quite clear. It could be
transsudate of maternal plasma through the chorion and amnion or transsudate of
fetal plasma through the quite permeable skin before it undergoes keratinization. The
causes of amniotic fluid formation in the second trimester are better understood.
44 Obstetrics
In the second trimester, the major producer of amniotic fluid is

NB! the fetus
The volume of amniotic fluid depends on the balance between fetal fluid produc-
tion (urine and alveolar fluid) and resorption of this fluid as the fetus swallows it
and it drains to the systems of maternal and fetal circulation through the chorionic
and amniotic membranes.
The lungs of a term fetus secrete about 300–400 ml of fluid per day. There is an
active transport of chlorides from alveolar capillaries into bronchial lumen, and then
the gradient makes the fluid pass into the bronchial lumen. Thus the pulmonary fluid
is a transsudate, almost completely protein-free, its osmolality equaling the osmo-
lality of fetal plasma. The pulmonary fluid has no direct relation to the regulation
of fluid homeostasis in the fetus. Thus, an increase in venous volume, for instance,
does not induce elevated secretion of pulmonary fluid. Most likely, the main role of
pulmonary fluid consists in promoting the expansion of lung tissue providing for lung
growth. The amount of pulmonary fluid should decrease by the moment of birth for
a transition to external respiration.
Interestingly enough, some hormones whose release by the fetus is noted at birth
(catecholamines, vasopressin) induce a decrease in pulmonary fluid production, too.
Along with reduced fluid secretion, the difference in osmotic pressure between fetal
plasma and pulmonary fluid leads to resorption of pulmonary fluid through pulmo-
nary epithelium and as a result of clearance through lymph vessels. A disorder in these
processes may help to explain the incidence rate of transient tachypnea in newborns
or wet lung syndrome in newborns after planned cesarean section.
Fetal urine is one of the main sources of amniotic fluid. The daily quantity of fetal
urine in term pregnancy is 400–1200 ml. At the age of 20–40 weeks the production
of urine by the fetus grows tenfold as a result of accelerated maturation of renal tis-
sue. Normally urine is a hypotonic solution; its low osmolality determines a greater
hypotonicity of amniotic fluid at late gestational ages in comparison with maternal
and fetal plasma. Many substances released by the fetus including vasopressin, atrial
natriuretic factor, angiotensin II, aldosteron and prostaglandins (II) affect renal cir-
culation, glomerular filtration or the rate of urinary excretion. In response to fetal
stress the content of various hormones changes, which can explain the fact that fetal
hypoxia is often accompanied by oligohydramnios.
It is supposed that swallowing of amniotic fluid by the fetus is the main cause of
its resorption, although what is swallowed is a mixture of amniotic and pulmonary
(tracheal) fluid. Swallowing of amniotic fluid by the fetus can be seen as early as at
18 weeks of gestation. The swallowing increases from 200 ml per day at 18 weeks to
500 ml at 40 weeks.
As neurobehavioral reactions of the fetus develop, fetal swallowing occurs mostly
during the active sleep phase (that is, in combination with respiratory movements
and eye movements). A moderate increase in osmolality of fetal plasma leads to
more frequent swallowing movements and greater volume of swallowed fluid, which
supports the physiological mechanism of «thirst» in a term fetus.
As the amniotic fluid is more hypotonic in comparison with maternal plasma, this
fact provides for elimination of excessive fluid and its transition through the chorionic
and amniotic membranes into maternal plasma. It should be noted, however, that the
role of maternal plasma in this process is not great. Of much greater importance in
the metabolism of amniotic fluid is its transmembraneous transition into the lumen
of placental vessels.
Transmembranous exchange and swallowing of amniotic fluid by

NB! the fetus, on the one hand, and production of urine and pulmonary
fluid, on the other hand, maintain a stable volume of amniotic fluid
The paraplacental route, or metabolism through extraplacental parts of fetal mem-

branes, plays an important role in the amniotic fluid metabolism. There is no
universal point of view about this issue. Passive transudation from maternal blood
is believed to be one of the sources of amniotic fluid origin; but this role is also as-
cribed to transudation occurring under the influence of major biological mechanisms
in accordance with the osmotic or hydrostatic gradient and difference of potentials.
1.6.2. Composition of the amniotic fluid

The biochemical composition of the amniotic fluid is relatively constant.
Insignificant fluctuations in the concentration of organic and mineral substances are
noted, depending on the gestational age (Table 1.2). The amniotic fluid has a weakly
alkaline or nearly neutral reaction. It was established that the pH of the amniotic
fluid at a gestational age under 12 weeks amounts to 7.32±0.028.
The amniotic fluid contains 0.71% of mineral substances: all the electrolytes pres-
ent in the mother’s body. Sodium provides for osmotic concentration of the amniotic
fluid. At early gestational ages the content of sodium in the amniotic fluid is nearly
the same as in the maternal blood.
Table 1.2. Composition of the amniotic fluid in the fi rst trimester of normal pregnancy
Parameter Value
pH 7.18–7.44
Bicarbonates, μmol/l 26.6±1.9
pO2, mm Hg 7–25
Sodium, mmol/l 134±2.3
Potassium, mmol/l 3.85 ±0.05
Calcium, mmol/l 1.39±0.17
Glucose, mmol/l 3.12 ±0.34
Bilirubin, mmol/l 1.26±0.12
Creatinine, mmol/l 5.7 ±1.04
Triglycerides, mmol/l 0.36 ±0.03
Urea, mmol/l 0.21±0.09
Alkaline phosphatase 35.5 ±12.27
Total protein, g/l 1.93 ±0.39
46 Obstetrics
Apart from electrolytes, osmotic concentration of the amniotic fluid is also main-
tained by other components, glucose and urea in the first place. At 7–12 weeks
gestation the concentration of glucose in the amniotic fluid amounts to 3.12 mmol/l.
Some authors attribute the relatively high glucose content in the first trimester to
the inability of the liver to synthesize glycogen from glucose. As the liver becomes
functionally mature, the content of glucose goes down.
In the second trimester of pregnancy the amount of amniotic fluid increases at a
maximum rate, and changes of its biochemical composition are most pronounced.
At gestational age 15–25 weeks the pH of amniotic fluid gradually decreases
from 7.17±0.004 to 7.14±0.04. As gestation progresses, the content of sodium and
potassium in the amniotic fluid reduces. At later stages of pregnancy the content
of calcium in the amniotic fluid decreases progressively. The total calcium content
decreases on the whole, while ionized calcium remains stable; its concentration is
the same as in the maternal blood.
Glucose content in the amniotic fluid and its relation to fetal metabolism in the
second trimester of pregnancy are of great interest. As pregnancy progresses, glucose
content in the amniotic fluid goes down, while the content of urea goes up. As early
as at 25 weeks of gestation the concentration of urea in the amniotic fluid is consid-
erably higher than in the maternal and fetal blood.
Thus, in the second trimester of pregnancy, when the main embryo organs and
systems have completed their formation, they continue their growth, specialization
of functions and formation of inter-organic relations. This process is helped along by
amplification of amniotic structures. Thus, in the uteroplacental region the second
wave of cytotrophoblast invasion takes place, which leads to an increase in the area of
placenta-uterus contact, involvement of myometrial segments of uterine arteries into
gestational restructuring. Uterine arteries are of larger size, and the inflow of arterial
maternal blood to the intervillous space increases considerably. Fetal membranes are
formed at the same time, and the volume of amniotic fluid around the fetus grows
rapidly: the paraplacental route of substance transport emerges. Differentiation of
stem and intermediate branches continues in the placenta.
On the whole the amniotic structures provide morphofunctional opportunities for
a rapid fetal growth; at 16 weeks fetal weight exceeds placental weight and retains its
leadership from now on.
1.7. CRITICAL PERIODS OF FETAL DEVELOPMENT
At critical periods the embryo is especially vulnerable to the damaging effect of

various factors. In mammals the vulnerable periods coincide with the times of im-
plantation and placentation.
• The first critical period falls on the end of the fi rst week and the beginning of
the second week after conception (3–4 weeks gestation). The ovum, morula
and blastocyst have no defense reactions. Probably this feature is practical from
the biological point of view as the ability of the species to survive is maintained
through massive culling (rejection of inferior organisms). The damaging factors
lead to congenital malformations, various diseases and death of the fetus.
• The second critical period takes up weeks 5–8 of gestation; it coincides with the
critical placentation stage when the placental bed is being formed as a result of
complex interrelations of developing villi and consecutive opening of spiral arteries.
• The third critical period covers the last four weeks of pregnancy when the placenta
stops gaining weight while fetal weight grows rapidly.
REMEMBER!
The lifespan of an ovum is no longer than 24 hours, of a spermatozoon — no longer
than 48 hours.
A developing follicle inhibits the growth of other follicles, so the other maturing
follicles undergo atresia (they die).
Fertilization is a process of union between male and female sex cells to produce a
new organism with a unique genetic makeup.
Implantation is only possible when the endometrium is most sensitive to the ovum;
thus the notion of implantation window emerged: a timespan from day 19 to 22 of
the period.
Extraembryonic structures:
chorion, or chorionic sac;
amnion, or amniotic membrane together with extraembryonic coelom;
yolk sac;
funiculus with allantois attached to it;
surrounding endometrium.
Critical periods:
first: end of week 3 and the entire fourth week of gestation;
second: 5-8 weeks gestation;
third: the last month of pregnancy.
1.8. FETAL PHYSIOLOGY

1.8.1. Fetal circulation
The circulation of blood in the fetus and placenta differs from that in adult hu-
mans.
• blood oxygenation takes place in the placenta;
• the right and left ventricles contract simultaneously rather than consecutively;
• the heart, the brain and the upper trunk receive the blood from the left ventricle;
the placenta and the lower trunk — from both ventricles.
The heart and vessels develop form splanchnomesoderm during the third week
after conception (5 weeks of gestation). Two primordial cardiac tubes fuse, and a
primitive tube capable of contracting constantly is formed during the fourth week.
The first system to function in a fetus is the cardiovascular system

NB!
48 Obstetrics
During the period of 5–8 weeks,

after a series of complex processes,
this primitive tube transforms into a
four-chamber heart. However, the fe-
tus, unlike the adult, has an opening
between the atria (interatrial foramen,
Lat. foramen ovale) whose only func-
tion it is to shunt the blood from right
to left until the pulmonary circulation
begins to function (Fig. 1.20).

As early as at 6 weeks of gestation
the embryo has three blood circula-
tion systems at the same time.
• Aortocardial circulation: the

embryonic blood flow proper, the
basis for future fetal circulation.
The left branch of the sixth aortal
(pulmonary) arch connects the
aorta to the left pulmonary artery.

Thus the embryo/fetus forms
the Botallo duct (Latin ductus
arteriosus). The Botallo duct,
like the foramen ovale, acts as a
right to left shunt transmitting
the blood from the right ventricle
to the aorta.
• Vitelline network developing at
the same time with the yolk sac. It
plays only an insignificant role in
the provision of the embryo with
nutrients, but it takes part in the
formation of vessels that nourish
the alimentary tract organs: the
spleen, liver and salivary gland.
• Allantoic circulation developing
at the same time with the growth
of chorionic tissue and the
Fig. 1.20. 1 — arch of aorta; 2 — carotid artery development of chorionic villi
and vein; 3 — subclavian artery and vein; (placental circulation). Initially
4 — Botallo duct; 5 — pulmonary vessels; 6 — the system of allantoic circulation
left atrium; 7 — pulmonary artery; 8 — left
consists of one umbilical artery
ventricle; 9 — descending vein; 10 — inferior
vena cava; 11 — umbilical arteries; 12 — and two umbilical veins. In a
umbilical ring; 13 — umbilical vein; 14 — human embryo the umbilical
Arantius’ duct; 15 — right ventricle; 16 — right vein splits in two at 6 weeks
atrium; 17 — superior vena cava; 18 — hepatic gestation; and in the period of
vein; 19 — umbilical arteries 6–10 weeks the right umbilical
vein disappears. Later the venous duct (Latin ductus venosus) emerges from a
portion of the venous network in the liver. This is the venous shunt which sends
more than a half of the umbilical blood flow [70–130 ml/(min×kg) in the third
trimester] directly to inferior vena cava bypassing the liver.
Thanks to the intensive placental exchange of gases, the umbilical cord carries
oxygen-rich blood from the placenta to the fetus (Fig. 1.21). At some distance from
the umbilical ring the intraabdominal portion of the umbilical vein splits into smaller
branches:
• the aforementioned venous duct;
• some branches supplying the left lobe of liver;
• a large branch supplying the right lobe of liver.
The blood from the left lobe of liver courses along the hepatic vein to the inferior
vena cava; there it mixes with the oxygenated flow from the venous duct. Due to the
fact that the blood from the right hepatic vein mixes with the blood form the portal
vein (only a small portion of portal blood mixes with the venous duct blood), it is
less oxygenated than the blood from the left lobe of liver. Thus, the combination of
drain from «right hepatic vein+portal vein» system and the blood coming from lower
limbs and pelvic organs and tissues, leads to reduction in oxygenation. Interestingly
Tricuspid valve
SVS
Foramen ovale
LHV
RHV
Ductus venosus
Umbilical vein
IVC
Portal vein
Fig. 1.21. Umbilical and hepatic ducts (schematic): SVC — superior vena cava; IVC — inferior
vena cava; LHV — left hepatic vein; RHV — right hepatic vein (Rudolph A.M. Hepatic and
ductus venosus blood flows during fetal life // Hepatology. — 1983. — 3:254; with permission)
50 Obstetrics
enough, two blood flows — from the venous duct and the blood coming from the
portal vein and lower limbs — scarcely mix upon passing from the inferior vena cava
to the right atrium. Furthermore, a portion of oxygenated blood from the venous duct
passes to the foramen ovale predominantly due to the valve cusp in the inferior vena
cava and the so called crista dividens located on a wall of the right atrium. In this
way the shunting of intensively oxygenated blood from the venous duct through the
foramen ovale is provided, as well as a minimum mixing with «spent» blood coming
from the superior vena cava.
As a result, the left atrium receives mostly blood from the venous duct with
a small admixture of blood returning from the lungs. In this way the oxygenated
blood is carried consecutively to the left atrium, then to the left ventricle, and from
there it comes mostly to the brain and upper trunk. The rest portion of blood, less
oxygenated, passes from the tricuspid valve to the right ventricle (Fig. 1.22). That is
where the blood from the superior vena cava and coronary sinus comes, too. Due to
elevated vascular resistance in the pulmonary circulation (vascular resistance in the
pulmonary artery is 2–3 mm Hg higher than in the aorta) the blood from the right
ventricle courses along the Botallo duct to the aorta.
Pulmonary arteries Pulmonary veins
Right
Left atrium
ventricle
2
Right Left
atrium ventricle
Intrathoracic Extrathoracic Intrathoracic

veins veins arteries
Extrathoracic
arteries
3
Placenta
Fig. 1.22. Cardiac shunts in the fetus (schematic): 1 — ductus arteriosus; 2 — foramen ovale;
3 — ductus venosus (Anderson D.F., Bissonnette J.M., Faber J.J., Thornburg K.L. Central
shunt flows and pressures in the mature fetal lamb // Am. J. Physiol. — 1981. — 241: H60,
with permission)
1.8.2. Organs and systems

1.8.2.1. Heart
In adults the average arterial blood pressure in the systemic and pulmonary
circulation is 95 and 15 mm Hg, correspondingly. Despite the high rate of cardiac
output from the left ventricle, the volume of cardiac output from both ventricles
is equal. The stroke volume is the portion of blood discharged by the left ventricle
upon each contraction; the cardiac output is stroke volume multiplied by the heart
rate (70 ml×72 per minute=5040 ml per minute). In an adult man with a mass of
70 kg the cardiac output is 72 ml/(min×kg) on average. Apart from the heart rate,
the cardiac output is influenced by the systolic output which, in its turn, depends on
the venous return (preload), pressure in the aorta and pulmonary artery (afterload)
and contractility.
In contrast to an adult heart where each ventricle pumps the blood to its separate
system, unique fetal shunts provide for unequal distribution of venous drainage
to corresponding areas. The ventricles discharge a mixture of highly and poorly
oxygenated blood. In this way the left and right ventricles function as two pumps
contracting simultaneously rather than alternately — the way it happens in adults.
Ejection from the left ventricle is considerably larger than from the left one (60 and
40% correspondingly). The blood comes to the descending portion of the aorta,
mostly along the Botallo duct (see Fig. 1.22). As a result, the pumping of blood
to the placental bed reflects the way the right ventricle works. Due to the high
vascular resistance in the pulmonary circulation, the pulmonary circuit receives
only 5–10% of the total ventricular ejection. The blood from the left ventricle is
directed mostly to the upper portions of the trunk and the head. Ejection from
the left ventricle is about 120 ml/(min×kg). Joint ejection from both ventricles
exceeds 300 ml/(min×kg). The placenta receives only about one half of the total
ventricular ejection.
NB! The umbilical vein returns a half of the total fetal blood to the heart
In this system at least a half of the blood from the umbilical vein bypasses the
liver along the venous duct; the rest of the blood passes through the hepatic blood
flow. Taken together, the blood from the umbilical vein, hepatic branch of the
portal vein and the blood returning from lower trunk and lower limbs accounts
for 69% of the total cardiac output. The foramen ovale conducts about 1/3 (27%)
of the total cardiac output. Only 7% of the total cardiac output passes from the
pulmonary circulation to the left atrium. Thus, only about 34% (27%+7%) of
the total ventricular output passes through the left atrium. Since only 27% of the
total ventricular output is discharged through the foramen ovale, 42% of blood
remains in the right atrium and contributes to ejection from the right ventricle.
Upon addition of 21% from superior vena cava and 3% from coronary vessels,
ejection from the right ventricle amounts to 66% of the total ventricular output.
However, only 7% passes to the pulmonary circulation, the remaining 59% pass
52 Obstetrics
to the aorta along the Botallo duct. From the left ventricle 24% of the total
ventricular flow passes to the upper trunk and brain, while 10% mix in the aorta
with the blood coming from the right ventricle. As a result, 69% of the total
ventricular ejection reaches the descending aorta while one half of the blood
enters the placental network, and the other half is distributed between abdominal
organs and lower limbs.
The fetal heart rate becomes somewhat less in the second half of gestation, espe-
cially during weeks 20–30; on average, it exceeds the heart rate of an adult at rest
twofold.
After 10 weeks of pregnancy FHR amounts to 140 beats per minute,

NB! on average
The fetal heart rate varies across 24 hours: it goes down between 2 to 6 AM and
surges in the period between 8 to 10 AM. In most cases the heart rate acceleration
occurs in response to limb movement, which shows the effects of the central nervous
system. Besides, reflex tachycardia develops as a result of reduced venous return as-
sociated with this limb movement.
The very first intake of breath induces significant changes in the distribu-
tion of blood in the bloodstream of the fetus / newborn. The alveoli expand,
oxygen concentration in alveolar capillaries increases causing a noticeable
drop of microvascular resistance in the lungs. This leads to two important
events:
• fi rst, the afterload and pressure in the right atrium go down;
• second, intensified pulmonary circulation results in increased venous return to
the left atrium and, consequently, in increased pressure there.
Both events produce a cumulative effect: increased pressure in the left atrium
exceeding the right atrium pressure, which ends in physiological closure of the
foramen ovale. The return of highly oxygenated blood from the lungs to the
left atrium, left ventricle and aorta, the decrease in vascular resistance in the
pulmonary circulation, and thence, in the pulmonary trunk too — all this re-
directs the flow of highly oxygenated blood in the Botallo duct. A local change
of oxygen concentration in the Botallo duct induces local vasoconstriction.
The accompanying spontaneous constriction of umbilical vessels arrests the
placental blood flow, reduces the venous return, which brings down the right
atrium pressure.
1.8.2.2. Fetal hemoglobin

The fetus develops in conditions of aerobic metabolism. Partial BP is within the
range 20–35 mm Hg. However, there is no metabolic acidosis. Adequate oxygen-
ation of fetal tissues is provided by several mechanisms. The most important one is
the increased fetal cardiac output and, correspondingly, increased blood flow in its
organs. Besides, a certain contribution is made by a higher hemoglobin concentration
(in comparison with adults) and the greater ability of fetal hemoglobin to transport
oxygen. As a result, a shift to left in the oxygen dissociation curve (in comparison
with adults) ends in increased oxygen saturation of the fetal blood while the pO2
value remains low1. For instance, at pO2 of 26.5 mm Hg in adults oxygen satura-
tion amounts to only 50%, and in the fetus — 70%. Thus, at a normal fetal pO2 of
20 mm Hg oxygen saturation of the fetus amounts to 50%.
At the gestational age 26–40 weeks fetal hemoglobin (HbF) concentration de-
creases while the concentration of «adult» hemoglobin (HbA) in the fetal bloodstream
goes up. HbF levels go down in a linear fashion from 100% to 70%, which means
that in a term pregnancy the level of HbA in the fetus amounts to 30% of total fetal
hemoglobin.
1.8.2.3. Kidneys
In the fetus, the general, electrolyte and fluid homeostasis depends primarily on
fetal-maternal metabolic processes taking place in the placenta. However, the sta-
bility of amniotic fluid volume and its composition are mostly associated with the
performance of fetal kidneys.
Despite the increase in values of the absolute glomerular filtration rate in the third
trimester, the absolute glomerular filtration rate values remain constant if calculated
with reference to 1 g of renal mass: the absolute glomerular filtration rate increases
alongside with kidney growth.
Formation of new renal glomerules in the fetus is complete by 36

NB! weeks gestation
Further increase in the values of absolute glomerular filtration rate reflects the
growth of glomerular surface participating in filtration, increase in effective filtration
pressure and the coefficient of capillary filtration. Despite the fact that glomerular
filtration depends on hydrostatic pressure and increased fetal arterial pressure in the
third trimester, both renal blood flow calculated with reference to 1 g of renal mass
and renal filtration fraction remain constant. At early gestational ages the fetus shows
some imbalance in the joint performance of glomerules and tubules. However, at
later stages the increased sodium and chlorine reabsorbtion in the tubules results in
a due balance between glomerular filtration and tubular reabsorbtion. Despite the
low rate of glomerular filtration, the daily urine output is quite high (60–80% of the
total amount of amniotic fluid).
1.8.2.4. Gastrointestinal tract

Intestinal rotation begins at week 8 and completes at week 12. From now on the
intestine is completely formed, its lumen is free.
Fetal intestinal peristalsis begins to function in the second trimes-

NB! ter of pregnancy
The swallowing reflex develops gradually. The fetus swallows the amniotic fluid
constantly and at an increasing rate, approximately 20 ml/h in term pregnancy. The
1 pO stands for partial oxygen pressure. In a mixture of gases, the partial pressure of each gas is the
2
pressure that gas would exert if it was the only one occupying that volume of space.
54 Obstetrics
amniotic fluid contains rather high concentrations of glucose, lactic acid and amino
acids. That is why one can suppose that the fetus swallows the fluid as nourish-
ment. The swallowing meets the fetus’ need for fluid, which is also necessary for
the development of gastrointestinal organs. The fetus receives 10–15% of nitrogen
needed for its growth and development from the amniotic fluid containing a certain
amount of protein.
Experiments on rabbits proved that an arrest of fetal swallowing after 24 days
of gestation (in rabbits pregnancy lasts 31 days) results in fetal mass falling behind
by 8% by day 28 of gestation. In experiments on sheep esophageal occlusion in a
90-day old fetus (in sheep pregnancy lasts 145–150 days) led to a 30% decrease in
the height of villi in the small intestine and reduced weight of the liver, pancreas
and intestine.
Apart from a certain amount of nutrients, the amniotic fluid contains some
growth factors. Data obtained by neonatologists support the presupposition that
there is an association between the swallowing movements and the development of
the gastrointestinal tract. It was noted that intrauterine growth restriction is more
likely to occur upon esophagus obstruction rather than upon obstruction of lower
intestinal portions.
Intrauterine defecation and hence the presence of meconium in

NB! the amniotic fluid usually indicate fetal hypoxia
By the moment of birth the large intestine is filled with meconium, but there is
no defecation.
While the content of fluid in the body gradually decreases, the store of glyco-
gen and fat grows about fivefold in the third trimester. In preterm babies there is
practically no fat, thence their poorer ability to endure starvation. This is further
compounded by incomplete development of the gastrointestinal tract, which is
manifested by weak, interrupted sucking, uncoordinated swallowing movements,
retarded stomach emptying, and disorder of asbsorption of carbohydrates, fats and
other nutrients.
1.8.2.5. Liver
By the end of pregnancy the placenta remains the main organ responsible for
bilirubin elimination. In experiment, 10 hours upon administration of bilirubin to
the fetus, only 10% was found in the bile ducts while 20% remained in the blood
plasma. These findings indicate that even in a term fetus the metabolism of bilirubin
and its derivatives is not yet full-fledged.
1.8.3. Gestational programming

The fetus develops in conditions of a sophisticated dynamic system. He receives
the nutrients exclusively from the mother. A hitch in any link of the system (genetic
disorders, lessened transport of nutrients, concomitant extragenital maternal disor-
ders) may cause low weight to the extent of fetal growth restriction accompanied by
perinatal complications (hypoglycemia, hypocalcemia, and polycythemia).
Low weight at birth has a profound impact on the general state of

NB! health and the subsequent duration of lifespan
A distinct association was noted between low weight at birth and the probability
of stroke, breast cancer, diabetes mellitus, idiopathic arterial hypertension, cardio-
vascular disease across the person’s lifespan.
In 1986 Barker and Osmond published findings supporting an association be-
tween the occurrence of ischemic heart disease in England and Wales in the years
1968–1978 in individuals born between 1921–1925, and high infant mortality in
these areas in the years 1921–1925. Similar evidence had been obtained by Rose
and Fordahl before them, who had conducted a comparable study in 1964–1977.
An analysis of data on about 16,000 people born in the years 1911–1930 showed
that mortality due to coronary artery lesion was inversely related to these people’s
body weight at birth. On the whole, mortality was higher in those who showed low
weight across the first year of life.
The most reliable association was noted between low weight at birth and hyper-
tonic disease at a mature age. The factors named above led Barker to formulate a
hypothesis that unfavorable deviations in nutritional and endocrine fetal status can
lead to disorders in metabolic adaptation in the fetus-newborn-infant-adult. Such
«programming» of metabolism, organ structure and physiological reactions of the
body lays a foundation for the development of cardiovascular and endocrine diseases,
metabolic disorders at a later and advanced age. This hypothesis somewhat chimes
with the thrifty hypothesis that states that intrauterine development in conditions of
malnutrition results in certain adaptive metabolic changes in the fetus / newborn.
These changes permit the most effective development of the body in given conditions
when there is nutritional deficiency. An abrupt transition to a more varied diet in the
postnatal period can trigger most undesirable reactions including the development of
diabetes mellitus type 2 and metabolic syndrome.
REMEMBER!
The amniotic fluid volume increases from 250 ml at 16 weeks to 800 ml at 32 weeks
and then decreases to 500 ml at 40 weeks.
About 40% of blood of the total cardiac output [300 ml/(kg×min)] passes to the
umbilical bloodstream of the fetus.
The umbilical bloodstream amounts to 70–130 ml / min after 30 weeks of gestation.
The fetus excretes 400–1200 ml of urine a day. This is the main source of amniotic
fluid.
In a term pregnancy the uterine blood flow is 750 ml/min (10–15% of maternal
cardiac output).
In a term pregnancy the placenta weighs 500 g on average, which amounts to 1/7
of the fetal weight.
56 Obstetrics
While the heart rate fluctuates within the range of 120–180 per minute, the fetal
cardiac output is constant.
The fetus develops in the conditions of aerobic metabolism.
Up to 20% [that is, 8 ml (kg×min)] of the consumed oxygen is used by the fetus
for formation of new tissue.
Inadequate living conditions (malnutrition) of the fetus can produce a long-term
negative effect. Children with fetal growth restriction run a higher risk of metabolic
syndrome development at an adult age.
CONTROL QUESTIONS
1. What are the periods of antenatal fetal development?

2. What is implantation window? Which days of the menstrual period does it
correspond to?
3. What determines the sensitivity of endometrium to implantation?
4. What peaks of cytotrophoblast activity do you know? What do they stand for?
5. In which trimester can one measure the length of the umbilical cord? How
can one do this?
6. In what way is the volume of the amniotic fluid maintained during pregnancy?
7. What is the biochemical composition of the amniotic fluid?
8. What critical periods of fetal development do you know?
9. What are the specifics of fetal blood circulation?
10. How does low weight at birth affect further life?
CHECK YOURSELF!
Level 1. Test
Select one correct answer
1. The first period of antenatal fetal development is called

a) cellular;
b) embryonic;
c) organogenetic;
d) fetal.
2. Intensive growth and maturation of cerebral cortex takes place at weeks

a) 20–24 of intrauterine development;
b) 3–8 of intrauterine development;
c) 15–20 of intrauterine development;
d) 7–8 of intrauterine development.
3. Embryology began to be distinguished as an independent science thanks to this

researcher
a) William Harvey;
b) Hippocrates;
c) Aristotle;
d) Darwin.
4. The human ovum was first observed and described by

a) William Harvey;
b) R. Graaf;
c) Mandel;
d) K.M. Baer.
5. The lifespan of a spermatozoon is

a) 78 h;
b) 16 h;
c) 2 days;
d) 6 h.
6. The pool of oocytes used by the woman during her lifetime originates
a) in the sixth week of intrauterine development;
b) in the eighth week of intrauterine development;
c) in the fourteenth week of intrauterine development;
d) the oocyte pool is replenished with new primordial follicles across the whole
lifespan of the woman.
7. The extracellular lifespan of an oocyte is

a) under 24 h;
b) 8 h;
c) 3–4 days;
d) 48 h.
8. This develops in place of a ruptured follicle

a) corpus luteum;
b) corpus albicans;
c) atretic follicle;
d) Graafian vesicle.
9. The implantation window is restricted to

a) day 6–9 of the menstrual period;
b) day 14 of the menstrual period;
c) day 19–22 of the menstrual period;
d) day 1–5 of the menstrual period.
58 Obstetrics
10. The first peak of cytotrophoblast invasion occurs at

a) 5–10 weeks after fertilization;
b) 4–6 weeks after fertilization;
c) 16–18 weeks after fertilization;
d) 1–2 weeks after fertilization.
11. The second peak of cytotrophoblast invasion occurs at

a) 5–10 weeks after fertilization;
b) 4–6 weeks after fertilization;
c) 16–18 weeks after fertilization;
d) 1–2 weeks after fertilization.
Level 2. Clinical situations

1. Patient A. had a spontaneous abortion at 9 weeks gestation. Biopsy of utero-
placental bed was made for a postmortem examination. It was revealed that a greater
part of spiral arteries had pronounced muscular and elastic component in the wall;
a small number of arteries showed signs of lysis of the musculoelastic component
and its replacement with fibrinoid tissue. Which pathogenetic mechanism of abortion
can one suggest in this case?
2. An ultrasound examination at 19 weeks gestation detected that the umbilical
cord had two vessels. Is this normal?
NOTES
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• Chapter 2
PHYSIOLOGICAL CHANGES DURING
PREGNANCY
A normal pregnancy implies overall average values of homeostasis and functional
tests, typical of uncomplicated pregnancy in a healthy woman.
The changes proceeding in the body of a pregnant woman are programmed geneti-
cally; they are of physiologic adaptive nature. The range of these changes involving
all the body’s systems is determined by the necessity to promote fetal vitality and
provide its protection; their extent is determined by the gestational age, the number
of fetuses and individual reserve force of the mother.
2.1. METABOLIC CHANGES DURING PREGNANCY
In pregnant women metabolic processes are characterized by an intensified course.

It is important that, alongside with activation of anabolic reactions, catabolism accel-
erates too, which is accompanied by increased excretion of metabolic waste products
from the body. Furthermore, in the existing unique situation the drift of catabolic
changes is aimed, in the first place, at providing chemical monomers for formation
of complex macromolecular structures in the developing fetus.
All types of metabolic processes undergo substantial changes. This is connected
directly with a change in the activity of numerous enzymes; this activity, in its turn,
depends on the qualitative and quantitative balance between regulatory biomolecules
(hormones, hormonoids, growth factors, cytokines and other).
Basal metabolism and oxygen consumption increase by 15–20% as early as by
16 weeks gestation reaching their peak values by the second half of pregnancy and
during delivery (Fig. 2.1).
2.1.1. Protein metabolism

Protein metabolism becomes noticeably intensified. In the body of a pregnant
woman nitrogen begins to be stored, which is necessary both for the mother and
Intensity of anabolism
Amount of assimilation products
Phosphatase and histaminase activity
Oxygen consumption
Cholinesterase activity
Fig. 2.1. Specifics of metabolism during pregnancy

60 Obstetrics
fetus. The need for nitrogen on the part of the pregnant woman and fetus is in the
ratio 2:1. Starting at 17 weeks of pregnancy nitrogen retention amounts to 1.84 g/
day (by the end of pregnancy — 4.0–5.0 g/day). The amount of residual nitrogen
in the blood does not grow; on the contrary, it diminishes. As insulin resistance
grows while the production of major nitrogen acceptors (pyruvate, 2-oxoglutarate)
reduces, the synthesis of urea and its urine excretion diminish, too. This effect
is also helped along by attenuation of transamination reaction of branched chain
amino acids. Thus, adaptive reactions in pregnancy are aimed at accumulation of
protein and its nitrogen-containing precursors first by the mother and then by the
fetus (Fig. 2.2).
Nitrogen accumulation
Nitrogen consumption
Release of ammonia
and amino acids with urine
Urea excretion with urine
Fig. 2.2. Specifics of protein metabolism in pregnancy
2.1.2. Carbohydrate metabolism

Glucose is the main substance that meets the energy requirements of the fetus
and mother. As pregnancy proceeds, glucose expenditure grows all the time, which
demands constant adjustment of the regulating mechanisms. At the beginning of the
second trimester when the placenta starts functioning, there is an increase in produc-
tion of hormones with a hyperglycemic effect (glucagon, estrogens, cortisol, pituitary
prolactin, placental lactogen, somatotropin). This results in intensified glucogenesis
in the liver and replenishing of the blood with glucose.
At the same time the body of a pregnant woman increases the production of
insulin, a hypoglycemic hormone, but cells show diminished resistance to insulin.
It appears that insulin resistance is an adaptive reaction aimed at forming a flow of
nutritive substrates directed to the fetus from the mother after she has had a meal
(Fig. 2.3).
Specifics of carbohydrate
metabolism during pregnancy
Glucose consumption
Hypoglycemic hormone secretion
Insulin excretion
Fig. 2.3. Specifics of carbohydrate metabolism during pregnancy

Chapter 2. Physiological changes during pregnancy 61
2.1.3. Lipid metabolism

The main specific feature of lipid metabolism in pregnant women is that there
should be conditions for nonstop steroid synthesis. Apart from this, fatty acids, cho-
lesterol, and phospholipids are the structural foundation for the development of fetal
tissues. The greatest concentration of lipids is noted in the placenta, adrenal glands,
and mammary glands. Hyperinsulinemia develops, and against this background the
total amount of lipids in the blood plasma of a pregnant woman increases 1.5 times
and more, and the content of triglycerides and low density lipoproteins grows con-
siderably. Total cholesterol content does not change or reduces insignificantly in the
first trimester of pregnancy; by the end of pregnancy it increases in a linear fashion.
Free fatty acid content also decreases at early stages of pregnancy to grow about
twofold at later stages.
Intensive storage of fat by the maternal body proceeds until 30 weeks gestation,
and then this process slows down. At the same time, while the transport of fatty
acids and glucose through the placenta increases considerably, the fetus shows an
intensive concentration of fats and other lipids during the concluding ten weeks
of gestation.
Changes in lipid metabolism can trigger deposition of subcutaneous fat and body
weight gain (Fig. 2.4).
Concentration of ether-soluble lipids,

TG and LDLP in particular
Concentration of total cholesterol,
free fatty acids starting in the third trimester
Accumulation of lipids in adrenals,
mammary glands and the placenta
Subcutaneous fat deposits
Fig. 2.4. Specifics of lipid metabolism during pregnancy: TG — triglycerides; LDLP — low
density lipoproteins
2.1.4. Mineral and water metabolism

The body of a pregnant woman retains and stores many inorganic substances
which promote fetal growth and development. There is an increase in the absorption
of phosphorus needed for the development of the fetal nervous system and skeleton,
calcium salts (calcium takes part in the formation of cartilage and bone tissue).
Iron retention increases; this element is needed both for the pregnant woman on
account of enhanced bone-marrow hemopoiesis and lactation, and for the fetus.
Other inorganic substances are retained by the pregnant woman’s body — macro
and microelements which are transported to the fetus and promote its normal growth
and development (potassium, sodium, magnesium, chlorine, cobalt, cuprum and
others). Intensive absorption of inorganic substances takes place across the entire
length of pregnancy.
62 Obstetrics
2.1.5. Acid-base balance

Acid-base balance is related to the metabolism of the main macromolecule groups,
water-electrolyte exchange and gas exchange. Oxygen requirements of the develop-
ing fetus are very high. To meet these requirements, the placenta develops specific
structure with a large respiratory surface, plenty of erythrocytes in the fetal blood,
and other adaptive mechanisms. Oxygen exchange is mostly provided for by the
uteroplacental circulation, which also meets the fetal need for oxygen. Besides, a
considerable portion of oxygen coming with maternal blood is consumed by the
placenta and the uterus. The pregnancy-related metabolic changes described above
induce an enhanced oxygen requirement on the part of the organs and tissues in the
maternal body.
2.2. PHYSIOLOGICAL CHANGES IN ORGANS DURING

PREGNANCY
In a pregnant woman’s body there proceed numerous physiological changes that
ensure fetal development, prepare the body for delivery and breastfeeding of the
newborn.
2.2.1. Central nervous system

Adaptive processes in the maternal body are associated with changes in higher
nervous vegetative regulation. It was suggested that, starting from an early gestational
age, the ovum causes stimulation of uterine interoreceptors thus creating a constant
source of afferent impulsation.
• In the first trimester cerebral cortex excitability is increased, which leads to
enhanced excitability of subcortical centers and the spinal marrow.
• In the second trimester the excitability of the cortex and subcortical centers is
just about equal.
• In the third trimester the excitability of the cortex increases and remains
unchanged until 38–39 weeks of pregnancy. One and a half weeks before the due
date the cortex excitability goes down again.
This is the way the pregnancy dominant is formed.
2.2.2. Endocrine system

2.2.2.1. Pituitary gland and hypothalamus
Adenocorticotropic hormone secretion
In the early stages of pregnancy the secretion of adenocorticotropic hormone
(ACTH) is considerably diminished; later it increases along with the level of plasma
cortisol. In the third trimester the content of cortisol increases 23 times compared
with the baseline. In this way, since there is no block on the secretion of factors
similar to ACTH in the placenta, fetal adrenal glands can accomplish their morpho-
functional development (Fig. 2.5).
Estrogens
ACTH in late pregnancy
Cortisol in the second
and third trimester
TTH in late pregnancy
Intensified vascularization,
thyroid hyperplasia calcitonin
Mineralocorticoids
ACTH in the first trimester

Somatotropic hprmone
TTH at early gestational ages
Fig. 2.5. Specifics of the endocrine profi le during pregnancy: ACTH — adenocorticotropic
hormone; TTH — thyreotropic hormone; STH — somatotropic hormone
Somatotropic hormone secretion

In the early stages of pregnancy the synthesis of thyreotropic hormone (TTH) is
suppressed on account of enhanced thyroid hormone content under the stimulating
impact of human chorionic gonadotropin (HCG). In the later stages of pregnancy
the stimulation of thyroid-binding globulin production in the liver under the impact
of estrogens promotes a potential decrease in the levels of free triiodothyronine
(T3) and thyroxin (T4), which results in secondary compensatory elevation of TTH
concentration; TTH is produced by the maternal pituitary gland. These changes
lead to enhanced vascularization and hyperplasia of the thyroid; the extent of this
phenomenon varies from individual to individual.
2.2.2.2. Thyroid gland

Increase of thyroid hormone secretion
In the first half of pregnancy the thyroid gland becomes activated («physiological
hyperthyroidism»). The content of T3, T4, and thyroxine-binding globulin increases
twofold; however, the content of free fractions of thyroid hormones remains un-
changed.
In uncomplicated pregnancy the thyroid clearance of iodine grows threefold,
renal clearance of iodine — twofold. At the same time free uptake of iodine by
the thyroid gland is constant, which maintains the basal metabolic rate within
adequate bounds.
Transient clinical manifestations typical of hyperthyroidism are possible; they
discontinue after childbirth (increased basal metabolic rate, warm limbs, palmar
erythema, lability of cardiac function).
Increase in calcitonin secretion

In pregnancy the growing concentration of estrogens induces an increase in cal-
citonin secretion. These changes help to avoid bone resorption and elevated calcium
content in the blood plasma.
The content of maternal parathyroid hormone remains unchanged in pregnancy.
64 Obstetrics
In later stages of pregnancy the concentration of calcitriol, the hormonally active

metabolite of vitamin D, increases twofold, which encourages calcium absorption
in the intestine.
At the same time, the uptake of calcium by the placenta is enhanced under the
impact of a protein similar to parathyroid hormone produced by the fetus. Thus, in
the third trimester the fetus receives 19 g of calcium and 10 g of phosphorus from
the mother, which is an equivalent of 260 and 140 mg per day, correspondingly. In
view of this the consumption of calcium by the mother in late stages of uncompli-
cated pregnancy doubles.
If these processes are decompensated, which may be associated with insufficient
consumption of calcium from the diet, some pregnant women note pain in bones
and joints, and demineralization of dental enamel.
2.2.2.3. Adrenal glands

Increase in cortisol secretion
Cortisol production by maternal adrenal glands is stably elevated from 12 weeks
gestation until the delivery; it is associated with activated metabolism and increased
cholesterol content.
In pregnant women the circadian rhythm of cortisol secretion gets disrupted, total
cortisol levels increase on account of stimulated transcortin production (the hormone
concentration doubles in pregnancy). The uterus and decidual membranes convert
inactive cortisol to an active form. Myometrial levels of cortisol increase nine fold,
while in the blood plasma — only threefold. This process promotes disorders of
carbohydrate tolerance, fat deposition and striae development on the skin.
Increase in mineralocorticoid secretion

On account of physiological hypervolemia, in uncomplicated pregnancy the levels
of rennin, angiotensinogen, angiotensin and aldosterone are elevated in proportion
to estrogen concentration so as to counter the natriuretic effect produced by proges-
terone. Secretion of aldosterone by the adrenal glands increases starting at 15 weeks;
in the third trimester it amounts to 1 mg per day. On account of these changes there
is fluid retention, elevated circulating blood volume.
2.2.2.4. Placenta
Human chorionic gonadotropin secretion
Local immunosuppression in the uterine cavity (emergence of local immu-
nologically privileged site), limited production of maternal antibodies or stimu-
lated production of blocking antibodies, limited T-helper function and other
changes in the system of cellular immunity induce immunological tolerance in
the mother’s body. As early as 9 days after ovulation, HCG can be revealed in
the maternal plasma; this time corresponds to completed blastocyst invasion in
endometrial stroma. In uncomplicated pregnancy HCG concentration in the
plasma grows twofold every two days reaching its peak value at weeks 8–10
(80,000–100,000 I.U. per litre).
After that the hormone level decreases (about twofold by weeks 18–20) to remain
stable until the end of pregnancy.
HCG concentration depends on the number of fetuses, trophoblast activity, and

the presence of placental insufficiency.
In later stages of pregnancy another peak of HCG concentration is possible, which
can be determined by compensatory reaction of the placenta if there is placental
insufficiency coupled with rhesus isoimmunization.
2.2.2.5. Ovaries
Once pregnancy has started, the ovaries discontinue their cyclic processes and
ovulation. Corpus luteum is active in one of them. The hormones produced by it
(progesterone and estrogens) provide conditions for a normal progress of pregnancy.
These hormones induce hypertrophy and hyperplasia of muscular fibers in the uterus.
Estrogens promote storage of contractile proteins (actin, myosin and others) in the
myometrium, increase of phosphorus compound deposits, which ensure carbohydrate
uptake by uterine muscle. Under the impact of estrogens vessels dilate. Progesterone
exerts a protective effect on the fertilized ovum and uterus. It works to slow down
the conduction of nervous excitation from one muscle fiber to another, which sup-
presses the activity of uterine neuro-muscular apparatus. Progesterone fosters uter-
ine growth during pregnancy and development of glandular tissue in the mammary
glands. Progesterone levels in the first weeks of pregnancy amounts to 10–30 ng/l,
at 5–6 weeks it somewhat goes down.
Corpus luteum is active in the first 10–12 weeks providing for the development
of pregnancy (see Fig. 1.10). After that it begins a gradual involution; by 16 weeks
of gestation its hormonal function has been taken over by the fetoplacental complex
almost completely.
2.2.3. Cardiovascular system

2.2.3.1. Circulating blood volume increase
Uteroplacental blood circulation, the so-called third circulating system, proceeds
in conditions of physiological hypervolemia, which maintains optimum conditions
for microcirculation in the placenta and other vital organs of the mother (the heart,
brain, liver, kidneys). At the same time, the number of corpuscular elements elevates,
and coagulation potential grows: the body prepares itself for blood loss during child-
birth. These processes are associated with activation of the rennin-angiotensin-aldo-
sterone system under the impact of placental estrogens and progesterone, increased
reabsorption of sodium and water in distal convoluted renal tubules, fluid retention
in the vascular bed, and increased volume of the circulating plasma.
This process remains intensive in the first and second trimester reaching its
maximum intensity by 29–36 weeks. On the whole, the circulating blood volume
grows by 40% (3500–5000 ml) by the end of pregnancy, the volume of circulating
plasma — by 35–47% leaving far behind the increase in the volume of circulating
erythrocytes (18–25%) (Fig. 2.6).
The total content of water in the body increases by 7–9 l. In multiple gesta-
tion the circulating blood volume is 500 ml higher than in singleton gestation, on
average.
66 Obstetrics
Blood + 40%
volume
Plasma + 35–47%
volume
Erythrocyte + 18–25%
volume
Fig. 2.6. Changes in the volume of circulating blood, plasma and erythrocytes
by the end of pregnancy
The cardiac minute output, heart rate, central venous pressure, and pressure in the
veins of lower limbs increase, and blood viscosity decreases as a part of compensatory
processes, while the total peripheral vascular resistance decreases.
2.2.3.2. Cardiac output increase

During pregnancy the stroke volume increases, the heart rate accelerates, the car-
diac cavities increase their volume, the left ventricle becomes hypertrophied while its
walls retain their normal thickness. Cardiac output begins to increase at 4–8 weeks
gestation and reaches its peak values by 28–32 weeks increasing by 40–50%. In
early pregnancy this is made possible at the expense of the stroke volume, and after
20–24 weeks — mostly due to the accelerated heart rate. In this situation estrogen
affects the myocardium in a way similar to cardiac glycosides providing optimum
blood supply to the fetus and maternal tissues compensating for chronic cardiac
overload and preparing the body for labor.
2.2.3.3. Blood pressure and microcirculation

In pregnancy total peripheral vascular resistance decreases due to diminished
sensitivity of peripheral vessels to the vasoconstrictor effect of angiotensin II under
the impact of placental estrogens and progesterone, maintenance of blood flow in
placental vessels on account of perfusion. Starting in the first trimester, diastolic BP
decreases; in the second trimester an insignificant decrease in BP is noted; in the
third trimester BP returns to the baseline values.
In the second trimester of gestation systolic BP and diastolic BP go down
by 5–15 mm Hg. The lowest systolic BP is noted at 28 weeks, then it increases
and by the end of pregnancy it becomes the same as pregestation values. Such
changes promote adequate angiogenesis and maintenance of optimum blood
circulation in the fetus, uterus, maternal organs and tissues across the gestation
period (Fig. 2.7).
Total circulating blood volume,

CO, SV, heart rate, central
venous pressure, minute volume
LV hypertrophy
Amount of corpuscular elements
Hypercoagulation
TPVR
Diastolic pressure
Systolic pressure in the second trimester
Fig. 2.7. Specifics of cardiovascular function in pregnancy: CO — cardiac output; LV — left

ventricle; TPVR — total peripheral vascular resistance
Thus angiogenesis in the fetal body and placental vascular network, in the myome-
trium and mammary glands proceeds in most favorable conditions; the uteroplacental
blood flow is maintained at an optimum rate.
2.2.3.4. Changing of the heart position

The heart changes its position in the chest on account of the pregnant uterus
pushing the heart beginning in the second trimester.
Upon that, a half of healthy pregnant women may show functional apical systolic mur-
mur (more often in the second half of pregnancy); 10% of women may show functional
systolic murmur at the pulmonary artery (more often in the second half of pregnancy).
2.2.4. Blood and hematopoiesis

2.2.4.1. Total blood volume increase
Starting in the first months of pregnancy, the woman’s blood flow shows elevated
levels of leukocytes and neutrophils, an accelerated erythrocyte sedimentation rate
(ESR), increased total blood volume. The purpose of these changes is to meet the
growing demands of the mother and fetus for corpuscular blood elements, to maintain
optimum conditions for microcirculation in the placenta (emergence of the «third
circulation system») and the mother’s vital organs (the heart, brain, liver, kidneys),
and to prepare for the imminent blood loss.
2.2.4.2. Red blood cells and hemoglobin increase

A progressive growth of the red blood cells number starts at the 10th week of gestation.
By the end of pregnancy the volume of circulating red blood cells increases by
18–25% amounting to about 1650 million (in nonpregnant women — 1400 million),
which helps to meet the mother’s and fetus’ increased oxygen requirements.
2.2.5. Respiratory system

Pulmonary capacity remains unchanged across pregnancy. Due to the need to
increase pulmonary gas exchange and to provide the mother and fetus with oxygen,
68 Obstetrics
the lungs of the pregnant woman function in hyperventilation mode (in pregnancy
oxygen tension in arterial blood drops to 30–32 mm Hg). pH of maternal blood
changes from 7.4 to 7.44, partial pressure of carbon dioxide — from 38 to 32 mm
Hg. The rate of carbon dioxide elimination and excretion of bicarbonates by kidneys
increase, too.
In late pregnancy, on account of considerable growth of the uterus size, functional
residual lung capacity and the total lung volume decrease, respiratory excursion of
lungs diminishes. This is followed by 10% respiratory rate acceleration so that even
insignificant exercise causes dyspnea. By the end of pregnancy the respiratory volume
grows in proportion to the 30–40% increase in oxygen consumption, the amount
of expired air increases by 26%. Residual volume drops to 20%. The pulmonary
minute volume increases from 8.4 l/min in the first trimester to 11.1 l/min in the
third trimester.
As gestation progresses, the diaphragm goes up propelled by the growing uterus,
the chest circumference increases, the substernal angle widens and diaphragm ex-
cursion intensifies, which is counteracted by a reduced vertical size of the chest
(Fig. 2.8).
Hyperventilation
pH of maternal blood
Respiratory rate at the end of pregnancy
pO2
pCO2
Total volume, residual capacity,
respiratory capacity
Fig. 2.8. Specifics of respiratory function in pregnancy
2.2.6. Digestive system

Reduced tone of inner organ musculature. Across the entire duration of preg-
nancy, progesterone concentration continues to rise, which reduces the rate of
food transit through the intestine, and increases fluid absorption in the colon.
Sometimes reduced acidity of the gastric juice is noted. Relaxation of cardiac
sphincter may lead to heart palpitations and reflux esophagitis. These changes
may result in hyperorexia or dysorexia, thirst, heartburn, nausea, salivation in the
mornings in the first trimester, predisposition for constipation, relative reduction
of urine excretion.
Changes in protein synthetizing function of liver. The total concentration of
plasma protein decreases throughout the entire pregnancy on account of diminished
albumin content, which is associated with reduced protein-producing function of
the liver. A considerable increase in sex steroid binding globulin, thyroxin bind-
ing globulin, transcortin and transferrin content is noted. At the same time, if the
pregnancy is uncomplicated, the ratio of albumins and globulins remains within

the range of 0.8–1.3.
In uncomplicated pregnancy the total concentration of plasma proteins is reduced
on average from 7.0 to 6.0 g%, albumin concentration — from 3.5 to 2.5 g%. Globulin
concentration rises from 2.75 to 3.0 g% (Fig. 2.9).
If, on account of reduced oncotic pressure, plasma proteins show pronounced
reduction, the pregnant woman may develop edema.
2.2.7. Immune system

Suppression of cellular immunity is aimed at preventing rejection of gestational
sac. The process consists in elevating the levels of cortisol, estrogens, progesterone,
HCG; it promotes physiological immunosuppression by way of inhibiting the activ-
ity of T-cells. Apart from suppressed immune reactions of the mother, rejection of
gestational sac is counteracted by immaturity of the fetal antigen system and the
presence of immunity barrier represented by the placenta. The surface of trophoblast
cells has no molecules of class II human leukocyte antigens, which ensures tolerance
of maternal tissues to fetal tissues.
The reverse side of the coin, so to say, is that pregnant women are more often
subject to viral infection; they are inclined to severer, more protracted course of the
disease.
Concentration of sex steroid-binding

globulin, thyroxine-binding globulin,
transcortin and transferrin
Smooth muscle tone in GI tract

Gastric juice acidity
Protein synthesizing function of liver
albumin concentration
Рис. 2.9. Specifics of alimentary function in pregnancy
2.2.8. Urinary system

For the purpose of retaining the levels of tubular reabsorption and excretion
of electrolytes with urine when the woman experiences elevated fluid load, renal
blood flow and glomerular filtration increase, the clearance of creatinine, urea and
uric acid intensifies. Under the impact of progesterone the urinary tract dilates,
renal pelvis expands considerably. The ureters become longer (20–30 cm); now
the ureter cannot fit into its bed and becomes convoluted. The bending commonly
takes place at the border between the upper and middle thirds of the ureter. The
capacity of renal pelvis grows from 5–10 ml to 50 and even to 100 ml. As a result
70 Obstetrics
of such expansion the dead space area increases twofold. In term pregnancy the
urinary bladder shifts upward.
In the first trimester renal blood flow and glomerular filtration first increase
by 30–52% to go down gradually afterwards. Dilation of urinary tracts be-
gins at 5–6 weeks, reaches its maximum by 32 weeks and decreases by the due
date.
For reference: in nonpregnant women renal blood flow is 1100 ml/min, in the
first trimester of pregnancy — 1460 ml/min, in the second trimester — 1150 ml/
min, in the third trimester — 1050 ml/min. 3 weeks prior to delivery the blood flow
decreases to 850 ml/min.
In the nonpregnant state glomerular filtration is 105 ml/min, in the first trimester
of pregnancy — 135 ml/min, in the second trimester — 115 ml/min, in the third
trimester — 110 ml/min, 3 weeks prior to delivery — 90 ml/min. Some pregnant
women develop glucosuria, which is associated with elevated glomerular filtration of
glucose, which exceeds the sugar excretion threshold of the kidneys. Interpretation
of urine tests may present some difficulty.
2.2.9. Skin
During pregnancy the skin undergoes peculiar changes. Deposition of brown pig-
ment is quite often noted on the skin of the face, the linea alba, nipples and mam-
mary areoles. Enhanced pigmentation during pregnancy is linked to the fact that
adrenal glands intensely produce yellowish-brown pigment that is close to melanin.
As the uterus grows, the anterior abdominal wall distends. Under the impact of
mechanical extension and hypercorticism, archlike lines tapering at the ends appear
on the abdomen. During pregnancy they are of reddish-pink color; after delivery it
changes to silver-white. These lines are localized at different sites: around the navel,
in lower stomach regions, not uncommonly they appear on the thighs or mammary
glands.
2.2.10. Reproductive system

2.2.10.1. Mammary glands
Starting at 6 weeks gestation and especially in the second half of pregnancy the
mammary glands increase in size as the number of glandular lobules grows, tubular
lobules transform to alveolar lobules. At the ends of ducts solid projections develop
where a lumen appears. The lumen extends to form an alveolus. Lipid droplets are
noted in alveolar lumen as well as in the epithelium lining. The number of lipid
droplets surges during lactation. During pregnancy the mammary glands produce
colostrum.
2.2.10.2. Cervical mucus

The amount of cervical mucus increases under the impact of estrogens while its
biochemistry changes due to the effect of progesterone; these processes constitute
mechanical and immunological protection of the uterine cavity, placenta and fetus
from ascending infection or contact with potential disturbing factors from the external
environment.
Throughout the entire pregnancy cervical mucus becomes viscous, sticky, and
opaque; it fills the endocervix network acting as an immunological and mechanical
barrier.
In the area of the external orifice cervical mucus contains few bacteria and many
leukocytes, in the middle portion of cervical canal it contains few leukocytes and no
bacteria; the upper portion of the cervical canal is sterile, there are no leukocytes.
The changes reach their peak before delivery, when the cervical mucus plug comes
out. By the moment of delivery in 50–80% of women the hyperactivity of cylindrical
epithelium leads to a shift of the transformation zone of cervical canal epithelium
simulating the manifestations of ectopy.
These processes may result in negative ferning or arborization: revealing artifacts
upon taking samples from the cervical canal for testing, especially for polymerase
chain reaction.
2.2.10.3. Vaginal biocenosis

Pronounced hyperplasia of vaginal epithelium developing under the impact of
estrogens serves to maintain the acidity of vaginal environment, to decrease bacte-
rial contamination resulting from contacts with the external environment. Vaginal
folds become deeper; papillas widen and begin to look like thin battered-down nails.
Proliferating epithelial cells desquamate quickly releasing glycogen which, under the
impact of lactobacteria, transforms to lactic acid thus promoting acidity of the envi-
ronment (pH 3.5–5.0). Among desquamated epithelial cells there appear navicular
cells with folded edges aggregated into groups; this is induced by the effects of pro-
gesterone; the process takes place throughout the entire pregnancy.
Throughout the entire pregnancy the internal vaginal medium is acidic, favorable
for yeast fungus proliferation; as pregnancy progresses the number of navicular cells
begins to exceed the number of superficial flat and basal cells. That is why pregnant
women typically show extremely low bacterial contamination of the upper vaginal
portion, or carrying yeast infection. One can use lab tests for navicular cells in preg-
nant women to diagnose imminent or habitual abortion, to assess the effectiveness
of progesterone therapy, in late pregnancy—to assess fetal maturity and termination
of pregnancy.
2.2.11. Musculo-skeletal system

In pregnant women relaxin produced in the placenta induces serous suffusion and
loosening of articular ligaments, cartilage and synovial membranes of the pubic and
sacroiliac joints. These changes are more pronounced in pubic symphysis, which
causes separation of pubic bones by 0.5–0.6 cm in the area of symphysis. Separation
by 1–2 cm and more is considered pathological.
The chest widens, costal arches move upward, the lower sternal end moves away
from the spinal column. As the uterus grows in size, the woman’s posture changes:
the head and shoulders are thrown back, lumbar lordosis of the spinal column be-
comes more accentuated (the «proud stance» of pregnant women).
72 Obstetrics
REMEMBER!
Changes on the part of the endocrine system in pregnancy:

• adenohypophysis mass increases two- or threefold; large acidophilic «cells of
pregnancy» are noted; pituitary function changes; the levels of follicle stimulating
and luteinizing hormones go down, while prolactin, TTH and ACTH levels increase;
• in the posterior pituitary lobe oxytocin produced in hypothalamus is accumulated;
oxitocin synthesis increases by the end of pregnancy and during delivery;
• the fact of pregnancy and its development are associated with the function of a
new endocrine gland, corpus luteum of pregnancy; corpus luteum produces
sex hormones progesterone and estrogens which play key role in implantation
and further development of pregnancy.
Changes on the part of the cardiovascular system in pregnancy:
• increase of blood volume;
• heart rate acceleration;
• increase of venous pressure.
Changes on the part of the respiratory system during pregnancy:
• in normal pregnancy the fetus receives a constant supply of oxygen, which
increases by more than 30–40% during pregnancy;
• the vertical chest size reduces; this is counteracted by increased chest
circumference and prolonged excursion of the diaphragm;
• limitation on diaphragm excursion encumbers pulmonary ventilation; this is
shown by hurried respiration (by 10%) and increase of respiratory volume by
30–40% by the end of pregnancy.
Changes on the part of the gastrointestinal tract in pregnancy:
• production of gastric secretin and its acidity decrease;
• on account of biosynthesis activation cholesterol content in the blood increases;
• functional activity of the liver decreases (the levels of total protein and fractions
diminish), signs of cytolysis (hyperenzymemia) are possible;
• inactivation of estrogens and other steroid hormones produced by the placenta
intensifies.
Changes on the part of the hemostasis system during pregnancy:
• platelets play the key role in retaining the integrity of vascular walls;
• the hemostasis system undergoes changes: elevated levels of VII, VIII X coagulation
factors and fibrinogen in blood plasma, reduced fibrinolytic activity of the plasma
until the due date followed by a return to the baseline 2–3 days after delivery
of the placenta.
Changes on the part of the locomotor system during pregnancy:

• serous suffusion and loosening of articular ligaments, cartilage and synovial
membranes of the pubic and sacroiliac joints;
• separation of pubic bones;
• anteroposterior diameter of the pelvic inlet changes on account of changes in
the joints.
Changes on the part of the skin during pregnancy:
• in uncomplicated pregnancy brown pigment is deposited on the face, nipples
and areoles, which is due to a changed adrenal function;
• separation of connective and elastic skin fibers gives rise to striae gravidarum;
• hair growth is noted on the skin of the face, thighs and abdomen, which is due to
elevated androgen production by the adrenal glands and, partially, the placenta.
Changes on the part of the mammary glands during pregnancy:

• blood supply intensifies;
• proliferative processes in the epithelium and acini intensify;
• hyperplasia and hypertrophy of lobules takes place;
• smooth musculature of nipples is activated;
• the weight of mammary glands increases from 150 to 500 g.
Changes on the part of the immunity system during pregnancy:
• in physiological pregnancy the humoral component of immune system as
evaluated on the basis of blood levels of IgA, IgM, IgG immunoglobulins does
not change significantly;
• the ratio of B-lymphocytes, T-helpers and T-suppressors does not change
significantly;
• choriogonadotropine, placental lactogen, glucocorticoids, progesterone and
estrogens, α-fetorpotein show a pronounced immunosuppressive effect;
• trophoblast antigens emerge in the fifth week of pregnancy, fetal antigens — in
the twelfth week. From this time on, the immune attack of the fetus progresses;
• the maternal body commonly shows immune tolerance to fetal antigens of
paternal origin.
Changes on the part of the kidneys in pregnancy:
• widening of renal pelvis;
• increase in renal pelvis capacity from 10 to 50–100 ml;
• widening of ureters to 20–30 mm;
• increase of renal blood flow and glomerular filtration by 50%.
Changes on the part of the genital system in pregnancy:
• increase of uterus weight 100 to 1000 g;
• fifty-fold increase of uterus capacity;
• increase of vascular network;
• increase of the number of various receptors;
• thickening of uterine tubes and intensified blood supply;
• thickening and elongation of uterine ligaments;
• hyperplasia and hypertrophy of vaginal muscles and connective tissue
components.
2.3. INFLUENCE OF HARMFUL FACTORS ON FETUS.

ANTENATAL CARE
Physiological changes arising in pregnancy work favorably in a healthy woman’s
body as they promote complete development of major functional systems. In such
conditions pregnancy is well tolerated, as a rule. However, poor hygiene, malnutri-
tion, excessive physical and emotional stress may induce dysfunction of physiological
processes and cause complications of pregnancy. This especially applies to women
with signs of retarded development of the genital system, who have abortions, gyne-
cological and extragenital diseases in past history, who are under stress or in other
unfavorable conditions. In such women complications of pregnancy may develop even
upon a slightest disturbance of lifestyle or hygienic requirements.
Effect of harmful factors. During pregnancy first the embryo, and then the fetus
can be subject to a harmful influence of a variety of factors. They affect the health
74 Obstetrics
of parents during gametes development and just before conception. In this respect
pregnancy should be planned for the time period when future parents are healthy,
have no harmful habits, are not exposed to occupational hazards, have a balanced
diet, and both wish for a child. The disturbing factors are most harmful during
embryogenesis; they can cause the death, malformation or disease of the fetus.
Certain factors are dangerous at any gestational age, like radiation, infection,
harmful effects of chemicals. It is desirable that a woman planning to get pregnant
should not be exposed to occupational hazards at work. In old times newlyweds were
not allowed alcohol, conception was out of the question during fast periods; while
pregnant women were allowed meat and dairy products during fast periods.
Harmful factors can be organized under the following headings.
Unhealthy working conditions, most commonly exposure to radioactive sub-
stances, X-rays, chemicals, microorganism strains, any excessive exercise. Thus
chemicals (like organophosphorous compounds) can accumulate in the body and
exert their influence even several years after the woman has quitted the hazardous
occupation.
Infection. All infections are dangerous, especially during embryogenesis. For in-
stance, rubella and cytomegalovirus induce malformations of the fetus. Infections
both with marked clinical manifestations (syphilis, hepatitis) and latent course (toxo-
plasmosis, mycoplasmosis) are equally dangerous. Antibacterial drugs administered
for treatment of infections can also have an unfavorable effect on the fetus.
In case of a severe infection during embryogenesis when intensive antimicrobial
therapy is administered, termination of pregnancy is indicated.
Environmental factors. Harm may come from environmental pollution if the
woman resides in an industrial area or an area with radiation pollution or chemical
contamination. All pregnant women must be evacuated from areas of environmental
disaster. Some areas have insufficient content of necessary mineral substances (io-
dine, calcium) in water, or elevated content of salts, etc. This can be corrected by
administering a special diet. An abrupt change of the environment (changing the
terrain elevation, climatic or weather conditions) can become a stress factor for the
pregnant woman.
Harmful habits (smoking, alcohol and drug abuse). Quite often women who in-
dulge in harmful habits do not care about their pregnancy, do not lead a lifestyle
suitable for their condition. According to statistics, the number of smoking women
is on the rise. If a pregnant woman gave up smoking during the period of morn-
ing sickness, she should not resume the habit as a smoking mother’s child shows
retarded growth, it is born low weight due to angiopathy of uterine vessels. If the
woman cannot give up smoking completely, she should cut down the number of
smoked cigarettes. The attitude to alcohol is based on this formula: all quantitative
and qualitative parameters of alcohol known to science do nothing but promote a
dreadful condition in the fetus: fetal alcohol syndrome. That is why the main recom-
mendation to a woman is easy to remember: If you drink, you should not get pregnant;
if you are pregnant, you should not drink!
Smoking and pregnancy. Humanity learnt about the health hazard of smoking as
early as in the 19th century. The attitude to smoking changed for the worse abruptly
in 1956 when 40 thousand doctors from different countries correlated case histories
of their patients. It was established that heavy smokers develop cardiovascular and
pulmonary diseases as well as lung cancer many times more often than non-smokers.
When they are inhaled by the pregnant woman, nicotine, carbon monoxide,
benzopyrene and even some radioactive substances from cigarettes, cause a spasm
of vessels, including the uteroplacental vessels, fetal hypoxia develops, and the toxic
substances enumerated above affect all fetal organs causing fetal growth restriction.
Smoking women more often have premature delivery.
Fetal growth restriction is the most common complication of pregnancy in
smoking mothers; it develops in early pregnancy and affects all fetal organs. Such
newborns have a weight that is 200 g below normal. The more cigarettes the preg-
nant mother smokes, the higher risk to the fetus. Pregnant women who smoked
less than one pack of cigarettes suffered from perinatal mortality 20% more often;
those who smoked more than one pack — 35% more often. It was impossible to
establish the number of smoked cigarettes that would not increase the risk of fetal
growth restriction.
Most infants born to smoking mothers are born low weight, they are often ill;
their development is slower than in their peers, they die in childhood more often.
Statistics testify that smoking during pregnancy (regardless of the number of smoked
cigarettes) increases the risk of an unfavorable outcome twofold!
By the end of the 20th century the medical world was shaken by new data about
the effect of smoking on health. It was revealed that nicotine has a negative effect
both on the physical and mental wellbeing of the fetus. German researchers proved
that children of smoking mothers typically showed lack of attentiveness, impulsive-
ness, useless hyperactivity; even their intelligence level was lower than in their peers.
That was not the end of bad news, though. In 2003 researchers revealed the fol-
lowing links:
• children of mothers who smoked during pregnancy run a risk of developing
diabetes or obesity by the age of 16 about 30% more often;
• boys born to smoking mothers have testicles of smaller size; the spermatozoa
concentration in sperm is 20% lower, on average;
• children of mothers who smoked during pregnancy start smoking themselves
several times more often (Fig. 2.10).
Alcohol during pregnancy. It was estimated that about 11% of pregnant women
abuse alcohol. Alcohol is absolutely contraindicated to pregnant women. Regular
consumption of alcohol can cause the development of fetal alcohol syndrome.
Presence of some sign of fetal alcohol syndrome points to alcohol induced fetal
damage. The amount of alcohol causing alcohol induced fetal damage or fetal al-
cohol syndrome is not exactly known. Fetal alcohol syndrome may develop both in
systematic alcohol abuse and after single episodes of heavy drinking.
Other complications include spontaneous abortion in the second trimester of
pregnancy, fetal hypoxia and low Apgar score. Alcohol consumption is often ac-
companied by smoking and drug abuse. This produces extra damaging effects on the
fetus increasing the risk of fetal growth restriction (Fig. 2.11).
Drug abuse and pregnancy. Drug abuse entails a substantially higher risk of peri-
natal morbidity, fetal growth restriction, hypoxia and neonatal abstinence syndrome
development.
76 Obstetrics
– FGR, low weight at birth

– 20-35% increase in perinatal
mortality
– Psychoemotional
disturbances
– Diabetes mellitus
– Obesity
– Sperm abnormalities
Fig. 2.10. Effect of smoking tobacco on physical wellbeing, progress of pregnancy and child’s
development
– FGR, low weight at birth

– Spontaneous abortion
– Psychoneurologic dis-
orders including mental
deficiency
– Malformations including
microcephaly, microph-
thalmy
Fig. 2.11. Effect of alcohol on the course of pregnancy and child’s development
Effect of alcohol on the fetus. The incidence of embryofetal

NB! alcohol syndrome is 1–2 per 1,000 pregnancies. It includes the
following signs:
• FGR;
• microcephaly;
• microphthalmia;
• mental deficiency and other neurologic disturbances;
• typical arrangement of facial features (flat nose bridge and
philtrum, narrow upper lip (fish-mouth), and union of eyelids in
the corners of eyes).
Undernutrition. This condition can be fought by informing the woman about

balanced nutrition and its importance; some women need social support. During
pregnancy both excessive and unbalanced nutrition are harmful.
Somatic disease (see Chapter 22 Pregnancy, labor and postpartum period in
women with extragenital disease).
Complications of pregnancy: preeclampsia, anemia, miscarriage and others.
Taking medications. During pregnancy taking medications other than administered
by the doctor is absolutely inadmissible. The first trimester is an especially tender
period for medication consumption. A healthy pregnant woman has no need for
medications except in case of life-threatening disease.
Stressful situations. A pregnant woman should be protected against stressful situ-
ations. This is the duty of the family, significant others, the obstetrician, and the
woman herself. The woman should avoid conflicts, excess negative information and
excessive socializing, make a thoughtful choice of reading matter, TV shows, con-
tacts with other people and topics for discussion. In old times they used to say that
a pregnant woman should see beautiful things, think of sublime things and behave
nobly so that to have a healthy, handsome child.
2.4. RATIONAL BEHAVIOR OF HEALTHY

PREGNANT WOMAN
2.4.1. Lifestyle and daily regimen
The main rule guiding the pregnant woman’s actions should be prevention of ef-
fects of manageable environmental factors that have a proven or potential negative
effect on the fetus. Critical periods of development are:
• 8 weeks gestation (organogenesis);
• 15–20 weeks gestation (intensive brain development);
• 20–24 weeks gestation (formation of major functional systems of the fetal body).
The woman should inform that she is pregnant when she deals with all health
professionals that provide health care for her, and pharmacists.
2.4.2. Daily recreation

The pregnant woman should adjust her daily routine in such a way so that to have
enough resting time. Starting in the second trimester she needs to sleep no less than
9 hours daily including daytime naps.
In all seasons it is advisable to take regular unfatiguing walks for 1–1.5 hours daily
and, if possible, before bedtime.
Exposure to warm air (22 °С) of about 25 min duration is indicated to pregnant
women. In autumn, winter and spring when people experience natural relative
hypovitaminosis, ultraviolet irradiation of the body at gestational ages 18–20 and
35–37 weeks is good for pregnant women. This measure can help to prevent phospho-
rus and calcium metabolism disorder, which is especially important if the pregnant
woman resides in northern regions.
78 Obstetrics
2.4.3. Diet
Rational nutrition is a balanced choice of various food products in accordance
with the gestational age, and correct distribution of meals across the day. The diet
should take into account the pregnant woman’s weight and height, fetal size, the
course of pregnancy, the nature of the woman’s occupation. An overweight woman
should plan her meals in such a way as to avoid excessive weight gain, that is, to
reduce the energy value of her diet by reducing carbohydrates and fats. Underweight
women should increase the energy value of their foods while retaining the correct
ratio between the main groups of foods.
The quantity and quality of food consumed by the pregnant mother determines
the wellbeing and development of the child. This does not imply that the pregnant
woman should «eat for two». Her diet should include a sufficient amount of protein,
carbohydrates, fats, mineral salts, and the meals should be balanced. It is advisable
to abstain from spicy and fried foods, to limit the intake of salt and sugar; stewed
and boiled foods are preferable.
2.4.3.1. Proteins, carbohydrates and fats

In the first months of pregnancy it is recommended to take four meals a day.
At this gestational age a woman of middle height and weight needs no less than
2400–2700 kcal/day where there is no less than 100 g of protein, 350 g of carbohy-
drates and 75 g of fats.
In the second half of pregnancy the best regimen is 5–6 meals a day, in small
portions. In this period one should increase the intake of proteins to 110 g, carbohy-
drates — to 400 g, and fats — to 85 g. Animal foods should predominate in the diet.
Protein rich foods are meat, chicken, fish, eggs, dairy products. Milk and cottage
cheese, yogurt and biokefir are most preferable. Dairy products should not be too
fatty; it is advisable to choose soft cheeses.
Carbohydrates are easily assimilated by the fetus; they are found in abundance in
bread, potatoes, rice, cooked cereal and other grain products. Intake of fruit should
be limited to 400–500 g per day; their excess promotes obesity. Sugar and sweets
should be limited; in the second half of pregnancy one should virtually give up
confectionery; a healthy pregnant woman needs no more than four teaspoonfuls of
sugar a day. 30 g of dark unsweetened chocolate a day is admissible; ice cream (no
more than 50 g a day) is admissible occasionally.
As a source of fats, one should give preference to vegetable oil (sunflower, corn,
olive, soya). These varieties of vegetable oil contain vitamin E which is necessary for
the normal course of pregnancy. Intake of butter can amount to 20–25 g per day.
Fatty foods should be given up altogether.
2.4.3.2. Fluids
During pregnancy the woman had better increase her fluid intake to 2 litres a day.
To prevent urinary tract infection pregnant women with renal disease would do well
to drink cranberry or cowberry water, lemon tea, Indian kidney tea.
Dietary rules for pregnant women:

NB! • meals should be frequent (5-6 times a day) but small;
• eat when you are hungry rather than according to the schedule
(better eat less than overeat);
• abstain from fried, smoked and preserved foods; boiled, baked
and steamed foods are preferable;
• do not eat much before bedtime (supper at 6 PM, after this time
have some kefir and fruit);
• a pregnant woman’s diet should be varied.
2.4.4. Attitude to air and urban transport and driving a car

During pregnancy the woman should preferably abstain from air flights, she had
better go by train or in a car. When going in a car, one should stop for rest every
hour or hour and a half. A pregnant woman should not drive for longer than two and
a half hours a day. When using public transport one should avoid the rush hour and
go out as little as possible during the period of epidemics of viral disease.
After 28 weeks one should avoid long trips in any kind of transport; the last two
weeks before due date the woman should keep at home.
There are several easy rules that provide safety and comfort when driving:
• the driver’s seat should be pushed back so that the distance between the steering
wheel and the pregnant belly is no less than 10 cm;
• the back of the driver’s seat should be somewhat inclined backwards but in a way
not to interfere with the view;
• the safety belt should always be worn;
• when buckling the safety belt one should ensure that it is in the correct position:
its upper part should go under the breast, its lower part — at the lower abdomen
(car manufacturers produce highly elastic safety belts intended for pregnant
women).
Sometimes the pregnant woman should abstain from driving:

NB! • when she had pronounced manifestations of toxicosis (riding in
a car and various smells may aggravate the malaise);
• when she is too agitated or irritated (a greater risk of inappropri-
ate behavior on the road);
• in the third trimester.
Do not attempt to get to hospital by yourself once labor has set in.
2.4.5. Physical exercise

For most pregnant women it would do good to walk, swim, do remedial gymnas-
tics (aerobics), which could be done in a gym or at home. In the third trimester of
pregnancy the load on knee and ankle joints should be as little as possible.
80 Obstetrics
In pregnancy exercise does the following:

• strengthening back muscles;
• increasing the mobility of the spinal column and coxofemoral joint;
• elimination and prevention of congestion in the small pelvis and lower limbs;
• increasing the elasticity of perineal muscles;
• learning breathing exercises and relaxation skills;
• reducing the risk of excessive weight gain;
• normalizing the tone and function of inner organs.
If during exercise the woman experiences shortness of breath, weakness, dizzi-
ness, dragging pain in the lower abdomen, blood tinged discharge or other unusual
symptoms, she should stop exercising at once and consult her physician.
Sports and exercise are contraindicated to pregnant women with
• acute disease;
• exacerbation of chronic disease;
• signs of threatened miscarriage;
• pronounced toxicosis;
• preeclampsia;
• miscarriage or polyhydramnios in past history;
• regular spasmodic pain developing after exercising.
Certain types of exercise should be suspended: horse riding,

NB! water skiing, surfing, platform diving, scuba diving, speed running,
mountain skis, cycling, team games.
2.4.6. Work and employment

The pregnant woman should not work night shifts, work overtime, go on business
trips after 3 months of pregnancy or do physically demanding jobs after 20 weeks.
The working day of a pregnant woman should not exceed 6 hours, there should be
no place for rush, urgency, trying to catch up with backlog. The period of profound
concentration should not exceed 25% of working time.
It is forbidden
NB! • to employ women for heavy and underground work;
• to have women carry or move heavy objects;
• to have women work at nighttime except for jobs where this is
highly necessary and is of temporary nature;
• to have women work overtime, at weekends, or go on business trips
2.4.7. Housekeeping and renovation

The pregnant woman can do house work, but without overstrain. Short rest is
advisable every hour or hour and a half. No more than 2 hours can be spent in the
kitchen, and this time should be evenly distributed during the day.
Moist mopping is done without using chemical detergents. The pregnant woman
is intent on making her home comfortable (nesting syndrome), which often includes
changes in the interior design, renovation and decoration. There should be no smell
of paint, lacquer, acetone or solvents in the home. The mother to be should avoid any
contact with organic solvents from the moment her pregnancy was diagnosed; if there is
forced necessity, the woman should wear protective equipment and air the room well.
2.4.8. Visiting of public places

The pregnant woman should spend no more than an hour a day in the shops. It
is advisable to avoid shopping when there is a rush of customers (festive days and
weekends, end of business day) and during epidemics of the flu and acute respira-
tory viral infections, as pregnant women show a suppressed resistance to infections.
During pregnancy one should avoid night clubs and any places where smoking is
allowed and where it is noisy. Psychologists recommend that pregnant women go to
exhibitions, theatres, concerts of classical music.
2.4.9. Clothes and shoes

Clothes should be loose, comfortable and ergonomic. Natural fabrics should be
given reference to. Compression of the chest and abdomen should be avoided, as well
as oppressing rubber bands or insertions, especially in the underwear. Loose-fitting
dresses or long billowing tunics are suitable for pregnant women. It would be ideal
to wear clothes and underwear designed and made especially for pregnant women.
Shoes should be comfortable, on low wide heels.
2.4.10. Hygiene
2.4.10.1. Oral cavity and teeth hygiene
During pregnancy one should choose a toothbrush with soft bristles and a remin-
eralizing toothpaste, or kids’ toothpaste. It is advisable to go to a dental appointment
at the beginning of each trimester.
2.4.10.2. Skin care and procedures

During pregnancy intradermal blood flow is enhanced, dermal respiration in-
tensifies, too. On account of this the skin functions under a greater load having to
eliminate harmful metabolic waste. The best hygienic hydrotherapeutic procedure
is a warm shower, which can be combined with sponge bath and rubdown with
lukewarm water.
Women can apply skin care products designed for pregnant women, or any care
products whose label does not say they are contraindicated in pregnancy.
All machine cosmetology procedures, mesotherapy treatment, photoepilation, sun
tanning parlor, invigorating massage are strictly contraindicated to pregnant women.
2.4.10.3. Nail care

Care of nails on hands and feet should not be dispensed with, it should be done
even oftener than usual as the cuticle has a tendency to get callous and prone to
82 Obstetrics
develop hangnails. During the first 14 weeks (period of organogenesis) hygienic

manicure without applying nail polish is preferable. Throughout the entire pregnancy
the woman should use nail polish remover that does not contain acetone.
It is contraindicated to have nail extension with acidic nail primer. The safety of
gels used for nail extension has not been studied.
2.4.10.4. Hair care

The question of hair care from the point of view of fetal safety has not been studied
well enough. Regular trimming of hair at the ends promotes its growth. Hair care
products and hair dyes should be excluded during the period of organogenesis, and
later it should be kept to a minimum. Natural hair dyes like henna and indigo can
be used. Visits to the hairdressers where the pregnant woman spends 1–3 hours in a
static position, with loud noise and a high concentration of toxic substances in the
air, are a negative influence on the body.
2.4.10.5. Care for mammary glands

It is recommended to wash the mammary glands every day with lukewarm water
using baby soap.
2.4.10.6. Intimate hygiene

Hygienic vaginal douche is contraindicated as it has a proven negative effect on
vaginal biocenosis. Underwear should be of natural fabrics only.
2.4.10.7. Physical intimacy

Abstinence is indicated when the pregnant woman has the following:
• habitual miscarriage in past history;
• threatened abortion;
• blood tinged vaginal discharge;
• low placentation or placenta previa;
• cervical insufficiency;
• membrane rupture;
• spontaneous preterm labor in past history;
• multiple pregnancy after 20 weeks gestation.
A pregnant woman does not have to abstain from sex if there are no contraindica-
tions and gestation proceeds uneventfully; however, excessive pressure on the abdo-
men should be avoided starting at 12 weeks, and deep penetration of the penis into
the vagina should be limited. If there is any risk of sexually transferred infection, the
condom should be used in any sexual contact.
A woman’s need for sex varies during pregnancy. The couple

NB! should choose sex positions that suit both. When the woman is
markedly tired, which is typical of the first months of pregnancy,
the couple should have sex at daytime reserving the night hours
for rest. No pain is admissible during intercourse.
2.4.11. Pharmaceuticals
During the stage of organogenesis (until 14 weeks) one should try to abstain from
any drugs, except for folic acid and potassium iodide to prevent open neural tube
defects and congenital hypothyroidism. Healthy women should avoid any pharma-
ceuticals throughout the entire pregnancy, except for the simplest over-the-counter
drugs listed under A by the Food and Drug Administration.
The following medications are absolutely contraindicated in

NB! pregnancy:
• certain antibiotics (streptomycin, tetracycline);
• antidepressants;
• hypotensive drugs like reserpine, hydrochlorothiazide;
• vitamin A at doses exceeding 10,000 U a day.
The question of taking vitamins developed purposefully for pregnant women re-
mains open. There is no level A evidence supporting the need for their consumption.
REMEMBER!
Pregnancy is a physiological process.
During pregnancy and delivery the body undergoes various anatomical and
physiological changes that involve most organs and systems. Early changes take
place, on the one hand, on account of increased metabolic requirements on the
part of the fetus, on the other hand — on account of elevated levels of pregnancy
hormones like progesterone and estrogens.
The main rule guiding the pregnant woman’s behavior should be prevention of the
effects of manageable factors of the external environment that have a proven or
potentially negative effect on the fetus.
Critical periods of development are as follows:

• the eighth week (organogenesis);
• 15–20 weeks (accelerated brain development);
• 20–24 weeks (formation of major functional systems of the fetal body).
CONTROL QUESTIONS
1. Who formulated the principle of pregnancy dominant? What does it say?

2. What is the role of prolactin hormone in the pregnant woman’s body?
3. What are the main functions of corpus luteum in pregnancy, at what gestational
age is it active?
4. What is true differentiation of mammary lobules, at what gestational age does
it take place?
84 Obstetrics
5. How does systolic and diastolic blood pressure change during pregnancy?
6. On what account does the area of dead space in kidneys increase?
7. What is the immunologic paradox of pregnancy?
8. What induces reduced hemoglobin concentration during pregnancy?
9. What are the changes in the hemostasis system during pregnancy?
10. How does pregnancy affect vaginal biocenosis?
CHECK YOURSELF!
Level 1. Test
Select one or more correct answer(s)
1. How many days does pregnancy last?

a) 280 days;
b) 334 days;
c) 116 days;
d) 360 days.
2. Striae gravidarum appear on the skin under the effect of elevated concentrations of:
a) TSH;
b) TSH+luteinizing hormone;
c) Somatotropic hormone+ACTH.
3. Corpus luteum is active

a) until 6 weeks gestation;
b) for 20 weeks;
c) for 12 weeks;
d) for 14 weeks.
4. By the end of pregnancy the uterus weighs

a) 2000 g;
b) 100–150 g;
c) 400 g;
d) 1000–1500 g.
5. CH can be revealed
a) in the third week of pregnancy;
b) in the fifth week of pregnancy;
c) in the 12th week of pregnancy;
d) in the 7th week of pregnancy.
6. Spasmodic contraction of gastrocnemius muscle in a pregnant woman indicates

reduced levels of
a) calcium;
b) sodium;
c) chlorine;
d) potassium.
7. During pregnancy cardiac output

a) increases;
b) decreases;
c) increases in the first and second trimesters and decreases in the third trimester;
d) remains unchanged.
8. The least hemoglobin concentration in the blood is noted

a) in the first trimester;
b) the same throughout the entire pregnancy;
c) in the second trimester;
d) in the third trimester.

1. At an appointment the patient showed a heart rate 96 beats per minute at rest.
What is the diagnosis and management?
2. At 34 weeks gestation the patient’s hemoglobin is 118 g/l. What is the diagnosis
and management?
NOTES
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• Chapter 3
ANTENATAL AND POSTPARTUM CARE
3.1. ANTENATAL CARE
3.1.1. Psychological features and behavior changes

of pregnant women
Pregnancy is not a disease; rather, it is a special time in the woman’s life when
her organs and systems function in intensive mode, sometimes approaching the criti-
cal mode. The need to provide for fetal development and to protect the fetus from
various negative influences of the internal and external environment is accompanied
by invariable strain on all vital functions.
In early pregnancy even a healthy woman may show vegetative or neurotic disor-
ders (weakness, undue fatigability, nausea, vomiting, salivation, hyperosmia, abrupt
mood swings, tearfulness). As pregnancy progresses, these signs are followed by those
induced by vagal effects, uterine growth and the effect of placental hormones on all
organs and systems (heartburn, constipation, frequent urination, heart palpitations,
muscular pain in legs). Nearer to the due date the woman may show dyspnea, edema,
pain in the lower back and pubic symphysis, emotional instability (see Chapter
2 Physiological Changes During Pregnancy). All these features should be taken into
account when consulting pregnant women and giving them recommendations about
their health, lifestyle, the course of pregnancy and fetal condition, as well as specific
features of postpartum period (including breastfeeding).
A mother’s-to-be lifestyle and behavior should be aimed at the

NB! greatest possible elimination and prevention of harmful factors
affecting the fetus.
Safety of the embryo during the first eight weeks of gestation and during critical
periods (see section 1.7. Critical Periods of Fetal Development) is of prime impor-
tance as this is the time of active organogenesis.
3.1.2. Standards of antepartum care

Antepartum care is the main function of a prenatal clinic. The quality of outpatient
observation aimed at preventing obstetric complications determines, to a great extent,
the outcome of pregnancy and delivery. It was established that in women who present
for antepartum care at early gestational age and see their doctor no less than 7 times,
the perinatal mortality rate is twice lower than in those who were not registered with
prenatal care clinic. A pregnant woman with uneventful course of pregnancy should
make no less than 7 visits to a prenatal care clinic.
Chapter 3. Antenatal and postpartum care 87
The pregnant women are examined by:

• Gynecologist-obstetrician at least 7 times;
• Therapist at least twice;
• Dentist at least twice;
• ENT and eye specialists at least once (not later than 7–10 days after the first
prenatal visit);
• Other specialists according to indications, considering concomitant extragenital
diseases.
Screening ultrasound is performed three times: at gestational age 11–14 weeks,
18–21 weeks and 30–34 weeks.
Principles of prenatal care

• Prenatal coverage of pregnant women. The woman should be registered with
the prenatal care clinic in the first trimester. After her booking visit to the
prenatal care clinic the gynecologist-obstetrician refers her to a therapist
and ophthalmologist for a preventive examination. Visit to a doctor at early
stages of pregnancy allows a timely diagnosis of extragenital disease, an
assessment of its severity, presence of remission or exacerbation. In this
way the issue of hospitalization for prevention of premature birth can be
dealt with in time, as well as issues of rational occupation, evaluating the
extent of obstetric and perinatal risk, developing an individual pregnancy
management protocol.
• Registering. At the booking visit the doctor takes the patient’s medical and
obstetric history and fills in her Case Sheet for Pregnant and Puerpera. In
Russian Federation the form includes passport data, details of the patient’s
medical history and any family history of illness, with special attention paid
to reproductive history, menstrual periods, somatic and gynecologic illnesses
or surgery in childhood and maturity, blood transfusions. The patient’s record
contains all findings of every test and examination and administrations and
recommendations issued at each visit.
• When the pregnant woman pays her booking visit irrespective of the gestational
age, the obstetrician should familiarize themselves with her outpatient case
record issued by the district clinic. Special attention should be paid to surgery on
reproductive organs; the obstetrician should obtain discharge summaries with a
detailed protocol of the surgery.
• Revealing factors of perinatal and obstetric risk with a repeated assessment of the
changing status. Despite the fact that pregnancy and delivery are a physiological
process, it is always associated with a certain risk. According to the World Health
Organization (WHO), most deliveries (85%) proceed without complications,
without assistance — such delivery is evaluated as normal (low perinatal risk).
According to the WHO, delivery is classified as safe when the necessary sanitary
requirements are met and there is a person present who has the skills to deliver
a baby.
• All risk factors summed up, the pregnant woman is assessed as pertaining to the
group of low, medium or high risk. For quantitative assessment of risk factors one
should use the prenatal risk factors score.
88 Obstetrics
• As the pregnancy progresses and new fi ndings about obstetric complications

and the nature of somatic illness course are revealed, the factors of prenatal and
obstetric risk should be given a dynamic reassessment.
• Timely examination (within 12–14 days). The early presentation for a booking
visit is fully effective if the woman undergoes complete examination shortly
afterwards. The clinical and laboratory fi ndings help to assess the chances of
carrying the pregnancy, the extent of prenatal risk, to make a plan of management
of the patient in advance.
• Follow-up on puerperant mother. In the postpartum period after the mother and
newborn have been discharged from the maternity hospital, a telephone message
is sent to the district gynecology clinic.
• Timely hospitalization during pregnancy and prior to delivery if there is an
emergency or elective indications. This simple measure helps to reduce perinatal
mortality rate 8 times in comparison with those women who needed hospital care
but were not hospitalized in due time.
• Frequency of appointments with obstetrician-gynecologist. In uncomplicated
pregnancy the woman sees her doctor at least 7 times; once a month in the fi rst
half of pregnancy, and once or twice a month after 28 weeks. The schedule
of appointments with the obstetrician-gynecologist is subject for change in
accordance with regulations by the local health care authorities.
• If extragenital disease is revealed or complications develop, there is a need for
more frequent appointments with the obstetrician-gynecologist.
• If need be, the pregnant woman is referred to a day patient facility.
• Childbirth education implies physical and psychological preparation for labor and
childbirth for all pregnant women and their husbands.
• Prevention of purulent septic complications including timely sanation of the oral
cavity and ear-nose-throat area.
3.1.3. Examination of a pregnant woman

The pregnant woman with physiological pregnancy is examined by an obstetrician-
gynecologist no less than 7 times.
If the doctor reveals internal organ diseases, their course complicated by
pregnancy, the therapist or another specialist is called in to discuss with the
obstetrician-gynecologist the possibility of carrying the pregnancy to term.
Additional investigations are administered if necessary, the attending doctors
deal with the issue of choosing the facility for care and desirability of pre-
serving the pregnancy, and the woman is referred to a hospital. At each visit
the obstetrician-gynecologist checks if the woman complies with all medical
recommendations. Medical advice and care are provided by maternity welfare
centers, hospitals, clinical sites of teaching hospitals, perinatal centers, relevant
departments of teaching hospitals.
Pregnant women who smoke, abuse alcohol or drugs require special attention.
If the fact of drug or alcohol abuse is revealed, the woman should be persuaded to
see an addiction psychiatrist, which is essential to promote her own health and that
of her child. During pregnancy and after childbirth such patients are managed by
obstetrician-gynecologist with consideration to recommendations given by the ad-

diction psychiatrist.
If a pregnant woman shows positive results of lab tests for human immunodefi-
ciency virus (HIV), the obstetrician-gynecologist refers her to the regional Centre
for AIDS Prevention and Management for detailed examinations, registration and
administration of chemoprevention of mother-to-child transmission of HIV infec-
tion (antiretroviral therapy). In places where a woman has no access to obstetrician-
gynecologist, the function of referral is performed by the therapist, family physician,
or staff of the rural health post.
HIV-infected pregnant women are hospitalized; they give birth in specialized
hospitals.
If the pregnant woman is under 18 and intends to have her baby, she is observed
by the obstetrician-gynecologist at the local prenatal clinic, and after delivery she
is referred to a pre-conception clinic or to a youth counseling centre for individual
selection of means of contraception.
If there are indications for therapeutic abortion and the woman consents to it, she
is given a medical commission certificate with complete clinical diagnosis signed by
the relevant specialist (depending on the nature of illness), obstetrician-gynecologist,
head of the prenatal clinic, with a seal affixed.
3.1.3.1. Prenatal screening

All pregnant women are referred for prenatal diagnosis for the purpose of prevent-
ing the birth of children with congenital and inherited anomalies.
The aim of prenatal screening is to determine for each pregnant woman her indi-
vidual risk of having a baby with genetic disorders (Down syndrome, Edwards syn-
drome, Patau syndrome, neural tube defects) taking into consideration the woman’s
age, levels of biochemical markers, nuchal translucency and nasal bone length.
Prenatal screening is performed twice.
• First screening (11–14 weeks). At gestational age 11–14 weeks the pregnant
woman is referred to health care facilities certified to offer prenatal diagnosis,
for complex prenatal diagnosis of fetal development disorders, which includes
ultrasound examination by certified specialists with a license from Fetal Medicine
Foundation for ultrasound examination in the fi rst trimester, determination of
maternal serum markers (pregnancy associated plazma protein A and β-HCG,
free β-subunit of chorionic gonadotropin) followed by computerized calculation
of the risk of birth of a child with chromosome anomaly (trisomy 21, trisomy 18
and trisomy 13).
• Second screening (18–21 weeks). This stage includes an ultrasound examination
of all fetal organs and systems, as well as an assessment of extraembryonic
structures. At gestational age 18–21 weeks the pregnant woman is referred to
health care facilities providing prenatal diagnosis for an ultrasound examination
to rule out fetal development anomalies that become manifest relatively late.
At gestational age 30–34 weeks the ultrasound examination is performed at
community-based facilities.
Physical examination. At the first examination of a pregnant woman the doctor
assesses her body build, asks about the initial body weight before pregnancy, and
90 Obstetrics
about her diet. Women who are under- or overweight should be given closer at-
tention.
During this appointment the woman’s BP is taken on both arms; the coloration
of her facial skin and mucosas should be noted, she should be checked for visible
edema. The doctor listens to her heart sounds and lungs, palpates her thyroid gland,
mammary glands, regional lymph nodes, checks the condition of her nipples.
Obstetric examination includes the following: measuring the external pelvic size
and rhombus of Michaelis, vaginal examination with inspection of the cervix and
vaginal walls with speculum, as well as inspection of perineum and anus, checking
for exostoses in the small pelvis, measuring the diagonal conjugate, checking for
anomalies of genital organs. If there are no abnormal changes in the vagina or cervix,
a woman with uncomplicated pregnancy needs only one vaginal examination; further
examinations are performed if there are indications. Palpation of the abdomen helps
to assess the condition of anterior abdominal wall and muscular elasticity.
External obstetric examination. When the uterus grows big enough to be palpated
from outside (13–15 weeks), one can assess the symphysis-fundal height (SFH),
uterine tone, fetal size, amniotic fluid volume (AFV), the presenting part. As preg-
nancy progresses, one assesses the fetal lie, position of its organs, fetal presentation
and position. Palpation is done using four classic obstetric maneuvers (Leopold’s
maneuvers).
Auscultation of fetal heart sounds is done starting at 20 weeks of pregnancy. Fetal
heartbeat is assessed using an obstetric stethoscope (Pinard horn) or pocket fetal
monitor (Fig. 3.1). It sounds as rhythmical double beats with an average rate of
130–140 bpm. Fetal heartbeat is also assessed with ultrasound equipment, dopple-
rometer, fetal cardiomonitor, which makes the investigation much more accurate.
If elevated BP is detected in early pregnancy, investigations should be performed
to rule out or confirm hypertonic disease. If the patient presents at the prenatal clinic
at advanced gestational age, differential diagnosis between hypertonic disease and
preeclampsia becomes complicated. Obviously, the earlier the woman comes to the
prenatal clinic, the more reliable data will be at the doctor’s disposal.
Determining the time for pre-maternity
and post-delivery leave is an important step
as it ensures that women in certain risk
groups may receive timely diagnostic, pre-
ventive or therapeutic services.
According to the laws in place in the
Russian Federation, a working woman, ir-
respective of her length of service, is en-
titled to a maternity leave beginning at
30 weeks gestation, of 140 days duration
(70 consecutive days before delivery, and
70 — after delivery). In multiple pregnancy
the maternity leave begins at 28 weeks for
194 consecutive days (84 consecutive days
before pregnancy, and 110 consecutive days
Fig. 3.1. Pinard horn after pregnancy).
If labor begins in the period 23–30 weeks and ends in a live birth, the sickness
certificate is issued by the prenatal clinic on the strength of discharge summary from
the maternity hospital which delivered the baby. The woman is given a maternity
leave of 156 consecutive days; in case of a still birth or the newborn’s death within
the first 7 days (168 hours) after delivery — 86 consecutive days. If the woman left
her place of residence and gave birth elsewhere, the sickness certificate is issued by
the maternity hospital (or department) where the childbirth took place.
If childbirth proceeds with complications, the sickness certificate for extra 16 con-
secutive days is issued by the maternity hospital (or department) or by the local
prenatal clinic on the strength of documentation from the healthcare facility which
delivered the baby.
The sickness certificates are entered in the register of sickness certificates. The
age of gestation can be determined most accurately by an ultrasound examination
in the first trimester.
In order to provide comprehensive information to the maternity hospital, the doc-
tor at the prenatal clinic hands out to the pregnant woman an exchange-notifiable
medical chart at 22–23 weeks gestation.
3.1.3.2. Role of exchange-notifiable medical charts of pregnant and

puerpera
To provide continuity of care for the pregnant woman by the maternity wel-
fare centre and maternity hospital, each pregnant woman with 22–23 weeks
gestation receives an exchange-notifiable medical chart that includes infor-
mation about the woman’s state of health, specifics of the pregnancy course,
findings of lab tests and additional examinations, whether the pregnant woman
is in any prenatal risk group (for each trimester). The doctor at the maternity
hospital enters in the chart all the data about the childbirth and the newborn’s
condition (Fig. 3.2).
The maternity welfare centre should pay special attention to pregnant women as-
signed to high risk groups for perinatal, obstetric complications and to patients with
extragenital disease.
If the pregnant woman has an exacerbation of extragenital disease or complications
of pregnancy, the obstetrician-gynecologist and therapist at the maternity welfare
centre should administer relevant treatment in outpatient settings or refer her to the
relevant hospital department.
Patients with tuberculosis, diabetes mellitus, cardiovascular, sexually transmitted
disease or infections are under the care of relevant specialists; as a rule, for delivery
they are referred to specialized maternity hospitals or hospital departments.
3.1.3.3. Laboratory methods

When a pregnant woman is registered with a prenatal clinic, certain lab tests have
to be done. They include general blood test, clinical urinalysis, blood grouping, Rh
affinity, syphilis markers, hepatitis B (HbsAg) and C (HCvAg), HIV. Blood sugar
level is tested, as well as vaginal discharge analysis for microflora, cytology of vaginal
and cervical scraping, tests for sexually transmitted infections (gonorrhea, trichomo-
niasis, chlamydiasis).
92 Obstetrics
EXCHANGE NOTIFIABLE CHART 14. Pelvis dimensions

Data on pregnancy filled D Sp D Cr D troch
in by maternity welfare centre C.ext C.diag C.vera
(issued to each pregnant woman and Height Weight
given to her at 30 weeks gestation) 15. Fetal lie
Presenting part: head, buttocks,
1. Name, patronymic, surname not determined
Fetal heartbeat: clear, rhtythmic
2. Age 3. Address Beats per minute in the right, left
16. Laboratory and other tests:
4. Previous somatic, gynecological RW1 “ ” 200 HBS1 “ ” 200
diseases and surgeries RW2 “ ” 200 HBS2 “ ” 200
RW3 “ ” 200 HСV1 “ ” 200
ВИЧ1 “ ” 200 HCV2 “ ” 200
5. Features of previous pregnancies, ВИЧ2 “ ” 200
deliveries, postpartum periods Rhesus: «+», «-», blood type
Antibody titer
Blood group
6. Parity Husband’s Rh affinity
7. Previous abortions Toxoplasmosis: complement fixation test,
Year gestational age skin test
8. Preterm delivery Year Clinical tests:
Gestational age term delivery Blood urine
9. Date of last period АналVaginal content
10. Gestational age test (smear)
Weeks at booking visit Ova and parasite exam
« » year 200 17. Childbirth education
11. Total appointments 18. Date of issuing medical incapacity
12. Date of quickening certificate due to pre-maternity leave
13. Features of present pregnancy « » 200
19. Estimated due date
« » 200
Obstetrician-gynecologist
Fig. 3.2. Exchange-notifiable medical chart. Data entered by the maternity welfare centre
After that laboratory tests are done at the following stages:

• general blood test once a month; starting at 30 weeks gestation — once every two
weeks;
• urinalysis at each visit
• blood sugar level after the booking visit to the prenatal clinic, at 22–24 and
36–37 weeks;
• coagulogram at 36–37 weeks;
• RW and HIV tests upon their booking visit to the prenatal clinic, at 30 weeks and
2–3 weeks before the due date;
• bacterioscopy (mandatory) and bacteriology (preferably) study of the vaginal and
cervical canal content at 30 weeks.
3.1.3.4. Instrumental methods
All pregnant women have electrocardiography (ECG) done upon their booking
visit, and then at 36-37 weeks. ECG is also done if there are indications. Ultrasound
examination is done repeatedly to follow dynamic changes of the developing pregnancy.
Ultrasound is planned for the following gestational age:
• 11–14 weeks (see below);
• 18–21 weeks (see below);
• 30–34 weeks to see whether the embryo’s physical parameters correspond to
the gestational age (signs of fetal growth restriction) and for an assessment of
extraembryonic structures.
Each visit of the pregnant woman to the prenatal clinic is reflected in her Case
Sheet for Pregnant and Puerpera. The Case Sheet contains the woman’s family and
medical history, findings of clinical and laboratory investigations, medical advice and
prescriptions, as well as the individual plan of management approved by the chief
medical officer. At each visit, the doctor writes down the diagnosis and the date of
the next visit, and signs it.
Case Sheets for Pregnant and Puerpera are kept in the obstetrician-gynecologist
office in a card index sorted by the woman’s next visit.
3.1.4. Vitamins and microelements

It is on very rare occasions that a pregnant woman requires synthetic vitamin
supplements. Effectiveness of vitamin supplements was proven only in case of imbal-
anced diet or for regions where the population is severely undernourished.
Folic acid intake should be recommended to all women; its routine consumption
in a daily dose 400 mcg for 12 weeks prior to conception and in the first 12 weeks
of pregnancy reduces the risk of neural tube defect development in the fetus.
There is no evidence in favor of routine intake of iron supplements to date. Intake
of iron supplements by pregnant women with hemoglobin level above 100 g/l has
no effect on the perinatal outcome. At the same time, prolonged consumption of
iron containing medications has a negative effect on the gastrointestinal tract caus-
ing irritation of gastric mucosa, constipation or diarrhea. Throughout the world,
therapeutic intake of iron supplements is considered justified if the hemoglobin level
is under 100 g/l.
A daily dose of vitamin A over 700 mcg can produce a teratogenic effect, so rou-
tine intake of vitamin A should be ruled out. Besides, the pregnant woman should
be informed about rational limits on consumption of foods with a high vitamin A
content (liver and others).
According to recommendations by the British Society for Obstetrics and
Gynecology, pregnant women should consume 10 mcg/day of vitamin D in the form
of dietary supplements or multivitamin preparations; this is especially applicable for
the following risk groups:
• women residing in Africa, South Asia, the Caribbean and Middle East;
• women who do not get enough sunshine;
• women whose diet does not ensure sufficient vitamin D consumption;
• obese women (body weight index over 30 kg/m 2).
94 Obstetrics
Iodine additives are indicated in regions where there is iodine insufficiency in the
environment and the population does not get enough iodine from their diet. This
risk is determined by the standards issued by public health authorities. As congenital
hypothyroidism (cretinism) is an irreversible condition, all pregnant and breastfeed-
ing women residing in iodine poor regions are assigned to the risk group; thus they
are in need of individual and collective iodine deficiency prevention with the aim of
ensuring an optimum level of iodine intake.
According to WHO recommendations, collective prevention implies consumption
of only iodine-treated salt. Individual prevention as prescribed by an endocrinolo-
gist is ensured by a daily intake of 200 mcg of potassium iodide by pregnant and
breastfeeding women.
Herbs, herbal infusions and extracts are also classified as medications, so they
cannot be taken without a doctor’s recommendation. To date there is not enough
known about such medications to determine their safety for the fetus or for the
mother.
3.1.5. Medications
It is desirable to avoid intake of any medications during pregnancy except for
cases when there is a threat to the patient’s health and life, and the benefit clearly
outweighs the risk.
Any doctor who prescribes treatment to a woman of reproductive age should keep
in mind the possibility of pregnancy. No medication can be regarded teratogenic or
non teratogenic without studying its dose, length of administration, gestational age
of the woman. Very few medications were tested for safety on pregnant women so as
to be recognized as completely safe. It is desirable to prescribe to pregnant women
only medications with established effectiveness (A, B levels) and safety; administra-
tion of new medications that just appeared on the pharmaceutical market should be
avoided, if possible. Pregnant women should take medications in minimally effective
doses, for minimum periods of time.
If the woman has a chronic extragenital disease, the treatment (choice of medica-
tion, dose, dosage frequency, length of therapy) is decided on in cooperation with
the relative medical professional.
3.2. PSYCHOPROPHYLAXIS AND PREPARATION

FOR LABOR
Family-oriented preparation. Psychoprophylaxis is a method of childbirth prep-
aration and pain management, which had been developed primarily by Soviet
psychotherapists I.Z. Velvovskii and A.P. Nikolaev. The technique was observed
in 1951 by a French obstetrician F.Lamaze and popularized by him in the Western
world. According to the technique, psychoprophylaxis — 5 conversations with
the doctor with the aim of stimulating the so called positive birth dominant in
the cerebral cortex — should start from the first visit of the pregnant woman
to the prenatal clinic, and complete 7–10 days before the due date. It is desir-
able to involve the pregnant woman’s husband to Expectant Fathers educational

program held at prenatal clinics where they use demonstration aids, technology,
infant care articles.
Psychoprophylaxis is not an independent method; it can be implemented
together with physical exercising for the pregnant women. The childbirth educa-
tion method includes hygienic gymnastics to be done daily or every other day
starting at early gestational age under the guidance of exercise physiologist or a
trained nurse.
After the primary examination the obstetrician-gynecologist and therapist refer the
pregnant woman to the therapeutic physical training room and inform the exercise
physiologist about her gestational age and health condition. Eight to ten women cho-
sen by the gestational age, form the exercise group. Classes are held in the morning,
for working pregnant women — in the afternoon. Exercises are divided into three sets
to fit gestational ages: under 16 weeks, 17–32 weeks, and 33–40 weeks. Each set of
exercises is aimed at formation of certain skills necessary for the body to adjust to
the current pregnancy stage. If the pregnant woman is not able to attend the exercise
class, she is familiarized with the sets of exercises so that she continues to do them
at home to be checked by the exercise physiologist every 10–12 days.
Pregnant women with diseases do the exercises with consideration paid to
their condition and specifics of disease. Exercise is contraindicated in acute
conditions or conditions with frequent exacerbations or decompensated somatic
disease, habitual abortion in past history or threatened miscarriage in the cur-
rent pregnancy.
Preparation for childbirth of pregnant women and their husbands (starting at
33–35 weeks) includes educating them about the physiology of childbirth, correct
behavior during childbirth; autotraining exercises and pinpoint self massage are also
taught for pain relief during labor.
Preparation for childbirth classes should be attended by all pregnant women start-
ing at the earliest gestational age. Women should be informed about the importance
of these classes. Information about the program and schedule of classes should be
widely available at the prenatal clinic. Midwives and pediatric nurses should be pres-
ent to help conduct the classes.
It is desirable to have 8–10 pregnant women per class, preferably with similar
gestational age. One group may include women observed by the same obstetrician-
gynecologist, or by different ones.
The head of the prenatal clinic organizes the classes with consideration to local
conditions; he/she oversees the Expectant Mothers classes, keeps in touch with the
regional wellness centre to obtain methodological support and handout materials.
The Expectant Mothers course includes 3 classes with an obstetrician-gynecologist,
2—with a pediatrician, and 1 class with a legal expert, if possible.
Psychoprophylaxis eliminates the fear of imminent childbirth, reduces painful
sensations, ensures an adequate behavior of the parturient woman and help on the
part of her husband; it allows a well-considered decision about administration of
anesthesia. It should be explained to the woman and her family that administration
of epidural anesthesia or other painkilling techniques is safe for the child if it is
performed in an orderly fashion.
96 Obstetrics
The interior of the therapeutic physical training room should promote a relaxed
atmosphere in the audience. There should be comfortable arm chairs, video, audio
and multimedia equipment.
It is desirable to provide opportunities for the pregnant women for independent
work with all sorts of materials on issues of hygiene during pregnancy, family involve-
ment into preparation for childbirth, breastfeeding, care for the newborn, contracep-
tion after childbirth, and so on.
3.3. POSTPARTUM CARE
The postpartum period is regarded uneventful if the puerpera is in general good state,
with normal body temperature, pulse rate and BP, appropriate uterus involution, normal
quantity and quality of lochia, sufficient lactation. The woman can experience stool re-
tention, discharge from the uterus (lochiometra), delayed or absent involution of uterus
(subinvolution), breast engorgement, scratches and bruises on the nipples, infection and
its complications. For prevention of infection complications it is necessary to provide
strict compliance with sanitary and epidemiological requirements and personal hygiene.
Organization of postpartum care. Puerperal women necessarily require medical
care as they may develop postpartum disease after childbirth. The pregnant woman
should be informed about this possibility prior to childbirth.
After she was discharged from the maternity hospital, the puerpera is expected
to come to the maternity welfare centre within 2–6 weeks. On the day she was dis-
charged a telephone message is sent from the maternity hospital where she delivered
to the maternity welfare centre.
When examining the puerpera, the obstetrician-gynecologist familiarizes him/
herself with discharge summary from the maternity hospital describing the course
and outcome of delivery, questions the woman about her complaints and how lacta-
tion proceeds, examines the condition of mammary glands, abdominal wall and the
quality and quantity of lochia.
Lactation is paid attention to in all puerperal women. It should be impressed upon
the woman how important breastfeeding is considering the significance of breast milk
for the child’s health and development. At the end of postpartum period the options
of contraception are discussed. All advantages and disadvantages of each method with
regard to breastfeeding should be weighed. The possibilities of the lactation amenor-
rhea method should also be considered.
In case of a home delivery the emergency team takes the puerpera and newborn
to the maternity hospital. If the woman refuses to go to hospital, she is examined at
home by an obstetrician-gynecologist from the maternity welfare centre; the findings
and recommendations are entered into the woman’s Case Sheet for Pregnant and
Puerpera. In 2–3 days the mother and child are visited at home by a pediatrician.
The pediatrician examines the newborn and makes an appointment with the puerpera
at the pediatric clinic, where a statement of live birth (with a counterfoil) is issued. If
there was a still birth or the new born dies within 168 hours after delivery, a medical
certificate of perinatal death (with a counterfoil) is issued by an anatomic pathologist
or a forensic expert upon completion of postmortem study.
3.4. BREASTFEEDING
It is a well known fact that biological and psychoemotional bond between mother
and child continues until the child becomes 18 months old, at least. If the mother
undertakes breastfeeding begins immediately the first minutes after birth and contin-
ues to breastfeed ad libitum and on demand even at nights, the baby is spared the
necessity of giving it milk substitutes and infant formulas.
Exclusive breastfeeding means feeding the child with only breast

NB! milk. If necessary, medications, salts and vitamins can be admin-
istered mixed with expressed breast milk.
Predominant breastfeeding means feeding the child with moth-
er’s milk plus giving water or juice in amounts of 30 g/day or
supplementing formulas in amounts no more than 100 ml/day.
Partial breastfeeding implies giving breast milk in combination
with formula (more than 100 ml/day) or additional foods (over
30 g/day).
If the infant is latched to the breast frequently, upon demand, this promotes
oxytocin and prolactin production in the mother’s body, reduces the risk of
postpartum hemorrhage, and is extremely important for successfull lactation
function.
The main WHO recommendations in the sphere of newborn and infant care:
• care without excessive intervention;
• skin to skin contact: touching the baby as often as possible, holding it and
carrying as long as possible; use of baby sling — a wrap carrying the baby and
leaving the mother’s hands free;
• involvement of both parents in baby’s care and communication with the
baby;
• prevention of discomfort and pain in the baby;
• care of premature and sick children that does not limit their movements;
• consulting the parents before they discharge from the maternity hospital.
3.4.1. Facts about breastfeeding

• Breast milk is the best food for the child; its quality does not depend on the
woman’s build or diet; breast milk protects the child from infections.
• Breastfeeding cannot make the woman’s body look worse. Childbirth always
changes the shape of the breast and body irrespective of whether she breastfeeds
or not. On the contrary, prolonged breastfeeding makes the woman lose
unwanted weight; smooth gradual weaning of the child helps to preserve the
breast in the best shape.
• Breastfeeding promotes a deep emotional bonding between mother and child,
which is important for their further relationship.
• In most cases the size and shape of breast, as well as the size and shape of nipples
(retracted, flat nipple) do not affect the process of breastfeeding.
98 Obstetrics
• There is no need to buy beforehand bottles, teats, milk pumps and other devices
for artificial feeding, as this will inspire anxiety in the mother concerning her
ability to breastfeed.
• Some time before delivery it should be explained to the mother why it is so important
to latch the child to the breast right after birth, and to stay in the same ward with
the child, which will encourage frequent breastfeeding and induce the flow of milk.
• Early, correct latching of the child to the breast in the maternity hospital helps to
avoid multiple problems of mother’s and child’s health in future.
3.4.2. Practical advice to lactating women

• The length of breastfeeding should be determined by the child; it should have the
opportunity to suck until it lets go; with correct latching technique there will be
no harm for the nipple. In the first 4–8 weeks after birth the child may breastfeed
literally round the clock, which does not indicate there is not enough milk. Once
the child acquires new skills, it will stop hanging at the breast and begin to be
interested in the world around, and the mother should be told about it.
• Frequent latching of the child to the breast is a necessary condition for successfull
lactation. It should be taken into account that night feedings provide sufficient
level of prolactin. During the fi rst 3 months of the child’s life one should
remember that in daytime the intervals between feedings should not exceed
2 hours, at nighttime — 3 or 3.5 hours; extremely prolonged intervals may lead
to development of lactostasis or lack of milk production.
• The child should remove all the milk from one breast before the mother gives
him the other: this ensures that the child receives enough milk with highly
concentrated fats as well as certain enzymes facilitating milk assimilation. It is
an important fact that upon frequent switching of breasts the child is overloaded
with lactose sugar while not getting enough fats, which can lead to secondary
lactase insufficiency. That is why there are no rules guiding how often the
breasts are switched; depending on which breast was emptied in the last session,
the mother decides which breast to offer now. If there is not enough milk, it is
admissible to offer both breasts in one feeding.
• There is no need for pumping out breast milk, frequent latching done properly
ensures milk production that meets the child’s needs exactly, which is the only
effective measure preventing hyperlactation (one of causes of lactostasis) or
hypogalactia.
3.4.3. Breastfeeding technique

The child should be breastfed on demand. The mother may be in a sitting or
reclining position, whatever is most comfortable. There are five most common
breastfeeding positions:
• football hold when the child is latched onto the breast from under the armpit;
• cradle and cross-cradle hold when the child’s head lies on the mother’s forearm
and his back along the inner arm and palm; in the first case the arm and breast
are homolateral, in the second case — contralateral;
• lying on the side;

• laid-back position when the child is on top and the mother is lying on her back;
this position is most appropriate when the flow of milk is too powerful and the
child chokes on it (Fig. 3.3–3.7).
Fig. 3.3. Breastfeeding position Fig. 3.4. Breastfeeding position

‘cradle hold’ ‘cross-cradle hold’
Fig. 3.6. Breastfeeding position ‘laid-back’
Fig. 3.5. Breastfeeding position

«football hold’
100 Obstetrics
“Cradle hold”
“Cross-cradle hold”
“Football hold”
“Lying on one side”

Fig. 3.7. Ways of latching the child to the breast
The child’s head is put on the forearm or enclasped under the head by the palm
(the thumb opposite all other fingers). One should watch that the child’s head is not
too inclined forward (there should be enough free space between the child’s chin and
his chest so that he can wide open his mouth). Irrespective of the chosen position
the whole child’s body should be facing the mother, tucked onto her; if the child is
on its back with a head turned to one side, breastfeeding will be a priori ineffective
as the child is uncomfortable.
The thumb supporting the breast is positioned above the areole, the other fin-
gers — below the areole; the areole and nipple are left free. To get the child to open
the mouth as wide as possible, one should stroke the nipple against the child’s upper
lip, then put the areole and nipple deep into the mouth (one should let the child at-
tach himself rather than leaning towards it). Latching should be asymmetrical: more
on the side of the lower lip, which, in its turn, should be everted.
During breastfeeding there should be no smacking or slurping sounds; one should
see to it that the child’s chin is pressed tightly to the breast; the nose may butt
against the breast or be free; even in the first case the physiologically snub nose of
a newborn ensures free unobstructed nasal respiration. After feeding one can express
some drops of milk from the breast and spread them over the nipple and wait till it
dries and forms a thin protective film.
The mother should exclude all possible allergens from her diet (caviar, citrus fruit,
chocolate, whole cow milk). Fluid intake should be about 1–2 day.
The optimum length of exclusive breast feeding is the first 6 months of the child’s
life. Even with other foods added, breastfeeding should remain until the child is at
least 12 months old (preferably 24 and more, if this option is suitable for the dyad
mother and child: to date there is no proven evidence that prolonged breastfeeding
may harm in any way the health of mother or child. Prolonged breastfeeding ensures
effective prevention of ovarian cancer and breast cancer in the mother.
Children who were breastfed for a long time show lower risk of metabolic disor-
ders, cardiovascular and allergic disease, disturbance of occlusion or speech devel-
opment (sucking the breast ensures proper development of the organs of speech).
Fig. 3.8. Proper latching to the breast
3.5. THE NEWBORN

3.5.1. Anthropometric data
Most term infants regain the initial physiological weight loss by day 10 after birth;
by 5 months they double their weight, by 12 month — treble. If the newborn has
not regained the lost grams by day 8–10, or continues to lose weight, he should be
seen by a pediatrician. Premature and macrosomic infants regain their initial weight
longer; this usually happens by the end of two weeks. During the first twelve months
of life a healthy infant grows 25–30 cm. During the first months his subcutaneous
fat increases markedly reaching its maximum by 9 months.
The infant’s weight is the most unstable and sensitive indicator of his physical
development and adequacy of food consumption. Any illness, loss of appetite, dis-
turbance in sleep or routine is reflected by weight fluctuations.
102 Obstetrics
Minor weight deviations from age norms should not give rise to anxiety. If weight
gain is too slow (less than 500 g per month) or too fast (over 2 kg per month), a
pediatrician should be consulted. If there is a suspicion that the child is not getting
enough milk, the weekly weight gain should be estimated; it should be no less than
125 g. Weight gain does not proceed at an even pace. If monthly weighing shows a
deviation from normal parameters, weighing should be done more often.
Occasional weight check is not informative enough: the child may remove 20 g at
one breastfeeding, and 120 g at another, so weighing should be done at an interval
of no less than 3 days. Pumping milk out is also uninformative for assessment of the
amount of milk produced. No pumping is as effective at removing milk as a suck-
ing child. The number of urinations per day can serve as another objective method
of assessment: from the 14th day of life there should be no less than 10 urinations.
Table 3.1 shows average values of infant normal weight and length in the first
year of life.
If there emerges a real need to supplement the feeding with pumped out milk or
formula, one should bear in mind that there are multiple ways of doing it without
using a bottle and teat (spoon, cup, syringe without a needle, finger feeding using
a thin nasogatral tube, supplementary nursing system, silicone attachable spoon);
however, all these methods require certain dexterity. The point is that after any, even
the most «anatomical» soft silicone teat or nipple the infant may begin to latch on
incorrectly or refuse to suck the breast altogether, and this event frustrates the ma-
jor lactation mechanism (offer and demand principle) when milk is produced only
upon its frequent, complete removal from the breast. As for a pacifier, one can easily
do without one; the mother should offer the breast at the slightest demonstration
of discomfort, including nighttime. Maternal breast is the most powerful means of
psychological support for the child.
Table 3.1. Average values of infant normal weight and length in the fi rst year of life
Age Average normal values

Weight, g Length, cm
At birth 3100–3400 50–51
By the end of 4 weeks 3700–4100 54–55
By the end of 8 weeks 4500–4900 75–59
By the end of 3 months 5200–5600 60–62
By the end of 11 months 9500–10 000 72–78
By the end of 12 months 10 000–10 800 74–80
3.5.2. Newborn care

3.5.2.1. Sleep
The child’s room has to be always aired before bedtime. For comfortable sleep
the temperature should be 20–24 °С. Radiators must not be left by the cot; on no
occasion can one use space heaters with glowing filament in the child’s room: these
devices are fire hazardous and consume oxygen from the air intensively. Before night-
time all toys should be removed from the cot, even crib hanging toys, as they excite
the child and can disturb his sleep accidentally.
In the beginning the daily routine is usually chaotic. From the outset, the parents
should show a difference between daytime and nighttime. When it is warm outside,
sleeping in the open in the shade of a tree is very good for health; in winter the time
of sleeping in the open should be cut down. If a child is sleeping on the balcony, he
must not be left alone. In summer the perambulator is covered with protective anti
mosquito net (it usually comes with the perambulator).
The parents should install going-to-bed routines and try to hold on to them at all
accounts. Bathing is a good prelude to falling asleep quietly; if bathing is followed
by feeding, the filled infant becomes sleepy. A 6-month old infant can fall asleep
in company of his best loved stuffed animal. The child should sleep in a position
comfortable for him.
3.5.2.2. Cot
In the beginning the child can be put to sleep in a perambulator with detachable
baby carrier. Such a carrier is convenient as it has handles for transportation of a
sleeping child. Starting at about 3 months the child will need a stationary cot. When
choosing a cot, one should be certain it is strong and durable; it will serve the child
for 3 years. When buying a cot, the parents should pay attention to its green passport.
The slat space should be no less than 2.5 cm (or the child can get stuck) and no
more than 6 cm so as the foot does not slip in between. The blocking fixator should
hold the drop side firmly in the chosen position.
When buying a used cot the parents should make sure that it does not contain
harmful paint or chipboard materials that can release harmful substances in course
of time; there must be no broken parts, chipping, sharp angles.
3.5.2.3. Bedding
The mattress should be a precise fit for the bed size and fit tightly to the walls so
that the head does not get entrapped. The mattress should be level, without bumps
or slants; its cotton case should be easily removable. Wooden bedrails can be covered
with cotton skirting firmly tied on the outside; this protects the child from draughts
and bruises. When it is cold, baby nests of easily washed material are convenient.
Children under 18 months should not be given eiderdown blankets; a child under
18 months does not need a pillow for sleep.
3.5.2.4. Crying
Most often the cause of discomfort that makes the child cry is hunger, need for
contact with mother or wet diaper.
104 Obstetrics
3.5.2.5. What to do to calm your baby?
First of all, offer your breast to the child, in most cases this does the job. Regular
smooth rocking movements have a calming effect as they remind the child of sensa-
tions he had in the womb. Swaddle the child rather tight: this will give him a pro-
tected feeling. A child older than 6 weeks can be distracted by showing something
interesting. Anything bright, sparkling will attract his attention and he will soon forget
the cause of distress. Children under 2 months can see clearly only objects placed
within 25 cm from the eyes. When talking to the child, the adult should bend down
to keep this distance.
3.5.3. Postnatal diagnostics. Hereditary diseases

Neonatal screening means mass examination of newborns to detect congenital or
hereditary disease. The common practice worldwide is to screen for 8–12 diseases.
Starting in 1994, in all maternity hospitals in Russia blood is taken from the new-
born’s heel to be tested for congenital hypothyroidism and phenylketonuria. In 2006
the screening program included tests for adrenogenital syndrome, galactosemia and
cystic fibrosis.
Disorders detected by neonatal screening are harmful and potentially fatal; if not
diagnosed and treated in the early stage, they lead to profound irreversible changes,
often with a fatal outcome or mental deficiency development. Early diagnosis and
correction of revealed disorders through the life course make it possible to avoid
unfavorable outcomes.
Pediatric care provides treatment for children with health disorders in all fields
(genetics, endocrinology, etc.). This multistage system is made effective by rapid
diagnostics and start of treatment at the preclinical stage.
3.5.3.1. Phenylketonuria
Phenylketonuria is a disease induced by disturbed metabolism of the amino acid
phenylalanine. This condition affects the CNS; it is accompanied by mental defi-
ciency development; there are no clinical presentations in the first days of life. The
incidence rate of this condition is 1:7200 newborns. In maternity hospitals all new-
born babies are examined with screening methods. On day 2–3 a specimen of blood
is taken from the child’s heel; the sample is placed on a form of chromatographic
paper and then sent to the laboratory for medical and genetic investigation.
A concentration of phenylalanine exceeding 2 mg suggests the possibility of phe-
nylketonuria. When the diagnosis is confirmed, treatment consists of dietary restric-
tion of phenylalanine; as early as in the first month various medical foods where
phenylalanine is totally or almost absent are administered. Such dietetic therapy
promotes normal neurological and verbal development.
3.5.3.2. Congenital hypothyroidism

Congenital hypothyroidism is a disorder of the thyroid gland whose function is
reduced or even absent. The condition leads to delayed development of all organs and
systems, the CNS in the first place. It becomes manifest late, not earlier than in the
4th — 6th month of the child’s life. The condition is seen in 1 of 4000–6000 newborns.
Early diagnostics helps to detect hypothyroidism in the first days of the child’s life.
For this purpose the content of TSH in the blood is determined. A TSH concentra-
tion above 50 mU/l suggests the possibility of hypothyroidism. Treatment of con-
genital hypothyroidism starts in the first month of the child’s life. Adequate timely
start of therapy helps to avoid the threat to the baby’s life and health.
REMEMBER!
Medical supervision of pregnant women is the main objective of maternal
welfare center. Women who are supervised from an early gestational age and see
the doctor 7–12 times during pregnancy show perinatal mortality rates twice lower
than women who are not registered with the maternal welfare centre.
The woman’s body in pregnancy and childbirth undergoes various anatomical and
physiological changes of most systems and organs. The objective of the doctor
at a maternal welfare centre is to reveal factors of prenatal and obstetric risk at
the first prenatal visit and then to dynamically assess the changing status.
In order to enhance the effectiveness of prenatal diagnostics and to prevent birth of
children with congenital and hereditary disease, prenatal diagnosis procedures
are performed on all pregnant women.
The aim of prenatal screening is to determine each pregnant woman’s risk of giving
birth to a child with genetic disorder (Down syndrome, Edwards syndrome, Patau
syndrome, neural tube defect) taking into consideration the woman’s age, levels
of biochemical markers, and nuchal translucency. Prenatal screening is performed
two times.
Family-oriented preparation. Psychoprophylaxis is a method of childbirth
preparation developed primarily by Soviet psychotherapists I.Z. Velvovskii and
A.P. Nikolaev and later propagated in the West by F. Lamaze as the Russian method.
The aim of psychoprophylaxis consisting of 5 conversations with the doctor is to
stimulate the so called positive birth dominant in the cerebral cortex; it should start
at the first prenatal visit of the pregnant woman to the maternity welfare centre,
and complete 7–10 days before the due date.
CONTROL QUESTIONS
1. What are the advantages of an early first prenatal visit at the maternal welfare
center?
2. What is prenatal screening, when is it performed?
3. Why should a pregnant woman avoid air flights?
4. What is the role of exchange-notifiable medical chart of the pregnant and puerpera?
5. What is the aim of administering folic acid to pregnant women? At what
gestational age is its intake advisable?
6. In what cases is iodine intake indicated during pregnancy?
7. What are the main principles of Expectant Mothers and Expectant Fathers course?
8. Terminology of breastfeeding.
9. Recommended daily routine of a breastfeeding mother (diet, exercise, walking).
106 Obstetrics
CHECK YOURSELF!
Level 1. Test
Select one or more correct answers
1. A pregnant woman should be registered with maternity welfare centre at gestational age
a) under 16 weeks;
b) 8 weeks
c) 12 weeks
d) 14 weeks.
2. Within what period after registering should the pregnant woman go through exami-
nations and tests?
a) 1 month;
b) 10 days;
c) 15–2 0 days;
d) 12–14 days.
3. How often should a pregnant woman see her doctor after 32 weeks gestation:
a) once a month;
b) every other day;
c) twice a month;
d) 6–7 times a month.
4. Prenatal screening is done twice at:

a) 6–8 weeks+18–21 weeks;
b) 11–14 weeks+18–21 weeks;
c) 18–21 weeks+30–32 weeks;
d) 16–18 weeks+23–25 weeks.
5. External palpation of uterus becomes possible at:

a) 8 weeks;
b) 9–10 weeks;
c) 13–15 weeks;
d) 6–7 weeks.
6. According to legislation in force, working women are entitled to a maternity leave of:
a) 156 consecutive days;
b) 70 consecutive days;
c) 86 consecutive days;
d) 140 consecutive days.
7. If there was a complicated childbirth, the post-delivery leave is prolonged by:

a) 70 consecutive days;
b) 16 consecutive days;
c) 8 consecutive days;
d) 86 consecutive days.
8. Folic acid is prescribed to pregnant women at a dose of:

a) 400 mcg every day;
b) 400 mcg twice a day;
c) 200 mcg every day;
d) 100 mcg every day.
9. The recommended length of solely breastfeeding is:

a) 3 months;
b) 6 months;
c) 9 months;
d) 12 months.
10. The recommended length of breastfeeding with other foods added:

a) 3 months minimum;
b) 6 months minimum;
c) 9 months minimum;
d) 12months minimum, 2 years preferably.
11. An admissible interval between breastfeedings at daytime:

a) 1 hour;
b) 2–2.5 hours;
c) 3 hours;
d) 4 hours.
12. An admissible interval between breastfeedings at nighttime:

a) 2 hours;
b) 3–3.5 hours;
c) 4 hours;
d) 6 hours.
13. Predominant breastfeeding implies that other foods are given in an amount no
more than:
a) 50 ml;
b) 100 ml;
c) 200 ml;
d) 300 ml.

1. Patient M. day 10 after childbirth presents with nipple painfulness when begin-
ning breastfeeding; examination reveals cracks in both nipples. What are you going
to do?
2. Patient N. 4 weeks after childbirth presents with low milk production: the baby
lets go of the breast crying, then latches to it again. The baby’s weight at birth was
3470 g, 4 weeks later — 4130 g. What do you recommend?
• Chapter 4
DIAGNOSTICS OF PREGNANCY.
ЕSTIMATION OF GESTATIONAL AGE
AND EXPECTED DATE OF DELIVERY.
METHODS OF EXAMINATION
If a woman of reproductive age presents with a missed menstrual period, and she
was not diagnosed with absolute infertility, the doctor should consider the possibility
of her being pregnant.
4.1. HISTORY
Early detection of pregnancy was a major concern from ancient times. In Ancient
Egypt a pregnancy test involved giving a woman some crushed melon mixed with
the milk of a woman who had born a male child. If the concoction made her sick,
she was considered pregnant. Ancient Jews made a woman walk on soft grass to
find out if she was pregnant. In their opinion, a
woman with a child left deeper imprints. Midwives
of Ancient Greece showed considerable knowledge
on the subject; they based their decision about
pregnancy on absence of menstruation, low appe-
tite, salivation, nausea, emergence of yellow spots
on the face. Hippocrates (460–377 BC) (Fig. 4.1)
believed a missed period to be the first sign of
pregnancy.
Soranus of Ephesus (1st century AD) estab-
lished the following signs of pregnancy: delayed
menstruation, engorgement of mammary glands,
cutaneous vessels of the breast become convo-
luted acquiring a bluish coloration; there is an
urge to vomit; there are dark circles under the
eyes and sometimes yellow spots on the face;
the abdomen distends in the course of time, and
the pregnant woman can feel the fetus moving
Fig. 4.1. Hippocrates (460–377 BC) inside.
Chapter 4. Diagnostics of pregnancy. Еstimation of gestational age and... 109
Diagnostics of pregnancy should be mastered by all health care

NB! providers. Pregnancy requires observation by specialists; this
condition implies limitations on the choice of therapeutic and
diagnostic procedures that are safe otherwise. When pregnancy
is suspected, the woman should be referred to an obstetrician
gynecologist.
From the obstetric point of view, early diagnostics of pregnancy is necessary for
the optimum management of the patient.
Clinical examination of a pregnant or puerperal woman involves findings of the
woman’s family, medical and reproductive history, general somatic and special ob-
stetric investigations.
Upon early diagnostics of pregnancy the doctor has a number of advantages:
• if uterine pregnancy was confirmed, one can start early prevention of exacerbation
of chronic conditions, of decompensation of somatic disease; this helps to reduce
the risk of complication development;
• if ectopic pregnancy was diagnosed, heavy blood loss can be avoided within the
time till the pregnancy is terminated or complications set on; thus there is a
chance to employ organ sparing treatment (reconstructive surgery, administration
of cytostatics) which improves the reproductive prospects of the patient;
• if the pregnancy is unwanted, in early stages preference is given to sparing
methods of pregnancy termination which involve a lower risk of complications
(medication-induced abortion, vacuum aspiration);
• the doctor should prescribe investigations and tell the patient about signs of
possible complications like spontaneous abortion, ectopic pregnancy, gestational
trophoblastic disease, which can initially present as normal uterine pregnancy.
4.2. CLINICAL SIGNS OF PREGNANCY
Clinical signs of pregnancy have no diagnostic value; they provide a basis for the
gold standard of pregnancy diagnostics.
Common clinical signs of pregnancy can be divided into three groups: presump-
tive, probable and positive ones. Nowadays they have all lost their value and can be
attributed to the historic aspects of obstetrics.
Missed menstrual period is an important sign, but it is equivocal as it can indicate
other conditions, especially in women with irregular periods. The informative value of
this sign increases if it is combined with swollen tender breasts and colostrum pro-
duction , cyanosis of the vagina and, most important, of the vaginal part of uterine
cervix, changes in the size and consistency of the uterus.
As the gestational age increases, the pregnant uterus grows in size. The change of
uterus shape can be determined by bimanual examination. In nonpregnant women
the uterus is of pear-like shape, somewhat condensed in the anteroposterior diameter.
Once it becomes pregnant, the uterus begins to change in shape. At 5–6 weeks gesta-
tion the uterus shape becomes globular. Starting at 7–8 weeks gestation the uterus
110 Obstetrics
becomes asymmetrical, one of its angles may protrude. By about 10 weeks gestation
the shape is back to globular, and by the third trimester it is ovoid. There is a rule
one can use conveniently: by 8 weeks the uterus body has increased twice compared
with baseline, by 10 weeks — three times, by 12 weeks — four times.
The following signs can indicate pregnancy.
Increase of uterus. It becomes noticeable at 5–6 weeks gestation; the uterus first
grows in the anteroposterior direction becoming globular, then its transverse dimen-
sion increases, too. The larger the gestational age, the more apparent uterine growth.
By the end of the second month of pregnancy, the uterus has increased to the size
of goose egg, at the end of the third month the uterine fundus is at the level of
symphysis or somewhat above (Fig. 4.2).
Horowits-Hegar’s sign: Uterine consistency becomes softer, and it may be pos-
sible to palpate or to compress the connection between the cervix and fundus; when
doing the bimanual examination, the fingers of both hands can meet almost without
resistance.
Snegirev sign: during bimanual examination the softened pregnant uterus becomes
denser and its size shrinks under the impact of mechanical irritation.
These and other clinical signs have been superseded by more precise and nonin-
vasive ultrasound examination.
Positive signs of pregnancy can be detected many weeks after pregnancy has
occurred. In clinical practice they are used as components of external obstetric
examination.
36 weeks
32 weeks 40 weeks
28 weeks
24 weeks
20 weeks
16 weeks
12 weeks
Fig. 4.2. Fundal height related to gestational age

• Palpation of fetal parts. In the second half of pregnancy palpation of the abdomen
can detect the head, back and limbs of the fetus.
• Clearly heard fetal heart sounds. Simple auscultation with obstetric stethoscope
reveals fetal heartbeat after 22 weeks.
• Fetal movements felt by the doctor when examining the pregnant woman.
4.3. GOLD STANDARD OF PREGNANCY DIAGNOSTICS
Establishing the fact of pregnancy in early stages basing on clinical signs presents
certain difficulties as some endocrine conditions, stress, consumption of certain
medications can imitate the presentations of pregnancy. A missed period may be
due to stress anorexia followed by weight loss, endocrine disorders (prolactinoma,
adrenal hyperandrogenism, severe hypothyroidism), intake of sex hormones or psy-
chotropic drugs.
Being familiar with clinical signs of pregnancy is necessary as it helps to make
a provisional diagnosis. Pregnancy is confirmed by instrumental and laboratory
methods.
The gold standard of diagnosing pregnancy of any localization is

NB! a combination of two methods:
• beta-HCG test;
• ultrasound examination to visualize the ovum (gestational sac)
and its localization.
This diagnostic approach has three advantages:

• first, it virtually excludes the possibility of a false positive or false negative result;
• second, besides just establishing the presence or absence of pregnancy in the
uterine cavity it gives an idea of the course of pregnancy and fetus/embryo
condition;
• third, it is less invasive and allows a series of investigations without a risk to the
pregnant woman or the fetus/embryo.
4.3.1. Human chorionic gonadotropin (hCG)

Human chorionic gonadotropin is produced by the syncytiotrophoblast of the
growing villous chorion. β-Subunit of this hormone is detected in the blood of a
pregnant woman as early as 8–9 days after conception, which coincides with comple-
tion of blastocyst implantation in the endometrium (3.5 weeks of pregnancy). The
concentration of β-hCG grows steadily reaching its peak value at 8–9 weeks, and then
drops two-three times and remains unchanged to the end of pregnancy (Table 4.1).
Two weeks after childbirth no hormone is detected in the blood. Quantitative deter-
mination of β-hCG, apart from early diagnosis of normally proceeding pregnancy,
enables one to distinguish a normally proceeding pregnancy from a pathological one
(ectopic pregnancy, imminent miscarriage) when quantitative determination is done
repeatedly.
112 Obstetrics
β-hCG level is measured in the blood (using an immunology method) or in urine

(test strips, Fig. 4.3). The first method yields more reliable results.
Control line
Test line
Fig. 4.3. Positive pregnancy test
Table 4.1. Changes in hCG concentration in the course of normal pregnancy

Gestational age, weeks hCG concentration, mU/ml
3–4 25–300
5–6 1500–5000
6–7 10 000–30 000
7–8 20 000–100 000
8–9 50 000–200 000
9–10 20 000–200 000
10–11 20 000–100 000
11–12 20 000–95 000
13–14 20 000–90 000
15–16 15 000–60 000
17–27 10 000–60 000
28–39 10 000–60 000
When not supported by corresponding ultrasound findings or clinical signs, de-
tection of hCG in a woman’s blood is not an absolute confirmation of pregnancy.
The causes of false positive hCG test can be as follows:
• intake of hCG medications to stimulate ovulation;
• gestational trophoblastic disease and choriocarcinoma;
• ovarian choriocarcinoma, a rare subtype of ovarian germ cell tumor.
4.3.2. Obstetric ultrasound

Transvaginal echography is instrumental in reliably revealing pregnancy at an age
of 4–5 obstetric weeks (that is, upon missing a period for over 1 day); the gestational
sac can be visualized in the uterine cavity (Fig. 4.4).
Fig. 4.4. 4–5 weeks gestation. Gestational sac in the uterine cavity (ultrasound)
It is at this time (under 4–5 obstetric weeks) that most diagnostic errors are
made. The rate of errors can be cut down if the ultrasound structure of gestational
sac is clearly understood. Glandular endometrial polyp, minor submucous myoma-
tous node, nabothian cyst in the region of isthmus, or accumulation of fluid in the
endometrium (pseudogestational sac syndrome) — all these can be mistaken for the
gestational sac. The following signs help to avoid an error.
• Decidual changes in the endometrium (typical three-layer pattern of M-echo
endometrium over 15 mm thick) (Fig. 4.5).
• The visualized formation is of fluidized structure (fluid is anechoic in ultrasound,
black color); it produces the effect of dorsal echo enhancement: a lighter zone
visualized as a cone-shaped structure directly behind the fluidized formation.
This sign allows a differentiation of gestational sac from a polyp or submucous
myomatous node.
• The fluidized structure is surrounded by hyperechoic rim («crown»). This
image is produced by the chorion whose thickness in millimeters is about equal
the gestational age in weeks. A clear hyperechoic contour helps in differential
diagnostics between the gestational sac and fluidized formations in the uterus
(Fig. 4.6).
Starting at 5 obstetric weeks (3 weeks after conception) a yolk sac can be
detected inside the gestational sac, starting at 6 weeks — the embryocomplex
(2–3 mm) begins to be distinguishable near the yolk sac. After 6 weeks and
2 days fetal heartbeat is detectable in the embryo, which facilitates diagnostics
(Fig. 4.7–4.8).
In cases when diagnosis presents difficulty, for instance when ultrasound findings
at 4–5 obstetric weeks do not give enough ground to confirm or rule out uterine
pregnancy or when missed abortion is suspected, a repeat examination should be
done in one or two weeks.
Pregnancy in later stages is diagnosed on the basis of fetus visualization and move-
ments of the fetus or fetuses.
114 Obstetrics
Fig. 4.5. Three-layer endometrial pattern (ultrasound)
Fig. 4.6. Pregnancy week 5. The arrow is pointing to the chorion (ultrasound)
Fig. 4.7. Pregnancy week 6. The arrow is pointing to the yolk sac (ultrasound)
Fig. 4.8. Pregnancy week 12.5. The interrupted line indicates the crown-rump length
(ultrasound)
4.4. ESTIMATION OF GESTATIONAL AGE

AND DATE OF DELIVERY
Gestational age is estimated on the basis of the patient’s history and objective
findings.
4.4.1. Last normal menstrual period (LMP)

Gestational age is traditionally estimated by the time that elapsed from the date of
the last menstrual period to the date of estimation (given the menstrual cycle is regular).
To work out the delivery date, subtract 3 months from the day of
NB! last period, and add 7 days.
Working from the ovulation: if the date of conception is known,
subtract 3 months and 7 days (a modification of Naegele’s rule),
or add 266 days (38 weeks).
Besides, the date of conception can be conditionally estimated on the basis of

basal body temperature rise, the date of in vitro fertilization, artificial insemination,
the findings of ultrasound ovulation monitoring.
4.4.2. Booking visit

For estimation of the gestational age the doctor takes into account the findings of
the patient’s medical history and examination at the patient’s booking visit.
4.4.3. Date of quickening

When estimating the gestational age and date of delivery one takes into account the
date of quickening, which can be felt from the 20th week of pregnancy by primiparous
116 Obstetrics
women, and by multiparous women — about 2 weeks earlier. However, this sensation
is subjective, and its informative value is limited.
To determine the date of delivery for a primipara, 20 weeks are added to the
date of quickening (20 weeks), for a multipara, 22 weeks are added to the date of
quickening (18 weeks).
For a quick estimation of gestational age and date of delivery by the date of quick-
ening and the date of last menstrual period, specially designed obstetric calendars
are made, gravidometers (Fig. 4.9). Recently, pregnancy due-dates calculators for
iPhone application have become available like OB Wheel and others.
Fig. 4.9. Gravidometer
4.4.4. Ultrasonic data

Ultrasound is done at different periods during pregnancy.
Before the fetus can be visualized, the gestational age is estimated by the gestation-
al sac diameter figuring out the arithmetic average for three mutually perpendicular
diameters. Once the embryo is visualized and the heartbeat is felt, its crown-rump
length becomes the guiding value. The measurement findings are compared with
average values from obstetric tables to find out, which gestational age fits the size
of gestational sac and embryo. By the beginning of the second trimester fetal head
circumference, abdominal circumference and the biparietal diameter become diag-
nostically informative. In the second trimester full scale fetometry is done: measure-
ment of the above mentioned diameters, as well as the length of tubular bones in
the femur, shin, arm, forearm, foot, transverse cerebellar diameter. Matching these
findings with fetometric tables one makes a conclusion about the gestational age.
Ultrasound done in the first trimester with obligatory estimation of crown-rump
length is of most informative value as far as estimation of gestational age is concerned.
As gestational age progresses, fetal size is indicative of whether the presumed gesta-
tional age fits the fetal size rather than indicating the gestational age itself.
4.4.5. Objective findings

Starting at 6 weeks a significant enlargement of uterus is noted. Before this time
noninstrumental methods of establishing pregnancy are of no use.
By eight weeks the uterine size grows twice, by 10 weeks — thrice, by 12 weeks —
4 times. At 12 weeks uterine asymmetry disappears, the fundus of uterus reaches the
superior edge of pubic arch.
Starting at 4 months the fundus of uterus can be palpated through the anterior
abdominal wall. Gestational age is estimated from fundal height measurement. The
fundal height can be affected by the fetal size, excessive amount of amniotic fluid,
multiple pregnancy, malposition of the fetus, other specific features of the preg-
nancy course or obesity. When estimating the gestational age, fundal height is taken
into consideration together with other signs (date of last menstrual period, date of
quickening, etc.) (Table 4.2). Fundal height above the symphysis pubis is measured
with a centimeter tape.
4.5. METHODS OF EXAMINATION
Management of pregnancy and childbirth is impossible without a clear idea of the

patient’s general health and obstetric status, without taking into account the risks of
obstetric and extragenital complications.
Examination of pregnant and puerperal women includes the findings of the pa-
tient’s past history, medical history and reproductive history; general somatic and
special obstetric examination is performed; findings of laboratory and accessory
investigations are carefully assessed.
4.5.1. Interview of pregnant and parturient woman

The interview of pregnant and parturient woman is done following a certain plan.
The interview includes a general and special part. All findings are entered into the
pregnant woman’s chart or delivery protocol.
History
• Identifying data: surname, name, patronymic, age, occupation and place of work,
place of birth and residential address.
Table 4.2. Fundal height at various gestational ages
Gestational age, Fundus position

weeks Anatomical reference point Height, cm
16 Midway between pubis and navel 6
20 Two transverse fingers below navel 11–12
24 At navel level 22–24
28 Two transverse fingers above navel 28
32 Midway between navel and xiphoid process 32
36 At the level of xiphoid process and costal arches 36
40 Midway between navel and xiphoid process 32
118 Obstetrics
• What made the woman apply for medical care (complaints)

• Life history. Weight and length at birth. Heredity (presence of hereditary disease
in the patient and close relatives), mental and malignant disease. Intake of
psychoactive substances (in particular, alcohol, smoking, drug and chemical
abuse). It is important to obtain data about all infections (including syphilis,
trichomoniasis, gonorrhea, chlamydiosis, hepatitis) and non-infectious diseases
and surgeries in early childhood, puberty and maturity, the methods and time of
treatment. Allergies. Hemotransfusion in the past. Epidemiological anamnesis.
• Working and living conditions (occupational hazards and environmental risks) of
the pregnant woman and her husband.
• Reproductive history
• Menstrual function: time of menarche and periods becoming regular, nature of
menstruation period (number of days, heavy/slight flow, presence of pain, etc.);
did the period change after starting sex life, after delivery, abortion; date of last
menstruation.
• Nature of vaginal discharge: amount, coloration, odor.
• Sexual function: age when sex life began, how many times married, duration
of marriage, the period between beginning sex life and pregnancy, date of last
intercourse.
• Contraception. Methods of contraception, length of their use, complications.
• Age and health of the husband (baby’s father), blood group, Rh factor, body
weight and length at birth, harmful habits.
• Gynecologic disease in past history: time of onset, length of disease, treatment
and outcome.
• Reproductive function: In this section one obtains detailed information about
previous pregnancies in chronologic order, what number is the current pregnancy;
the course of previous pregnancies (complications, course of chronic somatic
illnesses), their outcomes. One should obtain detailed information about
abortions in past history and their complications. One should fi nd out the
duration of each delivery, surgical intervention, the sex, weight and length of baby,
its condition at birth, length of maternity hospital stay, course of postpartum
period (complications, their duration and treatment). It is important to estimate
the lactation function after previous childbirth, to fi nd out the woman’s attitude
to modern perinatal approaches (rooming-in, solely breastfeeding, breastfeeding
on demand).
• Obstetric history provides valuable information for assessment of prenatal risk factors
(predicting obstetric complications, specific features of pregnancy and childbirth).
Complications from previous pregnancies and childbirth, and a short interval
between successive births increase the risk of complications. If there is a uterine scar
after a cesarean section, if there was enucleation of fibromatous node, closure of
perforation opening, one should specify the time of surgery, type of cesarean section
(corporeal or in the lower uterine segment), the course of postoperative period.
• The following notions describing pregnancy and childbirth are distinguished.
– Nulligravida (Latin): a female who has never been pregnant
– Primigravida (Latin): a woman who has conceived for the first time and has no
pregnancies in past history
– Gravida (Latin): a woman who is pregnant currently. If this is her first preg-
nancy, she is referred to as primigravida; in further pregnancies she is referred
to as multigravida.
– Nullipara, primipara (Latin): a woman who has never given birth
– Multipara (Latin): a woman who has given birth two or more times
– Grand multipara (Latin): a woman who has given birth five or more times
– Parity: the number of childbirths in past history.
• Course of current pregnancy (divided into trimesters):
– First trimester (till 13 weeks 6 days): systemic disease, complications of preg-
nancy (toxicosis, threatened miscarriage, etc.), date of booking visit to the
maternity welfare centre and gestational age established at the first visit, lab
test findings.
– Second trimester (14–28 weeks): systemic disease and complications of preg-
nancy, weight gain, BP values, lab test findings, date of quickening.
– Third trimester (29–40 weeks): total weight gain in the entire pregnancy, even-
ness of weight gain distribution, BP values, blood and urine tests findings,
diseases and complications of pregnancy.
• Causes of hospitalization, length of stay, treatment.
4.5.2. General objective examination

The pregnant woman can have her primary examination by a therapist or other
specialists only after the doctor has familiarized themselves with an abstract of her
outpatient medical record. Omission of this is only possible if the woman has no
medical record in the local clinic.
An objective examination of the pregnant woman includes
• thermometry;
• examination of skin and visible mucous membranes;
• anthropometry (measuring the height, determining body weight, pelvimetry);
• determining the constitutional type;
• taking BP to diagnose arterial hypertension;
• examination and palpation of mammary glands;
• examination and palpation of the abdomen;
• palpation of the pubic symphysis;
• examination of the organs of blood circulation, respiration, digestion, excretion,
of the central and nervous systems;
• routine examinations done by other specialists.
Finding the body mass index is important in diagnosis of obesity and detection
of invisible edema. The earlier one performs anthropometry, the more reliable the
findings in the progress of pregnancy.
The same remark can be made about measuring BP, as in late pregnancy dif-
ferential diagnosis between hypertonic disease and preeclampsia presents difficulty.
One must establish what BP values were before pregnancy, as diagnosis of arterial
hypertension during pregnancy is based on comparing baseline values with the reg-
istered findings (before pregnancy or in early pregnancy).
Specialist obstetric examination includes three main stages.
120 Obstetrics
• External obstetric examination:

– inspection;
– pelvimetry;
– after the first trimester — measuring the symphysis-fundal height;
– after 20 weeks — measuring the greatest abdominal circumference (at the level
of the navel);
– palpation of the uterus and fetus;
– auscultation of fetal heart tone.
• Internal obstetric examination:
– Inspection of external genitalia and perineum;
– Internal obstetric examination proper:
◊ Examination of vaginal walls and cervix with speculum;
◊ Single-handed vaginal examination.
• Additional investigations.
4.5.2.1. External obstetric examination

External obstetric examination means a combination of inspection, measurements,
palpation and auscultation.
An inspection helps to check if the pregnant woman’s appearance fits her age, to
evaluate her constitutional type, nutritional status, the condition of skin and mam-
mary glands. Special attention is paid to the size and shape of abdomen.
Obstetric measurement
External pelvimetry
The common pelvic planes and the technique of measuring them are shown in
Fig. 4.11
Distantia spinarum (Latin) is the distance between the farthermost points of
anterosuperior spines of iliac bones (spina iliaca anterior superior, Latin); normally
this size measures 25–26 cm (Fig. 4.11a). Distantia cristarum (Latin) is the distance
between the farthermost points of crests of iliac bones (crista ossis ilium); normally
this size measures 28–29 cm (Fig. 4.11b).
Fig. 4.10. Martin pelvimeter

а b
1
2
c d
Fig. 4.11. Pelvimetry: a — distantia spinarum; b — distantia cristarum; c — distantia
trochanterica; d: 1 — conjugata externa, 2 — conjugata vera
Distantia trochanterica (Latin) is the distance between greater trochanters of femo-

ral bones (trochanter major, Latin); normally this size measures 31–32 cm (Fig. 4.11c).
Conjugata externa (Latin) (Baudelocque diameter) is the distance in a straight line
between the depression under the V spinous process of the lumbar vertebra and the
upper edge of the pubic symphysis. In patients with normal pelvis the external con-
jugate is 20–21 cm (Fig. 4.11d). To measure the external conjugate the patient turns
on one side, the underlying leg bent in the hip joint and in the knee; the overlying
leg is straight. The pelvimeter button is placed between the spinous process of the
122 Obstetrics
V lumbar and I sacral vertebra (suprasacral fossa corresponding to the upper angle
of rhombus of Michaelis) behind and in the middle of the upper edge of pubic
symphysis in front.
To make an indirect assessment of the inner pelvic size, pelvimetry

NB! is performed.
Using a tape measure the abdominal circumference is measured at the umbilical

level (in late pregnancy it normally measures 90–100 cm). The symphysis-fundal
height is measured as a distance from the top of the pubic symphysis to the high-
est point in the midline at the top of the uterus (Fig. 4.12). In late pregnancy the
fundal height is 34–36 cm on average. Measuring the abdominal circumference
helps the obstetrician to determine the gestational age, the approximate birth weight
(by multiplying these two sizes), to detect disorder of lipid metabolism, to suspect
polyhydramnios or oligohydramnios.
The rhombus of Michaelis is a contour whose boundaries are formed by:
• suprasacral fossa above;
• apex of sacrum (place of separation of greater gluteal muscles);
• superoposterior spines of iliac bones (Fig. 4.13).
In a normal pelvis the rhombus is of a regular shape. Its size is measured with a
centimeter tape: the horizontal diagonal size is 10–11 cm, vertical size — 11 cm. In
case of some a variety of contracted pelvis, the diagonal sizes are different, which is
followed by a change in rhombus shape.
It is of utmost importance to work out the conjugata vera (the

NB! anteroposterior diameter) as early as at the booking visit; it nor-
mally measures 11–12 cm.
Reliable data can be obtained by ultrasound; however, this method is not wide-
spread enough yet, so indirect measurement of conjugata vera is still resorted to.
Fig. 4.12. Measuring the abdominal circumference and fundal height

Fig. 4.13. The rhombus of Michaelis
1. 9 cm are subtracted from the value of conjugata externa thus obtaining the
approximate value of conjugata vera.
2. The vertical size of rhombus of Michaelis corresponds to the size of conjugata
vera.
3. The Franck size (distance from the spinous process of VII cervical vertebra to
the middle of jugular notch) equals the conjugata vera.
4. Using the diagonal conjugate (Fig. 4.14), the distance from the promontory of
the sacrum to the inferior margin of the pubic symphysis; normally it measures 12.5–
13 cm; it is determined by vaginal examination. In pelvis of normal size the sacral
promontory cannot be reached. If it can be reached, 1/10 of wrist circumference1
(Soloviov’s index) is subtracted from the value of the diagonal conjugate.
For instance, the diagonal conjugate is 12, wrist circumference is 14 cm;
1.4 should be subtracted, thus the conjugata vera is 10.6 cm (first degree con-
tracted pelvis). When the diagonal conjugate is 10 cm and wrist circumference is
16 cm, 1.6 cm are subtracted, thus the conjugata vera is 8.4 cm (second degree
contracted pelvis).
If one or several sizes deviate from the normal range, additional measurements of
the pelvis become necessary:
• lateral conjugate, the distance between anterior and posterior spines of iliac bones
on one side (14–15 cm and more); if the lateral conjugate measures 12.5 cm and
less, vaginal delivery in term pregnancy can be supposed to be traumatic;
• oblique dimensions of lesser pelvis:
– from the middle of upper pubic symphysis margin to posterior superior spine
on both sides (17.5 cm);
1 Circumference of the wrist joint is the site in woman’s body that is least of all prone to change its
dimensions in obesity.
124 Obstetrics
Fig. 4.14. Measuring the diagonal conjugate: 1 — diagonal conjugate; 2 — conjugata vera
Fig. 4.15. Measuring the wrist circumference to calculate Soloviov’s index
– from anterosuperior spine on one side to posterior superior spine on the other
side (21 cm);
– from spinous process of V lumbar vertebra to anterosuperior spine of each iliac
bone (18 cm); the dimensions are compared in pairs.
A difference between dimensions of each pair over 1,5 cm indicates obliquely oval
contracted pelvis, which can have an adverse effect on the course of labor.
The pubic angle is measured: the angle formed between the inferior rami
of the pubic bones. The pubic angle is measured while the pregnant woman
is lying in the gynecological examination chair; the thumbs of both hands are
placed along the inferior rami of the pubic bones. Normally the pubic angle
measures 90–100 °.
Pelvic outlet diameter measurement has an informative value:
• anteroposterior outlet diameter (9 cm): from the coccyx apex to lower margin of
pubic symphysis; 2 cm (coccyx deflection due to mobility of sacrococcygeal joint)
are added to the obtained value (Fig. 4.16).
• transverse diameter of the outlet (11 cm) is measured with pelvimeter with crossed
branches or a hard ruler between inner surfaces of ischial tuberosities; 2 cm (the
thickness of soft tissues) are subtracted from the obtained value (Fig. 4.17).
Fig. 4.16. Measurement of anteroposterior pelvic outlet diameter
Fig. 4.17. Measuring the transverse diameter of pelvic outlet
Abdominal palpation
Abdominal palpation helps to assess the condition of anterior abdominal wall and
elasticity of muscles. When the uterus has grown so that it can be palpated externally
(13–15 weeks), one can assess uterine tone, fetal size, amount of amniotic fluid, the
presenting part; later, as pregnancy progresses, one can determine the attitude of the
fetus, its lie, position and visus.
When palpating the abdomen, one uses so called maneuvers of external obstetric
examination (Leopold’s maneuvers). The pregnant woman is lying on her back. The
doctor stands facing her.
• First maneuver of external obstetric examination: fundal grip. The fi rst maneuver
determines the fundal height and the large fetal part found in the uterine fundus.
The obstetrician places the palms of both hands on the uterus so that they grip
the fundus (the fi rst Leopold’s maneuver, Fig. 4.18a).
• Second maneuver of external obstetric examination. It determines the lie of the
fetus in the uterus, its position and visus. The obstetrician gradually slides the
palms from the fundus to the left and right sides of the uterus. Gently pressing
the palms and fi ngers of both hands against the lateral sides of the uterus one
126 Obstetrics
determines the fetal back on one side and the extremities (arms, legs) — on the
other (Fig. 4.18b).
• Third maneuver of external obstetric examination. It serves to determine the
presenting fetal part; fetal ballottement can also be determined. The presenting
part is gripped with one hand and the obstetrician determines whether this is the
head or the rump. In head presentation the ballottement sign is positive if the
head is above the inlet of the lesser pelvis (Fig. 4.18c)
• Fourth maneuver of external obstetric examination. This maneuver is in fact an
addition and extension of the third one; it helps to determine the presenting part
and the position of the head in relation to the inlet of lesser pelvis. To perform
this maneuver, the obstetrician stands facing the patient’s feet, puts the hands on
both sides of the lower uterus portion so that the fingers of both hands almost
meet over the inlet of the lesser pelvis, and palpates the presenting part. During
delivery it is important to establish where the fetal head is: above the inlet of the
lesser pelvis (which segment) or in the cavity of the lesser pelvis (Fig. 4.18d).
a b
c d
Fig. 4.18. Leopold’s maneuvers: a — fi rst; b — second; c — third; d — fourth
Leopold’s maneuvers mean palpation of the uterus made in a

NB! certain order.
The largest diameter of the head is the greater (functional) part of the head that
passes through the pelvic inlet upon its engagement:
• in vertex presentation the border of the cephalic prominence passes along the line
of suboccipitobregmatic diameter;
• in military presentation it passes along the occipitofrontal diameter;
• in brow presentation — along the occipitomental diameter;
• in face presentation — along the vertical dimension.
The lesser part of the head is any one part of the head located below the greater
part.
The diameters of the head are a conventional concept as these

NB! are just imaginary planes, and a relative concept as they are
determined differently depending on the engagement of fetal
head.
The relation of the head to the planes of lesser pelvis is determined with the third
and fourth maneuvers of external obstetric examination, and upon vaginal examina-
tion.
American obstetricians determine the relation of the presenting part to lesser
pelvis planes while it passes through the birth canal using Bishop’s notion of lesser
pelvis levels. The stages of fetal head passage through the birth canal are deter-
mined by the relation of the fetal head lower pole to linea interspinalis (Latin) (see
Fig. 8.11) — zero plane.
Auscultation
Fetal heartbeat is listened to using an obstetric stethoscope beginning in the second
half of pregnancy (after 20 weeks gestation). The obstetric stethoscope differs from
a regular one in that it has a wide funnel. Heart tones are listened to on the side
of maternal abdomen where the fetal back is, below the umbilicus in presentation,
above the umbilicus in breech presentation. In transverse or oblique cephalic lie the
heartbeat is determined on the umbilicus level, closer to the fetal head. In multiple
pregnancy the heartbeats of fetuses are usually heard distinctly in different portions
of the uterus. Fetal heartbeat has three main auscultation characteristics: rate, rhythm
and clarity. The normal heartbeat rate is 110–160 beats per minute. The heartbeats
should be rhythmic and clear.
A dynamic assessment of fetal heartbeat can be made with a fetal cardiomonitor
which can be stationary, portable or pocket.
4.5.2.2. Internal obstetric examination

Internal obstetric examination is performed in conformity with the following
conditions:
• the pregnant woman is lying in lithotomy position with legs spread apart bent in
the knees and femoral joints;
128 Obstetrics
• the pelvis is raised;

• the woman should be given an opportunity to empty her bowels and bladder;
• the examination is performed aseptically.
Examination of external genitals. When examining external genitals one notes
the pattern of hair distribution (whether it is feminine or masculine), the de-
velopment of labia minora and labia majora, the condition of the perineum
(whether it is high, trough-like or low)1; one also checks for the presence of
pathological processes: inflammation, tumor, condyloma, fistula, perineal scar-
ring after laceration. When inspecting the anal area, one checks for the presence
of hemorrhoids.
Having moved apart the labia minora one inspects the vulva and vaginal orifice,
assesses the condition of external urethral opening, paraurethral passage and excre-
tory ducts of greater glands in the vaginal vestibulum.
Speculum examination of uterine cervix. One blade (Sims) or two blade (Cusco)
vaginal specula are used for this procedure. One notes the color of vaginal and cer-
vical mucosa, its size and the shape of the external orifice of uterus; one checks for
the presence of pathological processes in the cervix of uterus (cicatricial deformity,
ectropion, ectopy, leukoplakia, cervical canal polyps, condylomas) and vaginal walls;
the nature of vaginal secretion is also assessed.
In the first trimester of pregnancy one performs bimanual (vaginoperitoneal)
obstetric vaginal examination; in the second and third trimester — single-handed
examination as there is no need for palpation through the anterior abdominal wall.
At the beginning of the examination one palpates to check the condition of the
perineum (its rigidity, presence of scars) and the vagina (its length and width, condi-
tion of vaginal walls, vaginal fornices). Then the cervix is inspected; one determines
its length, shape, consistency, presence of scars or lacerations, the condition of the
cervical os (whether it is closed, partially open; it admits a tip of the finger or patent
for one finger, etc.).
Bishop score (the degree of cervical ripeness) is determined

NB! before delivery. Cervical ripeness is an integral parameter indicat-
ing how prepared for labor the woman’s body is.
There are a variety of methods estimating the ripeness of uterine cervix; however,
each one of them considers the following:
• cervical consistency;
• length of its vaginal part and cervical canal;
• extent of patency of cervical canal;
• position and direction of cervix in the cavity of lesser pelvis.
Taking these signs into consideration, a number of classification systems and scores
for integral estimation of ripeness of uterine cervix were elaborated (for instance,
Bishop score, 1964) (see Table 8.1).
1 The perineum is called high if the distance between the anus and posterior labial commissure is 5
cm and more.
4.5.3. Laboratory and instrumental methods of

investigation
The procedures of examining pregnant women are similar in different countries.
The decision about the number of tests and their variety is taken, as a rule, on the
basis of economic considerations.
In case of normally proceeding pregnancy the minimum of laboratory and instru-
mental investigations in Russia includes the following methods.
4.5.3.1. Laboratory methods of investigation

Laboratory methods of investigation are used to reveal extragenital disease and
obstetric complications. That is why pregnant women undergo both routine investi-
gations (clinical blood count and biochemical blood assay with fasting blood sugar
determination, urine test, tests for syphilis, hepatitis C and B, HIV) and special
investigations aimed at assessing how pregnancy progresses, evaluating the fetal
condition, revealing the risk for congenital malformations and chromosome diseases
(trisomy 21, trisomy 18 and trisomy 13), the so called biochemistry screening in
combination with fetal ultrasound.
Clinical blood count

Clinical blood count helps to obtain a complex picture of the pregnant woman’s
condition.
In pregnancy blood counts yield somewhat different findings. One of the causes
triggering a change in hematological parameters is the hypervolemic autohemodilution.
From the point of view of physiology, this is a process of preparing the body for
postpartum blood loss. In the body of a healthy pregnant woman the volume of plasma
increases by 35–50%. The increase in the number of red blood cells falls somewhat behind
the gain in the fluid portion of the blood; the RBC increase is only 25% thus leading to
physiological anemia. As a natural result, hematocrit and hemoglobin content go down.
The misbalance between the plasma volume and corpuscular elements volume results in
the development of oligocythemic hypovolemia, reduction of blood viscosity and elevated
ESR (Table 4.1). Alongside this, moderate leukocytosis and neutrophilia develop.
Coagulogram, hemostasiogram
Hemostasis depends on the condition of the vascular wall (endothelium), blood
platelets, plasma coagulation factor, and the fibrinolytic system. In physiological
pregnancy the systems of fibrinolysis and coagulation undergo considerable changes.
The coagulation factors, fibrinogen in particular, become more active (Table 4.4).
Fibrin is deposited on the vascular vessels of the uteroplacental circulation, and
fibrinolysis is suppressed. These changes, together with increased circulating blood
volume, interfere with the blood flow upon placental detachment, promote the de-
velopment of intravascular platelet plug (primary hemostasis).
Clinical urine analysis

• Amount. The fi rst-morning portion of urine is usually 150–250 ml; it is not
indicative of diurnal diuresis. Measuring the amount of fi rst-morning urine is
only expedient for interpretation of its relative density.
130 Obstetrics
Table 4.3. Normal blood values in nonpregnant and pregnant women
Value Nonpregnant Pregnant women

women I trimester II trimester III trimester
Hemoglobin, g/l 139 (115–152) 131 (112-165) 120 (108–144) 110 (110–140)
Hematocrit, %: 37 36 0.36 35 0.33 34
arterial blood 0.4 (33–44) 0.32
venous blood
RBCs, ×1012/l 4.2–5.4 (3.5–5) 4.2–5.4 3.5–4.8 3.7–5.0
WBCs, ×109/l 7.4 (4–8.8) 10.2 10.5 10.4
stab (1–5)
segmented (40–70)
basophils, % 0.5 (0–1) 0.2 0.2 0.1
eosinophils, % 2.0 (1–5) 1.7 1.5 1.5
LYM, % 38.0 (20–45) 27.9 25.2 25.3
monocytes, % 4.0 (3–8) 3.9 4.0 4.5
ESR, mm/h 22 (under 20) 24 45 72
Table 4.4. Major physiological parameters of homeostasis in pregnancy
Parameters Trimester of pregnancy

First Late second Late third
Fibrinogen, g/l 2.98 ±0.08 3.11±0.31 5.95 ±0.62
aPTT, sec 39.2 ±4.1 36.5 ±2.1 34.1 ±2.5
ART, s 64.4 ±6.9 61.4 ±6.9 51.1 ±4.8
Prothrombin index, % 89.3 ±4.5 95.4 ± 5.3 108.8 ±3.3
Fibrinogen breakdown products, mcg/ml Under 2.0 Under 2.0 5.7 ±0.9
Antithrombin III, g/l 0.22 ±0.03 0.18 ±0.01 0.15 ±0.02
Platelets, ×109/l 302 ±14.5 288 ±12 250 ±14
• Color. The color depends on the diuresis amount and on pigment excretion.
Normally urine is of pale yellow, straw color, which is due to the presence of
urine pigment, urochrome.
• Transparency. Normally all urine constituents are in a solution, so fresh urine is
quite transparent.
• Specific gravity depends on the concentration of substances dissolved in urine
(protein, glucose, urea, sodium salts and other).
• Chemical examination of urine
– pH. Organic acids and acidic salts of inorganic acids dissociate in a water
medium releasing a certain amount of free H+ ions. The concentration (activ-
ity) of free H+ ions indicates the true urine reaction, active acidity (pH).
– Protein. In a healthy woman’s urine almost no protein can be found, which is
due to reabsorption of protein filtered in the glomerules. Despite a consider-
able increase of glomerular filtration, proteinuria does not develop in preg-
nancy, as this process is counterbalanced by enhanced tubular reabsorption of
protein or by increased resistance of glomerules to plasma protein. The pres-
ence of protein in urine (over 0.075 g/l) is called proteinuria, which can be of
physiological and pathological nature.
– Physiological proteinuria is a transient presence of protein in urine; this phe-
nomenon is not associated with any disease; it is due to consumption of large
amounts of protein-rich food or due to physical exertion, emotional upheavals,
epileptic attacks. Orthostatic proteinuria is regarded as a functional condition.
– Glucose. Normally glucose from primary urine is almost completely reabsorbed in
renal tubules and cannot be detected by conventional methods. Glucose appears in
urine after its concentration exceeds the renal threshold, that is, 8.88–9.99 mmol/l,
or upon reduction of renal threshold for glucose (renal diabetes). Short-term
(transient) glucosuria can be noted in healthy individuals after considerable
alimentary load with foods high in carbohydrates or as a result of stress.
– Bilirubin. Only bilirubin glucuronide can pass through the glomerular filter
as the blood of healthy people contains it in trifling concentrations, so the
urine of healthy people contains minimal amounts of bilirubin, which is not
detectable by qualitative assays employed in clinical practice. Unconjugated
bilirubin does not pass through the renal filter.
– Urobilinogen. Urobilinogen is formed in the intestine from bilirubin excreted
by the liver. Normally urine contains trace amounts of urobilinogen.
– Ketone bodies (product of insufficiently oxidized fatty acids). In normal
conditions they are absent in urine; they can be noted only if their concentration
in the blood is elevated.
• Microscopic study of urine sediment. One distinguishes organized (RBCs,
WBCs, epithelium and casts) and unorganized (crystalline and amorphous salts)
types of urine sediment.
– RBCs. The urine of healthy individuals contains no RBCs, or possibly very few
RBCs per urine sample. They do not pass through the glomerular filter, so they
commonly appear in urine when there is renal disease and/or urinary tract
disease. In females RBCs can appear in urine when there is vaginal bleeding.
– WBCs. WBCs are not present in urine, or very few per visual field can appear.
Leucocyturia (over 5 WBCs per visual field) is revealed in case of renal and
urinary tract disease.
– Epithelium. Very few epithelial cells per visual field can be occasionally noted;
epithelium is desquamated in various parts of the urinary tract: squamous epi-
thelial cells in the urethra, transitional epithelium in the renal pelvis, ureter,
and bladder. Renal epithelium from the tubules is not noted in the urine of
healthy people. Elevated urine level of certain epithelial cells may indicate the
localization of inflammation.
– Cast cells are generated in the small distal convoluted tubules and collecting
ducts of the kidney, they generally maintain their shape and composition as
they pass through the urinary system. Appearance of cast cells in urine is an
important indication of renal disease. Only hyaline casts consisting of protein
and formed due to physical exertion can occasionally be present in normal urine.
– Bacteria. Bacteria are normally not present in urine. Before collecting the
urine sample one should pay particular attention to the hygiene of external
genitals (Table 4.5).
132 Obstetrics
Table 4.5. Normal urine test values in pregnant women
Parameters Characterization or value

Amount 150–250 ml
Color Straw-colored to amber yellow
Lucidity Complete
Density 1.015–1.030
pH 5.0–7.0
Protein None or under 0.075 g/l
Glucose None
Bilirubin None
Urobilinogen Trace
Ketone bodies None
RBCs Very few per sample
WBCs Less than 5 per sample and visual field
Epithelium Few squamous and transitional epithelial cells per visual field
Placental hormones
A new endocrine organ begins to work during pregnancy — the placenta. Placental
hormone tests permit an assessment of how pregnancy progresses (prenatal diagno-
sis), a diagnosis of fetoplacental insufficiency and of impaired fetal development.
Placental lactogen is determined starting at 5–6 weeks gestation. A placental
lactogen concentration <4 mcg/ml later than 30 weeks gestation indicates impaired
fetal development threatening the life of fetus. Dynamic investigation of placental
lactogen permits a control of placental function throughout the entire pregnancy and
a diagnosis of placental insufficiency.
Estriol provides for uterine growth and development during pregnancy. In normally
progressing pregnancy estriol production and its concentration in the blood increase
alongside fetal development. In a complicated course of pregnancy reduced estriol
levels serve as early diagnostic markers of fetal condition disturbance. Reduced estriol
levels are observed in Down syndrome, intrauterine infections: toxoplasmosis, ru-
bella, cytomegaly. In case of intrauterine fetal demise estriol synthesis and its content
in the blood drop abruptly, by over 50%.
Progesterone. Reduced progesterone concentration in the blood is noted when
there is threatened abortion, missed miscarriage.
Testosterone. Testosterone concentration in the blood and amniotic fluid depends
on gestational age and fetal sex. Its concentration is elevated in gestational tropho-
blastic disease in pregnant women. Nowadays the concentration of hormones in
physiological fluids is determined with highly sensitive and highly specific methods.
Almost all of them are competitive binding methods; their sensitivity is very high.
Specific hormone values at different gestational ages should be specified directly
at the laboratory which performed the investigation.
For the purpose of prenatal screening, each pregnant woman has tests assessing
the risk of giving birth to a child with genetic disorder (Down syndrome, Edwards
syndrome, neural tube defect). The risk is worked out considering the pregnant
woman’s age, weight, ultrasound findings and biochemical markers level: pregnancy-
associated placental protein and human chorionic gonadotropin. The risk calculation
is done using computer software. Determination of fetal DNA in the maternal blood
is more precise; it is performed in controversial cases and in groups with a risk of
congenital disorders.
4.5.3.2. Instrumental methods

Methods of instrumental investigation are subdivided into
• invasive methods:
– amnioscopy;
– chorion biopsy;
– amniocentesis;
– cordocentesis;
• noninvasive methods:
– ultrasound;
– dopplerography;
– fetal cardiotocography (CTG).
Noninvasive methods of examination

Ultrasound
Ultrasound investigation (sonography) is now the only highly informative, safe
and noninvasive method that allows an objective observation of embryo development
from the earliest stages of its development and a dynamic observation of the fetal
condition (Fig. 4.19).
Ultrasound diagnostics is based on the
piezoelectric effect. Ultrasound waves emitted
by the transducer are reflected by the struc-
tures of the investigated object in different
ways as they are of different density; the waves
are intercepted by the probe placed inside the
same transducer and transformed into electric
impulses reproduced on the screen in propor-
tion to the distance from the transducer to the
structure that reflected the signal.
Two major methods are widely used in
obstetrics: transabdominal and transvaginal
scanning; they got their names according to
where the transducer is placed during inves-
tigation.
Use of transvaginal transducers (Fig. 4.20)
permits early confirmation of the fact of
pregnancy, a more precise study of gesta-
tional sac development (the embryo, extra-
embryonic structures); most major defects of
embryo/fetus development can be detected
by ultrasound as early as in the first tri-
mester. Fig. 4.19. Ultrasound device
134 Obstetrics
Ultrasound screening of pregnant wom-

en in the Russian Federation is performed
at 11–14, 18–21 and 30–34 weeks gesta-
tion.
The main objectives of sonography in ob-
stetrics are as follows:
• establishing the fact of pregnancy and
its progress, the number of gestational
sacs;
• embryo- and fetometry;
• diagnosis of development impairment;
Fig. 4.20. Transvaginal transducer • assessing the functional condition of
the fetus;
• placentography;
• revealing the specific features of the structure and development of extraembryonic
structures;
• visual control in invasive investigations (chorion biopsy, amniocentesis,
cordocentesis, intrauterine surgery).
The crown-rump length is the most accurate embryometric param-

NB! eter.
Ultrasound makes it possible to diagnose uterine pregnancy at the earliest stage

of gestation. As early as in the fifth week (obstetric gestational age) the gestational
sac can be visualized in the uterine cavity in the form of hyporechogenic structure
of rounded or ovoid shape 5–6 mm in diameter. At 6–7 weeks gestation one can
detect the embryo: a hyperechogenic strip 6–7 mm in size. The most accurate em-
bryometric parameter in the first trimester is the crown-rump length. In physiologi-
cal pregnancy it permits an accurate estimation of gestational age (the inaccuracy
amounts to ±3 days). Evaluation of embryo vital activity in early pregnancy is based
on registering fetal cardiac function (starting at 6.5 weeks) and motor activity.
At 11–14 weeks gestation it is extremely important to detect markers of chromo-
some abnormalities: nuchal translucency, hypoplasia or absence of nasal bone, non-
immune fetal hydrops, discrepancy between crown-rump length and gestational age.
Another screening ultrasound (18–21 weeks) is aimed at evaluating fetal growth
and anatomy (detecting congenital abnormalities, markers of chromosome disease,
fetal growth restriction); localization, thickness and structure of the placenta, am-
niotic fluid volume.
The third ultrasound is performed at 30–34 weeks gestation to reveal congenital
abnormalities of late manifestation, fetal growth restriction and to assess the func-
tional condition of the fetus (evaluation of respiratory and motor activity, dopple-
rometry of blood flow in the mother-placenta-fetus system).
When studying the growth and development of fetus in the second and third
trimester one performs fetometry (measuring fetal size). Fetometry always includes
measuring the biparietal diameter, head circumference, abdominal diameter, abdomi-
nal circumference, as well as femur and humerus length.
In the second and third trimesters sonography permits an examination of cere-

bral structures, the skeleton, facial skull, and fetal internal organs (the heart, lungs,
liver, stomach, intestine, kidneys and adrenal glands, the bladder), which permits a
diagnosis of most fetal congenital abnormalities. For a detailed assessment of fetal
anatomy one can opt to use 3-dimensional sonography that allows a volumetric im-
age of the studied organ.
The range of sonography markers of fetal chromosome defects detectable in the
third trimester includes changes on the part of various organs and systems: ventricu-
lomegaly, choroid plexus cyst in the lateral ventricles, anomalous shape of skull and
cerebellum (Arnold-Chiari malformation), hyperechogenic bowel, pyelectasis, single
umbilical artery, symmetrical fetal growth restriction.
Ultrasound signs of changes in the placenta as pregnancy progresses are based on
the grade of placental maturity (Grannum classification) (Table 4.6). This classifica-
tion is based on detecting characteristic sonographic changes in the chorionic plate,
placental parenchyma and basal plate starting at 26 weeks gestation.
If the placental maturity grade is higher than the normal value for this gestational
age, this is referred to as premature aging of the placenta, which is often accompanied
by functional placental insufficiency.
Ultrasound diagnosis permits diagnostics of premature detachment of placenta;
it is based on detecting echonegative space between the placenta and uterine wall.
Ultrasound is also helpful for assessing the condition of postoperative scar on the
uterus.
Ultrasound provides valuable information on the condition of uterine cervix
during pregnancy, which is important in predicting preterm labor. In transvaginal
sonography, which has certain advantages over finger vaginal examination and trans-
abdominal sonography, one can estimate the length of uterine cervix along its entire
length, the condition of the internal os (its width and shape) of the cervical canal.
Dopplerography
Over recent years dopplerography (assessment of blood flow in major fetal and
uterine vessels), alongside with cardiotocography, has become the principal method
for investigation of the fetoplacental system.
Table 4.6. Ultrasound assessment of placental maturity grade (P.Grannum)
Grade Parts of placenta

Chorionic plate Parenchyma Basal plate
0 Smooth, without Homogenous Not identifiable
indentations
1 Subtle indentation A small number of diffused Not identifiable
hyperechoic areas
2 Larger indentations Linear hyperechoic calcifica- Linear «dot-dash»
along chorionic plate tions (comma-like) configuration of small
hyperechoic areas
3 Complete indenta- Rounded calcifications with Large, partially merging
tions through to the translucency in the middle, hyperechoic areas with
basal plate large irregular calcifications shadowing
with significant shadowing
136 Obstetrics
The Doppler investigation method is based on the following physical phe-

nomenon. When objects (in our case it is RBCs) are moving at a certain rate
towards the source of ultrasound impulse, their reflecting surface comes in
contact with ultrasound impulses oftener than when the object is motionless. As
a result, the frequency of reflected oscillations exceeds the baseline frequency
of emitted ultrasound impulses. And vice versa, when the reflecting surface
is moving away from the emission source, the frequency of reflected oscilla-
tions is lower than the frequency of emitted impulses. The difference between
the frequency of emitted and reflected impulses is referred to as the Doppler
frequency shift.
Basic indications for Doppler investigation of maternal-placental-

NB! fetal circulation:
• extragenital disease;
• complications of pregnancy;
• post term pregnancy;
• multiple pregnancy.
Investigation of uteroplacental blood flow is of utmost practical value; one studies

the blood flow in uterine arteries, its branches (coiled arteries), umbilical artery, as
well as fetal hemodynamics in the aorta and cerebral vessels of the fetus. Investigation
of venous blood flow in the fetal ductus venosus is very informative. The vessel
studied most often during pregnancy is the umbilical artery. After 10 weeks gestation
an analysis of blood flow velocity curves in the umbilical artery has implications for
clinical practice. The diastolic component of blood flow in the umbilical artery may
not be present as late as at 14 weeks gestation. Fetuses with chromosome abnormali-
ties can show anomalous (reverse) diastolic blood flow in ductus venosus as early as
at the age of 10–13 weeks.
In Russia, for an objective estimation of blood circulation in the mother-placenta-
fetus system one uses the classification of uteroplacental and fetoplacental blood flow
disorders (Strizhakov et al., 1989):
• First degree
– A: disorder of uteroplacental blood flow (uterine arteries) while fetoplacental
blood flow (umbilical artery) remains intact.
– B: disorder of fetoplacental blood flow while uteroplacental blood flow
remains intact.
• Second degree
– Disorder of uteroplacental and fetoplacental blood flow that does not reach
critical values (the diastolic blood flow remains intact).
• Third degree
– Critical disorder of fetoplacental blood flow (zero or retrograde diastolic blood
flow while uteroplacental flow is disturbed or remains intact).
The diagnostic value of first and second degree disorder of uteroplacental blood
flow is doubtful.
The accuracy of diagnosing fetal disorders using dopplerography findings is about
70%.
Fetal cardiotocography (electronic fetal monitoring)

Fetal cardiac activity is the most accurate and objective indicator of fetal condition
in the ante- and intranatal period at the time of investigation. However, during preg-
nancy cardiotocography is of minimal prognostic value. Monitoring of fetal cardiac
activity is performed using specially designed equipment, fetal cardiomonitors. Modern
cardiomonitors operate on the Doppler principle, which permits a registration of
change in the interval between certain cardiac cycles, which are transformed into heart
rate changes appearing as a light signal, acoustic signal, digital signal and represented
graphically as a cardiotocogram. The device is fitted with tensometric indicator, which
also registers the contractile uterine activity. During labor the pressure on the tenso-
metric sensor placed on the pregnant woman’s abdomen increases in proportion to
intrauterine pressure and is transformed by the sensor into electric impulses registered
in the form of a curve. Thus, a cardiotocogram represents two curves aligned in time,
one showing fetal heart rate, the other—uterine activity. Besides uterine contractions,
the uterine activity curve also registers fetal motor activity.
An up-to-date expert class cardiomonitor makes it possible to register, apart from
the heart rate, the fetal ECG; and this, without doubt, is of more diagnostic value
in assessing the fetal condition.
The objective of CTG is timely diagnosis of functional distur-

NB! bances of the fetus, which permits a choice of optimal timing and
method of delivery.
Indications for CTG during pregnancy: presence of risk factors for fetal distress:
preeclampsia, hypertonic disease, diabetes mellitus, anemia, isoimmunization, post-
term pregnancy, multiple gestation pregnancy, fetal growth restriction, olighydroam-
nios, obstetric and gynecological complications in past history (perinatal loss),
reduced fetal motor activity, dopplerography findings suggesting hemodynamic dis-
turbance of the mother-placenta-fetus system. Continuing cardiomonitoring during
childbirth is indicated to all parturient women at a high risk; the procedure is of
considerable prognostic value.
One distinguishes external (indirect) and internal (direct) CTG. During pregnancy
only external CTG is used; nowadays it is also widely used during childbirth.
In external CTG the external ultrasound transducer is placed on mother’s ante-
rior abdominal wall where the fetal heart tones are heard best of all. The transducer
surface is covered with special purpose gel to ensure optimum contact with the skin.
The external tensometric sensor is placed in the area of the fundus; this one does
not require application of gel. The pregnant woman can register each episode of fetal
movement on her own using a special device for fetal movement registration during
pregnancy (Fig. 4.21).
CTG is performed while the pregnant (parturient) woman is on her side in a re-
cumbent or semirecumbent position so as to avoid the postural hypotensive syndrome
(inferior vena cava compression).
To obtain as accurate information about the fetal condition as possible, cardioto-
cography should be done for at least 20–30 minutes; such a lengthy observation is
necessary due to the periods of sleep and activity in the fetus.
138 Obstetrics
Uterine tone transducer Uterine tone

Uterine wall
Fetal heartbeat transducer Fetal heart
Fig. 4.21. External cardiotocography
Internal CTG is only used during labor after rupture pf membranes and the uterine
cervix has dilated to no less than 2 cm. When using internal sensors a special spiral
electrode is attached to the child’s head; sometimes an intrauterine pressure catheter
can be used to register the contractile activity of the uterus. Given the invasive nature
of internal CTG, it is not widely used in clinical practice nowadays.
CTG is considered a justified procedure starting at 32 weeks gestation. If one uses
a device with automatic interpretation of the cardiotocogram, fetal cardiac activity
can be assessed starting at 26 weeks gestation.
The cardiotocogram interpretation begins with determining the basal rate. Basal
rate is determined by approximating the mean fetal heart rate rounded to increments
of 5 beats per minute during a 10-minute segment excluding accelerations and de-
celerations (Fig. 4.22).
When characterizing the basal rate one should take into consideration its vari-
ability, that is, the frequency and amplitude of fetal heart rate changes over 1-min-
ute intervals (long-term variability). The count of the frequency and amplitude of
instantaneous fluctuations is done over each successive 10 minutes. Some modern
cardiomonitors perform a computerized assessment of beat-to-beat fluctuations,
which is one of the most accurate indicators of the presence or absence of hypoxia
(short-term variability) (Fig. 4.23).
The following classification of basal rate variability types is now most commonly
used in clinical practice:
• mute (monotonous) pattern characterized by low amplitude (less than 5 per
minute);
• slightly undulating (5–10 per minute);
• undulating (10–15 per minute);
• saltatory (25–30 per minute).
A presence of mute (monotonous) and slightly undulating pattern registered
for a prolonged time usually indicates a disorder of the fetal functional condition.
Undulating and saltatory patterns indicate a satisfactory fetal condition.
Fig. 4.22. Basal rate of heart contractions (red line): 1 — fetal cardiogram; 2 — tocogram
Fig. 4.23. Cardiotocography. Basal rate of about 135 beats per minute. The blue color
highlights the accelerations
In interpreting a cardiotocogram, apart from fluctuations, one takes into account

accelerations and decelerations.
Accelerations are a visually apparent abrupt increase in fetal heart rate by 15 bp-
mor more above the basal rate, of over 15 seconds’ duration. Accelerations appear
as a reaction to fetal movements, contractions, functional tests. Accelerations are a
reassuring sign indicating a satisfactory fetal condition.
Decelerations. A deceleration is an episode of decreased fetal heart rate by 15 bpm
or more below the fetal baseline heart rate for 15 seconds and longer. Three main
types of decelerations are distinguished:
• Early decelerations (type I) begin simultaneously with contractions or no
later than after 30 seconds; their onset and termination are gradual (Fig.
140 Obstetrics
4.24).The duration and amplitude of early decelerations correspond to the

duration and intensity of contraction. Early decelerations are a fetal ref lex
response to short-term cerebral ischemia due to the fetal head pressure
during the contraction. If there are no other pathological changes on the
cardiotocogram, early decelerations are not regarded as a sign of intrauterine
hypoxia.
• Late decelerations (type II) are also associated with contractions; however,
they develop 30 and more seconds later than the onset of uterine contraction
(Fig. 4.25). Late decelerations reach their peak after a maximum uterine tension;
their duration is often longer than the contraction. Late decelerations are an
indication of disturbed uteroplacental blood circulation and progressing fetal
hypoxia.
• Variable decelerations (type III) show a different onset in relation to the
beginning of contraction; they appear on the cardiotocogram in different
shapes: V-, U-, W-shape (Fig. 4.26). Emergence of variable decelerations is
associated with umbilicus compression due to contraction, fetal movement or
oligohydramnios.
Atrial stimulation Atrial stimulation

I Time period per minute Time period per minute
21 2140 21 240
18 2210 18 210
15 1180 15 180
12 12 150
9 1220 9 120
6 990 6 90
3 660 60
0 330 30
а
500 1000 500 100
375 775 375 75
250 550 250 50
125 225 125 25
0 0 0 0
II mm Hg mm Hg
Fig. 4.24. Early decelerations
Criteria of normal antenatal cardiotocogram:

NB! • basal rhythm 120 – 160 per minute;
• the amplitude of variability of basal rhythm 10 – 25 per minute;
• no decelerations;
• presence of two and more accelerations in 10 minutes of obser-
vation.
21 240 21 240
18 210 18 210
15 160 15 180
12 150 12 150
9 120 9 120
6 90 6 90
3 60 3 60
0 30 0 30
a
500 100 500 100
375 75 375 75
250 50 250 50
125 25 125 25
0 0 0 0
II mm Hg mm Hg
Fig. 4.25. Late decelerations
21 240 21 240
18 210 18 210
15 160 15 180
12 150 12 150
9 120 9 120
6 90 6 90
3 60 3 60
0 30 0 30
a
500 100 500 100
375 75 375 75
250 50 250 50
125 25 125 25
0 0 0 0
II mm Hg mm Hg
Fig. 4.26. Variable decelerations
A doubtful cardiotocogram shows the following features:

• basal rate within the range of 100–110 or 160–180 bpm;
• the amplitude of basal rate variability less than 10 per minute or over 25 per
minute;
• absence of accelerations;
• spontaneous shallow short decelerations.
142 Obstetrics
With this type of cardiotocogram another investigation is needed in 1–2 hours,

as well as accessory methods of investigating the fetal functional condition like the
mammary stimulation test.
A pathological cardiotocogram typically shows:
• basal rate of less than 100 per minute or over 180 per minute;
• the variability amplitude of basal rate is less than 5 per minute;
• pronounced variable decelerations;
• late decelerations;
• sinusoidal rhythm.
Various scoring systems were put forward for the purpose of unifying and ensur-
ing more accurate interpretation of antenatal cardiotocogram. The Fischer score
(W. Fischer, 1973) is currently one of the the preferred method for assessment of
antepartum CTGs:
• a score of 8–10 points indicates a normal condition of the fetus;
• a score of 5–7 points indicates initiation of fetal activity disturbance;
• a score of 4 points and less indicates alarming changes in the fetal condition
(Table 4.7).
Table 4.7. Fischer score for antenatal cardiogram assessment
Variable Score
0 1 2
Basal rate, bpm >180<100 100–119 161–180 120–160
Fluctuations ampli- <3 3–5 6–25
tude, bpm
Number of fluctua- <3 3–5 6 and more
tions per minute
Acceleration 0 1–4 sporadic or periodic 5 and more, sporadic
Decelerations Late or variable Early (severe) or variable None or early (slight,
(severe atypical) (slight, moderate) moderate)
The accuracy of correct assessment of fetal condition is 70–85% with different
methods of cardiotocogram interpretation.
Antenatal CTG nowadays often includes a non-stress test (NST). The test consists
in studying the response of fetal cardiovascular system to its movements.
• Non-stress test is reactive if 2 accelerations (increase in heart rate by 15 bpm
lasting no less than 15 seconds) associated with fetal movements are noted within
20 minutes.
• Non-stress test is areactive (fetal distress) if less than 2 accelerations are noted
during a 20 minute interval.
Functional tests are of great help in estimating fetal condition

NB! and its backup capacity: assessment of fetal cardiac activity in
response to movement (nonstress test); nipple stimulation (mam-
mary test), a stress test.
If the fetus is in the condition of physiological rest, non-stress test may turn out
to be false positive. In such cases the investigation should be repeated in 2–4 hours.
As a rule, almost 95% of pathological (areactive) antenatal CTGs become normal

(reactive) in 80 minutes.
If CTG findings are doubtful, stress tests are used.
For instance, there is a safe, reliable analogous test — mammary stimulation test
(stimulation of nipples followed by endogenous oxytocin release).
The test can be assessed if no less than three uterine contractions are noted during
10 minutes. If the fetoplacental system possesses sufficient compensatory ability, in
response to uterine contractions the fetus produces moderately pronounced short-
term acceleration or early brief deceleration.
Determining biophysical profile of the fetus
Nowadays the fetal condition is assessed using the so called fetal biophysical profile
(BPP). BPP can be used to obtain objective information as early as at the beginning
of the third trimester (Table 4.8).
Each variable is assessed with a score of 0 (abnormality) to 2 (normal). The points
are summed up to obtain the indicator of fetal condition.
• A score of 8 to 12 indicates a normal condition.
• A BPP score of 6 to 7 indicates an ambiguous condition of the fetus.
• A score of 4–5 and less is an indicator of pronounced intrauterine fetal hypoxia;
it suggests a high risk of perinatal complication development.
Table 4.8. Criteria for fetal biophysical profi le assessment (Vintzileos A., 1983)
Biophysical Score
variable 0 1 2
No stress 1 acceleration in less 2–4 accelerations asso- 5 and more accelera-
test than 20 min ciated with fetal move- tions associated with
ments, with an ampli- fetal movements, with
tude of no less than an amplitude of no less
5 beats of no less than than 15 beats and of no
5 s duration, in 20 min less than 15 s duration,
in 20 min
Fetal motor No episodes of gener- 1–2 episodes of general- No less than 3 episodes
activity alized fetal movement ized fetal movement in of generalized fetal
during 30 min 30 min movement in 30 min
Fetal No episodes of fetal No less than 1 episode of No less than 1 episode
respiratory respiratory movements fetal respiratory move- of fetal respiratory
movements or episodes less than ment of 30–60 s in movement of no less
30 s long in 30 min 30 min than 60 s in 30 min
Fetal mus- Limbs extended No less than 1 episode 1 and more episodes of
cular tone of active extension with active extension with
return to flexion of fetal return to flexion of fetal
limb(s) limb(s)
Amniotic 1 pocket of fluid mea- 2 and more pockets of A pocket of fluid
fluid vol- suring under 1 cm amniotic fluid measur- 2–8 cm in vertical dis-
ume ing 1–2 cm tance
Placental Placental grading 3 at – Corresponds to gesta-
maturity an age below 37 weeks tional age
grade
144 Obstetrics
The notion of BPP includes the findings of nonstress test (after

NB! CTG) and ultrasonic findings:
• respiratory movements;
• motor activity;
• fetal tone;
• amniotic fluid volume;
• degree of placental maturation.
High sensitivity and specificity of BPP are due to a combination of markers for
both acute fetal disorders (NST, respiratory movements, motor activity and fetal
tone) and chronic disorders (amniotic fluid volume, placental maturity grade). Even
without additional data, reactive NST indicates a satisfactory fetal condition; though,
when NST is areactive, one pays close attention to ultrasound findings and other
biophysical variables describing the fetal condition. Considering the time-consuming
nature of BPP investigation (it takes about 40 min.), a so-called modified BPP has
been used lately; it includes only such components as assessment of NST and the
of amniotic fluid volume (AFV).
Invasive methods of investigation

Amnioscopy
This method consists in a direct visual examination of the amniotic fluid in the
lowest part of the amnion using an optical instrument, amnioscope. Indications
for amnioscopy are as follows: signs of disturbed fetal condition and post-term
pregnancy. Contraindications include vaginitis, cervicitis, placenta previa, breech
presentation of the fetus. For this procedure the cervix should be ripe or effaced,
the amniotic sac — intact (Fig. 4.27).
Doing amnioscopy one notes the color of amniotic fluid, presence of blood or
meconium staining, floccules of vernix caseosa (Fig. 4.27). In case of low-lying
placenta vessels are visible on fetal membranes.
Fig. 4.27. Amnioscopy

Invasive perinatal diagnostics

When noninvasive diagnostic methods suggest chromosome disorders of the fetus,
there is a need for definitive verification of the diagnosis. In recent years this has be-
come possible and accessible through determining fetal DNA fragments in maternal
blood (noninvasive prenatal molecular karyotyping). The final diagnosis is made with
invasive methods of investigation followed by fetal karyotyping. All invasive procedures
are performed after the pregnant woman has given her voluntary informed consent.
Fig. 4.28. Amnioscopy. Clear amniotic fluid Fig. 4.29. Amnioscopy. Green amniotic fluid
The point of up-to-date invasive prenatal diagnostics is that markers of congenital
and hereditary diseases typical for postnatal period can be determined in utero.
Invasive prenatal diagnostics can be performed under the following conditions:
• high probability of giving birth to a child with severe hereditary disease that can
hardly be treated or not treated at all;
• the risk of giving birth to a diseased child outweighs the risk of complications due
to the prenatal screening;
• an accurate prenatal diagnostic test and a laboratory equipped with appropriate
devices and reagents are available;
• the family has given their consent to an invasive procedure.
Basic methods of invasive prenatal diagnosis:
NB! • chorion biopsy (8 – 11 weeks);
• placentocentesis (starting at 14 weeks);
• transabdominal amniocentesis (17 – 20 weeks);
• cordocentesis (20 – 22 weeks).
The main indications for invasive prenatal diagnostics are:
• structural chromosome rearrangement in one of the parents;
• maternal age over 35;
• previous fetal abnormality in the past;
• prenatally diagnosed single-gene disorder;
• ultrasound findings indicating the presence of markers of chromosome
abnormality or similar findings from maternal blood serum marker study;
146 Obstetrics
• complicated course of pregnancy (oligohydramnios, polyhydramnios, retarded

fetal development).
If one reveals fetal defects that are not manageable prenatally or postnatally, the
question of pregnancy termination arises. Subsequently, the findings of prenatal di-
agnostics should be verified with laboratory methods, and a postmortem and genetic
study of the fetus should be performed.
Invasive prenatal diagnostics reveals fetal abnormalities in about 3.2% of
cases; and the total amount of complications due to this procedure does not
exceed 1%.
All the procedures discussed above are contraindicated if there are clinical mani-
festations of miscarriage, acute infection, presence of genital infection, tumor-like
uterine mass of large dimensions.
Chorionic villus sampling. For chorionic villus sampling one makes ultrasound-
controlled aspiration of chorionic tissue using a needle. The optimum gestational
age for this procedure is 11–13 weeks. 5 mg of chorionic tissue are needed for a
laboratory study. The biopsy is performed in outpatient settings, if there are cor-
responding indications—in inpatient settings (a day patient facility would be ideal)
(Fig. 4.30).
Prerequisites for invasive investigations associated with obtain-

NB! ing fetal tissue:
• normal vaginal flora;
• negative tests for syphilis, HIV, hepatitis B and C;
• clinical blood test and urinalysis within normal;
• an ultrasound examination beforehand.
Sample of placenta Ultrasound

is withdrawn undwer transducer
ultrasound guidance
Fetus
Fig. 4.30. Chorionic villus sampling

The main complication of the procedure is threatened abortion. This may be due
to violating the integrity of the gestational sac, ingress of infection, or hematoma
formation after the procedure. At present the rate of these complications has declined
considerably as it is performed with visual ultrasound control; the complication rate
does not exceed 2%.
Amniocentesis. Transabdominal amniocentesis consists in collecting a sample of am-
niotic fluid with a needle inserted through the abdominal wall so as to obtain amniotic
fluid and fetal cells contained in it—amniocytes. Nowadays amniocentesis is the lead-
ing method for sampling fetal material in most prenatal diagnosis centers (Fig. 4.31).
The best gestational age for amniocentesis and fetal karyotyping is 17–20 weeks. The
main complication is the risk of miscarriage; however, its rate does not exceed 1%.
The drawback of this procedure is its complexity: cultivating a sufficient amount of
amniocytes for effective karyotyping. This prolongs the procedure time by 2–3 weeks; in
about 2% of cases this interferes with making a diagnosis. Difficulty can arise if maternal
blood mixes with the obtained sample after which cordocentesis has to be resorted to.
Cordocentesis. Cordocentesis is a diagnostic prenatal test in which a sample of the
baby’s blood is removed from the umbilical cord for testing (Fig. 4.32).
If the purpose of the study is fetal karyotyping, cordocentesis is done after
18 weeks gestation; the best gestational age is 20–21 weeks. The risk of miscarriage
does not exceed 2%.
Placentocentesis. Starting at 14 weeks gestation placentocentesis can be resorted to
for the purpose of obtaining fetal tissue. The method of performing this procedure
is the same as for chorion biopsy in the first trimester. When doing placentocentesis
one also runs a risk of obtaining cells of maternal origin.
Ultrasound
transducer
Amniotic fluid
Placenta
Fetus
Uterus
Cervix
Fig. 4.31. Amniocentesis

148 Obstetrics
1 2
Fig. 4.32. Cordocentesis: 1 — ultrasound transducer; 2 — aspirating needle; 3 — lumen of

umbilical cord vein; 4 — umbilical arteries
REMEMBER!
Objectives of ultrasound examination in the first trimester:

• diagnosis of uterine pregnancy on the basis of visualizing the gestational sac in
the uterine cavity, ruling out extrauterine pregnancy;
• diagnosis of multiple pregnancy, of placentation type: bichorial, monochorial;
• assessment of gestational sac growth (mean sac diameter, crown-rump length
of the embryo/fetus);
• assessment of embryo vital activity (cardiac activity, motor activity);
• study of embryo/fetus anatomy, detecting markers of chromosome disorders;
• examination of extraembryonic structures (yolk sac, amnion, chorion, umbilical
cord);
• diagnosis of pregnancy complications (threatened abortion, incipient abortion,
complete abortion);
• detection of disorders (molar pregnancy, myoma of uterus, abnormalities of
uterus structure, changes in endometrium, ovarian mass).
The gold standard in diagnosing pregnancy of any localization consists in com-
bining two methods: beta-hCG determination and ultrasound examination to visual-
ize the gestational sac.
Gestational age is established on the basis of historical information and objective
investigations:
• last menstrual period date;
• ovulation;
• ultrasound findings in the first trimester;
• fundal height and abdominal circumference in the second and third trimester.
For indirect estimation of internal dimensions of the lesser pelvis one performs
pelvimetry.
It is of utmost importance to work out the true conjugate (conjugata vera, Latin) as
early as at the first examination; that is, the shortest diameter through which the
head must pass; normally it measures 11–12 cm.
Leopold’s maneuvers for external obstetric examination are palpations of the
uterus performed in a certain order.
Head diameters are a conventional notion as these planes are only imaginary,
and a relative notion as they are determined differently depending on the head
engagement.
Before childbirth, the grade of cervical ripeness is determined. Ripeness of the
uterine cervix is an integral indicator of how ready the maternal body is for labor.
The main indications for Doppler investigation of blood circulation in the mother-
placenta-fetus system:
• extragenital disorders;
• pregnancy complications;
• post-term pregnancy;
• multiple pregnancy.
The objective of electronic fetal heart monitoring is timely diagnosis of disor-
ders in the fetal functional status, which permits a choice of the optimum time and
method of delivery.
Criteria of normal antenatal cardiotocogram:
• basal rate of 120–160 bpm;
• basal rate variability amplitude 10–25 per minute;
• no decelerations;
• presence of two and more accelerations during a 10 min. interval.
Function tests are a great help in evaluating the fetal status and the spare capac-
ity of the fetoplacental system: studying the response of fetal cardiac activity to
movement (non stress test), and a response to mammary stimulation (mammary
stimulation test), which is a stress test.
Biophysical profile of the fetus includes the findings of non stress test (in CTG) and
findings from ultrasound examination:
• respiratory movements;
• motor activity;
• fetal tone;
• volume of amniotic fluid;
• placental maturity grade.
The basic methods of invasive prenatal diagnostics are:
• chorionic villus sampling (11–13 weeks);
• placentocentesis (from 14 weeks);
• transabdominal amniocentesis (17–20 weeks);
• cordocentesis (20–22 weeks).
Prerequisites for invasive procedures associated with fetal tissue sampling:
• normal vaginal biocenosis;
• negative tests for syphilis, HIV infection, hepatitis B and C;
• clinical blood test and general urine test findings without abnormalities;
• preliminary ultrasound examination.
150 Obstetrics
CONTROL QUESTIONS
1. What are the advantages of early diagnosis of pregnancy?

2. What is the gold standard in pregnancy diagnostics?
3. What can cause a false positive hCG test?
4. What typical signs permit identification gestational sac by ultrasound?
5. What pregnancy signs are considered positive?
6. What are the methods of establishing the gestational age?
7. What is Naegele’s rule and how is it applied?
8. How does the fundal height change as pregnancy progresses?
9. What is special obstetric examination?
10. What is the rhombus of Michaelis?
11. What ways of calculating the true conjugate do you know?
12. What is the external obstetric examination? What maneuvers does it include,
what are they for?
13. In what relation to the pelvic planes can the head be?
14. What are the fetal attitude, lie, position, visus and presentation?
15. What is the grade of cervix ripeness? How can it be determined?
16. What are the specific features of clinical blood test in pregnant women?
17. What are the main objectives of ultrasound examination in the first
trimester?
18. What are the main indications for Doppler investigation of blood flow in the
mother-placenta-fetus system?
19. What is CTG, at what gestational age is it performed?
20. What does the notion of biophysical profile include?
21. What invasive methods of prenatal diagnosis do you know?
CHECK YOURSELF!
Level 1. Test
1. The gold standard in pregnancy diagnosis:

а) beta-hCG determination;
b) ultrasound examination to detect the gestational sac;
c) combining two methods: beta-hCG and ultrasound examination to detect the
gestational sac;
d) beta-hCG repeat testing (no less than 3 times at an interval of 5 days).
2. hCG is released by:

а) cytotrophoblast;
b) syncytiotrophoblast;
c) corpus luteum;
d) the pregnant woman’s pituitary gland.
3. Ultrasound transvaginal sonography can give a positive diagnosis of pregnancy at

the age of:
а) 4–5 obstetric weeks;
b) 6–7 obstetric weeks;
c) 3–4 obstetric weeks;
d) 10 obstetric weeks.
4. The decisive criterion for calculation of gestational age using ultrasound findings,
from the moment of embryo emergence:
а) mean sac diameter;
b) crown-rump length;
c) abdominal circumference;
d) thigh length.
5. The fundus of uterus is found at the umbilical level at the gestational age of:
а) 16 weeks;
b) 30 weeks;
c) 22 weeks;
d) 28 weeks.
6. To calculate the due date one has to:

а) subtract 3 months and 7 days from the date of LMP;
b) subtract 3 months and add 7 days to the date of LMP;
c) subtract 3 months from the conception date and add 7 days;
d) subtract 3 months and 3 days from the conception date.
7. Obstetric stethoscope helps to hear the fetal heartbeat after the gestational
age of:
а) 12–13 weeks;
b) 18–20 weeks;
c) 22 weeks;
d) 16–18 weeks.
8. Beta-hCG is detected in the pregnant woman’s blood on day:

а) 12 after conception;
b) 4–5 after conception;
c) 18–20 after conception;
d) 7–9 after conception.
9. The term nulligravida means:

а) a currently pregnant woman who had at least two pregnancies in past history;
b) a currently pregnant woman who had no pregnancies in past history (pregnant
for the first time);
c) a currently pregnant woman who had pregnancies in past history irrespective
of their outcome;
d) a woman who has never been pregnant.
152 Obstetrics
10. The first trimester of pregnancy lasts to the end of:

а) 16th week;
b) 14th week;
c) 12th week;
d) 8th week.
11. The second trimester is the period:

а) 14–28 weeks of gestation;
b) 10–20 weeks of gestation;
c) 8–16 weeks of gestation;
d) 29–40 weeks of gestation.
12. The third trimester is the period:

а) 13–28 weeks of gestation;
b) 10–20 weeks of gestation;
c) 8–16 weeks of gestation;
d) 29–40 weeks of gestation.
13. Distantia spinarum normally measures:

а) 25–26 cm;
b) 28–29 cm;
c) 14 cm;
d) 30–32 cm.
14. The true conjugate is the distance:

а) from the promontory to superior margin of symphysis pubis;
b) from the promontory to superointernal margin of symphysis pubis;
c) from intervertebral disk between II and II sacral vertebrae to the middle of
internal surface of symphysis pubis;
d) from coccyx apex to the inferior margin of symphysis pubis.
15. The third Leopold’s maneuver determines:

а) the attitude of fetus in the uterus;
b) fetal attitude and visus ;
c) fundal height;
d) the presenting fetal part.
16. Fetal position is:

а) the relation of fetal back to the left or right side of the uterus;
b) the relation of fetal back to the anterior or posterior side of uterus;
c) the relation of large fetal part to the lesser pelvis inlet;
d) the relation of fetal head to the limbs and trunk.
17. Normal fetal heart rate is:

а) 120–160 bpm;
b) 110–140 bpm;
c) 120–180 bpm;
d) 90–160 bpm.
18. Signs taken in consideration when determining the ripeness of cervix:

а) consistency of the cervix and its length;
b) length of cervix, extent of patency of cervical canal;
c) consistency of the cervix, length of its vaginal portion, extent of patency of
cervical canal, position and direction of cervical axis in the lesser pelvis cavity,
the condition of the lower segment and wall thickness of vaginal part of the
cervix;
d) none of the mentioned above.
19. Nuchal tranclucency as a marker of chromosome abnormality is estimated at the

gestational age of:
а) 20–22 weeks;
b) 18–21 weeks;
c) 11–14 weeks;
d) 30–32 weeks.
20. CTG is deemed justified starting at the age of:

а) 20 weeks;
b) 32 weeks;
c) 14 weeks;
d) 12 weeks.
21. Physiological anemia during pregnancy is due to:

а) reduced erythropoiesis intensity;
b) hypervolemic autodilution;
c) hormonal changes;
d) decreased overall immune reactivity of the body.
22. Gestational sac can be visualized by ultrasound in the uterine cavity at the
age of:
а) 4 weeks and 3 days;
b) 5 weeks and 0 days;
c) 6 weeks and 2 days;
d) 7 weeks and 0 days.

1. Patient N. is pregnant. Her LMP date is known to be September, 11. Calculate
the estimated date of delivery.
154 Obstetrics
2. An external examination and internal obstetric examination yielded the follow-

ing dimenstions:
• distantia spinarum 26;
• distantia cristarum 28;
• distantia trochanterica 30;
• conjugata externa 21;
• Soloviov’s index 1.4;
• the Franck size 12;
• conjugata diagonalis 13.4;
• the rhombus of Michaelis: vertical size 13, horizontal size 12.
What is your conclusion?
NOTES
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• Chapter 5
FEMALE PELVIS IN OBSTETRICS.
FETUS IN LABOR
5.1. FEMALE PELVIS IN OBSTETRICS
Bony pelvis is a solid receptacle for internal genitals, the rectum, bladder and the
surrounding tissues. The structure of pelvis is an important issue in obstetrics.
The pelvis is divided into two distinct portions:
• greater pelvis (or false pelvis; pelvis major, Latin);
• true pelvis (true, or small pelvis; pelvis minor, Latin).
The border between the false and true pelvis runs through:
• the upper brim of symphysis and pubic bones in front;
• the innominate lines on the sides;
• the promontory at the back.
The plane passing between the false and true pelvis is the plane of pelvic inlet
(Fig. 5.1). The female true pelvis forms the birth canal, the passageway through which
the fetus is expelled during parturition.
The false pelvis is considerably wider than the true pelvis; it is bounded by:
• the alae of iliac bones on the sides;
• the last lumbar vertebrae in the back;
• the lower portion of abdominal wall in front.
The capacity of the false pelvis can change depending on contraction or relaxation
of muscles in the anterior abdominal wall.
The false pelvis is accessible for external examination; its dimensions can be deter-
mined quite accurately. The greater pelvis size serves as an indirect indication of the
Fig. 5.1. Female pelvis

156 Obstetrics
size of true pelvis, which is less accessible for immediate examination. Meanwhile it
is the true pelvis dimensions that are of greatest importance as the fetus is delivered
through the unyielding bony channel of the true pelvis.
The true pelvis is the bony part of the birth canal:
• the posterior wall of the true pelvis consists of the sacrum and coccyx;
• the lateral walls are formed by ischial bones;
• the anterior wall is formed by the pubic bones and symphysis.
The posterior wall of the true pelvis is twice longer than the anterior wall. The
upper portion of the true pelvis is a solid unyielding bony ring. In the lower portion
the pelvis walls are not solid; they have obturatory openings and ischiadic notches
bounded by two pairs of ligaments: sacrospinous and sacrotuberal.
5.1.1. Planes and dimensions of true pelvis

One should know the dimensions of the true pelvis so as to understand the act of
delivery as the movements performed by the fetal head during delivery are related to
how well its size and shape correspond to the size and shape of true pelvis planes
through which it passes.
True pelvis cavity is a space between the lesser pelvis walls and
NB! limited by the planes of pelvic inlet and outlet below and above.
The true pelvis cavity is in the shape of a of cylinder truncated from front to back
where the anterior part facing the pubis is almost three times shorter than the poste-
rior part facing the sacrum. Due to this shape, various parts of true pelvis cavity are
different shapes and dimensions. These parts are imaginary planes passing through
reference points on the internal surface of the true pelvis.
Four planes of the true pelvis are distinguished:
• the plane of the pelvic inlet;
• the plane of the greatest pelvic dimensions;
• the plane of the midpelvis (plane of least pelvic dimensions);
• the plane of the pelvic outlet.
The inlet plane is in the shape of an indented, transversely positioned ellipse that
corresponds to the sacral promontory (Fig. 5.2). The boundaries of true pelvis inlet are:
• the superior symphysis margin and superointernal margin of pubic bones;
• the innominate lines on the sides;
• the sacral promontory behind.
All these structures form the innominate (terminal) line.
The innominate (terminal) line separates the true pelvis cavity from the false pel-
vis, bounds the superior pelvis aperture, which is called the inlet to the true pelvis
cavity.
In the inlet, there are the direct, transverse and oblique diameters.
The anteroposterior diameter of the true pelvis inlet plane: the distance from the
most protruding point of promontory to the most protruding point of superointernal
symphysis margin. This dimension is called the obstetric, or true, conjugate. We
also distinguish the anatomical conjugate, the distance from the promontory to the
Chapter 5. Female pelvis in obstetrics. Fetus in labor 157
2
3
4
1
Fig. 5.2. Plane of true pelvis inlet: 1 — terminal line; 2 — anatomical conjugate, or diameter
recta; 3 — transverse diameter of true pelvis; 4 — oblique diameter of true pelvis
middle of superointernal symphysis margin. The anatomical conjugate is somewhat

larger than the obstetric conjugate, by 0.3–0.5 cm. The obstetric, or true, conjugate
is 11 cm. The distance from the middle of superior margin of the pubic arch to the
similar point of the promontory is 11.5 cm; it is called the anatomical conjugate.
The transverse diameter of the true pelvis inlet plane: the distance between the
outermost points of innominate lines is 13 cm.
Oblique diameters of the true pelvis inlet plane:
• right diameter: from the right sacroiliac joint to the left iliopubic eminence;
• left diameter: from the left sacroiliac joint to the right iliopubic eminence; each
of these sizes measures 12 cm.
In order to understand the direction of oblique pelvic diameters in a parturient
woman, one can practice the following technique: both palms are joined at a straight
angle, the palms facing upwards; the finger tips are brought to the pelvic outlet of the
reclining woman. The left hand plane corresponds to the left oblique pelvic diameter,
the plane of the right hand — to the right diameter.
The pelvic plane of greatest dimensions passes through:
• the middle of internal surface of symphysis pubis in front;
• the middle of laminae acetabuli on the sides;
• the junction of II and III sacral vertebrae behind.
In its shape, the pelvic plane of greatest dimensions resembles a circle.
Only two diameters are distinguished in the pelvic plane of greatest dimensions:
• the anteroposterior diameter in the pelvic plane of greatest dimensions—from the
junction of II and II sacral vertebrae to the middle of symphyseal inner surface;
it measures 12.5 cm;
• the transverse diameter in the pelvic plane of greatest dimensions—between the
middle of cotyloid cavities; it measures 12.5 cm.
There are no oblique diameters in the pelvic plane of greatest dimensions as the
pelvis does not have a solid bony ring in this area. Oblique diameters in the pelvic
plane of greatest dimensions are conventional; they measure 13 cm.
158 Obstetrics
The plane of least pelvic dimensions passes through:

• the inferior margin of symphysis pubis in front;
• the ischiadic spines on the sides;
• the sacrococcygeal symphysis behind.
The plane of least pelvic dimensions is of elongated oval shape; it has two diam-
eters: direct and transverse:
• the anteroposterior diameter in the pelvic plane of least dimensions runs from
the scarococcygeal symphysis to the inferior margin of symphysis (apex of pubic
arch); it measures 11–11.5 cm;
• the transverse diameter in the pelvic plane of least dimensions joins the spines of
ischial bones; it measures 10.5 cm.
Fetal head meets with most difficulty when passing the narrowest
NB! portions of the pelvis: the anteroposterior diameter and transverse
diameter in the plane of least dimensions.
The pelvic outlet plane passes through:
• the inferior margin of pubic arch in front;
• the inner surfaces of ischial tuberosities on the sides;
• the apex of coccyx behind.
It is the motility of the coccyx that ensures the major difference of the outlet plane
from other pelvic planes: it consists of two planes joining at an angle along the line
connecting ischial tuberosities.
Two diameters—anteroposterior and transverse—are distinguished in the pelvic
outlet plane:
• the anteroposterior diameter of the pelvic outlet plane runs from the apex of
coccyx to the inferior symphysis margin; it measures 9.5 cm. When the fetal
head passes through the outlet of pelvis, the coccyx moves away by 1.2 cm thus
enlarging the direct diameter to 11.5 cm;
• the transverse diameter of the pelvic outlet plane joins the inner surfaces of
ischial tuberosities; it measures 11 cm (Fig. 5.3).
Thus in the true pelvis inlet the greatest diameter is the transverse one.
Fig. 5.3. True pelvis outlet plane: 1 — anteroposterior outlet diameter; 2 — transverse outlet
diameter
In the pelvic plane of greatest dimensions the direct and transverse diameters are
equal. The greatest diameter is the conventionally accepted oblique diameter.
In the pelvic plane of least dimensions the direct diameters are greater than trans-
verse ones. Mean diameters of true pelvis planes are shown in Table 5.1.
Table 5.1. Mean diameters of major planes in the true pelvis, cm
Diameters Planes
inlet greatest dimensions least dimensions outlet
anteroposterior 11 12.5 11.5 9.5–11
transverse 13 12.5 10.5 11
oblique 12 – – –
Except for the pelvic outlet plane, the diameters of true pelvic planes are unavail-
able for immediate measurement, thus pelvic dimensions are estimated indirectly
judging by the reference points available for measurement.
5.1.2. Pelvic axis

All classical planes of the true pelvis are bounded by this or that symphysis point
anteriorly, and posteriorly — by various points of the sacrum or coccyx. The sym-
physis is considerably shorter than the coccyx and sacrum, so the pelvic planes join
in the anterior direction and separate in a fan-like fashion in the posterior direction.
If one joins the middle of all direct diameters of all pelvic planes, one obtains, rather
than a straight line, a line concave in front in correspondence with the concavity of
the inner sacral surface. This conventional line joining the centers of all direct pelvic
diameters is referred to as the pelvic axis. Its shape resembles a fishing hook (Fig. 5.4).
6
3
5
4
Fig. 5.4. Pelvic planes and axis: 1 — anatomical conjugate; 2 — true conjugate; 3 — anteroposterior
diameter of pelvic plane of greatest dimensions; 4 — anteroposterior diameter of pelvic plane of least
dimensions; 5 — anteroposterior diameter of pelvic outlet with the coccyx in normal position; 6 —
anteroposterior diameter of pelvic outlet with the coccyx bent back; 7 — pelvic axis
160 Obstetrics
During labor the fetus passes along the birth canal following the
NB! pelvic axis.
5.1.3. Pelvic inclination

The position of bony pelvis in space is conventionally referred to as pelvic inclina-
tion (Fig. 5.5).
45–55°
Fig. 5.5. Pelvic inclination
Pelvic inclination is the angle between the inlet plane, and the
NB! horizontal plane when the body is in vertical position.
The size of this angle, on the one hand, is determined genetically, which
explains, in particular, the tradition of various positions for parturient women
in different nations. On the other hand, the angle of pelvic inclination can
change depending on the specific living conditions of a particular woman; fac-
tors like early sitting, early heavy manual labor, sedentary lifestyle, wearing high
heels daily, spinal curvature, injury etc. have their impact on the formation of a
woman’s skeleton.
In women of European race the angle of pelvic inclination in an upright position
is 45–55°.
This angle varies substantially upon changes in body position. For instance, it
can decrease if a recumbent woman draws her thighs to the abdomen to the utmost,
which raises the pubis. The angle of pelvic inclinations can be decreased if the woman
is semi-recumbent or sits on her haunches. The angle of pelvic inclination can be

increased if a bolster is put under the small of the back of a recumbent woman: this
leads to downward deflection of the pubis.
5.2. FETUS AS AN OBJECT OF LABOR
Fetus as an object of labor should be mature, carried to full term. The notion of
«term» is determined by the length of time the fetus stays in the uterus from concep-
tion to delivery. Maturity of the fetus is determined by a number of features of fetal
physiological development.
Mature fetus and term fetus are different things!

NB!
A fetus is regarded as full-term if it was born at 37 to 42 weeks gestation. The
mean birth weight of a term fetus is 3500 g, its length — 50 cm.
A mature fetus has a well developed subcutaneous fat, pink skin, solid cartilage
in the ear and nose, head hair 2–3 cm long. The lanugo hair remains only in the
area of the shoulder girdle and shoulder blades; the umbilical ring is situated mid-
way between the pubis and xiphoid process. In boys the testicles are descended in
their usual place in the scrotum; in girls the clitoris and labia minora are covered
with labia majora.
The fetal head deserves the closest attention, for the following reasons:
• during childbirth the head, due to its size and hardness, meets with most
opposition on the part of the maternal passages;
• the density and motility of cranial bones determines, to a great extent,
the possibility of injury to the mother (injury of the birth canal) and fetus
(intracranial hemorrhage);
• there are reference points on the head (the sagittal suture on the skull, the
anterior and posterior fontanelles) used for the purpose of diagnostics during
childbirth as head presentation occurs in 96% of all childbirths.
The head of a mature fetus consists of the facial and cranial parts. The cranial
part has 7 bones: two frontal bones, two temporal bones, two parietal bones and one
occipital bone (Fig. 5.6). The bones of facial skull have no considerable impact on
the mechanism of childbirth.
The head of a term fetus has certain features. Facial bones of the fetus are firmly
connected. The bones of the cranial part are connected with fibrous membranes—
sutures, which provide for certain mobility and displaceability of bones in relation
to one other. The space where the sutures overlap is called fontanelle. The bones in
the area of fontanelles are also connected with fibrous membranes. When the head
passes through the birth canal, the sutures and fontanelles allow considerable shift-
ing and sliding of each bone to accommodate the size and shape of maternal pelvis
as cranial bones in a fetus are less dense than in infants. This intrapartum process
is termed molding; it is extremely important for a successful passage of the head
through the birth canal.
162 Obstetrics
Fig. 5.6. Skull of a newborn: a — lateral view; b — overview: 1 — anterior fontanelle; 2 —

posterior fontanelle; 3 — sphenoid fontanelle; 4 — mastoid fontanelle; 5 — frontal bone;
6 — occipital bone; 7 — parietal bone; 8 — temporal bone; 9 — frontal suture; 10 — coronal
suture; 11 — sagittal suture; 12 — lambdoid suture
Four sutures are of importance in obstetrics:

• sagittal suture passing between the parietal bones; in front the suture merges into
the anterior fontanelle, behind — into the posterior fontanelle;
• frontal suture is situated between the frontal bones; it has the same direction as
the sagittal suture;
• coronal suture joins the frontal bones with parietal bones; it passes perpendicular
to the sagittal and frontal sutures;
• lambdoid suture joins the occipital bone and parietal bones.
The area of suture junction contains fontanelles (fontanelle is space free of ossified
tissue). Two fontanelles are of importance in obstetric practice:
• Anterior (large) fontanelle bregma is at the point of joining of the sagittal, frontal
and coronal sutures, it is of rhomboid shape. Four sutures fan out from the
anterior fontanelle:
– frontal suture goes anteriorly;
– sagittal suture goes posteriorly;
– the corresponding parts of the coronal suture go to the right and left.
• Posterior (small) fontanelle lambda is a small concavity of triangular shape. Three

sutures run from the posterior fontanelle:
– sagittal suture goes anteriorly;
– the corresponding parts of the lambdoid suture go to the right and left.
There are four fontanelles that are of secondary importance: two pairs on the right
and left side. The sphenoid fontanelle (pterion) is at the junction of the parietal, frontal
and temporal bones. The asterion is found at the junction of the parietal, temporal
and occipital bones. These fontanelles are of no diagnostic significance.
The fetal head has other landmarks, too; they are the occipital protuberance, two
parietal tubers and two frontal tubers.
Seven diameters are distinguished in the fetal head: two transverse

NB! and five longitudinal ones. Longitudinal diameters include three
oblique ones. In the cerebral portion of fetal skull, seven bones,
six fontanelles, five tubers and four sutures are distinguished.
Head dimensions in a mature fetus:

• suboccipitobregmatic diameter extends from suboccipital fossa to the middle of
anterior fontanelle; it measures 9.5 cm; the corresponding head circumference
is 32 cm;
• suboccipitofrontal diameter extends from the suboccipital fossa to the hairline
in the brow (anterior angle of the anterior fontanelle); it measures 10 cm; the
circumference is 33 cm;
• occipitomental diameter extends from the chin to the occipital protuberance; it
measures 13.5 cm; the circumference is 42 cm;
• occipitofrontal dimension extends from the glabella to the occipital protuberance;
it measures 12 cm; the circumference is 34 cm;
• vertical dimension extends from the middle of anterior fontanelle to the hyoid
bone; it measures 9.5 cm; the circumference is 32 cm;
• biparietal diameter is the greatest distance between outermost points of parietal
tubers; it measures 9.5 cm;
• bitemporal diameter is the distance between the outermost points of the coronal
suture; it measures 8 cm.
All dimensions of the fetal head in a full term fetus are shown in Table 5.2. Sagittal
dimensions of a fetal head are shown in Fig. 5.7.
In a term fetus, three diameters are the same, measuring 9.5 cm:
NB! suboccipitobregmatic, vertical, and biparietal diameter.
The following dimensions are distinguished in the trunk of a full term fetus:
• bisacromial diameter (shoulders) measuring 12 cm, in the circumference —
35 cm;
• bisiliac diameter (buttocks) measuring 9 cm, in the circumference — 28 cm.
The following terms are used for a detailed description of the way the fetus is
positioned inside the uterus during pregnancy and childbirth: fetal lie, presentation,
attitude, position, variety of position (visus, Latin).
164 Obstetrics
Table 5.2. Head dimensions of a full term fetus
Dimensions Value, cm Corresponding circumference, cm

suboccipitobregmatic diameter 9.5 32
suboccipitofrontal diameter 10 33
occipitomental diameter 13.5 42
occipitofrontal dimension 12 34
vertical dimension 9.5 32
biparietal diameter 9.5 –
bitemporal diameter 8 –
Fig. 5.7. Skull of a newborn (lateral view). Sagittal cranial dimensions: 1 —

suboccipitobregmatic diameter; 2 — suboccipitofrontal diameter; 3 — occipitomental
diameter; 4 — occipitofrontal dimension; 5 — vertical dimension
Fetal lie (latin — situs) is the relationship of the long axis of the fetus to the long
axis of the mother. Fetal axis is an imaginary line passing along the fetal back, from
the occiput to the coccyx. The long axis of the mother is an imaginary line passing
from the internal cervical os to the middle of the fundus of uterus body.
Fetal lie is the relation of longitudinal fetal axis to longitudinal axis

NB! of uterus.
Fetal lie can be longitudinal, transverse or oblique.
• Longitudinal lie is a physiological position when the fetal long axis is in line with
the mother›s uterus with its head down (Fig. 5.8).
• Transverse lie is a position when the fetal long axis and the mother’s long axis
cross at a straight angle while the head and breech of the fetus are above the crests
of iliac bones (Fig. 5.9).
• Oblique lie occurs when the fetal long axis and the maternal axis cross at an acute
angle while the head or pelvic pole is situated in one of iliac fossas (Fig. 5.10).
Transverse and oblique lie are noted in 0.5% of all cases; they are regarded as ab-
normal as they are associated with obstruction for fetal passage along the birth canal.
Fetal presentation (latin — presentatio) refers to which anatomical part of the
fetus is leading, that is, closest to the pelvic inlet of the birth canal. The fetal part
which descends first to the true pelvis plane during labor is called the presenting part.
Fig. 5.8. Longitudinal fetal lie
Fig. 5.9. Transverse fetal lie

166 Obstetrics
Fig. 5.10. Oblique fetal lie
Fetal presentation is the relation of the large fetal part (head and
NB! pelvic pole) to pelvic inlet1.
One distinguishes cephalic presentation when it is the head that leads the way and
finds itself over the pelvic inlet, and breech presentation when the pelvic pole is above
the inlet to true pelvis cavity. The third type of presentation is shoulder presentation
in a transverse fetal lie. In Russia, in case of an abnormal fetal lie (transverse or
oblique) obstetricians consider that there is no presenting part.
The notion of fetal attitude (latin — habitus) describes the relationship of fetal
body parts to one another.
Fetal attitude is the relation of fetal head and limbs to the trunk.
NB!
• Normal fetal attitude is when the head is tucked down to the chest with its arms
and legs drawn in towards center of chest — flexed attitude. In this attitude the
fetus is of ovoid (egg-like) shape and takes up the least space in the uterus.
• Extended (deflexed) attitude is an abnormality; it depends on multiple factors:
length of the umbilical cord, general condition of the fetus (presence/absence of
hypoxia), presence of tumors or other uterine malformations, etc. In some cases
extended attitude results in labor complications. This is an infrequent condition.
Fetal position (Latin — positio) is the relation of fetal back to the right or left side
of the uterus. Two positions are distinguished:
• first: fetal back facing the left side of uterus;
• second: fetal back facing the right side of uterus.
Fetal position is the relation of fetal back to the left (I position)
NB! or right (II position) side of the uterus.
1 In English-speaking countries obstetricians distinguish three types of presentation: shoulder

presentation comes in addition to cephalic and breech. Russian obstetricians defi ne shoulder presentation
as transverse lie.
In transverse and oblique lie the position is determined according to the fetal head:
• the head is to the left of the uterus — fi rst position;
• the head is to the right of the uterus — second position.
The variety of the position is the relationship of fetal back to the anterior or pos-
terior side of the uterus. The fetal back is turned not only to one of lateral uterine
sides, but somewhat to the front or to the back:
• anterior position — fetal back is turned somewhat anteriorly;
• posterior position — fetal back is turned somewhat posteriorly.
Variety of fetal position is the relation o fetal back to the anterior

NB! (anterior variety) or posterior (posterior variety) uterine wall.
If the fetal back is turned to the front, we speak of anterior variety, if to the back—
posterior variety. In English-speaking countries obstetricians use the relationship
of fetal occiput, or rather, of the posterior fontanelle, to the corresponding uterine
walls. Thus the anterior variety first position corresponds to left occipitoanterior
(LOA) position.
In the first half of pregnancy (and sometimes later, for instance, if polyhydramnios
develops) the fetus, while of relatively small dimensions, may change its lie in the
uterus. This is called an unstable fetal lie. As it develops, the fetus assumes a more
stable lie, which is helped along by the abdominal wall, the pregnant uterus tone,
the volume of amniotic fluid, etc.
By the onset of labor the longitudinal lie, once assumed, does not change.
Transverse (oblique) lie, after the onset of labor, sometimes changes to longitudinal
if there is polyhydramnios. Physiological (flexed) attitude persists in a viable fetus
until it is born.
REMEMBER!
The true pelvis cavity is a space contained within the true pelvis and bounded by
the inlet and outlet planes from above and below.
Four planes of the true pelvis are distinguished:

• inlet plane;
• the plane of greatest pelvic dimensions;
• the plane of least pelvic dimensions;
• outlet plane.
The head meets with the greatest difficulties when it passes through the true pelvis
in the anteroposterior diameter of the inlet plane, and in the transverse diameter in
the plane of least pelvic dimensions.
The imaginary line connecting the centres of all direct pelvic diameters is called the
pelvic axis. During childbirth the fetus passes through the birth canal following the
direction of the axis pelvic plane.
Pelvic inclination is the angle between the pelvic inlet plane and horizontal plane.
168 Obstetrics
Maturity of the fetus and its being full term does not mean the same thing!
Lie of the fetus is the relationship of longitudinal fetal axis to the uterine longitu-
dinal axis.
Presentation of the fetus is the relation of the head or pelvic pole to the inlet to
the small pelvis.
Attitude of the fetus means the relationship of the fetal head and limbs to the trunk.
Fetal position is the relation of the fetal back to the left (first position) or to the
right (second position) side of the uterus.
Variety of the position is the relation of the fetal back to the anterior (anterior
variety) or posterior (posterior variety) uterine wall.
CONTROL QUESTIONS
1. What are the greater and true pelvises?

2. What is the plane of the true pelvis?
3. What are the diameters in the inlet plane of the true pelvis?
4. What are the diameters in the plane of greatest pelvic dimensions?
5. What are the diameters in the plane of least pelvic dimensions?
6. What are the diameters in the outlet plane of the true pelvis?
7. What is the pelvic axis?
8. What is the angle of pelvis inclination?
9. Are the notions of maturity of the fetus and its being full term the same things?
10. Which part of the fetus has the greatest impact on the course of delivery?
11. What are the parts of the head in a full term fetus?
12. How are the bones of the cranial part of the skull connected?
13. What are fontanelles?
14. What diameters of the head in a full term fetus should the obstetrician know?
15. What obstetric terms are used to give an accurate description of the way the
fetus is positioned in the uterus?
16. Can the fetal lie in the uterus change in the course of pregnancy?
CHECK YOURSELF!
Level 1. Test
1. Using the diagonal conjugate size one can calculate:

a) transverse diameter of the inlet plane;
b) true conjugate;
c) external conjugate;
d) anteroposterior diameter of the plane of greatest pelvic dimensions.
2. The transverse diameter of 10.5 cm corresponds to a transverse diameter of:

a) the plane of true pelvis inlet;
b) the plane of greatest pelvic dimensions;
c) the plane of least pelvic dimensions;
d) the plane of true pelvis outlet.
3. The true conjugate should be no less than:

a) 10 cm;
b) 11 cm;
c) 14 cm;
d) 12 cm;
e) 13 cm.
4. The true conjugate cannot be calculated on the basis of:

a) diagonal conjugate;
b) vertical diagonal of the rhombus of Michaelis;
c) horizontal diagonal of the rhombus of Michaelis;
d) external conjugate.
5. The inferior margin of symphysis pubis, ischial spines and sacrococcygeal symphysis
bound the following true pelvis planes:
a) inlet plane;
b) plane of least dimensions;
c) plane of greatest dimensions;
d) outlet plane.
6. Fetal attitude is:

a) relationship of fetal limbs and head to the trunk;
b) relationship of fetal head to the trunk;
c) interrelations of various fetal parts;
d) interrelations of fetal legs and buttocks.

1. A pregnant woman presents to a maternity welfare clinic; a vaginal examination
reveals that the diagonal conjugate is 12 cm, Soloviov’s index — 1.5. Calculate the
true conjugate and verify it by three other ways.
2. An external obstetric examination of a pregnant woman with 35 week gestation
revealed that the uterus was of ovoid shape transversely extended. What is the
presumptive diagnosis?
NOTES
_________________________________________________________________
_________________________________________________________________
_________________________________________________________________
• Chapter 6
ORIGINS OF LABOR ONSET
6.1. MECHANISMS OF UTERINE CONTRACTIVE ACTIVITY
Labor is a process completing the pregnancy; it consists in expulsion of the fetus

and afterbirth from the uterine cavity through the birth canal ( after the fetus has
attained viability, after 22 weeks gestation).
Labor is a complex physiological genetically programmed process, an uncondi-
tioned reflex whose regulation is provided by virtually all organs and systems in the
female body. For various reasons pregnancy can be terminated at any stage. The fetus
can only survive once it has acquired certain anatomical and functional developmen-
tal features that depend on multiple conditions.
A fetus is considered viable starting at 22 weeks gestation when

NB! its weight is 500 g, and its length is 25 cm.
Until 22 weeks gestation the fetus is not viable. Termination of pregnancy prior to
22 weeks gestation is termed abortion rather than delivery.
Labor at term, normal labor and physiological delivery is considered as such when
it occurs at an age of 37 to 42 weeks, and a mature fetus is born whose adaptation
to external conditions is easy and fast.
A woman who gives birth for the first time is referred to as primiparous, the one
who has experienced one or more previous childbirths — multiparous. During labor
the woman giving birth is commonly referred to as parturient woman.
6.2. ONSET OF LABOR AND REGULATION OF UTERINE

ACTIVITY
The factors triggering the onset of labor and regulating the uterine activity have
not been studied well enough yet. Multiple theories were put forward to shed
light on the mechanism of labor onset: the theory of foreign body, the mechani-
cal, placental, immune and other theories; most of them are of merely historical
interest now.
In 1940–1950s investigations undertaken by Russian scientists broke new ground as to
the onset of labor and the way it is regulated; they substantiated the theory of neurohu-
moral regulation of the uterine function including labor (A.P. Nikolaev, A.I. Petchenko,
L.S. Persianinov, N.L. Garmasheva, I.I. Jakovlev and others). According to this theory,
the onset of labor is associated with changes taking place in the CNS and the blood of
the pregnant woman. The leading role here is played by the hypothalamus, pituitary
gland, and the limbic system (amygdoid bodies, etc.). The ovaries, placenta and other
glands of internal secretion have a regulatory effect on the uterine motor function, too.
Chapter 6. Origins of labor onset 171
The uterus itself as an effector plays a decisive role in the nature of labor and, by way
of feedback principle, it has an influence on all competent systems.
Nowadays it is the genetic program that is considered the foremost factor trig-
gering the onset of labor at term; the genetic program provides for a completion of
pregnancy once the fetus has achieved maturity.
Pregnancy and childbirth are the main stages of the reproductive function.
Physiological processes associated with conception, carrying and delivering the fe-
tus take place involving the uterus, its contractile apparatus represented by a host of
smooth cells or myocytes. A coordinated function of these cells ensures that the uterus
as a receptacle for the fetus is in appropriate tone, provides for uterine contractility
as an accelerator partus, uterine involution in the postpartum period and restoration
of fertility. Like pregnancy, the act of childbirth is a genetically determined function
of the entire body in its continuous interrelation with the ambience. Maternal and
fetal mechanisms of regulation are considered to be the source of regulation of the
uterine contractile apparatus.
Fetoplacental complex (hypothalamus-pituitary axis, fetal adre-

NB! nals, placenta, fetal membranes) plays an active role in labor
induction and development.
6.2.1. Regulation of uterine activity

According to physiology of visceral systems, the regulation of uterine activity is
effected through three basic mechanisms:
• humoral (biologically active substances including hormones);
• neurogenic (central and vegetative nervous system);
• local (myogenous).
A coordinated function of these mechanisms at each stage of the reproductive
process occurring in the female body (prepuberty, stabilization of menstrual function,
pregnancy and labor) ensures a contractile myometrial activity in agreement with the
function the uterus is performing at the given stage.
Nowadays the main role in the development of uterine activity during pregnancy and
childbirth is ascribed to humoral factors rather than to the nervous system (Fig. 6.1).
UTERINE
ACTIVITY
Nervous Myogenous
Humoral
Fig. 6.1. Mechanisms of uterine activity regulation

172 Obstetrics
6.2.1.1. Humoral regulation
As pregnancy progresses, the blood and tissues of the maternal body experience
a gradual accumulation of bioactive substances (estrogens, progesterone, adrenalin,
noradrenalin, acetylcholine, oxytocin, serotonin, prostaglandins, histamine and oth-
ers). A change in concentration of these substances affects both the excitability of
various parts of the central and vegetative nervous system innervating the uterine
musculature, and the content of calcium ions in myocytes (an indirect mechanism
triggering the uterine activity). Before childbirth, there is an increase in the produc-
tion of uterotonic compounds providing for labor contractions (oxytocin, prostaglan-
dins, serotonin and others).
It was established that fetus-released oxytocin, serotonin, bradykinine, histamine
and other bioactive substances have a proven effect on the induction of the childbirth
process and regulation of uterine activity.
Upon certain changes in the ratio of hormones and bioactive substances, an
alternating excitation of sympathetic and parasympathetic innervations centers is
formed; reflex excitability of the uterus arises. Neurophysiological changes occur in
the myometrium forcing the uterus to perform regular contractions—labor contrac-
tions (Fig. 6.2).
Biologically Enhanced synthesis

active substances of biologically active
substances in maternal body
Change in excitability
of CNS and VNS that Elevated
innervate the myometrium
Enhanced
uterine excitability
CONTRACTIONS
Fig. 6.2. Humoral mechanism of uterine activity regulation
6.2.1.2. Neurogenic regulation
Neurogenic regulation is provided for by the vegetative nervous system whose

function is subordinate to the cerebral cortex and limbic structures. All parts of the
uterus have double vegetative innervations:
• the sympathetic nervous system innervates the powerful external myometrial
layers in the fundus and body of the uterus;
• the parasympathetic nervous system innervates the internal (subvascular) layers

most prominent in the lower segment and cervix of uterus.
Several groups of receptors are present in the uterine muscle:
• in the body of uterus where the myometrium is the strongest, α- and
β-adrenoreceptors predominate in longitudinal muscular fibers;
• in the lower segment — M-cholinergic and D-serotonin receptors in circular
muscular fibers;
• in the cervix of uterus: chemo-, mechano-, and baroreceptors.
In the process of pregnancy, a physiological «desympathization» of the uterus
occurs due to a decrease in the number of sympathetic fibers and production of
catecholamines.
The dominant of childbirth is formed in the CNS prior to the onset of
labor: an excitation focus in the cerebral cortex, which suppresses responses
that are of lesser significance at this stage, and ensures the progress of labor.
Intensiveness of interhemispheric connections grows; they enhance the coordi-
nation of all systems of the body. The number of sympathetic fibers increases,
as well as production of catecholamines. Alternating excitation of sympathetic
and parasympathetic areas induces excitation and contraction of corresponding
myometrial layers, which is manifested by regular contractions of increasing
strength and duration.
Myometrium is activated through alpha-adrenoreceptors; it is sup-

NB! pressed through beta-adrenoreceptors.
6.2.1.3. Myogenic regulation

At all stages of reproduction, the muscular wall of the uterus, from the functional
point of view, is a homogenic structure whose structural and functional unit is the
myocyte, a smooth muscle cell. Myocytes form smooth muscle fibers — the basic
functional unit of the myometrium. Under the impact of the vegetative nervous sys-
tem and bioactive substances, myocytes can modify their tonic and phasic activity
thus generating phasic contractions while tonic contractions persist.
6.2.2. Physiology of muscle contraction

Contractile activity of myocytes depends on the concentration of free calcium ions
in the interfibrillar space.
The key role played by calcium in a number of biological reactions was first shown
as early as 1883 when Sydney Ringer noted that isolated frog muscles did not contract
in distilled water. For a muscle to respond with contraction to electric stimulation,
it requires the presence of calcium ions in the surrounding medium.
Myosin light-chain kinase stimulates an increase in calcium concentration; the
process is calmodulin-mediated.
Calmodulin is a quite large protein consisting of 148 amino-acid residues.
Like cyclic adenosine monophosphate, calmodulin was found in practically all
174 Obstetrics
studied cells. In smooth muscle cells it functions as the primary intracellular

receptor Ca 2+. Calcium itself, or rather, its ions, are bound with the calmodu-
lin protein inside the cell; calcium is one of the main intracellular secondary
messengers.
Uterine myocytes contain potential-sensitive and receptor-regulated ion channels:
calcium channels, sodium channels and potassium channels. The flux of sodium
and calcium ions into the cells along corresponding channels generates the electric
potential causing myocyte contraction.
Consequently, the contractile activity of myocytes increases upon an increase of
free Ca2+ ions concentration in them, which is achieved by increasing the influx of
Ca2+ ions into the cell at the expense of opening calcium channels and reducing the
effectiveness of calcium pump function; the pump forces Ca2+ ions into the intracel-
lular calcium stores or the extracellular space. Reduction of influx of Ca2+ ions into
the myocyte occurs due to closing calcium channels or activation of calcium pumps
removing Ca2+ ions into the stores (Fig. 6.3).
Unlike potential sensitive channels, receptor-regulated ion channels of myocyte
membranes change their permeability for Ca2+ ions upon a direct exposure to a bio-
active substance with specific receptors situated on the muscle cell surface (oxytocin
and M-cholinergic receptors, and others).
Muscular contraction involves the following series of events. In response to an
electric impulse arriving to the muscle along the nerve cell axon, stores of Ca2+
ions (membrane cisterns) open inside the muscle cell (myofibril). In the store the
concentration of Ca2+ ions can exceed their cytoplasm concentration a thousand
times, and more. The released calcium binds to troponin C protein, which is bound
to actin filaments lining the inner cellular surface. Troponin acts as a blocker im-
peding the sliding of myosin filaments along actin filaments. As a result of calcium
binding to troponin, the block detaches itself from the filament, myosin slides
along actin, and the muscle contracts. As soon as the act of contraction is over,
calcium ATPases — special proteins — pump calcium ions back into intracellular
stores (Fig. 6.4).
Initiation of smooth musculature contraction can take place in the following way.
Calcium ions released in response to an outer signal (nerve impulse) bind to calmod-
ulin; calcium binding to calmodulin activates it in the same way as cyclic adenosine
monophosphate stimulates the function of protein kinase. After that calmodulin
interacts with kinase enzyme and activates it. The kinase-calmodulin complex binds
to actin bringing it to a functional condition. As a result, smooth muscles contract.
Calcium-mediated route of the signal to striated skeletal muscles is longer; however,
smooth muscles, in contrast to striated ones, can remain in contracted state for
longer periods of time.
Other signals, apart from nerve impulses, can affect the concentration of intracel-
lular calcium. For instance, adenosine monophosphate can do this: in response to
appearance of adrenalin in the blood followed by an increase in cyclic adenosine
monophosphate in cardiac muscle cells, calcium ions are released, which results in
faster heartbeat.
Substances having an influence on calcium may be contained in the cellular
membrane directly. As we know, the membrane consists of phospholipids among
а Opening connecting T-tube lumen Plasma membarne
with extracellular ambience of muscle fiber
Transverse Segments of sarco- Myofibrils

tubules plasmatic reticulum
Sarcoplasmatic
b reticulum
Myofibrils
Plasmatic membrane
Cytosol
Transverse tubules
Lateral cisterns
Mitochondrion
c Action Longi-
tudinal Longi-
potential tudinal
tubule
system tubule
system Sarcolemma
Terminal Ryanodine
cistern receptor (RyR)
Dihydropyridine
receptor (DHPR)
Myosin Actin
Fig. 6.3. The myocyte and calcium channels: a — structure of muscular tissue; b — structure
of myocyte; c — mechanism of muscle contraction
which phosphoinositol-4,5biphosphate plays a particular role. Besides inositols, the

molecule of phosphoinositol-4,5biphosphate contains two long carbohydrate chains
consisting of 20 and 17 carbon atoms. Under the impact of certain extracellular signals
176 Obstetrics
Opening
Electric Ca2+
membrane
impulse release
cisterns
Са2+ binding
to calmodulin
Pumping Са2+
into intracellular Са2+ binding
cisterns to troponin C
Myocyte Actin gliding Eliminating

contraction along myosin the actin
filament block
Fig. 6.4. Mechanism of myocyte contraction
and under the control of G proteins they get detached thus forming two molecules:
diacylglycerin and inositol triphosphate. The latter participates in intracellular cal-
cium release.
Oxytocin can stimulate uterine contraction without calcium involvement, by way
of myosin phosphatase inhibition, which, in its turn, leads to enhanced phosphoryla-
tion of the myosin molecule.
Research has shown that contractile uterine activity is regulated by three systems:
• the system of uterine contractility activation;
• the system of uterine contractility inhibition;
• the system of modulating the properties of uterine monocytes.
Each system involves humoral, neurogenic and local mechanisms. The number of
components in a system and the power of each system depend on the stage of the
reproductive process.
• the system of uterine contractility activation involves the action of prostaglandins,
oxytocin, histamine and the uterine pacemaker (automatic increase of calcium
permeability of the surface membrane of myocytes).
• the inhibition system involves mechanisms of prostaglandin synthesis block,
β-adrenoreceptor inhibiting mechanism, progesterone mechanism, methyl
xanthine and calcium-inhibiting mechanisms.
• the system of myocyte properties modulation involves the action of estrogens,
progesterone, prostaglandins, extension of the uterus by the growing fetus,
endogenic modulators of adrenal function. There are changes in the morphological,
biochemical and physiological parameters; ion transport, receptor affi nity on the
membraneous surface of cells, the nexus number between myocytes, the intensity
and nature of innervations — all these are subject to change. Furthermore, one
half of modulators activate the contractile activity of the uterus while the other
half inhibits it.
Besides, there is a system of myometrium repair where progesterone can participate
as one of its components.
Changes in the condition of adrenoreceptors, ion- and receptor-

NB! controlled calcium channels in myocytes affect the contractile
activity of the uterus; these changes can be achieved using sub-
stances that stimulate or inhibit myocyte contractility.
Childbirth can begin once the myometrium, the cervix and the systems regulating
uterine contractility are ready. The fetus is the driving force of this process.
It was shown that the fetus plays the key role in initiating term labor in mam-
malians. However, in humans the role of the fetus in labor initiation has not been
explained satisfactorily.
In sheep term labor starts upon activation of the hypothalamic-pituitary-adrenal
axis. This activation results in release of adrenocorticotropic hormone and cortisol.
Fetal cortisol promotes estradiol production and suppresses progesterone production
due to the effect of placental 17a-hydroxylase on placental metabolism of cortisol.
A shift in the progesterone/cortisol ratio stimulates production of placental oxytocin
and prostaglandins (especially prostaglandin F2a). If there is no increase in fetal
ACTH or cortisol, labor does not set on.
In humans spontaneous onset of labor depends on the aggregate and consecu-
tive action of paracrine/autocrine hormones united in the so called parturition
cascade that provides for uterine contractions: prostaglandin E2; prostaglandin EM,
13, 14-dihydro 15-keto-prostaglandin E2, prostaglandin F2a; prostaglandin FM, 13,
14-dihydro 15keto-prostaglandin E2a (Fig. 6.5).
In some measure, activation of the uterus is promoted by dehydroepiandrostendiol
production by fetal adrenal glands, which undergoes conversion to estradiol and es-
triol in the placenta. Placental estriol stimulates production of prostaglandin F2a by
the mother (most probably, in the decidual tissue), formation of prostaglandin and
oxytocin receptors and gap junctions (Fig. 6.6).
Inhibitors Uterotropins Uterotonics Involution

Progesterone Estrogen Prostaglandins Oxytocin
Prostacyclin ? Progesterone Oxytocin ? Thrombin
Relaxin ? Prostaglandins
Uterine contractility
Nitric oxide ? Corticotropin-

Parathyroid hormone- releasing hormone
related peptide
? Corticotropin-
releasing hormone
? Human placental
lactogen
Time
Phase 0 Phase 1 Phase 2 Phase 3
(Quiescence) (Activation) (Stimulation) (Involution)
Parturition
Fig. 6.5. Regulation of uterine activity (Adapted from Challis J.R.G., Gibb W. Control of
parturition // Prenat. Neonat. Med. — 1996. — Vol. 1. — P. 283. — Taylor and Francis Ltd.)
178 Obstetrics
Fig. 6.6. Gap junction. Electronic photography (From Buhimischi C.S. et al. Forces
of labor // Fetal and Maternal Medicine Review. — 2003. — Vol. 14. N. 4. — P. 273–307)
In humans, no antenatal decrease in progesterone level was noted, that is, initia-
tion of labor does not require lower progesterone concentrations. However, judging
by recent findings, in humans we can suppose the presence of so called functional
progesterone withdrawal: there is a reduction in progesterone receptor concentration
as well as a shift in the ratio of progesterone receptor type A and B in the myome-
trium and fetal membranes.
Prostaglandins take part in initiation of labor; their synthesis increas-

NB! es drastically shortly before the onset of labor. Prostaglandins are
produced by uterine tissue, amnion, chorion, decidual tissue and
the fetus.
Significant differences in the concentration of oxytocin receptors in the myometrium

of uterine fundus, in the lower segment and cervix were revealed; the fundus shows con-
siderably greater concentrations of oxytocin receptors, as well as greater concentrations
of the muscular component (over 70% in the fundus and less than 20% in the cervix).
The amount of oxytocin receptors in the myometrium increases 100–200 times
during pregnancy reaching its peak before childbirth. At the same time, the uterus
becomes increasingly responsive to the circulating oxytocin. In humans, oxytocin re-
ceptors with high affinity were found in the amniotic sac and decidua parietalis. It can
be supposed that during delivery oxytocin plays a double role. First, oxytocin stimulates
uterine contractions directly via receptors. Second, oxytocin stimulates the production
of prostaglandins by the amnion and decidual membrane acting in an indirect way.
Indeed, even with adequate uterine activity labor induction in term pregnancy is only
effective if oxytocin infusion is accompanied by enhanced prostaglandin production.
Binding of oxytocin to specific receptors leads to phospholipase C activation. In its
turn, phospholipase C increases the concentration of intracellular calcium by activat-
ing intracellular calcium release from stores and promotes the influx of extracellular
calcium into the cell. Activation of phospholipase C by oxytocin can be impeded by a
high concentration of cyclic adenosine monophosphate. The growth of calcium con-
centration is stimulated by myosine light chain kinase and is calmodulin-mediated.
The process of fetal maturation and maternal signals regulating the circadian
rhythm are believed to play an important role. In most mammalians a distinct fluc-
tuation of uterine activity is noted: activation of uterine activity at night-time.
Research has suggested other explanations for the emergence and development
of uterine contractility. The myometrium is regarded as a single-layer structure as
smooth muscle fibers change their direction from one portion of uterine muscle to
another; that is, they are three-dimensional. The uterus consists halfway of connec-
tive tissue randomly interlaced with smooth muscle bands and fibers. The stroma of
connective tissue provides for uterus extension following a contraction. According to
recent research, the main role in the development of labor may be played by the cervix
which produces specific proteins prior to labor.
Prior to the onset of labor, oxidative phosphorylation (Krebs cycle), a more ef-
fective process for production of adenosine triphosphate, begins to dominate over
β-oxidation of fatty acids and anaerobic glycolysis in the mitochondria of uterine
myocytes. Before childbirth, the contractile apparatus of the myocyte (actin and
myosin) extends filling the entire cell, which appears dark under electron microscopy.
This cell is ready for effective functioning, and adenosine triphosphate ensures the
work of potential-sensitive myocyte channels — ion transport in the process of con-
traction. In normally proceeding labor «dark» myocytes dominate over «light» ones
(80% and 20%, correspondingly).
Billions of myocytes of different uterus parts are connected with highly perme-
able intercellular contacts and desmosomes; during a contraction they are involved
into the contraction all at the same time forming in the uterine cavity a force vector
aimed at overcoming the cervical «seal». There is an opinion that the mouth of the
womb opens due to blood storage in the cervix whose structure in childbirth is that
of a cavernous body. This process is triggered by protein(s) intensively researched
over recent years.
The properties of myometrium change during pregnancy: the extent of automatism
and conductivity decrease, sensitivity to oxytocin, serotonin, histamine, adrenalin as
stimulators of uterine contractions reduces; the number of β-adrenoreceptors grows.
On the one hand, the uterus ensures the bearing of the fetus, its growth and nutri-
tion; on the other hand, it prepares the contractile apparatus for labor (the systems
of activation and inhibition of uterine contractility).
Before childbirth the capacity of myocytes for automatism and their sensitivity to
bioactive substances (oxytocin, serotonin, histamine, prostaglandin F2a and prosta-
glandin E2, etc.) increase. During this period, due to hypoxia or other causes, the
fetus begins to produce the endogenous β-adrenergic blockers, dopamine and other
catecholamines, which causes enhanced prostaglandin production in maternal and
fetal tissues. At the same time, the cervix ripens, and the obturative mechanism
resolves («cervical seal»).
The onset of labor is a genetic signal occurring in limbic structures
NB! and resulting in a cascade of reactions causing a discharge of
uterotonic compounds before labor and providing for their pulsat-
ing synthesis during labor. These substances control the regularity
of uterine contractions.
180 Obstetrics
With the onset of labor uterine contractions are the result of phasic contractile
activity of myocytes in all parts of the uterus; the contractile activity develops due
to the effect of oxytocin, serotonin and histamine produced by the mother, under
the impact of fetal oxytocin. The wave of contraction begins at the site of minimal
β-reactivity of myocytes — the pacemaking mechanism.
REMEMBER!
Labor is a complex process programmed genetically, an unconditioned reflex whose
regulation is provided for by virtually all organs and systems in the female body. This
process is aimed at expelling of the gestational sac from the uterine cavity once the
fetus has reached viability.
The causes of labor onset have not been studied well enough yet. There are many
theories explaining the causes of labor onset, among them the genetic theory and
humoral theory.
An active role in labor induction and development is played by the fetoplacental

complex (hypothalamic-pituitary axis, fetal adrenal glands, placenta and parafetal
membranes).
The system activating the muscle contraction includes the prostaglandin, oxytocin,
histamine and pacemaker mechanisms (automatic increase of calcium permeability
of myocyte surface membranes). The mechanisms of chemoreceptor activation play
and additional role.
Activation of the myometrium occurs as α1-adrenoreceptors are acted on; the inhibi-
tion effect is ensured by β2-adrenoreceptors.
The amount of oxytocin receptors in the myometrium increases 100–200 times

during pregnancy reaching its peak before childbirth. At the same time, the uterus
becomes increasingly responsive to the circulating oxytocin.
Labor is triggered by the readiness of the myometrium, cervical tissues and the sys-
tems regulating uterine contractility. The fetus acts as an initiator of these processes.
The onset of labor is a genetic signal transmitted at the level of limbic structures;
it results in a cascade of reactions causing a release of uterotonic compounds be-
fore the onset of labor and providing their synthesis in a pulse mode, on which the
regularity of uterine contractions depends.
CONTROL QUESTIONS
1. What is labor?
2. What are the theories explaining the onset of labor?
3. What mechanisms are responsible for uterine contractile activity?
4. What are the features of oxytocin receptors during pregnancy?
5. What is the physiology of muscle contraction?
6. What receptors take part in myometrium activation?

7. Concentration of which ions regulates the contractile activity of myocytes?
CHECK YOURSELF!
1. The fetus is considered viable starting at the gestational age of:

a) 22 weeks;
b) 24 weeks;
c) 28 weeks;
d) 37 weeks.
2. Termination of pregnancy is termed abortion if the gestational age is less than:

a) 28 weeks;
b) 22 weeks;
c) 12 weeks;
d) 16 weeks.
3. Contractile activity of myocytes increases upon elevation of concentration of the

following ions in myocytes:
a) free Mg2+ ions;
b) free Ca2+ ions;
c) free Na+ ions;
d) free K+ ions.
4. The number of oxytocin receptors in the myometrium increases during pregnancy:

a) 10 times;
b) twofold;
c) 100–200 times;
d) 500 times.
NOTES
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• Chapter 7
MECHANISM OF LABOR IN CEPHALIC
(VERTEX) PRESENTATION
7.1. FACTORS DETERMINING THE MECHANISM OF LABOR
The greatest effort associated with childbirth is required of the parturient woman
at the end of the expulsion stage. Even in the most favorable match between the
shape and size of the fetal head, and the lesser pelvis dimensions, certain condi-
tions are necessary for the head to pass through the birth canal. In most cases the
fetus overcomes all the obstacles on the part of the birth canal as the progressive
advance of the fetus (and especially of its presenting part, the head) combines with
other motions: flexion, rotation, extension. Besides, the head undergoes moulding.
Background information. The mechanism of labor began to be studied by Ould as
late as in 1742. Ould pointed out that at the inlet of the true pelvis the fetal head is en-
gaged in the oblique diameter and is delivered through the anteroposterior diameter.
J.J. Fried and G.A. Fried, famous professors of obstetrics from Strasbourg, pub-
lished their works in 1742 and 1769 where they offered their explanation that fetal
head rotation was due to the difference in dimensions of different pelvic parts and
the need of the head to adapt to them.
At the beginning and in the middle of the 18th century a considerable contribution
to this field of obstetrics was made by Puzos (1686–1753) and especially by Smellie
(end of 17th century — 1763) who believed the relationship of pelvic dimensions and
the head to be the crucial factor in understanding the mechanism of labor.
Roederer (1726–1763) divided the mechanism of labor into 5 stages, and Stein
senior (1737–1803) called attention to oblique pelvic planes and invented the pelvim-
eter, an instrument to measure the fetal head, to determine its length and weight be-
fore childbirth, and to determine the angle of pelvic inclination as well (see Fig. 4.10).
Johnson in 1769 described the way to determine the diagonal conjugate, and
Saxtorph (1740–1800) showed that upon entering the pelvis the fetal head stations
itself in one of oblique diameters.
In Russia N.M. Maximovich-Ambodik (1744–1812) (Fig. 7.1) also explained the
mechanism of labor using the changing relationship between the fetal head and dif-
ferent parts of the pelvis; he was the first to teach obstetrics in the Russian language
and the first to use a wax manikin and a wooden doll for better demonstration.
In the 19th century research shed new light on the mechanism of labor.
F.K. Naegele (born in 1777) made himself prominent in the history of obstetrics
with his works on normal and pathological pelvis structure; he described a vari-
ety of head engagement — anterior asynclitism — which was named after him:
Naegele’s obliquity.
Chapter 7. Mechanism of labor in cephalic (vertex) presentation 183
The mechanism of labor as described by

A.J. Krassovsky (Fig. 7.2) is certainly of some
interest; it includes five stages:
• relative change of the presenting fetal
part;
• descent of the presenting part to the true
pelvis cavity;
• adaptation of the greatest dimensions
of the presenting part to the fitting
dimensions of the pelvic cavity by
changing the greater dimensions to lesser
ones;
• liberation of the presenting part or the
upper half of trunk form external genitals;
• expulsion of the aftercoming part of the
fetus.
Fig. 7.1. N.M. Maximovich-Ambodik
Krassovsky supplied detailed explanation
and description for each stage emphasizing the fact that in real life the stages do
not succeed in the given order being rather a continuous process.
His notions of the mechanism of labor were supplemented by Spiegelberg (1867),
Wochenfeld (1887), Schatz (1890), Farabef and Varnier (1923).
Major contribution to the teaching of practical obstetrics was made by Joseph
F. Jordania (Fig. 7.3). The training course involving use of phantoms developed by
him still remains the basis of obstetrics. Jordania introduced the term «mechanism
of labor» emphasizing that the progress of fetus during childbirth is provided for by
biological factors (fetal tone, maternal musculature of the uterus and its fundus, etc.)
in equal measure with mechanical factors derived from the anatomical structure of
the birth canal.
By the end of pregnancy the fundus, to-
gether with the pelvic pole of the fetus, be-
gins to experience increasing pressure from
the diaphragm and abdominal wall. Due to
its resilience and little pliability (especially in
primiparous women), the abdominal wall pre-
vents deflection of the fundus forward. Thus
the pressure from the diaphragm applied to
the fetal pelvic pole radiates along the fetal
spine and is transmitted to the head. The
head flexes, and in a slightly flexed position it
settles with its sagittal suture in one of oblique
diameters and engages with its minor segment
the true pelvis cavity at the level of -2 or even
-1 on Bishop’s score (Fig. 7.4).
In multiparous women the pressure exerted
by the diaphragm on the fundus and pelvic
pole of the fetus meets no opposition on the Fig. 7.2. A.J. Krassovsky
184 Obstetrics
part of the hyperinflated anterior abdominal

wall. In this connection the fundus deflects
forward while the head remains floating above
the pelvic inlet until the onset of labor. When
the head engages the pelvis, the sagittal suture
is situated at an equal distance from the sym-
physis pubis and the promontory. This type
of engagement is called synclitism (Fig. 7.5).
In other cases the sagittal suture is deflected
either forward, to the pubis, or backwards, to
the promontory. This off-axis engagement is
called asynclitism (see section 24.3 Asynclitic
cephalic presentation).
In vertex presentation the fetal head is flexed
and the occiput is the leading part. In vertex
presentation there are anterior and posterior
varieties. Anterior variety is more commonly
Fig. 7.3. J.F. Jordania observed in the first position; posterior vari-
ety — in the second. Vertex presentation ac-
counts for 96% of all childbirths. This is due to the fact that the spine is not connected
with the center of the head but closer to the occiput thus forming an asymmetrical
lever that is under pressure transmitted from the spine. This pressure affects mostly
the shorter shoulder of the lever, that is, in the part facing the occiput, and this
produces the flexion (Fig. 7.6).
Fig. 7.4. Position of fetal head pressed to the pelvic inlet (position I, anterior variety of vertex
presentation)
Fig. 7.5.
1 2
Fig. 7.6. The principle of asymmetrical lever in the mechanism of head flexion: 1 — the
long shoulder of the lever; 2 — the short shoulder of the lever; 3 — direction of the force
transmitted from the spine to the head
For better understanding of the mechanism of labor, one should regard the fetal
head as a kidney-shaped body (theory by S.D. Mikhnov) rather than an ovoid or el-
lipsoid body, as is customary in obstetrics. A head curved like a kidney has two poles:
the occiput and the chin. Both poles are connected by an imaginary line of head
curvature in the shape of an arch, with its convexity facing the area of the anterior
fontanelle (Fig. 7.7a). The birth canal and the axis pelvis plane, correspondingly,
look like an arch too, with the convexity facing backwards (Fig. 7.7b). The head
negotiates the pelvic cavity easily only if the lines of pelvic and cephalic curvature
coincide (are congruent) (anterior variety of vertex presentation) which is achieved
upon a correct internal rotation of the fetal head.
The mechanism of labor is a complex of all movements per-
NB! formed by the fetus during its expulsion.
186 Obstetrics
а b
Fig. 7.7. The shape of fetal head matching the birth canal shape (by S.D. Mikhnov): a — line
of cephalic curvature; b — axis pelvis plane
When it is delivered, the fetus makes motions under the impact of forces exercised
by the uterus, abdominal wall, diaphragm, pelvic floor musculature (the cumulative
effect of contractions and bearing down efforts) as well as the impact of counteracting
forces on the part of the birth canal (uneven distribution of obstruction in various
pelvic planes).
Along with these causes there are other additional factors promoting the progress
of labor. These include pelvic inclination, sutures and fontanelles on the fetal head,
and symphyses in the parturient woman’s pelvis.
7.2. OCCIPITOANTERIOR VARIETY

OF VERTEX PRESENTATION
In the occipitoanterior variety of vertex presentation the entire mechanism of labor
is divided into four steps; this division is but conventional, other handbooks name a
different number of steps (Fig. 7.8).
Step one: head flexion (Fig. 7.9). The cervical part of the spine bends, the chin
is tucked onto the chest, the occiput goes down, and the brow hovers above the
pelvic inlet.
As the occiput goes down, the posterior fontanelle positions itself below the an-
terior fontanelle so that the point of direction — the lowermost point on the head
which is on the axis pelvis plane — is now the point on the sagittal suture closer to
the posterior fontanelle. In occipitoanterior variety of vertex presentation the head
flexes to the suboccipitobregmatic diameter, and this diameter leads the way to the
pelvic inlet and to the pelvic plane of greatest dimensions. Consequently, the fetal
head is engaged in condition of moderate flexion in the transverse or one of oblique
diameters in the plane of true pelvis inlet.
Step two: internal rotation (normally with occiput facing forward). Continuing its
progressive advance in the pelvic cavity the head meets with opposition at the pelvic
Fig. 7.8. Position of fetal head before onset of labor
Fig. 7.9. Head flexion (the fi rst step in the mechanism of labor in occipitoanterior variety
of vertex presentation)
plane of least dimensions; the head starts rotating around its longitudinal axis as if
«screwing» itself into the pelvis. This happens as the pelvic plane of least dimensions
is of elongated oval shape, in contrast to the transverse oval shape of the lesser pelvis
inlet. Besides, rotation of fetal head to occiput anterior position aligns the axis pelvis
plane and the line of cephalic curvature. Head rotation begins during its descent
from the pelvic plane of greatest dimensions to the plane of least dimensions. Sliding
along the lateral pelvic wall the occiput draws nearer to the symphysis pubis, and
the anterior portion of the head shifts to the sacrum. The sagittal suture leaves the
oblique diameter and passes to the anteroposterior diameter of the pelvic outlet, and
the suboccipital fossa positions itself under the symphysis pubis; that is, the fixation
point and the point of bearing are established (Fig. 7.10).
Step three is head extension. The fetal head continues is progress along the birth
canal. In normal labor head extension occurs at the pelvic outlet when the head meets
188 Obstetrics
with opposition on the part of the perineum and proceeds forward in the direction
of the symphysis; the suboccipital fossa (fixation point) hits the inferior margin of
symphysis pubis (point of bearing), and after several bearing down efforts the head
extends. The head is delivered through the vulvar ring with its suboccipitobregmatic
diameter (9.5 cm). In consecutive stages, the occiput, crown, brow, face and chin
are delivered (Fig. 7.11).
Step four is restitution and external rotation. While the head extends, the shoul-
ders have reached the transverse diameter of pelvic inlet or one of its oblique
diameters. As the head progresses along the birth canal, the shoulders perform
corkscrew movements following the head, their bisacromial diameter passing from
Fig. 7.10. Step two in mechanism of labor in occipitoanterior variety of vertex presentation
Fig. 7.11. Fetal head extension (step three in the mechanism of labor in occipitoanterior
variety of vertex presentation)
oblique to anteroposterior diameter of the pelvic outlet. This rotation occurs as

the trunk passes through the plane of least pelvic dimensions, and the rotation is
transmitted to the already delivered head. The occiput turns to the side of fetal
position: facing the left (in first position) or right (in second position) thigh of the
mother (Fig. 7.12).
Now the anterior shoulder comes under the pubic arch. A second point of fixation
and bearing is formed between the anterior shoulder at the spot of deltoid muscle
insertion and the inferior margin of symphysis (Fig. 7.13, 7.14).
Once the shoulders are delivered, the rest of the trunk is delivered more easily, as
the birth canal has been prepared by the fetal head. The head of a fetus delivered in
the occipitoanterior variety of vertex presentation is of dolichocephalic (elongated)
shape due to molding and labor tumor (caput succedaneum) (Fig. 7.15).
Fig. 7.12. Step four in mechanism of labor
Fig. 7.13. Anterior shoulder delivered

190 Obstetrics
Fig. 7.14. Posterior shoulder delivered
Fig. 7.15. Head of a newborn after delivery (labor tumor)
7.3. OCCIPITOPOSTERIOR VARIETY

OF VERTEX PRESENTATION
If childbirth proceeds in the occipitoposterior variety of vertex presentation, the
fetal occiput faces the sacrum (Fig. 7.16). A vaginal examination detects the posterior
fontanelle at the sacrum, and the anterior fontanelle — at the pubis. Occipitoposterior
variety of vertex presentation may emerge due to a change in the shape and capacity
of the true pelvis, functional incompetence of uterine muscle, specific shape of fetal
head, preterm or dead fetus. Only in 1% of all vertex presentations the fetus is de-
livered in the occipitoposterior variety. In occipitoposterior variety the mechanism of
labor is composed of five steps. Step one is flexion of fetal head. In occipitoposterior
variety of vertex presentation (like in occipitoanterior variety) the sagittal suture is
stationed in one of oblique pelvic diameters — in the left one (first position) or in
the right one (second position). In this case the posterior fontanelle faces left and
backwards to the sacrum (first position), or right and backwards to the sacrum (sec-
ond position). Upon flexion the head passes through the inlet plane and the plane of
greatest pelvic dimensions with its suboccipitofrontal diameter (10 cm). The point of
direction is the point on the sagittal suture situated closer to the anterior fontanelle.
Step two is internal rotation of fetal head with occiput backwards. The rotation
proceeds so that the anterior fontanelle is placed posteriorly at the sacrum, and the
anterior fontanelle — anteriorly at the pubis.
Internal rotation takes place while passing through the plane of least pelvic dimen-
sions; it is completed in the plane of pelvic outlet once the sagittal suture is stationed
in the anteroposterior diameter.
Step three is further flexion of the head to the utmost. When the head passes with
its hairline (fixation point) below the inferior margin of symphysis pubis (point of
bearing), it becomes fixed. The head performs additional flexion, and the occiput is
delivered with its suboccipital fossa (Fig. 7.17).
Step four is extension of the head. A second point of bearing (anterior surface
of coccyx) and fixation point (suboccipital fossa) are formed. Under the impact of
labor forces the fetal head performs the extension, so first the brow, and then the
face turned to the pubis appears from under the pubis.
Step five is internal rotation of shoulders, external rotation of head. From now
on, the progress of labor is the same as in the occipitoanterior variety of vertex
presentation.
As the fetal head is engaged with a diameter which is more than the suboccipito-
bregmatic diameter, and an additional difficult step is added in the occipitoposterior
variety of vertex presentation to mechanism of labor, so the expulsion period becomes
protracted. This requires extra efforts on the part of the uterus and abdominal muscle.
Soft tissues of the pelvic floor and perineum undergo considerable expansion and are
often injured. Protracted labor and elevated pressure from the birth canal affecting
the fetal head doing maximum flexion — these factors often lead to fetal hypoxia,
mostly due to disturbed cerebral circulation.
Fig. 7.16. Occipitoposterior variety of Fig. 7.17. Maximum head flexion in left
vertex presentation occipitoposterior position
192 Obstetrics
REMEMBER!
Mechanism of labor is a complex of flexion, extension, progressive and rotational
movements of large parts of the fetus when passing through the birth canal.
Steps of labor mechanism in occipitoanterior variety of vertex presentation:

• step one — head flexion;
• step two — internal (correct) rotation of fetal head;
• step three — head extension;
• step four — internal rotation of shoulders and external rotation of head.
Steps of labor mechanism in occipitoposterior variety of vertex presentation:

• step one — head flexion;
• step two — internal (incorrect) rotation of head;
• step three — additional flexion of fetal head to the utmost;
• step four — head extension;
• step five — internal rotation of shoulders, external rotation of the head.
Fixation point is the spot on the fetal body resting against the pelvic bones of the
mother.
Point of bearing is the point on the bones of maternal pelvis with which the fixation
point (on the fetal body) is in contact.
CONTROL QUESTIONS
1. What factors affect the mechanism of labor?

2. What is the point of direction?
3. What are the specifics of fetal head position at the end of pregnancy?
4. What is synclitic and asynclitic engagement of fetal head?
5. What is referred to as vertex presentation?
6. What is referred to as point of fixation, point of bearing?
7. How does the first step of labor proceed in occipitoanterior variety of vertex
presentation?
8. What is the second step of labor in occipitoanterior variety of vertex presentation?
9. What is the third step of labor mechanism in occipitoanterior variety of vertex
presentation?
10. What is the fourth step of labor mechanism in occipitoanterior variety of
vertex presentation?
11. In which diameter is the head delivered in occipitoanterior variety of vertex
presentation?
12. What happens after the head is delivered?
13. How does the first step of labor proceed in occipitoposterior variety of vertex
presentation?
14. How does the second step of labor proceed in occipitoposterior variety of
15. How does the third step of labor proceed in occipitoposterior variety of vertex
presentation?
16. How does the fourth step of labor proceed in occipitoposterior variety of
17. How does the fifth step of labor proceed in occipitoposterior variety of vertex
presentation?
18. In which diameter is the head delivered in occipitoposterior variety of vertex
presentation?
CHECK YOURSELF!
Level 1. Test
1. The fourth step of labor in occipitoposterior variety of vertex presentation consists in:
a) head extension;
b) head flexion
c) internal rotation of the head;
d) additional head extension.
2. The point of direction in occipitoposterior variety of vertex presentation is:

a) brow;
b) a point on the sagittal suture situated closer to the posterior fontanelle;
c) chin;
d) a point on the sagittal suture situated closer to the anterior fontanelle.
3. The second fixation point in occipitoposterior variety of vertex presentation is:

a) suboccipital fossa;
b) hairline;
c) upper third of the shoulder.
4. Specific features of labor in occipitoposterior variety of vertex presentation are:

a) additional head flexion;
b) additional head extension;
c) asynclitic engagement;
d) persistent occiput direct position.

1. A vaginal examination in the second stage of labor revealed cervical opening
10 cm, the sagittal suture was stationed in the anteroposterior diameter in the plane
of least dimensions, the posterior fontanelle was felt under the pubis, the anterior
fontanelle could not be felt. What is the diagnosis?
2. A vaginal examination revealed cervical opening 5 cm, the sagittal suture sta-
tioned in the oblique diameter of pelvic inlet, the posterior fontanelle found closer
to the sacrum, the anterior fontanelle could hardly be felt. What is the diagnosis?
• Chapter 8
CLINICS AND MANAGEMENT OF LABOR
IN VERTEX PRESENTATION
8.1. BASIC CONCEPTS
Labor (delivery, childbirth) is the process of expulsion or extraction of gestational

sac (product of conception: the fetus and parafetal structures) from the cavity of
uterus after the fetus has become viable. In the light of this definition, any expulsion
or extraction (vaginal or abdominal) is considered to be delivery. When the fetus is
delivered, labor is not over as the afterbirth still remains in the uterus.
International classification codes:
• 047 False labor
• 060 Preterm labor and delivery
• 048 Prolonged pregnancy
• 080 Single spontaneous delivery
• 080.0 Spontaneous vertex delivery
The causes of labor onset are not studied well enough (see Chapter 6 Onset of
Labor and Regulation of Uterine Activity).
The onset of labor is preceded, as a rule, by precursors of labor, a complex of
clinical manifestations; their emergence four to two weeks prior to childbirth indicates
that childbirth is near:
• fundus of uterus sinks as the presenting part engages the lesser pelvis inlet; this
happens in primiparous women;
• relative decrease in amniotic fluid volume;
• «show»: profuse mucous vaginal discharge as the mucous plug is discharged from
the cervix of uterus;
• some reduction in body weight;
• emergence of irregular cramplike painless sensations in the lower abdomen;
• absence of weight gain over the last two weeks.
There is another notion accepted in obstetrics: labor readiness.
The extent to which the woman’s body is prepared for labor is

NB! determined by ripeness of the cervix.
Ripeness of cervix is commonly determined using various integral scores, Bishop’s

score (1964) among them (Table 8.1).
A vaginal examination determines the cervical consistency, its length (or degree
of effacement), patency of the cervical canal and the position of cervix in relation to
the pelvic axis. Fetal station is determined in relation to the ischial spines which are
Chapter 8. Clinics and management of labor in vertex presentation 195
Table 8.1. Bishop’s score evaluating the grade of cervical ripeness (E.H. Bishop, 1964)
Parameter Points
0 1 2 3
Cervical canal diameter, cm closed 1–2 3–4 5 and more

Cervical effacement, % 0–30 40–50 60–70 80 and more
Fetal station (Bishop, Fig. 8.11) -3 -2 -1…0 +1…+2
Cervical consistency firm medium soft
Relation of cervical axis to posterior intermediate along the pelvic axis
maternal pelvic axis
in the plane of least dimensions (see below). Each parameter is accorded from 0 to
2 points. The total of the points indicates the grade of cervical ripeness:
• a score of 0–2 points indicates that the cervix is unripe;
• a score of 3–6 points indicates insufficient ripeness;
• a score of 7–13 points indicates cervical ripeness.
In Russian obstetric tradition a notion of physiological preliminary period is dis-
tinguished. There is no such term abroad, but «protracted latent phase» can serve as
an equivalent. The preliminary period is not seen in all pregnant women. In contrast
to the precursors of labor, preliminary pains are limited to several hours (no less than
6 hours) immediately preceding the onset of labor; they should not interfere with
natural vital activity (sleep, nutrition, everyday activities) of the pregnant woman.
Preliminary pains occur almost without clinical manifestations: some irregular painful
contractions of the uterus are noted.
In some pregnant women these pains grow worse, more intensive and afterwards
they turn into labor contractions.
The preliminary period coincides with the time of dominant of labor formation in
the cerebral cortex, changes in the hormonal panel, and is accompanied by additional
ripening of the cervix. The cervix softens, assumes a central position along the pelvic
axis and rapidly shortens to 2 cm.
Abnormal preliminary period (of longer than 6 hours duration) is classified as an
anomaly of labor. The painful sensations disrupt the woman’s daily routine; for in-
stance, she becomes unable to sleep. It corresponds to the notion of «dystocia during
the latent phase» (Table 8.2).
Table 8.2. Differential diagnosis of labor and preliminary pain
Parameter Labor Preliminary pain
Regularity regular irregular

Interval between contractions growing less no change
Contraction intensity growing more intense no change
Pain localization abdomen and lumbar area low abdomen
Efficiency of pain killers no yes
Structural changes in the cervix yes no
(effacement and dilation of the cervix)
196 Obstetrics
8.2. DEFINITION
The description labor at term, normal labor and delivery is applied to childbirth
occurring at gestational ages 37 to 42 weeks, when a mature, term fetus is delivered
that can easily adapt to the external surroundings. Childbirth at gestational ages
22–36 weeks yields an immature, pre-term fetus; this delivery is considered pre-term,
while delivery at gestational age 42 weeks and more is regarded as post-term delivery.
In case of pre-term or delayed development of labor the delivery is often accom-
panied by complications; the newborn’s adaptation to the new living conditions has
its specifics; such children require special attention.
During childbirth the woman who is giving birth is referred to as parturient.
The woman giving birth for the first time is called primiparous; the woman who
has given birth two and more times is referred to as multiparous.
For various reasons, pregnancy can terminate at any gestational age. The fetus
can only survive if it has developed certain anatomical and functional features that
depend on multiple conditions.
Nowadays a fetus is considered viable starting at 22 weeks gestation

NB! when its weight is 500 g, and its length is 25 cm.
Until 22 weeks gestation the fetus is non-viable. Termination of pregnancy before

22 weeks gestation is referred to as abortion rather than childbirth.
8.3. HOSPITALIZATION FOR CHILDBIRTH
Upon admission to maternity hospital the woman is given a shaving of her ex-
ternal genitals and a cleansing enema if she wishes it. Shower is administered to all
patients; an individual set of clothing and beddings is issued to her (a nightshirt, a
gown, a towel, drawsheets). She is allowed to use her own shoes and underwear.
After an examination and history-taking the admission department midwife ac-
companies the parturient woman to the ward where the woman will stay before and
during childbirth.
8.4. STAGES OF LABOR
The act of childbirth is commonly divided into three stages:

• stage one — period of dilation — from the onset of labor to complete cervical
dilation (10 cm);
• stage two — period of expulsion — from complete cervical dilation to fetus
expulsion;
• stage three — placental expulsion period — from delivery of fetus to expulsion of
placenta.
Childbirth terminates with expulsion of the afterbirth. The onset of labor is a
different matter. Childbirth begins with labor contractions which, unlike common
irregular uterine pains, result in structural changes in the cervix: its dilation and ef-
facement. At the same time, cervical changes are typical as early as the last one-two
weeks before childbirth, and the rate of cervical change during the latent phase is so
slow that it takes no less than three hours to note it. That is why, the onset of labor
is considered to be the time when the rate of contractions becomes no less than one
in ten minutes, as proposed by E. Friedman.
8.4.1. The first stage of labor

The first stage of labor begins with appearance of regular contractions and ends
with complete cervical opening (10 cm). The characteristic sign of the first stage is
contractions.
Contractions are assessed against four parameters: their rate, duration, intensity
and painfulness.
Uterine contractions are involuntary rhythmical contractions of the

NB! uterine muscle at a rate no less than one in ten minutes.
At the beginning of labor contractions are rare, of short duration and not too pain-
ful: they occur every 10 minutes, of 10–15–20 s duration. Afterwards the intervals
gradually diminish to 1–2 minutes (at the end of the first stage). In the middle of
labor the duration of contractions is 30–40 s, at the end of labor it is 50–60 s. The
painfulness of contractions depends on their intensity, as well as on the quality of
psychoprophylaxis (childbirth education).
The tone and intensity of uterine contractions are assessed by palpation placing a
hand on the fundus and noting with a stopwatch the time from the beginning of one
contraction to the beginning of another. Instrumental methods of registering labor
(hysterography using fetal electronic monitor) are useful in obtaining more detailed
information about the intensity of uterine contractions (Fig. 8.1). A hysterogram
helps to assess the rate of contractions in 10 minutes, their duration, amplitude, and
the interval between contractions. The effectiveness of contractions can be evaluated
with a vaginal examination judging the structural changes in the cervix: its shortening,
effacement, and later its dilation.
Effacement and dilation of cervix proceed in different manner in primiparous and
multiparous women.
• In primiparous women dilation starts with the internal os; the cervical canal and
the cervix grow shorter, then the cervical canal stretches more and more, and the
cervix shortens and effaces; it is as if the cervix is pulled into the lower uterine
segment. Only the external os remains open. Then the external os begins to open.
Upon complete opening it appears as a thin border in the birth canal formed by
the vaginal walls and uterus fused into one whole.
• In multiparous women the opening of the canal and cervical effacement proceed
simultaneously, as a rule (Fig. 8.2).
The opening of the mouth of uterus occurs due to contraction and retraction
(shifting in relation to each other) of muscular fibers in the body of uterus and ex-
tension (distraction) of the cervix and lower uterine segment.
198 Obstetrics
240 240
210 210
CONTRACTIONS
180 180
150 150
90 90
UA UA
UA
60 100 60 100
12
30 75 10 30 75
FHR ppm 8 FHR ppm
50 6 50
25 4 25
2
Fig. 8.1. Registration of myometrial contractile activity (hysterography) using an electronic

fetal monitor
2 2
2
2
1
1 1 1
2 2
2
1 1
1
b
Fig. 8.2. Specifics of cervical dilation in primiparous (a) and multiparous (b) women: 1 —
external os; 2 — internal os.
The lower uterine segment is a portion of the isthmic area in the body of uterus that
forms the birth canal in the first stage of labor as a result of retraction and distraction
processes. As the birth canal is formed, a furrow called contraction ring emerges at
the border between the upper and lower uterine segments (see Fig. 8.7). The con-
traction ring is determined by palpation after the rupture of the amniotic sac. The
height of its station above the pubis corresponds to the degree of cervical opening.
The lower uterine segment hugs the presenting head tightly and forms the inner
belt of adherence, or contact. The belt of adherence divides the amniotic fluid into
«anterior waters» situated below the belt of adherence, and «posterior waters» situated
above the belt of adherence. When the head hugged by the lower segment presses
against the pelvic walls, an external belt of adherence is formed along the entire
circumference. That is why posterior waters do not pass when the gestational sac is
ruptured and anterior waters move away (Fig. 8.3).
Term rupture of membranes should occur when the cervix is almost completely
open. If membranes rupture during the first stage of labor while the cervix is not
dilated 7 cm, this rupture is considered early. Passing of waters before the onset of
regular labor is called preterm rupture of membranes, PROM.
Two phases are distinguished in the first stage of labor:
• latent phase: from the onset of contractions to cervical dilation 4 cm;
• active phase: from 4 cm to complete dilation.
The active phase, in its turn, is divided into the following periods:
• acceleration;
• maximum slope;
• deceleration.
The rate of cervical dilation is an important indicator that labor proceeds normally
(Fig. 8.4).
The rate of cervical dilation at the beginning of labor (latent phase) is 0.35 cm per
hour, in the active phase — 1.5–2 cm per hour in primiparous women, and 2–2.5 cm
per hour in multiparous women.
Cervical dilation (deceleration period) proceeds more slowly: 1–1.5 cm per hour.
The rate of cervical dilation depends on the contractile capacity of the myometrium,
the possibility of physiological remodeling of the cervix, which depends on endog-
enous factors and external influences.
Posterior waters
External belt
of adherence
Anterior waters
Fig. 8.3. Division of amniotic fluid into posterior and anterior waters
200
Cervical dilation, cm Obstetrics
Second stage of labor

Latent phase Active phase
Time, h
Fig. 8.4. Partogram. Phases of the fi rst stage of labor
Duration of the first stage of labor is 10–14 hours on average in primiparous

women, and it is twice as short in multiparous women. If the woman is active during
the first stage (she walks, takes a shower, rests in a sitting position) labor is almost
2 hours shorter compared with those parturient women who spend the time passively
in bed (lying flat on the back is most unfavorable).
Partogram. In order to perform a dynamic assessment of labor, one uses linear
graphic representation of cervical shortening and dilation depending on the duration
of labor. The same graph shows the progress of fetal head in relation to the planes
of the true pelvis (Fig. 8.5). The WHO partogram shows two lines: alert line and
action line. The alert line is the border beyond which the rate of cervical dilation is
less than 3 cm/hour, and he patient can be observed further. The dynamic represen-
tation of cervical dilation in physiological labor should go parallel to the alert line.
The action line is drawn four hours to the right of the alert line showing that if the
patient has crossed the action line, induction of labor should be started or the plan
of management should be revised.
Intranatal assessment of perinatal risk. Calculating the points of prenatal risk while
the pregnant woman receives care at a maternity welfare clinic helps to distinguish
the groups of perinatal risk (low, medium, and high risk groups). The next stage in
determining the risk strategy is taking into account the intranatal risk factors: com-
plications of labor affecting the perinatal outcomes. The act of childbirth affects the
perinatal outcome to a greater degree than the course of pregnancy.
S.J. Hobel (1973) who studied the effect of antenatal and intranatal factors on
labor outcomes established that intranatal complications affect perinatal morbidity
and mortality twice as much compared with the effect of antenatal factors, including
high risk situations.
Partogram
Name Gravida Para Hospital number
Date of admission Time of admission Ruptured membranes hours
Fetal
heart
rate
Amniotic fluid
Moulding
Action
t
Cervix (cm)
er io
n
[Plot Х]
Al t
Ac
Descent of head
[Plot 0] Latent phase
Hours
Time
Contractions
per 10 min
Oxytocin U/L
drop/min
Drugs given
and IV fluids
Pulse
BP
Temp °С
Protein
Urine Acetone
Volume
Fig. 8.5. Partogram (WHO)
The staff of the Chair of Gynecology and Obstetrics at PFUR developed an original
system for evaluation of risk factors based on a bulk of clinical data accumulated over
years of clinical practice. New risk factors were added to the prenatal score and, which
is most important, the main intranatal factors were determined and estimated. Based
on this study, it was established that the main intranatal factors affecting the perinatal
outcomes are fetal hypoxia, changed color of amniotic fluid, and anomalies of labor.
202 Obstetrics
That is why in the course of childbirth the obstetrician has to reevaluate the pre-
natal risk factors worked out by the end of pregnancy: as complications set in, the
parturient woman can be transferred from a low risk group to a medium, and even
to a high prenatal risk group.
If intranatal risks accrue at a considerable rate, the obstetric situation has to be
reevaluated, and sometimes the plan of childbirth management has to be changed
radically.
In the first stage of labor the obstetrician monitors the general condition of the
parturient woman and fetal heartbeat, the progress and painfulness of labor contrac-
tions, the condition of the cervix and mouth of the uterus. Special attention is paid
to the condition of the woman’s cardiovascular system: skin coloration should be
noted, arterial pressure measured regularly. One should ask the parturient woman
about her wellbeing, whether she feels tired, or has a headache, dizziness, vision
disorder, pain in the upper abdomen.
Fetal monitors are in widespread use nowadays; this device registers the contrac-
tions of smooth uterine musculature evaluating simultaneously the parameters of fetal
cardiac activity (heart rate) (Fig. 8.6).
An external obstetric examination during the period of dilation is done systemati-
cally, no less than once an hour. Data are entered into the woman’s record no less
than every three hours.
To monitor the pattern of labor, one performs external and internal obstetric
examinations.
Doing an external obstetric examination one notes the shape of the uterus, its
consistency during and outside contractions, fundal height, the condition of the
contraction ring.
The intensity and duration of contractions can be assessed with a hand placed at
the fundal area; the degree of its relaxation is assessed by palpation. After a contrac-
tion the uterus should relax completely.
Fig. 8.6. Fetal monitors: portable and pocket monitors

In normal labor the contraction ring is palpated as a transverse furrow which

goes upwards as the cervix dilates (Fig. 8.7). The height of contraction ring station
is indicative of the degree of dilation: the distance between the ring and pubis in cm
is approximately equal to the degree of cervical dilation in cm. At the end of dilation
period the contraction ring is situated 10 cm above the pubis (Schatz-Winterberg
sign). One should also determine the lie, position, variety and presentation of the
fetus, and the relation of the presenting part to the pelvic inlet.
However, an external obstetric examination alone does not always give an idea of
labor progress, which is why a vaginal examination is done as well.
A vaginal obstetric examination during the period of dilation is performed every
6 hours if there are no emergency indications. Irrespectively of labor duration a vagi-
nal examination should be done upon admission of the parturient woman to maternity
hospital, immediately upon rupture of membranes, and if there are signs of fetal
hypoxia, vaginal bleeding, before administering anesthesia, and on other indications.
A vaginal examination is done with two fingers: the index finger and middle finger
(like a gynecological examination, but with one hand, the inner one). The ring finger
and little finger are bent and tucked to the palm, the thumb is straight and drawn
aside. The obstetrician uses the other hand to separate labia majora and labia minora
baring the vaginal vestibule. First the middle finger is introduced into the vagina
pressing it against the posterior vaginal wall, and then the index finger is introduced.
The vaginal examination serves to determine the following:
• condition of the perineum (presence of scars, old lacerations, varicose veins;
• condition of the vagina (wide or narrow, short or long, presence of scars,
partitions, tumors) and muscles of the pelvic floor;
• condition of the cervix (intact, shortened, effaced, thickness and resilience of its
edges, degree of dilation);
Fig. 8.7. Contraction ring of the uterus

204 Obstetrics
• condition of the membranes sac (intact, absent; if it is intact, one checks for the
degree of its filling and tension during and outside contractions);
• condition of the fetal presenting part, its position in the true pelvis, sutures,
fontanelles and the leading point (Fig. 8.8);
• condition of the true pelvis bones (the shape of promontory and symphysis pubis,
depth of sacral fossa, mobility of sacrococcygeal symphysis, etc.);
• size of diagonal conjugate.
As the fetal head passes through the plane of pelvic inlet, the largest and least
head diameters are distinguished.
• Head above pelvic inlet. In this obstetric situation the head can be floating, or
pressed against the true pelvic inlet. Performing the fourth obstetric maneuver
one can place the fi ngers under the head (Fig. 8.9). During a vaginal examination
the true pelvis is free, innominate lines can be palpated as well as the promontory
and symphysis pubis. The sagittal suture is in one of oblique diameters, the
anterior and posterior fontanelles — at the same level.
• Head stationed with the small diameter in pelvic inlet. In this obstetric situation
the head is immobile, its greater diameter stationed above the inlet plane. In
external obstetric examination the fi ngers fan out (Fig. 8.10). In a vaginal
examination the promontory can only be reached with a bent fi nger. The inner
surface of symphysis and the sacral fossa are free. The sagittal suture is in the
oblique diameter.
• Head stationed with the greater diameter in pelvic inlet. In this obstetric situation
the head is stationed with its greater circumference in the inlet plane of true
pelvis. In external obstetric examination the fi ngers of both hands join upon
Fig. 8.8. Determining the localization of sutures and fontanelles by a vaginal examination
Fig. 8.9. Fetal head above the true pelvis inlet (fi ngers of both hands can be placed
under the head)
Fig. 8.10. Fetal head stationed with the small diameter above the true pelvis inlet
(gliding on the head the fi ngers of both hands fan out)
206 Obstetrics
a reverse movement of the palms. A vaginal examination reveals that the head
covers the upper third of symphysis pubis and sacrum, the promontory is not
palpated. The posterior fontanelle is below the anterior fontanelle, the sagittal
suture is in the oblique diameter.
• Head stationed in the plane of greatest pelvic dimensions. In this obstetric situation
the head is only slightly palpable above the pubis. A vaginal examination reveals
that a half of the inner surface of symphysis pubis and the upper third of sacral
fossa is occupied by the head. Ischial spines are palpable.
• Head stationed in the plane of least pelvic dimensions. Upon external examination
the head is not palpable. A vaginal examination reveals that the entire inner
surface of symphysis pubis and the entire sacral fossa are occupied by the head.
Ischial spines cannot be reached. The sagittal suture is situated in the oblique
diameter, but closer to the anteroposterior diameter.
• Head stationed in the pelvic outlet. In this obstetric situation the sacral fossa and
coccyx are completely occupied by the head. The inner surface of ischial spines
is not palpable. The sagittal suture is stationed in the anteroposterior diameter of
lesser pelvis outlet.
In American school of obstetrics one determines the relationship of the presenting
fetal part to the true pelvis planes as the head progresses through the birth canal,
using Bishop’s notion of true pelvis levels. The following levels are distinguished:
• the line passing through ischial spines: zero level (the fetal head is with its greater
diameter in the pelvic inlet);
• planes above the zero level are designated as negative levels: -1, -2, -3;
• planes below the zero level are designated as positive levels: +1, +2, +3; level
+3 indicates that the head is stationed at the pelvic floor (Fig. 8.11) modified
attitude to distinguish 5 levels above and 5 levels follow zero plane.
Monitoring fetal cardiac activity during labor
• regular auscultation of fetal heartbeat is the main and sufficient criterion for
monitoring the fetal condition during labor if there are no emergency indications;
Fig. 8.11. Relationship of fetal head to pelvic planes (Bishop)

• auscultation of fetal heartbeat (normal heart rate is 120–160 beats per minute) is
done in the fi rst stage of labor every 15–30 minutes for one full minute after the
contraction is over; during bearing down efforts — after each effort;
• routine administration of CTG to all parturient women is not justified, especially
in case of low risk as this technique yields a high rate of false positive results thus
increasing the incidence of interventions, operative delivery among them;
• continuous CTG monitoring should be administered to patients in the risk group
according to indications;
• the findings of monitoring the fetal cardiac activity and uterine activity should be
entered in the appropriate field of the partogram;
• ultrasound observation of fetus during delivery can be done if necessary.
During the first stage of labor one should monitor the function of the bladder and
bowels as their fullness interferes with normal progress of labor. Bladder fullness may
develop due to its atony or result from urethra being pressed to the symphysis by the
fetal head. The patient should be encouraged to empty the bladder every 2–3 hours,
if there is no spontaneous urination, catheterization can be resorted to.
The patient should remain active during the first stage of labor. The parturient
woman should employ non-medicamentous methods of pain killing that she was
taught at her psychoprophylaxis training classes. The notion of «childbirth with the
partner» implies the presence of the husband or other relatives. If the membranes
are intact, bed rest is only recommended in case of polyhydramnios, preterm delivery
and breech presentation.
Labor is always accompanied by pain of varying degree of intensity. If psychopro-
phylactic methods of pain killing are ineffective and the patient complains of acutely
painful contractions, the obstetrician can administer analgesia. Administration of
analgesia is more expedient when the latent phase of labor is over. The choice of
analgesia technique depends on the condition of the patient and fetus and the ob-
stetric situation (see Chapter 9 Obstetric Anesthesia).
The following is not recommended in the first stage of normally progressing labor:
• induction of labor with amniotomy and oxytocin;
• routine amniotomy if cervical dilation is less than 7 cm;
• medicamentous enhancement of uterine contractions in the fi rst stage of
normally progressing labor: routine administration of uterotonics (oxytocin) for
acceleration of labor should be given up;
• making the patient bear down before she herself complains of a sensation of
strong pressure in the rectum.
8.4.2. The second stage of labor

Once cervical dilation is 10 cm, the second stage of labor sets in: expulsion period,
which ends in delivery of the fetus. The end of the second stage of labor (besides
contractions) is characterized by bearing down efforts, or pushing.
Bearing down efforts are controlled contractions of straight
NB! abdominal muscles, diaphragm and pelvic floor which are simulta-
neous with uterine contractions.
208 Obstetrics
Bearing down begins when the presenting part drops to the pelvic floor. At this
instance the presenting part is found in the pelvic plane of least dimensions.
Bearing down recurs every 1–3 minutes lasting for 50–60 s.
The duration of the second stage is one hour on average (no more than 2 hours
at most) in primiparous women and 30 minutes on average (one hour at most) in
multiparous women.
In the second stage of labor the obstetrician should carefully watch the following:
• the patient’s condition;
• nature of labor;
• fetal heartbeat: heart rate should be auscultated after each bearing down; one
should also note the rhythm and volume of fetal heart tones;
• progress of the presenting part;
• nature of discharge from the birth canal.
During delivery, the fetal head begins to show through the vaginal opening with
each contraction. When the head remains visible without slipping back in, it is known
as crowning.
Normal spontaneous delivery in cephalic presentation does not imply administra-
tion of uterotonics or dissection of the perineum (episiotomy).
At present there are two rival approaches to managing the end of the expulsion
period.
• The first — traditional, so to say — approach when the obstetrician or midwife
render manual help to the delivering fetus in cephalic presentation.
• The second approach implies non-interference («hands-off»), no manipulations
with the head or perineum (hands-off approach), but verbal directions about
respiration and pushing can be given. With this management of childbirth the
patient can assume the position that is most comfortable, squatting or in the
knee-elbow position; this delivery is referred to as vertical.
Free position during labor. Vertical delivery. The term «vertical delivery» is mostly
applied to the patient assuming a vertical position during the second stage of labor
only. Free activity (position) during labor refers both to the first and second stage;
it means that the patient is free to do and move about as she likes.
During the first stage the patient can sit, stand, walk, lie down (lying on the back
protracts the duration of labor, so this is most unfavorable), take a warm shower or
a bath — all this promotes pain relief during contractions, shortens labor, reduces
administration of uterotonics, and has undeniable psychological advantages.
In the first stage the vertical position provides a greater pressure of gestational sac on
the area of lower segment and mouth of the uterus exciting the receptors of this area,
which makes contractions more effective and shortens the dilation period by 2–3 hours.
Besides, in a vertical position the uterus does not compress great vessels of the
abdominal cavity, which preserves good uteroplacental circulation without causing
fetal hypoxia during contractions, especially during the second stage1.
During the second stage any vertical position can be assumed: half squatting,
kneeling down, standing up or sitting in a transformer chair (Fig. 8.12).
1 In term pregnancy the weight of uterus is 6 kg on average (3,500 g accounting for the fetus, 1 kg for
the uterus per se, 1 l for the amniotic fluid, and 0.5 l—for the blood).
Fig. 8.12. Obstetric bed
When the patient is in a vertical position, she has a better coordinated function
of abdominal muscles, muscles of the back, pelvic floor and of the entire skeletal
musculature; its function is enhanced due to gravitation. The vertical position is more
physiological for pushing. No obstetric maneuvers are performed on a patient who
is giving birth in a vertical position. The midwife watches the patient’s condition,
fetal hearbeat and supports the fetus while the head is delivered, and after that she
takes the child out of the maternal passages. In some cases the parturient woman
can deliver the child herself (Fig. 8.13).
When managing delivery with the patient in a free position one can hardly employ
the traditional obstetric stethoscope for auscultation of fetal heartbeat, especially
when the patient is pushing. At this time it is preferable to use obstetric stethopho-
nendoscope, portable or pocket Doppler device.
During the second stage, any vertical position shortens its duration, reduces
the rate of operative delivery, episiotomy, painful sensations, the incidence of fetal
heartbeat disturbance.
The traditional position lying on the back (lithotomy position) is most convenient
for the midwife, but not so for the mother or fetus.
During the third stage the patient can assume a reclining position while breastfeed-
ing her newborn. This position promotes a faster placental separation and reduces
the blood loss.
In whatever position delivery takes place, this must not prevent an immediate
placing of the newborn on the mother’s breast (Fig. 8.14).
Obstetric maneuver is a complex of consecutive manipulations at the end of the
second stage of labor that are aimed at promoting the physiological delivery process
210 Obstetrics
Fig. 8.13. Vertical delivery
and preventing intrapartum injury of the mother. Traditionally, the patient is lying
on her back in a tilting bed with the head raised, her legs bent and drawn aside, her
feet bearing against the bed. Obstetric maneuver can be also given to a patient lying
on her side with her thighs drawn aside (Sim’s position) or squatting as it is done
in some maternity hospitals (Fig. 8.15).
In traditional delivery (the patient lying on her back) obstetric manual help is
given from the moment the head begins to crown.
• The first point in obstetric manual help is to prevent early head extension. This
is necessary for the head to be delivered in a flexed position with its smallest
circumference (32 cm) leading the way, passing in the suboccipitobregmatic
diameter (9.5 cm). The midwife places her left hand’s palm on the pubis so that
the palmar surfaces of her joined fi ngers are situated on the head preventing its
extension, but she must not press on the head on any account.
Fig. 8.14. Placing the newborn on the mother’s breast
• The second point is to deliver the head from the pudendal ring outside bearing down
efforts. As soon as bearing down is over, the midwife carefully stretches the vulvar
ring with the right thumb and index fi nger above the crowning head (Fig. 8.15a).
• These two actions are performed until the head approaches the level of ischial
tuberosities (transverse diameter of pelvic outlet) with its parietal tubers.
• The third point is reducing the tension of perineum during crowning and
delivery of parietal tubers. The midwife places her left hand’s palmar surface
on the perineum, so that her four fingers are in the area of the left labium
majus, and her thumb drawn aside, in the area of the right labium majus.
With all her fingers she carefully moves the soft tissues in the direction of the
perineum providing some spare tissue and thus reducing the perineal tension.
The palm of the same hand supports the perineum without pressing the palm to
the crowning head on any account. Thus the spare tissues reduce the perineal
tension restoring the blood circulation and preventing perineal laceration
(Fig. 8.15b).
• The fourth point is regulating the bearing down efforts (occurs simultaneously with
point three). This is necessary as perineal tissues experience maximum tension
during crowning. If the parturient woman does not suppress her pushing, her
perineum can be torn. The bearing down efforts are regulated in the following
way: when the fetal head with its parietal tubers is stationed in the pudendal
fissure, and its suboccipital fossa is under the symphysis pubis, the patient is told
to give deep frequent breaths with her mouth open. With this respiration pushing
becomes impossible. All the while the midwife carefully moves the perineum
above the fetae face with her right hand, and extends the head slowly and raises it
with her left hand. If pushing is needed at this moment, the patient is offered to
push with a force sufficient for delivering the head.
212 Obstetrics
b
Fig. 8.15. Obstetric maneuver in occipitoanterior variety of vertex presentation: the second
and third points
• The fifth point is freeing the shoulders and delivering the trunk. Now the midwife
waits for internal rotation of shoulders and external rotation of the head under the
impact of pushing, and then she starts upon the fifth point of maneuver. When
the external rotation of the head is complete, she needs to help the shoulders to
get out so she takes the fetal head with both hands and pulls it back slightly until
the anterior shoulder passes under the symphysis pubis. Then she grasps the head
with her left hand so that her palm is on the posterior fetal cheek. Lifting the head
forward, the perineum is carefully pushed from the posterior shoulder. As a result,
first the posterior shoulder is delivered, and then—the anterior shoulder (Fig. 8.16).
When the head is delivered, the head and shoulders should be given time to rotate
on their own, at the same time the midwife checks for cord entanglement. If the
cord is tight, it should be clamped in two places; if it is loose, it should be loosened
b
Fig. 8.16. The fi fth point of maneuver: a — the head is extended, the brow, face and chin are
delivered, the fi fth point is beginning; b — delivering the posterior shoulder
further; then the midwife waits for the next pushing (cyanosis of the face is not a
sign of danger).
Once the shoulder girdle is delivered, index fingers are introduced under the
armpits from the back side raising the trunk forward; as a result the lower part of
the trunk is delivered without a difficulty.
Physiological delivery is attended by a midwife.
Routine dissection of the perineum (perineo- and episiotomy)

NB! during labor is not advisable.
Dissection of the perineum during labor should not be done in patients with third
or fourth degree perineal tears in past history.
214 Obstetrics
At present the WHO limits intrapartum episiotomy to the following:

• complicated vaginal delivery (breech presentation, fetal shoulder dystocia,
application of forceps);
• cicatricial changes of the genitals due to female circumcision or poorly healed
third or fourth degree tears;
• fetal distress (acute hypoxia).
A neonatologist should always be present at a delivery; the specialist examines the
newborn immediately, desirably on the mother’s chest.
Care of the cord is performed in two stages. Primary care of the cord: after vascular
pulsation is over or in 1–3 minutes but not later than 10 minutes after the delivery
the cord processed with a skin antiseptic is cut between two clamps with a sterile
instrument (Fig. 8.17). The midwife performs the secondary care of the cord on a
heated newborn table having scrubbed and disinfected her hands and having put on a
sterile gown. A plastic clamp is applied to the cord aseptically; the optimum distance
from abdominal skin to the clamp is 1 cm. The cord is swabbed with a sterile gauze
napkin with an antiseptic. The umbilical stump is not covered with a gauze napkin.
During childbirth one should not do any of the following:
• transfer the parturient woman to the delivery room (on a delivery bed) until the
head crowns (the head is visible 2–4 cm in the pudendal fissure; between bearing
down efforts the head does not go away);
• perform early episio-, perineotomy. The notion of rigid perineum implies there
is obstacle to fetal head progress for 1 hour and longer;
• administer uterotonics to shorten the second stage of labor;
• counteract fetal head extension;
• regulate the pushing with breath-holding on a full inspiration (Valsalva’s
maneuver);
• try to deliver the baby during one pushing;
• lift the baby above the mother’s body (the level of the placenta) if the cord has
not been clamped;
• administer methylergometrine during the second stage of labor to prevent blood loss.
Fig. 8.17. Primary care of the cord

8.4.3. The third stage of labor

When the fetus has been delivered, the third—placental—stage of labor begins; it
lasts until the placenta is expelled. The placental stage lasts 10–15 minutes on aver-
age; it should not be protracted by more than 30 minutes.
There are three different notions which must not be con-

NB! fused:
• mechanisms of placenta separation, two of them;
• signs of placenta separation, several of them;
• techniques of afterbirth removal (several manual techniques).
8.4.3.1. Mechanism of placenta separation

Placenta separation begins in the centre where a retroplacental hematoma de-
velops, which promotes further separation of the placenta. This way of placenta
separation is referred to as central (Schultze mechanism). In central separation of
the placenta there is no external hemorrhage, and the retroplacental hematoma is
delivered together with the placenta.
Separation of the placenta can begin at its edge (Duncan mechanism), in this case
no retroplacental hematoma develops; however, each contraction increases the area
of placental separation. In this type of separation there is vaginal bleeding once the
separation process begins (Fig. 8.18).
Fig. 8.18. Placenta separation: a — by Schultze mechanism; b — by Duncan mechanism

216 Obstetrics
8.4.3.2. Signs of placenta separation
In certain cases the separated placenta can be retained. That is why it is essential
to know the signs indicating that the placenta has detached from the uterus and is
situated in its lower segment, in the cervix or vagina:
• Kustner sign: when the sharp of the hand is pressed over the symphysis pubis, the
cord is not pulled into the genital tract (Fig. 8.19);
• Alfeld sign: the detached placenta sinks to the lower uterine segment or
vagina so that the ligature or clamp placed on the cord when ligating it goes
down;
• Schroeder sign: change in the shape of uterus or fundal height. Immediately
upon delivery of the fetus the uterus becomes oval and positions itself along
the middle line. The fundus is at the navel level. After placental separation the
uterus extends, shifts to the right, and the fundus rises to the right subcostal
space.
As administration of uterotonics at the end of the second and at the beginning of
the third stage of labor has become widespread practice, Schroeder sign has lost its
utility. Other signs of placenta separation were proposed; however, they did not find
recognition in clinical practice:
• Dovzhenko sign: retraction of the cord upon deep respiration indicates that the
placenta has not detached;
• absence of cord retraction upon inspiration indicates separation of the placenta;
• Strassman sign: oscillating motions of blood in the placenta upon tapping the
uterus are transmitted along the cord if the placenta has not detached;
• Klein sign: upon pushing or slight pressing down on the uterus the cord moves
outside and does not retract if the placenta has detached.
The main function of the obstetrician is to provide aseptic management of the
delivery with continuous monitoring of the mother’s and fetal condition.
Delivery of fetus in vertex presentations is performed by the midwife. During the
expulsion stage the obstetrician monitors the fetal heartbeat and the progress of labor.
(S)he prescribes drugs, performs surgery (perineo-, episiotomy).
All abnormal deliveries, including those in breech presentation, are performed by
the obstetrician; (s)he manages forceps delivery, vacuum extraction of the fetus and
the like.
Fig. 8.19. Kustner sign

8.4.3.3. Methods of delivery of placenta (afterbirth)
If, according to all signs, placental separation has occurred, it should be delivered
at once: the patient is asked to push. Under the impact of abdominal muscles the
separated placenta is usually delivered without a problem. If this technique fails, one
resorts to delivery of the placenta by external techniques.
• Baier method: the abdominal wall is taken by both hands forming a longitudinal
fold, and the patient is asked to push.
• The separated afterbirth is then easily delivered due to a considerable increase in
the intraabdominal pressure (Fig. 8.20).
• Genter method: the fundus is brought to the middle line. The obstetrician stands
at the patient’s side facing her legs. The obstetrician clenches hands into fists
and places the dorsal surface of proximal phalanges at the fundus angles and
gradually presses on the fundus in the downside and inside direction. When this
technique is performed, the patient should not push (Fig. 8.21).
Fig. 8.20.
Fig. 8.21. Genter method of placenta delivery

218 Obstetrics
• Crede’s method: the uterus is brought to median position, applying gentle

massage the obstetrician induces uterine contractions. The fundus is grasped by
4 fi ngers behind and the thumb in front to squeeze the placenta. After that the
placenta is expressed: the uterus is compressed in the anteroposterior direction,
and the fundus is pushed downwards and backwards along the pelvic axis to expel
the placenta (Fig. 8.22).
The placenta is usually delivered as an entire whole, but sometimes the membranes
connected with the placenta are retained in the uterus. In this case the obstetrician
takes the delivered placenta and rotates it slowly in one direction. The membranes
are thus twisted, which promotes their detachment from the walls of uterus and
expression outside without a rupture.
There is another technique of membrane expression (Genter method). After the
placenta has been delivered, the patient is asked to bear down on her feet and raise
the pelvis. In this case the placenta hangs down, its weight making the membranes
detach and express.
If fetal membranes have ruptured, the obstetrician explores carefully the upper
portion of the vagina wearing sterile gloves; fenestrated forceps are operated to re-
move all the retained parts of fetal membranes that can be discovered.
8.4.3.4. Prevention of postpartum hemorrhage

According to WHO recommendations (2012) prevention of postpartum hem-
orrhage consists in routine administration of oxytocin (within the first min-
ute upon delivery of the fetus 10 units by intramuscular or slow intravenous
administration) and performing controlled cord traction (if there are trained
specialists).
• intravenous administration of 10 units of oxytocin 2 minutes after delivery of the
fetus;
• gentle external massage of the uterus;
• manual maneuver: one hand of the obstetrician above the pubis presses on
the contracted uterus and shifts in the direction of the navel; the other hand
Fig. 8.22. Crede’s method of placenta expression

performs traction of the cord (performed by a trained specialist) (Andrew-Brandt

manevues).
The opponents of this method believe that its disadvantage is the increased risk of
uterus inversion, cord rupture and retaining of placental tissue in the uterus.
Considering the fact that controlled cord traction has no significant effect on the
rate of massive bleeding, it should not be performed by untrained personnel; instead,
only oxytocin should be administered.
The upper limit of physiological blood loss is 0.5% of body weight (5 ml per 1 kg
of body weight).
Management of postpartum period should consist in expectant attitude and careful
observation of the patient. If the woman is in a satisfactory condition and there are
no signs of external or internal bleeding, one can expect spontaneous separation and
delivery of the placenta within 30 minutes.
The afterbirth period should not exceed 30 minutes.

NB!
After delivery of the placenta it should be carefully examined including the mem-
branes to make sure they are intact.
If the cord has ruptured or the placenta was not expressed within 30 minutes,
manual expression of the placenta is performed. When the placenta is delivered, the
tone of uterus is assessed at once through the anterior abdominal wall.
The uterine tone should be assessed every 15 minutes within the first 2 hours of
the postpartum period (early postpartum period). The midwife or the obstetrician
evaluating the uterine tone must make sure that the uterus has contracted satisfac-
torily and does not relax (become soft).
Duration of labor is:
• 12–16 hours in primiparous women:
– the first stage 10–14 hours;
– the second stage up to 2 hours;
– the third stage up to 30 minutes;
• 6–8 hours in multiparous women:
– the first stage 5.5–7 hours;
– the second stage up to 1 hour;
– the third stage up to 30 minutes.
Labor is considered rapid if it lasts less than six hours in primipa-

NB! rous women, and less than four hours in multiparous women. Labor
is termed precipitous if it lasts less than four hours in primiparous,
and less than two hours in multiparous women.
There is a notion of precipitous labor which lasts less than one to two hours.
The birth canal — the perineum, vagina and cervix — are inspected immediately
after childbirth to estimate possible maternal injury. If lacerations are detected, they
are repaired aseptically according to all rules of surgery. The puerpera (the woman
who gave birth is referred to as puerpera) should remain for 2 hours in the delivery
220 Obstetrics
room for observation. The obstetrician evaluates her general condition, tone of the
uterus (every 15 minutes), the nature of discharge from the genital tract, measures
her BP and pulse.
If all goes well, in 2 hours the puerpera is transferred to the postdelivery depart-
ment together with the newborn.
8.4.3.5. Care of newborn in the delivery room

While in the delivery room, heat loss by the newborn should be prevented, and
principles of modern perinatal care should be observed.
After birth the baby is wiped, the first wet diaper is replaced with a dry one. After
that it should be determined whether the baby requires rehabilitation procedures.
When examining the baby one pays attention to the following:
• presence of spontaneous respiration, cardiac contractions, skin coloration;
• presence of congenital defects or diseases;
• the degree of maturity and signs of fetal growth restriction.
Signs of satisfactory condition at birth:
• spontaneous respiration within 30 minutes upon delivery;
• loud crying;
• heart rate above 100 per minute;
• pink skin color.
The first examination of the newborn is best of all performed immediately after
birth, on the mother’s chest. Sanation of the upper airway is performed only if indi-
cated; the same applies to gastric intubation. If the baby is in a satisfactory condition,
after being wiped it is placed on the mother’s (father’s) abdomen and covered with
a thick diaper (blanket).
There is no need for special processing of the skin, removal of vernix
caseosa or complete washing of the newborn’s body. Vernix caseosa is not
removed in the delivery room. It is not recommended to wash the newborn
with tap water in the delivery room. If the baby’s skin is dirtied with blood
or meconium, it is removed carefully with a piece of cotton wool moistened
with warm water.
The newborn is covered with a thick dry diaper and / or blanket, a bonnet is put
on the head. The skin-to-skin contact with mother should last from 40 minutes to
2 hours. The mother and baby should be covered with one blanket.
The first breastfeeding of the newborn should take place as soon as possible
after delivery and not later than after 1.5 hour. At the end of the first hour after
birth preventive administration of ointment (prevention of gonoblennorrhea) to the
newborn’s eyes (1% tetracycline or 10 000 units per 1 g erythromycin in individual
container) or of eye drops (20% sulfacetamide solution) is performed. It is not
recommended to administer silver nitrate which can cause chemical conjunctivitis
and pain reaction in newborns. To date there is no evidence supporting the ef-
fectiveness of sulfacetamide.
Primary care of the newborn, anthropometry and wrapping is performed no earlier
than the first hour after birth, after skin-to-skin contact with the mother. In all new-
borns the temperature is measured 4 times during 2 hours in the delivery room and
after transfer to the postpartum ward. In 2 hours, if there are no complications on
the part of the mother or the newborn, the midwife takes them both in a wheelchair
or on a stretcher to the postpartum ward for rooming-in.
When the puerpera has been transferred, the delivery room is cleaned in the mode
of terminal disinfection.
REMEMBER!
Definitions Labor is the process of expulsion or extraction of gestational

sac (product of conception: the fetus and parafetal structures)
from the cavity of uterus after the fetus has become viable.
Precursors of labor constitute a complex of clinical
manifestations; their emergence four to two weeks prior to
childbirth indicates that childbirth is near
Classification The act of childbirth is commonly divided into three stages:

• stage one — period of dilation;
• stage two — period of fetus expulsion
• stage three — placental expulsion period (separation of
placenta, afterbirth delivery)
Clinical Effacement and dilation of the cervix proceed differently in

manifestations primiparous and multiparous women.
and management A vaginal obstetric examination during the period of dilation is
performed regularly every 6 hours if there are no emergency
indications. Irrespectively of the duration of labor, the patient
is given a vaginal examination upon admission to maternity
hospital, immediately upon rupture of membranes, developing
signs of fetal hypoxia, vaginal bleeding, before administering
anesthesia and for other indications. Obstetric maneuver is a
complex of consecutive manipulations at the end of the second
stage of labor that are aimed at promoting the physiological
delivery process and preventing intrapartum injury of the
mother.
The placental period lasts for 10–15 minutes on average; it
should not be protracted over 30 minutes. The upper limit of
physiological blood loss is 0.5% of body weight (5 ml per 1 kg
of body weight).
CONTROL QUESTIONS
1. What are precursors of labor?

2. What is the preliminary period?
3. What are the stages of labor?
4. What are the principles of managing a normal delivery?
5. What is an obstetric maneuver?
6. What signs of placental separation do you know?
7. What is the primary care of the cord?
8. What is the secondary care of the cord?
222 Obstetrics
CHECK YOURSELF!
Level 1. Test
1. The preliminary period corresponds to:

a) passing of amniotic fluid;
b) formation of delivery dominant;
c) onset of labor;
d) ripening of the cervix;
e) engagement of fetal head in the lesser pelvis inlet.
2. The beginning of labor is:

a) onset of contractions that leads to structural changes in the cervix;
b) passing of amniotic fluid;
c) progress of fetal head along the birth canal;
d) onset of cramp-like pain;
e) pushing.
3. During the second stage the following typically happens:

a) passing of amniotic fluid;
b) pushing;
c) cervical dilation 10 cm;
d) accelerated fetal heartbeat;
e) engagement of fetal head in the pelvic inlet.
4. The first stage ends with:

a) birth of the newborn;
b) birth of the placenta;
c) complete cervical dilation;
d) fetal head crowning;
5. Cervical dilation takes place due to:
a) contraction of muscular fibers;
b) shifting of muscular fibers;
c) shortening of the cervix;
d) passing of amniotic fluid;
e) firm adherence of the lower segment to the fetal head.
6. Obstetric maneuver during labor is rendered upon:

a) bleeding from the vagina;
b) fetal head delivery;
c) development of perineal edema;
d) fetal head crowning;
e) threat of perineal tear.
7. The afterbirth period begins upon:

a) delivery of the fetus;
b) separation of the placenta;
c) cutting the umbilical cord;
d) complete cervical dilation.
8. Baier method is applied if:

a) there are no signs of placental separation for 2 hours;
b) there are no signs of placental separation for 30 minutes;
c) there is vaginal bleeding;
d) there are signs of placental separation;
e) placental lobules are retained in the uterus.
9. Maximum blood loss in normal delivery is:

a) 600 ml;
b) 350 ml;
c) 0.5% of body weight;
d) 1000 ml.
10. The first toilet of the newborn does not include:

a) auscultation of fetal heartbeat;
b) treatment of the eyes;
c) two-step cutting of the cord;
d) treatment of the skin;
e) fetal anthropometry.

1. A primigravida aged 20 was brought to the maternal hospital with contractions
at 5–6 min interval, of 40–45 s duration, of medium strength and painfulness, which
had lasted for 7 hours. BP 115/70 mm Hg, pulse 80 bpm, of satisfactory strength.
Obstetric examination: abdominal circumference 96 cm, fundal height 32 cm, pelvis
dimensions 26–29–32–21. The fetus is in longitudinal lie, cephalic presentation,
fetal head tight at the lesser pelvis inlet. Fetal heartbeat clear, rhythmical, 146 per
minute, on the left below the navel. The cervix is effaced, dilation 5 cm, edges thin,
extensible. The gestational sac is intact, fills well upon contractions. The posterior
fontanelle is anterior and left, the anterior fontanelle—posterior and right, it is higher
than the posterior fontanelle; the sagittal suture is in the right oblique diameter. The
promontory is not palpable. No exostoses in the lesser pelvis. Mucous discharge.
What is your diagnosis? Substantiate it.
2. A secundigravida aged 26 was brought to the maternity hospital upon onset of
contractions. Her first pregnancy outcome was physiological delivery. Fetal weight
3200 g, length 52 cm. The present pregnancy is the second one. Pelvis dimensions
25–28–31–20. The fetus is in longitudinal lie. Fetal head is in the lesser pelvis
cavity. Fetal heartbeat clear, rhythmical, 132 per minute. The cervix is effaced,
complete dilation. No gestational sac. The fetal head is in the lesser pelvis cavity; it
224 Obstetrics
accommodates the entire surface of symphysis pubis, the entire sacral fossa, coccyx,
and ischial spines on the sides. The posterior fontanelle is anterior at the pubis, the
anterior fontanelle is posterior at the sacrum, above the posterior fontanelle. The
sagittal suture is in the anteroposterior diameter. What is your diagnosis? Substantiate
it. In which plane of the lesser pelvis is the fetal head stationed?
NOTES
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• Chapter 9
OBSTETRICAL ANESTHESIA
Relieving pain during labor is the basis of obstetric anesthesia. Pain is both a sen-
sory and emotional pathological condition. This fact led clinical practitioners to see
that a formal administration of analgesic drugs in response to a woman’s complaint
is unacceptable as analgesia implies more than mere administration of drugs. The
obstetrician should understand the cause of pain and explain it to the patient as lack
of mutual understanding can result in failed anesthesia.
Anesthesia with medications is not required in every labor;

NB! however, each parturient woman requires emotional support.
9.1. CAUSES OF PAIN IN LABOR
Immediate causes of pain during delivery are as follows:

• cervical dilation;
• contraction of the uterus and tension of round ligaments of the uterus, parietal
peritoneum which is an especially sensitive reflexogenic area;
• excitation of periosteum on the inner sacral surface due to the tension of
sacrouterine ligaments and mechanical compression of this area while the fetus
is passing through it;
• excessive contraction of the uterus as a sex organ when there are relative obstacles
to its evacuation, resistance of pelvic floor muscles;
• vascular constriction and expansion during uterine contractions; the vessels
form an extensive network, and their baromechanoreceptors are highly
sensitive;
• changes in the chemical activity of tissues: accumulation of underoxidized
products of tissue metabolism (lactate, pyruvate) that occurs during a prolonged
contraction; temporary ischemia of the uterus due to repeated contractions
(Fig. 9.1).
At present all methods of labor anesthesia are conditionally divided into two
groups.
• Group one: non-pharmaceutical methods of pain relief
• Group two: pharmaceutical methods of pain relief.
226 Obstetrics
Contraction
Altered chemistry,
and dilation
tissue ischemia
of blood vessels
Irritation
Myometrium
PAIN of sacrum
contraction
periosteum
Muscles Tension in round

of pelvic floor ligaments
resisting and peritoneum
Cervical
dilation
Fig. 9.1. Causes of labor pain
NB! It is not the purpose of analgesia to eliminate pain altogether.
9.2. NON-PHARMACEUTICAL METHODS OF PAIN RELIEF
Non-pharmaceutical methods of pain relief target the psychophysiological aspect

of pain. Individual perception of pain by the patient depends on a series of interrelated
compounding factors such as the patient’s physical condition, expectations, frustra-
tion, motivation and bringing-up. Non-pharmaceutical methods of pain relief are:
• psychoprophylaxis (childbirth education);
• the greatest possible support on the part of the family;
• providing information to the patient and her family about the progress of labor
making it as detailed as they need. The information should be truthful; when
talking about a proposed intervention or method of management both positive
and negative sides should be discussed;
• the patient should be free to move about during the first and second stages of
labor;
• vertical body position during labor pains (except when the waters have discharged
and the fetal head is not securely engaged). The personnel should encourage the
patient to assume vertical positions;
• massage;
• respiration technique combined with relaxation;
• taking a shower or a bath;
• music;
• aroma therapy;
• alternating heat and cold;
• acupuncture and acupressure.
Chapter 9. Obstetrical anesthesia 227
None of the methods of non-pharmaceutical pain relief have proven efficacy.

Rather, their value is in distracting the woman, leading her to perceive childbirth as
an extremely exciting, important event; at any rate, these methods can do no harm.
When expectant mothers attend classes in childbirth education, special attention is
paid to explaining the mechanism of labor pain and methods of pain relief. Labor pain
is fed by fear of the unknown, apprehension, previous negative experience. At the same
time, pain attenuates or is better tolerated if the patient has assurance, understanding of
the childbirth process, if her expectations are realistic enough; respiration techniques,
trained reflexes, emotional support and other methods of distraction are also of help.
For all physiological methods to succeed, the patient herself should make her choice.
Success of these methods is associated with sincere commitment on the part of the
parturient woman and personnel, with a substantial social, economic and educational
background, positive experience in the past and normal labor.
9.3. PHARMACEUTICAL METHODS OF PAIN RELIEF
Pain and anxiety in parturient woman are relieved with anesthetics, opioid and
non-opioid analgesics and their combinations with sedative and neuroleptic drugs.
The choice of drugs should be based on the following points:
• the administered drug should produce a strictly selective analgesic effect without
a pronounced narcotic action;
• the combination of analgesics with spasmolytic drugs decreases the duration of
labor, especially of its first stage;
• the analgesic effect can be prolonged by choosing a combination of drugs that
potentiate and mutually prolong each other’s effect in small doses;
• analgesia should not suppress labor or affect the fetus or newborn in a negative way;
• the method should be easily manageable and available.
Drugs administered in childbirth can be divided into three types:
• drugs of parenteral administration to relieve pain and anxiety;
• drugs administered for local infiltration and regional block;
• drugs used for inhalation analgesia and anesthesia.
All drugs pass the placental barrier at a different rate and in varying amounts; this
applies both to inhalation anesthetics and local anesthetics.
9.3.1. Opioid analgesics

Drugs of this type are the most effective powerful agents used in labor anesthesia,
although none of them can ensure effective pain relief without adverse reactions
affecting the mother and / or fetus. These drugs are administered to relieve rather
than to eliminate pain completely. The most severe adverse reaction produced by
opioid drugs is suppression of respiration both in the mother and fetus. Besides, all
opioid drugs produce orthostatic hypotension due to peripheral vasodilatation. They
can attenuate uterine contractions during the latent or early active phase of labor.
However, when labor is progressing stably, opioid drugs can improve uncoordinated
uterine contractions.
228 Obstetrics
Several opioid drugs are available. In a carefully chosen dose they produce a similar
analgesic effect; the choice is usually made on the basis of potential adverse effects
and the desired duration of analgesia. Intravenous administration is preferable, as a
rule, compared with intramuscular administration as intravenous infusion reduces
the effective dose by 1/3–½, and the effect sets in much faster (in 5–10 minutes
compared with 40–50 minutes).
Promedol is one of most commonly administered analgesics. Fentanyl is admin-
istered less often; it is given via intramuscular injections in a dose of 0.5–1.0 ml of
0.005% solution. The dose can be repeated in 3–4 hours, if necessary.
Like all morphinoid drugs, promedol and fentanyl show all the disadvantages
mentioned above. Fortral (pentazocine) that is now undergoing clinical trials does not
cause any of these adverse reactions. Preliminary findings indicate that it stimulates
hemodynamics and respiration, and hysterography findings indicate that it produces
a labor stimulating effect. By convention, this drug is considered non-opioid, unable
to cause addiction.
Tramadol is successfully administered for pain relief in spontaneous labor, in a
dose of 50–100 mg IM; it does not produce any negative effect on the progress of
labor or the newborn’s condition.
9.3.2. Ataralgesia
A combination of analgesics with sedative /tranquilizing drugs is used during labor
to diminish agitation, nausea and vomiting. The achieved sedative effect permits a
decrease in the dose of opioid drugs.
9.3.3. Inhalation analgesia

The advantage of inhalation analgesia is the possibility of administering low con-
centrations of substances with analgesic properties, which means achieving analgesia
without depression of consciousness or protective reflexes (retaining the ability to
follow instructions), reducing the risk of adverse reactions. The parturient woman
should start inhaling the gas or inhalation substance as soon as she perceives the be-
ginning of a contraction; continuous inhalation is also possible. Nowadays dinitrogen
oxide becomes increasingly popular for inhalation anesthesia. During labor a mixture
a b
Fig. 9.2. Inhalation anesthesia: a — inhalation device; b — self analgesia during labor
of 50% nitrous oxide and 50% oxygen can be administered by the patient herself as
self-analgesia. The mixture composition can be varied: from 30% nitrous oxide and
70% oxygen for patients who received parenteral analgesics, and 40% nitrous oxide
+ 60% oxygen for patients who received no other analgesia (Fig. 9.2).
9.3.4. Regional anesthesia

The main methods of regional anesthesia include:
• epidural anesthesia;
• pudendal block;
• local perineal infi ltration.
An ambition to achieve a full-scale analgesic effect during labor with least pos-
sible effect on the maternal and fetal body prompted the development of epidural
block. The epidural nerve block produces a pronounced analgesic and spasmolytic
effect while at the same time it does not suppress the function of respiration, cardiac
activity, renal or hepatic function.
The principle of epidural anesthesia consists in administering an analgesic
agent into the epidural space, which blocks the subdural nerves in segments
Th10-L1(Fig. 9.3).
In contrast to spinal anesthesia, epidural nerve block has a favorable effect
on the course of preterm labor; it shortens the period of cervical dilation and
prolongs the expulsion stage with a smoother progress of the head. The epidural
block promotes relaxation of perineal muscles thus decreasing the pressure on
the fetal head. Studies established a positive effect of epidural nerve block in
complicated labor.
It was noted that women who received opioid analgesics delivered babies with
considerably poorer neuroreflex activity compared with mothers who received epi-
dural nerve block during labor.
Nowadays epidural anesthesia includes both local anesthetics and opioid and non-
opioid analgesics. Epidural anesthesia provides a prolonged and effective pain relief
from the onset of labor to delivery of the fetus; however, it can produce complications
if the patient is not monitored carefully.
The most attractive effect of this type of analgesia is the fact that the woman
remains conscious and can take an active part in the process of labor; she can begin
caring for the newborn from the moment of birth.
Additional manipulations during and after labor, like episiotomy, perineorrhaphy,
manual examination of the uterus cavity can be easily performed if the woman re-
ceived epidural anesthesia. If a need for cesarean section arises during labor, it can
be performed with sole epidural block without additional general anesthesia.
Pudendal block (Fig. 9.4) is administered for the purpose of analgesia during
the second stage of labor, especially if it is preterm labor, when applying vacuum
extractor as the woman should remain conscious, as well as when dissecting the
perineum or repairing it. The block can be given via the perineum or the lateral
vaginal walls. 10 ml of 0.5-1% procaine (Novocain) solution or 4 ml of 1% lido-
caine solution is injected in the region of pudendal nerve branches (ischiorectal
space) on both sides.
230 Obstetrics
spi
nal
anes
thesi
a
epidural
b c
Fig. 9.3. Regional anesthesia: a — position of the parturient woman receiving epidural
anesthesia; b — installing the epidural catheter
a b
Fig. 9.4. Pudendal nerve block. Its types: a — via the perineum; b — via the lateral vaginal walls
Any method of pharmaceutical anesthesia in labor including

NB! regional anesthesia, has its downsides.
Local perineal infiltration is mostly administered for repair of the soft tissues of
the birth canal that were injured during childbirth.
REMEMBER!
Anesthesia is not required in every childbirth.
Analgesia during labor is not aimed at complete elimination of pain.
Non-pharmaceutical methods of analgesia include:

• psychoprophylaxis;
• providing information to the patient and her family about the progress of labor
making it as detailed as they need. The information should be truthful; when
talking about a proposed intervention or method of management both positive
and negative sides should be discussed;
• the patient should be free to move about during the first and second stages of
labor;
• vertical body position during labor pains (except when the waters have discharged
and the fetal head is not securely engaged). The personnel should encourage
the patient to assume vertical positions;
• massage;
• respiration technique combined with relaxation;
• taking a shower or a bath;
• music;
• aroma therapy;
• alternating heat and cold;
• acupuncture and acupressure.
Pharmaceutical methods of pain relief include the administration of:

• opioids;
• tranquilizers;
• anesthetics;
• inhalation anesthetics;
• local anesthetics.
Any method of pharmaceutical anesthesia during labor has its downsides.
Drugs administered during labor can be divided into three types:

• parenteral drugs for relief of pain and anxiety;
• drugs administered for local infiltration and regional block;
• drugs for inhalation analgesia and anesthesia.
CONTROL QUESTIONS
1. What are the causes of pain syndrome development during delivery?

2. What are non-pharmaceutical methods of anesthesia during labor?
3. What is the effect of acupuncture on labor pain?
4. What are the basic requirements to pharmaceutical analgesia during labor?
5. What are the types of regional anesthesia, what drugs are administered?
6. What are the advantages of epidural anesthesia?
232 Obstetrics
CHECK YOURSELF!
Level 1. Test
1. Neuroleptanalgesia requires administration of:
a) a neuroleptic drug;
b) combination of a neuroleptic and a sedative drug;
c) combination of a neuroleptic and an analgesic drug.
2. Non-pharmaceutical methods of analgesia include:

a) neuroleptanalgesia;
b) acupuncture;
c) regional anesthesia;
d) pudendal block.
3. Local infiltration of the perineum is used for:

a) repair of lacerated soft tissues of the birth canal;
b) cesarean section;
c) vacuum extractor application.
Epidural analgesia is used for:

a) the first stage of labor only;
b) forceps-assisted delivery only;
c) from the onset of labor to delivery of the fetus;
d) cesarean section only.

The parturient woman is in the first stage of labor. The rate of contractions is every
3 minutes. A vaginal examination reveals that the cervix is effaced, dilated 3 cm, the
least diameter of the fetal head is in the plane of pelvic inlet. In two hours dilation is
5–6 cm, the greatest diameter of the fetal head is in the plane of pelvic inlet. Labor
pains are frequent (5–6 in 10 minutes), painful. What is your diagnosis? What is the
plan of management?
NOTES
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• Chapter 10
BREECH PRESENTATION
10.1. BACKGROUND
The incidence rate of breech presentation decreases from 40% at 24 weeks ges-
tation to 3% at 40 weeks as most fetuses (over 90%) change their presentation to
cephalic spontaneously by the end of pregnancy. This apparently reflects a congenital
ability of a mature active fetus to assume the most convenient position that is con-
gruent to the uterine cavity whose shape is like that of pear turned upside down.
Breech presentation can be associated with anomaly of the fetus itself, pathological
volume of amniotic fluid, specific localization of the placenta, relative shortness of
the umbilical cord due to its entanglement. The higher rates of neonatal mortality
and morbidity in breech presentation are associated, first of all, with fetal immaturity,
congenital anomalies of development (predominantly of the CNS), as well as with
asphyxiation or trauma during labor.
The main method of decreasing the rate of adverse neonatal outcomes in breech
presentation is cesarean section. Over the recent decade in most countries of Western
Europe, USA and Canada elective cesarean section has become almost the only ac-
ceptable method of delivery in breech presentation. In 1970 about 14% of fetuses in
breech presentation were delivered via cesarean section. According to the National
Center for Health Statistics in the USA, in 2005 the incidence rate of cesarean sec-
tion in breech presentation amounted to 87.2%.
10.2. DEFINITION
Breech presentation is a situation when the fetus is in longitudinal lie, and the
presenting part is the pelvic pole (the buttocks, buttocks and feet, feet, knees).
10.3. ICD-10 CODE
O32.1. Maternal care for breech presentation
10.4. TERMINOLOGY
Terms
Breech presentation (Middle English breeches, from Old English brec, plural of
broc leg).
234 Obstetrics
Types of attitude in breech presentation (Fig. 10.1):

• frank breech presentation: the baby’s legs are up next to its abdomen, with its
knees straight and its feet next to its ears . This is the most common type of
breech, it accounts for 65% of all breech presentations;
• complete (flexed) breech is when the baby appears as though it is sitting crossed-
legged with its legs bent at the hips and knees; it is seen in 25% of cases;
a b
c d
Fig. 10.1. Varieties of breech presentation: a — frank breech; b — complete or flexed breech;
c — double footling presentation; d — single footling
Chapter 10. Breech presentation 235
• footling presentations:
– double (both legs are the presenting part) and single (one leg is the presenting
part) footling; this type is noted in 10% of cases;
– rarely seen knee presentation, which can be single or double (0.3% of cases).
10.5. PREVALENCE
On average, breech presentation is seen in 4–4.5% of all deliveries. In preterm

delivery or multiple gestation the prevalence of breech presentation increases two to
ten times (Fig. 10.2)
Methods of delivery in breech presentation. Until the middle of the 20th century
the main method of delivery was vaginal delivery assisted by obstetric maneuvers
to help along the delivery of the head and arms. As the rate of cesarean section
increased, the rate of abdominal delivery in breech presentation increased as well.
This trend grew strong in recent time (Fig. 10.3) after Mary Hannah et al. com-
pared perinatal outcomes of vaginal deliveries and elective cesarean sections for
term fetus in breech presentation.
The paper sets forth convincing evidence that perinatal mortality in elective
cesarean section is 3 compared with 13 for vaginal delivery, and neonatal morbid-
ity on the whole is 14 compared with 38, and in the population of low perinatal
risk—4 compared with 51, correspondingly. As a result, in the Netherlands the
rate of cesarean section in breech presentation grew from 50% in 200 to 80% af-
ter 2001 while the total rate of cesarean section grew from 5.2% in 1983 to 14%
in 2005.
Rate of breech presentation (%)
45
40
35
30
25
20
15
10
5
0 24 26 28 30 32 34 36 38 40 42
Gestational age, weeks
Boys Girls
Fig. 10.2. Dependence of breech presentation incidence on gestational age (Rietberg C., 2006)
236 Obstetrics
%
100
90
Total CS rate
80
70
60
Planned CS
50
40
30
Vaginal birth
20
10
0
1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005
Fig. 10.3. Method of delivery (in percentage) in breech presentation on an example

of the Netherlands before and after the publication of the study Term Breech Trial
(Hannah M. et al., 2000)
10.6. COMPLICATIONS OF VAGINAL DELIVERY

IN BREECH PRESENTATION
A breech baby can be born spontaneously, without complications.
NB! However, the course of labor in breech presentation has its specifics
which may pose a threat to the child, and sometimes – to the mother.
Perinatal mortality in breech presentation is 2 – 5 times higher.
10.6.1. Complications of the first stage of labor

Complications may develop from the very beginning of labor: cervical dilation
usually proceeds at a slower pace, buttocks spend quite a long time above the pelvic
inlet, no belt of adherence is formed, amniotic fluid is not divided into anterior and
posterior waters. This leads to preterm rupture of fetal membranes and often — to
cord prolapse, primary uterine inertia. Protracted duration of labor and a prolonged
rupture to delivery interval increase the rate of infectious complications in the mother
and newborn.
10.6.2. Complications of the second stage of labor

The expulsion period is often complicated by secondary uterine inertia.
This is especially dangerous if pushing stops at a time when the buttocks have
engaged the lesser pelvis cavity. If there emerges an urgency requiring a rapid deliv-
ery due to maternal or fetal indications (cesarean section or total breech extraction).
This is usually associated with a high risk of severe maternal and especially fetal
traumatism.
A severe complication of labor in footling presentation is preterm expulsion
of the fetus while cervical dilation is not complete: after rupture of membranes
the fetal legs descend to the vagina and irritate the cervix vigorously thus in-
tensifying labor. The legs followed by the buttocks and the trunk begin a rapid
progress along the birth canal while cervical dilation is only 5 cm. As a result the
head — the largest and hardest part of the body — is not able to pass through the
incompletely dilated cervix, which leads to fetal hypoxia and demise. Attempts
to extract the trapped head result in cervical rupture and even in rupture of the
lower uterine segment.
When the head passes through the birth canal, there is always occlusion of the
cord to pelvic walls by the head. If the head is not delivered fast enough, the situation
may end in fetal hypoxia and demise. Besides, there is a chance of such complica-
tion as nuchal arm entrapment: a disorder of attitude in which fetal arms, instead or
remaining flexed across the fetal chest, become raised up over the fetal head. If the
arms are placed in front of the face, it is degree 1, arms to the sides of head means
degree 2; arms thrown back behind the head — degree 3. That is why G.G. Genter
proposed distinguishing three degrees of arm entrapment. Traumatic injury of the
mother and fetus occurs during the second stage of labor when rendering assistance
for delivery of the arms and head. Fetal complications include fracture of arms during
the attempts to get them out, rupture of cerebellar tentorium and fetal death upon
excessive head extension, as well as lesion of various parenchymatous organs (the
liver, spleen, and adrenals).
Fetal complications: fracture of clavicles and arms when they

NB! are swept out, rupture of cerebellar tentorium and fetal demise
in case of excessive head extension.
Labor complications such as poor uterine contractions, fetal
hypoxia, and placenta previa are indications for emergency
cesarean section.
Earlier, breech presentation was considered as a transitional
stage between normal and pathological labor; nowadays breech
presentation is classified as abnormal labor.
10.7. ETIOLOGY
The established causes of breech presentation are shown in Table 10.1.

Possible causes of breech presentation can be inherited predisposition (the rate of
breech presentation reccurrence with the next pregnancy is 9.9%; after two breech
presentations — 27.5%), polyhydramnios, multiple gestation, congenital malforma-
tions (Table 10.2.; see Fig. 10.4).
238 Obstetrics
Table 10.1. Etiological factors of breech presentation
Predictor Explanation
Nullipara Resilient compact abdominal and uterine muscles
obstruct the flexion of extended legs. The flattened uterus
limits fetal freedom of movement
Uterine malformations Irregular shape of uterine cavity in abnormalities of
Mullerian ducts development
Oligohydramnios Limitation of fetal movement. Oligohydramnios is often
seen in congenital developmental defects, antenatal fetal
death
Placenta localization Placenta previa obstructs fetal head engagement.
Placental attachment in the area of one of uterine horns
results in the loss of pear-like shape of the uterus
Myoma of uterus On the whole, myoma leads to uterine cavity deforma-
tion. Myoma nodules localized in the lower uterine seg-
ment interfere with fetal head engagement
Contracted pelvis Obstacles to head engagement
Congenital malformations and Reduction in the general tone of the fetus and in motor
chromosome abnormalities activity is quite possible
(Table 10.2)
Multiple gestation Lack of space limits fetal movements
Consumption of alcohol and This may cause general reduced tone and motor activity
other psychoactive substances in the fetus
Multiparity Flabby muscles of the abdominal wall and uterus promote
unstable position of the fetus
Polyhydramnios Unstable fetal position
Preterm gestation Typical midgestational physiological polyhydramnios
(Fig. 10.4)
Fetal growth restriction, fetal An affected fetus is not inclined to move freely about.
death, relative cord shortness The effective cord length decreases by 20–30 cm on aver-
(coiling of the cord) age upon coiling around the neck once. As a result, the
short cord prevents the fetus from making the version
from breech to cephalic presentation
Table 10.2. Comparative rate of congenital malformations and chromosome abnormalities
in fetuses in cephalic and breech presentation, %
Congenital malformations Breech Cephalic

and chromosome abnormalities presentation presentation
Neural tube defect 0.22 0.06
CNS, eye, ear 0.70 0.22
Gastrointestinal organs 0.56 0.31
Bronchopulmonary system 0.24 0.10
Genitourinary organs 0.98 0.61
Anterior abdominal wall and skin 0.39 0.27
Locomotor apparatus 1.04 0.50
Chromosome abnormalities and hereditary syndromes 1.18 0.42
Total 4.40 2.42
Amniotic fluid volume, ml
3000
99%
2500
2000
g
t,
gh
ei
1500
lw
ta
fe
50%
1000
500
1%
0
8 12 16 20 24 28 32 36 40 44
Fig. 10.4. Amniotic fluid volume (1–50–90 percentile) and fetal weight in pregnancy.
From the middle of the second trimester and until 36 weeks the fetus is in conditions
of physiological polyhydramnios, which provides considerable freedom of movement
10.8. DIAGNOSTICS OF BREECH PRESENTATION
Detection of breech presentation presents no difficulty. The pregnant woman notes

fetal movements in the lower abdominal portion. An external examination (Leopold’s
maneuver) — palpating above the true pelvis inlet — reveals a mass or irregular shape
and softish consistency, and in the area of the fundus — a harder spherical structure
with clear-cut contours. The heart beat is usually auscultated above than the navel.
A vaginal examination detects a softish mass or small parts (the legs).
The final diagnosis of breech presentation and its varieties is made using sonog-
raphy.
10.9. MANAGEMENT OF PREGNANCY

IN BREECH PRESENTATION
The progress of pregnancy with breech presentation is not, on the whole, any
different from the progress of pregnancy with cephalic presentation. The pregnant
woman should be informed about the following:
• most fetuses move to head-down position spontaneously by the end of a term
pregnancy;
• breech presentation by itself is not an absolute indication for cesarean section
(Table 10.3); however, if the woman refuses point blank to give a vaginal
delivery, the obstetrician should not force her, and vice versa; in both situations
240 Obstetrics
Table 10.3. Zatuchni-Andros breech scoring index
Parameter Points
0 1 2
Parity 0 1 2 and more
Gestational age, weeks 39 38 37
Estimated fetal weight, g >3600 3200–3600 <3200
Previous breech no 1 2
Dilation, cm 2 3 4 and more
Station (Bishop score) -3 or higher -2 -1 or lower
Note: <4 points—cesarean section; 4 points—reestimation; >4 points—vaginal birth
an informed voluntary consent or refusal should be signed by the patient before

delivery;
• during a spontaneous moving of the fetus to head-down position the pregnant
woman can have sensations that are similar to clinical manifestations of preterm
labor.
It is known that there are many sets of exercises to turn the fetus from breech
to cephalic presentation. However, their pronounced effectiveness of 70–80% is
dubious, as it does not exceed the rate of a spontaneous version (turning that
occurs without exercises). A method with proven effectiveness is external cephalic
version (see Chapter 27 Operative Obstetrics) employed in some maternity care
institutions after 37 weeks gestation. The reported effectiveness of this method
is 30–80%.
If the fetus does not perform a spontaneous cephalic version by 38.5–39 weeks,
the pregnant woman is hospitalized for development of a management plan.
List of diagnostic procedures in breech presentation in hospital settings (after
38.5 weeks)
• Further evaluation:
– studying the obstetric history and revealing extragenital disease;
– ultrasonography: presentation, biometry, degree of head extension;
– X-ray pelvimetry (CT scan, MRI) if required;
– amnioscopy if required;
– evaluation of fetal condition (non-stress test and other);
– evaluation of the degree of preparedness for childbirth.
• Predicting labor outcome and choosing the plan of management.
The main decision to be made is choosing the method of delivery. An attempt to
have a vaginal delivery in breech presentation is justified if the fetus is of medium
weight, the pelvis is of normal dimensions, in the absence of severe disease or ob-
stetric complications in the mother; in all other cases cesarean section is indicated.
In breech presentation there can be an uncomplicated spontaneous

NB! delivery, but this type of presentation is always more insecure than
vertex presentation.
A high perinatal risk in a woman with breech presentation (25 points and more)
is an indication for elective operative delivery.
In most cases breech presentation is not the cause but rather

NB! a predictor of an unfavorable perinatal outcome or a marker of
certain problems existing from the outset; and a planned cesarean
section is not always able to eliminate these problems.
In the literature there exist a great variety of scoring systems to assess the degree
of prenatal risk in breech presentation.
Essential prerequisites for vaginal birth in breech presentation
• Estimated fetal weight 2000–3600 g
• Frank breech
• Pelvis of normal dimensions
• Fetal head is flexed
• Continuous CTG monitoring during labor
• Zatuchni-Andros breech scoring index ≥4 points
• Facilities for emergency cesarean section
• Adequate rate of cervical dilation and fetal progress through the birth canal
• Experience in delivering breech fetuses (!)
• Informed consent of the patient (!)
Indications for cesarean section in breech presentation
• Estimated fetal weight <1500 or >3600 g
• Footling presentation
• Head extended too much
• Zatuchni-Andros breech scoring index <4 points
• No experience in delivering breech fetuses (!)
• Abnormal changes in heart rate
• Cervical dilation and fetal progress too slow
• Informed consent of the patient (!)
10.9.1. Mechanism of labor in frank breech presentation

At the end of pregnancy and in the beginning of labor the intertrochanteric line
of buttocks is in one of oblique diameters of the pelvic inlet (in occipitoanterior
variety of the first position it is the left oblique diameter). In a vaginal examination
the intertrochanteric line serves as the sagittal suture while the sacrum and coccyx
act as the posterior fontanelle (Fig. 10.5). Additional reference points are ischial
tuberosities, intergluteal sulcus, anal opening, external genitals and feet of the fetus
(in footling presentation). Fetal progress through the birth canal usually begins after
rupture of the membranes and sufficient cervical dilation.
The onset of labor is preceded by the descent, engagement and compression of
buttocks.
• The first step is internal buttocks rotation. It begins when the buttocks pass from
the pelvic plane of greatest dimensions to that of least dimensions. The point of
direction is on the anterior buttock. The rotation ends in the intertrochanteric
line stationing in the anteroposterior outlet diameter (Fig. 10.6).
• The second step is lateral flexion of the lumbar section of vertebral column.
Further progressive advance of the fetus results in the formation of a fi xation
242 Obstetrics
a
c
d
Fig. 10.5. Dimensions and planes of the pelvis: a — bitrochanteric diameter in the left oblique
diameter. The pelvic pole usually passes the inlet pelvic plane with its bitrochanteric diameter
in one of oblique pelvic diameters. In this case the reference point is the point corresponding to
fetal sacrum (situated in the opposite oblique diameter); b — occipitoposterior vaiety of the first
position (left sacrum posterior); c — pelvic inlet plane; d — pelvic plane of least dimensions
Fig. 10.6. During labor, upon progressive advance of the fetus the rotation of fetal pelvis
brings the bitrochanteric diameter to the anteroposterior diameter in the pelvic plane of least
dimensions. The figure shows a rotation from occipitoposterior variety of the fi rst position
(left sacrolateral, LSL) to the fi rst position (left sacroposterior , LSP)
point (anterior iliac bone of the fetus) and a point of bearing (inferior margin of
symphysis pubis), and after that the lumbar section of fetal spine flexes laterally,
the posterior buttock moves to a point above the perineum, and the anterior
buttock follows it to come from under the symphysis pubis. At this time the
shoulders with their bisacromial diameter enter the same oblique diameter of
pelvic inlet, through which the buttocks passed (end of step two). The trunk now
rotates with the back somewhat anteriorly (Fig. 10.7).
• The third step is internal shoulder rotation and related external trunk rotation.
This rotation takes place in the pelvic plane of least dimensions and ends in the
shoulders stationing in the anteroposterior outlet diameter. The anterior shoulder
passes under the pubic arch, and the posterior shoulder stations anterior to the
coccyx above the perineum (Fig. 10.8).
• The fourth step is lateral flexion of cervico-thoracic segment of vertebral column.
Due to the progressive advance of the fetus a second fi xation point is formed: on
the anterior fetal shoulder at the site of deltoid muscle insertion (upper third of
the humerus). The point of bearing is the inferior pubic margin.
The forces of labor produce a flexion of the trunk in the cervico-thoracic section
of vertebral column, thus the shoulder girdle and arms are delivered. At this time
the head with its suboccipitobregmatic diameter enters the oblique diameter of pelvic
inlet, opposite to the diameter through which fetal shoulders passed.
Fig. 10.7. Completion of the second step of labor in breech presentation (lateral flexion of
lumbar section of vertebral column)
Fig. 10.8. Completion of the third step of labor in breech presentation (internal shoulder
rotation and external trunk rotation)
244 Obstetrics
• The fifth step is internal head rotation. When passing from the pelvic plane of
greatest dimensions to that of least dimensions the head makes an internal
rotation, as a result of which the sagittal suture is in the anteroposterior diameter
of the outlet, while the suboccipital fossa (the third fi xation point) is fi xed above
the symphysis pubis.
• The sixth step is head flexion. From the clinical point of view it is crowning of
the head: the chin, mouth, nose, brow and vertex of the fetus appear above the
perineum successively. The head crowns in its suboccipitobregmatic diameter as
it does in vertex presentation (Fig. 10.9).
Fig. 10.9. The fi fth step of labor in breech presentation (delivery of head in flexion)
When studying the mechanism of breech labor one can see a clear
NB! regularity: an alternation of three rotations and three flexions.
10.9.2. Mechanism of labor with mixed footling and breech

presentations
In this case the difference in the mechanism of labor is that the first to appear
from the pudendal fissure are either fetal buttocks and legs (in incomplete breech pre-
sentation), or fetal legs (in double footling presentation) or one leg (in single footling
presentation). In the latter case the extended (presenting) leg is the anterior leg, as a
rule. The labor tumor in breech presentations develops on the buttocks, which become
edematous, of bluish-purple color. The labor tumor often shifts from the buttocks to
external genitals of the fetus, which is manifested by scrotum or labial edema. In mixed
footling and breech presentations the labor tumor develops on the anterior leg.
10.9.2.1. Course and management of labor in breech presentations

Two most important conditions are continuous CTG monitoring and «hands-off»
approach until the moment when the trunk is delivered to the umbilical ring. When
labor is starting, a number of issues should be settled:
• need for emergency cesarean section;

• availability of anesthesia;
• surgical facilities fully operational;
• informed consent signed in due form;
• two obstetricians and a neonatologists present at the delivery;
• experience of managing labor in pelvic presentation (one of the most important
prerequisites);
• apart from the routine equipment for delivery, Piper forceps and accessory
warmed-up diapers.
Three types of vaginal delivery are traditionally distinguished in labor with pelvic
presentation.
• Spontaneous delivery without obstetric intervention. This scenario is mostly
typical of preterm and extremely preterm labor.
• Assisted breech delivery. This is the most common scenario. Labor proceeds
without obstetric intervention until the umbilical ring is delivered. Then
assistance is given to extract the trunk, arms and head of the fetus.
• Total breech extraction. After grasping the feet, the entire fetus is extracted using
energetic tractions. This approach is an option to deliver a non-cephalic second
twin, but it is unacceptable for singleton deliveries as the cervix may not be
adequately dilated to accommodate the passage of the fetal head. If one fetal leg
descends, expectant approach is assumed provided fetal heart rate is satisfactory.
One should wait for complete cervical dilation. Total breech extraction is associated
with a birth injury rate of 25% and a mortality rate of approximately 10%.
Management of the first stage of labor

The main objective in managing the first stage of labor in breech presentation is
to keep the gestational sac intact until complete or almost complete cervical dilation.
For this purpose the parturient woman is put on the side which the fetal back faces;
this prevents presentation and prolapse of the cord. The woman should urinate and
defecate using a bedpan.
If membranes rupture prematurely while the cervix is not ripe enough, the parturi-
ent woman should undergo cesarean section.
If uterine inertia develops, labor induction is only administered with cervical dila-
tion 5 cm and more; with less dilation it is better for the fetus to be delivered via
cesarean section.
Management of the second stage of labor

During the second stage the clinicians use an active expectant approach. The
patient lies on her back with her legs flexed in femoral and knee joints; the soles of
both feet rest against foot support. This position promotes good pushing, which is
an essential condition for correct management of breech delivery.
Four clinical phases are distinguished in breech delivery:
• spontaneous delivery of the infant up to the umbilicus;
• delivery from the umbilicus to the inferior scapular angle;
• delivery of the shoulder girdle;
• delivery of the head.
246 Obstetrics
As soon as the fetus is delivered up to the umbilicus, the head begins to engage the
lesser pelvis inlet and compresses the cord. If the delivery is not over within 5 minutes,
an asphyxiated fetus is born. If this time is 10 minutes and more, the fetus usually dies.
If CTG monitoring is unavailable during the second stage in pelvic presentation,
the fetal heart rate is auscultated with a stethoscope after each bearing down effort.
Fetal tachycardia is often noted during the expulsion stage; this is
NB! due to the n. splanchnicus irritated by the legs pressing against
the abdomen. In this case there is no indication for an operative
delivery.
Discharge of meconium is a common event in pelvic presentation.
The obstetrician does not interfere until the buttocks enter the vagina. As soon as this
happens the clinicians should be ready to initiate maneuvers assisting in the delivery.
During bearing down efforts the woman should press her thighs
NB! to the abdomen with her arms. This is especially important during
the expulsion stage: the diminished angle of pelvic inclination
facilitates the passage of fetal head through the pelvis.
Perineo- or episiotomy is performed if required. In frank breech once the buttocks
have emerged, assisted delivery begins.
All maneuvers and techniques proposed for the second stage management in pelvic
presentation can be divided into several groups:
• preventive maneuvers (by Tsovyanov and Bracht), maneuvers to assist in the
delivery of arms and legs (by Pinard, Lovset);
• maneuvers assisting in the delivery of the aftercoming head (Guilleme, Mauriceau-
Smellie-Veit , Levret, Lachapelle, Martin-Wiegand, the Prague method);
• Piper forceps application to the aftercoming head;
• Fetal extraction by the pelvic pole.
10.9.2.2. Great names
Jacques Guillemeau (1550 – 1613)

A French surgeon from Orleans who
rose to recognition due to his pioneering
work in ophthalmology and obstetrics.
He was a court surgeon at the Hotel-
Dieu hospital in Paris. He was a favourite
student of Ambroise Pare (1510 – 1590)
who was also his Godfather.
In 1609 Guillemeau published a
book on obstetrics entitled De l’heureux
accouchement des femmes which was the
first to provide a description of a maneuver
employed in breech presentation. This
method was later named Mauriceau-
Smellie-Veit maneuver.
Francois Mauriceau (1637 – 1709)

A renowned European obstetrician
who studied obstetrics at the Hotel Dieu
hospital in Paris.
In 1668 Mauriceau published Traite
des Maladies des Femmes Grosses et
Accouchees; the book was immediately
translated into other European languages.
Mauriceau is considered the inventor of a
classical maneuver to help deliver a breech.
Andre Levret (1703 – 1780)

Levret is considered to be the most
influential figure in French obstetrics
in the eighteenth century. He was most
respected for his rational approach to
obstetric surgery represented in his
book L’art des Accouchements (The art
of obstetrics). The so-called classical
maneuver for breech presentation is
often referred to as Mauriceau–Levret
maneuver; its other name is La Chapelle
maneuver after the famous midwife
Marie-Louise La Chapelle (1769 – 1921).
Marie-Louise La Chapelle (1769 –

1921)
This woman headed the obstetric
department at the Hotel Dieu hospital in
Paris; she made a stand against applying
obstetric forceps. In her book Pratique
des accouchements, which remained
an indispensible guide for generations
of obstetricians for a long time, she
advocated a natural birth as the best
method of delivery. She is considered to
be the founder of modern obstetrics.
248 Obstetrics
William Smellie (1697 – 1763), Scotland

Smellie studied medicine in Glasgow
and trained in obstetrics in London and
Paris. He is the inventor of an obstetrical
manikin for instructing his students.
Smellie described the mechanism of labor,
designed an improved version of obstetric
forceps. Reportedly, he also devised
a maneuver to help deliver the head of
a breech. He authored a handbook in
Obstetrics.
Aloys Constantin Conrad Gustav Veit

(1824 – 1903)
Veit was a German obstetrician-
gynecologist; he headed a chair of
obstetrics and gynecology in Rostock
and Bonn. His name is associated with
Mauriceau-Smellie-Veit maneuver, a
procedure defined as a classicasl method
of assisted breech delivery.
Adolphe Pinard (1844–1934)

French obstetrician gynecologist who
made a great contribution in his work
involving prenatal and maternal health.
Pinard established abdominal obstetric
palpation methods and invented a special
stethoscope which is still widely used the
world over. He described a method of
delivering legs in frank breech presentation.
The town of Nancy hosts the Maternité
Adolphe-Pinard Hospital. A boulevard in
Paris was named after him.
Jørgen Løvset (1896–1981)

Nor wegian obstetrician and
gynecologist whose name is associated
with a new way to release the child’s
shoulders at the breech birth (Løvset’s
maneuver).
Lovset J. Shoulder delivery by breech
presentation // J. Obstet. Gynaecol. Br.
Empire. — 1937. — Vol. 44. — P. 696–704.
Napoleon Arkadievich Tsovyanov

(1882–1965)
In 1928 Tsovyanov proposed a way
to manage a breech birth aimed at
maintaining the fetus’s attitude until
the head is delivered. Somewhat later,
a German gynecologist E.Bracht (1936)
proposed a similar method of managing
the delivery where pressure was exerted on
fetal head through the fundus during the
expulsion stage (Naujok maneuver). These
maneuvers have been widely used both in
Russia (Tsovyanov’s maneuver) and in
Germany (Bracht maneuver).
Erich Franz Eugen Bracht (1882–1969)
He was an assistant to Menge in
Heidelberg, and then to Pfannenstiel in
Kiel, and to Franz in Berlin. In 1922
Bracht became an associate professor at
the University of Berlin, and eventually
director of the Charité Frauenklinik.
Starting in 1945 he headed the Provincial
Frauenklinik in Berlin-Neukőlln which
became a major maternity and gynecology
clinic following World War II. He served as
a consultant of gynecology and obstetrics
during the American occupation of Berlin
and retired in 1955.
Bracht E. Zur manualhilfe bei
beckenendlage // Ztschr Geburtsh
Gynäk. — 1936. — Vol. 112. — P. 271.
250 Obstetrics
10.10. MANEUVERS IN BREECH PRESENTATION
10.10.1. Tsovyanov maneuver in frank breech presentation

(Tsovyanov I maneuver)
The main objective pursued by this maneuver in frank breech presentation is to
preserve the physiological fetal attitude (fetal legs are up next to its abdomen, with
knees straight and its feet next to its ears, arms crossed on the chest) and to ensure
the fetus follows the pelvic axis.
Once the buttocks have emerged, the obstetrician grasps them so that the thumbs
are placed on fetal thighs pressed to the abdomen, and the other four fingers of both
hands — on sacral surface. Grasping the fetus like that one promotes the physiologi-
cal course of the delivery: upward movement of the delivering trunk following the
line of pelvic curvature. As the trunk is delivered the obstetrician presses the fetal
legs gently to its abdomen gradually shifting the hands to the pudendal fissure; in
this way fetal legs are prevented from hanging down, and arm entrapment is pre-
vented as well, as the arms are now pressed to the chest by the feet of extended legs
(Fig. 10.10). Bearing down efforts promote a rapid delivery of the fetus up to the
umbilical ring, and then — to inferior scapular angles. Now the fetal breadth passes
to one of oblique pelvic diameters, by the moment of shoulder girdle delivery it is
in the anteroposterior outlet diameter.
a b
Fig. 10.10. Tsovyanov maneuver in frank breech presentation: a — grasping the fetal trunk;
b — as the trunk is born, it is threaded between the hands
Fetal buttocks should be directed somewhat posteriorly so as to

NB! bring the anterior fetal arm under the symphysis pubis and fix
it there. For the posterior arm to be delivered, the fetal trunk is
lifted anteriorly, and the posterior arm can be helped out of the
hollow of sacrum.
The shoulder girdle of the fetus is born. After that one can see fetal chin, mouth
and nostrils in the gaping pudendal fissure. If bearing down is normal, the fetal head
can be freed by directing fetal buttocks downward and anteriorly: this helps the head
to be delivered without accessory assistance.
This maneuver begins when the buttocks emerge.
This maneuver is over when the fetal feet emerge from the pudendal fissure.
10.10.2. Tsovyanov maneuver in footling breech

presentation (Tsovyanov II maneuver)
This technique helps to prevent the delivery of fetal legs before the cervix is fully dilated.
When the fetal feet emerge, the pudendal fissure of the parturient woman is covered
with a sterile diaper; the palmar surface of the obstetrician’s right hand is brought to the
pudendal fissure and blocks the early delivery of the legs (Fig. 10.11). As a result, during
each bearing down effort the fetus seems to squat inside the birth canal. Thus the buttocks
press on the cervical canal promoting its dilation. Fetal buttocks descend to the vagina
forming a mixed breech presentation with the legs that are already there. The delivering
legs should be blocked until the cervix is fully dilated, and this would be indicated by:
• pronounced protrusion of the perineum by the presenting part;
• incompletely closed anus;
• frequent energetic pushing;
• contraction ring stationed 5 transverse fi ngers above the pubis. When the
buttocks descend to the pelvic floor, fetal feet begin to protrude from under the
obstetrician’s palm despite the counteraction they meet.
These events designate a fully dilated cervix. As soon as we establish full dilation,
we no longer counteract the delivery of the legs, thus the legs followed by the but-
tocks, trunk and head are delivered without a difficulty.
This maneuver begins when the feet (or foot) emerge(s).
This maneuver is over when the cervix is fully dilated.
10.10.3. Bracht maneuver

Bracht maneuver is almost identical with Tsovyanov maneuver in breech presentation.
The only difference is that the obstetrician’s assistant performs additional manipulations.
In 1936 E.F.E. Bracht proposed the following maneuver: the obstetrician monitors
the delivery of the fetus up to the scapular angle after which (s)he gently grasps the
fetal trunk maintaining the upward and anterior rotation of the fetal body. When
the anterior rotation is nearly complete, the fetal body is held against the mother’s
Fig. 10.11. Tsovyanov maneuver in footling breech presentation

252 Obstetrics
symphysis. At the same time moderate pressure is exerted on the fetal head through
the abdominal wall to prevent its extension (Fig. 10.12).
Fig. 10.12. Bracht maneuver in fetal head delivery
When the trunk is delivered up to the inferior scapular angles, if there is nuchal
arm entrapment and / or difficulty in delivering of the head, one can resort to Lovset
maneuver and / or classical hand maneuver: freeing the shoulder girdle and freeing
the aftercoming fetal head.
10.10.4. Pinard maneuver

The main stages of this maneuver are shown in Fig. 10.13.
а b
Fig. 10.13. After a spontaneous delivery of the trunk up to the umbilicus one performs
sweeping/external rotation of each thigh (a) combined with rotating the pelvis in the opposite
direction resulting in the flexion of the knee and the delivery of each leg (b)
10.10.5. Løvset’s maneuver

Freeing the shoulder girdle is composed of two steps.
• Step one: delivery of posterior shoulder and arm. The fetus is held by its ankle
joints by one hand; the trunk is lifted and led in the direction opposite to the
fetal position until the legs are parallel to the inguinal fold. After that two or four
fi ngers are inserted into the birth canal from that side of sacral fossa to which the
fetal back is turned until they reach the fetal shoulder and the elbow joint. The
arm is flexed in the elbow joint and swept down across the fetal face and along the
anterior surface of the fetal chest (Fig. 10.14).
b
Fig. 10.14. Classical hand maneuver in pelvic presentation: when the shoulder
blades emerge under the pubis the obstetrician hooks the arm downwards (a)
to have it delivered (b)
254 Obstetrics
• The anterior arm is often delivered spontaneously at the same time as the
posterior arm is swept out. If this does not happen, one initiates the second
step of freeing the shoulder girdle: delivery of anterior shoulder and arm. For
this purpose, the anterior arm should be preliminarily moved backward: the
fetal trunk and the delivered arm are held by both hands in the chest area and
rotated to the oblique pelvic diameter opposite the one in which it is currently
(Fig. 10.15). One should ensure that the back and, consequently, the occiput
are facing the pubis.
Fig. 10.15. Classical hand maneuver in pelvic presentation: delivery of anterior shoulder
and arm
10.10.6. Mauriceau-Smellie-Veit (MSV) maneuver

Delivery of the aftercoming head is composed of two steps: flexing the head and
freeing it from the pudendal ring.
• Step one: flexing the head. The fetus is laid face down with the length of its body
over the obstetrician’s hand and arm. The second and third obstetrician’s fingers
of this hand are placed on the fetus’s cheekbones; the fingers of the other hand
are pressed to the fetus from the back: the third fi nger presses on the occiput,
and the other two second and fourth are placed on both sides of the neck without
compressing the clavicles. The palm is fi rmly against the fetal back. The fi ngers
maxilla gently presses it down to the chest, and the fi nger at the occiput exerts
gentle pressure, too. This combined impact brings about flexion of the head.
• At the same time while obstetrician’s hands are in the same position the second
step is performed: crowning of the head. For this purpose the head is pulled first
backward until the hairline is visible (the suboccipital fossa, fi xation point), and
then downward and forward. This causes the mouth, nose, brow and occiput to
deliver above the perineum (Fig. 10.16).
Fig. 10.16. Mauriceau-Smellie-Veit (MSV) maneuver to free the head in breech presentation.
Pressure on the maxilla (not the mandible!) promotes head flexion (black arrow). Successful
delivery of the head is ensured by gentle traction and additional careful pressure of the
assistant’s hand above the pubis
10.10.7. Martin–Wiegand maneuver

The fetus is placed on the obstetrician’s arms the way it is done for Mauriceau-
Smellie-Veit maneuver; the other hand exerts pressure over the pubis, which pro-
motes additional flexing of the head pressing it in the direction of the true pelvis
outlet.
10.10.8. Burns–Marshall maneuver

When the trunk is delivered, it is left hanging down for several seconds. Under the
impact of the trunk weight the head moves forward and flexes, and comes under the
symphysis pubis with its suboccipital fossa. Now is the time to begin the maneuver.
Both ankles are grasped with the second, third and fourth fingers of the right hand.
Performing gentle traction the obstetrician swings the feet upwards over the mother’s
abdomen (Fig. 10.17). If necessary, the obstetrician’s left hand pushes aside the peri-
neal tissue providing an access of air to the fetal air passages. Preferably, the fetal
head should be prevented from emerging too fast. At this stage one can combine
Burns-Marshall maneuver with pressure on the head from the mother’s abdomen
and application of obstetric forceps.
256 Obstetrics
Fig. 10.17. Burns-Marshall maneuver
10.10.9. Piper’s forceps

Piper’s forceps are unlike other models in that they have a perineal curve;
initially they were meant to be applied to the after-coming head in breech de-
livery. Their purpose is to facilitate the delivery of the head by applying traction
to the fetal head rather than the trunk or shoulders. In this way one avoids the
prospect of injuring the cervical section of the vertebral column due to overex-
tension (Fig. 10.18, 10.19).
Fig. 10.18. Applying Piper’s forceps: wrong assistance when applying Piper’s forceps.
Excessive upward sweeping of the trunk leads to hyperextension of the spine in the cervical
section (increased risk of neural trauma)
Fig. 10.19. Applying Piper’s forceps: the fetal trunk can be placed directly on the forceps.
The fetus is delivered in one piece due to gentle traction in the correct direction
258 Obstetrics
10.11. MANAGEMENT OF THE THIRD STAGE OF LABOR AND

POSTPARTUM PERIOD
Management of the third stage of labor and of postpartum period does not differ
from their management in cephalic presentation.
10.12. PROPHYLAXIS
Prophylaxis of pelvic presentation constitutes elimination of its causes.
REMEMBER!
Definition Breech presentation is the type of presentation in which the

fetal pelvic pole is situated above the true pelvis inlet
Etiology Change in the lower uterine segment (its extension and flac-
cidity).
Incompetent uterine musculature.
Contracted pelvis.
Extended and flaccid abdominal muscles.
Grand multiparous mother.
Incompetence of uterine ligaments.
Tumours of uterus, cervix, vagina and ovaries.
Multiple pregnancy.
Premature birth.
Placenta previa.
Polyhydramnios and oligohydramnios
Classification Frank breech presentation.

Mixed breech presentation.
Footling presentations:
— double;
— single
Mechanism Step one: internal rotation of the buttocks.

of labor in frank Step two: lateral flexion of the lumbar section of the fetal
breech spine
presentation Step three: internal rotation of shoulders and external rota-
tion of the trunk
Step four: lateral flexion of cervico-thoracic section of the
spine
Step five: internal rotation of the head
Step six: flexion of the head
Progress Preterm delivery is more common with breech presentations

of pregnancy than with cephalic presentation; the mother should be hospi-
and delivery talized 1–2 weeks prior to the onset of labor to work out the
plan of management
Complications Premature rupture of membranes

Poor uterine contraction strength
Prolapse of the cord or small parts of the fetal body
Premature expulsion of fetus (footling presentation) while the
cervix is not fully dilated
Nuchal arm entrapment
Rupture of cerebellar tentorium
Injury of parenchymatous abdominal organs
Fractures of tubular bones in fetus
Acute fetal hypoxia
Maneuvers Tsovyanov I and Bracht maneuvers in frank breech presenta-

tion.
Tsovyanov II maneuver in footling presentation.
Pinard maneuver: delivery of fetal legs.
Lovset maneuver: delivery of fetal arms.
Delivery of aftercoming fetal head (Mauriceau-Smellie-Veit,
Martin-Wiegand, Burns-Marshall maneuvers).
CONTROL QUESTIONS
1. What types of breech presentation do you know?

2. What complications are typical of breech presentation during the first stage
of labor?
3. What complications are typical of breech presentation during the second stage
of labor?
4. What are the principles of preventing complications during the second stage
of labor?
5. What is Tsovyanov I maneuver?
6. What is Bracht maneuver?
7. What is Tsovyanov II maneuver?
8. Fetus of what weight is considered large in breech presentation?
9. What complications are typical of a fetus delivered in breech presentation?
CHECK YOURSELF!
Level 1. Test
1. The share of breech deliveries in term pregnancy is:
a) 10%;
b) 20%;
c) 3.5%;
d) 30%;
e) 40%.
260 Obstetrics
2. Frank breech presentation is an obstetric situation where the following is stationed

above the true pelvis inlet:
a) fetal buttocks; legs extended in knee joints and flexed in femoral joints;
b) one fetal leg;
c) both fetal legs;
d) one fetal leg and one buttock;
e) fetal arm.
3. The first step in labor with breech presentation:

a) lateral flexion in the lumbar section of the spine;
b) lateral flexion in the cervico-thoracic section of the spine;
c) extension of fetal head;
d) flexion of fetal head;
e) internal rotation of the buttocks.
4. In uncomplicated frank breech presentation only this maneuver will suffice:

a) Tsovyanov I;
b) Mauriceau-Levret-LaChapelle;
c) Tsovyanov II;
d) Bracht
e) Smellie
5. Indications for planned cesarean section in breech presentation:

a) footling presentation;
b) frank breech presentation;
c) fetal weight over 3600 g;
d) fetal weight under 3600 g;
e) female fetal sex.
6. Which is the most accurate definition of complete (mixed) breech presentation:

a) legs flexed in femoral and knee joints;
b) legs flexed in femoral joints and extended in knee joints;
c) legs flexed in knees and femoral joints, arms flexed in elbows;
d) legs extended in knees and femoral joints.
7. How many steps are commonly distinguished in the mechanism of labor in breech
presentation:
a) 4;
b) 5;
c) 6;
d) 7.
8. What type of fetal attitude in breech presentation is the most favorable for vaginal
birth:
a) frank breech;
b) double footling;
c) single footling;
d) knee presentation.
9. What is the correct sequence of steps in the mechanism of labor in breech presentation:
a) rotation — flexion — rotation — extension — rotation — flexion;
b) rotation — flexion — rotation — flexion — rotation — flexion;
c) flexion — rotation — flexion — rotation — flexion — rotation;
d) rotation — flexion — extension — rotation — flexion — extension.
10. In a vaginal examination in breech presentation the following serves as the sagittal
suture:
a) sinus sagittalis
b) intertrochanteric line;
c) bisacromial diameter;
d) bipedal diameter;
e) interspinal diameter.
11. Labor tumor in breech delivery is most commonly situated on:

a) anterior buttock;
b) posterior buttock;
c) both buttocks;
d) perianal area.
12. Fetal head in breech delivery crowns in:

a) suboccipitofrontal diameter;
b) suboccipitobregmatic diameter;
c) vertical dimension;
d) intertrochanteric diameter.
13. Complication typical of the second stage in breech delivery:

a) cord prolapse;
b) premature rupture of membranes;
c) shoulder dystocia;
d) nuchal arm entrapment.
14. Tsovyanov I maneuver implies:

a) delivering the shoulder girdle;
b) change from footling presentation to mixed breech;
c) delivering the aftercoming head;
d) preserving the flexed attitude in the fetus.
15. Possible complications in the first stage of labor in breech presentation:

a) poor uterine contraction strength;
b) premature rupture of gestational sac;
c) cephalopelvic disproportion;
d) nuchal arm entrapment.
262 Obstetrics

1. Primiparous patient aged 17 was admitted with report of labor for 10 hours.
No disease in past history. Gestational age 40 weeks. Pelvis of normal dimensions.
Estimated fetal weight 3900 g. External examination findings: pelvic pole is above the
lesser pelvis inlet, fetal heart beat clear, rhythmical, 140 bpm. Vaginal examination:
cervical dilation 3 cm, cervical edges thin, gestational sac intact, footling presenta-
tion, promontory cannot be reached, no exostoses in the lesser pelvis. What is your
diagnosis? What is the plan of management?
2. Secundiparous patient aged 25 was admitted with report of labor for 2 hours.
Past history: second pregnancy, full term, the previous pregnancy 2 years ago resulted
in uncomplicated delivery (weight 3500 g, length 52 cm). External examination find-
ings: a softish structure is determined above the lesser pelvis inlet, it is pressed to
the inlet. Fetal heart beat 140 bpm, clear, rhythmical. Estimated fetal weight 3200 g.
Vaginal examination: cervical dilation 3 cm, gestational sac is intact, buttocks pre-
senting at the lesser pelvis inlet, promontory cannot be reached, no exostoses. What
is your diagnosis? What is the plan of management?
NOTES
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• Chapter 11
PHYSIOLOGY OF POSTPARTUM PERIOD
The postpartum (puerperal) period is the length of time beginning after placenta
delivery and lasting for 6 weeks. During this time all the organs and systems that
experienced pregnancy- and birth-related changes now undergo involution, with the
exception of the mammary glands whose function reaches its peak exactly during
the postpartum period. The most pronounced involution changes take place in the
genitals, especially in the uterus. The rate of involution changes is most pronounced
in the first 8–12 days.
The first pregnancy and delivery usually bring about stable changes that make it
possible to establish the fact of previous pregnancy even after a considerable lapse
of time (condition of the perineum and vagina, changes in the shape of the cervix
and external os, striae gravidarum on the skin).
11.1. CLASSIFICATION
The first 2 hours after delivery are viewed separately; this time period is called
early postpartum period. When it is over, late postpartum period begins.
In the English-language publications the postpartum period is usually divided into:
• immediate postpartum period that lasts for 24 hours after delivery. This is the time
of complications related to anesthesia or delivery itself;
• early postpartum period that lasts for 7 days after childbirth;
• late postpartum period that lasts for 42 days ending commonly in complete
involution of all organs and systems of the puerpera.
The chronologic division into periods is conventional; the division is based on the
fact that complications due to disturbed contractile activity accompanied by bleeding
most often set in during the first hours after childbirth.
11.2. ANATOMICAL AND PHYSIOLOGICAL CHANGES

IN POSTPARTUM PERIOD
Changes occurring in the postpartum period affect not only the genitals (the
uterus, vagina, ovaries, tubes, pelvic floor, mammary glands) but also all the systems
of the body (digestion, circulation, excretion, endocrine system, etc.).
11.2.1. Genitals
The most extensive involution processes take place in the genitals, especially in
the uterus. The rate of involution is at its highest during the first 8–12 days. After
264 Obstetrics
delivery of the fetus the uterus shrinks in size due to intensive contraction of its
musculature (Fig. 11.1).
The uterine body is almost spherical in shape; it preserves great mobility due to
decreased tone of the ligaments. The cervix of uterus looks like a thin-walled sac
with gaping external os with torn edges that hangs down into the vagina. Immediately
after delivery the cervical canal can easily accommodate a hand; the uterus weight
is 1000 g, its size corresponds to 20 weeks gestation. After delivery of the fetus the
fundus of uterus can be palpated 1–2 transverse fingers (2–4 cm) below the navel.
This station of the fundus persists for several hours. After that the restoring tone of
pelvic floor and vaginal muscles moves the uterus upwards. By the end of the first
day the fundus of uterus is palpated at the level of the navel.
During the first days of the postpartum period it is not uncommon for the uterus to
shift to the right and to slightly turn with its left aspect facing the anterior abdominal
wall. Its position in the lesser pelvis changes due to the condition of adjacent organs
(the bladder and intestine).
The entire inner surface of uterus is a vast wound surface with most pronounced
structural changes in the area of placental bed. Postpartum hemorrhage is arrested
due to:
• contraction of myometrium immediately after childbirth;
• formation of platelet plug and activation of plasma hemostasis afterwards.
Vascular lumen in the area of placental bed is constricted upon the contraction
of uterine musculature; thrombi are formed in them, which promotes the arrest of
Navel
Days
postpartum
Fig. 11.1. Involution of postpartum uterus

Chapter 11. Physiology of postpartum period 265
bleeding after the childbirth. The cytoplasm of some muscular cells undergoes fatty
degeneration, and later — steatosis. Involution takes place in the intermuscular con-
nective tissue as well. In the ensuing days the involution of uterus proceeds very fast.
The fundal height decreases by 2 cm on average with each passing day.
The rate of uterus involution depends on parity, the degree of

NB! uterus distension during pregnancy (fetal weight, polyhydramnios,
multiple pregnancy), the onset of breastfeeding within the first few
hours. The actual size of uterus and the rate of its involution can
be seen on ultrasound.
The process of uterine involution involves muscular cells, intermuscular connective

tissue and myometrial vessels (Fig. 11.2).
The process of healing on the inner uterine surface starts with the decomposition
and sloughing of the shredded decidual spongiosa, blood clots and thrombi. This
is helped along by phagocytosis and extracellular proteolysis. The decomposing
pieces of the decidua, blood clots and other sloughing tissue elements become the
constituents of lochia.
Lochia (after birth cleansings) are vaginal discharge (blood, mucus, waste product
of muscle cells and decidua). Over 6 weeks of puerperium, about 500–1500 ml of
lochia is discharged.
The pH of lochia is neutral or alkaline. During the first 2–3 days lochia are
blood tinged; RBCs predominate in their composition (lochia rubra, Latin). On day
3–4 they look bloody and serous, WBCs being the predominant constituents (lo-
chia serosa, Latin). A week after delivery the discharge shows mucus, decidual cells
and squamous epithelial cells while there are almost no RBCs (lochia alba, Latin)
Fig. 11.2. Late postpartum period. Clots in uterine cavity (sonography)

266 Obstetrics
(Table 11.1). With the postpartum period proceeding physiologically, lochia have a
peculiar musty odor; their discharge usually discontinues after 5–6 weeks.
Epithelization of the inner surface of uterus takes place at the same time with
sloughing of the decidual membrane; it is over by day 10 of the postpartum period
(except for the placental bed). The endometrium is fully restored 6 weeks after
childbirth. The tone of uterine ligaments is restored by the end of the third week of
the puerperium.
Involution of the cervix proceeds more slowly. The internal os contracts and re-
stores its shape before all other portions of the cervix. This is due to the contraction
of circular muscular fibers. After 3 days the internal os accommodates one finger.
Restoration of the cervical canal shape is over by day 10. By this time the internal
os is fully closed. The external os occludes by the end of the third week and becomes
slit-like. Epithelization of the vaginal portion of cervix continues for 6 weeks after
childbirth. Lacerations of cervix are a common complication of delivery; scars may
form in their place, which can cause cervical deformation.
For 3 weeks after childbirth the walls of the vagina remain edematous, its lumen
is extended. In about 3 weeks vaginal walls restore their initial tone. In breastfeeding
women the vaginal mucosa may become atrophied while the vaginal gland secretion
is reduced due to insufficiency of estrogens, which can lead to dryness and even de-
velopment of lactation atrophic vaginitis. Relics of torn hymen composed of sclerous
mucosal pieces are called carunculae myrtiformes (Latin).
During the first 2–3 days after childbirth perineal muscles contract slowly, after-
wards the process picks up. By day 10–12 the perineal tone is restored; however the
restoration is often incomplete. Lacerations or incisions of muscles of fascias during
labor promote the development of prolapse. Overextension of the anterior abdominal
wall during pregnancy can lead to ruptures of elastic skin fibers, appearance of striae
and flaccidity of straight abdominal muscles (Fig. 11.3). Restoration of the muscles
in the anterior abdominal wall lasts for 4–6 weeks on average.
2 weeks after childbirth the epithelium of uterine tubes undergoes atrophy due to
hypoestrogenism.
During the postpartum period the luteolysis completes in the ovaries, and fol-
licle maturation begins. Breastfeeding women produce a large amount of prolactin,
so menstrual periods are suppressed for several months or throughout the time of
breastfeeding. In non-lactating women the menstrual cycle is restored 6–8 weeks
after childbirth. As a rule, the first menstrual period after childbirth occurs while
the cycle is anovulatory: the follicle develops and matures, but there is no ovulation,
and no corpus luteum is produced.
Endometrium is the site of proliferation processes. Later the ovulatory cycles are
restored. The time of the first ovulation varies, but it is in direct relation to the regi-
Table 11.1. Nature of discharge (lochia) at various times after childbirth
Type of lochia Days Composition

Lochia rubra 0–3 Mostly RBCs
Lochia serosa 3–7 Mostly WBCs
Lochia alba Weeks 2–6 Mucus, decidual cells, squamous epithelial cells
Fig. 11.3. Overextension, striae of the anterior abdominal wall after childbirth
men of breastfeeding. In about 10–15% of non-lactating women the ovulation occurs

6 weeks after childbirth, in another 30% — in 12 weeks. The earliest time of ovula-
tion described in literature is 33 days after delivery. If a woman breast feeds and has
no periods, ovulation is uncommon in the period before 10 weeks. In about 20% of
women ovulation occurs 6 months after childbirth. The time of ovulation depends on
the pattern of breastfeeding and introduction of complementary foods (suppression
formula, see section 11.5. Contraception in Postpartum Period).
11.2.2. Lactation
The function of the mammary glands is at its highest after childbirth. During
pregnancy glandular tissue proliferates under the impact of progesterone. As is well
known, estrogen concentration is low at the beginning of gestation; it rises gradually
reaching its peak by the time of delivery. In particular, these changes are necessary as
it is the function of estrogens to modulate the expression and sensitivity of oxytocin
receptors both in the myometrium and in the mammary gland. In other words, by
the end of pregnancy the uterus becomes capable of regular contractile activity, and
the mammary gland — of lactation.
Secretion of breast milk takes place as a result of complex reflex and hormonal
effects; it is regulated by the nervous system and the lactogenic pituitary hormone,
prolactin. It ensures the intensive flow of milk to mammary glands. Thyroid and
adrenal hormones have a stimulating effect, as well as a reflex effect during suckling.
The first latching of the newborn to the mother’s breast triggers the mechanism
of lactation. The essence of lactation is determined by two major processes:
• secretion of milk in the gland under the impact of prolactin;
• emptying of the gland under the impact of oxytocin (Fig. 11.4).
268 Obstetrics
There are no proven means for stimulation of prolactin secretion

NB! except for frequent complete emptying of the mammary gland.
No prolactin analogs have been synthesized, so the only available
method to trigger and maintain lactation is effective suckling.
Hypophysis
Mammillary Secretion
stimulation of prolactin and oxytocin
Suckling Lactogenesis
Fig. 11.4. Lactation regulation
Oxytocin produced in this process enhances the contraction of myometrial smooth

musculature decreasing blood loss, hastening the detachment and birth of the pla-
centa, and ensures the highest rate of uterus involution. During breastfeeding a
woman may exeperience painful uterine contractions and an increase in the volume
of blood discharge. The infant receives the first drops of colostrum containing a
concentration of immunoglobulins and antibodies to the infectious matter that he
shares with his mother. From the areole, the lactoflora passes to the main locus of
biocenosis formation — intestine of the infant thus ensuring the contamination of
intestine with microflora, which is needed for physiological maturation of local and
systemic immunity, microbiocenosis and digestive function. Processing the nipples
with disinfectants or washing with water and soap before every breastfeeding is ex-
tremely unfavorable for the development of the child’s host defenses, so the woman
should do hygienic procedures only after feeding, no more than once or twice a day.
Thus early latching to the breast is a complex of preventive and therapeutic mea-
sures both for the mother and child. True, or primary hypogalactia occurs extremely
rarely, in 2–3%. It may be caused by hypoplasia of mammary glands, as well as con-
genital / acquired pituitary dysfunction (for instance, Sheehan’s syndrome: pituitary
infarction accompanying profuse blood loss during childbirth).
During the first day of postpartum period the mammary glands secrete colostrum.
Receiving colostrum is of special importance for the infant as it prepares the gas-
trointestinal tract for digestion of mature milk. Colostrum is a thick yellowish fluid
with alkaline pH. It contains colostrum bodies, WBCs, milk corpuscles, epithelial
cells from glandular vesicles and milk ducts. Compared with milk, colostrum is
richer in proteins (9%) and minerals (0.5%), but poorer in carbohydrates (4.5%); the
amount of fats is virtually the same (3.5–4%). It facilitates the newborn’s adapta-
tion to breastfeeding, produces a mild laxative effect helping the newborn’s intestine
to excrete meconium. Colostrum proteins are somewhere in between breast milk
fractions and blood plasma as to their amino acid composition; this fact apparently
facilitates the transition from placental nutrition breast milk feeding. Compared with
breast milk, colostrum has more iron-binding protein, lactoferrin, which is necessary
for the development of hemopoiesis in the newborn. It contains high amounts of
immunoglobulins, hormones (especially corticosteroids) and enzymes. This is very
important as during the first days of life the functions of certain organs and systems
in the newborn are still immature. Transitional milk produced on day 3–4 acquires a
stable composition at 2–3 weeks; now it is mature milk. Woman’s breast milk has an
alkaline pH, specific gravity 1026–1036 and contains 88% of water, 1.1% of proteins,
7.3% of carbohydrates, 2.1–5.3% of fats, 0.1% minerals (Fig. 11.5).
Apart from its nutritional value, breast milk promotes the development of both active
and passive immunity providing conditions for a transition from almost sterile intrauterine
medium to the non-sterile world where the infant is going to live, grow and develop.
Proteins are represented by albumins: partially unfolded lactalbumin and lacto-
ferrin; these two participate directly in anti-infectious protection of the newborn. In
1.1 7.3
2.1–5.3
0.1
88
Proteins Fats Carbohydrates Minerals Water

Fig. 11.5. Composition of breast milk (%)
270 Obstetrics
the conditions of low pH in the stomach of a breastfed infant the albumin molecule
partially unfolds (due to calcium release); at the same time milk triglycerides are
hydrolysed by acid-sensitive lipases, and oleic acid is released. These processes result
in HAMLET (Human Alpha-Lactalbumin Made Lethal to Tumor Cells) formation:
a complex capable of destroying germs and tumor cells both in vitro and in vivo.
In its turn, lactoferrin is capable of binding transition metals; besides, it shows
anti-inflammatory, antifungal, antiviral, antiparasitic and procoagulant effects.
Interestingly enough, lactoferrin concentration elevates (like the fat content of
milk does) with each passing year of breastfeeding compared with baseline values.
Immunoglobulins (IgG, IgM and secretory IgA), lymph cells, macrophages, lyso-
zyme, unsaturated fatty acids, oligosaccharides contained in breast milk retain all
their properties in the infant’s stomach and promote his health while his own immu-
nity is developing. These constituents of breast milk block the adhesion of pathogenic
bacteria to intestinal epithelium, support bifidobacteria — the so-called bifidus factor.
The well balanced content of enzymes, hormones, immunity factors and other
components varies throughout the process of lactation as the newborn has to adjust to
the effect of numerous environmental influences, many of them being harmful. This
food optimal in composition meets all the infant’s needs in the best way. That is why
breast milk is arguably considered to be gold standard surpassing all its substitutes.

Despite the blood loss during childbirth which should not exceed 0.5% of body
weight (300–400 ml), the stroke volume of the heart increases after delivery. The
cardiac minute output elevates by about 80% immediately after childbirth. This is
due to canceling the placental circulation, return of extravascular fluid to the systemic
circulation, and the increase of venous return. The heart rate decreases, cardiac
output increases insignificantly to return to normal values 2 weeks after childbirth.
During the postpartum period the hemodynamics depends on the age, mode of
delivery, anesthesia during labor, blood loss, the puerpera’s activity. During the first
5 days of puerperium there is a tendency for increased BP in most patients. This is
associated with increased resistance of uterine vessels. The circulating blood volume
becomes normal 3 weeks after childbirth. Hemodynamic changes are the same in
lactating and non-lactating women.
Fibrinogen concentration is noted to decrease as early as during labor; it continues
to do so during the puerperium. Its lowest value is noted on the first postpartum
day. On day 3–5 the concentration of fibrinogen becomes the same as before deliv-
ery; in 7–10 days it becomes the same as before pregnancy. The fibtinolytic activity
of plasma increases immediately after delivery; fibrin synthesis grows significantly.
During labor and the early postpartum period an increased WBC content is noted.
During the first hours after childbirth the amount of WBC may be 25×109/l, granu-
locytes predominating in the differential white blood cell count. The mechanism of
elevation of WBC number has not been studied well enough; it may be related to
labor stress. The level of iron in the blood serum goes down before labor and returns
to normal 2 weeks after childbirth. The number of RBCs is 15–20% higher than
before pregnancy.

Overextension and incomplete emptying of the bladder during labor lead to de-
creased bladder tone, which commonly occasions urine retention during the first days
of postpartum period. Renal blood flow and tubular reabsorption return to baseline
levels 6 weeks after childbirth.

The decreased gastrointestinal motility is usually restored during the first weeks
after delivery. Protein synthesis by the liver and protein levels in the blood return to
baseline values.

The vital capacity of the lungs changes fast as compared to the period of pregnancy.
The pulmonary residual volume increases, while the vital capacity and inspiratory
volume decrease. Oxygen consumption goes down as well, so it is advisable for the
puerpera to do respiratory exercises. Regulation of oxygen consumption depends on
the extent of anemia in the woman, emotional factors, and lactation.
11.2.7. Metabolism, fluid and electrolyte balance

In contrast to pregnancy, during the postpartum period one notes a decrease
in the content of all types of fatty acids in the blood, if the woman keeps to
a diet.
Cholesterol and triglycerides concentration returns to baseline levels in 6–7 weeks.
On day 2–3 of the postpartum period the concentration of glucose goes down
(compared to the values of pregnancy and labor). This should be taken into account
if the puerpera has insulin dependent diabetes mellitus; in this case a re-estimation
of the necessary daily insulin dose can be required.
Lactation is quite an energy consuming process; the lactating mother expends
500 kcal daily, which affects her metabolism. This explains the lower risk of type
2 diabetes mellitus, obesity and postmenopausal hyperlipidemia in women who
breast fed for over one year. A total weight loss of 4 kg during the puerperium and
the 6 months following childbirth is also associated with a decreased amount of fluid
and electrolytes accumulated during pregnancy. The total loss of fluid is 2 l during
the first 7 days and another 1.5 l during the following 5 weeks. Excretion of fluid
is mostly due to intercellular fluid. Aldosteron content in the blood elevates, and
progesterone content decreases, which promotes excretion of sodium.
11.3. CLINICAL FEATURES OF POSTPARTUM PERIOD
A physiological postpartum period is characterized by the following:

• satisfactory general condition of the woman;
• normal body temperature, pulse rate and BP;
272 Obstetrics
• satisfactory involution of uterus;

• normal amount and quality of lochia;
• sufficient lactation.
Weakness may persist for some hours following the childbirth. Fatigue after inten-
sive labor, sensation of soreness after the extension of the vulva and vagina commonly
wear off during the first days of the postpartum period. The puerpera needs rest,
peace and sound sleep which quickly restore her strength and general well-being.
Involution of the uterus can be accompanied by irregular but painful myometrial
contractions that take place over the first 2–3 days after childbirth; they are more
pronounced in multiparous women. These contractions are mostly intensive as she
is breastfeeding.
In some new mothers the beginning of the postpartum period is accompanied by
short-term shiver lasting for 5–10 minutes. Shiver can be due to the release of con-
siderable amounts of metabolic waste products in muscle cells (lactic acid), and by
entry of amniotic fluid through a tear in the placental membrane into the maternal
circulation. In such cases the puerpera should be actively monitored. The pulse rate
may go up to 100 a minute and even more, upon physical exercise.
Healthy puerperas usually have no fever. However, the work of the entire body
musculature during labor can increase the body temperature by several tenths of
a degree. This can explain the commonly noted temperature elevation over the
12 hours following the childbirth. This is the so called first physiological eleva-
tion of body temperature, which should not exceed 37.5 °С while the pulse rate is
normal and the general condition is satisfactory. The second physiological elevation
of body temperature can take place on day 2–3 after childbirth. The temperature
elevation can be due to massive ascending entry of microorganisms from the vagina
to the uterus and reabsorbtion of tissue lysis products in the uterine cavity. The
elevation of body temperature usually persists for some hours and resolves without
interference.
Enhanced sweat production is seen in many puerperal women. This leads to greater
thirst. Relaxation and extension of the anterior abdominal wall and pelvic floor
muscles promote decreased intestinal tone, which results in stools retention during
the first days of the postpartum period.
11.4. MANAGEMENT OF POSTPARTUM PERIOD
The first two hours after a physiological delivery (early postpartum period) are
spent by the puerpera in the delivery room. The obstetrician observes her general
condition, her pulse, BP, monitors the condition of the uterus: determines its con-
sistency, fundal height, watches the blood loss. During the early postpartum period
one examines the soft tissues of the birth canal: external genitals, perineum, vagina
and its fornices. The inspection of the cervix and upper vaginal portions is performed
with specula. All the detected lacerations should be repaired. When estimating the
amount of blood loss during delivery one should take into account the blood dis-
charged during the afterbirth and early postpartum periods. The average blood loss
is about 250 ml.
The maximum physiological blood loss should not exceed 0.5% of

NB! the puerpera’s weight; that is if her weight is 60 kg, the maximum
blood loss is 300 ml, if she weighs 80 kg – 400 ml, but no more
than 500 ml (WHO)!
In 2 hours the puerpera is taken to the postnatal ward in a chair or a cart, together
with the newborn.
Objectives in postpartum period management:
• the speediest possible return of the puerpera to active lifestyle, developing the
breastfeeding skills;
• prevention of postpartum complications;
• promotion of newborn’s health.
The postnatal ward should have all facilities for rooming in: this brings down the
rate of infant and maternal morbidity in the postpartum period considerably. The
mother takes active care of her newborn, which limits the newborn’s contact with the
hospital personnel, provides favorable conditions for colonization of the newborn’s
body with his own microflora, decreases the probability of infection with hospital
strains of opportunistic flora.
Rooming in is one of the most essential measures for prevention

NB! of hospital infection.
The personnel of the obstetric department should encourage breast feeding on

demand, provide education, consulting and practical help to mothers who encounter
difficulties with breast feeding.
The maternity hospital should provide free access of family to the woman and
her child.
The following is done on a daily basis during the puerperium:
• taking body temperature twice a day; the pulse rate and BP — twice a day;
• examination and palpation of mammary glands to assess their shape, condition
of nipples, checking for scratches and cracks (after breast feeding), presence or
absence of engorgement;
• assessing fundal height, its tone and subjective sensations during palpation;
• control of sutures in the perineum (presence of edema, hyperemia, infiltration).
Rhesus-negative patients (unsensitized) who delivered a Rhesus-positive infant
should receive a mandatory injection of Rho(D) immune globulin within 72 hours.
Rooming in of the mother and newborn, breast feeding on demand promote a
rapid adaptation of both to the postpartum period and early discharge. The time
of hospital stay should not exceed 4 days after a physiological delivery, 5 days in
particular cases. The recommended length of hospital stay is 3 days (until the child
receives BCG vaccination). In different countries the length of hospital stay var-
ies from 21 hours (USA, Sweden) to 4–5 days (Germany, Italy). Stitches in the
perineum (if interrupted stitches were placed) are no contraindication to discharge
from hospital as they can be taken out on day 5–7 by an obstetrician-gynecologist
at the district maternity welfare center, and sub-cuticular stitches are not taken out
at all. Early discharge is a valid preventive measure against hospital infection. This
274 Obstetrics
objective is also achieved by home delivery, which tradition is now being revived in
the Northern Europe. As medical supply for home delivery is very expensive, this
method cannot become predominant in most advanced countries.
There is evidence in favor of an active postpartum period; it consists in early get-
ting up of the puerpera (after 4–6 hours), which promotes better circulation, speeds
up involution in the genitals, return to normal function of the bladder and bowels,
as well as prevents thromboembolism complications.
When there is urine retention, one should try to induce it using the reflex response.
If this fails, oxytocin injections (1 ml twice a day IM) or catheterization of the blad-
der is administered. If there is a need to empty the bladder again, Foley catheter is
introduced for a day.
If there are no spontaneous stools, a laxative or cleansing enema is administered
on the third day after childbirth.
To prevent genitalia prolapse or urine incontinence, it is recommended that all
puerperal women do Kegel exercises. This set of exercises was developed to restore
the tone of pelvic floor muscles; the exercise consists in voluntary contraction of the
muscles. The main difficulty about the exercises is to reveal the required muscles and
to feel them. This can be done in the following way: trying to stop a stream of urine.
The muscles involved in the process are those to be trained.
The set of exercises consists of three parts:
• slow compression: contract the muscles as if to arrest urination, count slowly to
three, relax;
• contractions: contract and relax the muscles as quickly as possible;
• ejections: bear down the way it is done during defecation or labor.
Exercising should begin with 10 slow compressions, 10 contractions and 10 ejec-
tions 5 times a day. In a week increase each exercise by 5 continuing to do them
5 times a day. Afterwards increase each exercise by 5 every week until they are 30.
Only when the perineal muscle tone is restored, the puerpera is permitted exercises
that restore the tone of abdominal muscles.
After childbirth a healthy puerpera can return to her customary diet; a breastfeed-
ing mother is usually not required to keep to a specific diet. Alcohol consumption and
smoking are highly undesirable. Alcohol and nicotine can easily pass to the breast
milk, which can cause severe disturbances of the infant’s CNS and even mental
development retardation.
Prevention of infectious complication calls for scrupulous compliance with sani-
tary and epidemiologic requirements and maintaining strict personal hygiene.
When the puerpera is discharged, the attending doctor explains to her the ben-
efits of breastfeeding; speaks about the recommended length of breastfeeding (from
6 months to 2 years from the moment of birth) and prevention of unwanted preg-
nancy.
After discharge the puerpera is referred to a district maternal welfare clinic for
follow-up care during the postpartum period.
Prior to discharge, ultrasonography of pelvic organs can be done.
One should take into account some specific features of the postpartum period as-
sociated with lactation, presence of wound surface in the place of placental bed, and
the condition of physiological immunodeficiency. That is why the puerperal women
require a special daily regimen apart from medical supervision. In the postnatal
hospital department one should scrupulously observe the principle of cyclic filling of
the wards. This means that one ward accommodates mothers and infants delivered
within the same day. The principle of cyclicity is made easier to observe since there
are single-bed wards, semi-private rooms. Wards should be designated for puerperal
women whose stay at the maternity hospital will have to be prolonged due to their
health condition. Postnatal wards should be spacious, no less than 7.5 m2 per each
bed. Moist mopping and airing of the wards is done twice a day. After the puerperal
women are discharged, the ward is given a thorough cleaning: washing and disin-
fection of the walls, floor and furnishings. The beds and oilcloths are also washed
and disinfected. The bedding (mattresses, pillows and blankets) are processed in the
disinfection chamber.
Modern perinatal technology implies a complex of techniques

NB! based on methods of child rearing known in all traditional cultures.
Modern perinatal technology relies on exclusive breastfeeding.
Lack of breast milk is mostly due to violation of basic principles
of organizing breastfeeding in the maternity hospital, improper
breastfeeding technique, lack of support from the hospital
personnel or the family. In 97% of cases hypogalactia stems from
problems with breastfeeding!
Care for a healthy puerpera is integral with care for her healthy newborn; it is pro-
vided in accordance with modern perinatal technologies (see Chapter 13 Physiology
of the Newborn).
Modern perinatal technologies can minimize postpartum complications in the
mother and child.
Another outcome of rooming in — no less important — is the fact that the puer-
pera acquires the skills of caring for her newborn under the guidance of the personnel.
An essential role in developing the skill of breastfeeding and further successful
lactation is played by the personnel.
In this respect, the goals of the personnel center around the following:
• in most cases — merely observing, communicating, providing emotional and
psychological support;
• preparation for further breast feeding can be done together with the obstetrician
(explaining the benefits of breast feeding, educating the woman about the
technique of breast feeding and the processes taking place after childbirth) see
Chapter 3 Antenatal and Postpartum Care;
• giving help when the newborn is latched to the breast for the first time
immediately after delivery;
• at the early stages of breast feeding, if the mother has difficulties, she should
be given practical help (correcting her position, nipple latch); breast feeding
on demand should be encouraged; the mother should be reassured that she has
enough colostrum (milk) for successful breast feeding.
An absolute contraindication to breast feeding on the mother’s part is her HIV-
positive status. Alternative safe means of feeding the newborn should be provided.
276 Obstetrics
Situations requiring temporary suspension of breast feeding include:

• conditions that preclude the woman from caring for her newborn: preeclampsia and
eclampsia, massive bleeding during and after childbirth, sepsis, decompensation
of chronic extragenital conditions;
• exacerbation of herpes infection (herpes simplex virus type I) if the eruption is
localized right on the breast area: until clinical manifestations subside, direct
contact between the affected area and the infant’s mouth should be avoided.
During an exacerbation the infant can be given expressed mother’s milk (no
processing of the milk is required);
• active tuberculosis diagnosed for the first time (all antituberculous medications
are compatible with breast feeding; however in the given situation breastfeeding
should be suspended until chemotherapy cycle is completed);
• untreated brucellosis;
• if the mother takes certain medications:
– sedative psychotropic drugs, antiepilepsy drugs and opioids;
– radioactive iodine (breast feeding can be resumed 2 months after the therapy
is completed);
– iodine or its compounds (local administration in high doses);
– chemotherapy with cytotoxic drugs, including antimetabolites.
In case of suspension / discontinuation of breast feeding, complementary foods
should be given without using a sucking bottle (using an eyedropper, a spoon, a cup,
a syringe without a needle, complementary feeding system at the breast) so as to avoid
incorrect nipple latch by the infant, which increases the risk of hypogalactia (due to
reduced effectiveness of suckling) and of nipple injury (cracks).
Viral respiratory infections in the mother (including conditions with a high
temperature), presence of breast implants are no contraindications to breast
feeding.
Modern perinatal technology implies early discharge of mother

NB! and newborn from the maternity hospital.
Before discharge one should assess the condition of mammary glands, the nature
of lochia and condition of stitches. If there were complications during pregnancy
or delivery, the obstetrician should administer a complete blood count and a uri-
nalysis. If there are abnormalities during the puerperium, there may arise a need
for a vaginal examination. The obstetrician should be assured that the puerpera
has normal bowel movements and urination. She should be informed that lochia
will continue for no less than 3 weeks, and sometimes 4–5 weeks. On the eve
of the discharge one should talk to the woman about her daily regimen at home
and about postpartum contraception. The woman should continue observing the
same principles of personal and common hygiene as she observed in the maternity
hospital. Recommendations should be given to limit the extent of daily exercise,
ensure daytime rest for no less than 2 hours and daily walks in the open air. Regular
well-balanced nutrition is an important prerequisite for an uneventful course of the
puerperium. The time when the woman will resume her habitual routine, exercise
and work can vary in each particular case. The length of temporary work incapacity
is 6 weeks. The district pediatrician and nurse usually visit the newborn at home
over the first several days. At her first visit to the maternity welfare clinic, the
woman’s BP is taken and a sonography examination is performed. If there were
complications in the course of pregnancy or delivery, a complete blood count and
a urinalysis are administered. The woman is consulted about breast feeding (see
Chapter 3 Antenatal and Postpartum Care); all possible encouragement should be
given to breast feeding.
Doing an examination of external genitals one should note the condition of the
perineal scar (after laceration or episiotomy) and watch for signs of incompetence
of pelvic floor muscles. When doing a cervix examination with specula one should
take the PAP test.
During this visit contraception methods should be discussed; the gynecologist tries
to reveal possible complications of labor like back pain and postpartum depression.
A trust relationship between the woman and gynecologist promote the maintenance
of reproductive health for years to come.
11.5. CONTRACEPTION IN POSTPARTUM PERIOD
The postpartum period is the ideal time to solve the issues of family planning.
Anovulation persists for only 15 weeks in non-lactating women. About 1% of breast
feeding mothers get pregnant over the first year after childbirth.
The choice of contraception after childbirth is determined by breast feeding and
its regimen.
The method of lactation amenorrhea is a quite reliable and

NB! cost effective method of postpartum birth control. Exclusive
breastfeeding round the clock provides a secure protection
against pregnancy due to a high prolactin level which suppresses
ovulation.
The woman remains infertile over six months after childbirth provided she has
amenorrhea and her infant receives exclusively breast milk (without a nighttime in-
terval exceeding 3–3.5 hours or using pacifiers). Women who breast feed irregularly
may ovulate and get pregnant.
The main principle behind lactation amenorrhea is disturbance of the rhythm of
gonadotropin-releasing-hormone secretion in response to mechanical stimulation of
the nipple and areole. In its turn, this prevents the accumulation of luteinizing and
follicle-stimulating hormone concentrations necessary for follicle maturation.
This method requires four conditions to be met:
• breast feeding should take place no less than every 2–2.5 hours at daytime and
3–3.5 hours at nighttime (within the interval from 12PM to 7AM);
• persisting amenorrhea;
• no recourse to water, breast milk supplements or pacifier in the infants’ diet and
regimen;
• infant’s age under 6 months.
278 Obstetrics
If the method of lactation amenorrhea does not suit the breast feeding woman
for any reason, it is acceptable to prescribe purely progestine oral contraceptives
(they can be taken immediately after childbirth), parenteral contraceptives (implants,
Depo varieties are not contraindicated 6 weeks after childbirth), intrauterine devices
(4 weeks after childbirth), combination estrogen-gestagen contraceptives (6 weeks
after childbirth). As a means of emergency contraception, one can use both hormonal
and intrauterine contraceptives starting 4 weeks after childbirth.
REMEMBER!
The puerperium lasts for 6 weeks.
The maximum physiological blood loss should not exceed 0.5% of the woman’s
weight.
Involution is retrograde change of all organs and systems after childbirth.
The rate of uterus involution depends on parity, the extent of its distension during
pregnancy and breast feeding.
Lochia are postpartum discharge consisting of sloughing decidual membrane,

blood and other tissue components.
An unpleasant acrid odor of lochia indicates infection.
Modern perinatal technologies are based on rooming in and exclusive breast

feeding on demand.
Early discharge from maternity hospital is possible 12–20 hours after childbirth.
CONTROL QUESTIONS
1. Classification of the postpartum period.

2. Involution changes in the reproductive system.
3. Involution changes in the cardiovascular system.
4. Involution changes in the excretory system.
5. Involution changes in the respiratory system.
6. Modern perinatal technologies.
7. Regulation of lactation.
8. Benefits of breast feeding for the mother and infant, the underlying rationale.
9. Contraindications to breastfeeding on the part of the mother and infant.
10. What are the principles of active management of the postpartum period?
11. Acceptable methods of contraception in breast feeding women.
12. The method of lactation amenorrhea: the principle of its action, effectiveness,
prerequisites.
13. What is the composition of breast milk?
CHECK YOURSELF!
Level 1. Test
1. The postpartum period on average lasts for:
a) 2 hours;
b) 4 weeks;
c) 6 weeks;
d) 8 weeks.
2. According to Russian obstetric school, 2 hours after childbirth is the end of:
a) very early postpartum period;
b) early postpartum period;
c) late postpartum period;
d) very late postpartum period.
3. How long does the puerpera stay in the delivery room:

a) 1 hour;
b) 2 hours;
c) 3 hours;
d) 4 hours.
4. True hypogalactia can be caused by:

a) negative experience of breast feeding in close relatives (mother, grandmother);
b) hypoplasia of mammary glands in the puerpera;
c) non-compliance with the principles of breast feeding;
d) need to breast feed several infants at the same time (multiple pregnancy,
simultaneous breast feeding of the newborn and the elder child).
5. The method of lactation amenorrhea is applicable during the period of:

a) 2 months after childbirth;
b) 4 months after childbirth;
c) 6 months after childbirth;
d) 12 months after childbirth.
6. Absolute contraindication to breast feeding on the part of the mother is:

a) hepatitis B;
b) syphilis;
c) HIV infection;
d) chronic hepatic failure.
7. Contraindication to breast feeding on the mother’s side requiring suspension of

breast feeding is:
a) acute viral respiratory infection;
b) suppurative mastitis;
280 Obstetrics
c) active tuberculosis;
d) human papilloma virus infection.
8. The composition of breast milk becomes stable and the milk is mature:
a) on day 3–4 after childbirth;
b) during the third trimester of pregnancy;
c) during 2–3 weeks after childbirth;
d) during 5–6 weeks after childbirth.
9. What time after childbirth can combination oral contraceptives be prescribed to a

breast feeding mother:
a) in 2 months;
b) in 6 months;
c) in 12 months;
d) such medications are contraindicated to breastfeeding mothers.

1. The present case is the first physiological (uneventful) vaginal birth of a
singleton pregnancy. When should the newborn be latched to the mother’s breast?
2. It is the fourth day after a second spontaneous delivery complicated by massive
blood loss, the mother does not have enough breast milk. The elder child received
exclusively breast feeding until 6 months. What is your diagnosis? What is the plan
of management?
NOTES
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• Chapter 12
POSTPARTUM COMPLICATIONS
12.1. SEPTIC DISORDERS IN POSTPARTUM PERIOD
Although antibiotics found their way into obstetric practice almost a century ago,
which promoted a sharp decrease in the rate of postpartum infection, pyoinflamma-
tory complications of the puerperium still remain a major issue of modern obstetrics.
The rate of postpartum infection varies significantly due to the fact that there are no
universally accepted criteria for its diagnosis; the rate amounts to 2–10% in different
countries. An important role in the incidence of infectious complications belongs to
the level of social and economic development of the country, patterns of health care
(free of charge or private), local culture, educational background, religion, etc. On
the whole, the number of women who died of septic complications is higher than
the toll of all epidemics, pandemics or wars. Even nowadays, in the 21st century,
over 50 thousand women die of sepsis every year. In economically backward coun-
tries septic complications in the puerperium remain one of the three leading causes
of maternal death sharing the credit with obstetric hemorrhage and preeclampsia.
12.1.1. Definition
Postpartum infection is a disease of puerperal women related to pregnancy and
delivery and caused by infection.
Infections revealed during the puerperium but not associated with pregnancy and
delivery (the flu, dysentery) are not classified as postpartum conditions.
12.1.2. Historical background

The story of struggle against pyoinflammatory conditions dates back to ancient
times. However, the first scientifically reliable historical documents appeared in the
second half of the 18th century: contemporaries totally overlooked a small book
by a Manchester physician Charles White published in 1773 in his Treatise on the
Management of Pregnant and Lying-in Women; it discussed issues of patient’s hy-
giene, including washing and boiling of patients’ clothes and underwear. This could
be regarded as the first reform of medical practice comparable with smallpox vac-
cination if the principles stated by White had become widespread. Unfortunately,
this did not happen.
It is believed that a scientific impetus for elimination of puerperal fever (post-
partum sepsis) was provided by research performed by an obstetrician from Vienna
Ignaz Semmelweis (1818–1865) (Fig. 12.1). He merely suggested that when examining
puerperal women one should wash the hands with chlorine water. This measure alone
282 Obstetrics
resulted in a severalfold drop in the rate of puerperal

fever forestalling the discoveries by L. Pasteur and
J. Lister. This discovery was not accepted by con-
temporaries, as is often the case, so it did not lay a
foundation for aseptics. It took almost half a century
and hundreds of thousands of maternal lives until the
true origin of septic complications including puer-
peral complications was recognized. In the middle of
the 19th century the true cause of infectious disease
was revealed at last. An invaluable contribution to
studying the etiology of infection was made by Louis
Pasteur (1822–1895), professor at Lille University, and
English surgeon Joseph Lister (1827–1912). Besides,
Louis Pasteur proved that the bacteria that cause the
souring of milk and putrefaction of meat are spread
Fig. 12.1. I.F. Semmelweis everywhere, and their activity can be turned to human-
kind’s benefit (bread- and beer-making).
Microorganisms are important constituents of many foods as well as of the skin
and mucosa in the human body. Microorganisms populating the vagina were men-
tioned in the second half of the 19th century. In Russian literature the first report of
studying vaginal microflora was made by Dimitry Ott (1855–1929) in 1886. In 1887
a theory of self-cleaning of the vagina as a self-regulating system was proposed.
The first half of the 20th century was marked with some landmark events in sci-
ence. One of them was discovery of penicillin by Alexander Fleming. Nowadays tens
of thousands of new antibiotics are synthetized in laboratories all over the world;
however, despite the major advances of pharmacology, a progressively increasing rate
of postpartum infection is noted throughout the world.
It has dawned on people that antibiotics are not perfect for all cases. Moreover, anti-
biotics have played a low-down trick becoming a catalyzer in the evolution of antibiotic-
resistant strains of bacteria that can be put down by still newer drugs, and so on, and
so forth ad infinitum. To date, the case fatality rate of septic shock amounts to 50%.
A comprehensive study on human microbiology (a transregional project of 2007–
2012) and an escalation of infections caused by superbacteria afforded ground for the
WHO declaration that the «era of antibiotics came to an end» (2014).
12.1.3. Etiology and pathogenesis

Early 21st century saw a change in factors affecting the development of pyoinfam-
matory conditions during the puerperium. By that time most pregnant and puerperas
were women with chronic genital infection, severe extragenital disease, pregnancy
achieved using assisted reproductive tehcnology, with hormonal therapy or surgery
for miscarriage in past history.
An important factor is the change in the nature of microflora seen over recent de-
cades: due to a widespread administration of broad spectrum antibiotic drugs, which
is not always justified, as well as the use of means of disinfection, strains of bacteria
have developed that show multiple resistance to antibacterial drugs and disinfectants.
Chapter 12. Postpartum complications 283
Selection of infectious matter has occurred: strains less resistant to therapy have
subsided while antibiotic resistant strains multiply in maternal hospitals everywhere.
In early 2000s the term superbacteria was coined; it means bacteria showing resis-
tance to all antibiotics used in therapy. The therapy often results in a fatal outcome.
Any of the huge range of opportunistic infectious matter populating the human body
(microbiota1) can evolve to superbacteria.
Establishing large obstetric hospitals where infants were separated from mothers
has played a negative role in prevention of postpartum infection. Concentration of
large numbers of pregnant and puerperal women and infants under one roof produced
a much higher risk of infection.
In obstetrics, increase in the incidence of infectious complications is promoted by:
• widely used assisted reproductive technology, invasive diagnostic techniques
(amniocentesis, cordocentesis, chorion biopsy);
• introduction of surgical techniques to pregnancy management: surgical correction
of cervical incompetence in miscarriage;
• higher incidence of abdominal delivery.
12.1.4. Risk factors

Risk factors for postpartum pyoinflammatory disease (WHO, 2008):
• noncompliance with the principles of personal hygiene;
• noncompliance with the principles of aseptics;
• retention of dead tissue in the birth canal (prolonged pregnancy with a dead
fetus, retention of placental parts in the uterine cavity, etc);
• anemia and eating disorders in history;
• prolonged labor;
• prolonged membrane rupture to delivery period;
• frequent vaginal inspections;
• cesarean section or other surgery during delivery;
• sexually transmitted disease in history;
• diabetes mellitus;
• recurrent abortions.
One of the factors of nonspecific protection against microbial invasion is a person’s
own bacterial and viral «coat». To date, 10 000 infectious organisms are known that
populate the human body without any sign of disease whatsoever. The total num-
ber of genes of the entire microbiome2 exceeds the genome of the person himself
100 times. 1014 bacteria live in the body of one human. There are 10 bacterial cells
per each human cell; 100 bacterial genes per each human gene. The bacterial weight
in each human is about 3 kg3. Bacterial flora of various body parts prevents invasion
of pathogenic organisms. Any invasion to healthy epithelium was practically always
1 Microbial flora harbored by normal, healthy individuals

2 Microbiome is the total of genetic material of all microorganisms populating the macroorganism
(the human).
3 Data by National Institute of Health (USA) which launched the Human Microbiome consortium in
2007. Its objective is determining the species composition and numerical composition of microorganisms
populating the human body and their DNA sequences. The fi rst fi ndings were published in 2012.
284 Obstetrics
preceded by changes in the microflora. All female genital diseases as well as sexually
transmitted disease are accompanied by changes in vaginal ecology.
The skin and mucosas of a human, including the genital tract, can be imagined
as a totality of microareas of varying types, each one being a habitat or an ecologi-
cal niche populated by various microorganisms. Essentially, each habitat has its own
population of organisms different from all others. Despite the ability of organisms to
adapt well to the changing environment, the latter influences them both quantitatively
and qualitatively.
Normal biocenosis of the genitals is not a constant value; rather, it is a constantly
changing component of homeostasis. The genital tract of a healthy woman shows
considerable changes during menstrual periods, pregnancy, and the postpartum,
post-abortion and menopausal periods.
Natural barrier mechanisms protecting the female genitals and preventing infection
include the following:
• pubic and perineal hair;
• Bartholin’s gland secretion containing immunoglobulins;
• morphofunctional competence of perineal tissues — the closed pudendal fissure;
• vaginal secretion containing carbohydrates, proteins, lysozyme:
• the predominant components of proteins are albumins and immunoglobulins;
• glycogen produced under the impact of estrogens and gestagens is a substrate
to lactobacillus metabolism; lactic acid and traces of hydrogen peroxide are
produced during the process; lactic acid produces the acidity in the vaginal
medium (pH 3.8–4.4);
• cervical mucus which is secretion of glands in the cervical mucosa; it contains
IgA produced in response to the presence of bacteria in the vagina, the bacteria
acting as antigens;
• endometrium (sloughing every month during the menstrual period);
• secretion of uterine tubes containing lysozyme.
There are a number of barrier methods protecting against vaginal

NB! infection. The main method is maintaining the acidity of vaginal
contents provided by the presence of lactobacteria.
During pregnancy hormonal changes in the vaginal and cervical epithelium are
associated with progressively increasing acidity, which promotes the growth of nor-
mal vaginal microflora — lactobacilli — that are a factor of nonspecific protection.
Healthy pregnant women, compared with nonpregnant ones, show a tenfold increase
in lactobacillus population as pregnancy progresses.
The baby is born in a medium with microorganisms of low

NB! virulence and acquires the lactoflora, which provides the main
factor of resistance against the pathogenic microflora of external
environment.
The mechanism of disease development consists in disrupting the mechanism

of local immunity, which leads to lactobacilli suppression, and in some cases — to
their complete elimination and thus — to activation of opportunistic organisms that

can achieve high concentrations and cause the development of postpartum infection.
The development of postpartum infection stems primarily from

NB! the puerpera’s condition, virulence of the causative agent and the
extent of contamination.
Disturbed balance in the «body — microorganism» system can be caused by vari-

ous factors.
Factors predisposing to postpartum infection:
• factors present before pregnancy:
• endogenous extragenital infection foci in the nasopharynx, oral cavity, renal
pelvis;
• extragenital noninfectious disease (anemia, diabetes mellitus, disorder of lipid
metabolism, etc);
• factors developing during pregnancy: many of its complications like anemia of
pregnancy, preeclampsia, placenta previa, gestational pyelonephritis.
The invasive methods of investigating fetal condition discussed above, surgery for
cervical incompetence increase the risk of postpartum infection development (there
is not enough evidence).
Correction of microbiocenosis, the so called vaginal sanation

NB! in pregnant women using antibacterial drugs while there are no
valid diagnostic criteria, which is not followed by restoration of
normal biocenosis, increases the risk of postpartum infection
development.
Besides, at advanced gestational age of normally progressing pregnancy one notes

a considerable change in the concentration of certain immunoglobulins (G, A, M) in
the blood plasma, a reduction in absolute numbers of T- and B-lymphocytes. That
means that «secondary physiological immunodeficiency» develops. In this situation
the vaginal ecosystem is the vulnerable spot that is why bacterial vaginosis and vagi-
nitis develop in pregnant women.
Labor brings along other factors promoting the development of postpartum in-
fection. First of all, it is the discharge of mucous plug at the end of pregnancy, the
plug posing a mechanical and immunological barrier to microorganisms. Rupture
of membranes brings about a drop in the acidity of vaginal content; IgA is washed
away mechanically from the vaginal tract mucosa, which dramatically reduces local
secretory protection. It was established that 6 hours after the rupture of membranes
there is not one anti-infection barrier left in the female genital tract, while the de-
gree of colonization and the nature of microflora depend on the length of interval
between membrane rupture and delivery. Early rupture of membranes, prolonged
labor, abnormalities of uterine activity, frequent vaginal examinations (more than 3),
insufficient anesthesia, any surgical invasion — all these factors give a dramatic boost
to the risk of postpartum infection. Injury in labor and bleeding also predisposes to
the development of postpartum infection.
286 Obstetrics
Chorioamnionitis is a clinical manifestation of ascending infection during delivery.

When there is a protracted interval after the rupture of membranes, the parturient
woman shows malaise, increased body temperature, fever, rapid pulse; the amniotic
fluid becomes turbid and smelly, sometimes pus-like discharge is noted, the hema-
tologic status changes. In about 20% of cases the puerperas who had chorioamnio-
nitis during childbirth develop postpartum endomyometritis and other varieties of
puerperal disease.
During the postpartum period there is not one anti-infection barrier left in
the puerpera’s genital tract, except for the WBC margination emerging in the
placental bed area. The inner surface of postpartum uterus is a wound surface,
and the uterine contents (blood clots, epithelial cells, fragments of decidua)
provide a friendly medium to microorganism growth. The uterine cavity is eas-
ily infected due to ascension of pathogenic and opportunistic vaginal flora. As
mentioned above, in some puerperas the postpartum infection is a continuation
of chorioamnionitis.
The development of infection at puerperium is promoted by uterine subinvolution,
retention of afterbirth fragments, violation of sanitary and epidemiologic principles.
Postpartum infection is in most cases of the type of wound infection. The wound
serves as portal of entry for infection; the primary focus commonly emerges here,
most often it is localized in the uterus. Further development of infection depends
on the virulence of microorganisms and extent of contamination on the one hand;
on the other hand — on the condition of the woman’s host defenses. A factor pro-
tecting against dissemination of bacteria from the uterine cavity at puerperium is
the emergence of leukocyte margination in the placental bed area. Perineal, vaginal
and cervical tears contribute to infection development, especially when the tears
were not detected or repaired, another contributing factor is the surgical scar after
cesarean section.
12.1.5. Etiological structure

Characteristic feature of etiological structure of obstetric pyoinflammatory dis-
ease is its variability due to widespread administration of antibiotic drugs. Under
the impact of antibiotics strains of bacteria sensitive to them give way to resistant
strains. Thus, before the antibiotics were discovered, hemolytic streptococcus
used to be the most dangerous causative agent of postpartum complications. After
introduction of antibiotics to obstetric practice the staphylococcus sensitive to
the drug gave way to staphylococci which develop resistant strains more easily.
Starting in the 1970-s broad spectrum antibiotics highly active against staphylo-
cocci have been used in clinical practice, and since then the role of staphylococci
in infection causation has diminished; they have been replaced by gramnegative
bacteria and nonspore-forming anaerobic bacteria and their combinations resis-
tant to antibiotics.
Pyoinflammatory infection can be caused by both pathogenic and opportunis-
tic bacteria. The most common pathogenic bacteria are gonococci, Chlamydia,
Trichomonas. Opportunistic bacteria that populate many habitats in the human
body and serve as a factor of nonspecific anti-inflammatory protection can
themselves become, under certain conditions, causative agents of postpartum

infection.
Causative agents of postpartum infection can be aerobic bacteria: enterococci,
colibacilli, Proteus, Klebsiella, group B streptococci, staphylococci. The flora is
often represented by anaerobic bacteria: Bacteroides, fusobacteria, peptococci, pep-
tostreptococci. In modern obstetric practice one encounters Chlamydia and fungi
increasingly often.
In contrast to some other infections caused by a certain agent, postpartum infec-
tion is caused by a variety of agents. Various clinical forms of postpartum infection
can be due to different bacteria. Anaerobic gramnegative cocci are not especially viru-
lent. Anaerobic gramnegative bacilli promote the development of severe infection: the
most common causative agent of obstetric sepsis is Escherichia coli. Staphylococcus
aureus causes wound infection and postpartum mastitis. Most commonly, postpar-
tum infection is polymicrobial, aerobic and anaerobic; causative agents that can
form biofilms are especially dangerous. A biofilm is a thin layer of microorganisms
adhering to the surface of a structure; they can easily adapt to environmental changes
and medications.
Microbial associations that are more pathogenic than

NB! monocultures now play the leading role in the emergence of
postpartum infection (over 80%). The virulence of microorganisms
in an association is much higher, especially in case of aerobic-
anaerobic and biofilm infection.
Port of entry for infection is commonly the surface of placental bed and the surface
of birth canal injury.
In most cases of postpartum infection, there is no route of infection as such,
because it is the patient’s own opportunistic flora that is activated. In other cases
infecting with resistant hospital strains from outside takes place upon violation of
antiseptics principles.
One should remember that in case of postpartum infection the

NB! causative bacteria are mostly transmitted by the hands of the
personnel, articles of care and instruments.
If there is massive infecting with highly virulent microflora and / or considerable

reduction of the puerpera’s host defenses, infection leaves the primary focus and
spreads abroad. The following routes for spread of infection from the primary focus
are distinguished:
• hematogenic route;
• lymphogenic orute;
• longitudinal (intracanalicular) route;
• perineural route.
One should also mention the comparatively recent route of for spread of infec-
tion: intraamnial, associated with introduction of invasive investigation methods in
the obstetric practice (amniocentesis, cordocentesis).
288 Obstetrics
12.1.6. Classification
Classification of postpartum infection presents certain difficulty due to the variety
of causative agents, multiplicity of forms and clinical presentations and also the fact
that there are no universally accepted criteria or terminology.
The international classification of diseases, injuries and causes of death, tenth
version, provides a fairly detailed reflection of all postpartum infection of female
genitals as well as infection not related to childbirth; this classification is accepted
for statistical purposes all over the world.
ICD-10 codes
• Pregnancy, childbirth and the puerperium (O00–O99).
– Complications predominantly related to the puerperium (O85–O92).
– O85 Puerperal sepsis.
– O86 Other puerperal infections.
◊ O86.0 Infection of obstetric surgical wound.
◊ O86.1 Other infection of genital tract following delivery.
◊ O86.2 Urinary tract infection following delivery.
◊ O86.3 Other genitourinary tract infections following delivery.
◊ O86.4 Pyrexia of unknown origin following delivery.
◊ O86.8 Other specified puerperal infections.
– O87 Venous complications in the puerperium.
◊ O87.0 Superficial thrombophlebitis in the puerperium.
◊ O87.1 Deep phlebothrombosis in the puerperium.
◊ O87.2 Hemorrhoids in the puerperium.
◊ O87.3 Cerebral venous thrombosis in the puerperium.
◊ O87.8 Other venous complications in the puerperium.
◊ O87.9 Venous complication in the puerperium, unspecified.
– O88 Obstetric embolism.
◊ O88.3 Obstetric pyemic and septic embolism.
– ◊ O90 Complications of the puerperium, not elsewhere classified.
◊ O90.0 Disruption of caesarean section wound.
◊ O90.1 Disruption of perineal obstetric wound.
– ◊ O91 Infections of breast associated with childbirth.
◊ O91.0 Infection of nipple associated with childbirth.
◊ O91.1 Abscess of breast associated with childbirth.
◊ O91.2 Nonpurulent mastitis associated with childbirth.
However, this classification appears rather cumbersome for the purposes of
clinical practice, so in the absence of universally accepted clinical classification,
obstetricians in different countries use different terms and diagnoses describing
in various ways the prevalence of infection. In Russian school of obstetrics one
uses the classification of postpartum infection proposed by S.V. Sazonov and
A.V. Bartels.
According to Sazonov-Bartels classification of postpartum

NB! infection, various forms of postpartum infectious disease are
regarded as separate steps in a single dynamic process.
• Stage one: infection is limited to the area of postpartum wound:

– postpartum metroendometritis;
– postpartum wound infection located in the perineum, vaginal walls or cervix.
• Stage two: spread of infection beyond the postpartum wound, but it is still
localized:
– metritis;
– parametritis;
– salpingoophoritis;
– pelvioperitonitis;
– local thrombophlebitis (metrothrombophlebitis, thrombophlebitis of pelvic
veins, thrombophlebitis of femoral veins).
• Stage three: clinical presentation of the infection is similar to generalized infection:
– diffuse peritonitis;
– anaerobic gas infection;
– progressing thrombophlebitis.
• Stage four: generalized infection—sepsis (septicemia, septicopyemia).
• Postpartum (lactation) mastitis (serous, infi ltration or suppurative mastitis).
• Septic shock1.
Strictly speaking, this classification, although logical, does not answer the ques-
tions of infection management. It is the impossibility to distinguish stages in pyoin-
flammatory disease that constitutes the problem of maternal mortality of sepsis. In
most cases the diagnosis and therapy come too late and are not active enough.
Although the main links of clinical classification correspond to

NB! ICD-10 and are well organized to understand the dynamics of
infection spread, any specialist caring for a puerpera should be
guided by the formula: Infection can become generalized at any
stage of disease.
In the 22nd edition of Williams Obstetrics the following infection-related complica-

tions of the puerperium are stated:
• wound infections, infections of perineum, vagina and cervix;
• parametrial phlegmon;
• adnexal infection;
• pelvic abscess;
• peritonitis;
• septic pelvic thrombophlebitis;
• toxic shock syndrome.
The logistics of septic process is understood in the same way

NB! by practically all; however, sepsis at any stage, anticipating it
(risk strategy!) and providing early diagnosis poses a healthcare
problem of global importance.
1 In the classical classification by Sazonov-Bartels septic shock belongs to the fourth stage of infection;
however, this complication may accompany any infection irrespective of its stage.
290 Obstetrics
General clinical presentations of postpartum infection are extremely variable; this

variability is due to the polymicrobial nature of postpartum infection, different routes
for its spread, different responses of the puerperal women’s bodies. Although the
clinical course of both localized and generalized types of postpartum disease varies
considerably, there are a number of typical signs:
• tachycardia (sometimes discordant with the body temperature);
• elevated body temperature;
• fever;
• increased perspiration;
• sleeping disorder;
• headache;
• adynamia or euphoria;
• appetite suppressed or absent;
• manifestations of dysuria or dyspepsia;
• reduced BP (in septic shock or sepsis).
An important clinical sign of postpartum infection is tachycardia while the body
temperature is within normal or subfebrile.
Local signs:
• lower abdominal pain;
• retention of lochia or copious puruloid foul-smelling lochia;
• uterine subinvolution;
• suppuration of wounds in the perineum, vagina, anterior abdominal wall after
cesarean section.
Since antibiotics are widely administered due to changes in the

NB! nature and properties of major infectious agents of postpartum
infection, their clinical presentations are much different nowadays.
One notes suppressed, subclinical manifestations where
there is a discrepancy between the puerpera’s general state,
clinical presentations and severity of the disease, slowed-down
development of infection, poorly marked clinical signs.
12.1.7. Nosological forms of postpartum infectious disease

12.1.7.1. Puerperal ulcer
The notion of puerperal ulcer implies infection of the traumatic injury of the skin,
vaginal mucosa and cervix as a result of surgical delivery through the natural passages
or prolonged labor with a large fetus.
Factors promoting the development of puerperal ulcer are incorrect placing of
stitches, properties of suture material, disorder of tissue trophism, inadequate care.
Clinical presentations of this condition are mostly local signs: local tenderness, a
frequent sensation of itching due to skin irritation by the ulcer discharge. The ulcer
boundaries are clearly designated, somewhat edematous and congested, with inflam-
matory infiltration of surrounding tissue. The base of the ulcer is covered with dingy
grey incrustation with necrosis patches; the discharge is mucopurulent, smelly. The
wound can bleed easily.
The main principles of managing puerperal ulcer consist in local administration of
antiseptic and antiinflammatory drugs. First, the wound is swabbed with disinfectant
solutions (hydrogen peroxide, chlorhexidine) for several days. To provide a drain,
hypertonic solution of sodium chloride is administered. Enzymes are commonly
used to remove the necrotic incrustation and fibrinous deposit and to accelerate
regeneration. Local administration of ultraviolet is known to be effective. When the
wound has been cleansed, disinfectants and compounds that promote epithelization
are administered. If the area of lesion is large, and / or inadequate treatment was
administered, the infection may become generalized.
12.1.7.2. Suppuration of perineal sutures

In suppuration of perineal sutures the tissues show an inflammatory reaction
caused by the invasion and growth of the causative agent in the suture material.
Clinical presentations of suppuration of perineal sutures include edema, hyperemic
skin, acute tenderness. A slight pressing on the skin near the stitches produces leak-
age of serous purulent discharge.
Management of suppuration of perineal sutures consists in removing the sutures
and treating the wound applying the purulent surgery principles: removal of suture
material, cleansing out the purulent discharge and removing the fragments of necrotic
tissue if possible; further treatment is administered like in postpartum ulcer. When
the wound has been completely cleansed of pus and granulation is satisfactory, one
can place secondary sutures in the perineum.
12.1.7.3. Suppuration of the hematoma of external genitals and vagina

In suppuration of the hematoma of external genitals and vagina typical presenta-
tions are sensation of heaviness, pressure and acute pain. Pulsating pain develops.
External genitals become deformed. The surface of the skin or vaginal mucosa above
the hematoma becomes unfigured, glistening, and congested.
Suppurative hematoma should be treated surgically. The hematoma is opened,
the cavity is cleansed and drained well. The cavity of emptied hematoma is washed
with disinfectant solutions.
12.1.7.4. Infected wound after cesarean section

Infected wound after cesarean section is characterized by local and general manifesta-
tions, changes in the blood. If the postoperative wound is suppurating, the sutures should
be removed to provide drainage of the wound contents, purulent cavities are drained.
12.1.7.5. Puerperal endometritis (metroendometritis)

Puerperal endometritis (metroendometritis) means inflammation of the uterine
mucous membrane which involves, to a lesser or greater degree, its muscular layer
(mostly in the area of the WBC margination).
Postpartum metroendometritis is the most common complication

NB! of the postpartum period.
292 Obstetrics
Starting in the 19th century and till mid-20th century, four types of puerperal me-
troendometritis were distinguished: classical, abortive, inapparent, metroendometritis
after cesarean section.
• Classical metroendometritis is rarely seen in contemporary obstetric practice.
Clinical presentations develop on day 1–5: tachycardia 100 per minute,
body temperature elevated to 38–39 °С. General malaise, fever, dryness and
hyperemia of skin are noted. The uterus body shows subinvolution, tenderness;
there is purulent foul-smelling discharged. The hematological status changes:
leucocytosis to 10–15×109/l, left shift, increased ESR.
• Abortive metroendometritis is noted on day 2–4; however, if adequate treatment
is administered, the symptoms subside quickly.
• Inapparent metroendometritis is most common nowadays. Symptoms develop on
day 5–7. Clinical presentations are inapparent, all developments proceed slowly.
Body temperature does not rise above 38 °С, there is no fever. In most puerperas
the leucogram shows no change. Local signs are hardly noticeable (insignificant
uterus tenderness revealed by palpation). The course of endometritis becomes
undulating: recurrence develops on day 3–12 after «cure».
Nowadays metroendometritis is mostly noted in its inapparent

NB! variety.
Criteria of postpartum endometritis (two signs suffice to make the diagnosis).

• Elevated body temperature (38 °С and higher).
• Uterus tenderness in palpation.
• Foul-smelling discharge from the genital tract.
• Moderate bleeding from the genital tract is possible. An increased WBC count in
the blood has a low prognostic value to confi rm the presence of infection.
Body temperature elevation to 38 °С within 24 hours after delivery (including
cesarean section) is common. Most often it is caused by dehydration, so manage-
ment includes abundant drinking, infusion therapy (if indicated). Anti-inflammatory
therapy is not indicated.
If subfebrile body temperature to 37.5 °С persists over 24 hours after the second
postpartum day, and there are no clinical signs of endometritis, the following is
indicated:
• body temperature and pulse measurement every 3 h;
• uterine discharge culture test, determining the sensitivity of microflora to
antibiotics;
• differential diagnosis with possible causes of elevated body temperature.
Ultrasound diagnostics is required to reveal fragments of placental tissue, hema-
tometra, which are risk factors for endometritis.
Ultrasound of the uterus should not be administered for diagnosis of postpartum
endometritis; after spontaneous and especially operative delivery hysteroscopy is in-
dicated to all patients (Fig. 12.2).
The informative value of hysteroscopy is 91.4% in diagnosis of postpartum and
postoperative endometritis; this value is the highest for all investigation methods
including pathomorphology investigation (100%).
Fig. 12.2. Hysteroscopy of postpartum uterus
Post-cesarean metroendometritis always has a severe course. Besides, there are

pronounced signs of intoxication and enteroparesis. Most often these signs are noted
in puerperal women in whom the surgery was accompanied by copious bleeding, loss
of fluid and electrolytes.
Clinical presentations are complemented by oral dryness, intestinal distention,
reduced diuresis.
The main principles of managing metroendometritis include debridement of the
uterus cavity (the primary focus) while providing antibacterial, symptomatic and
multicomponent infusion therapy.
12.1.7.6. Puerperal metritis

Puerperal metritis is a more profound lesion of the uterus than in metroendo-
metritis. It develops when the WBC margination breaks through in the placental
bed area and infection spreads along lymphatic and blood vessels into the depth of
uterine muscular layer.
Metritis develops together with endometritis and constitutes its sequel. It cannot
be diagnosed earlier than day 7 postpartum. The disease starts with tachycardia,
fever, body temperature elevation to 39–40 °С. The general condition is disturbed
considerably. Palpation reveals enlargement of the body of uterus and its tenderness,
especially in the area of uterus sidewalls. The discharge is scanty, dark red with pus
admixture, smelly.
General principles of postpartum metritis therapy. When diagnosing metritis one
fills in a chart of observations: hourly control of body temperature, BP, pulse, di-
uresis, and all the administrations.
Therapy of pyoinflammatory disease during the postpartum period should be based
on general principles of therapy:
• debridement of the purulent focus (hysteroscopy-guided removal of necrotized
decidual fragments; in critical forms of the disease — hysterectomy); antibacterial
therapy;
• detoxifying therapy.
To administer adequate therapy, one should take into account all the features ac-
companying the onset of disease, the length and rate of development of the disease,
individual response to therapy, the features of pregnancy and delivery.
294 Obstetrics
Before administering antibacterial therapy one should obtain a

NB! sample of uterine discharge for bacteriology study. Upon revealing
the causative agent one determines its sensitivity to antibiotics for
further etiotropic therapy.
Empirical antibiotic therapy (2015–2016) includes:

• amoxicilline / clavulanate 1.2 g thrice a day IV;
• ampicilline / sulbactam 1.5 g 3–4 times a day IV;
• amoxicilline / sulbactam 1.5 g 3 times a day IV;
• cefoperazone / sulbactam 2–4 g twice a day IV;
• ceftriaxone 1–2 g once a day IV;
• cefotaxime 1–2 g thrice a day plus metronidazole 500 mg thrice a day IV;
• cefepime 1–2 g twice a day IV;
• ciprofloxacin 200–400 mg twice a day IV.
Alternative therapy:
• imipenem / cilastatin 500 mg 3–4 times a day IV;
• meropeneme 1 g thrice a day IV;
• piperacillin / tazobactam 4.5 g 4 times a day IV.
Antibacterial therapy is considered effective if major symptoms

NB! disappear within 48 – 72 hours.
If there are no clinical signs of improvement over this period, the following is done:
• rule out any other possible sources of infection, pus accumulation in the uterine
cavity, development of thrombosis of profound veins and pelvic veins;
• if the above mentioned causes of clinical ineffectiveness of therapy are ruled out,
it is advisable to change the regimen of antibacterial therapy taking into account
the findings of culture tests, if possible.
The criterion of therapy discontinuation is sanation of the focus, return of body
temperature to normal within 2–3 days.
Late diagnosis and inappropriate treatment can result in further

NB! spread and generalization of infection.
12.1.7.7. Puerperal salpingoophoritis
Puerperal salpingoophoritis is an inflammation where infection spreads form the

uterus cavity to uterine tubes and ovaries. Most commonly the process develops when
there was adnexal infection in history.
Clinical presentations of puerperal salpingoophoritis usually develop on day
7–10 after delivery. The puerpera’s general condition worsens abruptly; tachycardia,
pyrexia to 40 °С with fever are noted. There is pain in lower abdomen, signs of
irritable bowel, intestine distention. The uterus is enlarged, pasty, inclined in the
direction opposite to the infection focus. A vaginal examination detects an acutely
painful infiltrate in the area of adnexa without clear-cut contours.
On the first day the therapy of salpingoophoritis is conservative: antibacterial,

symptomatic and infusion therapy is administered. When the process becomes local-
ized developing pyosalpinx or pyoovar, laparotomy is performed with removal of the
abscess and sometimes of the uterus with its appendages.
12.1.7.8. Puerperal parametritis

Puerperal or postpartum parametritis is further spread of infection to the connec-
tive tissue and fat adjacent to the uterus. The route for spread of infection is the same
as in previous conditions, but the infection can be introduced due to deep tears of
the cervix or perforation of the uterus body in the area of parametrium.
Clinical presentations of puerperal parametritis set in on day 10–12 after childbirth.
First there is fever, pyrexia to 39–40 °С, the temperature persists for 8–10 days. The
patient’s general condition shows almost no change, she complains of dragging pain
in lower abdomen. A vaginal examination determines a moderately tender infiltrate
without clear-cut contours in the area of the broad ligament of uterus. On the side
of lesion the vaginal fornix is flattened. There are signs on the part of the iliopsoas
muscle: flexion of the leg in the coxofemoral joint produces pain. If therapy is not
initiated in good time, pus may spread above the inguinal ligament to the femoral
region, through the sciatic foramen to the buttock and to the pararenal area. The
abscess may open into the bladder and rectum.
In parametritis the therapy is the same as in salpingoophoritis. If abscess of
parametrial cellular tissue develops, it should be opened through the vagina or after
laparoscopy and followed by draining of the parametrium.
12.1.7.9. Postpartum pelvioperitonitis

Postpartum pelvioperitonitis means inflammation of the peritoneum limited to
the small pelvis cavity. It commonly develops after a cesarean section or traumatic
injury of the uterus.
Clinical presentations of postpartum pelvioperitonitis most often develop by day
3–4 after childbirth. At early stages pelvioperitonitis shows signs similar to clinical
presentations of diffuse peritonitis. As a rule the disease has a sudden onset, with
elevation of body temperature to 39–40 °С accompanied by acute pain in lower
abdomen, meteorism. The patient may have nausea, vomiting, painful defecation;
positive signs of peritoneum irritation in the lower abdomen are noted. The uterus
which is the source of infection is enlarged, tender; its anterior wall is tense so its
contours are unclear; its movements are limited; the posterior fornix bulges forth.
The inflammation can terminate in development of limited abscess in retrouterine
space or resolution of the infiltrate.
Postpartum pelvioperitonitis requires a complex therapy. It consists in massive
antibacterial, immune and multicomponent infusion therapy. When the infiltrate re-
solves, physiotherapy is recommended to eliminate adhesion formation. If an abscess
develops, it is opened, commonly through the posterior vaginal fornix (culdotomy).
12.1.7.10. Puerperal thrombophlebitis

Puerperal thrombophlebitis is one of severe complications of the postpartum pe-
riod. According to present view, pathogenesis of thrombus formation is due to the
296 Obstetrics
following factors: disturbance of hemodynamics, changes in vascular walls, infection,

changes in the blood coagulation system. All these factors may be present in the body
of an apparently healthy pregnant woman.
Any chronic condition that leads to changes in the biochemical and physico-
chemical properties of the blood can provide background against which throm-
boembolic conditions develop. As for extragenital disease, one should mention
varicose vein dilation, obesity, heart defects, anemia, disease of liver and bili-
ary tracts, hypertonic disease, arterial hypotension, uterine fibroid. The risk of
thromboembolic complications is increased at subsequent delivery, preeclampsia
of prolonged duration.
According to its localization, thrombophlebitis is divided into:
• extrapelvic:
– superficial vein thrombophlebitis in lower extremities;
– deep vein thrombophlebitis in lower extremities;
• extrapelvic (central):
– metrothrombophlebitis;
– pelvic vein thrombophlebitis.
Deep vein crural thrombophlebitis commonly develops 2–3 weeks after childbirth.
Clinical presentations are scarce: elevated body temperature, pain in gastrocnemius
muscles that gets worse upon movement in the talocrural joint on the side of the
lesion, moderate ankle edema on the side of lesion.
Superficial vein crural thrombophlebitis is characterized by pronounced presenta-
tions. As a rule, it develops in the presence of varicose veins of lower extremity. Its
signs are induration along the course of the vein, hyperemia, tenderness and infiltrate
in the affected area, ankle edema.
Metrothrombophlebitis is difficult to recognize. One notes quickened pulse, uterine
subinvolution, prolonged and copious discharge from vaginal tract. A vaginal ex-
amination detects that the uterus is enlarged and painful, especially at its sidewalls;
coiling cord-like indurations are noted on its surface.
Thrombophlebitis of pelvic veins is not usually detected before the end of the
second week. The most severe and life-threatening type of postpartum thrombo-
phlebitis is ileofemoral venous thrombus, its common outcome being pulmonary
vein embolism.
The main principle in the therapy of postpartum thrombophlebitis is admin-
istration of antibiotics. As the inflammation develops against the background of
vein thrombosis, anticoagulants are required to prevent further development of the
process. To avoid possible complications, strict bed confinement is recommended.
12.1.7.11. Generalized postpartum peritonitis

Generalized postpartum peritonitis is inflammation of the peritoneum associated
with infection spreading to the abdominal cavity and accompanied by a complex of
severe pathophysiological reactions that disrupt the functioning of all body’s systems.
Epidemiology. The incidence rate of generalized postpartum peritonitis varies
within a wide range of 0.05 to 0.3%. In a predominant number of cases peritonitis
develops after cesarean section which is now one of the most common obstetric
operations.
In 30% of observed cases peritonitis develops due to infection of the peritoneum

during surgery. In 15% of cases it is caused by disorder of intestinal barrier func-
tion as a result of prolonged paresis in postoperative endometritis. In 55% of cases
peritonitis develops due to deficient sutures in the uterus.
Classification. From the point of view of etiology and pathogenesis, peritonitis is
divided into:
• primary (a rare variety of hematogenic origin);
• secondary (a common variety; it includes postoperative peritonitis);
• tertiary (no specific source or causative agent).
According to the degree of generalization, we distinguish
• local peritonitis:
– limited (abscess);
– unlimited (pelvioperitonitis);
• diff use (generalized peritonitis).
Etiology. In peritonitis after a cesarean section, both grampositive and gram-
negative organisms are isolated, as well as nonspore forming anaerobes (most often,
Bacteroides). Grampositive organisms are isolated in 1/3 of cases, approximately.
The major causative agents are gramnegative bacteria (E. coli, Proteus, Klebsiella,
enterococci). The infection is most often polymicrobial.
Pathogenesis. The leading role in the pathogenesis of peritonitis is played by intoxi-
cation associated with the spread of causative agents in the abdominal cavity. Their
waste products cause the development of systemic inflammatory response syndrome
with signs of multiple organ failure. In a predominant number of cases, the source
of infection in obstetric peritonitis is in the uterus (endomyometritis, incompetence
of sutures in the uterus after a cesarean section).
A progressing decrease in the circulating blood volume is one of major hemodynam-
ic disorders. The increase in hypovolemia is promoted by exudation and transudation
into the gastrointestinal lumen, abdominal cavity, all body tissues as well as substantial
dehydration due to vomiting, respiration, perspiration. This leads to insufficiency of pe-
ripheral circulation, disturbed microcirculation, tissue hypoxia, acidosis and alkalosis.
Enteroparesis holds a special place in the pathogenesis of peritonitis after cesarean
section (Fig. 12.3). Overdistension of intestinal loops with fluid and gases leads to
intestinal dysfunction and dehydration of the whole body.
Massive loss of fluid, pyrexia and vomiting lead to further decrease in circulating
blood volume, cardiac output promoting the development of septic shock.
Clinical presentation of generalized postpartum peritonitis is characterized by the
patient’s critical condition, especially in suppurative peritonitis (Fig. 12.4).
The patient shows pronounced tachycardia; pulse arrhythmia is possible.
Respiration is quick, shallow; body temperature is elevated to 39–40 °С. There is
pronounced toxicosis, nausea, sometimes with vomiting; the abdomen is distended
due to retention of gases and absence of defecation. In most severe cases some signs
described above (elevated body temperature, irritable bowel) may be absent; the clini-
cal blood count shows leucopenia.
The course of obstetric peritonitis is divided into three phases.
• Phase one, reactive (24 h). Characteristic feature is progressing of local clinical
signs: abdominal pain, vomiting, diarrhea, tachycardia, tachypnea, decreased BP.
298 Obstetrics
Fig. 12.3. Enteroparesis (day 3 after cesarean section)
Fig. 12.4. Suppurative peritonitis. Relaparotomy after cesarean section
• Phase two, toxic (24–72 h). General reactions are predominant: disturbed
hemodynamics, microcirculation, hepatic and renal functions. Pain syndrome
subsides in the presence of suppressed peristalsis. Multiple organ failure
syndrome develops.
• Phase three, terminal (more than 72 h). Decompensation of syndrome disorders.
Septic shock develops.
Diagnosis. Early diagnosis of peritonitis is essential as therapy started during the

reactive phase produces good outcomes while if therapy was administered in the
intoxication phase, prognosis becomes doubtful.
When making a diagnosis it is important to assess the dynamics of clinical presen-
tations accompanying the administered therapy. One should consider the recurrence
of signs and progressing of intoxication symptoms.
A physical examination detects
• elevated body temperature >38 °С;
• tachycardia >90 per minute;
• abdominal tenderness on palpation;
• positive signs of peritoneum irritation;
• disturbed peristalsis, meteorism, absence of stools or passage of flatus, oral
dryness, nausea, vomiting;
• arterial hypotension <90 mm Hg;
• oliguria;
• changes in mental status.
There is a discrepancy between clinical presentation of postoperative peritoni-
tis and laboratory findings: while the presentations of peritonitis are pronounced,
changes of lab findings are seen with a delay.
Laboratory diagnostics:
• complete blood count: leucocytosis, leucopenia less often, left shift, toxic
neutrophils, anemia;
• blood biochemistry: hypo- and dysproteinemia, hypokalemia, metabolic
acidosis, positive procalcitonin test;
• coagulogram: coagulopathy, thrombocytopenia;
• common urine analysis: decreased density, proteinuria, hyaline and granulous casts;
• uterine and abdominal discharge culture.
Echography criteria of peritonitis:
• free liquid in rectouterine space, paracolic gutter, between intestinal loops,
under the liver and diaphragm;
• accumulation of gas and fluid in the overdistended intestinal loops;
• intestinal peristalsis diminished or absent.
X-ray findings:
• overdistention of intestinal walls;
• many asymmetrically located levels of liquid (Kloiber’s cups).
Management. Timely surgery is of key importance in the treatment of obstetric
peritonitis; in most cases surgery consists in excision of necrotized wound edges
and placement of sutures. Hysterectomy is performed in exceptional circumstances.
Adequate antibacterial therapy. The same combination of medications is adminis-
tered as in severe endometritis, as endometritis is the condition that most commonly
precedes obstetric peritonitis. Nasointestinal catheter is introduced.
It is extremely important to administer infusion therapy aimed at eliminating
hypovolemia and metabolic acidosis, correcting the balance of fluid, proteins and
electrolytes, detoxification of the body.
Prognosis is favorable if diagnosis was made in time and complex intensive therapy
was initiated.
300 Obstetrics
When does one raise the issue of hysterectomy in postpartum pyoinflammatory

disease?
• Apart from the uterus, no other focus of infection that could cause the critical
condition was detected.
• A discrepancy between deterioration of clinical presentations and the signs of the
primary condition.
• Progression of the systemic inflammatory response syndrome while receiving
intensive therapy: ineffectiveness of conservative therapy.
• Procalcitonin test increase by more than 2.0 ng/ml.
• Emergence or progressing of the signs of polyorganic insufficiency: decreased
BP, oliguria, acute respiratory distress syndrome, jaundice, encephalopathy,
disseminated intravascular coagulation syndrome, thrombocytopenia.
Above all, the focus of infection should be cleaned out as soon as

NB! possible, within the first 6 hours desirably!
When is the issue of hysterectomy not raised?

• A focus of infection of any localization (meningitis, phlegmon, abscess, sinusitis,
pyelonephritis, etc.) has been revealed and treated.
• The systemic infective reaction syndrome is not progressing which proves the
effectiveness of conservative therapy.
• No procalcitonin increase.
• Polyorganic insufficiency is not progressing.
• No clinical presentations of septic shock.
If we are dealing with a variety of peritonitis due to peritoneal infection after a
cesarean section, conservative therapy may prove ineffective. An intensive therapy
aimed at eliminating the cause of the condition can ensure a favorable outcome. In
this case one should take into consideration the fact that intensive therapy should
not be prolonged over one day.
Peritonitis due to enteroparesis may be prevented if adequate therapy was initi-
ated within the first day; however, if there are all clinical presentations of peritonitis,
surgery must not be delayed.
Peritonitis due to incompetent uterine sutures has a typical course; it develops
later and also requires an active surgical intervention.
Operative treatment in generalized obstetric peritonitis implies elimination of
the source of infection (excision of the necrotized wound edges, less often — total
hysterectomy).
The surgery has its specifics:
• separation of adhesions;
• prevention of bowel obstruction (transnasal intubation of the small intestine if
adhesive process is developing);
• careful lavage of the abdominal cavity with antiseptic solutions (chlorhexidine,
dioxidine, ozonated physiological saline);
• drainage of the abdominal cavity;
• closure of the anterior abdominal wall with interrupted sutures in layers
(prevention of eventration).
Infusion & transfusion therapy. Detoxification is performed by the method of con-

trolled hemodilution using crystalloids to 1000 ml/day in combination with colloids —
hydroxyethyl starch (modified gelatin), albumin. Administration of these medications
also promotes restoration of hemodynamics and elimination of the circulating blood
volume deficiency. If the condition is severe, large amounts of fluid (to the extent of
4 liters) are introduced in combination with aggressive diuretic administration.
To improve microcirculation and prevent disseminated intravascular coagulation,
anticoagulants are administered. The average daily dose of heparin is 10 000 units, low
molecular weight heparins produce a better effect: nadroparin calcium (Fraxiparine)
0.4 ml once a day, enoxaparin sodium (Clexane) 0.2 ml once a day. If there is meta-
bolic acidosis, one administers 150–200 ml of 4% sodium bicarbonate solution; if
there is hypokalemic alkalosis — potassium containing solutions (6–12 g/day) while
carefully monitoring its content in the blood serum.
Eliminating enteroparesis is an essential aspect of peritonitis treatment. If there
is hypokalemic alkalosis, administration of 6–12 g of potassium per day is indi-
cated. During the postoperative period it is advisable to provide mild, physiologi-
cal stimulation of the intestine which is achieved by adequate anesthesia (epidural
block), reasonable infusion therapy in the regimen of normovolemia or insignifi-
cant hypovolemia, administration of metoclopramide drugs (Cerucal, Reglan). If
these measures prove ineffective, the intestine can be stimulated with neostigmine
methylsulfate (Proserine), pyridostigmine bromide (Kalimin), distigmine bromide
(Ubretid). To eliminate persistent enteroparesis, hyperbaric oxygenation is admin-
istered. Hyperbaric oxygenation promotes the tone and contractile ability of the
intestine and accelerates gas diffusion from the intestinal lumen, while the periodic
change of pressure in the hyperbaric chamber acts as a stimulus of mechanical ir-
ritation like the pressure knock when giving an enema. Besides, the therapy includes
drugs that block histamine receptors and proton pump inhibitors.
12.1.7.12. Puerperal sepsis

Puerperal sepsis is the maximum degree of sepsis generalization; it is character-
ized by a systemic response to inflammation in conditions of constant or periodic
entry of bacteria to the circulating blood from the inflammation focus, which leads
to polyorganic insufficiency while the body’s resources are depleted and the immune
system is unable to localize the infection.
Epidemiology. There is no objective evidence about the incidence rate of sepsis in
Russia. It is believed that in obstetrics the rate of sepsis is 0.2–0.3% of all varieties
of postpartum infectious complications. In most cases puerperal sepsis follows en-
domyometritis, less often — mastitis, pyelonephritis or wound infection.
Classification. Two major varieties of puerperal sepsis are distinguished:
• without metastasizing — septicemia;
• with metastasizing — septicopyemia (purulent foci in other organs).
Regarding the course of disease, sepsis can be
• fulminant: day 1–3 after infectious invasion;
• acute: from the fourth day to 2 months after infectious invasion;
• subacute: 2–6 months after emergence of chronic focus;
• chronic: over 6 months.
302 Obstetrics
Etiology. Recent findings indicate that in 40–90% Escherichia coli, Bacteroides

spp., Clostridium klebsiella spp., Enterococcus fecalis and others are isolated. Some
types of B-hemolytic streptococcus and Staphylococcus aureus produce a powerful
exotoxin. Gramnegative bacteria like E. coli are isolated in blood cultures of 50%
of patients; this bacterium is endotoxin-producing. Sepsis caused by Pseudomonas
aeruginosa has a fulminant course, often septic shock develops. It has been observed
recently that cases of anaerobic sepsis are on the rise.
Pathogenesis. Sepsis is a secondary process, even if it has a fulminant course from
its very onset. Spread of infection from the primary focus (endomyometritis, mastitis,
peritonitis, etc.) can proceed by hematogenous or lymphogenous route.
The opinion held earlier that in sepsis bacteria are necessarily present in the blood
has changed. Bacteriemia is not a pathognomonic symptom of a septic process. Sterility
of blood cultures upon repeat investigations does not rule out the presence of sepsis.
According to contemporary views, sepsis does not develop due to a progressing infec-
tion; it is rather a result of a generalized (systemic) inflammatory response of the body.
The major trigger is lipopolysaccharide A, a universal component of microbial endo-
toxin. Certain exotoxins are competing substances. A systemic inflammatory response to
microbial endo- and exotoxins consists in releasing a considerable amount of mediators
of the class of antiinflammatory cytokines. The most important role is played by the
tumor necrosis factor which is synthesized in macrophages, monocytes and Kupffer
cells in the liver. Among other cytokines, the most prominent ones are interleukins-1,
-8, -6. All these mediators have a pro-coagulant, anti-inflammatory, genetic, immune
activity; they stimulate the release of hormones, produce a damaging effect on vascular
endothelium, suppress the synthesis of proteins (albumin, transferrin).
Besides, they take part in the synthesis of other inflammation mediators, pro-
teases, oxidants. Neutrophils are the source of lysosomal proteases; they «stick» to
the endothelium. Pathophysiological response to this cascade of reactions includes
selective vasodilation, platelet aggregation, blood flow disturbance. Damage to en-
dothelium promotes a spread of systemic inflammation beyond the vascular bed.
Toxic metabolites permeate cellular and vascular walls; they produce an unfavorable
effect on the tissues and organs of the whole body. Depending on the inflammatory
response associated with the toxin’s virulence and dose, clinical presentation develops
dependent on the degree of polyorganic insufficiency (Fig. 12.5).
Thus the following takes place successively:
• generalized lesion of endothelium;
• disturbance of homeostasis regulation;
• disturbance of vascular tone;
• immediate suppression of vital functions;
• lesion (alteration) of tissues.
Clinical presentations. Sepsis does not have any pathognomonic symptoms. Clinical
presentations are due to the extent of the body’s resistance, the extent of response,
the number and virulence of infectious agents.
Clinical presentations of puerperal sepsis are characterized by the patient’s critical
state. The temperature curve shows hectic fever; repeated shaking chills are noted.
The pulse is extremely rapid, 120 per minute and more. The pulse rate is often discor-
dant with the puerpera’s body temperature. The patient’s skin is pale, sallow. Signs of
CAUSATIVE AGENT
Monocytes/macrophages, T– B–
neutrophils, platelets lymphocytes lymphocytes
ARACHIDONIC TNF,
IL–2
ACID IL–1, IL–6
ICOSANOIDS
Inflammation, Elevated
edema, temperature,
hypercoagulation, Vascular dilation, left shift, anemia, Ig
allergy, sensitization, tissue ischemia C-reactive protein
endothelial lesion
Organ hypoperfusion
Polyorganic insufficiency
Fig. 12.5. Pathogenesis of sepsis
marked dehydration are noted. There are pronounced signs of CNS irritation: acute
headache, dizziness, excitation, fear. The endotoxin works to produce disturbance of
the blood coagulation system (DIC syndrome, thromboses). If metastases develop in
parenchymatous organs (septicopyemia), there are corresponding signs on the part
of the affected organs.
Infection can become generalized at any stage of infectious

NB! disease.
Sepsis is a systemic inflammatory reaction (systemic inflammation response syn-

drome) developing in response to clinically proven infection: sepsis=systemic inflam-
mation response+infection focus.
Systemic inflammation response can be confirmed by the following two or more
signs.
• Body temperature above 38 °С or below 36 °С.
• Tachycardia >90 per minute.
• Tachypnea >20 per minute or decrease in Pa CO2 <32 mm Hg.
• WBC count in peripheral blood >12×109/l or <4×109/l, or the count of immature
cells above 10%.
Severe sepsis and septic shock are varieties of sepsis.
• Severe sepsis is characterized by organ dysfunction, decreased tissue perfusion
and arterial hypotension.
304 Obstetrics
• Septic shock is sepsis accompanied by arterial hypotension despite an adequate

infusion therapy: severe sepsis+arterial hypotension (systolic arterial pressure <
65 mm Hg despite quite adequate fluid supply).
Clinical signs indicating sepsis are as follows (Bacterial Sepsis in Pregnancy //
Green-top Guideline. — #64a. — 1st edition. — April, 2012).
• Fever.
• Diarrhea and vomiting (may indicate production of exotoxin and the onset of
toxic shock).
• Rash (petechial, maculopapular rash or purpura).
• Abdominal / pelvic pain and tension.
• Pathologic vaginal discharge
• Productive cough.
• Urination disorders.
Signs of polyorganic insufficiency
• Changes in mental status.
• Hypoxemia (PaO2 <72 mm Hg when breathing the atmospheric air).
• Hyperlactatemia (>1.6 mmol/l).
• Oliguria (<30 ml/h).
• Arterial hypotension (BP <90 mm Hg or decreased by 40 mm Hg).
Even if adequate therapy is provided, mortality in septic shock is nowadays still
high: 15–30%.
Diagnosis. To make a diagnosis of obstetric sepsis, there should be a primary focus
of infection (endomyometritis, mastitis, pyelonephritis, etc.). Diagnosis is based on
assessing threshold values of systemic inflammation response syndrome. At least two
criteria for systemic inflammatory focus should be met, and one of them — abnormal
body temperature or the WBC count. One should determine the nature and severity
of hyperthermia, the type of fever (persistent high fever to 39–40 °С with an unfa-
vorable outcome; remittent fever with a fluctuation of 2 °С over 7–10 days which is
typical of septicemia; undulant fever due to insufficient drainage of purulent foci).
Respiratory insufficiency is seen in more than 50% of puerperas; it includes pneu-
monia, pulmonary edema, thromboembolism of pulmonary artery lesser branches,
abscess formation. However, despite clinical presentations of respiratory distress
(tachypnea, cyanosis, disturbance of acid-base balance and blood gases), X-ray
manifestations of the condition become discernible much later.
If there are signs of systemic inflammation response, the following investigations
are indicated:
• Complete blood count (platelet count by all means), urine test, coagulogram,
plasma electrolytes,
• Bacteriology investigation (cultures of the blood, lochia, urine, wound
discharge).
• X-ray of the lungs, ultrasound of abdominal organs, echocardiography.
If possible:
• acid-base balance and blood electrolytes;
• blood lactate (when findings > 4 mmol/l, mortality rate amounts to 100%);
• procalcitonin test;
• plasma C-reactive protein.
Blood culture is the key method of investigation; it should be done prior to ad-
ministering antibiotic therapy; however, antibiotic therapy should be initiated before
the findings are available.
Any relevant investigation should be done as soon as possible to establish the
source of infection, this may include X-ray of the chest, ultrasound or CT imaging
of lesser pelvis organs, etc.
Severe sepsis means sepsis plus one of the following complications: cardiovascu-
lar insufficiency, respiratory distress syndrome or other systems dysfunction (renal,
neurological, hematolytic or biliary system).
Sepsis markers:
• body temperature >38 or <36 °С;
• heart rate >90 per minute;
• tachypnea;
• change in mental status;
• hyperglycemia >7.7 mmol/l while the patient does not have diabetes mellitus;
• systolic arterial pressure <65 mm Hg or mean arterial pressure <70 mm Hg.
One of promising methods of improving the quality of septic condition diagnostics
is the laboratory method of determining procalcitonin concentration. This method is
highly sensitive (94%) and highly specific (73%). Other sepsis markers are presepsin
protein, C-reactive protein, leucogram changes (leucocytosis, left shift).
Procalcitonin test administration is only practical in problem cases when the classi-
cal signs of sepsis do not suffice for clear verification (for instance, in borderline cases
between sepsis and severe metritis or sepsis accompanied by immunodeficiency).
Besides, procalcitonin test is instrumental in justifying your decisions (indications
for surgery, adjustment of antibacterial therapy and other).
Treatment. It is important, first of all, to decide upon the individual tactics of man-
aging the puerpera’s condition. One should consider the specifics of pregnancy and
delivery, obstetric history, presence of extragenital disease, the nature of the primary
focus and causative agent. Treatment should be administered with consideration to
pathophysiological features of systemic inflammation.
General principles of sepsis management include:
• surgery to eliminate the primary infection focus;
• antibacterial therapy;
• detoxification including reasonable infusion-transfusion therapy and
extracorporal methods of elimination therapy (hemofiltration, hemosorption);
• adjuvant therapy (glucocorticoids, vasopressor, C-protein);
• normalizing the organ function: artificial lung ventilation, anticoagulants, anti-
inflammatory medications.
If there is acute or chronic renal failure accompanied by disorder of renal excre-
tion, hemodialysis is the method of choice.
12.1.7.13. Septic shock

Septic shock (bacterial or infectious toxic septic shock) is syndrome whose progress
coincides with generalized infection; it is a complication of postpartum pyoinflamma-
try disease of any localization. From the clinical point of view it is a collapse precipi-
tated by toxins of decomposing microorganisms. The notion of shock characterizes
306 Obstetrics
the biological nature of the syndrome and implies a condition due to disturbance
of regulation of vascular tone, microcirculation in organs and tissues on account of
thrombus formation and adequate tissue perfusion.
Septic shock can complicate the course of localized

NB! pyoinflammatory disease and of any generalized infection, as well.
Etiology. Septic shock often complicates the course of pyoinflammatory disease

caused by gramnegative flora: E. coli, Proteus, Klebsiella, Pseudomonas aeruginosa.
When they decompose, they release an endotoxin. A septic process caused by gram-
positive bacteria is much less often complicated by a shock. In this type of infection
the active part is played by exotoxins produced by live microorganisms.
Pathogenesis. Endotoxins and exotoxins (the latter less often) trigger shock devel-
opment. Besides the presence of infection, the development of shock is precipitated
by two other factors: reduced general resistance of the body and opportunity for
massive entry of the causative agents or its toxins into the blood. Processes related to
pregnancy and delivery often provide this opportunity. The septic focus is most com-
monly situated in the uterus. The portal for entry of infection is the large absorbing
surface of the placental bed. Severity of the condition is due to hyperergic reaction
of the body to the massive entry of bacteria. In a body trying to respond to acute
microbial invasion the entire homeostasis regulation system becomes disturbed. The
key factor here is change in hemodynamics producing persistent arterial hypotension
with typical disorder of tissue perfusion.
Risk factors for the development of septic shock are the same as in all other
postpartum pyoinflammatory diseases.
Clinical presentations. Clinical presentations of bacterial shock are divided into
two stages: the early one (6–8 h) and the late one, of several days to several weeks
duration.
Clinical presentations of the early stage of bacterial shock show the charac-
teristic sudden rise of body temperature to 39–40 °С, fever, copious perspira-
tion. Later, as the body temperature decreases, arterial hypotension develops.
Characteristic signs are tachycardia, rapid shallow respiration, skin pallor. The
patient complains of muscular pain, headache, sudden weakness. Petechial hem-
orrhage emerges, oliguria is noted. Blood test shows leucocytosis, thrombocyto-
penia, elevated ESR.
Clinical presentation of the late stage of septic shock typically shows further de-
crease in BP while the circulating blood volume increases, enhanced breathlessness,
moderate cyanosis, cold limbs. The patient becomes anxious, her consciousness is
disturbed; she develops general hemorrhagic diathesis with marked bleeding from
wounds and injections; hemorrhagic necrosis of skin develops. The amount of ex-
creted urine progressively decreases until complete anuria develops. Renal failure is
one of characteristic signs of bacterial shock.
Renal failure develops as a consequence of toxins affecting renal parenchyma and
of prolonged arterial hypotension and thrombosis, which leads to degeneration and
necrosis of canalicular epithelium with disorder or complete cessation of glomerular
filtration.
Among patients with septic shock lethality is as high as 60%.

NB!
Diagnosis. Septic shock=severe sepsis+signs of arterial hypotension (mean
BP <90 mm Hg despite adequate supply of fluid).
Monitoring patients with septic shock includes:
• control of BP, central venous pressure, heart rate — every 30 minutes;
• blood culture upon hospitalization and during fever;
• hourly control of diuresis;
• cardiac activity control (ECG);
• X-ray of the chest, abdominal cavity, ultrasound investigation to confirm the
localization of primary and secondary purulent foci;
• complete blood count over time (assessment of the leucogram), hematocrit test;
• dynamic control of coagulogram values;
• test for serum electrolytes, urea, creatinine, arterial blood gases, pH, glucose
control: below 8.3 mmol/l.
Treatment. Treatment of septic shock is based on antishock measures aimed at
supporting the body’s main functions: respiration, circulation, salt-water balance.
Fighting the intravascular blood coagulation is of key importance. Antibacterial
therapy is another key aspect in shock treatment.
When the infection has become generalized, all antibiotics are

NB! administered at their greatest single and daily doses.
Rehydration therapy requires administration of crystalloid and colloid solutions

in the amount of 30–40 ml/kg.
Glucocorticoids are indispensable as they block the trigger mechanism of shock,
promote the formation of immune complexes and produce a direct neutralizing effect
on the endotoxin; the daily dose is 2 g.
In septic shock one must ensure tissue saturation to the extent of 90%; for this
purpose application of positive end-expiratory pressure is undertaken.
To eliminate hemocoagulation disturbances one administers protease inhibi-
tors: aprotinin (Gordox) 300 000–500 000 units, Trasylol 125 000–200 000 units.
On account of chronic DIC syndrome anticoagulants are administered: heparin
20 000–60 000 units/day by drop perfusion or subcutaneously; nadroparin calcium
(Fraxiparine) subcutaneously 0.4 mg/day.
If conservative therapy produces no effect within 8 – 10 hours, the

NB! septic focus should be excised, and the abdominal cavity drained
extensively.
Initial therapy of septic shock

• Stabilizing the hemodynamics (infusion therapy with crystalloids or synthetic
colloids in the amount of 2000–3500 ml while controlling the central venous
pressure (over 80 mm H2O, in patients receiving artificial lung ventilation —
120 mm H2O) and diuresis (over 0.5 ml/kg per hour), vasopressor and inotropic
308 Obstetrics
agents: Norepinephrine (noradrenaline) 2–20 mcg/min. dopamine (Dopmin)

5–20 mcg/min — for initial treatment, epinephrine (adrenalin) 1–10 mcg/min,
phenylephrine (Mezaton) 40–300 mcg/min; if this fails — hydrocortisone no
more than 300 mg/day (level 1A). There is no evidence if one type of solutions
(crystalloids or colloids) has any advantage over the other.
• Intravenous antibacterial therapy should be initiated within an hour from making
the diagnosis.
– Empiric therapy:
◊ Meropeneme 1 g thrice a day IV;
◊ imipenem / cilastatin 500 mg 4 times a day IV;
◊ ceftriaxone 2 g once a day+metronidazole 500 mg thrice a day±amikacin
15 mg/kg IV;
◊ ceftazidime 2 g twice a day+metronidazole 500 mg thrice a day IV;
◊ cefepime 2 g twice a day+metronidazole 500 mg thrice a day IV;
◊ cefoperazone / sulbactam 2–4 g twice a day IV.
– Initial empiric antibacterial therapy includes one or more antibacterial drugs
that show activity against all probable infectious agents and can pass in
adequate concentrations to the presumed source of sepsis.
– If there is a high risk of methicillin-resistant S. aureus, one administers a com-
bination of carbopeneme drugs or cefoperazone / sulbactam with vancomycin
(local findings from resistance monitoring).
• Adjuvant therapy (glucocorticoids, renal replacement therapy, nutritive support,
prevention of stress ulcer by H2-blockers administration, proton pump inhibitors,
prevention of pulmonary artery thromboembolism with low molecular weight
heparin and other). Hemoglobin level is sustained at 70–90 g/l. Fresh frozen
plasma is only administered in hemorrhage, it is not used for correction of
laboratory fi ndings.
Objectives to be met within the first 6 hours after recognizing severe sepsis
(Dellinger R.P. et al., 2008)
• Obtaining blood culture before administering antibiotics.
• Broad-spectrum antibiotics within one hour after diagnosing severe sepsis.
• Determine lactate in the blood serum.
• In case of arterial hypotension and / or lactate level >4 mmol/l, crystalloid
infusion 20 ml/kg or its equivalent.
• Administer vasopressor in arterial hypotension that does not respond to the start
of infusion therapy to maintain the mean BP >65 mm Hg.
• In case of persistent arterial hypotension despite infusion therapy (septic shock)
and / or lactate level above >4 mmol/l:
– achieving central venous pressure ≥8 mm Hg;
– achieving central venous saturation (ScvO2) ≥70% or mixed venous saturation
(ScvO2) ≥65%.
Indications for transfer to intensive care:
• arterial hypotension or elevated serum lactate despite infusion therapy;
• edema of lungs;
• artificial lung ventilation;
• respiratory protection;
• polyorganic insufficiency;
• uncorrectable acidosis;
• hypothermia.
12.1.7.14. Puerperal lactation mastitis

Puerperal lactation mastitis means inflammation of the mammary gland developing
after childbirth when the patient breastfeeds; the condition is associated with invasion
of infectious agents into the gland.
Epidemiology. In most cases (80–85%) mastitis develops in primiparous women.
Manifestations of the disease most commonly develop at the end of the first week
to the fourth week postpartum.
Thanks to implementation of modern perinatal technology,
NB! rooming-in in particular, the rate of this complication has dropped
considerably.
Etiology. Nowadays the common causative agent (in 60–80% of cases) of lacta-
tion mastitis is Staphylococcus aureus characterized by high virulence and resistance
to many antibacterial drugs. Other bacteria act as causative agents much less often;
they are group A and B streptococci, E. coli, Proteus. In purulent varieties of mastitis
anaerobic bacteria are isolated as well.
However, in these cases various staphylococcus strains predominate, too. Infection
can be caught from staphylococcus vehicles, patients with inapparent forms of pyo-
inflammatory disease among those surrounding the patient as the infective agents
spread through hands, personal belongings, bedding, etc. hospital infection may also
be the cause of mastitis.
Pathogenesis. The structure of the mammary gland itself (profusion of cellular
tissue, sinuses, alveoli, a wide network of milk ducts and lymph vessels) promote the
tendency to a fast spread of inflammation to adjacent areas (Fig. 12.6).
The infective agent commonly enters the mammary gland tissues by a lymphog-
enous route through cracks in the nipples. The spread of infectious agents takes place
during breast feeding. This may proceed by hematogenous or lymphogenous route
from endogenous inflammation foci. The inflammatory process in the mammary
gland is promoted by lactostasis associated with milk duct occlusion, morphological
changes in the gland (tumor, mastopathy, scars), violation of hygiene. The woman’s
general condition and the strength of her host defenses are an important factor in
the pathogenesis of lactation mastitis.
When a purulent process occurs in glandular organs, one of its aspects is the poor
ability to limit the inflammation within certain boundaries; it spreads extremely rapidly.
Classification. Two types of lactation mastitis are distinguished:
• epidemic mastitis (develops in hospital settings);
• endemic mastitis (develops outside hospital 2–3 weeks after childbirth).
Russian clinicians mostly work with the following classification that regards mas-
titis as consecutive stages of an acute inflammation:
• serous (incipient) mastitis;
• infiltrative mastitis;
• purulent (infiltrative purulent, abscessed, phlegmonous, gangrenous) mastitis.
310 Obstetrics
Fig. 12.6. Mammary gland structure: 1 — thoracic wall; 2 — pectoral muscles; 3 —

mammary lobe; 4 — nipple; 5 — areole; 6 — milk duct; 7 — fatty tissue; 8 — skin
Violating the rules of breastfeeding is the major factor predisposing

NB! to mastitis.
Clinical presentations. Nowadays mastitis has the following features:

• late onset (4 weeks after childbirth);
• higher incidence of inapparent subclinical forms;
• predominance of infiltrative purulent mastitis;
• protracted course of the disease.
If lactostasis was not reversed within 3–4 days, mastitis usually develops as in the
presence of lactostasis the amount of microbial cells in milk grows several times,
which promotes a fast progress and spread of inflammation.
Clinical presentations of serous and infiltrative mastitis are characterized by a
sudden elevation of body temperature to 38–40 °С, sometimes accompanied by
shivering. There is headache, general weakness and malaise. As a rule, outflow of
milk becomes disturbed due to edema of milk ducts, there is pain in the mammary
gland. Palpation reveals induration in the breast; the skin above it is sometimes
hyperemic. If treatment is initiated too late or is inadequate, serous mastitis turns
to infiltrative form, which is characterized by more pronounced general and local
manifestations.
Clinical presentations of infiltrative purulent and abscessing mastitis are character-
ized by body temperature elevation to 38–39 °С with considerable fluctuations and
shivers. The patient’s condition deteriorates. The mammary gland is enlarged, its skin
is hyperemic and cyanotic. The superficial venous network stands out under the skin.
Palpation reveals an infiltrate with clear boundaries, painful on palpation; a fluctua-
tion is felt in its depth. Regional lymph nodes are enlarged, painful on palpation. A
pronounced left shift is noted.
Phlegmonous mastitis means fusion of several suppuration foci that developed in
one mammary gland. The patient’s general condition deteriorates, body temperature
elevates to 40–41 °С with shivers. The mammary gland is considerably enlarged,
acutely painful and edematous. Its skin is hyperemic and cyanotic. Emergence of a
pattern of inflamed lymph vessels is typical. One notes leucocytosis, an abrupt left
shift, aneosinophilia, lymphopenia.
If the signs are apparent, diagnosis presents no difficulty; it is based on the patient’s
presentations, estimation of clinical findings and additional investigations.
If signs typical of suppuration are underestimated, this results in unjustifiably pro-
tracted conservative treatment. In infiltrative abscessing mastitis seen in more than
half of all cases, the infiltrate is composed of multiple small purulent cavities while
the fluctuation sign is not often noted. In this situation a fine needle aspiration of the
infiltrate does not yield any pus, as a rule. Diagnostic value of this method increases
in subclinical forms of abscessing mastitis.
Additional methods of investigation include complete blood count, culture and
cytology studies of the milk (leucocytes 106/ml, bacteria >103 colony-forming units),
and ultrasound examination of the mammary glands. Sonography usually reveals an
infiltration zone of increased echogenicity in a certain area of the gland; if an abscess
develops, a rarefaction focus is formed in this area, and the infiltrate zone intensifies
around it. Later a surface with uneven borders and intersections is formed.
Treatment is administered according to the type of mastitis. General principles
of mastitis management consist in emptying the gland, adequate antibacterial
therapy, administration of symptomatic and detoxification therapy as well as lo-
cal therapy.
Conservative therapy is only possible in serous and infiltrative mastitis. When
managing serous mastitis, emptying the gland of milk every 3 hours is obligatory.
If treatment is ineffective and serous mastitis becomes infiltrative mastitis, lactation
suppression is recommended. Lactation can be suppressed only after lactostasis has
been eliminated. Suppression of lactation by tight bandaging of the breasts is dan-
gerous as the disrupted circulation may promote the development of severer forms
of mastitis (Fig. 12.7).
Lactation suppression is precipitated by:
• bromocriptine (parlodel) 2.5 mg twice a day for 10–14 days;
• cabergoline (dostinex) 0.25 mg twice a day for 2 days.
In incipient mastitis application of cold is recommended by some authors.
If the disease shows positive dynamics, physiotherapy can be started a day after the
initiation of treatment (laser, microwave therapy). These methods are contraindicated
if the patient has mammary gland disease prior to pregnancy.
Antibacterial therapy constitutes the foundation of mastitis treatment. Antibiotics
active against staphylococcus infection are mostly administered:
• amoxicilline+clavulanic acid (Amoxiclav) 1.2 g each 3–4 times a day;
• ampicilline / sulbactam 1.5 g 3–4 times a day;
• cefoperazone / sulbactam 4 g twice a day;
• cefazoline 2.0 g thrice a day.
312 Obstetrics
Fig. 12.7. Lactation mastitis
Antibiotics are given parenterally. The duration of therapy is 5–10 days. To in-
crease immunologic resistance of the body, antistaphylococcus -globulin is admin-
istered in a dose of 5 ml (100 units) every other day IM; 3–5 injections altogether.
If there are pronounced signs of general intoxication, infusion therapy is indicated
(to the extent of 2000–2500 ml/day) in hospital settings.
Despite the administered therapy, 4–10% of puerperas show suppuration.
Treatment of purulent mastitis implies prompt hospitalization and surgical treat-
ment while administering antibacterial and infusion therapy. Timely opening of the
abscess prevents further development of the process or its generalization. During
surgery one evacuates the pus, removes necrotic tissue, the cavity is cleansed with
antiseptics after which a drain and lavage system is applied for constant droplet
irrigation of the remaining cavity and for outflow of the lavage fluid. In total,
2–2.5 liters of fluid (0.02% sterile chlorhexidine solution) a day are required for
adequate lavage. The drain and lavage system is removed no earlier than 5 days
after surgery. Antibiotics are supplemented with imidazole drugs (metronidazole,
tinidazole).
In case of purulent mastitis lactation must be suppressed

NB! using medications. The newborn is transferred to formula
feeding.
Breastfeeding in mastitis. If the patient has serous mastitis, the infant can be
latched to the healthy gland. The diseased gland is emptied by decanting, usually
with a breast pump. The expressed milk can be used for feeding after pasteurization.
In infiltrative mastitis breastfeeding is completely canceled until full recovery. The
expressed milk should not be given to the infant.
REMEMBER!
Definition Lactation mastitis is inflammation of the mammary
gland due to invasion of infectious agents into its tissues
Epidemiology The incidence rate varies greatly depending on the
use of modern perinatal technology in hospitals. With
rooming-in arrangement the incidence of mastitis is
6–12 times lower
Etiology The main causative agent of lactation mastitis is

Staphylococcus aureus; it shows high virulence and
resistance to many antibacterial drugs
Pathogenesis The infectious agent enters the mammary gland tissue
by lymphogenous route through nipple cracks, and by
galactogenous route (through milk ducts)
Classification Serous (incipient) mastitis. Infiltrative mastitis.
Purulent mastitis (infiltrative-purulent, abscessing,
phlegmonous, gangrenous)
Clinical presentations Local and general presentations depend on the type of
mastitis. In incipient forms general signs predominate
over local signs
Diagnosis. Protocol If a puerpera develops fever, mastitis should be ruled
out first of all. Diagnosis is specified on the basis of
local presentations of the disease
The infiltrative and purulent forms of mastitis require
prompt hospitalization
Treatment Treatment should be etiological: administration of

antibiotics is obligatory!
Prevention As early as during pregnancy the woman should
be prepared for future lactation (educating her
about the advantages of rooming in, of exclusive
breastfeeding)
12.2. BASIC PRINCIPLES OF DIAGNOSING POSTPARTUM

INFECTIOUS DISEASES
Diagnosis of postpartum infection is made with consideration of the patient’s
complaints, past history findings, an estimation of clinical presentations, laboratory
findings as well as instrumental methods.
A thorough inspection of the mammary glands, external genitals, the perineum,
vaginal and cervical speculum examination is done as well as a vaginal examination.
Complete blood count in such patients commonly reveals a reduced con-
centration of RBCs and hemoglobin, elevated WBC count, increased ESR,
314 Obstetrics
decreased hematocrit. The leucogram shows a left shift with elevated count of
stab neutrophils. Sometimes considerable thrombocytopenia is noted (in septic
shock). The extent of blood changes runs parallel to the severity of the pa-
tient’s condition. However, when effective antibacterial drugs are administered,
there is often a discrepancy between blood test findings and the true severity
of infection.
Urine test helps to detect or rule out pyelonephritis, which is important in differ-
ential diagnosis. There is a close relationship between the severity of the disease and
the extent of required laboratory investigations. Apart from blood and urine tests, in
severe forms one administers a series of blood biochemistry studies (proteinogram,
ionogram, acid base balance and others).
To determine the immunologic status of the puerpera, humoral and cellular im-
munity is investigated.
As there is a possibility of disseminated intravascular coagulation development,
hemostasis should be also assessed in patients with postpartum infection (fibrinogen,
activated partial thromboplastin time, thrombin time, platelet count, hematocrit,
thromboelastogram, antithrombin III, accelerated fibrinolysis assay). The value of
these accessory laboratory methods of investigation is not so much diagnostic as
helpful in assessing the severity of disease and its outcome.
As the disease is of microbial nature, bacteriology study is of great importance
as it permits the so-called etiological diagnosis in most cases. It is desirable to
perform the primary withdrawal of samples (blood, lochia, wound discharge,
exudates, milk, urine) before antibiotic therapy is initiated, which helps to iden-
tify the isolated microorganisms and to determine their sensitivity to antibiot-
ics. Gram staining can give a preliminary idea of the bacteria contained in the
substrate under study.
Hardware and instrumental methods of investigation (ultrasound, computed to-
mography, hysteroscopy, magnetic resonance imaging, laparoscopy) render invalu-
able help in diagnostics of infectious complications.
12.3. MAIN COMPONENTS OF POSTPARTUM

INFECTION MANAGEMENT
Treatment of postpartum infection is provided in so-called observation depart-
ments of maternal hospitals. Treatment should be etiotropic, complex, systematic and
active. It should be initiated as soon as possible upon revealing the early manifesta-
tions of postpartum infection, which helps to prevent the development of more severe
generalized forms of the disease.
The patient should be confined to bed. She needs easily digested food, a varied
diet with sufficient but not excessive energy value. Taking into account the body’s
enhanced need for fluid the patient should receive fluid to the extent of 2–2.5 l a day
(considering the infusion therapy), if there are no contraindications (cardiovascular
disease and the like).
Antibacterial therapy constitutes the main component of complex treatment of
pyoinflammatory postpartum disease.
When administering antibiotics, a number of requirements should

NB! be met:
• mandatory isolation and identification of the causative agent;
• timely initiation and continuation of therapy until a lasting effect
is achieved;
• using sufficient doses and optimum methods of drug
administration;
• understanding possible complications and side effects,
prevention of the drug penetrating breast milk.
Therapy should be initiated at once before the etiologic diagnosis is made

but after samples for culture study have been taken. In view of the fact that the
main causative agents of postpartum infectious complications are opportunistic
aerobic and anaerobic bacteria isolated mostly in associations, treatment starts
with empiric administration of broad spectrum antibiotics. Adjustments can be
made in the administered therapy with consideration to the findings of culture
tests.
Empirical antibacterial therapy includes a combination of no less than two anti-
biotics at maximum doses administered at the same time. The intensity of therapy
is graded according to the clinical variety of the disease and its severity. In a severe
course of the disease one administers a combination of three antibiotics, in case of
moderate severity — a combination of two drugs. Combination antibiotic therapy
enhances the effectiveness of treatment, prevents or slows down the growth of strains
resistant to the action of administered drugs. At the same time, simultaneous admin-
istration of two and more drugs increases the risk of development of adverse effects
of antibiotic drugs.
The infant should not be regarded as a deterrent to rational etiotropic therapy. It
is contraindicated to give to a breastfeeding mother streptomycin, tetracycline drugs,
rifampicin, laevomycetin due to their adverse effects. In severe and moderately severe
cases of infection the breastfeeding should be suspended for the period of treatment.
‘Sparing’ antibacterial therapy is one of major causes of recurrent

NB! emdometritis followed by peritonitis and sepsis.
For prevention of candidiasis and dysbacteriosis antimycotic medications are in-

cluded in the therapeutic regimen.
Besides antibiotics drugs from other product groups are used in the therapy of
postpartum infections: metronidazole, antiviral medications.
If immunity is suppressed, administration of most powerful antibiotics may prove
useless. That is why one administers drugs enhancing specific immunologic reactiv-
ity and nonspecific defense of the puerpera’s body (complex immunosupportive and
immunostimulating therapy).
Cleansing the primary focus is the major component of treatment, alongside
with antibacterial therapy. Its goal is to eliminate the inflammatory debris and to
deliver medications to the focus. If some contents are revealed in the uterine cav-
316 Obstetrics
ity, which is seen in 70% of puerperas, it is preferable to perform hysteroscopy and

vacuum aspiration. Good clinical outcomes were achieved after aspiration-irrigation
drainage of uterine cavity with cooled solutions (4–8 °С) of antiseptics for 24 h
during 3–5 days.
Uterotonic drugs are indicated in endometritis which reduces the absorbtion of
decay products into the bloodstream. This measure helps to restore the contractile
ability of the uterus and to empty its cavity of infected lochia.
Anti-inflammatory therapy. Nonsteroid anti-inflammatory drugs constitute the
anti-inflammatory therapy.
Infusion and detoxication therapy. Multicomponent infusion therapy is adminis-
tered to achieve the following goals: eliminating hypovolemia, detoxification, cor-
rection of accompanying disorders of colloid-osmotic balance, normalizing micro-
circulation, rheologic and coagulant parameters of the blood. The composition of
infusion therapy is determined on the basis of the severity of the disease and the
patient’s condition. Infusion therapy includes well-balanced water-electrolyte solu-
tions (Disol, Trisol), hydroxyethylated starch, modified gelatin, blood components —
only if indicated.
To prevent complications of infusion therapy (pulmonary edema,

NB! left ventricular insufficiency) one should administer hydroxyethyl
starch solutions.
Other methods of treatment include hyposensitization therapy, prevention of he-

mocoagulation disorders, extracorporal detoxification, administration of uterotonics
and other.
Physical methods of treatment in combination with complex therapy are adminis-
tered on a case-by-case basis in various clinical forms of the disease.
Prevention of pyoinflammatory postpartum infection should be started in the first
weeks of pregnancy. At the maternity welfare clinic one should identify women at
high risk of infectious and inflammatory complications and administer therapeutic
and preventive measures.
Widespread implementation of modern perinatal technologies by

NB! maternity hospitals is an indispensable condition for decrease in
postpartum infection.
At an obstetric hospital the rules of aseptics and antiseptics must be observed

without fail. Modern technologies of delivery should be mastered and introduced
into practice properly:
• limitations on the means and methods of sanitization that disrupt the body’s
biocenosis in healthy women (local antiseptics, shaving of the pubis);
• early latching of the infant to the breast;
• rooming-in of the mother and infant followed by an early discharge from the
maternity hospital;
• exclusive breastfeeding (exclusive breastfeeding on demand without a nighttime
interval, without resorting to bottles or pacifiers).
REMEMBER!
Definition Postpartum infection is an infection-mediated disease
of the puerpera immediately related to pregnancy and
delivery. Infection revealed postpartum but not related to
pregnancy and childbirth in terms of pathogenesis (flu,
dysentery) is not regarded as postpartum infection
Epidemiology The incidence rate of postpartum infection is 2–10%. An
important role in the incidence of infectious complications
belongs to the level of social and economic development of
the country, patterns of health care (free of charge or pri-
vate), local culture, educational background, religion, etc.
Etiology Nowadays microbial associations play the leading role
in the etiology of postpartum infection (over 80%);
Staphylococcus aureus is the causative agent in almost
80% of mastitis cases
Pathogenesis In most cases what happens is activation of the body’s own
opportunistic microbial flora; in other cases it is exogenous
contamination with resistant hospital strains if rules of
aseptics and antiseptics are not observed. The decisive
role in the emergence of postpartum infection is played
by the puerpera’s condition, the virulence of the microbial
agent and their numbers, as well as the presence of portal
of infection like nipple cracks
Classification According to Sazonov-Bartels classification of postpar tum
infection, various forms of postpartum infection are regar-
ded as separate stages of one dynamic infectious process
(from postpartum ulcer and endometritis to sepsis)
Clinical Local and general presentations depend on the type of
presentation infection
Diagnosis Diagnosis of postpartum infection is made considering the
patient’s complaints, past history findings, and findings of
the laboratory tests as well as other investigation methods
Treatment Treatment should be etiotropic, complex, systematic and
active. It should be initiated as soon as possible upon
revealing the early manifestations of postpartum infection,
which helps to prevent the development of more severe
generalized forms of the disease. Antibacterial therapy
constitutes the main component of complex treatment of
pyoinflammatory postpartum disease. Therapy should be
initiated at once before the etiologic diagnosis is made, but
after samples for culture tests have been taken. Therapy
starts with broad-spectrum antibiotics. Purulent mastitis
requires surgical intervention (dissection and draining of
the focus)
Complications Possible complications are determined by the type of
infection: the process acquiring a chronic nature, fatality
318 Obstetrics
12.4. NON-INFECTIOUS POSTPARTUM DISEASE
Non-infectious postpartum disease is a condition whose development is not medi-

ated by microbial invasion. They include the following:
• subinvolution of uterus;
• lochiometra;
• retention of gestation sac fragments in the uterus;
• cracked nipples;
• lactostasis.
12.4.1. Subinvolution of uterus

Subinvolution of uterus means a slowed down rate of retrograde development of
uterus related immediately to disorder of its contractile ability. To a greater or lesser
extent, subinvolution of uterus accompanies postpartum disease.
Clinical presentations of subinvolution of uterus are characterized by enlarged
uterus whose consistency is not firm enough, copious turbid lochia of brownish
color. Subinvolution of uterus is often accompanied by subfebrile body tempera-
ture.
The postpartum uterus size depends on a number of factors

NB! which should all be taken into account: parity, method of
delivery, the time of the first latching to the breast, fetal weight
at birth, specifics of the course of pregnancy and childbirth,
etc.
Subinvoluiton of uterus is diagnosed on the basis of dynamic observation of the

puerpera.
The most informative method in diagnosis of uterine subinvolution

NB! is ultrasound examination done over time starting on day 2
postpartum.
Exclusive breastfeeding is the best method of preventing subinvolution of

uterus.
Treatment of subinvolution of uterus consists in measures promoting uterine con-
traction (application of icepack to the abdomen, chinine, ergometrine, oxytocin,
etc.).
12.4.2. Lochiometra
Lochiometra is retention of lochia in the uterine cavity. This often results from a
powerful anteversion of the uterus and due to mechanical obstruction of the cervical
canal with blood clots and membranes.
Clinical presentations. Lochiometra (hematometra) usually becomes manifest on
day 2–5 postpartum; it is characterized by a short-term insignificant increase in body
temperature (to 37.5 °С), decreased or discontinued discharge from genital tracts.
As a result, the uterus becomes considerably enlarged, acquires a spherical shape
and softish consistency. Its palpation through the abdominal wall detects the fundus
above the umbilicus. The patient may complain of cramp-like pain in the lower
abdomen. Ultrasound examination reveals an enlarged uterine cavity with hydrous
or non-homogeneous contents.
Treatment of lochiometra consists in facilitating the outflow of lochia by bring-
ing the uterus to median position when performing a bimanual examination. The
uterus can be emptied of its contents by vacuum aspiration or curettage, desirably
under hysteroscopy guidance. To enhance uterine contractility one can administer
uterotonic agents.
One should remember that both uterine subinvolution and

NB! lochiometra developing in conditions of diminished uterine
contractility are direct stakeholders in the pathogeny of postpartum
infectious complications (endometritis in particular).
12.4.3. Retained fetal membranes in the uterus

Clinical presentations of retained fetal membranes are only characterized by sub-
febrile body temperature as fetal membranes do not provide a favorable medium
for bacterial growth. However, if the membranes drop in the vagina, infection can
develop in the uterine cavity, which is always accompanied by body temperature rise
to 38–39 °С.
Treatment of retention of fetal membranes in the uterine cavity implies their
removal under hysteroscopy guidance, administration of antibiotics and agents pro-
moting uterine contraction.
12.4.4. Retained placental fragments in the uterus

Clinical presentations of retained placental fragments are characterized by pro-
longed subfebrile body temperature, periodic bloody discharge alternating with bleed-
ing, prolonged incomplete closure of cervical canal (until the second week postpar-
tum and later) as well as slowed down subinvolution of uterus.
Treatment of retained placental fragments consists in mandatory removal of pla-
cental fragments from the uterine cavity under hysteroscopy guidance, administration
of antibiotics and uterotonic agents.
Prevention is of key importance. Each afterbirth should be inspected thoroughly.
If retained placental fragments are suspected after delivery, should be undertaken
manual exploration.
12.4.5. Cracked nipples

Both nipples are affected, as a rule. In primiparous women this condition is seen
twice as often as in secundiparous women.
320 Obstetrics
The condition of nipples is affected by the technique and

NB! duration of breastfeeding, strength of sucking, intervals between
breastfeeding episodes, presence of alveolar papillary reflex.
Factors promoting cracking of nipples:

• defects of nipple development (inverted, retracted nipple);
• late latching of the infant to the breast, lactostasis;
• failure to prepare nipples for breastfeeding and resulting poor erection of nipples
during breastfeeding;
• hypo- and avitaminosis, complications of pregnancy and delivery;
• violation of sanitary and epidemiologic regimen.
Three stages of crack formation are distinguished in clinical practice:
• stage 1: maceration of nipple epidermis;
• stage 2: crust;
• stage 3: deep bleeding erosion.
• Methods of treatment:
• physical methods (helium-neon laser, ultrasound, ultraviolet irradiation);
• pharmaceutical treatment (application of fluid, ointment, aerosol), epithelization
promoting agents; the best method is multiple application of swabs moistened
with colostrum from the puerpera.
Breastfeeding hinders the healing while cancellation of

NB! breastfeeding results in milk congestion.
However, if there is deep bleeding erosion, breastfeeding from this mammary gland
should be suspended until complete epithelization of the crack. To prevent congestion
of milk, its regular outflow should be ensured.
Manual expression of breast milk is a more sparing method.

NB!
12.4.6. Lactostasis (congestion of milk)
This postpartum complication is associated with incorrect regimen and breastfeed-
ing technique. Lactostasis is common in hospitals where newborns are kept in nurser-
ies. If the mother is forced to give up breastfeeding, this complication often follows.
Clinical presentation of lactostasis is painful induration engorgement of mammary
glands. Lactostasis usually is bilateral. The patients note pain in the breast, edema
of areole, uneven or difficult outflow of milk.
Treatment consists in wearing a well chosen bra that ensures that the breasts are
raised, correcting the regimen of breastfeeding and expressing. Ice pack is applied
to the edema site for 15–20 minutes at an interval of several hours. Physiotherapy
(ultrasound, laser) can reduce congestion of milk and improve its outflow.
If these methods are ineffective, partial temporary suppression of lactation is
resorted to. A central acting drug, bromocriptine (Parlodel) is administered for this
purpose.
CONTROL QUESTIONS
1. What is the incidence rate of postpartum infection?

2. What is the most common infection?
3. Etiology of mastitis.
4. Etiology of endometritis.
5. Clinical presentations of endometritis.
6. What is sepsis?
7. Diagnosis of sepsis.
8. Principles of sepsis therapy.
9. What is septic shock?
10. Principles of septic shock therapy.
CHECK YOURSELF!
Level 1. Test
1. Risk factors for endometritis:

a) age over 30 and chronic pyelonephritis;
b) early toxicosis and intestinal dysbacteriosis;
c) delayed parturition and green amniotic fluid;
d) cesarean section and genital infection.
2. Endometritis is diagnosed on the basis of:

a) disorder of uterus involution and lochia outflow;
b) elevated body temperature and shivering;
c) high ESR values and low hemoglobin;
d) abdominal ultrasound findings.
3. Etiotropic therapy of postpartum infection:

a) detoxification;
b) antibacterial therapy;
c) hormone therapy;
d) immunoglobulin therapy;
e) vitamin therapy.
4. Which of these is not administered in sepsis?

a) detoxification;
b) antibacterial therapy;
c) eliminating the infection focus;
d) supporting vital functions;
e) haemostatic therapy.
322 Obstetrics
5. What signs provide the ground for sepsis diagnosis?

a) disorder of uterus involution and lochia outflow;
b) elevated body temperature and shivering;
c) high ESR values and low hemoglobin;
d) two and more inflammation foci.
6. What surgery is performed in sepsis?

a) curettage of uterine mucosa;
b) continuous irrigation of uterine cavity with disinfectants;
c) hysterectomy;
d) cleansing and draining the abdominal cavity.
7. Septic shock is:

a) sepsis and arterial hypotension;
b) sepsis and blood loss;
c) hemorrhagic shock against the background of severe endometritis.
8. Stages of septic shock are:

a) fibrillation and increased tone;
b) hyperthermia and arterial hypotension;
c) hypercoagulation and hypocoagulation;
d) slow and fast.
9. Clinical signs of mastitis are:

a) engorgement of both breasts;
b) hyperemia of both breasts;
c) disorder of milk outflow;
d) local hyperemia and infiltration.
10. Principles of purulent mastitis therapy:

a) antibacterial therapy;
b) massage and expression of milk;
c) suspension of breastfeeding from the affected gland;
d) opening the focus.

1. On day 3 the puerpera presents with turbid foul-smelling lochia. What is the
diagnosis? What is the plan of actions?
2. On day 4 the puerpera presents with local reddening and painful induration in
the upper external quadrant of the right breast. What is the diagnosis? What is the
plan of actions?
NOTES
_________________________________________________________________
_________________________________________________________________
• Chapter 13
PHYSIOLOGY OF NEONATE
13.1. INTRODUCTION TO NEONATOLOGY
Neonatology is a branch of pediatrics that studies anatomical and functional fea-

tures of children from the moment of birth over the first 28 days of their life. The
goal of neonatology is to provide physiological conditions for healthy development
of the child in all periods of his life; neonatology provides diagnosis and treatment
of disorders and diseases, and rehabilitation of children.
As an independent science neonatology emerged in the 20th century. The terms
neonatology and neonatologists were introduced by an American Alexander Schaffer
in 1960.
The background for neonatology development was laid in the 19th century; it
was obstetricians who made a considerable contribution to this field of expertise.
Obstetricians proposed methods of newborn resuscitation upon delivery, of care
and feeding of the premature newborn, disinfecting the milk to reduce mortality.
Introduction of principles of aseptics by I.F. Semmelweis and O.V. Holmes to obstet-
ric practice in 1860s and 1870s permitted a decrease in mortality of both puerperant
mothers and their newborns.
Considerable credit is due to R. Virchow for his works on pathological anatomy
of neonates which promoted the development of pediatrics at large and neonatol-
ogy in particular. R. Little established the pathogenetic role of neonate asphyxia in
the etiology of infantile paralysis. K. Schmorl developed the notion of kernicterus
(nuclear jaundice) in newborns based on his finding bilirubin crystals in cerebral
nuclei. Clinician D. Hutchinson described the triad of signs of congenital syphilis
(1858); French obstetrician S. Tarnier introduced oxygen inhalation into care for
premature infants.
Examination, vaccination and any treatment of a newborn requires

NB! his mother's informed consent to the procedures, or her refusal.
13.2. NEWBORN CHARACTERISTICS
The parameters of newborns’ physical development depend on the parameters and

age of their parents, specifics of nutrition, living conditions and parity1. Good build
and nutrition are essential for adaptation after delivery and for further development.
A full-term newborn weighs 3500 g on average; boys commonly weigh somewhat
more than girls. Body length in a newborn is 50 cm on average, head circumfer-
1 In obstetrics: the number of times a woman has given birth.

324 Obstetrics
ence—35 cm. In approximately 95% of children the body weight is 2500–4500 g,

body length — 46–55 cm.
Assessment of the neonate’s physical development is made on the basis of mean
parameters (body weight, length, head and chest circumference); the values are cor-
related with the gestational age.
NB! Body weight is no criterion for gestational age.
Gestational age of an infant (fetus) is the number of full weeks that elapsed from
the first day of last menstrual period, to the date of delivery.
Neonates are divided into the following groups:
• full term baby born at 37 to 42 weeks gestation (Fig. 13.1);
• post-term baby born at 42 weeks gestation or later (Fig. 13.2);
• pre-term baby born at 22 to 37 weeks gestation.
There is a notion of low birth weight (LBW); it means body weight under 2500 g
irrespective of gestational age (Fig. 13.3).
• Very low birth weight: a baby weighing less than 1500 g at birth, irrespective of
the gestational age.
• Extremely low birth weight: babies weighing less than 1000 g (Fig. 13.4).
• Extreme immaturity is noted in premature infants at a gestational age less than
28 full weeks.
Fig. 13.1. Full-term baby

Chapter 13. Physiology of neonate 325
Fig. 13.2. Post-term baby
Fig. 13.3. Newborn with stage II prematurity (signs of CNS lesion): the head thrown back,
enlarged, spastic positioning of bones
Fig. 13.4. Newborn with stage IV prematurity. Pronounced signs of morphofunctional

immaturity: almost no subcutaneous tissue, umbilical ring located in the lower abdominal
third closer to the pubis, the head constitutes 1/3 of body length; thin skin
326 Obstetrics
Neonates are classified as

• low weigh infants whose intrauterine growth correlates with their gestational age,
of normal body length;
• full-term and pre-term infants whose weight and length are too small for their
gestational age;
• macrosomic fetus and giant fetus are distinguished based on their body weight
(Fig. 13.5).
As there is a great difference between premature newborns and newborns with
IUGR, the assessment of a low weight full-term newborn is of great practical sig-
nificance as it helps to predict possible pathological conditions and disorders during
adaptation to extrauterine life.
In ICD-10 newborns with restricted fetal growth
Giant fetus and malnutrition are classified as P05 or small size
(5000 g and more) (weight and length) for gestational age (SGA). The
abbreviation IUGR widely used in neonatology
stands for Intra Uterine Growth Restriction; if the
Macrosomia
(4000 – 4999 g)
body weight and length are below 10th centile for
gestational age, the condition is termed small for ges-
tational age (SGA). In the recent decade we observe
Normal weight transition from JUGR-acronym to FGR1.
Birth weight
(2500 – 3999 g)
Large for gestational age is a condition when the
newborn has body weight exceeding 90th percentile
Low weight for gestational age. Maturity of newborn is one of the
(1500 – 2499 g) most important factors of intrauterine development. It
encompasses a series of morphological, clinical, func-
Very low weight tional and biochemical parameters in relation to gesta-
(1000 – 1499 g) tional age. At each stage of development starting with
zygote the morphological and functional condition of
Extremely low weight the fetus, newborn and infant matches its calendar age
(< 1000 g) together with the environment that surrounds it and
interacts with it. Apparently, it is essential to determine
Fig. 13.5. Classification of neo- for each infant whether it is mature or immature.
nates by body weight Immaturity is one of the signs of IUGR.
13.3. ANATOMICAL AND FUNCTIONAL FEATURES

OF THE NEWBORN’S ORGANS AND SYSTEMS
By 28–32 weeks of intrauterine development the fetal lungs have developed as an
organ of external respiration. The lungs produce a surfactant ensuring that the alveoli
are expanded during respiration. The surfactant system regulates itself; it influences
pulmonary microcirculation, permeability between the alveolus and pulmonary ves-
sels. Together with pulmonary secret, phospholipids of the surfactant system of the
1 FGR — fetal growth restriction.

fetus pass into the amniotic fluid. Determining the surface-active phospholipids in
amniotic fluid yields the grade of maturity of fetal lungs.
The respiratory system affects the development and regulation of

NB! other vital body functions such as hemodynamics, metabolism,
and water exchange.
The mechanism of the first breath is first of all associated with the neurological
component. When the child makes a contact with the ambient air, impulses pass to
the substantia reticularis in the brain and increase its activity abruptly. Afterwards
respiration is sustained by topic influence of the upper portion of brainstem. The
respiratory center of the fetus and newborn is under the influence of carbon dioxide
and acid pH of the blood, anatomical changes in the respiratory system and BP, the
ambient air temperature, pain, and medications.
During the first breath only 1/3 of alveoli expand. Complete expansion of the lungs
takes place over several days; it depends on the degree of maturity of the newborn.
When the first breath occurs and respiratory muscles (mostly the diaphragm) make
a reflex contraction, negative pressure results in the thoracic cavity which promotes
the inflow of atmospheric air into the airways. The vascular component is of great
importance in expanded lungs. As the pulmonary vessels fill with blood, smaller
branches of the pulmonary artery slowly expand, too. In its turn, this sustains the
opening and expanded state of the alveoli.
Functioning of pulmonary system vessels promotes the narrowing of the arterial
duct lumen. Exchange of gases between alveoli and the blood occurs by diffusion:
oxygen passes through the alveolar membrane, interstitial fluid, cellular membrane
of capillaries, through the plasma in vessels and erythrocyte membrane (Fig. 13.6).
Pulmonary External
circulation factors
is activated
Pulmonary
circulation
Systemic
circulation
Filling of lesser Reflex contraction

branches of respiratory
of pulmonary artery muscles
Alveoli expand
Fig. 13.6. Mechanism of alveolus expansion in neonate

328 Obstetrics
The rate, duration and depth of newborn’s respiratory

NB! cycle are extremely variable. Abdominal type of respiration
predominates. When the newborn is awake, the chest and
abdomen move simultaneously. Inspiration phase is shorter
than expiration phase. The respiratory rate is 40–60 per
minute.

During the intrauterine period the work of the heart is aimed at ensuring exchange
processes between the blood of the fetus and mother through the placenta.
Clamping of the cord and arrest of placental circulation lead to reorganization
of infant’s circulation: closing six fetal communications. When independent respira-
tion begins, blood flow through the lungs increases 5–10 times compared with the
intrauterine period. Blood return to the left atrium increases correspondingly where
the pressure rises as it does in the aorta. High pressure in the left heart chamber
promotes shutting of the valve of foramen ovale, closure of the arterial duct due to
the narrowing of its lumen. Bypass of the blood from left to right (from aorta to
pulmonary artery) may persist for the first 4 days of life and produce clinical pre-
sentations in the form of murmur.
BP varies depending on the infant’s postnatal age in days, and gestational age.
Normal heart rate is 120–140 beats per minute.
Various methods are employed for assessment of the functional condition of the
cardiovascular system. ECG shows the major myocardial functions (automatism,
excitability and conduction), disturbance of cardiac rhythm, overload of heart parts
and cardiac failure.

After birth the infant’s nutrition changes. While adapting to new living conditions
the digestive function of a neonate depends on its age. Metabolism is intensive; it
ensures fast growth, weight gain and development of the infant. Capacity of the
stomach is not large (7–10 cm3); it increases from day to day to amount to 90 cm3
by 10 days. Round muscles in the cardial part of the stomach are poorly developed,
which promotes regurgitation. During the first days the mother does not have a lot
of colostrum, but the amount is sufficient to meet the newborn’s need for nutrition.
Gastric digestion proceeds in a weak acid medium helped by enzymes (pepsin, ca-
thepsin, chemosine, lipase and others); for the most part they are contained in the
mother’s milk.
The infant’s nutrition should match its energy requirements, which can be achieved
by frequent breastfeeding: 10–15 times a day and more (on demand).
Low activity of the newborn’s own enzyme systems in the GI tract causes various
problems with newborn’s nutrition if the main organizational principles are not ob-
served (incorrect technique, frequent switching of breasts, limiting the breastfeeding
time; see Chapter 3 Antenatal and Postpartum Care).
Meconium is discharged upon delivery. It comprises a mixture of intestinal mucus,

sloughed epithelium and bile—a homogenous green odorless mass. In 2–3 days me-
conium is replaced by transitional stools, and after that stools common for breastfed
babies develops: doughy mass of yellow color. At an early neonatal age the stools
can be 6 times a day. The stool frequency must be correlated with the nature of fe-
cal masses and the presence or absence of pathological admixtures: mucus, watery
mass, green or yellow coloration.

Fetal kidneys are able to transport organic substances, reabsorb sodium, dilute and
acidify urine. However, their intrauterine function is of no practical value as it is the
placenta that excretes the waste products. Transition to extrauterine existence implies
that now kidneys will take over this function. An infant on exclusive breastfeeding
does not produce a large amount of urine within the first 2 days: to the extent of
30 ml a day (physiological oliguria). This is due to the small amount of colostrum
and provides a gradual adaptation of kidneys to the load. By the end of the first week
diuresis increases almost twice; it is important that this process take place gradually.
Abrupt load on the kidneys with large quantities if breast milk substitutes in the first
days of life substantially increases the risk of hardly manageable nephrogenous arte-
rial hypertension in future. Besides, one-time fluid load can increase the amount of
extracellular fluid without increasing the diuresis, which should be taken into account
if there is a need to give the infant infusion therapy: the excretory function of the
kidneys becomes adequate only by the end of the fifth day.
13.3.5. Endocrine system

The endocrine gland function is regulated by the CNS. By the time of full term
delivery the adrenal glands are sufficiently mature; they produce gluco- and min-
eralocorticoids. Adrenals speed up the development of the lungs and influence the
surfactant production. The development of adrenal cortex function is disrupted if
there is pathology of the neonate, especially in preterm babies.
Thyroid hormones are of great importance for normal growth and development of
the infant; they stimulate protein synthesis and cellular metabolism which has a bear-
ing on oxidation processes, the activity of enzyme systems and differentiation of body
tissues. Thyroid hormones are especially significant for the development of CNS;
they stimulate neuroblast proliferation and migration, growth of axons and den-
drites, promote the accumulation of lipids and glucoproteids by the nervous tissue.
At childbirth, the neonate’s blood contains up to 50% thyroxin of maternal origin.
The carbohydrate metabolism is regulated by a complex of glucocorticoids, insulin,
and glucagon.
13.3.6. Immune system

A full term neonate can produce an immune response to external stimuli. The
features of neonate’s immunity are due to the conditions of intrauterine development
330 Obstetrics
(immaturity, restricted growth, hypoxia and intrauterine infection). Full term neo-
nates show an elevated amount of T lymphocytes and T suppressors. They receive a
normal amount of IgG from the mother through the placenta, but there are few IgM
and IgA in the blood and secretions: they cannot pass through the placental barrier.
The amount of interferon is low. The blood shows an increased level of neutrophils,
but proliferation is poor, and the ability of the bone marrow to produce neutrophils
in severe infection is restricted.
In full term babies transient immunodeficiency is noted in the first days of life;
this is due to massive antigen stimulation. After delivery the intestine, skin and mu-
cosas of the infant are populated by microorganisms while the entry of hormones
and humoral factors through the placenta has now been arrested.
Infants with complicated intrauterine development (immaturity, growth restric-
tion, hypoxia, congenital infection, prematurity) show a more pronounced immu-
nodeficiency.
While adequate immune response to foreign agents (antigens) is developing, im-
mune protection by maternal milk is of crucial importance.
13.4. CLINICAL EXAMINATION OF THE NEWBORN
Clinical examination of the newborn includes external inspection, assessment of

the pose and position, motor activity, the ability to come in contact with mother,
crying, muscle tone, skin; all organs and systems are examined consecutively; a
neurologic examination is made. An adequate functioning of all departments and
personnel of the maternity hospital promotes successful breastfeeding that can con-
tinue for a long time. In hospitals with rooming-in conditions the puerpera is helped
to start breastfeeding within 30–120 minutes after childbirth (in most cases it can be
done irrespective of whether delivery was physiological or operative).
Immediately after cord dissection the newborn is wiped with a warm sterile napkin,
fitted with a cap and socks and put on the naked chest / abdomen of the mother his
face down and covered with a dry napkin or blanket. In this position the puerpera
holds the infant herself (or aided by the midwife).
The first latching to the breast occurs when thew baby shows he is
NB! ready to take the breast (rooting reflex, automatic crawling reflex).
The baby should not be forced to suck at once; he may develop
the inclination later.
After a physiological delivery a healthy neonate is capable of crawling to the

mother’s nipple and taking it with its mouth. Skin-to-skin, eye-to-eye contact
promotes a favorable sensation of emotional comfort in the puerpera, emergence of
emotional intimacy with the baby. The crucial issue in the method is facilitating the
neonate’s adaptation to extrauterine life by populating its skin and GI tract with ma-
ternal microorganisms. If the infant is healthy, it can be examined by a neonatologist
without breaking the contact with mother. If the scenario is different and the contact
is broken, this precludes adequate neutralization of birth stress in the newborn.
Measuring the body weight and length, processing of the eyes can be postponed
till transferring the infant to postpartum wards, if till now the infant is not ready for
the first feeding.
A second inspection is done in the ward, with the mother

NB! participating. The baby can be inspected in bed, on the changing
table, in the humidicrib in good natural lighting and at a t of
24–25 °C. The pediatrician’s hands should be dry and warm.
13.4.1. External inspection

The external inspection is made to reveal disorders of intrauterine development,
congenital disease and birth trauma.
The build of the infant is assessed in supine position. The middle point of body
length is located in the area of umbilical ring. One notes the length of limbs in rela-
tion to the trunk, head size, facial features. The examination helps to reveal
• hydrocephaly, microcephaly;
• choanal atresia, cleft lip, palate or upper jaw;
• torticollis, polydactylism, disorder of hand posture (main d’accoucheur, claw
hand, wrist drop), talipes, polydactylism;
• the thickness and condition of umbilical cord and ring (hemorrhage,
inflammation);
• disorder in the development and differentiation of genitals (clitoris hyperplasia,
malposition and hypospadia of testicles);
• skin condition (cyanosis, icterus, pallor, exfoliation, signs of inflammation,
hemangioma, edema, effusion of blood, subcutaneous tissue necrosis);
• oral mucosa (candidiasis).
Palpation is used to detect clavicle or other bone fracture, cephalohematoma size,
signs of hip and femur dysplasia.
The infant is turned onto its abdomen. Studying the back one can detect hair
growth, skoliosis, pilonidal sinus, meningocele, meningomyelocele, foot crease paral-
lelism, suspicion of coxofemoral dislocation, imperforation of anus.
Body weight is an indicator of intrauterine development; it can show macrosomy
(post-term, diabetic fetopathy) or SGA and IUGR.
Body weight measurement should be postponed until the first breastfeeding is
completed.
Immaturity may indicate disrupted intrauterine development: discrepancy between
morphological, functional signs and the infant’s gestational age.
Inspection of the newborn can give rise to suspicion of congenital disease.
Detection of 5 and more disembryogenetic stigmas indicates disrupted intrauterine
development.
13.4.2. Assessment of pose and position

The pose and position of a healthy newborn should be on its back with flexed
arms and legs with uncoordinated active movements. The infant reacts to stimuli by
332 Obstetrics
intensifying his motor activity (flexion and extension, crossing of legs). He spreads
his fingers wide; one can note transient minor tremor of the chin and hands.
When doing the examination one checks for the abnormal frog and fencer posi-
tions, opistotonus (throwing back of the head), asymmetry of the pose and move-
ments, abnormal posture of hands and feet (varus or valgus posture, heel position,
foot drop).
13.4.3. Evaluation of communicability

The ability to come in contact with mother or communicability is an important cri-
terion in newborn’s health assessment. One evaluates the change of facial expression,
eye-to-eye contact, irritation and pacification reactions in situations of discomfort
(wet diapers, forced awakening, hunger), response to sound.
13.4.4. Assessment of the infant’s cry

Baby crying can be an emotional response to handling, pain irritation. It stops
when the situation changes (picking the infant up, stroking, talking, etc.). When the
cry is weak, irritated, unemotional (monotonous), with a nasal twang, continuing
after the source of discomfort was removed, an analysis of these factors can be help-
ful in diagnosing a disease.
13.4.5. Assessment of muscle tone

Muscle tone of the newborn is determined by enhanced tone of flexors — embryo
pose. The arms are bent in all joints, pressed to the trunk, hands in a fist with the
thumb covered with four other fingers, legs splayed in coxofemoral joints and bent,
dorsal flexion of the foot is noted. If one places the infant with his chest on the
palm, the legs and arms will be adducted to the trunk due to the active muscle tone.
Muscular activity is characterized by head adduction (the chin touching the breast-
bone), extension of arms in elbow joints, flexion in radiocarpal joints, abduction of
thighs, leg flexion in the knee joint, foot flexion. Increased or decreased muscular
tone indicates a disease and causes abnormal positions.
13.4.6. Examination of the skin

The skin in healthy newborns is pink, delicate, somewhat dry due to low function-
ing of sweat glands, with good tissue tone. The skin of neonates has certain particu-
lar features. At birth the skin is covered with vernix caseosa which has protective
properties and so should not be removed within the first 6–12 hours after delivery.
There are whitish-yellow dots projecting above the skin (milia); lanugo hairs may be
found on the face, shoulders and back; cyanotic Mongolian spots are noted on the
sacrum and buttocks; vesicles with transparent contents (sweat gland cysts, miliaria
crystallina) can be seen on the face.
Skin color depends on the age after birth. In the first days there can be cyanosis
of hands and feet; skin around the mouth may be bright red (sign of circulatory
adaptation or vascular response to tactile or temperature exposure)—physiologic

erythema. On day 3 the skin acquires icteric coloration, mostly in the face and up-
per trunk — physiologic icterus (unconjugated bilirubin concentration not exceeding
220 μmol/l) (Fig. 13.7).
Fig. 13.7. Physiologic icterus of newborn
On a first examination one establishes the presence of anal opening and meco-
nium.
Body temperature in a healthy newborn should be stable, about 36–37 °С.
13.4.7. Examination of organs and systems

The head can be brachio- dolichocephalic or of irregular shape which depends
on its engagement during delivery. Cranial skull dominates over facial skull. Head
circumference is 34–37 cm, chest circumference is 1–3 cm less.
Head palpation can reveal labor tumor or head tissue edema (caput succedaneum)
after delivery in cephalic presentation, as well as cephalohematoma (blood effusion
under the periosteum of one of cranial bones). One checks for cranial bone density:
poor mineralization can make bones pliant in preterm babies; dense bones are seen
in post-term infants. One can detect areas of resorption and fractures in the skullcap.
The sutures and fontanelles are palpated. Bulging and pulsation in fontanelles and
sutures is regarded as a sign of pathology.
The size of the anterior fontanelle varies individually (1–3 cm from opposite bone
edges). The posterior fontanelle is mostly closed in full-term infants. The sagittal
suture is open; the distance between bones is not more than 3 mm.
The face is symmetrical, the eyes open, the cornea clear, pupil diameter
2–3 mm; the pupils react to light. Convergent strabismus and transient nys-
tagmus are possible. The conjunctiva is pink. Mucosas of the lips, tongue and
mouth are well supplied with vessels. In rare cases teeth can be found on alveolar
processes. One checks for defects like cleft lip (cheiloschisis ) (Fig. 13.8) and
cleft palate (palatoschisis) (Fig. 13.9) and other stigmata of disembryogenetic
development.
334 Obstetrics
Fig. 13.8. Cleft lip
Fig. 13.9. Cleft palate
The neck can be short due to trauma of cervical vertebrae during labor or due to
chromosome disorder. Palpation determines the causes of torticollis or asymmetry
of sternocleidomastoid muscle.
The chest helps to evaluate the respiratory and cardiovascular function. Findings
can include barrel-shaped thorax, costal position close to horizontal, symmetrical;
intervertebral spaces and sternal notch can be somewhat retracted. Lower portions
of the chest participate in the respiratory act. Chest deformities include pectus exca-
vatum, pigeon chest, asymmetry.
Palpation of the chest detects a fracture of clavicle and shoulder blade presenting
as local edema and crepitation, enhanced rigidity typical of pulmonary disease, the
apex beat of the heart heard in the fourth intercostals space 1–2 cm left of mid-
claviclular line outward.
Auscultation is performed with a special small size stethoscope. Auscultation de-
termines clear heart sounds, heart rate of 110–140 bpm. Puerile respiration is heard
above all pulmonary fields: the expiration is one third of inspiration. Respiratory rate
is 40–50 per minute. In the first minutes of life rales are heard above the lungs due
to the remaining portions of intrauterine pulmonary fluid; there can be short-time
breath-holding spells or apnea for 10 s.
The abdomen is of spherical shape; it participates in respiration. Abdominal dis-
tension, visible intestinal peristalsis, asymmetry and retraction, changed color in the
anterior abdominal wall are all pathological signs of digestive organ disease; they
are accompanied by the infant’s restlessness. Abdomen is accessible to palpation;
sometimes separation of straight abdominal muscles is determined. Palpation of a
newborn’s abdomen is made with gentle movements, with finger pads. In healthy
infants the liver extends below the costal margin 2 cm along the midclavian line;
the spleen is palpated at the costal arch margin. Sometimes kidneys are accessible to
palpation. For accessory determination of liver and spleen margin one uses percussion
of the abdomen. Auscultation is used for diagnosis of intestinal peristalsis disorders.
The umbilical vein and two arteries are palpated at the superior and inferior poles
of umbilical wound; inflammation in vessels may be diagnosed.
Genitalia. In full term girls labia majora cover labia minora. In genital crisis there
can be discharge of mucous and blood. In boys the balanus is covered by the fore-
skin, testicles are descended in the scrotum. On day 3–5 crystals of uric acid salts
can be noted at the urethral orifice. Scrotum edema can develop as a manifestation
of hormonal crisis. In boys one should determine whether the testicles are in the
scrotum or in the inguinal canal.
In healthy newborns the coxofemoral joints can be splayed until they touch the
table or bed surface. Limitation in splaying can indicate increased flexor tone or
coxofemoral dysplasia. There may be excessive movement in the joints.
When inspecting the lumbar region, one can discover hypertrichosis as a sign of
disrupted spine formation, and retraction of buttock on the side the lumbar portion of
spinal cord is affected. Palpation of buttocks reveals inflammatory changes in tissues.
13.4.8. Neurological examination

The neurological examination evaluates the general condition of the newborn
and provides a complex assessment of behavioral signs (pose, motor activity, com-
municability, muscle tone and other) and neurological signs. Newborns respond to
pathogenic exposure with nonspecific neurologic signs. Focal neurological signs are
rarely detected.
When performing a neurological examination one should consider

NB! the gestational age. Behavioral and neurological signs depend
on maturation of the nervous system and on the gestational age.
Transition to waking (within 1–30 min) and to sleep (1–2 h) are indicative of
health. Depending on the condition, the child’s response to stimulation varies.
When having a light shining into his eyes the newborn closes his eyes and throws
back the head. Motor reaction to a sound stimulation is detectable from 35 weeks
gestation.
336 Obstetrics
A number of unconditioned reflexes are evaluated in the newborn three times:

• oral automatism: rooting, snout reflex, grasp reflex, palm-mouth reflex;
• spinal automatism: Babinski sign, Galant, Perez reflex, supporting reflex, Moro
reflex, crawling response.
Tendineal reflexes are of medium activity.
Absence of reflex, asymmetry, an intensified, repeated and
NB! unusual reflex is indicative of abnormality.
Non-focal unspecific neurological disorders are manifested as suppression syn-
drome, heightened nervous-reflectory irritability and vegetative disorders.
Suppression syndrome: inertia, poor response to stimulation. Muscular hypotonia
and suppression of reflexes, including sucking and swallowing reflexes.
Syndrome of heightened nervous-reflectory irritability is manifested by spontaneous
irritability, starting, limb tremor, crying and reflex responses.
Vegetative disorders are manifested by changes in pupils, skin, BP, heart rate and
respiratory rate, intestinal peristalsis, salivation and tracheobronchial secretion.
Signs of lesion of 12 pairs of cranial nerves are assessed by checking their function.
When doing a complex evaluation of newborn’s development, evaluation of general
condition and neurological status, one should consider the mother’s health, exacer-
bations of infectious and somatic diseases during pregnancy, the course of pregnancy
and childbirth, the infant’s condition upon delivery.
Clinical examination begins with analysis of gestational age and specifics of intra-
uterine development (IUGR, immaturity, macrosomic fetus, etc.).
13.5. NEWBORN PRIMARY CARE IN DELIVERY ROOM

Thorough preparation of the delivery room and ensuring equipment integrity are
essential for the newborn’s health.
In the delivery room the necessary articles are a radiant heat source to warm the
baby, Apgar timer, sterile gloves, dry sterile diapers, scissors, scalpel, adhesive tape,
phonendoscope, electronic thermometer.
For the first toilete of the newborn one will need
• sterile beddings comprising a cotton blanket, three coarse calico diapers, a cap
and socks;
• individual sterile set for a newborn: clamps for umbilical cord remnant, silk
stitch, two clamps, dropper, 4–6 gauze balls, centimeter tape;
• sterile metal or enameled tray for newborn;
• pediatric tray scale to weigh the infant.
In the delivery room the infant receives primary care:
• drying with a warn diaper, placing on the mother’s epigastric region and covering
with another dry warm diaper and leaving the infant until he can take the breast
on his own (this usually takes 30–60 min);
• swabbing the umbilicus with a napkin moistened with 70 0 ethyl alcohol and
dissecting it;
• taking anthropometric measurements (at any time before transfer to postpartum
ward).
After birth it is not recommended to suck out the contents of

NB! the newborn’s mouth and nose. Prolonged aggressive sucking-
out can delay the onset of independent respiration and cause a
prolonged spasm.
Several seconds of evaporation from the newborn’s moist skin lead to moderate
cooling. This is an intensive sensory stimulation causing spontaneous respiration in
the infant.
The midwife washes the hands thoroughly and swabs them with alcohol,
wipes the infant’s eyelids with a sterile cotton ball. Then she pulls his lower
eyelid down and applies erythromycin or tetracycline ophthalmic ointment for
prevention of ophthalmic infection. This procedure is repeated in 2 hours in
the ward.
The newborn can see, feel pain, heat, cold, feel odors and taste, can cry. For
the first few hours the biological bond between the mother and child is preserved.
Separating the mother and newborn for as little as 1–2 days can have unfavorable
effects.
It is not advisable to remove vernix caseosa or wash the newborn while in the
delivery room. Vernix caseosa moistens and provides mechanical protection to the
skin; it has antibacterial, wound healing and antioxidant properties. The remains of
vernix caseosa that failed to absorb are removed in 6–12 hours. If the newborn’s
skin is dirtied with blood or meconium, the dirt should be removed carefully with a
cotton ball moistened in warm water.
The umbilical cord remnant is processed in two stages.
• First stage. As soon as cord vessel pulsation subsides (1–3 minutes but
not later than in 10 minutes), Kocher’s clamp is placed on it 10 cm from
the umbilical ring; another clamp is placed 2 cm outwards from the first,
the third Kocher’s clamp is placed as near as possible to mother’s external
genitals (for control of placental separation). The length of cord between the
first and second clamps is wiped with a ball moistened with 950 ethyl alcohol
and cut with sterile scissors.
• Second stage reduces the risk of infecting the umbilical cord remnant. Before the
secondary processing of the cord the midwife scrubs her hands as before surgery
and puts on a sterile gown. Processing is done on the infant table in compliance
with principles of aseptics under radiant heat. In secondary cord processing
a disposable plastic clamp is most reliable and safe; it is placed on the cord
remnant, the optimum distance from abdominal skin to the clamp being 1 cm.
After placing the clamp the cord tissue above the clamp is cut, and then the blood
is wiped (Fig. 13.10).
The umbilical cord remnant can be tied with silk stitch. The accuracy of clamp
placement is checked before the transfer of mother and infant to the ward.
The umbilical stump provides the main channel for postnatal

NB! infection. The stump is kept clean both in hospital and at home
(keeping it dry, not covering it or applying anything).
338 Obstetrics
Fig. 13.10. Final appearance of umbilical cord remnant
Taking anthropometric measurements. The infant is weighed swaddled in a diaper

on pediatric tray scale. Before weighing the tray is wiped with a disinfectant. The
body weight is arrived at by subtracting the diaper weight.
One measures the infant’s length, head and chest circumference with a sterile
oilcloth tape. The head circumference is measured along the line of superciliary arch
and posterior fontanelle, the chest circumference—along the nipple line. In some
countries (in USA for instance) footprints are taken while giving primary care and
taking anthropometric parameters (Fig. 13.11).
Fig. 13.11. Newborn’s footprints

One should wash the hands carefully, use sterile gloves,

NB! instruments and dressings during childbirth, care of the cord and
of the newborn.
After measuring the newborn is wrapped in diapers and a blanket. A tag stating
the mother’s name and surname, the infant’s sex and weight, the date and time of
birth is attached to the baby’s hand.
When providing care such as changing the nappies one should

NB! watch that the baby remains warm; all procedures should be done
quickly, the baby should be kept covered.
13.6. NEONATAL CARE

Sometimes early contact between the mother and child is impossible as the
mother needs rehabilitation after childbirth due to surgery or delivery complication;
sometimes the newborn requires intensive care. Early latching to the breast is not
recommended for asphyxiated babies or babies with cerebral circulatory disorder,
severe developmental defects. The length of separation should be as short as possible.
As soon as the mother feels better or the infant begins to recover, they should be
brought together so as the mother can start taking care of the infant immediately.
After an uneventful delivery the mother and baby are transferred from the delivery
room together. The infant’s toilet and care are performed during the first day of life,
apart from the mother, by the department nurse. She demonstrates the algorithm of
processing the infant’s skin and mucosas (the eyes, nasal passages, intimate wash)
and teaches the mother how to use sterile materials and disinfectants.
13.6.1. Rooming-in and breastfeeding

To ensure exclusive breastfeeding the following is important:
• latching the newborn to the mother’s breast immediately upon delivery;
• rooming-in of the mother and infant in maternity hospital;
• excluding all foods and fluids except breast milk;
• ban on teats, pacifiers and bottles that weaken oral motility in the newborn;
• breastfeeding on demand without night-time intervals;
• early discharge from maternity hospital.
Rooming in of mother and infant also limits the contacts of the newborn with
other children. Even in a four-bed ward this contact is limited to three rather than
20–25 as is the case in the nursery. It is desirable that the number of beds in room-
ing-in wards is no more than two beds for mothers and two beds for neonates. The
optimum number of beds is one for mother, one for infant. The newborn should not
be transported to various sections of the hospital without a good reason. Thus vac-
cination, blood sampling for neonatal screening, hearing screening and examination
by pediatrician are performed in the ward the infant rooms in.
340 Obstetrics
In caring for newborns receiving exclusive breastfeeding artificial quieting means

like teats, pacifiers should be avoided. No supplementary foods or fluids are required.
Moreover, supplementary feeding and drinking provided with bottles leads to dete-
rioration of oral motor activity, which is the main factor for adequate nourishment.
When sucking grows weaker, the myoepithelial area of nipple and alveoli cannot be
adequately emptied and thus there is no adequate stimulus for prolactin production
and as a result hypogalactia develops. Pacifiers work to produce the same effect.
Neither advertising formulas nor instructing groups of women
NB! on artificial feeding is admissible. Above all is providing the
opportunity to breastfeed on demand, which also precludes giving
the neonates water, glucose, etc.
Some infants (extremely pre-term, very low birth weight, with enhanced hypo-
glycemia risk) may require supplementary feeding. In the first two cases preserving
the sufficient amount of breast milk permits an effective prevention of a common
complication, necrotizing enterocolitis, which can worsen the prognosis considerably.
Neonatal hyperbilirubinemia (including its varieties due to Rhesus and antigen in-
compatibility in AB0 blood grouping) does not require discontinuation of breastfeeding!
It is congenital metabolic disorders of the infant that are considered an absolute
contraindication for breastfeeding: galactosemia, branched-chain ketoaciduria, phe-
nylketonuria. In the last case partial breastfeeding is possible with careful monitoring
of the infant’s condition.
13.6.2. Swaddling
At present there is no undivided opinion on the issue of swaddling of neonates.
Some authors believe that swaddling the infant, limiting his movement slows down
his mental and motor development. It is proposed to put on crawlers at once and
leave the infant to move about as he likes. Pediatricians cannot give an unequivocal
opinion which is better: swaddling or giving complete freedom. Each approach has
its pros and cons; every child should be assessed individually.
For swaddling there should be both warm and light nappies available. Choosing
the nappies one should consider the temperature in the room and prevent over heat-
ing of the infant. Before first use the nappies are boiled in soapy water; baby soap is
preferable. Washing should be done manually with baby soap or in washing machine
using baby antiallergic detergent powder.
Tight swaddling is not recommended as it suppresses the movement of the dia-
phragm, reduces lung ventilation, disrupts blood circulation, poorly preserves heat
due to a small air space, limits the infant’s movements, which slows down the de-
velopment of neuromuscular coordination. Tightly swaddled infants sleep more and
suck less, which interferes with the development of lactation function in the mother.
13.6.3. Sleeping of the newborn

The newborn usually sleeps as long as he needs. Comfortable conditions for a quiet
sleep should be provided. However, in certain cases (for instance, after complicated
vaginal birth, operative delivery, pronounced hyperbilirubinemia that produces a

sedative effect on the CNS, transient hypoglycemia) sleep can be excessively pro-
found and long. The mother should not hesitate to put the infant in her bed if she
finds it more convenient; there is no risk of strangulation or infection to the infant
once all safety measures are observed: a firm even mattress, full-term baby, he has his
own blanket and no pillow, elder children are not sleeping in this bed, both parents
are off strong drink, cigarettes or psychoactive drugs.
If the newborn is separated from the mother in the first days of his life, this in-
terferes with establishing breastfeeding routine, which is extremely important for the
infant’s well-being. Contact between the mother and newborn should be established
as soon as possible, and early discharge from hospital is preferable.
Kangaroo care is a safe and effective alternative to common care for pre-term infants
in a stable condition. It provides adequate thermoregulation, facilitates breastfeeding
and permits a close observation of the infant’s condition. The mother’s or father’s body
(like in marsupial animals) is in skin-to-skin contact with the vertically placed infant’s
body for 24 hours (mother for 18 h, father — 6 h), which ensures maximum protection
for the infant throughout his stay in the maternity hospital. This method decreases the
risk of hypothermia that leads to increased neonatal mortality, cross-infections, and
improves adaptation due to neurosensory stimulation (Fig. 13.12).
Fig. 13.12. Kangaroo care

342 Obstetrics
In many countries newborn boys receive circumcision which is done on day 1–2
by a specialist.
13.6.4. Care of umbilical cord remnant

The cord stump and umbilical wound are inspected by a pediatrician
(Fig. 13.13).
Fig. 13.13. Umbilical wound, day 3–5
The cord stump dries and mummifies in the air without the help of dressing or
bandage; this commonly happens 7–9 days after birth. It remains clean if the infant’s
clothes are kept clean, no urine or dirt come in contact with the wound. There is
no need for antiseptics for cleaning the stump. If it is dirtied, the cord stump can be
washed with clean water and dried with cotton or gauze. The infant can be discharged
home when the umbilical cord remnant has not detached yet.
Early dissection of the cord remnant is dangerous. It can produce complications
like bleeding, injury of intestinal wall in undiagnosed embryonal hernia, infection.
Dissecting the cord remnant is unjustified invasion.
Any changes in the appearance of umbilical wound—redness of skin around it,
edema, copious discharge, bleeding, appearance of masses or pus-like substance on
the bottom — require immediate medical advice.
Prolonged healing of the wound is also a cause for concern.
When the wound has completely healed (by day 15–17), a retraced skin fold re-
mains in its place — the navel. It is located on the abdominal midline in the middle
between the xiphoid process and pubis. Position of the umbilical ring helps a doctor
to evaluate the infant’s degree of maturity. Sometimes umbilical hernia may develop
due to specific features of transition between the skin fold and umbilicus. A wide
umbilical ring and pronounced hernia indicate umbilical hernia; for its diagnosis and
reduction surgical advice and help may be required.
13.7. TRANSIENT AND ADAPTIVE DYSFUNCTIONS

IN EARLY NEONATAL PERIOD
Almost a half of neonates show moderate neurological signs in the first
5–6 days of life: transient strabismus, floating movement of eyeball, decreased
muscle tone and reflex response due to psychophysiological stress and pain stress
during delivery.
Transient hyperventilation. The first breath takes place as after delivery the fetus
experiences increasing oxygen insufficiency, which is accompanied by various meta-
bolic changes and these, in their turn, lead to activation of the respiratory center.
The lungs are filled with air, and residual lung capacity is created; lungs are emptied
of fetal fluid (it is absorbed into the lymphatic system), pulmonary arteries dilate,
vascular resistance in the lungs drops, pulmonary blood flow increases, fetal bypasses
between systemic and pulmonary circulation close. Minute pulmonary ventilation
is twice as large in newborns as in older children; this is aimed at compensating
acidosis upon birth.
During the first minutes of life the infant experiences metabolic adaptation where
maternal placental hormones play the leading role. Infants may develop transient
hypothyroidism, genital crisis, desquamative vulvovaginitis.
Transient hypervolemia or increased circulating blood volume develops after birth
due to active absorbtion of fluid present in the lungs, into the blood and lymph
sinuses. The infant gets accessory blood volume due to placental transfusion, which
amounts to 20–30 ml per 1 kg of the infant’s weight. The volume of placental
transfusion also depends on the fetus’s position in relation to the level of placenta
position. If the fetus is put down below the placental level, it quickly receives an ac-
cessory blood volume. Full-term infants with transient hypervolemia develop edema,
tachycardia, breathlessness, pronounced transient icterus.
13.7.1. Physiological loss of body weight

Over the first 3–4 days of their lives almost all newborns lose weight. The change
in weight is directly related to the amount of food. Weight loss indicates the infant’s
metabolic adaptation; it does not exceed 6–10%. Optimum thermal environment and
early latching to the mother’s breast help to restore the body weight. Weight loss is
regarded as pathological if it amounts to more than 10%; it occurs upon violation
of rational feeding of the newborn.
13.7.2. Body temperature fluctuations

Newborns cannot sustain the body temperature by themselves that is why they can
be easily overheated or overcooled. The ability to endure environmental temperature
fluctuations develops as late as by 20–30 days of life.
13.7.3. Icterus
Icterus (jaundice) developing in the first week of life is noted in about 60% of
full-term newborns and in 80% of pre-term newborns. Conjugational icterus presents
the major problem of neonatal care. One should differentiate between physiologi-
cal and pathological jaundice. Normal level of unconjugated bilirubin in the blood
serum is below17.1–22.2 mcmol/l (1–1.3 g/dl); it grows by less than 85.5 mcmol/l
a day (<5 mg/dl a day). Jaundice only develops on day 2–3 and reaches its peak on
344 Obstetrics
day 3–4 in preterm babies when the conjugated bilirubin level in the blood is below
204 mcmol/l, and in breastfed infants — below 220 mcmol/l. On day 5–7 jaundice
subsides untreated.
In pathological jaundice bilirubin levels are higher than those in physiological jaun-
dice; for twenty years this condition has been treated using phototherapy. This is an
effective method that does not produce any unfavorable effects on the infant. Acted
on by the light, bilirubin found under the skin is transformed into its isomer which
is easily excreted by the liver. The effect depends on light intensity; the wavelength
should be 425–475 nm. For the phototherapy session the infant’s eyes should be
covered with a blindfold. The whole body should be irradiated by the lamplight; body
position should be changed from time to time. Breastfeeding can continue during
therapy sessions. Sunbathing produces a similar effect: the indicated wavelength is
within the visible rather than ultraviolet spectrum of sunlight.
13.7.4. Erythema
Simple erythema (physiological reddening of skin, Fig. 13.14) develops after re-
moval of vernix caseosa. During the first hours of life the redness may appear cya-
notic, its intensity and duration depending on the degree of the infant’s maturity.
On the second day erythema commonly turns brighter and by the end of the first
week it subsides altogether.
Toxic erythema. On day 3–5 of his life the newborn may develop single or
multiple bloodshot papules and spots in the face, outer surfaces of hands and
feet, on the back or buttocks; this occurs as a manifestation of an allergic reaction
(Fig. 13.15).
Small white vesicles with some reddening at the base can emerge. This benign rash
is usually located in the face, trunk and extremities; it disappears in a week, as a rule.
Over 1–3 days new rash may appear but it commonly subsides within 2–3 days. The
Fig. 13.14. Simple erythema

Fig. 13.15. Toxic erythema of newborn
infant does not feel any worse for it, his body temperature remains within normal.
Exclusively breastfed newborns develop toxic erythema extremely rarely.
After birth infants may sometimes have enlarged sweat glands: thin-walled vesicles
filled with caseous or clear contents. They can be seen in the area of neck and scalp,
more rarely—on the shoulders and chest. The vesicles can be easily removed with
cotton drenched in alcohol; the skin remains undamaged and the rash does not
reappear (Fig. 13.16).
Fig. 13.16. Toxic erythema
13.7.5. Physiological skin peeling

Physiological skin peeling can be macrolaminar or in the form of defurfuration; it
develops on day 3–5 of the infant’s life. Peeling is mostly seen in infants with bright
simple erythema after it has subsided; it commonly appears on the abdomen and
chest. In post-term infants peeling is more pronounced. Peeling does not require
treatment; it subsides on its own.
346 Obstetrics
13.7.6. Caput succedaneum

Caput succedaneum (labor tumor) (Fig. 13.17) resolves on its own within 2 days.
Sometimes small punctuate hemorrhage appears on the caput; it resolves spontane-
ously, too.
Fig. 13.17. Caput succedaneum
13.7.7. Genital crisis

Genital crisis is manifested by enlargement of mammary glands, irrespective
of the newborn’s sex. On day 8–10 of life there can be milk-like discharge from
mammary glands. The reverse process in both boys and girls begins in 1–2 weeks.
Besides, girls may have blood-tinged discharge from the vagina on day 4–6. Edema
of external genitals is seen in 10% newborns. It persists for 1–2 weeks and longer
and then resolves untreated.
13.7.8. Milia
Milia (Fig. 13.18) are whitish-yellow cysts or bumps 1–2 cm in size. They are
mostly located on the wings and bridge of the nose, forehead; rarely—across the
entire body.
Fig. 13.18. Milia

These are sebaceous glands with copious secretion and clogged ducts; they are
seen in about 40% of newborns. If there are signs of sight inflammation around the
cysts, 5% potassium permanganate solution should be applied to them.
REMEMBER!
To perform examination, vaccination and treatment of any newborn one should
obtain the mother’s informed consent to the proposed events (or her refusal).
Body weight is not a criterion of gestational age.
The respiratory system affects the development and regulation of other vital
functions of the body: hemodynamics, metabolism, fluid exchange.
The rate, depth and duration of respiratory cycles are changeable in newborns.
Abdominal type of respiration predominates. When waking, the infant shows
synchronized movements of the chest and abdomen. Inspiration phase is shorter
than expiration phase. Respiratory rate is 40–60 per minute.
According to the principles of modern perinatal technology, the first examination

of the newborn should be performed without breaking the infant’s skin-to-skin
contact with the mother, preferably after the first latching to the breast.
A second examination of the infant is performed in the ward, with the mother’s
participation. The infant can be examined in the bed, couveuse, on a swaddling
table with a good natural lighting and at air temperature of 24–26 °С. The
pediatrician’s hands should be warm and dry.
When performing a neurologic examination of a newborn, one must take into

account the gestational age. Behavioral and neurological signs depend on
nervous system maturity and gestational age.
Absence of reflex, asymmetry, reinforced reflex are considered as pathological

signs.
The umbilical cord stump remains the major channel for infection entry after
delivery. The stump is kept clean both in hospital and at home: keeping it dry, not
applying anything to it, not covering it with anything.
One should wash one’s hands carefully, use sterile gloves, instruments and dressing
materials during childbirth, dissecting the cord and caring for the newborn.
CONTROL QUESTIONS
1. How are newborns classified according to their gestational age?

2. Describe the features of newborn’s respiratory system.
3. What changes take place in the infant’s cardiovascular system after delivery?
4. Describe the changes in the newborn’s digestive system.
5. Describe the changes in the newborn’s immune system. How does the infant
acquire passive immunity?
348 Obstetrics
6. Justify the importance of exclusive breastfeeding for the infant’s urinary

system.
7. Describe the stages of primary care for the newborn.
8. How is gonoblennorhea prevented in newborns?
9. Describe the order of examining the newborn.
10. How is the newborn’s physical development assessed?
11. What is skin-to-skin contact, what are its advantages?
CHECK YOURSELF!
Level 1. Test
1. How long does the neonatal period last?

a) from birth to day 14;
b) from birth to day 28;
c) from birth to day 40;
d) from 38 week of gestation to day 30 after birth.
2. Gestational age is the time starting from:

a) the first day of the last menstrual period before childbirth;
b) the moment of birth;
c) 37 weeks gestation;
d) conception to birth.
3. An infant is referred to as post-term if he was born:

a) after the estimated date of delivery;
b) at 42 weeks or later;
c) at 38 weeks or later;
d) large for gestational age.
4. A newborn is referred to as immature if he:

a) was born at 36–37 weeks;
b) shows a discrepancy between morphological, functional parameters and
gestational age;
c) shows underdeveloped rooting reflex;
d) has sleeping periods of 4 hours and longer.
5. A newborn’s heart rate is:

a) 120–140 per minute;
b) 100–120 per minute;
c) 80–100 per minute;
d) 60–80 per minute.
6. In full-term babies one notes the following in the first days of life:
a) physiological autoimmune reactions;
b) transient immunodeficiency condition;
c) activation of immune system function;
d) temporary replacement of active immunity by passive immunity.
7. Immediately after delivery the following should be done to a newborn:

a) measure body weight and length;
b) evacuate mucus from the respiratory tract;
c) remove vernix caseosa from the skin thoroughly;
d) help him to latch to the mother’s breast.
8. What should be done to the cord stump from the point of view of modern perinatal
technology:
a) dissect immediately after delivery;
b) dissect on day 2–3 after birth;
c) manage by a dry method (without applying antiseptics until spontaneous detachment);
d) wait for spontaneous detachment applying antiseptics daily.
9. What is the name of method of caring for preterm newborns where continuous
skin-to-skin contact is maintained:
a) kangaroo care;
b) coala care;
c) mild perinatal adaptation method;
d) Wilson-Jobs method.
10. What weight loss after birth is considered physiological:

a) 300 g;
b) no more than 1/5 of weight at birth;
c) no more than 10% of weight at birth;
d) any weight loss.
11. What level of unconjugated bilirubin in the blood of a breastfed baby requires
phototherapy:
a) 300 mcmol/l;
b) 220 mcmol/l;
c) 100 mcmol/l;
d) 50 mcmol/l.

1. The newborn of a preterm vaginal delivery shows blood bilirubin level of
300 mcmol/l on day 4 of life. What is your diagnosis? Your plan of management?
2. The infant of a term delivery is in a hospital with rooming-in practices on the
third day of life. Body weight at birth was 3550 g, body weight upon examination is
3225 g. Explain the weight loss, justify your plan of management.
• Chapter 14
DISEASES OF THE NEWBORNS
14.1. NEWBORNS WITH INTRAUTERINE GROWTH

RESTRICTION
The term intrauterine growth restriction (IUGR) is applied to a newborn whose
weight at birth is lesser than 10% percientile ofexpected for the given gestational age.
14.1.1. Epidemiology
IUGR is regarded as a pressing issue in perinatology and pediatrics. The incidence
rate of IUGR is 3–17.6%; in pre-term infants IUGR is seen more often: 15.7–22%.
In the structure of perinatal morbidity 20% are unrecognized IUGR cases. Infants
with IUGR are classified at risk for a short, «miserable» life.
Infants with IUGR require special attention of a neonatologist, pediatrician, psy-
choneurologist and other practitioners.
Low body weight is a consequence of multiple causes: his parents’ genetic code,
ethnic and constitutional features; in these cases the condition of the fetus and new-
born is not compromised, and no consideration to IUGR is given.
ICD-10 codes
• P05.2 Fetal malnutrition without mention of light or small for gestational age
(Infant, not light or small for gestational age, showing signs of fetal malnutrition,
such as dry, peeling skin and loss of subcutaneous tissue).
• P05.9 Slow fetal growth, unspecified.
Slow fetal growth should not be confused with IUGR. Slow fetal growth describes
the condition of a fetus while IUGR describes a condition after delivery and refers
to the newborn infant.
14.1.3. Diagnostics of intrauterine growth restriction

in newborns
On their first day of life all newborns are evaluated against scales of physical
development. They include such parameters as body weight and length, head cir-
cumference in correlation with the gestational age (Fig. 14.1).
The main diagnostic criterion of IUGR is the body weight and other parameters
of the newborn’s physical development below 10th percentile on the evaluation
scale.
Chapter 14. Diseases of the newborns 351
Fig. 14.1. Infant with IUGR (left) and infant appropriate for gestational age (right) (AGA)
To evaluate the degree of trophism disorders in a newborn (which correlate with

the degree of growth restriction) one employs a nutrition score. It was established
that the volume of soft tissues is the first parameter to change when the fetal en-
vironment is disturbed. The score assesses the thickness of subcutaneous fat in the
face, under the shoulder blade, in the area of thighs and buttocks of the neonate.
Apparently, this score is of accessory importance when estimating the status of a
newborn with restricted growth and cannot be employed as the main diagnostic
tool.
Newborns with IUGR have poorly developed subcutaneous fat, thus they are
inclined to have hypothermia, hypoglycemia, hypoxia and hyperbilirubinemia. Inner
organs are of smaller size. There are various disturbances in the development of func-
tions accompanied by depletion of organs and systems. Transient immunodeficiency
and susceptibility to infections develop.
During the perinatal period various nonspecific complications develop: meconium
aspiration, infections, disorder of cerebral circulation, metabolism changes, hypogly-
cemia and others. A child with IUGR is eligible for long-term follow-up care due to
numerous abnormalities of physical, neurological and mental development.
Prevention. There is no specific prevention of IUGR at present. It is advisable
to detect obstetric complications and extragenital diseases early and provide timely
adequate treatment.
14.2. NEONATAL GASTROINTESTINAL DISORDERS
Neonatal gastrointestinal disorders include vomiting and regurgitation, intestinal

dysbiosis, alimentary dyspepsia.
352 Obstetrics
14.2.1. Vomiting and regurgitation

In a neonate vomiting is reflex discharge of stomach contents resulting from con-
traction of the diaphragm and abdominal muscles.
14.2.1.1. ICD-10 codes

• P92 Feeding problems of newborn.
• P78.8 Other specified perinatal digestive system disorders.
14.2.1.2. Pathogenesis
Neonates are predisposed to regurgitating a small amount of milk after feeding.
This has to do with poor function of the esophageal sphincter, horizontal position
of the stomach, horizontal position of the infant while he is being fed, and the
rather large amount of food at each feeding episode. Regurgitation is precipitated
by contraction of stomach and diaphragm muscles. The infant’s condition is not any
worse for regurgitation.
Vomiting can appear upon pressure elevation in the stomach and intestine, irrita-
tion of the intestine by chemoreceptors (toxins); from the bowel the impulses pass
to the vomiting center.
Functional disturbances manifested as vomiting and regurgitation

NB! are due to slowed-down evacuation of food from the stomach,
disorder of gastric and intestinal peristalsis caused by immature
motor regulation.
Vomiting and regurgitation may accompany gastrointestinal disease: pylorospasm,

gastroesophageal reflux disease, esophageal achalasia, gastritis. Regurgitation differs
from vomiting in that the ingested food is released without an effort. The infant’s gen-
eral condition is not any worse, there are no vegetative signs, no changes in behavior
or appetite. Regurgitation is promoted by overfeeding and aerophagia (swallowing a
large amount of air while sucking).
Vomiting and regurgitation may be secondary signs in infections, cerebral lesions
and metabolic diseases (galactosemia, adrenogenital syndrome, hereditary metabolic
diseases and congenital kidney disease).
In reactive changes of vegetative centers (elevated intracranial pressure, irritated
peritoneum, irritation of bile ducts and other) the vomiting center is activated; it is
located in the area of reticular formation near the main vegetative centers (respira-
tory, coughing, vasomotor centers).
14.2.1.3. Clinical features

Vomiting of neonates is manifested by restlessness, pallor, tachycardia, aversion
to food, pathological weight loss. If functional regurgitation and vomiting have to do
with intestinal colic due to intestinal muscular spasm and excessive gases, the infant
shows abdominal distension, increased bowel sounds, troubled crying, sleep disor-
ders. Defecation makes the infant’s condition better. These disorders can develop
when the food does not suit the infant’s age and functional capacity of his GI tract
(enzyme immaturity) or when the intestinal microbiocenosis has been disturbed.
14.2.1.4. Treatment
Functional disorders like vomiting and regurgitation can be relieved by improving
the infant’s position during feeding. After feeding the infant is placed on his back or
side on a mattress with head elevated by 30 °. The rate of feeding episodes must be
increased to 10–12 per day thus decreasing the amount of milk per feeding episode.
Maternal breast milk is assimilated best of all. One can supplement breastfeeding
with formulas containing thickening agents like rice starch or locust bean gluten.
This formula is given at the end of breastfeeding.
If the newborn has meteorism, the mother should give up foods promoting gas
formation. She can take medications reducing gas formation, adsorbents (Smecta),
enzymes (Creon, abomin), carminative drugs (Simeticon, espumisan), eubiotics,
spasmolytic drugs; abdominal massage is indicated.
14.2.2. Intestinal dysbiosis

Intestinal dysbiosis implies a change in the composition and quantitative relations
between normal and opportunistic intestinal microflora.
14.2.2.1. Classification
ICD-10 code
• P 78.8 Other specified perinatal digestive system disorders.
• P78.9 Perinatal digestive system disorder, unspecified.
14.2.2.2. Etiology and pathogenesis

The GI tract environment begins its development during delivery. It is believed
that the fetus receives the primary microbial populations when it passes through
the mother’s birth canal. In healthy women the microbial flora of the birth canal is
represented by lactobacilli; in newborns it is obligate bacteria of the upper sections
of the alimentary canal. Lactobacilli provide optimum acidity; they participate in
production of certain vitamins and in milk digestion; they influence the formation
of the mucosa, thus they influence the digestive, absorption and protection functions
by contributing to mucus layers formation; they stimulate the local immunity as well
production of immunoglobulins and lymph cells.
After birth the newborn’s GI tract is populated by environmental bacteria includ-
ing pathogenic and opportunistic bacteria. Local defense of the newborn’s digestive
system is ensured by mucous layers; this secretion contains immunoglobulins, lymph
cells and nonspecific defense factors.
Latching the baby to the breast within the first minutes after
NB! delivery (or expressed colostrum) is an essential step in the
formation of the neonate’s microbiological environment: local and
systemic immunity, gastrointestinal microbiocenosis.
Breast milk contains practically all immune factors and bifidogenic properties.
Intestinal microbiocenosis of neonates receiving breast- and bottle feeding differs in
the amount of lactobacilli and bifodobacteria. Bottle fed babies replenish the defi-
354 Obstetrics
ciency of lactobacilli and bifodobacteria with opportunistic enterobacteria, staphy-

lococci, fungi, clostridia and other anaerobes. In bottle fed infants the properties of
E. coli undergo unfavorable changes.

Physiological intestinal dysbiosis that emerges in the process of microenvironment
development should be differentiated from enterocolitis which can be manifested by
malfunction of digestion and absorption in the small intestine, enhanced peristalsis and
gas formation. This leads to pathological weight loss in the newborn. There emerges a
higher risk of complications of neonatal period and early childhood: anemia, rickets,
hypotrophy. Intestinal dysbiosis does not result in disturbance of weight gain.
14.2.2.4. Treatment
To normalize intestinal microflora, eubiotics are administered. Exclusive breast-
feeding should be maintained.
Breast milk provides the best possible nutrition for a newborn

NB! with dysbiosis of the intestine.
Formula can be given on indications only, if there is no other possibility to provide

the baby with breast milk. Formulas contain prebiotics (lactulose, oligosugars) and
probiotics (bifidobacteria).
Prevention of intestinal dysbiosis is based on developing vaginal microbiocenosis
in the mother (prior to and during pregnancy), early latching of the newborn to the
breast after delivery, rooming in, exclusive breastfeeding.
14.2.3. Nutritional dyspepsia

Nutritional dyspepsia in newborns develops upon any disturbance of feeding:
overfeeding, fast transfer to bottle feeding (or change of formula), giving glucose
drink, cow’s milk formula, violation of the rules of formula preparation or storage.
In these cases the digestion of food components is disrupted.
ICD-10 codes
• P78.3 Noninfective neonatal diarrhea.
• P78.9 Perinatal digestive system disorder, unspecified.

In each case, one should establish the cause of dyspepsia.
In lower intestinal portions uncleaved food components cause osmotic and elec-
trolyte disorders, intensify intestinal peristalsis. Bacterial fermentation of uncleaved
carbohydrates leads to meteorism. The stools are fluid, foamy, with acid odor. A
coprology study detects iodophile bacteria.
Acted upon by bacteria uncleaved proteins begin to decay. Stools are foul-smelling;
abdominal distension and constipation are noted. Disorder of digestion and utiliza-
tion of fats results in formation of soaps that disrupt the absorption of fat-soluble
vitamins, magnesium and calcium. The stools show white lumps, the coprogram —
neutral fat and fatty acids.
Newborns often have combined disorders of food components digestion.
Any disorder of intestinal function calls for a coprology study for differential di-
agnosis and ruling out intestinal infection.
Culture tests of breast milk can have a certain differential diagnostic value.
14.2.3.3. Treatment
Administration of glucose and salt solutions helps rehydration (if there is dehydra-
tion) and reduction of the share of breast milk in the diet; the therapeutic solutions
are reinforced with enzymes and eubiotics; breast milk may be completely substituted
for 2–3 days.
14.3. PREMATURE INFANTS
14.3.1. Definition and classification

A premature infant is a child born until expiration of full 37 weeks
NB! of gestation.
The incidence rate of pre-term deliveries has been stable over the recent decade in
most countries; it amounts to 5–10%. The causes of premature births are discussed
in Chapter 21 Miscarriage. Premature (Pre-term) Birth.
Neonatal morbidity and mortality of preterm infants are considerably higher in
comparison with full term infants. Survival and prognosis of future development de-
pend on gestational age and body weight, timely provision of adequate care. Preterm
infants should be delivered in perinatal centers.
Gestational age of an infant is calculated using methods described in Chapter 13
Physiology of Neonate.
When speaking about preterm infants one uses the notion of post-conception age
which is determined by summing gestational and postnatal age. Determining the
post-conception age of a preterm infant is necessary for an evaluation of its develop-
ment and neurological status.
WHO recommends the following classification:
• low weight at birth 1500–2500 g;
• very low weight 1000–1500 g;
• extremely low weight under 1000 g.
Depending on their body weight at birth, premature infants are regarded as match-
ing their gestational age or small for gestational age (AGA, SGA).
Assessment of preterm infants is performed using special techniques like Ballard
score. The score uses 6 physical and neuromuscular criteria for evaluation of gesta-
tional age from 20 weeks (total score 10 points) to 40 weeks (total score 50 points)
with a 2 weeks error.
356 Obstetrics
14.3.2. Care of preterm newborns
Care of preterm newborns has its specifics. Such infants can easily develop irre-
versible changes, so ideal conditions for survival should be provided.
Preterm newborns are at increased risk of hypothermia, infection, hypoglycemia
so their care provides, apart from pharmaceutical therapy, conditions for comfortable
existence and heat preservation:
• exclude exposure to outer factors like bright light, loud sound, low temperature;
limit manipulations;
• keeping the infant in couveuse, caring for the infant using the nest or kangaroo
care method;
• ensuring adequate calories intake for each preterm infant with consideration to
its weight at birth and the amount of breast milk;
• prevention and treatment of hypoglycemia.
Thermal comfort is ensured by placing the preterm baby in a couveuse, providing
radiothermy in open cribs. The infant should obligatorily wear a cap and socks from
the first moment of life. The temperature is constantly monitored.
The contact between mother and infant should start as early as possible.
Kangaroo care (see Chapter 13). Advantages of the method:
• reducing the risk of hypothermia which is also a risk of higher neonatal morbidity
and mortality;
• reducing the risk of hospital infection;
• enhancing general psychomotor development in response to neurosensory
stimulation from mother and father.
Early beginning of breastfeeding meets energy requirements and provides an
adequate condition of the infant. If the sucking reflex is poor, alternative feeding
methods can be employed (feeding with a syringe or gastric tube). Partial breast-
feeding is administered if the newborn’s condition permits it, since only sucking
can stimulate lactation. Preterm infants have a higher metabolism rate. After birth
the infant should never go hungry; feeding is provided on demand, more often than
with full-term infants. Absence of fat pool is compensated for by early breast milk
feeding for 1–2 h after birth.
Preterm infants’ nutritional requirements can be only met by breast milk which
contains the required amounts of proteins, vitamins, lipids, minerals; it supports
the newborn’s immunity which is essential for this category of infants who are at a
higher risk of infection.
Hypoglycemia is seen in 15% of preterm infants and in 67% of infants with
IUGR. If there is hypoglycemia (glucose level in the blood below 1.65 mmol/l
or 30 mg/dl) the infant may develop convulsions, apnea, hypotonia, poor sucking
and lethargy.
Early, frequent feeding (breast or breast milk given through the

NB! gastric tube when the infant is unable to suck) can reduce the
incidence of hypoglycemia to 5%.
The infant is usually able to suck the breast after 32 weeks gestation.
Weight gain in the early neonatal period and during the first year
NB! of life can conclusively influence the development of cognition in
prematurely born infants.
Any transportation of a preterm infant (for diagnostic purposes or transfer to

a pediatric hospital) should take place with observation of temperature regimen.
Healthy infants can be discharged from the department for preterm neonates once
their body weight amounts 1700.0 g and when they are able to suck the breast. Such
infants are not vaccinated against tuberculosis. An indication of health in a preterm
infant is his harmonious development.
14.4. INTRAUTERINE INFECTIONS OF NEWBORNS
Intrauterine infections cover a wide range of diseases of the

NB! newborns caused by microorganisms getting to fetus and
contaminating it.
ICD-10 codes
• P35 Congenital viral diseases.
• P36 Bacterial sepsis of newborn.
• P37 Other congenital infections and parasitic diseases.
The true incidence rate of intrauterine infection of newborn has not been established.
The fetus is most endangered by germs which the mother

NB! first encountered during pregnancy when her primary immune
response was depressed. Recurrence of a chronic disease poses
a lesser threat.
In a pregnant woman an infection can be acute, subclinical or latent (while the

causative agent persists). Genitourinary infections of the mother are of special im-
portance for the fetus. Placental insufficiency increases the risk of infection general-
ization in any acute or chronic maternal disease. Meanwhile the infected fetus does
not always show clinical manifestations of an infection after birth.
The conditions in which the infected infant finds himself are of great
NB! importance for the development and progression of the disease.
Routes of infection spread to the fetus:
• hematogenous (chorionic plate is affected);
• ascending (amniotic fluid gets infected);
• descending (with primary parietal deciduitis), transplacental and combined.
358 Obstetrics
Risk factors for antenatal intrauterine infection include:

• chronic endometritis;
• gynecologic or obstetric disease in past history;
• complications of the present pregnancy (threatened abortion, polyhydramnios,
premature birth, premature separation of placenta, fused placenta);
• prolonged interval after rupture of membranes.
Slow fetal growth, dysembryogenetic stigmata, developmental defects, acute hy-
drocephaly, skin exanthema, jaundice, fever and neurological signs starting to prog-
ress in several days — all these are also regarded as risk factors for intrauterine
infection development.
14.4.3. Clinical features and diagnosis

Clinical features of the condition encompass disruption of the infant’s general
condition: pathologic weight loss, hyperthermia, lack of appetite, apathy or agitation
and other. Local signs indicate lesion of certain organs and systems (pneumonia,
meningitis, omphalitis, sepsis and other).
Over the first 48–72 hours of life signs like thrombopenia, anemia, elevated ESR,
leucopenia or leucocytosis, C-reactive protein give grounds to suspect intrauterine
infection; infection is verified by isolating the causative agent and serological studies
repeated over time.
Outcomes of intrauterine infection depend on the infant’s response to the effect
of the causative agent. Embryos show only the alterative component of inflamma-
tory reaction. In early fetal period it is supplemented by the proliferative component
which produces sclerosis. In late fetal period the vascular component develops as
well. Accordingly, intrauterine infection outcome may include abortion, formation
of developmental defects. Cerebral structures can become affected by intrauterine
infection at any gestational age as organogenesis still continues during the neonatal
period.
Favorable factors improving the prognosis for the infected neonate are rooming
in, breastfeeding and early discharge from the maternity hospital.
Nosocomial infection and inflammatory diseases of newborn occur after birth
upon massive invasion of the newborn by any causative agents. The infection
may come from the mother or hospital personnel which almost inevitably occurs
when the mother and infant are not rooming in. The infectious and inflamma-
tory disease may come in any form; all organs, body systems and tissues are
affected.
14.5. BIRTH INJURY
Birth trauma means injury to tissues and organs occurring spontaneously or

resulting from surgical intervention or manipulation. Birth trauma can be caused
by excessive power of muscular contractions while there are predisposing factors:
abnormalities of fetal position, large fetal weight, decreased size of birth canal and
its rigidity which can occur in oxytocia (rapid parturition), impetuous or prolonged
labor. Predisposing conditions like prolonged hypoxia, disturbance of fetal nutri-

tion and growth, intrauterine infection, prematurity increase the probability of birth
trauma even if labor proceeds physiologically.
There is a notion of obstetric trauma which can occur during obstetric maneuvers.
ICD-10 codes
• P10 Intracranial laceration and hemorrhage due to birth injury.
• P11.5 Birth injury to spine and spinal cord.
• P14 Birth injury to peripheral nervous system.
• P12.0 Cephalohematoma due to birth injury.
• P15 Other birth injuries.
14.5.2. Birth injury to nervous system

This trauma includes intracranial epidural and subdural hemorrhage, and cerebel-
lar tentorium tear with hemorrhage into the posterior cranial fossa.
Presidposing factors are
• hypoxia;
• coagulopathy;
• prematurity;
• vascular malformation;
• abnormalities of labor;
• cephalopelvic disproportion;
• cord abnormalities;
• obstetric maneuvers and surgery;
• breech presentation.

Typical clinical manifestations of intracranial hemorrhage are vegetative-visceral,
pseudobulbar and motor disorders, disturbance of thermoregulation and metabolism,
and convulsions. The infant’s condition visibly deteriorates: after a short-term lucid
interval of 3–6 hours there develops an excitation, and after that — CNS suppres-
sion, apnea attacks, change in the nature of crying, oliguria, centralized circulation,
cardiovascular failure, edematous hemorrhagic syndrome, coma.
Birth trauma of the brain proceeds in stages where we distinguish the acute period
(under 10 days), early restorative period (under 6 months) and late restorative period
that lasts as long as 2 years.
Superimposed somatic and infectious disease aggravates the course and prognosis
of intracranial hemorrhage.
14.5.2.2. Treatment
During the acute period one should provide feeding with maternal milk, care for
the newborn, treatment of cerebral edema, of hemorrhagic, convulsive, algesic and
dismetabolic syndromes.
360 Obstetrics
14.5.3. Spinal cord injury

Spinal cord injury is more common than the intracranial injury. It is precipitated
by a forceful extension of the distance between the cranial base and shoulders while
performing head traction in shoulder dystocia, as well as upon excessive rotation,
administering obstetric maneuvers, applying obstetric forceps and vacuum extractors,
delivery of aftercoming head in breech presentation
Pathogenesis of spinal cord injury:
• abnormalities of vertebral development, defects of subluxation in joints,
dislocation of vertebra, fracture of vertebral body or transverse process;
• ischemia of the vertebral circulation in the area of brainstem, cerebellum and
cervical portion of the spine;
• hemorrhage in the spinal cord and its meninges upon vascular tear or increased
vascular permeability.
14.5.3.1. Clinical presentations

Clinical presentations depend on the localization and extent of lesion. Infants
with injury to cervical vertebrae present bulbar disorders (due to proximity of stem
structures), disturbance of sucking and rooting reflex, respiratory disorder, muscular
hypotonia, pain syndrome, torticollis, short (or elongated) neck, tension of occipital
muscles.
Injury to the spinal cord at the level of CIII–CIV vertebrae is accompanied by
paresis of diaphragm with respiratory disorder and complications in the form of
protracted pneumonia.
Injury to the upper thoracic spine presents as respiratory disorder; injury to lower
thoracic spine — as flattened abdomen syndrome due to weakness of anterior ab-
dominal wall muscles.
Injury to the spinal cord in the lumboscaral region presents as flail legs: frog pos-
ture, suppressed reflexes.
Clinical methods of diagnostics are supplemented with neurosonography to rule
out cerebral lesions, determination of brainstem evoked potentials, X-ray diagnosis
(X-ray, CT scanning), MRI, myography.
14.5.3.2. Treatment
The head and neck must be immobilized with a cervical collar or annular dressing
for 14 days. The infant should be handled gently; when swaddled, his head and neck
should be supported; analgesia is administered. During the subclinical phase one
administers medications that boost CNS functions, restore neuromuscular conductiv-
ity and improve myelinization as well as physiotherapy, massage, remedial exercises.
Prognosis depends on the extent and severity of injury.
14.5.4. Birth injury to peripheral nervous system

Birth injury to peripheral nervous system includes hemorrhage in the spinal cord
and its meninges, in epidural tissue upon tear or increased permeability of vessels,
partial or complete rupture of the spinal cord (Fig. 14.2). Depending on the extent
of injury to spinal cord radices the following lesions can result:
Fig. 14.2. Duchenne-Erb palsy
• injury to upper cervical vertebrae (CI–CIV );

• (CIII–CIV ) or diaphragm paresis;
• Duchenne-Erb palsy (C V–C VI or brachial plexus);
• Dejerine-Klumpke palsy;
• Kerer paralysis (C V–TI);
• injury to thoracic vertebrae (TI–T XII);
• lumbosacral region injury.
From the point of view of clinical presentations, there is upper flaccid paresis
(hypotonia, hyporeflexia), muscle weakness in the back and cervical region, sup-
pressed reflexes.
14.5.5. Birth injury to osteoarticular system

The most common lesion is clavicular fracture. The clavicle is often fractured in
case of shoulder dystocia or during delivery in breech presentation. This injury is quite
easily diagnosed by palpation (crepitation); the condition requires no treatment. The
humerus and femur fractures are seen less often. In each case there should be func-
tional immobilization, pain relief and early administration of restorative treatment.
14.5.6. Other birth injuries

Birth injury of scalp in the form of slight bruise or lesion (occurring mostly upon
surgery or manipulation), cephalhematoma (bleeding under the periosteum) and
hemorrhage in the sternocleidomastoid muscle are seen rather often.
Hemorrhage in the sternocleidomastoid muscle presents as a swelling of pasty
consistency located in the lower third of the muscle (Fig. 14.3). The infant’s head is
inclined to the side of lesion. This lesion is differentially diagnosed from myogenic
torticollis.
Cephalohematoma is subperiosteal hemorrhage that can be extensive and bilat-
eral; it occurs in 0.4–2.5% of cases. It is localized in the area of parietal bones,
less often — in the occipital bone area. Bleeding is limited by sutures between two
362 Obstetrics
3
1
2
4
4
11
6
8 7
11 9
10
Fig. 14.3. Localization of lesion in birth injury (schema): 1 — caput succedaneum; 2 —

cephalohematoma; 3 — epidural hematoma; 4 — hemorrhage in cerebral ventricles; 5 —
leptomeningeal hemorrhage; 6 — hemorrhage into cerebellar tentorium with a tear; 7 —
hemorrhage in sternocleidomastoid muscle; 8 — fracture of VI cervical vertebra; 9 — clavicle
fracture; 10 — epiphysiolysis; 11 — intracerebral hemorrhages
bones. The blood contained in cephalohematoma may not dissolve for up to several
weeks. Systemic lesions like coagulopathy are not related to this injury. The swelling
develops several hours after birth as a rule, as subperiosteal bleeding proceeds slowly.
If cephalohematoma is of a large size, it should be opened aseptically, emptied and
a pressure dressing should be applied. If cephalohematoma is small, no treatment
is required; this should be explained to the parents to assuage their fears. Subgaleal
hemorrhage develops below epicranial aponeurosis when a lot of blood accumulates
there. If the infant is supine, the swelling may remain unnoticed while a soft mass
develops in the occipital area.
The injury develops as a result of repeated efforts to pull out the fetus using vacuum
extraction. The condition requires a conservative treatment. In rare cases there may
be profuse hemorrhage which calls for blood transfusion.
Birth injury to abdominal organs mostly results from a faulty execution of obstetric
maneuvers with a fetus in breech presentation. The commonly injured organs are the
liver, adrenals, spleen and external genitals. Clinical presentations are due to disturbed
function of the affected organ and to posthemorrhagic anemia.
Fig. 14.4. Cephalohematoma
14.6. NEWBORN ASPHYXIA. RESUSCITATION AND

INTENSIVE CARE
According to the WHO definition (1974), «Live birth refers to the complete ex-
pulsion or extraction from its mother of a product of conception, irrespective of the
duration of the pregnancy, which, after such separation, breathes or shows any other
evidence of life — e.g. beating of the heart, pulsation of the umbilical cord or definite
movement of voluntary muscles — whether or not the umbilical cord has been cut
or the placenta is attached. Each product of such a birth is considered live born.»
This means that an infant with any four signs of life should receive resuscitation.
An asphyxiated newborn does not breathe independently after birth, or respiration
is laborious, which cannot provide an adequate gas exchange in the body.
ICD-10 codes
• P21.0 Severe birth asphyxia: pulse less than 100 per minute at birth and falling
or steady, respiration absent or gasping, color poor, tone absent. Asphyxia with
1-minute Apgar score 0–3. White asphyxia.
• P21.1 Mild and moderate birth asphyxia. Normal respiration not established
within one minute, but heart rate 100 or above, some muscle tone present, some
response to stimulation. Asphyxia with 1-minute Apgar score 4–7. Blue asphyxia.
• P21.9 Birth asphyxia, unspecified.

Asphyxia of newborn can develop resulting from fetal hypoxia, obstruction of
the airway due to aspiration of meconium, amniotic fluid, mucus, blood as well as
364 Obstetrics
upon a severe CNS lesion, functional immaturity of pulmonary tissue or inadequate

surfactant production, hemodynamic disorder in the pulmonary circulation and some
developmental defects of the fetus.
In acute asphyxia the reflex and automatic reactions are aimed at intensifying the
blood flow, increasing cardiac output and changing the excitability of the respiratory
center. At the stage of decompensation of acute hypoxia the fetus develops a shock.
Birth of an asphyxiated infant can be precipitated by any abnormalities in the
maternal body that result in limited oxygen supply to the fetus through the placenta:
• preeclampsia;
• diabetes mellitus;
• Rhesus sensitization;
• maternal infection;
• bleeding in the second and third trimesters;
• preterm and post-term birth;
• multiple pregnancy;
• fetal growth restriction;
• consumption of drugs, alcohol and certain medications by the pregnant mother.
During labor, acute asphyxia can be caused by:
• placenta previa or premature detachment of normally situated placenta;
• abnormal fetal presentation;
• prolapse of cord loops during delivery;
• anesthesia;
• cesarean section;
• abnormalities of labor (protracted labor, rapid parturition, precipitate labor,
dystocia);
• fetal heartbeat arrhythmia upon birth;
• aspiration;
• intrauterine infection.
The delivery room personnel should be prepared to perform resuscitation at any time.
Effectiveness of resuscitation depends on the efficiency of the medical person-
nel and available equipment in hospital. If an asphyxiated infant is anticipated, a
neonatologist must be present in the delivery room; if there is intensive care unit in
hospital, a neonatologist expert in resuscitation must be present, too.
Delivery room evaluation of the newborn’s functional condition is done at the
first and fifth minutes of life employing the Apgar score:
• score 4–6 moderate asphyxia;
• score 1–3 severe asphyxia;
• score 0 still birth.
In this score the parameters to be evaluated are spontaneous breathing, heartbeat,
cord pulsation and voluntary muscle movement. If none of these four signs is pres-
ent, the infant is considered stillborn.
14.6.3. Clinical presentations

Clinical presentations of asphyxia include complete absence of respiration or
inadequate respiratory movements, decreased rate and strength of cardiac contrac-
tions, cyanosis or pallor of skin, reduced neuroreflex excitability and muscle tone.
There is a direct relation between the extent of clinical presentations and changes
in biochemical parameters of the blood; these correlations permit an evaluation of
asphyxia severity and its monitoring over time.
14.6.4. Treatment
Primary resuscitation method. If the condition of the fetus causes concern during
delivery (intrauterine hypoxia, immaturity, complicated labor, etc.), a neonatologist
must be present in the delivery room.
Resuscitation algorithm can be formulated as ABC resuscitation (P. Safar, 19870):
• Airway: clear the airways (Fig. 14.5);
• Breathing: provide ventilation;
• Circulation: restore or support cardiac activity and hemodynamics.
Fig. 14.5. Position of the infant while clearing airways: 1 — correct; b — incorrect (flexion);
c — incorrect (excessive extension)
366 Obstetrics
All resuscitation procedures are made in aseptic conditions, with clean hands. The
time of birth is registered, and a timer clock is turned on. The newborn is carefully
dried with a warm dry diaper, wrapped in another warmed diaper (or towel) and
placed under a source of radiant heat. If there are no contraindications, the infant
is placed on the mother’s abdomen and covered with a second diaper.
The infant’s head should be covered with a cap (the head surface accounts for
over 20% of the entire body surface; thus a cap prevents considerable convection heat
loss); socks should be put on his feet. The newborn is observed for 20 seconds, and
then a decision about primary resuscitation is taken. The infant is put on his back;
one performs mild tactile stimulation of the feet and heels.
If respiration is absent or there is infrequent inadequate respiration, artificial lung
ventilation is started. It is performed using a sack, mask or by tracheal intubation.
Chest excursion and normal heartbeat indicate effectiveness of the undertaken
procedures. At heartbeat below 100 per minute ALV continues using a mask until
heart rate becomes normal. If ALV with a mask remains ineffective for 1 minute and
cardiac depression is noted (heart rate below 60 per minute), intubation of trachea
is initiated.
Closed-chest cardiac massage is indicated if the heart rate is below 60 per minute.
Cardiac resuscitation begins with ALV only if the heart rate is 15–30 per minute.
Absence of heartbeat or bradycardia (heart rate below 60 per minute) is an in-
dication for pharmaceutical therapy if ALV and closed-chest cardiac massage failed
for 30 seconds.
Epinephrine (adrenalin) can be administered intravenously to increase the strength
and rate of cardiac activity, to relieve vascular spasm in critical conditions of newborns.
If there is a need to restore the circulating blood volume and to increase the heart
rate to 100 bpm, isotonic sodium chloride solution is administered. Medications
for blood volume restoration are usually administered with a catheter placed in the
umbilical vein.
If resuscitation procedures fail to restore the infant’s heartbeat within 10 minutes,
resuscitation is discontinued.
Resuscitation in the delivery room is merely a primary measure of emergency aid.
The infant should continue to be monitored in an intensive care unit. Successful
primary resuscitation cannot prevent hypoxia-mediated complications (convulsive
disorder) or unfavorable outcomes; to reverse the condition one administers anticon-
vulsive medications. Convulsive syndrome treatment is performed under the guidance
of electroencephalography.
Metabolic disorders are corrected using solutions of dextrose (glucose), calcium
gluconate, Cytoflavin and magnesium sulfate.
Intraventricular hemorrhage is a severe hypoxia-mediated complication. Its clini-
cal presentations are shock, acidosis, skin pallor and anemia, apnea, bradycardia,
convulsions and other neurological signs. An insignificant hemorrhage can occur
asymptomatically. About 50% of intraventricular hemorrhages develop within the
first day of life, another half — over the first 3 days. Intraventricular hemorrhage
is in most cases complicated by hydrocephaly. Infants with severe intraventricular
hemorrhage show 50% mortality; 10% of survivors develop hydrocephaly; all infants
show encephalopathy manifestations.
Timely primary resuscitation, considerate care and dynamic observation of the

infants in intensive care units are instrumental in preventing most pathological
complications.
14.7. RESPIRATORY DISTRESS SYNDROME IN NEWBORNS
RDS of newborns or respiratory distress syndrome in newborns is a manifestation

of respiratory failure due to surfactant deficiency, development of primary atelectasis,
interstitial pulmonary edema. RDS is one of the most common severe disorders of
pre-term infants; it is detected in about 25% of all newborns who die; newborns with
extremely low birth weight show this condition in 80% of cases.
ICD-10 code is P22.0 Respiratory distress syndrome of newborn. Hyaline mem-
brane disease.

The respiratory system of a pre-term infant is immature, same as the surfactant
system in the lungs. Surfactant is composed of phospholipids, neutral lipids and
proteins. Its main functions are reducing the surface strain and maintaining me-
chanical stability of the alveoli during expiration; these functions are provided for
by phospholipids. Among them, lecithin plays the key role; it accounts for 5% of all
lipids in surfactant.
Surfactant provides expansion of the alveoli (and of the lungs at large) and their
filling with air (fetal alveoli are collapsed); it is also an essential component of the
immunity.
Insufficient synthesis and / or rapid inactivation of surfactant, small size of al-
veoli, pliability of the chest, poor thoracic compliance, reduced respiratory volume
Hydrophobic proteins Alveolus

at the moment
Dipalmitoylphos- of inspiration
phatidylcholine
Inspiration Expiration
А B
Alveolus Alveolus
during during expiration,
expiration surfactant lacking
Fig. 14.6. Mechanism of surfactant action

368 Obstetrics
and compensatory hurried breathing are the factors underlying the development of
atelectasis, which is the main cause of hypoventilation and inadequate oxygenation.
In consequence, hypercapnia, hypoxia and acidosis develop leading to pulmonary
arteriole spasm and bypassing the blood through fetal communications.
14.7.3. Clinical features

RDS is characterized by clinical features of respiratory failure, radiologic abnor-
malities in the lungs. Respiration gradually becomes shallow, nasal flaring is noted,
grunting and inspiratory stridor are noted as well as sternal rigidity, cyanosis, CNS
suppression. BP drops, body temperature goes down; muscle hypotonia, cyanosis,
skin pallor, chest rigidity progress increasingly. If irreversible changes occur in the
lungs, general edema can develop and build up; oliguria is noted. Auscultation of the
lungs reveals diminished respiratory sounds and crepitant rales.
In severe RDS there are, as a rule, signs of cardiovascular failure: tachycardia and,
less often, bradycardia, a fixed rhythm that does not change under load; it indicates a
profound disturbance of cardiac regulation on the part of the CNS. Possible scenarios
include cardiac enlargement, varying degrees of cyanosis, liver enlargement, changes
in the character of heart sounds, and quite often—heart murmurs. Hypovolemia
develops quite often, which is mostly due to hypoxia-mediated lesion of vascular
endothelium, which promotes extravasation of fluid to the tissues.
Diagnosis is verified by X-ray of chest organs.
14.7.4. Treatment
Treatment of pre-term infants with RDS includes additional oxygenation and / or
forced ALV, endotracheal administration of surfactant.
14.7.4.1. Additional oxygenation

At an early stage of the disease it is recommended to administer the method of
spontaneous respiration under continuous positive airway pressure which apparently
ameliorates the infant’s condition (cyanosis subsides, the skin becomes pink).
There is a danger of toxic effect of oxygen on the eye retina and retiniopathy
development (often resulting in blindness), especially in extremely pre-term infants.
Once the parameters and partial oxygen pressure in the blood improve, the rate of
oxygen supply should be cut down.
If the infant can breathe unassisted, it receives oxygen therapy through oxygen
nasal catheter and by way of maintaining positive end-expiratory pressure (variable
flow method). This ensures an effective increase in residual lung capacity and main-
taining a stable pressure in airways facilitating both the inspiration and expiration for
the newborn. Continuous positive end-expiratory pressure is achieved through nasal
prongs in the delivery room immediately after birth.
14.7.4.2. Artificial ventilation of lungs

Progressing respiratory failure requires ALV. The newborn’s condition (the extent
of respiratory disorder) is evaluated using Downes score (Table 14.1); the infant’s
Table 14.1. Newborn respiratory distress scoring system by Downes

Sign Points
0 1 2
Respiratory rate <60 60–80 >80 or apneic
per minute episodes
Cyanosis none Cyanotic in in-room air Cyanotic in 40% O2
Retractions none Mild Severe
Grunting none Audible with Audible without
stethoscope stethoscope
Auscultation of Clear Delayed or decreased Barely audible
respiration
lab findings are also monitored repeatedly, first of all the gas composition of arterial
blood (pO2, pCO2, and other).
Based on the Downes score, RDS is classified into mild (2–3 points), moderate
(4–6 points) and severe (over 6 points).
14.7.4.3. Surfactant replacement therapy

Surfactant is administered to newborns as early as possible for preventive purposes
when there is a high risk of RDS or with therapeutic purposes when RDS diagnosis
was made. All surfactant medications are administered to infants receiving ALV only
endotracheally. Repeated administration of surfactant to infants with RDS improves
the parameters of oxygenation and ventilation, reduces the risk of pneumothorax.
Repeated administration is recommended if the infant’s condition deteriorates within
48 hours and a need to increase oxygen concentration arises.
14.8. PREVENTION OF CONGENITAL MALFORMATIONS.

NEONATAL SCREENING FOR CONGENITAL
AND HEREDITARY DISEASE
ICD-10 code
• Q01–Q99 Congenital malformations, deformations and chromosomal abnor-
malities.
Congenital malformations take the lead in perinatal, neonatal and infant morbid-
ity, mortality and disability. According to WHO, 4–6% of infants with congenital
malformations are born annually throughout the world.
The etiology of malformations in over 60% of cases is associated with multifacto-
rial causes. In 20% of infants the causes remain unspecified, in 5–6% chromosomal
abnormalities are revealed.
Pathogenetic features of congenital malformations have been studied in depth.
They are classified depending on exposure to pathogenetic factors during pregnancy:
• gametopathy—mutation in parental sex cells including hereditary mutations;
• blastopathy occurs during the fi rst 15 days from the moment of fertilization; they
are manifested as double malformations and sirenomyelia;
370 Obstetrics
• embryopathy (all types of malformations) occurs within the period of 16–75 days
of gestation;
• fetopathy (organ hypoplasia and dystopia) occurs within the period from 9 weeks
gestation to the end of pregnancy.
Congenital defects are classified into isolated (one organ involved), systemic and
multiple; minor malformations do not affect the infant’s vital functions nor restrict
his activity.
In international systems of genetic monitoring congenital malformations are reg-
istered under nosological entity and ICD code.
Medical genetics is of primary importance in promoting the health

NB! of generations to come.
Prevention. Administration of folic acid during the period preceding conception

and in the first months of pregnancy reduces the rate of congenital malformations
(of neural tube defects mostly).
Prenatal diagnosis of congenital malformations in the fetus consists in ultrasound
examination repeated 3 times. To verify the diagnosis (especially in the presence of
hereditary disease) accessory methods are employed to determine fetal karyotype:
amniocentesis, cordocentesis, chorionic biopsy. Sometimes biochemical study of
amniotic fluid or fetal blood is undertaken.
Neonatal screening is performed in the maternity hospital: massive examination
of newborns to detect congenital and hereditary disease.
Neonatal screening service is a multilevel structure. In maternity hospitals (or at
pediatric clinics in case of early discharge from hospital) blood samples are taken
from all newborns. Specialized filter paper is soaked with the blood sample and sent
to genetic laboratory to study for disease markers. If the sample screens positive, the
pediatric service provides accessory investigations to confirm or rule out the diagnosis.
Newborns are screened for 8–12 conditions. In Russia screening is done for con-
genital hypothyroidism, phenylketonuria, adrenogenital syndrome, galactosemia and
cystic fibrosis.
Diseases detected by neonatal screening have a severe course; if there was no early
detection or adequate treatment, profound irreversible changes develop, and the
outcome is quite often fatality or mental deficiency. Early diagnostics and correction
of detected disorders over lifetime make it possible to avoid unfavorable outcomes.
REMEMBER!
IUGR is a diagnosis made after birth; prior to birth the diagnosis is slow fetal
development: low body weight and length compared to normal values for the
infant’s gestational age.
Functional disorders of the GI tract present with vomiting and regurgitation; they
are due to slowed-down evacuation of food from the stomach, disrupted peristalsis
in the stomach and intestine resulting from insufficient maturity of motor regulation.
Latching the newborn to the maternal breast within the first 20–30 minutes
after delivery is a crucial episode in physiological development of the
infant’s microenvironment: local and systemic immunity and gastrointestinal
microbiocenosis.
Weight gain of infant during the first year of life is a sound indicator of its well-being.
Conditions in which an infected neonate lives after delivery can prevent development
of a disease due to bacterial contamination and determine his health status for the
entire life.
Birth injury results from exposure to mechanical effects of obstetric forces; the
continuity of tissues and organs of the fetus is disrupted during delivery.
Asphyxia of newborn is inability to breathe unassisted or respiratory failure in the

newborn; it interferes with adequate gas exchange in the body.
ABC resuscitation of neonates:

• Airway: clear the airways (Fig. 14.5);
• Breathing: provide ventilation;
• Circulation: restore or support cardiac activity and hemodynamics.
RDS of newborn develops when there is primary atelectasis, interstitial edema

of lungs while surfactant is deficient. RDS is one of the most common and severe
conditions occurring in neonatal period in pre-term infants.
Neonatal screening means examination of all newborns to detect hereditary or

congenital disease: congenital hypothyroidism, phenylketonuria, adrenogenital
syndrome, galactosemia and cystic fibrosis and others.
CONTROL QUESTION
1. What is IUGR of neonates?

2. What precipitates regurgitation?
3. What bilirubin levels in an infant require therapy?
4. What is intrauterine infection?
5. What are the criteria of pre-term fetus?
6. What is immaturity of newborn?
CHECK YOURSELF!
Level 1. Test
1. IUGR is:
a) small length while body weight is large;
b) body weight and length are below normal gestational values;
c) same as pre-term;
d) occurs only in pre-term infants.
372 Obstetrics
2. Causes of peripheral birth injury:

a) incorrect behavior of parturient woman;
b) fetal immaturity;
c) vertical delivery;
d) faulty actions of obstetrician.
3. Regurgitation is a sign:
a) of infectious disease of the newborn;
b) of incorrect feeding of the newborn;
c) typical of pre-term infants;
d) that can occur in any newborn.
4. What weight loss is regarded pathological?

a) above 3% of weight at birth;
b) above 5% of weight at birth;
c) above 8% of weight at birth;
d) above 10% of weight at birth.
5. Downes score is used to determine:

a) muscle tone and reflexes;
b) immaturity;
c) respiratory disorders;
d) cardiac arrhythmia.
6. Neonatal screening is performed to detect:

a) congenital syphilis;
b) congenital nervous system defects;
c) hypothyroidism and phenylketonuria;
d) blood group and Rhesus factor.

1. A full-term newborn has body weight 2600 g and length 50 cm. What is your
diagnosis?
2. A full-term neonate was born with body weight 3600 g and length 52 cm. On
the 4th day the neonate’s body weight is 3200 g. What is your diagnosis?
NOTES
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• Chapter 15
HEMOLYTIC DISEASE OF FETUS
AND NEWBORN
Incompatibility of mother and fetus with respect to many antigens is a constant
feature of pregnancy as the fetus becomes a homeotransplant in relation to the ma-
ternal body having inherited 50% of its genes from the father. Nature has foreseen
many mechanisms that prevent this incompatibility from fulfilling itself. Nevertheless,
clinical practice has seen cases when the defense mechanism fails to work (early
toxicosis, antiphospholipid syndrome, hemolytic disease of newborn, and other).
15.1. DEFINITION
Allo- or isoimmunization is production of antibodies by the immune system in re-

sponse to foreign protein antigens of another (Lat. Allos — other, foreign) individual
of the same (Lat. Isos — same) species. This commonly occurs in the recipient’s
body in response to other person’s erythrocytes entering his blood carrying on their
surface antigens that the recipient does not have. This can occur in case of
• transfusion of whole blood or erythromass;
• sharing one syringe by two drug addicts;
• pregnancy.
A certain amount of fetal erythrocytes commonly enter maternal blood during
the third stage of labor when the placental barrier has been disturbed (detachment
of placenta), and fetal erythrocytes pass to maternal circulation through gaping ves-
sels in the placental bed, that is, feto-maternal transfusion actually happens. It was
established that the rate and extent of bleeding grows with gestational age. The rate
of feta-maternal transfusion amounts to 7, 16 and 29% in the first, second and third
trimesters, correspondingly.
15.2. EPIDEMIOLOGY
15.2.1. Prevalence (U.S. data)
Until modern approaches were adopted, 1% of all pregnant women developed Rh-
alloimmunization. As a consequence of routine anti-Rh-prevention the incidence rate
of Rh-sensitization dropped from 45 cases per 10 000 deliveries (4.5%) to 10.2 cases
per 10 000 deliveries (1%).
However, nowadays anti-D-Rh-antibodies remain the most common antibodies
detected during pregnancy.
AB0 incompatibility is often noted during the first pregnancy; it is seen in 12%
of all pregnancies. The rate of detection of immune antibodies amounts to 3% of
374 Obstetrics
all live births. Clinically significant hemolysis in AB0-incompatibility is noted in less

than 1% of all deliveries.
15.2.2. Morbidity and mortality

We know almost 50 various red cell surface antigens capable of causing hemolytic
disease of fetus and newborn (HDN, HDF). However, only three types of antigens
are detected in fetal lesions of severe degree: anti-RhD, anti-RhC and anti-Kell
antibodies. Approximately 50% of affected infants require no therapy as they dem-
onstrate merely insignificant anemia and hyperbilirubinemia after birth. They survive
and develop within normal. Approximately 25% of full-term infants who receive no
treatment develop pronounced icterus; in 90% of cases they die or become disabled
(10%) due to development of kernicterus. In the other 25% of affected infants the
condition aggravates to the extent of hydrops even before delivery. A half of these
fetuses become affected as early as before 34 weeks gestation.
On the whole, before the advent of modern invasive treatment methods perinatal
mortality amounted to 50%. On account of exchange blood transfusion employed
by Wallerstein in 1945 perinatal mortality dropped to 25%. Later Chown proposed
termination of pregnancy prior to 34 weeks followed by immediate exchange blood
transfusion when there was a severe form of incompatibility without hydrops. This
also improved survival rates. Further decrease in neonatal morbidity and perinatal
mortality (to 16%) was achieved thanks to intraperitoneal transfusion method developed
by William Liley in 1963, and intravascular transfusion first used by Rodeck in 1981.
If there is hydrops in any form, the mortality rate increases to 30%. Most fetuses
in whom hydrops development was prevented using intravascular transfusion, survive.
25% with pronounced hydrops die despite administration of intravascular transfusion.
The incidence rate of psychomotor development disorder amounts to 10%, which is
consistent with general population values.
15.2.3. Racial features

Incompatibility with respect to Rh-antigen system (anti-D or anti-C) is noted in
10–15% of observations approximately. This situation is seen much less often in Asia,
especially in Southeastern Asia.
15.2.4. Gender differences

Sexual identity of the fetus affects the power of response to maternal antibodies.
In case of incompatibility, male Rh(D+) fetuses develop hydrops 13 times more
often than girls.
15.3. HISTORICAL REVIEW

The history of Rh incompatibility is a striking illustration of progress in our
understanding of this condition from defining it for the first time to treatment and
prevention over just several decades. Milestones on this way are described below.
Chapter 15. Hemolytic disease of fetus and newborn 375
• 1932 Diamond, Blackfan, Batty reported that fetal hydrops, severe jaundice and
unicteric anemia of newborns were manifestations of the same pathological
condition. According to these authors, there were no cases of fetomaternal AB0
blood group incompatibility among the patients observed by them.
• 1938 Darrow et al supposed that erythroblastosis of newborn had underlying
immunologic causes.
• 1939 Levine and Stetson discovered atypical agglutinin in the blood of a woman
who had just given birth to a still born macerated fetus and later showed an
intractable response to transfusion of supposedly compatible blood. The authors
supposed that the mother had been sensitized by fetal antigens inherited from the
father and absent in the mother.
• 1940 Landsteiner and Wiener discovered Rh antigen localized on red cell
membrane thus opening the way to investigating Rh incompatibility.
• 1941 Levine et al established that HDN results from breakdown of fetal RBCs
effected by Rh antibodies.
• 1943 Levine pointed out that the probability of immunization of a woman with
Rh(-) blood is lower if she carries a fetus which is AB0 incompatible with her.
• 1944 Fisher and Race made an assumption that Rh antigen inheriting is
determined by a series of allelomorphic genes closely set on one chromosome
where genes D and d, C and c, E and e are in mutually exclusive relations.
• 1948 Mollison et al proposed exchange blood transfusion for treatment of HDN.
• 1956 Bevis employed spectrophotometry and established a clear
association between pronounced pigmentation of amniotic f luid and fetal
erythroblastosis.
• 1957 Kleihauer, Braun, Betke suggested a laboratory method to assess feto-
maternal hemorrhage.
• 1961–1964 Clark, Woodrow, Finn in Liverpool and Gorman, Freda, Pollack
in New York City independently discovered the preventive effect of IgG class
of human anti-RhD-immunoglobulin. An English geneticist Clark took into
account the observation made by Levine in 1943 that AB0 incompatibility
between mother and fetus provides certain protection against production of Rh
antibodies in the mother.
• In 1962–1963 fi ndings from studying gene interaction in mimetic butterfl ies
suggested to Clark that similar anti-D antibodies can also simulate a protective
AB0 effect upon administration to Rh-negative mother. At the same time
Freda and Gorman in New York studied antibody-mediated immunity
suppression—a phenomenon described by Smith in 1909; later they used this
method of administering anti-D gamma globulin to women for prevention of
Rh-immunization.
• 1963 Liley was the fi rst to administer intrauterine intraperitoneal transfusion of
donor blood to fetus as treatment of HDN.
• 1964 Liley suggested estimating the extent of fetal hemolysis by the change in the
height of optical density peak at wavelength 450 nm using spectrophotometry of
amniotic fluid.
• 1967 WHO expert committee stated on the grounds of extensive convincing
evidence, that passive administration of anti-D IgG within 72 hours after delivery
376 Obstetrics
prevents isoimmunization of Rh(D)-negative mother thus acting as prophylaxis

of HDN and hemolytic disease of fetus in subsequent pregnancy.
• Zipursky, Israels established that in feto-maternal hemorrhage to the extent less
than 0.1 ml the probability of isoimmunization is only 3%, whereas if more than
0.1 ml of blood entered maternal circulation, the risk increases to 14%.
• 1970 Woodrow established that almost 50% of women either during pregnancy or
immediately after childbirth showed signs of transplacental bleeding, and in a half
of cases the amount of fetal blood entering the maternal body is under 0.1 ml.
• 1971 Liedholm demonstrated that isoimmunization is also possible after ectopic
pregnancy as well.
• 1972 Asztalos established that the risk of isoimmunization after a therapeutic
abortion decreases if the gestational sac was extracted by vacuum aspiration
rather than by curettage.
• 1973 Mollison demonstrated that in pregnant women isoimmunization mostly
develops at a late gestational age and the process requires at least a month.
• 1978 Queenan described a syndrome when the fetus has a severe form of HDF
with pronounced hydrops, the mother shows a rapid weight gain, and she
develops edema, proteinunria and hypertonic disease. Protein concentration in
the blood serum decreases critically. Maternal syndrome, or mirror syndrome,
augurs ill for the fetus as it usually precedes its death.
• 1983 Daffos et al were the first to withdraw fetal blood using ultrasound-guided
umbilical vessel puncture (cordocentesis). This laid foundation for intravascular
intrauterine hemotransfusion for fetuses with HDF.
• 1989 A.V. Mikhailov et al was the fi rst in the USSR to perform intrauterine
hemotransfusion to fetus with edematous HDF.
• 1995 Mari et al proposed a noninvasive method to assess the extent of anemia in
fetus using middle cerebral peak systolic velocity.
• 1998 ACOG recommends routine antenatal prophylaxis at 28 weeks gestation,
apart from postnatal prophylaxis.
15.4. ISOIMMUNIZATION
Two conditions are needed for HDF to develop:

• previous alloimmunization (isoimmunization) to the same antigen that is found in
the fetus during the present pregnancy but which was not found in the mother
during previous pregnancy; thus she does not have it this time;
• antibodies produced as a result of alloimmunization should be in IgG class as
only they, due to their small molecular weight, are capable of penetrating through
the placental barrier to the fetus.
Alloantibodies to RBC antigens are found in 3–5% of all examined pregnant
women. Sensitization of pregnant women by RBC antigens of the Rh blood group
system presents the greatest interest as 95% of all clinically significant cases of HDF
are due to Rh-incompatibility.
Rhesus factor (the name was taken from Macacus rhesus monkeys) is a system
of human red cell antigens, independent of factors determining blood groups
(AB0 system) or other genetic markers. There are six major Rh antigens. Two
nomenclatures are in current use to designate this antigen system: Wiener nomen-
clature and Fisher-Race nomenclature. According to the first system, Rh antigens
are shown as Rho, rh′, rh′′, Hro, hr′, hr′′; according to the second one — letter
designations are used: D, C, E, d, c, e. Quite often both nomenclatures are
used simultaneously showing the symbols of one system in parentheses: Rho(D)
(Table 15.1).
Table 15.1. Matching Wiener and Fisher-Race nomenclature
Nomenclature Antigens
Wiener Rho rh′ rh′′ Hro hr′ hr′′
Fisher-Race D C E d c e
Synthesis of Rh antigens is controlled by p arm genes on the first pair of chro-

mosomes. The presence of Rh factor on red cell membrane is coded by six genes
linked in threes on one chromosome. Gene pairs are allelic if their genes control
D-d, C-c, and E-e antigens, that is, each individual has six genes controlling Rh
synthesis. However, a fewer number of genes can be found in the phenotype (5, 4,
3) which depends on the number of homozygous loci in the individual.
Rho(D) antigen is the major one in the Rh family; it has the greatest practical
importance. It is found on red blood cells of 85% of people residing in Europe.
Rh-positive blood type is distinguished on the basis of Rho(D) antigen present on
red blood cells. The blood of people whose RBC lack this antigen is classified as
Rh-negative.
A person is considered Rh-positive if his red blood cell membrane

NB! carries Rho(D) antigen.
Rho(D) antigen is not uniformly predominant in people of different races. In

Eurasia, in the direction from west to east its predominance declines consider-
ably. The incidence rate of persons with Rh(-) blood type is 15% among the
European population (34% among Basques), among negroid population — 7%,
and in Indochina it is below 0.5%. An overwhelming number of Asians are Rho(D)
antigen carriers, so among pregnant Asians immunologic Rh incompatibility is seen
much less often than in pregnant Europeans. The gene of Hro(D) antigen is allelic
to Rho(D) antigen. There is no evidence of existence of Hro(d) antigen as no cor-
responding serum was obtained.
15.5. FETAL HEMOLYTIC DISEASE
Fetal hemolytic disease is a condition caused by hemolysis of

NB! RBCs accompanied by anemia and increased numbers of blast-
type RBCs circulating in the blood.
378 Obstetrics
15.5.1. Etiology
The probability of Rh(-) woman getting pregnant by Rh(+) male is 85%, and the
probability of birth of Rh(+) fetus is about 60%. When fetal blood enters maternal
circulation, which usually occurs during the third stage of labor, alloimmunization
may take place. Immune response develops in the form of emergence of correspond-
ing lymphocyte clones producing antibodies. This immunization persists for life.
In 50% of births the volume of feto-maternal bleeding does not exceed 0.1 ml
(and so it cannot be detected by Kleinhauer’s test), and in only 2% of cases it is
more than 10 ml. The likelihood of a greater amount of fetal blood entering mater-
nal circulation increases in operative interventions (manual separation of placenta,
cesarean section and other).
Kleinhauer-Betke test is a microscopic study of maternal blood smear to count
the number of fetal RBCs in it. The underlying phenomenon is that fetal RBCs are
more resistant to acid medium, so processing of the smear with an acid reagent causes
maternal RBCs to break down, in contrast to fetal RBCs. Further calculation is easy.
For instance, detection of 80 RBCs per visual field at 50 x magnification indicates
a volume of bleeding of 4 ml (Fig. 15.1).
Kleinhauer-Betke test is the most widely used analysis; however, its sensitivity and
reproducibility are low.
Flow cytometry shows more precision and less subjectivity. Nevertheless, most
laboratories continue using Kleinhauer-Betke test as flow cytometry is not widely
available.
In feto-maternal hemorrhage to the extent less than 0.1 ml the probability of
immunization is less than 3%, at 0.1–0.25 ml the probability increases to 9.4%; at
0.25–0.3 ml it amounts to 20%; at hemorrhage of more than 3 ml the probability
is 50%. An average probability of Rh sensitization (without prophylaxis) is 16% if
the mother and fetus are AB0 system compatible, and 2% if they are incompatible.
Sensitization becomes manifest 3–6 months after delivery in only half of all those
sensitized. In other sensitized women the antibodies reach the detectable threshold
Pink fetal RBC
Shadow
of maternal RBC
а b
Fig. 15.1. Kleinhauer-Betke test: microscopic preparation (a), scheme (b)
only when the next pregnancy occurs. No more than 0.03 ml of Rh(+) fetal RBCs
entering the maternal circulation are capable of triggering an immune response in
a second pregnancy.
About 30% of all Rh-negative individuals fail to respond by

NB! antibody production even after repeated massive transfusion of
incompatible blood; they are referred to as non-respondents.
15.5.2. Pathological anatomy and pathogenesis

A consecutive pregnancy with Rh(+) fetus induces an increased antibody produc-
tion, or anamnestic reaction, in a previously sensitized woman: growth of titer of
antibodies detectable by indirect Coombs’ test. IgG class antibodies pass through
the placental barrier into fetal circulation due to their low molecular weight and
cause hemolysis of fetal red cells, which, in its turn, causes anemia and hyperbili-
rubinemia. Hyperbilirubinemia does not produce a significant effect on fetal condi-
tion as maternal liver takes on the function of neutralizing the produced bilirubin.
Hyperbilirubinemia becomes a pressing issue only after delivery, which is not the case
with anemia. Anemia affects the fetus through tissue hypoxia and cardiac failure with
a probable outcome of hydrops, ascites, hydrothorax, hepatomegaly, erythroblastosis.
Anemia is the major cause of fetal distress. Icterus does not cause
NB! distress as the produced bilirubin is neutralized by the mother’s
body. Once the baby is born, he loses this protection, so the
newborn suffers from both anemia and icterus.
Postmortem examination of infants who died of HDN and HDF shows charac-
teristic hydrops with abdominal distension and pronounced subcutaneous edema
(Buddha syndrome), ascites, excessively enlarged liver and spleen; their inferior
poles can reach the iliac bone crest. Both organs show pronounced extramedullary
erythropoiesis, a great number of erythroblasts. There is always pronounced anemia
with immature RBC predominance (erythroblastosis). Heart chambers are usually
distended, myocardium is hypertrophied. Erythropoiesis foci can be noted along
coronary heart vessels. Hydrothorax is often noted. Pulmonary congestion and a
large number of erythroblasts are seen in the lungs, in the kidneys—pronounced
erythropoiesis. Polycythemia is noted in bone marrow.
The fetus develops ascites due to hypertension in the portal and umbilical veins
caused by enlargement and anatomical changes in the liver. Due to erythropoiesis,
fetal hypoproteinemia develops at the same time in hepatic tissue as a result of hepatic
failure and inability of congested placenta to provide an adequate transportation of
amino acids and peptides. In its turn, this leads to progressive ascites followed by
generalized edema.
When cordocentesis method was developed, it became possible to throw light on
certain features of hydrops development. In fact, affected fetuses often show hy-
poproteinemia and hypoalbuminemia; in fetuses with hydrops this is an inevitable
finding as hypoproteinemia plays the key role in the origin of fetal hydrops. It was
380 Obstetrics
revealed that hydrops development is restrained as long as fetal hemoglobin persists

above 40 g/l. Mean hematocrit in hydrops is 10.2.
The characteristic appearance of placenta includes pronounced edema, enlarge-
ment, its weight often measures 50% of fetal body weight. The placenta and mem-
branes are to a greater or lesser extent colored yellow due to bilious pigments excreted
by fetal kidneys. Chorionic villi show edema, stromal hyperplasia, and increased
amount of capillaries.
When fetal hydrops is detected one can suppose HDF due to Rh-isoimmunization
or some other causes. When antibodies to red cell antigens are absent, the condition
is termed nonimmune hydrops fetalis. Its incidence rate is 1 per 2500–3500 deliver-
ies. In 25% fetuses nonimmune hydrops is caused by chromosomal abnormalities,
in 18% — by multiple malformations (cardiac malformation mostly). Cardiac ar-
rhythmia of fetus (supraventricular arrhythmia, for instance) can also be a cause of
nonimmune hydrops.
The gravity of HDN and HDF increases in consecutive pregnancies, as a rule.
Presentations of hemolysis and fetal hydrops develop at the same gestational age
as in previous pregnancy or earlier. In modern conditions the survival of newborns
and fetuses is over 80% due to adoption of up-to-date transfusion technologies and
intensive management of newborns.
Maternal morbidity and mortality are no different from general population, al-
though some authors describe the so-called mirror syndrome in which the mother
develops a complex of symptoms roughly similar to preeclampsia, while «intrauterine
disaster» keeps progressing.
15.5.3. Diagnostics
History taking. When taking history one should note stillbirths in combination with
fetal hydrops or live births with hydrops signs in past history. These findings call for
adequate immunology investigations during the present pregnancy.
Examination. When doing a physical examination one can only note the discrep-
ancy between symphysio-fundal height and gestational age due to possible polyhy-
dramnios.
Serum study. Blood grouping and screening for antibodies (indirect Coombs’ test)
that can cause HDF should be done as early as at the booking visit. Then the hus-
band’s (father’s) blood group and Rh factor are determined as well as his genotype
(hetero-, homozygous). If this study is unfeasible, one should suppose the infant’s
father to be Rh(+) homozygous, thus the fetus is assumed to be Rh(+).
Amniocentesis, spectrophotometry. Investigation of amniotic fluid promotes a
deeper understanding of the fetal lesion. Bilirubin, waste product of fetal RBCs, is
excreted by fetal kidneys and lungs; it passes to the amniotic medium and impreg-
nates fetal membranes.
In 1961 Liley pointed out that there is a high grade of correlation between bilirubin
concentration in amniotic fluid and the outcome for the fetus. Fluid obtained by am-
niocentesis is studied with spectrophotometry by analyzing changes of optical density
at wavelength 450 nm and matching the findings against normal values. Liley’s chart
is quite informative when the test is done at 26 weeks gestation (Fig. 15.2) and later.
1.0
0.8
0.6
Optic density of amniotic fluid
0.4
Zone 3
0.3
0.2
0.1
0.08 Zone 2
0.06
0.04
0.03
0.02 Zone 1
0.01
24 26 28 30 32 34 36 38 40
Fig. 15.2. Modified Liley’s chart (ACOG Technical Bulletin No. 90. — January 1986 // Am.
J. Obstet. Gynecol. — St.Louis: Mosby)
When a decision is to be made about pre-term termination of pregnancy due to

progressing HDF signs, the fluid obtained by amniocentesis can be also studied to
determine the degree of fetal lung maturity: lecithin-sphingomyelin ratio (L-S ratio),
phosphatidylglycerol concentration, foam test and others.
Maternal serum antibodies titer+ultrasound. When the titer is <1:16 in a woman
isoimmunized during the present pregnancy, the risk of HDF is not high. In con-
secutive pregnancies and with this titer the risk of HDF increases. After 16–18 weeks
gestation one checks every 2–4 weeks for a possible increase in antibody titer. The
serum remaining from the previous test should be kept as a control, which increases
the test accuracy. Amniocentesis makes a repeat testing for antibody titer redundant.
Ultrasound permits an accurate diagnosis of the extent of fetal lesion in pro-
nounced forms of HDF. In mild or moderate degrees of HDF no typical ultrasound
signs are detected.
In pregnant women with a low antibody titer (1:4; 1:8) a repeat ultrasound ex-
amination usually suffices to confirm a satisfactory fetal condition (the likelihood of
hydrops or polyhydramnios development is not strong).
In pregnant women sensitized during previous pregnancy and with a higher anti-
body titer the fetal condition is monitored by combining ultrasound with amniotic
fluid spectrophotometry. In a moderate or grave HDF the fetus can show polyhy-
382 Obstetrics
dramnios, hydropericardium, cardiomegaly. In grave HDF ultrasound is done over

time to monitor the changes in fetal condition, progressing or subsiding of HDF
signs.
Ultrasound markers of HDF. These markers include:
• placenta thickening by more than 50 mm in moderate or grave HDF; placental
structure is homogeneous;
• in mild or moderate HDF polyhydramnios (amniotic fluid index >24) is
not common; a combination of hydrops and polyhydramnios indicates an
unfavorable prognosis;
• hydropericardium is one of earliest signs of HDF;
• enlarged heart size is accompanied by progressing cardiac failure in grave HDF;
when the heart diameter to chest diameter ratio exceeds 0.5, cardiomegaly
diagnosis is justifiable;
• detection of ascites indicates a pronounced degree of HDF;
• hepatosplenomegaly due to intensified extramedullary erythropoiesis;
• edema of subcutaneous fat, especially marked on fetal head.
It was proposed in recent years to use Doppler estimation of middle cerebral
velocity in the fetus (increase in maximum velocity indicates anemia) (Fig. 15.3).
Cordocentesis. Still more precise information about fetal condition can be pro-
vided by immediate study of fetal blood obtained by cordocentesis. In particular,
this allows Rh blood grouping of the fetus (if the fetus turns out Rh-negative, no
further complex investigation is required), assessment of hemoglobin, hematocrit,
reticulocytosis, amount of bilirubin and serum protein in the fetal blood — that is,
the main diagnostic criteria of the degree of hemolysis.
Specifics of managing pregnancy with HDF. A pregnant woman without compli-
cations in obstetric history and with antibody titer > 1:16 detected before 26 weeks
gestation requires amniocentesis followed by spectrophotometry.
• If ΔOD 450 coincides with Liley’s zone 1, this indicates Rh-negativity or mild
HDF.
80
CMA, peak velocity, cm/sec
В 1.5МОМ
70
А 1.29МОМ
60
50 Median
40
30
20
20 25 30 35
А – mild anemia; В – moderate and severe anemia

Fig. 15.3. Middle cerebral peak systolic velocity depending on gestational age (Moise Jr.
Management of Rhesus Alloimmunization // Obstet. Gynecol. — 2002)
• ΔOD 450 estimate coinciding with the middle of Liley’s zone 2 indicates a
probability of moderate or grave HDF. Pre-term termination of pregnancy is
usually indicated in this situation.
• ΔOD 450 estimate coinciding with Liley’s zone 3 or ultrasound fi ndings of
hydrops require urgent delivery or intrauterine hemotransfusion to the fetus.
Management depends on gestational age, fetal condition and the possibilities of
neonatal care in the given institution.
If the patient has obstetric complications in past history, or her antibody titer
is more than 1:16 at a gestational age below 26 weeks, ultrasound examination is
required. Further management is decided upon with a perinatologist or by calling a
case conference. If a grave fetal condition is detected, it is indicated to administer
cordocentesis to determine hematocrit and perform rhesus-genotyping, especially if
the father is heterozygous for this antigen.
• If anemia is revealed, intravascular in utero hemotransfusion can be administered
simultaneously with primary cordocentesis.
• If no anemia is revealed, further management will be determined by obstetric
history and ultrasound fi ndings.
If pronounced anemia is noted in the second and third trimesters, intrauterine
hemotransfusion is indicated. Transfusion may be called for as early as at 18 weeks
gestation. Intravascular intrauterine transfusion considerably improves survival rates
in severely affected fetuses, increasing them to 86%.
Before the only two effective treatment options for HDF (intravascular intrauterine
transfusion and pre-term termination of pregnancy) had been introduced, a number
of other treatment strategies were proposed, which showed little or no effectiveness
at all. The objective of most was reducing the number of antibodies circulating in
maternal blood: plasmapheresis, hemosorption, husband’s skin grafting, so-called
nonspecific desensitizing therapy, etc. They should not be administered!
Two major interventions at fetal hemolytic disease are intrauterine

NB! transfusion to the fetus and pretrm delivery.
15.6. HEMOLYTIC DISEASE OF NEWBORN
Management of the newborn with HDN depends on multiple factors.
Classification of HDN requires the following to be determined:
• type of incompatibility (Rh, AB0, other red cell antigens);
• clinical variety of the disease (edematous, icteric, anemic);
• extent of severity in icteric and anemic HDN (mild, moderate or severe);
• complications:
– bilirubin encephalopathy: kernicterus, other neurologic disorders;
– hemorrhage or edema syndrome;
– involvement of liver, heart, kidneys, adrenal glands;
384 Obstetrics
– bile inspissations syndrome;

– metabolic disorders: hypoglycemia and others;
• accompanying disease and underlying conditions (pre-term fetus, intrauterine
infection, asphyxia, etc.).
The division of HDN into clinical varieties (edematous, icteric,

NB! anemic) is conventional. In fact, a child with HDN is always anemic
with anemia as the primary factor. Later, due to massive lysis of
RBCs, bilirubinemia begins to surge after delivery.
Evaluation of HDN severity is shown in Table 15.2.
Table 15.2. Criteria of severity of hemolytic disease of newborn
Main clinical Degree of severity, points

presentations 1 2 3
Anemia (Hb, g/l) >150 149–100 <100
Icterus <85.6 85.6–136.8 >136.8
(bilirubinemia,
mcmol/l)
Edema syndrome Pasty appearance of Pasty appearance Anasarca
subcutaneous tissue and ascites
1–3 points: mild disease; 4–6 points: moderate disease; 7–9 points: severe disease.
15.6.2. Diagnostics
When HDN is suspected, the plan of examinations includes:
• blood grouping and Rh phenotyping in the mother and child;
• analysis of the infant’s peripheral blood with reticulocyte count;
• determining bilirubin concentration in the infant’s blood serum over time;
• immunology studies (determining antibody titer with direct Coombs’ test).
When assessing the hemoglobin level one should remember that upon birth a
healthy full-term infant shows relative polycythemia with hemoglobin 170±20 g/l.
This is associated with specifics of intrauterine circulation, but unnecessary for extra-
uterine existence. Bone marrow function diminishes and the number of reticulocytes
goes down, on the feedback principle. As RBCs break down in the process of their
natural senescence (30–40), hemoglobin content at 8–10 weeks of life normally
amounts to 120 g/l. In pre-term infants this decrease in hemoglobin content is
more pronounced and occurs earlier. At low hemoglobin levels intensified reticu-
locytosis develops, which usually results in normal hemoglobin content restoration.
Hemoglobin levels requiring anemia treatment depend on the newborn’s age. At
the first week of life it is desirable that hemoglobin should not exceed 130 g/l. After
that a decrease by 1 g per week to 80g/l is quite acceptable. At hemoglobin below
70–80 g/l one considers the issue of hemotransfusion depending on the infant’s
clinical condition.
Immediately after birth a healthy term infant shows relative

NB! polycytemia with Hb of 170±20 g/l. In hemolytic disease of
newborn the Hb value may be 130 g/l and less, as early as on
the first day.
In infants with HDN hemoglobin can be 130 g/l and less in the first day of life,
so one should not wait for hemoglobin to drop to 80 g/l but initiate adequate treat-
ment much earlier (see Table 15.2).
The content of bilirubin in healthy newborn’s blood serum is almost the same as
in the mother. By day 4 it increases to 140 mcmol/l, by day 10 it gradually decreases
reaching 25 mcmol/l. The increase of bilirubin followed by its reduction is manifested
as physiological jaundice. There is a method of clinical assessment for jaundice by
Kramer’s rule (Fig. 15.4).
Icterus becomes discernible at bilirubin levels exceeding 140

NB! mcmol/l. In a healthy term baby an increase in bilirubin content in
the blood serum exceeding 205 mcmol/l during the first 48 hours
of life is considered a critical condition.
At unconjugated bilirubin level 428–496 mcmol/l 30% of full-term infants develop

kernicterus; at 518–684 mcmol/l, 70% of infants develop kernicterus.
As suggested by G. Schmorl (1904), the term kernicterus is applied to bilirubin-
induced encephalopathy, a condition in which unconjugated bilirubin effects a lesion
of basal nuclei. Post-mortem of such infants shows bright orange coloration of basal
ganglions (Fig. 15.5).
100
Icterus is restricted
to the neck – 100 mcMol/L
150 Icterus reaches the navel

and involves the upper third
of shoulder – 150 mcMol/L
250 250
Icterus involves the area from
the navel to the knees – 200 mcMol/L
200
Icterus involves arms and legs
>270 >270
to the wrist and ankle – 250 mcMol/L
250 250 Icterus affects the area

from the crown to the finger- and toetips –
>270 >270 over 250 mcMol/L
Fig. 15.4. Kramer’s rule of visual assessment for jaundice (Kramer, 1969)
386 Obstetrics
Fig. 15.5. Coloration of subcortical nuclei in kernicterus. Macropreparation
Even in pronounced Rh-incompatibility the fetus is born with normal or somewhat

elevated blood bilirubin levels. However, infants with HDN can show such a rapid
progressing of bilirubinemia that the correct way is to monitor its hourly increase
rather than check for bilirubin levels daily. On the basis of hourly findings of bilirubin
level increase, one can initiate treatment even when the absolute levels are not yet
critical, which can be seen on a chart proposed by K. Polacek (Fig. 15.6).
410.4 24
EBT is needed ABO
376.2 22
342.0 20
Rh
307.8 18
Bilirubin, mcMol/L
273.6 16
Bilirubin, mg/%
239.4 14
Сases requiring observation
205.2 12
171.0 10
136.8 8
EBT not indicated
102.6 6
68.4 4
34.2 2
0 24 48 72 96 120 144 168

Fig. 15.6. Acceptable bilirubin concentration in newborns’ blood (Polacek K., 1961). EBT –
exchange blood transfusion
The plan of laboratory studies also includes regular determination of glycemia

(no less than 4 times a day in the first 3–4 days of life), platelet count, transami-
nase activity (at least once) and other investigations determined by specific clinical
presentations.
15.6.3. Treatment
In HDN all actions are aimed at attaining three major objectives:
NB! • managing anemia;
• elimination of non-conjugated bilirubin;
• elimination of anti-Rh-antibodies.
The following means are at the disposal of a neonatologist:
• phototherapy;
• infusion therapy;
• adsorbents of unconjugated bilirubin in the bowel;
• phenobarbital;
• exchange blood transfusion.
Nowadays phototherapy is the most widely used method of HDN treatment. From
the moment of introducing phototherapy for HDN treatment by J. Kramer et al in 1958
it has been established that this method is practically completely safe and effective.
Phototherapy is usually initiated at unconjugated bilirubin levels in blood serum
85–110 mcmol/l less than the levels requiring exchange transfusion. In full-term in-
fants phototherapy is started at unconjugated bilirubin level 205 mcmol/l and more,
in pre-term infants — at a level of 171 mcmol/l and more.
The positive effect of phototherapy consists in enhanced bilirubin excretion with
feces and urine, reducing the toxicity of unconjugated bilirubin. The greater the
area and intensity of radiation, the greater the effect. Duration of phototherapy
is 72–96 hours, but it can last less if the unconjugated bilirubin level has reached
physiological values for the particular age (Fig. 15.7).
The effectiveness of phototherapy increases in combination with infusion therapy
as diuresis stimulation accelerates the excretion of water-soluble bilirubin photoderiv-
atives and photoisomers. 5% dextrose (glucose) solution and salt solutions are admin-
istered. Adding albumin solutions is only indicated in established hypoproteinemia.
Newborn’s meconium contains 100–200 mg of bilirubin while its content in the
blood at birth is only 10–15 mg. It is believed that a cleansing enema or a glycerin
suppository administered within the first 2 hours after birth to remove meconium
Fig. 15.7. Blue light phototherapy

388 Obstetrics
reliably decrease the manifestations of unconjugated bilirubin surge in the blood.

These procedures should be given to all newborns with jaundice at birth. However,
after a lapse of 12 hours such treatment is ineffective.
Phenobarbital administered after birth promotes bilirubin diglucuronide produc-
tion and bile outflow thus reducing the intensity of jaundice. This effect is noticeable
from day 4–5 of therapy.
No conservative treatment, phototherapy included, can eliminate the need for
exchange blood transfusion at very high levels of unconjugated bilirubin.
Indications for exchange blood transfusion are hyperbilirubinemia values shown in
Fig. 15.6 and in Table 15.3. Administering exchange blood transfusion the neona-
tologist at the same time achieves two other objectives: elevating hemoglobin levels
and decreasing the titer of circulating antibodies (Rh-antibody half life is 28 days).
Table 15.3. Maximum level of serum bilirubin (mcmol/l) as indication for exchange blood
transfusion in USA (Berman R.E., Kligman R.M., 1991)∗
Body weight at birth, g No complications Complications

or accompanying disease∗∗
<1250 222 171
1250–1499 257 222
1500–1999 291 257
2000–2499 308 291
2500 and more 342 308
∗ The presented data are typical of infants in the first 28 days of life.
∗∗Complications include perinatal asphyxia and acidosis, postnatal hypoxia and acidosis,
pronounced and prolonged hypothermia, hypoalbuminuria, meningitis and other grave
infections, hemolysis, hypoglycemia, signs of depression and suppression of the CNS.
15.7. PREVENTION OF RHESUS ISOIMMUNIZATION

To decrease perinatal morbidity and mortality associated with HDN one should
single out the risk group among pregnant women and implement anti-Rh prevention.
Teenage girls should have their AB0 and Rh typing performed so that all women
know about the risk of isoimmunization. In case of therapeutic or spontaneous abor-
tion all Rh-negative women should receive anti-Rh-Ig.
AB0 and Rh typing should be performed prenatally at each pregnancy. In Rh-
negative pregnant women with a negative antibody test the screening for antibodies
is repeated at 28 weeks gestation. A pregnant woman with a negative antibody test
should receive elective therapy with anti-Rh-Ig at 28 weeks (antenatal prevention).
After an abortion (be it operative, pharmaceutical or spontaneous) or ectopic
pregnancy the probability of Rh-sensitization is 4–5% on average. The required
anti-Rh-Ig dose is 50 mcg before 13 weeks, and 300 mcg at a later gestational age1.
Rh-antigen is detected in the embryo starting at 7 – 8 weeks

NB! gestation.
1 The dose of 300 mcg corresponds to 1500 IU of anti-D-immunoglobulin.

Immunoglobulin should be introduced no later than 72 hours after delivery, abor-

tion, premature placental separation (that is, feto-maternal hemorrhage).
Chorionic villus sampling can be a cause of feto-maternal hemorrhage; it is indi-
cated to administer 50 mcg of anti-Rh-Ig.
Amniocentesis can also precipitate Rh-sensitization. If no anti-Rh prevention was
administered before, Rh- negative, previously non-sensitized pregnant women receive
a standard dose of 300 mcg of anti-Rh-Ig. However, this does not exclude the need
for postpartum prevention.
When cordocentesis is planned in a Rh-negative, previously non-sensitized woman,
the fetus’ Rh affinity should be established. If the fetus is Rh-positive or Rh-affinity
was not determined, 300 mcg of anti-Rh-Ig are administered to the mother.
If a Rh-negative, previously non-sensitized woman has a uterine hemorrhage,
anti-Rh-Ig should be administered. To determine the volume of feto-maternal hem-
orrhage, Kleihauer-Betke test is done. If more than 15 ml fetal RBCs passed into
maternal circulation, an additional dose of anti-Rh-Ig is required, apart from the
standard 300 mcg. Indirect Coombs’ test is indicated 72 hours after immunoglobulin
administration to detect free Rh-antibodies.
Anti-D prevention (recommendations by British Blood Transfusion Society, 2014)
• Prevention with anti-D-immunoglobulin should be given to D-negative women
with no anti-D-antibodies who have signed their informed consent to anti-D-Ig
administration.
• At gestational age below 12 weeks (after bleeding, curettage of uterine cavity,
operative or pharmaceutical abortion or ectopic pregnancy) 250 IU of anti-D-
immunoglobulin are administered within 72 hours.
• At 12–20 weeks gestation, following potentially sensitizing events, 250 IU of
anti-D-immunoglobulin are administered within 72 hours.
• In pregnancies after 20 weeks and until full term following potentially sensitizing
events a Kleihauer test (test for feto-maternal hemorrhage, FMH) is carried
out, and 500 IU of anti-D-immunoglobulin are administered within 72 hours
after delivery. For routine antenatal anti-D prophylaxis (regardless of anti-D
immunoglobulin injection for potentially sensitizing events) 1500 IU of anti-D
Ig are administered at 28–30 weeks gestation, or 500 IU at 34 weeks gestation.
• A FMH test should be carried out after delivery. If the fetus is RhD-positive,
or samples of cord blood are unavailable, 500 IU of anti-D Ig are administered
within 72 hours. If FMH test indicated a need for further prophylaxis, additional
anti-D Ig is administered.
Childbirth is the most common significant cause of Rh-isoimmunization. If an
Rh-positive fetus is born from an Rh-negative, previously non-sensitized mother,
anti-Rh Ig administration is required. Table 15.4 shows consolidated data on prob-
ability of sensitization in case of various events.
When performing hemotransfusion one should always check the donor blood for
Rh-affinity. Rh-antigen is only noted on red cell membrane so technically transfu-
sion of plasma cannot precipitate Rh-immunization. However, in theory platelets
and granulocytes can contain an admixture of RBCs. If Rh-antigen was injected by
mistake, one should remember that 1 ml of Rh(+) erythromass can be blocked by
20 mcg of anti-Rh Ig.
390 Obstetrics
Table 15.4. Estimation of past history factors promoting the risk of Rh-immunization, %
Immunization risk factors Immunization risk

Spontaneous abortion 3–4
Induced abortion 2–5
Ectopic pregnancy <1
Full term pregnancy prior delivery 1–2
Delivery with AB0-compatibility 16
Delivery with AB0-incompatibility 2–3.5
Amniocentesis 1–3
Transfusion of Rh-positive blood Up to 70
Anti-Rho(D)-Ig is obtained from plasma of sensitized donors whose antibody titer

is no less than 1:128–256. The required amount of drug is provided by Rho(D)-
sensitized pregnant women as well as by persons who received Rho(D)-incompatible
blood through hemotransfusion by mistake, and in recent time — thanks to Rho(D)-
negative volunteer donors (men and women whose reproductive activity is over).
Thanks to widespread introduction of anti-Rh(D) prophylaxis, the incidence rate
of Rh(D)-sensitization has declined drastically in comparison with not so long ago.
Nowadays it is other red cell antigens that take the lead as etiologic factors of isoim-
munization and HDN.
In the system of CDE (Rh)-antigens, E-antigen comes second after D-antigen
in its ability to cause HDN. Antibodies to Kell-antigen are produced in response to
transfusion of Kell-positive blood to a Kell-negative patient. Kell-antibodies can be
a cause of pronounced HDN. About 90% of Earth’s population are Kell-negative, so
the probability of HDN is not high. Other antigens that can occasionally precipitate
isoimmunization and HDN are antigens Duffy, Kidd, MNSs, Lutheran, Diego, Xg,
Public and Private. In about 2% of women screening tests detect atypical antigens.
Only a small part of these antigens can be the cause of HDN.
In most cases the mother and baby are incompatible in the

NB! AB0 system. However, AB0-incompatibility, in contrast to
Rh-incompatibility, is almost always the problem of the newborn
rather than the fetus, although there are extremely rare reports of
fetal hydrops in AB0-incompatibility.
In 12–20% of all pregnancies there is AB0 incompatibility between mother and

fetus which accounts for 60% of all HDN cases. The rate of HDN due to AB0
incompatibility is 2% of all deliveries, severe HDN — 0.03% of all deliveries. The
infant usually shows moderate anemia and mild or moderate degree of hyperbiliru-
binemia over the first 24 hours after birth. AB0 incompatibility is mostly noted when
there is a combination of 0(I) blood group in the mother and A(II) or B(III) blood
group in the newborn. The situation may reoccur in consequent pregnancies. A and
B receptors on red cell membrane to α and β antibodies are produced in amounts
sufficient to trigger HDN only by the end of pregnancy or after delivery so there is
no question of HDF. Besides, before they encounter corresponding fetal red cells,
most antibodies are neutralized by A- and B-antigens found in great amounts in

other tissues and organs of the fetus.
REMEMBER!
HDF is a fetal condition caused by RBC hemolysis, characterized by anemia and
increased numbers of erythroblasts in the blood-stream.
For HDF to develop, there should be previous alloimmunization (isoimmunization) of

the mother to the same antigen that is found in the fetus at the present pregnancy.
Feto-maternal hemorrhage in the third stage of labor or during abortion is believed

to be the major cause of immunization.
A person is considered Rh-positive on whose red cell membrane Rho(D)-antigen

is present.
In advanced countries previously sensitized immigrants from Asia and Africa

constitute the major source of HDN.
The probability of sensitization of Rh-negative parturient woman who delivers

a Rh-positive fetus is 16% on average. If ante- and postnatal prophylaxis was
administered, the probability approaches zero.
The main diagnostic tools for HDF detection are indirect Coombs’ test, amniocen-
tesis followed by spectrophotometry, cordocentesis, fetal liver measurement under
ultrasound guidance, measuring middle cerebral peak systolic velocity.
Two main invasions used in HDF are intrauterine intravascular hemotransfusion to

the fetus, and pre-term termination of pregnancy.
HDN is classified into edematous, icteric and anemic forms.
Assessment of HDN severity is based on determining antibody titer (direct Coombs’

test), degree of anemia and hyperbilirubinemia.
HDN management is aimed at achieving three main objectives: management of

anemia, excretion of unconjugated bilirubin, elimination of anti-Rh antibodies.
The most effective methods of treating pronounced HDN are phototherapy and
exchange blood transfusion.
CONTROL QUESTIONS
1. What is the association between hemolysis and bilirubinemia?
2. What is necessary to perform blood typing?
3. Where is unconjugated bilirubin neutralized and in what way?
4. What is physiological jaundice of newborn due to?
5. Three forms of hemolytic disease of newborn.
6. What is Kleihauer-Betke test based on?
7. Why can IgG pass through the placenta?
392 Obstetrics
8. What is the objective of intrauterine hemotransfusion to the fetus?

9. To whom, when and why is anti-D Rho immunoglobulin administered?
10. What dose of anti-D Rho immunoglobulin is administered in the event of
20 ml fetal blood passing to maternal blood flow?
11. Is postnatal prophylaxis 100% effective? If not, why?
12. Which method of pregnancy termination carries a greater risk of immunization
(curettage or vacuum-extraction)?
13. Explain the notion of kernicterus.
14. Blood of which group can be used for intrauterine transfusion to the fetus
when there is Rh-incompatibility?
15. What is the effect of phototherapy based on?
CHECK YOURSELF!
Level 1. Test
1. The term isoimmunization stands for:
a) immunity stimulation;
b) immunity suppression;
c) antibody formation;
d) decreased reactivity of the body;
e) none of the above.
2. Isoimmunization can be caused by incompatibility:

a) between maternal and fetal blood groups;
b) Rh-incompatibility of maternal and fetal blood;
c) M-, Kell-, Duffy- antigen incompatibility (or other accessory antigens);
d) all of the above;
e) none of the above.
3. Conditions in which alloimmunization arises:

a) Rh-positive fetus in Rh-negative mother;
b) Rh-sensitization of the mother;
c) transfusion of incompatible blood in past history;
d) abortion in past history;
e) all of the above.
4. After the first pregnancy the average rate of immunization in Rh-negative women
without prophylaxis is:
a) 16%;
b) 20%
c) 30%;
d) 40%
e) 50%.
5. For a fetus, the combination of AB0- and Rh-sensitization in maternal body:

a) does not matter;
b) is more dangerous;
c) is less dangerous;
d) is very dangerous.
6. The most unfavorable HDF sign is:

a) progressive increase in antibody titer;
b) «jumping» antibody titer;
c) presence of nonprecipitating antibodies;
d) signs of ascites in the fetus;
7. In HDF the placental weight is:

a) 300 g;
b) 500 g;
c) 1000 g;
d) over 1000 g;
e) c and d answers are correct.
8. In HDF the following is noted, as a rule:

a) hepatic dysfunction;
b) hypoproteinemia development;
c) anemia development;
d) a and b answers are correct.
9. If no anti-rhesus antibodies are found in the blood 6 months after delivery, can one
say that specific prophylaxis was effective?
a) no;
b) yes;
c) depending on complications;
d) depending on parity.
10. For HDN diagnosis, the following is tested in newborn’s blood:

a) hemoglobin and RBC count;
b) hourly accretion of bilirubin;
c) blood group;
d) Rh-affinity of the blood;
11. The essence of HDF consists in:

a) kernicterus development;
b) RBC hemolysis;
c) anemia development;
d) hypoproteinemia development;
394 Obstetrics
12. Rhesus immunization in a pregnant woman develops under the following

circumstances:
a) Rh-positive maternal blood passes to fetal blood stream and stimulates fetal
antibody production;
b) Rh-positive fetal blood passes to maternal blood stream and stimulates
maternal antibody production;
c) Rh-negative fetal blood passes to maternal blood stream and stimulates
maternal antibody production;
d) R-negative maternal blood passes to fetal blood stream and stimulates fetal
antibody production.
13. In what dose was RhoGAM recommended to be administered in antenatal

prophylaxis at 28 weeks gestation?
a) 50 mcg to sensitized pregnant woman;
b) 50 mcg to non-sensitized pregnant woman;
c) 300 mcg to sensitized pregnant woman;
d) 300 mcg to non-sensitized pregnant woman.
14. At which stage of pregnancy does maternal blood usually mix with fetal blood?
a) upon conception;
b) at 9 weeks gestation if the fetal heart has developed enough;
c) in the third trimester at 32–34 weeks gestation;
d) maternal and fetal blood never mix.

1. Primagravida aged 24 presents at maternal welfare clinic at 12 weeks gestation.
Her blood group is A(H), Rh(-) (data stated in her passport). What investigations
does she require? What is the plan of management?
2. Secundigravida aged 32 was referred to pathologic pregnancy department with
the following diagnosis: 32 weeks gestation, pregnancy with Rh-incompatibility (anti-
body titer 1:32). What is the plan of management in hospital? What anti-Rh globulin
dose will be required for postnatal prophylaxis in this case?
NOTES
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• Chapter 16
MULTIPLE PREGNANCY
16.1. DEFINITION
Multiple pregnancy is a pregnancy where more than one fetus develops simultane-
ously in the womb.
ICD-10 codes XV Pregnancy, childbirth and the puerperium (O00–O99).

• O30 Multiple gestation.
– O30.0 Twin pregnancy.
– O30.1 Triplet pregnancy.
– O30.2 Quadruplet pregnancy.
• O31 Complications specific to multiple pregnancy.
– O31.0 Papyraceous fetus.
– O31.1 Continuing pregnancy after abortion of one fetus or more.
– O31.2 Continuing pregnancy after intrauterine demise of one fetus or more.
• O43 Placental disorders.
– O43.0 Twin-to-twin placental transfusion syndrome.
• O84 Multiple delivery.
– O84.0 Multiple delivery, all spontaneous.
– O84.1 Multiple delivery, all by forceps and vacuum extractor.
– O84.2 Multiple delivery, all by cesarean section.
– O84.8 Other multiple delivery.
– O84.9 Multiple delivery, unspecified.
• Z37 Outcome of delivery.
– Z37.2 Twins, both liveborn.
– Z73.3 Twins, one liveborn and one stillborn.
– Z37.4 Twins, both stillborn.
– Z37.5 Other multiple births, all liveborn.
16.3. HISTORICAL ASPECT
At all times a multiple delivery was surrounded by superstition and mysticism. It

was believed that twin infants could in some way affect nature, in particular, change
the weather. In some American Indian tribes twins were made to offer up their
prayers to the wind and rain. People believed that each wish of twins was gratified
396 Obstetrics
and they could curse their enemies, bring about plenty of fish in the river and even
heal sickness (Fig. 16.1).
The word for twins meant «providers of plenty». In some African tribes the twins’
mother was referred to as heaven, the twins themselves — offspring of heaven.
However, these are all myths and superstition, and here are historical facts: in 1775
Jacob Kirillov, a peasant from Vvedenskoye village, was introduced to the court. He
was 60 years old then and was married for the second time. His first wife was pregnant
21 times and gave birth to 57 live offspring (4 quadruplets+7 triplets+10 twins); the
other wife gave birth to 15 children after 7 deliveries (1 triplet+6 twins). Put together,
this makes him father of 72 children. On February 27, 1782 a statement was sent
to Moscow from Nikolsky monastery from Shuisk county that Fedor Vassiliev, a
peasant, twice married, had 87 children by both marriages. The first wife gave birth
27 times producing 69 offspring (4 quadruplets+7 triplets+16 twins), the second
one — 18 children (2 triplets and 6 twins). In that year Vassiliev was 75; 83 of his
children were still living. These unique incidents are confirmed by documents.
Delivery of quadruplets or quintuplets is a rare occasion, giving birth to sextuplets
happens next to never; in Germany in the town of Hammeln is a tomb with bas
relief and inscription: «Early in the year 1600 on January 9 in the morning she gave
birth to two boys and five girls» — a testimony to delivery of septuplets, which is a
truly unique occasion as, according to statistics, delivery of septuplets is preceded by
delivery of 262 billion people!
The second half of the 20th century saw an increase in the incidence of multiple
pregnancies due to introduction of ovulation-inducing medications into the practice
of gynecology. In 1968 in Birmingham 6 offspring were born: 2 boys and 4 girls.
One of them died an hour after birth. Their mother had been treated with new anti-
infertility medication. In England this was the first case of delivering sextuplets. In
1971 in Gdansk quintuplets were born: 3 boys and 2 girls. According to the press,
their development was normal. Closer to our time, a woman in Italy gave birth to
six pairs of twins.
Fig. 16.1. Ancient sculptures representing Siamese twins

Chapter 16. Multiple pregnancy 397
The question in what relation are infants of a multiple pregnancy (identical or

fraternal, in other words, monozygous or dizygotic), is sometimes hard to answer.
Sometime genetic tests have to be done. A curious incident happened in California
some time ago. A woman filed a legal claim for parentage testing as she had given
birth to twins. Genetic testing indicated that the children were by different fathers.
Such cases were registered from the 19th century. Several instances of this rare phe-
nomenon called superfecundation are known: fertilization of an ovum that ovulated
while a pregnancy already existed, within one menstrual period, by spermatozoon
of another male.
In 1922 a well-known Russian gynecologist V.S. Gruzdev collected all data relating
to superfecundation in late 19th–early 20th centuries, in his textbook. He reported
an interesting fact: in America a woman gave birth to twins where one was white,
the other — black.
There is another interesting phenomenon related to multiple pregnancy. Fraternal
twins are not always born at the same time. The second one may be delivered a
month after the first one. This is referred to as superfetation: fertilization of an ovum
that ovulated while a pregnancy was already developing, during the next menstrual
period. Thus, in India a second twin was born 45 days after the first one.
Siamese, or conjoined, twins deserve a separate remark (Fig. 16.2–16.4). As close
as Siamese twins, goes the saying (Fig. 16.5). In this rare condition approximately
one fifth of Siamese twins survive.
Fig. 16.2. Conjoined twins in medieval picture

398 Obstetrics
Fig. 16.3. Chang and Eng
Fig. 16.4. Poster announcing Chang and Eng show

а b c
Fig. 16.5. Variations of Siamese twins: a — ischiopagus; b — thoracopagus; c — craniopagus
(Patten B.M.)
Chang and Eng Bunker were born in Siam (from which the name Siamese twins is
derived) in 1811. They were joined at the chest, and at first they could only lie face
to face. Later, as they grew, their intersection stretched, and they were able to walk,
run and swim shoulder to shoulder. Each one led his own life; they could eat, work
or sleep at different times (see Fig. 16.3).
Their Chinese mother sold them to a circus, and for many years they were shown
as freaks in European and American shows (see Fig. 16.4). Having accumulated some
money they settled down in the USA, married two sisters and gave birth to 20 normal
and two deaf offspring. The Civil war between the North and South brought them
financial ruin; Chang took to drowning his sorrow in drink. In 1869 he was paralyzed,
but the twins lived for another 5 years. In 1874 Chang developed pneumonia and
died in his sleep. Having learned of his death, Eng died in two hours.
A festival is held annually in Twinsburg (USA) where fraternal, that is, identical
twins come together wearing identical clothes (Fig. 16.6).
Fig. 16.6. Twins Day Festival, Twinsburg, Ohio
16.4. EPIDEMIOLOGY
Multiple pregnancies account for 0.5–2.0% of all deliveries and result in a delivery
of twins as a rule, less often — of triplets. Triplets constitute about 1% of all multiple
400 Obstetrics
deliveries. A formula of the rate of twin deliveries is described by Hellin’s law; it is

a principle that one in about 80 pregnancies ends in the birth of twins; one in 802
(6 400), of triplets; one in 803 (512 000), of quadruplets. These figures are average
for the population, without recurrence to assisted reproductive technology. Identical
twins are seen at a mean rate of 0.2–0.4% all over the world. Among multiple preg-
nancies, the rate of identical and fraternal twins is 30 and 70%, correspondingly. In
contrast to fraternal twins, the rate of identical twins is quite constant; it does not
depend on parity, maternal age or other factors. Over recent decades a tendency
was noted for increased rates of multiple pregnancies, which is due to introduction
of assisted reproductive techniques, aging of the cohort of pregnant women when
patients fulfill their reproductive function at an age above 35 (the peak of controlled
ovarian stimulation).
In multiple pregnancy more than one half of ova undergo resorbtion

NB! at early gestational ages. Resorbtion of an embryo mostly occurs
during the first 7 weeks of gestation; it is not seen after 14 weeks
gestation (the vanishing twin syndrome).
Advanced countries have seen an increase in the rate of multiple pregnancies

over recent decades, in particular triplets, quadruplets and more. This phenomenon
is due to the widespread use of assisted reproductive technology (in vitro fertiliza-
tion, embryo transfer, stimulation of ovulation) that began in mid-1980s. The rate
of multiple pregnancies after resorting to assisted reproductive technology increases
10 times (Table 16.1).
Among other causes associated with multiple pregnancy one should also mention
these:
• high parity (the probability of multiple pregnancy is twice higher for the fourth
delivery than in the first pregnancy);
• genetically determined (the probability of twin delivery in families with twins in
history is 7.5% on the maternal side, and 1.7% on the paternal side);
• racial difference in the rate of multiple pregnancies (in China the rate of twin
deliveries is 0.3%, in Nigeria it is almost twenty times greater — 5.7%);
• the woman’s build (multiple pregnancies are mostly seen in tall heavyset
women);
• perigravid administration of folic acid;
• administration of combined oral contraceptives (withdrawal syndrome).
The outcomes of pregnancy and delivery are different for singleton and multiple
pregnancies: in the latter case the rate of pregnancy and delivery complications is
higher, and hence, higher perinatal morbidity and mortality.
Causes of unfavorable outcomes comprise pre-term delivery, hemorrhage, pre-
eclampsia and other complications. In case of multiple pregnancies, perinatal
mortality is 3–4 times higher than in singleton pregnancy. First of all this is due
to prematurity, chronic intrauterine hypoxia, slow fetal growth, a high rate of
chromosomal abnormalities, risk of fetal injury (cerebral circulation disorders are
noted 20 times more often). In twin pregnancies the infants are born with body
weight less than 2500 g in a half of cases. The risk of a twin demise during the
Table 16.1. Variants of multiple pregnancy and their rate after in vitro fertilization and embryo
transfer, %
Country Twins Triplets Quadruplets

Belgium 30 2.3 –
USA 29 6.0 0.6
Great Britain 27 5.2 –
Sweden 25 0.9 –
France 24 2.0 –
Latin America 22 6.3 0.8
Finland 22 1.6 –
Italy 21 7.1 –
Canada 21 4.4 –
Japan 19 4.4 –
Singapore 18 10.4 –
first year of life is 5 times higher than for singletons, and in case of triplets it is
14 times higher.
On account of high rates of complications seen during pregnancy and delivery,
multiple pregnancy should be regarded as pathological.
16.5. DEFINIITON
In a multiple pregnancy the fetuses can be identical, monozygotic or fraternal,

dizygotic.
• Identical twins develop from one ovum; they share sex, genotype, blood group,
and they look alike.
• Fraternal twins develop from different ova fertilized by different spermatozoa.
Their genetic makeup is the same as in common siblings.
There are two types of twins:

NB! • monozygotic, or identical twins;
• dizygotic, or fraternal twins.
Depending on placental-membrane relation, multiple pregnancy can be of the

following types:
• dichorionic-diamniotic (each fetus has its own chorion and amnion, the partition
between them consisting of four layers: two amnions and two interposed smooth
chorions while the placenta can be separated or fused);
• monochorionic-diamniotic (both amnions are enclosed in one common chorion,
the partition between fetuses consisting of two amnion layers);
• monochorionic-monoamniotic (the fetuses share one amniotic cavity, there is no
partition) (Fig. 16.7).
402 Obstetrics
Dichorionic diamniotic
Monochorionic diamniotic
Monochorionic monoamniotic
Fig. 16.7. Placenta-membrane relations in multiple pregnancy
There were instances of heterotopic pregnancy, an extremely rare phenomenon

of intrauterine and ectopic pregnancy developing simultaneously; both pregnancies
can be multiple.
16.6. ETIOLOGY AND PATHOGENESIS
Multiple pregnancies are caused by various factors, heredity being one of them.
There were families where multifetal pregnancies were seen across generations.
The probability of twins is 4–7 times higher for families with multiple pregnancies
in family history than in the general population. The older the pregnant woman
(35 and more), the more often multifetal pregnancy occurs. The risk of multiple
pregnancy is higher within the first month after oral contraceptive withdrawal if
they were taken no less than 6 months. Assisted reproductive technology (ovula-
tion stimulating medications, in vitro fertilization, embryo transfer) increase the
risk considerably.
Dizygotic twin pregnancy occurs:
• upon simultaneous fertilization of two eggs that matured in one or both ovaries
(several eggs can mature in one follicle) by spermatozoa from one or different
males;
• upon fertilization of an egg that ovulated while there was already a pregnancy
within one menstrual period (superfecundation);
• upon fertilization of an egg that ovulated while there was already a pregnancy
during the next menstrual period (superfetation).
Dizygotic twins can be of one (75%) or different sex. Their genotype is not the
same.
Monozygotic twin pregnancy occurs:
• upon fertilization of polynucleate egg;
• upon atypical cleavage of conceptus (pre-embryo): one ovum fertilized by one
sperm cell turns into two embryos (polyembryonism)
Three or four simultaneously developing fetuses can be arranged

NB! in various combinations of identical and fraternal twins.
Monozygotic twins occur more rarely than dizygotic twins. Monozygotic twins
share the genetic material, they look alike, have the same blood group, show histolog-
ical and immunological compatibility, but their fingerprints are individual (Fig. 16.8).
In dizygotic twin pregnancy the fertilized eggs develop independently from each
other. After implantation each embryo develops its own amnion and chorion; later
each fetus has its own placenta; their circulations are divided.
All dizygotic twins are dichorionic. If the embryos were implanted at some distance
from each other, their placentas do not adjoin. Upon implantation at a close distance
the embryos share the decidual membrane, placental edges adjoin, the partition be-
tween gestational sacs consists of four membranes (two chorions and two amnions).
Despite the fact that each placenta has its own vascular tree, sometimes anastomoses
are formed which may give rise to complications.
There are different types of placenta-membrane relations in monozygotic twin
pregnancy depending on the time passing from the moment of fertilization to the
cellular mass division (Table 16.2):
• 3–4 days (before morula formation and trophoblast differentiation): dichorionic-
diamniotic pregnancy;
• 5–8 days (morula has formed, chorion cells have differentiated, amnion has not
formed): monochorionic-diamniotic;
• 8–12 days: monochorionic-monoamniotic;
• 13 days and more: fused fetuses emerge — conjoined twins (Siamese twins)
Fig. 16.8. Identical twins
A monozygotic pregnancy can show any variety of placenta-

NB! membrane relations depending on the period of time elapsing
from the moment of fertilization to the cellular mass division (pre-
embryo).
404 Obstetrics
Table 16.2. Types and rate of membrane-placenta relation
Type and rate Monozygotic twins Dizygotic twins

Chorion one two two
Placenta one fused two fused two
Rate, % 20 6 7 30 37
Total rate, % 33 67
The type of placental complex has a direct effect on the progress and outcome
of the pregnancy: in monochorionic pregnancy perinatal mortality is higher than
in dichorionic pregnancy (Fig. 16.9). If the twins are monoamniotic, the umbili-
cal cords of both fetuses are attached to one placenta (close to each other), which
can result in their twisting and demise of both fetuses. There is a risk of conjoined
twins formation.
In the gender structure of twins female fetuses predominate (75%). Conjoined
twins are named according to the site of their fusion: craniopagus (head), thoracopa-
а b
c d
Fig. 16.9. Placenta-membrane relation in twin pregnancy: a — two placentas, two chorions,
two amnions; b — two fused placentas, two chorions, two amnions; c — one placenta, one
chorion, two amnions; d — one placenta, one chorion, one amnion
gus (chest), omphalopagus (abdomen) (Fig. 16.10), pygopagus (buttocks and inferior
part of the spine); combinations are possible, like thoraco-omphalopagus.
Fig. 16.10. Newborn conjoined twins (omphalopagus)
One third of conjoined twins are stillborn. Approximately another 1/3 dies within
the first day of life. Sometimes surgical separation of the twins is possible depending
on the site and extent of fusion.
16.7. DIAGNOSTICS
Ultrasound remains the gold standard of multifetal pregnancy diagnosis. Ultrasound

examination using a transvaginal sensor allows visualization of several gestational sacs
in the uterine cavity several days after a missed period (Fig. 16.11).
At early gestational ages it is sometimes recommended to determine hCG content
in the woman’s blood or urine. In multifetal pregnancy the hCG content is higher
than in singleton pregnancy at the same gestational age. Diagnostic value of this
method is rather low.
Ultrasonography is the gold standard in diagnosing a multiple

NB! pregnancy.
406 Obstetrics
а b
Fig. 16.11. 3D echogram of multiple pregnancy during the fi rst trimester:

a — triplets; b — twins
16.8. CLINICAL FEATURES
Clinical features of multiple pregnancy in

the second and third trimesters are as fol-
lows:
• uterine size growth too fast for the
estimated gestational age (a gravidogram
is used for the purpose);
• in late pregnancy an external obstetric
examination detects three and more large
fetal parts;
• fetal heart beat heard in two and more
sites, with an auscultatory gap between
them (Fig. 16.12).
Ultrasound permits differentiation between
multifetal pregnancy and polyhydramnios,
molar pregnancy, uterus tumor (myoma),
fetal macrosomia. Importance of ultrasound
increases since the rate of malformations
is much higher in multiple pregnancy, and
Fig. 16.12. Two foci of heart beat there is a risk of numerous complications
auscultation in twin pregnancy (Fig. 16.13).
Fig. 16.13. 3D echogram of twins in late pregnancy
16.9. MANAGEMENT OF PREGNANCY
The course of pregnancy, delivery and postpartum period has its specific features
in case of multifetal pregnancy.
16.9.1. Maternal and fetal complications

The risk of maternal complications is associated with specific adaptation of mater-
nal body to multifetal pregnancy. Due to elevated load the body has to cope with,
patients carrying several fetuses often note increased fatigue, breathlessness, urination
disorder, constipation.
In 70 – 85% of cases a multiple pregnancy shows complications.

NB! In multiple delivery perinatal mortality is 3 – 4 times higher than
in single deliveries.
In the first trimester the pregnancy is mostly endangered by miscarriage and

vomiting of pregnancy. In the second trimester, due to pronounced hypervolemia (on
account of physiological hemodilution) anemia is seen 2–3 times more often than in
singleton pregnancies. The risk of gestation diabetes is elevated considerably: its rate
is 7% for twin pregnancy, 9% for triplet pregnancy, and 11% in case of quadruplets.
The risk of urine tract infection is 1.5 times higher. Varicose veins are common; and
there is a greater risk of thrombus formation. Preeclampsia is 4 times more common
in multiple pregnancy than in singleton pregnancy.
In most cases multifetal pregnancy is accompanied by relative polyhydramnios.
The risk of antenatal fetal complications is much higher in multiple pregnancies.
Complications typical not only of multifetal pregnancy include fetal abnormalities
(2–4%) and fetal growth restriction, especially in case of identical twins.
408 Obstetrics
16.9.2. Complications of multiple pregnancy

These, first of all, include the vanishing twin; its rate can be up to 50%. Reduction
of one embryo occurs in the first trimester. At a later gestational age, however, there
still is a high risk of antenatal demise of one fetus; in this case one fetus undergoes
mummification while the other one develops within normal and is delivered at term.
If demise of one fetus occurred before 22 weeks gestation, the term missed twins is
applied. The demise may be brought about by complications that have to do with
specific relations between two fetal vascular systems.
Anastomoses can form between vessels of twin cardiovascular systems in case of
monochorionic twins, les often — in case of fused placentas. The pressure gradient
in vessels leads to occurrence of so-called twin-to-twin transfusion syndrome (TTTS)
when one fetus becomes the donor, and the other — recipient (Fig. 16.14).
TTTS is a specific complication of multiple pregnancy which
NB! mostly occurs in case of monochorionic twins, and less often – in
case of fused placentas.
Amniotic
Oligohydramnios membrane A
Donor
Polyhydramnios Recipient B
Fig. 16.14. Twin-to-twin transfusion syndrome. Superior left: ultrasound of twin-to-
twin transfusion: the fetus in the upper part shows decreased amount of amniotic fluid
(oligohydramnios); MEMB — membrane separating the upper fetus from the lower one whose
amniotic cavity contains excessive fluid (polyhydramnios). Below left: schematic representation
of TTTS: on the right is placenta (its vessels injected with dye); left fetus: yellow color shows
arteries, blue—veins; right fetus: red—arteries, green—veins; a — part of arterial network in the
right fetus is fi lled with yellow dye due to the presence of anastomosis artery (shown with an
arrow); b — close-up of part of placenta with anastomosis colored yellow
As a result of cardiac shunt from one circulation to the other, the donor fetus
develops anemia, slow growth, oligohydramnios while the recipient fetus develops
erythremia, cardiomegaly, congestive heart failure, non-immune hydrops, polyhy-
dramnios. Absolute polyhydramnios is an indirect sign of TTTS.
In this syndrome the perinatal mortality rate is 70–100%. The outcome depends
on the type of anastomoses (arterio-arterial, arteriovenous or veno-venous) and the
diameter of involved vessels, which determines the specific volume of twin-to-twin
transfusion.
In massive twin-to-twin transfusion antenatal demise of both fetuses is a possibil-
ity. Besides, if the twins are monochorionic and after the demise of one the other one
has non-immune hydrops due to necrotic lesions, almost each fourth surviving infant
dies. The risk of perinatal death of recipient fetus after the demise of the donor fetus
is 50% at gestational age before 34 weeks, and about 20% after 34 weeks gestation.
However, 1/3 of surviving recipient fetuses (after the donor fetus demise) dies in
early postpartum period. Death causes in such neonates (recipient fetuses) are pul-
monary hypertension, obstruction of right ventricular outflow tract, renal and hepatic
failure. Most surviving recipients show a pronounced psychomotor retardation. After
a live birth of a donor fetus early neonatal complications are associated with severe
forms of restricted fetal growth.
The only diagnostic tool for TTTS is ultrasound examination which helps to
identify some criteria of TTTS development:
• in recipient fetus: polyhydramnios, hydrops (subcutaneous edema over 5 mm,
pleural and pericardial exudation, ascites);
• in donor fetus: oligohydramnios, growth restriction.
The weight difference between fetuses can amount to 20% and more. Such twins
are termed discordant (Fig. 16.15). An accessory diagnostic tool is color flow map-
ping.
Methods of managing TTTS:
• amnioreduction: a series of therapeutic amniocentesis procedures that reduce
intra-amniotic pressure in the recipient fetus;
Fig. 16.15. Discordant monochorionic twins

410 Obstetrics
• septostomy: perforation of the amniotic partition that allows amniotic fluid to

freely circulate between two amniotic cavities. This method was proposed after
an accidental septostomy during therapeutic amniocentesis showed that the
amount of fluid in amniotic cavities settled to normal;
• selective fetal euthanasia is not a fully acceptable method as its perinatal mortality
is 50%. However, the option is there especially if demise of one fetus is imminent;
• endoscopic laser coagulation of placental vascular anastomoses (Fig. 16.16) is the
gold standard of TTTS management. Laser coagulation of anastmoses is performed
under combination guidance (endoscopy and sonography). Complications after
endoscopic laser coagulation of placental vascular anastomoses: demise of one
fetus (7%), demise of both fetuses (1%), recurrent development of TTTS (13%).
Another type of abnormal vascular relation between twins is the so-called twin
reversed arterial perfusion (acardiac twin, acardius, acardius acephalus, acardius
myelacephalus, acardius amorphous) (Fig. 16.17).
а b
Fig. 16.16. Endoscopic laser coagulation of placental vascular anastomoses: a — prior to
coagulation; b — after coagulation
Fig. 16.17. Acardiac monster and its development

Pathogenesis of this complication has

not been established definitely but it is
understood that anastomoses that emerge
at early embryogenesis stages between
umbilicus arteries lead to retrograde
blood circulation in one (recipient) fetus
and to secondary disturbance of organ
morphogenesis. From the placenta, the
blood flows to the recipient along umbili-
cal arteries rather than along the umbilical
vein, and thus blood supply to the upper a
portion of recipient fetus becomes insuf-
ficient (this fetus becomes unviable).
The recipient twin develops malfor-
mations. There are many varieties of ab-
normalities to the extent of absent brain,
limbs, chest, heart, lungs, esophagus,
liver, etc. The donor fetus is morphologi-
cally sound but his heart is overloaded so
it has hydrops, hypotrophy, cardiomegaly,
hepatosplenomegaly. Mortality of recipi-
ent fetuses is 100%, of donor fetuses —
b
50%.
Monoamniotic twins pose a serious
threat to the pregnancy outcome; perina-
tal mortality in this condition can be as
high as 40%. Besides TTTS, the risk of fe-
tal demise in case of monoamniotic twins
is associated with both fetuses placed in
one amniotic sack as in this situation the
cords may twist and cord entanglement
ensues (Fig. 16.18).
In multiple pregnancy there is practi-
cally no risk of post-term delivery. The c
chronologic criterion of post-term preg-
Fig. 16.18. Cord entanglement in
nancy in multifetation is a gestational age
monoamniotic twins: a — macroscopic
over 38 weeks (!). representation; b — ultrasongraphy; c —
The prognosis of outcomes for the color flow mapping of vessels in entangled
pregnancy and delivery in case of multife- cords
tation is much worse than with singleton
pregnancies. One should monitor women with multiple pregnancy closely recognizing
them to be at high perinatal risk. If there is a slightest sign of abnormality, hospitaliza-
tion is indicated. Women are admitted to antenatal department of maternity hospital
2 weeks before the estimated delivery date (at 36 weeks) to perform investigations
and to decide upon the time and mode of delivery. When the woman has triplets or
more fetuses, hospitalization is recommended starting at 26 weeks and until delivery.
412 Obstetrics
Such measures as administration of tocolytics, suturing the cervix of uterus, pes-

sary insertion failed to reduce the rate of pre-term deliveries, although research
continues. The main objective of antenatal monitoring of multiple pregnancy is early
diagnosis and prevention of obstetric complications.
16.9.3. The timing and mode of delivery

We discuss the timing of delivery only tentatively as 70% of multiple preg-
nancies end in pre-term delivery which in most cases was preceded by early
rupture of membranes. In case of multiple pregnancy, severe complications both
maternal (severe preeclampsia, extragenital disease decompensation, etc.) and
fetal (decompensated placental insufficiency resulting in pronounced growth
restriction, acute fetal hypoxia, TTTS, etc.) require emergency termination of
pregnancy.
If there are no emergency indications, the choice of mode of planned delivery is
mostly determined by the lie and presentation of the first fetus, estimated weight and
condition of fetuses, and gestational age.
The tactics of labor management in multiple pregnancy depends

NB! mostly on the position and presentation of fetuses, and on their
weight.
Indications for planned elective cesarean section:

• monoamniotic twins;
• triplets or more fetuses;
• breech presentation or unfavorable lie of the first fetus (transverse, oblique).
Abdominal delivery is preferable when the second twin is in breech presentation,
with an estimated weight 3500 g. If the second twin in breech presentation weighs less
than 1500 g, vaginal birth is admissible. After the first twin delivery, when the second
twin has sufficient amount of amniotic fluid and there are no contraindications, one
can perform external cephalic version (under ultrasound guidance) (if there is breech
presentation or unfavorable lie) or combination podalic version, if the second fetus
is in unfavorable lie. The suggested manipulations have a limited use in obstetric
clinical practice due to a high risk of fetal injury.
Podalic version of the fetus followed by extraction or cesarean section are methods
of choice when there is a need for emergency delivery.
A multiple pregnancy often ends in preterm delivery, so in case

NB! of an operative delivery it is recommended to extract the fetuses
in their amnitocs sac(s) intact.
In case of twins labor induction should be administered no later

NB! than at 38 weeks gestation. Perinatal mortality and neonatal
morbidity are the least within the ideal period for delivery: 36 – 37
weeks for twins, 34 – 35 weeks for triplets.
16.10. MANAGEMENT OF DELIVERY
It is recommended to begin tocolytic therapy (nifedipine, β-adrenomimetics,

oxytocin receptor inhibitors) at a gestational age below 34 weeks if there was early
rupture of membranes or during the latent phase of labor (cervical dilation less
than 4 cm); the purpose of therapy is to delay delivery by 24–48 hours. In the
interval, RDS prophylaxis with dexametazone or betametazone is administered
and the patient with multiple pregnancy is hospitalized to a hospital with adequate
specialized facilities. If there arise indications for emergency delivery, manage-
ment plan is reviewed. Indications for tocolytic therapy in the active phase of
labor include prevention of oxytocia or accelerated labor as well as intrauterine
resuscitation. Pre-term rupture of membranes in pre-term pregnancy requires
antibacterial therapy for prevention of chorioamnionitis or neonatal infection.
If there are no bacteriology study findings, empirical broad-spectrum antibiotic
therapy is preferable.
Complications of multifetal delivery:
• prolapse of small body parts or umbilical cord upon uncontrolled rupture of
membranes;
• unfavorable lie of fetuses;
• uterine inertia;
• fetal hypoxia;
• premature detachment of normally situated placenta after the first fetus has been
delivered.
Management of childbirth in case of multiple pregnancy requires concentration,
ability to respond to the changing obstetric situation and considerable expertise of
the doctor who should be able to perform any type of operative procedure.
During labor, a cardiomonitor should follow the condition of both fetuses. When
the first fetus is born, the second one’s condition continues to be monitored. In con-
nection with a high rate of labor abnormalities, the contractile activity of the uterus
must be registered using a monitor, as well as cervical dilation during the first stage
of labor (a partogram should be filled in).
Since there is a high risk of acute fetal hypoxia, labor should be

NB! managed with continuous CTG control.
Epidural analgesia with consideration to all particulars is the gold standard of

labor analgesia.
If there is uterine inertia, oxytocin is administered with care (slow administration
while assessing the fetal condition and progress of labor).
In the second stage of labor the uterine contractions often become hypotonic, so
for prevention of poor contractility oxytocin is administered IV at a rate of 0.0002 IU/
kg per minute during the stage of expulsion. As soon as the first fetus is delivered, the
cord is clamped and a vaginal examination is made. If the second fetus is in cephalic
presentation, the gestational sac should be opened, which promotes contraction of
the overdistended uterus and is an effective prevention of premature detachment of
the placenta.
414 Obstetrics
Headlock twins is a rare complication of twin labor. It occurs when one fetus is
in breech presentation and the other in cephalic presentation. Labor can progress
uneventfully until the first fetus’s trunk delivers but the first fetus’s head remains
above the pelvic inlet and cannot deliver as the second fetal head is wedged between
the first one’s head and trunk (above the shoulder). If headlock occurs, cesarean
section is performed, the heads are unlocked, one fetus is extracted and the other
one born vaginally (Fig. 16.19).
If headlock remain unrecognized, the common outcome is demise of the first
fetus, sometimes of both. In very early pre-term labor twins collision is sometimes
seen: a clinical situation when two heads of small premature fetuses descend into the
lesser pelvis cavity simultaneously.
A twin delivery should be attended by two midwives and two

NB! neonatologists.
The third stage of labor and early postpartum period are especially dangerous as
there is a risk of hemorrhage. Hypotonic hemorrhage after multifetal delivery occurs
4–5 times more often than after singleton delivery. The rate of hypotonic hemorrhage
in case of triplets is 12% of all deliveries, in case of quadruplets — 21%.
For prevention of hypotonic hemorrhage the administration of uterotonic medications
continues for 2 hours after delivery while closely observing the puerpera’s condition.
The third stage of labor and early postpartum period are most
NB! risky due to the possibility of hypotonic hemorrhage.
When the afterbirth is delivered, it is carefully inspected to check for integrity of

its lobes and membranes, to confirm chorionicity and preliminary determination of
Fig. 16.19. Twins in headlock

zygosity. Different sex of newborns indicates fraternal twins unequivocally. If the

newborns are of the same sex, dichorionic, their zygosity remains undetermined until
genetic testing is done. However, one should confirm the type of multiple pregnancy
upon examining the afterbirth after delivery. If there is one placenta and two layers
in the partition, one can state the twins to be monochorionic diamniotic, if there
are four layers — dichorionic twins and fused placentas.
For the same purpose, the place of fusion of the partition and placenta is exam-
ined sonographically (Fig. 16.20). Union of partition and placenta in the form of «T»
(T-zone) indicates monochorionic pregnancy, that in the form of «Λ» (Λ-zone)—
dichorionic pregnancy.
а b
Fig. 16.20. a — afterbirth, fraternal twins. The partition consists of 4 membranes: two
amnions (1) and two chorions (2); b — afterbirth, identical twins. The partition consists of
two amnion layers (1, 2)
Chorion Amnion
Chorion Amnion
Placenta
Placenta
Fig. 16.21. Membrane relations in twin pregnancy. On the left is monochorionic diamniotic
pregnancy (partition represented by two amnions), the place of placenta-partition fusion is in
the form of inverted T (T-zone); on the right is dichorionic diamniotic twin pregnancy (two
chorions and two amnions in the partition), the place of placenta-partition fusion is in the
form of «Λ» (Λ-zone)
416 Obstetrics
а b
Fig. 16.22. Echograms of twin pregnancies: a — Λ-zone; b — T-zone
16.11. COURSE AND MANAGEMENT OF POSTPARTUM

AND NEONATAL PERIODS
The management of early neonatal period in case of multiple delivery requires
special attention, but in essence it is the same as with singleton delivery, except for
cases of pre-term delivery or delivery of infants with pronounced hypotrophy. In
most cases rooming-in and exclusive breastfeeding are as desirable for twins as for
singletons (Fig. 16.23).
Fig. 16.23. Breastfeeding twins
A multiple pregnancy that ended in a preterm delivery poses

NB! no contraindications for rooming-in, except when the newborns
require rehabilitation.
16.12. MATERNAL AND FETAL OUTCOMES

OF PREGNANCY AND CHILDBIRTH
The outcome of pregnancy and childbirth for the mother is determined by the risk
of complications related to multifetal pregnancy: hypertension, thrombus formation,
operative termination of pregnancy, hypotonic hemorrhage, etc.
For the fetus, the outcomes depend on zygosity of multifetal pregnancy and related
complications, the timing and mode of delivery, the quality and extent of neonatal
care. High neonatal morbidity in multiple pregnancies is mostly associated with
an early gestational age. No significant difference was noted in the rate of RDS,
intraventricular hemorrhage or necrotizing colitis of newborn compared with the
outcomes of singleton deliveries.
16.13. PROPHYLAXIS
Prophylaxis of multiple pregnancy touches upon the issue of employing assisted

reproductive technology. One should mention here embryo reduction after in vitro
fertilization and European standard of IVF — planting only one fertilized ovum in
the uterine cavity. Fetal surgery, a successfully developing branch of medicine, is
also noteworthy; it permits correction of potentially threatening complications of
multiple pregnancy.
REMEMBER!
Definition A pregnancy is referred to as multiple if there are two or
more fetuses
Epidemiology Multiple pregnancies account for 0.5–2.0% of all childbirths,
triplets — 1% of all multifetal deliveries. Twin deliveries are
1:80 of all deliveries, triplets — 1:802, quadruplets — 1:803,
etc. (Hellin’s law). Use of assisted reproductive techniques
has increased the rate of multiple pregnancies several-fold
Etiology Heredity, high parity, advanced maternal age, use of oral
contraceptives and ovulation-stimulating medications, use
of assisted reproductive techniques.
Pathogenesis Dizygotic twins develop upon simultaneous fertilization of
two mature ova in one or both ovaries by spermatozoa of
one or different males; besides, several ova can mature
in one follicle; fertilization of an ovum that ovulated while
a pregnancy is in progress, within one menstrual period
(superfecundation); fertilization of an ovum that ovulated
while a pregnancy was in progress during the next menstrual
period (superfetation).
Monozygotic twins develop upon fertilization of a poly-
nucleate egg; upon atypical cleavage of conceptus (pre-
embryo): one ovum fertilized by one sperm cell turns into
two embryos (polyembryonism)
418 Obstetrics
Classification Identical (monozygotic, homologous) twins and fraternal

(heterologous, dizygotic) twins
Clinical Uterine size enlarged in relation to the estimated gestational

presentations age; external obstetric examination detects three large fetal
parts and many small ones by palpation; fetal heart beat
heard in two and more sites, with an auscultatory gap
between them
Diagnosis The most reliable method of diagnosing multiple fetuses in

the first half of pregnancy is ultrasound examination (starting
at 4.5 weeks gestation)
Management Multiple pregnancy is managed as a high perinatal risk

of pregnancy pregnancy as 70% of multiple pregnancies end in pre-term
delivery
Management In most cases the delivery is managed as pre-term delivery.

of delivery The choice of delivery mode depends on the lie and
presentation of the first fetus and the estimated body weight
of each fetus
Complications Complications accompany 70–85% of pregnancies (early

toxicosis, miscarriage, anemia of pregnant women,
pre-eclampsia, thrombophlebitis, gestational diabetes
and pyelonephritis); there is a high risk of hemorrhage
during labor. Perinatal mortality in multifetal delivery is
3–4 times higher than in singleton delivery; it is mostly
due to fetal immaturity, TTTS, reverse arterial perfusion
syndrome
Prophylaxis Early diagnosis and correction of pregnancy complications,

especially of those typical of multiple pregnancy
CONTROL QUESTIONS
1. What types of multiple pregnancies do you know?

2. What are the methods of diagnosing multiple pregnancy?
3. What is the most common type of multiple pregnancy?
4. What complications are typical of multiple pregnancy?
5. What are the principles of managing patients with multiple pregnancy?
6. What is referred to as discordant twins?
7. What is twins headlock?
8. What is the principle of headlock prevention?
CHECK YOURSELF!
Level 1. Test
1. The rate of multiple pregnancy occurrence grows due to:

a) environmental deterioration;
b) young age;
c) older reproductive age;
d) use of contraception.
2. Unfavorable outcomes of multiple pregnancy are due to:

a) pre-term delivery;
b) hemorrhage at early gestational age;
c) early toxicosis;
d) large weight gain.
3. Multiple pregnancy can be suspected if:

a) weight gain over the course of pregnancy is more than 12 kg;
b) there is pronounced anemia (hemoglobin value less than 70 g/l);
c) fundal height outstrips the gestational age;
d) disorder of gait (waddling gait).
4. The most commonly occurring type of twins:

a) monochorionic monoamniotic twins;
b) monochorionic diamniotic twins;
c) dichorionic monoamniotic twins;
d) dichorionic diamniotic twins.
5. Discordant twins are

a) of different sex;
b) of the same sex;
c) pre-term;
d) of different weight.
6. The main complications of multifetal delivery:

a) premature rupture of membranes;
b) labor abnormalities;
d) arterial hypertension in the second stage of labor.
420 Obstetrics
7. Headlock complicates the delivery

a) when the first fetus is in transverse lie and the second one in cephalic
presentation;
b) when the first fetus is in oblique lie and the second one is in cephalic
presentation;
c) when the first fetus is in cephalic presentation and the second one is in cephalic
presentation;
d) when the first fetus is in breech presentation and the second one is in cephalic
presentation.
8. The postpartum period is often complicated by:

a) pre-eclampsia;
b) hypogalactia;
c) hypotonic hemorrhage;
d) painful uterine contraction.

1. A pregnant woman aged 32 presents for her booking visit. Menstrual gestational
age 8–9 weeks. The uterus is enlarged to the size of 11–12 weeks. What is your di-
agnosis? Plan of investigations?
2. A parturient woman aged 35 was brought to hospital in an ambulance; she is in
the first stage of labor with twins. Ultrasound findings indicate the first fetus in breech
presentation, the second—in cephalic presentation. What is the plan of management?
NOTES
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• Chapter 17
ABNORMAL LABOR
17.1. ACTUALITY, EPIDEMIOLOGY
Abnormalities of uterine contractility constitute the most common complication of

labor diagnosed in 10–15% of parturient women; in about every third case it is an
indication for intrapartum cesarean delivery. Up to the present moment there are
no effective methods for prevention and treatment of various disturbances of uterine
contractility. Abnormalities of uterine contractility in labor can lead to dangerous
complications both for the mother and fetus: premature detachment of normally
situated placenta, lacerations of soft tissues in the birth canal, uterine rupture, fetal
hypoxia and injury, etc.
The first mention of commonly noted painful or protracted but inefficient

labor dates back to classical literature. Thus, Hippocrates in his work mentions
the procedure of instrumental and manual dilation of the cervix when labor is
ineffective.
In the 12th and 13th centuries a sponge drenched in opium solution was used to
relieve labor pain. The method was proposed by Hugh of Lucca and Theodoric.
In the 19th century famous obstetricians J. Simpson and A.J. Krassovsky (1889)
suggested administration of chloroform as obstetric anesthesia to treat precipitous
labor.
The Russian obstetrician N.N. Fenomenov (1907) proposed instrumental dissec-
tion of a rigid cervix if pharmaceutical therapy failed.
In his textbook on obstetrics A. Bumm pointed out in 1908 that therapy of spas-
modic pain requires administration of narcotic agents in large doses.
Oxytocin began to be administered in maternity departments for treatment of
hypotonic contractions in labor while β-adrenomimetics were administered in case
of hypertonic contractions.
The second half of the 20th century witnessed a new era in treatment of labor ab-
normalities. The rise of a new discipline, Anesthesiology and Critical Care, promoted
the development and introduction of methods for labor analgesia, management of
dystocia and precipitous labor, introduction of methods of regional anesthesia (epi-
dural nerve block).
422 Obstetrics
17.3. ETIOLOGY AND PATHOGENESIS
The causes of labor abnormalities are various. Conventionally, they can be divided
into the following groups.
Factors persisting prior to pregnancy onset:
• abnormalities of genitalia development;
• anatomical changes in the pelvis;
• genital infantilism;
• uterine tumors (myoma);
• scar on the uterus (after a cesarean, myemectomy) and cicatricial deformity of
the cervix;
• ovarian dysfunction including endocrine infertility;
• young or «old» age of the parturient woman;
• some extragenital illnesses (like obesity).
Factors emerging during pregnancy:
• multifetal pregnancy;
• polyhydramnios or oligohydramnios;
• fetal macrosomia;
• abnormalities in placenta situation;
• unfavorable fetal lie.
Factors emerging during labor:
• unripe birth canal;
• maternal exhaustion;
• inadequate analgesia for painful contractions;
• iatrogenic causes (inadequate management of labor).
Abnormalities of labor can develop resulting from a disturbance at any level in the
mechanism of initiation and progress of uterine contractility.
According to ICD-10, the following forms are distinguished.

• O62 Abnormalities of forces of labor.
– O62.0 Primary inadequate contractions.
– O62.1 Secondary uterine inertia.
– O62.2 Other uterine inertia.
– O62.3 Precipitate labor.
• O63 Long labor.
– O63.0 Prolonged first stage.
– O63.1 Prolonged second stage.
– O63.2 Delayed delivery of second twin, triplet, etc.
– O63.3 Long labor, unspecified.
In Russian obstetric practice, a simpler classification of uterine contractility ab-
normalities is in use:
• pathological preliminary stage;
Chapter 17. Abnormal labor 423
• poor uterine contractility (hypotonic contractions or uterine inertia):

– primary;
– secondary;
– hypotonic pushing efforts (primary or secondary);
• hypertonic labor;
• labor dystocia;
– uncoordination;
– hyperactivity of lower uterine segment;
– convulsive contractions (uterine tetany);
– circulatory dystocia (contraction ring).
In Russian obstetric practice such a clinical entity as pathological preliminary
stage is distinguished, which corresponds to prolonged latent phase of the first stage
of labor (cervical effacement and dilation) distinguished by foreign authors (see
Chapter 8 Clinics and Management of Labor in Vertex Presentation). It is supposed
that this abnormality occurs when the dominant of pregnancy fails to be formed in
the pregnant woman’s cortex before labor. Keeping a partogram helps the novice
doctor to make an early diagnosis of labor abnormality (Fig. 17.1).
The diagnosis of pathological prelimnary period is made on the

NB! basis of irregular contractions occurring in lower abdomen or the
small of the back, lasting over 6 hours but producing no changes
in the cervix (no dilation or effacement) (see Table 8.2).
Making a differential diagnosis between preliminary pain and the start of labor
after one examination presents considerable difficulty even to a very experienced
10
9
8
Cervical dilation, cm
7
e
as
ph
6
e
iv
5
t
Ac
4
3
e
2 tphas
Laten
1
0
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22
Time, h
Secondary uterine inertia Prolonged latent phase

Primary uterine inertia Normal delivery
Fig. 17.1. Variants of partogram in labor abnormality

424 Obstetrics
doctor. For a correct evaluation of what is going on, one should assess several signs
over 3–5 hour observation.
A pathological preliminary period disrupts the woman’s emotional state, disorga-
nizes the daily routine, leads to fatigue and sleeplessness. Inefficient uterine contrac-
tions impair fetal circulation causing fetal hypoxia.
The strategy of managing a pathological preliminary period consists in blocking
abnormal inefficient contractions. Intravenous infusion of β-adrenomimetics can be
used for this purpose.
One of major treatment objectives is relieving pain when regional analgesia can
be administered (epidural nerve block). Further procedures depend on the result
achieved by analgesia.
Three scenarios are possible.
• The patient presents no complaints; hysterography shows no uterine activity.
In this case, if the mother and fetus are in a satisfactory condition, and
there are no contraindications for labor induction, expectant management is
undertaken.
• Active management is undertaken when there are good, effective contractions
and / or cervical ripening has occurred permitting amniotomy to induce labor.
Further management of labor proceeds as usual, with monitoring of the fetal
condition and uterine contractions.
• There are no changes for the better: no effective contractions, no effacement
or dilation of the cervix. Ineffective management, in combination with other
prenatal maternal and fetal factors, promotes an increase in intranatal risk and
justifies termination of pregnancy via cesarean section.
Pathological preliminary period is seen in only 5% of patients before a physiologi-
cal childbirth; however, it precedes labor abnormality in 16–24% of women.
17.5. UTERINE INERTIA
The incidence rate of uterine inertia amounts to 8–10% of all deliveries; in pri-
miparous women uterine inertia is observed twice as often as in multiparas.
17.5.1. Primary uterine inertia

Primary uterine inertia means weak, ineffective contractions from

NB! the onset of labor and during the entire latent phase (until cervical
dilation 4 cm).
Clinical features of labor with primary uterine inertia are extremely varied. There
may be satisfactorily forceful contractions but too spaced-out; and conversely, the
contractions may be frequent but weak and short. Infrequent but sufficiently force-
ful contractions are most favorable for the delivery outcome. Diagnosis of primary
uterine inertia is confirmed by observing the patient: absence of structural changes in
the cervix (dilation and effacement) while contractions are regular; vaginal examina-
tion is done at an interval of 3–4 hours.
Primary uterine inertia is often accompanied by premature membrane rupture
(Fig. 17.2). A prolonged time period after membrane rupture can result in chorio-
amnionitis, hypoxia and intrauterine fetal demise.
Dynamic observation of the rate of contractions, their force and

NB! duration is done using partograms: one enters CTG and vaginal
examination findings onto the partogram.
10
Active Phase
Cervix 9
t
(cm) 8 er n
7 Al tio
Ac
6
5
4
Latent Phase
3
2
1
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
0
Time
Hours
Contractions 1
2
per 3
10 mins 4
5
Oxytocin U/L
10 Units /6 h
drops/min
180
170
Fetal 160
heart 150
140
rate 130
120
BP 110
100
90
80
70
60
Pulse 70 73 75 73 70 73 75
Temp °C N N N N N N N
protein – – – – – – –
Urine acetone – – – – – – –
volume 100 150 150 120 100 120 120
Fig. 17.2. An example of partogram showing primary uterine inertia

426 Obstetrics
Disorder of uterine contractility during the third stage of labor can cause abnor-
mality of placental detachment followed by pathological blood loss (over 0.5% of
patient’s weight). The same disorder can lead to hypotonic and even atonic hemor-
rhage during early postpartum period.
When labor progresses normally, the frequency of contractions is 3–4 in 10 min-
utes, of 40–60 s duration.
The average duration of labor in primiparous patients is 12–14 hours, with the
latent phase of the first stage lasting 8 hours, active phase — about 5 hours, and the
second stage of labor lasting about 60 minutes.
The average duration of labor in multiparous patients is 7–8 hours where the
latent phase is about 5 hours, active phase — about 2 hours, and the second stage
of labor—about 30 minutes.
If labor is ineffective and primary uterine inertia is diagnosed, labor induction
methods are resorted to.
There are two ways to enhance labor activity.
• The first way is non-pharmaceutical: amniotomy.
• The second way is pharmaceutical: administration of oxytocin.
17.5.1.2. Technique of labor induction with oxytocin

Amniotomy is performed preliminarily. Oxytocin administration first begins at
a rate of 0.001–0.002 U/min (1–2 mU/min) increasing the rate every 30 or more
minutes. The rate of oxytocin administration depends on the frequency of contrac-
tions, which should not exceed 3–4 in 10 minutes and can be achieved by oxytocin
infusion rate of 1–2 mU/min.
For induction and stimulation of labor oxytocin is administered only intravenously,
in hospital settings, under specialist surveillance. Simultaneous intravenous and intra-
muscular administration of the medication is contraindicated. The dose is calculated
with consideration to individual sensitivity of the patient and fetus.
The appropriate rate of infusion should be checked scrupulously. An infusion
pump or another similar device should be used during oxytocin administration
for labor induction, as well as monitoring of uterine contractility force and fetal
cardiac activity. If contractile activity of the uterus grows excessively strong, infu-
sion should be discontinued at once, and the excessive uterine contractility will
subside as a result.
Before oxytocin is started, physiological solution that contains no oxytocin should
be administered. A standard oxytocin infusion is made in the following way: dissolve
1 ml (5 U) of oxytocin in 500 ml of non-hydrating fluid and mix thoroughly by ro-
tating the bottle. 1 ml of an infusion made in this way contains 10 mU of oxytocin.
The rate of initial dose administration should not be more than 0.5–4 mU/min
(corresponding to 1–8 drops per minute as 1 drop of infusion contains 0.5 mU of
oxytocin). Every 20–40 minutes it can be increased by 1–2 mU/min until the de-
sired degree of contractions is achieved. Once the desired frequency of contractions
corresponding to spontaneous labor is achieved, as well as cervical dilation 4–6 cm
while no signs of fetal distress are noted, one can gradually reduce the rate of infu-
sion at the same rate at which it was increased. In late pregnancy a high rate infu-
sion requires great care; on very rare occasions a rate more than 8–9 mU/min can
be justified. In case of pre-term delivery a very high infusion rate may be needed,
sometimes exceeding 20 mU/min (40 drops per minute).
All the while one should monitor fetal heartbeat, tone of uterus at rest, the fre-
quency, duration and power of contractions.
When the uterus is hyperactive, of the fetus is distressed, oxyctocin should be
discontinued at once, and the patient should be given oxygen.
Contraindications for labor stimulation:
• threatening uterine rupture;
• transverse and oblique lie of the fetus;
• engagement of extended fetal head;
• fetal hypoxia;
• premature detachment of normally situated placenta.
If labor induction was effective, at the end of the latent phase of labor one faces
the issue of analgesia.
When a desired effect is achieved, the rate of oxytocin administration is not in-
creased any further, and in some patients IV oxytocin infusion is discontinued, and
uterine contractions are closely observed.
When labor becomes excessively powerful and signs of fetal

NB! hypoxia develop, oxytocin infusion is immediately discontinued.
Uncontrolled administration of oxytocin may lead to uterine hyperstimulation. In

this case one type of abnormality, uterine inertia, evolves into another abnormality,
convulsive contractions.
Oxytocin overdose leads to hyperactivity, can cause convulsive contractions, dis-
order of utero-placental circulation. When labor is too powerful, the placenta may
detach prematurely, fetal hypoxia or even uterine rupture may develop.
Labor induction requires observing uterine contractions and the

NB! rate of the progress made by the presenting part over time, and
mandatory CTG.
17.5.2. Secondary uterine inertia

Secondary uterine inertia is decrease in the vigor of uterine contractions (after nor-
mal contractions in the latent phase) during the active phase of labor (the frequency
of contractions less than 3 in 10 minutes) (Fig. 17.3). Subjectively the contractions
are assessed as painful, weak.
Hypotonic pushing efforts means a decrease in the vigor of labor during the second
stage of labor emerging due to muscle weakness in the anterior abdominal wall or
general exhaustion of the patient. When there is secondary uterine inertia, both the
first and second stages of labor become longer.
At the onset of labor the contractions are quite powerful, prolonged and fre-
quent, but later they become weaker and shorter with longer intervals between
them; sometimes contractions subside entirely. Cervical dilation slows down or
428 Obstetrics
10
Active Phase
Cervix 9 t
er
(cm) 8 Al n
7 tio
Ac
6
5
4
Latent Phase
3
2
1
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
0
Time
Hours
Contractions 1
2
per 3
10 mins 4
5
Oxytocin U/L
5 Units /3 h
drops/min
180
170
Fetal 160
heart 150
140
rate 130
120
BP 110
100
90
80
70
60
Pulse 70 73 75 73 70 73 75
Temp °C N N N N N N N
protein – – – – – – –
Urine acetone – – – – – – –
volume 100 150 150 120 100 120 120
Fig. 17.3. An example of partogram showing secondary uterine inertia
stops. The progress of the fetal presenting part along the birth canal also slows
down or stops.
Prolonged duration of labor results in pronounced maternal exhaustion, and the
interval after membrane rupture becomes protracted.
If labor and the associated fetal head descent weaken or stop entirely, the soft
birth canal tissues and adjacent organs (the bladder, urethra, rectum) undergo pro-
longed compression between the fetal head and maternal bony pelvis. This results
in disorder of venous return, edema of soft tissues in the birth canal, and later—
hypoxia-mediated changes of tissues. In the long term, the patient may develop a
fistula (rectovaginal fistula, for instance). The presenting fetal head also develops a
pronounced edema of soft tissues, a large caput succedaneum. The newborn may
develop cerebral circulatory disorders due to hypoxia and even cerebral hemorrhage,
also hypoxia-mediated.
Fetal head should not linger in one pelvic plane over 1 hour in
NB! a primiparous, and over 30 minutes in a secundiparous mother.
A prolonged interval after membrane rupture carries a risk of chorioamnionitis,

and during the puerperium — of endometritis.
The third stage of labor and early puerperium in patients with uterine inertia is
often complicated by hypotonic and atonic hemorrhage.
If the abnormalities of labor fail to improve, one should once again assess the
fetal size, specifics of head engagement (rule out engagement of extended head),
maternal pelvic dimensions so as to exclude secondary uterine inertia as a sign of
cephalopelvic disproportion.
If there are no contraindications, labor induction with oxytocin in

NB! the regimen described above is administered.
Patients for whom labor induction is contraindicated, and patients showing a

considerable intranatal progression of risk factors are given an emergency abdominal
delivery.
If the fetus shows signs of hypoxia while the mother has secondary uterine inertia
in the second stage, or hypotonic pushing efforts when the head is in the pelvic cavity
or at the pelvic outlet — these factors are an indication for emergency termination of
pregnancy through vaginal passages. The delivery is brought to an end by applying
obstetric forceps or vacuum extraction to the fetal head.
17.6. EXCESSIVE UTERINE ACTIVITY
Excessive uterine activity is characterized by powerful, high-amplitude, pro-

longed (over 1 min) and frequent (over 4 in 10 min) contractions with short intervals
(1–2 min) between them. The patient is, as rule, overwrought, crying and com-
plaining of unabating pain. Between contractions, the uterus relaxes for 30–60 s.
Labor may be quite normal at the onset, but sometimes excessively powerful
contractions are noted as early as in the first stage. Powerful contractions at short
intervals result in a rapid cervical effacement and dilation. During the second stage
of labor the pushing efforts are forceful like contractions, so the fetus is delivered
over 1–2 pushing efforts.
Uterine tetany develops less often; it is characterized by a high uterine tone and
powerful, high-amplitude, acutely painful contractions, but the interval between them
cannot be determined.
430
Fig. 17.4. Excessive uterine activity. Cardiotocogram

Obstetrics
When uterine activity is excessive, labor proceeds very fast: less

NB! than 6 hours in primiparas, and less than 4 hours in secindiparas;
this is called oxytocia. If labor lasts less than 4 hours in
primiparas and less than 2 hours in secindiparas, it is described
as precipitous labor.
Diagnosis is made on the grounds of clinical assessment of contractile activity or

CTG, and specified (like in case of any labor abnormality) on the basis of vaginal
examination findings (Fig. 17.4).
Excessive uterine activity is dangerous both for the mother and fetus. Vigorous
labor can result in premature placenta detachment. During excessively powerful
contractions the utero-placental circulation is disturbed, fetal condition deteriorates;
there appear signs of fetal hypoxia. A fast progress of fetal head along maternal pas-
sages interferes with the molding process. The head is exposed to strong compres-
sion, which often leads to craniocerbral fetal injury (disorder of cerebral circulation,
intracranial hemorrhage, etc.). Precipitous expulsion of the fetus is accompanied by
injury to maternal soft tissues of the birth canal. As the reserves of contractile uter-
ine activity have been depleted, the early postpartum period is often complicated by
hypotonic or atonic hemorrhage.
The condition is managed in this way: the puerpera lies on her side
NB! opposite to the fetus location. Uterine activity is brought to normal
using acute tocolysis with beta-adrenergic agonists [hexoprenaline
(Ginipral♠)] administered intravenously by droplet infusion.
Analgesia is provided via epidural nerve block, which is continued into the second
stage of labor. The patient is put on her side, and the perineum is protected by not
turning on the back. At the end of the second stage and after delivery one should
administer prolonged (2 h) prophylaxis of hemorrhage via IV droplet infusion of
oxytocin.
17.7. UNCOORDINATED UTERINE ACTIVITY (HYPERTONIC

DYSFUNCTION)
Uncoordinated uterine activity means absence of coordinated (unidirectional) uter-
ine contractions in separate muscular fibers in uterus, in some cases in the form of
muscular fibrillation.
This abnormality is seen in 1% of parturient women. Uncoordinated uterine activ-
ity is usually noted in the first stage of labor; it is manifested by uterine contractions
emerging in different parts due to displacement of regeneration zone and propagation
of activity impulses. Several such zones can arise at the same time. Meanwhile the
myometrium is no longer able to maintain synchronous contraction and relaxation
of certain parts. Basal tone of the myometrium becomes inadequately high, which
makes contractions less efficient. Despite quite powerful uterine contractions the
cervix fails to dilate. As a result, labor becomes ineffective.
432 Obstetrics
The following forms of hypertonic uterine dysfunction are distinguished:

• dystocia of uterine cervix: absence of cervical relaxation when the musculature of
uterine body contracts;
• hyperactivity of lower uterine segment: the contraction wave propagates from the
lower segment upwards.
Clinical presentations of uncoordinated labor include painful,

NB! irregular contractions of varying amplitude with irregular intervals
between them, constant pain in the back or lower abdominal
segment. Between the contractions the uterus does not always
relax completely. Cervical dilation is absent or insignificant. The
progress of labor slows down or comes to a standstill.
Premature rupture of membranes is quite common.

Diagnosis of uncoordinated uterine activity is made on the basis of clinical pre-
sentations of labor and CTG findings; it is specified upon a vaginal examination.
When uterine activity is uncoordinated, contractions of varying power occur
at different time intervals. The parturient woman complains of strong pain in the
lumbar region and in the lower abdomen which does not always subside when the
contraction is over.
A vaginal examination demonstrates no change in cervical effacement or dilation.
Treatment of uncoordinated uterine activity consists in eliminating pathological
labor. One of the main methods is effective analgesia with epidural nerve block and
intravenous tocolysis with β-adrenomimetics.
When treatment proves ineffective or signs of fetal hypoxia develop, the delivery
is terminated via emergency cesarean section.
Uncoordinated uterine activity produces the same maternal and fetal complica-
tions as those seen in excessive uterine activity.
REMEMBER!
Epidemiology 10–15% of deliveries
Etiology and pathogenesis Anatomically contracted pelvis, CPD, inade-
quate management of labor, overdistension
of uterus (polyhydramnios, multifetality,
fetal macrosomia), uterine malformations
and tumors, maternal exhaustion.
Clinical features and diagnosis Monitoring of contractions (CTG), par-
togrpahy, assessment of cervical condition
over time, patient’s complaints.
Algorithm and treatment Uterine inertia: medication-induced rest,
analgesia, labor induction. Pathological
preliminary period, excessive or uncoordi-
nated uterine activity: epidural analgesia,
tocolysis. If these fail — cesarean section.
Complications Premature detachment of normally situated

placenta, uterine rupture, maternal injury
during labor, prolonged period after mem-
brane rupture, chorioamnionitis, hypoxia,
fetal injury and intrauterine demise.
CONTROL QUESTIONS
1. What is referred to as pathological preliminary period?
2. What is uterine inertia?
3. What are the causes of labor abnormalities?
4. What types of disorders of uterine contractions are distinguished?
5. What is the therapy of uterine inertia?
6. What is the therapy of uncoordinated uterine activity?
7. What are maternal complications in labor abnormalities?
8. What are fetal complications in labor abnormalities?
CHECK YOURSELF!
Level 1. Test
1. Uterine inertia is divided into:
a) primary, secondary and tertiary;
b) spontaneous, iatrogenic;
c) acute, chronic;
d) primary, secondary.
2. Therapy for uterine inertia includes:

a) amniotomy, oxytocin;
b) amniotomy, prostaglandins;
c) oxytocin, prostaglandins;
d) amniotomy, analgesia.
3. Excessive contractile activity of the uterus means that contractions are:

a) 2–3 in 10 min, amplitude 35 mm Hg;
b) 3–4 in 10 min, amplitude40 mm Hg;
c) 5–6 in 10 min, amplitude 20 mm Hg;
d) 4–5 in 10 min, amplitude 60 mm Hg.
4. Therapy of uncoordinated uterine activity includes:

a) oxytocin;
b) analgesia;
c) amniotomy;
d) prostaglandins.
434 Obstetrics
5. Complications of uncoordinated uterine activity are:

a) fetal hypoxia, premature membrane rupture;
b) birth trauma in the fetus, difficult urination in the mother;
c) hypoxia and birth inside an intact amniotic sac;
d) precipitous delivery, fetal hypoxia.

1. Primipara aged 23 has been in labor for 9 h. Contractions come every 4–5 min-
utes, of 25–30 s duration. Fetal condition is satisfactory. A vaginal examination
detects a distinctly shortened cervix; 2 finger widths fit into the cervical opening; the
gestational sac intact; the presenting part is the head. What is your diagnosis? What
is your plan of management?
2. A secundipara aged 27 has been in labor for 2 h. Contractions come every 60 s,
of 55–60 s duration. Fetal condition is satisfactory. A vaginal examination detects
an effaced cervix, dilation 5 cm, no gestational sac, the presenting part is the head.
What is your diagnosis? What is your plan of management?
NOTES
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• Chapter 18
HEMORRHAGE IN OBSTETRICS
ICD-10 codes
• O44.1 Complete placenta previa with hemorrhage.
• O45.0 Premature separation of placenta with coagulation defect.
• O46.0 Antepartum hemorrhage with coagulation defect.
• O67.0 Intrapartum hemorrhage with coagulation defect.
• O69.4 Labor and delivery complicated by vasa previa.
• O71.0 Rupture of uterus (spontaneous) before onset of labor.
• O71.1 Rupture of uterus during labor.
• O71.2 Postpartum inversion of uterus.
• O71.3 Obstetric laceration of cervix.
• O71.4 Obstetric high vaginal laceration alone.
• O72.0 Third-stage hemorrhage.
• O72.1 Other immediate postpartum hemorrhage.
• O72.2 Delayed and secondary postpartum hemorrhage.
• O75.1 Shock during or following labor and delivery.
18.1. GENERAL INFORMATION
Obstetric hemorrhage is a common, dangerous complication of pregnancy and
childbirth. Any bleeding from the birth canal during pregnancy, labor or puerperium
is regarded as pathological.
Hemorrhage is inside the top five causes of maternal mortality: sepsis, ec-
lampsia, obstructed labor, and unsafe abortion (WHO). Over 50 000 women die
of hemorrhage every year. In the Russian Federation, hemorrhage ranks second
after extragenital disease in the structure of maternal mortality (according to the
Ministry for Health Care of Russian Federation, 2013) and accounts for 20% of
deaths.
Although delivery is nowadays managed in hospital settings using up-to-date
methods of hemostasis and replacement of the volume of lost blood, hemorrhage
remains one of the main causes of maternal mortality in Russia.
This is due to the specific nature of obstetric hemorrhage, its sudden onset and
massive flow of blood. Implicitly, obstetric hemorrhage cannot be arrested until ma-
gistral blood flow to the uterus is controlled or the uterus is removed as the source
of hemorrhage.
436 Obstetrics
1.6 0.5
а 3.3
3.3
30.7
6.1 Extragenital disease
Hemorrhage
9.4 Embolism
Abortion
Gestosis
Sepsis
10.7 Anesthesia complications
Uterine rupture
Ectopic pregnancy
Other
16.8 17.6
b 4.1 1.3
9.4
9.4 34.8
17.2
23.8
Fig. 18.1. Structure of maternal mortality causes in the Russian Federation, % (Ministry
for Health Care of Russian Federation, 2013): a — inclusive of abortions, rupture of uterus,
ectopic pregnancy; b — net causes
Profuse hemorrhage is always accompanied by hemorrhagic shock and consump-

tion coagulopathy (DIC syndrome).
In obstetrics, hemorrhage is classified according to the time of its onset. Somehow
or other, all classifications follow this rule stated by E.Bumm.
Classification of WHO
• intrapartum hemorrhage (obstetric and non-obstetric);
• third-stage and postpartum hemorrhage (immediate and late postpartum
hemorrhage).
Hemorrhage during pregnancy, the first and second stage of labor can be related
or unrelated to gestational sac abnormalities.
Classification accepted in Russia:
• hemorrhage in early and late pregnancy;
• hemorrhage during the first and second stage of labor;
Chapter 18. Hemorrhage in obstetrics 437
• hemorrhage during the third stage of labor;

• hemorrhage in the immediate and late postpartum period.
Classification accepted in the USA:
• antepartum hemorrhage (placenta separation, placenta previa);
• postpartum hemorrhage: hemorrhage in the third stage, hemorrhage due to
uterine atony, retention of placental fragments, placenta accreta, inversion of
uterus, genital tract lacerations, postpartum hematoma, rupture of uterus.
18.2. EARLY PREGNANCY BLEEDING
Definition. Vaginal bleeding occurring before 22 weeks gestation is referred to as

bleeding in the first half of pregnancy or early pregnancy bleeding (WHO, 2002).
Etiology. Hemorrhage during pregnancy can arise due to multiple causes, some
of them constituting a threat to the woman. Early pregnancy hemorrhage is one of
most common causes of hospitalization.
According to their etiology, vaginal bleedings in pregnancy are divided into those
related and unrelated to pregnancy, obstetric and non-obstetric bleeding (WHO,
2002). Hemorrhage can develop due to a combination of obstetric and non-obstetric
causes.
Non-obstetric causes of vaginal bleeding:
• cervical ectopia;
• cervical polyp;
• cervical cancer;
• vaginal and vulvar varices;
• vaginal and vulvar trauma.
Obstetric causes of vaginal bleeding:
• spontaneous abortion (incipient, inevitable, incomplete abortion)
• bleeding after abortion;
• criminal way of pregnancy termination (at any gestational age, often in early
pregnancy);
• interrupted ectopic pregnancy;
• trophoblastic disease;
• placenta previa, low lying placenta
• premature abruption of normally located placenta, placental abruption (placenta
attached to a scar, myomatous node, the bladder).
Bleeding due to placenta previa or premature abruption is rarely seen at an early
gestational age. It commonly occurs after 22 weeks gestation and can be massive.
The main cause of early pregnancy vaginal bleeding is spontaneous or artificial
abortion.
18.2.1. Pregnancy and bleeding cervical ectopy

In cervical ectopy the blood-tinged discharge is insignificant and painless. It can
occur spontaneously, upon tension (constipation, lifting heavy objects) or upon me-
chanical contact (coitus, vaginal examination).
438 Obstetrics
When a pregnant woman has bleeding cervical ectopy, incipient spontaneous

abortion and cervical cancer should be ruled out; the doctor makes a series
of specialized examinations: speculum examination of the cervix, colposcopy,
bimanual vaginal examination, vaginal smears for culture and cytology studies
(Fig. 18.2).
When these manipulations are performed with care, they usually do not affect
the pregnancy.
Treatment. If there is vaginitis and cervicitis, local antibacterial therapy is admin-
istered (vaginal tablets and suppositories) followed by restoration of normal vaginal
biocenosis.
18.2.2. Pregnancy and bleeding cervical polyp

When a pregnant woman has a cervical polyp, she complains of scanty blood-
tinged discharge from the vagina that occurs suddenly without an apparent cause,
sometimes after intercourse; the bleeding is painless.
In case of cervical polyp the doctor should rule out incipient abortion and cervical
cancer, so the patient is hospitalized.
Treatment. Polyps require surgical treatment, polypectomy. No endocervical cu-
rettage can be done in pregnancy. Decidual polyps can resolve spontaneously. A
removed polyp should be referred for histology examination.
18.2.3. Pregnancy and cervical cancer

If cervical cancer is detected in early pregnancy, the patient is immediately hos-
pitalized to an oncology department.
Termination of pregnancy is absolutely contraindicated as this
NB! may trigger massive hemorrhage and promote the spread of
malignancy.
Radical surgical treatment is resorted to in such cases: radical hysterectomy of
the pregnant uterus. At gestational age after 16 weeks first a cesarean delivery is
performed (sectio cesarea parva), and then the uterus, appendages and lymph nodes
Fig. 18.2. Bleeding cervical ectopy Fig. 18.3. Cervical polyp in a pregnant woman
are removed. If the condition is detected at the end of the second trimester or in
the third trimester, it is expedient to prolong the pregnancy to 34 weeks, perform a
cesarean section, and then, after an examination by oncologist, radical hysterectomy
is performed (Fig. 18.4).
18.2.4. Vaginal or vulvar injury, bleeding varices

during pregnancy
Vaginal bleeding may develop upon a mechanical injury (lacerations of vaginal
mucosa after a fall, traffic accident, rape, etc.), chemical injury (burns caused by
chemicals or drugs) or upon injury to varicose veins in the vagina or vulva (Fig. 18.5).
Fig. 18.4. Cervical cancer and pregnancy Fig. 18.5. Varicose vulvar veins
The pregnant woman is hospitalized. Management and extent of therapy are de-
termined by the degree and depth of injury and bleeding. In a mechanical injury the
source of hemorrhage is established, the bleeding vessels are identified and ligated.
When the bleeding has been arrested, and there are no signs of infection, the impaired
continuity of vaginal or vulvar tissues is restored.
Burns of vaginal or vulvar mucosa can be extensive or present as single or multiple
ulcerations; they bleed easily. In such cases therapy consists in administration of dis-
infecting solutions or ointments (gels) with anti-inflammatory action and promoting
epithelization of the injured surface.
In patients with varicose veins the bleeding can be profuse, so sometimes ligation
of bleeding vessels is required.
18.3. HEMORRHAGE IN II–III TRIMESTERS

AND IN I–II STAGES OF LABOR
Definition. Hemorrhage developing after 22 weeks gestation is referred to as bleed-
ing in late pregnancy, or antepartum bleeding (WHO, 2002).
Causes of hemorrhage in the first and second stages of labor are the same as
those after 22 weeks gestation. They can be obstetric or non-obstetric. All obstetric
hemorrhage is uterine bleeding.
440 Obstetrics
The gestational age 22 weeks is used as a conventional delimitation as management

of hemorrhage at any gestational age or during labor is based on the same principles.
The bleeding can be arrested completely only upon removing the gestational sac from
the uterus. Only this measure permits the uterus to contract and gives the chance to
render antishock procedures that can save the mother’s life. It is expedient to discuss
these hemorrhages in one chapter.
Classification. Hemorrhage is classified as obstetric and non-obstetric. At this
gestational age non-obstetric bleeding is a rare occasion.
The main cause of hemorrhage in the second and third trimester

NB! as well as in the first and second stage of labor is placenta previa
and PROM.
18.3.1. Placenta previa

18.3.1.1. Definition
Placenta previa means abnormal situation of the placenta; it is inserted in the lower
uterine segment below the presenting fetal part and occludes, partially or wholly, the
internal os. Placenta previa finds itself in the way of the delivering fetus (Fig. 18.6).
18.3.1.2. Statistics
There has been a rise in the incidence of placenta previa over the latest decade,
which is attributed to a greater incidence rate of abortions, cesarean sections, recon-
structive surgery on the uterus and intrauterine interventions.
In Russia the incidence of placenta previa is 0.95% of all deliveries. In multiparous
women it is seen more often (75%) than in primiparous patients. Pregnant women
with placenta previa have vaginal bleeding in 34% of cases, and during labor — in
66% of cases.
Placenta
Fetal head
Fig. 18.6. Complete placenta previa (ultrasound)

When massive bleeding due to placenta previa occurs, maternal

NB! morbidity amounts to 23%; preterm delivery is noted in 20% of
patients. Perinatal mortality rises manifold: from 170 to 260‰.
The causes of abnormal placental situation are not clearly understood. Some
authors associate it with pathological processes in the uterus, others — with specific
processes in the gestational sac. Thus there are two factors affecting the formation
of placenta previa: maternal and fetal, or rather the factor of the gestational sac.
Abnormalities of placenta implantation commonly arise when there are atrophic
and dystrophic processes in the endometrium that disrupt normal decidual endo-
metrial reaction. The fertilized egg (zygote) cannot implant in the pathologically
changed lining of the fundus and body of the uterus, and descends to the lower
segment.
Pathology of endometrium is possibly associated with chronic inflammation and
dystrophic changes after abortions and deliveries, scarring after uterine surgery (ce-
sarean section, conservative myomectomy, uterine perforation, etc.), multiparity,
advanced maternal age in primiparas, smoking, drug abuse, septic complications in
the puerperium and after abortions in past history.
Placenta previa is noted 3 – 5 times more often after a previous

NB! cesarean section.
Normal implantation of the zygote is disturbed when there is a disorder in spatial

relations inside the uterus and the condition of its walls in presence of myoma of
uterus, uterine malformations, infantilism. Maternal angiopathy secondary to cardio-
vascular, renal, hepatic disease, diabetes mellitus, smoking disrupts the circulation
in pelvic organs including the uterus, and promotes anomalous implantation of the
fertilized egg and formation of placenta previa. Intrauterine interventions impair the
structure and metabolism of endometrium and promote insufficiency of placental
bed and of the placenta.
Sometimes the development of placenta previa is associated with specifics of the
gestational sac. The fertilized egg cannot implant in the fundus area in due course
as the nidation function of the trophoblast is disturbed secondary to delayed enzy-
matic processes in the trophoblast. The egg acquires implantation capability only
upon descending to the lower segment, the villous chorion proliferating in the area
of internal os.
If the decidual membrane is not well-developed in the lower segment area, this
gives rise to adherent placenta or placenta accreta, especially if there is a scar on
the uterus after a previous cesarean section. When there is placenta previa, the lower
segment of uterus turns into spongy cavernous tissue that contracts poorly, is easily
injured upon surgical interventions and serves as an additional source of hemorrhage.
In placenta previa hemorrhage develops due to placenta separation from the uter-
ine wall. This situation of the placenta results in its insecure attachment and rupture
of placental vessels causing spontaneous bleeding that is not associated with injury.
442 Obstetrics
Early in the second half of pregnancy placental separation occurs when the isthmus
somewhat stretches two ways, the lower segment is formed, and the inextensible
placenta loses touch with the uterine wall. During the last weeks of pregnancy, as
Braxton Hicks contractions intensify or labor develops, placenta previa separates from
the uterine wall causing bleeding to begin, which grows worse in the course of labor.
Placenta previa is classified into complete, incomplete and low-lying placenta.
There is no clinical significance in distinguishing lateral and marginal placenta
previa. Low-lying placenta is the most favorable variety of all types of pathological
placental situation.
• Complete placenta previa is a clinical situation when the internal os is completely
covered by the placenta (Fig. 18.7a).
• Incomplete placenta previa is a clinical situation when the internal os is partially
covered by the placenta (Fig. 18.7b).
• The variants of placenta previa situation are of relative value for obstetric care
during labor. As the cervix dilates the situation of placenta previa can change as
the lower placental edge separation proceeds slower than cervical dilation.
• Low-lying placenta is a clinical situation when the lower placental edge is situated
less than 7 cm from the internal os but does not entrap its edge (Fig. 18.7c). In
а b c
Fig. 18.7. Placenta previa varieties: a — complete placenta previa; b — incomplete placenta
previa; c — low-lying placenta
a vaginal examination, fetal membranes are palpated behind the internal os,
sometimes the rough surface of fetal membranes is detected, which suggests a
closely situated placenta.
English-language textbooks (Williams Obstetrics, 2006) propose a similar clas-
sification distinguishing also marginal placenta previa when the placenta is next to
the cervix but does not cover the opening; at cervical dilation 4 cm only the lower
placental edge is palpated. The condition of vasa previa is considered separately.
This is a rare situation (velamentous cord insertion) when umbilical vessels situated
in fetal membranes cover the internal os (1:5200 pregnancies). When the amniotic
sac ruptures, the presenting vessels are ruptured too, which leads to fetal hemorrhage
and fetal demise (Fig. 18.8).
Fig. 18.8. Velamentous cord insertion

The main clinical sign of placenta previa is bleeding from the uterus. In placenta
previa uterine hemorrhage commonly develops at gestational age 28–30 weeks due
to the formation and distension of the lower segment.
When there is placenta previa, hemorrhage has its specifics. During pregnancy
hemorrhage has a sudden onset, it is painless; it can suddenly discontinue but reap-
pear after some time. The intensity of hemorrhage does not always indicate the degree
to which the placenta encroaches upon the cervical os: there may be insignificant
hemorrhage in complete placenta previa, while incomplete placenta previa can be
accompanied by profuse hemorrhage if the laceration passes in the area of marginal
venous sinus.
The lower the placenta is situated, the earlier and more powerful
NB! is the hemorrhage.
444 Obstetrics
Due to constant blood loss the pregnant women quickly develop progressing
anemia.
In complete placenta previa the hemorrhage is often of an early

NB! onset in the second trimester; the bleeding can be profuse at
once or show scanty discharge; it can discontinue for some time
and then recur.
During the last weeks of pregnancy when precursors of labor develop, the hemor-
rhage recommences and / or intensifies. Hemorrhage can first present with the first
contractions. If there was insignificant vaginal bleeding during pregnancy, the first
contractions enhance the hemorrhage.
During labor, when the cervix is fully dilated, abnormally situated placenta sepa-
rates more and more. A placenta that covers the internal os prevents the presenting
fetal part from engaging the pelvic inlet and pressing the bleeding portion to pelvic
walls. Acute anemia progresses fast.
In incomplete placenta previa the hemorrhage begins at the end

NB! of pregnancy, often in the early dilation period or even later when
the cervix is effaced and dilated 4 – 5 cm.
The intensity of hemorrhage depends on the separated area. Thus, the greater
the area of placenta previa, the earlier the hemorrhage sets on, and the heavier it is.
In case of placenta previa, when the head engages with its occiput, the hemorrhage
may attenuate or even halt for a time after the passage of amniotic fluid as the fetal
head descends into the pelvic inlet and presses the separated placental part to the
uterine and pelvic walls arresting the bleeding.
Upon unfavorable engagement the lower uterine segment cannot embrace the head
as tightly as in occipital presentation so the bleeding does not stop. In abnormal fetal
lie (transverse or oblique), when there is no presenting part, the bleeding can even
grow worse.
Low-lying placenta is the most favorable variety of placenta

NB! previa. Hemorrhage often begins at the end of dilation period; it
is not so profuse as in case of other varieties.
Low-lying placenta is also diagnosed by ultrasound examination; it can be con-

firmed by an inspection of the delivered placenta: the rupture of fetal membranes is
at a small distance from the placental edge. The following complications are possible
during pregnancy: pre-term delivery, placental insufficiency, chronic hypoxia and
slow fetal growth, maternal anemia.
Fetal hypoxia is the second main sign of placenta previa; it can be chronic or acute.
Chronic fetal hypoxia develops during pregnancy due to placental insufficiency sec-
ondary to reduced blood supply to the lower uterine segment. Recurrent insignificant
uterine bleeding can be another cause of chronic hypoxia; this bleeding results in
exclusion of a major part of vessels of separated placenta from placental circulation.
Placenta
Internal os
Fig. 18.9. Low-lying placenta, ultrasound
The separated part of placenta does not participate in the system of utero-placental
blood circulation so the expression of hypoxia depends on the area of separated
placenta previa and some other factors.
When placental separation progresses and the patient bleeds

NB! profusely, acute fetal hypoxia develops.
When placenta previa is not accompanied by bleeding, other presentations are

scarce. An external obstetric examination often detects oblique or transverse fetal
lie, unstable fetal lie, breech presentation, high fetal station.
Delivery is often accompanied by bleeding due to abnormal placental separation
secondary to partial tight attachment (less often — ingrowth) of chorionic villi to the
lower uterine segment, uterine atony, amniotic fluid embolism, thromboembolism,
ascending infection. The bleeding can continue into the puerperium.
18.3.1.6. Diagnosis
Diagnosis is made on the basis of history findings, clinical signs, obstetric inves-
tigations and ultrasound examination.
History taking. The main sign of placenta previa is painless vaginal bleeding that
occurs when the uterus is «undisturbed», often after physical strain (defecation, uri-
nation, intercourse) or upon the onset of labor. It can be profuse at once or present
in the form of scanty vaginal bleeding.
The pregnant woman presents with vaginal bleeding that occurred spontaneously,
during sleep or at rest. There is no pain. Scarlet, bright red blood discharges from
the vagina. When the discharge is scanty, the blood is dark red.
Questions about obstetric and gynecologic past history are aimed at finding out
about previous infections of the uterus and appendages, septic complications after
delivery or abortion, parity, the number of abortions and surgeries (myomectomy,
446 Obstetrics
cesarean section, perforation of uterus), uterine malformations, ovarian dysfunction.

One should find out about the course of the present pregnancy, if there was threat-
ened abortion, vaginal bleeding in early pregnancy, anemia, unstable fetal lie, etc.
The gestational age when the hemorrhage developed also matters; in the second
trimester the bleeding is usually associated with complete placenta previa, in late
pregnancy or at the beginning of the first stage of labor it is mostly due to incomplete
placenta previa or low-lying placenta.
Special obstetric examination. When doing an external obstetric examination, one
notes the uterus condition (its tone, tenderness), fetal lie in the uterus, its heartbeat.
The uterus is usually in normal tone, with even contours, soft to palpation, painless
in all parts. Unfavorable fetal lie (transverse or oblique), breech presentation, high
fetal station are frequent findings. When the pregnant woman presents with hemor-
rhage at the maternal welfare clinic, she is only given a general examination and
external obstetric examination.
At the maternal welfare clinic no cervical or vaginal examination

NB! is performed if the patient presents with vaginal hemorrhage
as the manipulations can aggravate the condition.
Ultrasound helps to clarify the degree of overlap, the area of placental separation,
and fetal condition. Vaginal examination is contraindicated. The pregnant woman is
hospitalized immediately.
If a pregnant woman or woman in early labor shows vaginal

NB! bleeding, emergency hospitalization is indicated.
When a pregnant woman with vaginal bleeding is admitted to hospital to make a

final diagnosis, speculum examination of the cervix is required.
Speculum examination of the cervix is only performed at a

NB! maternity hospital, with major surgical facilities standing by.
Speculum examination is needed to rule out other sources of vaginal bleeding:

ectopy, polyp, cervical malignancy, varicose veins and vaginal injury.
In presence of placenta previa the cervix and vagina are cyanotic, lucid; scarlet
blood is discharged from the cervical canal.
If a diagnosis of placenta previa was made and confirmed using

NB! ultrasonography, no vaginal examination is performed.
In presence of low-lying placenta a vaginal examination detects only gestational

sac membranes. The membranes are thick, with a rough surface as the chorionic villi
do not undergo complete atrophy near the placenta but persist in the form of small
papillas until the end of pregnancy. They are localized only in the part of membranes
that immediately adjoins the placental edge. Placental tissue is not palpated as the
placental edge is above the internal os.
18.3.1.7. Laboratory tests and instrumental investigations
The diagnosis of placenta previa should be established at the maternal welfare
clinic using ultrasound, prior to hemorrhage development. Ultrasound permits a
precise assessment of placenta localization and the degree of the overlap. Transvaginal
sonography (performed only if there is no bleeding) provides more reliable evidence.
Determination of placenta localization is in the protocol of screening ultrasound
examination at 11–14, 22–22 and 32 weeks gestation. If in the second trimester the
lower placental edge is found to be localized in the area of internal os, later in 95%
of patients it shifts to the fundus of uterus. In fact, the placenta itself does not shift;
rather, the shift occurs due to conversion of the uterine isthmus to the lower uterine
segment at the beginning of the third trimester.
Ultrasound diagnosis of complete placenta previa is made when it fully covers the
internal cervical os passing onto uterine walls. In case of incomplete placenta previa
it partially covers the internal os or is localized at its edge.
18.3.1.8. Differential diagnosis

One should not strive to establish the ultimate cause of hemorrhage in the mater-
nity welfare clinic setting, as complete examination of the patient is impossible due
to the threat of bleeding growing worse. This is the objective of hospital caregivers.
Placenta previa should be differentially diagnosed from the following conditions:
• late spontaneous abortion or pre-term delivery;
• premature separation of normally situated placenta;
• laceration of marginal placental sinus;
• laceration of umbilical vessels when they are attached to placental membranes;
• uterine rupture;
• injury of soft tissue in the birth canal;
• varicose vein rupture;
• cervical ectopy;
• cervical polyp;
• genital wart.
A speculum examination of the vagina and cervix suffices to rule out non-obstetric
causes.
When there is abruption of placenta, clinical presentations depend on the area and
localization of the abruption. The first presentation is pain in the area of uterus;
external bleeding may not be present or be scanty. The uterus is tense, tender to
palpation; it does not relax. Fetal heartbeat can vary (Fig. 18.10).
When there is rupture of marginal sinus the bleeding develops suddenly at the end
of pregnancy or in the first stage of labor. The escaping blood is of bright red color.
The bleeding can arrest or start again.
When there is umbilical vessels rupture, the bleeding develops following membrane
rupture or immediately upon amniotomy: scarlet blood flows from the vagina while
fetal heartbeat changes suddenly or subsides altogether.
Rupture of uterus along the scar can be complete or incomplete.
• When the rupture is incomplete, the uterine walls slowly dehisce along the scar.
The fetus commonly survives. Vaginal bleeding appearing due to incipient uterine
448 Obstetrics
rupture is mistaken for low-lying placenta. Clinical presentations of deficient

uterine scar are inapparent: insignificant tenderness in the scar area upon palpation
or fetal movement. Nausea and, less often, vomiting is a typical sign.
• In complete rupture the fetus usually dies. It can fi nd itself entirely in the
abdominal cavity and so that the fetus can be felt immediately behind the anterior
abdominal wall. The pregnant woman is in shock (see Chapter 26 Maternal
Obstetric Trauma).
18.3.1.9. Treatment
Pregnant women with placenta previa are regarded to be at high obstetric risk.
Ultrasound during pregnancy helps to detect the low localization of the placenta as
well as reveal, using dopplerometry, the signs of placenta accreta. Beginning in the
second trimester, sonography helps to follow the process of placental shifting, to
detect signs of abruption.
Treatment is provided only in hospital settings where the pregnant or parturient
woman is admitted when vaginal discharge begins.
The aim of treatment is to arrest the bleeding. Upon admission, examination and
making the diagnosis the management plan and the mode of delivery are decided
upon, and the patient is referred to the team on duty.
Management is determined by the type of placenta previa, gestational age or stage
of labor, and, above all, by the rate of bleeding and the amount of lost blood.
When there are no indications for surgery, conservative treatment is used. In other
cases emergency surgery is indicated.
Conservative treatment is an option in any variety of placenta

NB! previa when the pregnancy is preterm, there is no or only
slight bleeding, and as long as the woman’s general condition
is satisfactory (systolic blood pressure above 100 mm Hg,
hemoglobin content in the blood no less than 100 g/L).
The patient should observe strict bed rest, avoid any physical strain; pharmaceuti-
cal therapy is administered. When the uterus is in hypertone or blood discharge is
scarce, oral or intravenous tocolysis is administered. When there are no indications
for speedy termination of pregnancy and in preterm pregnancy (before 34 weeks),
prevention of RDS in the fetus is initiated.
If the pregnancy is preterm and there is no vaginal bleeding, the patient and fe-
tus are in a satisfactory condition, the patient can be discharged to be observed by
maternal welfare clinic gynecologist.
Indications for surgery in placenta previa at any gestational age: profuse bleeding,
acute fetal hypoxia, maternal anemia.
If the woman experiences one episode of bleeding of 250 ml and
NB! more, emergency cesarean section is indicated irrespective of
the degree of placenta previa or gestational age.
Placenta previa is an absolute indication for planned cesarean
section.
When there is complete placenta previa and no or scarce discharge of blood the
pregnant woman is admitted to antepartum department where they receive conserva-
tive treatment aimed at prolongation of pregnancy. At 38 weeks gestation they are
given a planned cesarean section. Considering the high risk of massive bleeding, the
surgery should be performed at hospitals with appropriate facilities and personnel
qualifications.
If a patient receiving conservative treatment develops massive bleeding, shows
progressing anemia or signs of fetal hypoxia, she is given emergency cesarean section.
In case of complete placenta previa a bleeding is an absolute

NB! indication for cesarean section irrespective of the gestational
age.
Complete placenta previa without clinical manifestations is not

NB! an absolute indication for hospitalization (if the woman refuses
to go to hospital); the rule of thumb is not to leave her alone or
wherever she cannot reach the hospital.
Patients with moderate discharge of blood and incomplete placenta previa

have a chance of a vaginal birth. If effective labor is present, cervical dilation
is 4–5 cm, amniotomy is performed to arrest the bleeding. The rupture of fetal
membranes promotes the descent of fetal head to the pelvis where the head
presses upon the area of abruption, prevents further abruption and arrests the
bleeding. If bleeding continues after amniotomy, emergency cesarean section is
performed. If the delivery began as a vaginal birth, the third stage should be ac-
tively managed. Immediately after delivery of the fetus, it is indicated to perform
manual separation of the placenta and to express the afterbirth. This is obligatory
as it helps to perform early verification of the abnormality of placental attach-
ment (adherent placenta or true placenta accreta), uterine hypotonia or rupture
of the lower uterine segment.
In whatever way the delivery proceeds, the patient requires special attention.
18.3.1.10. Complications and outcomes of placenta previa

If the cesarean section is performed, the emptied uterus can become atonic; this
condition requires surgical treatment. In a vaginal delivery the reduced contractility
of lower uterine segment and/or true placenta accreta can lead to massive bleeding
in the third stage of labor or puerperium. Infection develops more commonly during
the puerperium than after a normal childbirth.
Embolism is the most serious complication of placenta previa

NB! separation that can result in sudden death during pregnancy, labor
or postpartum period.
Embolism develops due to passage of air bubbles, fragments of infected blood

clots or amniotic fluid into the maternal blood stream from the open veins of the
placental bed.
450 Obstetrics
Favorable prognosis for the mother and fetus depends on early diagnosis and quali-
fied care (delivery via cesarean section) as well as many other factors that have an
impact on the delivery outcome. One should also take into consideration the body’s
reaction to blood loss, the condition of the cardiovascular system and hemopoietic
organs.
18.3.1.11. Prophylaxis
Prophylaxis of placenta previa consists, above all, in combating abortions, espe-
cially criminal abortions, prevention and treatment of genital infections, endometritis
in particular.
18.3.2. Placental abruption

Placental abruption is separation of normally situated placenta from the site of its
attachment, prior to delivery of the fetus.
Placental abruption is a severe condition noted in 0.4–1.4% of pregnant women;
it can occur during pregnancy or delivery and lead to life-threatening complica-
tions for the mother and fetus. Fatality amounts to 1.5–15%. The mother’s death
occurs mostly due to hemorrhagic shock followed by multiple organ failure. In
grand multiparous patients it occurs twice as often as in primiparous women.
In fact placental abruption has a much higher incidence than registered. Thus,
spontaneous abortion at an early and late gestational age is often due to placental
abruption, but it is entered into statistical records as abortion. When there are no
clinical presentations while the abruption takes place on a small area, the maternal
surface of the placenta after delivery shows small dark blood clots and impressions
from the hematoma.
18.3.2.3. Etiology
Etiology of placental abruption is not clearly understood. Placenta is a spongy
elastic plate which is intimately connected with the functional endometrial layer
by connective tissue partitions that separate cotyledons. Placenta is continuously
worked upon by the uterine wall and gestational sac. Besides, at the site of placenta
attachment the contractile ability of the myometrium is reduced. The gestational
sac occupying the entire uterine cavity exhibits resistance to the compressing uter-
ine walls and presses the placenta to the placental bed. If these forces maintain a
physiological balance, placenta does not separate from the placental bed. If there
is increased pressure on the part of the uterine wall, or decreased resistance on the
part of the gestational sac (for instance, upon gestational sac rupture and passing of
waters), premature separation of the placenta begins which is always accompanied
by hemorrhage.
Placental abruption can occur during pregnancy, the first or second stage of labor
(Fig. 18.10).
Fig. 18.10. Retroplacental hematoma
Hypothetically, placental abruption should be preceded by severe lesion of the

maternal cardiovascular system, disorder of vascular endothelium followed by hemor-
rhage into the placental bed, and myometrium tone elevation.
Besides, during pregnancy and especially in labor there can be factors that
change the balance of forces maintaining the placenta at the placental bed;
these factors can be also of external origin. However, placental abruption often
occurs in young primiparous women with a low perinatal risk, without previous
disease. This presumably occurs secondary to insufficiency of the placental bed
(Fig. 18.11).
The following risk factors for placental abruption are known.
• Maternal extragenital disease and complications of pregnancy accompanied by
changes in the maternal vascular system (angiopathy, capillaropathy) causing
uterine angiopathy followed by placental bed insufficiency (insufficiency of the
first and second wave of cytotrophoblastic invasion). These changes develop
in hypertonic and hypotonic disease, heart defect, thyrotoxicosis, diabetes
mellitus, inferior vena cava syndrome, renal disease (glomerulonephritis,
pyelonephritis), tuberculosis, syphilis, malaria and other chronic infections.
Placental abruption is possible in autoimmune conditions (antiphospholipid
syndrome, lupus erythematosus), allergic reactions. Placental abruption is most
common in severe pre-eclampsia.
• Hyperplastic processes, inflammatory and degenerative changes in the uterus
and placenta disrupting the interface between the uterus and placenta: chronic
inflammation of the uterus (endomyometritis), submucous myomatous nodes,
uterine malformations (uterine septum, bicornuate or arcuate uterus), post-term
pregnancy, etc.
• Excessive distension of uterus leading to thinning-out of its wall and increase of
the placental bed, which promotes expansion and thinning-out of the placenta
itself (polyhydramnios, multiple pregnancy, fetal macrosomia).
452 Obstetrics
b
Fig. 18.11. Superficial layers of placental bed bioptate in placental abruption: a — a layer of
well-differentiated decidual cells is noted below the Nitabuch’s fibrinoid, hematoxylin and
eosin staining, x400; b — narrow lumen of the endometrial segment of utero-placental artery
upon complete replacement of its wall by fibrinoid, hematoxylin and eosin staining, ×63
• Immediate injury: a fall, a blow to the uterus, external version of the fetus, rough
handling during examination, vaginal surgery, etc.
• Indirect injury: absolutely or relatively short umbilical cord, late rupture of fetal
membranes, rapid discharge of amniotic fluid in polyhydramnios, precipitous
delivery of the fi rst fetus in multiple pregnancy, accelerated or precipitous labor.
• Nervous and emotional factors: fear, stress, arousal during intercourse and other.
Placental cotyledons are washed by maternal blood. When the interface between
the uterus and placenta is in any way disrupted, bleeding develops. At first it is ret-
roplacental, so for some time it remains inapparent. When capillary membranes are
damaged and vessels rupture, the circulation in the intervillous space is disturbed,
bleeding develops resulting in retroplacental hematoma. Thrombi emerge in utero-
placental arteries, fibrin deposits appear in the intervillous space, which leads to red
(hemorrhagic) placental infarctions first, and then to white infarctions. Multiple
infarctions, in their turn, further disturb placental circulation and promote further
placental abruption. Under the impact of tissue thromboplastin that is released from
the injured tissues of the decidua and villi, the blood coagulates.
If the abruption area is not large, thrombi develop in uterine vessels, and villi
become compressed secondary to the formation of retroplacental hematoma. Further
abruption discontinues, and infarctions form at the site of abruption, which gradually
become calcified. They are detected upon inspection of the placenta after delivery.
If the abruption area is extensive, massive bleeding ensues. If the placental edges
interface with the uterus, retroplacental hematoma, while growing, shifts together
with the placenta to the amniotic cavity and increases the intrauterine pressure
provided the amniotic sac is intact. Uterine walls distend. All layers in the uterine
walls become soaked with blood which sometimes effuses to the parauterine tissue
and even to the abdominal cavity if the continuity of the uterine serosa has been
disturbed. There is no external bleeding while occult bleeding is quite considerable.
The uterus drenched with blood loses its contractile ability, the muscular and
serous surface of uterus are damaged. Sometimes the entire uterus is drenched with
blood rather than at the site of placental bed. This condition is known as uteropla-
cental apoplexy or Couvelaire uterus [after a French obstetrician Couvelaire who
described two episodes he observed in 1912 (Fig. 18.12)].
If communication between the uterus and placenta is disturbed at

NB! the placental edge, the blood escapes between fetal membranes
and uterine wall, and comes to the vagina; thus external bleeding
develops.
Fig. 18.12. Couvelaire uterus

454 Obstetrics
The blood can escape to the amniotic fluid if the fetal membranes are no longer
intact thus increasing the amniotic fluid pressure which is manifested by acute strain
at the lower pole of the gestational sac.
Separation of more than 2/3 of placental surface results in a
NB! fast fetal demise.
It is believed that tissue thromboplastin, fibrinolysine and their activators inhibit-
ing coagulation pass to the maternal circulation from the damaged uterus as a result
of its impaired circulation and thus massive hemorrhage is promoted even more.
DIC always follows PROM as fibrin is deposited in the retroplacental

NB! hematoma, and fibrin-free blood comes to the maternal body
along uterine veins (consumption coagulopathy).
We distinguish:
• complete placental abruption when its entire maternal surface is separated;
• partial placental abruption when a part of maternal surface of the placenta is
separated from the placental bed.
Partial abruption can be progressing and non-progressing. According to the degree
of expression, the following forms of placental abruption are distinguished:
• mild (separation of a small area);
• moderate (separation of ¼ of placental surface);
• severe (separation of more than 1/3 of placental surface.
Clinical classification of placental abruption is based on the type of hemorrhage:
• abruption with external bleeding (blood discharge from the vagina);
• abruption with internal bleeding (retroplacental hematoma formation, no blood
discharge from the vagina);
• abruption with combination bleeding (external and internal bleeding) (Fig. 18.13).

Clinical presentations of placental abruption depend on the area of separation,
the rate and volume of bleeding.
The major signs of PROM are pain in the placentation area

NB! (separation of placenta), hypertone of uterus, signs of internal
bleeding (diminished BP, tachycardia), and fetal hypoxia due to
hemorrhage.
The patients present with abdominal pain of varying localization and inten-
sity, anxiety, dizziness, weakness, short fainting spells. They note a constant
tension of the uterus, feel changes in fetal behavior. The fetus can become too
active or, on the contrary, become less active, and then the woman stops feel-
ing its movement.
а b c
Fig. 18.13. Clinical varieties of placental abruption: a — partial abruption with external
bleeding; b — central abruption (retroplacental hematoma, internal bleeding); c — complete
abruption with external and internal bleeding
Pain develops due to distension of uterine wall and irritation of uterine serosa by
the hematoma formed at the site of placental separation. The pain can be mild or
quite acute, first it is localized and then radiates to the whole abdomen.
In case of mild abruption the pain sign is not pronounced. If abruption goes along
the placental edge, the pain is insignificant or absent as the blood escapes outside
and the intrauterine pressure does not increase. In case of sudden, extensive abrup-
tion there are acute bursting pains in the entire abdomen, the patient complains of
a sensation that «something has burst», there is a burning sensation at the site of
abruption. The abdomen grows tense, enlarged. The pain can irradiate to the thigh,
pubis, lumbar region.
Uterine hypertonia is associated with retroplacental hematoma distending the
uterine wall. The uterus grows tender and tense to palpation. Tenderness can be
generalized or local, at the site of placenta attachment.
If abruption occurs during pregnancy, the uterus is continually in hypertone, the
fetus cannot be palpated due to the tenseness and tenderness of the uterus. If abrup-
tion occurs during labor, the uterus cannot relax between contractions.
Acute fetal hypoxia is due to placental abruption, disorder of uteroplacental cir-
culation secondary to uterine hypertone, maternal and fetal hemorrhage. If 1/3 of
maternal surface of the placenta separates, the fetus is afflicted, and then dies of
hypoxia. In complete placental abruption fetal demise occurs rapidly.
When the abruption passes through the centre of placental bed, the bleeding often
remains contained inside, retroplacental hematoma develops. The blood discharged
from the vagina is of varying color. If bleeding started immediately after abruption
or the blood had to pass a considerable distance from the separated lower placental
pole to the vagina, it is of scarlet color. If some time elapsed after abruption, the
blood becomes dark, it contains clots.
When ¼ of the placenta separates, the mother develops signs of anemia and hemo-
dynamic disorder. The patient complains of dizziness, weakness; a short fainting spell
456 Obstetrics
is possible developing secondary to hypovolemia and coagulopathy. The expression

of clinical features depends on the type of placental abruption.
If abruption is limited to a small area (¼ of placental surface), there are no pain-
ful signs.
A pregnant woman with placental abruption can have insignificant abdominal
pain, increased uterine tone, dark blood discharge from the vagina.
If insignificant abruption occurs during delivery, the uterus can relax between
contractions, fetal heartbeat remains unchanged. The only sign is scanty dark red
discharge from the vagina.
If placental abruption occurs at the end of the first or second stage of labor, bleed-
ing develops, labor grows weak, contractions become irregular, signs of fetal hypoxia
develop. Delivery usually proceeds unassisted, and the signs of placental abruption
are detected upon inspecting the placenta (the maternal surface of placenta shows
depressions covered with dark blood clots; in these areas the placenta is markedly
thinner).
During pregnancy or labor abruption can be detected accidentally by ultrasound
examination. Ultrasound shows a retroplacental hematoma whose changes over time
are indicative of progressing or non-progressing partial abruption (Fig. 18.14).
In moderate degree of abruption when ¼–1/3 of placental surface has separated,
clinical presentations can develop gradually; sometimes there is a sudden onset. An
apparently healthy pregnant woman develops abdominal pain which is first localized
and then spreads to the entire abdomen. The uterus is tense. The nature of fetal
movements changes. The patient can complain of weakness, dizziness, nausea: signs
of hemorrhagic shock. Blood discharge from the vagina can be of varying intensity
and color. Abruption occurring during labor produces the same presentations.
Severe degree of abruption means that more than 1/3 of placental surface has
separated. Abruption of a large area or the entire placenta occurs suddenly causing
intense pain in the abdomen.
Hematoma Placenta
Fig. 18.14. Placental abruption. Ultrasound

The patient grows restless, moans and cries with pain. Massive internal bleeding
produces the signs of hemorrhagic shock. Severe degree of placental abruption is
indicated by:
• disturbed hemodynamics: fall in arterial pressure, frequent weak pulse, pallor,
cold sweat, seeing spots, a short spell of unconsciousness or dizziness;
• pain syndrome: the pain is fi rst limited to the area of abruption and then spreads
to the entire surface of uterus; it is strong, dull, continuous; vomiting develops;
the abdomen is markedly distended;
• changes in the consistency and configuration of uterus: the uterus is hard, its
surface tender, the uterus protrudes at the area of abruption, this site is of elastic
consistency;
• fetal hypoxia or demise;
• signs of hypovolemia, coagulopathy.
18.3.2.7. Diagnostics
Diagnosis is made on the basis of patient’s complaints, findings of general and
obstetric history (pre-eclampsia, frequent episodes of threatened abortion in the
present pregnancy), clinical presentations (signs of internal bleeding, abdominal pain,
uterine hypertone, disorder of fetal cardiac activity), general and special examination;
laboratory tests.
The main clinical signs of PROM: abdominal pain, hypertone of

NB! uterus, signs of internal bleeding, disturbed fetal heartbeat.
Only 10% of women show classical presentations of placental abruption; every

other patient shows only blood discharge and signs of fetal hypoxia. In 1/3 of patients
there is no pain syndrome, so diagnosis of placental abruption is made difficult.
When the patient presents no complaints of pain or blood discharge, mild abrup-
tion during pregnancy can be only detected after delivery; ultrasound examination
is of low informative value. Considerable abruption is always accompanied by pro-
nounced presentations and is unequivocally established with the help of ultrasound
examination.
An objective examination detects signs of hemorrhagic shock; abdominal palpation
reveals a tense tender uterus with local swelling at the site of placenta attachment;
fetal parts cannot be palpated.
A vaginal examination reveals blood discharge from the uterus and a constantly
tense gestational sac. When it is opened or ruptures spontaneously, the amniotic fluid
can show admixture of blood.
Fetal heartbeat grows fast but then becomes slower, arrhythmic, and disappears.
When normally situated placenta separates during the first stage
NB! of labor, the nature of contractions changes: they grow more
or less powerful, or become irregular. The uterus cannot relax
between contractions. Fetal heartbeat changes as the fetus is
suffering from hypoxia and can die. Signs of hemorrhagic shock
develop.
458 Obstetrics
It is rather difficult to diagnose placental abruption during the second stage of

labor. While the patient has contractions and bears down, she may have bad pain in
the uterus, but this does not occur often. Abruption is commonly accompanied by
bright red vaginal discharge and acute fetal hypoxia.
Early diagnosis of placental abruption is possible with the help of accessory in-
vestigation methods, ultrasound in the first place as it shows the area of abruption,
its progressing and the size of retroplacental hematoma as well as signs of acute
fetal hypoxia. CTG administered during pregnancy and labor helps to monitor fetal
condition.

Differential diagnosis and laboratory investigations are only made in hospital set-
tings. Placental abruption should be differentially diagnosed from
• late spontaneous abortion or preterm delivery;
• placenta previa;
• rupture of placental marginal sinus;
• rupture of umbilical vessels when there is velamentous cord insertion;
• rupture of uterus;
• injury of soft birth canal;
• varicose vein rupture;
• cervical ectopy;
• cervical polyp;
• genital wart.
If there is external bleeding, placental abruption should be differentially diagnosed
from placenta previa and conditions unrelated to pregnancy but accompanied by
external hemorrhage.
When the patient presents with external bleeding and hemorrhagic shock signs,
one should rule out other causes of intraperitoneal bleeding: spleen rupture, rupture
of sacculated tumor of uterine tube or ovarian rupture.
18.3.2.9. Treatment
Placental abruption is a severe, dangerous complication of pregnancy and labor.
Early detection of this condition, adequate treatment of abruption and its sequelae
(uterine atony, anemia, hemorrhagic shock, DIC) can save the mother’s and fetus’s
life.
The choice of treatment method is determined by the time of placental abrup-
tion (during pregnancy or labor), the expression of clinical features and the obstetric
situation.
Objectives of treatment
• arresting hemorrhage;
• at the same time: restoring circulating blood volume, antishock therapy if
indicated;
• managing fetal hypoxia.
The hemorrhage and progressing abruption can be only arrested

NB! by a fast, gentle emptying of the uterus. If clinical features and
signs of internal bleeding continue to increase (acute premature
detachment of normally situated placenta), cesarean section is
performed at any gestational age or in the first or early second
stage of labor, irrespective of the fetus condition (viable or
demised fetus). At the same time, anti-shock, antianemic therapy
and normalization of homeostasis is administered.
If the greater portion of uterine wall is drenched with blood of dark purple color,
its muscle is flaccid, unresponsive to mechanical or pharmaceutical stimulation
(Couvelaire uterus, uteroplacental apoplexy), hysterectomy is indicated removing the
uterus without appendages. When pronounced uteroplacental apoplexy is not pres-
ent, one should ligate uterine vessels, and if that fails—ligate internal iliac arteries
(Fig. 18.15). If the hospital has an angiosurgery department, vascular embolization
can be performed. When the areas of blood extravasation are not large, the uterus
contracts well and no additional procedures are required.
If clinical features of placental abruption are pronounced (acute abruption dur-
ing the second stage of labor), a vaginal delivery is possible, but this can be only
undertaken in a large hospital complete with diagnostic and therapeutic equipment.
When the fetus is alive, in cephalic presentation, and its condition allows it, the
second stage of labor is urgently terminated by applying obstetric forceps; if the fetus
is in pelvic presentation, total breech extraction is performed.
When the patient with placental abruption has given a vaginal birth manual re-
moval of placenta with careful inspection or manual examination of uterine walls is
indicated in all cases. This is done immediately after delivering the fetus to rule out
Uterine tube Broad ligament

Proper ovarian Body of uterus of uterus
ligament
Ovarian
artery
and vein
Ovary
Ureter
Uterine artery
Internal iliac
artery
Vaginal artery
and vein Area of incision
Vagina in uterus
Fig. 18.15. Sites to place ligatures in case of uterine ischemia by consecutively applying
ligatures to vascular bundles in the uterus and ovaries (а, b, c, d)
460 Obstetrics
uterine rupture, hypotonia, and to remove retained placental fragments and blood
clots, which promotes uterine contraction. Speculum examination of the vagina and
cervix is done. Medications promoting uterine contraction are administered as well
as antibiotics for prevention of infection; if anemia is present, appropriate treatment
is administered.
18.3.2.10. Prophylaxis of placental abruption

Prophylaxis consists in prevention of abortions, early detection and timely treat-
ment of preeclampsia, hypertonic disease and chronic infection.
18.4. HEMORRHAGE IN III STAGE OF LABOR
According to WHO classification (2002), postpartum hemorrhage is bleeding

developing after the birth of fetus; hemorrhage of the third stage is not classified
separately.
In Russian obstetric practice the bleeding of the third stage of labor is considered
separately from postpartum hemorrhage. However, the main causes of these types
of hemorrhage are identical: disrupted contractility of the uterus and disorder of
placenta separation and delivery. As a result, the uterus cannot empty completely,
blood with clots is accumulated inside, the entire placenta or its fragments are re-
tained. In these conditions the uterus is incapable of fully contracting and providing
a physiological arrest of postpartum hemorrhage. Hemorrhage begins from the open
vessels of the placental bed.
Hemorrhage developing after delivery of the fetus and until the

NB! placenta is born, is referred to as hemorrhage of the III stage
of labor.
Statistics. Postpartum hemorrhage is encountered in 3–5% of deliveries.

Etiology. Causes of hemorrhage in the third stage of labor:
• retention of placenta in the uterus secondary to disorder of uterine contractility;
• retention of placenta secondary to partial adherent placenta or placenta accreta;
• injury of soft tissues in the birth canal (cervical, uterine, vaginal, vulvar rupture,
hematoma);
• acquired and congenital coagulopathy.
18.4.1. Prolonged III stage of labor due to abnormality

of uterine contractility
When the III stage of labor proceeds physiologically, the uterus contracts distinctly
which causes a sudden decrease in the area of placental bed so that is becomes less
than the placenta. During the afterbirth contractions the uterine muscular layers
retract in the area of placental bed so that the spongy layer of decidua ruptures and
the placenta separates. The process of placental separation is intimately associated
with the intensity and duration of retraction.
Duration of the third stage of labor is 5 – 15 minutes in most

NB! puerperas; but it does not exceed 30 minutes. Physiological
blood loss is no more than 0.5% of body weight.

Uterine contractility becomes disrupted due to secondary changes of its wall
after previous genital infections and inflammatory diseases, multiple deliveries and
abortions, after surgery on the uterus, in uterine myoma, uterine malformations,
preeclampsia and hormone dysfunction. The contractile activity of uterus is affected
by overdistension of uterus by fetal macrosomia, in polyhydramnios and multiple
pregnancy. The contractile ability of myometrium is impaired by inadequate admin-
istration of uterotonics and conduction analgesia during labor, fast emptying of the
uterus (accelerated and precipitous labor, surgical assistance ) and prolonged labor
(inertia or uncoordinated uterine activity).
The myometrium cannot develop adequate contractions and detach the placenta
fully in the presence of placenta previa, low-lying placenta, its localization in one of
tubal angles of uterus or at the uterine septum. Structural features of placenta itself
are of primary importance, as well as the size of its area of attachment to the uterine
lining. A large surface of attachment interferes with normal myometrial contractions
and placental separation from the uterine walls. The placenta can occupy a very large
uterine area if it has such abnormalities as placenta circumvallate, bilobed, succen-
turiate , membranacea, duplex.
A conmmon cause of postpartum hemorrhage is inappropriate

NB! (aggressive) management of the third stage of labor.
If there are no signs of placenta separation and no bleeding,

NB! intravenous administration of oxytocin is indicated.
When the contractile activity is disturbed, the uterus cannot detach the placenta
completely. Only a portion separates, the uterus does not contract, and a hemorrhage
begins from the open vessels of the placental bed devoid of placenta.
The rate of hemorrhage and the volume of lost blood depend on the size of sepa-
rated placenta: the greater the separated portion, the worse the bleeding.
The rate of hemorrhage also depends on the site of placenta attachment: the
bleeding is more copious where the myometrium is thinner and the contractility is
less (low-lying placenta, its localization at the uterine septum or in tubal angle). If
after the birth of placenta a fragment or its accessory lobe is retained in the uterus,
the hemorrhage can be intensive.
When the external orifice develops a spasm, the placenta that has detached from
the uterine wall cannot deliver. Having a «foreign body» inside, the uterus cannot
contract adequately, which causes hemorrhage in the end.
It is not only retained placental fragments or accessory lobes that prevent uterine
contraction, but also accumulation of blood clots in the uterine cavity.
462 Obstetrics
Once the fetus has been born, the puerpera is usually in a satisfactory condition
and presents no complaints. A moderate outflow of dark blood from the vagina is
noted. When there is a disorder of placental separation and delivery, the amount of
lost blood increases rapidly. The hemorrhage can be external or internal (if the blood
is accumulated inside the uterus).
• In external hemorrhage the vaginal bleeding is intensified, the blood acquires
bright scarlet color; it is discharged in portions, blood clots are seen.
• Internal hemorrhage develops when the internal os is stopped by a blood clot
and fragments of fetal membranes or when the os is in spasm. Having no outlet
the blood accumulates in the uterus and, together with the placenta that failed
to separate it prevents the uterus from contracting. The uterus grows in size
because of blood accumulation becoming tense, tender to palpation; the fundus
is at the level of umbilicus or higher. The puerpera complains of abdominal
pain.
The main sign of placenta retention is vaginal hemorrhage in the absence of signs
of placenta separation. If the volume of lost blood amounts to 300 ml or 0.5% of the
patient’s weight and the hemorrhage persists, it should be regarded abnormal and a
manual examination of the uterine cavity is performed.
The hemorrhage can be so profuse that hemorrhagic hock develops (arterial pres-
sure fall, rapid pulse, pallor, etc.).
Delayed placental separation from uterine walls is diagnosed on the basis of exter-
nal signs of placenta separation (Schroeder, Alfeld, Kustner signs) prior to afterbirth
delivery. Retention of placental fragments in the uterus is determined by inspecting
the placenta and membranes after the placenta is delivered.
If inspection of the smooth lustrous maternal surface of the placenta reveals rough-
ness, depressions oozing dark blood, this is considered placental defect. Ruptured
vessels on the fetal surface and both membranes indicate an accessory placental lobe
which is retained in the uterus.
If inspection of the afterbirth gives rise to doubts about its integrity, the diagnosis
of doubtful placenta integrity is made.
Placenta retention is differentially diagnosed from hemorrhage from ruptured soft
birth canal and coagulopathy.
If there is an injury, hemorrhage develops immediately upon delivery of the fetus,
the blood flows out in a stream; it is of scarlet color and coagulates well. In case of
coagulopathy the blood flowing from the uterus cannot clot for a long time.
18.4.1.4. Treatment
When hemorrhage develops during the third stage of labor, the uterus should be
emptied, and then it contracts and hemorrhage is arrested. When placenta is retained
in the uterus, conservative and operative treatment is administered, when only pla-
cental fragments are retained, only operative treatment is administered.
Conservative methods include intravenous infusion of 5 IU of oxytocin to stimulate
post-labor contractions promoting placental separation and arrest of hemorrhage.
Ergot-containing medications should not be administered as they induce spasm of

the internal os.
When placental separation is established by external signs, there is a risk of pla-
centa retained in the uterine cavity. In case of retained placenta, external methods
of placenta delivery are employed: Genter, Crede, Andrew-Brandt, Baier methods
(see Fig. 8.20; Table 18.1).
If conservative methods fail and the volume of lost blood exceeds 300 ml or 0.5%
of the patient’s weight, operative methods are resorted to. If placenta defect is de-
tected after delivery of the placenta, a manual examination of uterine walls is done
at once to remove placental fragments or blood clots.
Surgical methods imply manual separation of the placenta and delivery of the
afterbirth followed by a control manual examination of uterine walls (see sec-
tions 27.4.4.4 and 27.4.5).
After a manual examination and complete emptying of the uterus it should con-
tract well, become compact. Intravenous administration of uterotonics continues.
From time to time, palpation of the uterus is done through the abdominal wall to
check its tone; the volume of discharged blood is also monitored.
If placental fragments are retained in the uterus (defect, retained

NB! accessory lobule), and there are doubts about the integrity of
the placenta, only operative treatment is resorted to: manual
examination of uterine walls, detachment and removal of placental
fragments and blood clots that interfere with contraction of the
uterus.
Table 18.1. Diagnostic criteria of hemorrhage in the third stage of labor

Condition of pla- Placenta Retention Adherent Placenta Birth canal
centa, maneuvers retention of placenta placenta accreta injury
and surgery in uterine fragments
cavity
Afterbirth In cavity delivered In cavity In cavity –
Signs of placenta + + – – +
separation
Integrity of deliv- – +
ered afterbirth
Maneuvers and Methods Control Manual separation of Inspection
surgeries of pla- manual placenta and expression and repair
centa examination of afterbirth (if placenta of lacera-
delivery of uterine accreta was not diagnosed tions
cavity walls prior to labor)
Laparotomy / Organ-sparing Upon uter-
cesarean section techniques. ine rupture
Complete hys-
terectomy or
amputation of
uterus
464 Obstetrics
Antibacterial therapy is administered in the puerperium in all cases of surgery for

prevention of infection.
If the blood loss is 0.7–1% of the patient’s weight, infusion-transfusion therapy for
replacement of circulating blood volume is initiated; symptomatic therapy is initiated
if required. The volume of infusion-transfusion therapy is determined by the amount
of blood loss and the patient’s condition.
Diagnostic criteria of hemorrhage causes in the third stage of labor are shown in
Table 18.1.
18.4.1.5. Prevention
The main point of prevention is adequate management of the third stage of labor.
Prevention of abortions, treatment of gynecologic and chronic infections also con-
tributes to the prevention of retention of the placenta or its fragments in the uterus.
18.4.2. Abnormalities of placenta attachment

Abnormalities of placenta attachment to the uterine wall (adherent placenta or
placenta accreta) are causes of hemorrhage in the third stage of labor.
Placenta accreta is a severe complication seen relatively seldom: 1 case per 3000–
5000 deliveries, mostly in multiparous patients and after a previous cesarean section.

The conditions of adherent placenta or placenta accreta occur upon structural and
morphological changes in uterine walls, in the uterus itself or upon disorder of the
enzymatic (proteolytic) function of the chorion.
The group of risk for these conditions includes pregnant women with previous
inflammatory disease (endomyometritis), scars in the uterus, frequent deliveries and
abortions, tumors (myoma), uterine malformations. Development of degenerative
processes in the uterus is promoted by chronic infection, preeclampsia, postterm
pregnancy.
Enhanced proteolytic activity of the chorion (hyaluronidase activity) can lead to
villi growing into the compact layer of the deciduas, in some cases they grow even
deeper — to the endometrial basal membrane and muscular layer of the uterus, even
as far as the serous layer.
18.4.2.4. Screening
Ultrasound (MR imaging) is done in late pregnancy to patients with operated
uterus syndrome, placenta previa and placenta attachment to the scar.
The classification is based on the degree to which chorionic villi penetrate the
layers of uterine walls. We distinguish the following variations:
• adherent placenta;
• placenta accreta, increta, percreta (Fig. 18.16).
In case of adherent placenta the chorionic villi do not go deeper than the compact
layer of decidua, but are firmly attached to it due to atrophy of the spongy decidual
layer.
In case of placenta accreta there is no spongy decidual layer so chorionic villi
penetrate the myometrium growing through it, sometimes as far the uterine serosa
(Fig. 18.17).
PLACENTA
DECIDUA
NITABUCH MEMBRANE
MYOMETRIUM
ADHERENS ACCRETA VERA INCRETA PERCRETA
PLACENTA ACCRETA
Fig. 18.16. Variants of abnormal placental attachment
Fig. 18.17. Placenta accreta. Ultrasound with color flow mapping

466 Obstetrics
Adherent placenta and placenta accreta can be complete when the entire maternal
surface is firmly attached to the uterine wall, or incomplete when only a part of its
surface or some lobules are firmly attached, which affects the clinical course of the
postpartum period.
When adherent placenta or accreta is complete, the placenta is not capable of
spontaneous separation from the uterine wall. There is no hemorrhage.
When adherent placenta or accreta is incomplete, the placenta partially separates
from the uterine wall. Placental fragments firmly attached to the wall or ingrown
cannot separate from it. Due to the retained parts the uterus cannot contract and
the hemorrhage cannot stop. Blood discharge from the vagina develops at once.

In case of incomplete adherent placenta or placenta accreta the hemorrhage de-
velops without fail. The severity of hemorrhage depends on the area of placental
bed with which the placenta lost contact, the condition of uterine neuromuscular
apparatus, and the blood coagulation system. Hemorrhage can be profuse at once
as intervillous spaces open up at the already detached placental area, and are con-
tinuously filled with maternal blood. There are no signs of placental abruption. The
patient’s response to hemorrhage depends on the volume of lost blood and her condi-
tion prior to the onset of hemorrhage (presence of preeclampsia, anemia, obesity and
other somatic diseases). If the hemorrhage is prolonged, hemorrhagic shock develops.
There is no hemorrhage in the presence of complete adherent placenta or placenta
accreta as the placenta is intimately connected with the uterus along its entire surface.
Clinical features include absence of the signs of placenta separation for 30 min and
longer after delivery of the fetus.
18.4.2.7. Diagnostics and treatment

Antepartum diagnosis of abnormal placental implantation is only possible in
case of placenta accreta when patients from high risk groups (previous surgery on
uterus, placenta previa) have ultrasound examination for this particular purpose, in
combination with dopplerometry and MR imaging. Sonographic findings that can
be suggestive of placenta accreta include:
• expanded intervillous spaces in the suprabasal area;
• pronounced thinning of the myometrium in the area of placental bed;
• tuberous appearance of the maternal surface of the placenta;
• disorder of vascular structure in the area of placental bed;
• the distance between uterine serosa and retroplacental vessels less than 1 mm;
• multiple vascular lacunae (irregular vascular spaces) within placenta producing
«Swiss cheese» appearance.
Reliable findings can be only obtained using color Doppler flow mapping tech-
nique. MRI provides the most accurate investigation; it is done when there are
ultrasound findings suggestive of placenta accreta.
If there is no hemorrhage and no signs of placental separation, conservative therapy
is initiated promoting uterine contraction and separation of placenta from its walls:
intravenous administration of uterotonics, use of modern perinatal technology—
latching the newborn to the breast immediately upon delivery (endogenous oxytocin).
If there are still no signs of placenta separation, hemorrhage persists and the volume
of blood loss amounts 0.5% of the patient’s weight, surgical methods of hemostasis
are resorted to (manual separation of the placenta and delivery of the afterbirth).
If there is no hemorrhage and conservative therapy aimed at placental separation
from uterine walls fails, manual separation of the placenta and delivery of the after-
birth is also performed after 30 minutes.
A diagnosis of adherent placenta or accreta can be established only during the
procedure of manual detachment of the placenta.
In case of adherent placenta it is manually detached from the uterine wall, the
uterus contracts, hemorrhage stops. However, after removal of the afterbirth there is
a risk for uterine hypotonia, intensifying of the hemorrhage.
In case of complete or incomplete accreta the placenta cannot be manually detached
from the uterine wall.
If one persists in the attempt to detach an accreta vera from the

NB! uterine wall, profuse bleeding develops that can endanger the
woman’s life, so manual detachment of the placenta should be
discontinued at once.
This situation requires emergency surgery: laparotomy, excision of the portion of

placental bed with accreta. Other methods of surgical hemostasis are employed if
necessary.
Modern technologies make it possible to spare the uterus.
If placenta accreta was diagnosed before labor, the patient receives planned cath-
eterization of uterine arteries and a cesarean section followed by immediate emboliza-
tion of uterine arteries (Fig. 18.18) (or temporary balloon occlusion of iliac arteries).
Then the accreta is excised, transfixion sutures are made in the uterine wall, and if
Fig. 18.18. Uterine artery embolization

468 Obstetrics
there is no hemorrhage, the uterus can be spared. Intraoperative balloon tamponade

of the uterus is an option for prevention of hypotonic hemorrhage.
If these measures prove ineffective, hysterectomy is indicated.
The outcome of treatment is determined by the volume of lost blood, presence
of hemorrhagic shock and consumption coagulopathy. Simultaneously with surgical
treatment, procedures for compensation for circulating blood volume, hemorrhagic
shock and DIC prevention (blood saving technology) are undertaken.
18.5. POSTPARTUM HEMORRHAGE
Postpartum hemorrhage according to WHO (1990) is a loss of over 500 ml of

blood after a vaginal birth , or over 1000 ml after a cesarean section; that is, a loss
exceeding 0.7–0.8% of the patient’s weight.
In most cases the amount of blood loss is established approximately, which ends in
underestimating the true blood loss. According to WHO, in most countries even the
loss of 500 ml is regarded as a real threat to the mother’s life due to a high rate of
anemia. In this respect a blood loss is regarded physiological if it is less than 0.5% of the
patient’s weight. It is pointed out that even lesser blood loss can cause a grave condi-
tion in the mother in the presence of anemia, preeclmpsia and cardiovascular disease.
Hemorrhage develops not only after abnormal but also after normal childbirth
when the mother loses 500 ml of blood; that is, when the blood loss is not massive
but acute.
A large blood loss within several minutes results in disorder of vital functions:
cerebral, pulmonary and renal. In the presence of extragenital disease the mother
can develop other complications. The effect of massive blood loss is dangerous due
to vascular spasm in the anterior pituitary gland (Sheehan’s syndrome).
Classification. In Russian obstetric practice postpartum hemorrhage is classified
according to the time of onset: early hemorrhage within 24 h after delivery; late hem-
orrhage after 24 hours postpartum; besides, there are such distinctions as hemorrhage
of the early postpartum period (within 2 hours after childbirth) and late postpartum
period (up to 42 days after childbirth).
WHO classification:
• primary postpartum hemorrhage;
• secondary postpartum hemorrhage;
• retained placenta.
18.5.1. Early postpartum hemorrhage

Early postpartum hemorrhage is abnormal vaginal blood discharge occurring
within 2 hours after childbirth.
Early postpartum hemorrhage is noted in 2–5% of deliveries.
18.5.1.3. Etiology
In Russian obstetric practice the following causes of hemorrhage are distinguished:
• uterine hypotonia and atonia;
• retention of placental fragments in the uterine cavity;
• injury to soft tissues in birth canal;
• acquired and congenital disorder of blood coagulation system.
The rule of four T’s is used to determine the etiology of hemor-

NB! rhage:
• tone (decreased uterine tone);
• tissue (presence of afterbirth fragments in the uterus);
• trauma (ruptures of soft birth tract and uterus);
• thrombin (congenital coagulopathy, hemostasis disorder).
From the point of view of obstetric practice, another cause should be added:
therapy (massive infusion of solutions, long-term ingestion of spasmolytic and to-
colytic medications or disaggregants, anticoagulants, etc.).
Hemorrhage can be brought about by a combination of several causes, and then
it becomes threatening.
Arresting of postpartum hemorrhage is provided for by manifold factors. First of
all it is contraction of uterine muscle and formation of thrombi in the placental bed
vessels. Contraction and retraction of the myometrium produce tightening of uter-
ine vessels and their drawing into the depth of myometrium, which promotes their
compression and arrest of hemorrhage. Under the impact of coagulating factors and
tissue activators thrombi begin to be formed in uterine arteries of the placental bed,
and the thrombi occlude the vascular lumen. First the thrombi are unconsolidated,
loosely attached to vascular walls; they can be easily detached and washed away
by the blood flowing from the placental bed if the uterine contractility is reduced.
Formation of solid fibrin thrombi firmly attached to the vascular wall takes time.
Reliable hemostasis helped along by thrombus formation is achieved after 2–3 hours.
Disorder of one of the factors mentioned above leads to hemorrhage in the early
postpartum period.
18.5.2. Uterine hypotonia and atonia

The most common cause of postpartum hemorrhage is disorder of uterine contrac-
tility when it loses its tone, cannot contract; thus physiological hemostasis becomes
impossible. The other major cause of postpartum hemorrhage is injury to the soft
birth canal.
Uterine hypotonia is a dramatic reduction in uterine tone and contractility.
Uterine atonia is complete absence of uterine tone or contractility. The neuro-
muscular apparatus of the uterus is paralysed. The uterus does not respond to the
470 Obstetrics
measures that stimulate its tone. Uterine atonia is a rare condition, but it causes
massive hemorrhage.
On the whole, this distinction is conventional. It is difficult to tell at once a hy-
potonic hemorrhage from an atonic hemorrhage, thus it is reasonable to apply one
term, hypotonic hemorrhage, and discuss uterine atonia after all measures have failed
and the hemorrhage persists. Uterine hypotonia is a reversible condition.
18.5.2.2. Etiology
Etiology of hypotonic and atonic hemorrhage is varied. Some risk factors are asso-
ciated with previous pregnancies and gynecological disease, others—with the present
pregnancy, and some develop during labor. Careful history taking and examination of
the patient upon admission help to reveal risk factors, to attempt to prevent hemor-
rhage and be ready to give emergency care.
• Factors associated with previous pregnancies, gynecological disease and causing
anatomical incompetence of the uterus: hypoplasia and malformations of uterus,
myoma, scars on the uterus after surgery (conservative myomectomy, closure
of the perforative opening after a surgical abortion, cesarean section), previous
inflammation and infection during post-abortion and postpartum periods.
Multiple abortions and deliveries result in replacement of a considerable
portion of uterine myometrium by connective tissue, which reduces myometrial
contractility and elasticity. The most threatened group are primiparous and grand
multiparous patients who experienced protracted labor or dystocia, abnormal
separation and delivery of the placenta. Underlying extragenital disease (diabetes
mellitus, obesity, cardiovascular disease, disorders of the coagulation system,
anemia) affect uterine contractility and limit the compensatory reserves of the
patient’s body in case of hemorrhage.
• Factors developing during the present pregnancy and causing functional
incompetence of the uterus: overdistension of the uterus by polyhydramnios,
multiple pregnancy, fetal macrosomia; functional incompetence of the uterus and
its lower segment at placental abruption, placenta previa or low-lying placenta.
Severe preeclampsia, eclampsia and fetal demise are often accompanied by
coagulopathy-mediated uterine hemorrhage.
• Factors emerging during labor: maternal exhaustion due to prolonged painful labor,
persistent uterine inertia, accelerated and precipitous labor. Disorder of uterine
contractility is promoted by a rapid extraction of the fetus at obstetric surgery and
excessively active management of the postpartum period. Myometrial contractility
is affected by chorioamnionitis during labor, prolonged administration of oxytocin
and tocolytics, general anesthesia and epidural nerve block.
Uterine hypotonia and atonia and even shock uterus can develop as a second-
ary condition in case of multiple organ failure (severe preeclampsia, cardiovascular,
hepatic, renal disease, neuroendocrine disorder, acute and chronic infection, critical
conditions like trauma and severe infection). Hemorrhage can accompany shock of
varying origin (toxic, pain, anaphylactic shock), inferior vena cava syndrome, am-
niotic fluid embolism.
Uterine hypotonia and atonia can be precipitated by a combination of several
causes mentioned above.
Clinical features of uterine hypotonia show the main sign, massive hemorrhage
from the uterus after delivery. Bright red blood flows in a stream or is discharged in
clots. Hemorrhage can be continuous or undulating.
• In continuous hemorrhage the uterus remains flaccid, it does not respond to
attempts to stimulate its tone (administration of uterotonics, external massage,
manual examination of uterine walls). Massive hemorrhage soon produces signs
associated with hemodynamic disorder and acute anemia. Presentations of
hemorrhagic shock progress gradually.
• Hemorrhage episodes alternate with temporary restoration of uterine tone, but
the disorder of myometrial contractility keeps progressing. Despite the fact that
the uterus responds to conservative treatment, the volume of lost blood grows.
In undulating hemorrhage the parturient woman temporarily adapts to insidious
hypovolemia. BP does not usually decrease, but there is tachycardia, pallor of
skin and visible mucosas.
The extent of clinical features depends on the rate and duration

NB! of bleeding, and the initial condition of the puerpera.
In case of massive (over 1.5% of body weight) but slow blood loss the signs of
acute anemia are not pronounced, and the patient copes with the condition better
than if she quickly lost the same or even less amount of blood .
The greatest portion of maternal deaths does not result from fast,
NB! massive blood loss; it is rather due to ineffective management
of a prolonged, undulating bleeding of low intensity, when the
gynecologist deters decisive actions for psychological reasons.
In case of prolonged, nonmassive hemorrhage when the patient’s general condition

is not disturbed apparently, at a certain stage the compensatory mechanisms break
down acutely and irreversibly.
If the patient’s strength is depleted and her reactivity is reduced, even insignificant
hemorrhage within the physiological range (0.3% of body weight) can produce severe
clinical presentations (hemorrhagic shock) in patients with deficient circulating blood
volume (preeclampsia, cardiovascular disease, obesity) and anemia.
Diagnosis of uterine hypotonia is made by the sign of uterine hemorrhage and
objective findings about its tone. Palpation shows an enlarged flaccid uterus; its con-
tours are sometimes poorly defined through the anterior abdominal wall. External
massage can lead to some uterine contraction and lessening of hemorrhage. Then
the uterus relaxes again, and the hemorrhage resumes. Contours of atonic uterus
can hardly be defined.
In order to provide comprehensive care, it is important to make
NB! a correct estimate of the blood being lost.
472 Obstetrics
A readily available technique is collecting the blood discharged from the vagina
into basins placed under the puerpera and measuring its volume in a graduated glass
with a capacity of 1–2 l. The drawsheets soaked with blood are also weighed, and
the total is worked out. Despite all attempts to determine the volume of lost blood
accurately, in obstetric practice the real blood loss is always underestimated.
One should make a quick assessment of the patient’s condition: the color, mois-
ture and temperature of the skin, BP, pulse, heart rate, diuresis by the hour. It is
desirable to make the count of RBCs, hemoglobin, hematocrit, blood coagulation
time and time of hemorrhage by express method, prothrombin ratio. To rule out a
coagulation disorder, a bedside express test1 or coagulogram is done.
If the hemorrhage persists, the patient’s condition is constantly monitored to
diagnose hypovolemic shock in good time and initiate its treatment.
Signs of incipient shock: pallor, restlessness, weak frequent pulse (110 and more
per min), dyspnea (respiratory rate 30 and more), BP decrease to 90 mm Hg, reduced
diuresis but not less than 30 ml/h (WHO, 2002).

In the early postpartum period hypotonic hemorrhage is differentially diagnosed
from hemorrhage due to injury of soft tissues in the birth canal, retained placental
fragments and coagulopathy.
Injury to soft tissues in the birth canal can be followed by considerable hemor-
rhage, especially in case of lacerations in the clitoris area. Hemorrhage is also profuse
when there are cuts and lacerations of the perineum, cervical lacerations. In contrast
to hypotonic hemorrhage, in these cases the uterus remains compact. Injury of
external genitals is detected by external examination. Speculum examination of the
cervix and vagina, manual exploration of uterine walls confirm the diagnosis of tears
of soft tissues in the birth canal, and associated hemorrhage. Manual exploration
of the walls of uterine cavity permits the diagnosis of uterine rupture and retained
placental parts in the uterus.
When there is coagulopathy, the blood flowing from the uterus is bright red and
forms no clots.
18.5.2.6. Treatment
Treatment is aimed at controlling the hemorrhage and replacing the circulating
blood volume, early diagnosis of hypovolemic shock, supporting vital functions.
The main objective of management is arrest of bleeding.

NB!
Treatment of hypotonic hemorrhage includes conservative and surgical methods,
it is initiated without delay. Treatment can be effective if adequate care is provided
in certain order.
1 Blood sample collected in a vial is warmed in hands for 7 min. If there is no clot formation, hypo-
coagulation is present.
The average time elapsing from the onset of postpartum bleeding

NB! to the death of puerpera is two hours.
First one makes sure that the delivered placenta is intact. Once its integrity is
verified, conservative methods of hemorrhage control are initiated.
If these are of little effect, one resorts to surgical methods immediately to the ex-
tent of performing laparotomy and hysterectomy to remove the source of hemorrhage,
the uterus. The rule of thumb goes that blood loss under 1 liter requires conservative
therapy; blood loss of more than 1 liter requires a resort to surgery.
All actions aimed at hemostasis are performed simultaneously by

NB! the whole attending team (according to the plan agreed on). They
are aimed at increasing the tone and contractility of uterine muscle
while restoring the circulating blood volume and the volume of
circulating RBCs.
Measures to control hemorrhage

In case of hypotonia, hemostasis procedures are always accompanied by con-
tinuous measuring of the lost blood. The preliminary stage includes the following
measures (10 steps).
• Recruiting more personnel. Without leaving the patient unattended, one calls
an experienced obstetrician gynecologist competent in all surgical techniques,
anesthesiologist and intensive care specialist, lab assistant.
• Initial assessment of the volume of lost blood: this is done visually or using a
kidney dish +20% (if the patient is brought in an ambulance, one can use the
shock index provided she has no preeclampsia) (Fig. 18.19).
• Initial assessment of the patient’s condition and monitoring of vital functions (BP,
pulse, body temperature, respiratory rate).
• Depending on the gravity of the patient’s condition, define the place where she
will be managed, and transport her there.
• Establishing allergy history (if the patient’s condition permits).
• Emptying the urinary bladder and leaving a permanent catheter.
• Catheterization of one or more peripheral veins (catheters 14–16G) to start an infusion.
• If necessary, do Rh testing and blood typing, obtain blood samples for compatibility
testing, if necessary — for bedside test.
• Check the availability of blood products and order them if needed (according to
the fi ndings or Rh testing and blood typing).
• Desirably, establish the cause of hemorrhage (four T’s: tone, tissue, trauma,
thrombin).
The extent of care is determined by the volume of lost blood. If the volume is no more
than 300–400 ml, external massage of the uterus through the anterior abdominal wall is
performed: grasping the fundus with a palm, circular massaging movements are made
without applying force. The uterus becomes compact; the blood clots accumulated in the
uterus and preventing its contraction are removed by gently pressing on the fundus. The
massage continues until the uterus contracts completely and hemorrhage stops. The puer-
pera’s condition is assessed (pulse, BP, the color of skin and mucosas, consciousness, the
474 Obstetrics
ml
ml
Fig. 18.19. Blood collection basin

volume of lost blood). Simultaneously, uterotonics are administered: oxytocin, synthetic
analogs of prostaglandin E (Misoprostol per rectum). Intravenous infusion of salt solutions
is started; at signs of shock — stream infusion (1 l/15 min). For restoration of uterine tone,
WHO proposes to dilute 40 IU of oxytocin in 1000 ml of isotonic sodium chloride solu-
tion and inject the mixture intravenously at a rate of 40 drops per minute, in two veins.
If external massage fails to help the uterus to contract, or the uterus contracts
and then relaxes again, manual examination of the uterus cavity is done (see sec-
tion 27.4.5). The manual examination makes sure there are no placental fragments
or fetal membranes in the uterus and its walls are intact. Having confirmed there
is no placenta retention one can administer a single dose of carbetocin, a powerful
uterotonic, synthetic analog of oxytocin with an effective duration of 6 hours.
In case of persistent hemorrhage bimanual uterine compression is recommended
(see section 27.4.6).
• Bimanual uterine compression: the left hand grips the fundus, and the right hand
which was properly processed and gloved is introduced into the anterior vaginal
fornix, and the fist is clenched. The uterus is now gripped between two hands.
When the hands move to meet each other, the pressure on the uterus promotes
its contraction, and the hemorrhage stops (Fig. 18.20).
Fig. 18.20. Bimanual uterine compression

Nowadays, bimanual uterine compression is not resorted to when

NB! performing a manual examination of uterine walls. According to
the opponents of this method, it leads to destruction of thrombi in
the vessels and to release of thromboplastin into maternal blood
flow, which disrupts the coagulating function and aggravates the
bleeding.
If the hemorrhage is now arrested, the success should be consolidated by other

conservative methods helping to preserve the tone of contracted uterus. A latex in-
trauterine balloon is introduced into the uterine cavity (hydrotamponade of uterus)
(Fig. 18.21) (see section 27.4.7).
Fig. 18.21. Intrauterine hemostatic balloon
Thanks to the system regulating the amount of fluid and its elasticity, the bal-
loon fills the entire uterus cavity and takes on its shape. Pressed to the walls of
uterus the balloon produces mechanical stimulation causing uterine contractions
and promotes the formation of mural thrombi. The balloon can be left inside for
24 hours.
The choice of care method in early postpartum hemorrhage is shown in Table 18.2.
One must not perform tamponade of uterus with a bandage soaked in normal
saline solution as this misleads the physician. Uterine vascular clamping (methods
by Baksheyev, Henkel-Tikanadze, Quantiliani) is regarded unacceptable due to little
efficiency and risk of injury.
A repeat manual examination of the uterus is unacceptable as it produces no effect
and delays the onset of surgical treatment.
If all the above mentioned methods prove ineffective, one should immediately
initiate surgical hemostasis.
476 Obstetrics
Table 18.2. Choice of care method in early postpartum hemorrhage
Cause: ‘T’s Care method

Tone Manual exploration of the walls in uterus cavity: bimanual compression
Tissue Manual exploration of the walls in uterus cavity
Trauma Examination of the birth canal, repairing the tears. If uterine rupture is
detected, laparotomy is performed
Thrombin Infusion of coagulation factors (Q-FFP, cryoprecipitate, platelet concen-
trate). Antifibrinolytics
If the bleeding is controlled, one should consolidate the success

NB! by other conservative methods that help to preserve the tone of
contracted uterus. For this purpose IV cabetocin is administered,
and an intrauterine latex balloon (uterine tamponade) is inserted.
This is only acceptable after control of bleeding!
In case of heavy bleeding one should perform manual compression of the

aorta with control of the femoral artery. If aorta compression is adequate, the
pulse on the femoral artery is undetectable, and the hemorrhage should at-
tenuate.
Ineffective manual exploration of the uterus cavity in the form of

NB! renewed or continuing bleeding (loss of 1.5% of body weight and
more) permits a diagnosis of atonic hemorrhage and a start of
laparotomy and surgical hemostasis. A repeat manual exploration
of the uterus is unacceptable.
The algorithm of uterotonics administration is shown in Table 18.3.
Surgical phase
Surgical treatment is always associated with laparotomy. Methods of surgical he-
mostasis are as follows:
• administration of Dinoproston (prostenon) into the myometrium after
laparotomy;
• uterus ischemization by placing clamps and ligatures on vascular bundles of
uterine and ovarian arteries;
• hemostatic compression sutures on the uterus (B-Lynch, Pereira sutures and
their Rymashevsky-Radzinsky modification);
• ligation of internal iliac arteries (if blood loss exceeds 1500 ml, immediate
ligation of internal iliac arteries is advisable);
• angiography-guided embolization of uterine arteries (in a clinic where adequate
equipment and personnel is available);
• amputation or complete hysterectomy of uterus.
The first stage of surgical treatment includes administration of Dinorposton (pro-
stenon) into the myometrium and ligation of uterine vessels. Having opened the
Table 18.3. Algorithm of uterotonics administration
Features of admin- Uterotonic (prioritized)

istration Oxytocin Methylergometrin prostaglandins
Initial dose and 5 IU IV (slow) 0.2 mg IM or IV Dinoproston (pros-
route of adminis- (slow) tenon) 0.25 mg IM or
tration into the cervix.
Misoprostol 800–
1000 mcg per rectum
as a single dose
Repeat doses (if Carbetocin as a sin- 0.2 mg IM every 0.25 mg every 15 min
there is no hemor- gle dose or 20 IU of 15 min
rhage) oxytocin IV droplet
in 500 ml of solution
at a rate of 60 drops/
min
Maximum dose No more than 3 l of 5 doses (1 mg) 8 doses (2 mg)
oxytocin-containing
fluid
Contraindications, Preeclampsia, No IV administra-
warnings arterial hyper- tion. Bronchial
tension, cardiac asthma, glaucoma,
disease arterial hypertension
abdominal cavity one places ligatures on uterine vessels and proper ovarian ligaments
on both sides, and for the next 30–40 minutes one waits.
Sometimes additional sutures on round ligaments of uterus are required to stop
blood supply along their arteries. Myometrial hypoxia develops which promotes an
increase in the tone of uterus.
If the bloos loss is over 1500 ml and/or coagulopathic hemorrhage

NB! develops, ligation of internal iliac arteries is indicated in the
first place.
The up-to-date approach is to apply B-Lynch or Pereira sutures (and their

Rymashevsky-Radzinsky modification) to the uterus that bind and compress it, which
also promotes reflex contraction (Fig. 18.22).
Due to hypoxia the myometrium contracts in a reflex manner, hemorrhage stops,
the uterus can be spared. The technique of surgery is easier, and the course of post-
operative period is more uneventful than in the case of cesarean section.
If coagulopathy develops, the volume of lost blood can be reduced by ligating the
internal iliac arteries.
Modern organ-sparing techniques in most cases permit achieving hemostasis.
Organ-sparing methods for postpartum hemostasis are an essential condition. Only
if they fail, radical measures are justified.
If compression sutures and vessel ligation fail to arrest the hemorrhage and the
uterus does not contract, the only way to save the puerpera’s life is to remove the
478 Obstetrics
а b
Fig. 18.22. Types of hemostatic compression sutures: a — B-Lynch; b — Pereira
source of hemorrhage, the uterus (hysterectomy). The extent of surgery depends on

hemostasis, localization of the placental bed, presence of deep cervical lacerations,
signs of inflammation.
Embolization of uterine vessels is preferable to vessel ligation and removal of
uterus, if possible.
Simultaneously, procedures are undertaken to regulate or restore macro- and
microcirculation which provides for normal functioning of all organs and systems,
prevention of hemorrhagic shock and DIC. It is highly recommended to perform
autologous blood transfusion (using Cell Saver device; blood is taken from the
abdominal cavity). Success of this therapy depends on observing the stage-by-stage
approach, monitoring vital functions, especially hemostasis.
All actions should be started as soon as possible; they must be

NB! done in a complex; one must consider the initial condition of the
puerpera.
• Active management of the third stage of labor.
• Inserting an intravenous infusion drip at the end of the first stage of labor to
patients from a group of high risk for hemorrhage.
• Administration of tranexamic acid 15 mg/kg to patients with baseline disturbance
of hemostasis.
• Autologous plasma transfusion is an effective method for prevention and
treatment of obstetric hemorrhage, especially in women who are at a risk for
hemorrhage and for whom cesarean section is planned.
• Intraoperaive autologous blood transfusion is an effective way of restoring the
globular volume at cesarean section.
Administration of a single carbetocin dose, 100 mcg (analog of long-term effect

oxytocin) and latching the newborn to the mother’s breast immediately upon delivery
is a method of hemorrhage prevention.
For prevention of hemorrhage in the early postpartum period one resorts to the rec-
ommendations for active management of the third stage of labor by the International
Confederation of Midwives and the International Federation of Gynecology and
Obstetrics (FIGO). The recommendations imply the following procedures.
• IM administration of 10 IU of oxytocin. Oxytocin is preferable to all other
uterotonics as its effect sets on 2–3 minutes upon administration, with minimum
side effects. The medication is economically viable (cheap). Carbetocin produces
a more pronounced effect but its clinical use is limited by its high cost. Misoprostol
(400–600 mcg per os) is administered when parenteral administration of
oxytocin and ergot alkaloids is impossible. The patient should be consulted about
the side effects of uterotonic drugs.
• Controlled cord traction (Fig. 18.23). The gravest complication of this technique
is inversion of uterus, thus this technique has many opponents.
18.5.3. Hemorrhage in late postpartum period

Hemorrhage in late postpartum period develops within 2 hours to 42 days after
delivery. Late postpartum hemorrhage — 24 hours after delivery.
Most commonly late postpartum hemorrhage develops 7–12 days after delivery
(WHO, 2002) when the puerpera has been discharged home.
Fig. 18.23. Controlled cord traction

480 Obstetrics
When the puerpera is in satisfactory condition and her uterus involution progresses
well, bloody discharge from the uterus continues for 3–4 days postpartum, in mod-
erate amounts, of dark color. Serosanguineous discharge persists for up to 7 days.
More prolonged blood discharge in moderate amounts or profuse hemorrhage
from postpartum uterus as well regular relapse of hemorrhage of varying intensity
until 42 days postpartum is regarded as late postpartum hemorrhage.
18.5.3.2. Etiology
Late postpartum hemorrhage develops when there is disorder of endometrial
epithelization (especially in the placental bed) or of uterine involution. These
processes are slowed down by complications during labor inducing decreased
contractility of uterine musculature (polyhydramnios, multiple pregnancy, pro-
longed labor, hypotony of uterus, retention of placental fragments, etc.), and
by postpartum infection. Sometimes the cause of hemorrhage is not associated
with pregnancy or labor as is the case in the presence of benign or malignant
uterine disease.
Causes of hemorrhage in late postpartum period:
• uterine hypotony;
• retention of placental lobule in the uterus;
• undiagnosed incomplete rupture of uterus;
• incompetent scar after a cesarean section;
• postpartum infection (metroendometritis);
• placental polyp;
• chorionepithelioma;
• submucous myoma of uterus;
• congenital coagulopathy.
According to WHO, late postpartum hemorrhage develops due to retention of
placental fragments in the uterus, abruption of necrotized tissue, separation of wound
edges on the uterus after a cesarean section or rupture or uterus.
18.5.3.3.
The main sign is hemorrhage from the uterus which can present as profuse or
scanty, and develop gradually. Blood discharge can be continuous or appear at in-
tervals. Subinvolution of uterus is always a concomitant sign. Hemorrhage is often
accompanied by infectious complications.
The puerpera complains of vaginal blood discharge, pain in the lower abdomen or
in the entire abdomen; the pain can be nagging, cramp-like, constant or inconstant.
In case of infection the patient has headache, hyperhidrosis, shiver, increased body
temperature.
The patient’s condition depends on the amount of lost blood, the rate of bleeding
and the presence of infection.
In case of uterine hypotonia or retention of placental fragments, hemorrhage
develops within the first several days after delivery; it is commonly profuse. The
uterus loses its tone, sometimes becomes flaccid. If there is massive hemorrhage,
presentations of hemorrhagic shock and DIC develop.
In case of submucous myoma, chorionepithelioma hemorrhage has a sudden onset

and heavy flow. Bright red blood with or without clots flows from the uterus. The
uterus may remain compact and painless.
In case of postpartum infection, placental polyp, cervical cancer, blood discharge
appears at regular intervals; it is prolonged and scanty. If the blood flow is not heavy,
the patient’s condition is not compromised.
A progress of infection is indicated by the patient’s feverish condition, tachycardia,
low abdominal pain and foul-smelling vaginal discharge, which can be heavy or light.
In this condition the puerpera should be immediately taken to hospital.
Early, correct diagnosis and immediate initiation of treatment can save the puer-
pera’s life. To achieve this, she is thoroughly questioned, her general condition and
the nature of bleeding is assessed.
When taking the patient’s history one notes the patient’s complaints, previous
gynecologic disease and abortions, parity, multiple pregnancies, polyhydramnios,
fetal macrosomia in the present pregnancy, the nature of labor: precipitous labor,
prolonged uterine inertia, features of the postpartum period.
The patient’s general condition is assessed (skin coloration, pulse and respiratory
rate, BP). The abdomen and postpartum uterus are palpated noting the size of uterus,
its consistency, tenderness. The rate and volume of hemorrhage are estimated.
A speculum examination of cervix can reveal a bleeding tumor (cancer), bleed-
ing polyp in the cervical canal or nodes of chorionepithelioma localized in the
cervix, vaginal wall or external genitals. A bimanual vaginoabdominal examina-
tion reveals that the uterine size is greater than normal for the particular day of
puerperium (subinvolution). Subinvoluted uterus can remain large, insufficiently
compact or have uneven consistency with unformed cervix and open cervical ca-
nal. If secondary infection develops, the uterus and abdomen are usually tender
to palpation.
Ultrasound examination finds that the uterine size is greater than normal for the
particular day of puerperium; other findings include enlarged uterine cavity contain-
ing mural blood lcots, thin blood or placental tissues, seldom—nodes of myoma or
chorionepithelioma (Fig. 18.24, 18.25).
Diagnosis of trophoblastic disease is confirmed by hCG test, its qualitative and
quantitative parameters.
The final diagnosis and the cause of hemorrhage are often established only by
histology study of material obtained by D&C.
18.5.3.5. Treatment
The principles of treatment are the same as in early postpartum period: early
adequate care. Hemorrhage commonly develops when the patient is at home, so the
first thing to be done is hospitalizing her.
Upon admission one assesses the severity of puerpera’s condition and starts infu-
sion of colloid solutions simultaneously doing complete blood count, investigation
of the coagulation system. When the blood discharge is scanty, bacteriology and
bacterioscopy study of uterine discharge is obligatory.
482 Obstetrics
Polyp
3D polyp in uterus
Fig. 18.24. Placental polyp. 3D ultrasound, polyp in uterus
9.8 cm/s
-9.8 cm/s
Fig. 18.25. Chorionepithelioma. Ultrasound, color flow mapping
In case of uterine hypotonia and profuse hemorrhage developing 1–2 days after
delivery, the main method of treatment is bimanual examination of uterus walls with
general anesthesia. In uterus hypotonia the cervix remains dilated, so a hand or its
half can enter the uterus cavity. One carefully examines all uterus walls removing the
fragments of placenta or fetal membranes, or blood clots and necrotized tissue. The
uterus contracts, hemorrhage stops. If it is later than 2 days after delivery, one per-
forms hysteroscopy. If necessary, after sounding, determining the length and direction
of uterus, one carefully curettes the walls with a large blunt curet; this is followed
by hysteroscopy control. During this procedure uterotonic drugs are administered
intravenously or immediately to the cervix and body of uterus. The content of uterus
is sent for pathomorphology study.
If there is a heavy blood loss, a complex of antishock and antianemic procedures
as well as hemostasis control are undertaken alongside with surgery and after it.
Uterotonic drugs (oxytocin, prostaglandins), antibiotics are administered; in case of
anemia — antianemic therapy.
If there is a placental polyp and light bleeding, first antibacterial therapy is admin-
istered, and after that — D&C and pathomorphology study of the material obtained.
In endometritis and scanty uterine hemorrhage D&C — a surgical method of treat-
ment — is only indicated once anti-inflammatory therapy fails.
If the patient is running a high temperature or there are inflammatory foci in the
true pelvis, the uterine walls are only scraped in the presence of profuse bleeding that
threatens the patient’s life, while administering antibacterial and infusion-transfusion
therapy.
Having detected chorionepithelioma one prescribes appropriate investigations and
administers chemotherapy. Difficulties arise when the hemorrhage is profuse, and to
save the patient’s life the uterus must be removed.
If there are bleeding due to unrepaired lacerations of vulva, vagina and cervix and
no signs of infection, one ligates the bleeding vessels and repairs the wound. If the
wounds are infected, hemostasis is performed while the wounds are left open; they
heal by secondary intention. Having eliminated infection one can place secondary
sutures, for instance in the perineum. If uterus rupture is detected, the extent of
surgery is deliberated. In modern obstetric practice the uterine wound is commonly
repaired as one usually tries to preserve the woman’s reproductive function.
18.5.3.6. Prophylaxis
One should ensure early detection of women with a risk for hemorrhage: mul-
tiparous, with uterus overdistension (multiple pregnancies, polyhydramnios, fetal
macrosomia), preeclampsia, previous abortions, genital infections and coagulopathy.
Adequate management of labor and puerperium, careful inspection of the afterbirth,
preventive administration of uterotonics (carbetocin, oxytocin), modern perinatal
technologies, early detection and treatment of genital infections constitute the basis
of preventing late postpartum hemorrhage.
18.6. HEMORRHAGIC SHOCK
18.6.1. Definition
Hemorrhagic shock is a pathological condition occurring secondary to acute and/
or massive hemorrhage accompanied by drastic decrease in the circulating blood
volume, cardiac output and tissue perfusion, multiple system organ failure when
adaptive compensatory mechanisms become overwhelmed.
484 Obstetrics
18.6.2. Etiology
Massive hemorrhage during pregnancy and labor results from placenta previa, pla-
centa abruption, rupture of the uterus or sacculated structures of uterine appendages,
lacerations of soft tissues in the birth canal, hematoma, disorder of placenta separa-
tion or retention of pregnancy products in the uterus, adherent placenta or placenta
accreta, intrauterine fetal demise, disrupted contractility of the uterus, congenital
and acquired disorders of the coagulation system.
Hemorrhage from the uterus can develop as secondary bleeding after toxic, ana-
phylactic or pain shock, collapse due to inferior vena cava syndrome, Mendelson’s
syndrome1, amniotic fluid embolism. These conditions are always accompanied by
coagulopathy which causes a block of contractile protein in the myometrium, and
thus — uterine hypotony and hemorrhage. In severe preeclampsia and extrageni-
tal disease massive hemorrhage results from multiple organ failure (shock uterus).
Microcirculatory disorders lead to ischemia, dystrophic changes and myometrial
hemorrhage which causes uterus paralysis and blocks its contractile activity.
Life-threatening hemorrhage:
NB! • loss of 100% of circulating blood volume over 24 hours or 50%
of circulating blood volume over 3 hours;
• blood loss at a rate of 150 ml/min or 1.5 ml/kg per minute
(20 min);
• one-time blood loss > 1500 – 2000 ml (25 – 35% of circulating
blood volume).
18.6.3. Pathogenesis
Childbirth always involves hemorrhage; lacerations of soft tissues in the birth
canal are a possibility. Labor-related trauma and hemorrhage can lead to hemor-
rhagic shock.
The pregnant woman’s body undergoes changes that provide for adequate response
to blood loss during labor, and hemostasis.
The pregnant woman’s weight gain is 10 kg on average. The circulating blood vol-
ume begins to increase in the first trimester, and by the end of the third trimester it
exceeds the baseline by 40–50%. Intravascular plasma volume increases by 40 weeks
gestation from 2.5 to 3.8 liters, and the volume of circulating RBCs — from 1.4 to
1.65 liters. The increase in these values leads to physiological hemodilution or di-
lutional anemia when the concentration of hemoglobin and hematocrit goes down.
Hemodilution prevents thrombus formation in the pregnant woman’s body.
Hemodynamic changes promote intensification of maternal blood flow and life
support for the fetus. In the first trimester the cardiac output increases from 4.5 to
6.8 l/min due to an increase in ventricular ejection and heart rate. Simultaneously,
peripheral and pulmonary resistance decreases, central venous pressure remains
1 Mendelson’s syndrome is acute exudative pneumonitis (aspiration syndrome) caused by aspiration of
acid gastric content into the lower respiratory tract followed by inflammatory response caused by a burn
of the mucosa.
within normal. Uterine blood flow increases from 50 ml/min in early pregnancy to
700 ml/min at its end.
During pregnancy there is a growing tendency for hyperventilation: the respira-
tory minute volume increases by 50% on average alongside the growing supply and
consumption of oxygen. One third of oxygen accretion is used up by the enhanced
cardiac function, the rest — by the uterus and placenta. Hypocapnia during labor
ensures normal transplacental CO2 diffusion from the fetus to the mother.
Considerable changes take place in the coagulation system: increase in plasma
coagulation factors (factors I, VII, VIII, IX, X), decrease in coagulation inhibitors.
The levels of prothrombin and antithrombin III, aPTT, bleeding time stay within
normal. Plasminogen activator inhibitor (PAI-2) produced in the placenta passes to
maternal plasma and together with another inhibitor, PAI-1, it blocks tissue plas-
minogen activator preventing plasmin formation. These changes protect the pregnant
woman from thrombosis, and the puerperal — from hemorrhage.
Hypovolemia, tissue hypoperfusion, hypoxia of vital organs,

NB! dystrophic changes in organs due to disrupted hemodynamics
and tissue metabolism determine the pathogeny of hemorrhagic
shock.
Circulating blood volume in pregnant women is 6% of body weight, on average.

The circulating blood volume decreases in hemorrhage, as well as blood return to
the heart and cardiac output; the oxygen supply to organs reduces. When there is a
bleeding, the body, on the one hand, works to arrest it, on the other hand—to ensure
vitally necessary transport of oxygen to organs and tissues.
At a blood loss of 500–700 ml (up to 10% of circulating blood volume or 0.6%
of body weight) compensation is achieved by increasing the tone of venous vessels
whose receptors are most sensitive to hypovolemia. Under these circumstances arte-
rial tone and heart rate do not change, tissue perfusion is preserved.
Hemorrhagic shock develops after a blood loss of 700–1300 ml (1.0–1.5% of
body weight or 15% of circulating blood volume, or 15 ml/kg) when significant
hypovolemia develops which is a powerful stress factor. The body attempts to retain
normal BP and to maintain the circulating volume by centralizing the circulation and
autotransfusion (release of RBCs from the spleen depot, skin, muscular capillaries).
The excitability of sympathetic system increases, catecholamines are released. When
hemorrhage continues, and the cardiac minute output cannot be maintained, the
normal BP level is maintained by way of increasing peripheral resistance (vasocon-
striction). Expression of vasoconstriction is uneven; it occurs only in the organs that
are not of vital importance: the liver, kidneys, intestine, pancreas, muscles and skin.
The lymph and interstitial fluid flood into the blood stream increasing the circulating
volume but enhancing hemodilution. During the first hours of acute massive blood
loss hemoglobin can remain at baseline despite the skin pallor. Fluid is retained in the
body due to increased production of antidiuretic hormone and aldosterone. The main
bulk of blood is channeled to the heart and brain. This is the way the body replaces
the circulating volume for some time and ensures oxygen supply to organs and tis-
sues. Immobility is important since it reduces the demand for circulating blood and
486 Obstetrics
oxygen. If circulating volume was not replaced fast enough and the bleeding persists,
the effects of vasoconstriction begin to set in. Vasoconstriction promotes an increase
in RBC aggregation, blood viscosity, hypercoagulation development (fibrinogen el-
evation, accelerated blood coagulation). These changes slow down the blood flow still
more thus reducing tissue perfusion. When the hemorrhage is arrested and adequate
therapy is administered, the body compensates for all disturbances on its own.
When blood loss is 1300–1800 ml (1.5–3.0% of body weight or 30% of circulat-
ing blood volume), macro- and microcirculation are disturbed still more. Blood
flow slows down first in the venous, and then in the arterial end of the capillary.
The capillary is eliminated from the circulation, arteriovenous shunts open, blood
flow slows down which aggravates tissue hypoxia. Due to slower blood flow and
hemoconcentration, cellular aggregates of RBCs and platelets are formed in vessels;
they accumulate on the walls, and fibrin deposits develop there. Fibrin is dissolved
by fibrinolysis, and new fibrin deposits grow, which leads to fibrinogenemia. Blood
clotting disorders increase progressively. At this stage DIC begins, and the patient’s
life is now threatened.
Due to circulatory decomposition and hypoxia, metabolic acidosis develops be-
cause of anaerobic glycolysis. A large amount of acid metabolites and aggressive
polypeptides enter the blood stream; they produce a toxic effect and suppress the
myocardium, which promotes a decrease in cardiac output and an increase in vas-
cular wall permeability.
In this way simultaneous disorders of macro- and microcirculation, of the coagula-
tion system keep progressing at the same time; they result in functional disturbances
first, and then—in fatal lesion of all organs and systems.
A massive blood loss is a loss of blood equaling 1.5% of the body weight, and more.
If hemorrhage progresses or its therapy is inefficient, multiple organ and system
failure develops (shock uterus, shock lung, shock kidney, liver necrosis, disturbance
of pituitary and fetoplacental circulation, fetal hypoxia and demise, DIC) resulting
in the patient’s death.

Depending on the volume of lost blood the presentations of hemorrhagic shock
are divided into three stages: mild, moderate and severe. These stages of hemorrhagic
shock development are not always clearly definable. In case of acute, massive blood
loss (placenta abruption, complete placenta previa, uterine rupture in labor) decom-
pensation develops quite soon, and the fatal outcome occurs within 10 minutes. If the
hemorrhage is constant, with a moderate flow, it is difficult to define the borderline
when decompensation of all organs and systems sets in leading to the patient’s death.
Medical personnel should be able to recognize the signs of hemorrhagic (hypo-
volemic) shock (Table 18.4).
• Stage 1 (mild, compensated shock): blood loss is 750–1200 ml (0.5–1.5% of body
weight, or 15–25% of circulating blood volume). At this stage the compensation
is provided by the cardiovascular system; it is of short duration and passes
unnoticed. Clinical features: the patient is conscious showing skin pallor,
tachycardia (up to 100 per min). BP is unchanged or somewhat decreased. The
Table 18.4. Stages of hemorrhagic shock
Value Mild (I) Moderate (2) Severe (3)

Blood loss, ml 750–1200 1300–1800 1800 and more
% of body weight 1.0–1.5 1.5–3.0 3.0 and more
Circulating blood 15–25 25–35 35 and more
volume loss, %
Pulse, per min. under 100 up to 120 over 120
BP, mm Hg Normal or some- 90–100 60 and less
what less
Shock index 0.5–1.5 1.5–2.0 2.0 and more
Central venous pres- 5–15 under 5 almost 0
sure, cm H2O
Hemoglobin, g/l 100 and more 80–100 under 80
Hematocrit, % Somewhat 25–35 under 25
decreased
shock index is 0.5 and more, central venous pressure 5–15 cm H2O. Hemoglobin
100 g/l, hematocrit somewhat decreased. Oliguria. Iso- or hypercoagulation.
• Stage 2 (of medium severity; decompensated reversible shock): blood loss is
1300–1800 ml (1.5–3.0% of body weight, or 25–35% of circulating blood
volume). As hemorrhage progresses, there are signs of vital organ dysfunction.
The patient is conscious, restless. There is skin pallor, the skin is moist.
Acrocyanosis develops; limbs become cold, which indicates peripheral vascular
spasm. The heart rate is 120 per min, dullness of cardiac sounds is noted; ECG
shows ST segment depression and flattening of T wave; respiratory rate is up
to 20 and more. Developing dyspnea indicates a shock lung. Systolic BP drops
to 90–100 mm Hg. The shock index increases to 1.5 and more, central venous
pressure is less than 5 cm H2O. Hemoglobin 80 g/l, hematocrit decreased to
25–30%. Coagulation time (Lee and White method) over 10 min. Signs of DIC
develop: thin blood without clots flows from the uterus; there are hemorrhages
in the skin and mucosas; coffee ground vomiting, melena, hemorrhage from
injections and surgical wounds are a possibility.
• Stage 3 (severe, decompensated, irreversible shock): blood loss is 1800 ml and
more (3% of body weight or 35% and more of circulating blood volume). The
patient’s consciousness is impaired. The skin becomes acutely pale, marble-like.
Heart rate over 120 per min, respiratory rate over 30 per min, systolic BP under
60 mm Hg. Shock index 2.0 and more, central venous pressure almost zero,
hemoglobin under 80 g/l, hematocrit under 25%, anuria. Coagulation time (Lee
and White method) over 15 min. If this stage of decompensation continues for
over 12 hours, the shock becomes irreversible despite the administered therapy.
A terminal condition develops: preagonal state, agonal state, and clinical death.
• In obstetric settings the clinical presentations of hemorrhagic shock have certain
particular features depending on the cause of bleeding.
488 Obstetrics
18.6.5. Diagnosis
In case of hemorrhagic shock one should detect the cause of bleeding, estimate
the volume of blood loss and its dynamics; the stage of shock is established on the
basis of objective data and laboratory findings (complete blood count, blood bio-
chemistry, hemostasiogram).
Hemodynamics can be assessed by the coloration, moisture and temperature
of skin (especially in limbs), the pulse, respiratory rate, central venous pressure,
Allgower shock index, central venous pressure, hourly diuresis, hemoglobin level,
hematocrit, acid-base balance and blood protein (Table 18.5).
The following methods serve for more accurate estimation of blood loss: hemo-
stasiogram, ultrasound during pregnancy (placenta previa and placenta abruption),
dopplerometry (fetal condition) (Table 18.6.).
Hemostasiogram:
• hypercoagulation phase: elevated thromboplastin and prothrombin, coagulation
time less than 4 min, paracoagulation tests (ethanol, protamine-sulphate,
β-naphthol) show no change;
• transition phase: fibrinogen concentration less than 2 g/l, paracoagulation
tests positive, fibrin degradation products increased, thrombin time >30–35 s,
prothrombin time >20 s, antithrombin III level <75%;
• hypocoagulaiton phase: fibrinogen level <1.5 g/l, paracoagulaiton tests often
negative, fibrin degradation products content >2×10 –2 g/l, thrombin time
Table 18.5. Estimate of blood loss extent (WHO, 2002)
Early hypovolemic shock Late hypovolemic shock

(under 1000–1300 ml) (1500–2000 ml)
Sleeplessness, anxiety, restlessness Confused or unconscious
Weak, frequent pulse (110 or more per min) Very frequent weak pulse
Respiration somewhat increased (respiratory Very rapid shallow breathing
rate up to 30 or more)
Pallor Skin pallor and coldness
Relatively low BP (systolic BP under 90 mm Very low BP (systolic BP under 60 mm
Hg) Hg)
Diuresis decreased, but exceeds 30 ml/h Diuresis less than 30 ml/h
Table 18.6. Objective assessment of blood loss
Parameter Extent of blood loss

mild moderate severe
RBC count, x 1012 g/l 3.5 Under 2.5 2.5
Hemoglobin content, g/l 100 80–100 80
Hematocrit value, % 30 25–30 25
Heart rate, per min Under 80 80–100 100
Systolic BP, mm Hg 110 110–90 90
>35 s, prothrombin time 22 s, antithrombin III amount 30–60%, platelet count

decreased.
D-dimers are products of fibrin degradation, markers of thrombus formation and
fibrinolysis (dissolution of intravascular thrombi and extravascular thrombin deposi-
tion). Their acceptable concentration during pregnancy is 248 g/l. In late pregnancy
their content exceeds the baseline 3–4 times. Their content increases at preeclampsia,
DIC, thrombosis and other conditions.
18.6.6. Treatment
Management of hemorrhagic shock consists in adequate

NB! restoration of circulating blood volume and timely correction of
coagulopathy.
Restoration of circulating blood volume begins from the moment when a pathologi-
cal blood loss was established (more than 0.5% of body weight). This procedure is
based on a dynamic assessment of the amount of lost blood and what continues to
be lost. Delivery has its own specifics, so attempts to invent special equipment to
measure blood loss (scales and other instruments) ultimately failed. The so-called
gravimetric method using basins shows an error of about 20%, almost always under-
estimating the value. Thus to the amount obtained gravimetrically one should add
these 20%, which will approximate the estimated volume to the real figure.
If hemorrhage developed outside a hospital, one can get an idea of the amount of
lost blood using the shock index. Shock index is the ratio of pulse rate to systolic BP.
The normal value of shock index is 0.5 on average. When there is hemorrhage, it
increases (Table 18.7).
The extent of infusion-transfusion therapy is determined on the basis of circulating
volume deficiency, which means the circulating blood volume lost with hemorrhage
expressed as a percentage. The circulating volume deficiency is calculated on the
basis of the lost blood volume and the patient’s body weight.
In pregnant women the circulating blood volume is approximately 6% of body
weight. For instance, a pregnant woman weighing 70kg has a normal circulating blood
volume 4200 ml (70×6/100). At a loss of 800 ml the circulating blood volume defi-
ciency is 19% (800×100/4200). The following formula makes the calculation easier:
There are special tables for calculating the circulating blood volume deficiency
(Table 18.9).
Table 18.7. Estimating blood loss by shock index
Shock index Blood loss, % of circulating blood volume

0.8 and less 10
0.9–1.2 20
1.3–1.4 30
1.5 and more 40
490 Obstetrics
It is easier to be guided by the percentage of lost blood volume in relation to the

patient’s body weight.
For instance, a puerpera weighing 70 kg had a blood loss of 700 ml (0.7 l); the
blood loss in relation to her weight is 1.0% (0.7×100/70).
Critical blood loss is 30 ml per each kilo of body weight, or 1.5%

NB! of body weight.
A dynamic assessment of blood loss underlies the plan of infusion-transfusion

therapy and its adjustments; the therapy is administered simultaneously with con-
servative and surgical methods of obstetric hemorrhage management. The aim of
therapy is maintaining a circulating blood volume sufficient for homeostasis, and the
volume of circulating blood cells.
Circulating blood volume is more important than the volume

NB! of circulating RBCs; one can die of hypovolemia rather than
of anemia.
In clinical settings, it is desirable to ensure control of the main homeostasis param-

eters (hemodynamics, levels of hemoglobin, hematocrit, RBCs, hemostasiogram).
If this kind of control is not available, the following plan of infusion-transfusion
therapy is recommended (Table 18.8).
Infusion transfusion therapy of hemorrhage constitutes the first stage of prevention
and therapy for multiple organ failure in the post-resuscitation period. When restor-
ing the circulating blood volume and eliminating hypovolemia one should take into
account the ratio of infused media, and the volume, rate and duration of infusion
(Tables 18.9, 18.10).
If 70% of the lost blood volume is restored within the first 1–2 hours, one can
hope for a favorable outcome.
Restoration of circulating blood volume begins with administration of high mo-
lecular mass blood substitutes, which can remain in the blood stream for a long time.
Table 18.8. Infusion-transfusion therapy in pathological blood loss (by deficiency of circulating
blood volume)
Circulating blood Restoration volume, Infusion media

volume deficiency, % % of blood loss
10–15 150–200 Crystalloid/colloid (3:1)
15–30 200–250 Crystalloid/colloid (2:1)+FFP (50% of
blood loss)
30–40 300 Crystalloid/colloid (1.5:1) )+FFP (100% of
blood loss) + packed red cells (20–30% of
blood loss)
>40 >350 Crystalloid/colloid (1:1) )+FFP (100% of
blood loss)+packed red cells (30% of blood
loss)+platelets, cryoprecipitate
Table 18.9. Table for calculation of circulating blood volume loss in obstetric hemorrhage, %
А 50 52 54 56 58 60 62 64 66 68 70 72 74 76 78 80 82 84 86 88 90 92 94 96 98 100
Б
3000 3120 3240 3360 3480 3600 3720 3840 3960 4080 4200 4320 4440 4560 4680 4800 4920 5040 5160 5280 5400 5520 5640 5760 5880 6000
В
300 10 10
350 12 11 11 10 10 10
400 13 13 12 12 11 11 11 10 10 10 10
450 15 14 14 13 13 13 12 12 11 11 11 10 10 10 10
500 17 16 15 15 14 14 13 13 13 12 12 12 11 11 11 10 10 10 10
550 18 18 17 16 16 15 15 14 14 13 13 13 12 12 12 11 11 11 11 10 10 10 10 10
600 20 19 19 18 17 17 16 16 15 15 14 14 14 13 13 13 12 12 12 11 11 11 11 10 10 10
650 22 21 20 19 19 18 17 17 16 16 15 15 15 14 14 14 13 13 13 12 12 12 12 11 11 11
700 23 22 22 21 20 19 19 18 18 17 17 16 16 15 15 15 14 14 14 13 13 13 12 12 12 11
750 25 24 23 22 22 21 20 20 19 18 18 17 17 16 16 16 15 15 15 14 14 14 13 13 13 12
800 27 26 25 24 23 22 22 21 20 20 19 19 18 18 17 17 16 16 16 15 15 14 14 14 14 13
Chapter 18. Hemorrhage in obstetrics
850 28 27 26 25 24 24 23 22 21 21 20 20 19 19 18 18 17 17 16 16 16 15 15 15 14 14
900 30 29 28 27 26 25 24 23 23 22 21 21 20 20 19 19 18 18 17 17 17 16 16 16 15 15
950 32 30 29 28 27 26 26 25 24 23 23 22 21 21 20 20 19 19 18 18 18 17 17 16 16 16
1000 33 32 31 30 29 28 27 26 25 25 24 23 23 22 21 21 20 20 19 19 19 18 18 17 17 17
1100 37 35 34 33 32 31 30 29 28 27 26 25 25 24 24 23 22 22 21 21 20 20 20 19 19 18
1200 40 37 37 36 34 33 32 31 30 29 29 28 27 26 26 25 24 24 23 23 22 22 21 21 20 20
1300 43 42 40 39 37 36 35 34 33 32 31 30 29 29 28 27 26 26 25 25 24 24 23 23 22 22
1400 47 45 43 42 40 39 38 36 35 34 33 32 32 31 30 29 28 28 27 27 26 25 25 24 24 23
1500 50 48 46 45 43 42 40 39 38 37 36 35 34 33 32 31 30 30 29 28 28 27 27 26 26 25
1600 51 49 48 46 44 43 42 40 39 38 37 36 35 34 33 33 32 31 30 30 29 28 28 27 27
1700 52 51 49 47 46 44 43 42 40 39 38 37 36 35 35 34 33 32 31 31 30 30 29 28
1800 51 50 48 47 45 44 43 42 41 39 38 38 37 36 35 34 33 33 32 31 31 30
1900 51 49 48 47 45 44 43 42 41 40 39 38 37 36 35 34 34 33 32 32
2000 52 51 49 47 46 45 44 43 42 41 40 39 38 37 36 35 35 34 33
2200 – deficient volume of circulating blood 10–15 % 54 52 51 50 48 47 46 45 44 43 42 41 40 39 38 37 37
2400 – deficient volume of circulating blood 15–30 % 53 51 50 49 48 47 45 44 43 42 42 41 40
2600 – deficient volume of circulating blood 30–40 % 53 52 50 49 48 47 46 45 44 43
2800 – deficient volume of circulating blood > 40 % 53 52 51 50 49 48 47
3000 52 51 50
Note: A — body weight; B — circulating blood volume; C — blood loss.

491
492 Obstetrics
Table 18.10. Infusion transfusion therapy upon abnormal blood loss (by blood loss of body
weight, %)
Volume of loss, % Volume of restoration, Infusion transfusion

of body weight % of blood loss, ml therapy composition
0.6–0.8 80–100/800 Saline
0.8–1.0 100–120/1200 Saline, hydroxyethylated starch
1.1–1.5 130–180/up to 2800 Saline, hydroxyethylated starch, FFP,
Dextran, Perftoran
1.5–2.0 250–300/up to 6000 Starch, FFP, Perftoran, packed red cells
At present the drugs of choice are hydroxyethylated starches (HAEC-steril, volecam,

refortan, infucol).
Efficacy of treatment is assessed judging by the skin color, body

NB! temperature, pulse, BP, central venous pressure, hourly diuresis,
hematocrit, and the acid-base balance in the blood.
Infusion transfusion therapy is composed of the following:

• Infusion starts with administration of hydroxyethylated starch, 20 ml per 1 kg of
body weight a day, usually 500–1000 ml/day. The daily dose is calculated on the
basis of blood loss and hematocrit. The starch increases the circulating volume,
cardiac output, the rate of remaining RBC circulation; they improve the flow
properties of blood and microcirculation within 6–8 hours.
• During starch administration FFP is defrosted; it contains coagulation factors.
Plasma is administered in a dose of 15 ml per one kg of body weight.
• If hemorrhage continues or at massive blood loss, it is indicated to infuse packed
red cells conserved for no longer than 3 days. The ratio of transfused FFP and
packed red cells is 3:1.
• In case there is prolonged hemorrhage, massive blood loss but no blood or
its products at the hospital, perfluorocarbons (Perftoran) are administered.
This medication considerably enhances the spare reserves of the remaining
circulating blood volume thus providing a cushion of time (2–6 hours) to
prepare infusion of packed red cells. Perftoran is an inert hydrocarbon,
insoluble in water and soluble in lipids. This transfusion medication with a
high oxygen capacity increases and maintains partial oxygen content in venous
and arterial blood; it decreases myocardial ischemia, prevents and reverts DIC
and peripheral circulatory disorders. 400 ml (30 ml/kg) are administered to a
bleeding patient on the fi rst day (after a biological assay: 5 drops followed by
30 drops in 3 min followed by the rest in 3 min). Perftoran cannot be combined
with other colloids. Packs contain 200 ml of the medication. It can be stored
for 5 years in a frozen state at a household refrigerator temperature (-18 °С).
Perftoran must not be mixed with other colloids, but can be

NB! administered alongside fresh-frozen plasma.
• Proteolysis inhibitors (like Contrical no less than 10 000 IU) are administered to
suppress excessive fibrinolysis. In coagulopathy this medication alone does not
suffice, the whole range of fibrinolysis is required. One administers medications
that do not fi x to fibrin, block plasmin and plasminogenesis thus preventing
fibrinogen degradation (tranexamic acid drug: tranexam 500–750 mg).
• Glucocorticoids are administered: prednisolone and hydrocortisone (10 mg/kg)
increasing BP.
• Stimulation of the vascular-thrombocytic component of hemostasis is performed:
NovoSeven, Prothromplex.
• If the blood loss is massive, hypoglycemia is triggered, thus 10 or 20% dextrose
(glucose) solution should be administered with Panangin (no more than 15 ml/kg).
• Cardiotonic drugs are administered only after having restored the blood loss.
Upon restoration of the circulating blood volume and arrest of hemorrhage the
therapy is continued.
18.6.7. Prophylaxis
Prevention of hemorrhage in puerperium should be started during pregnancy. It
includes the following:
• detecting and hospitalizing patients with anatomical and functional incompetence
of uterus, placenta previa;
• early detection of patients with preeclampsia and providing timely delivery;
• adequate, non-aggressive management of labor and postpartum period;
• timely prevention of uterine atony by administration of uterotonics.
18.7. DISSEMINATED INTRAVASCULAR

COAGULATION (DIC)
18.7.1. Definition
DIC is a change in the blood coagulation system of a secondary order.
18.7.2. Etiology
This condition was described occurring upon placenta abruption. DIC complicates
many severe diseases and critical conditions including massive blood loss. Resulting
from tissue hypoxia and metabolic acidosis of any origin—injury or toxins entering
the blood stream — blood and tissue thromboplastin is activated, which leads to dis-
order of hemostasis. In obstetrics DIC is mostly seen in severe forms of preeclampsia,
placenta abruption, hemorrhagic shock, amniotic fluid embolism, thromboembolism,
sepsis, cardiovascular, hepatic, renal disease, incompatible blood transfusion, non-
developing pregnancy, dead fetus in utero, etc. In all these obstetric complications
DIC is caused by:
• lesion of blood cells resulting in phospholipid release;
• lesion of tissues resulting in a great amount of thromboplastin entering the blood
stream;
494 Obstetrics
• lesion of vascular endothelium activating Hageman factor;

• hemodynamic disorders accompanying shock and resulting in hypoxia.
Development of DIC includes three phases.
• Phase one: active thromboplastin formation, the most prolonged hemostasis
phase. Both plasma factors (XII, XI, IX, VIII, X, IV, V) and platelet factors (III,
I) participate in it.
• Phase two: transformation of prothrombin into thrombin. This occurs with a
participation of active thromboplastin and calcium (factor IV).
• Phase three: fibrin polymer formation. Added by calcium (factor IV) and platelet
factor, thrombin transforms fibrinogen to fibrin monomer, which turns into
insoluble strands of fibrin polymer under the impact of plasma factor VIII and
platelet factor.
Change in procoagulants in the hemostasis process and activation of platelet
component of hemostasis lead to platelet aggregation releasing biologically active
substances: kinines, prostaglandins, catecholamines, etc. They affect the cardiovas-
cular function.
When the blood flows slowly along minor vessels, it breaks down into plasma and
RBCs which fill different capillaries. Devoid of plasma RBCs lose the ability to move
and aggregate in the form of slowly circulating, and then non-circulating formations.
This is followed by stasis, aggregation and their lysis; blood thromboplastin linked
to red cell stroma is released. Thromboplastin entering the blood stream causes
intravascular blood coagulation. Precipitated fibrin strands entangle RBC masses
forming sludge: lumps deposited in capillaries that disturb the homogeneity of blood
structure still more (Fig. 18.26). The development of sludge is helped along by two
interconnected phenomena — reduced blood flow and increased blood viscosity.
Blood supply to organs and tissues becomes disturbed.
In response to coagulation system activation, protective mechanisms come into
play: fibrinolytic system and cells of reticuloendothelial system. Fibrin deposited in
thrombus undergoes fibrinolysis (enzymatic degradation). The products of fibrinogen
Fig. 18.26. RBC aggregation (sludge) in capillaries

degradation have fibrinolytic properties. If the cause of massive thrombus formation

(hypercoagulation phase) is not established, large amounts of fibrinogen degrada-
tion products emerge in the blood, and they begin to dissolve the newly-formed
thrombi energetically. Thus diffuse bleeding develops, and hypocoagulation phase of
DIC begins. The coagulation factors that are formed in the thrombi are intensively
consumed, and this, alongside with fibrinolysis, leads to coagulation factor deple-
tion. If fibrinolysis prevails over blood coagulation, the patient’s life can be only
saved by transfusion of consumed coagulation factors that are contained in donor
FFP, NovoSeven and Prothromplex medications, cryoprecipitate, that is, factors and
concentrates of coagulation factors.
In presence of DIC, excessive bleeding develops due to increased consumption of
procoagulants and intensified fibrinolysis.
Several classifications of DIC stages were proposed, although in clinical practice
DIC is difficult to break down into clear stages.
Stage 1, hypercoagulation. Duration of this stage varies. Blood clotting time
decreases, fibrinolytic and anti-coagulant activity reduces, thrombin-test becomes
shorter. Clinical presentations of this stage include skin hyperemia alternating with
cyanosis, mottled skin (especially in upper and lower extremities), sometimes shiver,
restlessness, tachycardia.
Stage 2, hypocoagulation. A coagulogram shows consumption of coagulation fac-
tors, there are fibrin and fibrinogen degradation products, decreased platelet con-
tent, increase in thrombin time; the time of fibrin clot lysis shortens; antithrombin
III activity decreases. Clinical presentations include intensified vaginal hemorrhage
and hemorrhage from wounds; skin hemorrhages emerge; nasal bleeding develops;
petechiae appear on lateral surfaces of the chest, thighs, upper eyelids. The blood
flowing from the uterus contains loose clots that break down rapidly.
Stage 3, hypocoagulation with generalized activation of fibrinolysis. A coagulogram
shows a decreased amount and reduced function of platelets, decreased concentration
and activity of procoagulants; fibrin and finbrinogen degradation products circulate in
the blood in large amounts; fibrinolytic activity surges; free heparin content continues
to grow. Thin non-clotting blood is discharged; sometimes single minor clots are
formed that are lysed rapidly. One notes generalized bleeding in the site of injection,
venesection, surgical field, hematuria, hemorrhagic exudation in the abdominal and
thoracic cavity and pericardium.
Stage 4 — terminal — complete non-clotting of blood. Extreme hypocoagulation
combined with intensive fibrinolytic and anticoagulant activity. Clinical presentations
are the same as in stage 3: generalized bleeding.
One should note that in real life these stages of DIC do not always follow in a
clear sequence. There are many clinical and laboratory varieties of this phenomenon.
The progress of DIC depends on the underlying obstetric condition that caused
hemorrhage, accompanying somatic diseases, specifics of the course of pregnancy,
and so on. For instance, if fibrinogen is low or its activation occurred only 6–8 h
after the onset of thrombus formation, there may be no generalized bleeding. In this
496 Obstetrics
case disorder of microcirculation in parenchymatous organs mediates necrosis with

development of renal, hepatic and pulmonary failure, cerebral edema, shock uterus.
As for the clinical course of DIC, acute and chronic forms of DIC are distin-
guished.

There are no specific signs of DIC as it develops secondary to certain obstetric
complications; however its most common signs are hemorrhage, shock, thrombosis,
vital organ dysfunction.
Clinical presentations of DIC can persist for 7–9 hours and longer. Hemocoagulation
changes determined by laboratory methods persist longer than clinical changes.
Laboratory diagnosis of DIC is the highest priority; it permits an

NB! accurate assessment of the degree or stage of the condition and
choosing adequate management.
Acute and chronic forms of DIC are distinguished.
18.7.5.1. Acute DIC syndrome

Causes of acute DIC: placenta abruption, hypotonic and atonic hemorrhage, am-
niotic fluid embolism, uterine rupture.
Clinical features of acute DIC: bleeding from the site of injections and surgical field,
necrosis of the skin and mucosa, CNS dysfunction, acute renal and pulmonary failure.
18.7.5.2. Chronic DIC syndrome

Chronic form of DIC syndrome develops when there is dead fetus in utero,
preeclampsia, diseases of cardiovascular system, liver, kidneys, Rh incompatibility.
During labor chronic DIC can become acute. For instance, chronic DIC with
generalized arteriole spasm and prolonged moderately expressed hypercoagulation is
a link in the pathogenesis of preeclampsia of pregnant women. Platelet microclots
(sludge) are formed in the system of microcirculation; in severe preeclampsia this
leads to necrosis and hemorrhage in parenchymatous organs, the brain and placenta,
and this, in its turn, results in placental insufficiency; if local acute DIC develops,
placental abruption results.
Clinical features of chronic DIC are not pronounced. Intradermal and subcutane-
ous hemorrhages, gum and nose bleeding are possible.
Chronic DIC is diagnosed on the basis of laboratory findings of the hemostasis
system.
18.7.6. Treatment
Treatment of DIC consists in achieving three major goals simultaneously:
• eliminating the main cause of DIC;
• normalizing hemodynamics;
• normalizing blood coagulation.
In treating acute DIC at obstetric hemorrhage one should consider the phase of
syndrome when therapy begins, and the obstetric cause. Treatment is administered
under control of laboratory findings.
Acute DIC is combined, as a rule, with hemorrhagic shock, and the measures for
restoration of central and peripheral hemodynamics have a lot in common. Alongside
with normalizing central and peripheral hemodynamics, acute DIC requires restora-
tion of coagulation properties of the blood. For this purpose, intravascular clotting of
the blood should be arrested, fibrinolytic activity should be reduced, and coagulation
properties should be restored. This is done under coagulogram control. Restoration
of coagulation properties of the blood is achieved by replacement therapy: transfusion
of FFP, Perftoran, fresh frozen RBCs, fresh citrated blood, antihemophilic plasma,
fibrinogen, cryoprecipitate of NovoSeven and Prothromplex.
Inhibition of fibrinolytic activity is achieved by administration of proteolysis in-
hibitors: tranexamic acid drugs.
In case of progressing chronic DIC in pregnant women with preeclampsia, dead
fetus in utero, non-developing pregnancy it is expedient to perform an early termina-
tion of pregnancy via a vaginal birth.
Intensive therapy continues even after DIC was eliminated, for restoration of pro-
tein and water-electrolyte balance, prevention of infection complications.
18.7.7. Complications
• renal failure
• hepatic failure
• pulmonary failure
• infection
• fatality
18.8. AMNIOTIC FLUID EMBOLIZATION
18.8.1. Definition
Amniotic fluid embolization (AFE) is a critical condition caused by passage of
amniotic fluid or its components into maternal blood stream resulting in shock of
combined origin and disorder of blood coagulation.
Clinical presentations of AFE were first described in 1926. In 1941 Steiner and
Luschbaugh first reported 8 cases of maternal fatality of AFE as an obstetric syn-
drome diagnosed at autopsy and microscopic study of lungs. A total of 88 AFE cases
were described until 1960.
In 70–90% AFE results in the woman’s death. AFE is regarded as the cause
of death when the diagnosis is confirmed by histology studies. In 10% of patients
498 Obstetrics
embolism develops at a physiological course of pregnancy and in 20% — prior to

labor onset or rupture of membranes, somewhat more often at the end of the first
stage of labor or in the second stage. In 50–80% at pronounced clinical presenta-
tions of AFE fetal death occurs secondary to hypoxia. Of these, 90% of fetuses
die during labor.
Nowadays 1 case of AFE occurs per 8000 deliveries.
When pregnancy and delivery proceed uneventfully, amniotic fluid cannot pass to
maternal blood flow as venous pressure in uterine vessels always exceeds the amniotic
pressure. Venous pressure is 10 mm Hg at rest while amniotic pressure is 8 mm Hg;
when labor starts, it is 40 and 20 mm Hg, correspondingly.
Therefore, amniotic fluid can pass to maternal blood stream only in case of
• considerable excess of amniotic pressure compared with the pressure in maternal
venous system due to elevated intrauterine pressure;
• open veins in the uterus.
Intrauterine pressure elevates at violent labor (oxytocin stimulation, accelerated
and precipitated labor), polyhydramnios, fetal macrosomia, multiple pregnancy,
unfavorable fetal lie or head engagement, cervical rigidity, early rupture of amniotic
sac, insufficient analgesia in labor, amnioscopy, amniocentesis, rough handling dur-
ing delivery.
Open uterine vessels occur due to cervical and uterine injury, manual exploration
of uterine cavity, placenta previa and placental abruption, postpartum uterine atony,
cesarean section.
Amniotic fluid passes to maternal venous system by the following routes:
• transplacental route: through injured placental vessels;
• through intervillous space at placenta previa and placental abruption;
• transcervical route: through injured cervical vessels upon cervical rupture;
• through injured vessels in any portion of uterus at operative delivery (cesarean
section, forceps delivery) and uterine rupture.
From there, amniotic fluid is carried by the blood stream to the pulmonary artery,
minor vessels, capillaries and alveoli of the lungs.
Amniotic fluid constitutes a complex biological medium. It contains biologically
active substances produced both by maternal and fetal bodies. The fluid contains
mucoproteids with a high protein content, protein in concentration 210–390 mg%,
glucose, vitamins, enzymes, microelements, lipids, adrenalin, noradrenalin, thyroxin,
estradiol and other steroid hormones, histamine, nitrogen compounds, prostaglan-
dins. There are always components of the gestational sac — meconium, vernix ca-
seosa, furfur, mucus, fetal urine and chorionic villi.
The extremely aggressive composition of amniotic fluid plays the key role in the
pathogenesis of embolism; the fluid causes a grave anaphylactic reaction.
Two phases are distinguished in AFE pathogenesis:
• phase one — anaphylactic reaction to amniotic fluid antigens which leads to mast
cell degranulation and release of histamine, leukotrienes, cytokines, endothelin.
This explosive release of mediators leads to bronchospasm, pulmonary vessel
spasm, right and left ventricular failure with development of pulmonary edema
and shock of varied origin;
• phase two — acute coagulopathy with massive hemorrhage, which is due to a
large amount of tissue thromboplastin and the effect of mediators.
Mechanical stimulation of interoreceptors in pulmonary vessels by organic sub-
stances causes a reflex spasm of vessels in the pulmonary system, which disrupts
microcirculation in pulmonary capillaries, ventilation-perfusion relations and leads
to hypoxia. Biologically active substances precipitate vascular enlargement in the
systemic circulation and a drop in general peripheral resistance thus causing a
collapse. In the pulmonary circulation (pulmonary artery and right ventricle) the
pressure increases, the right ventricle becomes overloaded, and acute right ventricle
failure develops decreasing venous return to the left heart. Therefore, cardiac output
decreases, BP goes down, collapse develops and hypoxia aggravates. Thromboxane
and prostaglandins cause a coronary spasm.
Amniotic fluid has thromboplastin activity. Adding one drop of amniotic fluid to
a vial with blood shortens the clotting time twofold.
Tissue thromboplastin of amniotic fluid precipitates the coagulation phase. A large
amount of thrombin and fibrin is formed rapidly and thus multiple thrombi emerge,
especially in the lungs. Amniotic fluid contains a factor accelerating clot retraction.
Rapid depletion of coagulation factors, thrombocytopenia, hypofibrinogenemia and
compensatory activation of anti-clotting and fibrinolytic systems bring about the
hypocoagulation phase with massive profuse hemorrhage. The reticuloendothelial
system is blocked and becomes unable to excrete proteolysis products which have an
anticoagulant effect. Thrombohemorrhagic syndrome develops. Shock becomes the
first stage of thrombohemorrhagic syndrome.
These changes in the blood at AFE are described as DIC syndrome with its stages
of hyper- and hypocoagulation.
Once the fluid enters maternal blood flow, the fetus is immediately affected; it
develops hypoxia. In hypoxia the fetus releases meconium, which passes to the
amniotic fluid. Amniotic fluid becomes more aggressive, and hemodynamic changes
aggravate still more.

Clinical features are determined, in the first place, by the aggressiveness of for-
eign amniotic fluid, rather than by the rate of its passing to maternal blood flow.
We distinguish fulminant AFE with a violent malignant course as well as collaptoid,
hemorrhagic, convulsive and edematous clinical forms of AFE.
Basic AFE signs are retrosternal pain, dyspnea, fear of dying,

NB! skin pallor and cyanosis, suffocating sensation, cold sweat,
low BP, collapse. The patient is in mental confusion, she can
faint or sink into a coma. There can be motor agitation, tonic or
clonic convulsions, signs of pulmonary edema and acute right
ventricular insufficiency.
500 Obstetrics
Presentations of shock include acute right ventricular failure with a steep fall of
BP and increase in central venous pressure as a result of pulmonary hypertension,
reduced cardiac output. Low cardiac output promotes tachycardia, decrease in BP
and peripheral vascular spasm. Pulmonary edema then develops.
Instant fatality is a common occurrence. 30% of patients die within the first hour
after the first signs appeared. If the patient does not die within the first minutes, in
half an hour or within several hours coagulopathy develops. Massive uterine bleeding
begins; there are hemorrhages from the gums, injection sites, hemorrhagic diathesis.
The patient’s condition deteriorates rapidly due to the combination of cardiogenic
and hemorrhagic shock. The woman dies of multisystem and multiple organ failure.
When an insignificant amount of amniotic fluid passes to maternal blood flow,
the presentations are inapparent. The main signs are not pronounced, the patient
is conscious. She may complain of general weakness, shivers, moderate retrosternal
pain. She shows pallor of skin and mucosas, somewhat decreased BP, dyspnea. Later
uterine hemorrhage develops. Sometimes the only sign of AFE is vaginal hemorrhage.
18.8.5. Diagnostics
If a patient, who was in a satisfactory condition initially, develops

NB! cardiopulmonary insufficiency during or after labor, one should
first of all consider AFE.
Diagnosis, which is unfortunately mostly retrospective, is based on a careful

analysis of clinical presentations and the chronology of pathophysiological changes.
Additional methods of investigation are ECG (rhythm changes: sinus or paroxys-
mal tachycardia, flattening of waves), X-ray of the chest (interstitial edema, infarc-
tions).
Dynamic monitoring of the blood clotting system is essential:
• blood clotting time is usually within normal or shorter;
• fibrinogen content > 4.5 g/l;
• shortened aPTT;
• decreased antithrombin III content;
• increased content of fibrinogen degradation product.
An accurate intravitam diagnosis is only possible upon histological

NB! study of the blood taken from the central vein after inserting
a catheter; of the sputum and tracheal washing. The study
reveals components typical of amniotic fluid; an immunological
study detects syncytiotrophoblast cells and megakaryocytes in
pulmonary vessels.
After the patient’s death pulmonary vessels show components of amniotic fluid,
fetal EBCs, trophoblast cells; enlargement of the right ventricle is detected as well
as edema and hemorrhage in the lungs.
AFE is differentially diagnosed from pulmonary artery thromboembolism.
18.8.6. Treatment
A complex approach is required; all manipulations should be performed quickly
and, if possible, simultaneously.
The puerpera’s life dpends on the efficacy of anti-shock

NB! procedures!
The respiratory function should be restored immediately. When spontaneous res-

piration is absent, intubation and artificial lung ventilation are indicated.
At the same time, anaphylactic shock is managed: prednisolone IV 300–400 mg or
hydrocortisone up to 1000 mg, antihistamine and cardiac drugs, infusion-transfusion
therapy.
To replace the insufficient clotting factors, FFP, fresh donor blood, concentrates
of coagulation factors are transfused.
To control abnormal fibrinolysis one administers tranexamic acid drugs (manage-
ment of acute DIC) and supports blood circulation.
At the same time one performs a rapid, careful delivery, a vaginal birth prefer-
ably. The method of delivery is dictated by the obstetric situation; one can resort
to cesarean section, forceps, total breech extraction. In case of uterine hemor-
rhage, internal iliac arteries are ligated or embolized; complete hysterectomy is
performed.
Treatment is considered effective upon the following conditions:
• arrest of hemorrhage;
• systolic BP no less than 100 mm Hg;
• no abnormalities of cardiac rhythm;
• no cyanosis;
• circulating blood volume stabilized (RBCs 2×1012 g/l, hemoglobin ≥70 g/l,
hematocrit ≥25%);
• diuresis >30 ml/h;
• platelets ≥70x109/l;
• fibrinogen 1.5 g/l;
• blood clotting time ≤10 min;
• thromboelastogram values show iso- or hypercoagulation.
To date, no absolutely clear predictors of AFE have been

NB! established.
According to Abenhaim et al. (2008), the following risk factors for embolism were
identified on the basis of analyzing 3 mln deliveries in the USA:
• maternal age over 35 (risk ratio 2.2);
• cesarean section (5.7);
• placenta previa (30.4);
• preeclampsia (7.3);
• placental abruption (8.0);
• obstetric forceps (4.3);
• labor induction (1.5).
502 Obstetrics
According to Kameretal (Lancet, 2006), additional risk factors are polyhydram-

nios, cervical dilation, uterine rupture and fetal distress in labor.
18.8.7. Prophylaxis
Passage of amniotic fluid into maternal blood flow is promoted by early rupture
of membranes, excessive uterine activity, excessive oxytocin stimulation, fetal mac-
rosomia, placenta previa and placental abruption, cervical injury, operative delivery.
Accelerated and precipitous labor should be managed in due time; administer oxy-
tocin with caution, perform amniotomy strictly if indicated.
REMEMBER!
Definition Hemorrhage developing prior to 22 weeks gestation is referred

to as hemorrhage in the first half of pregnancy, or hemor-
rhage in early pregnancy (WHO, 2002).
Hemorrhage developing after 22 weeks gestation is referred to
as late pregnancy hemorrhage or antepartum hemorrhage
(WHO, 2002). Postpartum hemorrhage is bleeding after child-
birth; bleeding in the third stage of labor is not distinguished.
Hemorrhage in late postpartum period (secondary or late
postpartum hemorrhage) is discharge of blood developing from
24 hours to 42 days after childbirth
Etiology Non-obstetric causes of vaginal hemorrhage:

cervical ectopy;
cervical polyp;
cervical cancer;
varicose veins in vagina and vulva;
vaginal and vulvar trauma.
Obstetric causes of vaginal hemorrhage:
spontaneous abortion (incipient, inevitable, incomplete);
missed abortion;
bleeding after abortion;
criminal pregnancy termination (at any age, commonly at an
early gestational age);
interrupted ectopic pregnancy;
trophoblastic disease;
placenta previa, low placentation;
premature abruption of normally located placenta — placental
abruption;
uterine rupture.
Causes of hemorrhage in the first and second stage of labor
are the same as those after 22 weeks gestation. They can be
obstetric and non-obstetric. All obstetric hemorrhages are due
to uterine bleeding
Classification WHO’s classification:

hemorrhage during pregnancy (obstetric or non-obstetric);
hemorrhage in the third stage of labor and puerperium (early
and late postpartum hemorrhage)
Hemorrhage during pregnancy and in the first and second
stages of labor may or may not be associated with gestational
sac abnormalities.
Russian classification of hemorrhage:
Hemorrhage in the first and second half of pregnancy;
Hemorrhage in the first and second stage of labor;
Hemorrhage in the thirds stage of labor;
Hemorrhage in the postpartum period: early and late.
USA classification of hemorrhage:
antepartum hemorrhage (placental abruption, placenta
previa);
postpartum hemorrhage: hemorrhage in the third stage of
labor, uterine atony, hemorrhage due to retention of placental
fragments, placenta accreta, uterine inversion, birth canal
ruptures, postpartum hematoma, uterine rupture
Clinical Most cases of obstetric hemorrhage present as blood discharge

features from the vagina, except for the following:
cases of placental abruption when there is no apparent
hemorrhage as the blood accumulates behind the placenta or
membranes;
complete uterine rupture accompanied by intraabdominal
hemorrhage;
intraabdominal hemorrhage in case of interrupted ectopic
pregnancy.
External bleeding is absent when there develops hematoma
of soft tissues secondary to injury during delivery. In massive
bleeding presentations of hemorrhagic shock develop.
Hemorrhage during pregnancy or labor can be accompanied by
presentations of acute fetal hypoxia
Diagnosis Diagnosis is based on patient’s history, clinical evidence,

obstetric and ultrasound examination findings. One should
not strive to establish the final cause of hemorrhage in the
settings of maternal welfare clinic as a complete work-up is
impossible due to the risk of aggravating the hemorrhage;
this is the task of hospital personnel. At a maternal welfare
clinic one does not perform cervical or vaginal examination
as this can aggravate the bleeding. Speculum and vaginal
examination is only performed in hospital in conditions of
surgical preparedness as hemorrhage may intensify during
examination, and emergency delivery (cesarean section)
will be needed. Early diagnosis of placental abruption is
extremely important as this condition often requires immediate
therapeutic intervention.
504 Obstetrics
Diagnosis is made on the basis of patient’s complaints,

general and special history findings (preeclampsia, threatened
abortion), clinical features (signs of internal bleeding,
abdominal pain, uterus in hypertone, disorder of fetal cardiac
activity), general and special examinations; laboratory
diagnostic methods are employed. When clinical presentations
are pronounced and the signs of internal hemorrhage (acute
placental abruption) keep progressing, cesarean section is
performed at any gestational age, in the first or early second
stage of labor irrespective of fetal condition (live or dead
fetus); after that the issue of sparing the uterus is considered.
The surgery is performed while active antishock, antianemic
therapy and DIC prevention are provided. When hemorrhage
develops in the third stage of labor, delayed separation
of placenta is diagnosed by external signs of placental
separation (Schroeder, Alfeld, Kustner signs) before the
placenta is delivered. Retention of placental products in uterus
is diagnosed by inspecting the placenta and membranes after
the placenta has been delivered. Massive hemorrhage in
postpartum period is mostly due to uterine hypotonia or
atony. The diagnosis of uterine hypotonia is made by the signs
of uterine hemorrhage and objective findings about uterine
tone
Investigation With a bleeding patient, it is important to diagnose hemorrhagic

methods shock in time. At hemorrhagic shock one establishes the
cause of bleeding, estimates the volume of lost blood, and
determines the stage of shock on the basis of objective and
laboratory findings (complete blood count, blood biochemistry,
hemostasiogram)
Complications Massive hemorrhage, hemorrhagic shock, cardiogenic shock,

multiple organ failure, death
CONTROL QUESTIONS
1. What are the typical causes of hemorrhage in the third trimester of pregnancy?
2. What is abnormal location of placenta?
3. What are abnormalities of placentation?
4. What are the principles of diagnosis of abnormal placentation?
5. What are the specifics of obstetric hemorrhage?
6. Name the causes of hemorrhage in the third stage of labor.
7. Name the causes of postpartum hemorrhage.
8. What is the algorithm of action at hypotonic hemorrhage?
9. What is DIC syndrome?
10. What are the principles of blood loss restoration in obstetrics?
CHECK YOURSELF!
Level 1. Test
1. Specific features of obstetric hemorrhage are:
a) coagulopathy;
b) sudden onset;
c) massive bleeding;
d) associated with extragenital disease.
2. When cervical cancer is detected in early pregnancy, one should:

a) terminate the pregnancy immediately;
b) perform radical hysterectomy;
c) prolong the pregnancy to 34 weeks;
d) prolong the pregnancy to 28 weeks.
3. The main causes of hemorrhage in the second and third trimesters:

a) placenta previa;
b) placental abruption;
c) cervical ectopia;
d) vaginal injury.
4. Placenta previa can be of the following types:

a) complete;
b) constant;
c) temporary;
d) progressing.
5. Placental abruption occurs:

a) during pregnancy;
b) only in the first stage of labor;
c) only in the second stage of labor;
d) only in term pregnancy.
6. Vaginal blood discharge during pregnancy requires:

a) hemostasiogram;
b) examination of the patient at maternity welfare clinic;
c) hospitalization to obstetric hospital;
d) strict bed regimen.
7. Uterine rupture mostly occurs:

a) along the scar;
b) resulting from injury;
c) in fetal macrosomia;
d) in the presence of uterine myoma.
506 Obstetrics
8. To arrest hemorrhage in the third trimester one should:

a) transfuse erythromass;
b) transfuse plasma;
c) place clamps on the cervix;
d) perform cesarean section.
9. Placenta accreta requires:

a) careful manual separation of placenta from the uterine wall;
b) careful removal of placenta from the uterus with an obstetric curet;
c) laparotomy and hysterectomy;
d) embolization of vessels supplying the uterus.
10. The following algorithm is used for the therapy of hypotonic hemorrhage:
a) balloon tamponade of uterus, oxytocin IV, ice pack to the lower abdomen;
b) oxytocin IV, ice pack to the lower abdomen, transfusion of blood substitutes
and blood products;
c) oxytocin IV, external massage of uterus, manual exploration of uterus;
d) examination of the birth canal, oxytocin IV, external massage of uterus,
manual exploration of uterus.

1. A pregnant woman aged 34 presents at maternal welfare clinic with uterus in
hypertone and vaginal blood discharge. What is your diagnosis? What is your plan
of management?
2. An inspection of afterbirth reveals placental defect. What is the plan of man-
agement?
NOTES
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• Chapter 19
EARLY TOXICOSIS — HYPEREMESIS
GRAVIDARUM
Early toxicosis is a disease of pregnant women whose development is associated

with the growth of gestational sac or its components; the condition is characterized
by many signs. When the gestational sac or its components are removed, the disease
discontinues, as a rule.
Early toxicosis develops in the first weeks of pregnancy; the signs subside after
12–13 weeks gestation, as a rule.
19.1. EPIDEMIOLOGY
Nausea and vomiting are the most common, unpleasant signs of the first trimester
of pregnancy; however, not all pregnant women with these signs develop toxicosis.
Nausea and vomiting in pregnancy are due to changes in the digestive system as the
vagal effect increases, as well as the content of hCG and steroid hormones (Fig. 19.1).
The incidence rate of toxicosis is 2–3%; in 85–90% of pregnant women toxicosis
presents as vomiting, but no more than 8–10% of them require treatment. Severe
forms develop in 0.5% of patients.
200 000
Peak of Symptoms
150 000
HCG mIU/ml
100 000
50 000
Onset
of NVP Symptoms
0
0 10 20 30 40
Weeks Gestation
Fig. 19.1. β-hCG concentration and nausea and vomiting of pregnancy

508 Obstetrics
19.2. ICD-10 CODES
O21 Excessive vomiting in pregnancy

• O21.0 Mild hyperemesis gravidarum.
• O21.1 Hyperemesis gravidarum with metabolic disturbance.
• O21.2 Late vomiting of pregnancy.
• O21.8 Other vomiting complicating pregnancy.
• O21.9 Vomiting of pregnancy, unspecified.
19.3. HISTORICAL REVIEW
The term toxicosis was introduced in the early 20th century; it does not re-
flect the essence of abnormality nor agrees with present-day views of its causes.
Some authors attributed the cause to toxins and «abnormal» metabolism in the
pregnant woman’s body. Other authors stated that toxins are formed in the pla-
centa or chorion whose fragments pass to maternal blood stream, degrade there
and produce a toxic effect. Multiple attempts to isolate toxic substances in the
body of a pregnant woman with toxicosis failed. However, the term «toxicosis»
is still in use; it covers the whole range of disorders from nausea of pregnancy
to jaundice of pregnancy.
Early toxicosis is divided into:

• commonly encountered forms: hypersalivation, vomiting of pregnancy;
• rare forms:
– chorea gravidarum and bronchial asthma;
– osteomalacia;
– dermatosis;
– tetany;
– acute yellow dystrophy of liver.
There is a group of risk for early toxicosis (vomiting of pregnancy); it includes
pregnant women with concomitant somatic disease and specifics of pregnancy itself.
Risk factors are:
• extragenital diseases:
– digestive tract disease;
– diabetes mellitus;
– metabolic syndrome;
– thyroid disease;
• obstetric causes:
– multiple pregnancy;
– gestational sac malformations.
Chapter 19. Early toxicosis — hyperemesis gravidarum 509
19.5. ETIOLOGY
To date the etiology of this condition is not clearly understood. There are about
ten theories, the major ones are;
• neurogenous;
• hormonal;
• allergic;
• immune;
• corticovisceral.
19.6. PATHOGENESIS
Pathogenesis is not known to date. It was established that an increase in early

toxicosis signs correlates with hCG growth, with progesterone level (effect through
smooth muscle fibers), with steroid hormone level, with thyroid and adrenal hor-
mones.
19.7. COMMON FORMS
The predisposing factors are chronic diseases of the digestive tract and a positive
Helicobacter pylori test (gramnegative bacterium affecting the stomach mucosa).
Clinical presentations of hyperemesis gravidarum show the leading sign, vomiting.
Depending on the degree of this sign, mild, medium and severe forms are distin-
guished. Severe hyperemesis gravidarum is also called intractable vomiting.
• In mild degree, the general condition remains satisfactory. No more than
5 episodes of vomiting a day are observed; it is associated with meals. The
patient’s appetite is suppressed, her mood is depressed. The body temperature
remains within normal. Urine and blood tests show no abnormality.
• In moderate degree the general condition is markedly worse. Vomiting can
occur 10 times a day; it is not associated with meals. Weight loss is 2–3 kg a
week; tachycardia up to 100 per min and ketonuria are noted; subfebrile body
temperature is not common. There are no pronounced changes in the acid-base
balance. A study of electrolytes shows insignificant decrease in sodium content
while potassium content is within normal.
• In severe degree there is pronounced intoxication, sleep disorder; adynamia
develops. There can be 20–25 vomiting episodes a day. By this time the patient
becomes dehydrated. The skin is dry, flaccid. The weight decreases by 2–3 kg
a week. Tachycardia can be up to 110–120 per minute. Arterial hypotension
is often noted. Body temperature rises to subfebrile. Pronounced ketonuria,
a shift of the acid-base balance in the direction of acidosis are common. A
study of electrolytes shows moderate concentrations of potassium, sodium
and calcium. The blood shows hypo- or dysproteinemia, hyperbilirubinemia,
elevated creatinine, hemoglobin and hematocrit (hemoconcentration). The
patient’s general condition aggravates (Table 19.1).
510 Obstetrics
Table 19.1. Scale of severity of hyperemesis gravidarum
Signs and symptoms Degree of severity of hyperemesis gravidarum

mild moderate severe
Appetite Moderately poor Considerably none
reduced
Nausea Moderate Considerable Constant, nagging
Hypersalivation Moderate Pronounced Thick viscous
Vomiting episodes Up to 5 6–10 11–15 and more (to
a day the extent of con-
tinuous)
Heart rate, per min 80–90 90–100 Over 100
Systolic BP, mm Hg 120–110 110–100 Below 100
Food retention Mostly retained Partially retained Mostly not retained
Weight loss Very seldom by 5% 3–5 kg (1 kg a Above 5 kg (2–3 kg
week, 6–10% of a week, over 10% of
baseline) baseline)
Lightheadedness Seldom In 30–40% of In 50–60% of
patients (moderate patients (consider-
expression) able expression)
Subfebrile tempera- – uncommon In 35–80 % of
ture patients
Icteric sclerae and – In 5–7% of patients In 20–30% of
skin patients
Hyperbilirubinemia – 21–40 mcmol/l 21–60 mcmol/l
Dryness of skin ± ++ +++
Stools Once every Stool retention
2–3 days
Diuresis 900–800 ml 800–700 ml Below 700 ml
Acetonuria – In 20–50% of In 70–100%
patients occasion-
ally
Diagnostics of this complication of pregnancy presents no difficulty. Careful his-

tory taking and patient surveillance make it possible for the doctor to make an ac-
curate diagnosis and to assess the degree of severity. Blood and urine test findings
are important in diagnostics of this complication. Urine tests show acetone in urine.
Urine test for acetone (ketone bodies) is the most informative

NB! and accessible tool for diagnosis and assessment of the degree
of severity of early toxicosis.
Besides acetone, urine shows protein and casts. Blood tests show elevated hemo-
globin and hematocrit, which indicates blood thickening, elevated residual nitrogen
content, bilirubin, decreased content of chlorides and presence of acidosis.
Progressing ketonuria and proteinuria, icteric coloration of the

NB! skin and sclerae, elevated body temperature are prognostically
unfavorable signs indicating the patient’s grave condition and
ineffectiveness of administered therapy.
The following medications are administered for hyperemesis gravidarum:

• affecting the CNS;
• eliminating dehydration;
• antiemetic;
• normalizing the electrolyte balance;
• relieving the effects of prolonged starvation.
Hypersalivation starts with the sign of excess saliva in the pregnant woman’s
mouth. The woman swallows it which leads to stomach repletion. In its turn, this
causes vomiting and aggravates the patient’s condition. In some cases hypersalivation
can be an independent condition; it is easily tolerated if its degree is moderate. In
severe forms of hypersalivation the daily saliva production can be as much as several
liters. This leads to loss of proteins, carbohydrates, vitamins, salts and dehydration
of the body.
Anti-salivation therapy is the same as antiemetic therapy. In severe cases hospital-
ization is recommended as hospital provides conditions for a therapeutic and protec-
tive regimen, administration of medications regulating the CNS function; in case of
dehydration infusion therapy is administered. At the same time, mouth rinse with
chamomile and clary infusions, 0.5% Procain (Novocain) solution is recommended.
In case of intensive salivation one can administer atropine 0.0005 g twice a day. To
prevent maceration, Vaseline or baby cream is applied to face skin.
According to NICE1 recommendations (2008), for the sake of severe hyperemesis
gravidarum prevention, at the stage of pregnancy planning it is worthwhile to take
multivitamin supplements; pyridoxine (vitamin B6), ginger, P1 blockers, phenothi-
azine derivatives, and methyl prednisolone are administered as last-resort treatment
for hyperemesis gravidarum. Hydration, correction of ketosis and avitaminosis as well
as parenteral nutrition are administered to patients with low body weight.
In mild forms of hyperemesis gravidarum the patient can receive treatment at
home, while the doctor monitors her weight dynamics and controls the content of
ketone bodies in urine.
As the appetite is poor, it is recommended to take any foods at will. Meals should
be taken in small portions every 2–3 hours in supine position; the food should be
cool; it is recommended to drink 1 liter of cooled ginger and common balm infu-
sion during the day.
Small amounts of alkaline mineral water without gas 5–6 times a day are indicated.
It is recommended to cut down foods high on protein and fat, to limit exposure to
strong odors, to increase the consumption of dry carbohydrates. Habitual meals can
be resumed if emesis does not reoccur for 24 hours (dry diet).
Nonpharmaceutical methods like acupuncture, acupressure, physiotherapy (for
instance, phonophoresis of thiamine bromide solution), psychotherapy, hypnother-
1 NICE—National Institute for Health and Care Excellence

512 Obstetrics
apy can be helpful for normalization of cerebral cortex function and elimination of
vegetative dysfunction.
If no effect is noted, one administers drugs that block the vomiting reflex di-
rectly: m-cholinolytic agents (atropine), dopamine receptor blockers (haloperidol and
droperidol — neuroleptics, phenothiazine derivatives — Torecan) as well as direct
dopamine antagonists (Reglan, cerucal).
If emesis gravidarum is of medium severity, the patient should be

NB! hospitalized. One ward should not have two patients with early
toxicosis.
In hospital settings additional investigations can be performed: complete blood

count and blood biochemistry, hemostasiogram, acid-base balance, ultrasound of
the liver and kidneys).
Electrically induced sleep and electroanalgesia can be administered to patients with
both mild and severe hyperemesis for the purpose of normalizing the CNS function.
Proton pump inhibitors (Omeprazol and others) are included into complex thera-
py; they pose no risk for the fetus. Commonly administered antihistamine, anticho-
linergic drugs, dopamine and serotonin antagonists and other drugs (dexamethasone)
do not have any proven effectiveness.
To control dehydration and hypoproteinemia, one administers crystalloid solutions IV
by drop infusion — sodium chloride isotonic solution, 5% dextrose (glucose) solution,
Disol and others. In case of pronounced hypoproteinemia one can introduce amino acid
solution, 100 ml of 10% albumin solution. The pregnant woman should receive 2–2.5 li-
ters of fluid a day. When giving IV infusion of 5% dextrose (glucose) solution in the
amount of 1000 ml, insulin in the amount 1 IU per 4 g of dry glucose is added, as well
as 5% ascorbic acid in the amount of 4–6 ml. Besides the above mentioned drugs, one
administers equilibrated Ringer-Locke solution (up to 1000 ml) and 5% sodium bicar-
bonate solution (200–300 ml) while monitoring the patient’s electrolytes and acid-base
balance. In case of potassium deficiency potassium supplements are also administered.
When there is severe hyperemesis gravidarum, the neuroleptic Droperidol is ad-
ministered to inhibit excitation of the vomiting center. Droperidol affects cerebral
cortex and reticular formation, produces an antiemetic effect, suppresses vasomotor
reflexes, improves peripheral blood flow due to vasodilation.
Management of early toxicosis should continue until a pronounced

NB! effect or complete cure is achieved. After all medications have
been withdrawn, the patient’s condition should be followed for
three to five days.
If a permanent effect is achieved, the patient can be discharged home. If the effect
is negative and toxicosis progresses, acetone content in urine grows, signs of hepatic
failure begin to show, the pregnancy should be terminated.
Indications for pregnancy termination:
• intractable vomiting (despite the administered therapy);
• progressing dehydration;
• progressing weight loss;

• ketonuria progressing for 3–4 days;
• pronounced tachycardia;
• disorder of CNS function (adynamia, apathy, delirium, euphoria);
• bilirubinemia (up to 40–80 mcmol/l); critical bilirubinemia of 110 mcmol/l;
• icteric coloration of sclerae and skin;
• persistent subfebrile temperature.
19.8. RARE FORMS
19.8.1. Dermatosis gravidarum

Dermatosis gravidarum presents as itching of the skin all over the body; the itching
is often most pronounced around the vulva. Scratching produces inflammatory foci
with bright red coloration and local edema.
In rare cases the itching can be so unbearable that the pregnancy has to be ter-
minated.
To relieve the itching, local phototherapy is used as well as ointments contain-
ing antihistamine drugs, benzocaine (anesthesine); in severe cases — prednisolone
and hydrocortisone, vitamin B and C therapy. To reduce the reactivity of the CNS,
sedative drugs (preferably herbal medications) are administered.
19.8.2. Tetany gravidarum

Tetany gravidarum presents as upper extremity muscle cramp (main d’accoucheur),
more seldom — in lower extremities or in the face.
This condition is caused by decreased or failed function of parathyroid glands
leading to calcium metabolism disorder.
When this complication has a severe course or when latent tetany exacerbates
during pregnancy, the pregnancy should be terminated.
Therapy is administered with drugs like parathyroidin, dihydrotachysterol, vitamin
D.
19.8.3. Osteomalacia gravidarum

Pronounced osteomalacia garvidarum is encountered extremely seldom. In these
cases pregnancy is an absolute contraindication. The condition is associated with
calcium and phosphorus metabolism disorder, bone decalcification and softening. A
suppressed form of osteomalacia — symphysiopathy — is encountered more often;
the presentations include leg pain, pain in pelvic bones and muscles; palpation of the
pubis is painful, too. Sometimes separation of pubic bones is noted; however, unlike
true osteomalacia, the bones show no destructive change. Suppressed osteomalacia
is a manifestation of vitamin D hypovitaminosis.
Administration of vitamin D, cod liver oil, general and local ultraviolet therapy,
progesterone shows a good effect in treatment of this complication.
514 Obstetrics
19.8.4. Bronchial asthma gravidarum

This condition is seldom encountered. It is caused by hypofunction of parathyroid
glands and disorder of calcium metabolism.
It is differentially diagnosed with bronchial asthma that is not associated with
pregnancy.
Therapy includes administration of calcium preparations, vitamins B group, seda-
tive drugs.
19.8.5. Acute yellow atrophy of the liver

Acute yellow atrophy of the liver is a severe manifestation of toxicosis. Intoxication
leads to fatty degeneration of hepatic cells, liver atrophy. The liver shrinks in size;
first icterus develops followed by acute hepatic failure accompanied by convulsive
attacks and comatose condition. Two phases are distinguished in the disease: non-
icteric and icteric phase (Fig. 19.2).
Fig. 19.2. Macropreparation: fatty degeneration of the liver: acute yellow atrophy
Biochemical markers of acute fatty atrophy are hyperbilirubinemia due to the

direct fraction, hypoproteinemia (<6 g/l), hypofibrinogenemia (<200 g/l), insignifi-
cant increase in transaminase activity. Maternal lethality amounts to 75% (including
fatality after delivery).
Acute yellow atrophy of liver is an absolute indication for termination

NB! of pregnancy.
As pregnancy develops, the disease progresses alongside with it and leads to a

lethal outcome.
REMEMBER!
Early toxicosis develops at the first weeks of pregnancy; as a rule, its signs subside
after 12–13 weeks gestation.
Early toxicosis is classified into common forms (hypersalivation, emesis

gravidarum) and rare forms (chorea, bronchial asthma gravidarum, osteomalacia,
dermatosis, tetany, acute yellow atrophy of the liver).
Vomiting is the leading sign among clinical presentations of hyperemesis

gravidarum. Depending on the degree of expression of this sign, mild, moderate
and severe degrees of the condition are distinguished. Severe form of hyperemesis
gravidarum is also referred to as intractable vomiting of pregnant. Urine test for
ketone bodies is the most informative and accessible method in diagnostics and
assessment of the degree of early toxicosis severity.
Progressing ketonuria and proteinuria, development of icteric coloration in the

skin and sclerae, elevated body temperature — these are unfavorable prognostic
signs indicating the patient’s critical condition and ineffectiveness of administered
therapy.
Acute yellow atrophy of the liver is an absolute indication for termination of

pregnancy.
CONTROL QUESTIONS
1. What are the common forms of toxicosis?

2. What are the rare forms of toxicosis?
3. What are the diagnostic methods for hypersalivation and hyperemesis
gravidarum?
4. For what length of time should one treat a patient with early toxicosis?
5. What is the indication for termination of pregnancy in early toxicosis?
6. What are clinical presentations of the mild form of hyperemesis gravidarum?
7. What are clinical presentations of the moderate form of hyperemesis
gravidarum?
8. What are clinical presentations of the severe form of hyperemesis gravidarum?
9. What are the principles of management in hyperemesis gravidarum?
10. How is hypersalivation managed?
11. What is the extent of therapy at a mild form of hyperemesis gravidarum?
12. What is the extent of therapy at a moderate form of hyperemesis gravidarum?
13. What is the extent of therapy at a severe form of hyperemesis gravidarum?
14. What is the indication for termination of pregnancy?
15. What are clinical presentations and therapy of dermatosis gravidarum?
16. What are clinical presentations of acute yellow atrophy of the liver?
516 Obstetrics
CHECK YOURSELF!
Level 1. Test
1. The most common forms of early toxicosis are:
a) dermatosis;
b) acute yellow atrophy of the liver;
c) vomiting;
d) hypersalivation.
2. The most informative investigation in early toxicosis:

a) ultrasound;
b) urine test for ketone bodies;
c) blood biochemistry;
d) ophthalmoscopy.
3. Indications for termination of pregnancy in hyperemesis gravidarum:

a) more than 10 vomiting episodes a day;
b) hemoglobin <110 g/l;
c) hyperbilirubinemia;
d) weight loss over 5 kg a week.
4. Management of patients with mild form of hyperemesis gravidarum includes:

a) hospitalization;
b) changing the dietary regimen;
c) therapist consultation;
d) gastroenterologist consultation.
5. The volume of infusion therapy in severe hyperemesis gravidarum:

a) no less than 0.5 l;
b) no less than 1.0 l;
c) no less than 1.5 l;
d) no less than 2.0 l.
6. Acute yellow atrophy of the liver absolutely requires:

a) liver biopsy;
b) tracer study of the liver;
c) termination of pregnancy;
d) administration of hepatoprotector drugs.

1. At a therapist appointment a woman aged 23 presents with nausea and occa-
sional morning sickness. She has ulcerative disease in past history. Her periods are
irregular, the last one was 42 days ago. What is the presumptive diagnosis? What is
your plan of management?
• Chapter 20
PREECLAMPSIA
About 10% of pregnant women around the world have hypertension; in Russia,
according to the Department of Health, the figure is 5–30%. Preeclampsia holds a
special place in the structure of hypertensive conditions.
Preeclampsia (PE, from Greek eclampsia, lightning) is a multisystem abnormality
manifested in the second half of pregnancy (after 20 weeks); it is characterized by
arterial hypertension in combination with proteinuria (over 0.3 g/l in daily urine),
often by edema and manifestations of multiple organ failure.
20.1. EPIDEMIOLOGY
Mild preeclampsia is noted in 3–18% of women; as a rule, it does not compro-

mise the mother’s or fetus’s health. Among them, in 1–2% of pregnant women
preeclampsia becomes severe. In 2013 in Russia preeclampsia complicated the course
of 15.9% of pregnancies (Fig. 20.1).
The incidence rate of sever PE was 2.1% in 2005, and 1.5% in 2013. Severe PE
affects the kidneys, liver, blood coagulation system and brain in the first place, as
well as the fetoplacental system. Severe PE and eclampsia can seriously compromise
the mother’s and fetus’s health and even result in a lethal outcome.
In advanced countries eclampsia is noted at a rate of 1/2000 pregnancies, in
developing countries — at a rate of 1/100–1/1700 deliveries. Eclampsia and its
25
22.2 22.3
20
18.1
15.9
15
11.2
9.0
10
5
1985 1990 2000 2005 2010 2013
Fig. 20.1. Dynamics of preeclampsia incidence rate in Russian Federation, %

518 Obstetrics
complications persist as the main causes of maternal mortality around the world
(10–15%).
The share of PE in the structure of maternal mortality in Russian Federation is
on the decline ceding the first place to somatic disease, hemorrhage and embolism;
however, PE consistently accounts for 10% of deaths (Fig. 20.2).
3.3 1.6 0.5

3.3
6.1
Extragenital disease
30,7 Hemorrhage
9.4
Embolism
Abortion
Gestosis
Sepsis
Anesthesia complications
10.7 Uterine rupture
Ectopic pregnancy
Other
17.6
16.8
Fig. 20.2. Structure of maternal mortality causes in Russian Federation, %

(according to Department of Health, 2013)
PE is still the leading cause of neonatal morbidity (640 – 780‰)

NB! and mortality (18 – 30‰). According to WHO, every fifth child born
from a mother with PE has developmental disorders. In later life,
women who had PE develop hypertension and coronary disease
eight times more often.
ICD-10 codes
• O10 Pre-existing hypertension complicating pregnancy, childbirth and the
puerperium.
• O11Preeclampsia superimposed on chronic hypertension.
• O12 Gestational (pregnancy-induced) edema and proteinuria without
hypertension.
• O13 Gestational (pregnancy-induced) hypertension.
• O14 Preeclampsia.
– O14.0 Mild to moderate preeclampsia.
– O14.1 Severe preeclampsia.
– O14.9 Preeclampsia, unspecified.
Chapter 20. Preeclampsia 519
• O15 Eclampsia.
– O15.0 Eclampsia in pregnancy.
– O15.1 Eclampsia in labor.
– O15.2 Eclampsia in the puerperium.
– O15.9 Eclampsia, unspecified as to time period.
• O16 Unspecified maternal hypertension.
There is no universal classification of PE, which testifies to the complexity of the
problem. There are many various recommendations as to the terminology describing
hypertensive conditions detected during pregnancy. Terms «nephropathy», «gestosis»
and «EPH-gestosis» (gestosis with edema, proteinuria and hypertension) are used
alongside with the term «preeclampsia» in Russian Federation.
Abroad, the following terminology is used: preeclampsia, eclampsia, pregnancy-
induced hypertension.
At present the diagnosis of preeclampsia in Russian Federation is verified on the
basis of the 10th revision of the International Statistical Classification of Diseases and
Related Health Problems by the World Health Organization (2004).
According to ICD-10, preeclampsia (hypertension caused

NB! by pregnancy, showing significant proteinuria) is defined as
hypertension (systolic BP > 140 and/or diastolic BP  90 mm Hg
after 20 weeks gestation in women with initially normal BP) and
proteinuria (loss of 0.3 g and more of protein daily).
In clinical practice PE is also divided into combination forms, that is, superim-
posed on pre-existing chronic condition, and pure forms. In the total structure of
PE combination forms account for about 70%.
Combination PE has a more severe course. Commonly, there is an early onset,
more persistent and pronounced manifestations, with predominant signs of the dis-
ease on which PE was superimposed.
The following forms of PE are distinguished abroad:
• gestational arterial hypertension;
• PE;
• severe PE;
• eclampsia;
• PE and eclampsia superimposed on chronic arterial hypertension;
• chronic arterial hypertension;
• hypertonic disease;
• secondary arterial hypertension.
20.3. ETIOLOGY
The causes of PE development are multiple, varied and not clearly understood.
The association with pregnancy is apparent as termination of pregnancy before seri-
ous complications set in always promotes a recovery.
Factors that increase the risk of preeclampsia
520 Obstetrics
• Social and demographic: early and advanced reproductive age, low-socioeconomic

standing, some ethnic groups (like negroid race, for instance).
• Genetic predisposition to PE development
• Specific features of pregnancy: multiple pregnancy, fi rst pregnancy, PE in
previous pregnancies.
• Diseases of the mother: obesity, chronic renal disease, chronic arterial
hypertension, diabetes mellitus, thrombophilia.
A hypothesis was put forward stating that immunological incompetence is im-
plicated in the pathogenesis of PE. This hypothesis was confirmed after detecting
depositions of immunoglobulins G, M, A in 93% of pregnant woman with previous
PE, even when their kidneys showed no abnormal structural changes.
Genetic predisposition to PE has long been traced among close relatives. About
50 genes are contemplated as culprits, but to date the genetic component has not
been studied well enough.
The role of thrombophilia in PE pathogenesis is indisputable; they are due to
genetic changes in certain blood coagulation factors:
• protein C resistance;
• congenital deficiency of S protein and antithrombin;
• other genetic disorders in the blood coagulation system.
Research data published in 2013 show evidence that angio- and antiangiogenesis
factors are implicated in PE pathogenesis: vascular endothelial growth factor, pla-
cental growth factor 1/PIGF, and tyrosine kinase like factor.
The following physiological processes in late pregnancy predispose to PE devel-
opment:
• increase in circulating blood volume to 150% of the baseline;
• increase in pulmonary blood flow with predisposition to hypertension;
• partial occlusion in the inferior vena cava system;
• moderate hypercoagulation;
• progressing rate of glomerular filtration due to increased renal plasma flow;
• decrease in tubular absorption;
• delay of sodium reabsorption due to elevated progesterone;
• 20-fold increase in aldosterone concentration in the blood.
Extragenital disease holds the leading place (64%) among risk factors for PE. The
most significant conditions are as follows:
• arterial hypertension outside of pregnancy (25%);
• renal disease (in 80% of primigravid women PE was preceded by renal disease
confirmed by biopsy);
• vascular disease (50%) including chronic venous insufficiency (10%);
• endocrine disease (diabetes mellitus 22%, dyslipidemia 17%, obesity 17%);
• autoimmune disease (67%);
• congenital and acquired thrombophilia;
• PE in previous pregnancy;
• the pregnant woman’s age below 20 and over 35;
• PE in the pregnant woman’s mother and sisters;
• PE in the husband’s ex-wives.
Other PE risk factors:

• polyhydramnios, fetal malformations;
• occupational hazards;
• low economic status;
• perinatal morbidity and mortality during the previous pregnancy.
There are no accurate laboratory and diagnostic predictors of PE in the first and
second trimesters when the clinical presentations have not yet developed. However,
pregnant women with the following features are classified at high risk:
• circulatory disorder in the vessels of uteroplacental circulation (on the basis of
pulsation index);
• decrease in PAPP-A level below 0,5 MoM;
• increase in β-hCG level in the second trimester to more than 3 MoM;
• increase in inhibin A in the first or second trimester;
• increase in the ratio between tyrosine kinase like factor and placental growth
factor 1/PIGF or vascular endothelial growth factor;
• progressively decreasing platelet concentration (to 150×109/l and less);
• hypercoagulation in the cellular and plasma components of hemostasis:
– platelet aggregation increase to 76%;
– decrease in APTT below 20 s;
– hyperfibrinogenemia to 4.5 g/l;
– decreased anticoagulant content:
◊ endogenous heparin to 0.07 IU/ml;
◊ antithrombin III to 63%.
Presence of 2–3 signs mentioned above indicates a high probability of PE devel-
opment after 20 weeks gestation.
20.4. PATHOGENESIS
Research into PE pathogenesis extended the notion of when PE begins to develop.

It is supposed that in pregnant women with PE the immune control over realization
of genetic program is lost or disrupted.
Over the last decades it was asserted that the foundation for the disease is
laid at early gestational age and is associated with gestational sac implantation.
Cytotrophoblast invasion is incomplete; it is followed by incomplete gestational trans-
formation of uterine spiral arteries while angiogenesis factors and blockers undergo
abnormal changes. Incompletness of gestational transformation at early gestational
age is aggravated by the fact that uterine vessel receptors to vasopressors are retained
(normally they disappear), which promotes local ischemia of the uteroplacental zone.
The following disturbing factors in patients with PE have been

NB! identified: generalized vascular spasm following endothelial
dysfunction and accompanied by hypovolemia, disorder of
rheological and coagulation properties of the blood, which results
in (sometimes critical) reduction in perfusion of vital organs and
the placenta.
522 Obstetrics
Endothelial dysfunction acts as a trigger of intravascular platelet aggregation com-

mon to all types of PE.
The modern view of the order of abnormal events can be briefly represented in
this way:
• suppression of trophoblast migration;
• no transformation of the muscular layer in spiral arteries; they retain the
morphology of non-pregnant vessels;
• spiral artery spasm;
• decrease in intervillous blood flow;
• angiogenesis disorder;
• disorder of placental microcirculation;
• hypoxia developing as a result.
In its turn, hypoxia developing in the tissues of uteroplacental complex leads to
• generalized vascular spasm;
• hypovolemia;
• disorder of rheological and clotting properties of the blood;
• endothelial lesion, disorder of endothelial thromboresistant and vasoactive
properties;
• release of mediators (endothelin, serotonin, thromboxan) that play key role in the
regulation of hemostasis and vascular tone;
• insufficient release of endothelium-derived relaxing factor identified as nitric
oxide — the most powerful dilatators synthesized by endothelial cells;
• disorder and imbalance of prostanoids of maternal and fetal origin (prostaglandins
class E and F, prostacyclin, thromboxan, etc.);
• non-decrease in total peripheral vascular resistance; in physiological pregnancy
it decreases;
• reduced cardiac output;
• decrease in blood flow and glomerular filtration in kidneys;
• generalized compensatory arterial hypertension;
• tissue hypoperfusion;
• disorder of structural and functional properties of cellular membranes and
changes in cellular vital activity;
• multiple organ failure (Fig. 20.3).
20.5. CLINICAL FEATURES AND DIAGNOSTICS
In present day literature there is no convincing evidence that the disease has a
preclinical stage of development.
Despite the vast variety of clinical presentations, there is not one pathognomic
sign of PE. The classical triad of signs (Zahngemeister’s triad, 1912) is noted in
25–40% of pregnant women while 60–75% of patients with PE show an inapparent
course of the disease.
Clinical signs are caused by pathogenetic factors that are closely interrelated.
Pregnant women with moderate PE present no complaints or complain of edema,
insignificant BP elevation.
Genetic Extragenital
predisposition disease
Physiological Thrombophilia
changes
accompanying Other
pregnancy risk factors
Incomplete Preserving
trophoblast vasopressor
invasion receptors
Generalized
vascular spasm,
Incomplete Ischemia, hypovolemia,
transformation hypoxia endotheliosis,
of spiral arteries of uteroplacental Gestosis disturbed
of uterus area hemorheology
and coagulation,
humoral disorder
Reduced
Hyperfusion, blood flow No reduction
Polyorganic ischemia,
insufficiency and glomerular in peripheral
tissue necrosis filtration resistance
Dysfunction of cellular Generalized Decrease

membrane, disturbed compensatory in cardiac output
cellular activity hypertension
Fig. 20.3. Etiology and pathogenesis of preeclampsia
In severe PE the above mentioned signs are complemented by headache, nausea,

vomiting, vision disorder in the form of seeing spots, sensation of heat and hyper-
thermia, excitation or sleepiness, epigastric pain.
It is important to note that edema developing at the end of a day and subsiding
after a night’s rest does not justify the diagnosis «preeclampsia». In this case un-
necessary administration of therapy and unnecessary hospitalization lead to unfa-
vorable outcomes, as a rule. Moderate edema in the evening is noted in 50–80% of
pregnant women with physiological pregnancy. In the morning physiological edema
disappears.
PE can be manifested by BP increase as a single sign, as well as in combination
with proteinuria and/or edema developing after 20 weeks gestation.
Arterial hypertension (at systolic BP ≥140 and/or diastolic BP ≥90 mm Hg) is a
sign developing during pregnancy or in the first 24 hours after delivery in women with
previously normal BP. It emerges secondary to vascular spasm and hyperdynamic
systolic function of the heart.
524 Obstetrics
Rules of blood pressure measuring

• The most accurate values can be obtained with mercury sphygmomanometer;
all devices in use should be calibrated from it. Automatic methods of measuring
should be used with care as in patients with PE they can yield inaccurate BP
readings.
• The patient should be relaxed, preferably after a rest (no less than 10 minutes).
• The patient is in semisitting position or sitting at an angle of 45 ° (the cuff is at the
level of her heart), or lying on her side.
• The BP cuff should fit the diameter of the patient’s shoulder (a little loose is better
than tight).
• Measuring on one arm is enough.
• Systolic BP is evaluated by the first Korotkoff sound, diastolic BP — by the fi fth
sound (termination).
• The findings should be registered within the accuracy of 2 mmHg. If BP is
persistently higher on one arm, then all BP measurements are made on the arm
with higher BP.
Ambulatory daily BP monitoring can be useful to detect isolated-office arterial
hypertension (white gown symptom).
Proteinuria (loss of protein 0.3–0.5 g/day) is a sign developing during pregnancy;
it is not associated with organic lesion of kidneys. Ideally proteinuria should be de-
termined by protein content in 24-hour collection urine. Proteinuria is not considered
abnormal until it reaches or exceeds 0.3 g/day or 0.3 g/l in three samples obtained
at an interval of 4 hours.
Edema is general, excessive accumulation of fluid in tissues after 12-hour rest in
bed. Edema develops secondary to disturbance of capillary permeability and escape
of fluid from the blood stream to the interstitial space as a result of renal glomerular
lesion with increased permeability of the basal membrane of their capillaries, and
due to decreased oncotic pressure (with underlying hypoalbuminuria) (Fig. 20.4).
Fig. 20.4. Swollen legs

In physiological pregnancy moderate swelling is noted in 50 – 80%

NB! of women.
PE showing no generalized edema is considered more dangerous for the mother
and fetus than PE with edema. Rapidly progressing generalized edema, especially in
the lumbar area, the face and hands, is an unfavorable prognostic sign of PE severity.
Stable edema is an early PE sign. It is classified in the following way:
• invisible edema (abnormal weight gain by 500 g and more within a week, positive
ring symptom, nocturia, decrease in diuresis below 900–1000 ml while fluid
intake is 1400–1500 ml);
• visible edema divided into stages:
– stage I: edema of upper and lower extremities;
– stage II: edema of upper and lower extremities, abdominal wall;
– stage III: edema of upper and lower extremities, abdominal wall and face;
– stage IV: anasarca.
Criteria for diagnosing severe PE: if at least one of the following signs is present:
• systolic BP >160 mm Hg, diastolic BP >110 mm Hg after two measurements
made within 6 hours;
• proteinuria >5g/day;
• oliguria <500 ml/day (or less than 30 ml/h);
• neurological and/or vision disorders (persistent headache, hyperreflexia, nausea
and vomiting);
• pulmonary edema / cyanosis;
• epigastric / right subcostal pain;
• extensive edema (especially of sudden origin);
• hepatic dysfunction of unknown origin: increased alanine aminotransferase
(ALT) and aspartate aminotransferase (AST) over 70 IU/l;
• thrombopenia <100×109/l;
• pronounced hypoproteinemia <50 g/l;
• serum creatinine >90 mcmol/l;
• fetal distress: fetal growth restriction stage II and more, reverse outflow in
umbilical artery; areactive non-stress test, pronounced oligohydramnios.
Bright light, noise and pain can provoke a convulsive attack — eclampsia attack.
All signs show a progressing increase: BP elevates to 180/110 mm Hg and more,
proteinuria increases, edema progresses. BP commonly elevates rapidly while its
amplitude grows smaller. A study of the ocular fundus reveals acute arteriole angio-
spasm, hemorrhages, edema and retinal detachment. Azotemia and hypoxia increase,
pronounced acidosis develops; all vital functions deteriorate; uteroplacental blood
flow decreases; chronic DIC progresses.
Eclampsia is emergence of one or two cramps that are not

NB! associated with other manifestations of cerebral disorder (epilepsy
or insult) in patients with PE.
Convulsions can develop during pregnancy, childbirth or in the puerperium. In

16% eclampsia develops within the interval 48 days to 4 weeks postpartum.
526 Obstetrics
Eclampsia is the most dangerous stage characterized by progressing cerebral signs

and convulsive attacks. The danger of eclampsia attack is that a hemorrhage into the
retina, brain or other vital organs can occur during the seizure leading to blindness
and lethal outcome. The fetus can die of hypoxia secondary to disorder of uteropla-
cental circulation, which can be acute — placental abruption, or chronic — aggrava-
tion of angiospasm and progressing of DIC.
Four stages are distinguished in the clinical course of eclampsia:
• fibrillary tremor of muscles;
• tonic convulsions;
• clonic convulsions;
• resolution of the attack.
Algorithm of management of developing eclampsia attack
When a seizure develops, management begins on the spot.
Intensive therapy is provided at the delivery department or the patient is urgently
hospitalized to the resuscitation department.
The patient is laid on an even surface on her left side to reduce the risk of aspirat-
ing gastric contents, vomit and blood; her airways should be freed rapidly by opening
the mouth and drawing the mandible forward. At the same time, the contents of the
mouth should be evacuated (aspirated). The patient should be protected from injury
during convulsions but without restraining her actively.
If the patient can breathe on her own, an oropharyngeal airway is introduced
to perform an inhalation with moisture laden oxygen mix by applying a nasofacial
mask.
If respiratory apnea develops, forced ventilation is immediately started with a
nasofacial mask supplying 100% oxygen, in the mode of positive end expiratory
pressure. If convulsions reoccur or the patient remains comatose, myorelaxing
agents are administered and artificial lung ventilation is started in the mode of
normoventilation.
Indications for ALV: inability to sustain adequate spontaneous respiration
(eclamptic status, eclamptic coma, pulmonary edema, saturation reduced below
80%).
The peripheral vein is catheterized. Immediately after a convulsive attack the fol-
lowing is done:
• clear the mouth and larynx with an aspirator, if needed;
• start magnesium sulfate therapy at once:
– initial dose 4–6 g of dry substance (20 ml of 25% solution) IV slow stream
infusion for 5–10 min;
– if seizure reoccurs, IV infusion of 2 g of magnesium sulfate for 5 min;
– maintaining dose 1–2 g/h through an infusion pump;
• if the above fails, IV administration of 0.5% diazepam (seduxen) solution 2.0 ml
or barbiturates (sodium thiopental in a dose of 0.2–0.3 g);
• register vital parameters (heart rate, BP, oxygen saturation) continuously with a
monitor or every 5 min:
– CTG continues only after the seizure is over;
– drain the bladder with Foley catheter; it is left in the bladder until diuresis
returns to normal.
Eclampsia is an indication for emergency delivery. However, one

NB! must first of all stabilize the woman’s condition over one to three
hours.
When the mother’s condition becomes stable, magnesium sulfate infusion should
be continued, and the question of emergency or planned delivery is considered.
Cesarean section is not the only option. It is believed that adequately managed
spontaneous delivery puts less stress on the mother’s hemodynamics and reduces
the rate of respiratory complications in preterm neonates.
The patient’s fluid balance is monitored. In case of preterm pregnancy less than
32–34 weeks gestation, at the same time one should decide whether, after the mother
and fetus are brought to a stable condition, the patient should be referred to a peri-
natal center or tertiary care maternity hospital.
In severe PE and gestational age less than 34 weeks, prophylaxis of RDS should
be provided in advance.
If convulsions repeat, slow IV infusion of additional 4–6 g of magnesium sulfate
is administered.
Indications for emergency delivery (irrespective of gestational age):
• eclampsia;
• deteriorating fetal condition;
• progressing PE signs.
The degree of severity is judged, first of all, by BP level and proteinuria; however
the doctor assessing the risks should bear in mind that other organs may be involved
including placental abnormalities and fetal disorders. Hypoxia of the uteroplacental
zone leads to FGR which is noted in 30% of pregnant women with PE.
Laboratory and instrumental investigations of patients with PE
Obligatory investigations:
• register the changes in body weight;
• BP and pulse on both arms;
• measuring the fluid balance (intake, ml; diuresis, ml);
• complete blood count;
• urinalysis;
• daily loss of protein with urine;
• blood biochemistry (total protein, albumin, urea, glucose, electrolytes, creatinine,
residual nitrogen, uric acid, cholesterol, conjugated and unconjugated bilirubin,
ALT, AST, alkaline phosphatase, triglycerides).
Additional investigations:
• daily BP monitoring;
• hemostasiogram (thromboelastography, APTT, platelet count and aggregation,
fibrinogen and its degradation products, endogenous heparin concentration,
antithrombin III);
• ultrasound of mother’s vital organs;
• ultrasound fetometry;
• CTG;
• dopplerometry of maternal and fetal hemodynamics;
• ocular fundus examination;
528 Obstetrics
• lupus anticoagulant;
• ECG.
The extent and frequency of investigations depend on the nature and severity of
clinical presentations.
Complications of severe PE and eclampsia:
• acute renal failure;
• respiratory failure;
• retinal detachment;
• placental abruption;
• HELLP syndrome;
• acute fatty liver of pregnancy;
• cerebral hemorrhage;
• cerebral coma.
Nowadays the diagnosis of atypical PE forms — HELLP syndrome and acute
fatty liver of pregnancy — is assuming great importance. The issue whether HELLP
syndrome is a distinct disease or a complication of pregnancy remained controversial
for a long time; however in obstetrics the generally accepted approach is to regard
HELLP syndrome as a variety of severe PE. It is encountered both alongside with
PE and as an isolated condition.
20.6. HELLP SYNDROME
HELLP syndrome is a complex of symptoms including

• hemolysis;
• elevated liver enzymes;
• low platelet count.
It is noted in 0.3% of all pregnancies. In case of severe PE and eclampsia it
develops in 4–12% of cases; it is characterized by high maternal (up to 25%) and
perinatal mortality.
HELLP syndrome typically develops in the third trimester at 33–39 weeks, mostly
at 35 weeks gestation. In 30% of patients HELLP syndrome presents in the post-
partum period.
Clinical features include a rapid, aggressive progression of signs. Initial manifesta-
tions are not specific: headache, weakness, vomiting, and abdominal pain localized
mostly in the right subcostal area or diffuse. Later there appear blood-tinged vomit-
ing, hemorrhages at the sites of injections, progressive jaundice and hepatic failure,
convulsions, marked coma.
Rupture of liver with hemorrhage into the abdominal cavity is not a rare occasion.
HELLP syndrome can be manifested as total placental abruption followed by
massive coagulopathic hemorrhage and rapid development of hepatorenal failure.
With high probability, disorders of the coagulation system lead to profuse uterine
hemorrhage in the postpartum period.
Laboratory findings indicative of HELLP syndrome:
• elevated aminotransferase activity (AST >200 IU/l, ALT >70 IU/l, lactate
dehydrogenase >600 IU/l;
• thrombocytopenia (<100×109/l);
• decrease in antithrombin III below 70%;
• intravascular hemolysis and elevated bilirubin concentration;
• increased prothrombin time and APTT;
• decrease in fibrinogen concentration below the levels necessary in pregnancy;
• increased nitrogenous waste content in the blood;
• blood glucose fall to the extent of hypoglycemia.
HELLP syndrome can develop as an acute condition without underlying arterial
hypertension and/or proteinuria.
To date there are no methods of conservative treatment for this complication.
Glucocorticoid therapy did not prove helpful in decreasing maternal or perinatal
mortality. The only effect produced by glucocorticoids is elevating the platelet content.
Similar to PE, the only treatment method is delivery. At a gestational age below
34 weeks delivery is provided within 48 hours (prevention of fetal RDS), at 34 weeks
and more it should be emergency delivery.
20.7. ACUTE FATTY LIVER OF PREGNANCY
This is a rare condition encountered at a rate of 1 per 13 000; however, it is a

dangerous complication of pregnancy typically developing in primigravid women.
Maternal mortality amounts to 60–85%; the fetus dies even more often. Acute fatty
liver of pregnancy was first described in 1940 by H.L. Sheehan.
The cause of this complication is unknown as yet. Fat accumulates in the liver;
its content grows by 13–19% (5% is the normal value). Fatty degeneration of hepa-
tocytes proceeds without necrosis; the liver shrinks in size, hepatic failure develops.
Three stages are distinguished in the course of the disease.
• The pre-icteric stage begins at 30–34 weeks gestation, as a rule. Nonspecific
PE signs develop. Typical presentations are nausea, vomiting, poor appetite,
abdominal pain, weakness, apathy, skin itch, and heartburn, which is at fi rst
short-lived, transient and then becomes excruciating, intractable and ends in
coffee grounds vomiting. This process is caused by ulceration of the esophageal
mucosa upon development of DIC.
• 1–2 weeks from the onset of the disease, the icteric stage begins. Icterus is
usually intensive, but sometimes it is moderately expressed. By this time the
patient shows increasing weakness, heartburn, nausea and vomiting (often with
blood), tachycardia 120–140, retrosternal burning sensation, abdominal pain,
fever, oliguria, peripheral edema, accumulation of fluid in serous cavities; signs
of hepatic failure increase progressively. Hepatic failure of varying expression
develops resulting from renal lesion. Clinical features are combined with rapid
decrease of the liver size.
• The stage of severe fulminant hepatic failure and acute renal failure develops
1–2 weeks after the onset of icterus. The patient remains conscious for a long
time, until the terminal stage of the disease. Severe DIC syndrome develops with
intensive hemorrhage from the uterus and other organs and tissues. Acute fatty
liver is often complicated by ulceration of mucosa in the esophagus, stomach
530 Obstetrics
and intestine. Massive hemorrhage into the brain and pancreas occurs, which
precipitates the fatal outcome. Hepatic coma with cerebral dysfunction often
develops ranging from slight alteration of consciousness to unconsciousness
with reflex repression. Unlike common hepatic coma, metabolic acidosis rather
than alkalosis, develops in this condition. The disease lasts from several days to
7–8 weeks.
Biochemical signs of acute fatty liver of pregnancy:
• hyperbilirubinemia on account of the conjugated fraction;
• hypoproteinemia (<60 g/l);
• hypofibrinogenemia (<2 g/l);
• non-pronounced thrombocytopenia ;
• insignificant increase in amino transferase activity;
• a dramatic drop in antithrombin III;
• elevated uric acid concentration in the blood serum;
• leucocytosis (up to 20–30×109/l);
• metabolic acidosis.
Ultrasound sign of acute fatty liver is enhanced echogenicity of the liver. The
diagnosis can be finalized by computer tomography; the sign of acute fatty liver is
reduced radiological density of liver parenchyma.
Liver biopsy is impossible as a rule due to pronounced disturbance of the blood
coagulation.
Morphological signs of acute fatty liver are specific: the centrobular part of liver
shows pronounced fatty degeneration of hepatocytes while necrosis is absent. Hepatic
cells in the central lobes have a swollen, foamy appearance due to accumulation of
fat droplets in the cytoplasm.
To date, there are no methods of conservative treatment for this complication.
Similar to PE, the only way of managing this condition is delivery; however, even
after the delivery the prognosis for the mother is doubtful.
Fetal assessment. In emergency cases primary fetal assessment should be done with
CTG. This method provides information about the fetal condition at the moment of
investigation, but permits no prognosis of the outcome.
Patients with severe PE in labor should have continuous cardiomonitoring of the
fetus.
When providing conservative treatment one assesses fetal condition by ultrasound
examination determining fetal size, amniotic fluid volume, umbilical cord dopple-
rometry. A dynamic assessment helps to optimize the timing of delivery.
Significance of dopplerometry of other fetal vessels has not been established to
date.
20.8. DIFFERENTIAL DIAGNOSTICS OF PREECLAMPSIA
Elevated BP during pregnancy can be due to arterial hypertension existing before

pregnancy (usually it is hypertonic disease), diabetes mellitus, renal disease, hypo-
thyroidism, obesity and PE. Despite common manifestations, these are distinctly
different diseases. They have different pathogenesis, management and prognosis for
the mother and fetus. However, one should bear in mind that these diseases can be
encountered in combinations.
20.9. THERAPY OF PREECLAMPSIA
The only radical treatment of preeclampsia is delivery; thus all

NB! other methods are aimed at curbing the progress of PE and
preventing eclampsia.
If the patient presents with edema of pregnant or mild PE, treatment is provided
in the mode of day patient department. Patients with more severe degrees of PE
should be hospitalized at once.
Patients with severe PE and eclampsia should be hospitalized

NB! at specialized obstetric departments within the framewok of a
multifield hospital with facilities for resuscitation and special
neonatal care, or at perinatal centres.
Hospitalization is made through the ambulance service; the patient is accompanied

by an emergency medical care provider who immediately starts magnesium sulfate
infusion.
In Russian Federation the indication for hospitalization is newly diagnosed pre-
eclampsia.
Severe forms of PE and arterial hypertension are absolute indications for hospi-
talization.
In hospital the patient is under full-time surveillance (monitoring of BP, body
weight, diuresis), and the question of the timing and mode of delivery is considered.
Discharge from hospital is not recommended.
Management of severe PR is based on careful assessment of the patient’s con-
dition, stabilizing the condition, continuous monitoring and delivery at the time
optimal for the mother and fetus.
At the admission department one assesses the severity of PE: BP, consciousness,
headache, convulsions, dyspnea, abdominal pain, vaginal bleeding, fetal heartbeat.
A specialist in intensive care is always invited to the admission department who
begins to provide care to patients in the following condition:
• development of convulsions (convulsions in history);
• unconsciousness;
• BP elevated above 160/110 mmHg;
• respiratory disorder;
• vomiting;
• signs of placental abruption, vaginal bleeding;
• hemorrhagic shock.
The main issue in managing a pregnancy complicated by PE is the issue of the
timing and mode of delivery. Preterm delivery is indicated if the severity of PE aggra-
vates. In severe PE delivery should ideally occur before complications like eclampsia
532 Obstetrics
or HELLP syndrome set in but at a gestational age when the fetal surfactant system
is mature enough (with pharmaceutical stimulation).
Prevention of fetal respiratory distress syndrome. If gestational age is less than
34 weeks, glucocorticoids are administered. Antenatal glucocorticoid therapy should
be administered to all patients with PE before 34 weeks as well as to patients with
gestational arterial hypertension even in the absence of proteinuria, if delivery is
planned within the next 7 days.
20.9.1. Drug-free treatment

At present there is no conclusive evidence that pregnant women with PE should
limit salt consumption or keep to a protein-rich diet.
There is not enough evidence to recommend salt limitation to women with previ-
ous arterial hypertension or watching the energy value to obese women, or exercising,
limiting the physical or emotional load.
Strict bed confinement is not recommended to patients hospitalized with PE
(gestosis).
20.9.2. Drug therapy

According to meaningful empirical data, only two variants of symptomatic treat-
ment can be recommended at present: anticonvulsant and antihypertensive therapy.
Magnesium sulfate is recommended as the only first line drug in

NB! the treatment of eclampsia, prevention of eclampsia in women
with severe PE, and in women with moderate PE.
Magnesium sulfate:
• suppresses catecholamine release from peripheral nerve endings (thus it is
important to decrease peripheral vascular resistance due to reducing the effect of
catecholamines on smooth vascular muscles);
• increases the prostacycline level;
• induces a diuretic, hypotensive, anticonvulsant, and spasmolytic effect;
• decreases the intracranial pressure.
The following regimens of administering magnesium sulfate are effective: load-
ing dose of magnesium sulfate 4 g over 5–10 min administered with an infusion
pump; after that the dose is 1 g/h for 24 hours. Patients with severe PE and preterm
pregnancy should continue the therapy until delivery, during delivery and 24 hours
postpartum.
Magnesium sulfate infusion should be provided prior to delivery and during de-
livery and continued for at least 24 h after delivery or 24 h after the last convulsive
episode (depending on which occurred later) except for cases when there are clinical
indications for continuation of the therapy.
Recurring attacks require bolus infusion of 2 g magnesium sulfate or increase in
the rate of infusion to 1.5–2.0 g/h; alternative medications like diazepam, sodium
thiopental can be administered additionally.
When managing eclampsia the daily dose of dry magnesium sulfate

NB! powder can amount to 50 g: 4 – 6 g are administered within the
first hour. The loading dose is 4 – 6 g of dry substance over
10 – 15 minutes (a possible regimen: 20 ml of 25% solution – 5 g
of dry substance). The maintenance dose is 1 – 2 g of dry substance
hourly.
Accurate dosing and rate of administration is provided by using an infusion

pump. Magnesium sulfate acts through blocking calcium channels and thus
makes up for its own quite poor hypotensive effect as it potentiates other an-
tihypertensive medications. Administration of magnesium sulfate in antenatal
period should be accompanied by continuous monitoring of fetal heart rate
through CTG.
When magnesium sulfate is infused intravenously, it is necessary to monitor diure-
sis, tendon reflexes and respiratory rate which should be no less than 14 per minute,
to assess magniemia. Magnesium toxicity starts at its concentration in the blood
5 mEq/l (ECG changes appear); at 10 mEq/l tendon reflexes disappear, respiration
is suppressed at >15 mEq/l, and at levels >25 mEq/l cardiovascular collapse develops.
In case of magnesium sulfate overdose the infusion must be discontinued imme-
diately; one starts IV administration of 10 ml of 10% calcium gluconate (antidote)
for 10 min; in rare cases ALV may be required.
Benzodiazepines are not administered in treatment and prevention of eclampsia,
except when there are contraindications for magnesium sulfate or it proves ineffec-
tive. Short-term administration of benzodiazepines before delivery is associated with
floppy baby syndrome1 in the fetus; perinatal administration of this drug increases
the risk for cleft palate.
Drugs of secondary importance in achieving the anticonvulsant effect in eclampsia
should be administered as an auxiliary for a short-term administration.
Sodium thiopental is considered as a means of sedation and anticonvulsant therapy
when administering ALV.
The BP values at which antihypertensive therapy should be started are determined
in each particular case individually.
Antihypertensive therapy is mandatory if systolic BP amounts

NB! to 160 mm Hg, or diastolic BP rises to 110 mm Hg. If there is a
potential for a severe disease, the decision to initiate the therapy
can be made at lower BP values.
According to recommendations by European Society of Hypertension/European

School of Hematology (ESH/ESH) (2013), it is expedient co consider the issue of
pharmaceutical therapy for all pregnant women with BP >150/95 mm Hg. Besides,
according to recommendations by the working group of ESH/ESH (2013), in case of
1 Floppy baby syndrome (congenital amyotonia) a condition when the infant’s muscles are weak and
hypotonic.
534 Obstetrics
gestational arterial hypertension, chronic arterial hypertension and superimposed PE,

as well as arterial hypertension and asymptomatic lesion of target organs, or presence
of manifestations at any gestational age at BP > 140/90 mm Hg, one should consider
early initiation of antihypertensive therapy.
In the interest of the fetus one should not allow BP to drop abruptly
NB! since this carries a risk of impairing uteroplacental circulation.
Treatment of non-severe arterial hypertension in pregnant women has no advan-

tage as it does not improve the perinatal outcome.
Most sources recommend hydralazine and nifedipine for a rapid BP decrease in
presence of PE.
Drugs of choice for planned therapy are methyldopa, metoprolol, nifedipine.
Antihypertensive drugs for planned therapy
• First line. Methyldopa (Dopegit), a central α-adrenomimetic (methyl tyrosine
derivative). Initial dose 250 mg/day, every 2 days the dose is increased by 250 mg/
day. Maximum daily dose is 2.5 g.
• Second line. Dihydropyridine calcium antagonists, preferably of prolonged
action: nifedipine (Cordipine retard, Corinfar retard, Cordaflex) 30–40 mg/day.
• Third line. Β-adrenergic blockers: metoprolol (Betaloc, Metocard, Egiloc,
Corvitol) 25–100 mg/day.
Atenolol, angiotensin-converting enzyme inhibitors, angiotensin receptor blocking
drugs and diuretics should be avoided. Angiotensin-converting enzyme inhibitors are
contraindicated in pregnancy due to the risk for renal failure in the fetus, and its
demise. Atenolol administration promotes FGR development, so it is contraindicated
for pregnant women.
Antihypertensive drugs for rapid BP decrease
• Dihydropyridine calcium antagonists: nifedipine (Cordipine, Corinfar). Initial
dose 10 mg (never place under the tongue or chew!); it is repeated in 15 min
thrice to bring down diastolic BP to the range 90–100 mm Hg (maximum
dose is 60 mg). If this is ineffective, the antihypertensive drug is replaced or
supplemented by another one. Maximum daily dose is 120 mg.
• Β- adrenergic blockers: metoprolol (Metoprolol-Akri, Betaloc, Metocard,
Egiloc) 50–100 mg/day (avoid their administration in bronchial asthma).
• Clonidine (Clofelin, Hemiton), central α-adrenomimetic (imidazoline
derivative) 0.15 mg thrice a day or IV slow infusion 100 mcg dissolved in 10 ml of
0.9% sodium chloride solution for 1 min, thrice a day.
Infusion therapy is administered in the minimum required extent (daily volume of
infusion is 10–15 ml/kg a day), mostly to provide a carrier medium for hypotensive
drugs, postoperative preparation after operative delivery or in presence of apparent
signs of hemostasis disorder confirmed by laboratory findings. Fluid infusion is not
for routine administration in oliguria (at diuresis <15 ml/h). Over the last 20 years
pulmonary edema has been a significant cause of death in severe PE/eclampsia.
Fatality is often associated with inadequate fluid infusion.
Moderate dehydration is better than hyperhydration. The infusion volume is about
1–1.2 l/day; only balanced crystalloids are used for infusion.
The following is not recommended for patients with PE:

• increasing plasma volume;
• administering dopamine and furosemide in persistent oliguria;
• administering acetylsalicylic acid (Aspirin) or heparin in low doses;
• administering hydroxyethyl starch, albumin, dextran, Actovegin, spasmolytic agents.
There is not enough evidence in favor of administering activated protein C, anti-
thrombin III (Antithrombin), heparin, dipyridamol, arginine (L-arginine), prolonged
epidural nerve block, acetylcysteine (N- acetylcysteine).
To date there is not enough evidence to support recommendations to administer
vitamins C and E for prevention and treatment of PE.
During labor and in the puerperium it is recommended to limit fluid intake so as
to avoid an overload on the right heart.
One should take into account that in obstetric settings PE and

NB! its complicated varieties present the highest risk of massive
hemorrhage. When providing emergency care to such patients
one should be ready to provide surgical, local and conservative
hemostasis, intensive care for massive blood loss (blood
components, blood reinfusion systems).
The following can be administered:

• tranexamic acid drugs as a means of prevention if there is a risk for coagulopathy
development; routinely before operative delivery (for the main indication 500–
1000 mg);
• carbetocin;
• plasma factor drugs (factors II, VII, IX, X) at corresponding doses, in case of
coagulopathy (deficiency of procoagulant clotting factors).
In order to monitor the hemostasis system, patients with PE (accompanied by
DIC) may need thromboembolism prevention (under control of thromboelastogram
or hemostasiogram), and bed rest.
Prevention of thromboembolic complications is administered in case of moder-
ate or severe PE accompanied by a high risk for thromboembolism (thrombophilia,
obesity, age over 35, bed rest, etc.):
• indications for administration of low molecular weight heparins: hemostasiogram
showing hypercoagulation, activation of intravascular thrombi formation;
• criteria of low molecular weight heparins withdrawal: satisfactory condition with
stable BP readings, absence of proteinuria and normal hemostasiogram findings
over 5–7 days;
• duration of low molecular weight heparin therapy is adjusted individually.
20.10. ALGORITHM OF LABOR MANAGEMENT IN

PREGNANT WOMEN WITH PREECLAMPSIA
The decision about delivery is made when the patient is in a stable condition, in
the presence of senior obstetric personnel.
536 Obstetrics
At gestational age under 34 weeks, when there is an option to

NB! postpone the delivery, one should administer glucocorticoids for
prevention of fetal respiratory distress, and assess the effect of
conservative treatment in 24 hours.
At preterm age conservative treatment may improve the perinatal outcome; how-
ever, this should be weighted against the risk for the mother.
The mode of delivery depends on fetal presentation, its condition and maturity
of the birth canal.
Upon admitting the patient to the delivery department, one performs the follow-
ing procedures:
• summon the responsible obstetrician-gynecologist on duty, intensive care
specialist, neonatologist;
• fill out the intensive surveillance chart;
• provide the intravenous access: peripheral vein catheterization (18G);
• BP monitoring: at moderate arterial hypertension once an hour at least, at severe
hypertension — continuous monitoring;
• continue antihypertensive and anticonvulsant therapy (if it was initiated earlier)
at previous doses, and adjust them according to indications;
• provide adequate analgesia of labor (pharmaceutical analgesia as indicated). The
gold standard of analgesia is epidural nerve block;
• perform early amniotomy;
• do not routinely limit the duration of the second stage of labor if the mother’s and
fetus’s condition is stable.
Antihypertensive therapy is continued during labor; systolic BP should be less than
160 mm Hg, diastolic BP — less than 110 mm Hg.
For prevention of hypotonic hemorrhage in the third stage of labor and early
puerperium, IV administration of oxytocin is required.
Administration of ergometrine is contraindicated as the drug has

NB! a hypertensive effect.
20.11. POSTPARTUM PERIOD MANAGEMENT
One should remain vigilant as in some patients eclamptic convulsions (with

the worst outcome) develop after delivery. A puerpera with moderate and severe
PR should be closely followed up by experienced personnel in intensive care unit
(at least for 24 hours) or until her general condition and BP stabilizes. Oxytocin
infusion is continued into the early postpartum period as there is a high risk for
hemorrhage.
Depending on the BP level, antihypertensive therapy and magnesium sulfate
therapy are continued after delivery until stable water balance and BP readings are
achieved.
20.12. PREVENTION OF PREECLAMPSIA
As early as at the first contact with the woman one should assess the risk for PE
so as to determine her individual plan of management.
Women with a high PE risk should be provided with obstetric consultations and
referred for clinical and laboratory investigations.
Considering that PE pathogenesis implies vascular disorders of the placental bed,
PE prevention should be started before pregnancy. The main issue here is treatment
of extragenital diseases.
An effective preventive method for patients in the high risk group is taking low
doses of aspirin (acetylsalicylic acid) after 12 weeks gestation (100 mg daily).
According to ESH/ESH recommendations (2013), aspirin (acetylsalicylic acid)
intake at a dose of 75 mg/day starting at 12 weeks gestation and until delivery can
be recommended to women with a high PE risk (arterial hypertension in previous
pregnancies, chronic renal disease, systemic lupus erythematosus, antiphospholipid
syndrome, diabetes mellitus, chronic arterial hypertension) providing the risk for
gastrointestinal hemorrhage is low.
Calcium in the form of food supplements is recommended at a dose of up to 1 g
daily, on condition the woman does not get enough calcium in her meals.
Search for more effective preventive methods has not been successful so far.
There is not enough evidence that PE prevention can be achieved by limiting
caloric intake in obese women, limiting salt intake, by physical exercise, antihyperten-
sive therapy, vitamins C and E, heparin (even in the presence of thrombophilia and
PE in previous pregnancies), selenium, zinc, iron, polyvitamins, nitric oxide donors
(nitroglycerine), progesterones, diuretics, cod liver oil, garlic (in tablets), magnesium,
changing the diet (consuming carbohydrates and proteins), bed rest.
REMEMBER!
Preeclampsia (PE) is a multisystem abnormality developing in the second half
of pregnancy (after 20 weeks gestation) characterized by arterial hypertension
combined with proteinuria (over 0.3 g/l in daily urine), often with edema and
manifestations of multiple organ failure.
The leading disturbing factors in PE are generalized vascular spasm in the

presence of endothelial dysfunction, changes in rheological and clotting properties
of the blood which leads to (sometimes critical) decrease in perfusion of vital
organs and the placenta.
The only truly effective method of treatment is delivery, thus all other therapy
methods are aimed at restraining PE progress and preventing eclampsia. PE and its
complicated forms present the highest risk for massive hemorrhage in obstetrics.
At gestational age less than 34 weeks and given the possibility to delay delivery
one should administer glucocorticoids to prevent fetal RDS and assess the effect of
conservative therapy in 24 hours. At preterm gestation conservative treatment can
improve the perinatal outcome; however this benefit should be weighted against
the risk for the mother.
538 Obstetrics
CONTROL QUESTIONS
1. What is preeclampsia (PE)?

2. What are the criteria of moderate PE?
3. What are the criteria of severe PE?
4. What are the principles of managing delivery in patients with PE?
5. What is HELLP syndrome?
6. What is acute fatty liver of pregnancy?
7. What are modern principles of gestosis therapy?
8. What is background therapy of PE?
9. What is eclampsia?
10. What is the algorithm of emergency care in convulsions?
11. What are the means of PE prevention?
CHECK YOURSELF!
Level 1. Test
1. The most threatening sign of PE is:
a) swollen legs;
b) anterior abdominal wall edema;
c) arterial hypertension;
d) hypoproteinemia.
2. In PE, the most informative additional investigation is:

a) ultrasound;
b) Nechiporenko test;
c) complete blood count;
d) ophthalmoscopy.
3. Indications for termination of pregnancy are:

a) weight gain over 2 kg a week;
b) hemoglobin <70 g/l;
c) fetal RDS;
d) loss of protein over 3 g/l in one portion;
4. Minimum clinical criteria of PE are:

a) end-of-day edema
b) arterial hypertension after 16 weeks gestation;
c) proteinuria;
d) arterial hypertension after 20 weeks gestation.
5. Clinical criteria of severe PE are:

a) systolic BP >160 mm Hg;
b) proteinuria >1g/l in daily urine;
c) headache;
d) nausea/vomiting.
6. The main principle of PE therapy is:

a) hypotensive drugs;
b) diuretic drugs;
c) vitamin therapy;
d) osmotic therapy.
7. During an attack of eclampsia the doctor should:

a) perform vaginal examination;
b) perform amniotomy;
c) prevent aspiration and asphyxia;
d) restrain the pregnant woman’s hands.
8. After an eclampsia attack one should:

a) perform cesarean section immediately;
b) initiate magnesium sulfate therapy;
c) provide prevention of fetal RDS
d) infuse FFP.
9. In the presence of PE, the postpartum period can be complicated by:

a) hemorrhage;
b) placental abruption;
c) hypogalactia;
d) eclampsia.

1. The pregnant woman with 32 weeks gestation presents at a maternity welfare
clinic with a headache. There is no edema. Weight gain is 300 g per week, pro-
teinuria 0.99 g/l, BP 150/95 mm Hg. What is your diagnosis? What is the plan of
management?
2. The pregnant woman with 38 weeks gestation was brought to maternity hospital
in an ambulance. At home she had a seizure with fainting; her BP is 155/90 mm
Hg. After the ambulance team administered magnesium sulfate solution, her BP
decreased to 130/90 mm Hg. Ultrasound findings: fetal size corresponds to 34 weeks
gestation, a retroplacental hematoma 7–8 cm is present. What is your diagnosis?
What is the plan of management?
NOTES
_________________________________________________________________
_________________________________________________________________
• Chapter 21
MISCARRIAGE. PREMATURE (PRETERM)
BIRTH
Miscarriage is spontaneous termination of pregnancy (spontaneous abortion)

before 22 weeks gestation. Spontaneous preterm labor is spontaneous termination of
pregnancy at 22 to 37 weeks gestation counting from the first day of last menstrual
period. In English language literature authors propose the following definition of
abortion: any termination of pregnancy ending in birth of immature nonviable fetus.
Spontaneous miscarriage is involuntary termination of pregnancy before the time
when the fetus is able to survive independently.
Miscarriage is classified into early miscarriage (before 12 weeks), late miscarriage
(at 12–21 weeks) and premature birth (at 22–36 full weeks) (Fig. 21.1).
Early pregnancy loss Late miscarriage Preterm birth

(before 12 weeks) (12–22 weeks) (22–37 weeks)
0 12 22 37
Fig. 21.1. Classification of miscarriage and premature birth: before 12 weeks — early
miscarriage; 12–21 weeks — late miscarriage; 22 to 36 weeks — premature birth
The term habitual abortion in Russian Federation is applied to spontaneous

miscarriage for two times in a row at a gestational age before 22 weeks. In other
countries habitual abortion means termination of pregnancy for three and more
times in a row; however, it is recommended to perform investigations after two
miscarriages.
Preterm birth, according to WHO, is spontaneous termination of pregnancy at
gestational age from full 22 weeks to full 36 weeks, birth of a fetus with a weight
more than 500 g.
Loss of a desired pregnancy occurs in almost every fifth pregnant woman. The
rate of spontaneous abortion amounts to 10–20% of clinically diagnosed pregnan-
cies. Miscarriage is associated with obstetric history; its rate is higher in women with
primary miscarriage and lower in those who has given birth (Fig. 21.2).
Chapter 21. Miscarriage. Premature (preterm) birth 541
Implantation Postimplantation Spontaneous Live births

loss loss abortion
Medical control stage
Preclinical stage
Fig. 21.2. Distribution of early miscarriage
The incidence of miscarriage at early gestational age when

NB! pregnancy has not been diagnosed, is 2 – 3 times higher than at
diagnosed pregnancy; it amounts to 30% and more.
The rate of miscarriage also varies depending on the age: 12% of women under
29 and up to 50% of women over 45. The mother’s advanced age probably promotes
the rate of chromosome abnormalities and leads to rejection of the gestational sac.
About 80% of miscarriages occur at a gestational age before 12 weeks.
If a pregnancy terminates in premature birth of a viable but preterm fetus, the rates
of perinatal mortality and neonatal morbidity are very high. The severity of disorder
in the premature fetus is greater in more premature babies.
21.1.2. Historical aspect

Miscarriage became a topic of interest in the twentieth century as the number
of large families declines. Reduced parity is not exclusively associated with medi-
cal problems; to a greater extent it is due to the changes in women’s social status.
Despite the availability of new effective means of contraception in the last century,
the rate of induced abortions remains quite high. The ratio of delivery to abortion,
according to official statistics, is 1:0.5; according to expert estimates — 1:1.6–1.7.
Pregnancy developing after a primary surgical abortion develops in conditions of
chronic endometritis, implantation defects, at a high risk of miscarriage or preterm
birth. Thus the value of each pregnancy has grown considerably.
In mid-1930s a hypothesis linking hormonal disorders with complications of gesta-
tion was put forward, and pregnant women had to take hormones to avoid miscar-
riage. Hormonal therapy was actively introduced into clinical practice without pre-
liminary controlled studies. Synthetic diethylstilbestrol was administered to pregnant
women for over 30 years. Only in mid-1950s concurrent cohort controlled studies
showed that the drug does not reduce the risk of spontaneous abortion or premature
birth, nor does it increase the probability of giving birth to a live fetus. Despite these
conclusive findings, obstetricians continued to administer diethylstilbestrol until in
mid-1960s it was proved that there exists an association between diethylstilbestrol
542 Obstetrics
administered to pregnant women and vaginal adenocarcinoma (a very rare type) in

girls born by these mothers. Later it was demonstrated that the drug increases the
risk of breast cancer, mental disease and genitourinary disorders (including tumors
and infertility) in children of both sexes. That is why absence of evidence-based data
about the effect of hormones including progestin on prolongation of early pregnancy
should be accepted as a scientific fact.
21.1.3. Classification of miscarriage

ICD-10 codes
• O03 Spontaneous abortion.
• O02.1 Missed abortion.
• O20.0 Threatened abortion.
In clinical pregnancy miscarriage is classified depending on the stage when it
occurs:
• spontaneous abortion;
• abortion in progress;
• incomplete abortion;
• complete abortion.
In case of fetal demise the pregnancy is called missed abortion.

Spontaneous abortion occurs due to various causes. The following factors are
commonly distinguished:
• genetic;
• anatomical;
• endocrine;
• immune;
• infectious;
• thrombophilic.
When the cause of abortion is not established, this is referred to

NB! as an idiopathic case.
Genetic and, in part, infectious factors lead to formation of abnormal em-

bryo. The damaging effect of other factors (anatomical, endocrine, immune)
consists in providing a background unfavorable for the development of geneti-
cally sound gestational sac, in depleting the capacity of the chorion and arrest-
ing the embryo development (embryogenesis disorder). The critical stages in
the first trimester are 6–8 weeks (embryo death) and 10–12 weeks (gestational
sac expulsion).
Among spontaneous abortions occurring before 9 weeks gestation about 1/3 are
due to missed abortion. About 50% of women presenting with vaginal bleeding or
nagging pain in lower abdomen have a gestational sac in the uterine cavity, which
cannot yet be visualized by sonography. In most cases this gestational sac is mor-
phologically defective.
The high incidence of spontaneous abortion in case of embryo

NB! anomaly is selection that eliminates 95% of morphological and
cytogenetic “errors”.
On these grounds no management of spontaneous abortion is attempted in many

countries believing that 85% of miscarriages are genetically determined before
7 weeks, and before 12 weeks—78%.
21.1.4.1. Genetic causes of miscarriage

Termination of 70–80% of pregnancies in the first trimester is associated with
chromosome defects; by the end of 24 weeks gestation their rate decreases to 7%.
In some cases the abnormal embryo undergoes resorption. The rate of chromosome
abnormalities is higher in case of anembryonic gestation.
A genetic examination of the parents usually reveals no anomaly

NB! of the karyotype; these are so-called sporadic chromosome
mutations.
In sporadic miscarriage the effect of damaging factors is transient; it does not

disturb the woman’s reproductive function in the future. For instance, disorder of
gamete formation results in abnormal ovum and/or spermatozoon. Genetically ab-
normal nonviable embryo is in itself the cause of spontaneous abortion, as a rule.
In such cases miscarriage will not reoccur.
The probability of chromosome abnormality in subsequent pregnancy is about 1%.
In contrast, 7% of couples with habitual abortion show chromosome abnormalities.
Thus disease runs in the family: hereditary disease, congenital malformations, birth
of mentally retarded children, infertility and/or miscarriage of unknown origin are
noted not only in the given couple but also in close relatives; the same holds true for
cases of perinatal mortality. A genetic consultation is required in such cases.
The less the gestational age at the moment of ovum demise, the
NB! more often its cause is choromosome mutation.
In case of chromosome aberration embryogenesis is often impossible or becomes

thwarted at an early stage. Maldevelopment due to chromosome aberration can be
associated with the reduced cellular ability to multiply. In this case there is dramatic
desynchronization in the processes of embryo or placenta development, cellular dif-
ferentiation and migration.
When the karyotype of one parent shows balanced chromosome rearrangement,
the probability of having a baby with unbalanced chromosome abnormality is 1–15%
(the difference has to do with the nature of rearrangement, the size of involved seg-
ments, the sex of the carrier and family history). Autosomal trisomy is encountered
most commonly (52%); it first develops secondary to gametogenesis disturbance
544 Obstetrics
upon chromosome non-disjunction in the process of mitotic division in parents with

normal karyotype.
The percentage of various trisomy types differs widely. Trisomy 6 (1/3 of all tri-
somy cases mediating spontaneous abortion) is not noted in live-birth infants; thus
it is absolutely fatal. Trisomy types next in importance (according to their incidence
rate) are trisomy 22 and trisomy 21.
The second most frequent disorder is monosomy 45X followed by triploidy, tet-
raploidy, translocation and mosaicism.
In rare cases one parent is the carrier of balanced translocation; in such a marriage
repeated miscarriage is possible.
Infections, abuse of coffee, alcohol, chemical substances and narcotic drugs do
not increase the rate of miscarriage in any significant way. There is no reliable evi-
dence that external factors can affect anything else apart from a small number of
early abortions.
When abnormal karyotype is detected in even one parent during pregnancy, one
should use all available methods to reveal congenital disorders of embryogenesis.
21.1.4.2. Anatomical causes of miscarriage

Anatomical causes include congenital uterus malformations, diseases and injuries
of the cervix and body of uterus.
Uterus malformations (mullerian duct anomalies) can be presence of two dis-
tinct uteri (uterus didelphus), bicornuate uterus, unicornuate uterus, partially or
completely septated uterus, arcuate uterus. The malformations increase the rate of
miscarriage in the second trimester as well as the rate of premature birth. Acquired
anatomical defects include submucous myoma of uterus, less often—intrauterine
synechiae (Asherman syndrome) (Fig. 21.3).
Means of diagnostics include:
• ultrasound;
• hysterosalpingography;
а b
Fig. 21.3. Uterine malformations: a — bicornuate uterus, ultrasound; b — Asherman

syndrome, hysteroscopy
• hysteroscopy;
• MRT.
Cervical incompetence is the most common cause of miscarriage

NB! in the second trimester.
Isthmico-cervical insufficiency (cervical incompetence) means incompetence of

the internal os and cervix of uterus. The rate of this abnormality in patients with
habitual abortion is 13–20% (Fig. 21.4).
Cervical incompetence can be organic (or anatomical) and functional (or hor-
monal).
Organic cervical insufficiency can be congenital (in the presence of genital infantil-
ism, uterine malformations) or acquired as secondary traumatic lesion of the cervix
due to therapeutic and diagnostic manipulations on the cervix as well as traumatic
delivery followed by deep lacerations of the cervix.
The main causes of organic (acquired) cervical incompetence:
• trauma of the cervix in abnormal and operative vaginal delivery (forceps delivery,
fetal macrosomia, breech presentation, embryotomy, etc.);
• invasive methods of treating the cervix (conization, amputation of the cervix);
• artificial abortions (rough dilation of the cervical canal during an instrumental
abortion), termination of pregnancy at a late gestational age.
It is supposed that functional cervical incompetence develops in women with
progesterone deficiency, connective tissue dysplasia.
As a rule, cervical incompetence does not cause any clinical presentations. Cervical
effacement and dilation proceed painlessly, unobserved by the patient.
Patients with suspicion of servical incompetence or with habitual

NB! miscarriage in the second trimester should receive a weekly or
fortnightly examination of the cervix starting at 12 weeks gestation.
а b
Fig. 21.4. Normal uterine cervix (a) and cervix in cervical incompetence (b)
546 Obstetrics
Later the inferior pole of the gestational sac descends to the external os or into
the vagina (prolapse). In this case there is a high risk of gestational sac rupture due
to infection and excessive mechanical pressure on the inferior pole. The amniotic
membranes rupture.
Cervical incompetence is mainly treated surgically. Surgery should consist in placing
circular sutures with synthetic filaments once there develop clinical manifestations of
cervical incompetence; there should be no signs of infection or contraindications for
prolongation of pregnancy. An alternative to circular sutures is obstetric support pessary
used in different modifications starting at 14–15 to 22 weeks gestation (see Fig. 27.2).
In non-pregnant patients with anatomical cervical incompetence one performs
plastic surgery on the cervix. The chair of obstetrics and gynecology at the PFUR
prefers the method of dissection and repair of the cervix proposed by Prof. Yeltsov-
Strelkov.
21.1.4.3. Endocrine causes of miscarriage

Endocrine causes of miscarriage account for 8–20%, the most significant causes
are luteal-phase defect prior to pregnancy, luteinizing hormone hypersecretion,
thyroid dysfunction, diabetes mellitus, hyperandrogenism of ovarian, adrenal or
combined origin.
As a rule, luteal-pase defect results from a wide range of unfavorable factors:
disturbed secretion of follicle stimulating and luteinizing hormones in the follicu-
lar phase of menstrual period; early or late peak of luteinizing hormone release,
hypoestrogenism secondary to incomplete folliculogenesis which is mostly due to
hyperprolactinemia, hypothyroidism, hyperandrogenism. For this reason, treatment
of luteal-phase defect prior to pregnancy requires a differentiated approach.
Examination of women with endocrine-mediated habitual miscarriage starts with
assessment of functional diagnostics tests outside of pregnancy: measuring the basal
temperature, evaluation of cervical mucus (length of mucus filament), ferning. One
also investigates excretion of thyroid, adrenal, ovarian hormones (the last one is of
least informative value). Folliculogenesis is monitored using ultrasound. The main
treatment is hormone therapy until the patient gets pregnant.
21.1.4.4. Immunological causes of miscarriage

Immunological causes of miscarriage account for 80% of all inexplicable cases of
repeated miscarriage. We distinguish autoimmune (antiphospholipid syndrome) and
alloimmune (abnormal activity of natural killers, charged ratio of T-helpers-1-Th-1
and T-helpers-2-Th-2 and other) disorders. The main antiphospholipid syndrome
complications are thrombosis and miscarriage. Therapy includes antiaggregants (ace-
tylsalicylic acid, aspirin) and direct anticoagulants — heparin, enoxaparin sodium
(Clexane), nadroparin sodium (Fraxiparine). Unfortunately, none of these methods
is supported by a body of evidence.
Outside of pregnancy, 31% of women with habitual miscarriage demonstrate auto-
antibodies to thyroglobulin, thyroid peroxidase. In these cases the risk of spontaneous
abortion during the first trimester is as high as 20%. Patients with habitual miscarriage
showing antinuclear and antithyroid antibodies should have further investigations to
reveal an autoimmune process and verify the diagnosis.
The blood of ¼ of women with habitual miscarriage shows hCG antibodies; they
have a high affinity and thus inhibit the formation of hCG-receptor complex and
realization of its biological action. This is the cause of disorders in chorion implan-
tation and placentation, and at a later gestational age — retarded rate of placenta
maturation.
Diagnostics of antiphospholipid syndrome (Sydney, 2006). Its clinical criteria are
as follows:
• venous or arterial thrombosis in past history;
• three and more spontaneous abortions at an age before 10 weeks when anatomical,
genetic and hormonal causes of miscarriage are at work;
• one and more cases of structurally normal fetus demise after 10 weeks gestation;
• one and more preterm deliveries before 34 weeks gestation due to severe PE and/
or severe placental insufficiency.
Laboratory criteria:
• a standard enzyme immunoassay showing medium and high titer of anti-
cardiolipin antibodies detected in two and more assays at an interval of 12 weeks;
• lupus anticoagulant in plasma detected by two and more tests at an interval of
12 weeks;
• IgG or IgM antibodies to β2-glycoprotein I detected by two and more tests at an
interval of 12 weeks.
The diagnosis of antiphospholipid syndrome is established

NB! when there is one clinical, and one serological criterion of the
condition.
21.1.4.5. Infectious causes of miscarriage
If primary infection occurs at an early gestational age, it can become the cause of a
spontaneous abortion. The source of infection can be acute or chronic inflammatory
processes of various organs and systems: dental caries, acute respiratory viral infec-
tion, chronic tonsillitis, pyelonephritis and other extragenital diseases. The primary
focus of infection can be located in the genitals — endometritis, cervicitis, vaginitis.
Pregravid examination of patients with habitual miscarriage in history should in-
clude pH-metry of vaginal discharge, bacterioscopy and bacteriology study of cervical
mucus, tests for specific infections (Trichomonas, gonorrhea, etc.).
Treatment consists in cleansing the focus of acute infection. After treatment of
vaginitis or vaginosis the vaginal microbiome should be restored which is achieved
by intake of eubiotics (yoghurt, biokefir, etc.) and medications that decrease vagi-
nal pH.
Women with diagnosis of habitual miscarriage, when they are not

NB! pregnant, often show chronic endometritis.
Chronic endometritis causes disorder of placentation and tightening of placen-

tal vessel lumen, which leads to FGR at least, and in most cases—to miscarriage
(Fig. 21.5). There is no infectious agent in this case, but a faulty immune response.
548 Obstetrics
а b
Fig. 21.5. Structural features of placental bed: a — normal gestational changes in spiral
artery segment located in the myometrium; b — changes induced by chronic endometritis:
edema, narrow vascular lumen, membranes remaining elastic in the endometrial segment
Habitual miscarriage occurs more often when opportunistic flora

NB! persists in the endometrium.
Habitual miscarriage occurs less often at chronic endometritis caused by mixed

bacterial and viral infection (herpes simplex virus, cytomegalovirus, Coxsackie A
and B virus, enterovirus). Later immune abnormalities can come into play, and the
infectious agents pale into insignificance. To confirm or rule out the infectious causes
of miscarriage one performs endometrial biopsy on day 7–8 of menstrual period
followed by histology study of the material, PCR and culture test of the bioptate.
Treatment of chronic endometritis is provided according to standards of managing
chronic pelvic inflammatory disease.
In chronic endometritis, correcting the immunity disturbance

NB! and restoring the biocenosis of the reproductive tract is more
important than curing the focus (the role of the infectious agent
is only relevant during the acute stage).
21.1.4.6. Polymorphism in hemostasis-related genes and miscarriage

The most common types of polymorphism in hemostasis-related genes in general
population:
• factor V Leiden mutation (5–9%);
• protein C and S deficiency (0.2–0.5% and 0.08%, correspondingly);
• prothrombin gene G20210A mutation (2–4%);
• hyperhomocysteinemia (1–11%);
• antithrombin III deficiency (0.02–0.2%).
All patients with polymorphism in hemostasis-related genes should undergo an
individual risk assessment to make a decision about practicability of administering
unfractionated heparin (low-molecular weight heparin). One should adjust the dose
of low-molecular weight heparins according to anti-Xa activity or the APTT.
In patients with thrombophilia, the criteria of therapy effecicy

NB! are normal hemostatic values and absence of thrombotic
complications.
21.2. SPONTANEOUS ABORTION
Termination of pregnancy from conception to 22 weeks gestation without outside

intervention is referred to as spontaneous abortion. Spontaneous abortion is one of
the main complications of pregnancy; it occurs in 15–20% of all desired pregnancies.
Pathogenesis of spontaneous abortion can vary depending on the cause. In some
cases it starts with uterine contractions which precipitate detachment of the ges-
tational sac. In other cases uterine contractions are preceded by collapse of the
gestational sac (missed abortion). Sometimes detachment of the gestational sac and
uterine contractions occur at the same time.
21.2.2. Diagnostics
Diagnostics presents no difficulty; it is based on presentations, findings of general
and gynecologic examinations, ultrasound.
At threatened abortion the woman has a sensation of heaviness or slight drawing
pain in the lower abdomen or in the sacral area. There are no specific signs.
In the second trimester threatened abortion produces cramp-like pain. A gy-
necologic examination shows that the uterine size matches the length of delayed
period. The uterus reacts to palpation by contracting. No structural changes of
the cervix are noted, there is no vaginal discharge. Ultrasound examination is
not informative.
At incipient abortion the cervix can be somewhat effaced (Fig. 21.6) with slightly
open external os. The body of uterus becomes compact, but it still matches the length
of delayed period. At incipient abortion the cramp-like pain is more pronounced
than at threatened abortion, there is vaginal bleeding. The gestational sac detaches
at a small area, so the uterus size matches the gestational age.
In case of cervical incompetence the cervical canal is somewhat enlarged, so the
pain is less pronounced or absent. The patient’s general condition in threatened and
incipient abortion remains satisfactory.
Ultrasound examination detects partial detachment of the chorion (placenta) along
the edge or formation of retrochorionic (retroplacental) hematoma (Fig. 21.7).
Ultrasound examination permits an assessment of the internal os condition and
the cervical length. In case of cervical incompetence the internal os is more than
8 m open, the cervix is effaced to 25 mm or less.
If the inferior pole of the gestational sac can be easily reached through the cervical
canal, we are dealing with ongoing abortion (abortion in progress).
550 Obstetrics
1.4 cm
Fig. 21.6. Cervical effacement (ultrasound)
Distance
Distance
Fig. 21.7. Pregnancy at 7 weeks. Retrochorionic hematoma (ultrasound)
At abortion in progress, complete or incomplete abortion, the

NB! woman’s condition depends on the volume of lost blood. Massive
blood loss can be complicated by hemorrhagic shock.
Ongoing abortion is accompanied by cramp-like pain in the lower abdomen, pro-

nounced hemorrhage. The cervical canal is open, the gestational sac is in the cervical
canal, its inferior pole can protrude into the vagina. In case of cervical incompetence
the abortion commonly begins with premature rupture of the membranes. The ges-
tational sac descends to the opened cervical canal, the membranes get infected and
rupture. The progress of miscarriage is usually rapid and painless.
At incomplete abortion, when the gestational sac is only partially expelled from
the uterus cavity, there is cramp-like pain and hemorrhage of varying intensity. The
cervical canal is open, the uterus is of soft consistency, and its size is less than the
estimated gestational age. The retained conception products are fetal membranes,
the chorion (placenta or its fragments) (Fig. 21.8).
а b
Fig. 21.8. Incomplete abortion. Ultrasound (a) with color flow mapping (b)
At complete abortion, which is mostly noted in late pregnancy, the gestational sac
is completely expelled from the uterus cavity. The uterus contracts, and the hemor-
rhage subsides.
If threatened or incomplete spontaneous abortion becomes prolonged, vaginal
microflora can pass to the uterus cavity and cause development of chorioamnionitis,
endometritis.
Septic abortion can be the cause of generalized pyoinflammatory

NB! disease, and even sepsis or septic shock.
21.2.3. Laboratory and instrumental methods of

examination
Laboratory and instrumental methods of examination are used to diagnose the
initial stages of miscarriage:
• measuring the basal temperature;
• dynamic assessment of hCG levels;
• ultrasound.
Ultrasound examination performed in the first trimester permits a more precise
definition of the gestational age, detection of multiple pregnancy, malformations of
the uterus and gestational sac, placenta separation or placenta previa. The gestational
sac can be visualized from 4.5–5 weeks gestation (menstrual age). At an earlier ges-
tational age, when the sonographer fails to visualize the gestational sac in the uterus,
this can lead to the erroneous diagnosis of ectopic pregnancy. In dubious cases one
should monitor β-hCG with repeated tests followed by ultrasound. At 5–6 weeks
552 Obstetrics
gestation one can detect the yolk sac and gestational sac with a vaginal transducer.
Soon after that one can visualize the embryo and assess its cardiac activity.
The following ultrasound findings indicate miscarriage:
• discrepancy between the gestational age, and the size of gestational sac and yolk sac;
• transabdominal scan shows absence of embryo while the gestational sac is more
than 25 mm in three orthogonal planes (more than 188 mm at transvaginal scan)
(Fig. 21.9);
• irregular shape or shifting of the yolk sac;
• small size of the embryo;
• absence of embryo heartbeat while the CRL is more than 5 mm;
• slow heartbeat (<100 per min) at gestational age 5–7 weeks;
• retrochorionic hematoma of a large size: more than 25% of gestational sac
surface.
Fig. 21.9. Anembryonic gestation. Gestational age 7 weeks 5 days. Absence of embryo
complex (ultrasound)
Normal embryo size and normal heartbeat are favorable signs

NB! even at uterine hemorrhage as two-thirds of such embryos remain
viable.
If a live embryo is detected at 8 weeks gestation while there are signs of threatened
abortion, in 95% of women the pregnancy continues; if this happens at 14–16 weeks,
the probability of spontaneous abortion decreases to 1%, that is, it is preserved in
99% of cases.
21.2.4. Differential diagnostics

Miscarriage is differentially diagnosed from ectopic pregnancy, molar pregnancy,
menstrual dysfunction, benign and malignant diseases of the cervix, vagina and body
of uterus.
21.2.5. Treatment
The possibilities of therapy in the first trimester are limited due to the possible
toxicity and teratogenic effects of medications during the organogenesis period
(18–55 days from the moment of conception).
In Russia a pregnant woman with threatened abortion in early pregnancy is of-
fered hospitalization while abroad it is considered that this condition does not require
hospital care. It has been established that bed rest is ineffective for prolongation of
pregnancy at any gestational age.
Hospitalizing a woman at early gestational age when there is a

NB! diagnosis of threatened abortion made on the basis of of gnawing
pain or discomfort in lower abdomen, can do no good and even
harm. In such a condition, hospitalization increases the risk of
thromboembolism, pyoseptic infection (hospital infection); the
woman’s social adaptation is disturbed: she regards herself as a
patient rather than an expecting mother.
At threatened abortion a protective regimen is initiated; it is indicated to regulate

the intestinal function (prevention of constipation associated with elevated serotonin
production), to administer physiotherapy, gestagens (didrogesterone 20–40 mg/day
or micronized progesterone) until 16–20 weeks gestation.
Effectiveness of the above procedures has not been proved evidentially; they do
not produce a reliable increase in the rate of preserved pregnancies. However, since
no adverse effect of this therapy on the mother or fetus has been shown, and the
therapy has been successfully used in Russian obstetric practice for decades, we can-
not give it up. First of all, the pregnant woman in this situation cannot bear not to
receive any treatment, and the conservatism of obstetrician-gynecologists is a deeply
rooted feature.
Prior to the start of therapy or simultaneously with it the patient is examined to
find out the cause of threatened abortion. Knowing the cause and understanding
the pathogenesis of miscarriage one provides care with more success. In most cases
the pregnancy is preserved, which can be due to the absence of clear cut criteria of
«threatened abortion» and ensuing hyperdiagnostics.
At threatened abortion in the first or second trimester the care is limited to semi-
bed rest (controlled studies showed ineffectiveness of bed rest as treatment for threat-
ened abortion). The woman herself should decide whether she will keep to bed or not.
• Physical, emotional and sexual rest.
• Gestagen support until 20 weeks gestation (didrogesterone 20–40 mg, micronized
progesterone 200–400 mg/day in vaginal suppositories).
NB! There is no conclusive proof in favor of gestagen therapy.
• At late gestational age calcium antagonist therapy is possible. Blocking calcium

channels (or competing with calcium ions) the drug suppresses myocyte
554 Obstetrics
contraction decreasing the myometrial contractile activity. Nifedipine has a

good effect administered sublingually 10–20 mg thrice a day. The drugs are
contraindicated in case of tachycardia.
• 25% solution of magnesium sulfate is often administered (10–20 g of dry
substance, IV droplet infusion or with infusion pump). Magnesium sulfate
is not certified as a tocolysis drug but it is cheap and is widely used in poor
countries.
• Therapy depending on the detected cause of threatened miscarriage
(antiphospholipid syndrome, exacerbation of infection, anemia, and other).
• Prevention and treatment of constipation normalize the vaginal biocenosis
(populating it with lactobacteria from the colon), decreases the physical effort
during defecation.
• At gestational age 16–31 weeks it is admissible to administer indomethacine and
its analogs per rectum or per os no more than 200 mg/day for no longer than
5 days. Clinical trials did not show any effect on the rate of spontaneous abortion;
the same effect was shown by spasmolytic drugs.
• Starting at 26 weeks tocolysis with β2-adrenomimetics is indicated; their
administration should be only intravenous.
• Atosiban, blocker of oxytocin receptors, is a patented medication against
preterm childbirth (starting at 23 weeks gestation). It does not show any
advantage compared with β2-adrenomimetics or calcium channel blockers as to
prolongation of pregnancy, but it has virtually no adverse effects. The drawback
of this drug is its rather high cost compared with other tocolytic drugs.
Complete abortion. Patients with threatened abortions should be instructed that if
spontaneous abortion occurs at home, they should keep all expelled tissues for spe-
cialist examination. Soon after complete abortion the pain subsides and hemorrhage
arrests. If the diagnosis is confirmed by sonography and raises no doubt, no further
procedures for hemorrhage arrest are required.
In all cases ultrasound examination is administered for evaluation of the uterus
cavity contents. In dubious cases it is advisable to perform vacuum aspiration of the
retained fragments of the gestational sac as complete removal of necrotized decidual
tissue reduces the blood loss, prevents development of puruloseptic complications
and reduces the rehabilitation period.
Septic abortion. The role of septic abortions as a leading mortality cause in the
world is now on the decrease, mostly thanks to legislation that allows medical (in-
cluding pharmaceutical) abortion for patients with unwanted pregnancy.
However, any spontaneous abortion can be complicated by infection. In most
cases endometritis develops, but in unfavorable course of the process panmetritis and
pelvioperitonitis are possible followed by further spread of infection to the extent of
generalization (sepsis).
At puruloseptic complications the patient’s general condition is compromised;
there develop local symptoms. The body temperature runs high, there is abdominal
pain, bloody and sometimes pus-like vaginal discharge. A physical examination
detects tachycardia, tachypnoea, muscular guarding in the anterior abdominal wall;
a bimanual examination demonstrates a tender uterus of soft consistency. In severe
cases septicemia and septic shock develop.
The culture of uterine contents demonstrates polybacterial infection and shows

endogenous vaginal flora. As a rule, this is E. coli and other anaerobic bacte-
ria, gramnegative bacilli, hemolytic streptococcus group B, anaerobic streptococci,
Bacteroides, staphylococci.
Sequence of actions at septic abortion:
• general and gynecologic examination; cervical canal specimen, Gram staining;
• count of blood elements, determining electrolytes, uric acid and creatinine
levels;
• blood grouping;
• culture of cervical canal discharge, blood and gestational sac fragments;
• catheterization of the bladder (Foley catheter);
• IV infusion of crystalloids with large bore angiocatheter;
• subcutaneous administration of 0.5 tetanus toxoid to vaccinated patients or IM
injection 250 IU antitetanus globulin.
Optimum treatment encompasses instrumental evacuation of uterine contents and
rational administration of antibiotics before, during and after curettage or vacuum
aspiration (the latter is more preferable).
Careful evacuation of uterine contents is extremely important; it should be started
only several hours after the initiation of antibacterial therapy.
The condition of patients with septic abortion improves critically if

NB! treatment was initiated in good time. Septic shock remains a risk
of serious complications requiring intensive care.
21.2.6. Prognosis
A spontaneous abortion occurring once is not regarded a risk factor for habitual
miscarriage.
The risk increases upon reoccurring spontaneous abortions. Thus, after three
spontaneous abortions the risk of a fourth one amounts to 25–50%.
According to data from evidence-based multicentral randomized studies, there is
no reliable evidence that women with habitual miscarriage increase their parity after
administration of prolonged bed rest, progesterone and its analogs, low molecular
weight heparin, etc.
Even without treatment the rate of a favorable outcome of a subsequent pregnancy
is within the range 82–86%.
21.2.7. Prevention
There is no specific prevention of spontaneous miscarriage.
Neural tube defects may be the cause of early spontaneous abortion; prevention
of this defect consists in taking folic acid 3 menstrual periods prior to conception
and into the first 12 weeks of pregnancy at a daily dose of 400 mcg.
If neural tube defects were noted in previous pregnancies, the preventive dose is
increased to 4 mg/day.
556 Obstetrics
21.3. MISSED ABORTION

Missed abortion means demise of the embryo or fetus without expulsion of the
conception products from the uterus cavity before 22 weeks gestation. The gestational
sac fails to be expelled despite the quite long period elapsed after the moment of
embryo demise. The causes why complete abortion does not take place are not well
understood.
A theory describing the changes in regulatory mechanism of the immune system
during pregnancy hypothesizes that there is a switch of immune response mediated
by Th1 subtype of T helper cells to immune response mediated by Th2 subtype
cells. It is known that inflammation develops with direct involvement of the cy-
tokine system which plays a major role in regulating inflammatory reactions and
intercellular interactions in the endometrium. In the presence of chronic inflamma-
tion (including autoimmune inflammation) the anti-inflammatory cytokines grow
in numbers exceeding the normal values more than twofold. Anti-inflammatory
cytokines produced by T-helper lymphocytes-1 do not only show a direct embryo-
toxic effect, but also suppress trophoblast invasion disrupting its normal formation.
Their excessive numbers result in prothrombinase activation which causes throm-
bosis, infarction and detachment of trophoblast ending in miscarriage in the first
trimester. Increased synthesis of the damaging cytokines and decreased synthesis
of growth factors promote abnormal invasion and lesion of trophoblast at an early
gestational age.
Viral infections of female genitals mostly develop in the presence of immune
deficiency; they themselves promote aggravation of secondary immune deficiency.
Some viruses (human papillomavirus, cytomegalovirus) can affect the trophoblast
and vascular endothelium directly causing increased production of prothrombinase
and interleukin-8 which promote further endothelial lesion. At the same time anti-
miscarriage mechanisms are disrupted: HLA-G expression by trophoblast and secre-
tion of growth factors decreases, while no activation of Th2 pathway of lymphocyte
differentiation takes place.
The leading cause of missed abortion is persistent viral and

NB! bacterial infection.
Study of the species and quantitative composition of vaginal and cervical micro-
cenosis showed a certain association between the dysbiotic condition and persistence
of opportunistic organisms in the endometrium.
21.3.2. Diagnostics
Diagnostics of missed abortion is based on the findings from a gynecologic exami-
nation, ultrasound, hCG levels (Fig. 21.10). The major signs are uterus too small for
gestational age, absence of embryo cardiac pulsation or fetal heartbeat, no-growth
Fig. 21.10. Missed abortion, embryo demise. Ultrasound
of gestational sac, low hCG level. In multiple pregnancy demise of one fetus is a
possibility.
21.3.3. Treatment
In case ultrasound detects only insignificant conception products in the uterus
while hemorrhage is not intensive and there is no sign of infection, expectant attitude
is allowed by western obstetricians. This approach is adopted since surgical treatment
implies a high risk for cervical injury, uterus perforation, development of synechiae,
pelvic inflammatory disease development, adverse effects of anesthesia. As a result,
the gestational sac is expelled from the uterus. However, this expectation becomes
an emotional stress so most patients prefer artificial removal of the gestational sac.
Development of intensive bleeding, incomplete abortion, infection signs are indica-
tions for evacuation of uterine contents.
At early gestational age the sac is removed by pharmaceutical

NB! means using antigestagens (mifepriston) and prostaglandins
(mesoprostol). Single-step instrumental evacuation is indicated
when there is hemorrhage.
In case of missed abortion pharmaceutical evacuation of the gestational sac is

indicated. One-step instrumental emptying of the uterus following cervical dila-
tion and vacuum aspiration is traumatic (curettage being still more traumatic)
and offers no advantages compared with pharmaceutical termination. Despite
the fact that one still sometimes has to resort to instrumental evacuation after
administering pharmaceutical methods, the rate of early and delayed compli-
cations after a pharmaceutical abortion is scores of times lower than after a
surgical invasion.
Instrumental evacuation of uterine contents requires hysteroscopy guidance.
Hysteroscopy assesses the condition of endometrium, absence of gestational sac
fragments; the uterine cavity is irrigated with antiseptics (Fig. 21.11).
558 Obstetrics
Fig. 21.11. Hysteroscopy fi ndings after removing the gestational sac from uterine cavity
When uterus contents are removed without hysteroscopy guidance, the patients
run a higher risk of postoperative complications: hematometra, endometritis, retained
conception products.
Patients showing a prolonged retention of gestational sac in the uterus (more than
3–4 weeks) may have coagulopathy related hemostasis disturbances. In such patients
preparation for surgery encompasses hemostasis study, blood typing and Rh testing.
One should have at one’s disposal everything needed for arresting coagulopathy
hemorrhage.
In case of late term abortion the following medications are administered: anti-
gestagen (Mifepristone) in combination with E2 prostaglandins (misoprostol). If
there are no signs of vaginal, cervical or uterine infection, mechanical methods
of cervical dilation can be used: Foley catheter introduction, dilapan, laminaria
sticks.
Intraamniotic or intravenous administration of 5-methyl-PG (dinoprost, Enzaprost)
is less effective. Intraamniotic administration of prostaglandins at missed abortion is
rendered difficult due to reduced volume of amniotic fluid and postmortem changes
of fetal membranes, which increase absorption of the drug into maternal myometrium
and blood stream in an unpredictable way.
Administration of prostaglandins is not recommended to patients with bronchial
asthma and arterial hypertension.
Large doses of oxytocin (up to 40 IU) can be administered for stimulation of
uterine contractions, intravenously through an infusion pump or by droplet infusion.
However, this method is second in effectiveness compared with other pharmaceutical
methods. Its complications encompass water intoxication due to the antidiuretic ef-
fect of oxytocin. In late term pregnancy termination analgesia can be achieved with
epidural nerve block or narcotic analgesics.
The gestational sac is referred for histology and, desirably, genetic study to deter-
mine the fetal karyotype.
To avoid immunization, rhesus-negative patients should receive

NB! antirhesus immunoglobulin within 72 hours after removal of the
gestational sac: 50 mcg in the first trimester, and the standard
300 mcg in the second trimester.
It is recommended that patients with pelvic inflammatory disease in past history

should receive preventive antibacterial therapy with broad spectrum antibiotics for
no less than 7 days during the post-abortion period.
Desirably, the patient should attempt subsequent pregnancy no earlier than
in three months, so contraception is advised and therapy for chronic endo-
metritis is started as endometritis always occurs upon expulsion of necrotized
chorionic villi, despite of the mode of evacuation of the collapsed gestational
sac (FIGO, 2006).
21.4. PRETERM BIRTH
Preterm termination of pregnancy is spontaneous termination of pregnancy from

22 to 36 weeks gestation.
According to the Helsinki Convention, a birth is considered preterm if it occurs
at gestational age 22–36 weeks delivering a fetus weighing 500–2500 g, with body
length 35–45 cm and signs of immaturity.
10% of all births around the world have a preterm termination, and 50–70% of
perinatal mortality cases are associated with immaturity-related complications.
Neonatal morbidity of preterm newborns is much higher than morbidity of
term newborns. Almost every third infant with cerebral paralysis was born pre-
term. In case of preterm fetus the prognosis depends on the gestational age and
body weight.
The main objective of care in case of incipient and actual preterm

NB! birth is to prolong the pregnancy so as to transfer the patient to
a facility of higher order (e.g., to a perinatal centre), and prevention
of fetal respiratory distress.
Up to 30% of preterm births occur after premature rupture of membranes. As a

rule amnion membranes undergo changes and then rupture due to their infection
with organisms form the vagina (ascending infection). The risk of fetal membrane
infection is higher in case of cervical incompetence.
ICD-10 codes
• O.60 Preterm labor and delivery.
• O.42 Premature rupture of membranes.
560 Obstetrics
Preterm birth is classified according to the gestational age:
• 22–27/6 weeks extreme preterm birth;
• 28–30/6 weeks very early preterm birth;
• 31–33/6 weeks early preterm birth;
• 34–36/6 weeks late preterm birth.
This division is associated with different management approach and different
outcomes for the fetus.
Termination of pregnancy at 22–27 weeks and delivery of extremely low
weight fetus (500–1000 g) accounts for 5% of all preterm births. The causes
of pregnancy termination at this gestational age are infection of the lower pole
of the gestational sac, cervical insufficiency with prolapse of the sac and its
preterm rupture.
Termination of pregnancy at 28–33 weeks (newborn’s weight 1000–1800 g) is
noted in 30–35% of cases. The causes are multiple. Prognosis for newborns in this
group is more favorable than in the preceding one. Preterm newborns require care
in intensive care settings equipped with modern technology.
Most commonly a preterm birth takes place at a gestational age 34–36 weeks
(60%). Causes are varied: preeclampsia, placental abruption, Rhesus incompatibility,
multifetality, polyhydramnios, maternal disease (diabetes mellitus, arterial hyperten-
sion) and other factors.
As to the mechanism of development, preterm births are classified into
• spontaneous;
• induced: performed for medical indications in the mother or fetus. Labor induction
is preformed irrespectively of the gestational age when there are conditions
threatening the woman’s health and life, or in case of fetal malformations.
As to the clinical course, we distinguish:
• threatened preterm birth;
• ongoing preterm birth.
21.4.3. Etiology
The etiology of preterm birth is complex and varied, which presents difficulty in
diagnostics, choice of management approach and prevention.
Besides causes of preterm birth identical to those at gestational age under 22 weeks,
the following risk factors are important:
• gestational sac infection (over 60% in the structure of causes);
• maternal extragenital disease (diabetes mellitus, arterial hypertension, renal
disease, endocrine disease, anemia, acute and chronic infection);
• obstetric complications:
– hemorrhage at early and late gestational age associated with placenta previa,
chorionic migration and detachment;
– PE;
– Rh- and AB0 incompatibility;
– placental insufficiency;
– hypoxia and FGR;
– abnormalities of fetal development;

– polyhydramnios or oligohydramnios;
– multiple pregnancy.
21.4.4. Prediction of preterm birth

When screening pregnant women it is important to single out those at risk for
pregnancy termination. Still more important are diagnostic procedures that can
determine the probability of realization of the worst scenario. Nowadays there are
several methods allowing prediction of preterm birth.
Estimation of cervical length. Estimation of the cervix length using transvaginal
sonography is a prognostically valuable tool. A shortened cervix detected by trans-
vaginal sonography is a significant prognostic criterion of preterm birth, even in
patients from low risk groups.
• At cervical length <25 mm one should resort to the entire range of diagnostic
methods;
• At cervical length <15 mm the risk of preterm birth before 32 weeks is 50%.
The main risk factor is preterm birth in past history. The main
NB! diagnostic criterion is cervical effacement to 25 mm and less.
Determination of vaginal pH. Increased pH of the vaginal medium, its alkalization

is a prognostic sign of preterm birth. Any express method can serve for verification
(test strips, special gloves or vaginal speculum with an indicator) (Fig. 21.12) as well
as laboratory findings supplementing the culture studies of the cervical contents and
contents of the posterior vaginal fornix. Culture tests are done to determine possible
infective agents and their sensitivity to antibiotics.
Fetal fibronectin is high molecular weight glycoprotein which is normally produced
by chorionic cells. Fibronectin is an extracellular matrix protein contributing to the
Fig. 21.12. Glove and vaginal speculum with an indicator to determine pH of vaginal discharge.
562 Obstetrics
process of fetal membrane attachment to uterine decidua. This protein passes to the
cervical canal and vaginal discharge in conditions of threatened abortion. No fetal
fibronectin in vaginal discharge at gestational age 22–35 weeks guarantees no preterm
birth within the next 14 days with 99.2% confidence. An alternative method deter-
mining the risk of preterm birth is a test for highly phosphorylated protein binding
the insulin-like growth factor, which is a decidual protein. When the chorion and
membrane separate, the decidual protein passes to the cervical canal.
On the whole, diagnostics of preterm birth per se is not difficult; it is based on
the pregnant woman’s presentations, findings of external and internal obstetric ex-
amination.
Despite the established risk factors and availability of a broad range of tocolytic
medications, the rate of preterm births all over the world remains quite high (an
average of 10%) and shows no tendency to decline.
Since there is no single pathogenetic factor for preterm birth, nor

NB! a clear understanding of its pathogenesis, no ethiopathogenetic
therapy is possible.
To date, the functional specifics of the cervix, 75% of whose morphology is rep-
resented by connective tissue, have not been fully estimated. We do not yet fully
understand the role of relaxin, the major pregnancy hormone (a polypeptide consist-
ing of A and B chains), and of its receptors in the pathogenesis of preterm birth; the
same refers to a number of proteins initiating cervical ripening in preterm pregnancy.
Thence the failure of all measures for prevention and treatment of preterm birth.
When coping with this problem the emphasis is on the preterm infant, both from the
medical and social point of view, on the choice of obstetric institution and methods
of rational management of preterm birth, care for preterm infants and prevention of
postnatal complications.
21.4.5. Clinical features and diagnostics

Threatened preterm birth presents with lumbar and lower abdominal pain. The
excitability and tone of uterus are elevated. Transvaginal sonography shows the
cervix less than 25 mm; the probability of labor onset is much greater at cervical
length <15 mm.
An accessory important prognostic criterion of preterm birth is determining fetal
fibronectin in vaginal discharge. Ultrasound cervicometry combined with fetal fibro-
nectin findings improves the prognostic value. A vaginal examination shows an intact
cervix and closed external os. In secundipara it can accommodate a fingertip. The
fetus may show elevated motor activity. The presenting fetal part is low or pressed
to the pelvic inlet.
A pregnant woman classified at risk for preterm birth should see a doctor im-
mediately in case of
• low abdominal or lumbar pain (nagging or cramp-like pain), sensation of
pressure;
• more frequent urination episodes;
• change in the quantity, coloration or odor of vaginal discharge;

• local tenderness of the uterus;
• weaker or stronger fetal movements.
When preterm birth is in progress, contractions in the lower abdomen are noted.
Transvaginal sonography shows a cervix shorter than 15 mm. A vaginal examination
also shows a shorter cervix, often its effacement (latent phase of labor).
Diagnostics of preterm birth is not complicated; it is based on presentations, ul-
trasound findings and the data of external and internal obstetric examination.
Laboratory testing is of major significance when there is

NB! suspicion of amniotic fluid leaking.
Elements of amniotic fluid are determined in native smear.

The test for placental α1-microglobulin (PAMG-1) in vaginal discharge is more
sensitive. Amniotic fluid leakage is also diagnosed by the test for protein-1 binding
insulin-like growth factor (IGFBR-1) in the cervical canal.
Ultrasound helps to monitor the index of amniotic fluid.
The course of preterm birth has some specific features. They encompass
• premature membrane rupture (30–40%);
• labor abnormalities (inertia, dystocia);
• accelerated or precipitated labor in presence of cervical incompetence, or
protracted labor due to unripe cervix, neuroendocrine regulation mechanisms
not ready;
• fetal hypoxia;
• antepartum hemorrhage resulting from detachment of low-lying or normally
located placenta;
• hemorrhage in the third stage of labor and early postpartum period due to labor
abnormalities or retention of placenta fragments;
• infectious complications during labor (chorioamnionitis) and postpartum period
(endometritis, phlebitis, etc.).
21.4.6. Treatment. Clinical management of preterm birth

To date, there is not a single medication in the world whose pregnancy-prolong-
ing effect can bear scrutiny from the point of view of evidence-based medicine.
Effectiveness of bed rest, any forms of spasmolytic drugs, lymphocytotherapy lacks
evidence. The attitude to routine administration of progesterone and prednisolone
drugs has now changed.
Depending on the situation, the approach to preterm pregnancy is expectant
conservative (prolongation of pregnancy) or active.
• Expectant conservative approach is indicated in case of threatened and ongoing
preterm delivery, unless pregnancy prolongation is contraindicated.
• Active approach to management to the extent of emergency abdominal delivery
is indicated upon premature placental separation, eclampsia, acute fetal hypoxia
and other severe obstetric complications threatening maternal and/or fetal life,
decompensation of severe extragenital diseases.
564 Obstetrics
Complex management of threatened and ongoing birth is based on the following

principles.
• Bed rest or semi-bed rest (there is no evidence that bed rest reduces the risk of
premature birth).
• Acute tocolysis with drugs reducing the contractile activity of the myometrium
(tocolytics):
– atosiban (oxytocin receptor inhibitor);
– β2-adrenomimetics fenoterol (Partusisten), terbutalin (Bricanyl), hexopren-
alin (Ginipral), ritodrine (USA) and others;
– calcium channel blockers nifedipine, verapamil (Isoptin, Finoptin);
– prostaglandin synthetase inhibitors: indomethacin and others.
• Fetal RDS prevention with glucocorticoids:
– betamethasone 12 mg once or dexamethasone 6 mg twice a day for 2 days
(48 h). The total glucocorticoid dose is 24 mg.
• Prevention of cerebral abnormalities in fetus.
• Antibiotic prevention of chorioamnionitis and endometritis upon premature
rupture of membranes. Broad-spectrum drugs are administered. If studies of the
species composition of vaginal flora were conducted, laboratory findings serve as
guidance (sensitivity to antibiotics).
21.4.6.1. Tocolysis
β2-adrenomimetics are first-line tocolytic drugs in the treatment of threatened
premature birth. Their effectiveness is 86%; however, these drugs produce a range of
adverse effects dangerous for the mother (pulmonary edema, hyperglycemia, hypoka-
liemia, arterial hypotension, arrhythmia, myocardial ischemia), fetus and newborn.
These drugs act through β2-adrenergic receptors that emerge after 25 weeks
gestation (at 26–27 weeks), so their administration before this gestational age is
not expedient.
For the purpose of tocolysis β2-adrenomimetics are administered via IV droplet
infusion starting at 6–8 drops per minute gradually increasing the rate of infusion
to 15–20 drops per minute.
Clinical controlled studies indicate that β2-adrenomimetics (Ginipral) reduce the
percentage of deliveries occurring within 24 hours and within 48 hours after the start
of therapy.
When administering β2-adrenoreceptor agonists one should monitor
NB! the woman’s heartbeat, respiratory rate, fluid balance (especially
upon IV droplet infusion), fetal condition and uterine contractions.
Contraindications for β2-adrenomimetics administration: thyrotoxicosis, diabetes
mellitus, cardiovascular disease, bronchial asthma, intrauterine infection, polyhy-
dramnios, premature separation of normally located placenta or of placenta previa,
disorder of fetal cardiac rhythm.
When administering calcium channel blockers one should monitor
NB! the BP (arterial hypotension is a possibility), fetal condition and
uterine contractions.
Calcium channel blockers

The tocolytic effect of nifedipine is based on blocking calcium channels (in
Western obstetrics this is the first-line drug in management of threatened premature
birth). Its effectiveness is as high as that of β2-adrenomimetics; its advantage is less
adverse effects. Nifedipine is administered at a dose of 10–20 mg sub linguam thrice
a day.
Atosiban
Atosiban is a first-line drug but its mechanism of action is based on different
principles. It inhibits oxytocin receptors. Its administration is justified when uterine
contractions have been registered and cervical dilation is less than 4 cm, as well as
in patients with amniotic fluid leakage at gestational age 23–30 weeks. Its effect is
comparable to the effect of β2-adrenomimetics. No adverse effects of this drug have
been registered.
Magnesium sulfate
The tocolytic effect of magnesium sulfate (although it was not registered as a to-
colysis drug) is based on its assumed but not proven competition with calcium ions.
Magnesium is not a tocolytic agent, but its effectiveness is 67%; it is cheap and pro-
duces less adverse effects on the mother and fetus so it is widely used. Its beneficial
effect can be attributed to hyperdiagnostics of threatened premature birth (which
amounts to 90%): abdominal pain raises alarm in obstetricians and patients, which
leads to unjustified hospitalization and polypragmasia (Fatkullin I.F., 2014). 25%
solution of magnesium sulfate (10–20 g of dry substance) is administered in therapy
of threatened premature birth due to its proven ability to reduce the rate of cerebral
disorders in the fetus. The solution is introduced with an infusion pump (Fig. 21.13),
Fig. 21.13. Infusion pump

566 Obstetrics
the rate of infusion is determined by the safe dose of the drug, 1–2 g/h. Magnesium
sulfate can be also administered in 5% glucose (dextrose) solution intravenously, by
droplet infusion, rate of infusion 1–2 g/h.
Contraindications for magnesium sulfate administration: disorder of intracardiac
conductivity, myasthenia, severe cardiac insufficiency, chronic renal failure.
When administering magnesium sulfate one should monitor the

NB! diuresis (no less than 30 ml/h), BP, patellar reflex, respiratory rate,
fetal condition and uterine contractions, check the fluid balance
every 2 – 4 hours, and test the content of magnesium in peripheral
blood.
Prostaglandin synthetase inhibitors

The mechanism of tocolytic effect of indomethacine is based on blocking prosta-
glandin synthesis; the effectiveness is 72%. The total dose should not exceed 1000 mg,
the length of therapy—no more than 5 days. Indomethacine is administered at ges-
tational age 16–31 weeks.
Specifics of prostaglandin synthetase inhibitors (indomethacin) administration for
tocolysis.
• Indomethacin is only administered if the gestational age is below 32 weeks, and
the amniotic fluid volume is within normal. The initial dose is 100 mg per rectum
or 50 mg per os. If ineffective, the dose is repeated in an hour.
• The drug is administered at a dose of 25–50 mg every 4–6 h for 48 h.
• Prior to initiating tocolysis, one determines the volume of amniotic fluid; the
study is repeated in 48–72 h. In case of oligohydramnios the drug is discontinued
or the dose is reduced.
The therapy can be repeated after a 5-day interval, if needed. Therapy should be
discontinued if signs of threatened preterm birth increase progressively.
Fetal contraindications for indomethacin: growth restriction, kidney malforma-
tions, chorioamnionitis, oligohydramnios, cardiac malformations involving the pul-
monary trunk and transfusion syndrome in multifetality.
When administering indomethacin therapy one should check the blood flow in
the pulmonary trunk and assess the expression of regurgitation at the tricuspid valve.
The investigation is repeated no less than once a week; if the shunting decreases,
therapy is discontinued. The amniotic fluid volume should be assessed twice a week.
It is not recommended to combine tocolytic medications when

NB! managing a threatened preterm birth.
Tocolysis is contraindicated in case of

• intrauterine infection or suggestion of one;
• polyhydramnios;
• bloody discharge in placenta previa;
• premature detachment of normally situated placenta;
• disorder of fetal cardiac rhythm;
• fetal teratomorph;
• antenatal fetal demise;

• suspicion of uterine scar incompetence;
• cervical dilation 4 cm and more.
21.4.6.2. Prevention of respiratory distress syndrome

When threatened preterm birth occurs, one should provide prevention of newborn
RDS. The patient receives glucocorticoids which promote surfactant synthesis and
accelerate the maturation of fetal lungs. RDS prevention is provided at gestational
age of full 23–43 weeks. The cycle of treatment requires 24 mg of betamethasone
or dexamethasone. Betamethasone 12 mg once a day or dexamethasone 6 mg twice
a day for 2 days (48 h).
The most pronounced favorable effect was noted in infants born no sooner than
24 hours after the onset of betamethasone therapy, and 48 hours—after dexametha-
sone therapy.
Glucocorticoids are contraindicated in chorioamnionitis, ulcerative stomach and
duodenum disease, diabetes mellitus, severe PE or severe arterial hypertension, en-
docarditis, acute pyelonephritis.
21.4.6.3. Prevention of intraventricular hemorrhage of the newborn

Effect of administering Phenobarbital and vitamin K to parturient women in
ongoing preterm labor was studied as a means of preventing intraventricular hemor-
rhage of the newborn. The obtained data provide sufficient evidence to regard both
methods effective enough. Magnesium sulfate exerts a more beneficial effect as a
neuroprotector for the fetus.
21.4.6.4. Preterm premature rupture of membranes (pPROM)

Premature rupture of membranes is noted in 30–40% of patients with preterm
birth. If premature rupture of membranes occurs at 23–34 weeks gestation, the
mother and fetus feeling well, there are no signs of infection or severe obstetric
complications and/or extragenital diseases, one should adopt conservative expectant
approach.
Prolongation of the period after membranes rupture promotes maturation of fetal
lungs, progressing of pregnancy and thus — advance of the gestational age.
One of the likeliest causes of PROM is intrauterine infection or infection ascend-
ing from the cervical canal. It is obligatory to perform a culture test of cervical and
vaginal contents immediately after amniotic sac rupture.
Management of pregnant women should be approached in a differentiated manner.
Conservative management requires the following conditions to be met:
• daily change of underwear;
• change of sterile drawsheets 3–4 times a day or as they become dirty;
• evaluation of the mother’s condition (daily measuring the abdominal
circumference, fundal height, the nature and quantity of passing amniotic fluid,
thermometry and other) and fetus (respiratory movements and motor activity);
• ultrasound evaluation of amniotic fluid;
• daily WBC count and hemogram of the mother;
• vaginal discharge culture for flora and sensitivity to antibiotics every 5 days;
568 Obstetrics
• preventive correction of vaginal biocenosis and stimulation of its population by

lactobacilli (prevention of constipation);
• giving up vaginal examinations.
Preventive administration of antibiotics leads to statistically significant reduction
in the risk of maternal and fetal infection within the first week after premature
membrane rupture. On the other hand, controlled clinical studies showed no effect
of preventive antibiotics administration on perinatal mortality.
Premature rupture of membranes can lead to other complications: compression
or prolapse of the cord, fetal lung malformation or hypoplasia (if the period of pro-
nounced oligohydramnios extends). The benefit of amnioinfusion upon premature
membrane rupture has not been studied well enough.
Administration of tocolysis before the onset of labor after premature membrane
rupture remains disputable.
Active management of pregnancy, labor induction after premature membrane
rupture impair the outcomes for the fetus even if glucocorticoids were administered
for RDS prevention.
Absolute contraindications for conservative expectant management upon pPROM:
• unfavorable fetal lie (oblique, transverse);
• placenta previa and placental abruption;
• chorioamnionitis;
• acute fetal hypoxia;
• grave maternal condition.
Indications for delivery in prolonged premature membrane rupture:
• signs of infection: latent (leucocytosis or left shift, pathological microflora in the
cervical canal) or apparent (elevated body temperature, passing of turbid foul-
smelling fluid from the vagina);
• signs of fetal distress by findings of functional tests;
• gestational age over 34 weeks;
• decrease in amniotic fluid index.
Emerging signs of infection require an alteration of antibacterial

NB! therapy, and a delivery.
Broad-spectrum antibiotics are administered.

Antibiotic therapy prior to delivery permits a 5-fold reduction in newborn mortality
form sepsis compared with postnatal treatment.
21.4.6.5. Management of preterm labor

Management of preterm birth is determined individually depending on the gesta-
tional age, maternal and fetal condition, the particular obstetric situation.
Cesarean section performed at 22–26 weeks gestation does not reduce perinatal
mortality and grave morbidity of newborns, irrespective of fetal presentation. After 26
and till 34 weeks gestation cesarean section significantly improves perinatal outcomes.
Abdominal delivery at preterm pregnancy has some specific features. The lower uter-
ine segment of great thickness prior to labor onset implies difficulty in fetus extraction.
Some authors recommend a vertical incision, but no controlled studies were conducted.
The objective in cesarean section is to ensure a free, gentle

NB! delivery of fetal head; this can be achieved by extracting the fetus
en caul through a sufficiently large incision.
The apparently «easy» cesarean section can be complicated by a difficult extrac-
tion traumatic for the premature fetus. Extraction of fetus with intact membranes
(en caul) (Radzinsky V.E., 2007; Fatkullin F.I., 2010) for hydrostatic protection from
frequent natal trauma, and even extraction with the placenta (Bashmakova N.V.,
2014) to preserve the warmth continuity allows a rapid extraction and transfer of the
fetus under the source of radiant heat where the membranes are opened (Fig. 21.14).
Preserving the warmth continuity is beneficial for the premature newborn reducing
the need for resuscitation procedures and their length.
Despite the lack of systematic reports of controlled studies, this technology is win-
ning more supporters in this country, especially in perinatal centers, when extracting
preterm and low weight infants of multifetal pregnancy.
а b
с d
Fig. 21.14. En caul delivery at preterm cesarean section: a — preterm birth, twins
(Radzinsky V.E., Moscow, 2009); b — preterm birth (Fatkullin I.F., Fatkullin F.I., Kazan,
2010); c — preterm birth, triplets (Sudakov A.G., Blagoveshchensk, 2010); d — preterm birth,
quadruplets (Yevtushenko I.D., Tomsk, 2015)
570 Obstetrics
If a vaginal delivery is decided upon, one should closely monitor fetal well-being,
cervical dilation, the nature of labor, head engagement.
In the first stage of labor analgesia should be administered, the method of choice
is epidural nerve block.
Even when labor is regular, one should preferably continue the

NB! administration of tocolytics (intranatal tocolysis) so as to prevent
precipitate labor and to boost uteroplacental circulation.
Preterm birth requires continuous fetal heart monitoring and filling in a par-
togram as anomalies of labor are a common complication in preterm deliveries.
Uterine hyperactivity and accelerated cervical dilation is most traumatic for the
preterm fetus. In addition, analgesia may not produce the desired effect of slow-
ing down the labor. In these cases intravenous tocolysis with β2-adrenomimetics is
administered. The rate and mode of drug administration is the same as when man-
aging threatened preterm birth. In case of uterine inertia one can remain expectant
(no treatment) for 5–6 hours, and then start a slow administration of uterotonic
drugs. Administration of agents contracting the uterus is discontinued as soon as
regular labor has been achieved.
In preterm birth obstetric maneuvers are not resorted to as there

NB! is a high risk for fetal injury.
In case of pelvic presentation no obstetric maneuvers are performed either.

Epidural block is effective in eliminating preterm pushing and reducing the pelvic
floor muscle resistance.
To prevent hemorrhage at the moment of crowning, oxyctocin is administered in-
travenously. A neonatologist should be present at the delivery. The air in the delivery
room should be warm. The newborn is quickly put into a couveuse.
A preterm infant has signs of prematurity:
• body weight under 2500 g;
• length under 45 cm;
• a lot of vernix caseosa on the body;
• subcutaneous tissue is not well developed;
• the entire body covered with lanugo hairs;
• hair on the head not very long;
• soft ear and nose cartilage;
• nails do not surface above fingertips;
• umbilical ring located nearer to the pubis;
• boys’ testicles undescended, girls’ clitoris and labia minora not covered with labia
majora;
• thin squeaky cry.
The neonate’s respiratory function is assessed using Silverman score. Preterm in-
fants have frequent asphyxia attacks; respiratory failure is a common development as
well as respiratory distress syndrome (hyaline membrane disease), thermoregulation
disorder, hyperbilirubinemia. The newborns have a tendency for infections.
Preterm infants, especially those with very low and extremely low weight, hold
the first place in the structure of perinatal mortality. Neonatal morbidity of preterm
infants amounts to 800–900‰. Prematurely born infants are classified at high risk
for disability.
Newborns of greater weight and gestational age have a better

NB! prognosis.
21.4.7. Prevention of premature birth

Patients with premature termination of pregnancy in past history need specialized
care. For this purpose the following is done:
• regular medical check-ups of women with habitual miscarriage;
• specialized investigations outside of pregnancy to detect the causes of spontaneous
abortion;
• determining the risk for miscarriage, developing a complex of therapeutic
and preventive procedures and management of the present pregnancy with
consideration to the risk;
• rehabilitation of patients with habitual miscarriage and pregravid preparation
(meaningful empirical data in favor of its effectiveness are lacking).
REMEMBER!
Definition Miscarriage is a spontaneous termination of pregnancy at

various gestational ages before 22 weeks. Preterm birth is
spontaneous termination of pregnancy at various gesta-
tional ages before full 37 weeks counting from the first day
of the last menstrual period
Etiology Factors:
• genetic;
• anatomical;
• endocrine;
• immune;
• infectious
Classification Before 22 weeks:

• incipient abortion;
• abortion in progress;
• incomplete abortion;
• complete abortion;
• septic abortion.
In case of embryo/fetus demise the condition is termed
missed abortion. From 22 to 37 weeks:
• threatened preterm birth;
• ongoing preterm birth
572 Obstetrics
Diagnostics Presentations (pain, vaginal bleeding before 22 weeks ges-

tation).
• Measuring basal temperature (before 22 weeks gestation)
• B-hCG test
• Ultrasound cervicometry
• Estimation of cervical incompetence signs
• Tocography (in late pregnancy)
• Test for fetal fibronectin in vaginal contents or other
markers of preterm birth
Treatment • Physical and sexual rest

• Surgery if cervical incompetence is present, or obstetric
pessary
• Tocolysis if threatened preterm birth
• Prevention of fetal RDS
Complications Fetal/embryonic demise, hemorrhage, chorioamnionitis,

endometritis, septic condition, preterm infant delivery
CONTROL QUESTIONS:
1. What is referred to as habitual abortion?

2. What is early miscarriage?
3. What is late miscarriage?
4. What birth is referred to as preterm?
5. What complications are typical of preterm birth?
6. What are the specific features of preterm neonates?
7. What are the principles of therapy of preterm birth?
8. Algorithm of management of preterm birth upon rupture of membranes.
9. What is intranatal tocolysis?
CHECK YOUSELF!
Level 1. Test
1. Signs of threatened abortion:
a) bloody discharge;
b) low lying chorion;
c) pressure sensation in the lower abdomen;
d) shortened cervix.
2. Signs of abortion in progress:

a) bloody discharge;
b) low lying chorion;
c) pressure sensation in the lower abdomen;
d) shortened cervix.
3. Missed abortion is:

a) no embryo in the gestational sac;
b) no cardiac activity in the embryo;
c) no cardiac activity in the fetus;
d) restricted fetal growth.
4. The most common causes of early miscarriage:

a) endocrinopathy;
b) genetic abnormalities;
c) genital infection;
d) somatic disease.
5. Diagnosis of missed abortion is based on:

a) patient’s presentations;
b) laboratory findings;
c) ultrasound findings;
d) no change in uterine growth.
6. Preterm birth occurs at a gestational age:

a) before 28 weeks;
b) before 37 weeks;
c) before 23 weeks;
d) before 20 weeks.
7. Tocolytic drugs are:

a) oxytocin;
b) methylergometrin;
c) Atosiban;
d) Ginipral.
8. Preterm infant’s body weight is less than:

a) 500 g;
b) 1000 g;
c) 2000 g;
d) 2500 g.

1. Patient N with pregnancy 7 weeks gestation had an ultrasound; the uterine
cavity has a gestational sac, no embryocomplex. What is your diagnosis? What is
the plan of management?
2. Pregnant patient A at 18 weeks gestation shows cervical shortening to
1.5 cm, cervical dilation 20 mm. What is your diagnosis? What is the plan of
management?
• Chapter 22
PREGNANCY, LABOR AND POSTPARTUM
PERIOD IN WOMEN WITH EXTRAGENITAL
DISEASES
Starting at puberty female morbidity grows to reach 82% of accumulated dis-

ease by early adulthood. Nowadays childhood and adolescence is the time when
young people start experimenting with psychoactive substances, alcohol, smok-
ing. Unreasonable reproductive behavior aggravates the situation: the mean age
to start sex life is 15.9 in girls; almost 40% of them have their first abortion at
the age 16–17. These negative phenomena reduce the reproductive potential of
teenage girls.
Among young women with childbirth ahead of them, 42% are anemic, 21% have
chronic pyelonephritis, 11% — hypertonic disease, etc.
Smoking and alcohol abuse by ailing women aggravate the systemic changes in
the body during pregnancy.
These factors of ill health combined with reproductive disorders (first abortion
sequelae, gynecologic disease, etc.) produce a population at high obstetric and peri-
natal risk, that is, at high risk for maternal and perinatal morbidity and mortality.
In advanced countries maternal mortality from extragenital disease holds the first
or second place.
This burden can be reduced by promoting women’s health prior to and during
pregnancy, which is the objective of physicians in all specialities, first of all in the
field of therapy, cardiology, cardiosurgery, nephrology, hematology. In case of a so-
matic or infectious disease the physician (perinatal consilium) should consider the
possibility of carrying the pregnancy to term, methods of treating the main condition
and providing early diagnostics of fetoplacental insufficiency that develops in virtually
all unhealthy women.
Prevention of obstetric and perinatal complications in unhealthy pregnant women
is the major objective confronting the entire health care system. The objective of
obstetrics is to prevent obstetric and perinatal complications in unhealthy women
considering the specifics of the extragenital condition.
Anemia should be treated by therapists and hematologists. Hypertonic disease —
by therapists and cardiologists, pyelonephritis — by therapists and urologists, and so
on. In uncomplicated cases the care can be provided by general practitioners where
they are available. An obstetrician is not supposed to treat cardiac defects and related
circulatory disorders, but (s)he should understand the pathogenesis of these condi-
tions and, most importantly, the pathogenesis of gestational complications, clinical
presentations and methods of diagnostics, critical periods for timely prevention of
conditions threatening the pregnant woman, fetus and newborn.
Chapter 22. Pregnancy, labor and postpartum period in women with... 575
22.1. BLOOD DISORDERS AND PREGNANCY
22.1.1. Anemia in pregnancy

Anemia in pregnancy means anemia developing during pregnancy (mostly in the
second or third trimester) as the enhanced demands of the maternal and fetal body
for substances necessary for hemopoiesis cannot be met adequately. ICD-10 code is
O99.0 Anemia complicating pregnancy, childbirth and the puerperium.
22.1.1.1. Epidemiology
The incidence rate of anemia determined by reduced hemoglobin in the blood
using the WHO standard varies within the range 21–80% in different regions of the
world. Anemia develops in patients with rheumatism, diabetes mellitus, gastrointes-
tinal tract diseases, renal disease and infections.
75 – 90% of anemias in pregnancy are accounted for by iron

NB! deficiency anemia; other varieties of anemia are noted much less
often.
According to its severity, the disease is classified in the following way (WHO, 1992;
Ministry for Public Health of Russian Federation, 2005):
• mild anemia: Hb 109–70 g/l, RBCs 3.9–2.5×1012 g/l, hematocrit 37–24%;
• moderate anemia: Hb 69–40 g/l, RBCs 2.5–1.5×1012 g/l, hematocrit 23–13%;
• severe anemia: Hb below 40 g/l, RBCs 1.5×1012 g/l, hematocrit below 13%
(Table 22.1).
Two types of anemia are distinguished: anemia diagnosed during pregnancy and
anemia existing prior to pregnancy. The first type is noted more often.
Anemia is also divided into acquired (deficiency of iron, protein, folic acid) and
congenital (sickle cell anemia).
22.1.1.3. Etiology
Iron and protein deficiency anemia is a condition at which the content of iron
in the blood serum, bone marrow and blood pool is dramatically reduced due to its
insufficient intake and protein deficiency in the body.
Anemia of pregnancy is the result of multiple causes including those related
to pregnancy: high estrogen level, early toxicosis interfering with absorption
Table 22.1. Anemia classification (WHO, 1992; Ministry for Public Health of Russian
Federation, 2005)
Anemia, degree Hb, g/l RBCs, ×1012 Hematocrit, %
Mild 109–70 3.9–2.5 37–24
Moderate 69–40 2.5–1.5 23–13
Severe <40 <1.5 <13
576 Obstetrics
of iron, phosphorus and magnesium needed for hemopoiesis, physiological

hemodilution.
Risk factors for anemia of pregnancy:
• unbalanced diet and insufficient intake of iron, vitamins, folic acid, micronutrients
in the meals;
• anemia in past history;
• short intervals between pregnancies;
• prolonged breastfeeding;
• blood loss in past history;
• chronic infection;
• chronic gastrointestinal disease;
• occupational and environmental hazards;
• chronic intoxication, including heavy metal salts.
Food is the natural source of iron. A pregnant woman’s daily requirement for iron
is 1300 mg; of these, 300 mg are needed for the fetus.
In most pregnant women at 28 – 30 weeks gestation a moderate

NB! anemia is associated with predominant rise of circulating blood
plasma in relation to the corpuscular volume. The content of RBCs
and hemoglobin declines (physiological dilution, polycythemic
dilution).
Such changes in blood composition do not compromise the pregnant woman’s

condition or well-being.
If the intake of iron is not sufficient or it is not adequately assimilated by the
body, the woman develops an iron deficiency anemia with Hb level under 110 g/l.
During pregnancy the body undergoes changes that promote anemia develop-
ment:
• enhanced expenditure of iron by maternal body which is necessary for appropriate
fetal development;
• elevated estriol content which suppresses erythropoiesis;
• accumulation of intermediary metabolic waste that has a toxic effect on the bone
marrow;
• sideropenia (iron shortage in the body);
• deficiency of vitamin B12, folic acid and protein;
• oxygen deprivation that disrupts the oxidation and reduction processes in the
pregnant woman’s body.
Iron deficiency disrupts hemopoiesis, metabolism and tissue respiration. Anemia
triggers circulatory, hemic and tissue hypoxia leading to functional and structural
changes in all organs and tissues. The regenerating tissue — epithelium of the skin,
respiratory and digestive systems, the immune system and the brain as well as the
reproductive system—are impaired most severely. The degree of disease and clinical
presentations are determined by the expression of anemia rather than by the time of
its onset (Fig. 22.1).
Iron deficiency anemia is characterized not only by hemoglobin shortage but also
by disorder of protein metabolism: hypoalbuminemia in case of mild degree of the
disease, and hyporpoteinemia in case of severe degree of the disease.
22.1.1.5. Gestational complications

Due to anemic angiopathy, a pregnant woman with anemia in the first trimester
shows disturbance of placental bed formation, primary fetoplacental insufficiency.
Fetoplacental insufficiency mediates hypoplasia of the chorion and amnion, anoma-
lies of placentation, placental separation, threatened abortion and missed abortion.
In the second and third trimesters circulatory and hemic hypoxia due to disturbed
uteroplacemntal circulation and fetoplacental insufficiency can give rise to preterm
termination of pregnancy including preterm birth (11–40%), fetal growth restriction
and fetal hypoxia, placental abruption and PE (40–50%), mostly the edematous-
proteinuric form.
If there are no obstetric complications, vaginal delivery is a possibility. Uterine
inertia is noted in 10–15% of parturient women, hemorrhage in the third stage of
labor and in early postpartum period — in 10%. In 12% puerperas the postpartum
period is complicated by puruloseptic conditions, in 38% — by hypogalactia. Early
placental insufficiency increases the risk for hypotrophy signs in infants. Up to 29%
of neonates are born asphyxiated. High perinatal mortality is only associated with
severe disease. Severe anemia increases perinatal losses to 140–150‰, and neonatal
mortality — to 1000‰.
NB! Anemia that preceded pregnancy is most unfavorable.
Iron deficiency
Disturbed Disturbed Disturbed

tissue
hemopoiesis metabolism respiration
Tissue Hemic Circulatory

hypoxia hypoxia hypoxia
Functional and morphological changes

in organs and tissues
Fig. 22.1. Pathogenesis of abnormal change in anemia

578 Obstetrics
22.1.1.6. Pathogenesis of pregnancy complications
Hypoxia of maternal tissues and utero-feto-placental complex, deficiency of pro-
tein and iron-containing enzymes underlie the emergence and development of preg-
nancy complications. Hemic and circulatory hypoxia compromises the function of
all organs and systems in the mother’s body, which increases the risk of pregnancy
complications.
In conditions of anemia pregnancy develops in inadequate endometrium with
developing insufficiency of the placental bed, chorion and utero-feto-placental cir-
culation.
In the third trimester insufficient vascularization leads to structural and func-
tional changes in the endometrium: decidual transformation lingers at the stage of
intermediate-type loose decidual cells in the subepithelial zone and around spiral
arteries; pronounced edema and fibrosis of the stroma is predominant; diapedetic
hemorrhages and hemosiderosis are noted; inflammatory infiltration of the endo-
metrium is a possibility. All these changes lead to superficial implantation of the
gestational sac. The chorion and early placenta show disturbance of chorionic villi
development, hypoplasia of the placenta. Insufficiency of the first wave of trophoblast
invasion develops, which leads to embryo demise, missed abortion, preterm birth.
In the second trimester gestational transformation of spiral arteries is lacking. In
the area of basal membrane, in the fetal portion of the placenta, fibrinoid is laid in
the intervillous space, which seals a portion of the villi. The vascular link of placental
barrier becomes disturbed followed by a spasm of arterioles and capillary sphincters.
Spiral, and then utero-placental arteries show pronounced angiopathy leading to less
elasticity and reduction in diameter, decrease in nitric oxide production: insufficiency
of the second wave of invasion. If the pregnancy was not terminated in the first trimes-
ter, it is terminated or complicated in the second trimester. Upon anemia develop-
ment in the second trimester the complications of gestation are also mediated by the
hypoxia syndrome, but they develop later. Fetoplacental insufficiency is, as a rule,
of secondary nature; it leads to chronic hypoxia, FGR, preterm birth (Fig. 22.2).
а b
Fig. 22.2. Placental bed in severe anemia: a — active invasion of multinucleate giant cells
and villous cytotrophoblast in the endometrium and myometrium, hematoxylin and eosin
staining, ×150; b — lack of second wave of invasion in the myometrium, presence of single
multinucleate giant cells, hematoxylin and eosin staining, ×300
Inadequate immune defense due to pregnancy and hypoxia secondary to anemia

result in immunodeficiency and a high rate of infections in the pregnant, puerperant
women, puerperas and newborns (Fig. 22.3).
Tissue hypoxia, deficiency of protein

and iron-containing enzymes
First
trimester
Disturbed Disorder
Structural
Superficial development of the first wave
and functional
implantation of chorionic villi, Embryo demise
changes of cytotrophoblast
of ovum placental invasion
in endometrium
hypoplasia
Pregnancy loss
Angiopathy Fetoplacental
of spiral uterine Disorder of the second wave
insufficiency,
and uteroplacental arteries of cytotrophoblast invasion
IUGR, fetal hypoxia
Second
Preterm birth
and third
trimester
Compromised immunity Infectious
complication
Fig. 22.3. Pathogenesis of pregnancy complications in anemia
In the presence of anemia hemorrhage is especially threatening during labor and

in the puerperium; even a physiological blood loss can be followed by hemorrhagic
shock.

Clinical features are a combination of signs associated with hemoglobin insuf-
ficiency and caused by deficiency of iron-containing enzymes.
Signs associated with hemoglobin deficiency are due to a low supply of oxygen to
tissues; they are present in anemia of any other origin:
• weakness;
• dizziness;
• headache;
• palpitations;
• shortness of breath;
• fainting spells;
• lethargy;
• insomnia.
Presentations typical of iron deficiency anemia (however, not inevitable) are as
follows:
• pica chlorotica;
• massive hair loss, brittle nails;
• difficult passage of food along the esophagus (dysphagia);
• urine incontinence;
• pallor and dryness of skin and mucosas;
580 Obstetrics
• bluish sclerae;
• subicteric coloration of the sclerae, nasolabial triangle, palms;
• thinning of the nails;
• swelling;
• angular stomatitis;
• glossitis;
• abnormal skin pigmentation;
• abdominal bloating, tenderness to palpation of stomach, small and large
intestine;
• loose stools;
• burning an itching of the vulva.
Presentations typical of anemic syndrome:
• shortness of breath upon the slightest exercise;
• heart murmurs;
• tachycardia;
• orthostatic hypotension;
• emergence / more common occurrence of angina attacks.
In moderate anemia the pregnant woman may present no complaints; the condi-
tion is only revealed by laboratory methods. Clinical signs are noticeable in moderate
anemia.
When taking the history one notes risk factors for the development of iron defi-
ciency anemia:
• subsequent pregnancy and childbirth at a short interval, prolonged breastfeeding;
• gynecological disease accompanied by chronic blood loss: endometriosis,
myoma of uterus, etc.;
• diseases manifesting as chronic nosebleed: idiopathic thrombocytopenic
purpura, thrombocytopathy, Rendu-Osler disease (hereditary hemorrhagic
teleangiectasia);
• renal diseases: pyelonephritis, glomerulonephritis, urolithiasis;
• vegetarianism;
• chronic infection.
Indications for hematologist consultation:
• severe anemia;
• no effect of antianemic therapy, or progressing of anemia;
• signs of aplastic or hemolytic anemia;
• onset of hemorrhagic syndrome manifestations.
A gastroenterologist consultation is required if the patient has gastrointestinal tract
conditions.
Laboratory and instrumental methods. Laboratory investigations, and clinical blood
count first of all, are an important tool in diagnostics of anemia and in determining
upon the plan of management.
The basis of diagnosis in iron deficiency anemia is isolated decline of hemo-
globin content in the complete blood count. Diagnostic criteria are decreased
hemoglobin in complete blood count (<110 g/l), decreased ferritin in the blood
serum (<40 mg/dl). Findings may encompass decreased mean cell volume, de-
creased hemoglobin content in the RBC (microcytosis).
Signs of iron deficiency anemia in a complete blood count (clinical guide Blood
Saving Technology in Obstetric Practice, Moscow, 2014):
• decreased color index which reflects the hemoglobin content in a RBC; it serves
as a calculated value;
• decreased mean corpuscular volume (normal value 80–95 fl);
• decreased hemoglobin content in the RBC (normal value 27–31pg);
• decreased reticulocyte count.
One also makes tests for:
• iron content in the blood serum: the iron content is decreased (normal findings
are within the range of 12–25 mcmol/l);
• the total iron bonding capacity of serum. A difference between the values of total
iron binding capacity of serum and serum molecular iron indicates the latent iron
binding capacity; its normal value is 30–85 mcmol/l;
• ferritin in blood serum is a protein iron-containing complex serving for storing
iron in tissues; its decrease is a typical laboratory sign of iron deficiency (normal
value 12–300 mcg/l);
• transferrin (normal value 23–45 mcmol/l);
• transferrin saturation with iron (normal value 16–45%).
NB! To find the index of soluble transferrin receptor and ferritin ratio
is a new strategy in diagnosing iron deficiency anemia.
In hypochromic anemia the presence of iron deficiency anemia is confirmed by

the following findings:
• decreased serum iron (<12–25 mcmol/l);
• elevated total iron-binding capacity of blood serum (>30–85 mcmol/l);
• decreased ferritin in blood serum (<15–150 mcg/l);
• elevated latent iron-binding capacity of blood serum;
• decreased transferrin saturation with iron (<16–50%). It is noteworthy that
the quality of laboratory diagnostics depends on the way the blood sample was
obtained and on complying with the diagnostic protocol. The obtained fi ndings
do not show true values if the investigation was made:
• while the patient received iron supplements (diagnostics should be made prior to
therapy initiation or no earlier than 7 days upon its completion, except for tests
for blood transferrin);
• after transfusion of packed red blood cells or washed erythrocytes;
• upon inadequate storage of the sample (tests for serum iron require plastic tubes
with a stopper);
• upon improper sample withdrawal: blood for testing should be obtained in the
morning as there are daily fluctuations of iron concentration in the blood serum
(in the morning the iron content is higher).
Patients with anemia should have their blood tested every month, blood biochem-
istry—once in a trimester, and when a dynamic surveillance is required.
582 Obstetrics
Complete blood count is indicated for all patients with iron deficiency anemia to
rule out microhematuria.
For evaluation of the cardiovascular system in anemia, ECG is done.
Endoscopic methods of gastrointestinal tract investigation are only administered
if indicated.
22.1.1.9. Differential diagnostics

Iron and protein deficiency anemia should be differentially diagnosed from he-
moglobinopathy, thalassemia, other forms of anemia and anemization syndrome
due to other extragenital diseases and pregnancy complications (diabetes mellitus,
pyelonephritis, hemorrhage in labor and other).
22.1.1.10. Treatment
Treatment of patients with anemia should promote:
• correction of deficiency of iron, protein, micronutrients, vitamins (B12);
• relieving hypoxic conditions;
• normalizing the hemodynamic, systemic, metabolic and organ disorders;
• prevention of complications of pregnancy and childbirth;
• early rehabilitation in the postpartum period.
Treatment should be initiated even if the disease is of mild degree.
Nonpharmaceutical therapy includes an appropriate diet rich in iron and proteins.
However, normalizing the blood iron through mere balanced diet is rather difficult
as only a certain percentage of iron is absorbed from foods (20% from meat, 0.2%
from vegetable foods). Therapeutic protein diet is recommended to replenish the
protein insufficiency.
Treatment starts with oral intake of drugs; it should be prolonged until the store
of iron is replenished (ferritin concentration >50 mcg/l).
Pharmaceutical therapy is aimed at
• arresting anemia (restoring the normal hemoglobin values);
• replenishing the iron store in the body (saturation therapy);
• preserving the iron stores at normal levels (supporting therapy).
When treating the mild form of anemia, the daily dose is 50–60 mg; in pronounced
anemia it is 100–120 mg. Iron supplements are taken in combination with ascorbic
and folic acid.
Indications for parenteral administration of iron supplements:
• intolerance of oral iron supplements;
• disorder of iron absorption;
• active gastroduodenal ulcer;
• severe anemia and vital necessity for iron deficiency correction.
Duration of drug therapy is the same in case or oral and parenteral admin-
istration.
When treating pregnant patients it is acceptable to administer recombinant human
erythropoietin in combination with parenteral administration of iron supplements
in case of severe and moderate anemia. This method of therapy is an alternative to
hemotransfusion or in case of resistant anemia when therapy with only iron supple-
ment is absolutely ineffective.
Hospitalization to perform blood transfusion becomes necessary when hemoglobin

concentration is below 70 g/l, and there are signs of anemia-mediated cardiovascular
instability; in the latter case hospitalization provides an opportunity for in-depth
hematological and general clinical investigations.
22.1.1.11. Treatment of gestational complications

Treatment is provided by an obstetrician gynecologist with a therapist. The ob-
stetrician monitors the signs of preterm birth and miscarriage, early signs of feto-
placental insufficiency and restricted fetal growth.
Special emphasis is put on prevention of hemorrhage in the third stage of labor
and in early puerperium (administration of uterotonic drugs). The rate of hemor-
rhage and, what is more important, its severity grows alongside with aggravation
of anemia.
Anemic puerperas constitute a group of high risk for maternal and fetal
puruloseptic disease. If treatment is initiated early enough, the prognosis is
favorable.
Evaluation of effectiveness of therapy for iron deficiency anemia. In mild anemia
the visits to the maternal welfare clinic are paid with the same regularity as in un-
complicated pregnancy.
In case of severe anemia monitoring with laboratory tests is performed every
week.
In evaluating the efficacy of therapy the most informative parameter

NB! is ferritin content (when administering iron supplements).
22.1.1.12. Prevention of iron deficiency anemia
Prevention includes diagnostics and treatment of anemia, gastrointestinal disorders

and other extragenital disease before the woman gets pregnant.
Prevention and prognosis of gestation complications. Prevention of maternal and
fetal complications in case of anemia implies early diagnosis and balanced diet of
the pregnant woman.
That is why an early booking visit and prompt examination of the pregnant woman
are so important.
Measures taken after 17 – 18 weeks gestation (utero-placental-

NB! fetal circulation complete) aimed at health improvement of the
mother and fetus do not produce much effect.
Prevention of iron deficiency anemia is indicated to pregnant women who

• reside in areas where iron deficiency is a common problem;
• have a short interval between gestations;
• carry several fetuses;
• breastfeed for a long time.
584 Obstetrics
REMEMBER!
Anemia is the most common complication of gestation; it is noted in 21–80%
of pregnant women. During pregnancy most women develop iron and protein
deficiency anemia.
The total iron requirement during pregnancy, childbirth and lactation is 1100–
1300 mg where 300 mg are for the fetus.
Gestational complications in anemia:

• preterm loss of pregnancy;
• feto-placental insufficiency;
• chronic hypoxia;
• restricted fetal growth.
The complication of the third stage of labor and early postpartum period is
hemorrhage.
Treatment: dietetic therapy (protein alimentary therapy in protein deficiency), iron

supplements.
Treatment is discontinued upon replenishing the iron stores. Ferritin concentration

is the main indicator of therapy effectiveness.
22.1.2. Idiopathic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura is an autoimmune disorder due to formation
of antiplatelet antibodies and/or circulating immune complexes that have an impact
on membrane glycoprotein structure of platelets and cause them to be destroyed by
the cells of reticuloendothelial system.
ICD-10 code
• D 69.3 Idiopathic thrombocytopenic purpura.
There are no precise data about the rate of idiopathic thrombocytopenic purpura
in pregnant women. In most cases pregnancy does not compromise the woman’s
condition. Exacerbation of idiopathic thrombocytopenic purpura due to pregnancy
develops in about every third woman.
On the basis of the course of the disease, the following types are distinguished:
• acute disease (of less than 6 month duration);
• chronic disease showing
• frequent recurrence;
• rare recurrence;
• continuously recurring course.
Pregnant women predominantly show chronic idiopathic thrombocytopenic pur-
pura (80–90%); acute disease is noted in 8% of patients.
On the basis of its nature, the course of disease can be

• exacerbation (crisis);
• clinically compensated disease (no manifestations of hemorrhagic syndrome
while thrombocytopenia persists);
• clinical hematological remission.

Etiology of this disease is unknown. The assumption is that it is caused by a com-
bination of environmental factors (stress, photosensitization, radiation, unbalanced
diet, etc.), genetic and hormonal factors. Viral activation may serve as a trigger.
In idiopathic thrombocytopenic purpura platelet destruction is typically enhanced
due to production of antibodies to their membrane antigens. Such platelets are
eliminated from the blood by spleen macrophages. The main signs of the disease
encompass thrombocytopenia, shortened life cycle of platelets, normal or elevated
megakaryocyte concentration in bone marrow and absence of splenomegaly.
Pathogenesis is founded on thrombocytopenia and related decrease in platelet
components in the blood clotting system. Platelets participate in all phases of he-
mostasis. Plasma factors of coagulation and fibrinolysis can be absorbed by platelets.
Besides, platelets secrete endogenous products that actively participate in hemostasis
(Fig. 22.4).
In conditions of platelet deficiency microcirculatory hemophilia develops due to
enhanced fragility of small vessels as well as due to RBCs passing from the blood
stream through the capillaries. Hemophilia becomes manifest upon platelet concen-
tration decrease to 5×104 per 1 mcl.
Formation of antibodies
to RBC membrane antigens
Platelet lesion
Elimination of compromised platelets by spleen
Thrombocytopenia
Hypocoagulation
Fig. 22.4. The main pathogenetic links of idiopathic thrombocytopenic purpura

586 Obstetrics
In pregnant women idiopathic thrombocytopenic purpura mostly takes a chronic
course with a gradual onset, prolonged recurrent course and relative resistance to
most treatment methods.
The main sign of the disease is a sudden onset of hemorrhagic syndrome, of
microcirculatory type, in an apparently healthy subject:
• skin hemorrhages (petechiae, purpura, ecchimosis);
• mucosal hemorrhages;
• bleeding from mucous membranes (nasal and gingival bleeding, bleeding from the
socket of an extracted tooth, uterine hemorrhage, less often — melena, hematuria).
A physical examination does not reveal any other signs of the disease (intoxication,
liver and spleen enlargement, enlargement of lymph nodes).
Deterioration in the course of disease is only seen in 27% of pregnant patients.
The rate of exacerbations is determined by:
• the stage of disease at the time of conception;
• degree of severity.
Exacerbations are accompanied by various manifestations of hemorrhagic syn-
drome: multifocal petechial skin rash, hemorrhages on the mucosa of the nose, gums,
eye globes, as well as bleeding in the nose, stomach, intestine and genitourinary tract.
Subarachnoid hemorrhage is also possible (2%).
Exacerbation and deterioration of the course of idiopathic thrombocytopenic pur-
pura mostly occur in early pregnancy and 1–2 months after childbirth or abortion.
Recurrence of the disease may be associated with production of antiplatelet antibodies
by fetal spleen. In most cases, no dangerous hemorrhage develops during pregnancy.
When taking history one should note periodical nasal and gingival bleeding, heavy
menstrual bleeding, appearance of petechial rash on the skin and mucosas, small
bruises developing even upon slight pressure (applying a cuff, palpation of organs, etc.).
Physical examination. Hemorrhages are located on the skin of limbs, especially legs, on
the abdomen, chest and other body parts. The liver and spleen size are within normal.
Laboratory tests. Complete blood count shows thrombocytopenia of varying sever-
ity: during an exacerbation the platelet content varies within the range 10–30 000/
mcl, in 40% single platelets are noted. A hemostasiogram shows structural and
chronometric hypocoagulation.
Instrumental investigations. Bone marrow aspiration; the punctate shows an el-
evated number of megakaryocytes.

Idiopathic thrombocytopenic purpura is differentially diagnosed from the following
conditions (diagnostics is performed in hospital settings):
• symptomatic varieties of thrombocytopenia due to effect of medications
(diuretics, antibiotics), infection (sepsis), allergy;
• other diseases of the blood (acute leucosis, megaloblastic anemia).
All pregnant women with pronounced changes in blood parameters should see a
therapist and hematologist.
Gestational complications develop upon exacerbation of chronic recurrent type of
the disease; they are seen two- threefold more often than in the population:
• PE (34%);
• spontaneous abortion (14%);
• feto-placental insufficiency (29%);
• placental abruption and hemorrhage in the third stage of labor and in the early
puerperium (4.5%). Hemorrhage immediately after childbirth is from the
ruptures rather than from the placental bed (a contracted uterus arrests the
hemorrhage).
Childbirth is often complicated by uterine inertia and fetal hypoxia (25%).
The newborn demonstrates signs of hypoxia, restricted growth, early adaptation
disorder, neonatal thrombocytopenia due to transplacental passage of antiplatelet
antibodies from mother to fetus during pregnancy. Newborns mostly die of extreme
immaturity and intracranial hemorrhage.
In most patients pregnancy results in delivering a healthy baby.
22.1.2.8. Pathogenesis of gestational complications

The decreased platelet count leads to changes in microcirculation, hemor-
rhagic diathesis, hypoxia of organs and tissues including the uterus and placenta.
Complications arise due to circulatory hypoxia and hemorrhage in the placenta and
uterine wall.
Hemorrhagic diathesis and hypoxia compromise the first and second wave of
invasion causing primary and secondary uteroplacental insufficiency, which may
become the cause of an early miscarriage or placenta separation in the second or
third trimester, restricted fetal growth (Fig. 22.5).
Reduced
platelet count
Circulatory Hemorrhage
hypoxia in uterus and placenta
Disorder of the first and second

wave of cytotrophoblast invasion
Uteroplacental
insufficiency
Pregnancy Placental
FGR
loss abruption
Fig. 22.5. Pathogenesis of gestational complications in idiopathic thrombocytopenic

purpura
588 Obstetrics
NB! Pregnancy is contraindicated if the condition recurs often.
22.1.2.9. Treatment
On an outpatient basis, one can only administer preventive procedures and

glucocorticoid supporting therapy. Pregnant patients with idiopathic thrombocy-
topenic purpura receive the main treatment in specialized hospital departments.
Thrombocytopenia without hemorrhagic syndrome does not always require treat-
ment.
Treatment objective is prevention of severe hemorrhage that can threaten the
patient’s life.
Pathogenetic treatment of pregnant women with idiopathic thrombocytopenic pur-
pura includes glucocorticoids, immunoglobulins. Glucocorticoids provide a complex
effect on all links of the pathogenesis: they prevent antibodies formation, disrupt their
binding to platelets, produce an immunosuppressive effect, and have a beneficial
effect on platelet production by bone marrow cells. Treatment is first directed at
reducing hemorrhagic manifestations, and then — at increasing the platelet count.
Hemotransfusion of red cell packed mass is only administered in presence of pro-
nounced anemia.
If hormone therapy proves ineffective, splenectomy is performed, which is prefer-
ably done in the second trimester or after the childbirth.
Treatment of gestational complications is conventional.
Treatment of complications during delivery or in the puerperium. Labor can be
accompanied by uterine inertia, fetal hypoxia; conventional treatment is admin-
istered. In the third stage of labor and early postpartum period there is a risk
for hemorrhage, so hemorrhage prevention (uterotonic administration) should
be undertaken.
22.1.2.10. The timing and mode of delivery
The patient gives a vaginal birth at term supported by glucocorticoid adminis-

tration. Cesarean section is performed for obstetric indications. Preterm delivery
via cesarean section and simultaneous splenectomy is indicated in case of a severe
exacerbation of the main illness with intractable hemorrhage or a threat of hemor-
rhage in the CNS.
22.1.2.11. Prevention and prediction of gestational complications
In case of thrombocytopenia, one should take care to prevent injury, infection,

avoid medications that reduce the platelet function. Acetylsalicylic acid and other
antiaggregant drugs, anticoagulants and nitrofuran antibiotics are contraindicated to
all patients with thrombocytopenia.
REMEMBER!
Etiology of this disease is unknown.
Pregnancy and its outcomes do not compromise the patient’s condition in most
cases; an exacerbation due to pregnancy develops in every third patient.
Exacerbation and deterioration in the course of idiopathic thrombocytopenic
purpura mostly develop in early pregnancy or 1–2 months after childbirth or
abortion.
Delivery usually takes place at term, the patient continues on glucocorticoids.
Abdominal delivery is required for obstetric indications or upon a severe
exacerbation of the main illness. In case of profuse bleeding or a sever variety of
the disease, splenectomy is indicated.
Acetylsalicylic acid and other antiaggregant drugs, anticoagulants and nitrofuran
antibiotics are contraindicated to patients with thrombocytopenia
22.2. URINARY TRACT DISORDERS

Of all extragenital diseases of pregnancy, urinary tract infection comes third after
anemia and cardiovascular disease. According to modern views, there are infections
of the lower urinary tract (cystitis, urethritis) and upper urinary tract (pyelonephritis)
which can be complicated and uncomplicated. There are five factors that complicate
the course of urinary tract infection (UTI).
• Anatomical abnormality of the urinary tract: congenital malformation and/or
malposition of kidneys, renal pelvis, ureters, bladder, strictures of the ureter,
urethra, kidney stone disease.
• Functional disorders: hyperactive bladder, vesicoureteral and/or ureteropelvic
reflux.
• Severe accompanying disease (diabetes mellitus, cardiac failure, acquired
immunodeficiency syndrome, etc.).
• Instrumental (invasive) methods of urological examination and treatment.
• Mechanical injury and trauma of the urinary tract.
When at least one of the above mentioned factors is present, UTI is considered
to be complicated. UTI can develop in apparently healthy women with normal renal
function and no structural changes in the urinary tract.
Under the impact of pregnancy-related hormonal changes, the structure and
function of the kidneys and urinary tract change as well, and the following factors
emerge, that promote UTI:
• hypotonia and hypokinesia of renal pelvis and ureter, dilation of ureter, especially
on the right (progesterone effect);
• hypotonia and enlargement of the bladder, increase in residual urine;
• increased rate of vesicoureteral reflux;
• increased pH of urine, glucosuria;
• weaker urethral sphincter (in late pregnancy);
590 Obstetrics
• increase in renal blood flow by 50–80% in the fi rst trimester and gradual decline
afterwards;
• increase in glomerular filtration rate by 50% (tubular absorbtion is constant);
• transitory immunodeficiency, increased glucocorticoid concentration.
Three main types of UTI of pregnancy are distinguished: asymptomatic bac-
teriuria, acute cystitis and pyelonephritis. Due to their infectious nature, inflam-
matory diseases of kidneys and urinary tract pose a considerable risk for the
mother and fetus.
22.2.1. Asymptomatic bacteriuria

Asymptomatic bacteriuria is diagnosed upon obtaining findings of two consecu-
tive urine culture tests showing the same infective agent while there are no clinical
presentations of infection of the kidneys or urinary tract.
ICD-10 code
• O23.0 Infections of kidney in pregnancy.
The incidence of bacteriuria increases alongside with the intensity

NB! of sex life.
Asymptomatic bacteriuria is detected in 2–10% of pregnant women. In most cases

bacteriuria is present before the onset of pregnancy; its rate is approximately the same
in pregnant and nonpregnant women.
Pregnant women with permanent bacteriuria often demonstrate chronic pyelone-
phritis (8–33%). In bacteriuria a high rate of congenital abnormalities of the urinary
tract is noted, as well as nephrolithiasis, ureterectasia.
22.2.1.2. Etiology
The main infective agent of asymptomatic bacteriuria is E. coli. Less often other
representatives of Entrobacteriaceae family are detected: Klebsiella spp., Enterobacter
spp., Proteus spp., as well as Staphylococcus epidermidis, Staphylococcus saprophyticus,
Enterococcus faecalis and group B streptococci.
Persistent bacteriuria is promoted both by the host’s specific features (local host
defenses disorder: insufficient production of neutralizing antibodies), glucosuria pro-
moting bacterial growth, and specific features of the bacteria with certain virulence
factors (adhesins, hemolysin, K-antigen and other). The incidence rate of bacteriuria
in pregnant women is also determined by the anatomical and functional condition
of the urinary tract: progesterone-mediated dilation of the renal collecting system,
reduced contractility of the ureters and insufficiency of the urethral sphincter. In most
patients bacteriuria indicates colonization of the periurethral area that was present
prior to the onset of pregnancy. In 30–40% of women with bacteriuria untreated
before pregnancy, acute gestational pyelonephritis develops.
Asymptomatic bacteriuria does not produce apparent clinical presentations. In a
big majority of patients bacteriuria is detected in early pregnancy upon the booking
visit. Only in 1% of cases bacteriuria develops at later gestational ages. It can subside
without causing an inflammation of the kidneys.
Pregnancy does not affect the incidence of bacteriuria; however,

NB! functional changes in urinary organs that occur in pregnancy
promote the development of UTI.
22.2.1.5. Diagnosis
Most pregnant women report bacteriuria in past history; it was detected by
an examination related to genital infection, infertility or urinary tract disease.
Asymptomatic bacteriuria should not be considered an inoffensive condition; it can
become a marker in predicting gestational problems. The objective of diagnostics is
to rule out renal and urinary tract disease or malformations, or gynecologic infection.
The rate of false-positive findings can be as high as 40%, so pregnant women with
positive urine cultures should repeat the test in 1–2 weeks.
Asymptomatic bacteriuria typically shows the following:
• presence of bacteria in midstream urine ≥105 CFU/ml detected twice at an
interval of 24 h (the same species of organisms);
• absence of clinical signs;
• presence or absence of leucocyturia (pyuria).
Double detection of bacteriuria helps to identify the patients for whom therapy is
absolutely indicated; it decreases the rate of unjustified antibiotic therapy administra-
tion. The presence or absence of pyuria in asymptomatic bacteriuria does not have
any clinical significance, and in both cases the therapy is identical.
Reaction with triphenyl tetrazolium chloride is used as a screening test in
examination of pregnant women; the test is simple and economically feasible.
The rate of positive findings in the test with triphenyl tetrazolium chloride when
determining true bacteriuria (105 and more in 1 ml or urine) amounts to 90%
and more.
To rule out inflammatory disease and malformations of the urinary system, vaginal
dysbiosis, genital infection, one administers the following investigations:
• blood biochemistry;
• urinalysis;
• Nechiporenko test;
• urine culture test;
• culture of vaginal contents;
• ultrasound of kidneys;
• dopplerometry of renal vessels.
Neither plain nor excretory urography is indicated for pregnant women. To rule
out disease of kidneys and urinary tract the pregnant woman is referred to an urolo-
gist or nephrologist.
592 Obstetrics
Bacteriuria can be caused by contamination of urine samples which should be
suspected if the the culture shows different infecting agnets or non-uropathogenic
organisms.
Asymptomatic bacteriuria can be a sign of vaginitis or cervicitis,

NB! if the sample was taken incorrcetly.

Gestational complications are associated with the infective agents acting
on the woman’s body and the uteroplacental complex. It was not proved
that bacteriuria predisposes to development of chronic renal disease, arterial
hypertension or preeclampsia, anemia, amnionitis, endometritis. However,
20–40% of pregnant women with asymptomatic bacteriuria demonstrate devel-
opment of pyelonephritis during pregnancy. Pregnant women with untreated
asymptomatic bacteriuria are at risk for delivering low-weight infants and
preterm birth; this risk is 1.5–2 times higher than in women without bacteri-
uria as prostaglandins produced locally and systemically are major mediators
of uterine contractility.
Prevention of gestational complications. Treatment of bacteriuria before 22 weeks
gestation prevents development of pyelonephritis in 70–80%, and preterm birth in
30% of patients.
22.2.1.8. Treatment
After doing bacterial culture and drug-susceptibility tests, pharmaceutical therapy
is administered to pregnant women with asymptomatic bacteriuria (oral administra-
tion):
• single-dose of a highly effective, safe antibiotic (an economical regimen, less risk
of adverse effects);
• 3-day antibiotic regimen;
• in 2 weeks — urine culture test;
• if urine is sterile (bacteriuria ≤104 CFU/ml), the pregnant woman is observed on
a regular basis;
• if there are risk factors for UTI, supporting therapy with herbal formulations is
indicated;
• if bacteriuria recurs, a different medication is administered.
Treatment of bacteriuria encompasses restoration of normal vaginal and intestinal
biocenosis.
Estimation of therapy effectiveness: urine culture test 28–42 days after completion
of therapy, and in 7–10 days.
Criteria of therapy effectiveness:
• recovery (sterile urine cultures or presence of bacteria at concentrations below
104 CFU/ml);
• persistence of infection (isolation of the same agent in urine at concentrations
104 and more CFU/ml).
In some patients reinfection is possible: detection of a new bacterial species in

urine at concentrations 103 and more CFU/ml at any visit to the maternity welfare
clinic.
Treatment of gestational complications is conventional.
22.2.1.9. Timing and mode of delivery

If prevention was provided in due time, the patient gives a vaginal birth at term.
Cesarean section is only performed for obstetric indications.
Urine culture test and kidney ultrasound should be included in the list of obliga-
tory screening tests for patients with bacteriuria.
REMEMBER!
In most cases bacteriuria exists prior to pregnancy; its rate is approximately the
same in pregnant and nonpregnant women.
The incidence rate of bacteriuria in pregnant women is determined by the

anatomical and functional condition of the urinary tract: progesteronemia, bladder
hypotony, dilation of the renal collecting system, incompetence of the urethral
sphincter and others.
Bacteriuria indicates that the pregnant woman’s genitourinary system is

compromised.
Treatment of bacteriuria prevents development of gestational pyelonephritis in

70–80%, and preterm birth in 30% of pregnant women.
22.2.2. Cystitis
Cystitis is inflammation of mucous membrane of the bladder; it accompanies
various conditions of the urinary system and genitals in women.
ICD-10 code
• O30 Cystitis.
Acute cystitis develops in 1–3% of pregnant women.
• By course of the disease: acute and chronic cystitis.
• By origin: primary and secondary.
22.2.2.3. Etiology
Cystitis is more often noted in women, which is due to the anatomical structure
of the female urethra which presents more opportunity for ascending infection.
594 Obstetrics
We distinguish cystitis of infectious and noninfectious nature.

Cystitis of noninfectious origin occurs upon irritation of the mucosa of the uri-
nary bladder by chemicals excreted with urine, including medications taken in large
doses for a long time, in case of tumors, upon injury of the mucous membrane by
a foreign body (urinary stone). In most cases an infection is soon superimposed on
the initially aseptic inflammation.
More than a half of cystitis cases (58%) in women are related to defloration. A
girl infected upon the first sex contact becomes a cystitis patient or a carrier of sexu-
ally transmitted infection. As the interval between infection onset and initiation of
treatment encompasses several months, and sometimes years, the process becomes
chronic and persists before the start of pregnancy.
The routes of infection spread can be ascending, descending, lymphogenous,
hematogenic and contact.
Infection passes to the woman’s bladder from the urethra. Female urethra is short
and wide, which cuts down on the distance bacteria must travel to reach the bladder.
Bacteria get to the urethra mostly from the vagina or intestine. Infection can occur
due to catheterization of the bladder when obtaining urine specimens. Catheterization
of the bladder in pregnant and parturient women is especially dangerous when the
bladder is hypotonic.
Cystitis can be the first clinical presentation of pyelonephritis or urolithiasis.
The disease is most often caused by E. coli (80%), Klebsiella (3.7%), staphylococ-
cus (5%), streptococcus (2.5%), enterococcus (2.2%) and Proteus vulgaris (8.2%),
sometimes gas-producing organisms. Cystitis directly related to genital infections
(Chlamydia, gonococcus, Ureaplasma) is not uncommon.
NB! Specific cystitis can be caused by such organisms as tuberculosis

mycobacteria, gonococcus and, rarely, Treponema pallidum.
The mucosa of the urinary bladder shows considerable resistance to infection, so

infecting the bladder does not produce cystitis. Besides infection, development of
cystitis is determined by additional predisposing factors:
• getting cold often;
• hypovitaminosis, chronic fatigue;
• anatomical malformations;
• failure to follow the rules of personal hygiene;
• sexual promiscuity;
• secondary immunodeficiency;
• surgery;
• hormonal disorder;
• hypodynamia;
• constipation.
During pregnancy there are changes in the body’s hormone homeostasis, the dis-
order of vaginal microflora deteriorates, the immunity is decreased. Structural and
physiological changes of various parts of the urinary system (physiological hydrone-

phrosis and hydroureter of pregnancy, hypotonia of the bladder, its greater capacity,
a tendency to incomplete emptying) as well as changes in chemical composition of
urine (glucosuria, increased pH) are linked to a combined effect of gestational hor-
mone shift (increased progesterone, estrogen, CG, E2 prostaglandin), hypertrophy
of longitudinal muscle bundles in the lower part of ureters, weakening of urethral
sphincter by the end of pregnancy.
When there is no infection, no disease develops. If a genitourinary bacterial agent
is present, bacterial vaginosis, hypotony of the bladder and «thermostat» conditions
(t=37 °С and sufficient humidity) combine to promote an inflammatory process:
acute cystitis of pregnancy.
A pregnant woman with chronic cystitis is always at risk for its regular or out-of-
turn exacerbation.
During labor, the passage of fetus along the birth canal leads to circulatory
disorder in the pelvis, which is an additional predisposing factor for acute cystitis.
Catheterization of the urinary bladder after childbirth can promote contact infec-
tion.
It is recommended that a puerpera should empty her bladder every 2 hours as
accumulation of urine predisposes to bladder inflammation. Postpartum cystitis
develops due to passage of E. coli, less often — staphylococci and streptococci — to
the urinary bladder.
Predisposing factors are retention of urine in the bladder, changes

NB! in the bladder wall mucosa at prolonged labor or injury.

Acute cystitis has a sudden onset, some time after the individual got cold or
was exposed to another causative factor. Clinical presentations of acute cystitis
encompass a compromised general condition (fever, weakness, reduced working
efficiency) and local signs that allow a prompt diagnosis. The signs include fre-
quent (every 30–60 min) and painful urination in small portions (20 ml), lower
abdominal pain getting worse upon palpation and filling of the bladder. Urination
makes the pain worse. The pain can grow almost continuous, but most commonly
it is associated with urinating (during the entire act of urination or appearing at
the beginning or at the end). Due to the frequent urge to urinate (urination does
not depend on the part of day, movement or rest), patients are not always able
to contain urine.
When inflammation is at the bladder neck, the most intense pain appears at the
end of urination which is associated with tenesmus and convulsive contraction of
the sphincter. The patients have to empty the bladder often, and the pain becomes
constant.
In acute cystitis the expression of clinical signs varies. In mild cases patients just
have a sensation of heaviness in the lower abdomen. Moderate pollakiuria (frequent
urination) is accompanied by insignificant pain at the end of urination. These signs
are present for 2–3 days and resolve without treatment. With early initiation of
596 Obstetrics
therapy the course of acute cystitis runs for 6–8 to 10–15 days. A longer course
indicates the presence of a concomitant condition that supports the inflammation
and requires additional examination.
In severe forms of acute cystitis the typical presentations are high temperature,
pronounced intoxication, hematuria, oliguria. The duration of disease in such cases
is much longer. Severe complications may develop.
In acute cystitis, macro- and microhematuria (presence of blood cells in urine) are
possible, besides pyuria (leucocyturia). Hematuria is, as a rule, of terminal nature
(appearing at the end of urination) which is associated with injuring the inflamed
mucosa in the bladder neck and Lieutaud body at the end of urination (hemorrhagic
cystitis).
Postpartum cystitis causes urinary retention, pain at the end of urination, turbidity
of the first pass urine.
Clinical presentations of chronic cystitis are varied; they depend on the patient’s
general condition and effectiveness of therapy. The main clinical signs are the same
as in acute cystitis, but they are less pronounced. Chronic cystitis can be a continu-
ous process with constant, more or less pronounced, presentations and changes in
urine (leucocyturia and bacteriuria); another possibility is a recurrent course with
exacerbations presenting like acute cystitis, with remissions when there are no mani-
festations altogether.
In acute cystitis there is evidence of a sudden onset and rapid progression of signs
with maximum expression in the first days; in chronic cystitis the patient reports
previous history of cystitis.
Physical examination. Palpation reveals tenderness of the urinary bladder, percus-
sion — its overflow.
Laboratory and instrumental investigations. In acute cystitis the findings encompass
pyuria (WBCs ≥104 /ml of unspun urine), bacteriuria (E. coli ≥102 CFU/ml, other
urinary pathogens ≥106 CFU/ml). Diagnosis of acute cystitis cannot be made with-
out clinical findings. Bacteriuria is not an obligatory sign of acute cystitis. Typical
presentations and pyuria while there are no bacteria in midstream urine indicate
urethritis rather than acute cystitis.
Cystoscopy is not usually required in acute cystitis as the procedure can aggravate
the disease. In chronic cystitis cystoscopy reveals edema, hyperemia, hemorrhage,
rough mucosal surface due to foci of thickening, and areas covered with fibrinopu-
rulent membranes and ulcerations.

Acute cystitis is differentially diagnosed from disease of the kidneys, urinary stones,
cystalgia, urethritis and female genital infection.
When there are stones in the bladder, the signs resemble those of cystitis. At the
same time, in urolithiasis the pain is prompted by walking or harsh riding; it irradi-
ates to the perineum.
Disorder of urination manifests as a frequent urge becoming more intense when
the body is in motion. Sleep does not bring relief to pain.
In cystalgia there are no structural changes in the urinary bladder, pyuria is

absent while pain can be quite intense. The diagnosis of cystalgia is made on
the basis of presentations typical of cystitis while there is no pyuria, no bacteria
in urine; cystoscopy shows no changes of mucosa of the urinary bladder typical
of cystitis.
Cystitis can be the first clinical manifestation of pyelonephritis. In acute pyelo-
nephritis the body temperature suddenly runs high to 38–39 °С with shaking chills.
Patients often complain of lumbar pain, nausea and vomiting. One should remember
that acute pyelonephritis requires immediate hospitalization.
In urethritis urination is painful with discharge of pus from the urethra. Urethritis
can be combined with cervicitis or bartholinitis. Urethritis is most commonly caused
by sexually transmitted disease.

Untreated bladder infection can become the cause of threatened abortion, preterm
birth and other complications.
Infection of lower urinary tract can spread in an ascending way

NB! and cause pyelonephritis.
22.2.2.9. Treatment
Therapy with oral drugs is administered on outpatient basis by an urologist. If
the first episode occurs during pregnancy, a single-dose of highly effective, safe
antibiotic, or a 3-day regimen is administered. If the condition recurs, the drug is
replaced. Antibacterial drugs are administered in case of bacteriuria, hematuria and/
or leucocyturia. Local therapy includes instillations (introduction of solutions to the
bladder) with antimicrobial drugs.
Vaginal disbiosis and sexually transmitted disease are treated only if indicated.
Estimation of treatment effectiveness. 2 weeks after treatment a control urine cul-
ture test is done. Criteria of recovery: absence of clinical presentations and normal
urine findings.

In case of early diagnosis and treatment, a vaginal birth takes place at full term;
cesarean section is only performed for obstetric indications.
22.2.2.11. Prevention of gestational complications

Prevention of gestational complications encompasses observation of the rules of
personal hygiene, early (preferably before pregnancy) detection and treatment of
cystitis and other inflammatory conditions of the urinary tract and female genitals,
constipation, disorders of vaginal biocenosis and urodynamics, avoiding getting cold,
following the rules of aseptics upon endovesical investigations or catheterization of
the bladder.
Prevention of chronic cystitis consists in adequate treatment of acute cystitis, early
detection and treatment of urinary tract disorders.
598 Obstetrics
REMEMBER!
In pregnant women the development of cystitis is favored by the structure of the
urethra and hormone changes.
The routes of infection spread are ascending, descending, lymphogenous,

hematogenic and contact.
Untreated cystitis during pregnancy can promote threatened abortion, preterm

birth, pyelonephritis.
Postpartum cystitis develops due to specifics of the delivery process. Causative

agents are E. coli (most often), enterococci, les soften — staphylococci and
streptococci.
Signs of cystitis: urine retention, pain at the end of urination, turbidity of the first
pass urine.
Treatment: if it is the first episode, single-dose or 3-day antibiotic regimen, upon

recurrence — 7-day regimen.
Effectiveness of therapy: absence of clinical signs, normal urine findings. Control

test is done 2 weeks after therapy.
22.2.3. Pyelonephritis
Gestational pyelonephritis means pyelonephritis newly diagnosed during pregnancy.
Gestational pyelonephritis is an acute disease developing in a healthy woman with-
out chronic pyelonephritis in past history; its course includes a recovery stage and
recurrence.
ICD-10 code
• O23.0 Infections of kidney in pregnancy
According to epidemiology studies, the prevalence rate of upper urinary tract
infection among pregnant women is 1–3.5%. The rate of gestational pyelonephritis
is 3–10%. Pyelonephritis more often develops in prmigravidas. The condition can
occur in puerperant women (up to 15%) and in puerperas (over 20–30%).
• By pathogenesis:
– primary pyelonephritis;
– secondary pyelonephritis.
• By its course:
– acute pyelonephritis;
– chronic (latent or recurring) pyelonephritis.
22.2.3.3. Etiology
The disease is caused by various agents (bacteria, protozoa, viruses, fungi). The
inflammation is commonly caused by E. coli, less often — by enterococci, Proteus,
staphylococci and streptococci. Their disease-inciting power in kidneys is due to the

tropism to renal parenchyma, the phenomenon of sticking to urinary tract epithelium,
the ability to reproduce in acid medium, etc. However, in 5–30% of patients urine
culture tests do not show any pathogens. The virulence of opportunistic organisms
is not high, they cause the disease in patients with decreased immunity.
The infection spreads by hematogenous and urinogenous route;

NB! the infectious matter ascends to the bladder and enters the renal
pelvis via the ureter.
The lymphogenous route of infection spread is possible in case of retrograde lymph

flow in lymphadenitis.
Bacteriuria and previous pyelonephritis are risk factors for acute

NB! pyelonephritis in pregnancy.
Development of gestational pyelonephritis is due to a presence of an infection

focus and disturbed urodynamics in the upper urinary tract.
69% of pregnant women with gestational pyelonephritis report infection of the
urinary system in past history. Risk factors for pyelonephritis are as follows:
• previous urinary tract infection;
• urinary stone disease;
• abnormalities of the urinary tract;
• female genital inflammatory disease;
• carrying pathogens and opportunistic organisms;
• low socio-economic status.
Pathogenesis of gestational pyelonephritis is to a great extent determined by the
anatomy and function of the female urinary tract, disorder of urodynamics in the
upper urinary tract, vaginal dysbiosis, asymptomatic bacteriuria in the pregnant
woman and asymptomatic bacteriospermia in her husband. Infections developing
during pregnancy can also influence on the development of pyelonephritis.
In bacteriuria urine cultures can turn out sterile due to emergence

NB! of L-form bacteria.
Hematogenous spread of infection is of rare occasion; it becomes possible when

significant bacteriuria combines with disorder of urodynamics or venous outflow.
Ascending infection affects the urethra and bladder first. The passage of urine is
disturbed under the impact of progesterone, hydrostatic pressure in the collecting
system increases, and the blood flow in the organs changes which favors the spread
of pathogens. If vesicoureteral reflux develops, the infected urine passes to the pelvis
where pathogens adhere to urothelium, and pyelonephritis develops.
Inflammatory changes in the kidney begin as a focal process; after each new attack
it becomes more diffuse; the inflammation which was first serous becomes purulent
600 Obstetrics
and reduces the filtration capacity of the kidneys the amount of urine decreases
(oliguria, anuria), the quality of excreted urine changes (turbid urine, pyuria). A
unilateral process can spread to the other kidney. Ureteral occlusion leads to urine
retention and hydronephrosis. As the process in the kidneys progresses, purulent
foci emerge. Intensive development of infection in the presence of ureteral occlu-
sion can cause septic shock. The infection becomes generalized when the pathogen
is highly active and urodynamics is disturbed (ureteral occlusion due to edema and
inflammatory detritus).
In pyelonephritis there is a systemic involvement. Intoxication and anemia im-
pair the cardiac contractile activity. Left ventricular insufficiency and pulmonary
edema, anemia, tachycardia, arrhythmia can develop. Hepatic function is im-
paired due to the toxic impact of urea, methyl guanethidine, products of nitrogen
metabolism, increased gastrin secretion, etc. Gastrorenal syndrome development
is promoted by vascular and trophic disorders in the gastrointestinal mucosa,
changes in the protein metabolism, water-electrolyte balance, acid-base balance,
hyperaldosteronism, immunity disorders. Patients with UTI run a higher risk of
superimposed preeclampsia.

Acute and chronic pyelonephritis is distinguished in the clinical course of
the disease. Acute pyelonephritis is noted in 2–10%, more often in primigravid
patients. When the chronic condition exacerbates, it is regarded as acute inflam-
mation. In puerperas pyelonephritis develops on day 4, 6, 12 of the postpartum
period.
Critical time for exacerbation of the condition: the first and seconf
NB! trimesters (due to progesterone in one case and due to the peak
concentration of corticosteroids in the other case), 32 – 36 and
39 – 40 weeks gestation, and the postpartum period.
Clinical presentations of acute pyelonephritis. General reaction (in case of infec-

tion): intoxication, high temperature, shivers, headache, weakness, sweating, nausea,
vomiting.
Local signs: lumbar pain irradiating to lower abdomen and vulva (the pain re-
sembles renal colic), dysuric phenomena (not always), reduced amount of urine,
cloudy urine. The pregnant woman tries to assume a forced position of the body:
lying on her side with legs pressed to the abdomen. In the second and third trimester
the pain is usually less intensive.
Acute serous pyelonephritis can proceed asymptomatically; it is detected by labo-
ratory tests.
Purulent pyelonephritis presents serious danger:
• diffuse purulent pyelonephritis: nondestructive form;
• focal purulent pyelonephritis is destructive: suppurative nephritis, carbuncle and
abscess of the kidney.
When chronic pyelonephritis recurs, clinical presentations are the same as in
acute inflammation; in latent pyelonephritis the disease can be only diagnosed from
laboratory findings. Pregnancy aggravates the course of chronic pyelonephritis; in

1/3 of patients exacerbation occurs.
Pregnant women with pyelonephritis should be hospitalized

NB! upon exacerbation of the disease irrespective of the gestational
age.
Diagnosis is based on clinical, laboratory and instrumental investigations. When
taking history, one reveals previous urinary system diseases, pyelonephritis signs
(localization and nature of pain, diuresis, body temperature, etc.).
In acute course of the disease or exacerbation of chronic disease lumbar tenderness
is revealed on the affected side or bilaterally.
Treatment by specialists is indicated:
• urologist;
• nephrologist.
Laboratory investigations include:
• complete blood count (leucocytosis, left shift of leukocyte formula, sometimes
leucopenia, hypochromic anemia);
• blood biochemistry (dysproteinemia, positive C-reactive protein, in severe
cases — increased urea, residual nitrogen);
• urinalysis (alkaline reaction, bacteriuria, E. coli ≥10 4 CFU/ml,
pyuria ≥104 WBCs/ml of unspun urine);
• Nechiporenko test (leukocyturia >4000/ml);
• Roberg assay (reduced reabsorbtion in severe cases);
• Zimnitskiy’s test (hypo- or hyperstenuria, nicturia: in chronic pyelonephritis the
concentration capacity of kidneys is disturbed early);
• urine culture test (growth of the infective agent to 105 and more CFU/ml, drug-
susceptibility test);
• vaginal contents culture.
A severe course of pyelonephriutis can be aggravated by renal

NB! abscess or carbuncle which are managed surgically.
Instrumental investigations:
• ultrasound of kidneys to detect malformation, malposition, parenchyma
echogenicity, enlargement of the collecting system;
• chromocystoscopy;
• cystoscopy.
Catheterization of ureters is of diagnostic and therapeutic significance as it elimi-
nates the renal block. Chromocystoscopy shows that the involved kidney does not
excrete the dye.
Survey and excretory urography as well as radionuclide methods (renography,
scynthygraphy) and magnetic resonance imaging are administered strictly if indi-
cated, their use in pregnant women is limited.
602 Obstetrics
Pyelonephritis is differentially diagnosed from acute appendicitis, acute cholecysti-

tis, renal or hepatic colic, exacerbation of gastroduodenal ulcer, urinary stone disease,
renal carbuncles, general infections (food poisoning and foodborne infection, the flu,
etc.) and gestational complications.

Obstetric and perinatal complications develop at 21–30 weeks gestation. The
rate and severity of complications is associated with the degree of kidney involve-
ment.
Obstetric complications:
• spontaneous abortion;
• preterm birth;
• PE;
• anemia;
• fetoplacental insufficiency;
• polyhydramnios;
• postpartum endometritis.
Fetal complications:
• chronic fetal hypoxia;
• FGR;
• intrauterine infection.
Pregnant women with pyelonephritis and UTI are regarded at high risk for intra-
uterine infection, miscarriage, still birth and early neonatal mortality.
22.2.3.9. Pathogenesis of pregnancy complications

In acute pyelonephritis or exacerbation of chronic pyelonephritis, threatened abor-
tion and preterm birth are induced by pain syndrome, feverish state, exotoxins of
gram-negative intestinal bacteria as they increase uterine excitability (prostaglandin
release).
In most cases gestational pyelonephritis is accompanied by anemia developing
due to reduced hematopoietic renal function; anemia can complicate the course of
pregnancy, childbirth and postpartum period.
In the presence of renal disease PE often develops which manifests as edematous-
nephrotic or hypertensive forms. In severe PE, secondary to renal disease, there is
edema and separation of fibers in perivascular and intermediate tissue, noncoronary
myocardiosclerosis (uremic myocardiopathy) which later transforms to cardioscle-
rosis. There are signs of pulmonary hypertension, slowing-down and decrease of
capillary blood flow.
Intoxication and anemia, metabolic disorder and hypoxia disrupt formation of
the placental bed which leads to placental insufficiency and thus — to spontaneous
abortion at early gestational age, hypoxia and FGR, preterm birth.
Polyhydramnios develops due to infection of amniotic membranes. Infection of
the fetus and newborn is also possible (Fig. 22.6).
Pregnancy
Predisposing factors loss or preterm
not related birth
to pregnancy
Bacteriuria Anemia
Factors Preeclampsia
arising
during gestation
+ Infection = Cystitis
Placental
insufficiency, FGR,
fetal hypoxia
Pyelonephritis
Chemical
irritation, Polyhydramnios
trauma
Intrauterine infection
Fig. 22.6. Pathogenesis of gestational complications in UTI
Objectives of treatment are as follows:

• reversing the main signs of the disease;
• restoring the urinary tract function;
• bringing laboratory finding to normal range;
• choice of antibacterial therapy considering the gestational age, severity and
duration of the disease;
• prevention of recurrence and complications of the disease.
The main treatment encompasses antibacterial and detoxifying therapy once urine
passage is normal or restored to normal. Symptomatic therapy is also included into
the complex treatment. When treating acute pyelonephritis or exacerbation of chronic
pyelonephritis in pregnant patients with hyperthermia and dilation of upper urinary
tract, a stenting catheter and antimicrobial therapy are advisable followed by preven-
tion with uroseptic drugs until childbirth.
Antimicrobial therapy. The choice of drug is made depending on the organisms’
sensitivity to antibiotics and uroseptics, considering the effect on the fetus. Before
urine culture findings for sensitivity to antibiotics are available, therapy begins with
broad-spectrum antibiotics (IV or IM administration for 48 h). Depending on the
urine culture test, the drug is replaced with another if required, the one to which the
pathogens are sensitive. Duration of the therapy is from 5–7 to 10–15 days followed
by prevention with herbal medicines for 3–6 months.
Nonpharmaceutical therapy:
• diet #7;
• abundant intake of low mineral concentration water;
• knee-elbow position for 10–15 min several times a day;
• sleeping on the unaffected side.
Surgical treatment is provided in hospital settings in the following cases:
• disturbed urine passage: ureter catheterization using ureteric stents, transcutaneous
puncture nephrostomy, operative pyelonephrostomy, renal decapsulation;
604 Obstetrics
• purulent destructive inflammation: suppurative nephritis, kidney carbuncle and

abscess.
Estimation of treatment effectiveness: urine culture and urinalysis to confirm elimi-
nation of the pathogens, after that — urinalysis once every 2 weeks, urine culture
test once a month.
NB! Criteria of healing: three negative tests for leucocyturia in a row.
Indications for hospitalization:

• pyelonephritis exacerbation;
• superimposed PE;
• decreased renal function;
• threatened abortion or threatened preterm birth;
• signs of FGR;
• asymptomatic bacteriuria or leucocyturia resistant to therapy.
Indications for preterm termination of pregnancy:
• pyelonephritis combined with severe PE;
• ineffectiveness of administered therapy for pyelonephritis;
• purulent destructive inflammation (carbuncle of kidney, etc.);
• acute renal failure;
• fetal hypoxia.
Treatment of gestational complications is conventional. Vaginal delivery is prefer-
able. Cesarean section is only performed for obstetric indications.
After discharge the patient is under urologist’s surveillance for 3–5 years.
When pregnancy is planned, it is advisable to have an ultrasound scan of the
kidneys and urine culture test.
Prevention and prediction of gestational complications. Prevention of gestational
pyelonephritis is aimed at revealing asymptomatic bacteriuria, disorder of urodynam-
ics, initial signs of the disease.
Nonpharmaceutical procedures for prevention of pyelonephritis exacerbation en-
compass adequate fluid intake (1.5–2.0 l/day), postural therapy (knee-elbow posi-
tion), herbal medicine therapy. Antibacterial therapy of asymptomatic bacteriuria in
pregnant women reduces the risk of pyelonephritis considerably.
In case of chronic pyelonephritis the pregnant woman has to undergo planned
examinations:
• in the first trimester: an urologist administers a thorough examination of the
urinary tract function to conclude if it is possible to preserve the pregnancy and
to issue recommendations about management of the condition;
• at the end of the second trimester and early in the third trimester (24–30 weeks)
when acute pyelonephritis and its obstetric complications commonly develop,
the woman undergoes a repeat examination to detect gestational complications
and to check the urinary tract condition;
• before childbirth (at 38–40 weeks) to decide upon the timing and mode of delivery.
REMEMBER!
Gestational pyelonephritis more often develops in primigravid women.
Etiology: mostly opportunistic pathogens.
Acute and recurrent gestational pyelonephritis are distinguished.
General and specific signs are typical (leucocyturia and bacteriuria).
Principles of treatment: sanation of the urinary tract, normalizing the passage of
urine, symptomatic therapy.
Pregnancy is terminated before term if pyelonephritis combines with severe PE,
the administered treatment shows no effect, there is acute renal failure, fetal
hypoxia.
22.2.4. Glomerulonephritis
Glomerulonephritis is an infectious allergic renal disease with predominant lesion
of glomerular vessels involving the tubules and interstitial tissue.
ICD-10 code
• N03.2 Chronic nephritic syndrome with diffuse membraneous glomerulonephritis.
Glomerulonephritis occurs in 0.1–0.2% of pregnant women.
• Acute glomerulonephritis:
– cyclic glomerulonephritis;
– acyclic glomerulonephritis.
• Chronic glomerulonephritis:
– malignant form (subacute, rapidly progressing);
– mixed form;
– hypertonic form;
– latent form;
– terminal form.
22.2.4.3. Etiology
In most cases the causative agents are hemolytic streptococci group A and B
(type 12 and 49), so called nephrogenous streptococcus strains isolated mostly in
the oropharynx of patients with acute nephritis. Glomerulonephritis development
is usually associated with streptococcal infection in past history (quinsy, scarlet
fever, chronic tonsillitis, furunculosis). Dermal streptococcal infection (pyodermia,
erysipelas) is not uncommonly the cause of infection. The streptococcal origin of
glomerulonephritis is confirmed by immunologic studies: streptococcal antigens are
detected in the blood in more than a half of patients with acute glomerulonephritis.
Much less often, the infective agents are represented by staphylococci, diphtheria
bacillus, meningococci, viruses, etc.
606 Obstetrics
Predisposing factors are getting cold, stress, preeclampsia.
The immune response of the body to the infection plays the key role in the de-
velopment of glomerulonephritis.
The latent period spanning from the actual infection to emergence of clinical
signs of nephritis is accompanied by the body’s reduced resistance, formation of
antibodies to organisms and antigen-antibody complexes or autoantibodies (com-
plexes of endogenous antibodies with proteins, glomerule antibodies). Interacting
with the complement, they fix under the epithelial cells and on the basal membrane
of glomerular vessels and disrupt vascular wall permeability, activate the complement
system, coagulation and kinine systems causing fibrin deposition in the capillary wall.
The immunobiologic process lasts for 2 – 3 weeks; after that the

NB! patient develops edema, arterial hypertension, hematuria and
proteinuria.
The pathogenesis of this condition is complex. Development of edema in glomerulo-

nephritis is associated with lesion of glomerular vessels which leads to reduced glomerular
filtration. Sodium and fluid are retained in the body. There is an increase in the activity
of hyaluronidase which depolimerizes the protein-mucopolysaccharide complexes in the
intercellular substance; in its turn, this enhances the capillary permeability to fluid and
protein. The porosity of vascular wall can be inferred from the presence of protein in
the edema fluid. Fine protein fractions pass to the interstitial space, which decreases the
oncotic pressure of the blood plasma leading to fluid retention in tissues.
Pregnant women with pyelonephritis are prone to edema; there are common
edema-causing mechanisms in glomerulonephritis and in pregnancy: increased per-
meability of the blood-tissue barrier and markedly increased hydrophilism of tissue
colloids, enhanced activity of the hyaluronic acid-hyaluronidase system, elevated
hydrostatic pressure in the capillaries. Reduced glomerular filtration in kidneys in
late pregnancy decreases the filtration capacity of kidneys and leads to sodium and
fluid retention in the body.
Arterial hypertension can be present in acute and chronic glomerulonephritis (hy-
pertonic and mixed forms). In acute glomerulonephritis the pathogenesis of arterial
hypertension is associated with increased circulating blood volume due to reduced
glomerular filtration and retention of sodium and fluid.
As the blood flow to the heart increases, the minute volume of the heart increases
too, while the peripheral resistance to blood flow decreases. In chronic glomerulone-
phritis, peripheral resistance to the blood flow grows as the gestational age increases.
Reduced renal blood flow triggers the renin angiotensin aldosterone system whose
pressor effect promotes greater peripheral resistance to the blood flow due to arteriole
tightening.
In chronic glomerulonephritis (hypertonic and mixed forms), apart from a pro-
found disturbance of regional renal circulation, there are pronounced changes in the
blood circulation system.
Proteinuria is a sequence of glomerular capillary lesion. The amount of protein
lost with urine depends on the degree of involvement: just the endothelium or the
endothelium+basal membrane, which can only occur in a long-term process. In

pregnant women it can occur in any form of the disease, sometimes becoming mas-
sive, especially in case of the nephrotic form of glomerulonephritis.
At early stages of glomerulonephritis the hemopoietic function is disturbed which
leads to normochromic anemia, less often — hypochromic anemia. When assessing
blood test findings of pregnant women one should take into account the effect of
physiological hemodilution.
Thus a vicious circle is created: the diminished hemopoietic function leads to
anemia and hypoxia which disrupts the tubular function.
Pregnancy does not affect the course of glomerulonephritis strongly. An increase
in proteinuria, superimposed or progressing arterial hypertension and renal insuf-
ficiency are noted in 1/3 of patients only; after child birth these phenomena can
resolve spontaneously.

Acute glomerulonephritis is rarely seen during pregnancy as it affects mostly children and
teenagers. Besides, pregnancy-related hyperproduction of glucocorticoids precludes the
development of acute glomerulonephritis. It should be differentially diagnosed from PE.
The cyclic form of acute glomerulonephritis shows a typical sudden onset: head-
ache, lumbar pain, shortness of breath, facial edema, oliguria, increased BP, fever,
reddish brown coloration of urine (macrohematuria). Macrohematuria, proteinuria
and cylindruria are noted in all patients.
The acyclic form commonly shows a gradual onset, less evident leg swelling, slight
shortness of breath, proteinuria and hematuria detected by chance.
Chronic glomerulonephritis of pregnant women is noted in milder forms: latent in
63%, mixed in 25%, hypertonic in 7%, nephritic in 5%. Exacerbations of chronic
glomerulonephritis are not commonly seen in pregnancy; the clinical presentations
of exacerbation are similar to those of the acute disease.
• Latent glomerulonephritis is characterized by scanty urine syndrome; it can
persist for 10–20 years and change to hypertonic or nephritic glomerulonephritis.
This variety is the most common one.
• Mixed glomerulonephritis: inflammatory and vascular changes as well as related
arterial hypertension are quite pronounced; dystrophia progresses causing
proteinuria, hypoproteinemia, hypercholesterolemia and edema. Arterial
pressure is moderately elevated. In some patients hypertonic signs predominate
while in others nephrotic signs do, and this fact influences the development of
certain gestational complications.
• Hypertonic glomerulonephritis commonly shows elevated BP and mild changes
in urine (proteinuria, cylindruria, hematuria are not pronounced or constant).
• The nephrotic variety of chronic diffuse glomerulonephritis is characterized by four
signs: massive edema, pronounced proteinuria, hypoproteinemia and hypercholes-
terolemia. BP remains within normal. In severe cases there is pulmonary edema,
ascites, cerebral edema with convulsions, retinal edema and blindness. Pregnancy
aggravates the course of nephrotic glomerulonephritis (effect of glucocorticoids);
the edema and proteinuria can be corrected by adequate therapy. The outcome of
pregnancy depends on the expression of arterial hypertension and azotemia.
608 Obstetrics
Subacute malignant diffuse glomerulonephritis of 6–18 months duration results in

the patient’s death. It develops in pregnant women extremely seldom.
The terminal stage is the end stage of nephritis. All varieties of chronic glomeru-
lonephritis in the end pass to the terminal stage, chronic uremia. At this stage, the
renal parenchyma is badly affected, the reproductive function diminishes to render
pregnancy impossible. A pregnancy that began in a woman on hemodialysis very
seldom ends in a positive outcome for the fetus and leads to the aggravation of the
mother’s condition.
Contraindications for gestation. Patients with acute glomerulonephritis seldom have
positive pregnancy outcomes. In most cases fetal demise occurs, or the disease leads
to a preterm birth. Both complications are tied to the variety of glomerulonephritis,
the one with arterial hypertension or with azotemia. Acute glomerulonephritis with-
out arterial hypertension or azotemia offers a more favorable prognosis. The disease
calls for prolonged intensive treatment which in most cases affects the fetus and the
further progress of pregnancy adversely. At the same time, inadequate treatment
results in the disease becoming chronic.
Acute glomerulonephritis experienced a year or more before

NB! pregnancy and treated successfully does not usually affect the
fetus, nor does it cause a noticeable impairment of renal function
in later life.
In other words, cured acute nephritis does not affect the course of pregnancy,
maternal and fetal condition. After an episode of acute glomerulonephritis the woman
should become pregnant no earlier than in 3–5 years.
Exacerbation of chronic glomerulonephritis is not often seen

NB! during pregnancy.
If glomerulonephritis with nephrotic syndrome shows a favorable course, preg-

nancy can be prolonged. Compared with latent glomerulonephritis, in mixed and
hypertensive glomerulonephritis the systemic circulatory disorders lead to a six-fold
increase in PE rate, disorder of uteroplacental circulation; they promote premature
placental separation and a ten-fold increase in perinatal mortality. In these types of
glomerulonephritis prolongation of pregnancy is contraindicated.
Contraindications for pregnancy prolongation are acute glomerulonephritis and
chronic glomerulonephritis at the stage of exacerbation, with pronounced arterial
hypertension and azotemia.
Acute glomerulonephritis and exacerbation of chronic

NB! glomerulonephritis are contraindications for pregnancy. Termination
of pregnancy is indicated irrespective of the gestational age.
Contraindications for pregnancy:

• acute glomerulonephritis;
• exacerbation of chronic glomerulonephritis;
• hypertonic and mixed glomerulonephritis;

• any variety of glomerulonephritis with signs of azotemia.
Diagnosis is made on the basis of past history findings (glomerulonephritis mostly
develops prior to pregnancy; it seldom exacerbates during pregnancy), clinical in-
vestigation, urine tests and kidney function test. When the signs are pronounced,
diagnosis does not present any difficulty.

Acute glomerulonephritis is differentially diagnosed from PE.
Chronic glomerulonephritis is differentially diagnosed from arterial hypertension,
urinary system diseases, normochromic anemia, etc.
Differential diagnosis between acute glomerulonephritis and exacerbation of chron-
ic glomerulonephritis is difficult: one takes into account the time period from the
onset of infection to acute expression of glomerulonephritis, the urinary syndrome.

Glomerulonephritis produces an adverse effect on the course of pregnancy and
fetal condition so patients with glomerulonephritis seldom see a positive outcome.
Common gestational complications in glomerulonephritis include spontaneous abor-
tion at an early gestational age, preterm birth, PE, anemia, fetoplacental insufficiency,
placental abruption, chronic hypoxia, FGR and fetal demise. The risk of gestational
complications increases if glomerulonephritis is accompanied by arterial hypertension
and renal function impairment. Patients with normal BP show obstetric complica-
tions and fetal demise 4–10 times less than patients with arterial hypertension.
In glomerulonephritis the endothelial lesion and activation of the clotting system
show a local and systemic nature. Endothelial and thrombocytic disorders in the
capillaries of renal glomerules cause nephrologic complications (renal insufficiency,
uremia), and in uterine and placental vessels — obstetric complications. Structural
signs of circulatory placental insufficiency are noted in more than a half of glomeru-
lonephritis pregnant patients, even when there are no clinical manifestations. The
ischemic placenta produces angiotropic substances that show properties of endothe-
lial toxins.
Systemic lesion and generalized vascular spasm, microcirculatory disorder, and
uterine ischemia affect the placental bed, disrupt the implantation of the gestational
sac, cause primary and secondary feto-placental insufficiency, provoke miscarriage
and preterm birth, PE, FGR, fetal demise.
PE develops in almost one half of pregnant patients with glomerulonephritis
prior to the common time (after 20 weeks). When diagnosing PE in the presence of
glomerulonephritis, one should assess the degree of arterial hypertension and pro-
teinuria which can indicate critical manifestations (eclampsia, HELLP syndrome,
DIC, placental abruption, fetal demise, renal failure).
In glomerulonephritis, arterial hypertension and azotemia lead to fetal demise
and preterm birth. Infants born to women with glomerulonephritis often show renal
disease (Fig. 22.7).
610 Obstetrics
Renal
insufficiency
Uremia
Endothelial Pregnancy loss

lesion, or preterm birth
hypercoagulation
Preeclampsia
Placental
insufficiency,
FGR, fetal hypoxia
Renal disease
in newborn
Fig. 22.7. Glomerulonephritis outcomes in pregnancy
Three degrees of risk are distinguished for women with glomerulonephritis:

• degree 1, minimal: pregnancy aggravates the course of the extragenital disease in
less than 20% of patients; gestational complications arise in no more than 20%
of women (latent, focal glomerulonephritis);
• degree 2, pronounced: the course of extragenital disease aggravates during
pregnancy or childbirth in more than 20% of patients; in 20–50% the
extragenital disease causes gestational complications: PE, spontaneous
abortion, preterm birth, often FGR, elevated perinatal mortality (nephrotic
glomerulonephritis);
• degree 3, maximum: pregnancy poses a threat to maternal life and well-being,
50% of women develop gestational complications. Infants are seldom born at
term, high perinatal mortality (hypertonic and mixed glomerulonephritis,
azotemia in any variety of glomerulonephritis, acute glomerulonephritis and
exacerbation of chronic glomerulonephritis) is noted.
22.2.4.9. Treatment
The conventional therapy for glomerulonephritis using cytostatics and immunode-
pressants is not administered to pregnant women due to the embryo- and fetotoxic
effects of the medications. A complex symptomatic therapy is administered including
diet, osmotherapy, hypotensive drugs, anticoagulants, antiaggregants, antioxidants,
protein supplements, and glucocorticoids if indicated.
Pregnant women with glomerulonephritis are managed jointly by

NB! a nephrologist and obstetrician-gynecologist.
During pregnancy women retain the same daily routine that was before pregnancy.
Women can continue on their job if it is not associated with getting cold. Sedentary
jobs are preferable as being in a vertical position for too long impairs the renal
function: the renal blood flow reduces, glomerular filtration and diuresis decrease,
proteinuria increases. Any exercise except for the complex recommended to pregnant
women should be discontinued. If the disease exacerbates or certain signs start pro-
gressing, the patient should keep to bed.
The diet of a pregnant woman should be adjusted to the variety of glomerulo-
nephritis; the main point is limiting sodium chloride and fluid intake. In case of
nephrotic glomerulonephritis accompanied by great losses of protein with urine and
hypoporteinemia, food rich in protein (120–160 g/day) is indicated to promote fetal
growth and development. It should be remembered that excess of protein foods in the
diet attenuates the appetite as soon as within a week, enhances proteinuria which in
some cases can be mistaken for superimposed nephropathy. Patients with mild latent
glomerulonephritis do not need any drug therapy. Antibiotics are not indicated in
chronic glomerulonephritis.
22.2.4.10. Management of pregnancy complicated by

glomerulonephritis
Follow-up examinations are made three times.
• Workup 1: pregnant women with chronic glomerulonephritis should have a
workup before 12 weeks gestation to specify the variety of glomerulonephritis
and to settle the question of carrying the pregnancy to term. Unwell patients
are hospitalized to a therapeutic hospital or a specialized nephrology
department.
• Workup 2 is performed at 28–30 weeks gestation when the body is under the
maximum pregnancy load; the objectives are diagnostics, prevention and
treatment of gestational complications.
• If pregnancy proceeds favorably, workup 3 is performed at 36–37 weeks gestation
to settle the timing and mode of delivery.
At any gestational age, once the patient’s general condition deteriorates or there
is a risk of miscarriage, PE, hypoxia or FGR, hospital care is indicated. If glomeru-
lonehritis or PE show no exacerbations, hospitalization is not required.
Patients with nephrotic glomerulonephritis are admitted to hospital as many times
and stay there as long as their condition requires.
Patients with nephrotic, mixed or hypertonic glomerulonephritis are at
risk for preterm fetal demise, so it does not seem expedient to wait till the
end of pregnancy. Preterm termination of pregnancy serves the interest of
the fetus.
• exacerbation of chronic glomerulonephritis with renal dysfunction;
• disorder of protein metabolism with progressing azotemia;
612 Obstetrics
• elevated BP;
• ineffectiveness of administered therapy;
• superimposed severe PE;
• deterioration of fetal condition.
If patients with hypertonic or mixed glomerulonephritis reject preterm termination
of pregnancy, they are managed according to the principles of nephrotic glomeru-
lonephritis therapy.
22.2.4.11. Management of labor and puerperium

Patients give a vaginal birth. During labor one closely watches the changes in BP,
provides adequate analgesia, hypotensive therapy, early amniotomy. Management of
the second stage of labor depends on BP values and fetal condition. In case of arte-
rial hypertension, hypotensive drug infusion is administered and once normal BP is
achieved. it is maintained at the required level. In case of latent glomerulonephritis
delivery at term without obstetric assistance is possible.
Cesarean section is mostly performed for obstetric indications.
During the puerperium, if the patient’s condition deteriorates, she is transferred to
a specialized department, and later she is followed up by a therapist or nephrologist.
Prevention is based on early treatment of acute glomerulonephritis, elimination
of infection foci.
22.2.4.13. Prognosis
For a pregnant woman, prognosis depends on the variety of glomerulonephritis
considering renal function values, rather than single signs of the disease. A favorable
prognosis is only possible when the patient shows normal BP, glomerular filtration
above 60 ml/min, the relative urine density over 1023, proteinuria below 5 g/day,
mild hematuria, no edema or eye fundus changes.
REMEMBER!
Glomerulonephritis is noninfectious allergic condition of kidneys involving mostly
glomerular vessels affecting the tubules and interstitial tissue.
In most cases the pathogens are hemolytic streptococci group A and B.
Glomerulonephritis development is usually associated with streptococcal infection
in past history (quinsy, scarlet fever, chronic tonsillitis, furunculosis). Dermal
streptococcal infection (pyodermia, erysipelas) is not uncommonly the cause of
infection.
Common gestational complications in glomerulonephritis encompass early
spontaneous abortion, preterm birth, PE, anemia, placental insufficiency, preterm
separation of placenta, fetal hypoxia and demise.
The risk of gestational complications is higher when glomerulonephritis is
accompanied by arterial hypertension and renal dysfunction. Patients with normal
BP show obstetric complications and fetal or neonatal demise 4–10 times less
often than patients with arterial hypertension.

• exacerbation of chronic glomerulonephritis with renal dysfunction;
• disorder of protein metabolism with progressing azotemia;
• elevated BP;
• ineffectiveness of administered therapy;
• superimposed severe PE;
• deterioration of fetal condition.
Contraindications for pregnancy in women with renal disease: acute

glomerulonephritis, hypertonic and mixed glomerulonephritis, any variety of
glomerulonephritis with signs of azotemia.
CHECK YOURSELF!
Level 1. Test
Select one correct answer
1. In pregnant women anemia is often due to:
a) vitamin deficiency;
b) iron deficiency;
c) excess of micronutrients;
d) residing in urban areas.
2. Common variety of anemia in pregnant women:

a) megaloblastic anemia;
b) hypoplastic anemia;
c) iron and protein deficiency anemia;
d) sickle cell anemia.
3. Immediate causes of iron deficiency anemia:

a) iron deficiency;
b) frequent common colds;
c) frequent blood loss;
d) immunodeficiency conditions.
4. Clinical features of anemia in pregnant women:

a) skin pallor;
b) arterial hypertension;
c) puffy face;
d) proximal myopathy.
5. Typical gestational complications in anemia:

a) FGR;
b) polyhydramnios;
c) gestational diabetes mellitus;
d) PE.
614 Obstetrics
6. Common complications of childbirth in anemia:

a) uterine inertia;
b) arterial hypertension;
c) arterial hypotension;
d) acute fetal hypoxia.
7. Methods of anemia treatment:

a) iron supplements;
b) surgery;
c) infusion therapy;
d) plasmapheresis.
8. Termination of pregnancy is indicated in

a) acute glomerulonephritis;
b) acute cystitis;
c) asymptomatic bacteriuria;
d) urinary stone disease.
9. In pregnancy with kidney disease a diet should:

a) not be followed;
b) be followed by all means;
c) contain protein;
d) contain no salt.
10. Workup of pregnant patients with pyelonephritis includes:

a) urine culture to determine drug susceptibility;
b) weekly urine test for protein;
c) BP measuring;
d) measuring intraocular pressure.
11. Which gestational pyelonephritis develops more often:

a) right-sided;
b) left-sided;
c) bilateral.
12. Gestational pyelonephritis develops at the following critical periods:

a) 14–22 weeks;
b) the first trimester of pregnancy;
c) gestational age does not matter;
d) the third trimester of pregnancy.
13. Contraindications for carrying pregnancy to term in pyelonephritis:

a) pyelonephritis of the only kidney;
b) bilateral pyelonephritis;
c) pyelonephritis combined with diabetes mellitus;
d) pyelonephritis combined with severe anemia.
14. Normal RBC value in a healthy woman:

a) 4.0–5.5×1012/l;
b) 1.5–2.5×1012/l;
c) 5.5–6.0×1012/l;
d) 3.2–3.7×1012/l.
15. Risk factors for anemia development in pregnant women:

a) short interval between childbirths;
b) residing in urban area;
c) great physical load;
d) smoking, alcohol abuse during pregnancy.

1. Pregnant woman A. aged 22, gestational age 27–28 weeks, cephalic presenta-
tion, presents at maternal welfare clinic with weakness, dizziness. Objective findings:
BP 90/60 mm Hg, heart rate 78 per min, rhythmical, skin pallor, angular cheilitis.
Uterine tone is normal. The patient feels the fetal movements well. Heart beat is
clear, rhythmical, 136 per min. Mucous discharge from the vagina. Complete blood
count: Hb 80 g/l, RBCs 2.8×1012/l, hematocrit 24 g/l. Make your diagnosis, define
the plan of management.
2. Pregnant woman K. aged 28, gestational age 28 weeks was brought to the admis-
sion department with presentations of right lumbar and lower abdominal pain, pain-
ful urination, body temperature elevated to 38.2 °С. Past history: primigravid, acute
cystitis and nonspecific vaginitis in the first trimester. Objective findings: satisfactory
condition, temperature 38.3 °С, abdomen painless to palpation, no peritoneal signs,
right costovertebral angle tenderness; vaginal transducer ultrasound: cervix shortened
to 25 mm, internal os closed, body of uterus enlarged to 28 weeks, excitable, mucous
discharge. Complete blood count: WBCs 14×109/l, Hb 110 g/l, RBCs 3.44×1012/l;
urinalysis: relative density 1020, protein 1 g/l, WBCs 50–60, RBCs not present, large
amount of bacteria noted. Make your diagnosis. What additional investigations are
required? What is the adequate treatment?
22.3. PREGNANCY AND LABOR

WITH DIABETES MELLITUS
Diabetes mellitus is a condition with insulin deficiency in the body. The deficiency
is absolute when the pancreas produces the hormone in small amounts; it is relative
when the patient’s tissues are not responsive to insulin although the secretory func-
tion of the pancreas is not disturbed.
Gestational diabetes mellitus (GDM) is a transient disorder of glucose tolerance
newly diagnosed during pregnancy.
ICD-10 code
• O24.4 Diabetes mellitus arising in pregnancy.
616 Obstetrics
22.3.1. General information

The incidence rate of GDM is growing steadily all over the world. In the
general population of various countries the rate of GDM amounts to 1–14%,
and 7% on average. The fluctuations are due to different methods of DM diag-
nostics; they are directly related to the incidence rate of DM type 2 in certain
ethnic groups.
The rate of this condition is 0.5% per the entire number of deliveries; the number
of diabetic pregnant women increases due to the similar tendency in the general
population. In the first trimester DM is newly diagnosed in 2.1%, in the second
trimester — in 5.6%, in the third trimester — in 3.1%. According to the American
Diabetes Association, about 70% of all pregnancies (over 20 000 cases annually) are
complicated with GDM. GDM presents an urgent medical and social problem as it
considerably increases the rate of adverse pregnancy outcomes for the mother, fetus
and newborn.
Specific features of GDM:
• GDM is a risk factor for the development of obesity, DM type 2 and cardiovascular
disease in the mother and future progeny;
• pregnancy is a condition of physiological insulin resistance, so pregnancy itself
poses a considerable risk factor for a disorder of carbohydrate metabolism.
The notions of diabetes mellitus, overt diabetes mellitus and GDM require a clear
definition in clinical and laboratory terms.
Three main types of DM are distinguished in clinical practice:
• DM type 1, insulin dependent diabetes;
• DM type 2, non-insulin-dependent diabetes;
• DM type 3, GDM that develops after 28 weeks gestation; it is a transient disorder
of glucose utilization in pregnant women
According to the WHO classification, the following types of DM are distin-
guished:
• DM type 1 (insulin dependent):
– autoimmune DM;
– idiopathic DM;
• DM type 2 (non-insulin-dependent);
• other specific types of DM:
– genetic defects of β-cell function;
– genetic defect in insulin action;
– disorder of endocrine portion of the pancreas;
– endocrinopathy;
– drug- or chemical-induced diabetes;
– infection;
– unusual types of immune-mediated diabetes;
• other genetic syndromes that sometimes combine with diabetes;
• GDM.
22.3.1.3. Etiology
Diabetes mellitus type 1 is an autoimmune disorder with destruction of beta-cells
in the pancreas. It develops in children and teenagers who typically show absolute
insulin insufficiency, labile course of the disease, predisposition to ketoacidosis, an-
giopathy, autoantibodies to one’s own antigens of beta pancreatic cells. The risk of
diabetes in the offspring of a diabetic mother is 2–3%, of a diabetic father — 6.1%,
in case both parents are diabetic — 18%.
Diabetes mellitus type 2 develops in people over 30, often in presence of obesity;
relative insulin insufficiency is common: tissues show decreased sensitivity to endog-
enous insulin (insulin resistance). If metabolic disorders are mild, this type of DM
with its late onset does not compromise the reproductive function.
Insulin affects all types of metabolism. Insulin is an anabolic hormone. When
insulin is deficient as a factor promoting glucose utilization and biosynthesis of gly-
cogen, lipids, proteins, the metabolism of glucose is disrupted and gluconeogenesis
increases resulting in hyperglycemia, the main sign of DM.
In a physiologically proceeding pregnancy, carbohydrate metabolism changes to
adjust to the growing fetal demand for energy, mostly glucose. A normal pregnancy
in the second and third trimester typically shows a decreased glucose tolerance and
decreased sensitivity to insulin (due to contra-insular placental hormones), enhanced
insulin breakdown and increase in free fatty acid content.
Placental and fetal demand for energy is met at the expense of glucose passing to
the fetoplacental system from the mother. Due to the decreased glucose level, the
sensitivity of maternal tissues to insulin increases in the first trimester. At later ges-
tational ages, there is an increase in the content of placental hormones suppressing
glucose utilization by maternal tissues, which provides for sufficient glucose delivery
to the fetoplacental system. That is why after a meal even healthy pregnant women
show elevated blood glucose compared with non-pregnant women. A persistent mild
hyperglycemia leads to compensatory hyperinsulinemia. At the same time, there
develops physiological insulin resistance mediated by placental hormones: proges-
terone, estrogens, prolactin and placental lactogen. Insulin resistance also promotes
hyperinsulinemia.
Hyperglycemia inhibits glucagon secretion, so a considerable portion of glucose
turns into triglycerides — lipid metabolism is disrupted.
By 10–12 weeks gestation fetal pancreas produces differentiated beta-cells capable
of secreting insulin. Mild hyperglycemia in the mother causes elevation of fetal blood
glucose, which stimulates the secretion of fetal insulin.
NB! Maternal insulin does not permeate the placenta.
In late pregnancy lipolysis becomes more intensive under the impact of placental
lactogen, which results in elevated levels of glycerin and free fatty acids in the plasma,
and thus ketogenesis increases. Another cause of ketogenesis increase is the effect
of placental hormones on maternal hepatocytes. Ketone bodies (beta-oxybutyric and
618 Obstetrics
acetoacetic acids) can pass freely through the placenta; they are utilized by fetal liver
and brain as a source of energy.
The changes in carbohydrate metabolism discussed above are similar in their na-
ture to changes induced by DM, so pregnancy is regarded as a factor predisposing
to diabetes. This tendency promotes the development of a transient glucose tolerance
disorder, GDM.
Pregnant women may show transient glucosuria associated with changes in renal
filtration function rather than with carbohydrate metabolism disorder. Transient
glucosuria does not require therapy; however, it should be differentially diagnosed
from GDM.

Predisposition to DM can be inherited during the preimplantation period.
Inherited chromosome mutations can be the cause of disease development. Genetic
mutations during this period result in zygote destruction.
GDM, disorder of cellular metabolism and angiopathy affect embryogenesis.
Maternal insulin does not pass through the placenta, and the fetus cannot produce its
own insulin until 8–12 weeks gestation. Excess glucose passing from mother to fetus
leads to a pronounced metabolic disorder including intensified lipid peroxidation,
formation of substrates with a teratogenic effect. That is why at the very beginning
of organogenesis hyperglycemia causes dysfunction in the anlage of body systems and
organs, that is, diabetic embryopathy develops.
Placental bed is the first to bear the brunt of hyperglycemia development. Typically,
hypoplastic types of placenta develop: succenturiate or annular placenta. Angiogenesis
disorders are possible, like formation of a single umbilical artery instead of two, emer-
gence of arteriovenous anastomoses. In a pregnant diabetic patient the myometrial
segment of uteroplacental arteries does not undergo appropriate gestational changes.
Due to functional insufficiency of the second wave of cytotrophoblast invasion, these
arteries retain their regular wall structure with a narrow lumen and become unable
to provide for an adequate increase in uteroplacental blood flow during the second
and third trimesters. Insufficiency of trophoblast invasion, disorder of uteroplacental
circulation and some variants of villi immaturity are regarded as the initial stage in the
development of primary placental insufficiency. Vascularization becomes inadequate,
the chorionic tree development is disrupted, cotyledon formation lags behind, which
results in placental hypofunction. Later, villi maturation slows down; their develop-
ment is restricted and dissociated. Immature terminal villi reduce the metabolism
and synthesis of hormones.
Thus, there arise unfavorable conditions for trophoblast and embryo development,
which can result in miscarriage in the first trimester or in placental insufficiency if
the pregnancy persists.
In a healthy pregnant woman the fasting plasma glucose declines

NB! as pregnancy progresses.
In late pregnancy DM often causes PE which is promoted by diabetic mi-

croangiopathy affecting vessels in the lesser pelvis, placenta and uterus, and by
DIC. PE mostly manifests as arterial hypertension and edema; however, severe

forms to the extent of eclampsia are not uncommon. When PE combines with
diabetic nephropathy, the threat to maternal life increases manifold, as uremia
may develop.
The pathogenesis of polyhydramnios encompasses fetal polyuria, reaction of the
amnion to the increased glucose content in the amniotic fluid as glucose can pass
through the placental barrier.
The hormone-producing placental function decreases, uteroplacental blood supply
reduces, fetal DIC and diabetic fetopathy develop, multiple malformations and even
intrauterine fetal demise are possible.
In polyhydramnios, fetal demise is associated with progressing anoxia due to
placental ischemia resulting from the mechanical pressure of amniotic fluid. Fetal
demise usually occurs at 36–39 weeks gestation. This outcome is more common in
case of macrosomia, ketoacidosis, vascular disease and PE. When DM combines with
PE, the rate of stillbirths amounts to 18–25%.
Hyperglycemia intensifies the production of a number of hormones needed by
the fetus. In particular, it influences the synthesis of somatotropic hormone which
produces its effect mostly by stimulating somatomedin/insulin-like factors. They are
noted in early pregnancy and become functional in the second trimester when fetal
growth is especially active.
When maternal DM is sub- or decompensated, fetal blood shows a stably elevated
glucose concentration, which stimulates hyperplasia of beta-cells in fetal pancreas.
Until 28 weeks gestation the fetus cannot synthesize most fatty acids receiving ma-
ternal acids from the placenta, so in the second trimester almost no excess glucose
is expended for lipogenesis.
In case of maternal DM the fetus shows excessive buildup of fatty tissue, but the
muscle bulk and bone thickness are relatively normal. Phenotypical signs of diabetic
fetopathy develop; their emergence was predetermined much earlier. Alongside with
hypertrophy of the insular pancreatic cells, the fetus shows a relative decrease in the
weight of the brain and thymus.
The heart, adrenals and kidneys increase in proportion to the growth of fetal
weight, but this is not always the case. Sometimes the fetus continues to grow slowly.
Dysfunction of many organs is due to enzymatic immaturity.
Chronic fetal hypoxia manifests as low oxygen saturation of the blood, acidosis,
enhanced erythropoiesis, foci of extramedullary hemopoiesis, high level of glycated
hemoglobin, large amount of RBCs and polycythemia.
The syndrome of neonatal respiratory disorder is due to fetal hyperinsulinemia
which blocks the activating effect of cortisol on enzymes participating in phospho-
lipid synthesis in alveolar epithelial cells, and this results in decreased surfactant
production (Fig. 22.8).
22.3.2. Gestational diabetes mellitus

Gestational diabetes mellitus is hyperglycemia newly diagnosed during preg-
nancy but this condition does not meet the criteria of overt DM (Tables 22.2,
22.3).
620 Obstetrics
Preimplantation Predisposition
period for DM
Compromised
Metabolism disorder,
primordium of organs
teratogenic substrate
and systems
accumulation
(diabetic embryopathy)
Insufficient Pregnancy
cytotrophoblast loss or preterm
invasion birth
Intrauterine
demise
Placental
Insufficiency
insufficiency,
of placental bed
fetal hypoxia
Diabetic
Hyperglycemia
fetopathy
Diabetic
Preeclampsia
microangiopathy
Malformations
Hyperconcentration
of glucose
Polyhydramnios
in amniotic fluid,
fetal polyuria
Elevated somatotropin
synthesis, accumulation
Macrosomia
of adipose tissue
in fetus
Hyperinsulinemia, Respiratory
reduced surfactant disorder
production syndrome
Fig. 22.8. Pathogenesis of gestational disorders in diabetes mellitus
Pregnant women are classified at high risk if they show at least

NB! one of the following signs:
• obesity (initial BMI  30.0 kg/m2);
• type 2 DM in close relatives;
• any disturbance of carbohydrate metabolism (gestational DM in
previous pregnancy);
• disturbed glucose tolerance (disturbed fasting glycemia) in past
history;
• glucosuria.
The fasting glucose level in venous plasma is <5.1 mmol/l, and in one hour (dur-
ing an oral glucose tolerance test) <10.0 mmol/l, and in two hours ≥7.8 mmol/l and
<8.5 mmol/l which indicates disorder of glucose tolerance in nonpregnant individuals
while in pregnant women it is within normal.
Table 22.2. Threshold values of venous plasma glucose in diagnostics of GDM
Venous plasma glucose*, ** mmol/l mg/dl

Gestational DM at presentation
Fasting ≥5.1, but <7.0 ≥92.0 but <126
Gestational DM, oral glucose tolerance test with 75 g glucose
In one hour ≥10.0 ≥180
In two hours ≥8.5 ≥153
* Only glucose level in the venous plasma is studied. It is not advisable to use whole capillary
blood specimens.
** At any gestational age (one abnormal finding of venous plasma glucose is enough).
*** When the findings of oral glucose tolerance test with 75 g of glucose are available, the
diagnosis of gestational DM is made if at least one out of three values of venous plasma glucose
is equal to or higher than the threshold value. When abnormal values are obtained at the
baseline measuring, glucose load is not administered; when abnormal values are noted at the
second point, the third measurement is not required.
Table 22.3. Threshold values for venous plasma glucose in diagnostics of overt (new-onset)
GDM (Russian National Consensus Gestational Diabetes: Diagnosis, Treatment, Postpartum
Followup, 2012)
Overt (new-onset) gestational DM*

Fasting venous plasma glucose ≥7.0 mmol/l (126 mg/dl)
HbA1c** ≥6.5%
Venous plasma glucose irrespective of the time of day or ≥11.1 mmol/l (200 mg/dl)
meals when hyperglycemia signs are present
* If abnormal findings are noted for the first time and there are no hypoglycemia signs, the
presumptive diagnosis of GDM should be confirmed by the levels of fasting venous plasma glu-
cose or HbA1c using standardized tests. When hyperglycemia signs are present, the diagnosis of
GDM is made on the basis of one value within the diabetic range (glycemia or HbA1c). If overt
DM is detected, it should be defined according to the active classification by WHO as soon as
possible, for instance, DM type 1, DM type 2, etc.
** HbA1c, glycated hemoglobin, is a biochemical parameter of the blood indicating the mean
content of blood sugar over a prolonged time period (up to 3 months) in contrast to the blood
glucose value which reflects the glucose level merely at the moment of investigation (using a
test method with NGSP certification and standardized to the DCCT reference range).
The test findings are interpreted by an obstetrician-gynecologist, therapist, general

practitioner. An endocrinologist consultation is not required to establish the fact of
carbohydrate metabolism disorder in a pregnant patient.
22.3.2.1. Diagnostics of carbohydrate metabolism disorders during

pregnancy
Diagnostics of carbohydrate metabolism disorders during pregnancy is a two-stage
process.
622 Obstetrics
• Stage one takes place at the first visit. At the first antenatal visit at any gestational
age before 24 weeks each pregnant woman without fail has one of the following tests
– fasting venous plasma glucose;
– glycated hemoglobin (HbA1c);
– venous plasma glucose at any time of day irrespective of meals intake.
– If the test findings correspond to the category of overt DM (see Table 22.3), its
variety is specified, and the patient is immediately referred to an endocrinolo-
gist.
– If HbA1c <6.5%, or accidentally detected plasma glucose <11.1, fasting venous
plasma glucose test is administered.
– If fasting venous plasma glucose ≥5.1 mmol/l, but <7.0 mmol/l, diagnosis of
GDM is made (see Table 22.2).
– If fasting venous plasma glucose <5.1 mmol/l, all pregnant women at a high
risk of GDM are immediately administered an oral glucose tolerance test with
75 g glucose (see below).
• Stage two takes place at 24–28 weeks gestation.
All women showing no disorders of carbohydrate metabolism in early pregnancy
have an oral glucose tolerance test with 75 g glucose.
Oral glucose tolerance test principles

An oral glucose tolerance test with 75 g glucose is a safe loading diagnostic test
for detection of carbohydrate metabolism disorder during pregnancy.
• The test findings can be interpreted by an obstetrician-gynecologist, therapist,
general practitioner or endocrinologist.
• The subject continues with her usual diet (no less than 150 g carbohydrate a
day) for at least three days before the test. The test is made in the morning on an
empty stomach after 8–14 hours fasting. The last meal should contain 30–50 g
of carbohydrates. There is no limitation of water intake. Medications that can
affect the blood glucose level (polyvitamins and carbohydrate-containing
iron supplements, glucocorticoids, beta-adrenoblockers, beta-adrenomimetics)
should be taken after the test is over, if possible.
An oral glucose tolerance test is not administered:

• in early toxicosis of pregnancy (nausea, vomiting);
• when the patient has to stay in bed (the test is not made until the patient can freely
move about);
• in the presence of an acute inflammatory or infectious disease;
• in the presence of chronic hepatitis exacerbation or dumping syndrome
(postgastrectomy syndrome).
The test for venous plasma glucose is only made in laboratories using chemistry
analyzers or glucose analyzers. Self-monitoring blood glucose test systems (glucom-
eters) cannot be used for the oral glucose tolerance test.
In exceptional cases the oral glucose tolerance test with 75 g glucose can be ad-
ministered at gestational ages until 32 weeks gestation (high risk for GDM, fetal size
by ultrasound tables for intrauterine growth assessment ≥75 percentile, ultrasound
signs of diabetic fetopathy).
Oral glucose tolerance test administered in late pregnancy can be

NB! dangerous for the fetus.
22.3.2.2. Management and treatment of pregnant women with GDM

The patient is observed by a gynecologist, endocrinologist, therapist, general
practitioner for 1–2 weeks.
• Diet therapy excluding easily digested carbohydrates and limiting fats; breaking
down the daily ration into even portions for 4–6 meals.
• Graduated exercise (walking) no less than 150 min a week, swimming.
• The patient performs self-monitoring and submits the readings to the doctor
(Table 22.4). Self-monitoring encompasses:
– fasting test for glycemia using glucometers before and one hour after the main
meals (Fig. 22.9);
– fasting test for ketonuria and ketonemia in the morning;
– BP measuring;
– noting fetal movements;
– measuring the weight;
– keeping food records and test records.
If the tests show ketonuria or ketonemia, additional intake of carbohydrates (about
15 g) before sleep or at nighttime is indicated.
Indications of insulin therapy
• inability to achieve the target glycemia level (2 and more non-target glycemia
values) over 1–2 weeks of self-monitoring (see Table 22.4);
• signs of diabetic fetopathy by the findings of an expert ultrasound examination
which is indirect evidence of chronic hyperglycemia.

Diabetic patients typically have mouth dryness, polydipsia, increased fluid intake
(over 2 l), polyuria, skin itch, particularly in the area of the anus and genitals, tran-
sient vision disorder, weight loss, sleep disorder. There is a pronounced tendency for
pyoderma, furunculosis, vaginitis.
Table 22.4. Target glycemia levels for self-monitoring
Parameter Target level

Glucose Findings calibrated against plasma
Fasting <5.1 mmol/l
Before meal <5.1 mmol/l
Before sleep <5.1 mmol/l
At 3 AM <5.1 mmol/l
1 hour after a meal <5.1 mmol/l
Hypoglycemia none
Ketone bodies in urine none
BP <130/80 mm Hg
624 Obstetrics
Fig. 22.9. A hand-held glucometer
by 33% by 75%
Prior First Second Third

to pregnancy trimester trimester trimester
Fig. 22.10. Insulin requirement in pregnant women
Most pregnant women with diabetes show no changes; sometimes improved glu-
cose tolerance is noted (due to estrogens) which stimulates insulin production by
the pancreas. In its turn, peripheral assimilation of glucose improves, too. Glycemia
levels go down, even to the extent of hypoglycemia, which calls for lesser insulin
doses in diabetic patients. The reduced insulin requirement is associated with inten-
sive utilization of glucose by the fetus, so in the first trimester the condition of the
carbohydrate metabolism should be watched closely and efforts should be taken to
prevent hypoglycemia and ketoacidosis (Fig. 22.10).
Due to the effect of contriunsular hormones (glucagon, placental lactogen, prolac-
tin), in the second trimester carbohydrate tolerance deteriorates, diabetic presenta-
tions intensify, the glycemia level and glucosuria increase, ketoacidosis is possible.
During this period the insulin dose should be increased.
In the third trimester the contrinsular hormone level decreases leading to a bet-
ter carbohydrate tolerance; glycemia and the administered dose of insulin decrease.
Improvements in the course of diabetes are associated with the effect of fetal insulin
on the mother, and with enhanced glucose utilization by the fetus, glucose passing
from maternal blood through the placenta.
The specifics of diabetes course determine the recommended hospitalization time
in the second and third trimesters (see below).
Pregnancy has an adverse effect on the course of DM: vascular complications
start progressing; in particular, diabetic retinopathy is diagnosed in 35% of patients;
diabetic nephropathy promotes superimposition of PE; pyelonephritis exacerbations
recur. Asymptomatic bacteriuria is noted in pregnant women with DM two-three
times more often than in non-diabetic women. Urinary tract infection is noted in
16%, and pyelonephritis — in 6–31% of pregnant women. However, in most diabetic
patients the first half of pregnancy proceeds without particular complications, except
for threatened abortion: its risk increases if during the first 3 months of pregnancy the
glycated hemoglobin concentration or fasting blood glucose are 12% and 6.7 mmol/l,
correspondingly.
In late pregnancy PE often develops (30–70%). Spontaneous abortion occurs in
15–31% of women at 20–27 weeks. A preterm birth is associated with decompen-
sation of DM and its complications, and severe obstetric complications like PE.
Polyhydramnios is diagnosed in 20–60% of pregnant women. Polyhydramnios often
combines with fetal malformations and still birth (29%).
During labor diabetic patients show uterine inertia (10–15%) due to uterus
overdistention by a large fetus, and polyhydramnios. For the same reasons, cepha-
lopelvic disproportion, asphyxia and frequent injury of the fetus (clavicle fracture,
shoulder dystocia, intracranial trauma) and mother (rupture of cervix, vaginal wall,
perineum) are noted. Premature membrane rupture is seen in 20–30% of pregnant
women.
Comatose conditions — ketonemic and hypoglycemic coma — are dangerous DM
complications of pregnancy.
Diabetic fetopathy is a complex of signs including a distinctive appearance, func-
tional immaturity of fetal organs and systems, accelerated fetal weight gain, a high
rate of congenital abnormalities, abnormalities in the puerperium course, high peri-
natal mortality.
Two variants of diabetic fetopathy are distinguished:
• hypertrophic fetopathy (fetal macrosomia while the fetal body length is within
normal; increased size and weight of the placenta (fig. 22.11));
Fig. 22.11. Newborn with diabetic fetopathy

626 Obstetrics
• hypoplastic fetopathy (placental insufficiency manifests as FGR, low birth

weight, small placental size and more pronounced signs of intrauterine hypoxia
and asphyxia at birth.
The rate of newborns weighing 4 kg and more is greater than in the general
population. Fetal weight gain before 28 weeks gestation does not differ from normal
values essentially. The peak weight gain is noted at 28–36 weeks gestation. Over the
last two weeks weight gain decelerates, so immature newborns of diabetic mothers
show a weight considerably higher that the value appropriate for their gestational
age.
Ultrasound signs of diabetic fetopathy:
• large fetus — macrosomia (abdomen circumference ≥75 percentile);
• hepatosplenomegaly;
• cardiomegaly/cardiopathy;
• double contour of fetal head;
• edema and thickening of subcutaneous fat;
• increased nuchal translucency.
One should give consideration to a new-onset or progressing polyhydramnios
when GDM diagnosis has been made (if other causes of polyhydramnios have been
ruled out).
22.3.2.5. Diagnosis
The most accurate method of diagnosing the disease is doing fasting plasma glu-
cose test and random plasma glucose test.
Despite the fact that the urine of healthy individuals contains no sugar, pregnant
women may show glucosuria associated with changed renal filtration rather than
with carbohydrate metabolism disorder. To make sure that in this particular case
glucosuria is not a sign of GDM, fasting plasma glucose test is done. If the kidney
function is unimpaired, glucosuria becomes noticeable only when the blood sugar is
higher than 8.88–9.99 mmol/l.
Ketonemia (elevated amount of ketone bodies — acetone, acetoacetic and
beta-oxybutyric acid — lipid metabolism products, in the blood) and acetone
in urine emerge upon DM decompensation. Ketone bodies detected in urine
cannot pass to the fetus while ketone bodies contained in the blood do pass
to the fetus.

Achieving stable compensation of DM 2–3 months before conception and over
the first 7 weeks of pregnancy constitutes prevention of congenital malformations.
Pregnant diabetic patients receive care in outpatient and inpatient settings. The
algorithm of fetopathy and perinatal mortality prevention in expectant mothers with
DM is as follows.
• All women with DM and planning pregnancy should be referred to an
endocrinologist 5–6 months before conception to specify the extent of DM
compensation, verifying the presence and extent of late DM complications,
receiving training on self-monitoring skills and settling the question of their
ability to carry pregnancy to term.
• Once pregnant, the woman should have multiple workups, and hospitalized if
situation so requires:
– At an early gestational age (at 4–6 weeks preferably):
◊ clinical workup;
◊ adjusting the insulin dose;
◊ receiving diabetes education;
◊ specifying the presence and extent of late diabetes complications;
◊ detection and management of obstetric complications;
◊ geneticist consultation;
– at 12–14 weeks when the insulin requirement decreases, and the rate of hypo-
glycemic episodes increases;
– at 23–24 weeks gestation:
◊ adjusting insulin dose;
◊ monitoring the course of diabetic complications;
◊ etection and management of newly developed gestational complications
(threatened abortion, polyhydramnios, genitourinary infection);
◊ assessment of the fetoplacental complex condition;
◊ a cycle of symptomatic therapy;
• at 34–36 weeks gestation:
◊ insulin therapy adjustment;
◊ detection and management of diabetes complications;
◊ prevention of hyaline membrane disease of fetal lungs;
◊ preparation for childbirth;
◊ choosing the timing and mode of delivery.
The question of the possibility of pregnancy, its preservation or termination is
settled in consultation with obstetrician gynecologist, therapist, endocrinologist be-
fore 12 weeks gestation.
Contraindications for pregnancy in DM
• Presence of rapidly progressing vascular complications that are usually
noted in severe disease (retinopathy, nephropathy); they complicate the
course of pregnancy and aggravate the prognosis for the mother and
fetus.
• Presence of insulin resistant DM and labile DM.
• Combination of DM and Rh-sensitization in the mother, which considerably
aggravates the prognosis for the fetus
• Combination of DM and active tuberculosis of lung in which case pregnancy
often results in severe exacerbation of tuberculosis.
When GDM is revealed or insulin therapy is initiated, hospitalization is not always
required; it depends on the presence of obstetric complications. Antepartum hospital-
ization of pregnant women with GDM compensated by a diet and showing no signs
of fetopathy takes place at 37 weeks gestation. If insulin therapy is administered,
the pregnant woman is managed by an endocrinologist, obstetrician gynecologist
and therapist.
Administration of peroral antihyperglycemic drugs to pregnant or
NB! lactating women is contraindicated!
628 Obstetrics
Pregnant women receiving insulin therapy or showing signs of diabetic fetopathy

are hospitalized at 36 weeks.
22.3.2.7. Delivery
If DM is compensated and the fetus is in satisfactory condition, preterm termina-
tion of pregnancy is not expedient. The obstetrician gynecologist and endocrinologist
determine the timing and mode of delivery. Compensated DM is not an indication
for a planned cesarean section except for certain cases of macrosomia and/or breech
presentation. If diabetic fetopathy signs are prominent (even with an estimated fetal
weight <4 kg), a planned cesarean section can be considered so as to avoid labor-
related injury.
22.3.2.8. Postpartum care and planning subsequent pregnancy

All women with GDM should have their venous plasma glucose tested obligatorily
over the first 3 postpartum days so as to reveal possible disorders of carbohydrate
metabolism.
Patients with GDM in past history are at a high risk for its development during
subsequent pregnancies and DM type 2 in future. Consequently, such patients should
be followed up by an endocrinologist.
• 6–12 weeks after childbirth all women with fasting plasma glucose <7.0 mmol/l
have an oral glucose tolerance test with 75 g glucose (fasting glucose test and 2 h
after a load) so as to reconsider the extent of carbohydrate metabolism disorder
by glycemia categories (normal, disturbed glucose tolerance, disturbed fasting
glycemia, DM).
• If blood sugar levels are within normal, another oral glucose tolerance test is
done in 3 years, and if glycemia tolerance or fasting glycemia is disrupted, it is
done in 6 months.
• Diet aimed at weight loss if overweight.
• Increasing physical activity.
• Planning subsequent pregnancies.
Pediatricians and adolescent doctors should be informed about the need to moni-
tor carbohydrate metabolism and provide DM type 2 prevention in an infant of a
mother with GDM.
Satisfactory diabetes compensation permits prevention of complications both in
the mother and fetus. It is important to prevent the development of hyperglycemia,
ketoacidosis and severe hypoglycemia.
22.4. ARTERIAL HYPERTENSION
Hypertensive disorders of pregnancy (including PE) are noted in 2–8% of preg-

nancies.
Hypertensive complications of pregnancy remain a major cause of maternal and
perinatal mortality the world over (26% in Latin America, 9% in Africa, 15% on
average). Over 50 000 pregnant women die annually due to arterial hypertension-
related complications. According to the Ministry for Public Health of the Russian
Federation, over the last decade hypertensive complications have ranked No. 3 and
4 in the structure of causes of maternal mortality, arterial hypertension increases the
risk of placental abruption and massive hemorrhage; it can precipitate a disorder of
cerebral circulation in the woman as well as retinal detachment or eclampsia. Arterial
hypertension also causes such complications as progressing placental insufficiency
and IUGR, in severe cases — asphyxia and fetal demise. A long term prognosis
for women experiencing hypertensive gestational complications encompasses an in-
creased incidence rate of obesity, DM, ischemic heart disease, stroke. Children of
such mothers also show various metabolic, hormonal, cardiovascular disorders.
22.4.1. Classification of hypertensive disorders during

pregnancy
ICD-10 codes are represented in Table 22.5.
Chronic arterial hypertension (pre-existing hypertension) refers to AH diagnosed
before the onset of pregnancy or before 20 weeks gestation; this is hypertonic disease
or secondary (symptomatic) hypertension. In pregnant patients with chronic AH the
degree of AH is not simple to determine as the first and second trimesters commonly
demonstrate a physiological decrease in BP.
AH can be:
• primary;
• symptomatic.
Stages of hypertonic disease (pre-existing essential hypertension):
• stage I: target organs are not involved;
• stage II:
– left ventricular hypertrophy;
– local or generalized narrowing of retinal vessels;
Table 22.5. Classification of hypertensive disorders during pregnancy by ICD-10
Nosological entity Code

Chapter: pregnancy, childbirth and the puerperium
Block: edema, proteinuria and hypertensive disorders in pregnancy, childbirth and the
puerperium
Pre-existing hypertension О10
Pre-existing essential hypertension О10.0
Pre-existing secondary hypertension О10.4
PE superimposed on chronic hypertension О11
Gestational hypertension О13
Pre-eclampsia О14
Mild to moderate pre-eclampsia О14.0
Severe pre-eclampsia О14.1
Eclampsia О15
Eclampsia in pregnancy О15.0
Eclampsia in labor О15.1
Eclampsia in the puerperium О15.2
630 Obstetrics
– microalbuminuria, proteinuria, elevated creatinine concentration in the blood

plasma;
– signs of atherosclerosis of the aorta, coronary, carotid or femoral arteries;
• stage III:
– heart: angina pectoris, myocardial infarction, cardiac failure;
– brain: transient disorder of cerebral circulation, stroke, hypertonic
encephalopathy;
– kidneys: renal failure;
– vessels: dissecting aneurism, signs of peripheral arteries occlusion.
PE/eclampsia with pre-existing AH. When there is pre-existing AH, PE is diag-
nosed in pregnant women in case of:
• first emergence of proteinuria after 20 weeks (0.3 g and more of protein in daily
urine) or a prominent increase of pre-existing proteinuria;
• progressing AH in women whose BP was easily controlled before 20 weeks
gestation;
• signs of multiple organ failure after 20 weeks gestation.
Gestational AH is increased BP level first noted after 20 weeks gestation while the
proteinuria values are within normal.
Pre-eclampsia/eclampsia. PE is a pregnancy-specific syndrome that emerges after
20 weeks gestation, is recognized by the presence of AH and proteinuria (over 0.3 g
in daily urine).
The diagnosis of eclampsia is made when a patient with PE

NB! develops convulsions which cannot be attrubuted to anything
else.
AH criteria in pregnancy
• Diastolic blood pressure is a more valuable diagnostic parameter of PE than
systolic BP as it is less subject to fluctuations.
• In pregnant women the diagnosis of AH is justified when diastolic BP ≥90mm
Hg or systolic BP ≥140 mm Hg obtained twice on the same arm at an interval no
less than 4 hours.
• Upon a repeated measurement during the same appointment or daily monitoring,
30–70% of patients show normal BP values.
• Diastolic BP 90 mm Hg and systolic BP 140 mm Hg are considered border-line
values; they indicate a need for more thorough monitoring of the maternal and
fetal condition.
• Despite elevated BP, a considerable portion of pregnancies proceed uneventfully;
to a certain extent, pregnancy produces a beneficial effect on the utero-
placental-fetal circulation in a situation of enhanced vascular resistance acting
as a compensation mechanism.
• A diagnosis of severe AH is justified at systolic BP ≥160 mm Hg and diastolic
BP ≥110 mm Hg registered upon serial measurements (interval of determinations
once in 15 min).
• A relative elevation of BP (by 30 mm Hg from baseline systolic BP, and by

15 mm Hg from baseline diastolic BP) is not of a great prognostic value due to
considerable individual BP fluctuations during pregnancy, thus producing a great
number of false positive results.
• The mean BP value can be used as an indicator for prognosis of PE development
(Table 22.6).
This classification can be used to determine the degree of BP elevation in any
variety of AH during pregnancy (chronic AH, gestational AH, PE).
22.4.2. Pathogenesis of gestational complications
Starting at early gestational age, patients with hypertonic disease

NB! develop morphological and functional anomalies of the placenta,
and fetoplacental incufficiency develops. As a result, metabolism of
gases, nutrients and waste products in the placenta deteriorates,
which promotes fetal hypotrophia and even demise.
AH causes functional and structural changes in the vessels associated with a nar-
rowing of their lumen (Fig. 22.12).
Fig. 22.12. Parietal decidual bioptate. Prominent hypertrophy of muscular layer and
narrowing of the lumen in spiral arteries are equivalent to systemic arterial hypertension.
Hematoxylin and eosin staining, ×100
Table 22.6. Classification of the degree of BP elevation in pregnancy
BP category Diastolic BP, mm Hg Systolic BP, mm Hg

Normal BP <90 and <140
Moderate AH 90–109 and/or 140–159
Severe AH ≥110 and/or ≥160
632 Obstetrics
In this case the placental bed shows abnormalities at an early gestational age which
later may result in placental insufficiency, IUGR. AH increases the risk of placental
abruption, development of PE with typical complications for the mother and fetus
(Fig. 22.13).
Ischemia of the placenta can develop as a metabolic, hormonal and hemody-
namic response. A microscopic study of the placenta reveals thrombosis of vessels
and intervillous spaces, signs of sclerosis and obliteration, narrowing of the lumen,
arterial atheromatosis, edema of villous stroma, necrotic changes in the placenta,
predominance of chaotic sclerotic villi. Spiral vessels of the placental bed retain the
muscular and elastic layers along the entire length of the vessel or at certain portions.
One should remember the hypotensive effect of pregnancy in the first trimester. It
is known that BP values show consistent changes at different stages of a physiological
pregnancy. During the first trimester BP (systolic BP in particular) shows a tendency for
decline, while in the third trimester it gradually rises. Besides, moderate tachycardia is
noted during pregnancy and especially in labor, while immediately after childbirth, that
is, in the early postpartum period, bradycardia develops. It has been established that BP
levels reach their peak during pushing efforts due to occlusion of the distal aortic portion.
Pregnant patients with hypertonic disease demonstrate BP fluctuations, a consis-
tent elevation and decline at different gestational ages. In some patients a high BP
does not change considerably, in others it elevates even higher, and in still others BP
becomes normal or even below normal. Increase in previously elevated BP is often
due to a superimposed PE, and then edema and albuminuria are noted.
A temporary BP decline in hypertensive patients is usually noted in the first or
second trimester. In the third trimester and after childbirth, once the hypotensive
influence has been eliminated, BP elevates again and can exceed the values registered
before pregnancy.
The high rate of PE in hypertonic patients is associated with the common patho-
genetic mechanism of vascular tone disregulation and renal dysfunction. Placental
abruption is one of severe gestational complications.
Placental inefficiency,
hypoxia, fetal
hypotrophy
Insufficiency
of cytotrophoblast
invasion Preeclampsia
Arterial Incompetence
hypertension of placental bed
Premature
detachment
Microangiopathy of placenta
Pregnancy loss
or preterm birth
Fig. 22.13. Pathogenesis of gestational complications in arterial hypertension

PE of varying severity develops in 28 – 89.2% of pregnant women

NB! with hypertonic disease; it often manifests itself quite early,
at 24 – 26 weeks gestation.
PE superimposed on hypertonic disease is dangerous both for the mother and
fetus as it creates a higher risk of still birth, premature birth, placental abruption,
eclampsia, acute renal failure, disorder of cerebral circulation. Stroke, eclampsia and
hemorrhage due to DIC caused by placental abruption are the main causes of death
in pregnant and parturient women with hypertonic disease.

Hypertonic disease is determined by the degree of BP elevation, the functional
condition of the neuroendocrine system and different organs (parenchymatous organs
in the first place), the condition of hemodynamics (macro- and microcirculation)
and hemorheology.
The patients’ complaints are diverse: undue fatigability, headache, dizziness, pal-
pitations, sleep disorder, shortness of breath, chest pain, vision disorder, tinnitus,
cold extremities, paresthesia. Sometimes there emerge thirst, nicturia, hematuria,
groundless fear. Nosebleeds are noted less commonly.
The main sign of the disease is elevated BP, both systolic and diastolic. At first BP
elevation is transient, then it becomes constant, and its degree corresponds to the severity
of the disease. In most cases there is evidence of elevated BP existing before pregnancy.
When past history data are inconclusive, hypertonic disease can be presumed from a
family history of hypertonic disease, early BP elevation (before 20 weeks gestation) while
there was no edema or albuminuria, the patient’s advanced age , retinal angiosclerosis,
left ventricular hypertrophy, evidence of elevated BP during previous pregnancies.
22.4.4. Diagnostics
Physical examination. Pulse measurement on both arms and legs, BP measurement
on both arms and legs (normal BP findings on the legs should be 20–40 mm Hg
higher than on the arms). When performing auscultation of the heart and vessels one
should note the condition of the aortic valve, carotid and femoral arteries. Frequent
or slow pulse is noted. Kidney palpation is performed.
Laboratory tests:
• urinalysis and Nechiporenko test;
• fasting plasma glucose test, concentrations of potassium, uric acid, creatinine,
total cholesterol in the blood plasma;
• potassium, phosphorus, uric acid content in the blood serum;
• creatinine content in the blood serum or urea nitrogen;
• determining the potassium/sodium ratio.
Instrumental examinations:
• ECG;
• EchoCG;
634 Obstetrics
• eye fundus examination;

• 24-h ambulatory BP monitoring;
• ultrasound of kidneys and adrenals;
• chest X-ray.
Indications for consultation by other specialists:
• Therapist, ophthalmologist consultation (obligatory).
• Endocrinologist, nephrologist, urologist consultation.
22.4.5. Differential diagnosis

Hypertonic disease is differentially diagnosed from polycystic kidney, chronic
pyelonephritis, diffuse diabetic glomerulosclerosis with renal failure and AH, re-
novascular hypertension, kidney malformations, nodular periarthritis, aortic coarc-
tation, pheochromocytoma, thyrotoxicosis, Conn syndrome, Cushing syndrome,
acromegaly, encephalitis and brain tumor.
22.4.6. Gestational complications
PE plays the leading role in the structure of hypertonic disease complications.

As a rule, PE shows an extremely severe course, its response to therapy is poor; it
recurs during consequent pregnancies.
In the presence of hypertonic disease labor becomes accelerated or, on the con-
trary, prolonged.
As the underlying condition aggravates, the incidence of

NB! spontaneous abortion and preterm births increases.
22.4.7. Treatment of hypertension

A pregnant woman with AH receives three investigations during
NB! pregnancy, in hospital if necessary.
• prior to 12 weeks gestation. If the revealed disease is at stage
1, pregnancy can be preserved; stages 2 and 3 are indications
for termination of pregnancy;
• at 28 – 32 weeks gestation, which is the time of peak load on the
cardiovascular system. The patient receives a thorough work-up;
the administered therapy is adjusted, obstetric complications
are attended to;
• at 38 – 39 weeks gestation the woman is hospitalized to prepare
for delivery.
Gestational AH management. The pregnant woman should be consulted about the

alarming signs (signs of deteriorating condition or of severe PE).
• Primary care level: arrange a consultation with a specialist from secondary or

tertiary care level. Hospitalization is indicated for a profound workup and if the
patient resides in a far away area.
• Secondary and tertiary care level: ambulatory management is a possibility
(provided emergency care is available around the clock) with appointments at the
maternity welfare clinic once every three days and regular tests and examinations:
microalbuminuria, proteinuria, fetal ultrasound and dopplerometry.
Monitoring of fetal condition (starting at 26 weeks):
• continuous cardiotocography until BP becomes stable (after that daily or on
indications);
• ultrasound: fetometry, placentometry (later, once a week);
• dopplerometry of umbilical arteries (additionally, on indications).
Pregnancy is prolonged as long as there is an adequate condition of the intrauter-
ine medium necessary for fetal growth and development without compromising the
mother’s condition.
In severe AH care is provided by an obstetrician gynecologist and a specialist in
intensive care, preferably at a specialized intensive care department.
Patients who received angiotensin-converting enzyme inhibitors or angiotensin
II receptor blockers before pregnancy should be informed by the therapist (car-
diologist) about the higher risk for fetal congenital malformations in mothers
receiving these drugs as early as at the stage of planning their pregnancy. The
pregnant patient should discontinue taking these drugs and have them replaced
by others.
Patients receiving chlorothiazide diuretics should be informed about the increased
risk for fetal congenital abnormalities and neonatal complications when exposed to
these drugs.
Choice of hospital for delivery of patients with AH:
• in case of uncomplicated AH and no gestational complications — institutions of
secondary or tertiary care;
• in the presence of any complications — institutions of tertiary care.
The timing of delivery is chosen individually:
• no grounds for preterm (before 37 weeks gestation) delivery;
• at >37 weeks and BP <160/110 mm Hg delivery takes place considering the fetal
and maternal conditions and with regard to the mother’s wishes.
22.4.7.1. Drug-free treatment

An integral part of complex treatment of hypertonic disease is educating the pa-
tients so as to achieve informed participation of the patient and ensure the maximum
effectiveness of treatment.
Drug-free treatment includes physiotherapy (electrosleep, short-wave diathermy
on the feet and shins, and pararenal area).
Recommendations about lifestyle and diet:
• educate the patients about healthy nutrition (Food Guide Pyramid), especially
about reducing salt consumption to 5 g/day;
• giving up smoking and alcohol;
• adequate psychotherapy;
636 Obstetrics
• reducing the intake of vegetable and animal fats, increasing the portion of
vegetables, cereals, dairy products with reduced fat content (1.5–2%);
• staying out of doors several hours a day;
• regular checkups should preferably start before pregnancy;
• the patient and her family should be informed about the increased risk for PE
development, the specific care during pregnancy, the importance of an early first
prenatal visit, contraindications for certain hypotensive drugs during pregnancy,
puerperium and the entire duration of breastfeeding.
If there is a need for diagnosis verification, choice of therapy, medication dose
adjustment, additional investigations, the patient should have an opportunity to be
transported to an institution of tertiary care.
22.4.7.2. Antihypertensive drug therapy

Antihypertensive drug administration is obligatory at BP >150/95 mm Hg (severe
arterial hypertension). The target value is BP level <150/80–100 mm Hg.
At BP within the range 150/95 mm Hg (moderate arterial hypertension) the deci-
sion of initiating drug therapy is taken on a case-by-case basis.
According to ESH/ESH recommendations (2007), it is advisable to consider
administration of drug therapy to all patients with BP >150/95 mm Hg. Besides,
according to recommendations by the working group of ESH/ESH (2013), in case
of gestational arterial hypertension, chronic arterial hypertension and superimposed
PE, arterial hypertension with asymptomatic lesion of target organs or presence of
signs at any gestational age with BP >140/90 mm Hg one should consider an early
start of antihypertensive therapy.
The main medications administered nowadays to hypertensive pregnant patients is
methyldopa (first-line drug), labetalol (α-, β-adrenergic antagonist, not registered in
the Russian Federation), calcium antagonists (nifedipine) and β-adrenergic antago-
nists as well as certain vasodilators of myotropic action. Hydrochlorothiazide, cloni-
dine (clofeline), prazosin can be administered, if there are appropriate indications.
Angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, spi-
ronolactone, calcium antagonists diltiazem and felodipine are contraindicated during
pregnancy.
Fast-acting antihypertensive drugs
• There is no conclusive evidence a certain drug has more advantages in
reducing BP in pregnant patients with severe arterial hypertension. The choice
of medication should be guided by the experience of its administration in a
particular institution.
• The most commonly administered drugs around the world are hydralazine and
labetalol (parenteral administration).
• Nifedipine. A possible regimen: initial sublingual dose 10 mg, repeat in 30 min
three times (maximum daily dose 60 mg). If ineffective, the drug should be
changed.
• No contraindications for combined administration with magnesium sulfate.
• Antihypertensive drugs with more slow action
• Methyldopa. Initial dose 250 mg/day, every 2 days the dose is increased by
250 mg/day. Maximum daily dose 2.5 g.
Possible regimens:
• Methyldopa: initial dose 750 mg/day, maximum daily dose 4 g/day;
• Labetalol: initial dose 300 mg/day, maximum daily dose 2400 g/day;
• Atenolol: initial dose 50 mg/day, maximum daily dose 200 g/day
The objective of antihypertensive therapy at uncomplicated chronic hypertension
is to maintain BP below 150/100 mm Hg. Diastolic BP should not be brought below
80 mm Hg. The target value of therapy in secondary hypertension is 140/90 mm Hg.
The main medications for antihypertensive therapy in pregnant patients are shown
in Tables 22.7–22.9.
Magnesium sulfate is not a hypotensive medication proper. Simultaneously with
emergency care one starts planned antihypertensive therapy with prolonged-action
drugs aimed at preventing a recurrence of BP elevation.
22.4.8. Treatment of complications in childbirth and

puerperium
Preterm birth is a common obstetric situation in this cohort of patients. Arterial
hypertension is one of the main causes of placental abruption. When the administered
therapy is inadequate, PE in the presence of AH of any origin can result in eclampsia.
Stroke, eclampsia and hemorrhage due to DIC caused by placental abruption are
the main causes of mortality in pregnant and parturient women with AH.
The first and especially the second stage of labor show a considerable BP elevation
associated with psychoemotional stress and pain during labor. Compensatory mecha-
Table 22.7. Main medications for planned therapy of arterial hypertension in pregnancy
Medication Drug form, dose, mode Category of fetal Note

of administration risk by FDA
Methyldopa Tablets 250 mg. 500– В First-line drug. The best
2000 mg/day divided studied antihypertensive
into 2–3 intakes, mean drug for arterial hyperten-
daily dose 1500 mg sion therapy in pregnancy
Nifedipine Prolonged-action С The best studied calcium
tablets 20 mg, modi- antagonist drug, it is inter-
fied release tablets nationally recommended
30/40/60 mg. for administration to
Mean daily dose hypertensive patients as a
40–90 mg divided into first or second-line drug
1–2 intakes depending in pregnancy. Short-action
on the dosage form; varieties should not be
maximum daily dose administered for planned
120 mg therapy
Metoprolol Tablets С At present, a drug
25/50/100/200 mg of choice among
25–100 mg 1–2 times β-adrenergic antagonists
a day, maximum daily
dose 200 mg
638 Obstetrics
Table 22.8. Stand-by drugs for planned antihypertensive therapy in pregnancy
Drug Drug form, dose, mode Category of Note

of administration fetal risk by
FDA
Amlodipin Tablets 5/10 mg. С Available evidence insufficient
5–10 mg once a day to assess safety. The drug is only
administered when nifedipine
therapy proves ineffective or
nifedipine is poorly tolerated
Verapamil Tablets 40/80 mg, С Administered as an antihy-
prolonged-action pertensive and antiarrhythmic
tablets 240 mg. Dose medication. There are a few
40–480 mg 1–2 times studies on its administration in
a day depending on the pregnancy including adminis-
drug form. Maximum tration in the first trimester
daily dose 480 mg
Bisoprolol Tablets 5/10 mg. Dose С Available evidence insufficient
5–10 mg once a day. to assess safety. The drug is only
Maximum daily dose administered when metorpolol
20 mg is poorly tolerated
Clonidine Tablets 0.075/0.150 mg. С Third-line drug in case of
Maximum single dose refractory hypertension
0.15 mg, maximum
daily dose 0.6 mg
Hydro- Tablets 25 mg. Dose С Third-line drug in case
chloro- 12.5–25 mg/day of chronic hypertension.
thiazide Contraindicated in case of PE,
disorder of uteroplacental circu-
lation, IUGR
Furosemide Tablets 40 mg. Dose С Administration is justified if
20–80 mg/day pregnancy is complicated by
renal or cardiac failure
Prazosin Tablets 1/5 mg. Initial C Indicated in case of pheochro-
dose 0.5 mg, 2–20 mg mocytoma
divided into two-three
intakes
Note. Stand-by drugs are administered when the main antihypertensive drugs for pregnant
patients are poorly tolerated; their administration should be substantiated and approved by the
medical board
nisms fail to ensure the optimal BP level, it increases steadily; cerebral circulation
disorder is possible.
Labor sometimes becomes complicated; it often becomes

NB! precipitate.
Table 22.9. Medications for a fast decrease of BP at severe arterial hypertension in pregnancy
Drug Dose, mode of Time of onset Note

administration of hypoten-
sive effect
Nifedipine 10 mg per os 30–45 min, Sublingual administration not rec-
repeat in ommended
45 min Take care when administering
together with magnesium sulfate
Clonidine 0.075–0.15 mg 2–15 min Treatment in refractory AH:
per os 0.075 mg 3 times a day, maximum
IV administration single dose 0.15 mg, maximum
is possible daily dose 0.6 mg
Nitroglycerin IV droplet infu- 1–2 min Drug of choice in case of pul-
sion 10–20 mg in monary edema at elevated BP.
100–200 ml of 5% Systolic BP should be maintained
dextrose (glucose) at no less than 100–110 mm Hg.
solution, rate of Duration of administration no
infusion 1–2 mg/h, longer than 4 h due to the risk of
maximum rate adverse fetal effects and cerebral
8–10 mg/h edema in the mother
Sodium IV droplet infusion 2–5 min Administered seldom, only if above
nitroprusside in 250 ml of 5% mentioned medications prove
dextrose (glucose) ineffective or if there are signs of
solution, beginning hypertonic encephalopathy.
with 0.25 mcg/kg If administered for longer than
per min, maximum 4 h, the fetus can show effects of
up to 5 mcg/kg per cyanide intoxication, transient
min bradycardia
Note. When administering active antihypertensive therapy, one should be apprehensive about
excessive BP decrease which can disturb placental perfusion and cause an aggravation of fetal
condition.
In the third stage of labor, as intraabdominal pressure has declined steeply and
aortic compression has decreased, blood redistribution occurs which promotes a
lower BP compared with the preceding two stages.
Not uncommonly, hypotonic hemorrhage develops during labor; it is often ac-
companied by vascular insufficiency.
NB! Natural delivery occurs most often.
In the first stage of labor one should watch carefully the changes in BP, provide
adequate analgesia, hypotensive therapy, early amniotomy. During the expulsion
stage hypotensive therapy is intensified. In the third stage of labor one provides pro-
640 Obstetrics
phylaxis of hemorrhage (IV oxytocin infusion). Throughout the entire labor process
fetal and maternal cardiomonitoring is performed.
22.4.10. Antihypertensive therapy during lactation

In the first 5 days after childbirth, as the circulating blood volume increases physi-
ologically, there is an increased risk for BP elevation.
Management in the postpartum period
• BP measurement at least twice a day for 3–5 days postpartum.
• Antihypertensive therapy as indicated (see above), therapy discontinued at
BP <140/90 mm Hg.
• Before discharging the patient, inform her about alarming signs.
• Follow-up examination in 2 weeks (if no emergency arises).
• When hypertension persists longer than 2 weeks postpartum, the patient should
be seen by a therapist (cardiologist).
AH treatment after childbirth
• Abandon pharmaceutical therapy when target organs are not involved, there
are no associated clinical conditions, BP is below 140/90 mm Hg. Lactation is
possible in this case.
• Low-dose pharmaceutical therapy when target organs are not involved, there are
no associated clinical conditions, BP is at 150/95–179/109 mm H, which permits
continuation of breastfeeding. In this situation the target BP values are not likely
to be achieved; however, the total cardiovascular risk is lower.
• Antihypertensive therapy including combination therapy aimed at achieving
target BP values in high-risk patients (AH with involvement of target organs
and/or associated clinical conditions, BP ≥80/110 mm Hg, DM, metabolic
syndrome). In this situation breastfeeding should be discontinued (Table 22.10).
Table 22.10. Relative dose of drugs administered to lactating patients
Drug Relative dose, % Drug Relative dose, %

Nifedipine 2–5 Metoprolol* 3.2
Methyldopa 3.2 Propranolol* 0.4
Labetalol* 0.3 Oxprenolol* 1.5
Captopril** 0.014 Nadolol* 5
Enalapril** 0.1 Timolol* 3.3
Verapamil 1 Hydrochlorothiazide*** 2.2
Diltiazem 1 Spironolactone*** 1.2
Note.The relative dose (percentage of maternal dose per body weight) is the amount of a drug that a baby receives daily per
1 kg of its weight.
*One should monitor the infant’s condition for early diagnosis of possible clinical presentations associated with beta-adre-
noreceptors block. The American Academy of Pediatrics classifies propranolol, timolol, nadolol, oxprenolol, labetalol♠ as
compatible with breastfeeding. Metaprolol intake is considered compatible with breastfeeding although it accumulates in
breast milk; acebutolol and atenolol should not be administered to breastfeeding women.
**Can be administered at severe course of AH, AH combined with DM, renal disease, in proteinuria persisting in patients
with previous PE.
***Administration of diuretics can cause reduced milk production.
22.4.11. Prognosis
When the process is compensated, prognosis is favorable.
22.4.12. Prevention
Intake of salicylic acid (aspirin) in low doses 75 mg/day after 12 weeks gestation
until childbirth, provided there is a low risk for gastrointestinal hemorrhage (ESH/
ESH, 2013), prevents thrombotic complications.
REMEMBER!
AH is diagnosed when systolic BP is 140 and more mm HG, diastolic BP — 90 and

more mm HG in patients who do not receive antihypertensive drugs.
According to WHO, the following AH stages are distinguished:

• I: BP elevated in the range 140/90–159/99 mm Hg;
• II: BP elevated in the range 160/100–179/109 mm Hg;
• III: BP elevated 180/110–159/99 and more mm Hg.
We distinguish:
• primary AH;
• symptomatic AH.
A pregnant woman with AH has a workup three times during pregnancy; she is
hospitalized in the following cases:
• before 12 weeks gestation. When stage I of disease is revealed, pregnancy can
be preserved, stage II and III are indications for pregnancy termination;
• at 28–32 weeks, the period of the greatest load on the cardiovascular system. The
patient is thoroughly examined, the administered therapy is adjusted, pregnancy
complications are managed;
• 2 weeks before the due date to prepare the woman for delivery.
22.5. ARTERIAL HYPOTENSION
Synonym: hypotonic disease.

No particular ICD-10 code.
In the general population, the disease is noted in 5–7%, among pregnant wom-
en — in 10–12%.
22.5.2. Screening
AH screening consists in measuring the patient’s BP at each antenatal visit.
Prevention of complications consists in maintaining normal PB levels.
642 Obstetrics
• Physiological and abnormal arterial hypotension;
• Acute and chronic arterial hypotension;
• Neurocirculatory and symptomatic arterial hypotension.
It was suggested that emergence of accessory uteroplacental

NB! circulation is a factor promoting arterial hypertension in pregnant
owmen.
22.5.4. Etiology
Etiology of arterial hypotension is not yet absolutely clear. Pregnancy aggravates
the course of arterial hypotension as the placenta produces hormones that suppress
the pituitary function thus decreasing the production of pressor substances, which
promotes the onset of this disease.
Immune response to placental and fetal antigens is important in the development of
arterial hypotension in pregnancy. The immune response leads to a decrease or increase
in production of certain biological substances, catecholamine, acetylcholine, serotonin,
histamine in particular. Acetylcholine is regarded as a factor promoting BP decrease.

Pregnancy produces conditions favorable for hypotonic disease development: in-
creased tone of the parasympathetic nervous system, changes in higher vegetative cen-
ters of vasomotor regulation, inhibition of all functions prevailing over their excitation
(urokinetic and peristaltic function), reduced vascular peripheral resistance, presence
of additional blood pool (uteroplacental circulation), multiple changes in the hor-
mone and neurotransmitter systems where vasodilation prevails over vasoconstriction.
Arterial hypotension is regarded as one of manifestations of disorder of supraseg-
mentary vegetative regulation; this disorder promotes a background against which
early toxicosis of pregnancy develops.
The main complication of pregnancy at arterial hypotension is

NB! spontaneous abortion. Arterial hypotension promotes IUGR due
to diminished uteroplacental blood flow.

Clinical features of abnormal arterial hypotension are varied; presentations are
diverse and multiple:
• lethargy;
• apathy;
• weakness and morning fatigue;
• memory loss;
• headache;
• palpitations, pain in the heart area;
• orthostatic phenomena: dizziness, blackouts, particularly in the process of
standing up, fainting — while the overall wellbeing is satisfactory.
Patients present with nausea, vomiting, cold sweat, skin pallor, coldness of extremi-
ties, meteosensitivity. Neurological disorders encompass irritability, emotional instabil-
ity, ill humor. Cardiovascular presentations include pulse instability, bradycardia, apical
systolic murmur, increased cardiac and systolic output while ECG shows no abnor-
malities. Hypotonic disease that first arises during pregnancy has a more severe course.
Decompensated form of the disease with frequent hypotonic crises is most common.

7–25% of women develop early toxicosis and PE. 7.5% patients have a miscarriage;
and of these, 56.5% have a spontaneous abortion. The rate of IUGR detection is
8–33%. Women with arterial hypotension have low weight newborns (under 2500 g)
twice as often as women with normal BP; perinatal mortality is twice higher in case
of maternal hypotension. 17% of women show a combination of arterial hypotension
and anemia (Fig. 22.14).
22.5.9. Diagnostics
Taking past history. Arterial hypotension may be the main manifestation of a dis-
ease or a sign of another disease (gastric ulcer, infection, allergy, etc.). The onset of
disease can be associated with an emotional trauma, stress, overstrain.
Toxicosis
gravidarum
Enhanced function
of parasympathetic
nervous system Placental
inefficiency,
Changes in vasomotor hypoxia,
regulation centers fetal hypotrophy
Arterial Inhibition
Preeclampsia
hypotension of excitation
Reduced general
peripheral vascular Premature
resistance detachment
of placenta
Formation
of uteroplacental
circulation Pregnancy
loss
or preterm birth
Fig. 22.14. Pathogenesis of gestational complications in patients with arterial hypotension

644 Obstetrics
Physical examination. Women with arterial hypotension are usually of asthenic

body build, with skin pallor and acrocyanosis. The extremities are cold to the touch,
the pulse unstable, deficient; bradycardia is noted not uncommonly as well as left
ventricular hypertrophy, apical systolic murmur. In most patients, cardiac percussion
or auscultation reveal no abnormalities. The minute volume is increased, peripheral
resistance to blood flow is inadequately decreased which reduces the BP.
Laboratory tests
• urinalysis;
• thyroid hormones.
Instrumental investigations
• measuring BP 2–3 times a day; BP monitoring;
• ECG;
• kidney and adrenal gland ultrasound.
Example of diagnosis. 10 weeks gestation. Threatened abortion. Essential arterial
hypotension. Indications for consultation by two specialists
• therapist consultation
• endocrinologist consultation.
22.5.10. Differential diagnosis

Arterial hypotension is differentially diagnosed from gastric ulcer, infections, al-
lergy, hypothyroidism, adrenal insufficiency.
22.5.11. Prevention of gestational complications

Exercise therapy is an effective method for prevention and treatment of arterial
hypotension; morning exercises are very important. Hydrotherapeutic procedures are
beneficial: shower, dousing, hot-and-cold feet baths, massage. Sleep should be of
10–12 h duration every day. Both night sleep and 1–2 h daytime napping is good.
The condition is aggravated by prolonged standing on one’s feet, hot baths, remaining
in stuffy hot quarters for a long time.
22.5.12. Treatment of gestational complications in each

trimester
Pregnant women with arterial hypotension are classified at risk for miscarriage,
increased perinatal and maternal morbidity and mortality.
In the first trimester there is a risk of miscarriage. Conventional therapy is used.
In the second and third trimesters there is a high risk for the development of
fetoplacental insufficiency, IUGR, chronic hypoxia, PE, threatened premature birth.
Asymptomatic arterial hypotension does not require treatment. Decompensated
hypotension calls for hospital treatment.
Treatment of pregnant women with arterial hypotension begins with nonphar-
maceutical methods: adequate work and rest schedule, keeping regular hours (night
sleep no less than 6 h, daytime sleep 2–3 h). Exercise therapy combined with hy-
drotherapeutic procedures can be administered. It is advisable to eliminate exposure

to harmful factors, emotional and physical overstrain; the diet should be balanced
and varied with 4 meals a day; tea or cold coffee should be taken in the morning or
afternoon (not in the evening!). Aerotherapy, physiotherapy (blue light therapy, cal-
cium electrophoresis on the collar zone), psychotherapy, massage and self-massage,
electrosleep are recommended. Appropriate treatment of concomitant diseases and
elimination of infection foci are very important.
Drug therapy is administered individually with consideration to the extent of mani-
festations. One administers biogenic stimulators: pantocrin, infusions of ginseng root,
lemongrass, eleutherococcus twice a day before the meal or immediately after meals.
22.5.13. Treatment of complications in childbirth and

puerperium
Patients with arterial hypotension typically show slow delivery, which can be
mistaken for uterine inertia. This condition is due to a considerable depletion of the
body’s energy resulting from slowed-down metabolism typical of hypotensive indi-
viduals. In such cases augmentation of labor results in dystocia. To cope with this
condition, the parturient woman should be provided with rest and sleep.
Parturient women with arterial hypotension tolerate blood loss poorly; they show
severe collaptoid conditions even upon a comparatively insignificant blood loss.

Most often the patient gives a vaginal birth. When managing a term delivery, one
should provide appropriate analgesia and prevention of hemorrhage.
22.5.15. Prevention
The most effective way of preventing arterial hypotension is observing the appro-
priate work and rest schedule.
REMEMBER!
Hypotensive patients show BP below 100/60 mm Hg and corresponding signs.
Classification
• Physiological and abnormal arterial hypotension.
• Acute and chronic arterial hypotension.
• Neurocirculatory and symptomatic arterial hypotension.
Exercise therapy is an effective method for prevention and treatment of arterial
hypotension; morning exercises are very important. Hydrotherapeutic procedures
are beneficial: shower, dousing, hot-and-cold feet baths, massage. Sleep should
be of 10–12 h duration every day. Both night sleep and 1–2 h daytime napping is
good.
Parturient women with arterial hypotension tolerate blood loss poorly; they show
severe collaptoid conditions even upon a comparatively insignificant blood loss.
646 Obstetrics
22.6. HEART DEFECTS
22.6.1. Mitral valve prolapse

Mitral valve prolapse is displacement of an abnormally thickened mitral valve
leaflet into the left atrium during systole.
Synonyms: floppy mitral valve syndrome, systolic click murmur syndrome, billow-
ing mitral leaflet, Barlow syndrome.
ICD-10 code
• I34.1 Mitral (valve) prolapse.
Mitral valve prolapse is the most common disease of pregnant women. Its in-
cidence rate in the general population is 5–10%; it is more often noted in women
(6–17%).
In young women an insignificant prolapse produces no signs; it is detected by
echocardiography; it is regarded as a variety of normal condition.
Mitral valve prolapse can be primary and secondary or acquired.
Primary mitral valve prolapse is due to incompetency of connective tissue struc-
tures and minor abnormalities of the valve structure.
Secondary mitral valve prolapse emerges upon an overload of pressure in the left
ventricle, for instance, upon aortic valve stenosis.
Depending on the extent of mitral leaflet displacement into left atrium, three
degrees of mitral valve prolapse are distinguished:
• Degree I: leaflet displacement by less than 0.6 cm;
• Degree II: leaflet displacement into the left atrium by 0.6–0.9 c;
• Degree III: leaflet displacement by more than 0.9 cm.
Depending on the presence or absence of hemodynamics disorder, mitral valve
prolapse can include mitral regurgitation or not. Regarding the clinical course, mitral
valve prolapse is divided into asymptomatic, mild, moderate and severe.
22.6.1.3. Etiology
In most cases the condition is hereditary (congenital insufficiency of connective
tissue) in Ehlers-Danlos syndrome, Marfan syndrome; it can be due to mixomatous
lesion of the mitral valve. Mitral valve prolapse can be associated with metabolic
disorder in collagenosis; with valvular and subvalvular abnormalities (annular dila-
tion, enlargement of leaflet surface, elongation of chordae tendineae, malformations
of papillary muscles). Mitral valve prolapse can be a part of congenital heart defects
(atrial septal defect, ventricular septal defect, Ebstein’s anomaly).
Secondary mitral valve prolapse can be caused by regional disorders of left ven-
tricular myocardial contraction and relaxation associated with inflammatory changes
(myocarditis, pericarditis) or its hypertrophy and degenerative changes. There has
been noted an association with disorder of vegetative innervation and impulse con-
duction in neurosis, hysteria, myocarditis, extrasystole, Wolff-Parkinson-White syn-
drome; with reduced elasticity of mitral valve tissue due to asymmetric left ventricular
contraction and ischemia of papillary muscles and chordae tendineae; consequences
of blunt injury of the heart.
Mitral valve prolapse is not rheumatic heart disease; rather, it is

NB! an anomaly that can be congenital, acquired or idiopathic.
When mitral regurgitation is absent, prolapse of mitral valve can remain asymp-
tomatic. The degree of mitral regurgitation can be accompanied by hemodynamic
disorders similar to those in mitral valve insufficiency (hypertrophy and dilation of
the left atrium and left ventricle). Mitral leaflet displacement is caused by reduced
tissue elasticity, insufficiency of connective tissue in the valve.
During diastole, an excess blood returns to the left ventricle, so the left atrium
and ventricle continuously suffer from volume overload. A prolonged impact of this
hemodynamic factor on the heart results in left ventricular and left atrial hypertro-
phy, that is, myocardial hypertrophy in combination with compensatory dilation of
these heart chambers.
Changes in hemodynamics in the course of mitral valve prolapse are associated
with disorder of the closing function of valve and mitral regurgitation.

During pregnancy, the increased cardiac output and reduced peripheral vascular
resistance, physiological enlargement of the left ventricular cavity and the ensuing
changes in the size, length and tension of chordae can promote a reduction in the
degree of mitral valve displacement. So the signs revealed by auscultation disappear
to return 1 month after childbirth.
A physiological pregnancy promotes reduced total peripheral vascular resistance
thus normalizing the intracardiac hemodynamics. However, an increased total pe-
ripheral vascular resistance (for instance, in AH) causes mitral regurgitation to in-
crease so the underlying disease can worsen (increased degree of mitral regurgitation,
very seldom — cardiac rhythm disorder: supraventricular and ventricular arrhythmia).
An acute pressure increase in the left ventricle (leaflet detachment in mixomatous
mitral valve) can lead to a rapid development of pulmonary edema.
AH causes structural and functional changes in vessels associated with vascular lu-
men narrowing. At early gestational ages there are disorders of the placental bed which
later can result in placental insufficiency, hypoxia and IUGR. AH elevates the risk of
premature placental separation, PE with characteristic maternal and fetal complications.
Certain developments in a pregnant body can promote a reduction

NB! in mitral valve prolapse: increased cardiac output and diminished
peripheral vascular resistance, physiological growth of the left
ventricular cavity followed by a change in the size, length and
tension of chordae. As a result, auscultation signs disappear to
re-emerge four weeks postpartum.
648 Obstetrics
Clinical features of mitral valve prolapse depend on the duration of the condition,
and prominence of mitral regurgitation. 20–30% of pregnant women with mitral valve
prolapse show no signs. About 70–80% of pregnant women with mitral valve prolapse
can have bouts of paroxysmal tachycardia and various types of cardialgia. In mitral
valve prolapse, pregnancy does not have characteristic complications.
Clinical presentations are varied, four major syndromes are distinguished: vegeta-
tive dystonia, vascular disorder, hemorrhagic and psychopathologic syndrome.
The vegetative dystonia syndrome includes:
• left chest pain (stabbing, nagging pain not related to exercise; stabbing pain of
several seconds duration, nagging pain lasts for hours);
• hyperventilation syndrome (shortness of breath, desire to take a full deep breath);
• disorder of cardiac vegetative regulation (palpitations, sensation of infrequent
heartbeat, sensation of irregular heartbeat, heart flutter);
• gastrointestinal disorder (irritated bowel syndrome, functional gastric indigestion,
etc.);
• psychogenic dysuria (frequent or, vice versa, infrequent urination in response to
psychoemotional stress);
• excessive sweating.
One should naturally rule out all possible somatic causes that can produce similar
presentations.
Vascular disorder syndrome includes:
• syncope, vasovagal state (fainting in a stuffy atmosphere, after prolonged
standing, etc.), orthostatic and precollaptoid state in similar conditions;
• migraine;
• «crawling skin» sensation in the legs;
• cold feet and hands;
• morning and evening headaches (due to venous engorgement);
• dizziness;
• idiopathic edema or pastosity.
The theory that syncope arises due to arrhythmia has not been confirmed to date.
Syncope is considered as a vagoval disorder (disorder of vegetative regulation of the
vascular tone).
Hemorrhagic syndrome encompasses easily appearing bruises, frequent nosebleeds,
gum bleeding, heavy and/or prolonged menstrual bleeding in women. Pathogenesis
of these conditions is complex; it includes a disorder of collagen-induced platelet
aggregation (due to collagen defect in these patients) and/or thrombocytopathy and
vasculitis.
Patients with mitral valve prolapse and hemorrhagic syndrome often show throm-
bocytosis and enhanced platelet aggregation which are considered hypercoagulation-
like reactive changes in the hemostasis system (a compensatory response to chronic
hemorrhagic syndrome).
The psychopathology syndrome is accompanied by neurasthenia, anxious phobic
disorders, mood disorders, mostly in the form of changing moods.
changes in the size, length and tension of chordae tendineae can promote a reduc-
tion in the degree of mitral valve displacement. Thus, signs revealed by auscultation
disappear to return 1 month after childbirth. Pregnant women show more frequent
attacks of paroxysmal tachycardia; the chordae tendineae in the valves can rupture
during childbirth.
However, women show great tolerance to physical exercise, so when mitral insuf-
ficiency is not prominent, in most cases pregnancy proceeds uneventfully.

In most cases it is a benign disease. Rare complications encompass mitral valve insuffi-
ciency, ventricular extrasystole, rupture of chordae tendineae, superimposition of myocar-
dial infarction, embolism of minor cerebral vascular branches and (rarely) sudden death.
More commonly, complications are in the form of PE, premature membrane rup-
ture, uterine inertia; the newborn may show intrauterine asphyxia, sometimes IUGR.
History taking. History findings and medical records permit a differentiation be-
tween primary and secondary mitral valve lesion.
Physical examination. A general examination, palpation of the heart does not reveal
any specific signs in patients with mitral valve prolapse. Heart percussion detects an
upper shift of the superior border of relative heart dullness; in the presence of mitral
regurgitation, left ventricular dilation is detected.
Auscultation reveals the following:
• mesosystolic click caused by strain of mitral valve leaflet or chordae tendineae at
the moment of precipitate displacement of the leaflet in the left atrium;
• late apical systolic murmur — the major auscultative sign of mitral valve prolapse.
Any maneuver that increases left ventricular volume — such as physical exercise —
can delay the onset of clicks, and shorten murmur duration.
Laboratory tests do not have any diagnostic value.
Instrumental investigations. ECG permits detection of signs of left atrial myocardial
hypertrophy as well as various cardiac rhythm disorders (tachysystole). Transthoracic
and stress echocardiography permit a confirmation of the displacement of one (usu-
ally posterior) or both mitral valve leaflets in the left ventricle cavity during left
ventricular systole.
A chest X-ray shows an enlargement of the left ventricle (if mitral valve prolapse
is present); Doppler echocardiography of transmitral flow — blood regurgitation, and
the degree of mitral regurgitation can be estimated.
Indications for consultation by other specialists. When mitral valve prolapse is
suspected, a therapist and cardiologist consultation is required to make a diagnosis,
specify the degree of regurgitation and intracardiac hemodynamic disorder.
Example of diagnosis. 20 weeks gestation. Mitral valve prolapse without distur-
bance of intracardiac hemodynamics.
22.6.1.9. Screening
Mitral valve prolapse is diagnosed accidentally when heart murmur and click are
heard at a planned examination by the therapist at the maternal welfare clinic.
650 Obstetrics
To reduce the risk of emergence (progression) of mitral regurgitation in patients
with mitral valve prolapse, it is advisable to provide prevention of infection and AH.
When mitral regurgitation is present, one provides prevention and management of
cardiac rhythm and conduction disturbance.
Treatment objectives:
• management of the main clinical manifestations of mitral valve prolapse;
• management of cardiac rhythm disorder;
• prevention of complications;
• prevention of myocardial neurodystrophy.
Indications for hospitalization

Hospitalization of pregnant women with mitral valve prolapse is necessary in
case of PE or deterioration of the underlying condition (progressing signs of mitral
regurgitation), sudden BP increase in the left atrium (pulmonary edema).
Nonpharmaceutical treatment:
• keeping regular hours, avoiding psychoemotional stress;
• adequate psychotherapy;
• physiotherapy (hydrotherapeutic procedures);
• limiting physical activity;
• therapy with herbal formulations;
• diet with limited sodium salt intake.
Pharmaceutical therapy is indicated in case of cardiac rhythm disorder and de-
velopment of pulmonary edema. Sinus tachycardia, which in the presence of mitral
regurgitation promotes increased pressure in the left atrium and pulmonary blood
congestion, is an indication for administration of medications with a negative chrono-
tropic effect like β-adrenergic antagonists. To prevent thromboembolism which pro-
motes microthrombi formation on the altered leaflets, one administers therapy with
medications acting on the rheological blood properties (low doses of acetylsalicylic
acid). The therapeutic decisions are determined by the extent of leaflet displacement,
and the nature of vegetative cardiovascular changes.
Cardialgia can be varied; it may imitate angina pectoris, among other things.
However, nitrate administration should be avoided as they can aggravate the extent
of displacement.
The condition does not call for surgical treatment.
Objectives of treatment:
NB! • managing the basic clinical manifestations of mitral valve
prolapse;
• reversing the disturbance of cardiac rhythm;
• preventing myocardial neurodystrophy.
Treatment of gestational complications in trimesters. In case of threatened abortion

tocolytic therapy is administered.
If PE develops in the second and third trimester, appropriate therapy is admin-

istered.
If fetoplacental insufficiency and chronic fetal hypoxia develop in the second and
third trimester, the issue of preterm termination of pregnancy is considered.
Management of complications during labor and puerperium. If uterine iner-
tia develops, labor-inducing agents should be administered at an appropriate
time.

Mitral valve prolapse does not compromise pregnancy, so it should be prolonged
to 40 weeks and terminate in a vaginal birth. Cesarean section is performed for
obstetric indications.
Prominent displacement of leaflets with large amplitude does not show particular
changes during pregnancy. As cardiac signs in such patients are pronounced, bear-
ing down efforts must be eliminated. When various obstetric complications combine
(uterine inertia, fetal macrosomia, etc.), cesarean section is indicated.
• Diet ensuring a sufficient intake of protein, vitamins and micronutrients.
• Limited intake of salt and fluid.
• Prevention of respiratory and urinary tract infection.
• Adequate work and rest schedule.
• Limiting physical exercise.
• Administration of sedative medications.
22.6.1.13. Information for patients

Pregnant women with a congenital mitral valve prolapse carry a higher risk of
their offspring having the same disease than in the general population. Thus, during
pregnancy special emphasis should be put on highly qualified prenatal diagnostics
of congenital heart defects.
A therapist (cardiologist) consultation should take place before pregnancy or dur-
ing it.
If mitral regurgitation is present, the patient should be referred to obstetric and
cardiologic specialized care institutions.
Mitral valve prolapse is a condition that favors a physiological pregnancy.
When mitral valve prolapse is not accompanied by mitral regurgitation, the risk
of gestational complications is not higher than that in the general population.
Acutely developing rhythm disorder and pulmonary edema compromise a favor-
able outcome.
In case of compensated disorders the prognosis is favorable. At subcompensation
there is a higher risk for multiple organ failure. Decompensated conditions are an
indication for termination of pregnancy to save the patient’s life.
652 Obstetrics
REMEMBER!
Mitral valve prolapse is displacement of one or both mitral valve leaflets in the
left atrium during the ventricular systole.
changes in the size, length and tension of chordae can promote a reduction in
the degree of mitral valve displacement. So the signs revealed by auscultation
disappear to return 1 month after childbirth.
• management of the main clinical manifestations of mitral valve prolapse;
• management of cardiac rhythm disorder;
• prevention of complications;
• prevention of myocardial neurodystrophy.
Indications for hospitalization
Hospitalization of pregnant women with mitral valve prolapse is necessary in case
of PE or deterioration of the underlying condition (progressing signs of mitral
regurgitation), sudden BP increase in the left atrium (pulmonary edema).
Mitral valve prolapse is a condition that favors a physiological pregnancy. In case of

mitral valve prolapse without prominent mitral regurgitation the risk of gestational
complications is not higher than in the general population.
22.6.2. Mitral valve stenosis

Mitral valve stenosis is narrowing of the left atrioventricular orifice leading to
disturbed emptying of the left atrium and increased diastolic BP gradient between
the left atrium and left ventricle.
Synonyms. Left atrioventricular orifice stenosis, stenosis of the mitral orifice,
bicuspid valve stenosis.
ICD-10 codes
• I05.0 Mitral stenosis.
• I34.2 Nonrheumatic mitral (valve) stenosis.
Mitral stenosis prevails among acquired heart defects accounting for up to 80%.
Total mortality is 10%. Upon pulmonary edema development mitral stenosis in-
creases considerably (up to 50% of total mortality of rheumatic heart defects).
By the area of mitral orifice narrowing, mitral stenosis is classified as:
• mild mitral stenosis; the orifice area 2–4 cm 2;
• moderate mitral stenosis; the orifice area 1–2 cm 2;
• severe mitral stenosis; the orifice area is less than 1 cm 2.
The course of rheumatic mitral stenosis depends on the extent of left venous orifice
narrowing and the prominence of myocardial dystrophy.
Classification by the degree of stenosis goes as follows:

• moderate stenosis: mitral valve orifice diameter over 1 cm;
• considerable stenosis: orifice 0.5–1 cm;
• severe stenosis: orifice less than 0.5 cm.
22.6.2.3. Etiology
The leading cause of acquired mitral valve stenosis is rheumatic endocarditis. Stenosis
signs develop 1–2 years after the endocarditis episode; it takes 2–3 years for this heart
defect to fully develop. Besides, mitral stenosis can also result from septic endocarditis
and systemic lupus erythematosus. Unmixed mitral stenosis and mitral valve disease with
prominent stenosis prevalence is seen much oftener than unmixed mitral insufficiency.
Prolonged hypertension in the pulmonary circulation causes,

NB! alongside with changes in pulmonary vessels, morphological
changes in pulmonary parenchyma, a phenomenon referred to as
«mitral lung». Reduced elasticity of lungs results in reduction of
their total and vital capacity, and in decreased respiratory volume.
While mitral stenosis develops, pregnancy is most dangerous.

A half of pregnant women with mitral stenosis show an emergence or progression
of circulation insufficiency of varying stages.
When myocardium undergoes dystrophy and sclerosis, and
NB! especially once atrial fibrillation is superimposed, the right ventricle
dilates, chronic right ventricular insufficiency develops followed by
edema, liver enlargement and ascites. Such bedridden patients
are rarely keen on preserving the pregnancy.
During pregnancy the unhealthy heart faces the need to transport a considerably
greater amount of blood as the circulating blood volume increases by 30–50% irre-
spective of the heart condition. The situation may lead to pulmonary edema in case
of second barrier insufficiency as the minute output of the right ventricle increases
while minute volume of the right ventricle does not change due to the narrowing
of the left atrioventricular orifice. Thus the pressure in pulmonary capillaries rises
steeply which results in an attack of cardiac asthma developing into pulmonary
edema. When pulmonary hypertension is present, edema can develop during sleep
as venous return increases when the patient is in a horizontal position.
An increase in pulmonary blood congestion can be complicated by hemoptysis
which is more often noted in pregnant patients than in nonpregnant. Patients with
mitral stenosis show a deterioration due to development of atrial fibrillation and
thromboembolism in late pregnancy when the left atrium becomes most distended.
Exercise, even within reasonable limits, emotional strain (excitement, alarm) can
trigger the development of cardiac asthma and pulmonary edema. These complica-
tions can emerge in patients with compensated mitral stenosis and signs of pulmonary
hypertension.
654 Obstetrics
Pulmonary edema often develops during childbirth or in the puerperium; it can

be caused by intravenous infusion of large amount of fluid.

Shortness of breath is the earliest sign; it is associated with blood congestion in
pulmonary circulation and pulmonary hypertension. Shortness of breath first arises
upon physical (psychoemotional) strain and fever; that is, in conditions when the
sympathoadrenal system is activated. Later tachycardia is superimposed on shortness
of breath. Shortness of breath often acquires the features of orthopnea: it arises or
deteriorates when lying flat and is relieved in the upright position.
Undue fatigability and muscle weakness upon physical exercise are associated with
failure to provide an adequate stroke volume increase and with increased pulmonary
vessel resistance (arterial pulmonary hypertension).
Irregularity of the heart function is noted when the defect is decompensated.
Cardiac malfunction is due to fibrillation and atrial flutter as well as supraventricular
extrasystole. Women with mitral stenosis seldom note pain in the heart area; however,
they complain of edema, heaviness in the right subcostal area, dyspeptic disorders
(anorexia, nausea, vomiting) typical of advanced stages of the disease marked by right
ventricular insufficiency, blood congestion in the venous bed of systemic circulation
and disorder of organ perfusion.
History taking. One typically reveals quinsy episodes in past history and ensuing
rheumatism. Rheumatism is inherited, but environmental factors also play a role; all
people are streptococcus carriers and many people have quinsy, but only 1–3 out of
100 individuals who had quinsy develop rheumatism.
Physical examination. A general examination reveals asthenic, delicate build.
The extremities are thin, cold to the touch, muscles are poorly developed.
Acrocyanosis and facial cyanosis is noted (bluish discoloration of the lips, ear-
lobes, nose tip, fingers and toes). Patients with prominent pulmonary hyperten-
sion and low cardiac output show a typical facies mitralis (cyanosis of the lips,
nose and ears combined with cyanotically flushed cheeks, mitral blush) as well
as general skin pallor (sometimes with ashen-grey tinge), which indicates in-
sufficiency of peripheral circulation. The condition is also marked by a forced
orthopnea position due to blood congestion in the pulmonary circulation. When
there is right ventricular insufficiency and blood congestion in the systemic
circulation, the patient can develop edema in the lower limbs or lumbar area as
well as jugular venous distension.
Laboratory tests
• Complete blood count.
• Coagulogram.
• Blood biochemistry, rheumatoid factor assay.
Instrumental investigations. ECG detects signs of myocardial hypertrophy of the
left atrium and right ventricle. One may also detect rhythm and conduction distur-
bance (supraventricular extrasystole, paroxysmal supraventricular tachycardia, atrial
fibrillation, right His bundle branch block).
Chest X-ray in three standard projections shows enlargement of the left atrium
and right ventricle, as well as radiological signs of pulmonary hypertension.
Stress echocardiography shows two signs typical of mitral stenosis: reduced rate
of diastolic closure of the anterior leaflet and unidirectional motion of its anterior
and posterior leaflets.
Indications for consultation by other specialists. The issue whether pregnancy is
acceptable is settled together by a cardiosurgeon, cardiologist (rheumatologist) and
obstetrician-gynecologist before the onset of pregnancy or before 12 weeks gestation,
and at any gestational age in case of decompensation. If there is a suspicion that
the rheumatologic process is active, hospitalization to a therapeutic (cardiologic)
department is indicated for diagnosis specification and treatment. Diagnosis example.
12 weeks gestation. Rheumatic heart disease: stenosis of left atrioventricular orifice.
Circulation disorder degree 1.

Mitral stenosis is differentially diagnosed from combined mitral disease, that is,
a combination of stenosis and insufficiency of the mitral valve. Combined mitral
disease is noted in clinical practice much more often than isolated mitral stenosis or
mitral insufficiency. In case of combined mitral disease the hemodynamic disturbance
comprises signs typical of each defect; the extent of hemodynamic disturbance is
determined mostly by predominance of stenosis or mitral valve insufficiency.

In case of mitral stenosis pregnancy is complicated by PE, hypochromic ane-
mia, threatened abortion and fetoplacental insufficiency. Pregnancy can aggravate
the severity of the main disease promoting the development of thromboembolism
(mostly in case of atrial fibrillation), right ventricular cardiac insufficiency, pulmo-
nary hypertension, pulmonary edema (mostly at 26–34 weeks gestation and during
childbirth). Common complications are rhythm and conductivity disturbance (in
40–50% of patients associated with thrombus formation in the left atrium), acute
increase of pressure in the left atrium which can lead to bronchial vein rupture
and sudden pulmonary hemorrhage. Rheumatic fever exacerbation is also possible.
Critical periods of rheumatic fever exacerbation are the first 14 weeks, 20–32 weeks
gestation, and the puerperium.
22.6.2.9. Treatment
Pharmaceutical treatment. Glucocorticoid and nonsteroid anti-inflammatory drugs
administered in rheumatism have a nonspecific anti-inflammatory effect; these are
symptomatic rather than pathogenetic drugs.
Surgical treatment. In case of mitral stenosis pregnancy should be considered
contraindicated if from its very beginning there are signs of circulatory insufficiency
or rheumatic activity.
Prognosis for the pregnancy and childbirth for most women improves after surgi-
cal correction of mitral stenosis. Pregnancy should be best planned 1–2 years after
mitral valvotomy as 2 years after surgery restenosis signs often develop and thrombi
appear at commissural edges due to rheumocarditis exacerbation. During pregnancy
656 Obstetrics
the severity of the patient’s condition is determined by the extent of heart defect
prominence and clinical outcomes of surgery.
Women can become pregnant if they show excellent surgery outcomes, complete
circulation compensation, mild myocardial changes, sinus rhythm, no pulmonary
hypertension or rheumatism activity.
Pregnancy is absolutely contraindicated to patients with poor surgery outcomes, in-
adequate mitral valvotomy, restenosis, circulatory insufficiency, pronounced myocardial
changes, atrial fibrillation, high pulmonary hypertension, recurring rheumocarditis, a
combination of mitral defect with aortic stenosis or tricuspid defect. This category of pa-
tients develops stable circulatory insufficiency that is not amenable to medical treatment.
If a pregnant patient shows compensated circulation, surgery is not indicated.
In case of circulatory insufficiency degree 1 and 2, mitral valvotomy is indicated to
pregnant patients; in case of insufficiency degree III surgery is ineffective.
Bakulev Center of Cardiovascular Surgery defines the following indications for
mitral valvotomy during pregnancy:
• intensified dyspnea;
• liver enlargement;
• hemoptysis;
• attacks of acute left ventricular insufficiency with pulmonary edema.
Mitral valvotomy is technically acceptable at any gestational age but it should be
preferably performed at 10–11 weeks or at 16–18 weeks gestation. It is advisable to
avoid the gestational age when the risk for pregnancy termination is the highest. These
are the days corresponding to the menstrual period, the second and third month when
the corpus luteum regresses, the period after 19–20 weeks when the uterus increases
due to distension of muscles by the growing fetus rather than due to the growth of
muscular elements. Cardiac surgery is not advisable at 26–28 weeks gestation when
the hemodynamic load on the heart is the highest. After 28 weeks gestation surgery
is undesirable as there is little time left before childbirth and the maternal and feta
cardiovascular system has no time in which to adapt to new hemodynamic condi-
tions. 16–28 weeks gestation is considered the best time for cardiosurgery as it takes
no less that 60–75 days for regional hemodynamics to improve, and the respiratory
function improves within 80–90 days. After successful surgery performed within this
time period, healthy full-term infants are born. Surgical elimination of the defect at a
later time does not restore circulation entirely, nor does it eliminate hypoxia or IUGR,
despite certain improvements in hemodynamics and respiratory function.
Mitral valvotomy during pregnancy is contraindicated to women above 30, to
patients with valvular calcification, subvalvular adhesion, limited motility of mitral
valve leaflets, restenosis, exacerbation of rheumatic process. In these cases open heart
surgery is required which is too dangerous for the fetus.
Treatment of gestational complications in each trimester. If PE arises in the second
or third trimester, appropriate therapy is administered. In case of threatened preterm
birth tocolytic therapy is administered. If anemia develops, iron supplements and
folic acid are administered.
Treatment of complications in childbirth and the postpartum period. If obstetric
complications develop during childbirth, one administers therapy aimed at elimina-
tion of abnormal manifestations.
The patients have cesarean delivery.
Preventive treatment is recommended at varying time; usually

NB! thrice during pregnancy or in spring and autumn irrespective of
the gestational age.
Prevention and prediction of gestational complications. Preventive treatment is

suggested at different gestational ages, usually 3 times during pregnancy or in spring
and autumn, irrespective of the gestational age. Hospitalization takes place at the
following time:
• the first hospitalization before 12 weeks gestation: to specify the diagnosis, check
the condition of the cardiovascular system and rheumatic process, to settle the
issue of pregnancy continuation;
• the second hospitalization at 28–32 weeks gestation, the period of the greatest
load on the cardiovascular system; the patient receives a thorough workup, the
administered therapy is adjusted;
• the third hospitalization should take place 2–3 weeks prior to the estimated
childbirth to prepare the woman for delivery, to make a plan of management, to
administer cardiac and antirheumatic therapy.
Primary diagnosis of mitral stenosis during pregnancy is associated with physi-
ological increase in the rate of blood flow through the narrowed mitral orifice.
Normal myocardial function before pregnancy or in the first trimester does not ensure
a favorable prognosis for the future.
During pregnancy the circulating blood volume, cardiac output and transmitral blood
flow increase considerably. This leads to exponential pressure growth in the left atrium
and pulmonary circulation, acutely developing abnormalities of the cardiac rhythm and
pulmonary edema, which suggests a poorer outcome of the disease and pregnancy itself.
REMEMBER!
Mitral valve stenosis is narrowing of the left atrioventricular orifice leading to
disturbed emptying of the left atrium and increased diastolic BP gradient between
the left atrium and left ventricle.
A half of pregnant women with mitral stenosis show an emergence or progression
of circulation insufficiency of varying stages. If myocardial dystrophy and sclerosis
arise, especially upon superimposition of atrial fibrillation, the right ventricle dilates,
chronic right ventricular insufficiency with concomitant edema, liver enlargement
and ascites develop. Such patients have to keep to bed; they seldom desire to
continue with the pregnancy.
Patients have a cesarean delivery.
658 Obstetrics
22.7. GASTROINTESTINAL DISEASE

22.7.1. Gastroesophageal reflux disease
Synonym. Heartburn.
Gastroesophageal reflux disease is noninflammatory and/or inflammatory disorder
of the distal part of esophagus when the stomach or duodenum contents repeatedly
come back into the esophagus and related sign develop.
ICD-10 code
• K21 Gastroesophageal reflux.
It is seen in women 3–4 times less often than in men; it first develops during
pregnancy in 20–80% of cases, mostly in multiparas.
NB! This condition ranks 2nd or 3rd among gastrointestinal diseases.
The following varieties are distinguished:
• reflux esophagitis (lesion of gastric mucosa observable by endoscopy);
• gastroesophageal reflux disease without esophagitis.
Esophagitis is classified as
• acute esophagitis;
• subacute esophagitis;
• chronic esophagitis.
22.7.1.3. Etiology
The most common cause is reflux of gastric juice into the

NB! esophagus due to cardial insufficiency. This is essentially an
aseptic burn of the esophagus by the acid in giastric juice.
The following are important factors in the developing of this condition:
• disorder of gastric and esophageal motor function;
• aggressive components of the gastric contents.
Pregnancy promotes an increase of intragastric pressure which, helped along by
other mechanisms of gastric contents regurgitation (like cardial incompetence, axial
hiatal hernia) predisposes to gastroesophageal reflux. Pregnant women mostly de-
velop so-called reflux esophagitis.
Pathogenesis of reflux esophagitis is determined by decreased pressure in the lower
esophageal sphincter, regurgitation of acid contents, and by a disrupted mechanism
of esophagus clearing of acid contents.
The esophagus is separated from the stomach by the lower esophageal sphincter,
a round muscle acting as a gatekeeper which upon contracting closes the opening
between the stomach and esophagus.
Pregnant women show an elevated progesterone content in the blood which relaxes
smooth muscle organs including the lower esophageal sphincter thus eliminating the
barrier against gastric contents leaking to the esophagus. Besides, as the uterus grows
in size, intraabdominal pressure rises which also promotes regurgitation of gastric
contents to the esophagus (Fig. 22.15).
Heartburn has no adverse effect on the course and outcome of

NB! pregnancy.
• Heartburn (upon physical strain, bending, lying down, after meals).

• Regurgitation of acid contents.
Heartburn is commonly noted in the second and third trimester, mostly after con-
suming fatty, fried and spicy foods; it lasts from several minutes to hours occurring
several times a day; bending down triggers its onset.
The sensation of heartburn is accompanied by a sense of longing, dejection. Long-
lasting heartburn can be accompanied by retrosternal pain, belching.
Heartburn is the most common symptom; it arises in at least 75% of patients with
gastroesophageal reflux disease.
Esophageal signs include heartburn, regurgitation, belching, odynophagia, pain in
the chest and/or epigastric area.
Extra-esophageal signs of gastroesophageal reflux disease are conventionally di-
vided into three groups:
• pulmonary signs (chronic cough, choking fits);
• otolaryngopharyngeal signs (hoarseness, persistent dysphonia, strained voice,
throat pain, excessive mucus production in the larynx, hypersalivation, etc.);
• dental signs (burning sensation in the tongue and cheeks, taste perversion, lesion
of hard dental tissue);
• gastric signs (sensation of stomach fullness, early satiety, flatulence, nonspecific
pain).
Elevated Progesterone
intragastric relaxing the esophageal
pressure sphincter
GERD
Elevated Reduced
intraabdominal esophageal
pressure peristalsis
Fig. 22.15. Factors predisposing to gastroesophageal reflux disease (GERD) during pregnancy
660 Obstetrics
Clinical presentations in most cases provide enough evidence to make a diagnosis.
History taking. Patients give evidence of gastrointestinal disease, sometimes the
first onset of the disease occurs during pregnancy.
Physical examination. The main objective methods of examination do not help
much in diagnosing esophageal disease.
Laboratory tests:
• urinalysis.
Instrumental investigations. Positive alkaline test (rapid relief of heartburn in re-
sponse to intake of absorbable antacids) is an indirect indication of reflux esophagitis.
To specify the cause of heartburn, the pregnant woman is referred for esophago-
gastroduodenoscopy, pHmetry, manometry, bilimetry.
The involvement of esophagus in reflux esophagitis can be best assessed using
endoscopy.
Example of diagnosis. 25 weeks gestation. Gastroesophageal reflux disease.

Gastroesophageal reflux disease is differentially diagnosed from the most common
causes of heartburn: functional dyspepsia, gastric and duodenal ulcer. Abnormal
gastroesophageal reflux is noted in 80% of bronchial asthma patients; 25% of these
patients show a good effect after administration of antisecretory medications.
22.7.1.9. Treatment of gestational complications in each trimester

Objectives of treatment:
• maximum protection against gastroesophageal reflux and attenuation of the
aggressive acid peptic effect;
• elimination of concomitant dyskinesia.
Pharmaceutical therapy. Therapy of reflux esophagitis in pregnant patients admits
administration of non-absorbable antacids, plant-derived medicines with a coating
and astringent properties (almagel, phosphalugel, infusions of alder and chamomile,
starch), prokinetics, H2 receptor blockers.
Good results are achieved by administering a combination of antacids with as-
tringent medicines. To eliminate the concomitant dyskinesia and improve the gas-
trointestinal tract tone, metoclopramide is administered at a dose of 10 mg orally
2–3 times a day for 10–14 days. Magnesium containing antacids can produce a
laxative effect.
Sodium hydrocarbonate is contraindicated; it causes belching and rebound phe-
nomenon.
Prolonged administration of aluminum-containing antacids in large doses should
be avoided.
Assessment of therapy effectiveness. Elimination of symptoms is the criterion of
therapy effectiveness.

The patient gives a vaginal birth at term.
The patient should adhere to certain lifestyle and diet principles.
• Avoid postures that promote heartburn: sleeping propped up is recommended
provided there are no contraindications.
• Prevention of constipation as any straining leads to an increase in intraabdominal
pressure, acid gastric contents coming up to the esophagus, and heartburn
development.
• Keeping to a strict diet, frequent small-portion meals, avoiding overeating.
Abstaining from fat, fried foods and chocolate: these foods promote additional
relaxation of esophageal sphincter. Avoid black and red pepper and other spices
when cooking. Decaffeinated tea and coffee are recommended. Carbonated
drinks are contraindicated as they can promote heartburn.
• Wearing loose clothes that do not compress the stomach area.
• During the fi rst two hours after a meal the stomach produces acid necessary for
digestion. This is the time when heartburn is most probable so it is recommended
not to lie down immediately after a meal. Walking after meals promotes a
faster passage of food from the stomach to the intestine, and helps to prevent
constipation.
Prognosis is favorable.
REMEMBER!
Gastroesophageal reflux disease is a noninflammatory and/or inflammatory
disorder of the distal part of esophagus when the stomach or duodenum contents
come back into the esophagus repeatedly, and related signs develop.
Heartburn does not produce any adverse effect on the outcome of pregnancy.
Clinical presentations:
• Heartburn (upon physical strain, bending, lying down, after meals).
• Regurgitation of acid contents.
• maximum protection against gastroesophageal reflux and attenuation of the
aggressive acid peptic effect;
• elimination of concomitant dyskinesia.
Patients give a vaginal birth at term.
22.7.2. Peptic ulcer

Peptic ulcer is a chronic disease with a cyclic course; it is marked by varied clinical
presentations and ulceration of gastric and duodenal mucosa during exacerbation.
ICD-10 codes
• K25 Gastric ulcer.
• K26 Duodenal ulcer.
662 Obstetrics
8–10% of Russian population have peptic ulcer; 10% of them are operated on
annually. Women have peptic ulcer 3–10 times less often than men. A rise in pep-
tic ulcer among women has been noted over recent years; this is due to the effect
of stress factors, increasing rate of marital breakdowns and more prominent social
activity of women.
Peptic ulcer is noted in 1 pregnant woman out of 4000. This may

NB! be an underestimation since diagnosis of peptic ulcer during
pregnancy is difficult. It is believed that the risk of ulcer is lower
during pregnancy.
22.7.2.2. Screening
No screening is done.
By localization:
• Gastric ulcer;
• Duodenal ulcer.
22.7.2.4. Etiology
Helicobacter pylori, a spiral-form microorganism, plays the leading role in the
development of the disease; it impairs gastric and duodenal mucosa. Despite the
fact that this organism can be detected in more than 80% of Russian people, much
fewer individuals develop the disease. The ulcer needs certain conditions to develop:
• stress, anxiety, depression;
• poor heredity;
• unbalanced nutrition: intake of rough, hot food, alcohol abuse;
• smoking;
• unregulated intake of certain medicines: glucocorticoids, acetylsalicylic acid
(aspirin);
• «operator performance» when people work in conditions that require making
decisions within a time limit.
Helicobacter pylori is one of the main causative factors; this is

NB! a bacterium causing destructive processes in gastrointestinal
mucosa.
Helicobacter pylori is passed from human to human upon a close, long-standing

contact like kissing, sharing dishes and towels, poor personal hygiene. Once in the
stomach, Helicobacter pylori begins to reproduce releasing enzymes (urease, protease)
that injure the protective inner layer of gastric and duodenal mucosa, disturb cellular
function and metabolism, and cause ulceration. On the other hand, constant stress
can alter the functioning of the nervous system, which results in a spasm of gastric
blood vessels. Local tissue hypoxia results, and the mucosa becomes vulnerable, the
walls begin to be digested by the acid gastric juice.
Pregnancy has a beneficial impact on the course of peptic ulcer

NB! due to changes in secretion (reduced acidity, increased mucus
production) and in motor and voiding function of the stomach
(reduced motor activity), as well as enhanced blood supply.
22.7.2.6. Pathogenesis of gestational complications.
Pregnancy has a favorable effect of the course of the disease, although it is believed
that patients who smoke and have unbalanced diet more often show such complica-
tions as early toxicosis, iron deficiency anemia (evidence is lacking). Peptic ulcer
exacerbation is noted in spring and autumn, in the first trimester, 2–3 weeks before
delivery and in the postpartum period.
Gestational vomiting is one of the most common complications. There is no
evidence that peptic ulcer can compromise gestation.

The main sign of peptic ulcer is pain in the middle or upper stomach, mostly
of mild or medium strength. The pain is associated with meals; what is important,
they show a certain rhythm developing at about the same time after a meal. «Empty
stomach» pain is typical of peptic ulcer. Patients may have heartburn, acid belch-
ing; very intense pain at its peak results in vomiting that brings immediate relief.
Constipation is common.
Exacerbations of the disease commonly occur in the first and third trimester and
early postpartum period.
In some cases peptic ulcer remains asymptomatic.

Women with peptic ulcer may develop vomiting of pregnancy, iron deficiency
anemia and gastrointestinal hemorrhage.
22.7.2.9. Complications of peptic ulcer disease during pregnancy

Gastrointestinal bleeding
Gastrointestinal bleeding elevates dramatically the risk of fetal demise and mater-
nal obstetric complications. Massive bleeding during pregnancy is an indication for
emergency surgery.
Bleeding complicates the course of disease irrespective of its duration; some-
times bleeding is a manifestation of the so-called silent (asymptomatic) ulcer. When
bleeding is profuse, one notes vomiting tinged with dark blood or coffee grounds,
skin pallor, dizziness and even fainting of varying duration. Over the next few days
the patient shows decreased BP, dark loose stool. Hemoglobin may remain within
normal. Massive bleeding can be arrested only in hospital settings; it is very seldom
664 Obstetrics
bad enough to cause death within minutes. Moderate gastric bleeding can resolve
spontaneously; the patient’s general state is not compromised, only the stool acquires
dark coloration.
Perforated ulcer
Perforated ulcer is a condition when an untreated ulcer can burn through the wall
of the stomach or duodenum. As a result, the contents of these organs can leak into
the abdominal cavity causing peritonitis. Perforated ulcer often develops upon alcohol
intake, full stomach, excessive physical strain, injury. Sometimes perforated ulcer is
the first sign of peptic ulcer, usually at a young age.
Clinical presentations. The pain is very bad, excruciating, knifelike, accompanied
by signs of collapse: sticky cold sweat, skin pallor, cold limbs, thirst and dry mouth.
Vomiting is not common. BP goes down. In several hours flatulence develops as
gases fail to pass. In 2–5 hours a false improvement develops: the pain subsides,
the tense abdominal muscles relax. The misleading well-being can stretch for up to
24 hours. Over this time the patient develops peritonitis, and the condition aggravates
dramatically. Medical help should be sought within hours from the onset of disease.
Perforation of ulcer into the abdominal cavity that does not receive surgical treat-
ment ends within 3–4 days after the onset with the patient’s death due to diffuse
purulent peritonitis.
Penetrated ulcer
Penetrated ulcer is a condition when perforation takes place in the adjacent pan-
creas, omentum, intestinal loops so that inflammation leads to a fusion of gastric
or duodenal wall with the surrounding organs. It is not often seen in women. The
condition is marked by night attacks of pain in the middle or upper stomach; the
pain often irradiates to the back. Even most active therapy cannot relieve the pain.
Diagnosis is made on the basis of clinical findings, past history; in marginal cases
endoscopy of the stomach and duodenum is performed to rule out hemorrhage and
perforation.
Past history. Past history has evidence of previous peptic ulcer or its periodic
exacerbations.
Physical examination. At a time of exacerbation, superficial palpation reveals
tenderness in the middle or upper stomach and muscle tension which indicates
peritoneal involvement; a positive Mandel sign is a confirmation. Detection of late
splashing sound to right of the middle line (Vasilenko’s sign) suggests gastric outlet
obstruction or considerable interdigestive secretion.
Abdominal palpation often reveals tenderness in the middle or upper stomach (up
to 53.7%), and by the end of pregnancy — in the right subcostal area (40.7%) which
can be attributed to superimposition of gallbladder dyskinesia.
Laboratory tests
• Complete blood count (decreased hemoglobin).
• Blood biochemistry.
• Fecal occult blood test.
• Esophagogastroduodenoscopy.
• Mucous biopsy and test for Helicobacter pylori.
• Stomach ultrasound.
X-ray examination is contraindicated to pregnant women.
Indications for consultation by other specialists. Therapist and gastroenterologist
consultations are indicated.
Example of diagnosis. Gestation 30 weeks. Cephalic presentation. Peptic ulcer in
remission. Gestational anemia degree 1.

Ultrasound is the main method permitting a differential diagnosis between peptic
ulcer and exacerbation of chronic cholecystitis, gallstone disease. Peptic ulcer is dif-
ferentially diagnosed from chronic gastroduodenitis, chronic appendicitis, pancreati-
tis, symptomatic gastric ulcer, ulcerated tumor (including primary ulcerous cancer),
tuberculous and syphilitic ulcer, ulceration in collagenosis and amyloidosis.

In most cases the course of peptic ulcer during pregnancy is benign, although
exacerbation is possible in 25% of cases. Noncomplicated course of peptic ulcer
does not compromise the fetal condition. If peptic ulcer develops complications
that require an operative intervention, it is admissible without termination of
pregnancy.
Pregnant patients with gastric and duodenal ulcer should be

NB! followed by a therapist, preferably a gastroenterologist. Preventive
antiulcerative therapy should be administered in spring and
autumn, early toxicosis, 2-3 weeks before the due date and
immediately after delivery.
Treatment is followed under professional surveillance only. If anemia is revealed,

iron supplements are taken together with ascorbic acid and folic acid. Prolonged
parenteral administration of drugs is preferable.
Nonpharmaceutical treatment. Bed rest, diet #3, intake of mineral water, split
meals 3–6 times a day.
Pharmaceutical therapy. Pharmaceutical therapy for peptic ulcer in pregnant
patients is only administered during exacerbation episodes verified by clinical,
instrumental and laboratory methods. Drug therapy is also indicated when bal-
anced diet, meal regimen, food-derived antacids prove ineffective, or complica-
tions develop.
If the patient shows flatulence, manifestations of intestinal indigestion, ad-
ditional enzymatic drugs are recommended; H2 histamine receptor blockers and
proton pump inhibitors are effective, but their impact on the fetus has not been
studied in depth.
666 Obstetrics
22.7.2.14. Treatment of complications in childbirth and puerperium
Prevention of infectious complications during childbirth and puerperium.
Assessment of treatment effectiveness. The criteria of treatment effectiveness are
elimination of presentations, negative fecal occult blood test, endoscopy revealing
ulcer cicatrization.

A vaginal delivery is managed using adequate analgesia (peridural nerve block).
Cesarean section is performed for obstetric complications.
One should follow work and rest regimen, have a balanced diet, abstain from
smoking and alcohol abuse. Patients should be actively followed up receiving anti-
relapse therapy in spring and autumn. Preventive therapy should be followed for
3–5 years even when there are no marked exacerbations.
REMEMBER!
Peptic ulcer is a chronic disease with a cyclic course; it is marked by varied

clinical presentations and ulceration of gastric and duodenal mucosa during
exacerbation.
Helicobacter pylori, a spiral-form microorganism, plays the leading role in the

development of the disease; it impairs gastric and duodenal mucosa.
The disease shows exacerbations mostly in the first and third trimester and in the
early postpartum period.
Patients with gastric and duodenal ulcer should be observed not only by an
obstetrician gynecologist but also by a therapist (gastroenterologist preferably). In
spring and autumn, when pregnancy is complicated by early toxicosis, 2–3 weeks
before estimated delivery, and immediately after childbirth patients require
preventive anti-ulcerative therapy.
22.7.3. Constipation
Constipation is disorder of passage through the large intestine; the condition is
marked by stool decrease to less than 3 times a week and at least one of the fol-
lowing signs:
• incomplete emptying of the bowel;
• small quantity and compactness of stool;
• straining as long as ¼ of defecation and longer.
Constipation is a multifactorial syndrome of retained defecation.
ICD-10 code
• K59.0 Constipation.
Constipation is the most common bowel disorder in pregnancy. Almost 60% of
pregnant women have this condition.
Constipation is classified as acute (under 6 months) and chronic (over
6 months). Both types can be functional or organic in nature, organic constipa-
tion being due to tumors, strictures of large intestine, diverticulosis, anatomical
malformations, etc.
Functional constipation means that there are no structural or metabolic changes
detectable by modern diagnostics. Functional constipation can be an independent
entity, or a secondary symptom accompanying various abnormal conditions of the
gastrointestinal tract and other systems (irritated bowel syndrome, diverticulosis,
hypothyroidism, DM, etc.).
In clinical practice it is essential to differentiate between constipation types by the
specifics of colonic transit and evacuation; this distinction is important in making
therapy decisions. The following constipation subtypes are distinguished:
• cologenic, associated with slowed-down transit through the colon;
• proctogenic, associated with disorder of defecation and feces evacuation.
22.7.3.3. Etiology
The nature of constipation can be
• neurogenic (in functional or organic CNS disorders, frequent voluntary
suppression of defecation, specific living or working conditions: absence of toilet,
working as a driver, shop-assistant and the like);
• reflex (upon lesion of digestive organs and other organs and systems), including
the proctogenic type;
• toxic (upon chronic intoxication with lead compounds, morphine, nicotine,
nitrobenzene, prolonged intake of spasmolytic and cholinolytic drugs in large
doses);
• endocrine (suppression of pituitary function, the thyroid gland and ovaries);
• alimentary (receiving insufficient amount of dietary fiber with food);
• hypokinetic (insufficient physical exercise, sedentary lifestyle);
• mechanic (bowel narrowing due to tumor or cicatricial tissue, congenital
abnormal elongation of the large intestine, hypoplasia of intramural ganglia in
the large intestine — megacolon, or Hirschsprung’s disease).
These factors can cause motor disorder of the bowel, disrupted absorption se-
cretion, vasomotor disorders. In most cases clinical presentations of constipation
combine several disorders.
Constipation often becomes a problem at an early gestational age; however, most
patients develop constipation at 17–36 weeks gestation.
668 Obstetrics
Causes of constipation in pregnancy:

NB! • increased content of progesterone and its metabolites, which
activates the inhibiting hormone in substances that stimulate
peristalsis (gastrin, cholecystokinin, serotonin, enkephalins, P
substance);
• reduced motilin content (its content returns to normal a week
after delivery);
• other possible mechanisms stem from the united nature of
blood supply and neurohumoral regulation of the uterus and
large intestine.
Intestinal hypotonia is a defense reaction of the body during pregnancy. This re-
action often leads to constipation: dyskinesia of the intestine, disorder of intestinal
evacuation. Constipation is often a persisting condition.

The substances that stimulate intestinal contraction become ineffective during
pregnancy as the sensitivity of intestinal muscle to the stimulation is decreased con-
siderably. This occurs because the intestine and uterus share the innervations, thus
any excessive activation of intestinal peristalsis can stimulate uterine contractions
causing a threatened abortion. Unfortunately, this defense reaction brings about an
undesired result, constipation.
It is not easy to single out the cause and effect in the development of constipa-
tion. On the one hand, modern medicine has evidence that constipation, especially
in pregnant patients, is to a considerable degree mediated by psychological factors.
On the other hand, constipation itself can cause anxiety, especially in women with
habitual miscarriage or long-standing infertility. Anxiety, in its turn, does not pro-
mote a normal bowel function.
Interestingly enough, in the puerperium women have constipation less often; per-
haps because their emotional state undergoes a rapid, dramatic improvement. It is
also characteristic that the rate of constipation is about the same as the rate of general
neurosis both in puerperant and pregnant women. Constipation is also promoted by
allergy, auto immune disorders and disorders of endocrine regulation.
When constipated, the body shows less frequent defecation (less

NB! than thrice a week), changes in stools consistency; there can
be abdominal pain and discomfort (usually in the left portion),
sensation of incomplete evacuation.
In atonic constipation feces masses are large, sausage-shaped. The first portion is
often very compact, of a larger diameter, and the end portion is half-shaped.
Defecation is very difficult and painful. The surface of feces may show streaks
of fresh blood due to lacerations of the mucous lining in the anal canal. In spastic
constipations the feces look like sheep dung (fragmented stools). Constipation is
often accompanied by flatulence, sensation of distension, spastic pain in the abdo-
men. Long-standing constipation often brings about a sensation of fatigue, apathy,
reduced working capacity.
Pain can develop without a cause or after strong emotions or physical exercise.
As a rule, negative emotions cause an attack of violent pain or an exacerbation of
continuous pain in the abdomen. Sometimes pain irradiates to the small of the back,
rectum, a leg, genitals. Some women feel a burning sensation in the rectum and an
itch in the anus, alongside with pain. Presentations like nausea, bitter taste in the
mouth, difficult passage of flatus are quite common.

The following complications are possible: vaginitis (disorder of lactobacilli
passage from the rectum to the vagina), threatened abortion, spontaneous mis-
carriage, premature membrane rupture, preterm birth, low birth weight infants
(Fig. 22.16).
Chronic congestion of the large intestine not only activates opportunistic intesti-
nal bacteria, but also alters genital microflora. These changes are considered to be
risk factors, in some cases they are the cause of severe infectious complications of
pregnancy, labor and puerperium.
In pregnant women constipation can lead to anal fissures, recurring hemorrhoids,
sphincteritis.
Bacterial vaginosis,
vaginitis, cervicitis
Premature rupture
of membranes
Intestinal
hypotonia,
dyskinesia
Pregnancy loss
Constipation or preterm birth
Stress
Intrauterine
infection
Postpartum
puruloseptic
infection
Fig. 22.16. Gestational complications in constipation

670 Obstetrics
Diagnosis is made on the basis of the pregnant woman’s presentations.
Laboratory tests:
• urinalysis;
• smear for bacterial culture;
• stools for bacterial dysbiosis;
• immune status
• bacteriology study of cervical canal contents (drug susceptibility test).
Instrumental investigations. Proctosigmoidoscopy is performed. In certain cases
colonoscopy is indicated. X-ray investigation is contraindicated during pregnancy.
Indications for consultation by other specialists. A therapist consultation is indi-
cated, and if necessary — consultation by a gastroenterologist and proctologist.
Example of diagnosis. Gestation 28 weeks. Cephalic presentation. Threatened
preterm birth. Functional constipation.

In pregnant women constipation can be also caused by colitis, megacolon, doli-
chosigma, abnormalities and malformations of the large intestine, effect of medicines.
Nonpharmaceutical treatment. Recommendations include a change of lifestyle:
increasing exercise, sports, remedial exercise, diet rich in fiber, normalizing the water
balance, managing neurotic disorders.
If constipation is a sequence of other diseases, compensation of the underlying
disease is important for improvement of the intestinal function. If constipation was
brought about by medications, they had better be discontinued.
Only if the above mentioned measures prove ineffective, one can resort to therapy
with laxative medications.
Pharmaceutical treatment.
Classification of laxative medicines
• medicines increasing the volume of intestinal contents which elevates the
intraluminal pressure and stimulates intestinal peristalsis;
• medicines stimulating the intestinal motor function;
• medicines softening the stools.
When administering laxatives to pregnant women one should

NB! comply with the strictest standards of safety to ensure normal
fetal growth. The laxative should be chosen with extreme care.
Treatment of gestational complications. In the first trimester there may be signs

of threatened abortion. Conventional therapy is administered, mostly using herbal
medicines with proven effectiveness, methylcellulose. When threatened abortion
develops at a more advanced gestational age, tocolytic therapy is administered.
Psychotherapy is the major tool in constipation treatment, medications being of
secondary importance. The woman should be aware that she does not have any
serious illness, that constipation lends itself to treatment quite effectively. Diet helps
to subdue constipation.
Assessment of treatment effectiveness. Treatment is considered effective if the fre-
quency of defecation and stools consistency become normal, and when concomitant
clinical presentations are eliminated.

If early preventive measures were provided, the patient gives a vaginal birth at
term. Cesarean section is performed for obstetric indications.
REMEMBER!
Constipation is disorder of passage through the large intestine; the condition is

marked by defecation reduced to less than 3 times a week and at least one of the
following signs:
• incomplete emptying of the bowel;
• small quantity and compactness of stool;
• straining as long as 1/4 of defecation time and longer.
Constipation mostly develops at 17–36 weeks gestation.
Gestational constipation not only impairs the quality of life, it also poses a threat
to maternal and fetal well-being.
22.7.4. Hemorrhoids
Hemorrhoids means varicose veins in the anal area.
ICD-10 code
• I84 Hemorrhoids.
Hemorrhoids is revealed in the first trimester in 33% of pregnant women, in the
second trimester — in 35%, in the third trimester — in 42%, after childbirth — in
41% of puerperas.
Hemorrhoids is mostly noted during the first and second pregnancy.
By localization:
• external («fringe»);
• internal;
• mixed;
• complicated.
By the course:
• acute;
• chronic.
672 Obstetrics
22.7.4.3. Etiology
Hemorrhoids is determined by blood congestion in venous plexuses of the intestine
due to increased intraabdominal pressure. This is promoted by a sedentary lifestyle,
chronic constipation, inflammation or tumor of the rectum and other pelvic organs.
Pregnancy and childbirth are two main causes of hemorrhoids

NB! in women. Congestion can be caused by the uterus pressing
on intestinal wall, blood congestion in portal circulation, and the
need for systematic increase in intraabdominal pressure during
urination (urological conditions), defecation and other.
Absence of valves in the portal system also plays a role. Congenital or acquired
connective tissue incompetence is also implicated, as well as changes in the nervous
system and in the rectal nervous apparatus.
Constipation leads to congestion of stools in the ampulla of rectum, elevated pressure
around the intestine and sphincter involving the abdominal muscle, diaphragm and
m. levator ani. The inflow and outflow of blood in cavernous sinuses of the rectum is
disturbed, which leads to blood congestion. In the process of embryogenesis, cavernous
tissue with a large amount of arteriovenous communications forms in the submucous
layer of the rectum. Prolonged hyperemia of cavernous sinuses causes dilation and
thinning of their walls and covering tissues so that they become vulnerable develop-
ing minor erosions and lacerations easily. Hemorrhoid formation during pregnancy is
promoted by the progesterone effect (reduced tone of smooth muscle venous wall).
As a result, bleeding develops during defecation or washing the anus. Formation
of erosions or fissures promotes development of infection and inflammation in the
thrombosed hemorrhoids.

During labor the fetal head descends into the small pelvis and compresses the
vessels including rectal veins. If labor is protracted, blood congestion increases.
Hemorrhoids become swollen and tense. The anal sphincter opens during the bearing
down efforts, and a considerable portion of the rectum becomes visible. Internal and
external hemorrhoids can be seen. When the woman pushes, the hemorrhoids rapidly
enlarge, somewhat receding between bearing down efforts. The crowing is accompa-
nied by a shift of large internal hemorrhoids downward and outside, sometimes they
rupture. After childbirth the anal orifice gradually contracts.
Hemorrhoids develops upon pathological changes in cavernous

NB! tissue of the colon due to dysfunction of atriovenous anastomoses.
This is brought about by a number of causes: constipation,
pregnancy, prolonged labor, hard manual labor, etc.
A prolonged active inflow of arterial blood in the anastomoses leads to hyperplasia

of cavernous bodies and formation of internal rectal piles. Lesion of minor veins in
the rectal mucosa that are intimately connected with cavernous bodies of the sub-
mucous layer and filled with arterial blood causes hemorrhage.
Major factors causing venous disorder in pregnancy
• hormonal changes;
• sensitization and allergy;
• functional condition of the venous wall;
• increase in circulating blood volume;
• emergence of uteroplacental circulation;
• changes in the coagulating system of the blood;
• hyperproduction of tissue hormones;
• increase in intraabdominal pressure;
• reduced physical activity.

External hemorrhoids (or piles) are a milder form of the disease; complications
are less common. External hemorrhoids are marked by emergence of hard lumps that
do not recede when pressed. Such lumps do not give much trouble to the patient;
sometimes unpleasant sensations and itching around the anus develop, bleeding
is not common. When infected, the hemorrhoids become compact, tender; bowel
movement causes bad pain.
In case of internal hemorrhoids the lumps are located between the mucosal folds.
They can be singular or form a rim of several lumps. They have a wide base; when
pressed, they recede; when the patient strains or coughs, they fill. Such lumps are
painful, they irritate the perianal skin with the mucus they produce. Bluish-purple
prolapsed hemorrhoids can be incarcerated in the anus, which makes the pain worse,
promotes necrosis of the mucosa, thrombosis, intoxication and fever. Intoxication is
manifested by headache, loss of appetite, belching, skin itch. Prolapse of hemorrhoids
through the anus carries a risk of thrombophlebitis of enteric plexuses.

Hemorrhoids have no effect on the course of pregnancy.
Past history. One should ask purposefully about hemorrhoids as patients sometimes
withhold information about it feeling embarrassed or believing that hemorrhoids are
inevitable in pregnancy. Diagnosis is made on the basis of typical presentations,
detection of prolapsed bumps in the anal area.
Physical examination. Digital investigation of the rectum.
Laboratory tests
• urinalysis;
• coagulogram.
Instrumental investigations. Proctosigmoidoscopy is performed.
Indications for consultation by other specialists. Considering the variety of hemor-
rhoids forms and stages, specifics of the particular case, probability of complications,
management decisions are made with a qualified proctologist.
674 Obstetrics
Example of diagnosis. Gestation 36 weeks. Cephalic presentation. External hemor-

rhoids, non-acute.

Hemorrhoids should be differentially diagnosed from bleeding polyps, inflamma-
tory lesions, rectal tumor and diverticulosis.
Nonpharmaceutical treatment. When making management decisions, hemorrhoid
patients are classified into three categories.
• Category one: patients with asymptomatic hemorrhoids. Only preventive
procedures are indicated: diet, remedial exercise, walking, washing the anus
after bowel movement, laxative herbs, laxative medications.
• Category two: patients presenting with constipation, bleeding, painful defecation,
itch around the anus. These are patients whose condition has advanced to degree
I-II. Treatment encompasses suppositories, warm baths with a diluted potassium
permanganate solution, herbal infusions, oral medications.
• Category three: patients with prolapsed internal hemorrhoids and frequent
exacerbations. They are eligible for hospitalization and instrumental treatment,
sometimes surgery (when hemorrhage does not respond to conventional therapy).
Minimally invasive methods are preferable (minor or closed surgery).
Surgical treatment. External hemorrhoids do not require surgery. Internal hem-
orrhoids call for a surgical intervention in case of prolonged moderate bleeding or
recurring profuse hemorrhage promoting anemia in the patient; prolapse of bumps
and mucosa of the rectum, presence of rectal cracks and fistulas. The surgical ap-
proach is chosen individually. If hemorrhoids are manifested by hemorrhage with
signs of pronounced anemia, sclerosing injections are made. Surgery is preferable at
an early gestational age, using a conservative approach.
Treatment of gestational complications. Conservative management is adopted at
any gestational age: warm baths, ointments and suppositories containing procaine
and benzocaine, belladonna, tribenoside. These methods provide an analgesic, anti-
inflammatory, desensitizing, venotonic effects.
Treatment of complications in childbirth and puerperium. Adequate treatment pro-
vides an improvement in the patient’s condition so that delivery proceeds without
hemorrhoids exacerbation. In puerperas hemorrhoids are treated in the same way as
in pregnant patients.
Indications for hospitalization. Emergency hospital admission is required upon
a heavy hemorrhoid bleeding, incarceration and necrosis of prolapsed hemorrhoid
bumps.
Assessment of treatment effectiveness. When condition is attended to at an early
stage, it can be stabilized and even eliminated. Surgery is followed by recovery in
most cases. 4–6 weeks after surgery the working capacity is fully restored.

In case of asymptomatic hemorrhoids the patients should achieve a regular emp-
tying of bowels (having defecation daily at the same time), eliminate constipation
by dietary means, do exercises for the pregnant women. Diet should be rich in veg-
etable fiber, vegetables and fruit with limited amounts of meat and carbohydrates.
Depending on the season, the daily meals should include beetroot, cabbage, pump-
kin, carrots, water-melon, melon. Low-fat dairy products, brown bread and bread
with bran are good.
Washing the anus with cool water after each bowel movement is obligatory.

When debating the issue of the mode of delivery, hemorrhoid is not a factor.
The patient gives a vaginal birth. Cesarean section is performed for obstetric
indications or after surgery for hemorrhoids. A common manifestation of varicose
disease is enlargement of uterine veins, which can cause hemorrhage upon a cesarean
section, thromboembolism, puruloseptic complications in the postpartum period.
22.7.4.13. Information for the patient

The following lifestyle is a good prevention of hemorrhoids:
• increasing physical activity, doing sports;
• diet rich in fiber;
• adequate intake of fluids;
• limiting alcohol and spicy food consumption;
• correction of neurotic disorders.
REMEMBER!
Hemorrhoid is determined by blood congestion in venous plexuses of the intestine
due to increased intraabdominal pressure. This is promoted by a sedentary lifestyle,
chronic constipation, inflammation or tumor of the rectum and other pelvic organs.
Pregnancy and childbirth are the main factors promoting hemorrhoids in women.
Hemorrhoids develop upon abnormal changes in the rectal cavernous tissue
related to dysfunction of arteriovenous communications.
The patient gives a vaginal birth.
A common manifestation of varicose disease is enlargement of uterine veins, which
can cause hemorrhage, thromboembolism, puruloseptic complications.
Prevention of hemorrhage and puruloseptic complications should be provided.
22.7.5. Liver disease

Even when pregnancy has a physiological course, the liver function is under strain.
This has to do with the necessity to detoxify both maternal and fetal waste. Changes in
the bile passages are due to mechanical (increased intraabdominal pressure, reduced
diaphragm excursion) and neuroendocrine factors. The tone and motor function of
the gallbladder and bile ducts are decreased, bile duct permeability is increased, the
content of bile acids, cholesterol and phospholipids diminishes, bile becomes more
676 Obstetrics
viscous. This promotes cholestasis which is regarded as a physiological phenomenon,

in contrast to other diseases of the liver and bile passages.
All gestational liver diseases fall into two categories.
• Category one embraces pregnancy-mediated liver dysfunction. Such conditions
are noted in severe early toxicosis (vomiting of pregnancy), PE/eclampsia,
HELLP. Acute abdomen and fatty hepatosis are only seen in pregnancy.
• Category two embraces liver dysfunction nonspecific for pregnancy. It could
exist prior to pregnancy or show a first onset. These include viral hepatitis, acute
and chronic cholecystitis, gallstone disease, biliary dyskinesia.
22.7.5.1. Biliary dyskinesia

Biliary dyskinesia is a disorder of the motor function of the gallbladder and bile
passages due to neuroendocrine disregulation.
It is classified as hyperkinetic and hypokinetic dyskinesia.
Clinical presentations. Hyperkinetic dyskinesia is mostly noted in early gestation,
hypokinetic dyskinesia — in late gestation. Hyperkinetic dyskinesia is marked by
recurrent short-term attacks of pain in the right subcostal area irradiating to the
right shoulder blade, clavicle and shoulder; they are often accompanied by neuro-
vegetative signs (tachycardia, hypotonia, sweatiness, weakness, headache, irritability,
etc.). Hypokinetic dysinesia presents with a dull gnawing pain and heaviness in the
right subcostal area, loss of appetite, nausea, belching, bitter eructation, constipa-
tion, bitter taste in the mouth, abdomen distension, weakness; the gallbladder area
is somewhat tender.
Biliary dyskinesia promotes the development of cholecystitis, cholelithiasis, cho-
lestatic hepatosis, vomiting, salivation, gestational anemia.
Diagnostics. Diagnosis is made on the basis of clinical presentations, ultrasound
findings, a general examination, duodenal intubation (performed in early pregnancy).
Treatment. Patients with biliary dyskinesia can receive ambulatory or hospital
treatment at a gastroenterology department.
Screening of pregnant women with biliary dyskinesia can be performed by a thera-
pist at a maternal welfare clinic.
Prevention consists in following recommendations about hygiene and diet.
22.7.5.2. Acute cholecystitis

Acute cholecystitis is an acute inflammation of gallbladder wall. In some cases an
acute inflammation develops in the presence of a gallbladder disease; in this case it
is referred to as calculous cholecystitis.
Etiology. In pregnant women the condition is caused by hematogenous or lym-
phogenous passage of infection to the gallbladder.
Classification:
• catarrhal cholecystitis;
• phlegmonous cholecystitis;
• gangrenous cholecystitis.
Clinical presentations:
• pain in the right subcostal area;
• nausea;
• vomiting;
• hyperthermia.
After acute cholecystitis pregnancy is complicated by miscarriage, anemia, cho-
rioamnionitis, PE, chronic fetal hypoxia.
Diagnostics:
• urinalysis;
• blood biochemistry;
• ultrasound of liver and gallbladder.
Treatment. For treatment the pregnant woman is hospitalized to a surgical depart-
ment.
22.7.5.3. Viral hepatitis

Epidemiology. The rate of viral infections is now on the rise, including sexually
transmitted disease. Despite the rather rare occurrence of viral hepatitis, pregnant
women contract it 5 times more often than nonpregnant women, which can be at-
tributed to a greater susceptibility of the pregnant women to the infectious hepatitis
virus due to altered hepatic function, reduced immunity. In pregnant women hepatitis
has a more severe course than in nonpregnant ones; it poses a serious danger to the
mother and fetus. Pregnant women with this disease are classified at a high obstetric
and perinatal risk.
Classification. Several types of viral hepatitis are recognized at present: A, B, C,
D, E (the former «neither A nor B»).
Viral hepatitis A.
Etiology and pathogenesis. The disease is caused by a RNA containing virus with
fecal-oral route of transmission. 70–90% of population show antibodies to hepatitis
A virus; most people have the infection in childhood.
The infection is spread by a diseased person. The route of transmission is
through feces and mouth. The main transmission factors are water, food, dirty
hands, household items, etc. Catering department staff are most dangerous from
the point of view of epidemiology. The incubation period is 9–40 days. The
most massive release of virus occurs during the last 7–10 days of the incuba-
tion period. The disease shows seasonal fluctuations: July-August, October-
November. In pregnant women the disease has its specifics: the premonitory
symptoms are mostly latent, there is generalized skin itch, cholestasis is more
pronounced.
Clinical course
Pre-icteric period lasts for 2–10 days; it is manifested in several ways: dyspepsia,
flu-like condition, asthenovegetative syndrome, mixed condition.
Icteric period consists of a progressive phase, peak and regression; each phase
lasting for 7 days on average.
The concluding, post-icteric, period is also referred to as convalescence.
Pregnant women demonstrated a longer pre-icteric period lasting for 2–3 weeks;
it is marked by predominance of dyspeptic manifestations: poor appetite, food
aversion, heaviness in the middle or upper abdomen, nausea, vomiting, and skin
itch.
678 Obstetrics
It is important to make a differential diagnosis with PR, HELLP,

NB! and acute fatty hepatosis.
Diagnostics
• Complete blood count: hemoglobin, RBCs, WBCs, leucocytosis, neutrophilosis,
elevated ESR.
• Blood biochemistry: hyperbilirubunemia, dysproteinemia (decreased albumins
and increased globulins), tenfold increase in amino transferase activity, increased
rates of thymol in the thymol turbidity test.
• Specific serological diagnostics of acute hepatitis A is done by determining IgM
antibodies that are detectable as early as 14 days after contracting the infection,
in 2–12 months at most.
Treatment. Hepatitis A therapy is administered in accordance with symptom-
atic criteria. Hepatitis A prevention consists in IM immunoglobulin administration
0.02 ml/kg once, not more than 2 ml. If the mother has acute hepatitis A at the time
of childbirth, the priority is passive immunoprophylaxis of the fetus.
Termination of pregnancy is not indicated.
Viral hepatitis B
Etiology and pathogenesis. Despite the available effective prevention, this condition
poses a health care problem the world over. This is due to continuously increasing rate
of incidence and a common occurrence of unfavorable outcomes: chronic persisting
and active hepatitis, liver cirrhosis and hepatocellular carcinoma. The death toll of
these diseases is over 1 mln people annually. The greatest danger of hepatitis B is
potential vertical transmission of infection. Infants are usually infected by HBsAg-
positive mothers during childbirth due to contact with the blood and infected vaginal
discharge; they are at a high risk of becoming chronic carriers of hepatitis B.
Patients with acute and chronic hepatitis and virus carriers are the source of in-
fection. The virus is transmitted parenterally, sexually, through the placenta, during
labor, via the breast milk. One can also get infected through household items shar-
ing toothbrushes, combs, handkerchiefs, and through improperly sanitized medical
appliances.
Clinical presentations. The incubation period is from 6 weeks to 6 months fol-
lowed by acute viral hepatitis, although asymptomatic infection is more common.
Acute viral hepatitis can be followed by a chronic carrier status (mostly in case of
unicteric hepatitis). The signs of acute hepatitis are fever, weakness, anorexia, vomit-
ing, pain in the right subcostal area and upper abdomen. Hepatomegaly and icterus
are pathognomic signs of the disease. Urine becomes dark (the color of beer) due
to bilirubinemia while stools become pale (acholic stools).
The course of acute hepatitis B during pregnancy can be particularly severe show-
ing the so-called fulminant course.
When myocardium undergoes dystrophy and sclerosis, and

NB! especially once atrial fibrillation is superimposed, the right ventricle
dilates, chronic right ventricular insufficiency develops followed by
edema, liver enlargement and ascites. Such bedridden patients
are rarely keen on preserving the pregnancy.
If the mother is an HBsAg carrier, the risk of infecting the fetus is 20–40%.
Diagnostics. Serological diagnostics is based on revealing antigens and antibodies
to hepatitis B virus.
Prevention. The main prevention measures are as follows.
• Screening for hepatitis B virus during pregnancy (at the first prenatal visit and in
the third trimester).
• When a serum-negative pregnant woman comes in contact with hepatitis B virus,
she receives passive prevention with Hepatect (not registered in the Russian
Federation) over the first 7 days after contact and in 25–30 days. Prevention of
postnatal transmission consists in abstaining from breastfeeding unimmunized
infants.
The main prevention of neonatal viral hepatitis is administering

NB! a test for HBsAg three times during pregnancy. If there is a risk
of infection, the serum-negative woman should receive a triple
vaccination with recombinant vaccine against hepatitis B virus.
Treatment. If acute hepatitis B develops during pregnancy, therapy consists in sup-

porting treatment (diet, maintaining water-electrolyte balance, bed rest).
In the Russian Federation hepatitis B is not an indication for cesarean section as
the surgery does not rule out the possibility of infection transmission through contact
with the infected blood.
Viral hepatitis C
Epidemiology. Hepatitis C virus was isolated in 1989; the rate of infection is high
all over the world and it is on the rise. Hepatitis c is marked by a tendency for
chronicity, limited clinical presentations and a poor response to antiviral therapy.
Etiology and pathogenesis. The infective agent is a virus containing RNA; its
specific feature is that there is a great variety of genotypes and subtypes, over 30.
The source of infection is the patient with acute and chronic hepatitis C, as
well as latent virus carriers. The route of transmission is parenteral and vertical,
from mother to fetus. As blood donors are obligatorily screened for hepatitis C
and all blood products are disinfected, the virus is practically not transmitted
via blood transfusion. Transmission of infection through household items or
sexual contact is not common. Sex partners of individuals with hepatitis C are
seldom infected even after long-standing contacts. The risk of infection through
contaminated needles is no more than 3–10%, so the main route of infection is
vertical transmission.
Risk factors for pregnant women:
• intravenous injections and drug abuse in past history;
• blood transfusion in past history;
• sex partner who is a drug-taker;
• tattoos and body piercings;
• dialysis;
• antibodies to hepatitis B and C;
• several sex partners;
• detection of hepatitis C in the pregnant woman’s mother.
680 Obstetrics
Diagnostics. The incubation period is 2–27 weeks, 7–8 weeks on average. 1 week
after introduction of infection hepatitis C virus can be detected using PCR.
Clinical presentations. In most cases the acute phase remains unrecognized. Icterus
develops in 20% of infected women. Other signs are poorly pronounced; they are
typical of types of viral hepatitis. Antibodies appear several weeks after exposure to
infection. Both latent and clinically manifest types of acute hepatitis C in 30–50%
of patients result in recovery with complete elimination of hepatitis C virus. In most
cases, however, it is followed by a latent phase and a long-lived persistence of the
virus. During the latent phase infected individuals believe themselves healthy and
present no complaints.
Treatment. No vaccine against hepatitis C is available as the virus is highly
mutagenic and we do not know enough about its interaction with the immune
system.
Despite the risk of vertical transmission, hepatitis C is no

NB! contraindication for pregnancy.
Pregnancy does not produce any adverse effect on the course of viral hepati-
tis C. All women undergo a screening test for hepatitis C virus three times during
pregnancy.
Screening for hepatitis C virus is done in Russia; in most countries these investi-
gations are not considered reasonable as there is no prevention for pregnant women.
Delivery. There is no universal opinion about the best mode of delivery for patients
with viral hepatitis C. Some specialists are of the opinion that cesarean section re-
duces the risk of infecting the fetus while others hold a contrary opinion. Premature
rupture of membranes followed by a long period before delivery increase the risk of
infection transmission.
Hepatitis C virus is detected in breast milk, so the debate whether breast feeding is
safe or not is still under way. The concentration of virus in the milk depends on the
extent of viral replication in the blood, so breast feeding can be continued provided
there is no virusemia.
Prevention of the disease consists in general sanitary precautions, early detection and
isolation of patients, disinfection of foci, and surveillance of individuals who were in
contact with patients over the preceding 4–6 weeks, thorough examination of blood
donors, using disposable instruments, observing the principles of personal hygiene.
When the diagnosis has been confirmed, the patient is transferred to a specialized
hospital.
REMEMBER!
Viral hepatitis is not a common disease; however, pregnant women get infected
5 times more often than nonpregnant women. During pregnancy hepatitis has a
more severe course; it poses a serious threat for the mother and fetus.
The following epidemiologic procedures are taken when viral hepatitis is suspected:
• isolation of the patient in an individual cubicle;
• individual use of dishes and instruments;
• calling in an infectious disease specialist;

• lab tests: complete blood count, urinalysis with tests for bile pigments and
bilirubin, blood test for cell membrane antigen, bilirubin, total protein and
protein fractions, prothrombin time, prothrombin index, ALT activity, alkaline
phosphatase, cholesterol.
When the diagnosis has been confirmed, the patient is transferred to a specialized
hospital.
Although transmission of infection to the fetus is possible, hepatitis C is not a
contraindication for pregnancy.
When a serum-negative woman is at a risk of infection, she should receive HBV-
recombinant vaccine three times.
22.8. THYROID DISEASES

Thyroid hormones are necessary to provide a physiological course of pregnancy:
they participate in trophoblast formation, regulate the embryogenesis processes, dif-
ferentiation and maturation of almost all organs and systems, the anlage and forma-
tion of major cerebral functions.
Albuminous and steroid hormones (hCG, placental lactogen; estrogens, progesterone)
secreted by the placenta into the mother’s body promote hepatic synthesis of thyroxine-
binding globulin, which results in an increase in related fractions of T3 and T4.
A specific feature of hCG is structural similarity to pituitary TSH, which promotes
an enlargement of the thyroid. Another factor promoting thyroid enlargement during
pregnancy is relative iodine deficiency arising due to transmission of a certain amount of
iodine to the fetus, and an increase in glomerular filtration and renal clearance of iodine.
22.8.1. Diffuse toxic goiter

Synonyms. Graves disease, hyperthyroidism.
Diffuse toxic goiter is an autoimmune condition developing due to production of
antibodies to TSH. It is manifested by a lesion of the thyroid gland, thyrotoxicosis
syndrome combined with extrathyroid diseases (endocrinous ophthalmopathy, pretibial
myxedema, acropathy). It is marked by increased thyroid function (hyperthyroidism)
and enlargement of the thyroid gland due to its hypertrophy and hyperplasia (goiter).
ICD-10 codes
• E01.0 Iodine-deficiency-related diff use (endemic) goiter.
• E01.1 Iodine-deficiency-related multinodular (endemic) goiter.
• E01.2 Iodine-deficiency-related (endemic) goiter, unspecified.
The condition is mostly seen in people aged 20–50; in women 7 times more often
than in men. 90% of patients show toxic goiter, 10% — nodular goiter.
Incidence rate among pregnant women is 0.05–4%.
The min method of large-scale prevention of iodine-deficiency-related conditions
is consumption of iodized salt.
682 Obstetrics
The only significant contraindication for iodine prevention during pregnancy is

abnormal thyrotoxicosis.
22.8.1.3. Screening
Interpreting lab test findings from pregnant patients has its own important
specifics. There are high chances that the patient will show deviations that are
either relatively harmless and only require observation (like antibodies to thyroid
peroxidase in euthyroidism), or downright normal for pregnancy (TSH sup-
pressed in the first trimester or elevated total T4). Failure to correctly interpret
these findings is likely to send the woman along a vicious circle of unnecessary
investigations resulting in administration of unsafe medications (thyrostatics) and
incur a psychotrauma.
According to WHO recommendations, a simplified classification of thyroid size
has been in use since 1994:
• Stage 0: no goiter;
• Stage 1: goiter is invisible but palpable; its lobe size is larger than the nail bone of
the patient’s thumb;
• Stage 2: goiter is palpable and can be seen.
Five stages of thyroid enlargement are distinguished:
• 1 stage: thyroid isthmus and parts of a lobe are palpable, the gland is not visible;
• 2 stage: the gland is easily palpable and visible;
• 3 stage: «thick neck» noticeable upon examination;
• 4 stage: pronounced goiter disfiguring the neck;
• 5 stage: extremely large goiter.
Insignificant enlargement of the thyroid gland is possible in normal pregnancy;
however, only a qualified specialist can decide whether the condition is normal or
abnormal.
22.8.1.5. Etiology
The disorder often develops after an infection; the predisposition may run in the
family (50%).
Diffuse toxic goiter is now regarded as an autoimmune disorder; it is marked
by autoantibodies to certain components of thyrocytes — thyroid gland cells that
produce thyroid hormones. These antibodies are referred to as thyroid-stimulating
immunoglobulins; they are classified as a class of IgG.
Immunoglobulins have the property to bind to foreign molecules (proteins, lipo-
proteids) found both in a dissolved state and on the surface of viruses, bacteria, etc.
Foreign molecules can be found on the membranes of their own cells if these cells
mutated or were infected by viruses. So far the antigen to which thyroid-stimulating
antibodies are produced in diffuse toxic goiter, has not been established. The antigen-
antibody complex formed on the thyrocyte membrane has cytotoxic properties, that
is, the ability to harm the cell.
The thyroid function alters as early as in the first weeks of pregnancy. It is affected
by multiple factors; most of them stimulate the thyroid directly or indirectly. This
mostly occurs in the first half of pregnancy when the fetal thyroid is not yet func-
tioning, and embryogenesis is entirely provided for by maternal thyroid hormones.
On the whole, thyroid hormone production increase by 30–50% during pregnancy
is within normal. HCG produced by the placenta is the most powerful stimulator of
the thyroid in pregnancy. HCG is a hormone structurally related to TSH (identical
α-subunits, different β-subunits); when elevated it can produce TSH-like effects
resulting in stimulation of thyroid hormone production.
Due to the effect of hCG, thyroid hormone production increases in the first tri-
mester, which, in its turn, precipitates suppression of TSH production. In the first
trimester the concentration of hCG is quite high, and the concentration of TSH is
reduced. As pregnancy progresses, production of these hormones undergoes reverse
changes, and TSH content becomes normal. No less than 20% of women in early
pregnancy show a decreased TSH content (Fig. 22.17).
During pregnancy estrogen production increases; estrogens have a stimulating
effect on the production of thyroxin-binding globulin in the liver. Besides, thyroxin-
binding globulin shows enhanced binding to sialic acids, which results in its reduced
clearance. As a result, by 18–20 weeks gestation the level of thyroxin-binding globulin
doubles. In its turn, this leads to thyroxin-binding globulin binding to additional free
thyroid hormones.
A transient decrease in the thyroid hormone levels causes additional stimulation
of the thyroid gland by TSH; thus free fractions of T3 and T4 remain at normal
levels while the level of total T3 and T4 is normally elevated in all pregnant women.
Physiologically, this can be needed for emergence of additional store of thyroid
hormones in the pregnant woman’s body.
In early pregnancy the volume of renal blood flow and glomerular filtration gradu-
ally increases, which results in increased excretion of iodine with urine and causes
additional indirect stimulation of the thyroid. Besides, an enhanced iodine require-
ment develops due to transplacental passage of iodine to the fetus for synthesis of
thyroid hormones by the fetal thyroid gland.
60 1.6
HCG content (IU/L x 1000)
50 1.4
TTH content (IU/L)
1.2
40
1.0
HCG TTH
30 0.8
20 0.6
0.4
10
0.2
0 0.0
5 10 15 20 25 30 35
Weeks gestation
Fig. 22.17. Altering hCG and TTH content during pregnancy

684 Obstetrics
Thyroid hormones stimulate the corpus luteum function, which is important in

maintaining pregnancy at an early gestational age.
The placenta is an active participant in thyroid hormone metabolism and the
transfer of hormones and iodine from mother to fetus. The placenta contains several
types of deiodinase, the most active one is 5-deiodinase type III (D3) that catalyzes
deiodinaiton of maternal T4 to reverse triiodothyronine (rT3) which is contained in
the amniotic fluid in high concentrations. Thus, thyroid hormones of the pregnant
woman can serve as an additional source of fetal iodine which is very important in
conditions of iodine deficiency.
An excess of thyroid hormones leads to increased metabolism producing a cata-
bolic effect on the body.
In the first trimester hCG acts as a weaker TSH counterpart; in 1–2% of women
it produces a slight increase in serum levels of free T3 and T4 while reducing the TSH
concentration which causes clinical presentations of thyrotoxicosis. Thyrotoxicosis is
often accompanied by severe vomiting of pregnancy, which hampers its diagnosis.
This condition is transient; it resolves by the second trimester.
Most patients with diffuse toxic goiter pregnancy show gestational complications.
The most common ones are miscarriage and premature birth. 46% of patients develop
signs of threatened abortion or premature birth. Threatened abortion mostly occurs
at an early gestational age which can be associated with a significant increase in
thyroid function and elevated production of thyroid hormones. Excessively produced
thyroxin is likely to affect implantation and further development of the gestational
sac resulting in an abortion.
Imbalance of thyroid hormones in a pregnant woman plays a key

NB! role in psychoneurological disturbances of children.

Among the multitude of manifestations, four major signs are noted: goiter, tremor,
exophthalmos, tachycardia (atrial fibrillation).
The tremor of fingers is particularly noticeable when the woman closes her eyes
and stretches out her arms.
Exophthalmos (bulging of the eyes) is pronounced in 60% of women; its degree is
mostly moderate. Other signs are often noted: von Graefe’s sign (eyelid lag), Mobius
sign (poor convergence), Kocher’s sign (convulsive retraction of the eyelid upon a
fast downwards or upwards movement), Stellwag’s sign (infrequent or incomplete
blinking), Dalrymple sign (abnormal wideness of palpebral fissures), Jellinek’s sign
(brownish pigmentation of eyelids).
Pressure fluctuations are noted. Thyrotoxicosis can be accompanied by subfebrile
temperature ; in the first months of gestation it is hard to differentiate from gesta-
tional subfebrile temperature.
Exacerbation of the disease may appear as thyrotoxic crisis: acute manifestation
of all signs. The crisis is marked by the patient’s agitation, disorientation, hyperther-
mia, arterial hypertension, jaundice, arrhythmia, moist skin, suddenly developing
exophthalmos.
Starting at 28–30 weeks most women develop signs of cardiac failure. The follow-
ing hemodynamic changes are typical of this gestational age: increased circulating
blood volume and cardiac output, tachycardia; due to the hyperactive thyroid, these
factors lead to cardiac activity disorder.
Clinical signs of mild thyrotoxicosis are very similar to common gestational mani-
festations: shortness of breath, tachycardia, increased fatigability, weakness, sleep
disorder, emotional lability, irritability, excessive sweat. In pregnant women these
signs of thyrotoxicosis are more severe; besides, more specific symptoms appear:
goiter and exophthalmos.
In the first trimester early gestational toxicosis is quite common. It usually coin-
cides with the exacerbation of the underlying disease. Sometimes early toxicosis is
particularly severe, not responding to treatment, and pregnancy has to be terminated.
In late pregnancy patients with pronounced thyroid dysfunction and predominat-
ing hypertensive syndrome often develop PE. Systolic BP increases secondary to a
surge in stroke and minute volume. Diastolic BP decreases due to growth of micro-
circulatory blood stream under the impact of excess thyroid hormones.

Complications of decompensated gestational thyrotoxicosis are shown in
Table 22.11.
The most common complication is miscarriage. Threatened abortion mostly oc-
curs at early gestational ages, which can be associated with considerable thyroid
hyperactivity, enhanced production of thyroid hormones. Patients with diffuse toxic
goiter quite often develop PE.
In rare cases, when the patient shows a malignant thyroid tumor, termination of
pregnancy and treatment at oncology department is indicated.
Signs of threatened abortion or peterm birth develop in 46% of

NB! patients.
Past history. Most patients report Graves disease in past history. Familial predis-
position plays a key role.
Table 22.11. Complications of decompensated thyrotoxicosis in pregnancy

Maternal complications Fetal complications
AH IUGR
PE Low birth weight
Placental abruption Still birth
Premature birth Malformations
Spontaneous abortion Fetal and neonatal thyrotoxicosis
Anemia
Cardiac failure
Thyrotoxic crisis
686 Obstetrics
• Physical examination:
– patient’s facial expression;
– anterior neck surface;
– distribution of subcutaneous fat.
• Thyroid gland palpation.
• Auscultation of the thyroid gland.
• Auscultation of the heart (murmurs).
When examining the patient one notes her behavior particularly: she is fidgety
with frequent uncoordinated movements, speaks fast, unable to concentrate on one
topic, emotionally unstable. Characteristic signs are warm moist palms that serve to
differentiate thyrotoxicosis from neurocirculatory dystonia in which the palms are
cold and moist.
Laboratory tests
• Tests for TSH, T4 and free T3 in the blood every month.
• Coagulating system of the blood in every trimester.
• Test for protein-bound iodine in the blood.
• Antibodies to thyroglobulin.
Instrumental examinations
• Thyroid gland ultrasound (thyroid gland size: no more than 18 ml normally in
women; the size and echostructure of nodules)
• Thin needle biopsy is indicated for differential diagnosis (upon detection of
palpable nodules whose diameter exceeds 1 cm)
• ECG.
The most informative methods of diffuse toxic goiter diagnosis are tests for thy-
roglobulin antibodies, thyroid hormones in the blood, thyroid gland ultrasound.
Pregnant women with diffuse toxic goiter show a considerably elevated content of
free T3 and T4 while pituitary TSH is decreased.
Radiological studies and functional assays with thyroid releasing hormone are not
done in pregnant women. Blood biochemistry reveals hypocholesterolemia, moderate
hyperglycemia.
Indications for consultation by other specialists. The case is managed by an en-
docrinologist.
Example of diagnosis. Gestation 7–8 weeks. Early toxicosis. Diffuse toxic goiter,
mild.

Diffuse toxic goiter is differentially diagnosed from vascular dystonia, autoimmune
thyroiditis, transient gestational hyperthyroidism.

The optimum time to plan parenthood is when thyrotoxicosis has been completely
eliminated, the blood showing no thyroid-stimulating immunoglobulins until the
start of pregnancy. Otherwise, if thyroid-stimulating immunoglobulins pass to the

fetal blood, its thyroid will be stimulated and congenital thyrotoxicosis will develop.
Thus pregnancy is undesirable until thyrotoxicosis has been eliminated (one should
use contraceptives).
If thyrostatic therapy of 12–18 month duration was decided upon, pregnancy is
postponed for about 24 months. When planning radioiodine (I-131) therapy, preg-
nancy is postponed for 12 months. Surgery offers the fastest resolution as in case of
Graves’ disease it guarantees no thyrotoxicosis recurrence, and this also applies to the
planned pregnancy. Having had her thyroid removed the patient receives a complete
replacement dose of L-thyroxine and can plan her pregnancy as soon as she wishes.
When the patient plans to resort to reproductive technology (IVF and other), first
the illness should be compensated, and only then assisted reproductive technology
can be started.
A dynamic assessment of thyroid function and the gland size is done every 8 weeks
(no less than once a trimester).

In case of a mild diffuse toxic goiter pregnancy can be saved; the patient should
be observed by an obstetrician-gynecologist and endocrinologist; in the second half
of pregnancy treatment is required.
A case of moderate severity can be an indication for surgery at the end of the first
trimester and early in the second trimester, or pregnancy termination followed by
obligatory treatment of thyrotoxicosis.
Pregnancy is contraindicated in case of severe toxic goiter.
In the first trimester pregnancy is often complicated by early toxicosis, threatened
abortion; conventional treatment is administered. In the third trimester PE and
threatened preterm birth is possible.
The main objective of thyrostatic therapy during pregnancy is maintaining free
T4 level in the upper normal range (21 pmol/l) or somewhat above normal using
minimal medication dose.
The principles of treating Graves’ disease in pregnant patients consist in the following.
• Endocrinologist appointment every 4 weeks.
• Free T4 test every 4 weeks.
• Propylthiouracil is the drug of choice.
– In case of moderate thyrotoxicosis newly diagnosed during pregnancy,
propylthiouracil is administered at a dose of 200 mg 4 times a day.
– Having achieved a decrease of free T4 to the upper normal level, a maintaining
dose of propylthiouracil is administered (25–50 mg/day).
There is no need to try to achieve normal TSH levels or to test this parameter
frequently.
If free T4 goes down to lower normal or below normal values, the thyrostatic drug
is temporarily withdrawn, free T4 tests continue every 4 weeks; the drug is admin-
istered again when appropriate.
As gestation continues, thyrotoxicosis appropriately becomes milder, the need for
thyrostatic drug declines, so in most cases the drug, depending on the free T4 level,
is withdrawn in the third trimester.
688 Obstetrics
As a rule, 2–3 months after childbirth the woman experiences recurrence and
aggravation of thyrotoxicosis, which calls for administration of the thyrostatic drug
and increasing its dose.
If the patient is on small doses of propylthiouracil (about 100 mg/day), breast
feeding is safe for the infant.
The patient should keep regular hours, avoid emotional strain if possible. Sedative
medications like valerian root infusion, motherwort infusion are widely administered.
Beta-adrenergic blockers (propanolol 20 mg 4 times a day) soften the manifestations
of thyrotoxicosis, especially tachycardia and tremor.
Nowadays there are three approaches to managing diffuse toxic goiter: thyrostatic
drug therapy, surgery and radioactive iodine therapy. The last one is unacceptable
for pregnant women.
Thyrostatic therapy uses thiamazole (Mercazolil) at a dose of 0.005–0.01 g
3-4 times a day after meals for 2–3 weeks; having achieved remission the dose is
gradually decreased to 1 tablet (0.005 g) once every 3–4 days.
During pregnancy surgery is indicated in case of
• no effect of conventional therapy of diffuse toxic goiter of moderate severity;
• nodular goiter;
• a need for high dose of thyrostatic drugs to maintain euthyroidism;
• suspicion of malignancy;
• very large goiter.
Surgery is most reasonable at the beginning of the second trimester. Surgery at
an earlier gestational age can provoke a spontaneous abortion.
When any disorder of the thyroid is detected during pregnancy, it is unequivo-
cally inacceptable to exert pressure on the woman making predictions about her
child’s future development. Any remark about the future child’s health can cause a
psychological trauma.
22.8.1.14. Treatment of complications in childbirth and puerperium

Delivery should be managed in condition of euthyroidism so as not to provoke a
thyrotoxic crisis. Managing the labor one adopts expectant approach; monitoring of
the cardiovascular function is essential.
In the third stage of labor and early postpartum period prevention of hemor-
rhage is needed as thyroid dysfunction precipitates disturbance of the hemostasis
system.
If the condition aggravates after childbirth, lactation should be suppressed and
antithyroid drugs administered.
Assessment of treatment effectiveness. To prevent complications, euthyroidism
should be maintained.

Most patients with diffuse toxic goiter have an uncomplicated delivery at term.
Rapid childbirth is typical; in most primiparous women the duration of labor does
not exceed 10 hours.
Cesarean section is performed for obstetric indications.
REMEMBER!
Delivery should be managed in condition of euthyroidism so as not to provoke a
thyrotoxic crisis.
Managing the labor one adopts expectant approach; monitoring of the cardiovascular
function is essential.
The patient should keep regular hours and avoid emotional strain if possible.
22.8.2. Hypothyroidism
Synonyms. Advanced stages of hypothyroidism are referred to as myxedema; cretin-
ism develops in case of euthyroidism.
Hypothyroidism is a complex of symptoms that arises upon limited production of
hormones by the thyroid gland.
ICD-10 codes
• E03.0 Congenital hypothyroidism with diff use goiter.
Goiter (nontoxic) congenital: not otherwise specified, parenchymatous. Excl.:
transitory congenital goiter with normal function (P72.0).
• E03.1 Congenital hypothyroidism without goiter.
Aplasia of thyroid (with myxedema). Congenital: atrophy of thyroid, hypothyroid-
ism not otherwise specified.
The incidence rate of hypothyroidism among pregnant women is about 2%.
Since pregnancy is the time of the greatest risk for development of severe iodine
deficiency conditions, women should start individual programs of iodine deficiency
prevention as early as at the stage of family planning. Prevention is constituted by physi-
ological doses of iodine: 200 mcg per day in the form of accurately dosed medications.
Iodine deficiency can be supplied by various methods. The most

NB! effective method is the one recommended by the WHO and
other international organizations: mass-scale iodine deficiency
prevention using iodinated dietary salt.
It is advisable to continue iodine prevention throughout the entire pregnancy and

lactation. The diet should include sea fish twice a week. Iodine-containing dietary
supplements should not be included into the individual prevention program.
• Primary hypothyroidism
– Reduced volume of the functioning thyroid tissue:
◊ chronic autoimmune thyroiditis;
◊ transient («silent») autoimmune thyroiditis;
690 Obstetrics
◊ hypothyroidism after total or subtotal thyroidectomy;

◊ infiltrative disorder of the thyroid.
– Disorder of thyroid hormone biosynthesis:
◊ congenital disorder;
◊ iodine deficiency;
◊ prolonged intake of excessive iodine;
◊ antithyroid factors.
• Secondary hypothyroidism:
– pituitary hypothyroidism;
– hypothalamic hypothyroidism.
In laboratory diagnostics the notions of overt and subclinical hypothyroidism are
employed.
Subclinical hypothyroidism means an isolated episode of TSH elevation while free
T4 is within normal; overt hypothyroidism means a combination of elevated TSH
and reduced free T4 content.
22.8.2.4. Etiology
Deficiency of thyroid hormones is determined by structural or functional changes
in the thyroid gland, or disturbed stimulation on the part of pituitary TSH and
hypothalamic thyrotropin-releasing hormone. Hypothyroidism due to resistance of
peripheral tissues to thyroid hormones is noted much less often.
Causes of primary hypothyroidism comprise the following:
• thyroid gland malformations;
• iodine deficiency disorder;
• immune thyroiditis, postpartum thyroiditis;
• thyroidectomy;
• radioactive iodine therapy and thyroid gland irradiation;
• congenital hypothyroidism;
• prolonged intake of excessive iodine amounts (amiodarone);
• tumor and cancer of the thyroid.
Physiological alteration of thyroid function during pregnancy:
• Hyperstimulation of the thyroid by hCG:
– physiological reduction in TSH level during recent pregnancy;
– increased production of thyroid hormones.
• Increased production of thyroxin-binding globulin by the liver:
– increased portion of total thyroid hormone fractions;
– increase in the total content of thyroid hormones in the pregnant woman’s body.
• Enhanced excretion of iodine with urine and transplacental transfer of iodine.
• Deiodation of thyroid hormones in the placenta.
Pregnancy increases the need for thyroid hormones which promotes relative iodine
deficiency; both factors aggravate the existing hypothyroidism and lead to decom-
pensation of subclinical hypothyroidism.
Decline in the content of thyroid hormones that regulate physiological functions

and metabolism results in suppression of all types of metabolism, utilization of oxygen
by tissues, reduced activity of various enzyme systems, diminished gas exchange and
basal metabolism. The slowing-down of protein catabolism and synthesis and of its
excretion leads to significant increase in the protein degradation products in organs
and tissues, skin and musculature.
Pregnant women experience iodine deficiency that is within borderline ranges,
while there are no adequate adaptation mechanisms. Free T3 and T4 levels keep
decreased until the middle of gestation and persist at low levels till childbirth.
These changes are due to a compensatory increase in fetal thyroid activity and
the passage of thyroid hormones from mother to fetus. At later gestational ages the
existing hypothyroidism may go into remission.
A specific feature of the disease in pregnant women is diminishing

NB! of hypothyroidism signs as the pregnancy progresses. Patients
taking thyroid hormones at certain doses on a permanent basis
show clinical presentations of thyroid hyperfunction, which is first
of all manifested by tachycardia.

Since practically all tissues have receptors to thyroid hormones, hypothyroidism
signs are multiple and varied. Their prominence depends on the extent and duration
of thyroid hormone deficiency.
If gestational hypothyroidism is not compensated sufficiently, women present
with apathy, decreased work capacity, sleepiness, chilliness, weight gain, persistent
constipation, impaired memory, attention and hearing, dryness of skin, frail nails,
hair loss.
In conditions of thyroid hormone deficiency energy production is not so intensive
which leads to constant chilliness and hypothermia. Predisposition to frequent infec-
tions is another sign of hypothyroidism; this is due to the lack of thyroid stimula-
tion of the immunity. Patients have frequent headaches; joint and muscle pain is
common. Numbness of hands is due to compression of nerves by edematous tissues
in the carpal tunnel. Alongside with physical retardation patients show intellectual
retardation and forgetfulness.
Due to tissue edema in hypothyroidism, sense organs are affected. Patients present
with vision disorder, hearing impairment, tinnitus. Due to edema of vocal cords the
voice becomes deeper; patients often snore in their sleep due to edema of tongue
and larynx. Slowing-down of digestion results in constipation.
Heart problem is one of major serious signs of hypothyroidism. Many patients
show a slowed-down cardiac rhythm below 60 per minute. Another cardiovas-
cular manifestation of hypothyroidism is elevated blood cholesterol, which can
lead to atherosclerosis of cardiac vessels, ischemic disease and intermittent
claudication.
There is no considerable clinical difference between pronounced manifestations
of primary, secondary and tertiary hypothyroidism.
692 Obstetrics
Alcohol consumption, exposure to cold, and stress can bring

NB! about a hypothyroid (myxedema) crisis: a fast deterioration of
the condition, especially in patients with myxedema. The crisis
is manifested by hypothermia, progressing CNS suppression,
alveolar hypoventilation with hypercapnia, bradycardia, arterial
hypotension and patient’s demise.
Hypothyroidism suppresses the generative function of women. Metabolism and

trophism are reduced; this affects the ovaries: primordial follicle maturation is re-
tarded, ovulation and corpus luteum development are disrupted. Before 6–8 weeks
gestation early stages of embryogenesis are provided for by maternal thyroid hor-
mones. If there is prominent thyroid hormone deficiency, both gestation and embryo
development are absolutely impossible.
Untreated or decompensated hypothyroidism affects the conception and increases
the rate of spontaneous abortion and still births. Conception disturbance can be due
to secondary hyperprolactinemia that causes anovulation.
In literature there are descriptions of cases when myxedema patients went through
pregnancy and delivery. In all observed cases the outcome of pregnancy was unfa-
vorable.
Hypothyroidism of pregnant women is dangerous for fetal development, its CNS
development in the first place.
Hypothyroidism of pregnant women (including hypothyroidism due to severe
iodine deficiency) can produce more adverse effects on fetal CNS than congenital
hypothyroidism of infants (aplasia, thyroid gland dystopia) when replacement therapy
is initiated immediately after birth. At early gestational ages fetal thyroid hardly
functions at all, and when maternal thyroid functions normally, the nervous system
development is provided for both in a normal fetus and one without a thyroid gland
(with congenital hypothyroidism). At later gestational ages, in presence of congenital
hypothyroidism, transplacental transfer of maternal T4 intensifies. Myelination of
CNS continues after childbirth and comes to completion during the first year of life.
Thus, if an infant with congenital hypothyroidism, who did not experience hypo-
thyroxinemia in early pregnancy, starts receiving replacement therapy with sodium
L-thyroxine within the first days of life, his CNS development may not show any
significant deviation from normal. Cerebral myelination continues for twelve months
after birth: even if anlage of the fetal thyroid was normal, after-effects of hypothy-
roxinemia of early pregnancy are considered irreversible.
Besides, transplacental transfer of antithyroid antibodies is possible. Infants by
mothers with elevated antibodies to thyroid peroxidase show a higher risk for mental
retardation, even when their thyroid function is normal. Weight gain and growth in
such neonates are much smaller.

Unlike earlier time, gestational and delivery complications in women with hypo-
thyroidism are virtually not seen if early, adequate therapy was provided.
In presence of subclinical hypothyroidism, even insignificant fluctuations of thy-

roid hormone in the blood definitely increase the rate of gestational complications
and carry a threat to both maternal and especially fetal health. Hypothyroidism can
complicate gestation with AH, PE, eclampsia and fetal demise (Fig. 22.18).
22.0
Hypertension, preeclampsia
15.0
5.0
Placental abruption
0.0
16.6
Low weight
8.7
6.6
Fetal demise
1.7
3.3
Fetal malformations
0.0
6.6
Postpartum hemorrhage
3.5
0 10 20 30
Overt hypothyroidism
Subclinical hypothyroidism
Fig. 22.18. Complications of decompensated hypothyroidism in pregnancy, %
Even subclinical varieties of hypothyroidism are accompanied by miscarriage.

Iron- and folic acid deficiency anemia is common. Women with hypothyroidism give
still birth twice more often than healthy ones.
Past history. According to WHO, about 30% of the world population run the risk
of iodine deficiency conditions, including 500 million people residing in iodine-
deficient areas and a high incidence rate of endemic goiter. About 20% of population
resides in iodine endemic areas (including Russia) where iodine prevention is not
provided actively enough. The average intake of iodine in Russia is 40–80 mcg per
day while the recommended daily dose is150 mcg, that is, three times higher. The
recommended daily iodine intake during pregnancy is 200 mcg (WHO).
One comes across familial hypothyroidism with partial peripheral resistance to
thyroid hormones (autosomal dominant inheritance).
Physical investigations
• Examination:
– patient’s facial expression;
– anterior neck surface;
– distribution of subcutaneous fat.
694 Obstetrics
• Thyroid gland palpation.

• Measuring the pulse.
• Taking BP.
On examination the patient shows pallor and edema of the skin and subcutaneous
tissue. The skin is dry, flaky, cold. One notes puffiness, pastosity of the face and ex-
tremities. The speech is slowed down, the voice is hoarse, the movements are slow.
The patients show bradycardia (52–60 per min), arterial hypotension, reduced cir-
culating blood volume, slow blood flow. Congenital hypothyroidism entails retarda-
tion of physical growth and mental development to the extent of feeble-mindedness.
Greater or lesser extent of mental disorder is noted in all patients.
Laboratory tests
• TSH, T4 and free T3 in the blood every month.
• Coagulation system of the blood in each trimester.
• Protein-bound iodine in the blood.
In primary hypothyroidism the TSH level is increased, in secondary hypothy-
roidism it is decreased or within normal. Secretion of T4 and T3 thyroid hormones
is reduced. The amount of protein-bound iodine is considerably lower in hypo-
thyroidism.
60–70% of patients show abnormal findings in blood tests: lymphocytosis, in-
creased ESR. Suppression of bone marrow metabolism underlies thyrogenic anemia
which can be hypochromic, normochromic and hyperchromic. The parameters of
basal metabolism and protein synthesis are reduced; beta-lipoproteid and cholesterol
content is increased to 9.36 mmol/l. Patients are predisposed to hypercoagulation due
to enhanced plasma tolerance to heparin and increased content of free fibrinogen.
• Ultrasound of the thyroid gland (determining the thyroid volume; in women it
normally does not exceed 18 ml), the number, size and echostructure of nodules.
Dopplerometry. A dynamic assessment of thyroid function and its volume is
performed every 8 weeks (no less than once in every trimester).
• ECG.
• Heart ultrasound.
Indications for consultation by other specialists. Treatment by endocrinologist.
Example of diagnosis. Gestation 34 weeks. Cephalic presentation. Threatened
abortion. Primary hypothyroidism.

Hypothyroidism is differentially diagnosed from ischemic heart disease. Severe
cases of myxedema should be differentiated from chronic nephritis or nephrotic
syndrome.
One should bear in mind the possibility of hypothyroidism development in indi-
viduals at risk like persons with previous surgery on the thyroid, radioactive iodine
therapy for thyrotoxicosis.
Individual iodine prevention is administered without discontinuing regular iodine
prevention. Even if the pregnant woman receives levothyroxine sodium but resides in
endemic area, this should not rule out the intake of potassium iodide as levothyroxine
does not pass the placental barrier.
Management of pregnant patients with hypothyroidism is based on the proposi-
tion that such women are classified at high risk for perinatal morbidity. If a pregnant
woman develops hypothyroidism after surgery on the thyroid, one should provide
functional assessment of the gland and replacement therapy with thyroid hormones,
and regular lab tests.
Once euthyroidism is achieved, both the mother and fetus have a lesser risk of
complications.
Congenital hypothyroidism requires special approach when deciding the issue of
pregnancy continuation. Medical and genetic consultation is required in such cases
as the woman has a rather high risk of giving birth to disabled progeny; there is
evidence linking thyroid disease to chromosomal aberrations.
NB! Since 1992 all newborns in Russia are screened for hypothyroidism.
On day 5–6 of the infant’s life the test for TSH level is done; in low birth weight
infants and those with a low Apgar score — on day 8–10. If TSH is elevated, T3
and T4 in the plasma are determined (in hypothyroidism their values are decreased).
Ultrasound of the thyroid is an important method in diagnostics of congenital
hypothyroidism. In case of congenital hypothyroidism there is a discrepancy between
actual age and bone age; bone age is determined by the knee rather than by the
wrist. Treatment consists in administering levothyroxine 10–15 mg per 1 kg of body
weight for 12 months.
The main principle of treating patients with hypothyroidism is replacement of the
deficient thyroid function. Therapy is administered and monitored by an endocrinologist.
Replacement therapy in hypothyroidism during pregnancy.
Compensated hypothyroidism is no contraindication for planning pregnancy.
During pregnancy T4 requirement increases, which calls for an increased levothy-
roxine sodium dose.
The dose of levothyroxine sodium should be increased by 50 mcg immediately
upon establishing pregnancy in a woman with compensated hypothyroidism.
TSH and free T4 tests should be done every 8–10 weeks.
If replacement therapy is adequately administered, the patient shows low normal
TSH values (<2mU/l) and a high normal free T4 level.
If hypothyroidism was newly diagnosed during pregnancy, a full replacement dose
of levothyroxine sodium is administered (2.3 mcg per 1 kg of body weight), without
a gradual increase which is a routine procedure in management of hypothyroidism
outside of pregnancy.
There is no difference between approaches to managing manifest and subclinical
hypothyroidism in pregnant patients.
696 Obstetrics
After childbirth the dose of levothyroxine sodium is decreased to a routine replace-

ment dose (1.6–1.8 mcg per 1 kg of body weight).
Treatment of gestational complications in each trimester is administered according
to general principles, while the patient continues her hormone therapy. Women with
congenital, acquired hypothyroidism (after thyroid surgery) and cerebral hypothy-
roidism of cerebropituitary origin do not get pregnant easily. In the first trimester
the patient may show threatened abortion, in the third trimester — PE, gestational
anemia. When managing anemia one should remember that administration of iron
sulfate decreases the effect of thyroid hormones, apparently due to iron binding to
thyroxin. That is why it is recommended to make an interval of no less than 2 hours
between the intake of these medications.
Treatment of complications in childbirth and puerperium. The most common com-
plication of labor is uterine inertia. The mode of delivery depends on the obstetric
situation. In the third stage of labor and early postpartum period prevention of
hemorrhage should be provided as thyroid dysfunction is accompanied by disorder
of the hemostasis system.
Assessment of treatment effectiveness. Normal fetal growth requires a stable com-
pensation of the disease. The requirement for the drug increases by 30–50%, which
is indicated by an increased TSH concentration in the blood. Therapy is administered
throughout the entire pregnancy achieving euthyroidism.
Prevention and early initiation of treatment of thyroid disease in pregnant women
promotes a decrease in the rate of maternal and fetal complications and enhances
the health indices and intellectual promise of the nation.

Most patients with compensated hypothyroidism give a term birth without com-
plications.
Cesarean section is performed for obstetric indications.
REMEMBER!
Replacement therapy for hypothyroidism during pregnancy.
Compensated hypothyroidism is not an obstacle to family planning.
T4 requirement grows during pregnancy, which calls for a greater levothyroxine
sodium dose.
The levothyroxine sodium dose should be increased by 50 mcg immediately after
the patient with compensated hypothyroidism gets pregnant.
TSH and free T4 tests are done every 8–10 weeks.
If replacement therapy is adequately administered, the patient shows low normal
TSH values (<2mU/l) and a high normal free T4 level. If hypothyroidism was newly
diagnosed during pregnancy, a full replacement dose of levothyroxine sodium is
administered (2.3 mcg per 1 kg of body weight), without a gradual increase which
is a routine procedure in management of hypothyroidism outside of pregnancy.
There is no difference between approaches to managing manifest and subclinical
hypothyroidism in pregnant patients.
After childbirth the dose of levothyroxine sodium is decreased to a routine
replacement dose (1.6–1.8 mcg per 1 kg of body weight).
22.9. TUBERCULOSIS
Tuberculosis is a chronic infection caused by the bacterium Mycobacterium tu-

berculosis (bacillus Kochii). Tuberculosis generally affects the lungs; genitourinary,
eye, bone and joint tuberculosis is prominent among extrapulmonary forms of the
disease.
ICD-10 code
• O98.0 Tuberculosis complicating pregnancy, childbirth and the puerperium.
The incidence of tuberculosis in pregnant women is relatively higher than in the
general population: 72 per 100 000 of population, and 106 per 100 000 of pregnant
women. In certain regions of Russia the morbidity rate is 100 and more per 100 000
of population. These data indicate that the epidemic tuberculosis situation in Russia
is stably alarming. In Moscow the tuberculosis morbidity rate among girls aged 18–20
is 1.7 times higher than in men.
More than 646 mln women in the world are infected by Mycobacterium tubercu-
losis; every year 3.1 mln develop tuberculosis. In developing countries tuberculosis
holds the third place among causes of morbidity and mortality in women of repro-
ductive age.
For women tuberculosis is the most common cause of lethality

NB! due to infection: over 1 million women die every year.
22.9.2. Prevention
Sanitation measures are provided by TB dispensaries in cooperation with general
health care and institutions for disease surveillance and control.
TB dispensaries pay special attention to patients with active mycobacteria releasing
tuberculosis and their relatives. Persons who were in contact with diseased animals
are also followed up for 12 months.
Infection is transmitted when TB patients do not follow the rules of personal
hygiene, do not receive adequate therapy, and their relatives do not receive chemi-
cal prophylaxis.
Specific prevention is aimed at boosting the body’s resistance to tuberculosis
infection by administering active BCG immunization or antitubercular drugs
(chemical prophylaxis). Immunized persons develop the disease 4–10 times less
often than those not immunized. Those immunized with BCG vaccine show
a more benign course of tuberculosis. 40–45 years ago it was any physician’s
axiom that a girl with tuberculosis should not get married or get pregnant or
give birth; if she gives a birth, she should not breast feed. These beliefs hold
certain truth; in fact one should postpone marriage and parentage until com-
plete recovery. The existing preventive measures are mostly aimed at ensuring
the child’s health.
698 Obstetrics
22.9.3. Screening
Preventive checkups are important in tuberculosis detection.
For detection of pulmonary tuberculosis, chest X-ray is made annually; children
and pregnant women have tuberculin diagnostics. An examination by a therapist is
obligatory during pregnancy, and an X-ray after childbirth.
According to a classification adopted in 1974, the following types of pulmonary
tuberculosis are distinguished:
• primary tuberculous complex;
• tuberculosis of intrathoracic lymph nodes;
• disseminated pulmonary tuberculosis;
• focal pulmonary tuberculosis;
• cavernous pulmonary tuberculosis
• infi ltrative pulmonary tuberculosis;
• fibrous cavernous pulmonary tuberculosis;
• cirrhotic pulmonary tuberculosis;
• tuberculosis of upper airways, trachea and bronchi;
• pulmonary tuberculosis combined with pneumoconiosis.
Classification by the course of the disease:
• acute;
• subacute;
• chronic.
Stages of tuberculosis:
• infi ltration;
• resorbtion;
• scarification;
• calcification.
Regarding bacterioexcretion:
• TB with bacterioexcretion;
• TB without bacterioexcretion.
22.9.5. Etiology
The causative agent is Mycobacterium tuberculosis of human
NB! variety, less often – of bovine, and most rarely – of avian variety.
Mycobacterium tuberculosis is resistant to the impact of external environment

factors. Mycobacteria retain their vitality both in liquid and dry sputum for several
months and then getting into a human body they are still capable of causing infection.
The hallmark of Mycobacterium tuberculosis is its acid resistance: they retain their
coloration upon staining with acid, alkali, alcohol. This infective agent has the shape
of a rod (Latin bacillus) 1.5–6 mcm long and 0.2–0.6 mcm thick. Mycobacterium
tuberculosis is curved along its length, sometimes arcuate, thickened at both ends. In
pathological samples they are placed parallel each other, sometimes at an angle or
in bundles and aggregations of varying shapes. The bacteria reproduce by transverse

fission, branching and budding.
The major source of infection is the diseased people and animals, mostly cows.
Infection is usually transmitted via bacteria containing droplets of sputum released by
the host. Besides, infection can enter the body with consumption of milk, meat and eggs
from infected animals and poultry. A majority of those infected for the first time show
Mycobacterium tuberculosis in their sputum; the bacteria are sensitive to anti-TB drugs,
in 5–10% the bacteria are drug resistant. In the latter case infection came from people
who received inadequate therapy and developed resistant strains of M. tuberculosis.
Pathogenesis is complex; it depends on the variety of conditions in which the
infective agent and the person interact. Transmission of M. tuberculosis does not
always result in the development of the disease. Unfavorable living conditions and
suppressed immunity are trigger factors in tuberculosis development.
Tuberculosis development is divided into primary and secondary stages that unfold
in conditions of different reactivity of the body.
Primary tuberculosis is marked by enhanced sensitivity of tissues to mycobacteria
and their toxins. Where M. tuberculosis enters the body (in the respiratory organs,
GI tract, skin) an inflammatory focus, or Ghon’s primary lesion can develop. In
response to its formation, as the body becomes sensitized, a specific process develops
in the lymph nodes, and the primary complex develops. It is mostly revealed in the
lungs and intrathoracic lymph nodes.
From the first day of infection the patient shows bacteriemia, the immune system
becomes activated fighting against the causative agent. As primary tuberculosis foci
are developing, the infection spreads through the blood and lymph forming tuber-
culosis foci in the lungs, bones, kidneys and other organs. Healing of the primary
tuberculosis foci is accompanied by changes in the immune system, developing the
immunity. When immunity is suppressed, the foci can become activated and begin
progressing, thus secondary tuberculosis begins.
The morphological manifestations of tuberculous inflammation are varied.
Depending on the body’s reactivity, the tuberculous focus shows predominance of
proliferation, exudation or necrosis. A typical productive reaction takes place mani-
fested by emergence of tubercles or granuloma consisting of epithelioid and lymphoid
cells as well as specific giant Langhans cells.
When tuberculosis foci heal, their contents grow compact, specific granulous tis-
sue is replaced by fibrous tissue, a connective tissue capsule grows around the focus,
and the focus itself becomes calcified. As the disease progresses, the caseous necrotic
masses dissolve and degrade, the infection spreads further, and destructive forms of
the disease develop.

Pregnancy mobilizes all the body’s reserves. Development of fetal bone system
entails enhanced utilization of calcium by the mother, which triggers demineraliza-
700 Obstetrics
tion that can lead to softening of Ghon’s primary lesions, or calcified foci, in lymph
nodes, and a latent disease turns active: endogenous activation.
The first three months of gestation are most unfavorable; they account for 1/3 of
exacerbations noted during gestation, childbirth and lactation. Tuberculosis diagnosis
is difficult during this period as the infection can be disguised as manifestations of
early toxicosis.
An increased rate of early toxicosis can be due to tuberculosis intoxication that
leads to hypofunctioning adrenal cortex and disorder of electrolyte balance. Over
the period of pregnancy, childbirth and lactation each woman loses up to 700–800 g
of iron. The higher rate of anemia is associated with tuberculosis intoxication and
expenditure of iron required for fetal development.
In pulmonary tuberculosis, once infiltration and pulmonary tissue destruction
has begun, anemia of moderate severity is noted almost 3 times more often than in
a subdued specific process: in 12.5% of cases if it is active tuberculosis, 2.7% — if
tuberculosis is inactive.
In case of active tuberculosis the rate of gestational complications is higher than in
case of inactive tuberculosis. As the blood is insufficiently saturated with oxygen and
the woman experiences hypoxia due to pulmonary and cardiac failure, fetoplacental
insufficiency develops and a premature birth takes place. Tuberculosis intoxication
promotes these processes.
A common complication in labor is premature membrane rupture due to infection
of fetal membranes and a reduction in their strength. The total duration of labor is
shorter in tuberculosis patients than in healthy women.
Intrauterine infection can be transmitted via the umbilical cord or infected am-
niotic fluid. In the former case, typical primary inflammation foci appear in the
liver, in the latter case infectious foci can develop in different organs. If a woman
got pregnant while already having tuberculosis, gestation can have a favorable ef-
fect on the disease.
In literature there are examples of tuberculosis stabilization and regression dur-
ing pregnancy. This is linked to the fact that the hormone balance in a pregnant
woman has a shift towards anabolism, the diaphragm has a high station simulating
the therapeutic effect of pneumoperitoneum. In the last weeks of pregnancy the TB
patient may feel better than before pregnancy. At the same time, this well-being may
be misleading; in late pregnancy even severe exacerbations can occur without fever
or marked intoxication while the organs and systems are extensively involved.
There is an opinion that in extreme conditions like hypoxia when the main
compensatory and defensive mechanisms are rapidly depleted, activation of uterine
contraction serves as a last resort to protect the fetus.
The course of labor is usually complicated due to limited respiratory reserves in
the mother and inadequate nourishment. Another typical complication of labor in ac-
tive tuberculosis is hemorrhage. Such patients lose more blood in labor than healthy
women. Besides, TB patients may develop hypertension in the pulmonary circulation,
which entails a risk of such grave TB complications as pulmonary hemorrhage or
spontaneous pneumothorax.
The greater blood loss in labor is due to the presence of iron deficiency anemia
in most parturient TB patients.
In the postpartum period an exacerbation of TB is often caused by ineffective

treatment the patient received during pregnancy and by the fact that childbirth brings
about a rapid transformation in all major systems of the body, and breastfeeding en-
tails a higher expenditure of fats and proteins by the woman’s body. Besides, as the
diaphragm goes down after delivery, the infection can travel from pulmonary foci to
unaffected pulmonary areas, and a rapid sinking of the diaphragm precipitates the
syndrome of abdominal compression.
In TB patients the puerperium is dangerous in that it carries the risk of acute
hematogenous dissemination of Mycobacterium and passage of caseous masses to un-
affected portions of the lung and development of bronchogenous spread of infection.
Infants born of mothers with TB show low birth weight as a rule; this is due to
fetoplacental insufficiency accompanied by IUGR and the high rate of premature
births. Such neonates show disorder of adaptation in the first days postpartum, CNS
abnormalities, respiratory disorders, a greater initial weight loss and a delayed weight
gain. These phenomena are due to maternal TB intoxication, low birth weight, insuf-
ficient amount of suckled milk. In the early neonatal period these infants commonly
show CNS abnormalities due to hypoxia, elevated bilirubin, circulation disorder,
hemorrhage and edema syndrome.
Tuberculosis per se is not the only culprit certainly, other factors are at play like
degree of involvement and localization of the disease (pulmonary or extrapulmo-
nary), and the presence of TB complications (cardiopulmonary failure, hemoptysis,
cachexia, anemia). The graver the underlying disease, the more critical complications
in the mother and newborn.

Nowadays clinical features of pulmonary TB exacerbation are quite inapparent;
they can be disguised as gestational toxicosis and respiratory infections.
TB intoxication is manifested by weakness, night sweat, reduced working capacity,
subfebrile temperature or occasional temperature rise to 38–39 °С, poor appetite,
absence of weight gain, or weight loss. TB exacerbation is often associated with
emotional and physical strain, respiratory infection, childbirth.
If a pregnant woman presents with such symptoms as a cough with or without
sputum for over 3 weeks, hemoptysis, chest pain, shortness of breath, pulmonary
TB can be suspected.

• Threatened abortion.
• Early toxicosis.
• Gestational anemia.
• Fetoplacental insufficiency.
• Threatened preterm birth.
• Premature membrane rupture.
In case of disseminated pulmonary TB perinatal mortality is 6 times higher than
in the general population; birth of premature and small for date infants is twice as
702 Obstetrics
common. If the pregnant woman has «minor» TB, the risk of fetal complications is
not higher than in all other women.
22.9.10. Diagnostics
Past history. The following risk groups are distinguished.
Risk group
NB! • Patients with a recent episode of tuberculosis: less than 1 year
after cessation of therapy.
• Patients under 20 and over 35 with tuberculosis of any localization.
• Pregnant women with diffuse tuberculosis irrespective of its
stage.
• Pregnant women who were in contact with individuals with
established tuberculosis, with or without bacterioexcretion.
• Pregnant women with recently established conversion of
tubercular tests, hyperergic or progressing tuberculin sensitivity
(Mantoux test with 2 tuberculin units).
• Pregnant women with concomitant disease: DM, chronic
nonspecific respiratory or renal conditions, gastric or duodenal
ulcer; those consuming alcohol, nicotine and marginalized
individuals.
From the legal point of view, there are no limitations on marriages between men
and women with TB. Moreover, future spouses often meet at TB hospitals or sana-
toriums. Female patients often get pregnant while staying at hospital or sanatorium.
Sometimes TB is detected in an already pregnant or breastfeeding woman.
Physical examination
• Examination of chest shape.
• Chest palpation.
• Comparative and topographic percussion.
• Lung auscultation.
Laboratory tests. The findings of complete blood count (elevated ESR, leucocy-
tosis, left shift, sometimes lymphopenia, monocytosis) and urinalysis (proteinuria,
cylindruria) do not allow detection of specific TB signs; however, in combination
with other methods they are important in diagnostics and monitoring of TB disease.
Studies of specific and nonspecific immunity of pregnant women with TB showed
a disorder of T-cell immunity.
Instrumental investigations. Diagnostics of TB in pregnancy can be also delayed
because both physicians and patients beware of X-ray examinations during preg-
nancy. In fact, the standards of radiation safety forbid screening investigations at
any gestational age. However, in critical situations diagnostic investigations are
permissible, and investigations for TB in the presence of clinical features or after
contact with infectious individuals can be regarded as emergency X-ray investiga-
tion. A single X-ray of the chest does not entail any risk for the pregnant mother
or fetus if it was conducted with regard to radiation safety standards and fetus
protection: shielding the abdomen with lead rubber apron. The X-ray lab assis-
tant should position the patient adequately and perform an accurate X-ray beam
collimation. Large format X-ray films are indicated, or computer-aided low dose
digital radiography.
Fluorography is not done on pregnant patients as even up to date digital fluoro-
graphs produce a threefold higher radiation exposure than conventional radiography.
When tuberculous pleuritis is suspected in a pregnant patient, the method of choice
is the ultrasound as it produces no radiation exposure and permits a multiple view
scanning, differentiating between fluid and pleural thickening. Fine needle aspiration
of pleural cavity is done under ultrasound guidance as the diaphragm is stationed
higher during pregnancy causing the risk of liver injury.
Tuberculin test is done for diagnostic purposes during pregnancy. In Russia where
practically the entire population is infected with M. tuberculosis, Mantoux test can be
informative as a method of TB diagnostics only when it is hyperergic (over 21 mm
or emergence of vesicles, lymphangitis or regional lymphadenitis). It is also note-
worthy that pregnant women show physiological immunity suppression, and that
includes delayed-type hypersensitivity reaction of which Mantoux test is a variety.
Contraindications for Mantoux test are as follows: allergy, all acute and chronic
conditions (especially bronchial asthma for 4 weeks after a decline of the condition,
and epilepsy. The tuberculin reaction is regarded as
• negative in the absence of an infiltrate or skin hyperemia in 48–72 h;
• doubtful in the presence of an induration 2–4 mm in diameter or just hyperemia;
• positive in the presence of an induration 5 mm and more in diameter;
• hyperergic in the presence of an infiltrate 17 mm and more in diameter.
Bacteriology test is aimed at isolating the causative agent from sputum, urine,
etc. Bacteriology test includes bacterioscopy, culture and a bioassay. Luminescence
microscopy is the most informative bacterioscopic diagnostic tool. Mycobacteria
culturing is more sensitive than bacterioscopy; it permits obtaining a pure myco-
bacterial culture, identifying it and determining its susceptibility to medications. If
sputum is scanty, provoking inhalations are provided. Bioassay is the most sensitive
method of detecting M. tuberculosis when guinea pigs are infected with pathological
material. Guinea pigs show tuberculous changes when 1 ml of sample contains just
a few mycobacteria.
Indications for consultation by other specialists. A pregnant woman with TB is
managed on a collegiate basis by a TB specialist and obstetrician gynecologist; any
concomitant disease requires consultation by appropriate specialists.
Example of diagnosis. Gestation 26 weeks. Gestational anemia degree 1. Tuberculosis
of intrathoracic lymph nodes. No bacterioexcretion.

Tuberculosis is differentially diagnosed from chronic nonspecific pulmonary dis-
ease, bronchiectasis, pulmonary actinomycosis, lung cancer, lung-fever, viral pneu-
monia, thrombosis and embolism of the pulmonary artery or its ramifications fol-
lowed by pulmonary infarction.
704 Obstetrics
22.9.12. Prevention and prediction of gestational complications

The patient has planned hospitalization at specialized institutions 3 times: during
the first 12 weeks of gestation, at 30–36 weeks and 38–40 weeks. During the remain-
ing time the patient receives management at TB dispensary.
The time of hospitalization at a specialized institution depends on the course of
the disease. If the pregnancy is not complicated, until 30 weeks gestation the patient
can receive treatment at a day patient department.
If the pregnancy is complicated, the patient is hospitalized at a regional anti-TB
health care facility; the management is provided by TB specialists and obstetricians-
gynecologists. Hospitalization at 30 weeks gestation is obligatory; the purpose is
preparation for childbirth; the patient stays in hospital until the due date and af-
terwards for no less than 8 weeks. In case of mild tuberculosis the patient can be
transferred to day patient department a week after childbirth.
If the patient was not treated of new-onset TB during pregnancy, after childbirth
she has to be referred to an anti-TB care facility and isolated from the child. If in-
dicated, fluorography after childbirth can be administered at the maternity hospital
or anti-TB care facility; on the whole, it is indicated for all puerperas. Fluorography
does not compromise lactation.
Nowadays most women with TB can preserve their pregnancy. Strict adherence
to treatment regimen ensures a favorable outcome of pregnancy and delivery for the
mother and fetus. All newborns should undergo preventive BCG vaccination.
Outcome of pregnancy depends mostly on where tuberculosis

NB! is localized, how diffuse it is; when it was revealed; whether
the patient has it for the first time or is a chronic tuberculosis
patient.
Tuberculosis of lymph nodes, pleuritis, «minor» pulmonary tuberculosis have no

impact on the pregnancy outcome. However, in case of disseminated pulmonary
TB, especially one complicated by massive destruction and hemoptysis, the risk of
maternal death is 4–9 times higher than in the general population.
It should be pointed out that if the patient is predisposed to hemoptysis and
pulmonary hemorrhage, endovascular embolisation of bronchial arteries can be per-
formed after 26 weeks gestation despite the high radiation exposure (the abdomen
is mandatorily shielded with several layers of lead aprons) as the risk of maternal
mortality in case of heavy hemorrhage is about 50%.
Patients with disseminated pulmonary TB are at high risk for puruloseptic com-
plications.
Termination of pregnancy in patients with TB is indicated in the following cases:
• fibrous cavernous pulmonary TB resulting from progression of any type of TB
with cavern formation;
• active TB of the spine, pelvis, especially when abscess or fistula are present;
• TB of coxofemoral, talocrural and knee joint;
• advanced bilateral TB of kidneys.
Termination of pregnancy can aggravate the condition. In case of disseminated
TB termination of pregnancy is contraindicated. Besides, an artificial abortion is
indicated if past history has evidence of TB exacerbation in previous pregnancies,

during the first 2 years after miliary TB and tuberculous meningitis; if the condi-
tion is accompanied by DM, kidney disease and cardiopulmonary failure. Artificial
abortion is performed during the first 3 months of gestation. Any type of TB with
bacterioexcretion is a contraindication for pregnancy.
Patients with tuberculosis are hospitalized three times in a planned

NB! way. During the first 12 weeks of gestation, at 30 – 36 weeks and
at 36 – 40 weeks patients are treated in hospital, throughout the
rest of the time – at the tuberculosis dispensary.
22.9.13. Treatment of gestational complications

in each trimester
Treatment is administered while the patient is on anti-relapse or intensive anti-
tuberculous therapy.
In the first trimester threatened abortion occurs. Conventional therapy is admin-
istered.
In the second and third trimester the patient may develop fetoplacental insuf-
ficiency, IUGR, chronic hypoxia, PE, anemia, threatened preterm birth.
Nowadays pulmonary tuberculosis in pregnant women is treated with isoniazid,
rifampicin, ethambutol, pyrazinamide and others. These drugs do not cause any
severe handicaps in the fetus. However, they should not be administered in early
pregnancy, during the organogenesis period (3–12 weeks).
The duration of therapy in pulmonary TB can cover the entire length of pregnancy
and stretch to the lactation period. This is especially applicable to patients with new-
onset tuberculosis.
Termination of pregnancy at tuberculosis is indicated

NB! • in case of fibrous-cavernous pulmonary tuberculosis which
develops following a progressive course of any cavernous form
of tuberculosis;
• active tuberculosis of the spine or pelvis, especially in case of
abscess or fistula formation;
• tuberculosis of hip, knee or talocrural joint;
• advanced bilateral tuberculosis of kidneys.
22.9.14. Treatment of complications in childbirth

and puerperium
The puerperium holds the greatest threat to the sick woman’s health and life. Two-
thirds of all TB exacerbations noted during pregnancy, childbirth and breastfeeding
occur in the first 6 months after delivery. Labor trauma, blood loss, endocrine altera-
tions, lactation, emotional stress are all risk factors for aggravation of TB course and
its generalization. If untreated, a slowly progressing disease exacerbates, local lesions
can lead to a generalized lesion with prominent intoxication and fever. That is why
706 Obstetrics
the woman should be followed up closely by a TB specialist for at least 2 months

after childbirth; if the disease is complicated, she should stay in hospital. On day 7
after childbirth the woman has an X-ray.
After childbirth more active therapy can be administered, especially if the patient
is not breastfeeding. When she does breastfeed, aminolgycosides are ruled out.
Isoniazid is administered in combination with pyridoxine. If the patient has destruc-
tive TB, pneumoperitoneum is indicated in the puerperium.
Antitubercular drugs pass to maternal milk to a lesser or greater degree and thus
come to the infant’s body. If the infant received BCG vaccine, these drugs can
suppress the strain and prevent premunity development. BCG strains resistant to
isoniazid are available in some countries.
According to WHO experts, the infant should not be separated from the mother
except for cases when she is in a hopelessly critical state. If the mother shows no
bacterioexcretion, the infant should receive BCG vaccine; if the mother excretes
bacteria, tuberculin test is done first, and if negative after BCG administration, it
is recommended to separate the infant from the mother for 6 weeks of her inten-
sive therapy. European physicians believe breastfeeding combined with maternal
chemotherapy to be optimal. In this case the infant receives chemoprophylaxis
with isoniazid over the entire period of bacterioexcretion in the mother. BCG is
administered 6–8 weeks after completing chemoprophylaxis, if the infant remains
tuberculin-negative.
Patients with disseminated pulmonary TB show a higher risk of puruloseptic
complications, thus a single administration of a cephalosporin antibiotic is recom-
mended (the remaining spectrum will be covered by rifampicin). If necessary, full-
scale anti-TB therapy is administered. Unfortunately, since HIV infection is on the
rise, the number of TB cases with HIV coinfection will increase, which is occurring
in certain countries, so strict observance of all infection control procedures is the
best way to protect the personnel.
Certainly, unlike specialized institutions, a regular maternity hospital cannot pro-
vide opportunities for a thorough clinical and radiological examination of pregnant
and puerperant women. That is why large cities should make provisions for special-
ized maternity hospitals or hospital departments for pregnant women with TB of
any localization.
Assessment of treatment effectiveness. If adequate therapy was initiated early
enough, by the time of delivery and puerperium the patients usually show an im-
provement: elimination of bacterioexcretion, healing of pulmonary foci, resorption
of infiltrates and elimination of abnormal fluid accumulation in pleuritis.
Patients who excrete TB bacteria before the onset of therapy, should be repeatedly
tested for bacterioexcretion with sputum tests and inoculation of sputum specimens
on a medium.
22.9.15. Timing and mode of delivery

Patients with TB give a vaginal birth; cesarean section is only performed for ob-
stetric indications or in case of decompensated pulmonary function. It is advisable to
avoid labor analgesia with narcotic analgesics as they suppress the respiratory center.
The method of choice for labor analgesia is epidural nerve block with low doses of
local anesthetics.
If there is a need for a cesarean section in TB patients, general anesthesia should
be avoided, first, in the context of probable complications, and second, from the
point of view of infection control. All personnel assisting at the childbirth should
wear masks, and the anesthesiologist who performs intubation must wear a carbon-
filter face mask.
Due to the high risk of infection spread regional anesthesia is the method of choice
for analgesia of cesarean section in such patients.
Obstetric forceps are applied only for obstetric indications and in the presence of
cardiopulmonary failure.
Breathing exercise is not advisable in labor; pain killing and spasmolytic drugs
are administered.
Before the puerpera is discharged, she and all people residing in her home where
the newborn is coming should have fluorography of X-ray of the chest.
REMEMBER!
Tuberculosis is a chronic disease caused by Mycobacterium tuberculosis.

Pulmonary TB is most common; extrapulmonary lesions include TB of the
genitourinary system, eyes, bones and joints.
The incidence rate of TB in pregnant women is relatively higher than in the general
population: 72 per 100 000 in the general population, and 106 per 100 000 among
pregnant women.
Risk groups:
• patients with recent TB in past history: less than 12 months after completion of
therapy;
• under 20 and over 35 with TB of any localization;
• disseminated TB irrespective of its stage;
• those in contact with persons in whom TB with or without bacterioexcretion was
established;
• those with newly diagnosed conversion of tuberculin tests, hyperergic or
progressing tuberculin sensitivity (Mantoux test with 2 TU);
• those with such concomitant conditions as DM, chronic nonspecific diseases of
respiratory organs and kidneys, gastric and duodenal ulcer;
• those taking alcohol, nicotine and narcotic substances, marginalized individuals.
The patient has planned hospitalization at specialized institutions 3 times: during
the first 12 weeks of gestation, at 30–36 weeks and 38–40 weeks. During the
remaining time the patient receives care at TB dispensary.
Patients with TB give a vaginal birth; cesarean section is only performed for
obstetric indications or in case of decompensated pulmonary function. It is
advisable to avoid labor analgesia with narcotic analgesics as they suppress the
respiratory center. The method of choice for labor analgesia is epidural nerve block
with low doses of local anesthetics.
708 Obstetrics
If there is a need for a cesarean section in TB patients, general anesthesia should

be avoided, first, in the context of probable complications, and second, from the
point of view of infection control. All personnel assisting at the childbirth should
wear masks, and the anesthesiologist who performs intubation must wear a
carbon-filter face mask.
Block anesthesia is a method of choice at cesarean section in such patients, due
to the high risk of infection spread.
CONTROL QUESTIONS
1. What is the low normal value of hemoglobin in pregnancy?

2. What blood parameters are looked at in anemia?
3. Is viral hepatitis an indication for pregnancy termination?
4. Principles of preventing constipation.
5. AH criteria.
6. Principles of examination of pregnant patients with kidney disease.
7. Indications for pregnancy termination in case of DM.
8. Indications for pregnancy termination in case of TB.
CHECK YOURSELF!
Level 1. Test
1. Which of these is part of pregnancy management in the first trimester in case of
cardiovascular disease?
a) complete clinical and instrumental workup to specify the diagnosis;
b) the issue of pregnancy termination before 12 weeks is not related to the
prominence of cardiac defect or the cardiovascular condition;
c) prediction of pregnancy outcome is made depending on the type of cardiac
defect;
d) if pregnancy continues, therapy aimed at eliminating obstetric complications
is administered.
2. In what case is vaginal birth possible for patients with cardiovascular disease:
a) vaginal birth is admissible in case of compensated circulation in patients with
mitral valve prolapse, mitral valve insufficiency;
b) septic endocarditis;
c) vaginal birth is admissible on condition that adequate analgesia at each stage
of labor is provided to prevent the emergence of aggravation of heart failure;
d) rheumatic heart disease degree II and III;
e) vaginal birth is admissible in presence of compensated circulation in patients
with aortic heart defect, ventricular septal defect.
3. How many times and at what gestational age is a pregnant woman with hypertonic
disease hospitalized:
a) a pregnant woman with hypertonic disease is hospitalized 3 times during
pregnancy;
b) hospitalization occurs at 12 weeks, 24 weeks and 35 weeks;
c) the purpose of the third hospitalization is preparation for childbirth and
deciding the issue of mode of delivery;
d) a pregnant woman with hypertonic disease is hospitalized 2 times during
pregnancy;
e) the first hospitalization occurs before 12 weeks, the second — at 28–32 weeks.
4. What are the measures for prevention and treatment of placental insufficiency in
pregnant women with anemia:
a) a diet including protein foods;
b) administration of acidophilic lactobacilli to normalize the birth canal flora;
c) treatment of all concomitant diseases;
d) treatment of anemia with iron supplements.
5. What are the main principles of pyelonephritis management:

a) pregnant patients with pyelonephritis should be hospitalized upon exacerbation
of the disease;
b) pregnant patients with pyelonephritis should be hospitalized upon revealing
this disease in past history;
c) principles of management include improving urine passage, eliminating its
congestion, intensive elimination of microorganisms and their toxins;
d) the main principle of pyelonephritis management is vitamin therapy.
6. What are the indications for preterm termination of pregnancy in glomerulonephritis?

a) pelvic presentation of the fetus;
b) superimposition of severe PE;
c) ineffectiveness of administered treatment;
d) exacerbation of chronic glomerulonephritis accompanied by renal dysfunction.
7. What are the main recommendations about management of pregnant women with
DM?
a) planning for pregnancy, pregravid preparation;
b) hospitalization of pregnant women at 7–8, 21–25, 30–32, and after
36 weeks;
c) hospitalization of pregnant women at 12, 28 and 36 weeks;
d) mandatory compensation of DM before pregnancy, during pregnancy, during
labor and puerperium;
e) follow-up of the offspring of DM patients is not required.
8. What are the main principles of treating hypothyroidism in pregnant women?

a) replacement therapy which is administered over the entire pregnancy;
b) replacement therapy administered in the first trimester;
710 Obstetrics
c) the dose of hormones is decreased, which is due to the passage of maternal

thyroid hormones to the fetus;
d) the dose of hormones should be increased in the third trimester;
e) hypothyroidism management has 2 stages: 1) eliminating the deficiency of
thyroid hormones; 2) maintaining the compensated state.
9. What are the indications for pregnancy termination in TB?

a) fibrous cavernous pulmonary TB arising secondary to a progressing TB with
cavern formation;
b) active TB of the spine, pelvis, especially with abscess or fistula; TB of
coxofemoral, talocrural and knee joints;
c) advanced bilateral TB of kidney;
d) compensated TB;
e) tuberculin test conversion.

1. Pregnant patient N aged 33 was admitted with premature membrane rupture,
contractions every 10 min. First pregnancy, 39 weeks gestation, the coming child-
birth is the first. Past history: the patient was registered with the cardiologist from
childhood, had acute respiratory viral infections, chickenpox. During the present
pregnancy she had three planned hospital stays at a specialized hospital department.
The patient reports an improvement in the main illness during pregnancy. What is
your diagnosis and plan of management?
2. A pregnant woman with 26 weeks gestation was admitted to a multi-specialty
hospital presenting moderate lumbar pain of 2 days duration. Body temperature
37.4 °С, BP 130/90 mm Hg. Chronic pyelonephritis in past history. What is your
diagnosis and plan of management?
NOTES
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• Chapter 23
POSTTERM PREGNANCY
The diagnosis of postterm pregnancy may be erroneous if the gestational age was
not determined correctly. Nowadays an erroneous diagnosis is made very seldom due
to the use of sonofetometry in the first and second trimesters.
Postterm pregnancy is marked by an exponential increase of complications in the
mother, fetus and newborn as the gestational age advances.
The major cause of the rise of maternal complications is the cesarean section as it
increases the risk of postpartum infection, hypotonic hemorrhage, septic and embolic
complications. The rate of cesarean section after 42 weeks is 2 times higher than at
38–40 weeks gestation. Maternal complications also include injury due to giving a
vaginal birth to a macrosomic fetus (rupture of the cervix, vaginal walls, third-degree
perineal rupture). These complications can result in urine retention, fistula, hem-
orrhage, infection, postpartum ulcer. Postterm infants show greater morbidity and
mortality compared with term infants.
Neonatal complications encompass chronic hypoxia, birth trauma (due to mac-
rosomia), meconium aspiration.
23.1. DEFINITION
A pregnancy is described as postterm if it extends to 42 and more weeks beyond
the gestational (menstrual, obstetric) age. The birth following this pregnancy is de-
scribed as postterm.
An infant born of such pregnancy quite often (but not always!) shows signs of
postmaturity. Postterm pregnancy can end in a birth of neonate without signs of
postmaturity; on the other hand, a term birth producing a postmature infant is a
possibility, too.

The scientific approach to postterm pregnancy was first defined by 1902 when
Ballantyne, and then Runge (1948) described the signs of postmaturity in a neonate.
In 1954 Clifford described a syndrome encountered at a rate of 10% in true post-
term pregnancy.
23.3. EPIDEMIOLOGY
Postterm pregnancy is seen in 4–14% women in the population. Going by the
gestational age determined by ultrasound in the first trimester, the rate of true post-
term pregnancy (42 and more weeks) is only 1–3%.
712 Obstetrics
Postterm pregnancy shows increased perinatal mortality, especially

NB! intranatal and neonatal mortality.
Meconium aspiration syndrome is very common in situations of postterm preg-

nancy. Infants born after 41 weeks gestation show prominent CNS lesions 2–5 times
more often. In postterm pregnancies the rate of fetal macrosomia amounts to 30%,
which promotes the higher rate of labor complications.
Regarding the gestational age, all pregnant women in clinical practice can be
conditionally divided into the following groups:
• tendency for postterm pregnancy (at the gestational age 41 weeks — 41 weeks
6 days);
• true postterm pregnancy (at the gestational age 42 weeks and more).
In English language literature authors employ terms prolonged, postterm and post-
date pregnancy. There is no difference in the meaning of prolonged and postterm,
they stand for a gestational age extending beyond 42 weeks; postdate stands for a
gestational age more than 40 weeks.
23.5. ETIOLOGY
Postterm pregnancy should be regarded as a result of interaction of multiple fac-

tors, but the leading factor is neurohumoral regulation.
The causes of postterm pregnancy can be related to the fetus or placenta rather
than the primary inertia of maternal body.
Alterations in the placenta in postterm pregnancy appear to be secondary
(Fig. 23.1). However, later they affect steroidogenesis, fetal condition and onset of
labor. The developing placental insufficiency leads to disorder of fetal metabolism.
In view of the intimate connection between the fetus and placenta, a reduced fetal
vitality affects placental function. This the way a vicious circle of postterm abnor-
malities emerges.
23.6. CLINICAL FEATURES
The most important signs of postterm pregnancy are these:

• abdominal volume decreased by 5–10 cm, usually after 290 days gestation
(dehydration);
• reduced skin turgor in the mother;
• maternal weight loss of 1 kg and more;
• increased uterus density due to a reduced fluid volume and retraction of uterine
musculature;
Chapter 23. Postterm pregnancy 713
а b
c
Fig. 23.1. Microscopy of placenta in postterm pregnancy: a — degeneration of villi and
chorion, sirius red staining; b — diff use calcification, hematoxylin and eosin staining; c —
perivascular fibrin deposit, hematoxylin and eosin staining
• oligohydramnios;
• mascrosomia;
• a vaginal examination shows increased density of fetal cranial bones, narrow
sutures and fontanelles;
• release of milk instead of colostrum from mammary glands;
• unfavorable cervix.
23.7. DIAGNOSTICS
Precise diagnosis of postterm pregnancy is only possible with accurate informa-

tion about the gestational age. It is important to employ all clinical data helping to
specify the gestational age and the estimated date of delivery:
• last menstrual period date;
• date of fertilization;
• ovulation;
• first antenatal visit to the maternity welfare clinic;
• the date of quickening;
• ultrasound findings in the first and second trimesters (the most accurate method).
714 Obstetrics
The established or estimated date of conception corresponds

NB! to the obstetric gestational age of 2 weeks; that is, on the first
morning of productive coitus the gestational age is 2 weeks and
7 hours.
A bimanual examination in the first trimester does not allow an accurate estima-
tion of the gestational age (±2–3 weeks). Other possibly helpful methods are the
date of the first positive beta-hCG test, the date of the first hearing of heart tone
(at 12 weeks using a Doppler sensor, and after 18 weeks using a stethoscope), the
date of fundal height at umbilical level (20 weeks).
An effective method is determining the gestational age using

NB! ultrasound in the first trimester (measuring the gestational sac
diameter before 6 weeks, and then measuring the CRL before 14
weeks).
Routine ultrasound in the first and second trimesters of pregnancy permitted

a decrease in registered postterm pregnancy. The earlier the ultrasound is done,
the more accurate the gestational age assessment. The crown rump size of the
embryo in the first trimester yields an accurate gestational age to a precision of
±3–5 days. After 12 weeks estimating the gestational age by the crown rump
length becomes less accurate. However, at this time and to the end of the second
trimester one can estimate the gestational age by several fetometric values (bipa-
rietal and occipitofrontal diameter, transverse cerebellar diameter, femur length,
etc.). The accuracy of estimation increases considerably if one takes into account
the fetal sex. In the third trimester the error in gestational age estimation is in
the range ±3–4 weeks.
In the third trimester the objective of fetometry is not to specify

NB! the gestational age (!); rather, it is done to compare the fetal size
against the known or estimated gestational age.
23.8. MANAGEMENT OF PREGNANCY AND CHILDBIRTH
An active approach to managing pregnancy and childbirth in postterm pregnancy

has yielded a two-fold decrease in perinatal mortality. At the gestational age 40 weeks
it is recommended to perform the woman’s workup. If the fetal condition is sat-
isfactory, hospitalization is postponed till 41 weeks. During this week the Cardiff
count to ten method is used to monitor fetal motor activity. After that the woman
is admitted to a maternity hospital to decide about the mode of delivery. The mode
of delivery depends on cervical ripeness, fetal condition, concomitant diseases, past
history findings, etc.
If pregnancy is uncomplicated and there are no significant risks,

NB! hospitalization before 40.5 – 41 weeks is counterproductive,
and sometimes harmful due to nosocomial infection, obstetric
interventions, etc.
Postterm pregnancy per se is a relative indication for a surgical delivery; other

factors like cervical unripeness, fetal hypoxia, extragenital disease, obstetric compli-
cations, primipara’s age, findings of her obstetric, gynecologic, social history taken
together can require a planned cesarean section.
Postterm pregnancy poses certain threat to the fetus. The woman

NB! is hospitalized at 41 weeks gestation to monitor fetal condition.
The principles of hospital care for pregnant women with an accurately estimated
gestational age and a tendency for postterm pregnancy can follow one of two routes.
• If the cervix is ripe, labor induction is indicated. Unfortunately, this is rare in
postterm pregnancy: only 8% of women with postterm pregnancy show 7 and
more points on the Bishop score of cervical ripeness.
Two major reasons for labor induction exist in this case. The fetus continues to
grow after 40 weeks gestation and macrosomia may result. In its turn, macrosomia
increases the risk of cephalopelvic disproportion and shoulder dystocia in labor.
Despite the fact that antenatal monitoring using ultrasound, CTG, Doppler imaging
and other method permits a quite precise assessment of fetal condition, there is still
a risk of sudden intrauterine fetal demise in conditions of postterm pregnancy when
everything appears quite satisfactory (0.5–1 case per 1000 pregnancies).
When the cervix is ripe and gestational age is over 41 weeks, labor
NB! induction is the method of choice.
• If case of unfavorable cervix and an accurately estimated gestational age one

can do antenatal monitoring of the fetal condition and wait for spontaneous
labor or cervical ripeness. To accelerate cervical ripening, one administers
mifepristone (antiprogestine), mechanical methods like dilapan, laminaria
sticks, bagging of uterus, Foley’s catheter. When the cervix is ripe enough,
labor induction begins.
In postterm pregnancy the management begins with amniotomy (artificial rupture
of membranes). Amniotomy can be only performed when the cervix is ripe enough.
If spontaneous labor is not initiated within 4 hours after amniotomy, one tries
labor induction by oxytocin administration (using an infusion pump or droplet
infusion). A combined administration of amniotomy and uterotonics is referred to
as combination labor induction. If combination labor induction fails, the delivery is
ended by a cesarean birth.
In case of postterm pregnancy it is recommended to initiate
NB! programmed labor to prevent perinatal complications.
716 Obstetrics
Programmed labor is artificially induced labor for maternal, fetal or mixed indi-
cations. It can be preterm, term, or postterm. The notion of programmed labor is
widely used, although the term «induced labor» is also encountered in literature;
this also means labor induced artificially for certain indications. Internationally, pro-
grammed (elective) labor means delivery at 39–40 weeks when the fetus is mature,
the cervix ripe, at an arbitrarily chosen time that is optimal for the mother, fetus
and the institution.
Many studies show a high rate of unsuccessful labor induction in postterm preg-
nancy as it is just in conditions of postterm pregnancy that the cervix remains unfa-
vorable. Preparation of the cervix with mifepristone increases the rate of successful
labor inductions.
Mifepristone, a synthetic steroid antigestagen, is administered at a dose of 200 mg
twice. In 48–72 hours the birth canal is examined. When the cervix is ripe enough,
amniotomy is performed; in 4–6 hours oxytocin is administered if needed. Over the
entire time of antigestagen administration the fetal condition has to be monitored
by several methods (see section 4.5.3. Laboratory and Instrumental Methods of
Investigation).
Investigations are recommended in different combinations, no less than twice a
week. A vaginal examination is periodically performed to assess cervical ripeness.
When doing a vaginal examination, one can hope for Ferguson reflex: mechanical
excitation of cervix and digital stripping of membranes from the walls of lower uter-
ine segment promotes a release of a certain amount of endogenous progesterone. In
some cases this works to trigger the labor dominant.
If situation so requires and the cervix is favorable, labor induction can be started
on the next day. Immediately before starting induction uterine activity and fetal heart
rate are registered using CTG. If fetal condition is unsatisfactory, labor induction is
given up in favor of cesarean section taking into account the perinatal risk.
In postterm pregnancy labor is managed with continuous monitoring of contrac-
tions, fetal cardiac activity and cephalopelvic proportions; fetal hypoxia or labor
abnormalities should be detected early.
When reading fetal heart rate values (CTG) one should remember that shallow,
short variable decelerations are commonly noted during labor due to umbilical thin-
ning and oligohydramnios in postterm pregnancy; these signs are not indicative of
hypoxia.
Emergence of late decelerations indicates fetal hypoxia. In presence of short-term
and shallow late decelerations an expectant approach is admissible. When frequent
prolonged late decelerations are combined with reduced heart rhythm variability while
there is no prospect of a speedy delivery, emergency cesarean section is indicated.
The main complication of labor in postterm pregnancy is fetal hypoxia (meconium
aspiration). When meconium is released into the amniotic fluid, this is often followed
by meconium aspiration. Meconium is found in the amniotic fluid in 25–30% of all
postterm pregnancies, which is 4 times more often than in a term birth. Meconium
aspiration syndrome is one of the main causes of neonatal mortality. In postterm
pregnancy meconium can be released into the amniotic fluid due to a more promi-
nent vagus reflex. Fetuses with postmaturity signs more often develop hypoxia when
placental insufficiency arises. Besides, in situations of postterm pregnancy the amount
of amniotic fluid decreases which leads to «thick meconium» and thus, to a greater
probability of airway obstruction.
In certain cases meconium aspiration can even occur antenatally.
Postterm pregnancy is often accompanied by macrosomia. About 25–30% of
postterm newborns show a birth weight over 4000 g (macrosomia), which is three
times higher than the rate of large fetuses in a term birth. When a macrosomic
infant is being delivered, the duration of dilation and expulsion stages increases,
and there is a higher risk of birth trauma. Shoulder dystocia is noted twice more
often.
In postterm birth with a macrosomic infant it is important to prevent a birth
trauma. The fetal weight is estimated immediately before delivery or in the first stage
of labor, if a vaginal birth is planned. An accurate assessment of fetal weight in post-
term pregnancy is rather difficult, even when using ultrasound.
When macrosomia is suspected, the following principles of management should
be observed.
• Use of midpelvic forceps should be avoided, especially when the second stage is
protracted. It was established that in this situation midpelvic forceps increase the
risk of shoulder dystocia from 0.2 to 4.6%.
• A neonatologist and anesthesiologist should be on hand.
• An obstetrician with good expertise in shoulder dystocia management should be
present at the childbirth.
• If the estimated fetal weight exceeds 4500 g, cephalopelvic disproportion is
suspected, there is evidence of macrosomia in previous deliveries, a timely
decision about a cesarean section should be made.
After delivery, the obstetrician and neonatologist together estimate the signs of
postmaturity:
• the skin, fetal membranes and umbilical cord stained with meconium;
• macerated skin, especially on the palms and soles (Fig. 23.2);
• decreased amount of vernix caseosa and subcutaneous fat, reduced skin turgor,
looking «old»;
• large size of the fetus (hypotrophy is less common), long fingernails;
• head molding poorly pronounced, compact cranial bones, narrow sutures and
fontanelles.
A fetus is considered postmature when at least 2–3 of the signs above are noted.
According to Clifford, 3 degrees of postmaturity are distinguished:
• I degree: the newborn is dry, its skin is of normal color. Vernix caseosa is poorly
pronounced. Amniotic fluid is light, its amount is decreased. The newborn’s
general condition is satisfactory.
• II degree: very dry skin, signs of hypotrophy. The amniotic fluid, umbilical cord
and skin are of greenish coloration from meconium staining. Perinatal mortality
is high.
• III degree: amniotic fluid of yellow color. The newborn’s skin and nails are of
yellow coloration. These are signs of profound hypoxia, but such infants show
lower mortality rates.
There is a high risk of hemorrhage in the third stage of labor and early postpartum
period, so prevention of hemorrhage should be emphasized.
718 Obstetrics
Fig. 23.2. Signs of postmaturity in a newborn: skin maceration, desquamating skin, long nails
23.9. PREVENTION OF POSTTERM PREGNANCY
• Ultrasound fetometry in the first trimester and/or in early second trimester

performed by a certified diagnostician.
• Gender fetometry (when determined via ultrasound, in male fetuses the
gestational age is usually overestimated by 1–2 weeks).
• When the gestational age by ultrasound differs from the age by LMP date, one
should be guided by the fetometry findings.
• The pregnant woman should be hospitalized at 41 weeks even when the pregnancy
proceeds uneventfully.
23.10. PROGNOSIS
Prognosis depends on complications arising during labor. Postterm pregnancy per

se does not affect future health.
REMEMBER!
Definition Pregnancy is referred to as postterm if it extends to 42 and

more weeks beyond the gestational (menstrual, obstetric) age
Terminology Postterm pregnancy is a notion related to the calendar while

postmaturity describes the physiological status of the fetus
and neonate
Epidemiology According to evidence cited in literature, postterm pregnancy is

seen in 4–14% women in the population. Going by the gestation-
al age determined by ultrasound in the first trimester, the rate
of true postterm pregnancy (42 and more weeks) is only 1–3%
Complications In conditions of postterm pregnancy perinatal mortality is higher,

especially intranatal and neonatal mortality; meconium aspira-
tion syndrome is noted more often. Infants born after 41 weeks
gestation show prominent CNS lesions 2–5 times more often. In
postterm pregnancies the rate of fetal macrosomia amounts to
30%, which promotes the higher rate of delivery complications
Classification In case of a tendency for postterm pregnancy (at the gestational

age 41 weeks — 41 weeks 6 days) the delivery occurs at term.
The true postterm pregnancy occurs when the gestational age
is 42 weeks and more, and the delivery is postterm
Diagnostics Precise diagnosis of postterm pregnancy is only possible with

accurate information about the gestational age
Tactics The pregnant woman should be hospitalized at 41 weeks even

when the pregnancy proceeds uneventfully.
If the cervix is ripe, programmed labor is initiated.
If the cervix is unfavorable, the woman is hospitalized for an
active observation of the fetus and preparation for delivery.
If the cervix is unfavorable after 42 weeks, cesarean section is
performed with the woman’s informed consent
CONTROL QUESTIONS
1. What methods of determining the gestational age do you know?
2. What are the methods of diagnosing postterm pregnancy?
3. What are the most common maternal complications?
4. What are the most common fetal complications?
5. What are the principles of managing labor in patients with postterm pregnancy?
6. What is postterm delivery?
7. What are the signs of fetal postmaturity?
8. What are the principles of preventing postterm pregnancy?
CHECK YOURSELF!
Level 1. Test
1. Postterm pregnancy is
a) fetal hypoxia;
b) oligohydramnios;
c) gestational age extending beyond full 40 weeks;
d) gestational age extending over 42 weeks.
720 Obstetrics
2. The most reliable method of estimating the gestational age:

a) by menstrual period;
b) by uterine size;
c) ultrasound in the first trimester;
d) ultrasound in the second trimester.
3. What is postterm delivery?

a) delivery after 40 weeks;
b) delivery when the woman is admitted to hospital with bearing down efforts;
c) delivery complicated by fetal hypoxia;
d) delivery at 42 weeks and later.
4. In postterm pregnancy the delivery is commonly complicated by:

a) fetal hypoxia;
b) precipitated labor;
c) hypertension;
d) cephalopelvic disproportion.
5. The signs of postmaturity are:

a) fetal macrosomia;
b) maceration of skin;
c) loud cry;
d) acrocyanosis.
6. The management of postterm pregnancy first of all depends on:

a) whether the gestational sac is intact;
b) cervical ripeness;
c) ultrasound findings;
d) laboratory test findings.
7. In case of unfavorable cervix and postterm pregnancy the following is indicated:

a) amniotomy;
b) labor induction with oxytocin;
c) observation of the patient at abnormal pregnancy department;
d) preparation of the cervix for delivery.

1. The pregnant woman aged 32 is at her first antenatal visit. Gestational age from
her LMP is 38–39 weeks. The cervix is not ripe. What is your diagnosis? What is
the plan of management?
2. An ultrasound at a maternity welfare clinic detects oligohydramnios in a preg-
nant woman with 40 weeks gestation. CTG shows signs of moderate fetal distress.
What is your diagnosis? What is the plan of management?
• Chapter 24
ABNORMAL FETAL LIE AND PRESENTATION
24.1. ABNORMAL FETAL LIE
ICD-10 code
• O32.2 Maternal care for oblique or transverse lie.
Labor in abnormal fetal lie or abnormal presentation of fetal head

NB! should be regarded as pathological.
Abnormal fetal lie is seen in 0.2–0.7% of all deliveries, in secundiparas it occurs

ten times more often than in primiparas. Oblique and transverse lie are regarded
as abnormal. In abnormal lie the long axis of the fetus crosses the long axis of the
uterus at an angle.
• In a transverse lie the long axis of the fetus crosses the uterine long axis at a right
angle while large fetal parts are above the iliac crests (Fig. 24.1).
• In an oblique lie the long axis of the fetus crosses the uterine axis at an acute
angle while one of large fetal parts is in one of iliac fossas of the greater pelvis.
Oblique lie is in most cases transient (unstable): during labor it changes to
transverse or longitudinal lie (Fig. 24.2).
Fetal position in transverse or oblique lie is determined by the fetal head: if it is on
the left, the fetus is in the first position, if it is on the right, it is the second position.
Fig. 24.1. Transverse fetal lie. First anterior position

722 Obstetrics
Fig. 24.2. Oblique fetal lie. First anterior position
If the fetal back faces forward, this is an anterior position, if it faces backward, this
is a posterior position (Latin, visus).
24.1.1. Etiology
Causes of abnormal fetal lie:
• decreased uterine tone;
• incompetence of abdominal muscles;
• discrepancy of the uterine cavity shape (like in uterine myoma) and fetal size
(Fig. 24.3);
Fig. 24.3. Pregnancy and bicornuate uterus (left), uterine myoma (right)
Chapter 24. ABNORMAL FETAL LIE AND PRESENTATION 723
• polyhydramnios;
• premature fetus;
• developmental disorder and uterine tumor;
• contracted pelvis;
• fetal malformations (hydrocephalus, anencephaly);
• absolutely or relatively short umbilical cord.
24.1.2. Diagnostics
Transverse or oblique lie can be detected by external examination (Leopold ma-
neuvers of external obstetric examination).
• When the fetus is in transverse lie, the uterus is of transverse-oval shape, the
fundus is considerably lower than in longitudinal lie, there is no large presenting
part (head or pelvic pole). In English language textbooks the presenting part —
face or arm — is distinguished in a transverse lie.
• When the fetus is in oblique lie, the uterus is of oblque-oval shape. The head or
buttocks are below the level of iliac crest. One of large fetal parts is in one of iliac
fossas of the greater pelvis. The abdominal circumference measures more than
normal for date while the fundal height is less than normal.
The diagnosis is specified by a vaginal examination: the presenting part cannot be
determined. Ultrasound is the most informative method for diagnosis of abnormal
fetal lie.
In an abnormal fetal lie fetal heartbeat is heard mostly in the area of the
navel.
Diagnosis of transverse and oblique lie is not usually difficult but its cause is not
always established.
24.1.3. Course and management of pregnancy and

childbirth
In early pregnancy and in its second half until 32 weeks the fetal position is
unstable. At a gestational age beyond 32 weeks the obstetrician carefully observes
a woman with transverse or unstable fetal lie. During the period 32–36 weeks ex-
ercises are recommended to improve an abnormal fetal lie. Exercises are indicated
in oblique fetal lie if the head is at the top. The correction exercises (developed by
I.I. Grischenko and A.E. Shuleshova) are done when there are no contraindications
like uterine scar, myoma, threatened premature birth, placenta previa, placental
abruption in the present pregnancy, abnormalities of fetal growth. The exercises are
done under the guidance of an instructor at the maternal welfare clinic; they provide
for rhythmical contraction of abdominal muscles and corresponding trunk muscles
in combination with correct rhythmical profound respiration.
For prevention of complications the woman is admitted to a maternity hospital
7–10 days before delivery to decide on the mode of delivery.
724 Obstetrics
Transverse or oblique fetal lie is an absolute indication for planned

NB! cesarean section.
24.1.4. Pregnancy and childbirth complications

Absence of an inner belt of adherence increases the rate of complications dur-
ing pregnancy: premature membrane rupture, preterm birth (25–30%), prolapse of
small fetal parts. A long period between membrane rupture and onset of labor and
umbilical cord prolapse can lead to uterine cavity infection (chorioamnionitis) and
fetal hypoxia.
After the onset of labor the first possible complication is premature membrane
rupture which can be followed by fetal arm of umbilical cord prolapse. Attempts to
push them back are ineffective and, which is worse, increase the risk of fetal injury
and chorioamnionitis.
If labor proceeds and cesarean section is performed untimely, persistent transverse
lie emerges: the uterus grips the fetus tightly limiting its motility, fetal shoulder drives
into the pelvic inlet, the prolapsed arm swells and becomes cyanotic, hypoxia devel-
ops followed by fetal demise (Fig. 24.4). Expulsion of a term fetus in a transverse or
oblique lie is not possible, absence of progress along the birth canal promotes uterine
overdistension to the extent of its rupture.
Other operative interventions and maneuvers like external / internal podalic ver-
sion of a vital fetus followed by total extraction is not applied nowadays due to birth
trauma of the fetus and a risk of uterine rupture.
Fig. 24.4. Impacted transverse fetal lie. Arm prolapse. Overdistension of lower uterine segment
In transverse lie delivery can end spontaneously only in case of very premature
fetus or so-called partus соnduplicato corpore (delivery of a doubled up body). The
prognosis of vitality of such a fetus is doubtful.
Absence of fetal mobility (in case of its transverse lie), arm

NB! prolapse and shoulders impacted at the pelvic inlet are referred
to as impacted transverse fetal lie (see Fig. 24.4).
In case of a transverse lie, one should administer anesthesia
immediately so as to arrest labor, and perform cesarean section.
Without urgent care there develop signs of threatened or
progressing uterine rupture, fetal hypoxia and demise.
24.2. MALPRESENTATION OF HEAD
ICD-10 code
• O32.3 Maternal care for face, brow and chin presentation.
Extended presentation is presentation of an extended fetal head at the pelvic inlet
(pathological attitude).
24.2.1. Etiology
Common causes of head malpresentation:
• polyhydramnios;
• premature membrane rupture;
• maternal spine deformity;
• incompetence of anterior abdominal wall (flabby, sagging abdomen) and pelvic
floor muscles;
• submucous uterine myoma;
• tumor in the area of fetal neck;
• too large or too small fetal head;
• loss of fetal resilience (fetal demise), etc.
Fetal head extension (irrespective of its degree) is mostly seen in secundiparous
women. Three degrees of head extension are distinguished.
• Degree 1 of extension: military (mild) extension. The point of direction is
the area of anterior fontanelle, the head is delivered by the occipitofrontal
diameter.
• Degree 2 of extension: brow (moderate) presentation. The point of direction is
the area of brow, fetal head is pressed to the pelvic inlet with its occipitomental
diameter.
• Degree 3 of extension: face (prominent) presentation. The point of direction is
the chin area. Fetal head is pressed to the pelvic inlet with its vertical diameter
(Fig. 24.5).
726 Obstetrics
а b c
Fig. 24.5. Three degrees of head extension: a — military position; b — brow presentation;
c — face presentation
24.2.2. Sinciput presentation (military position)

In sinciput presentation the fetal head is stationed above the pelvic inlet with its
occipitofrontal diameter. Sinciput presentation accounts for 44.7% in the structure
of extension malpresentations.
The diagnosis is made upon a vaginal examination detecting the

NB! anterior and posterior fontanelles stationed at one level, or the
anterior fontanelle stationed above the posterior one.
The diagnosis is confirmed after childbirth by the fetal head shape and the location
of caput succedaneum over the first hours and days of the infant’s life. In sinciput
presentation the head is brachicephalic (tower head), caput succedaneum located in
the area of the anterior fontanelle (Fig. 24.6).
Mechanism of labor in sinciput presentation

• Step 1: moderate extension of the head. The head is stationed in the transverse
pelvic diameter with its sagittal suture and a part of frontal suture; very seldom
it is stationed in the one of oblique pelvic diameters (Fig. 24.7). The head is
engaged with its occipitofrontal diameter measured from the nasal bridge to
the occipital protuberance; it is 12 cm. The head circumference (circumferentia
frontooccipitalis) is 34 cm. As the head moves along, the anterior fontanelle
becomes the point of direction.
Fig. 24.6. Molding of the head in sinciput engagement. FO — diameter frontooccipitalis
Fig. 24.7. Mechanism of labor in sinciput presentation. Step 1
• To overcome the reduced spatial relation between fetal head and maternal pelvis,
asynclitical engagement is often encountered.
• Step 2 in the mechanism of labor: internal incorrect rotation of the head.
The sagittal suture passes from the transverse diameter of pelvic inlet to the
anteroposterior outlet diameter with the occiput turning backwards to the
sacrum. The head performs a rotation when passing from the broad to narrow
part of the lesser pelvis cavity (Fig. 24.8).
• Step 3 in the mechanism of labor: flexion of the head. Flexion of the head occurs
in the cervical part of the spine. The fi xation point is the glabella, and the point of
728 Obstetrics
Fig. 24.8. Mechanism of labor in sinciput presentation. Step 2
bearing — lower edge of symphysis pubis. This is the way the vertex and occiput
of the fetus are delivered (Fig. 24.8).
• Step 4 in the mechanism of labor: extension of the head. The point of fixation is
the occipital protuberance, the point of bearing — anterior sacral surface. This is
the way the fetal face is delivered (Fig. 24.9).
• Step 5 in the mechanism of labor: internal rotation of the shoulders and external
rotation of the head occur in the same way as in occipital presentation.
Sinciput presentation entails prolonged labor, especially during

NB! the expulsion stage so complications are quite common: uterine
inertia, cephalopelvic disproportion and even threatened uterine
rupture, birth trauma and fetal demise.
The doctor watches the passage of the head along the birth canal and estimates
the signs of cephalopelvic disproportion, threatened uterine rupture, fetal hypoxia. If
these complications develop, emergency abdominal delivery is indicated.
24.2.3. Brow presentation

In brow presentation the fetal head hovers above the pelvic inlet with its occipi-
tomental diameter. Brow presentation is encountered much less often than sinciput
Fig. 24.9. Mechanism of labor in sinciput presentation. Steps 3 (a) and 4 (b)
presentation: 5% in the structure of all extension presentations, or 0.03% in the total

structure of deliveries (1:3000 deliveries). The head engages with its occipitomental
diameter (measured from the chin to the furthermost point on the occiput; 13.5 cm).
The head circumference (circumferentia mentooccipitalis) is 42 cm.
Brow presentation is diagnosed upon a vaginal examination: the

NB! brow and frontal suture are detected at the pelvic axis adjoined by
the nose bridge and eyebrow ridge on one side, and the anterior
angle of anterior fontanelle on the other side.
Caput succedaneum is located in the brow area extending from the bridge of the
nose to the anterior fontanelle (Fig. 24.10).
730 Obstetrics
Fig. 24.10. Molding of the head in brow presentation. MO — diameter mentooccipitalis
In brow presentation the fetal head presents at the pelvic inlet with its greatest
diameter (occipitomental diameter), so in brow presentation delivery via the natural
birth passages is impossible.
NB! Brow presentation is an absolute indication for cesarean section.
Even when the fetus is not large and pelvic size is normal, delivery is accompanied
by grave complications: maternal injury, severe fetal trauma, neonatal mortality and
morbidity.
24.2.4. Face presentation

Face presentation is encountered more often than brow presentation: 39.7% in the
structure of all extension presentations. Face presentation is difficult to diagnose by
external examinations: in the third Leopold’s maneuver the thrown-back occiput is
palpated as a hard tuber (tumor) divided from the back by a deep notch. Fetal heart-
beat is best heard from the side of the chest rather than from the side of fetal back.
Vaginal examination is most informative; it helps to feel the chin, nose, supercili-
ary ridges, and the frontal suture. When the face has a considerable edema, there
is a risk of an erroneous diagnosis of breech presentation. Specific information is
obtained using ultrasound.
Diagnosis of face presentation: a vaginal examination detects the

NB! nose, mouth and chin which is the point of direction.
The head crowns with its vertical diameter (diameter sublinguobregmaticus or

tracheobregmaticus, verticalis) measured from the hyoid bone to the middle of the
anterior fontanelle, 9.5 cm. Head circumference (circumferentia sublinguobregmatica,

tracheobregmatica) is 32 cm.
Face presentation of the fetus in mentoanterior position poses an insurmountable
obstacle to its delivery, as a united whole is formed consisting of the extended head
and shoulder girdle of the fetus (Fig. 24.11).
In case of face presentation delivery is only possible in mentoposterior position
when the fetal back faces the posterior uterine wall.
Mechanism of labor in face presentation

• Step 1 in the mechanism of labor in face presentation is the maximum extension
of the head. Extension occurs in the cervical part of the spine making the face the
presenting part (Fig. 24.12). A fully extended head passes through the birth canal
with a circumference that corresponds to the vertical diameter 9.5 cm.
Fig. 24.11. Mentoanterior position
a b
Fig. 24.12. Mechanism of labor in face presentation. Step 1, ending (a), step 2, beginning (b)
732 Obstetrics
• Step 2 in the mechanism of labor: internal rotation of the head with occiput
posteriorly. The facial line gradually passes from transverse to oblique diameter,
and when the head reaches the outlet, it comes to the anteroposterior outlet
diameter. The hyoid bone rests against the lower edge of the symphysis pubis.
• Step 3 in the mechanism of labor: flexion of the head. The chin has delivered
and is followed by the mouth, nose, brow, vertex and occiput emerging over the
perineum successively (Fig. 24.13).
• Step 4 in the mechanism of labor: internal rotation of the shoulders and external
rotation of the head. In mentoposterior position delivery via natural birth passages
is possible. After delivery the head shows a pronounced dolichocephalic shape,
the face is prominently edematous, deformed (Fig. 24.14–24.15). However, in
mentoposterior position, term pregnancy and normal pelvic dimensions the
delivery is accompanied by greater perinatal morbidity and mortality. Thus
delivery via a cesarean section is reasonable in the interest of the fetus.
At mentoanterior position a vaginal delivery is not possible as
NB! the head and shoulders enter the pelvic inlet simultaneously
(impacted shoulder). Emergency cesarean section is necessary.
Mechanism of labor in case of extension presentation is shown in Table 24.1.
Fig. 24.13. Above: A — superciliary ridges in left oblique diameter; B — further extension of
the head makes the mouth palpable; C — superciliary ridges in the transverse diameter. Below:
mechanism of labor in face presentation, step 3 (a — emerging point of fi xation in the area of
hyoid bone; point of bearing is the lower edge of symphysis pubis; b — flexion of the head)
Table 24.1. Mechanism of labor in case of extended presentations
Criteria Presentation
sinciput brow face
Step 1 First degree of extension Second degree of exten- Third degree of exten-
sion sion
Step 2 Internal rotation of the Internal rotation of the Internal rotation of
head when passing from head when passing from the head resulting in
broad to narrow part of broad to narrow part of posterior position (chin
the pelvis resulting in the pelvis resulting in anteriorly)
posterior position posterior position
Step 3 Flexion of the head Flexion of the head Flexion of the head
Step 4 Extension of the head Extension of the head Internal rotation of the
shoulders and external
rotation of the head
Step 5 Internal rotation of the Internal rotation of the
shoulders and external shoulders and external
rotation of the head rotation of the head
Point of Anterior fontanelle Brow Chin
direction
Point of Bridge of the nose at Maxilla at the symphy- Hyoid bone at the sym-
bearing the symphysis pubis; sis pubis; occipital pro- physis pubis
occipital protuberance tuberance at the coccyx
at the coccyx apex apex
Diameter Occipitofrontal, 12 cm Occipitomental, Vertical, 9.5 cm
by which 13.5 cm
the head is
delivered
Caput suc- At anterior fontanelle At the brow At the chin
cedaneum
Head Tower Triangular Substandard
shape
Fig. 24.14. Molding of the head in face presentation: SLB — diameter sublinguobregmaticus;
SLO — diameter sublinguooccipitalis
734 Obstetrics
Fig. 24.15. Face presentation accompanied by face edema (caput succedaneum), sometimes
by hemorrhage
24.3. ASYNCLITIC CEPHALIC PRESENTATION
ICD-10 code
• O32.8 Maternal care for other malpresentation of fetus.
24.3.1. Definition
Asynclitism is the position of the fetal head at the pelvic cavity or inlet when the
sagittal suture deviates anteriorly or posteriorly (to the pubis or sacrum) from the
median position. At the beginning of a normal labor the head is stationed above
the pelvic inlet or engages the inlet so that the sagittal suture aligned with the pelvis
axis is situated at an equal distance from the symphysis pubis and the promontory
(synclitic engagement). This axial or synclitic engagement is favorable for its passage
along the birth canal.
Abnormal asynclitism occurs in 0.1–0.3% of all deliveries.
24.3.2. Etiology
Causes of off-axis engagement of the head include relaxed muscles of the anterior
abdominal wall so that it cannot counteract the anterior deflection of the fundus,
dimensions of the fetal head and maternal pelvis (the pelvis can be contracted or
flattened; the angle of its inclination is also a factor).
24.3.3. Asynclitism variants

The following variants are distinguished:
• anterior, or Naegele asynclitism (when the sagittal suture approaches the
promontory, Fig. 24.16);
• posterior asynclitism (Litzmann’s obliquity, when the sagittal suture approaches

the pubis, Fig. 24.17).
In case of extension presentation, fetal macrosomia, anatomical peculiarities of the
pelvis the head engages the inlet so that one of parietal bones is lower than the other,
and the sagittal suture deflects to the pubis (Litzmann’s posterior asynclitism) or to
the promontory (anterior Naegele’s asynclitism). Poorly or moderately pronounced
asynclitism favors the passage of the birth canal that is not wide enough for it.
Sometimes asynclitism is so prominent that it prevents further passage of the head
along the birth canal. The degree of asynclitism is determined in a vaginal examina-
tion by the location of the sagittal suture and its attainability.
Pronounced degrees of off-axis engagement of the head result in the situation of
cephalopelvic disproportion.
Anterior asynclitism is more favorable for birth outcomes in contrast to posterior
asynclitism. However, the decisive role in the birth outcome is certainly played by
the lateral flexion of the head, that is, the prominence of asynclitic engagement.
In pronounced degrees of asynclitism (sagittal suture is hardly detected or cannot
be detected) delivery proceeds in the same way as in case of contracted pelvis; and
the greater the degree of asynclitism, the more difficult the delivery. In case of in-
significant asynclitism in the wide part of pelvic cavity the head assumes a synclitic
station again; as a rule, this occurs due to flexion. In case of pronounced asynclitism
the delivery is accompanied by the same complications as in case of cephalopelvic
disproportion.
Pathological asynclitism should be regarded as a sign of

NB! cephalopelvic disproportion and thus – as an indication for
cesarean section, without waiting for other signs of CPD to
develop.
Fig. 24.16. Abnormal anterior asynclitism, Fig. 24.17. Abnormal posterior asynclitism,
flat rachitic pelvis (Naegele’s asynclitism) flat rachitic pelvis (Litzmann’s asynclitism)
736 Obstetrics
When diagnosis is made belatedly and the time for surgery has been missed, the
possibl scenario includes threatened uterine rupture and fetal hypoxia.
24.4. PERSISTENT OCCIPUT POSITION
ICD-10 code
• O32.4 Maternal care for high head at term.
Persistent occiput position includes a high (at the inlet) and low (at the outlet)
respectively direct or transverse station of the sagittal suture (Fig. 24.18). In either
case grave complications are possible.
а b
Fig. 24.18. High direct station of sagittal suture: a — anterior view; b — posterior view
24.4.1. Persistent occiput direct position

In case of persistent occiput direct position the fetal head is stationed with its
sagittal suture in the anteroposterior inlet diameter. Later, after the rupture of mem-
branes, it can become persistent occiput direct engagement. Occiput direct position
usually leads to grave complications of labor as the head fixed with its occipitofrontal
diameter (12 cm) in the anteroposterior inlet diameter (11 cm) encounters a formi-
dable obstacle on the part of the symphysis pubis and promontory. This obstetric
situation differs from normal presentation when the head engages the least — an-
teroposterior — inlet diameter with its least — bitemporal — dimension, while its
greatest diameter (suboccipitobregmatic or suboccipitofrontal in occipitoanterior or

occipitoposterior position, correspondingly) engages the greatest outlet dimensions:
oblique or transverse. Depending on whether the posterior fontanelle faces anteriorly
to the pubis, or posteriorly to the promontory, persistent occiput direct position can
be anterior or posterior.
Etiology of high head is varied. Causes encompass a discrepancy between the head
and pelvis (contrcated or wide pelvis), fetal prematurity (small head), fetal head
malformation (wide flat skull), pelvis abnormality (round shape at the inlet while it
is contracted transversely), occasional (transient) occiput direct position at the mo-
ment of membrane rupture.
High fetal head is typical of labor in women with transversely contracted pelvis
when the transverse inlet diameter is the same or less than the anteroposterior di-
ameter. If the fetus is not large, a vaginal birth is possible.
Persistent occiput direct position diagnosed during labor is in

NB! most cases an indication for cesarean section.
24.4.2. Persistent occiput transverse position

Persistent occiput transverse position occurs when the head with its sagittal suture
is stationed in the transverse diameter of the narrow part of cavity or pelvic outlet
(Fig. 24.19). Passage along the birth canal becomes impossible; one observes pro-
longed (over 2h) head station in the same pelvic plane despite satisfactory uterine
contractions.
Etiology. The head cannot perform the internal rotation due to contracted pelvis
(flat pelvis, especially simple flat pelvis), small fetal head dimensions, reduced tone
of pelvic floor muscles.
Even with active labor the delivery cannot resolve spontaneously despite it being
a term pregnancy and the fetus being of normal or large size. Expectant approach
(until maternal or fetal complications develop) is admissible only with a low weight
or premature fetus.
Fig. 24.19. Persistent occiput transverse position

738 Obstetrics
The prognosis for fetal health is doubtful. Diagnosed persistent occiput transverse
position is an indication for an operative delivery (cesarean section); however, in
this case extraction of the fetus from the cavity of pelvic outlet is very difficult, it is
always accompanied by severe fetal birth trauma and a high risk of maternal injury.
Attempts to verify the diagnosis of malposition of the occiput and malpresentation
using external maneuvers and vaginal examination (prominent caput succedaneum
on the presenting part, difficult palpation of reference points on the head) can fail.
Any auxiliary method is admissible in this case: ultrasound, radiocephalopelvimetry,
MRI (the benefit outweighs maternal and fetal risks!).
REMEMBER!
Definition Fetal malposition and malpresentation include trans-
verse and oblique fetal lie, presentation of extended
head, asynclitic engagement, persistent occiput trans-
verse position and persistent occiput direct position
Epidemiology Fetal malposition 0.5–0.7%, presentation of extended

head 0.5–1.0%
Etiology Causes of fetal malpositions and malpresentations:

• uterine malformations; uterine myoma; decreased tone
and uncoordinated contraction of uterus
• oligohydramnios, polyhydramnios;
• multiple gestation;
• maternal scoliosis;
• weak musculature in the anterior abdominal wall (flabby,
pendulous abdomen) and pelvic floor;
• tumor in fetal neck area;
• too large and too small fetal head;
• loss of tone in the fetus (fetal demise) etc.
Diagnostics Diagnosis is made by an external obstetric examination,

vaginal examination and ultrasound
No chance of spon- Transverse and oblique fetal lie, brow presentation, men-
taneous delivery toanterior position, prominent asynclitism, persistent
occiput transverse or direct position
Algorithm of actions Emergency cesarean delivery. Embryotomy in case of

fetal demise
Complications Maternal complications: premature rupture of mem-

branes, uterine inertia, impacted transverse fetal lie,
functionally contracted pelvis, threatened uterine rup-
ture, infection, trauma of soft tissues in birth canal.
Fetal complications: hypoxia, asphyxia, intracranial
trauma, demise
CONTROL QUESTIONS
1. What causes presentation of extended fetal head?

2. In what situation is presentation of extended fetal head an absolute indication
for cesarean section?
3. What maternal complications arise in case of presentation of extended fetal head?
4. What are the complications in an infant delivered with presentation of
extended head?
5. Causes of asynclitic engagement.
6. What types of asynclitic engagement do you know?
7. Mode of delivery in persistent occiput direct position.
8. Name the causes of fetal malposition.
9. Methods of diagnosing fetal malpositions.
10. What are the complications of pregnancy and delivery in case of fetal
malposition?
CHECK YOURSELF!
Level 1. Test
1. Extension presentation is presentation of:
a) occiput;
b) sinciput;
c) face;
d) brow;
e) pelvis.
2. Step 1 in mechanism of labor with extended head:

a) flexion of head;
b) extension of head;
c) internal head rotation;
d) external head rotation;
e) progress of the head.
3. Absolute indication for cesarean section in case of presentation of extended head:

a) sinciput presentation;
b) nasoanterior position of the brow;
c) mentoanterior position;
d) nasoposterior position of the brow;
e) mentoposterior position.
4. Anterior asynclitism is an obstetric situation where:

a) anterior parietal bone is deeper than the posterior parietal bone, the sagittal
suture is closer to the symphysis pubis;
b) posterior parietal bone is below the anterior parietal bone, the sagittal suture
is closer to the promontory;
740 Obstetrics
c) anterior parietal bone is below the posterior parietal bone, the sagittal suture
is closer to the promontory;
d) the sagittal suture is in the anteroposterior outlet diameter;
e) the sagittal suture is in the transverse outlet diameter.
5. Malpresentation of the head includes:

a) sinciput presentation;
b) brow presentation;
c) face presentation;
d) persisitent occiput direct position;
e) persistent occiput transverse position.
6. The point of fixation during step 3 of labor mechanism with sinciput presentation:
a) glabella;
b) acromion of the anterior arm;
c) anterior trochanter;
d) hairline;
e) suboccipital fossa.
7. The point of fixation during step 3 of labor mechanism with face presentation:
a) suboccipital fossa;
b) anterior trochanter;
c) acromion of the anterior arm;
d) hyoid bone;
e) glabella.
8. Management of impacted transverse fetal lie:

a) cesarean section;
b) embryotomy;
c) application of obstetric forceps to the fetal head;
d) continue the vaginal delivery;
e) vacuum extraction of fetus.
9. Step 3 of labor mechanism with face presentation:

a) fetal head flexion;
b) fetal head extension;
c) internal rotation of shoulders, external rotation of the head;
d) internal incorrect rotation of the head;
e) internal correct rotation of the head.
10. Management of face presentation:

a) vaginal birth;
b) cesarean section;
c) obstetric forceps on fetal head;
d) vacuum extraction of fetus;
e) Tsovyanov maneuver.

1. The patient is a secundipara aged 33, gestation 38 weeks; she was admitted to
maternity hospital after 3 hours of satisfactory labor. Pelvic dimensions are normal,
the fetal head is in the pelvic inlet with its small segment. Estimated fetal weight
is 3500 g, heartbeat is clear, rhythmical 140 per min. Vaginal examination: cervical
dilation 4 cm, amniotic sac absent, sagittal suture in the transverse diameter, anterior
fontanelle on the right, posterior fontanelle on the left, below the anterior fontanelle.
Promontory cannot be reached, no exostoses. What is your diagnosis? What is your
plan of management?
2. The patient is a secundipara aged 25 brought to hospital by an ambulance with
diagnosis of 38 weeks gestation, cephalic presentation, premature rupture of mem-
branes, first stage of labor. Membranes ruptured an hour ago. Fetal heartbeat 140 per
min. clear, rhythmical. Vaginal examination: complete cervical dilation, amniotic sac
absent, cephalic presentation, the head pressed to the pelvic inlet, frontal suture in
the transverse pelvic diameter; anterior angle of anterior fontanelle, orbits and root
of nose are palpable. Promontory cannot be reached, no exostoses. What is your
diagnosis? What is your plan of management?
3. A grand multiparous patient presents with powerful, painful contractions with-
out relaxation in between. Gestation 40 weeks, labor ongoing for 6 h. Examination:
anterior abdominal wall overdistended, pendulous abdomen, fetal head pressed to
the pelvic inlet. After a contraction fetal heartbeat increases to 180 per min and
restores poorly. Estimated fetal weight 4500 g. Vaginal examination: complete cervi-
cal dilation, amniotic sac absent, cephalic presentation, sagittal suture in transverse
diameter close to the pubis, a contraction causes a pronounced molding, posterior
parietal bone overlaps the anterior one. Promontory cannot be reached. What is your
diagnosis? What is your plan of management?
4. Primiparous patient aged 35 presents with cramp-like pain persisting over
14 h. Gestation 38 weeks. Pelvic dimensions are normal. While in the admission
department, the membranes ruptured, light amniotic fluid escaped in the amount of
1.5 l. Vaginal examination: complete cervical dilation, amniotic sac absent, cephalic
presentation, sagittal suture in the anteroposterior inlet diameter, anterior fontanelle
in front, posterior fontanelle behind. Promontory cannot be reached. No exostoses.
NOTES
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• Chapter 25
CONTRACTED PELVIS
ICD-10 code
• O33 Maternal care for known or suspected disproportion.
– O33.0 Maternal care for disproportion due to deformity of maternal pelvic
bones.
– O33.1 Maternal care for disproportion due to generally contracted pelvis.
– O33.2 Maternal care for disproportion due to inlet contraction of pelvis.
– O33.3 Maternal care for disproportion due to outlet contraction of pelvis.
– O33.4 Maternal care for disproportion of mixed maternal and fetal origin.
• O65 Obstructed labor due to maternal pelvic abnormality.
Up till now, management of labor in presence of pelvic abnormalities presents the
greatest difficulty in obstetrics. Contracted pelvis is one of the causes of perinatal
morbidity and mortality, maternal injury.
Fetal malposition and face presentation are seen in puerperas with

NB! anatomically contracted pelvis three times more often, and cord
prolapse – four to six times more often than in puerperas with
normal pelvic dimensions.
The number of women with prominently contracted pelvis is on the decline;

however, the average birth weight and the rate of fetal macrosomia are on the rise.
Contracted pelvis is not always an obstacle in labor. Labor complications are often
related to a disproportionally large fetal head when the pelvis becomes functionally
contracted.
That is why we distinguish:
• (anatomically) contracted pelvis;
• functionally contracted pelvis (cephalopelvic disproportion).
Contracted pelvis is seen in 1–7% of pregnant women; it occurs in 3% of all labors;
its incidence rate shows no tendency for declining. Cephalopelvic disproportion is
diagnosed at a rate of 1.3–1.7%.
Chapter 25. Contracted pelvis 743
25.1.2. Definition
The pelvis is considered anatomically contracted if one or all

NB! external dimensions differ from normal values by 2 cm and more
while internal pelvic dimensions are 0.1 – 0.5 cm less than normal.
Abroad, the inlet plane is considered contracted if the conjugate diameter is un-
der 10 cm (the diagonal conjugate under 11.5 cm) and/or the transverse diameter
of the inlet plane is under 12 cm. The true pelvis cavity is considered contracted
if the total of interspinous (transverse diameter of the narrow pelvic portion) and
anteroposterior diameter traced from its middle to the junction of IV and V sacral
vertebrae is under 13.5 cm (15.5 cm normally). The outlet plane is assessed by the
transverse diameter; it is considered contracted if the diameter is equal or less than
8 cm. A contracted pelvic outlet not related to narrowing of any other pelvic planes
is noted extremely seldom.
Fractures and rare pelvic contractures are classified as a separate class. They are
mostly caused by traffic accidents.
Contracted pelvis may interfere with physiological labor. Irregular

NB! pelvic shape, its lesser dimensions may pose an insurmountable
obstacle on the way of fetal passage.
When taking external measurements the criterion for pelvic contraction is a

change in dimensions of 2 cm as this is the range admitting a technical error. When
measuring the diagonal conjugate and using additional means of diagnosing pelvic
abnormalities (ultrasound, X-ray pelvimetry, CT) one assumes 0.5 cm as the value
determining contraction of pelvis in external measurements.
Functionally, or clinically contracted pelvis (cephalopelvic

NB! disproportion) is the case when anatomical dimensions of
particular pelvis preclude the passage of particular fetus.
25.1.3. Historical aspect

Anatomical structure of female pelvis was studied from the 18th century. Many
labor abnormalities can occur due to bony pelvis abnormalities: umbilical cord
prolapse, labor abnormalities, cervical dystocia, premature rupture of membranes.
The first complete teaching about contracted pelvis was developed by a Dutch
physician H. Deventer (1651–1724). J.-L. Baudelocque (1747–1810) extended con-
temporary knowledge of anatomical varieties of pelvic structure. Baudelocque was
the first to use external pelvimetry the way it is used nowadays; he suggested dif-
ferentiating between the greater (false) and lesser (true) pelvis. French obstetrician
Levret gave a quite accurate description of rachitic pelvis in 1747. English obstetrician
W. Smellie suggested measuring the diagonal conjugate by which he worked out the
true conjugate. German obstetricians developed the teaching about the contracted
pelvis and the mechanism of labor. In 1839 F. Naegele described obliquely contracted
744 Obstetrics
pelvis and pointed out one variety of incorrect asynclitic engagement. In 1842 H.
Roberts singled out and defined transversely contracted pelvis.
A considerable contribution to the study of female pelvis was made by an out-
standing Russian obstetrician A. Krassovsky. In his monograph Operative Obstetrics
Including a Study of Female Pelvis Abnormalities he systematized the evidence about
contracted pelvis and proposed a system of classification. A remarkable Russian ob-
stetrician H.Genter who studied bony pelvis abnormalities noted, «It is not so easy
as it might seem, to give an accurate definition of contracted pelvis». A monograph
on contracted pelvis and cephalopelvic disproportion by R. Kalganova is still valuable
although it was published in 1950-s.
25.2. ANATOMICALLY CONTRCATED PELVIS
Anatomically contracted pelvis is classified regarding the shape and degree of
contraction.
The shapes of contraction can be common or uncommon.
Commonly occurring shapes of contracted pelvis:
• transversely contracted pelvis;
• pelvis contracted in its anteroposterior diameters:
– simple flat pelvis (all anteroposterior diameters are diminished):
– flat rachitic pelvis;
– pelvis with reduced anteroposterior dimension of the wide part;
– generally contracted pelvis, etc.
Rarely occurring shapes of contracted pelvis:
• obliquely dislocated pelvis;
• funnel shaped pelvis;
• osteomalatic pelvis;
• kyphotic pelvis;
• spondylolisthetic pelvis.
X-ray pelvimetry permits revealing pelvis shapes that escaped notice before, like
assimilated or long pelvis, a result of a congenital abnormality (partial or complete
sacralization).
Maternity hospitals, as a rule, do not do a good job of detecting contracted pelvis,
especially the varieties that are difficult to diagnose like transversely contracted pelvis
and pelvis with diminished capacity.
Regarding the degree of contraction all pelvises are classified by the shortening of
the true conjugate , except for transversely contracted pelvis.
The true or obstetric conjugate is measured
• by the external conjugate: depending on the size of wrist circumference (less
than 14 cm, 14 cm or more than 14 cm), 8 or 9 or 10 cm, correspondingly, are
detracted from the external conjugate thus arriving at the size of true conjugate;
• by the diagonal conjugate: having measured the diagonal conjugate one detracts
Soloviov’s index (1/10 of wrist circumference) from its size;
• by the vertical size of the Michaelis’ rhomboid;

• by the Frank size: the distance between the spinous process of VII cervical
vertebra and the jugular notch measured by a pelvimeter.
Regarding the degree of contraction the pelvis (except for transversely contracted
variety) is classified by the shortening of true conjugate.
Classification by Krassovsky describes three degrees of contraction:
• degree 1: the true conjugate measures 11–9 cm;
• degree 2: the true conjugate measures 9–7 cm;
• degree 3: the true conjugate lesser than 7 cm.
A decrease of the true conjugate to 7 cm and more indicates an absolutely con-
tracted pelvis. In this case a vaginal birth is impossible even upon decreasing fetal
size by embryotomy. Thus, distinguishing degree 4 of contraction makes no sense.
Regarding the degree of contraction the transversely contracted pelvis is classified
by the shortening of transverse inlet diameter (R. Kalganova). 3 degrees of contrac-
tion in this type of pelvis are distinguished:
• degree 1: transverse inlet diameter 12.5–11.5 cm;
• degree 2: transverse inlet diameter 11.5–10.5 cm;
• degree 3: transverse inlet diameter less than 10.5 cm.
Nowadays, degree 1 of contraction predominates: the so-called

NB! inapparent case which is difficult to diagnose by an obstetric
examination.
Grossly deformed pelvis with degree of contraction 3–4 is hardly ever encountered.
а c
Fig. 25.1. Basic pelvis shape by Caldwell-Moloy (1935). Lesser pelvis types: a — gynecoid;
b — android; c — anthropoid; d — platypelloid
746 Obstetrics
In English-language literature the pelvis is classified by Caldwell-Moloy (1935)

system. Classification is based on radiology findings; it describes 4 basic types of
female pelvis:
• gynecoid (generally characteristic of a woman);
• android (generally characteristic of a man);
• platypelloid (flat);
• anthropoid (apelike).
Conventionally pelvis is divided by a plane passing through the anteroposterior
inlet diameter and through the posterior edge of ischial spines, into two segments:
anterior (A) and posterior (P). Their combinations yield 14 additional pelvis types.
Regarding the size, the Caldwell-Moloy system classifies the pelvis into medium and
small (small corresponds to contracted pelvis).
25.2.2. Etiology
The causes of contracted pelvis formation are multiple.
Formation of the bony pelvis starts during intrauterine development stage; how-
ever, puberty plays a special role in the girl’s life. In childhood the bony pelvis
structure is affected by diseases like rickets, osteomyelitis, injuries of the pelvis and
lower limbs as well as nutrition.
Contracted pelvis arises due to varied causes depending on multiple influences
of the external and internal environment on the girl’s body during her intra- and
extrauterine existence. During intrauterine development pelvic deformity can arise
due to disorder of metabolism between mother and fetus, especially of mineral me-
tabolism. The pregnant mother’s nutrition, vitamin deficiency and other factors are
very important.
During infancy and early childhood pelvic deformity can be secondary to
unbalanced formula feeding, poor housing conditions, poor nutrition, rickets,
heavy manual labor, infections (tuberculosis of bone, poliomyelitis), pelvic
injuries.
The childhood period until the pelvis is completely ossified is

NB! crucial for the formation of bony pelvis.
During puberty the formation of bony pelvis proceeds under the impact of ovarian
and adrenal hormones. Estrogens induce transverse pelvic growth, androgens — lon-
gitudinal pelvic and skeletal growth.
Various diseases, prolonged psychoemotional strain, doing sports professionally in
puberty disrupt the endocrine function and the formation of female pelvis.
Developmental acceleration is also a factor in contracted pelvis formation (the
height of females in midland Russia was 156 cm in 1900-s, and 163 cm — in 1990-
s): the skeleton grows longitudinally while increase in transverse pelvic diameters is
delayed. Formation of transversely contracted pelvis can be affected by wearing tight
pants of strong fabrics during puberty. At some time obstetricians invented the term
«jeans pelvis».
25.2.3. Diagnostics
Early detection of contracted pelvis permits a choice of the optimal management
and prevention of labor complications. Diagnosis of bony pelvis abnormalities is
made by past history findings, anthropometry, external measurements, vaginal ex-
amination findings and additional investigations (radiology, ultrasound, CT, MRI).
• General past history: rickets and other diseases or injuries in childhood affecting
the formation and structure of the skeleton;
• gynecologic history: menarche and its nature, previous pregnancies and deliveries,
birth weight of previous children and other data allowing an estimate of the
woman’s reproductive function before pregnancies and in previous deliveries;
• objective general findings: the woman’s height and weight, her body build, joint
motility, structure of her spine and other data permitting an assessment of her
skeleton for the present moment;
• objective specific findings: abdomen shape in late pregnancy (pointed in
primiparous, and pendulous in multiparous women), the angle of pelvic
inclination (45–55 ° normally, in case of contracted pelvis greater inclination
is noted; the sacrum, buttocks and external genitals are retroflected; marked
lordosis of lumbar area is noted).
The shape of lumbosacral rhombus (Michaelis’ rhomboid) is an important factor
in obtaining objective specific data in diagnostics of contracted pelvis (Fig. 25.2).
Fig. 25.2. Michaelis’ rhomboid (a) and its shapes in different types of contracted pelvis (b):
1 — normal pelvis; 2 — flat rachitic pelvis; 3 — generally contracted pelvis; 4 — transversely
contracted pelvis; 5 — obliquely oval contracted pelvis (asymmetrical pelvis)
748 Obstetrics
A traditional way of pelvis examination is measuring it with a pelvimeter, although

it is not always possible to reveal a correlation dependence between the sizes of greater
and lesser pelvis (Table 25.1).
Table 25.1. Basic dimensions of a normal pelvis in common varieties of contracted pelvis, cm
Pelvis shape D. sp. D. cr. D. tr. C. ext. C. diag. С. vera
Normal 26 29 31 21 13 11
Transversely contracted 23 26 29 20 13 11
Simple flat 26 29 31 18 11 8
Flat rachitic 26 26 31 18 11 8
Generally contracted 24 26 28 18 11 9
When the common dimensions are diminished (d. spinarum, d. cristarum, d. tro-
chanterica, conjugata externa), additional dimensions are measured.
Additional obstetric sizes of the body, including the pelvis:
• lateral conjugate: distance between anterosuperior and posterosuperior ischial
spines on one side 14.5–15 cm;
• symphysis height 5–6 cm normally; the higher the symphysis pubis, the shorter
the true conjugate;
• pelvic circumference 85 cm normally;
• Soloviov’s index 1.4–1.5 normally; thick wrists indicate reduced pelvic capacity;
• Michaelis’ rhomboid:
– spinous process of V lumbar vertebra above;
– sacrum apex below;
– posterosuperior spines of iliac bones on the sides. Size of Michaelis’ rhomboid:
10 cm wide, 11 cm high.
The shape of Michaelis’ rhomboid is a factor in diagnostics of contracted pelvis.
In case of generally contracted pelvis (all dimensions reduced) and transversely con-
tracted pelvis the rhomboid is elongated vertically; in case of flat pelvis it is flattened
(see Fig. 25.2).
When measuring the transverse outlet diameter (11 cm) the pelvimeter is placed
on inner edges of ischial tuberosities; the obtained value of 9.5 cm is increased by
1–1.5 cm to allow for the thickness of soft tissues.
When measuring the anteroposterior outlet diameter (9–11 cm) the pelvimeter
is placed on the sacral apex and the lower symphysis border; the obtained value of
12–12.5 cm is decreased by 1.5 cm to allow for the thickness of sacrum and soft
tissues (see Fig. 4.15).
The diagnosis of contracted pelvis and the degree of its contraction are established
on the basis of external pelvimetry and vaginal examination.
A vaginal examination provides more reliable information which

NB! can throw light on pelvic size and capacity.
Having found the diagonal conjugate and subtracting Soloviov’s index from it one
obtains the true conjugate dimension. Using palpation one assesses the ischial spines,
ischial tuberosities and the distance between them, examines the sacral fossa, notes
the presence of exostoses and deformities in the lesser pelvis, false promontory. A
narrow rim of pelvis less than 900 indicates pelvic contraction.
Besides, internal dimensions of the lesser pelvis are determined using radiology
(X-ray pelvimetry) and ultrasound. X-ray pelvimetry permits determining anteropos-
terior and transverse pelvic diameters with a minimum error of 2 mm.
Indications for X-ray pelvimetry (Fig. 25.3):
• reduced dimensions of the greater and lesser pelvis detected by external and
internal obstetric examinations;
• fetal macrosomia (4000 g and more);
• complications in previous deliveries (protracted labor, injury of fetus and
neonate, intranatal fetal demise, forceps delivery, etc.);
• pelvic presentation.
Computed tomography is a more precise investigation; it is easier to perform than
X-ray pelvimetry.
Use of magnetic resonance imaging in obstetrics is admissible, the method is not
associated with radiation exposure; it permits an accurate estimation of fetal and
pelvic size and an assessment of soft tissues.
Deviations in the normal course of labor require a specification of pelvic shape
and size.
The shape of contracted pelvis determines the specifics of labor

NB! and of head engagement: asynclitism, persistent occiput direct or
transverse position.
Fig. 25.3. X-ray pelvimetry, anteroposterior view: 1–4 transverse dimensions of pelvic
planes, 5 — occipitofrontal diameter of fetal head
750 Obstetrics
The mechanism of labor in inapparent varieties of contracted pelvis and average

sized fetus may not be any different from women with normal pelvis. In case of differ-
ent shapes and marked contraction of the pelvis ,labor follows a specific mechanism
typical of the given variety of contraction.
25.2.4. Transversely contracted pelvis

Transversely contracted pelvis has a contracted dimension of the inlet plane
(Fig. 25.4).
Fig. 25.4. Varieties of transversely contracted pelvis
Approximate external and internal dimensions of a transversely contracted pelvis,

degree 1 of contraction:
• distantia spinarum 23 cm;
• distantia cristarum 26 cm;
• distantia trochanterica 28 cm;
• conjugata externa 20 cm;
• conjugata diagonalis 13 cm;
• conjugata vera 11 cm.
In case of transversely contracted pelvis the first step of labor shows head flex-
ion like in physiological delivery; however, due to the contracted transverse inlet
diameter the engagement occurs asynclitically in one of oblique diameters. This
engagement is referred to as oblique asynclitic. It is followed by all the steps of
physiological labor.
When the anteroposterior inlet diameter is enlarged while the

NB! transverse diameter is markedly contracted, the head is engaged
with the saggital suture in the anteroposterior inlet diameter.
This type of engagement is referred to as persistent occiput direct position (see sec-
tion 24.4.1). At the same time, the head flexes moderately while gradually advancing
to the pelvic outlet without doing the internal rotation. During steps 2, 3 and 4 the
head performs internal rotation, and deflexion. This is followed by internal rotation
of the shoulders and external rotation of the head like in physiological labor.
Persistent occiput posterior position is most unfavorable in case of occipitoposte-
rior position of the vertex. In these situations the delivery had better be terminated
by a cesarean section so as to reduce maternal traumatism.
The delivered head is of dolichocephalic shape. If engagement was asynclitic, ca-
put succedaneum is on one of parietal bones, which makes the head a symmetrical.
25.2.5. Flat pelvis

Pelvis is termed flat if only its anteroposterior dimensions (one or several) are
shorter, while transverse dimensions are normal. Three varieties of flat pelvis are
distinguished:
• flat rachitic pelvis;
• simple flat pelvis;
• pelvis with reduced anteroposterior diameter in the wide part of pelvic cavity.
It should be noted that flat rachitic pelvis is not commonly encountered in women
in developed countries due to effective rickets prevention in childhood.
25.2.5.1. Flat rachitic pelvis

Flat rachitic pelvis has the following characters:
• reduced anteroposterior inlet diameter;
• altered sacrum shape: it is shortened, flattened, thinned-out and widened; the
promontory encroaches upon the cavity; the coccyx is bent forward in a hook-
like fashion;
• iliac wings are flat, poorly developed; their crests are spread out so that distantia
spinarum is the same as distantia cristarum;
• pelvic bones show rough protuberances; at the point of muscle attachment they
look like exostoses (Fig. 25.5).
Approximate external and internal dimensions of flat rachitic pelvis in minor
degrees of contracted pelvis:
With this type of pelvis the first step of labor mechanism consists in head exten-
sion; the head persists in the transverse inlet diameter with its sagittal suture as this
is the most «advantageous» position: in the given situation it is the longest diameter
measuring 13 cm (the first specific feature). The head passes the reduced anteropos-
terior inlet diameter with its least diameter, the bitemporal measuring 8 cm. Due to
extended head the anterior fontanelle goes down and approaches the axis pelvis plane;
the posterior fontanelle is higher than the anterior one and it is hardly palpable.
Another specific feature is off-axis engagement of the head termed asynclitism
(see Section 24.3).
752 Obstetrics
Fig. 25.5. Flat rachitic pelvis

As the head is engaged asynclitically (depending on the type of asynclitism), the
presenting parietal bone develops caput succedaneum; the parietal bone that lags
behind flattens under the impact of pressure from the promontory or pubis and thus
characteristic molding occurs: the head flattened in bitemporal diameter adapting to
the reduced anteroposterior dimension.
In step 2 the head slips from the promontory, the sagittal suture assumes a median
position, the head flexes, the occiput turns to the symphysis (internal rotation), and
fetus expulsion occurs like in occipitoanterior position (with the posterior fontanelle
as the point of direction). Fetus expulsion proceeds rapidly due to increased outlet
dimensions.
In some cases the head persists in extended position, and the head is delivered
in sincipital presentation. If rotation was incorrect — occiput rotates posteri-
orly and head flexes — labor proceeds in the same way as in occipitoposterior
position.
In case of pronounced posterior asynclitism a vaginal delivery

NB! is impossible as the anterior parietal bone sort of “saddles” the
symphysis pubis and cannot clear this barrier.
On the whole, labor is protracted, mainly due to the prolonged first step of labor
mechanism. Floating fetal head persists for a long time; then it molds, adapts to a
passage through the inlet plane reduced in the anteroposterior direction. So it is
recommended to a parturient woman with flat rachitic pelvis to lie on the side op-
posite the fetal position which promotes a quicker engagement.
Labor is complicated by an early membrane rupture, prolapse of small fetal parts,
uterine inertia. When contractions are adequate, as soon as the head overcomes
promontory resistance, delivery may become accelerated and even fulminant due to
the increased cavity and outlet dimensions. In its turn, this can lead to rupture of
soft tissues in the birth canal and to birth trauma of the fetus.
25.2.5.2. Simple flat pelvis
Simple flat pelvis (Deventer’s pelvis) shows reduced anteroposterior diameters
of the inlet, cavity and outlet while the sacrum is close to the anterior pelvic wall
(Fig. 25.6).
Approximate external and internal dimensions in a simple flat pelvis with minor
degrees of contracted pelvis:
In this situation the mechanism of labor is the same as in case of flat rachitic
pelvis. The difference is that the head finds obstruction along the entire passage: at
the inlet, in the cavity and in the outlet. The cause is that in case of simple flat pel-
vis the anteroposterior diameter is reduced in all pelvic planes, not just at the inlet.
• Step 1 of the mechanism of labor has its specific features.
– First, the head extends and persists over the inlet with its sagittal suture in
transverse inlet diameter.
– Second, the head molds and engages the inlet with one of its parietal bones:
asynclitic engagement occurs.
• Step 2: the progressive and rotational fetal advance are only possible in presence
of satisfactory contractions and average sized fetus. Delivery ends in the same
way as in occipitoanterior position.
In other cases the head may not perform the internal rotation due to reduced
anteroposterior diameters, and then the third specific feature of the mechanism of
labor is noted: the sagittal suture is in the transverse diameter with all its planes.
A specific feature of labor with simple falt pelvis: persistent

NB! occiput transverse position (see section 24.4.2).
In case of simple flat pelvis labor is prolonged as the head passing through the
bony ring meets with resistance in all pelvic planes.
Fig. 25.6. Simple flat pelvis

754 Obstetrics
Labor is complicated by premature rupture of membranes, which increases the

risk of maternal infection. When the head passes through the pelvic ring, soft tis-
sues are compressed, their circulation is disturbed, edema and sometimes necrosis
results with fistula formation. Sometimes pubic or sacroiliac symphysis is damaged.
A common complication is rupture of the perineum, vaginal walls and cervix. The
most dangerous complication is rupture of the uterus.
Fetal prognosis is unfavorable. Persistent occiput position in all pelvic planes
and its enhanced molding can result in vein rupture and intracranial hemorrhage.
Excessive compression of the head threatens rupture of cerbellar tentorium. In rare
cases the pressure by the promontory causes spoon-like impression on parietal bones.
25.2.6. Generally contracted pelvis

Generally contracted pelvis has a normal gynecoid shape but all its dimensions
are reduced by 2 and more cm respectively.
External and internal dimensions in a minor degree of generally contracted pelvis:
Thus this type of pelvis shows an altered capacity rather than shape. The mecha-
nism of labor and clinical features of labor are altered too; it is expedient to consider
them stepwise.
Step 1 in the mechanism of labor shows a maximum head flexion (Roederer’s
asynclitism) at the pelvic inlet so that the posterior fontanelle is aligned with the
pelvic axis (Fig. 25.7). At the same time, the head molds markedly, cranial bones
overlap, fontanelles and sutures are hardly palpable. During this time the head per-
sists at the inlet with its small segment. As a result, considerable caput succedaneum
develops in the area of the posterior fontanelle.
As the head begins to advance progressively along the birth canal, the second step
of labor begins.
Fig. 25.7. Maximum head flexion in case of generally contracted pelvis

Like in physiological delivery, the head advances along the birth canal simultane-
ously performing correct rotation (occiput to the symphysis). However, in case of
generally contracted pelvis the process takes much longer, with especially prolonged
arrest of the head in the pelvic plane of least dimensions. Step 2 in the mechanism
of labor ends like in physiological labor with the head in anteroposterior outlet di-
ameter with its sagittal suture.
Like in physiological labor, step 3 shows head extension. However, in physiological
labor the point of fixation on the head (suboccipital fossa) is always in contact with
the lower border of symphysis pubis and fills the entire space of the pubic angle, so
extension of the head and its delivery produces a moderate distension of the pudendal
fissure and perineum. In presence of a contracted pelvis with a more acute pubic
angle the head does not come in contact with the lower border of symphysis pubis
(Fig. 25.8). The head cannot assimilate the entire space of the pubic angle so it
distends the perineum excessively which commonly results in perineal muscle injury.
This step in the mechanism of labor corresponds to delivery of the head.
а b
Fig. 25.8. Head passing under the pubic arch: a — in case of adequate pelvis; b — in case of
generally contracted pelvis
Step 4 in the mechanism of labor does not show any marked difference from the
course of physiological labor.
The delivered head has a marked dolichocephalic shape due to molding, caput
succedaneum and its wedgelike engagement in the lesser pelvis (Fig. 25.9).
Fig. 25.9. Dolichocephalic head shape

756 Obstetrics
25.3. MANAGEMENT OF LABOR IN PATIENTS WITH

ANATOMICALLY CONTRACTED PELVIS
Women with contracted pelvis often have various complications in labor requiring
operative delivery. The parturient woman should be carefully observed, especially at
the end of the first stage and during the second stage of labor.
To manage labor in patients with contracted pelvis one assumes

NB! an active expectant approach which requires a lot of self-
possession and professionalism; thus one must be knowledgeable
in the specific course and mechanism of labor with pelvic
abnormalities.
25.3.1. Clinical course of the first stage of labor

• Fetal head remains f loating above pelvic inlet and takes a long time to
adapt before engaging. The belt of adherence does not emerge so there is
communication between hindwaters and forewaters which produce pressure
on the gestational sac that is greater than normal. Premature rupture of
membranes is possible which sometimes leads to prolapse of the cord or
small fetal parts. If the head does not descend into the pelvis after membrane
rupture, the edges of the external os distended by the sac get incarcerated
between the head and pelvis and hang down into the vagina in the form of
edematous f laps.
• Since the gestational sac is absent, there are no conditions promoting contractions,
cervical effacement and dilation. As a result, primary or secondary uterine
inertia may develop.
• Protracted cervical dilation after rupture of membranes is the cause of a long
rupture to delivery interval; there is communication between the vagina and
uterine cavity where microorganisms can enter. Chorioamnionitis can develop
during labor.
• Fetal head begins to function as the gestational sac: a prominent caput
succedaneum develops on the head. Molding is pronounced: one parietal bone
overlaps the other, and they both overlap the frontal and occipital bones.
When pelvic dimensions are normal, a fetus is regarded as

NB! macrosomic if its weight is 4,000 g and more; a fetus of 5,000 g
and more is referred to as gigantic.
In breech presentations a fetus is regarded as macrosomic if
its weight is 3,600 g and more. The criteria of macrosomia are
the same for head presentations in women with anatomically
contracted pelvis.
Management of labor in presence of contracted pelvis is still the most challenging

department of the art of obstetrics.
The strategy of managing labor with contracted pelvis depends on

NB! the degree of contraction, the estimated fetal weigh, concomitant
obstetric complications and extragenital disease.
Labor differs with every variety of contracted pelvis; however, there are gen-
eral principles of managing the first stage of labor. It is recommended that the
woman keep to the bed to avoid premature rupture of membranes. To ensure
better engagement the woman should lie on the side corresponding to fetal
position.
Careful analgesia and instrumental monitoring of fetal condition and uterine
contractions are necessary. At the end of the first stage and during the entire sec-
ond stage of labor functional assessment of the pelvis is performed (estimating the
cephalopelvic proportions).
If the head persists in one pelvic plane up to one hour, one should
NB! assess the nature of labor and watch for signs of cephalopelvic
disproportion.
If there is no functional incompetence of the pelvis or uterine inertia, it is admis-

sible to administer short-term induction with oxytocin (at a rate of no more than
12–15 drops per minute).
The progress of labor is also assessed using tocography. One should watch the
uterine shape (when the lower segment overdistends, the uterus becomes hourglass-
shaped) and urination. If difficult urination or hematuria is noted, the obstetric
situation should be revised and a new plan of management elaborated. One ob-
serves the presenting part, whether it is above the inlet or gradually descends into
pelvic cavity.
If signs of cephalopelvic disproportion or fetal distress emerge, the delivery is
terminated by a cesarean section.
Nowadays neither vaccum extraction nor obstetric forceps are

NB! resorted to in case of contracted pelvis due to the high injury
rate.
25.3.2. Clinical course of the second stage of labor

The clinical course of the second stage of labor has the following specifics distin-
guishing it from physiological labor:
• the fetal head progress through all parts of pelvis is slowed down which often
causes fetal hypoxia;
• protracted course of the first stage leads to the woman’s nervous exhaustion
and physical fatigue and in the expulsion stage secondary uterine inertia may
develop;
758 Obstetrics
• if the head persists in one of pelvic planes due to its reduced size, there is a
risk of cervical incarceration and compression of adjacent organs which can
result in later emergence of genitourinary, cervicovaginal and intestinogenital
fistulas;
• in case of powerful contractions the bones of pubic and/or iliac symphysis can
separate, the cervix and perineum can tear;
• in some cases labor is complicated by powerful contractions and even uterine
tetany; excessive labor can result in uterine rupture, placental abruption, fetal
demise;
• in case of protracted labor (18 hours and more) and a prolonged rupture to
delivery interval there is a risk of an ascending infection (chorioamnionitis
during labor).
25.3.3. Mode of delivery

The outcome of labor depends on pelvic and fetal dimensions. To determine the
estimated fetal weight one measures fundal height and abdominal circumference,
performs ultrasound fetal biometry. Besides fetal size, the outcome is influenced
by the shape of contracted pelvis and, which is more important, the degree of its
contraction.
• In minor degree of contracted pelvis, small or average-sized fetus and occipital
position a spontaneous delivery occurs as a rule.
• In moderate degree of contracted pelvis the cesarean section is generally opted
for in the interest of the fetus.
• In severe degree of contracted pelvis the woman cannot give a live vaginal birth;
elective cesarean section is indicated.
If degree 1 of contraction is combined with fetal macrosomia

NB! (3,600 g and more), with pelvic presentation, hydrocephaly and
other complications of pregnancy, a planned cesarean section is
performed (prior to the onset of labor) at gestational age 38.5 –
39.5 weeks.
25.4. FUNCTIONALLY CONTRACTED PELVIS

(CEPHALOPELVIC DISPROPORTION)
Functionally contracted pelvis has dimensions that cannot provide the passage of
this particular fetus.
Possible causes of cephalopelvic disproportion are as follows:
• structural reduction in the pelvis;
• large fetal head;
• presenting an extended head;

• a combination of the above factors.
The classification of functionally contracted pelvis proposed by R. Kalganova
foresees three degrees of cephalopelvic disproportion. At present this classification
is not in use.
Cephalopelvic disproportion is mostly seen in case of average sized fetus. A study
conducted by Parkland Hospital showed that 2/3 of neonates had a birth weight
below 3700 g.
Specifics of the second stage of labor in cephalopelvic disproportion (macrosomic
fetus, occiput malpresentation) require a careful observation of the course of labor,
fetal progress and its heartbeat.
One should never allow fetal head persisting in one plane for an
NB! hour.
Prolonged period of unengaged head in one plane is one of the leading signs of
cephalopelvic disproportion. When CPD is detected, emergency cesarean section
should be performed. If early, adequate obstetric care is not provided, there is a risk
of rupture of uterus.
CPD can be only diagnosed when labor is in progress:
• with satisfactory contractions;
• after rupture of membranes;
• almost complete cervical dilation;
• the head pressed to the inlet;
• signs of disproportion between the head and pelvic inlet.
Besides the common methods of examining the presenting part, Vasten’s and
Zangemeister’s signs help to determine CPD.
Examination by Vasten’s sign is performed in the following way: with your
fingertips, perform motions from symphysis pubis upwards to the head pressed
to pelvic inlet determining the proportions between the fetal head and mother’s
pelvis.
• If the head and pelvis are proportionate to each other, the anterior symphysis
surface is higher than the anterior surface of the pressed head — negative Vasten’s
sign.
• If the anterior symphysis surface is on the level with the anterior head surface —
Vasten’s sign at the same level.
• If the anterior head surface is above the symphysis, it is a positive Vatsen’s sign:
cephalopelvic disproportion is present (Fig. 25.10).
For examination by Zangemeister’s sign, one measures the external conjugate
with a pelvimeter and then shifts the anterior end of pelvimeter to the most
prominent point of the head (the other end of pelvimeter remains in the same
place).
• If the obtained value is less than the external conjugate, it is a negative
Zangemeister’s sign.
760 Obstetrics
а b c
Fig. 25.10. Vasten’s sign: a — positive; b — at the same level; c — negative
• If the obtained value is greater than the external conjugate, this indicates CPD:
positive Zangemeister’s sign.
• If the obtained values are equal, there is a relative CPD.
With negative Vasten’s or Zangemeister’s sign a physiological

NB! vaginal delivery occurs, as a rule.
In case of equal values a vaginal delivery is doubtful.
With positive Vasten’s and Zangemeister’s signs a live fetus cannot
be delivered vaginally and thus should be delivered via a cesarean
section.
Other findings of objective examination and signs indicating CPD:

• high contraction ring (a borderline separating the lower and upper uterine
segments) which is associated with overdistension of the lower uterine segment
and a risk of its rupture;
• tenderness of the lower segment to palpation;
• compressed bladder sign: the parturient woman cannot pass urine independently;
there is admixture of blood in urine;
• edema of external genitals;
• vaginal examination findings: complete or almost complete cervical dilation,
edema on the borders of external os, no gestational sac, large caput succedaneum
on the head pressed to the inlet.
In case of CPD labor is terminated by a cesarean delivery to avoid uterine rupture.
In case of fetal demise embryotomy is performed.
Management of labor with contracted pelvis requires great skill

NB! and high professionalism. One should detect labor complications
in good time and take steps to control them. Of great importance
are an attentive attitude to the birthing woman and guarding her
emotions.
25.5. COMPLICATIONS
When managing labor in women with contracted pelvis one should remember
that an excessively conservative approach can lead to severe complications and an
urgently required embryotomy, so it is important not to miss the time favorable for
cesarean section.
In the early postpartum period the woman often develops atonic hemorrhage due
to overstrain and secondary weakening of contractility and low uterine tone.
The late postpartum period can be complicated by postpartum infection, genito-
urinary and intestinogenital fistulas, lesion of pelvic symphysis.
25.6. PROPHYLAXIS
At the maternal welfare clinic the gynecologist and midwife should detect a con-
tracted pelvis early, determine the degree of contraction, and hospitalize the pregnant
woman 7–10 days prior to the estimated delivery date for a detailed examination and
elaboration of the plan of management.
Prophylaxis of contracted pelvis begins in the girl’s infancy; it is aimed at preven-
tion of infection and rickets. Exercise, balanced diet with adequate vitamin intake,
observing personal hygiene at school, safety at workplace — all these factors promote
a reduction in the rate of various pelvic abnormalities.
REMEMBER!
Definition Anatomically contracted pelvis shows one or all external

dimensions reduced by 2 or more cm; the internal dimensions
of the lesser pelvis are reduced by 0.1–0.5 cm
Functionally contracted pelvis, CPD is a pelvis in which one
or more of its main diameters are reduced so that it interferes
with the normal mechanism of labor
Etiology In childhood the bony pelvis structure is influenced by diseases
like rickets, osteomyelitis, pelvic and lower limb injury, and
nutrition. During puberty it is disease, prolonged psychoemo-
tional strain, going in for sports professionally
Classification Commonly occurring shapes of contracted pelvis:
• transversely contracted pelvis;
• pelvis contracted in its anteroposterior diameters:
• simple flat pelvis (all anteroposterior diameters are diminished):
• flat rachitic pelvis;
• pelvis with reduced anteroposterior dimension of the wide part
• generally contracted pelvis, etc.
Regarding the degree of contraction all pelvises (except for
transversely contracted type) are classified by the shortening
of conjugata vera (three degrees)
762 Obstetrics
Clinical fea- Off-axis engagement (asynclitism), persistent occiput direct or

tures transverse position, marked caput succedaneum changing the
head shape (asymmetrical, dolichocephalic, etc.)
Diagnostics Reduced external and internal pelvic dimensions, woman’s
height under 158 cm
Research External pelvimetry, 4 ways of measuring conjugata vera, hos-
methods pitalization 7–10 days prior to delivery, estimating fetal weight,
functional assessment of pelvis during labor
Complications CPD, uterine rupture, acute hypoxia and trauma of fetus,
abnormalities of labor, premature rupture of membranes, hem-
orrhage in the postpartum period, injury of soft tissues in birth
canal, rectogenital and genitourinary fistulas
CONTROL QUESTIONS
1. Define the notion of anatomically and functionally contracted pelvis.
2. Causes of contracted pelvis.
3. Classification of anatomically contracted pelvis.
4. Methods of diagnosing anatomically contracted pelvis.
5. Specific features of mechanism of labor in case of flat pelvis.
6. Specific features of mechanism of labor in case of transversely contracted pelvis.
7. Specific features of mechanism of labor in case of generally contracted pelvis.
8. Labor complications in presence of bony pelvis abnormalities.
9. Principles of labor management in case of contracted pelvis.
10. Causes and signs of cephalopelvic disproportion.
CHECK YOURSELF!
Level 1. Test
Select one or more correct answer
1. Which of the pelvis types below are commonly occurring varieties?
a) obliquely oval contracted pelvis;
b) funnel pelvis;
c) generally contracted pelvis;
d) osteomalatic pelvis.
2. Which parameter is not used for determination of conjugata vera?

a) external conjugate: depending on the circumference of radiocarpal joint (less
than 14 cm, 14 cm or more than 14 cm), 8 or 9 or 10 cm, correspondingly, are
detracted from the external conjugate thus arriving at the size of true conjugate;
b) diagonal conjugate: having measured the diagonal conjugate one detracts
Soloviov’s index (1/10 of radiocarpal joint circumference) from its size;
c) by the vertical size of the Michaelis’ rhomboid;
d) by the Krassovsky dimension.
3. Which of these is not included in the Caldwell-Moloy classification:

a) platypelloid;
b) humanoid;
c) gynecoid;
d) android.
4. Which of these is not a sign of false rachitic pelvis:

a) only transverse inlet diameter is reduced;
b) only anteroposterior inlet diameter is reduced;
c) altered sacrum shape: it is shortened, flattened, thinned-out and widened;
the promontory encroaches upon pelvic cavity; the coccyx is bent forward in a
hook-like fashion;
d) iliac wings are flat, poorly developed; their crests are spread out so that distantia
spinarum is the same as distantia cristarum.
5. Which variety of contracted pelvis corresponds to these dimensions?

distantia spinarum 23 cm;
distantia cristarum 26 cm;
distantia trochanterica 28 cm;
conjugata externa 20 cm;
conjugata diagonalis 13 cm;
conjugata vera 11 cm;
a) simple flat pelvis with minor contraction;
b) flat rachitic pelvis with minor contraction;
c) transversely contracted pelvis with minor contraction;
d) simple flat pelvis with moderate contraction.


764 Obstetrics

8. Which of these statements is incorrect:

a) when the head persists in one pelvic plane for a long time (up to 1 hour), one
should carefully assess the nature of labor and check for signs of cephalopelvic
disproportion;
b) when the head persists in one pelvic plane for a long time and the pelvis is
contracted, obstetric forceps or vacuum extraction is indicated;
c) the principles of labor management depend on the degree of contracted pelvis,
pelvic shape, estimated fetal weight, concomitant obstetric and extragenital disease;
d) due to the high rate of trauma, vacuum extraction and obstetric forceps are
not used in case of contracted pelvis nowadays.
9. Which is not a cause of CPD:

a) anatomic reduction in pelvis size;
b) tocolytic therapy;
c) large fetal head;
d) deflected head presentation.
10. Which of the signs below is not a sign of CPD:

a) positive Vasten’s and Zangemeister’s signs;
b) high contraction ring;
c) absence of uterine contractions;
d) sign of bladder compression.

1. A pregnant woman aged 25 was admitted to maternity hospital. The present
pregnancy is the second one; the first pregnancy terminated in a stillbirth; fetus
3800 g with intracranial hemorrhage. The woman’s height is 160 cm; external pelvic
dimensions 26–28–30–17 cm, Soloviov’s index 1.6; the Michaelis’ rhomboid dimen-
sions: vertical 9 cm, horizontal 10 cm, abdomen circumference 110 cm, fundal height
41 cm. What is your diagnosis? What is the plan of management?
2. Primiparous woman aged 23 was admitted to maternity hospital in labor, fetus
in longitudinal lie, cephalic presentation. External pelvic diameters 26–29–31–20;
abdomen circumference 96 cm; fundal height 38 cm. A dynamic observation showed
that 10 h after the onset of labor the patient began to push uncontrollably. The pa-
tient complains of continuous acute pain in the lower uterine segment, cannot pass
urine independently, Vasten’s sign at the same level. A vaginal examination showed
cervical dilation 8 cm, no gestational sac, fetal head pressed to pelvic inlet. Fetal
orbits, root of nose, brow and anterior fontanelle angle are palpable. What is your
• Chapter 26
MATERNAL OBSTETRIC TRAUMA
During pregnancy the soft tissue of the birth canal undergoes considerable changes
under the impact of hormonal transformation so they can withstand considerable
pressure and distension during childbirth. Sometimes bruises and cracks arise in
external genitals, perineum, vagina and cervix. These superficial lesions are asymp-
tomatic and heal spontaneously over the first days after childbirth. When labor gets
complicated, there can be lacerations of external genitals, perineum, vagina and
cervix, edema can develop. On the whole, trauma is noted in every fifth parturient
woman. Sometimes there are life threatening lesions that can end in the parturient
woman’s death or long-term incapacitation or disability (rupture of uterus, bladder
and rectum, inversion of uterus, genitourinary and intestinogenital fistulas, lesions
of pubic symphyses, injury of pubic bones). In about 20% of puerperas the trauma
of soft tissues in the birth canal is accompanied by infection.
Epidemiology. Tears of soft tissues in the birth canal often occur in primiparous
women, and uterine rupture — in multiparous women mostly. There are no accu-
rate data on vulvar lesions. Cervical tears occur in 6–15% of childbirths, third and
fourth degree perineal tears occur at a rate of 3:10,000, uterine rupture — at a rate
of 1:10,000.
Causes of obstetric trauma:
• mechanical (excessive distension of tissue);
• structural (histopathological alterations in tissue);
• mixed (mechanical and histopathological).
Obstetric trauma can be spontaneous or forced, brought about by obstetric in-
tervention.
Etiology. Causes of obstetric trauma of soft tissues in the birth canal, cervix and
body of uterus are similar; they are as follows:
• incorrect obstetric assistance;
• contracted pelvis and CPD;
• prolonged abnormalities of labor;
• accelerated or precipitous labor;
• occiput malposition;
• pelvic presentation;
• rigidity, inflammation or scars in birth canal tissue, or uterine scar;
• operative delivery.
26.1. VULVAR LACERATIONS

Lacerations of external genitals (vulva) are traumatic lesions of labia minora and
majora, clitoris and vaginal vestibulum during labor.
766 Obstetrics
Classification:
• regarding the causes of occurrence: spontaneous and forced.
• regarding their localization: lacerations of labia minora and labia majora,
clitoris and vaginal vestibulum; there can be superficial bruises or deep tears of
underlying tissue accompanied by hemorrhage.
ICD-10 code
• O71 Other obstetric trauma.
Clinical features. Lacerations occur at the end of the second stage of labor (fetal
expulsion). Vulvar lesions are often combined with vaginal and perineal tears; they
are accompanied by hemorrhage at the end of the second stage, in the third stage
of labor or in early postpartum period. The intensity of hemorrhage depends on the
laceration’s localization and depth as different parts of organs have different blood
supply. The most copious hemorrhage occurs when clitoris area is traumatized.
Diagnostics. Vulvar lesions are diagnosed upon inspection of the genital tract.
Treatment. Superficial lesions (bruises) that are not accompanied by hemorrhage
do not require operative intervention. In case of deep or massive lesions one admin-
isters surgical hemostasis and repair of injured tissue.
All minor obstetric surgery like repair of lacerations is performed in situ; if there
are no individual birthing rooms — in the special room for minor operations.
Operation. The bladder is emptied via a catheter; the surgical area is swabbed
with antiseptics.
Anesthesia: local infiltration or IV anesthesia, or continuing epidural block if the
catheter was introduced during labor.
Surgical technique. All detected lacerations are repaired with interrupted or con-
tinuous sutures. Single hemorrhaging vessels are clamped and then ligated or repaired
with transfixion suture. In case of deep lacerations in clitoris area a urinary catheter
should be introduced into the urethra. If the urethra is damaged, a urologist con-
sultation is required.
When closing the wound near clitoris one introduces a catheter

NB! into the urethra so as not to pierce the urethral wall. Single stitches
are placed without engaging the underlying tissue so as to avoid
bleeding from cavernous bodies.
Postoperative period. In the postnatal ward the puerpera is taught how to care for
the sutures; dry care of the sutures is performed daily. Physiotherapy administered
on the suture area has a good healing effect.
Complications: suture line disruption, wound infection, healing by secondary
intention.
Prognosis is favorable.
26.2. VAGINAL LACERATIONS
Vaginal laceration is disruption of tissue continuity in vaginal walls occurring in

the process of fetus expulsion.
Chapter 26. MATERNAL OBSTETRIC TRAUMA 767
Classification
• Regarding the cause of occurrence: spontaneous or forced.
• Regarding their localization: lacerations in the upper, middle or lower third
portion, anterior, posterior and lateral walls, unilateral and bilateral:
– laceration in the lower third portion is often accompanied by perineal tears;
– laceration in the upper third portion can pass to vaginal fornix, cervix or lower
uterine segment;
– the middle third portion of the vagina is most expansible, least fixed and so it
tears most seldom.
ICD-10 code
• O71 Other obstetric trauma.
– O71.4 Obstetric high vaginal laceration.
Clinical features consist in hemorrhage from the wound, its intensity depending
on the depth and length of laceration. Longitudinal vaginal tears are most common,
transverse ones are less common. In case of deep lacerations all layers of vaginal
wall are damaged, to the extent of pelvic fat exposure. In rare cases lacerations can
extend to the rectum wall.
Diagnostics. Laceration of vagina is detected during speculum examination of the
birth canal.
Treatment. Vaginal lacerations always require surgical repair of vaginal walls and
arrest of bleeding.
Preparation for surgery is the same as in the case of vulvar trauma.
Anesthesia: local infiltration anesthesia or IV anesthetic, or epidural block if the
catheter was introduced during labor.
Surgical technique. Repair is performed under visual control which requires ex-
posure of the wound with vaginal speculums. If there is no one to assist in exposing
the wound and repairing it, the vagina is opened by the index and middle fingers
of the left hand.
To ensure thorough hemostasis, sutures are placed retreating 0.7 cm above the
wound angle. When superficial lacerations have been repaired, hemorrhage stops;
their repair is painless for the woman. Deep lacerations and lacerations of the up-
per vaginal third extending to paravaginal fat are only repaired with IV anesthetic or
continuing epidural block if the catheter was introduced during labor.
Repair of such lacerations is challenging from the technical point of view; it re-
quires good knowledge of anatomy and topography. Deep lacerations can be com-
plicated by extensive hematoma.
When closing the laceration in posterior vaginal wall one should

NB! bear in mind the underlying rectal wall. Upon completing the
surgery one should do a digital examination of anterior rectal wall
to rule out its piercing.
Postoperative period. In the postnatal ward the puerpera is taught how to care for
the sutures; dry care of the sutures is performed daily.
If the puerpera was classified at high risk for puruloseptic disease and her lacera-
tions are deep and extensive, antibacterial therapy can be administered.
768 Obstetrics
Complications: suture line disruption, postpartum ulcer development, healing by

secondary intention.
Prognosis is favorable in most cases. If the postoperative period becomes compli-
cated and the wound heals by secondary intention, cicatricial deformity of vaginal
walls is possible: narrowing of vaginal lumen, increased risk of trauma in subsequent
childbirth.
26.3. PERINEAL TEARS
Perineal tear is disruption of tissue continuity in the perineum occurring in the

process of fetus expulsion.
26.3.1. Statistics
Perineal tears are the most common type of obstetric trauma; they are seen in
7–15% of all deliveries, in primiparous women 2–3 times more often than in mul-
tiparous women.
Inadequate repair of third and fourth degree perineal tear, or its healing by second-
ary intention can result in anal incontinence of flatus or feces, and later — in incom-
petence of pelvic floor muscles, prolapse of the walls of uterus, bladder and rectum.
Perineal tears can be spontaneous or forced (Fig. 26.1). Forced tears occur result-
ing from inadequate management of labor (aggressive obstetric approach) or due to
incorrect technique when performing obstetric surgery.
Fig. 26.1. Second degree perineal tear

Regarding the extent of damage, perineal tears can be divided into four degrees
(Fig. 26.2).
• First-degree tear: disrupted continuity of the lower vaginal third, posterior
commissure and skin of perineum, no more than 2 cm (without involving
perineal muscles).
1
3
1
2
3
4 4
5
5
I II
3
3
4 4
6 7
7
8
III
Fig. 26.2. First, second and third-degree perineal tears: 1 — anterior vaginal wall; 2 —
posterior vaginal wall; 3 — upper border of tear; 4 — posterior commissure; 5 — perineal
skin; 6 — mucosa of rectum; 7 — external sphincter of rectum; 8 — anus
770 Obstetrics
• Second-degree tear: disrupted continuity of the posterior vaginal wall, posterior

commissure, perineal skin and pelvic floor muscles.
• Third-degree tear: besides lesion of above mentioned organs, the external
sphincter of rectum becomes involved.
• Fourth-degree tear: besides lesion of above mentioned organs, the anterior wall
of rectum gets torn. When labor is managed adequately, this degree of tear is not
commonly seen.
Central perineal tears. Neither the posterior commissure nor the external sphincter
of rectum is involved; it is the tissues located between them that get torn. As a result,
the fetus can be delivered through the available opening rather than the pudendal
fissure.
Classification by clinical course:
• threatening perineal tear;
• ongoing perineal tear;
• accomplished perineal tear.
ICD-10 code
• O70 Perinea laceration during delivery (including episiotomy extended by
laceration.
Soft tissues in the birth canal are extensible to a certain extent; extensibility is
considerably reduced in conditions of dysbiosis and inflammation of the vagina
and cervix. The presenting part advancing along the birth canal presses on the sur-
rounding organs distending them, which first produces a threatening trauma, and
then — laceration of tissues. A perineal tear occurs upon crowning of the head, less
often — upon crowning of the shoulders.
The mechanism of perineal trauma proceeds in the following order.
The venous plexus is compressed, which disturbs the outflow of venous blood
and lymph. This is manifested by cyanotic perineal skin (venous congestion) and/or
edema of skin (vascular leakage).
Later ischemia of tissues develops due to compression of arteries. The skin acquires
characteristic glitter and pallor.
Metabolic disorders occur, the turgor and strength of tissues diminish, and the
perineum gets torn.
A perineal tear can begin with a laceration of the posterior or lateral vaginal wall;
however, it commonly starts at the posterior commissure extending to the perineum
and posterior vaginal wall.

Signs of perineal tear:
• marked protrusion;
• cyanosis;
• edema;
• glitter and pallor of skin.
It is important to remark here that the signs of threatening tear sometimes indi-
cate that the tear has occurred at all levels except in the skin. Episiotomy performed
at this stage provides none of the benefits of an incised wound, and repair of the
perineum and pelvic floor becomes a challenging task. This should be performed by
a qualified specialist.
Emergence of insignificant minor cracks in the epidermis indicates an ongoing
perineal tear.
When a perineal tear is accomplished, gaping vulva and vulvar asymmetry are
noted; in fourth-degree tears — flatus and feces incontinence.
In most cases tears are accompanied by hemorrhage; in presence of varicose veins
the hemorrhage can be massive.
26.3.5. Diagnostics
After delivery the condition of birth canal should be carefully assessed. A rectal
examination is performed if necessary.
26.3.6. Surgical treatment

All perineal tears and incisions are only treated surgically: layer-by-layer repair of
damaged tissues (hemostasis is performed simultaneously).
A timely perineotomy prevents a tear of rectum and its sphincter;

NB! the smooth edges of a cut wound can be better put together, and
they heal better.
Perineal tears are repaired immediately after the birth of placenta. Before inspec-
tion of the cervix and vaginal walls the puerpera is given analgesia, and then the
tears are repaired.
Detected perineal tears should be repaired within one hour after

NB! delivery.
Repair is performed observing all rules of aseptics and antiseptics in the birthing
room or in the room for minor operations. The surgical field, the hands of the surgeon
and assistants are processed according to common principles of surgery.
The surgery requires help from a surgical nurse and an assistant; one needs sterile
material (cotton balls, wipes) instruments for vaginal surgery, suture material (syn-
thetic absorbable stitches for perineal repair and cosmetic stitch in the skin).
Anesthesia:
• first-degree perineal tear is repaired with local infiltration anesthesia;
• second-degree tears require thorough analgesia (regional, infiltration or pudendal
anesthesia);
• third- and fourth-degree tears require IV or regional anesthesia.
If epidural nerve block was used in labor, it is extended for the period of exami-
nation and repair.
772 Obstetrics
Technique of surgery. First-degree tears are commonly regarded as insignificant

(the muscular perineal layer is not involved); they can be repaired with single-layer
interrupted suture using absorbable stitches.
In first-degree tears the wound is exposed using vaginal speculums. A stitch is
placed on the upper angle of the wound; the ends of sutures are gripped with a clamp
and drawn upwards. The wound is opened, dried with cotton balls and inspected. The
crushed portions of wound edges are excised. Continuous or interrupted sutures are
placed on the vaginal wall at a distance of 1 cm. The needle should pass under the
entire depth of tissues; otherwise there will be pouches where blood will accumulate
and interfere with healing (Fig. 26.3).
The edges of the skin wound are joined with intradermal cosmetic stitch using
synthetic dissolvable stitch. The line of stitches is swabbed with an antiseptic.
In second-degree tears the lesion commonly involves, besides the skin and mu-
cosa, superficial bulbocavernous and transverse muscles of the pelvic floor while the
external anal sphincter is not affected. 3–4 absorbable stitches are placed, pelvic floor
(perineal) muscles are repaired with 3–4 interrupted implanted sutures with absorb-
able stitches. The skin should be repaired with continuous absorbable subcuticular
stitches (in order to prevent wound infection).
In most countries first- and second-degree perineal tears are repaired layer-by-
layer with continuous sutures using atraumatic needles.
First- and second-degree perineal tears can be closed using Schute’s method
(1959). Eight-like sutures are placed from top downward at a distance of 1 cm going
through all perineal layers (including the deep layer) (Fig. 26.4).
Repairing third- and fourth-degree tears is a demanding

NB! procedure which requires good knowledge of perineal anatomy
and topography, and considerable surgical skill so it should be
performed by an experienced surgeon.
а b
c d
Fig. 26.3. Technique of suture placement: a, b — correct; c, d — incorrect
As a result of repair performed by this method there are no stitch knots, and all
layers of perineal tissue are in close contact.
In third-degree tears one should first retrieve the ends of the torn rectal sphincter
and join them with interrupted U-shaped sutures. Then the perineal wound is closed
in the same order as in second-degree tears (Fig. 26.5).
In fourth-degree tears the surgery consists of two stages.
• First the rectal wall is closed with interrupted sutures using synthetic stitches
going through the depth of mucosal and muscular layers; the sutures are tied in
the rectal lumen.
• Now all the «soiled» instruments, material and gloves are replaced with clean
ones, scrub-up is performed, and the torn rectal sphincter and perineal tears are
repaired.
Postoperative period. The sutures should be kept clean. Perineal area should be
cleaned after each urination or defecation. The sutures are not washed but carefully
Fig. 26.4. Placing of Schute stitches
Fig, 26.5. Perineal tear (lacerated edges of the wound)

774 Obstetrics
dried with sterile cotton balls and processed by a dry method. If perineal tissues
develop edema, an ice pack is applied and/or physiotherapy is administered (laser,
ultrasound, etc.).
Patients with first and second-degree tears are allowed to walk in 6 hours. The
puerpera should abstain from vegetables, fruit or fresh bread to detain defecation. If
there is no bowel movement on day 3, a laxative is administered.
Patients with third- and fourth-degree tears keep bed rest for 2 days. Over the first
6 days the puerpera receives fluid foods promoting delayed defecation: broth, raw egg,
tea, paraffinum liquidum (one tablespoonful thrice a day). Antibacterial therapy is
also administered. A laxative is administered on day 6 after childbirth. The patient
can start the common diet on day 10.
Complications: suture line disruption, wound suppuration, healing by secondary
intention. In third- and fourth-degree tears and suture line disruption rectovaginal
fistulas can develop.
Perineal tears are easily infected; they can be the source of

NB! postpartum septic infection.
26.3.7. Prognosis
With correct surgical repair and uneventful postpartum and postoperative period
the prognosis is favorable.
If perineum is not adequately repaired, this can result in sinking

NB! and prolapse of genitals. In third- and fourth-degree tears the
patient may develop gas and feces incontinence or vaginorectal
fistula.
26.4. HEMATOMA OF EXTERNAL GENITALS AND VAGINA
Hematoma is a localized collection of blood outside the blood vessels (in external
genitals, vagina) without disruption of tissue continuity, or leakage of blood to the fat
surrounding the vagina and uterus due to hemorrhage from a damaged vein or artery.

Hematoma of external genitals and vagina develops during the expulsion period
of after delivery. The cause is mostly associated with alterations in the vascular wall:
enhanced angiasthenia, varicose vein disease, inflammation of the vagina.
Hematoma is promoted by:
• protracted or accelerated advance of fetal head along the birth canal;
• obstetric maneuvers (fetal head extraction with obstetric forceps or vacuum
extractor);
• episiotomy or perineal tear.
A trauma brings about distension and rupture of vessels in the depth of soft tissues
while the surface tissue remains intact. The blood accumulates in the depth of tissue
and loose connective tissue forming a hematoma whose size may be greater than the
fetal head. Hematoma can spread down to the buttocks, perineum, and upward to
the retroperitoneal space reaching paranephral fat. Patients with coagulopathy are at
a higher risk of hematoma.
Hematomas are classified by:
• localization (hematoma of external genitals, vagina, pelvic fat and other);
• the clinical course (progressing and non-progressing);
• size (small: under 2 cm in diameter, large: 4–5 and more cm in diameter).
ICD-10 code
• O71.7 Obstetric hematoma of pelvis.

Small-size hematomas (under 2 cm) do not trouble the puerpera, as a rule;
larger ones cause discomfort, sensation of pressure, distension in the vagina
and perineum. The function of adjacent organs is not compromised. Large or
progressing hematomas give severe pain in the lesser pelvis and lumbar area
irradiating to the leg. The puerpera complains of sensation of pressure in the
rectum or bladder and tenesmus. In case of a massive hematoma (blood loss of
more than 1% of body weight) presentations of hemorrhagic shock develop. In
certain cases the hematoma opens spontaneously, and a large amount of fluid
blood with clots escapes.
Each puerperant woman with pain in the perineum, lesser pelvis

NB! or the small of the back should be examined to rule out the lesser
pelvis hematoma (inspection, ultrasound).
26.4.4. Diagnostics
Hematomas are diagnosed upon examination of external genitals and vagina, and
by a vaginal examination. A bluish-purple tumor is revealed in the area of external
genitals or vagina, vaginal orifice may be off-center. Sometimes a hematoma can be
only detected by palpation of vaginal fornix. If the hematoma progresses extending to
the retroperitoneal space, acute anemia signs develop rapidly followed by manifesta-
tions of hemorrhagic shock. Disturbed hemodynamics (a drop in BP, tachycardia)
while there is no external bleeding requires emergency differential diagnostics to rule
out uterine rupture and internal hemorrhage from other organs. Additional diagnostic
methods are ultrasound and laparoscopy.
776 Obstetrics
26.4.5. Treatment
The algorithm and extent of invasion is determined by the size of hematoma.
Minor hematomas about 2 cm in diameter are not opened, they

NB! resolve spontaneously.
Progressing hematoma and hematoma with a diameter more than 4–5 cm require
opening to reveal the source of hemorrhage, ligation of the bleeding vessel, removal
of blood clots and repair of the wound (Fig. 26.6).
Prerequisites and preparation for surgery are the same as in case of perineal trauma.
As there is a risk for hemorrhagic shock, if considerable blood loss is supposed, sur-
gery is performed with a connected infusion set and a Cell Saver system on the ready.
Anesthesia: epidural nerve block, IV anesthesia.
Technique of operation. The hematoma is opened at the point of most protruding
fluctuating surface. The incision should go in the direction of tissue to provide resto-
ration of normal structure. The hematoma is emptied removing clots and fluid blood.
The bleeding vessel is ligated, the incision is closed. If the bleeding vessel cannot be
detected, one places deep sutures and performs vaginal tight tamponade (controlled
balloon tamponade). Blood loss restoration is performed using blood substitutes and
blood products, in accordance with the protocol for infusion-transfusion therapy.
NB! If the hematoma is infected, repairing the wound is contraindicated.
When the hematoma progresses and extends to pelvic fat, laparotomy is sometimes
performed.
Postoperative period. After emptying large hematomas antibacterial therapy and re-
peated monitoring (examination, ultrasound) are administered. Symptomatic therapy
is provided if needed, anti-anemic therapy.
Complications. Recurrence of hemorrhage, suppuration of hematoma. In this case
the hematoma is opened and treated in accordance with purulent surgery principles.
Fig. 26.6. Emptied and repaired perineal hematoma

26.5. CERVICAL TEARS
Cervical tear is disruption of tissue continuity in the cervix during labor.
26.5.1. Statistics
Cervical tears during childbirth are quite common; according to different authors,
their rate is 6–15%; in primiparous women they are seen 4 times more often than
in multiparous ones.
Regarding the mechanism of tear:
• spontaneous cervical tears occurring in labor without surgical assistance;
• forced cervical tears occurring upon operative intervention.
Regarding the localization:
• lateral (unilateral and bilateral);
• in the labium anterius;
• in the labium posterius.
Cervical tears can be single or multiple. Depending on their length and extent of
damage, cervical tears are divided into three stages.
• Stage I: cervical tear no more than 2 cm in length.
• Stage II: tears over 2 cm; they do not reach the vaginal fornix.
• Stage III: tears reaching the vaginal fornix or involving it.
ICD-10 code
• O71.3 Obstetric laceration of cervix.
During labor the cervix becomes effaced, the edges of external os become greatly
distended and thinned-out. The orifice edges develop superficial tears that occur in all
primiparas; they do not bleed, or if they do, the bleeding is insignificant. Deep tears
of the cervix occur in abnormal labor; they cause significant hemorrhage. Cervical
tears usually begin at the edge of external os spreading upward to the vaginal fornix,
and can involve the vaginal fornix and even the lower uterine segment affecting the
parametrium and peritoneum; in such cases this means a uterine rupture.

The only sign of cervical tear is bleeding from the birth canal developing mostly
after delivery of the fetus or placenta, when the uterus has contracted. Superficial
tears 0.5–1.0 cm in length can remain asymptomatic or present insignificant bleeding.
Deeper tears are usually accompanied by a hemorrhage of varying intensity. When
the efferent cervical branch of uterine artery is involved (in case of lateral cervical
tear) hemorrhage is intensive, starting immediately after delivery of the fetus. In case
of third-degree cervical tears hematoma may develop in parametrial fat.
778 Obstetrics
In cervical lacerations the extent of bleeding is not always

NB! proportional to the degree of laceration. The size of damaged
blood vessel is of decisive importance.
26.5.4. Diagnsotics
Cervical tear after delivery is detected with a speculum examination. In Russia the
examination is performed on all puerperas irrespective of their parity.
Technique of cervix speculum examination. After delivery the cervix is examined
under good lighting in the birthing room or in the operating room, in lithotomy
position. External genitals are swabbed with an antiseptic. The cervix is exposed with
speculums and clasped with fenestrated forceps first by the labium anterius. Then
the forceps are moved one by one every 2 cm clockwise. The edges of external os
are distended by the forceps, and the entire length of the cervix is inspected in a
circular fashion (Fig. 26.7).
Fig. 26.7. Application of fenestrated forceps and bringing down the cervix
In prmiparas, superficial (up to 1 cm) cervical lacerations are

NB! always present resulting in the external os later becoming slit-like.

All cervical tears, apart from superficial lacerations without bleeding, require
surgical treatment. Tears are closed aseptically. In third-degree cervical tears (before
repair) a control manual examination of the uterine cavity is obligatorily performed
to rule out involvement of the lower uterine segment.
Prerequisites for surgery and preparation are the same as in case of gynecological
reparative surgery.
Anesthesia. In first-degree tears the cervical wound is repaired without anesthesia.
In second- and third-degree tears general anesthesia is indicated.
Surgical technique. When repairing the tears, it is important to achieve good ap-
position so as to restore the anatomical shape of the cervix and ensure healing of
the wound by primary intention. The cervix is exposed with speculums and grasped
with two soft fenestrated forceps at a distance of 1.5–2 cm from the tear edge. The
edges of tear are drawn apart so as to ensure a good view of the wound angle and
provide access for repairing.
Interrupted sutures are placed 0.7 cm upward from the tear angle: the first pro-
visional clamp is led somewhat above the tear edge so as to grasp the contracted
vessels, and then one advances in the direction of the external os.
In repairing cervical tears one places single-layer interrupted sutures using syn-
thetic absorbable stitches. Sutures are placed through the entire mass of the cervix
(Fig. 26.8).
Fig. 26.8. Repair of cervical tears, common technique (single-layer interrupted sutures)
Postoperative period. The cervix does not require special care.

Complications. After delivery the cervical wall has multiple folds, so some tears
can escape notice and remain unrepaired. In such cases they can get infected form-
ing a postpartum ulcer that acts as a source of ascending infection (portal of entry
of infection). Secondary healing of unrepaired tears produces gross scars that cause
deformation of the cervix and formation of ectropion: a condition in which the
central (endocervical) columnar epithelium protrudes out through the external os
of the cervix.
26.6. UTERINE RUPTURE
Uterine rupture is disruption of uterine wall continuity during pregnancy or labor.
26.6.1. Statistics
According to various authors, uterine rupture occurs at a rate of 1 — 2:3000–
4000 deliveries. According to WHO (2006), the average rate of uterine rupture is
780 Obstetrics
0.05–0.31% the world over, after cesarean section — up to 1.0%. Uterine rupture
occurring during pregnancy is not common: about 10.0% in the structure of all
ruptures. Maternal mortality due to uterine rupture is 1–2 per 100 rupture cases
when the woman receives medical care, and amounts to 100% without care, fetal
mortality — 70%.
In Russia a classification by L.S. Persianinov (1964) is used. By the time of oc-
currence:
• during pregnancy;
• during labor.
During pregnancy ruptures mostly occur along the scar in the body and fundus of
uterus that form after uterine surgery (after cesarean section, myomectomy, perfora-
tion of uterus during abortion or D&C).
By etiology and pathogenesis:
• spontaneous (occurring without any external influence);
• forced (associated with incorrect assistance or trauma).
By localization:
• in the fundus of uterus;
• in the body of uterus;
• in the lower uterine segment;
• separation of uterus from vaginal fornix.
By the nature of lesion:
• complete rupture;
• incomplete rupture.
Complete uterine rupture is encountered 9 times more often than incomplete; it
occurs at the place where the serous coat is fused with the myometrium. In complete
rupture all uterine layers are damaged (Fig. 26.9).
Fig. 26.9. Complete uterine rupture in the area of lower uterine segment
In incomplete rupture only the mucosal and muscular layers are torn while the
peritoneum remains intact (the rupture does not extend to the abdominal cavity).
Incomplete rupture can be localized anywhere, but it mostly occurs in the lower
uterine segment on the anterior or lateral wall. In such cases hematoma of parame-
trial fat can develop.
By the clinical course:
• threatening rupture;
• ongoing rupture;
• accomplished rupture.
ICD-10 codes
• O71.0 Rupture of uterus before onset of labor.
• O71.1 Rupture of uterus during labor.

Causes of uterine rupture are varied. Two major theories explaining uterine rup-
ture exist.
26.6.3.1. Mechanical obstruction for fetal passage

In 1875 Bundle put forward the mechanical theory of rupture; it occurred due to
spatial disproportion between the presenting part and maternal pelvis.
This disproportion can occur in the following cases:
• deflected presentation and asynclitic engagement of the head;
• fetal hydrocephalus;
• contracted pelvis, especially in moderate degree;
• transverse fetal lie;
• pelvic tumor;
• scarry stricture of the cervix and vagina;
• various surgeries fixing the position of the uterus.
When there is disproportion between the presenting fetal part and maternal
pelvis, and the uterus develops powerful contractions, the body of uterus con-
tracts more and more, the main mass of muscles gradually shifting upwards to the
fundus (retraction). The mass of muscle fibers in the walls of the lower uterine
segment decreases. The lower segment thins out and distends excessively (marked
distraction). The fetus gradually advances to the thin-walled, overdistended lower
uterine segment. The cervix gets incarcerated between the fetal head and pelvic
walls (incarceration of the labium anterius mostly) which results in still greater
distension of the lower uterine segment. As labor continues, the lower segment
thins out critically, a crack develops that breaks vessels, and a hematoma develops
in the wall. The uterus gets ruptured
After complete uterine rupture and lesion of large vessels has occurred, an
abdominal hemorrhage begins. In obstetric this situation is referred to as Bandl’s
uterine rupture which corresponds to typical clinical presentations of threatening,
ongoing and accomplished uterine rupture. In incomplete uterine rupture he-
matomas develop in different places depending on the rupture location (between
782 Obstetrics
sheets of the ligamentum latum uteri, under the serous coat, in the prevesical mass).
Obstetric interventions can also serve as causative factors: excessive administration
of uterotonics, the so-called Kristeller’s maneuver, substandard performance of
vaginal obstetric surgery.
26.6.3.2. Histopathological changes of myometrium

N.Z. Ivanov in 1901, and J.D. Verbov in 1911 put forward a theory of uterine
rupture that saw the main cause of rupture in profound histopathological changes
in the myometrium developing due to inflammatory, atrophic and dystrophic pro-
cesses.
The following causes of histopathological changes are distinguished:
• scar on the uterus after previous surgery (cesarean section, myomectomy,
tubectomy in case of ectopic pregnancy) which removed the interstitial
portion of the tube, perforation resulting from intrauterine manipulations,
etc.;
• multiple intrauterine interventions (instrumental abortion, D&C);
• infantilism and malformation of genitals;
• chronic uterine infection (endomyometritis);
• grand parity (over four deliveries in history);
• polyhydramnios, multiple pregnancy;
• placenta previa or accreta;
• choioadenoma destruens.
A combination of several factors above is most common.
Verbov’s uterine rupture can present with few symptoms or asymptomatically as
they are not accompanied by pronounced clinical manifestations like Bandl’s (me-
chanical) rupture.
When the rupture is determined by histopathological changes, the altered tis-
sue in the uterine wall (like uterine scar) separates slowly (scar dehiscense) during
pregnancy or labor. Neither fetus nor mother feel any distress until the moment of
complete rupture, if there is no marked hemorrhage. Such ruptures commonly oc-
cur after abortion, uterine inflammation or uterine surgery; they account for 60%
of all ruptures.
Histopathological causes now predominate in the pathogenesis of uterine rupture,
which is associated with
• expanded indications for cesarean section which is performed on almost every
fourth pregnant woman;
• increased rate of organ-sparing surgeries in uterine rupture or uterine scar
dehiscence in previous deliveries; in uterine myoma, especially after myomectomy
through laparoscopic access without an adequate repair of suture bed;
• increased rate of reparative and plastic surgery for uterine malformations.
In modern conditions uterine scar holds the leading place in the structure of
indications for abdominal delivery.
In modern obstetric settings the major causes of uterine rupture
NB! during pregnancy are histopathological changes in the myometrium
or a combination of histopathological and mechanical forces.
26.6.4. Threatening uterine rupture

Threatening uterine rupture is an obstetric situation when no rupture or endome-
trial tear has occurred but there are signs indicating possible rupture.
Clinical features develop with the start of expulsion stage of labor; they are most
pronounced in presence of mechanical obstruction to expulsion, and somewhat less
in presence of histopathological alteration of uterine wall. Labor can be powerful
with frequent painful contractions. Outside of contractions the uterus cannot relax
completely. The parturient woman becomes restless, she shows fear of death, cries
with bad non-stopping pain in the abdomen and lumbar area, she clasps her abdo-
men, her pulse quickens.
An examination and objective investigation reveals characteristic signs of threaten-
ing uterine rupture:
• powerful labor (strong, frequent, acutely painful contractions);
• the uterus is elongated, its fundus deviates from the median line, round ligaments
are tense and tender; they can be located asymmetrically;
• high and/or oblique contraction ring (at the level of umbilicus), the uterus shows
an hour-glass shape (Fig. 26.10);
• the lower uterine segment is overdistended and thinned-out; it is tense and
acutely tender to palpation; as a result, the presenting part cannot be palpated;
• a protrusion or swelling emerges over the pubis due to edema of prevesical mass;
• spontaneous urination is made difficult by the fetal head pressing the bladder or
urethra to pelvic bones;
• the woman starts pushing involuntarily, nonproductively — in case of high head;
• vaginal examination reveals cervical edges edematous, hanging into the vagina.
There is no vaginal blood discharge; if it appears in a situation of threatening
rupture, this indicates the beginning of rupture. Continuous contractions lead to
fetal hypoxia.
Without timely, adequate intervention threatened rupture becomes

NB! uterine rupture in progress.
Fig. 26.10. High oblique position of retraction ring. Threatening uterine rupture
784 Obstetrics
26.6.5. Ongoing uterine rupture

Ongoing uterine rupture is a tear slightly involving the myometrium.
Clinical features. In this situation pronounced signs of threatening rupture are
complemented by new signs caused by myometrial trauma and development of a
hematoma in it: signs of pain shock, external bleeding.
Fetal condition deteriorates (fetal tachycardia or bradycardia, increased motor
activity, meconium seen in amniotic fluid when the fetus is in cephalic presentation),
and fetal demise occurs.
NB! If immediate care is not provided, the uterus ruptures.
26.6.6. Accomplished uterine rupture

Accomplished uterine rupture is partial or complete loss of continuity in uterine wall.
Classification. Accomplished uterine rupture can be complete or incomplete.
• Accomplished incomplete rupture is rupture of the mucous and muscular layers
while the serous coat continuity is intact.
• Accomplished complete uterine rupture is rupture going through all three layers
in uterine wall.
Ruptures commonly occur in the lower uterine segment.
Clinical features. At the moment of rupture the parturient woman experiences
acute stabbing pain, sensation of bursting. Labor discontinues immediately.
According to Genter, an accomplished uterine rupture is when
NB! in the delivery room an ominous silence hangs following the
puerperant woman’s cries and agitation.
The patient stops crying, becomes apathetic. Characteristic signs of pain and/
or hemorrhagic shock develop. First the shock is due to critical irritation of the
peritoneum, a change in intraabdominal pressure. Later the shock is aggravated by
hemorrhage and development of hemorrhagic shock. The skin becomes pale, the
pupils dilate, the eyes become sunken, the pulse grows more frequent, its strength
decreases, BP drops, the patient shows cold sweat, her respiration becomes shallow,
she develops nausea, vomiting, dizziness, loss of consciousness. The severity of the
patient’s condition depends on the volume of blood loss and the nature of rupture
(complete or incomplete); as a rule, fetal demise ensues.
In case of complete uterine rupture the abdomen shows a different shape, the
abdominal wall is no longer tense, contraction ring and strain of round uterine liga-
ments disappear. The fetus escapes to the abdominal cavity, completely or partially,
so palpation distinctly detects fetal parts immediately behind the abdominal wall.
The placenta separates from the uterine wall and prolapses into the abdominal cavity
together with the fetus. Well contracted uterus is palpated near the fetus. The fetus
dies at once, its heartbeat ceases. External bleeding is not usually intensive as the
blood escapes to the abdominal cavity.
In case of incomplete uterine rupture the presentations are less pronounced as
there is no intraabdominal hemorrhage. The rupture is localized in the lower uterine
segment, usually along the sidewall; hematoma develops in the parametrial mass
between the sheets of ligamentum latum uteri. There may be no external bleeding. As
a hematoma develops, the patient feels acute pain in the lower abdomen irradiating
to the sacrum and leg. If a large vessel ruptures and blood loss is considerable, there
develop signs of internal hemorrhage, hemorrhagic shock develops. When incomplete
uterine rupture is undiagnosed, the fetus can be born by a vaginal delivery. In this
case there are the following signs of incomplete rupture:
• grey coloration of skin;
• apparently groundless tachycardia;
• arterial hypotension;
• uterine bleeding;
• possible presence of a tense elastic mass in the pelvis, near a well-contracted
uterus.
The final diagnosis is made by a manual examination of uterine walls in the early
postpartum period or by ultrasound in the late postpartum period.
When incomplete uterine rupture remains undiagnosed, endometritis signs develop
several days after childbirth:
• frequent pulse;
• elevated body temperature;
• hemorrhage;
• lower abdominal pain irradiating to the leg;
• abdominal distension;
• lochia not typical of the postpartum day;
• progressing anemia, etc.
Clinical presentations depend on localization, size and nature of
NB! rupture, intensity of bleeding.
26.6.7. Rupture in deficient uterine scar

A deficient uterine scar implies a constant risk of its rupture. Regarding clinical
presentations, the rupture is classified as threatening, ongoing and accomplished.
Ruptures occur during pregnancy, in the first and second stage of labor.

Abnormal alterations in myometrial tissue obscure the signs of uterine rupture.
Pregnant and parturient women with scar on the uterus do not show marked clinical
manifestations of threatening and ongoing uterine rupture.
• In pregnancy ruptures occur less often than in labor. As the fetus grows, the
uterus distends, cicatricial tissue also stretches and dehisces.
• In threatened uterine rupture along the scar the manifestations are associated with
excessive stretching of cicatricial tissue and the peritoneum that covers it: nausea,
vomiting, pain in the upper abdomen and at the site of the scar that intensifies upon
fetal movements. Palpation of the scar reveals its tenderness, pits and protrusions.
• In ongoing uterine rupture a hematoma develops at the site of cicatricial tissue.
The woman complains of nausea, vomiting, dizziness, pain at the site of the scar.
Palpation of the abdomen shows increased uterine tone, its tenderness and signs
of acute fetal hypoxia. Discharge of blood is seen from the vagina.
786 Obstetrics
• In accomplished uterine rupture the manifestations develop gradually, not all

signs are present. There may be no marked signs of hemorrhagic and pain shock.
Fetal demise occurs often, but not always.
If a pregnant or parturient woman has a uterine scar, one should assess its com-
petence in advance, preferably before the onset of pregnancy. Methods of diagnosing
the competence of uterine scar outside of pregnancy are as follows:
• hysterosalpingography;
• hysteroscopy on day 4–5 of menstrual period;
• ultrasound (bicontrast echography);
• MRI.
Uterine scar is considered deficient, if
• previous cesarean section was performed less than 2 years ago;
• there was fever in the postoperative period;
• the scar healed by secondary intention;
• previous corporeal cesarean section;
• the placenta is located in the area of the scar;
• the patient had abdominal pain in the present pregnancy or vaginal bleeding long
before delivery;
• the scar is tender to palpation or upon fetal movements;
• in the area of the scar the skin has fused with underlying tissue of the anterior
abdominal wall, the scar has uneven surface, the niche sign develops.
In most pregnant patients the condition of the scar is assessed by ultrasound; the
examination checks for niches, alterations in the thickness and structure of cicatricial
tissue, presence of connective tissue. A scar is considered deficient if it is less than
1 mm thick along the entire length or in some areas. There are no reliable criteria
for assessment of scar deficiency in pregnancy. The condition of the scar can be
verified using MRI.
In case of threatening rupture during childbirth the signs noted during pregnancy
are complemented by uncoordinated labor, apathy. Contractions or pushing efforts
attenuate or subside, and blood is discharged from the vagina.
While the cervix is fully dilated, contractions are painful and unproductive,
the fetal advance is detained. Clinical presentations can be marked or inap-
parent.
In the postpartum period uterine rupture can be suspected only from abnormal
blood loss, progressing signs of hemorrhagic shock.
The diagnosis of uterine rupture is made by clinical signs. Diagnosis is difficult in
case of rupture along the scar, incomplete rupture, especially in the lower segment
when clinical signs are not pronounced. Such ruptures may remain undiagnosed for
some time after delivery. There are two or three distinctly pronounced signs helping
to distinguish uterine rupture along the scar.
Such pronounced signs are as follows:
• peritoneal irritation: tenderness to palpation, spontaneous abdominal pain,
abdominal distension, hiccups, nausea, vomiting;
• crunching sensation when palpating the anterior abdominal wall;
• progressing subperitoneal hematoma in the form of soft tumor located near the
uterus and spreading upward along the lateral pelvic wall;
• sudden skin pallor, frequent pulse, loss of strength while the patient is fully
conscious;
• floating fetal head which was previously fixed at the pelvic inlet;
• sudden bleeding after cessation of labor;
• absence of fetal heartbeat;
• the fetus or its parts are palpable right under the abdominal wall.
In marginal cases, if uterine rupture is suspected after delivery,

NB! as well as after vaginal surgery, one should always perform a
manual examination of uterine walls and speculum examination
of the cervix.
Uterine rupture in pregnancy is differentially diagnosed with acute appendicitis,

renal colic, bowel obstruction and placental abruption. Carefully taken history, ob-
jective examination, ultrasound and fetal assessment are helpful in making the final
diagnosis.
26.6.7.4. Treatment
When signs of threatening uterine rupture develop, labor should

NB! be immediately terminated with a cesarean section.
Before surgery begins, heavy sedation is administered so as to stop labor. The

operating unit should have equipment for autoerythrocyte reinfusion.
At ongoing and accomplished uterine rupture immediate

NB! laparotomy is indicated. The less time until surgery, the better
immediate outcomes.
The extent of surgical intervention depends on the puerpera’s condition, the na-
ture and location of the rupture. Nowadays organ-saving surgery is often performed.
During surgery, the fetus, placenta and escaped blood are removed from the ab-
dominal cavity. After debriding the wound edges the rupture is repaired; hysterectomy
is performed very seldom.
After extracting the fetus and afterbirth one should examine

NB! uterine walls carefully; the detected lacerations are repaired.
After closing the uterine rupture a thorough revision of abdominal
organs is indicated.
788 Obstetrics
Prior to the start of surgery and after its completion one administers anti-shock
therapy and blood loss restoration according to general principles, and antibacterial
therapy is initiated.
If accomplished uterine rupture is not diagnosed during labor or early postpartum
period, over several days the patient develops signs of severe puruloseptic process or
hemorrhage in late postpartum period.
26.6.8. Surgical techniques used in uterine rupture

In uterine rupture the abdominal cavity is opened with an incision along the
middle line from the pubis to umbilicus (lower midline access). If the fetus is in the
abdominal cavity, it is removed together with the secundines. The uterus is grasped
with a hand and carefully drawn out of the wound. It is inspected; the size and nature
of rupture is established to determine the extent of surgery.
First of all, one should achieve complete hemostasis. In case of incomplete rupture
and hematoma under its peritoneal cover, the peritoneum is dissected, fluid blood
and clots are removed, damaged vessels are ligated. If rupture occurred in the side-
wall and there is a hematoma in parametrium, one has to ligate the uterine artery at
the site of its separation from internal iliac artery or ligate the internal iliac artery.
Once hemostasis has been achieved, one excises the crushed wound edges or the
remnants of old scar with scissors or scalpel, which promotes satisfactory apposition
of wound edges. The wound is repaired by the same method as in cesarean sec-
tion. Peritoneal repair is done by placing running sutures. For peritoneal autoplasty
one can use the peritoneum of uterovesical fold or round ligament. The peritoneal
cavity is dried, the anterior abdominal wall is repaired layer-by-layer. If anatomi-
cal continuity of the uterus cannot be restored, supracervical uterus amputation or
hysterectomy is indicated.
26.7. ACUTE UTERINE INVERSION
Acute uterine inversion is a rare, severe obstetric complication when the body of
uterus escapes beyond the vagina turning with its mucosa inside out, together with
the attached placenta.
The rate of uterine inversion is 1:40,000 deliveries.
Complete and incomplete uterine inversion are distinguished:
• in incomplete inversion the fundus does not escape outside the external os;
• in complete inversion the entire uterus is in the vagina sometimes coming out of
the pudendal fissure; sometimes complete uterine inversion is accompanied by
inversion of the vagina.
Uterine inversion can be acute or chronic. Acute inversion is more common; 3/4
in the postpartum period, ¼ — during the first day after childbirth.
Regarding its cause, uterine inversion is divided into:
• forced inversion (abrupt tugging at the cord, rough handling when doing Crede
maneuver, failure to follow the algorithm of managing the third stage of labor;
• spontaneous inversion (abrupt relaxation of uterine muscle and elevated
intraabdominal pressure upon coughing or vomiting).
ICD-10 code
• O71.2 Postpartum inversion of uterus.
26.7.3. Etiology
Forced uterine inversion occurs during active management of the third stage of
labor or Crede maneuver (after the placenta has separated) when one does not fol-
low the strict order of actions. Crede maneuver requires a stage-by-stage approach:
emptying the bladder, bringing the uterus to median position, patting the uterus
lightly to promote its contraction, gripping the fundus with hands while simultane-
ously pressing on the uterus in two crisscross directions. Fundal attachment of the
placenta predisposes for inversion.
The main cause of spontaneous uterine inversion is relaxation of all uterine com-
partments and ligaments, loss of myometrial elasticity. In this condition, inversion
can be triggered even by elevated intraabdominal pressure upon pushing, coughing or
sneezing. Rarely, inversion occurs upon expulsion of a tumor on a short inextensible
peduncle (polyp, submucous myoma or sarcoma) from the uterine cavity.
First a recess is formed in the area of fundus (funnel of inversion); it draws in
uterine tubes, round and broad uterine ligaments, and sometimes the ovaries. Then
the funnel increases, the inverted uterine body can descend to the vagina through
the cervical canal.

Sudden acute pain develops in the lower abdomen followed by shock and uterine
hemorrhage. Hemorrhage can begin before inversion due to atony, and persist after
inversion has completed. In incomplete inversion the patient’s general condition does
not show a fast, abrupt deterioration.
26.7.6. Diagnostics
Uterine inversion is followed by acute abdominal pain and pain shock. Bright red
uterine mucosa turned inside out emerges from the pudendal fissure; sometimes the
uterus turns inside out together with the attached placenta. Complete uterine inver-
sion can be accompanied by inversion of the vagina. In this case the uterus is outside
the vulva, and diagnosis is easy. In incomplete inversion the uterus is detected in the
790 Obstetrics
vagina during a speculum examination. In both cases the uterus cannot be palpated
above the pubis.

Uterine inversion is differentially diagnosed from other complications (uterine
rupture, for instance) by bimanual examination which detects upper uterine border
in a position unusually low for the third stage of labor or postpartum period , and
a funnel-like depression in place of uterus.
26.7.8. Treatment
The postpartum uterus is replaced manually following manual removal of the
placenta under anesthesia.
Before surgery, anti-shock therapy is administered, the bladder is emptied. Uterine
mucosa and vaginal walls are swabbed with antiseptics and Vaseline oil, which pro-
motes replacement.
Under anesthesia, the uterus is carefully replaced through the external orifice.
Stages of surgery
• The inverted uterus is grasped by a hand so that the palm is at the fundus, and
fingertips — at the cervix resting against the posterior vaginal fornix.
• Pressing on the uterus with the entire hand one first replaces the inverted vagina in
the pelvic cavity, and then replaces the uterus starting with the fundus or isthmus.
• The left hand is on the lower abdominal wall and moves to meet the replaced
uterus.
In recent uterine inversion the replacement is not usually problematic. All manipula-
tions are performed with extreme care without rough handling since, given the shock
and hemorrhage, release of thromboplastic substance from the uterus into the blood-
stream can result in disorder of coagulation and intensified hemorrhage. Uterotonics
are administered immediately after surgery and continued for several days.
If manual replacement fails, laparotomy is performed, and the inverted uterus is
replaced by extero-internal technique.
Postoperative period. Antibiotic therapy, uterotonics for no less than 5 days are
indicated.
Complications: puruloseptic disease, thromboembolism.
26.7.9. Prognosis
With timely diagnosis and adequate treatment the prognosis is favorable. Without
emergency care the patient dies of shock and blood loss, in subsequent days — of
infection (peritonitis, sepsis).
26.7.10. Prevention
Prevention of uterine inversion consists in adequate management of the third stage
of labor, manual removal of the afterbirth once there are signs of placenta separation.
26.8. OVERSTRAIN AND RUPTURE OF PELVIC JOINTS
Lesser pelvis trauma is a sprain or tear of the pubic or sacroiliac symphysis dur-
ing labor.
ICD — 10 codes
• O71.5 Other obstetric injury to pelvic organs.
• O71.6 Obstetric damage to pelvic joints and ligaments.
Etiology and pathogenesis. Excessive softening of pubic symphysis sometimes de-
velops in pregnancy (symphysitis, symphysiopathy). These alterations are considered
to be suppressed osteomalacia. In presence of fetal macrosomia or postterm fetus,
contracted pelvis or CPD, assisted delivery (obstetric forceps, vacuum extraction,
total breech extraction, embryotomy) the softened symphysis begin to stretch, pubic
bones separating for more than 0.5 cm. When the pubic symphysis ruptures, pubic
bones can be displaced damaging the urethra, clitoris and bladder. Sacroiliac sym-
physis stretches as well. Hemorrhage develops in the joints followed by inflammation
in the late postpartum period.
Clinical features. Pelvic injury causes pain in the area of pubic symphysis, sacrum,
and coccyx in the first 3 days postpartum; the pain gets worse when the patient
spreads her legs apart or walks. Her gait is disordered. Signs of inflammation in the
traumatized area can appear: hematoma, hyperemia, edema of surrounding tissues.
Diagnostics. Injury of pelvic symphysis is detected upon examination and palpa-
tion; one reveals edema, tenderness, depression between the separated ends of pubic
bones. The diagnosis is confirmed by ultrasound and X-ray of pelvic bones.
Treatment is administered by a traumatologist; it can consist in conservative
therapy (rest, tight pelvic dressings, wearing a support). In case of rupture of pubic
symphysis or considerable separation of bones surgery is required. A history of such
complications is an indication for an abdominal delivery.
REMEMBER!
Uterine rupture
Definition Uterine rupture is loss of continuity of uterine walls in

pregnancy or labor.
Epidemiology 1–2 per 3000–4000 deliveries. In pregnancy it accounts
for 10.0% of all ruptures. Maternal mortality is 1–2 per
100 ruptures
Etiology and patho- Bandl’s theory (mechanical theory of rupture). Verbov’s
genesis theory (histopathological theory of rupture)
Classification By the time of occurrence, etiology and pathogenesis,
location, extent of damage, clinical course (threatening
rupture, ongoing rupture, accomplished rupture)
Clinical features Threatening and ongoing rupture is accompanied by active
labor, accomplished rupture — by cessation of labor.
792 Obstetrics
Diagnostics Past history, clinical presentations, objective findings,

ultrasound findings.
Algorithm of actions Threatening rupture: arresting labor, fast abdominal
delivery.
Ongoing and accomplished rupture:
Immediate laparotomy. The extent of surgery depends on
the patient’s condition, nature of damage and location of
rupture. Organ-saving surgery is preferable
Complications Hemorrhagic and pain shock, DIC
Perineal tear
Definition Perineal tear is loss of continuity of perineal tissue during
expulsion of fetus
Epidemiology The most common obstetric trauma occurring in 7–15%
of all deliveries; in primiparas noted 2–3 times more often
than in secundiparas
Etiology Inadequate assistance in labor, precipitous labor, labor
abnormalities, contracted pelvis, fetal macrosomia,
deflected presentation, obstetric maneuver, tissue rigid-
ity, disorder of genital microbial ecology (vaginitis, vagi-
nosis)
Classification By etiology, extent of damage (4 degrees), by clinical
course (threatening tear, ongoing tear, accomplished tear)
Clinical features Threatening tear: bulging of perineum, cyanosis,

edema, blanching. Ongoing tear: cracks in epidermis.
Accomplished tear: asymmetry and gaping of the vulva
Diagnostics Examination
Treatment Surgical treatment: repair of the perineal tear. Repair

of third- and fourth-degree tears is a demanding task
requiring expertise in anatomy and good surgical skills
(repair is performed by the attending obstetrician-
gynecologist)
Complications Infection of the wound, scar dehiscence, healing by

secondary intention
CONTROL QUESTIONS
1. Causes of uterine rupture.

2. Classification of uterine rupture.
3. Clinical presentations of threatening uterine rupture.
4. Management of threatening uterine rupture.
5. Clinical presentations of ongoing uterine rupture.

6. Management of ongoing uterine rupture.
7. Clinical presentations of accomplished uterine rupture.
8. Management of accomplished uterine rupture.
9. Causes of vaginal laceration.
10. Classification of vaginal laceration.
11. Methods of repairing vaginal laceration.
12. Classification of perineal tears.
13. Causes of perineal tears.
14. Clinical manifestations of threatening perineal tear.
15. Technique of repairing first- and second-degree perineal tear.
16. Technique of repairing third- and fourth-degree perineal tear.
17. Diagnostics and management of postpartum hematoma.
18. Diagnostics and management of injury to pubic symphysis.
19. Diagnostics and management of injury to vagina.
20. Diagnostics, management and prevention of postpartum fistula.
CHECK YOURSELF!
Level 1. Test
Select one or more corrects answers
1. According to Bandl, uterine rupture is caused by:
a) uterine scar;
b) inflammatory disease of uterus;
c) polyhydramnios;
d) uterine inertia;
e) cephalopelvic disproportion.
2. According to J.D. Verbov, uterine rupture is caused by:

a) infantilism and malformation of uterus;
b) premature membrane rupture;
c) scar on uterus after previous surgery;
d) transverse fetal lie;
e) amniotomy.
3. Accomplished uterine rupture is accompanied by:

a) cessation of fetal heartbeat;
b) premature rupture of membranes;
c) involuntary urination;
d) acute abdominal pain;
e) cessation of labor.
794 Obstetrics
4. In case of threatening uterine rupture one should:

a) apply obstetric forceps;
b) augment labor by oxytocin;
c) arrest labor;
d) terminate the delivery with cesarean section.
5. Causes of uterine rupture in labor:

a) inflammatory and cicatricial alterations;
b) manual examination of uterine cavity;
c) fetal macrosomia;
d) obstetric forceps;
e) amniotomy;
6. Cervical laceration is diagnosed by:

a) vaginal hemorrhage;
b) manual exploration of uterine walls;
c) speculum examination of birth canal;
d) ultrasound.
7. Causes of perineal tear in labor:

a) tissue rigidity, high perineum;
b) uterine inertia;
c) late amniotomy;
d) head crowning with its largest diameter;
e) precipitous labor.
8. Fourth-degree perineal tear may result in:

a) cicatricial deformity of cervix;
b) rectovaginal fistula;
c) urine incontinence;
d) flatus incontinence.
9. Causes of vaginal tear in labor:

a) fetal macrosomia;
b) precipitous labor;
c) amniotomy;
d) uterine inertia;
e) vaginitis.
10. Management of progressing postpartum hematoma:

a) observation;
b) opening the hematoma and ligating the vessels;
c) examination of cervix;
d) vaginal tight tamponade;
e) antianemic therapy.

1. In the second stage of vaginal delivery the parturient woman complains of inces-
sant contractions. An examination reveals that the lower uterine segment does not
relax. Fetal heart rate 180–200 per minute. Vasten’s sign at the same level. What is
your diagnosis? What is your plan of management?
2. At the end of the first stage of labor the parturient woman complains of acute
abdominal pain. Fetal heartbeat cannot be heard. Blood discharges from the vagina.
NOTES
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• Chapter 27
OPERATIVE OBSTETRICS
27.1. PREGNANCY-PRESERVING SURGICAL PROCEDURES
Pregnancy-preserving surgery is aimed at surgical correction of anatomical mal-

formations that promote miscarriage.
The rate of structural alterations of cervix in patients with recurrent miscarriage
requiring surgery is 10–16%. Structural causes of recurrent miscarriage include cer-
vical insufficiency which is recognized as the most common cause of miscarriage in
the second trimester (see Section 21.1.4.2).
Pregnancy-preserving surgery can be performed both during and outside of preg-
nancy. Its objective is eliminating structural causes of miscarriage.
All surgeries aimed at treating structural cervical insufficiency are divided into:
• those performed in pregnancy:
• surgery on the internal os (cervical cerclage);
• surgery on vaginal part of cervix;
• surgery closing the external os (no longer performed nowadays);
• those performed outside of pregnancy:
• plastic surgery on the cervix.

Indications for surgical treatment of cervical incompetence:
• spontaneous abortion in the second trimester and preterm delivery in past
history;
• progressing cervical incompetence (findings of clinical examination): altered
cervical consistency, shortened cervix (ultrasound findings), gradual dilation of
cervical canal and internal os.
Prerequisites for surgical treatment of cervical incompetence in pregnancy:
• gestational age 12–16 weeks;
• no fetal malformations;
• intact gestational sac;
• normal uterine tone;
• o genital inflammation, normal vaginal flora;
Chapter 27. Operative obstetrics 797
• no severe somatic disease or severe complications of pregnancy;

• no vaginal bleeding.
Contraindications for surgical treatment of cervical incompetence:
• disease or abnormal condition incompatible with pregnancy;
• hemorrhage during pregnancy;
• increased uterine tone;
• fetal malformations;
• acute infection of the lower genitourinary tract.
To enhance the effectiveness of surgery, standard medicinal

NB! therapy is administered a week before and after surgery. The
therapy is aimed at controlling uterine hypertone and preventing
infectious complications: bacteriological study and elimination
of microflora implicated in development of chorioamnionitis and
endometritis.
27.1.3.1. Treatment of cervical insufficiency in non-pregnant women

Outside of pregnancy, the cervix is difficult to assess; an assessment cannot provide
reliable information about the possibility of cervical insufficiency (or incompetence)
in pregnancy. Such an assessment is only possible in case of posttraumatic cervical
incompetence accompanied by gross deformity.
Whether it is worthwhile to have plastic reconstruction of the cervix is a decision
made by an obstetrician gynecologist after studying the patient’s history (number of
late abortions, ineffectiveness of other methods of treatment including repair of cervix
during pregnancy), the condition of cervix, the possibilities offered by surgery in each
particular case. Plastic reconstruction of the cervix performed outside of pregnancy
does not exclude surgery on the cervix during pregnancy.
In patients with recurrent miscarriage and cervical incompetence preoperative
preparation for pregnancy should begin with vaginal culture test. An examination
prior to surgery includes culture test of vaginal and cervical canal discharge, and
correction of detected abnormalities.
Anesthesia. If there are no contraindications, epidural nerve block or spinal an-
esthesia are preferable as the safest methods of analgesia. Nitrous oxide anesthesia
with artificial lung ventilation is administered less often.
Technique of plastic reconstruction of the cervix by Yeltsov-Strelkov dissection
method (Fig. 27.1).
• The first stage of surgery consists in exposing and bringing down the cervix (after
appropriate swabbing of external genitals, vagina and cervix); the cervix is fixed
with bullet forceps vulsellum and brought down to the maximum.
• The second stage is dissection of the cervix (by sharp dissection full length
along the lateral walls in old lacerations or according to the location of glandular
muscular hypertrophy) [Fig. 27.1 (1, 2)].
• The third stage is dissection of the cervix with excision of pathologically altered
tissue and edges of old lacerations from both flaps (anterior and posterior flaps
are dissected full length along the muscular layer) [Fig. 27.1(3)].
798 Obstetrics
• The fourth stage is constructing a cervical canal (with internal flaps) [Fig. 27.1
(4, 5)].
• The fifth stage is conclusive construction of the vaginal portion of cervix as a
whole (with external flaps). The newly constructed cervical canal has a spindle
shape which allows preservation of the mucus plug [Fig. 27.7 (6)].
27.1.3.2. Treatment of cervical insufficiency in pregnant women

The research on and technique of surgery for cervical incompetence was first pro-
posed by Shirodkar and McDonald. Shirodkar cerclage consists in placing a circular
suture (made of nylon) on the cervix in the area of internal os after dissecting the wall
and elevating the bladder. This technique is widely used in contemporary obstetric
practice for recurrent miscarriage in pregnant women at high risk.
1 2 3
4 5 6
Fig. 27.1. Plastic reconstruction of the cervix by Yeltsov-Strelkov (digits indicate the stages of
the procedure)
The XXIInd congress of the International Federation of Gynecology and Obstetrics

(FIGO) recognized the technique of Shirodkar cerclage (placing circular sutures in
internal os area burying the stitches in the cervical mucosa almost completely) the
most effective method of prolonging pregnancy.
U-shaped sutures on the cervix by A. Lyubimova method. The cervix is punctured
with a needle with permanent suture at the mucosal border of anterior vaginal fornix
retracting 0.5 cm from the middle line; the needle goes the whole depth and exits
at the posterior fornix. The suture end is passed to the lateral fornix on the left, the
needle goes through the mucosa and a part of cervix; the entry hole is 0.5 cm left
of the middle line. The end of the other suture is passed to the lateral fornix on
the right; the needle goes through the mucosa and a part of uterus and exits at the
anterior fornix.
Repair of cervix by V. Sidelnikova method (in case of gross tears of cervix on one
or two sides). The first purse-string suture is placed somewhat above the cervical
tear. The second purse-string suture is placed 1.5 cm below the first one through
the depth of cervix from one edge of tear to the other passing the suture circularly
along the circumference. The sutures are tied.
Prolapse of the gestational sac requires a quite challenging technique of placing
sutures in the cervix. A technique proposed by A.M. Fuks is an effective modifica-
tion of the cerclage technique: repair of the cervix with a metreurynter introduced
into the cervical canal which supports the prolapsing gestational sac and safeguards
against amniotic rupture during surgery.
Randomized studies showed no statistically significant evidence in favor of preg-
nancy prolongation after surgery for cervical incompetence.
In Europe vaginal pessary (Vitsky, 1961) was used instead of cerclage for
cervical incompetence as an alternative to the invasive treatment (Fig. 27.2).
In Russia this method is now used in the second and third trimesters (before
34 weeks gestation).
If there are signs of bacterial vaginosis or vaginitis, adequate

NB! therapy and restoration of vaginal flora is administered before
surgery or pessary introduction.
Management of postoperative period in pregnancy.

• The patient can get up and move about immediately after surgery.
• The vagina and cervix are swabbed with antiseptics for the first 3–5 days.
Fig. 27.2. Vaginal pessaries in cervical insufficiency

800 Obstetrics
• The following medicines are administered for the purpose of treatment and
prevention:
– progesterone line medicines;
– nonsteroid anti-inflammatory drugs (indomethacin 50 mg or 100 mg once
rectally in case of increased uterine tone) as emergency therapy.
• The patient is discharged on day 5 (in case of uneventful postoperative period).
• The condition of cervix is assessed in outpatient settings.
Complications of surgery:
• threatening spontaneous abortion;
• hemorrhage;
• rupture of amniotic membranes;
• necrosis;
• sutures cutting through the cervix;
• bedsores, fistulas;
• circular separation of the cervix (sutures in the cervix, onset of labor).
If uterine hypertone persists and the pregnant woman has

NB! cramplike pain, she should be hospitalized. Stitches in the cervix
should be taken out.
Indications for suture removal:

• gestational age 37 weeks;
• at any gestational age:
• leakage of amniotic fluid, rupture of membranes;
• vaginal bleeding;
• sutures cutting through the tissues (development of fistula);
• onset of regular labor.
REMEMBER!
Pregnancy-preserving procedures are aimed at surgical correction of structural
alterations that promote miscarriage.
Classification:
Surgery performed outside of pregnancy (plastic reconstruction of the cervix by
Yeltsov-Strelkov dissection method).
In pregnancy surgical procedures consist in placing sutures on the cervix. Vaginal
pessary is an alternative to surgical treatment of cervical incompetence.
Indications for intervention: cervical insufficiency
Prerequisites:
gestational age 12–16 weeks;
intact gestational sac;
no genital inflammation; vaginal flora within normal;
no severe somatic disease or severe complications of pregnancy;
no vaginal bleeding.
Preparation: complete clinical investigation before surgery, ultrasound repeated

over time.
Anesthesia: epidural nerve block, spinal anesthesia, endotracheal narcosis with
nitric oxide.
The objective of surgery is artificial construction of anatomical continuity in the
internal os of cervix.
Complications: abortion, hemorrhage, cervicovaginal fistula.
27.2. OBSTETRIC VERSION
Obstetric version is a procedure that manually changes an unfavorable fetal posi-

tion (presentation) over to another, more favorable, always longitudinal, position.
ICD-10 code
• O32 Maternal care for known or suspected malpresentation of fetus.
Classification
Procedures improving fetal presentation include:
• external cephalic version;
• classical external / internal podalic version upon full cervical dilation.
27.2.1. External cephalic version

External cephalic version is a process by which the fetus is brought from unfavor-
able lie or malpresentation to longitudinal lie and cephalic presentation with the help
of manipulations through the anterior abdominal wall.
Labor with unfavorable lie and pelvic presentation is always accompanied by
multiple complications which prompted obstetricians and midwives to search for
prevention from the earliest times. One of such methods is preventive cephalic version
performed in pregnancy. This technique fell into oblivion from time to time and then
was rediscovered. In mid-1950s B. Arkhangelsky advocated its use in breech presen-
tation. In late 1980s obstetricians both in Russia and abroad deemed it appropriate
to give up external cephalic version as the procedure is not always effective and can
cause severe complications (premature rupture of membranes, placental abruption,
uterine rupture, acute hypoxia and fetal demise). Nonetheless, over the recent decade
external cephalic version has regained popularity as a means of decreasing the rate
of cesarean section.
The mean rate of successful attempts is 50%; the success rate is higher in mul-
tiparous women.
The optimum gestational age for cephalic version is 37 weeks as in

NB! case of complications and emergency delivery the fetus will be viable.
Indications: transverse, oblique lie and breech presentation.

Prerequisites: gestational age 37 weeks (term pregnancy), satisfactory mater-
nal and fetal condition, accurately diagnosed fetal lie, position, attitude and
802 Obstetrics
presentation, no tension in the abdominal wall or uterus, fetus mobile in the

uterus (amniotic fluid intact), head size matches the pelvis, possibility of to-
colysis and CTG, available operating room, a team of qualified specialists on
call, empty bladder.
Contraindications: PE, threatened abortion, multiple pregnancy, polyhydramnios,
oligohydramnios, placenta previa, contracted pelvis, spontaneous abortion and pre-
term birth in history, uterine malformations, scar on uterus, myoma of uterus, ma-
ternal extragenital disease, fetal macrosomia, hemorrhage in the preceding 7 days,
areactive CTG.
Preparation. The version is performed by an experienced doctor with the patient’s
consent, in maternal hospital setting only. The patient comes to surgery in fasting
state after emptying the bowel with a laxative and enema on the eve. The bladder is
emptied right before surgery.
The pregnant woman wearing only a shift is laid on a hard coach on her back.
The doctor sits down on her right, establishes fetal lie, position, attitude and aspect
using external manipulations. For more accurate diagnosis ultrasound is used. CTG
is done for no less than 20 minutes.
Anesthesia is not indicated. IV administration of tocolytics is indicated during the
procedure.
Technique of manipulation. Talcum powder is applied to the patient’s abdomen.
In case of transverse or oblique lie the hands are placed of the head and pelvic pole
of the fetus. The head is slowly moved to the iliac region and then — to the pelvic
inlet. The other hand moves the pelvic pole to the fundus.
In case of pelvic presentation one manipulates carefully using both hands: the
buttocks are moved from the pelvic inlet high upward, above the iliac crest and the
head is moved downward. The version is considered complete when the head is above
the pelvic inlet and the buttocks are at the fundus. A control ultrasound examination
is done immediately after completing the version (Fig. 27.3).
An ultrasound is administered for more precise diagnosis of fetal

NB! lie, position, position variety and presentation.
Fig. 27.3. External cephalic version

Possible complications:
• acute fetal hypoxia;
• placental abruption;
• premature membrane rupture;
• fetomaternal transfusion.
After a successful or failed attempt at cephalic version a Rh-negative patient should
be administered a preventive dose of Rh0(D) immunoglobulin (300 mcg).
A non-stress test is adminsitered immediately upon performing the

NB! version.
27.2.2. Classical external & internal podalic version

Classical podalic version is a procedure that manipulates the fetus within the
uterus into a longitudinal lie, and always to pelvic presentation. In contemporary
obstetric practice it is employed in case of twin pregnancy after the first fetus has
been delivered when the second fetus is in unfavorable position.
The procedure is performed during labor. One hand that will perform the version
is introduced into the uterus while the other one is helping through the anterior
abdominal wall.
Podalic version has a long history. It was used in labor when the fetus showed
unfavorable lie, presentation or engagement (brow presentation, mentoanterior posi-
tion, persistent occiput direct position). Delivery was often brought to a completion
using this technique in case of prolapse of the cord or small fetal parts in transverse
lie and cephalic presentation as well as in maternal and fetal conditions that required
a prompt termination of labor.
In contemporary obstetric practice such unfavorable situations are resolved by a
cesarean section.
Indications: transverse and oblique lie while cesarean section is not possible.
Such a situation occurs when the second twin of a twin pregnancy is in transverse
or oblique lie. Podalic version must be followed by the procedure of total breech
extraction which is often associated with severe fetal complications, so in twin preg-
nancies indications for cesarean section are extended to the second twin, especially
in primiparous women.
Podalic version is dangerous for the fetus so it is resorted to in

NB! a transverse lie only if the fetus is extremely premature or if the
second twin is in malposition after the first twin has been delivered.
Contraindications:
• uterine scar;
• impacted transverse lie.
Prerequisites:
• fully dilated cervix;
• fetal mobility;
804 Obstetrics
• accurate information about fetal position;

• appropriate condition of the uterus and pelvis;
• possibility of a vaginal birth;
• satisfactory fetal condition, intact gestational sac or recent rupture of membranes.
The first two prerequisites are absolute ones. If the cervix is not fully dilated, one
cannot reach one’s hand into the uterine cavity.
If fetal mobility is limited, and especially if it is immobile, podalic

NB! version is contraindicated as uterine rupture is imminent in this
case.
Preparation. Fetal position and condition of birth canal are carefully examined
using ultrasound and a vaginal examination. The bladder must be emptied.
Technique. The procedure consists of three steps (Fig. 27.4):
• choice of hand and its introduction into the uterine cavity;
• locating and capturing the leg;
• version proper.
The first step is choice of the hand and its introduction. The obstetrician uses
the more skilled hand, usually the right one. It is believed that in left fetal position
it is more convenient to introduce the left hand, and in right fetal position — the
right hand. The other hand remaining outside draws the vulvar lips apart and fixes
the uterus during the version. During the first step one should pay attention to the
following.
To introduce the hand one stretches and draws all fingers together to give the
hand a cone shape. The fingers of the other hand draw the vulvar lips apart; and the
cone-shaped hand with the dorsal surface facing backward easily slips into the uterine
cavity through the vagina. The hand must be introduced outside of contractions. If
the gestational sac is intact, it is opened in the center, and the hand is immediately
introduced into the uterus trying to prevent a rapid passage of waters. The hand
should pass by the promontory. If the presenting head obstructs the passage of the
hand, it is gently pushed upward with the internal hand and drawn in the direction
of the back helping with the outside hand. In case of a transverse lie the presenting
shoulder is moved away in the same fashion.
The second step of procedure is capture of the leg. The step consists of three con-
secutive stages. The leg located anteriorly, that is, closer to the maternal abdominal
wall, is more favorable for further manipulations. This leg is usually below the other
one, so it is easy to locate. To locate the leg, the hand whose palmar surface is fac-
ing fetal ventral surface advances along the fetus while there is no contraction. The
hand inside the uterus either moves directly to the site where the legs are supposed
to be (short way), or glides laterally of the head or axilla to the gluteal area; here the
hand passes to the anterior thigh and lower leg (long way). Following the long way
the obstetrician consecutively determines fetal parts starting with the head and to the
target leg. The foot is differentiated from the hand by the calcaneal tuber, short toes
placed in a row; unlike the thumb the great toe cannot be drawn aside significantly.
In case of cephalic presentation it is preferable to look for the leg going the long
way, in transverse lie — going the short way. To capture the leg more effectively, the
3 4
Fig. 27.4. Classical external & internal

podalic version: 1 — obstetrician’s hand;
2 — introducing the hand for internal
version; 3 — leg captured by two fingers;
4 — leg captured by the whole hand; 5 —
leg brought down (version complete) 5
806 Obstetrics
external hand is placed at the fundus and tries to push the legs to the internal hand by
pressing on the pelvic pole. One had better capture the located leg by the crus with
the whole hand placing the thumb along its length, so as to avoid fracture of the leg.
Step three of the procedure is version itself which is performed by bringing down
the leg after capturing it. Simultaneously, the external hand slowly and carefully draws
the fetal head to the fundus.
Both hands are working in conjunction. The version is considered complete when
one limb has been drawn through the pudendal fissure to the hollow of the knee and
the head is at the fundus; that is, incomplete footling presentation has been achieved.
When delivery is over, it is indicated to perform a control manual

NB! examination of uterine walls to rule out uterine injury.
Possible complications and management:

• Prolapse of pulsating cord after opening the amniotic sac:
– trying to avoid compressing the cord one continues with the version followed
by total breech extraction.
• Spasm of external os when the hand enters the uterus or while performing the
version when the hand becomes compressed and cannot budge:
– administration of deeper anesthesia eliminates this complication. If the spasm
persists, the procedure is discontinued as attempts to execute the version can
cause uterine rupture.
• Bringing down an arm instead of a leg:
– one puts a gauze loop on the prolapsed arm and holds it; the hand is again
introduced into the uterus and executes the version.
• Acute fetal hypoxia:
– version should be accomplished as quickly as possible followed by total breech
extraction.
• Version impossible due to insufficient mobility of fetus:
– procedure discounted due to the risk of uterine rupture.
• Placental abruption:
– If terminating the delivery by cesarean section is impossible, the version is
continued followed by total breech extraction.
• Rupture of uterus:
– emergency laparotomy.
REMEMBER!
Obstetric version is a procedure that manually changes an unfavorable fetal

position (presentation) over to another, more favorable, always longitudinal,
position.
Procedures improving fetal presentation include:
• external cephalic version;
• classical external / internal podalic version upon full cervical dilation.
Indications for external cephalic version: transverse and oblique lie, breech
presentation.
Prerequisites for external cephalic version: viable fetus without malformations,
gestational age 35–36 weeks.
Contraindications for external cephalic version: multiple pregnancy,
polyhydramnios, oligohydramnios, placenta previa, contracted pelvis, fetal
macrosomia, fetal hydrocephalus, uterine malformations, myoma of uterus, uterine
scar, preeclampsia, severe extragenital maternal disease, spontaneous abortion
and preterm delivery in history, threatened abortion in the present pregnancy.
Classical external & internal podalic version is a procedure by which the fetus
is brought to longitudinal lie and pelvic presentation with the help of manipulations
in the uterus and through the anterior abdominal wall.
Indications for podalic version: transverse and oblique fetal lie while the
prerequisites for cesarean section cannot be met; second twin in a transverse lie.
Contraindications for podalic version: uterine scar, threatening uterine rupture,
birth canal unfavorable for fetal passage (cervical dilation, contracted pelvis, etc.),
impacted transverse lie.
Prerequisites for podalic version: fully dilated cervix, absolute fetal mobility,
accurate information about fetal position, uterus and birth canal favorable for fetal
passage, satisfactory fetal condition, gestational sac intact or recently ruptured.
Anesthesia: heavy sedation.
Stages of procedure:
• choice of hand and its introduction into the uterus;
• locating and capturing the leg;
• executing the version.
Complications: prolapse of umbilical cord, spasm of external os, bringing down
an arm instead of a leg, acute fetal hypoxia, placental abruption, uterine rupture.
27.3. DELIVERY OPERATIONS
27.3.1. Cesarean section

Cesarean section is the use of surgery to deliver the fetus and placenta through an
artificially made incision on the uterus.
This is one of the oldest techniques in abdominal surgery. Its evolution covered
multiple stages gradually perfecting the technique.
Cesarean section is the most common abdominal surgery; its rate is higher than
that of appendectomy and herniotomy taken together. Over the last twenty years
the rate of cesarean section has risen 1.5–2 times approximately. According to sta-
808 Obstetrics
tistics, in Europe cesarean section is performed in 25% of all deliveries, on average

(2013). The prevalence of this surgery in the USA (2014) is 30%, in the countries
of Latin America — 40% (2013). In private hospitals of Brazil the rate of cesarean
section amounts to 80%. In Russian Federation the rate of cesarean section is 25%
(Fig. 27.5).
27.3.1.2. History
In olden times cesarean section was made on grounds of religious beliefs; a woman
who died in labor was sectioned as burying her with a fetus in utero was deemed
inadmissible. What a scary sight it was when a fetus rigid with cadaveric spasm was
extracted from the womb tearing all tissues on its way! It is believed that the decree
was passed by the Roman king Numa Pompilius (717 BC). At that time cesarean
section was performed by people without any medical background.
In late 16th and early 17th century the surgery began to be executed on a living
woman. The first reliably known surgery was performed by I. Trautmann in 1610.
According to other sources, a sow gelder, Jacob Nufer performed the operation on
his wife. Interestingly enough, the mother lived for another 77 years and subse-
quently gave birth normally to five children. A famous French obstetrician Francois
Mauriçeau wrote at that time that «performing cesarean operation is equivalent
to murdering the woman». Those were times when antiseptics was not known.
Fig. 27.5. Rate of cesarean section by countries (WHO)

Indications and contraindications for the surgery were not clearly defined, no an-
algesia was administered. The contents of uterus escaped to the abdominal cavity
from the gaping uterine wound causing peritonitis and sepsis that brought about the
woman’s death. All operated women died of hemorrhage and septic disease.
In Russia the first cesarean section was performed in 1756 by Erasmus, the second
one — in 1796 by Zommer, both with favorable outcomes. According to evidence
compiled by A. Krassovsky, only 12 cesarean section were performed in Russia until
1880.
Introduction of aseptics and antiseptics, administration of analgesia in vari-
ous forms, elaboration and perfection of uterine stitching technique decreased
maternal mortality to 20% by the end of the 19th century. Indications for this
surgery were gradually expanded, and later it became ingrained into routine
obstetric practice.
There are at least three hypotheses how the word «cesarean section» came about.
• It is commonly believed to be derived from the surgical birth of Julius Caesar;
however, this seems unlikely.
• The name of surgery is derived from the Roman code of laws by a mythical
Roman king Numa Pompilius who lived in the eighth century BC. Among other
laws, there was a rule that every woman who died in labor should be cut open to
extract the fetus for a separate burial.
• Cesarean section is incorrect translation of the term sectio caesarea. The word
caesarea derives from ab utero caeso (Plinius). The term caesones (those cut
out) was applied to infants born by postmortem operations. Sectio derives from
seco, to dissect; and caesarea is cognate with caedere, to cut. Thus, the exact
translation of sectio caesarea should go as «section that cuts out».
ICD-10 code
• O82 Single delivery by cesarean section.
– O84.2 Multiple delivery, all by cesarean section.
Types of cesarean section:
• Abdominal cesarean section:
– intraperitoneal methods: cesarean section by dissecting the abdomen (classical
cesarean section, corporeal cesarean section in situ, cesarean section in lower
uterine segment by transverse incision modified by Yeltsov-Strelkov, Stark;
isthmico-corporeal cesarean section);
– methods of abdominal cesarean section with temporary delimitation of the
abdominal cavity;
– methods of abdominal cesarean section without dissection of the abdomen:
extraperitoneal cesarean section;
– vaginal cesarean section by Duhrssen (no longer used in contemporary
practice).
27.3.1.4. Types of operation

Classical cesarean section is no longer used nowadays.
The main stages of performing classical cesarean section are as follows.
810 Obstetrics
• Stage one: dissection of the abdomen. Incision is made along the abdominal
midline traveling the same distance up and down from the umbilicus skirting it
on the left; the incision is 20 cm long.
• Stage two: dissection of the uterus. The uterus is exposed and incised along the
anterior wall (in the body) with a longitudinal incision along the midline for
12 cm.
• Stage three: careful rupture of fetal membranes, extraction of the fetus by the leg
and removal of the placenta are performed by conventional methods.
• Stage four: the wound on the uterus is repaired with three-layered closure
with interrupted stitches (muscle to muscle, muscle to serous, serous to serous
stitches). After that the uterus is placed in the abdomen, the anterior abdominal
wall and a complete closure in layers is performed.
Classical cesarean section has a number of disadvantages:
• a large abdominal incision promotes adhesions between the uterus, intestinal
loops and anterior abdominal wall, development of postoperative hernia;
• incision in the body of uterus is accompanied by great blood loss and often
causes wound disruption in early postpartum period, scar dehiscence due to its
deficiency in subsequent pregnancy.
In case of corporeal cesarean section in situ the incision of anterior abdominal
wall is made between the pubis and umbilicus, the uterus is not exposed for extrac-
tion of fetus. The uterine wound is closed in three layers; muscle to muscle stitches
without biting the mucosa, muscle to serous stitches and serous to serous stitches.
This method has the disadvantage of coinciding incisions on the uterus and abdo-
men which promotes adhesion formation. Incision in the body of uterus often leads
to scar deficiency in subsequent pregnancies.
Corporeal cesarean section is now used in rare cases when fetal extraction should
be followed by supracervical uterus amputation or subtotal hysterectomy on indica-
tions (multiple myoma of uterus, Couvelaire uterus, etc.); this method also provides
for a more simple and gentle extraction of the fetus from the uterus in twin pregnancy
or preterm delivery of low weight infants, Joel-Cohen transverse fetal lie.
Nowadays the most common method is cesarean section in the

NB! lower uterine segment with a transverse incision. Laparotomy in
this case is performed using transverse suprapubic Pfannenstiel
or Joel-Cohen incision (Fig. 27.6).
Advantages of cesarean section with transverse incision in the lower uterine seg-
ment.
• Surgery is performed in the thinnest part of uterine wall (lower segment) so
that a quite insignificant number of muscle fibers get in the wound. Along with
involution and lower segment formation the surgical wound retracts drastically
too, and a small scar results at the site of incision.
• Blood loss is not large, even when the placental bed is encountered in the
incision. In this case the bleeding dilated vessels should be ligated independently.
• Perfect peritonization of the closed uterine wound is achievable, on account of
the vesociuterine fold.

Fig. 27.6. Types of laparotomy: 1 — Pfannenstiel incision; 2 — Joel-Cohen incision; 3 —

lower midline incision
• Incisions of parietal and visceral peritoneum do not coincide, so there is not

much risk of adhesions between the uterus and the anterior abdominal wall.
• Minimum risk for uterine rupture in subsequent pregnancies and vaginal
deliveries as in most cases the scar shows no tendency for dehiscence.
Nowadays cesarean section is considered a quite safe, simple operative procedure,
but the rate of complications remains quite high. The most severe one is peritonitis
which results from scar disruption in the uterine wall.
Indications for cesarean are absolute (maternal and fetal) and

NB! relative (maternal and fetal).
Absolute indication is a situation when cesareans section is performed to save the

mother’s and/or fetus’ life, and to prevent maternal incapacitation.
Relative indications are situations when cesarean section improves the perinatal
outcome (compared with the vaginal birth) for the mother and fetus. One absolute
indication suffices to opt for cesarean delivery.
If maternal indications are established before labor, cesarean

NB! section should be performed at an optimum gestational age.
Intrapartum cesarean section should be initiated immediately
upon establishing the diagnosis, but absence of contraindications
is a prerequisite.
Absolute maternal indications for cesarean section:

• third- and fourth-degree contracted pelvis (true conjugate 7.5 cm and less), rare
shapes of contracted pelvis (obliquely oval contracted pelvis, osteomalatic pelvis,
spondylolisthetic pelvis, etc.);
• complete placenta previa;
812 Obstetrics
• incomplete placenta previa with marked bleeding while a rapid delivery is not
possible;
• placental abruption while a rapid delivery is not possible;
• threatening and ongoing uterine rupture;
• two and more scars on uterus;
• uterine scar with tendency for dehiscence (prior cesarean section, myomectomy,
uterine closure after rupture, penetration during an abortion, etc.);
• placenta located in the area of scar after a prior cesarean;
• uterine scar after corporeal cesarean section;
• pelvic tumors interfering with delivery;
• prior surgery for genitourinary and rectogenital fistula;
• scarry stricture of vagina and cervix;
• perineal scar after a third-degree tear;
• marked varicose veins in cervix, vagina and vulva;
• extragenital malignancy and cervical cancer.
Relative maternal indications for cesarean section:
• fi rst degree contracted pelvis;
• abnormalities of labor not responding to conservative therapy;
• severe PE;
• extragenital diseases (high degree myopia, encephalopathy, severe cardiovascular,
renal, endocrine disease);
• uterine and vaginal malformations;
• pelvic and lumbar fractures in history;
• uterine scar after previous lower segment cesarean section;
• uterine scar after plastic surgery prior to or during pregnancy (myomectomy,
removal of a uterine septum, removal of a rudimentary horn etc.).
Absolute fetal indications for cesarean section:
• acute fetal hypoxia while rapid delivery is not forthcoming;
• transverse lie after rupture of membranes;
• deflected head presentation: brow presentation, mentoanterior position, sincipital
presentation, persistent occiput direct position;
• maternal agony or death while the fetus is viable.
Relative fetal indications for cesarean section:
• chronic placental insufficiency;
• pelvic presentation, deflected head and weight above 3500 g;
• multiple pregnancy with the first fetus in transverse lie;
• cord prolapse;
• prolonged infertility in history, pregnancy achieved using assisted reproductive
technologies;
• postterm pregnancy;
• macrosomic or giant fetus;
• first and second degree contracted pelvis and fetal weight over 3500 g.
Cesarean section for relative indications is only possible at certain

NB! combnination of indications constituting a high perinatal risk.
Owing to advances in general surgery and anesthesiology, use of broad-spectrum

antibiotics, maternal and fetal surgical risks in cesarean section have diminished
significantly.
Nowadays most cesarean sections are performed for a sum of

NB! relative indications in pregnant women with a high prenatal risk.
Presence of only one relative indication allows conservative management of labor

or other varieties of delivery. How many relative indications it takes to turn the bal-
ance, is left to the discretion of the doctor in each particular case.
Contraindications for uteroperitoneal intraperitoneal cesarean section:
• acute infection of any location, outside of the genitourinary system as well;
• ante- or intranatal fetal demise (except for placental abruption, uterine rupture).
In a situation posing a threat to maternal life these contraindications are consid-
ered relative.
Performance of cesarean section calls for certain surgical and obstetric prerequi-
sites to be met.
Surgical prerequisites include availability of fully equipped and fully functional
operating room and qualified personnel. In extreme cases, with absolute indications
and no chance of transferring the patient to a specialized care institution, one can
organize an operating room on the spot.
Obstetric prerequisites include the following:
• no endometritis signs in labor (elevated body temperature, frequent pulse, foul
smelling discharge);
• viable fetus (this requirement cannot be met always). In case of a threat to the
mother (complete placenta previa or acute placental abruption) cesarean section
is performed with nonviable fetus as well.
Previously, in extreme cases when the mother’s condition required an urgent de-
livery (prolonged period from membrane rupture to delivery, intrapartum chorioam-
nionitis), extraperitoneal cesarean section was practiced. When powerful antibiotics
and synthetic sutures became available, and due to common damage to the bladder
and ureters, this method was almost given up altogether.
When an elective cesarean is to be performed, the night before surgery the patient
should have a cleansing enema, take a shower and a sleeping pill before going to
bed. Preanesthetic medication is administered an hour prior to surgery; immediately
before surgery — catheterization of the bladder.
If emergency cesarean is decided on, the patient needs hygienic preparation,
evacuation of the stomach, IV administration of histamine H2 receptor antagonists
(in case endotracheal anesthesia is planned), as well as premedication and catheter-
ization of the bladder. The anesthesiologist or the patient’s condition may call for
other procedures.
Anesthesia in cesarean section.
The method of choice at a planned surgery is regional anesthesia.
NB! If a rapid delivery is needed, spinal or combination spinal-epidural
and epidural anesthesia is administered.
814 Obstetrics
If regional anesthesia is not possible, endotracheal anesthesia is administered.

Contemporary technology implies intraoperative autotransfusion when consider-
able blood loss is expected (placenta previa, true placenta accreta). The method
implies collecting the blood lost by the patient during surgery and reinfusing it to
the patient.
Modern technique of abdominal cesarean section
The skin and subcutaneous tissue are incised transversely along the lower abdomi-
nal fold (Pfannenstiel incision) for 15 cm (Fig. 27.7).
An aponeurosis 2–3 cm long is then dissected transversely with a scalpel crossing
the abdominal midline (1–1.5 cm on the right and left of the midline). Then the
aponeurosis incision is continued with scissors for another 1–1.5 cm in both direc-
tions (Fig. 27.8).
Kocher’s clamp is placed on the superior aponeurosis edge; the aponeurosis is
bluntly stripped from the rectus muscle with fingers. The connective tissue intersec-
tion placed in the midline is dissected with scissors. The upper edge of aponeurosis
is elevated with a clamp and dissected further in a wedge-shaped manner, the apex of
the wedge originating at the abdominal midline, and side surfaces — sharply upward.
Fig. 27.7. Transverse incision of the skin and subcutaneous tissue
Fig. 27.8. Aponeurosis incision

Wedge-shaped dissection of aponeurosis makes the wound not so tight, and the
incision now equals the longitudinal incision from the pubis to umbilicus. This apo-
neurosis dissection provides free access to the abdominal cavity and easier extraction
of fetal head. After dissecting the aponeurosis the rectus muscles are separated bluntly
(Fig. 27.9). The peritoneum is grasped with two forceps, elevated and dissected lon-
gitudinally, and then fixed to the sterile drapes.
This incision of anterior abdominal wall allows for a more active management of
postoperative period in comparison with the longitudinal (lower midline) incision.
This incision provides for a better cosmetic effect but requires a longer time to per-
form, gives less opportunity for broad access, and can be accompanied by significant
blood loss.
When dissecting the abdomen the peritoneum of uterovesical fold is elevated with
forceps and notched at the border with uterus, and then dissected in both directions
transversely; the total incision length is 12–13 cm. The fold is elevated, the bladder
is brought down bluntly and fenced off with a broad suprapubic speculum inserted
under the uterovesical fold thus exposing the lower uterine segment. This access to
the uterus allows a reliable peritonization of uterine scar.
The uterus is dissected through all myometrial layers in the lower segment with
a small transverse incision 2–2.5 cm long (Kerr incision) and 1.5–2 cm below the
incision of the uterovesical fold.
Index fingers of both hands are introduced into the wound stretching it gently in
transverse direction to 10–12 cm (Gusakov modification) (Fig. 27.10).
Another method of making uterine incision is used, Derfler modification. After
making Kerr incision the incision is extended with scissors in a curvilinear fashion
to the right and left from the midline to achieve the desired length.
After dissecting the uterus the gestational sac is opened and fetal extraction begins.
In cephalic presentation the hand introduced into the uterus elevates the fetal head
Fig. 27.9. Blunt separation of rectus muscles

816 Obstetrics
towards the incision, simultaneously pressing on the fundus through the anterior
abdominal wall (Fig. 27.11). To avoid injury to the cervical spine it is recommended
that once the head has been delivered the fetus should be extracted by its underarms
with fingers placed there. In pelvic presentation the fetus is extracted by the nearest
leg. The pelvic pole is elevated towards the incision, grasped, and the fetus is extracted
to the shoulder girdle. Then both legs are grasped and the delivered trunk is held up.
The other hand introduced into the uterus frees the arms and pushes up the head.
It is unacceptable to deliver the head by traction on the trunk as this stretches the
cervical vertebrae and injures the spinal cord.
This technique of fetus extraction is the most sparing for the fetus and helps to
avoid fetal birth trauma.
In a transverse or oblique lie, once the head or, more commonly, the pelvic pole
has been elevated to the incision, further technique is no different from the one
described above.
Fig. 27.10. Blunt separation of the wound
Fig. 27.11. Elevating fetal head into uterine incision in cesarean section
When an attempt to elevate the head to the incision fails, it is advisable to extend
the access to the uterus dissecting it 2–3 cm in the direction of the fundus. The
incision is in the form of T upside down, also referred to as anchor incision.
Then one starts the closure of uterine walls. Nowadays one places single- or two-
layer continuous suture of synthetic absorbable stitch (Polyglycolide, Polysorb, Vicryl,
Dexon) (Fig. 27.12).
Fig. 27.12. Continuous uterine suture
Peritonization of uterine scar is performed using the peritoneum of uterovesical

fold which is stitched up 1.5–2 cm above the uterine incision with continuous suture
to the visceral peritoneum covering the uterus.
When peritonisation is over, revision of the abdominal cavity is carried out. One
should note the condition of the ovaries, uterine tubes, posterior uterine surface,
vermiform process and other abdominal organs accessible to inspection.
The abdominal wall is oversewn in layers. The peritoneum, muscles, and aponeu-
rosis are closed with continuous suture. Subcutaneous fat is sutured with separate
stitches, if needed. A continuous cosmetic stitch is placed in the skin, and aseptic
dressing or adhesive bandage.
After surgery one monitors the patient’s general condition, hemodynamics (BP
and pulse are measured every two hours), condition of the abdomen, postoperative
dressing, vaginal discharge.
In modern obstetrics one manages the postoperative period

NB! actively. In several hours the puerpera can sit up, in 12 hours she
can get up and walk about. If there are no contraindications, the
woman cares for the newborn on her own.
Over the last 20 years a series of innovations in cesarean technique have been
proposed. Some authors provided clear evidence that patients who do not undergo
closure of the visceral and parietal peritoneum during gynecological surgery do not
show any additional postoperative complications; moreover, there is also a decrease
in adhesion found at repeat operation when the visceral and parietal peritoneum is
not closed.
818 Obstetrics
Widespread use of synthetic absorbable sutures in surgical practice implies more

common use of single-layer continuous suture when closing the uterine incision in
cesarean section.
These factors underlie the modification of cesarean section elaborated at Misgav-
Ladach hospital1 in 1994; in Russia this method is referred to as Stark operation.
Separate stages of this surgery do not show anything new. It is a combination of
known techniques and elimination of some conventional steps that makes the method
a new modification showing a number of advantages compared with traditional ap-
proaches. The advantages are these:
• quicker extraction of fetus;
• shorter surgery time;
• lesser blood loss;
• less risk for injury to surgeon’s and assistants’ hands with piercing and cutting
instruments;
• reduced need for postoperative administration of pain killers;
• reduced rate of intestinal paresis, reduced rate and extent of other postoperative
complications;
• earlier discharge;
• considerable financial benefit due to economizing on suture material.
Owing to these advantages and the simplicity of technique, Misgav method is
quickly gaining popularity.
Misgav-Ladach cesarean section technique. The abdominal wall is dissected with
Joel-Cohen incision (see Fig. 27.6). Laparotomy is performed with a straight trans-
verse incision 2–3 cm below the line joining anterosuperior iliac spines. The scalpel
deepens the incision along the midline in subcutaneous tissue and notches the
aponeurosis simultaneously. Then aponeurosis is dissected to the sides under the
subcutaneous fat with slightly open branches of straight scissors. The surgeon and
assistant draw the incision aside by traction along the skin incision. The peritoneum
is opened with the index finger in transverse direction; it should be noted that there
is no risk of injuring the bladder. Compared with Pfannenstiel incision, this technique
has advantages: it is performed faster, provides lesser injury and less blood loss. The
uterine incision is made along the uterovesical fold up to 12 cm long without dis-
secting it beforehand. Extraction of the presenting part and placenta is performed
like in all other methods of uterine incision.
The uterine wound is closed with single-layer continuous Vicryl suture, the
distance between bites is 1.5 cm. No closure of the visceral and parietal perito-
neum is performed; continuous locking Vicryl suture is placed on aponeurosis.
The skin and subcutaneous tissue are apposed with interrupted silk sutures at
large intervals (3–4 sutures per the incision) using Donati coaptation sutures
or metal clips.
1 Misgav-Ladach hospital was established in Jerusalem, Israel in the 19 th century; it exists nowadays.
The fi rst building was erected in 1854 (the new building is in the Katamon district of Jerusalem). In 1879
the institution was given the name Misgav-Ladach. The hospital worked out a new cesarean section
technique. The hospital is also renowned for its innovative approach to natural birth, encouraging the
presence of fathers in the delivery room.
Shortening the surgiacal time is one of advantages of the Misgav

NB! Ladach method; however, one should bear in mind that a shorter
time and good outcome of any surgery depend on the skill and
concerted action of all parties.
27.3.1.5. Complications
Complications can arise at any stage of the procedure. One most common com-
plication following a transverse Pfannenstiel incision of skin, subcutaneous tissue and
aponeurosis is hemorrhage from superficial epigastric arteries; in the postoperative
period this can lead to formation of supra-aponeurotic hematoma.
Another complication of cesarean section, especially of repeat c-section, is injury
to adjoining organs: the bladder and intestine.
Hemorrhage is the most common complication of cesarean section. It can be
noted upon dissecting the uterus to prolong the incision laterally and injuring the
vascular bundle. Hemorrhage caused by uterine hypotony or atony or disorder of
blood coagulation is a very serious complication.
Complications occur in less than 5% of cesarean sections. Elective cesarean sec-
tions show complications 2–5 times less often than emergency sections.
Uterine scar after cesarean section can complicate the course of subsequent preg-
nancies; deficiency of the scar is the most prominent complicating factor.
A relative safety of cesarean section, the opportunity of cotrolling

NB! fetal condition using electronic devices, modern surgical
techniques – all these factors allow for a vaginal birth after a
previous cesarean section, if the present pregnancy did not show
the complications that prompted the previous cesarean or nor
presented new indications for an abdominal delivery.
In the postoperative period antibacterial therapy is not administered routinely

unless there are indications. Inhibitor-protected penicillins or cephalosporins are
commonly administered due to their low toxicity and broad spectrum of action.
REMEMBER!
The most common method of cesarean section nowadays is lower uterine segment
surgery with transverse incision. Laparotomy is performed with transverse
suprapubic Pfannenstiel or Joel-Cohen incision.
Indications for cesarean sections are divided into maternal and fetal absolute
indications, and maternal and fetal relative indications.
When absolute indications are established before delivery, cesarean section
should be performed at an optimum gestational age. Intrapartum cesarean section
should be initiated immediately upon establishing the diagnosis, but absence of
contraindications is a prerequisite.
820 Obstetrics
In case of relative indications, cesarean section is performed when there is a

combination of several such indications.
At present most cesarean sections are performed for a combination of relative
indications in patients from a group of high prenatal risk.
The relative safety of cesarean section, opportunities of instrumental monitoring
of fetal condition, modern surgical techniques make it possible for patients with
previous cesarean section to give a vaginal birth, if the present pregnancy showed
no complications that required cesarean in previous pregnancy nor any new
conditions requiring abdominal delivery.
27.3.2. Operative vaginal delivery

Operative vaginal delivery refers to a delivery in which the operator uses forceps
or a vacuum device to extract the fetus from the vagina.
The incidence of operative vaginal delivery has been on the decline as the rate of
cesarean section has been growing. In contemporary obstetrics perinatal protection
of the fetus is the paramount consideration when debating the mode of delivery.
In the early 20th century forceps deliveries accounted for 20% while cesarean
section was an exclusive surgery; however at present the situation has reversed. At
the same time, when there is a need to terminate labor rapidly in the second stage,
operative vaginal delivery is a method of choice.
27.3.2.1. Forceps
Historical background
It is believed that forceps were invented by a self-styled «doctor»1, son of a French
doctor (died in 1631), a Huguenot who emigrated from France and settled down in
Southampton (England) in 1569.
For many years obstetric forceps were kept a family secret passed down from fa-
thers to sons as they brought the owner high profits. The secret was subsequently sold
at a good round price. However, greed predominated: the cynical family sold only
one branch of forceps, which did not let other doctors terminate labor successively.
After 125 years, in 1723 obstetric forceps were «reinvented» by a surgeon anatomist
from Geneva I. Palfyn and immediately publicized, so the priority of inventing ob-
stetric forceps goes to him by right. Palfyn submitted to the Academie des Sciences
Royale in France an instrument consisting of two straight non-crossing branches
connected with a chain. The instrument and its use soon gained popularity, and by
the 19th century over two hundred modifications were known. The most widely used
ones were Levret’s forceps in France, Smellie’s and Simpson’s in England, Naegele’s
and Busch’s in Germany, Naegele’s and Simpson’s in the Russian Empire.
In Russia obstetric forceps were first used in 1765 in Moscow by I. Erasmus, pro-
fessor of the Moscow University. However, the credit for introducing forceps to ob-
stetric practice belongs inherently to Nestor Maximovitch-Ambodik (1744–1812). He
1 The medical community made a decision never to mention the name of the impostor who violated
the Hippocratic oath

encapsulated his experience in his book Art of Obstetrics, Or Science of Midwifery

(1784–1786). Using his drawings a mechanic Vassiliy Kozhenkov fabricated the first
model of obstetric forceps in Russia. Later the theory and practice of performing
forceps delivery were developed by Russian obstetricians Anton Krassovsky, Ivan
Lazarevitch and Nikolay Fenomenov.
Forceps is an instrument applied to extract a live term fetus by the head out of the
birth canal. The forceps cradles the head firmly and replaces the expulsive maternal
pushing by the operator’s traction force. An operative delivery when a live term fetus
is extracted from the birth canal using forceps is referred to as application of forceps.
Obstetric forceps are a tool with tractive force rather than rotational
NB! or compressive.
Construction of forceps. Forceps consist of two symmetrical parts, branches that

can differ in the structure of the left and right parts of the lock. The branch grasped
by the left hand and introduced into the left part of maternal pelvis is called the left
branch; the other one is the right branch.
Each branch has three parts: the blade, lock and handle.
The blade is a curved plate with a wide cut-away (fenestration). Curved edges
of the blade are referred to as borders (upper and lower one). The blade can be of
varying shape to conform to the shape of fetal head or maternal pelvis. The cephalic
curve is the convolution of the blade in the frontal plane replicating the shape of fetal
head. The pelvic curve is convolution of the blade in the sagittal plane conforming
to the shape of sacral fossa and, to a certain extent, the axis pelvis. If forceps have
blades without a pelvic curve, they are referred to as straight forceps (Lazarevitch,
Kielland forceps).
The lock joins the forceps branches. Locks of various forceps models have differ-
ent structures. The distinctive feature is the degree of mobility that the lock allows
in the branches:
• Russian forceps (Lazarevitch): the lock slides freely;
• English forceps (Smellie): the lock is moderately mobile;
• German forceps (Naegele): the lock is almost immovable;
• French forceps (Levret): the lock is fi xed.
The handle is for holding the forceps and applying traction. It has smooth inner
surfaces, so when the branches are locked, the surfaces adhere tightly. The outer sur-
face of handles are scalloped which prevents the operator’s hands from slipping when
applying traction. The handle is made hollow so that the instrument is not so heavy.
The upper parts of handles have lateral protrusions called Busch’s hooks. When per-
forming traction they provide support to the operator’s hands. Besides, Busch’s hooks
can indicate inadequate position of forceps if upon closing the branches the hooks
are not opposite each other. However, their symmetrical position is not a criterion
of correct positioning of forceps on the fetal head. In Russia Simpson-Fenomenov
forceps are used most often (Fig. 27.13).
Classification of operations. Depending on where the fetal head is in the pelvis
there are the following variants: outlet forceps and low/mid forceps. They also differ
in the technique of applying and operating them.
822 Obstetrics
Fig. 27.13. Simpson-Fenomenov forceps
Forceps delivery is indicated in case of maternal or fetal danger during the expul-
sion stage that can be eliminated totally or partially by a fast termination of labor.
Indications for forceps delivery can be conventionally divided into two groups: ma-
ternal and fetal indications.
Maternal indications can be those related to pregnancy and labor — obstetric in-
dications (severe PE, persistent uterine inertia, and/or weak pushing, hemorrhage in
the second stage, endometritis in labor) and those related to the patient’s extragenital
disease requiring elimination of pushing — somatic indications (decompensated car-
diovascular conditions, respiratory disorder due to pulmonary disease, high degree
myopia, acute infection, severe mental disorder, intoxication or poisoning). Not
uncommonly, a combination of indications is encountered.
Fetal indications: acute fetal hypoxia in the expulsion stage.
Prerequisites. Certain conditions should be met; if even one of the prerequisites is
absent, forceps delivery is contraindicated. The prerequisites are as follows:
• live fetus;
• full cervical dilation;
• membranes must be ruptured;
• no disproportion between the size of the head and the size of the pelvis;
• fetal head should be in the pelvic outlet with sagittal suture in the anteroposterior
diameter, or in pelvic cavity with its sagittal suture in one of oblique diameters.
Application of obstetric forceps is only possible if all the above

NB! mentioned prerequisites are met.
An obstetrician beginning a forceps delivery should have a clear idea of the mecha-
nism of labor which (s)he will have to simulate. One should clearly understand which
stages the head has already accomplished and which have to be performed during
tractions.
Preparation for forceps delivery includes several aspects:
• choice of analgesia;
• preparation of the patient;
• preparation of the obstetrician;
• vaginal examination;
• testing the forceps.
For forceps delivery the patient should be in lithotomy position. The bladder
must be empty. External genitals and inner thighs are swabbed with antiseptic. The
obstetrician’s hands are scrubbed in the same way as for surgery. The forceps itself
should be checked before starting.
As the risk of peritoneal tear increases upon extraction of fetal head with forceps,
application of forceps should be preceded by mediolateral episiotomy.
Immediately before applying the forceps one should perform

NB! a thorough vaginal examination to confirm the presence of
conditions for the surgery and to determine the position of fetal
head in relation to pelvic planes.
Analgesia. The choice of anesthetic depends on the patient’s condition and indica-
tions for the procedure. When the patient’s active participation in labor is deemed
useful (uterine inertia and/or acute fetal hypoxia in a somatically healthy woman),
long-lasting epidural nerve block or inhalation of nitrous oxide with oxygen can be
administered. If pushing is contraindicated, the patient receives general anesthesia.
The effect of analgesia should not be over immediately upon extracting the fetus as
the forceps procedure is followed by peritoneal repair, sometimes by a control manual
examination of uterine walls.
Technique. The procedure consists of five steps:
• first: inserting and positioning the blades;
• second: locking the blades;
• third: tentative traction;
• fourth: extraction of the head;
• fi fth: removing the forceps.
Step 1. Forceps are inserted using the first «treble rule» (three on the right, three
on the left):
1) the left blade is taken by the left hand and applied on the left side of maternal
pelvis controlled by the right hand;
2) the right blade is taken by the right hand and applied on the right side of maternal
pelvis controlled by the left hand.
To control the position of the left blade the obstetrician inserts a half-hand, that
is, four fingers of the right hand, except for the first one. The palmar surface should
face the head; it is introduced between the head and left lateral pelvic wall. The right
thumb remains outside, it is drawn aside. After inserting the half-hand one begins
applying the left blade.
The handle is grasped the way one holds a pen or fiddlestick. This special way of hold-
ing the blade helps to avoid application of force when the blade is inserted (Fig. 27.14).
Before inserting the handle into the birth canal one draws the handle aside and
positions it parallel to the opposite inguinal fold, and vice versa. The blade’s toe
(tip) is placed on the palm of the half-hand inserted into the vagina. The posterior
border of the blade is placed on the lateral surface of the IV finger and rests against
the drawn-aside thumb.
The blade should slip inside the birth canal under the impact of its own weight
and due to the right thumb nudging the inferior border of the blade. The handle
end should move in an arch. As the blade moves in, the handle is brought down and
assumes a horizontal position (Fig. 27.15).
824 Obstetrics
а b
Fig. 27.14. Techniques of holding the forceps handle: a — like a pen; b — like a fiddlestick
Fig. 27.15. Position of the left branch when inserting the blade
The half hand inserted into the birth canal acts as a guide; it controls the accurate
direction and position of the blade. Using this half-hand the obstetrician ensures that
the blade’s toe is not aimed at the fornix or lateral vaginal wal,l and does not graze
the edge of cervix. Once the first blade is inserted, it is passed over to the assistant
so as to avid shifting it. The other (right) blade is inserted using the same technique
and observing the «treble rule»: the right blade is taken by the right hand, applied
on the right side of maternal pelvis controlled by the left half-hand.
Blades applied to the head should meet the second «treble rule»:
• the long axis of the blades goes from the occiput to the chin through the ears
along the occipitomental diameter (Fig. 27.16);
• the blades cradle the head in the greatest diameter so that parietal tubers are in
the fenestration of forceps blades;
• the line of forceps handles is aimed at the point of direction on the head.
Step 2 of the procedure is locking the forceps. If the blades are positioned asym-
metrically and it takes a certain effort to lock them, it means that their position is
inaccurate. The forceps should be drawn out and reapplied.
Step 3 of procedure is tentative traction. This indispensable step ensures that the
forceps are applied accurately and are not likely to slip. With his right hand the ob-
stetrician grips the handle from above so that the index and middle fingers are on
the Busch’s hooks. The left hand is applied to the dorsal surface of the right hand,
stretches the index or middle finger and touches the head at the point of direction
area (Fig. 27.17).
Fig. 27.16. Accurate application of forceps to fetal head in occipital presentation
Fig. 27.17. Tentative traction

826 Obstetrics
If the forceps are accurately placed, the fingertip keeps the contact with the head
during the entire tentative traction. If it lets go ofmm7 the head, it means the forceps
are positioned inaccurately and there is a risk of their slipping during traction. The
forceps have to be reapplied.
Step 4 of the procedure. After a tentative traction one begins extraction of the
head. The right index and third finger are placed on Busch’s hooks, middle finger
between the separating forceps branches while the thumb and little finger clasp the
handles on the sides. The left hand grips the handle from below.
When extracting the head one should consider the nature, force and direction of
tractions. Traction of the head by forceps should imitate natural contractions. To
this end, one should:
• imitate the force of contraction: never start the traction abruptly but with a slight
pull, increasing and decreasing the strength gradually;
• never apply excessive force when performing tractions by throwing back the
trunk or propping the foot against the table edge;
• make pauses between tractions for 0.5–1 min;
• unlock the forceps after 4–5 tractions and let the head rest for 1–2 min;
• try to synchronize tractions with uterine contractions thus augmenting the
natural expelling force. If the patient was not given analgesia, she should be asked
to push during tractions.
The direction of traction is guided by the third «treble rule». The rule is fully
applicable to placing forceps on a head stationed in the widest pelvic part (cavity
forceps):
• the first direction of traction (from the greatest to least pelvic dimension) is down
and backward following the axis pelvis (Fig. 27.18)1;
• the second direction of traction (from least pelvic dimension to the outlet plane)
is downward (Fig. 27.19);
• the third direction of traction (sweeping the head out) is forward (Fig. 27.20,
27.21).
One should remember that forceps are a tractive instrument; tractions should be
executed smoothly in a certain direction. No oscillating, rotating or pendular move-
ments must ever be made.
Step 5 of the procedure. The sequence of removing the forceps for the head to
crown is as follows:
• take the right handle by the right hand, the left handle — by the left hand and
unlock the forceps by drawing the hands apart;
• retrieve the blades in the inverse order of how they were inserted: first retrieve the
right handle and then the left one; when removing the blades the handles should
deflect in the direction opposite the inguinal fold.
Difficulties. Problems can be encountered at every stage of the procedure. Difficulty
in inserting the blades can be associated with vaginal tightness and pelvic floor rigidity
which requires dissection of the perineum.
Locking the forceps can also be difficult. The forceps cannot be locked if the
blades are on the head in different planes or when one blade is above the other. In
1 All directions of traction are indicated relative to the patient’s vertical position
Fig. 27.18. Direction of tractions with the head in the greatest pelvic dimension
Fig. 27.19. Direction of tractions with the head in the least pelvic dimension
Fig. 27.20. Direction of tractions with the head in the pelvic outlet
828 Obstetrics
Fig. 27.21. Extracting the head in forceps (traction directed forward)
this case one should insert a hand in the vagina and place the blades accurately. One
can pull the blades towards oneself.
Inaccurate placement of blades is associated with mistakes in diagnosing the posi-
tion of the head in the pelvis and of sutures and fontanelles on the head, so often
one should remove the blades, make a vaginal examination again and reinsert the
bladders accurately.
Outlet forceps. Outlet forceps are the type of forceps applied to the head stationed
in pelvic outlet with its sagittal suture in the anteroposterior diameter. The internal
head rotation has been accomplished. The head is at the pelvic floor, the entire
sacral fossa as well as the coccygeal area is filled by the head, ischial spines cannot
be reached. The sagittal suture is in the anteroposterior outlet diameter. The posterior
fontanelle is palpated below the anterior one (head flexed — occipital presentation)
and placed anteriorly (anterior position) or posteriorly (posterior position).
The blades are inserted following the rules described above, in transverse outlet
diameter. Forceps handles are placed parallel to each other (Fig. 27.22).
Fig. 27.22. Outlet forceps (occipitoanterior position)

Traction is first performed down and forward until the suboccipital fossa comes
under inferior symphysis border. The traction is more and more directed forward so
that the head deflects and crowns with the circumference of the suboccipitobregmatic
diameter.
In case of occipitoposterior position tractions are performed horizontally until
the anterior edge of anterior fontanelle comes in contact with the inferior border
of symphysis pubis (first fixation point). Then forward tractions are performed until
the suboccipital fossa is fixed at the coccygeal apex (second fixation point). Now the
forceps handles are dipped behind, the head deflects and the brow, face and chin are
delivered from under the symphysis pubis.
Low/Mid forceps
Low/mid forceps are applied to a head stationed with its sagittal suture in one of
oblique pelvic diameters (pelvic greatest or least dimension). This type is also referred
to as atypical. Obstetric forceps are applied in the opposite oblique diameter so that
the blades grasp the head at the site of parietal tubers.
When low/mid forceps are applied, the sequence of inserting the blades remains
the same. First the left blade is inserted, then the right one. However, insertion of
blades has its specifics depending on fetal position and whether it is left or right. Thus
in left occipitoposterior position the left blade is inserted, under the guidance of the
right hand, to the left and somewhat backwards (to the posterolateral pelvic part,).
The blade is positioned on the area of left parietal tuber. This blade is referred to as
fixed as it is positioned accurately immediately upon insertion.
The right blade is inserted to the right pelvic part by the conventional method,
and then, guided by the left hand, it is introduced into the vagina; the blade moves
forward until it reaches the right parietal tuber. The blade is moved by carefully
pressing on its inferior border with the second finger on the left hand. In this situ-
ation the right blade is referred to as wandering. In the end both blades are placed
opposite each other in the left oblique pelvic diameter (Fig. 27.23).
In case of right occipitoanterior position the left blade comes in first; it is inserted
in the left pelvic part and then moved forward to the anterolateral pelvic part (wan-
dering blade). The fixed right blade is at once inserted to the right posterolateral
pelvic part. In this way the blades are positioned biparietally in the right oblique
pelvic diameter (Fig. 27.24).
Tractions are directed down and backward, the head makes an internal rotation,
the sagittal suture gradually advances to the anteroposterior outlet diameter. Now
tractions are first directed down until the parietal tuber comes from under the pubis,
and then forward until the head deflects.
After low/mid forceps delivery a control manual examination of uterine walls is
recommended to check for possible complications induced by the procedure.
If obstetric forceps were applied in compliance with all prerequisites and principles
of use, no maternal or fetal complications ensue, as a rule. In some circumstances
forceps delivery causes certain complications.
Complications. The following complications arise upon forceps delivery.
Slipping of the forceps can be vertical (over the head in outside direction) or
horizontal (backward or forward). Forceps can slip due to incorrect grasping of
830 Obstetrics
Fig. 27.23. Low/mid forceps (left occiput anterior)
Fig. 27.24. Low/mid forceps (right occiput anterior)
the head, incorrect locking, fetal head disproportion. Slipping carries a risk for
severe injury to the birth canal: ruptures in the perineum, vagina, clitoris, rectum,
and bladder.
Birth canal injury. These include injury to the vagina and perineum, less often — to
the cervix. Rupture of the lower uterine segment and injury to pelvic organs present
a severe complication: the bladder and rectum are usually affected when prerequisites
for the procedure are not met or the technique is not executed appropriately.
Fetal complications. After the procedure the soft tissue on the fetal head usually
shows edema with cyanotic coloration. If the head was compressed excessively, a
hematoma may develop. A forcible pressure of the blade on facial nerve can cause
its paresis. Severe complications are injury to fetal skull bones whose degree varies
from indention on the bone to fractures. Cerebral hemorrhage constitutes a serious
threat to fetal life.
Postpartum infectious complications. In itself, forceps delivery does not cause post-
partum infection; however, the procedure increases the risk of infection development
so it requires adequate prevention during the puerperium.
27.3.2.2. Vacuum extraction

Vacuum extraction is a type of assisted delivery by extracting the fetus by the head
using a vacuum device that creates negative pressure between the inner surface of
the cup and fetal head.
Historical background
The first attempts to employ the force of vacuum for extraction of the fetus from
the birth canal were made in 1850s. The invention of Simpson’s «aerotractor» dates
back to 1849. The first modern model of vacuum extractor was designed by a Yugoslav
obstetrician Victor Finderle in 1954. However, the model proposed by Malstrőm in
1956 gained the greatest popularity. In the same year Russian obstetricians Chachava
and Vashakidze publicized their original model. Vacuum extraction devices used
in contemporary obstetric practice are much more compact and easier to operate
(Fig. 27.25). Manufacture of easy-to-use disposable devices at the turn of the 21st
century resulted in vacuum extraction prevailing over forceps delivery.
In contrast to forceps application, vacuum extraction requires an active participa-
tion of the parturient woman when tractions are performed, so the list of indications
is quite short.
Indications for vacuum extraction of fetus:
• uterine inertia not responding to conservative therapy;
• acute fetal hypoxia.
Contraindications for vacuum extraction:
• preeclampsia;
• conditions incompatible with pushing (decompensated heart defect, hypertonic
disease, pulmonary disease, high degree myopia, etc.);
• deflected head;
• marked prematurity (under 36 weeks).
Fig. 27.25. Modern vacuum extractor

832 Obstetrics
The last two contraindications are related to the specific physical effect of vacuum,
so applying the cup to a preterm fetal head or to posterior fontanelle area may result
in severe complications.
Prerequisites for vacuum extraction:
• live fetus;
• head stationed in the lesser pelvis;
• complete cervical dilation;
• head engaged in occiput position.
Preparation for the procedure is the same as in case of forceps delivery (see Section
27.3.2.1. Forceps).
Immediately before the procedure one should do another vaginal examination to
specify the obstetric situation: extent of cervical dilation, head station, head engagement.
Analgesia. The patient is required to participate actively during vacuum extrac-
tion, so general anesthesia is not indicated. Peridural or pudendal block can be
administered.
Technique of vacuum extraction consists of the following steps:
• inserting the cup and placing it on the head. The extractor cup is inserted into
the vagina under the guidance of the hand; the cup is pressed to the head with its
working surface as close to the posterior fontanelle as possible but never on the
fontanelle (Fig. 27.26);
• building up pressure. When the cup is in place, negative pressure is built up to
0.7–0.8 atm (500 mm Hg). Different models of vacuum extractor show different
mechanisms of building up pressure;
• traction of the head. Before starting the traction a tentative traction should be
made. When performing tractions the obstetrician works in the direction of
natural advance of the head, that is, depending on the location of the head in
the pelvis (Fig. 27.27). No traction is done in the intervals between contractions;
3 cm
3 cm
Fig. 27.26. Placing vacuum extractor cup on fetal head: 1 — point of direction
Fig. 27.27. Direction of tractions in vacuum extraction
• removing the cup. When parietal tubers crown through the vulvar ring, vacuum
is released and the cup can be removed; the head is delivered with manual
assistance.
Complications. The cup slipping off the head is the most common complication
which occurs when the technique is violated or airtightness is faulty. A slipping cup
can be reapplied again, but if this happens again, the procedure cannot be continued
and another mode of delivery should be considered.
The fetus is sometimes injured: cephalhematoma develops on the head, cerebral
signs, convulsions can develop. These complications are caused by faulty technique
and poor timing of the procedure.
REMEMBER!
Forceps are an instrument employed to extract a live term fetus by the head from
the vagina.
A procedure that assists in vaginal delivery of a live term fetus by means of forceps
is referred to as forceps delivery.
Forceps consists of two symmetrical parts: the right and left branch.
Each branch has three parts: the blade, lock and handle.
The cephalic curve is convolution of the blade in the frontal plane replicating the
shape of fetal head.
The pelvic curve is convolution of the blade in the sagittal plane conforming to
the shape of sacral fossa and, to a certain extent, the axis pelvis.
834 Obstetrics
Depending on the fetal head position in the pelvis, forceps are divided into outlet
forceps and low/mid forceps.
Forceps application is indicated when there is a threat to the mother’s of fetus’
wellbeing in the second stage of labor which can be partially or completely
eliminated by rapid termination of labor.
Maternal indications can be classified into those related to pregnancy and labor
(obstetric indications: severe gestosis, persistent uterine inertia, hemorrhage
in the second stage of labor, endometritis in labor) and those related to the
patient’s extragenital disease that require elimination of pushing (somatic
indications: decompensated cardiovascular conditions, respiratory disorder due
to pulmonary disease, high degree myopia, acute infection, severe mental
disorder, intoxication or poisoning). Not uncommonly, a combination of different
indications is encountered.
Fetal indications: acute fetal hypoxia in the expulsion stage.
Prerequisites for forceps delivery:
• live fetus;
• ruptured membranes;
• no cephalopelvic disproportion;
• the head stationed with its sagittal suture in anteroposterior outlet diameter or
with the sagittal suture in one of oblique pelvic diameters.
Forceps delivery can be executed only if all the prerequisites are met.
Preparation for forceps delivery:
• choice of analgesia;
• preparation of the patient;
• preparation of the obstetrician;
• vaginal examination;
• testing the forceps.
Right before starting to insert the forceps one should do a thorough vaginal
examination to ensure the conditions for the procedure are there and to determine
the relation of fetal head to pelvic planes.
The procedure consists of five main steps:
• step 1: inserting and placing the blades;
• step 2: locking the blades;
• step 3: tentative traction;
• step 4: extraction of the head;
• step five: removing the forceps.
There is a «treble rule» to guide insertion of the blades («three on the right, three
on the left»).
Accurately placed blades should comply with the second «treble rule»:
• the long axis of the blades goes from the occiput to the chin through the ears
along the occipitomental diameter;
• the blades cradle the head in the greatest diameter so that parietal tubers are in
the fenestration of forceps blades;
• the line of forceps handles is aimed at the point of direction on the head.
Direction of tractions is determined by the third «treble rule».

Complications of forceps delivery: slipping of forceps, birth canal injury, fetal
complications (hematoma, paresis of facial nerve, cranial bone injury, cerebral
hemorrhage), postpartum infection.
Vacuum extraction is a type of assisted delivery by extracting the fetus by the
head using a vacuum device that creates negative pressure between the inner
surface of the cup and fetal head.
Indications for vacuum extraction:
uterine inertia not responding to conservative therapy;
acute fetal hypoxia.
Contraindications for vacuum extraction:
• preeclampsia;
• conditions incompatible with maternal pushing (decompensated heart defect,
hypertonic disease, pulmonary disease, high degree myopia, etc.);
• deflected head;
• marked prematurity (under 36 weeks).
Prerequisites for vacuum extraction:
• live fetus;
• head stationed in the lesser pelvis;
• head engaged in occiput position.
The patient is required to participate actively during vacuum extraction, so general
anesthesia is not indicated. Peridural or pudendal block can be administered.
Vacuum extraction consists of the following steps:
• inserting the cup and placing it on the head;
• building up negative pressure;
• traction of the head;
• removing the cup.
Complications of the procedure: slipping of the cup, birth canal injury,
cephalhematoma, cerebral symptoms, convulsions.
CONTROL QUESTIONS
1. What are forceps?

2. What is forceps delivery?
3. What is the structure of forceps?
4. What are the types of forceps delivery?
5. What are maternal indications for forceps delivery? What are maternal
indications for vacuum extraction?
6. What are fetal indications for forceps delivery? What are fetal indications for
vacuum extraction? What are the prerequisites for operative vaginal delivery?
836 Obstetrics
7. What are the specifics of preparing for forceps delivery?

8. What analgesia is administered for forceps delivery?
9. What steps does forceps delivery consist of?
10. What is the first «treble rule»?
11. What is the point of the second step (locking the forceps)?
12. What is the third step (tentative traction) needed for?
13. What are the features of traction when performing the fourth step?
14. What is the third «treble rule»?
15. What are the specifics of applying outlet forceps?
16. What are the specifics of applying low/mid forceps?
17. What is vacuum extraction of fetus?
18. What are indications for vacuum extraction?
19. What are the prerequisites for vacuum extraction?
20. What are the specifics of analgesia in this procedure?
21. What is the technique of procedure; what steps does it consist of?
22. What are the complications of vacuum extraction?
23. What are the complications of assisted vaginal delivery?
CHECK YOURSELF!
Level 1. Test
1. The most common causes of operative vaginal delivery:
a) fetal hypoxia;
b) fetal malposition;
c) fetal malpresentation;
d) high perineum in the mother.
2. Operative delivery means:

a) removal of pessary;
b) forceps;
c) removal of cervical stitches;
d) vacuum extraction.
3. Indications for vaginal delivery:

a) uterine inertia;
b) severe extragenital maternal disease;
c) fetal distress;
d) vaginal bleeding.
4. Prerequisites for operative delivery:

a) intact gestational sac;
b) cervix dilated 7 cm and more;
c) live fetus;
d) fetal weight less than 2500 g.
5. Contraindications for operative delivery:

a) macrosomic fetus;
b) fetal malformations;
6. The following are NOT complications of operative delivery:

a) uterine rupture;
b) fetal injury;
c) hypotonic hemorrhage;
d) slipping of the retrieval instrument.
7. Analgesia in operative vaginal delivery:

a) endotracheal anesthesia;
b) pudendal block;
c) psychoprophylaxis;
d) short-term IV anesthesia.
8. In contemporary obstetric practice forceps are used in case of:

a) impossibility of cesarean section;
b) mentoanterior position;
c) prolapse of small fetal parts
d) not used at all.
9. The purpose of forceps in contemporary obstetrics:

a) to improve fetal presentation;
b) for faster extraction;
c) in case of CPD;
d) in case of eclampsia.
10. The following is indicated after operative delivery:

a) examination of the cervix;
b) administration of antibiotics;
c) manual examination of uterus;
d) uterus ultrasound.

1. The puerperant patient is in the second stage of labor; fetal heartbeat 136 per
minute. Vaginal examination detects no amniotic sac. Fetal head has been stationed
with the occiput in the plane of least pelvic dimension for an hour. What is your
diagnosis? What are you going to do?
2. Primiparous patient aged 30. Term pregnancy. Pelvic dimensions 26–26–31–19.
Arterial pressure 140/90 mm Hg. The fetus is in longitudinal lie, fetal head in pelvic
outlet, fetal heartbeat 100 per minute, rhythmical. Vaginal examination shows an ef-
faced cervix, dilation 10 cm, no amniotic sac. What is your diagnosis? What is your
plan of management?
838 Obstetrics
27.4. MINOR OBSTETRIC OPERATIONS (MANIPULATIONS)
Minor obstetric operations include:

• artificial rupture of membranes (AROM, amniotomy);
• perineotomy, episiotomy;
• transcervical amnioinfusion;
• manual removal of placenta;
• manual inspection of uterine walls;
• operated balloon tamponade;
• hysteroscopy during puerperium.
27.4.1. Amniotomy
Amniotomy is artificial rupture of fetal membranes.
Amniotomy is performed in pregnancy and labor to induce and accelerate labor,
eliminate the negative impact of membranes or their waters on the course of labor
and to meet prerequisites for vaginal operative delivery.
Indications.
• In a pregnant woman: induction of labor provided there are obstetric indications.
• In labor: flat amniotic bag, oligohydramnios, polyhydramnios, excessively
tough fetal membranes while the cervix is dilated more than 7 cm, hemorrhage
in presence of low-lying placenta, uterine inertia. Amniotomy is performed in
labor complicated by PE, hypertonic disease, DM and other underlying maternal
disease in which a decrease in uterine volume sets the maternal hemodynamics
right.
Contraindications: fetal malposition and malpresentation, cord presentation, all
contraindications for vaginal birth, exacerbation of genital herpes, unripe cervix.
Prerequisites for AROM depend on the particulars of each case of labor and can-
not be generalized. Amniotomy in pregnancy requires a ripe cervix (over 6 points on
Bishop score).
When the cervix is unripe, amniotomy for the purpose of labor

NB! induction increases the rate of labor complications 16 times, the
rate of cesarean section – 6 times.
Preparation. The patient is in the same position as for a vaginal examination. Fetal
heart activity is monitored; the cervix is assessed.
Surgical technique. Amniotomy is performed during a vaginal examination. The
branch of bullet forceps (ear forceps, amniotome) is inserted aseptically along fingers
introduced into the vagina, to reach the cervix and then the cervical canal or external
os until it reaches the amniotic sac (Fig. 27.29).
The point of the branch is placed between the index and middle fingers thus
avoiding trauma of soft birth canal tissues. Between contractions the membranes are
punctured eccentrically, with a forward motion. The operator inserts the index and
middle fingers in the opening widening it, and guides out the amniotic fluid slowly
without removing the hand.
Fig. 27.28. Amniotome varieties: a — disposable; b — multiple use
Fig. 27.29. Amniotomy: 1 — amniotic sac; 2 — amniotome
At polyhydramnios the amniotic fluid is slowly guided out along

NB! a needle or catheter. After amniotomy fetal heart beat should be
checked!
Complications: prolapse of small fetal parts or the cord, injury to cord vessels in
case of velamentous insertion of the umbilical cord, trauma of fetal head skin, prema-
ture separation of the placenta. If the indications and prerequisites for this operation
were assessed correctly, no complications develop, as a rule.
840 Obstetrics
27.4.2. Perineotomy and episiotomy

Dissection of the perineum is performed during labor to prevent injury to the
mother (threat of perineal tear, operative delivery) and fetus (premature fetus, etc.).
NB! A cut wound heals better than a lacerated wound.
The rate of episiotomy in labor now shows a tendency for decline. Episiotomy is
the most common obstetric intervention. Inadequate regeneration of the dissected
perineum promotes incompetence of pelvic floor muscles in future.
At perineotomy there is no quickening of the third stage nor a

NB! decrease in perinatal asphyxia, RDS or shoulder dystocia.
Definition: depending on direction of the incision, we distinguish median episi-

otomy, mediolateral and lateral episiotomy (Fig. 27.30, 27.31).
• Median episiotomy is dissection of the perineum along the median line (from
posterior labial commissure toward the anus) where the number of vessels and
nerve endings is minimal.
• Mediolateral episiotomy is incision of the perineum at an angle of 30–40 ° from
posterior labial commissure extending toward the right ischial tuber (Fig. 27.32).
• Lateral episiotomy is incision of the perineum running through the labium
majus 2–3 cm above the posterior labial commissure extending toward the right
ischial tuber. In this incision one sometimes dissects peripheral branches of the
neurovascular bundle which can disrupt innervation and promote hematoma
development. Bartholin’s gland or its duct can also be injured by this surgery, so
the technique is now almost outdated.
The type of incision depends on the obstetric situation and condition of the
perineum.
Indications:
• threatening perineal tear, high, rigid or scarred perineum, operative vaginal
delivery, etc.
3
2
1
Fig. 27.30. Varieties of episiotomy incision: Fig. 27.31. Mediolateral episiotomy

1 — median; 2 — mediolateral; 3 — lateral
Surgical
scissors
Fetal head
is crowning
Vaginal orifice
Mediolateral
episiotomy
Perineotomy
Anus
Fig. 27.32. Varieties of episiotomy
Contraindications:
• low perineum as the crowning can promote the incision becoming a rupture of
the external sphincter and anterior rectal wall.
Prerequisites. Episiotomy is performed at the end of the second stage when the
head crowns, at the peak of a contraction.
Analgesia. Local infiltration anesthesia or pudendal block are recommended as
well as local aerosol anesthetics.
Preparation: swabbing the perineum with an antiseptic.
Technique. When the head is crowning, at the peak of contraction and perineal
stretching an incision no less than 3 cm long is made with scissors, a finger having
been first inserted between the presenting part and vaginal wall (Fig. 27.32).
If the incision is shorter than 3 cm, it becomes a lacerated perineal

NB! wound.
When the delivery is over, the dissected perineum is repaired.
27.4.3. Amnioinfusion
Amnioinfusion refers to installation of fluid into the amniotic cavity.
Amnioinfusion was first used in the 19th century; it fell into oblivion and was re-
discovered again. From 1950s the technique was used in case of meconium-stained
amniotic fluid and oligohydramnios as preventive measure against fetal hypoxia
and fetal aspiration syndrome. However, some randomized studies (2005) showed
uncertainty about the role of amnioinfusion in prevention of aspiration syndrome.
Indications. Transcervical amnioinfusion is administered in case of oligohydram-
nios, fetoplacental insufficiency, passage of meconium-stained waters. Dilution and
842 Obstetrics
lavage of the amniotic fluid constitutes treatment and prevention of decelerations

(cord compression) and fetal aspiration syndrome.
Contraindications: placenta previa, separation of normally placed placenta, uterine
hemorrhage.
Analgesia is not indicated.
Prerequisites. Insertion of soft catheter to uterine cavity should be possible.
Technique. Sterile soft uterine catheter and intravenous tubing are needed. Uterine
lavage is performed using warm sterile 0.9% normal saline at room temperature in
the amount of 500–1000 ml.
After swabbing the external genitals and the vagina with an antiseptic the sterile
soft catheter is inserted into the uterus behind the fetal head with the right hand
gradually passing between the head and uterine wall. The catheter is connected to
the IV tubing, the clamp is removed, and the fluid flows into the uterus. The initial
rate of infusion is 10.0–20.0 ml/min, then 2.0 ml/min.
During the procedure fetal condition and uterine discharge are

NB! continuously monitored.
The procedure is discontinued when no meconium shows in the fluid flowing out
of the vagina, or fetal heartbeat restores.
Complications. Separation of normally placed placenta, acute fetal hypoxia.
27.4.4. Manual separation of the placenta and afterbirth

Manual separation of the placenta (or placental lobe) and afterbirth is a manipula-
tion when a hand introduced into the uterus forcibly separates the placenta (placental
lobe) from uterine walls and removes the placenta (placental lobe).
Indications:
• hemorrhage in the third stage of labor due to disorder of placenta separation;
• no signs of placenta separation for 30 min after delivery of the fetus (without
hemorrhage);
• retained placenta or its parts in the uterus.
Preparation. The patient’s position in the surgery chair is the same as for other
obstetric surgeries. The bladder is drained with a catheter. The surgery is performed
aseptically, preferably using a long surgical glove.
Analgesia: IV, inhalation anesthesia or epidural nerve block.
Technique. The labia are separated with the left hand and a cone-shaped right hand
is inserted into the vagina. The left hand is placed on the fundus to fix it. The other
hand follows the cord to get into the uterus, finds the site of cord attachment to the
placenta and follows the fetal surface to the edge of the placenta. The placenta is
separated from its bed with saw-like motions until it fully detaches. The manipulation
is performed by stretched out, compressed fingers whose palmar surface faces the
placenta, and the dorsal surface — the placental bed. The motions are controlled by
the left hand that exerts moderate pressure at the same site from outside. When the
placenta has been detached completely, the assistant guides it out of the birth canal
by pulling at it (Fig. 27.33).
Fig. 27.33. Technique of manual separation of the placenta
When the placenta has been removed, the hand remaining in the uterus carefully
evaluates uterine walls. Intravenous droplet infusion of uterotonics (oxytocin) is
initiated, if necessary.
The hand is drawn out of the uterus only when one has ensured that no placental
fragments are left and that the uterus shows good contractility.
Complications. Intensification of hemorrhage in case of true placenta accreta.
It is not advisable to enter the uterine cavity again as this increases

NB! the risk of infection and does nothing to improve contractility.
27.4.5. Control manual examination of the uterus walls

Control manual examination of the uterus walls is a manipulation performed by
a hand inserted into the uterus to evaluate the continuity of its walls and check for
presence of retained placental fragments.
Indications. Doubt about placental integrity, doubt about continuity of uterus walls
after operative delivery or embryotomy, third degree cervical laceration, hemorrhage
in the third stage of labor and puerperium, uterine scar, myoma of uterus, uterine
malformations, antenatal and intranatal fetal demise.
Analgesia: intravenous or inhalation anesthesia.
Technique. The labia are separated with the left hand, and a cone-shaped right
hand is inserted into the vagina and then — into the uterus. The left hand fixes the
uterus to the right hand from outside through the anterior abdominal wall. The right
hand consistently explores the entire surface of uterine walls and the fundus to evalu-
844 Obstetrics
ate the continuity of uterine walls and check for retained placental fragments. Tubal
angles, the area of the thin, soft lower uterine segment are assessed most thoroughly.
Any detected placental lobes, membrane fragments or blood clots are removed. The
exploration of the walls promotes excitation of neuromuscular uterine apparatus
which mediates its better contraction and arrest of hemorrhage. The procedure is
concluded by administration of uterotonics.
Postoperative management. Uterotonic drugs are administered practically always;
antibiotics — in the presence of a high risk of infection.
27.4.6. Bimanual uterine compression

Bimanual uterine compression is a manipulation that causes the body of uterus
to compress in the anteroposterior direction between a hand inserted into the vagina
and a hand located on the anterior abdominal wall (Fig. 27.34).
Indications: hypotonic hemorrhage (stage of conservative treatment).
Preparation for the procedure and prerequisites are the same.
Analgesia: not required.
Technique. A cone-shaped hand is inserted into the vagina; it forms a fist in the
anterior vaginal fornix. The external hand is applied to the anterior abdominal wall;
it guides the uterus to anteflexion position (approaching the uterus to the pubis). The
same hand presses on the posterior uterine wall through the anterior abdominal wall
in the direction of the internal hand; thus the body of uterus becomes compressed.
Compression is maintained until the hemorrhage is controlled and the uterus contracts.
27.4.7. Intrauterine balloon tamponade

Intrauterine balloon tamponade is an auxiliary method to control hemorrhage
from uterus into vagina during the postpartum period.
Fig. 27.34. Bimanual uterine compression

A balloon inserted into a postpartum uterus is filled with fluid, increases its vol-
ume and fills the entire uterine cavity causing reflex contraction of the uterus and
increasing its tone. The balloon pressed against the walls of uterus (vagina) promotes
formation and preservation of intravascular blood clots which results in hemorrhage
arrest (Fig. 27.35).
Classification: intrauterine and intravaginal balloon tamponade are distinguished.
Indications. In presence of obstetric uterine bleeding, balloon tamponade is either
an intermediate step while preparing for laparotomy, or a means to control bleeding
after a control manual exploration of uterus and complete evacuation of its contents.
In case of vaginal injury balloon tamponade is used to control the bleeding and to
prevent hematoma formation after repair of lacerations.
Contraindications: doubt about complete evacuation of uterine contents and about
continuity of its walls.
Preparation for the surgery and prerequisites are the same as in other obstetric
surgeries.
Analgesia is not required.
The tamponade procedure requires a sterile disposable latex balloon catheter, a
receptacle with 150.0 ml capacity and a tube no less than 1.0 m long (both sterile),
and clamps. There are models with double lumen tube: one lumen is for filling the
balloon, the other — for the outflow of blood from the uterus.
Technique. The puerpera is on the operating table or delivery bed in lithotomy
position.
• The receptacle is placed on a support 40–45 cm above the puerpera level, fi lled
with warm sterile normal saline, and the clamp on the tube is closed.
• The balloon catheter is connected to the tube without removing its package. By
pressing on it one removes air bubbles into the tube and receptacle, and closes
the clamp.
• Under direct vision and ultrasound gidance the cervix is exposed aseptically
using speculums. The balloon catheter is inserted into the uterus as far as the
fundus (into the vagina as far as the fornix), and the clamp is removed. The level
Fig. 27.35. Intrauterine hemostatic balloon

846 Obstetrics
of the saline decreases as the balloon catheter fills with the fluid and expands to
fill the entire uterine (or vaginal) cavity, so the fluid is added to the receptacle
to stabilize its level. Under ultrasound guidance one makes sure that no blood
is accumulated in the uterus (vagina). The uterus contracts squeezing out the
fluid from the balloon to the receptacle. As a rule, uterine tone restores within
30 minutes, and the level of fluid in the receptacle increases. The receptacle
is brought down to the level of the balloon which makes the balloon fall out
spontaneously, or it can be easily removed from the uterus or vagina.
Once the bleeding has been controlled, the balloon catheter is left in the uterus
or vagina for several hours (as long as 6–8 hours) to confirm a complete arrest of
bleeding.
27.4.8. Hysteroscopy in puerperium

Hysteroscopy means inspection if the uterine walls using a hysteroscope.
Indications: subinvolution of uterus, suspicion of postpartum endometritis and
submucous myoma of uterus. Hysteroscopy guidance is needed for certain procedures
like uterus sanation, antiseptics installation or biopsy.
Preparation for the procedure and prerequisites are the same as in gynecologic
surgery.
Analgesia: intravenous or mask anesthesia.
Technique. After swabbing the external genitals and vagina with an antiseptic the
lip of cervix is grasped with bullet forceps and uterine sounding is done to determine
the length and direction of uterine cavity; then the cervical canal is dilated. Under
direct vision and ultrasound the hysteroscope is inserted into the uterus; all the walls
are inspected, and diagnostic and therapeutic manipulations are performed. When the
manipulations (surgery) are over, the hysteroscope is retrieved, bullet forceps removed
from the cervix, the cervix and vagina swabbed with an antiseptic.
Complications: perforation of uterus.
REMEMBER!
Minor obstetric operations include amniotomy, perineo- and episiotomy,
transcervical amnioinfusion, manual removal of placenta, manual inspection
of uterine walls, operated balloon tamponade, and hysteroscopy during the
puerperium.
Amniotomy
Amniotomy is artificial rupture of fetal membranes.
Indications. In a pregnant woman: induction of labor in patients with PE, postterm

pregnancy, antenatal fetal demise while there is a chance of vaginal birth, abortion
on therapeutic grounds.
In labor: flat amniotic bag, oligohydramnios, polyhydramnios, excessively tough

fetal membranes while the cervix is dilated more than 6 cm, hemorrhage in
presence of low-lying placenta, uterine inertia.
Contraindications: fetal malposition and malpresentation, cord presentation, all

contraindications for vaginal birth, exacerbation of genital herpes.
Complications: prolapse of small fetal parts or the cord, injury to cord vessels
in case of velamentous insertion of the umbilical cord, trauma of fetal head skin,
premature separation of the placenta.
Episiotomy
Depending on the direction of the incision, episiotomy can be median, mediolateral

or lateral.
Episiotomy is performed at the end of the second stage of labor when the head is
crowning, at the peak of contraction force.
Indications: threatening perineal tear, high perineum, rigid or scarred perineum,

operative vaginal delivery etc. (an incised wound heals better than a lacerated
wound).
Contraindications for median episiotomy: low perineum.
Analgesia: local infiltration anesthesia or pudendal block.
Amnioinfusion
Amnioinfusion is installation of fluid into the amniotic cavity.

Indications:
• in a pregnant woman: oligohydramnios;
• in the first stage of labor: oligohydramnios, premature rupture of membranes,
treatment and prevention of decelerations (cord compression) and aspiration
syndrome in the presence of chronic fetal hypoxia.
Complications: separation of normally placed placenta, fetal hypoxia.
Manual separation of placenta
Manual separation of placenta (or its lobe) is a manipulation when a hand
introduced into the uterus forcibly separates the placenta (placental lobe) from
uterine walls and removes the placenta (placental lobe).
Indications:
• hemorrhage in the third stage of labor due to disorder of placenta separation;
• no signs of placenta separation or hemorrhage for 30 min after delivery of the
fetus;
• retained placenta or its parts in the uterus.
Complications: uterine hypotonia and hemorrhage in case of true placenta
accreta.
Manual examination of the uterus walls
Manual examination of the uterus walls is a manipulation performed by a hand
inserted into the uterus to evaluate the continuity of its walls and to remove the
uterine contents (retained placental fragments, blood clots, membrane fragments).
848 Obstetrics
Indications. Doubt about placental integrity, doubt about continuity of uterus

walls after operative delivery or embryotomy, third degree cervical laceration,
hemorrhage in the third stage of labor and puerperium, uterine scar, myoma of
uterus, uterine malformations, antenatal and intranatal fetal demise.
Bimanual uterine compression
Bimanual uterine compression is a manipulation that causes the body of uterus
to compress in the anteroposterior direction between a hand inserted into the
vagina and a hand located on the anterior abdominal wall.
Indications: conservative treatment of hypotonic hemorrhage.
Intrauterine balloon tamponade
Indications: hypotonic hemorrhage, hemorrhage upon injury to vagina.
Hysteroscopy
Hysteroscopy is inspection of uterus walls using a hysteroscope.
Indications: postpartum endometritis, submucous myoma of uterus.
27.5. FETUS DESTROYING OPERATION (EMBRYOTOMY)
Embryotomy is a surgery aimed at dismembering the fetus to minimize its size so

that it can be removed through the birth canal.
Embryotomy is one of the oldest types of surgery; in old times the operation was
sometimes performed on a live fetus. Development of obstetrics, especially advances
in cesarean section technique made it possible to decrease the rate of embryotomy
significantly. In contemporary obstetric practice the surgery is performed in ex-
traordinary circumstances, only on a demised fetus when removal of the fetus as it
is through the birth canal is associated with a great risk for the mother. As a rule,
nowadays embryotomy results from inadequate obstetric care.
Embryotomy associated with fetal demise means stress for the mother; psycho-
logical counseling may be required. At the time of surgery one should explain to
the mother and family that the infant is dead and the mother’s life has to be saved.
After the event the woman and her family should be persuaded that there was no
alternative to embryotomy.
ICD-10 code
• O83.4 Destructive operation for delivery.
Classification. The following types of embryotomy are distinguished.
• Operation to decrease the fetal body size. Body cavities are emptied of organs
contained in them: cerebral substance is removed in craniotomy, abdominal
organs — in exenteration, thoracic organs — in evisceration.
• Operations dismembering the fetal body to be removed in parts. The procedures
include decapitation and rachiotomy (spondylotomy).
• Operations that inflict reversible injury to the fetus: cleidotomy — surgical
division of the clavicle, puncture of the head in hydrocephaly that are done both
on a live and demised fetus.
Typical embryotomies are craniotomy, cranioclasy, decapitation

NB! and cleidotomy.
27.5.1. Craniotomy
Craniotomy is disruption of cranial continuity by perforation of the head and
removal of cerebrum from it.
Indications:
• cephalopelvic disproportion detected in the second stage of labor;
• intranatal fetal demise in the presence of other obstetric pathology (uterine
inertia in the second stage of labor); threatened uterine rupture; incarceration of
soft tissues of the birth canal;
• failure to extract the aftercoming head in pelvic presentation;
• critical maternal condition requiring prompt termination or acceleration of
labor.
Prerequisites:
• fetal demise;
• birth canal allowing for the passage of fetal parts (true conjugate more than
6.5 cm);
• cervical dilation no less than 6 cm;
• ruptured amniotic sac;
• fetal head tightly fixed to pelvic brim.
Craniotomy requires vaginal speculum (2) with retractors (2), sponge forceps
(2), bullet forceps (2), Fenomenov scissors (1), Blot’s lanceolated perforator or
Fenomenov perforator, spoon or curette to remove cerebrum, Braun cranioclast
(Fig. 27.36).
The patient’s position and preparation are the same as for other vaginal surgeries.
Analgesia. General anesthesia to kill the pain and relax the abdominal wall and
uterus, and to prevent psychological trauma to the mother.
а b c
Fig. 27.36. Perforators: a –Fenomenov’s; b — Blot’s; c — Braun cranioclast
850 Obstetrics
Technique. The operator performs the surgery in a sitting position. Two assistants
are needed: one to fix vaginal speculums, and the other to fix the head at pelvic brim
through the anterior abdominal wall.
The surgery consists of exposing the head, dissecting soft tissues of the head,
perforation itself and removal of the brain (excerebration).
Step 1, exposing the head, is done using flat obstetric vaginal speculums so that
the external os and head are visible.
Step 2, dissecting soft tissues in the head. The skin on the head is grasped in the
center with two pairs of two-pronged tools or bullet forceps, stretched and incised
for 2–3 cm between them with scissors or scalpel. It is more convenient to run the
incision perpendicular to the sagittal suture. Incision edges are rolled back exposing
the bone or fibrous tissue (fontanelle or suture).
Step 3, perforation of the head. An inexperienced operator had better begin the
perforation at the sutures or fontanelles. They are easy to locate if one guides a finger
under the incision edge and strips off the skin to a side. An opening in the head is
made under direct vision. Pulling the bullet forceps one achieves additional fixation
of the head. Simultaneously the assistant fixes the head at the pelvic brim pressing
on it through the anterior abdominal wall. The perforator is taken by the right hand;
the tip put to the head center, suture or fontanelle so that the instrument is stationed
perpendicular to the head and not at an angle (Fig. 27.37, 27.38).
In case of brow or face presentation the perforator is put at the frontal suture or
orbit, correspondingly.
Perforation is performed with careful drilling motions until the widest part of the
perforator tip reaches the hole edges. No puncturing or pushing motions should be
Fig. 27.37. Perforation of presenting head under direct vision

Fig. 27.38. Perforation of presenting head under guidance of the hand (at left: correct; at
right: incorrect)
done as they can end in the tip slipping off the head and injuring the patient badly.
After that both hands with Blot’s perforator are drawn together, sharp edges of the
tip are drawn aside. Drawing them together and aside in different directions one
makes 4–5 incisions on the head. Having drawn the tip edges aside to the full one
makes rotator motions at the level of perforation edges which can now accommodate
1–2 fingers.
Step 4, removal of the brain. A large blunt spoon is inserted through the newly
made hole, and the brain is destroyed and scooped out. Special attention should be
paid to destruction of the myelencephalon. The destroyed brain can be removed by
flushing it with sterile solution through a catheter inserted in the cranial cavity. Here
the perforation ends.
If perforation was performed with insufficient cervical dilation, vaginal speculums
should be removed leaving the bullet forceps that bite the head skin. The forceps
rings are drawn together and tied with a gauze bandage which is thrown over a pulley
attached to the bed. A weight of 300–500 g is attached to it.
852 Obstetrics
If the patient’s condition is satisfactory and labor is active, delivery can terminate
spontaneously. Otherwise, as soon as the cervix dilates fully or almost so, labor is
terminated by cranioclasia.
27.5.2. Craniotomy of aftercoming head

Perforation of the aftercoming head is a procedure performed on a demised fetus
in pelvic presentation and unfavorable fetopelvic proportions.
Indications: CPD, fetal hydrocephaly, failure to extract the aftercoming head by
manual maneuvers.
Prerequisites: demised fetus, not absolutely contracted pelvis, complete cervical
dilation, the head firmly engaged at pelvic brim.
Preparation. The patient’s position and preparation are the same as in other
vaginal surgeries.
Analgesia. General anesthesia to kill the pain and relax the abdominal wall and
uterus.
Technique. Like in case of craniotomy in cephalic presentation, this procedure
requires firm fixation of the head at the pelvic inlet. This fixation is achieved by pull-
ing the fetus down by the feet and pressing down on the head through the anterior
abdominal wall (see Fig. 27.39).
The assistant pulls the trunk by the leg steeply downward inserting a flat blade
speculum between fetal occiput and the anterior vaginal wall.
Fig. 27.39. Perforation of aftercoming head

Protected by the speculum the skin is gripped by forceps at the border of the scalp
and neck, and incised. A finger is put under the dissected skin to strip it off the bone
until foramen magnum is exposed. The perforator tip is put to it and a hole is made
in the skull. This manipulation, like all those that follow, is performed in the same
sequence as in perforation of a presenting head.
If one fails to reveal foramen magnum, the head is perforated at the border between
the neck and occiput. The head deflated after excerebration can be easily removed
through the birth canal.
27.5.3. Cranioclasy
Cranioclasy is removal of perforated head diminished in size, using a special in-
strument — cranioclast.
The cranioclast is designed like obstetric forceps; it consists of two branches
crossed and locked in the middle. The blades of the branches have a curve to com-
ply with fetal cephalic curve. One of the branches is solid and has a rough surface;
it is intended for insertion into cranial cavity. The other one is fenestrated; it is for
gripping the head from outside. The handles have Busch’s hooks and a sturdy lock
(Fig. 27.40).
Indications for the surgery and patient’s position on the operating table are the
same as for craniotomy.
Prerequisites: full or almost full cervical dilation; other prerequisites are the same
as for craniotomy.
Analgesia. General IV anesthesia or inhalation anesthesia.
Fig. 27.40. Braun cranioclast

854 Obstetrics
Technique:
• Step 1, insertion and placement of the blades. The inner cranioclast blade is
inserted into the skull through perforated the hole with the convexity facing the
fetal face, as deep as possible. The insertion is guided by a hand introduced in
the vagina to protect the vaginal walls. The cranioclast handle is passed to the
assistant. The outer (fenestrated) blade is inserted in the same way as the second
blade of obstetric forceps. The other hand is inserted into the vagina to guard
against injuring the vagina or incarcerating an edge of external os or vaginal wall
between the head and cranioclast. The blade is applied to the outer surface of the
head in concordance with the other blade inserted into the cranial cavity, Busch’s
hooks acting as reference points (Fig. 27.41a, b).
• Step two, locking the branches. The notch of the external branch is put on
the prong of the internal branch, a compression screw is put on the handles
and tightened. A correctly applied cranioclast should compress the facial skull
firmly. The hand inserted into the vagina checks the position of the cranioclast
(Fig. 27.42c).
• Step 3, extraction of the head. After a tentative traction the head is extracted.
Traction is performed in the same way as in forceps delivery. Using palpation
one makes sure that bone fragments protruding from the perforation hole do
not injure maternal tissues, that the cranioclast does not break off cranial bones
which commonly occurs when the blades have been applied parietally or not deep
enough. If this is the case, the cranioplast is retrieved and the blades are reapplied
deeper to capture the face or occiput (Fig. 27.41d).
• Step 4, removing the cranioclast. The cranioclast is carefully removed, one
branch after the other, after the head has emerged in the pudendal fissure. The
rest of the fetal body is extracted by conventional methods.
27.5.4. Decapitation
Decapitation is severing fetal head from the trunk in the area of cervical vertebrae
followed by extraction of the trunk and the head.
Indications: impacted transverse lie, demised fetus.
Contraindications: insufficient cervical dilation ≤6 cm, fetal neck out of the reach of
obstetrician’s hand, true conjugate <6–6.5 cm, scarry stricture of the vagina, placenta
previa, uterine hemorrhage, uterine scar, uterine malformation (bicornuate uterus).
Prerequisites:
• demised fetus;
• complete or almost complete cervical dilation;
• fetal neck within the reach of obstetrician’s hand;
• birth canal allowing for the passage of the fetus decreased in size (true conjugate
no less than 6 cm, no scarry stricture in the vagina).
Preparation and patient’s position on the operating table are the same as in other
vaginal surgeries.
Decapitation is performed using Brown’s decapitation hook (Fig. 27.42). It con-
sists of a solid metal centerpiece; at one end it is bent at an acute angle and shows
a bulging at the tip. The other end is a massive handle.
а b
c d
Fig. 27.41. Cranioclasy: a — inserting the solid cranioclast blade into cranial cavity after
perforation; b — applying the other cranioclast blade; c — fetal head fi rmly fi xed by
tightening the cranioclast screw; d — bringing down the perforated head by cransioclast
Analgesia. General intravenous or inhalation anesthesia.

Technique. The procedure consists in inserting and placing the decapitation hook,
severing the head and extraction of dismembered fetus (Fig. 27.43).
• Step 1, inserting and placing the decapitation hook.
• The assistant grasps the prolapsed fetal hand and pulls it down and away from the
head until the shoulder girdle and neck become attainable for the decapitation
hook. The other assistant fi xes the trunk at the pelvic inlet through the anterior
856 Obstetrics
Fig. 27.42. Brown’s decapitation hook.
Fig. 27.43. Decapitation
abdominal wall. If impacted transverse lie is not accompanied by prolapse of the

hand, this stage is bypassed and one starts with the next procedure, inserting the
hand into the birth canal, grasping the neck with the thumb in front, the index
and middle fi ngers placed behind.
• Decapitation hook protected by the palm of the obstetrician’s hand is introduced
into the birth canal; the hook slides along the thumb and passes over the neck.
One had better grasp the neck with the left hand while the right one works the
handle of decapitation hook.
• Step 2, decapitation itself. The assistant presses on the head trying to bring it to
the abdominal midline and fi x there. Thus the head is fi xed by the inside hand
grasping the heck, and from outside by the assistant’s hand on the abdominal
wall. After that the operating obstetrician forcibly pulls the instrument towards
oneself and down. The hook adheres to the spine tightly and is fi xed here. The
external obstetrician’s hand rotates the handle of the hook by 90 ° in one and then
the other direction until the spine is broken. Throughout these manipulations
and later the hand inside protects maternal tissues form injury. A characteristic
crepitation sound indicates that the spine is broken. The head is now connected
to the trunk with soft tissues only. By pulling the hook or prolapsed hand the soft
tissues are brought down as far as possible and dissected by embryotomy scissors
with a blunt tip until the head is completely severed from the trunk; this is done
under direct vision or guarded by fi ngers. Decapitation is now over, the hook is
drawn out of the birth canal sliding it along the inner hand.
• Step 3, extraction of dismembered fetus. The assistant keeps pressing on the
uterine fundus to prevent the head or trunk from changing their position at the
pelvic inlet. The decapitated trunk is easily delivered by traction on the arm. To
extract the head remaining in the uterus, the assistant presses on the fundus until
the head is stationed at the inlet. Speculums are inserted into the vagina exposing
the presenting head; it is grasped by two-pronged forceps and brought out. One
can also insert a hand into the uterus, hook a fi nger into fetal mouth and guide
the head out.
27.5.5. Cleidotomy
Cleidotomy (life saving surgery) is division of fetal clavicle to reduce the biacromial
diameter and facilitate delivery.
Indications: shoulders making no advance (after obstetric maneuvers were per-
formed) when they are stuck in the birth canal and labor does not progress. This
complication is mostly noted in pelvic presentation, but in cephalic presentation it is
possible, too (macrosomic or giant fetus, mistakes in obstetric maneuver). The sur-
gery can be done on a live fetus with macrosomia or shoulder dystocia (Fig. 27.44).
Contraindications: absolutely contracted pelvis or CPD, scarry stricture of the
vagina, placenta previa, uterine hemorrhage.
Prerequisites: fetal clavicle attainable for the obstetrician’s hand, birth canal allow-
ing for the passage of fetus decreased in size. No special preparation for the surgery
is required. The surgery can be performed with or without analgesia.
Technique. The surgery is performed by sharp dissection (with scissors) on a dead
fetus and by blunt dissection (with a finger) on a live fetus. The obstetrician inserts
four fingers of the left hand into the vagina that will serve as guide and protection.
The obstetrician reaches the clavicle that is closer to the pelvic outlet, brings scis-
sors with a blunt tip to the clavicle and dissects (breaks) it with one or two motions.
This makes the shoulder girdle collapse so that it can easily pass through the birth
canal. If this does not happen, the other clavicle is dissected.
858 Obstetrics
Fig. 27.44. Cleidotomy
27.5.6. Evisceration, eventration and exenteration

Evisceration, eventration and exenteration mean removal of fetal inner organs from
the thoracic and abdominal cavities to reduce the size of the trunk.
Indications: significant increase in the size of fetal abdominal or thoracic cavity as
in ascites, hydrothorax, hepatosplenomegaly, tumor, etc. Sometimes exenteration is
performed as an auxiliary surgery in case of impacted transverse fetal lie and impos-
sibility to perform decapitation.
Contraindications: true conjugate less than 6–6.5 cm, scarry stricture in the vagina,
placenta previa, uterine hemorrhage, live fetus.
Prerequisites:
• ruptured membranes;
• fetus accessible for the obstetrician’s hand;
• birth canal allowing for the passage of the fetus reduced in size (true conjugate
no less than 6 cm, no scars in the vagina that would constrict it significantly).
vaginal surgeries.
Analgesia: general intravenous or mask anesthesia.
Technique. The surgery is performed under direct vision or under control of fingers
using long scissors or Blot’s perforator. A slit-like incision is made at the most acces-
sible site on the chest or abdomen. Thoracic or abdominal organs are removed with
a finger introduced into the perforation hole or with bone forceps. After complete
removal of inner organs the fetus is extracted.
27.5.7. Spondylotomy
Spondylotomy is a rare type of surgery consisting in dissection of the spine.
Dissection of fetal spine is performed if there are no conditions for other varieties
of embryotomy, for instance, decapitation impossible in impacted transverse fetal lie
when fetal neck cannot be reached by a hand. Spondylotomy is an auxiliary procedure
when performing evisceration (Fig. 27.45).
Fig. 27.45. Cleidotomy

860 Obstetrics
Indications: impacted transverse fetal lie, dead fetus.

Contraindications: insufficient dilation of cervix ≤6 cm, fetus out of reach of ob-
stetrician’s hand, true conjugate less than 6–6.5 cm, scarry stricture in the vagina,
placenta previa, uterine hemorrhage, uterine scar.
Prerequisites:
• dead fetus;
• completely or almost completely dilated cervix;
• ruptured amniotic sac;
• fetal neck accessible to obstetrician’s hand;
• birth canal allowing for the passage of the fetus reduced in size (true conjugate
no less than 6 cm, no scarry stricture in the vagina).
vaginal surgeries.
Analgesia: general anesthesia.
Surgical technique. Spondylotomy can be performed with long scissors
(Fenomenov’s, Siebold scissors) under direct vision or controlled by fingers
of the left hand inserted into the uterus. The scissors dissect the interverte-
bral ligaments and fetal trunk, the inner organs are removed and the spine
is dissected.
27.5.8. Complications of fetus-destroying operations

The most serious complications of all types of embryotomy are associated with
slipping of sharp instruments employed in surgery. The incident leads to injury of
maternal inner genitals and even injury to adjacent organs (the rectum, bladder and
other).
To prevent injury one has to follow the technique carefully and perform the sur-
gery under direct vision whenever possible. General anesthesia eliminates maternal
motions, attenuates the tone of anterior abdominal wall and uterus.
27.5.9. Postpartum management

All cases of delivery terminating in embryotomy require manual separation of
placenta and expression of the afterbirth, control examination of uterine walls, in-
spection of the vagina and cervix in speculums so as to evaluate for their continuity.
Catheterization of the bladder is obligatory so as to prevent injury to the urinary
tract. Antibacterial therapy is indicated in the postoperative period.
REMEMBER!
Embryotomy is a surgery aimed at dismembering the fetus to minimize its size so

that it can be removed through the birth canal.
Types of embryotomy: craniotomy, cranioclasy, decapitation, cleidotomy,

exenteration, evisceration, eventration, spondylotomy.
Indications
Craniotomy and cranioclasy: threatening uterine rupture, incarceration of soft
tissue in the birth canal (risk of fistula), failure to extract the aftercoming head
in pelvic presentation, critical maternal condition requiring prompt termination or
acceleration of labor.
Decapitation: impacted transverse lie, dead fetus.

Cleidotomy: large size of shoulders delayed in the birth canal and arresting the
delivery.
Evisceration: significant increase in abdominal or thoracic cavity of the fetus.
Spondylotomy: impacted transverse lie while there is no possibility of performing
another embryotomy procedure.
Prerequisites:
fetal demise;
birth canal allowing for the passage of the fetus decreased in size;
cervix dilated no less than 6 cm or complete dilation;
ruptured amniotic membranes.
Analgesia: general anesthesia.
Postoperative management: manual separation and expression of the placenta,

examination of uterine walls, speculum examination of the vagina and cervix,
catheterization of the bladder.
Complications: injury to inner genitals and adjacent organs upon slipping of the
instrument.
CONTROL QUESTIONS
1. What are pregnancy preserving surgeries?

2. What is the most common cause of pregnancy termination in the second
trimester?
3. What is the classification of pregnancy preserving surgery?
4. What are the indications for surgical treatment of cervical insufficiency?
5. What are the contraindications for surgical treatment of cervical insufficiency?
6. What are the prerequisites for surgical treatment of cervical incompetence?
7. What surgery is commonly used for elimination of cervical malformations
outside of pregnancy?
8. What gestational ages are most favorable for surgical treatment of cervical
incompetence?
9. What are possible complications of surgery for cervical incompetence?
10. What are the indications for removing sutures in the cervix?
11. Classical external / internal podalic version upon full cervical dilation: what
are the indications, contraindications and prerequisites?
12. Classical external / internal podalic version upon full cervical dilation: what
are the preparation, analgesia, technique, complications?
862 Obstetrics
13. Maternal complications in classical external / internal podalic version.

14. Fetal complications in classical external / internal podalic version.
15. Definition of cesarean section.
16. Classification of cesarean section.
17. Technique of cesarean section in the lower uterine segment.
18. Advantages of lower segment cesarean section in comparison with corporeal
cesarean section.
19. Derfler incision.
20. Absolute indications for cesarean section.
21. Relative indications for cesarean section.
22. Prerequisites for cesarean section.
23. Complications of cesarean section.
24. What are the disadvantages of corporeal cesarean section?
25. What are the specifics of Stark operation?
26. Management of patients in the postoperative period.
27. Classification (types) of embryotomy.
28. Main steps of craniotomy.
29. Cranioclasy: its definition and technique.
30. Decapitation: its definition and technique.
31. Possible complications of embryotomy surgery.
32. What are the indications for manual separation and expression of the
placenta?
33. Manual examination of uterine walls: indications, preparation, technique.
34. Perineo- and episiotomy: what are the indications and technique?
35. Artificial rupture of membranes (amniotomy): indications, preparation and
technique.
CHECK YOURSELF!
Level 1. Test
1. The most common causes of miscarriage in the second trimester:
a) increased uterine tone;
b) gestosis;
c) cervical incompetence;
d) placental abruption.
2. Pregnancy preserving surgeries are:

a) pessary insertion;
b) Yeltsov-Strelkov reparative plastic surgery on the cervix;
c) placing sutures on the cervix;
d) female condom.
3. Indications for surgical treatment of cervical insufficiency:

a) cramp-like pain in lower abdomen;
b) prolapsed gestational sac;
c) cervical effacement and dilation;
4. Prerequisites for pregnancy preserving surgery:

a) intact gestational sac;
b) cervix shortened by less than 2.5 cm;
c) live fetus;
d) gestational age less than 12 weeks.
5. Contraindications for surgical treatment of cervical insufficiency:

a) hypertonic disease;
b) fetal malformations;
c) gestational DM;
6. Indications for suture removal:

a) gestational age 34–35 weeks;
b) estimated fetal weight over 2000 g;
c) amniotic fluid leakage;
d) contractions.
7. The following are NOT absolute indications for classical external / internal podalic
version
a) complete cervical dilation;
b) absolute fetal mobility;
c) IUGR;
d) fetopelvic proportion;
e) term fetus.
8. In contemporary obstetric practice external/internal podalic version is performed

in case of:
a) brow presentation;
b) mentoanterior position;
c) prolapse of small fetal parts or the cord;
d) transverse fetal lie;
e) impossibility to perform cesarean section.
9. Which method of cesarean section is most common:

a) classical (corporeal) cesarean section;
b) lower segment cesarean section;
c) extraperitoneal cesarean section;
d) vaginal cesarean section.
864 Obstetrics
10. Indications for cesarean section:

a) complete placenta previa;
b) chorioamnionitis;
c) intrauterine fetal demise;
d) CPD.
11. Absolute indication for cesarean section with a live term fetus:
a) pelvic presentation;
b) transverse lie;
c) chronic placental insufficiency;
d) mentoanterior position.
12. As a rule, elective cesarean section is performed if the following is present:

a) pelvic presentation of macrsomic fetus;
b) gestosis;
c) pyelonephritis;
d) first degree contracted pelvis.
13. Indications for corporeal cesarean section:

a) CPD;
b) uterine scar;
c) maternal moribund state;
d) placenta previa.
14. Joel-Cohen method refers to:

a) technique of closure of the visceral and parietal peritoneum;
b) laparotomy technique;
c) placing cosmetic stitches on the skin;
d) technique of fetus extraction.
15. Non-typical complications of cesarean section:

a) injury to ureter;
b) injury to intestine;
c) hemorrhage;
d) difficulty in fetus extraction.
16. Analgesia in embryotomy:

a) infiltration anesthesia;
b) IV anesthesia;
c) endotracheal anesthesia;
d) pudendal block;
e) conduction anesthesia.
17. Indications for embryotomy:

a) live fetus;
b) uncoordinated labor;
d) impacted transverse lie.
18. Common prerequisites for all embryotomy types:

a) live fetus;
b) cervix dilated no less than 6 cm;
c) dead fetus;
d) ruptured membranes.
19. Embryotomy is followed by:

a) only observation;
b) external massage of uterus;
c) examination of cervix and vagina;
d) manual examination of uterine walls.
20. Possible complications of embryotomy:

a) injury to the bladder and/or rectum;
b) injury to inner genitals;
c) perineal trauma;
d) retained placenta.
21. Placental defect requires:

a) IV administration of oxytocin;
b) manual examination of uterine walls;
c) D&C;
d) vacuum aspiration;
e) speculum examination of the cervix.
22. Indications for manual separation of placenta and expression of the afterbirth:
a) hemorrhage in the third stage of labor;
b) uterine inertia;
c) late rupture of membranes;
d) no signs of placenta separation or bleeding for 30 minutes;
e) retained placenta or its fragments.
23. The following is not an indication for manual examination of uterine walls:
a) doubt about placental integrity;
b) doubt about uterus integrity;
d) hypotonic hemorrhage.
866 Obstetrics

1. The patient had childbirth 5 min ago; the first fetus of monochorionic biamni-
otic twins, cephalic presentation, gestational age 38 weeks. Upon a vaginal examina-
tion the amniotic sac of the second twin was ruptured, the waters are of light color.
The fetus is presenting its back at the pelvic inlet. Fetal heartbeat clear, rhythmical,
140 per minute. What is your diagnosis? What is your plan of management?
2. Primiparous patient aged 30, term pregnancy. The patient was admitted to ma-
ternity hospital with the onset of labor, her contractions are regular. Pelvic dimensions
26–26–31–19. The fetus is in longitudinal lie, the head presenting at the pelvic inlet,
fetal heartbeat 136 per min, rhythmical. Vaginal examination shows effaced cervix,
dilated 4 cm, amniotic sac intact. Head presentation. A pulsing loop of the cord is
palpated before the head. What is your diagnosis? What is the plan of management?
3. Primiparous patient aged 19 was admitted to the delivery department with con-
tractions every 5–7 min for 15 hours. Her waters broke 10 hours ago. Gestational
age 32 weeks. Examination findings: abdominal circumference 95 cm, fundal height
30 cm, pelvic dimensions 25–27–30–19. Fetal head is palpated on the right, pelvic
pole — at the left uterine wall, heartbeat is not heard. Light waters are leaking in
moderate amount from the vagina. Vaginal examination: narrow vagina of a nullipa-
rous woman, fetal left arm is in the vagina. Complete cervical dilation. No amniotic
sac. The left shoulder is presenting, fetal shoulder blade is palpated at the pubis.
The promontory cannot be reached, no exostoses in the lesser pelvis. What is your
NOTES
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ANSWERS TO TESTS AND CLINICAL SITUATIONS
Chapter 1. Fertilization, implantation and organogenesis

Tests: 1 — a; 2 — a; 3 — a; 4 — d; 5 — c; 6 — b; 7 — a; 8 — a; 9 — c; 10 — b;
11 — c; 12 — a.
Situations. 1. Insufficient first wave of cytotrophoblast invasion in spiral arteries.
2. No, the umbilical cord should have three vessels: two arteries and one vein.
Chapter 2. Physiological changes during pregnancy

Tests: 1 — a; 2 — d; 3 — c; 4 — d; 5 — a; 6 — a; 7 — a; 8 — d.
Situations. 1. Compensatory heart rate increase typical of this gestational age.
2. Physiological hemodilution that requires no treatment.
Chapter 3. Antenatal and postpartum care

Tests: 1 — c; 2 — d; 3 — c; 4 — b; 5 — c; 6 — d; 7 — b; 8 — a; 9 — b; 10 — d;
11 — b; 12 — b; 13 — b.
Situations. 1. Provide adequate latching to the breast.
2. Recommend the patient to see a pediatrician to establish the cause of the in-
fant’s restlessness: weight gain of over 500 g indicates that the mother has enough
breast milk.
Chapter 4. Diagnostics of pregnancy. Estimation of gestational age and expected

date of delivery. Methods of examination
Tests: 1 — c; 2 — b; 3 — c; 4 — b; 5 — c; 6 — b; 7 — c; 8 –d; 9 — b; 10 — c;
11 — a; 12 — d; 13 — a; 14 — b; 16 — d; 16 — a; 17 — a; 18 — c; 19 — d; 20 —
b; 21 — b; 22 — a.
Situations. 1. The due date is June 6.
2. Normal female pelvis dimensions.
Chapter 5. Female pelvis in obstetrics. Fetus in labor

Tests: 1 — b; 2 — c; 3 — b; 4 — c; 5 — b; 6 — a.
Situations. 1. 12 cm — 1.5 cm = 10.5 cm.
2. Transverse fetal lie.
Chapter 6. Origins of labor onset

Tests: 1 — a; 2 — b; 3 — b; 4 — c.
Chapter 7. Mechanism of labor in cephalic (vertex) presentation

Tests. 1 — a; 2 — d; 3 — b; 4 — a.
Situations. 1. Second stage of labor, occipitoanterior position.
2. First stage of labor, occipitoposterior position.
Chapter 8. Clinics and management of labor in vertex presentation

Tests: 1 — b; 2 — a; 3 — b; 4 — c; 5 — a; 6 — d; 7 — a; 8 — d; 9 — c; 10 — a.
Situations. 1. Diagnosis: gestation 40 weeks, left occipitoanterior position, first
stage of labor. Substantiation: cervical dilation 5 cm indicates the first stage of labor;
868 Obstetrics
the posterior fontanelle in front and to the left indicates left anterior position; the
posterior fontanelle below the anterior one indicates occiput presentation.
2. Diagnosis: gestation 40 weeks, occiput presentation, left occipitoanterior posi-
tion, second stage of labor. Substantiation: complete cervical dilation indicates the
second stage of labor; the posterior fontanelle in front and below the anterior one
indicates occipitoanterior position. The head occupies all the reference points in the
outlet plane, the sagittal suture in the anteroposterior diameter indicates the head
stationed in the outlet plane.
Chapter 9. Obstetric anesthesia

Tests: 1 — c; 2 — b; 3 — a; 4 — c.
Situations. 1. Excessively intensive labor. Analgesia or tocolysis is indicated.
Chapter 10. Breech presentation

Tests: 1 — c; 2 — a; 3 — e; 4 — a, d; 5 — a, c; 6 — a; 7 — c; 8 — a; 9 — b;
10 — b; 11 — a; 12 — b; 13 — d; 14 — d; 15 — a, b.
Situations. 1. Diagnosis: gestation 40 weeks, double footling presentation, first
stage of labor, young primipara. Management: emergency cesarean section consider-
ing fetal macrosomia (3900 g) and double footling presentation.
2. Diagnosis: gestation 40 weeks, frank breech presentation, first stage of labor.
Management: continue expectant management of vaginal delivery, in the second
stage render Tsovyanov I maneuver considering frank breech and estimated fetal
weight (3200 g).
Chapter 11. Physiology of postpartum period

Tests: 1 — c; 2 — b; 3 — b; 4 — c; 5 — c; 6 — c; 7 — c; 8 — a; 9 — b.
Situations. 1. Immediately after delivery.
2. Sheehan syndrome. Secondary hypogalactia. The infant needs supplementary feeding.
Chapter 12. Postpartum complications

Tests: 1 — d; 2 — a; 3 — b; 4 — e; 5 — d; 6 — c, d; 7 — a; 8 — b; 9 — d;
10 — a, d.
Situations. 1. Endometritis. Antibacterial therapy. Irrigation-aspiration drainage
of uterus.
2. Mastitis. Antibacterial therapy. Suppression of lactation.
Chapter 13. Physiology of neonate

Tests: 1 — b; 2 — a; 3 — b; 4 — b; 5 — a; 6 — b; 7 — d; 8 — c; 9 — a; 10 — c; 11 — b.
Situations. 1. Icterus of newborn requiring phototherapy.
2. Weight loss under 10%. Repeated weighing of the infant.
Chapter 14. Diseases of newborns

Tests: 1 — b; 2 — d; 3 — d; 4 — d; 5 — c; 6 — c.
Situations. 1. IUGR. 2. Pathological weight loss (over 10%).
Chapter 15. Hemolytic disease of fetus and newborn

Tests: 1 — c; 2 — d; 3 — e; 4 — a; 5 — c; 6 — d; 7 — e; 8 — e; 9 — b; 10 — e;
11 — b, c, d; 12 — b; 13 — d; 14 — d.
Situations. 1. Repeated blood test for antibodies. Rh affinity of the husband (the
baby’s father). If the husband is Rh(+), antenatal (at 28 weeks) and postnatal pre-
vention.
2. Administer ultrasound (hepatomegaly, systolic rate of blood flow in the middle
cerebral artery and other signs of hemolytic disease), amniocentesis to determine
bilirubin content in the amniotic fluid, respiratory distress syndrome prevention. The
issue of preterm termination of pregnancy depends on examination findings. Anti-Rh
prevention is meaningless in this case.
Chapter 16. Multiple pregnancy

Tests: 1 — c; 2 — a; 3 — c; 4 — d; 5 — d; 6 — b; 7 — d; 8 — c.
Situations. 1. Multiple pregnancy? Molar pregnancy? Ultrasound.
2. Cesarean section as prevention of twins collision.
Chapter 17. Abnormal labor

Tests: 1 — d; 2 — a; 3 — d; 4 — b; 5 — a.
Situations. 1. Primary uterine inertia. Amniotomy.
2. Excessively powerful labor. Epidural nerve block or acute tocolysis with beta-
adrenoreceptor agonists.
Chapter 18. Hemorrhage in obstetrics

Tests: 1 — b, c; 2 — b; 3 — a, b; 4 — a; 5 — a; 6 — c; 7 — a; 8 — d; 9 — c, d;
10 — c.
Situations. 1. Placental abruption. Emergency hospitalization.
2. Manual exploration of postpartum uterus walls. Removing fragments of pla-
cental tissue.
Chapter 19. Early toxicosis—hyperemesis gravidarum

Tests: 1 — c, d; 2 — b; 3 — c; 4 — b; 5 — d; 6 — c.
Situation 1. Pregnancy? Exacerbation of peptic ulcer? Test for choriogonadotro-
pine, ultrasound of uterus and appendages.
Chapter 20. Preeclampsia

Tests: 1 — c; 2 — d; 3 — c; 4 — c, d; 5 — c, d; 6 — d; 7 — c; 8 — b; 9 — a.
Situations. 1. Preeclampsia. Osmotherapy.
2. Eclampsia, placental abruption, intrauterine growth restriction. Cesarean section.
Chapter 21. Miscarriage. Premature (preterm) birth

Tests: 1 — d; 2 — a, d; 3 — b, c; 4 — b; 5 — c, d; 6 — b; 7 — c, d; 8 — d.
Situations. 1. Anembryonia. Termination of pregnancy.
2. Cervical insufficiency. Placing sutures on the cervix.
870 Obstetrics
Chapter 22. Pregnancy, labor and postpartum period in women with extragenital
disease
Tests on sections 22.1 and 22.2: 1 — b; 2 — c; 3 — a; 4 — a; 5 — a; 6 — a;
7 — a; 8 — a; 9 — b; 10 — a; 11 — a; 12 — d; 13 — a; 14 — a; 15 — a.
Situations. 1. Diagnosis: gestation 27–28 weeks, cephalic presentation, moderate
anemia. The patient requires investigations in the prenatal clinic setting: serum iron,
total protein tests. Therapy with iron supplements.
2. Diagnosis: 28 weeks gestation, threatened preterm labor, exacerbation of ges-
tational pyelonephritis. Investigations: urine culture and blood biochemistry tests,
ultrasound of kidneys, catheterization of ureters. Treatment should include restora-
tion of urine passage (ureteral stenting in case of urine passage disorder), antibacterial
therapy considering culture sensitivity, detoxifying therapy, uroseptic medications,
pregnancy-preserving therapy.
Tests on sections 22.3–22.9: 1 — a, b; 2 — a, c; 3 — a, c; 4 — a, c; 5 — a, c;
6 — b, c, d; 7 — a, b, d; 8 — a, c, e; 9 — a, b, c.
Situations. 1. Diagnosis: 39 weeks gestation, cephalic presentation, first stage of
labor, premature rupture of membranes, congenital heart defect (aortic insufficiency).
Management:
• vaginal delivery;
• adequate analgesia at all stages of labor;
• continuous monitoring of hemodynamic values and CTG monitoring;
• prevention of fetal hypoxia and hemorrhage;
• if maternal and/or fetal condition deteriorates, forceps delivery and/or episiotomy
are indicated to suppress/attenuate pushing in the second stage of labor.
2. Diagnosis: 26 weeks gestation, cephalic presentation, exacerbation of chronic
pyelonephritis, PE?
Management:
• hospitalization;
• antibacterial therapy;
• detoxifying therapy;
• balanced vitamin-rich diet;
• knee-elbow position for 10–15 min several times a day; sleeping on the
unaffected side;
• diathermy of pararenal area;
• drinking low mineral content water, cranberry water;
• prevention of dysbiosis and vaginitis.
Chapter 23. Postterm pregnancy

Tests: 1 — d; 2 — c; 3 — d; 4 — a; 5 — b; 6 — b; 7 — d.
Situations. 1. Term pregnancy. Examination of the fetus. Appointment in 7 days.
2. Term pregnancy. Fetoplacental insufficiency. Fetal hypoxia. Emergency hospi-
talization.
Chapter 24. Abnormal fetal lie and presentation

Tests: 1 — b, c, d; 2 — b, c, d; 4 — c; 5 — d; 6 — a; 7 — d; 8 — b; 9 — a; 10 — b.
Situations. 1. Diagnosis: 38 weeks gestation, sinciput presentation, first stage of
labor. Management: conservative management, functional assessment of the pelvis,
prevention of intrapartum hemorrhage.
2. Diagnosis: 38 weeks gestation, brow presentation, end of the first stage and
beginning of the second stage. Management: emergency cesarean section.
3. Diagnosis: 40 weeks gestation, pathological posterior asynclitism, fetal macro-
somia, end of first stage of labor. Management: emergency cesarean section.
4. Diagnosis: 38 weeks gestation, persistent occiput direct position, end of the first
stage, polyhydramnios. Management: emergency cesarean section.
Chapter 25. Contracted pelvis

Tests: 1 — c; 2 — d; 3 — b; 4 — a; 5 — c; 6 — a; 7 — b; 8 — b; 9 — b; 10 — b.
Situations. 1. Simple flat pelvis, fetal macrosomia. Cesarean section.
2. CPD. Cesarean section.
Chapter 26. Maternal obstetric trauma

Tests: 1 — e; 2 — a; 3 — a, d, e; 4 — c, d; 5 — a, c, d; 6 — c; 7 — a, d, e;
8 — b, d; 9 — a, e; 10 — b, d.
Situations. 1. CPD. Imminent uterine rupture. Emergency cesarean section.
2. Uterine rupture. Intranatal fetal demise. Hemorrhage, laparotomy. Repair of
uterine wall.
Chapter 27. Operative obstetrics

Tests: 1 — c; 2 — c; 3 — b, d; 4 — a, b, c; 5 — b, d; 6 — a, c, d; 7 — c, e;
8 — e; 9 — b; 10 — a, d; 11 — b, d; 12 — a; 13 — c; 14 — b; 15 — a; 16 — b;
17 — d; 18 — b, c, d; 19 — d; 20 — b, c; 21 — b; 22 — a, d; 23 — c.
Situations. 1. The second fetus in a transverse lie. Podalic version.
2. Cord presentation. Emergency cesarean section.
3. Second stage of preterm labor. Impacted transverse lie. Antenatal fetal demise.
Embryotomy.
Tests on section 27.4: 1 — a; 2 — b, d; 3 — a, b, c; 4 — c; 5 — b, c; 6 — c;
7 — b, d; 8 — d; 9 — b, d; 10 — a, c.
Situations. 1. Second stage of labor. Occiput position. Secondary uterine inertia.
Vacuum extraction.
2. Second stage of labor. Arterial hypertension. Acute fetal hypoxia. Anesthesia.
Forceps delivery.
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Textbook
ОBSTETRICS
Edited by V.E. Radzinskiy, A.M. Fuks, Сh.G. Gagaev
Главный редактор издательства Т.А. Андреева

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© Коллектив авторов, 2018

Cheleby G. Gagaev, Igor N. Kostin,

Radzinskiy Victor, MD, Professor, Head of Department of Obstetrics and

until the 17th century. For a long time, the ideas

describe the ovum of mammals and humans

1.1.1. Germ cells

Fig. 1.6. Spermatozoa

The mean lifespan of a spermatozoon after ejaculation is 48

The amount of follicles is not restored during a human lifetime; it

Atresia of follicles means their destruction

The lifespan of extrafollicular existence of an ovum is no longer

This premise is of fundamental importance in dealing with practical issues of

Corpus luteum (ultrasound)

Fertilization (conception) is a process when the male and female

Fig. 1.11. Spermatozoa attempting to penetrate the ovum (photomicrography)

Fig. 1.12. Spermatozoon penetrating the ovum (photo Lenart Nilsson)

1.2. EARLY PREGNANCY (FIRST TRIMESTER)

The primary trophoblast is a stem cell for most placental cells

Fig. 1.13. Morula 50–60 hours after fertilization

The embryoblast presented as an aggregation of a number of cells (inner cell

Blastogenesis includes the stage of free blastocyst and implanta-

The blastocyst invades energetically between epithelial cells of the endometrium

Fig. 1.15. Implantation complete: day 8 (photo Lenart Nilsson)

Implantation is only possible when endometrium is ready for

If blastocysts start interacting with insensitive (unprepared) endometrium, they

Implantation can only occur during the implantation window, a

1.3. SECOND TRIMESTER

1.3.1. Changes in the fetus and extraembryonic structures

Reaching its peak at 16-18 weeks, the second wave of cytotropho-

As a result, the cytotrophoblast invasion, taken all round, is a unique short-term

1.3.2. Development of placenta

In regards to its structure, the placenta meets the demands of

1.4. PLACENTAL PHYSIOLOGY

1.5. UMBILICAL CORD DEVELOPMENT

In the second trimester the umbilical cord shows the typical

Fig. 1.17. Twisting of umbilical vessels. Ultrasound color ﬂow mapping

Table 1.1. Umbilical length at diﬀerent gestational ages*

Gestational age, weeks M±SD, cm

cal diameter in late pregnancy is due to physiologic reduction of Wharton’s jelly in

1.6. AMNIOTIC FLUID COMPOSITION

By the end of week 20 the smooth chorion fuses with parietal

GESTATIONAL AGE (weeks)

Fig. 1.18. The volume of amniotic ﬂuid depending on gestational age

In the second trimester, the major producer of amniotic fluid is

Transmembranous exchange and swallowing of amniotic fluid by

The paraplacental route, or metabolism through extraplacental parts of fetal mem-

1.6.2. Composition of the amniotic fluid

1.7. CRITICAL PERIODS OF FETAL DEVELOPMENT

At critical periods the embryo is especially vulnerable to the damaging eﬀect of

1.8. FETAL PHYSIOLOGY

The first system to function in a fetus is the cardiovascular system

 During the period of 5–8 weeks,

Pulmonary arteries Pulmonary veins

Intrathoracic Extrathoracic Intrathoracic

1.8.2. Organs and systems

After 10 weeks of pregnancy FHR amounts to 140 beats per minute,

1.8.2.2. Fetal hemoglobin

Formation of new renal glomerules in the fetus is complete by 36

1.8.2.4. Gastrointestinal tract

Fetal intestinal peristalsis begins to function in the second trimes-

Intrauterine defecation and hence the presence of meconium in

During the period of 5–8 weeks,