O&G4 Notes - Terminology 2010 PDF

THE CHINESE UNIVERSITY OF HONG KONG MEDICAL YEAR IV
OBSTETRICS & GYNAECOLOGY MODULE
Terminology
2010
By
Class of 2011
Terminology 2010 Obstetrics & Gynaecology Module
IMPORTANT
This Terminology 2010 is based on the previous edition by Dr. Edward Chu on 1st January 2004. Without
previous contributions by our seniors and collegues, this book cannot be produced so successfully.
In this edition, reference was made to:-
(1) Obstetrics Illustrated (6th Ed.) by Hanretty, K.P. in 2003;

(2) Gynaecology Illustrated (5th Ed.) by Hart, D.M. & Norman, J. in 2000;
(3) Protocol for Obstetrics and Gynaecology of Prince of Wales Hospital, by Department of Obstetrics and
Gynaecology of The Chinese University of Hong Kong, last retrieved by class 2010 on January 2009,
Materials from the above stated sources were incorporated into this edition. The copyright belongs to the
authors and publishers of the respective sources. This Terminology 2010 solely serves as a self-study
material for medical year four students in obstetrics and gynaecology module, which is not intended for any
sales or profit making purposes. Students should refer to standard textbooks and the most updated guidelines
in case of any doubt or discrepancies. The author shall bear no responsibility to any consequences of using
this book.
5 September 2009
NOTICE FOR FIRST DRAFT EDITION
This is a preliminarily published draft version intended for peer review by colleagues in Obstetrics and
Gynaecology III Module 2009/10. Due to time constrains, this booklet, edited in three weeks time, is yet to
be perfect. I am sure that there must be typos, wrong figures or data in this book as proof-reading cannot be
done in such a short time. Please do write down anything wrong about this book and let me know. Any
comments to it are also appreciated.
11 October 2009
NOTICE FOR SECOND DRAFT EDITION

It comes to my attention that Terminology 2007 was uploaded to the medical students forum in early
November. I personally had taken no part in editing it, and Terminology 2010 was edited based on
Terminology 2004 with addition of illustrations and protocol. In this second edition, new changes made in
the Terminology 2007 were incorporated into Terminology 2010 with the best effort. I hereby pay my
acknowledgement to the yet unidentified editors of Terminology 2007. Pleases feel free to inform me if you
are one of them.
9 November 2009
I hope you will find this book useful Terminology, Protocol and Illustrated all in one.
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DEDICATION
For ladies, wives, mothers, and our future generations.
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Brief Content
GENERAL OBSTETRICS ............................................................................................................................. 18
0. Obstetrics................................................................................................................................................................................. 18
1. Foetal anatomy ........................................................................................................................................................................ 19
2. Maternal anatomy .................................................................................................................................................................... 24
3. Antepartum .............................................................................................................................................................................. 30
4. Malpresenation ........................................................................................................................................................................ 41
5. Preterm labour and PPROM .................................................................................................................................................... 47
6. Postpartum............................................................................................................................................................................... 53
7. Obstetric statistics.................................................................................................................................................................... 62
8. Miscellaneous topics in General Obstetrics............................................................................................................................. 65
FOETAL MEDICINE .................................................................................................................................... 70
0. Foetal medicine ....................................................................................................................................................................... 70
1. Chromosomal disorders ........................................................................................................................................................... 71
2. Congenital abnormalities ......................................................................................................................................................... 78
3. Genetic disorders ..................................................................................................................................................................... 83
4. Foetal Haemolytic Diseases .................................................................................................................................................... 85
5. Foetal diagnosis and therapy ................................................................................................................................................... 88
6. Foetal growth and Monitoring ................................................................................................................................................. 92
7. Amniotic fluid ......................................................................................................................................................................... 99
8. Foetal well-being ................................................................................................................................................................... 106
9. Multiple pregnancy................................................................................................................................................................ 108
MATERNAL MEDICINE ............................................................................................................................ 114
1. Changes in pregnancy ........................................................................................................................................................... 114
2. Diabetes mellitus ................................................................................................................................................................... 118
3. Preeclampsia.......................................................................................................................................................................... 124
4. Other maternal medical diseases ........................................................................................................................................... 133
LABOUR MANAGEMENT ......................................................................................................................... 146
0. Intrapartum management ....................................................................................................................................................... 146
1. Normal Labour ...................................................................................................................................................................... 148
2. Inducation of Labour and Failure to Progress ....................................................................................................................... 162
3. Pain relief and maternal monitoring ...................................................................................................................................... 172
4. Intrapartum foetal monitoring ............................................................................................................................................... 173
5. Operative delivery ................................................................................................................................................................. 181
GENERAL GYNAECOLOGY ...................................................................................................................... 193
0. Gynaecology.......................................................................................................................................................................... 193
1. Menstrual problems ............................................................................................................................................................... 194
2. Birth control .......................................................................................................................................................................... 214
3. Disorders of early pregnancy................................................................................................................................................. 224
4. Endometriosis and Adenomyosis .......................................................................................................................................... 237
5. Benign gynaecological tumours ............................................................................................................................................ 241
6. Gynaecological infection ....................................................................................................................................................... 246
7. Growth and Development...................................................................................................................................................... 250
8. Menopause and HRT ............................................................................................................................................................. 252
9. Gynaecological surgery & investigations .............................................................................................................................. 256
10. Miscellaneous topics in gynaecology .................................................................................................................................... 267
REPRODUCTIVE MEDICINE ................................................................................................................... 269
0. Reproductive medicine and Endocrinology .......................................................................................................................... 269
1. Anovulation and endocrinopathy .......................................................................................................................................... 270
2. Assisted reproductive procedures .......................................................................................................................................... 276
3. Male infertility....................................................................................................................................................................... 281
4. Sexual dysfunction ................................................................................................................................................................ 283
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ONCOLOGY ................................................................................................................................................. 284
0. Gynae-oncology .................................................................................................................................................................... 284
1. Malignant neoplasms of vagina and vulva ............................................................................................................................ 285
2. Malignant neoplasms of ovary .............................................................................................................................................. 288
3. Malignant neoplasms of uterine cervix ................................................................................................................................. 291
4. Malignant neoplasms of uterine corpus ................................................................................................................................. 304
5. Trophoblastic diseases ........................................................................................................................................................... 310
6. Disease monitoring and treatment in gynae-oncology .......................................................................................................... 315
UROGYNAECOLOGY ................................................................................................................................. 317
0. Urogynaecology .................................................................................................................................................................... 317
1. Genital prolapse..................................................................................................................................................................... 318
2. Urinary incontinence ............................................................................................................................................................. 329
3. Other topics in urogynaecology............................................................................................................................................. 333
DRUGS .......................................................................................................................................................... 338
0. Drugs ..................................................................................................................................................................................... 338
1. Oxytocics............................................................................................................................................................................... 339
2. Tocolytic ............................................................................................................................................................................... 344
3. Anti-hypertensives................................................................................................................................................................. 350
4. Anticonvulsants ..................................................................................................................................................................... 352
5. Steroids and Hormonal Replacement Therapy ...................................................................................................................... 355
6. Antibiotics ............................................................................................................................................................................. 359
7. Anticoagulants ....................................................................................................................................................................... 361
8. Others .................................................................................................................................................................................... 362
MISCELLANEOUS ...................................................................................................................................... 363
1. English usage......................................................................................................................................................................... 363
2. Basic clinical skills ................................................................................................................................................................ 364
3. Infections ............................................................................................................................................................................... 373
INDEX ........................................................................................................................................................... 396
FIGURE LEGEND ....................................................................................................................................... 401
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Detailed Content
GENERAL OBSTETRICS ............................................................................................................................. 18
0. Obstetrics ............................................................................................................................................................................... 18
1. Foetal anatomy ...................................................................................................................................................................... 19
Foetal skull ................................................................................................................................................................................... 19
Fontanelle ..................................................................................................................................................................................... 19
Sagittal suture............................................................................................................................................................................... 19
Sinciput ........................................................................................................................................................................................ 19
Vertex ........................................................................................................................................................................................... 19
Lie ................................................................................................................................................................................................ 19
Presentation .................................................................................................................................................................................. 20
Position ........................................................................................................................................................................................ 20
Denominator................................................................................................................................................................................. 20
2. Maternal anatomy ................................................................................................................................................................. 24
Levator ani ................................................................................................................................................................................... 24
Urogenital diaphragm................................................................................................................................................................... 24
Pelvis ............................................................................................................................................................................................ 24
Pelvic Inlet ................................................................................................................................................................................... 24
Pelvic Cavity ................................................................................................................................................................................ 24
Pelvic Outlet ................................................................................................................................................................................. 24
Ischial spine.................................................................................................................................................................................. 25
Pubic symphysis ........................................................................................................................................................................... 25
Subpubic arch ............................................................................................................................................................................... 25
Intertuberous diameter ................................................................................................................................................................. 25
Shape of pelvis ............................................................................................................................................................................. 26
Gynaecoid .................................................................................................................................................................................... 26
Anthropoid ................................................................................................................................................................................... 26
Android ........................................................................................................................................................................................ 27
Platypoid ...................................................................................................................................................................................... 27
Funnel pelvis ................................................................................................................................................................................ 27
Contracted pelvis.......................................................................................................................................................................... 28
Cephalopelvic disproportion ........................................................................................................................................................ 28
Pelvimetry .................................................................................................................................................................................... 28
Rickets.......................................................................................................................................................................................... 28
Lordosis........................................................................................................................................................................................ 28
Os ................................................................................................................................................................................................. 29
Lower segment ............................................................................................................................................................................. 29
Dextrorotation of uterus ............................................................................................................................................................... 29
3. Antepartum ............................................................................................................................................................................ 30
Pre-conception counselling .......................................................................................................................................................... 30
Antepartum care ........................................................................................................................................................................... 31
Pregnancy test .............................................................................................................................................................................. 32
Dating of pregnancy ..................................................................................................................................................................... 33
Antepartum haemorrhage (APH) ................................................................................................................................................. 35
Placenta praevia ........................................................................................................................................................................... 35
Abruptio placentae ....................................................................................................................................................................... 38
Couvelaire uterus ......................................................................................................................................................................... 39
Velamentous Insertion of the Cord .............................................................................................................................................. 39
Vasa praevia ................................................................................................................................................................................. 39
APH of unknown origin ............................................................................................................................................................... 40
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4. Malpresenation ...................................................................................................................................................................... 41
Malpresentation ............................................................................................................................................................................ 41
Breech presentation ...................................................................................................................................................................... 41
External Cephalic Version (ECV) ................................................................................................................................................ 44
Cord prolapse ............................................................................................................................................................................... 46
5. Preterm labour and PPROM ............................................................................................................................................... 47
Preterm labour .............................................................................................................................................................................. 47
Braxton Hicks contractions .......................................................................................................................................................... 48
Preterm delivery ........................................................................................................................................................................... 48
Rupture of membranes ................................................................................................................................................................. 49
Amniostrix ................................................................................................................................................................................... 50
Chorioamnionitis .......................................................................................................................................................................... 50
Cervical incompetence ................................................................................................................................................................. 52
6. Postpartum............................................................................................................................................................................. 53
Postpartum care ............................................................................................................................................................................ 53
Postpartum fever .......................................................................................................................................................................... 54
Postpartum haemorrhage .............................................................................................................................................................. 54
Uterine atony ................................................................................................................................................................................ 55
Uterine rupture ............................................................................................................................................................................. 56
Uterine inversion .......................................................................................................................................................................... 57
Sheehan syndrome ....................................................................................................................................................................... 58
Puerperium ................................................................................................................................................................................... 59
Involution ..................................................................................................................................................................................... 59
Lochia .......................................................................................................................................................................................... 59
Engorgement of breasts ................................................................................................................................................................ 59
Colostrum ..................................................................................................................................................................................... 59
Lactation ...................................................................................................................................................................................... 60
Breast-feeding .............................................................................................................................................................................. 60
Breast milk ................................................................................................................................................................................... 60
Postpartum depression ................................................................................................................................................................. 61
Postpartum blue............................................................................................................................................................................ 61
Postpartum psychosis ................................................................................................................................................................... 61
7. Obstetric statistics ................................................................................................................................................................. 62
Maternal mortality........................................................................................................................................................................ 62
Perinatal mortality ........................................................................................................................................................................ 62
Stillbirth ....................................................................................................................................................................................... 62
Intrauterine death ......................................................................................................................................................................... 63
Neonatal death.............................................................................................................................................................................. 64
8. Miscellaneous topics in General Obstetrics......................................................................................................................... 65
Advanced maternal age ................................................................................................................................................................ 65
Fecundity...................................................................................................................................................................................... 65
Postterm ....................................................................................................................................................................................... 66
Gravid .......................................................................................................................................................................................... 67
Grand multipara ........................................................................................................................................................................... 67
Trimester ...................................................................................................................................................................................... 67
Placenta ........................................................................................................................................................................................ 67
Obstetric surgery .......................................................................................................................................................................... 67
Obstetric emergency..................................................................................................................................................................... 67
Birth trauma ................................................................................................................................................................................. 68
Subaponeurotic haematoma ......................................................................................................................................................... 68
Cerebral palsy .............................................................................................................................................................................. 68
Jehovahs witness ......................................................................................................................................................................... 69
Consanguinity .............................................................................................................................................................................. 69
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FOETAL MEDICINE .................................................................................................................................... 70
0. Foetal medicine ...................................................................................................................................................................... 70
1. Chromosomal disorders ........................................................................................................................................................ 71
Chromosomal abnormalities ........................................................................................................................................................ 71
Biochemical screening ................................................................................................................................................................. 72
Alpha-feto protein ........................................................................................................................................................................ 72
Human chorionic gonadotropin .................................................................................................................................................... 73
Nuchal translucency ..................................................................................................................................................................... 73
Trisomy ........................................................................................................................................................................................ 73
Non-dysjunction ........................................................................................................................................................................... 73
Down syndrome ........................................................................................................................................................................... 74
Edward syndrome ........................................................................................................................................................................ 75
Patau syndrome ............................................................................................................................................................................ 76
Klinefelter syndrome .................................................................................................................................................................... 76
Turner syndrome .......................................................................................................................................................................... 77
2. Congenital abnormalities ...................................................................................................................................................... 78
Neural tube defect ........................................................................................................................................................................ 78
Gastroschisis ................................................................................................................................................................................ 79
Omphalocele ................................................................................................................................................................................ 79
Hydrops foetalis ........................................................................................................................................................................... 80
Renal agenesis .............................................................................................................................................................................. 81
Potter syndrome ........................................................................................................................................................................... 82
Teratogen ..................................................................................................................................................................................... 82
3. Genetic disorders ................................................................................................................................................................... 83
Genetic disorder ........................................................................................................................................................................... 83
Haemophilia ................................................................................................................................................................................. 83
4. Foetal Haemolytic Diseases................................................................................................................................................... 85
Thalassemia .................................................................................................................................................................................. 85
Rhesus .......................................................................................................................................................................................... 86
Rhesus D iso-immunisation ......................................................................................................................................................... 86
5. Foetal diagnosis and therapy ................................................................................................................................................ 88
Amniocentesis .............................................................................................................................................................................. 88
Chorionic villus sampling (CVS) ................................................................................................................................................. 88
Cordocentesis ............................................................................................................................................................................... 89
Genetic counselling ...................................................................................................................................................................... 89
Ultrasound (Obstetrics) ................................................................................................................................................................ 90
Doppler effect .............................................................................................................................................................................. 91
Doppler studies ............................................................................................................................................................................ 91
6. Foetal growth and Monitoring ............................................................................................................................................. 92
Small-for-gestational-age (SGA) ................................................................................................................................................. 92
Intrauterine growth restriction (IUGR) ........................................................................................................................................ 93
Macrosomia .................................................................................................................................................................................. 96
Crown-rump length ...................................................................................................................................................................... 97
Abdominal circumference ............................................................................................................................................................ 97
Biparietal diameter ....................................................................................................................................................................... 98
Femur length ................................................................................................................................................................................ 98
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7. Amniotic fluid ........................................................................................................................................................................ 99
Amniotic fluid .............................................................................................................................................................................. 99
Amniotic fluid index (AFI) ........................................................................................................................................................ 100
Oligohydramnios ........................................................................................................................................................................ 101
Oligohydramnios sequence ........................................................................................................................................................ 102
Polyhydramnios ......................................................................................................................................................................... 102
Meconium stained liquor (MSL) ................................................................................................................................................ 104
Amnioinfusion ........................................................................................................................................................................... 105
Amnioreduction ......................................................................................................................................................................... 105
8. Foetal well-being .................................................................................................................................................................. 106
Foetal well-being........................................................................................................................................................................ 106
Biophysical profile ..................................................................................................................................................................... 107
Foetal movement ........................................................................................................................................................................ 107
Contraction stress test ................................................................................................................................................................ 107
9. Multiple pregnancy ............................................................................................................................................................. 108
Multiple pregnancy .................................................................................................................................................................... 108
Twin pregnancy.......................................................................................................................................................................... 108
Conjoint twin.............................................................................................................................................................................. 113
Twin-twin transfusion ................................................................................................................................................................ 113
Lamda sign ................................................................................................................................................................................. 113
MATERNAL MEDICINE ............................................................................................................................ 114
1. Changes in pregnancy ......................................................................................................................................................... 114
Physiological changes in pregnancy .......................................................................................................................................... 114
Pharmacology in pregnancy ....................................................................................................................................................... 116
Maternal medicine...................................................................................................................................................................... 117
2. Diabetes mellitus .................................................................................................................................................................. 118
Diabetes mellitus ........................................................................................................................................................................ 118
Gestational diabetes ................................................................................................................................................................... 119
3. Preeclampsia ........................................................................................................................................................................ 124
Hypertension in pregnancy ........................................................................................................................................................ 124
Blood pressure measurement ..................................................................................................................................................... 125
Preeclampsia .............................................................................................................................................................................. 125
Eclampsia ................................................................................................................................................................................... 130
HELLP syndrome ...................................................................................................................................................................... 132
4. Other maternal medical diseases ....................................................................................................................................... 133
Heart disease .............................................................................................................................................................................. 133
Mitral stenosis ............................................................................................................................................................................ 134
Anaemia ..................................................................................................................................................................................... 135
Macrocytosis .............................................................................................................................................................................. 135
Iron deficiency ........................................................................................................................................................................... 136
Asymptomatic bacteriuria .......................................................................................................................................................... 136
Disseminated intravascular coagulopathy (DIC)........................................................................................................................ 136
Thrombocytopenia ..................................................................................................................................................................... 137
Thromboembolism ..................................................................................................................................................................... 138
Pulmonary embolism ................................................................................................................................................................. 139
Amniotic fluid embolism ........................................................................................................................................................... 140
Systemic Lupus Erythematosus (SLE) ....................................................................................................................................... 140
Antiphospholipid syndrome ....................................................................................................................................................... 141
Epilepsy...................................................................................................................................................................................... 141
Acute fatty liver ......................................................................................................................................................................... 143
Appendicitis ............................................................................................................................................................................... 143
Thyroid disorder ......................................................................................................................................................................... 144
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LABOUR MANAGEMENT ......................................................................................................................... 146
0. Intrapartum management .................................................................................................................................................. 146
Partogram ................................................................................................................................................................................... 147
1. Normal Labour .................................................................................................................................................................... 148
Labour ........................................................................................................................................................................................ 148
Second stage of labour ............................................................................................................................................................... 150
Drinking during labour ............................................................................................................................................................... 152
Caput succedaneum.................................................................................................................................................................... 153
Moulding .................................................................................................................................................................................... 153
Engage........................................................................................................................................................................................ 153
Station ........................................................................................................................................................................................ 154
Third stage of labour .................................................................................................................................................................. 155
Neonatal Resuscitation ............................................................................................................................................................... 156
Controlled cord traction ............................................................................................................................................................. 156
Routine management of placenta after delivery ......................................................................................................................... 157
Retained placenta ....................................................................................................................................................................... 158
Morbid adherence of placenta .................................................................................................................................................... 158
Manual removal of placenta (MROP) ........................................................................................................................................ 159
Neonatological consultation ....................................................................................................................................................... 160
Postnatal discharge ..................................................................................................................................................................... 161
2. Inducation of Labour and Failure to Progress ................................................................................................................. 162
Induction of labour ..................................................................................................................................................................... 162
Bishop score ............................................................................................................................................................................... 163
Amniotomy ................................................................................................................................................................................ 163
Amnihook .................................................................................................................................................................................. 163
Uterine hyperstimulation ............................................................................................................................................................ 164
Failure to progress ...................................................................................................................................................................... 165
Incoordinate uterine contraction................................................................................................................................................. 165
Trial of labour ............................................................................................................................................................................ 165
Obstructed labour ....................................................................................................................................................................... 165
Deep transverse arrest ................................................................................................................................................................ 166
Dystocia ..................................................................................................................................................................................... 166
Shoulder dystocia ....................................................................................................................................................................... 167
Asynclitism ................................................................................................................................................................................ 169
Occipito-posterior ...................................................................................................................................................................... 169
Vaginal breech delivery ............................................................................................................................................................. 170
Loveset maneuver ...................................................................................................................................................................... 171
3. Pain relief and maternal monitoring ................................................................................................................................. 172
Obstetric anaesthesia .................................................................................................................................................................. 172
Entonox ...................................................................................................................................................................................... 172
Narcotic analgesia ...................................................................................................................................................................... 172
Pethidine .................................................................................................................................................................................... 172
Epidural anaesthesia ................................................................................................................................................................... 172
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4. Intrapartum foetal monitoring ........................................................................................................................................... 173
Intrapartum foetal monitoring .................................................................................................................................................... 173
Intermittent auscultation............................................................................................................................................................. 174
Cardiotocogram (CTG) .............................................................................................................................................................. 174
Foetal heart rate pattern .............................................................................................................................................................. 175
Foetal bradycardia ...................................................................................................................................................................... 178
Foetal scalp electrode ................................................................................................................................................................. 178
Foetal scalp blood sampling ....................................................................................................................................................... 179
Amnioscope ............................................................................................................................................................................... 179
Foetal distress ............................................................................................................................................................................. 179
Apgar score ................................................................................................................................................................................ 180
Birth asphyxia ............................................................................................................................................................................ 180
5. Operative delivery ............................................................................................................................................................... 181
Episiotomy ................................................................................................................................................................................. 181
Cervical Tear .............................................................................................................................................................................. 182
Perineal tear................................................................................................................................................................................ 182
Operative delivery ...................................................................................................................................................................... 183
Instrumental delivery ................................................................................................................................................................. 183
Forceps ....................................................................................................................................................................................... 185
Vacuum extraction ..................................................................................................................................................................... 188
Caesarean section ....................................................................................................................................................................... 189
Trial of scar ................................................................................................................................................................................ 192
GENERAL GYNAECOLOGY ...................................................................................................................... 193
0. Gynaecology ......................................................................................................................................................................... 193
1. Menstrual problems ............................................................................................................................................................ 194
Menstrual disorders .................................................................................................................................................................... 194
Menstrual cycle .......................................................................................................................................................................... 194
Amenorrhea................................................................................................................................................................................ 195
Oligomenorrhea ......................................................................................................................................................................... 198
Cryptomenorrhea ....................................................................................................................................................................... 198
Polycystic Ovarian Disease (PCOD).......................................................................................................................................... 199
Kallman syndrome ..................................................................................................................................................................... 202
Anorexia nervosa ....................................................................................................................................................................... 203
Prolactin ..................................................................................................................................................................................... 204
Hyperprolactinaemia .................................................................................................................................................................. 204
Galactorrhoea ............................................................................................................................................................................. 206
Bromocriptine ............................................................................................................................................................................ 206
Testicular feminisation syndrome .............................................................................................................................................. 206
Asherman syndrome................................................................................................................................................................... 206
Menorrhagia ............................................................................................................................................................................... 207
Metropathia haemorrhagia ......................................................................................................................................................... 208
Dysfunctional uterine bleeding .................................................................................................................................................. 208
Postcoital bleeding ..................................................................................................................................................................... 211
Postmenopausal bleeding ........................................................................................................................................................... 211
Dysmenorrhoea .......................................................................................................................................................................... 212
Mittelschmerz............................................................................................................................................................................. 212
Premenstrual syndrome .............................................................................................................................................................. 213
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2. Birth control......................................................................................................................................................................... 214
Contraception ............................................................................................................................................................................. 214
Pearl index.................................................................................................................................................................................. 214
Life table analysis ...................................................................................................................................................................... 215
Effectiveness .............................................................................................................................................................................. 215
Method ....................................................................................................................................................................................... 215
Calendar method ........................................................................................................................................................................ 216
Condom ...................................................................................................................................................................................... 216
Combined oral contraceptives .................................................................................................................................................... 217
Seven-day rule............................................................................................................................................................................ 219
Progestogen-only pill ................................................................................................................................................................. 219
Progestogen injectable ............................................................................................................................................................... 219
Intrauterine contraceptive device (IUCD) .................................................................................................................................. 220
Levonorgestrel intra-uterine system ........................................................................................................................................... 222
Emergency contraception / Postcoital contraception.................................................................................................................. 222
Sterilisation ................................................................................................................................................................................ 223
Vasectomy .................................................................................................................................................................................. 223
3. Disorders of early pregnancy ............................................................................................................................................. 224
Viable ......................................................................................................................................................................................... 224
Termination of pregnancy .......................................................................................................................................................... 224
Early pregnancy complications .................................................................................................................................................. 225
Abortion ..................................................................................................................................................................................... 226
Recurrent abortion...................................................................................................................................................................... 228
Septic abortion ........................................................................................................................................................................... 230
Ectopic pregnancy ...................................................................................................................................................................... 231
Pseudo gestational sac ................................................................................................................................................................ 234
Corpus luteal cyst ....................................................................................................................................................................... 234
Hyperemesis gravidarum ........................................................................................................................................................... 234
Minor disorders of pregnancy .................................................................................................................................................... 235
4. Endometriosis and Adenomyosis ....................................................................................................................................... 237
Endometriosis............................................................................................................................................................................. 237
Adenomyosis .............................................................................................................................................................................. 240
5. Benign gynaecological tumours .......................................................................................................................................... 241
Benign ovarian tumour ............................................................................................................................................................... 241
Physiological cysts ..................................................................................................................................................................... 241
Follicular cyst............................................................................................................................................................................. 241
Ovarian cystadenoma ................................................................................................................................................................. 241
Dermoid cyst .............................................................................................................................................................................. 242
Teratoma .................................................................................................................................................................................... 242
Nabothian cyst............................................................................................................................................................................ 242
Fibroid ........................................................................................................................................................................................ 243
6. Gynaecological infection ..................................................................................................................................................... 246
Pelvic inflammatory disease....................................................................................................................................................... 246
Bartholins Gland ....................................................................................................................................................................... 249
Pyometra .................................................................................................................................................................................... 249
7. Growth and Development ................................................................................................................................................... 250
Adolescence ............................................................................................................................................................................... 250
Puberty ....................................................................................................................................................................................... 250
Precocious puberty ..................................................................................................................................................................... 250
Tanner staging ............................................................................................................................................................................ 250
Hirsutism .................................................................................................................................................................................... 251
Virilism ...................................................................................................................................................................................... 251
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8. Menopause and HRT .......................................................................................................................................................... 252
Menopause ................................................................................................................................................................................. 252
Climacteric ................................................................................................................................................................................. 252
Osteoporosis ............................................................................................................................................................................... 252
Oestrogens and Progesterone ..................................................................................................................................................... 253
Hormonal replacement therapy .................................................................................................................................................. 254
9. Gynaecological surgery & investigations .......................................................................................................................... 256
Gynaecological surgery .............................................................................................................................................................. 256
Curettage .................................................................................................................................................................................... 257
Hysterotomy ............................................................................................................................................................................... 257
Endometrial ablation .................................................................................................................................................................. 258
Myomectomy ............................................................................................................................................................................. 259
Hysterectomy ............................................................................................................................................................................. 260
Hysteroscopy.............................................................................................................................................................................. 263
Cryotherapy................................................................................................................................................................................ 264
Electrocautery ............................................................................................................................................................................ 264
Cold coagulation ........................................................................................................................................................................ 264
Marsupialisation ......................................................................................................................................................................... 264
Endometrial sampling ................................................................................................................................................................ 265
Endometrial sampler .................................................................................................................................................................. 265
Hysterosalpingogram ................................................................................................................................................................. 266
10. Miscellaneous topics in gynaecology .................................................................................................................................. 267
Retroversion of uterus ................................................................................................................................................................ 267
Chronic pelvic pain .................................................................................................................................................................... 267
Imperforate hymen ..................................................................................................................................................................... 267
REPRODUCTIVE MEDICINE ................................................................................................................... 269
0. Reproductive medicine and Endocrinology ...................................................................................................................... 269
1. Anovulation and endocrinopathy ....................................................................................................................................... 270
Infertility .................................................................................................................................................................................... 270
Anovulation................................................................................................................................................................................ 272
Ovulation.................................................................................................................................................................................... 273
Spinnbarkeit ............................................................................................................................................................................... 273
Ferning ....................................................................................................................................................................................... 273
Fertilisation ................................................................................................................................................................................ 273
Conception ................................................................................................................................................................................. 274
Luteal phase ............................................................................................................................................................................... 274
Luteal phase insufficiency.......................................................................................................................................................... 274
Follicular phase .......................................................................................................................................................................... 274
Basal body temperature .............................................................................................................................................................. 274
Postcoital test ............................................................................................................................................................................. 275
2. Assisted reproductive procedures ...................................................................................................................................... 276
Assisted Reproductive Technology (ART) ................................................................................................................................ 276
Ovulation induction.................................................................................................................................................................... 277
Confirmation of ovulation .......................................................................................................................................................... 277
Clomiphene ................................................................................................................................................................................ 278
In vitro fertilisation(IVF) ........................................................................................................................................................... 279
Insemination ............................................................................................................................................................................... 279
Intra-cytoplasmic sperm injection (ICSI) ................................................................................................................................... 279
Ovarian Hyperstimulation Syndrome (OHSS) ........................................................................................................................... 280
3. Male infertility ..................................................................................................................................................................... 281
Spermatogenesis......................................................................................................................................................................... 281
Male infertility ........................................................................................................................................................................... 281
Semen analysis ........................................................................................................................................................................... 282
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4. Sexual dysfunction............................................................................................................................................................... 283
Sexual dysfunction ..................................................................................................................................................................... 283
Libido ......................................................................................................................................................................................... 283
Vaginismus................................................................................................................................................................................. 283
Dyspareunia ............................................................................................................................................................................... 283
ONCOLOGY ................................................................................................................................................. 284
0. Gynae-oncology ................................................................................................................................................................... 284
1. Malignant neoplasms of vagina and vulva ........................................................................................................................ 285
Staging of CA vagina ................................................................................................................................................................. 285
Staging of CA vulva ................................................................................................................................................................... 287
2. Malignant neoplasms of ovary ........................................................................................................................................... 288
Ovarian cancer ........................................................................................................................................................................... 288
Borderline malignancy of ovary ................................................................................................................................................. 289
Germ cell tumour ....................................................................................................................................................................... 289
Dysgerminoma ........................................................................................................................................................................... 290
Yolk sac tumour ......................................................................................................................................................................... 290
Krukenberg tumour .................................................................................................................................................................... 290
3. Malignant neoplasms of uterine cervix .............................................................................................................................. 291
Transformation zone .................................................................................................................................................................. 291
Cervical intraepithelial neoplasm (CIN) .................................................................................................................................... 292
Pap smear ................................................................................................................................................................................... 293
Spatula........................................................................................................................................................................................ 294
Cyutobrush ................................................................................................................................................................................. 294
Bethesda ..................................................................................................................................................................................... 295
Colposcopy................................................................................................................................................................................. 296
Dyskaryosis ................................................................................................................................................................................ 297
Koilocyte .................................................................................................................................................................................... 297
Acetowhite ................................................................................................................................................................................. 297
Loop electrosurgical excisional procedure (LEEP) .................................................................................................................... 297
Cervical cancer ........................................................................................................................................................................... 298
Exenteration ............................................................................................................................................................................... 302
Staging of CA cervix .................................................................................................................................................................. 303
4. Malignant neoplasms of uterine corpus............................................................................................................................. 304
Endometrial hyperplasia............................................................................................................................................................. 304
Endometrial carcinoma .............................................................................................................................................................. 306
Staging of CA endometrium ...................................................................................................................................................... 309
5. Trophoblastic diseases ........................................................................................................................................................ 310
Gestational trophoblastic disease (Molar Pregnancy) ................................................................................................................ 310
Hydatiform mole ........................................................................................................................................................................ 310
Invasive mole (Destructive mole, Villous choriocarcinoma) ..................................................................................................... 312
Choriocarcinoma ........................................................................................................................................................................ 313
Residual trophoblastic disease ................................................................................................................................................... 313
Bagshawe score .......................................................................................................................................................................... 314
Staging of GTD .......................................................................................................................................................................... 314
6. Disease monitoring and treatment in gynae-oncology...................................................................................................... 315
Tumour marker .......................................................................................................................................................................... 315
CA125 ........................................................................................................................................................................................ 315
Chemotherapy ............................................................................................................................................................................ 315
Radiotherapy .............................................................................................................................................................................. 316
Palliative .................................................................................................................................................................................... 316
- 14 -
UROGYNAECOLOGY ................................................................................................................................. 317
0. Urogynaecology ................................................................................................................................................................... 317
1. Genital prolapse................................................................................................................................................................... 318
Genital prolapse ......................................................................................................................................................................... 318
Cystocele .................................................................................................................................................................................... 320
Urethrocele ................................................................................................................................................................................. 320
Rectocele .................................................................................................................................................................................... 320
Enterocele................................................................................................................................................................................... 321
Uterine prolapse ......................................................................................................................................................................... 321
Vault prolapse ............................................................................................................................................................................ 321
Examination of genital prolapse ................................................................................................................................................. 322
Sims speculum .......................................................................................................................................................................... 322
Pad test ....................................................................................................................................................................................... 323
Ring pessary ............................................................................................................................................................................... 323
Colporrhaphy ............................................................................................................................................................................. 324
2. Urinary incontinence........................................................................................................................................................... 329
Urgency ...................................................................................................................................................................................... 329
Incontinence ............................................................................................................................................................................... 329
Urinary incontinence .................................................................................................................................................................. 329
Stress incontinence ..................................................................................................................................................................... 329
Urodynamic Stress Incontinence (USI)...................................................................................................................................... 329
Genuine stress incontinence ....................................................................................................................................................... 329
Urge incontinence ...................................................................................................................................................................... 330
Overflow incontinence ............................................................................................................................................................... 330
True incontinence ....................................................................................................................................................................... 330
Reflex incontinence.................................................................................................................................................................... 330
Colposuspension ........................................................................................................................................................................ 330
3. Other topics in urogynaecology .......................................................................................................................................... 333
Frequency of micturition ............................................................................................................................................................ 333
Nocturia...................................................................................................................................................................................... 333
Dysuria ....................................................................................................................................................................................... 333
Interstitial cystitis ....................................................................................................................................................................... 333
Voiding disorder ........................................................................................................................................................................ 333
Detrusor Overactivity (DO) ....................................................................................................................................................... 333
Detrusor Overactivity Incontinence (DOI)................................................................................................................................. 333
Detrusor instability ..................................................................................................................................................................... 334
Urodynamic study ...................................................................................................................................................................... 334
Uroflowmetry ............................................................................................................................................................................. 334
Cystoscopy ................................................................................................................................................................................. 334
Cystometry ................................................................................................................................................................................. 335
- 15 -
DRUGS .......................................................................................................................................................... 338
0. Drugs .................................................................................................................................................................................... 338
1. Oxytocics .............................................................................................................................................................................. 339
Oxytocin ..................................................................................................................................................................................... 339
Syntocinon ................................................................................................................................................................................. 340
Syntometrine .............................................................................................................................................................................. 340
Ergometrine ................................................................................................................................................................................ 341
Prostaglandin .............................................................................................................................................................................. 341
Misoprostol ................................................................................................................................................................................ 341
Misoprostol (Cytotec) ................................................................................................................................................................ 342
Gemeprost (Cervagem) .............................................................................................................................................................. 342
Prostaglandin E2 (Dinoprostone) ............................................................................................................................................... 343
Sulprostone................................................................................................................................................................................. 343
Hemabate (Carboprost) .............................................................................................................................................................. 343
2. Tocolytic ............................................................................................................................................................................... 344
General Guideline ...................................................................................................................................................................... 345
Nifedipine (as tocolytics) ........................................................................................................................................................... 346
Sulindac...................................................................................................................................................................................... 346
Atosiban ..................................................................................................................................................................................... 347
Salbutamol ................................................................................................................................................................................. 348
Hexoprenaline ............................................................................................................................................................................ 348
Ritodrine .................................................................................................................................................................................... 349
3. Anti-hypertensives ............................................................................................................................................................... 350
Methyldopa ................................................................................................................................................................................ 350
Hydralazine ................................................................................................................................................................................ 350
Nifedipine .................................................................................................................................................................................. 350
Labetolol .................................................................................................................................................................................... 351
4. Anticonvulsants ................................................................................................................................................................... 352
Diazepam ................................................................................................................................................................................... 352
Phenytoin ................................................................................................................................................................................... 353
Magnesium Sulphate .................................................................................................................................................................. 353
5. Steroids and Hormonal Replacement Therapy ................................................................................................................ 355
Dexamethasone .......................................................................................................................................................................... 355
Steroid Cover ............................................................................................................................................................................. 356
Tibolone ..................................................................................................................................................................................... 356
Danazol ...................................................................................................................................................................................... 356
GnRHa ....................................................................................................................................................................................... 357
GnRH ......................................................................................................................................................................................... 358
Gonadotropin ............................................................................................................................................................................. 358
Gonadotropin therapy................................................................................................................................................................. 358
6. Antibiotics ............................................................................................................................................................................ 359
Antibiotics Prophylaxis (Heart Disease) .................................................................................................................................... 359
Antibiotics Prophylaxis (Caesarean Section) ............................................................................................................................. 360
7. Anticoagulants ..................................................................................................................................................................... 361
Enoxaparin ................................................................................................................................................................................. 361
Fraxiparine (Nadroparin) ........................................................................................................................................................... 361
Warfarin ..................................................................................................................................................................................... 361
8. Others ................................................................................................................................................................................... 362
HyperHep (Hepatitis B Immune Globulin) ................................................................................................................................ 362
Naloxone .................................................................................................................................................................................... 362
Vitamin K................................................................................................................................................................................... 362
Methrotrexate ............................................................................................................................................................................. 362
- 16 -
MISCELLANEOUS ...................................................................................................................................... 363
1. English usage ....................................................................................................................................................................... 363
English usage ............................................................................................................................................................................. 363
Acronym .................................................................................................................................................................................... 363
Eponym ...................................................................................................................................................................................... 363
2. Basic clinical skills ............................................................................................................................................................... 364
History taking (Obstetrics) ......................................................................................................................................................... 364
Symptomatology (Obstetrics) .................................................................................................................................................... 364
Examination (Obstetrics) ........................................................................................................................................................... 365
Obstetric abdominal exam.......................................................................................................................................................... 365
Fundal height.............................................................................................................................................................................. 368
Doptone ...................................................................................................................................................................................... 368
Pinard stethoscope...................................................................................................................................................................... 368
History taking (Gynaecology) .................................................................................................................................................... 369
Symptomatology (Gynaecology) ............................................................................................................................................... 369
Examination (Gynaecology) ...................................................................................................................................................... 370
Lithotomy ................................................................................................................................................................................... 372
Speculum.................................................................................................................................................................................... 372
3. Infections .............................................................................................................................................................................. 373
Foetal infection .......................................................................................................................................................................... 373
Hepatitis ..................................................................................................................................................................................... 374
Hepatitis B ................................................................................................................................................................................. 374
Hepatitis C ................................................................................................................................................................................. 375
HIV ............................................................................................................................................................................................ 376
Group B streptococcus ............................................................................................................................................................... 381
Rubella ....................................................................................................................................................................................... 382
Chickenpox ................................................................................................................................................................................ 384
Toxoplasmosis ........................................................................................................................................................................... 388
Cytomegalovirus ........................................................................................................................................................................ 389
Parvovirus .................................................................................................................................................................................. 390
Listeriosis ................................................................................................................................................................................... 391
Sexually transmitted disease ...................................................................................................................................................... 392
Gonorrhea .................................................................................................................................................................................. 392
Syphilis ...................................................................................................................................................................................... 393
Trichomonas vaginalis ............................................................................................................................................................... 394
Bacterial vaginosis ..................................................................................................................................................................... 394
Human papillomavirus (HPV) ................................................................................................................................................... 394
Chlamydia .................................................................................................................................................................................. 395
INDEX ........................................................................................................................................................... 396
FIGURE LEGEND ....................................................................................................................................... 401
- 17 -
General Obstetrics
0. Obstetrics
What is Obstetrics
In Latin obstre means to stand opposite to (oba:-opposite to; stre:-stand). It originally pertained to a midwife standing opposite to
a parturiting woman and assisting in delivery. Now Obstetrics does not just concern of delivery, but a branch of medicine that
deals with pregnancy, labour and puerperium. In general, it has been subdivided into general obstetrics, maternal medicine and
foetal medicine.
Aims of obstetric care

To minimize maternal and foetal morbidities and mortalities (see maternal mortality and perinatal mortality) by early
identification of problems, actual and potential, and instituting appropriate management. To prepare, psychologically and mentally,
the mother and her husband (or partner) for pregnancy, labour and parenting, by providing them with support and education about
pregnancy and childbirth and childcare.
There are three phases of obstetric care:

1. Antepartum care
a. To detect and monitor any risk factors and manage it accordingly.
i. Majority of women are healthy. However, they may carry some risk factors that may affect the pregnancy. Common
examples are carrier of thalassaemia genes; maternal obesity and family history of diabetes are associated with
gestational diabetes.
ii. In addition, some women may have subclinical diseases that may not reveal until during pregnancy. For example, an
asymptomatic alular heart disease may deteriorate because of increased cardiac demand during pregnancy.
iii. Many antenatal disorders are not predictable or preventable, but their complications can be reduced by early
recognition, through regular monitoring. For example, regular blood pressure measurement and urinalysis during
every antenatal visit can pick up the evolution phase of pre-eclampsia.
b. To decide the optimal time and mode of delivery.
The normal time and mode of delivery is spontaneous labour at term (37 to 41 weeks of gestation) followed by
vaginal cephalic delivery. However, maternal or foetal complications may arise and preterm delivery, either by
induction of labour or caesarean section is required. The risks of continuation pregnancy to both the mother and
foetus should always be balanced against the risks of early delivery.
2. Intrapartum care
a. To ensure maternal and foetal well-being during labour and delivery.
b. To provide adequate labour pain relief.
c. To deliver the baby in the safest way for both the mother and the baby. Sometimes operative delivery may be required.
3. Postpartum care
a. To ensure normal recovery from pregnancy and childbirth.
i. Common early complications are postpartum haemorrhage and postpartum fever.
ii. One of the important late complications is postpartum depression.
b. To look for any problems in childcare and feeding.
c. To advise on contraception and family planning.
d. To follow up any antenatal problems and provide appropriate referral, counselling and management.
In addition to the above three parts, some couples will also be benefited from pre-conception counselling, particularly those who
have pre-existing chronic diseases, or family history of genetic disorders.
Other important topics in general obstetrics

1. Antepartum haemorrhage, postterm;
2. Besides, it is important to understand the physiological changes in pregnancy, the anatomy of the maternal pelvis and the
foetal skull.
- 18 -
1. Foetal anatomy
Foetal skull
The foetal skull is made up of the vault, face and the base. The vault is formed from parts of the frontal, occipital and the pair of
temporal bones and parietal bones. Between these bones there are four membranous sutures:-sagittal, frontal, coronal and
lambdoidal sutures.
Fontanelle
The foetal skull consists of a number of bones, and there are two fontanelles on the head, each being where a number of bones
meet.
1. Fontanelles is the membranous structure between margins of cranial bones of a foetus.
2. The anterior fontanelle is where the two parietal and two frontal bones meet.
a. This is a large space, and can be identified because 4 sutures run from it.
b. The anterior fontanelle is in the centre of the head, and is the presentation when the head is in the military of deflexed
position. When the head undergoes flexion, the presentation is the vertex.
3. The posterior fontanelle is where the two parietal and the single occipital bone meet.
a. It lies at the junction of the sagittal sutured and the lambdoidal sutures between the two parietal bones and the occipital
bone.
b. Usually it cannot be felt as a space, rather where 3 sutures meet.
4. The two fontanelles define the anterior and posterior limits of the vertex. These sutures and fontanelles allow moulding
during labour, and facilitate in assessment of the position of the foetal head during vaginal examination in labour.
Sagittal suture
This is the suture on the foetal skull where the two parietal bones meet, and is between the anterior and posterior fontanelles.
Sinciput
The part of the foetal head in front of the anterior fontanelle. It is part of head between the eyebrows and hairy scalp.
Vertex
A well-defined area of the foetal skull, bounded by the anterior and posterior fontanelles, and the two parietal eminences. The
vertex presentation is the normal and the most common one. It occurs once the head has undergone flexion, when the foetal head
will present with the smallest diameter to the birth canal.
Lie
This defines how the longitudinal axis of the baby is aligned with that of the mother. (Figure 2)
1. Longitudinal lie (98%) is when the baby is up and down, so the baby is in either cephalic or breech presentation. It is the
normal lie as the uterine cavity is longitudinal in shape.
2. Transverse lie (0.2%) is when the foetal poles are on the sides of the mother's abdomen. Causes are those that distort the
shape of uterine cavity:-lower segment fibroid, placenta praevia
3. Oblique lie (0.1%) is when one of the foetal poles is over one of the iliac fossae. The causes are similar to transverse lie.
4. Unstable lie is when the foetal lies change frequently from and to longitudinal, transverse or oblique. It implies that there is
too much room for the baby, such as in polyhydramnios, or the mother has a very lax abdomen (such as in grand multipara);
or in pelvic inlet contraction where the foetal poles fail to engage.
- 19 -
Presentation
Definition This is the part of the baby most easily felt by vaginal examination during labour.
Different types of presentation

1. Cephalic presentation
It is when the foetal head presents first. It is an imprecise term as it does not specify which part of the head is presenting,
and is usually used after abdominal palpation.
2. Vertex presentation (95%)
Vertex is the normal one, and occurs when the head is well flexed. Anterior fontanelle presentation is also normal,
especially in early labour before the head is fully flexed. It is also common in occipital posterior position. Presentations
other than this are malpresentations.
3. Brow presentation (0.02%)
It occurs when the head is extended. This sometimes occurs naturally, especially in multipara where the baby is not fixed
in position. More commonly it is associated with an obstruction in the birth canal such as disproportion, fibroid, ovarian
cyst, or placenta praevia. Unless the baby is very small, brow presentation makes the foetal diameters too large to deliver
vaginally. The head usually cannot enter the pelvic brim, so that when the membranes rupture, there is a high risk of cord
prolapse.
4. Face presentation (0.04%)
It is when the head is fully extended, and this occurs in very small babies, when the head enters the pelvis as a brow, but
extends into a face at the outlet and delivers. Although it can occur spontaneously, more commonly it is associated with
many loops of cords around the neck, or with thyroid goitre so the baby is forced into an extended position. Face
presentation can deliver vaginally if the head is rotated to a mentum anterior position. If rotation is to mentum posterior,
then the baby cannot bend its neck any further to fit the curvature of the pelvic canal, and so obstructed labour results.
5. Breech presentation (3%)
Breech presentation is when the baby's bottom comes out first. This can be a frank breech, flexed / complete breech or a
footling breech.
6. Other types of presentation
If the baby is in the transverse lie then the presentation would be the shoulder, elbow, or the hand. If the baby is floating
free, sometimes the umbilical cord is the presentation.
Position
The relationship of a defined area on the presenting part called the denominator, to the maternal pelvis. The most common
presenting position in cephalic presentation is occipto-anterior. Occipito-posterior position occurs in one-third of the cases.
Denominator
It is a defined area of the foetal presenting part, used to describe the position of the foetal presenting part in relation to the
maternal pelvis.
Presentation Denominator
Vertex Occiput
Face Mentus
Breech Sacrum
- 20 -
Figure 1 Attitude Figure 2 Lie
Figure 3 Position Figure 4 Breech and Cephalic Presentation
Figure 5 Brow Presentation Figure 6 Shoulder Presentation Figure 7 Vertex Figure 8 Face Presentation
presentation
The presenting diameters of the skull

Depends on the degree of flexion of the foetal head, it may present to the birth canal (maternal pelvis) in different longitudinal
diameters and presentation:
Foetal neck Longitudinal diameter (cm) Presentation
Fully-flexed suboccipito-bregmatic (9.5) vertex
Semi-flexed suboccipitao-frontal (10) vertex, usually with occiputo-posterior position
Mildly-extended occipito-frontal (11.5) vertex, usually with occipito-posterior position
Moderately-extended mento-vertical (13) brow
Fully-extended submento-bregmatic (9.5) face
Remark:
- Suboccipito-bregmatic:-from the suboccipital region to the centre of the anterior fontanelle
- Suboccipitao-frontal:-from the suboccipital region to the prominence of the forehead
- Occipito-frontal:-from the posterior fontanelle to the root of the nose
- Mento-vertical:-from the chin to the furthest point of the vertex
- Submento-bregmatic:-from below the chin to the anterior fontanelle
- 21 -
Figure 9 Foetal Skull
Figure 10 Measurements of foetal skull
- 22 -
Figure 11 Sutures
Figure 12 Circumferences
- 23 -
2. Maternal anatomy
Levator ani
Levator ani muscles is a pair of broad flat muscles, each arises from the inner surface of the antero-lateral pelvis, passes
downwards and inwards, from the lateral sides and meet each other at the midline. The muscles together constitute the pelvic
diaphragm. Each muscle is also divided into three parts:-pubococcygeus anteriorly, ischiococcygeous and iliococcygeus
posteriorly. The nerve supply is by the pudendal nerve (S2-4) on each side.
The exact origins of the muscles are:-

- The lower part of the body of the os pubis
- The tendinous arch of the parietal pelvic fascia (white line)
- The pelvic surface of the ischial spine
The site of midline insertions are:-
- The pre-anal raphe and the central point of the perineum where one muscle meets the other on the opposite side
- The wall of the anal canal, where the fibres blend with the deep external sphincter muscle
- The postanal or anococcygeal raphe, where again one muscle meets the other on the opposite side
- The lower part of the coccyx
Clinical role of levator ani

1. The pubococcygeus muscles support the pelvic and abdominal viscera, including the bladder. Weakness of the support results
in genital prolapse.
2. The medial edge passes beneath the bladder and runs laterally to the urethra, into which some of its fibres are inserted.
Together with fibres from the opposite muscle they form a loop which maintains the angle between the posterior aspect of the
urethra and the bladder base. During micturition this loop relaxes to allow the bladder neck and upper urethra to open and
descend. Failure to maintain the angle results in urinary stress incontinence.
3. The medial borders of the pubococcygeus muscles pass on either side from the pubic bone to the pre-anal raphe. They thus
embrace the vagina, and on contraction have some sphincteric action. Spasm of the muscle results in vaginismus.
Urogenital diaphragm
It is a triangular-shaped ligament lying below the levator ani muscles, and filling the gap between the descending pubic rami. It
consists of two layers of pelvic fascia, with the deep transverse perineal muscle (compressor urethrae) lying between the layers.
The diaphragm is pierced by the urethra and the vagina.
Pelvis
It is composed of a pair of iliac bones, a pair of ischial bones, a pair of pubic bones and a sacrum. Together with the pelvic
ligaments, they form the birth canal, with an inlet, cavity and an outlet.
Pelvic Inlet
Also known as the pelvic brim, the upper limit of the true pelvis. It consists of the pubic symphysis in front, the upper edge of the
pubic bones and the iliac bones on both sides, and in the back the sacrum (usually the S1). The normal diameters of the brim are
said to be 11cm anteroposteriorly, and 12cm laterally. An AP diameter of 10 cm is usually considered to be narrowed, and 9cm
would be diagnosed to be a contracted pelvis.
Pelvic Cavity
The walls of the pelvis are partly bony and partly ligamentous. The posterior boundary is the anterior surface of the sacrum, and
the lateral limits are formed by the inner surface of the ischial bones and sacrosciatic notches and ligaments. In front the pelvis is
bounded by the pubic bones, the ascending superior rami of the ischial bones and the obturator foramina.
Pelvic Outlet
The lower end of the bony birth canal. Marked by the pubic symphysis in the front, the lower edges of the pubic rami, limited
laterally by the ischial tuberosities, and posteriorly by the coccyx. In women with android pelvis, the pelvic outlet is narrowed
from side to side, and this sometimes prevents the baby from being delivered in the second stage, resulting in a failed instrumental
delivery.
- 24 -
Ischial spine
The sharp posterior-medical protrusion from the ischial bone. It is halfway between the pelvic inlet and outlet. The ischial spines
are of great obstetrical importance because the distance between them represents the shortest diameter of the pelvic cavity. They
are readily felt vaginally or rectally and therefore serve as valuable landmarks in assessing the station of the presenting part. It is
also a landmark to identify the site of pudendal nerve during pudendal anaesthesia.
Pubic symphysis
Where the two pubic rami join in the front. It forms the anterior border of the pelvic canal.
Subpubic arch
This is formed by the inferior borders of the pubic rami, ending at the ischial tuberosities. Normally this has an angle of 90
degrees. The shape of this arch is important in that it determines whether the foetal head has difficulty in coming out of the pelvic
outlet. As the baby's head is more or less round, a narrowed arch will force the baby's head backwards, so that the available
antero-posterior diameter is much less than as measured in the pelvimetry. The unavailable part of this AP diameter is called the
waste space of Morris. A good way to envisage this is to draw the pubic arch, and try to put a circle 9.5cm inside it. The distance
between the circumference and the apex of the arch is the waste space. The pubic arch is best assessed clinically, by feeling for the
arch and estimating its angle. Also, the distance between the ischial tuberosities should be about 10cm, which is usually the width
of the doctor's knuckles. A narrowed pubic arch will lead to difficulty in the second stage, and is a common cause of failed
instrumental delivery.
Intertuberous diameter
The distance between the tuberosity of the ischial bones. It is the transverse diameter of the pelvic outlet and normally measured
9cm. It can be assessed clinically by putting a fist to the perineum. The intertuberous diameter is normal when it can
accommodate 4 knuckles of fingers.
Figure 13 Levator Ani (Perineum)
Figure 14 Pelvic Floor
- 25 -
Figure 15 Pelvic Brim; Pelvic Inlet
Shape of pelvis
The pelvis is classified according to different pelvic shapes and the size is assessed by clinical pelvimetry.
A normal pelvis
- The brim is round, and the sacral promontory is not prominent
- The angle of inclination is about 55 degree to the horizontal
- The cavity is shallow with straight, non-converging walls
- The sacrum is smoothly curved
- In the outlet the sacro-sciatic notches are wide and shallow
- The sacrum does not project forwards
- The ischial spines are not prominent
- The pubic arch is wide and domed
- The sub-pubic angle is about 90 degree
- The inter-tuberous diameter is wide
Pelvic shapes
Four major pelvic shapes have been described:-Gynaecoid, Anthropoid, Android and Platypoid
Gynaecoid
This is the normal and most common type of pelvis. The brim is oval in shape, with the lateral diameter larger than the
antero-posterior diameter. The sacrum is well curved, and tilted in such a manner as to render the antero-posterior diameter of the
outlet slightly larger than the inlet. The midcavity is wide, the anteroposterior diameter being generous because of a good sacral
curve, and the lateral diameters are also good, with a good distance of 3-4 cm between the ischial spines and the sacrum. The
outlet has an antero-posterior diameter larger than the lateral diameter, and the subpubic arch is more than 80 degrees. Such a
pelvis fits naturally into the diameters of foetal skull with a normal vertex presentation.
Anthropoid
This is a variant of the normal pelvis. Its shape is very similar to that of the gynaecoid pelvis, except that the inlet is ovoid shape,
with a long antero-posterior diameter, and the lateral diameter near the back is slightly larger than that in front. Such a shape tends
to encourage occipito-posterior position.
- 26 -
Android
It is a male-like pelvic shape which tends to have a triangular inlet with beaking near the front. This encourages an occipital
posterior position. It is also a funnel pelvis, where the outlet is smaller than the inlet, and a side to side narrowing of the pelvic
canal. The outlet has a narrow subpubic arch. Typically women with android pelvis may have other android features, such as
having broad shoulders, are muscular, and sometimes hirsute.
Android pelvis can be diagnosed by pelvimetry, with the following features:-

1. The antero-posterior diameter at the outlet is smaller than that at the inlet
2. A narrowing of the distance between the ischial spines
3. A narrowed sacrosciatic notch
For this type of pelvis, the foetus tends to present with occipital posterior position, and the head has difficulty in rotating to the
anterior position as the pelvic canal is narrowed. The funnel shaped pelvis also results in obstructed labour. As the narrowest part
is at the outlet, the worst situation is the arrest at the second stage of labour. This would lead to a failed instrumental delivery with
all its disastrous consequences.
Platypoid
One of the pelvic shapes. 'Plat' is derived from a Greek word meaning flat. This type of pelvis is a result of clinical or subclinical
rickets. The pelvic brim is narrowed from front to back, so appearing flat, and this sometimes is associated with an exaggerated
lumbar lordosis. The combination of these causes the pelvic inlet to be small, and this contracted pelvis makes it difficult for the
foetal head to enter the pelvis. This is classically the situation of cephalopelvic disproportion. The softening of the bones caused
by rickets also leads to a splaying of the subpubic arch, so that the pelvis is usually only narrowed at the brim while the rest
presents no difficulty. This is responsible for the old obstetric adage that if the head will go in the brim it will come out the outlet.
Sometimes the head will angle sideways in an attempt to enter the pelvis, and this is called asynclitism.
Figure 16 Gynaecoid (Left) and Anthropoid (Right)
Figure 17 Android (Left) and Platypoid (Right)
Funnel pelvis
This describes a pelvis where the outlet diameter is smaller than the inlet, especially the antero-posterior diameters as seen on the
pelvimetry. Funnel pelvis occurs in the android pelvis. Women with funnel pelvis have difficult labours, because the birth canal
gets tighter as labour progresses, and the smallest part of the pelvis is only encountered at the second stage of labour.
- 27 -
Contracted pelvis
This denotes a pelvis which is smaller than normal, to the extent that it may cause difficulties in labour. Contraction may occur at
the inlet, and this is usually associated with a platypoid pelvis. Contraction can also occur at the outlet, and this is usually
associated with the android pelvis. The android pelvis may also be contracted in midpelvis, with a side to side narrowing of the
pelvis, which can be seen as a narrowed sacral sciatic notch on pelvimetry, or as a narrowed distance between the ischial spines.
Cephalopelvic disproportion
This describes the situation where the foetal head is too big for the birth canal. Before World War II, when nutrition was poor,
many women had rickets and so developed platypoid pelvis. These lead to inlet disproportion. Women who have android features
however may have an adequate pelvic inlet, but a narrow outlet. They tend to have difficulty in delivering the baby at the second
stage, and are said to have outlet disproportion.
Pelvimetry
Definition
Measurement of the size of the pelvis, either clinically or radiographically.
Clinical pelvimetry
Clinical method is as follow:
1. Inlet assessment:
Assess the diagonal conjugate diameter by inserting the index and middle fingers to reach the sacral promontory. If the
sacral promontory can be reached, it means the inlet is small (usual length of the index finger is 10cm).
2. Mid cavity assessment:
a. Assess the sacral curvature by digital examination.
b. Assess the ischial spines.
3. Outlet assessment:
a. Assess the intertuberous diameter. It should be as wide as a normal fist (9cm)
b. Assess the subpubic arch which is normally 90 degree.
Clinical assessment of pelvic size and shape is only likely to be of benefit if the pelvis is severely contracted
Radiological pelvimetry
- By X-ray, CT, MRI
- CT is the most common way as it has less radiation and more accurate when compared with X-ray, but cheaper and more
available than MRI
- Criteria for normality have not yet been set
- Pelvimetry is of no reliable evidence of benefit for the traditional indications of primigravid breech presentation, or after
caesarean section for suspected disproportion
Rickets
A softening of the bone due to vitamin D deficiency. The weight of the upper torso then pushes the sacral promontory towards the
pubis, and the lumbar spine develops an exaggerated lordosis. As a result the pelvic inlet appears flattened, and this is called the
platypoid pelvis. Women with rickets and platypoid pelvis develop inlet disproportion. Rickets should be differentiated from
osteoporosis.
Lordosis
An exaggerated anterior curving of the lumbar spine. Often occurs in rickets.
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Os
Greek word meaning opening. In obstetrics means where the cervical canal is. The internal os is the end of the cervical canal at
the uterine end, and external os the vaginal end.
Lower segment
The thin expanded lower portion of the uterus which forms from the isthmus during the last trimester of pregnancy. It is located
between the attachment of the peritoneum of the uterovescial pouch superiorly and the level of the internal os inferiorly. It
provides the usual method of approach to the baby in the operation of caesarean section. When abdominal delivery is necessary in
a preterm pregnancy when the lower segment is not yet formed, a classical caesarean section is then the method of approach. The
lower segment is less contractile as there are fewer muscle fibres. When the placenta is located there (placenta praevia), bleeding
from the placental bed is more difficult to control.
Dextrorotation of uterus
The pregnant uterus is usually rotated towards the right side, due to the presence of the rectum and sigmoid colon on the left side.
This is relevant that to avoid injury to uterine vessels during lower segment caesarean section, the operation table should be tilted
towards the left side.
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3. Antepartum
Pre-conception counselling
Aim
1. To ensure women are in good and healthy condition before being pregnant
2. It is important as the most critical phase of foetal development is complete by the time of the first antenatal clinic attendance,
and adverse factors may have already begun to produce their effects
Elements
1. General health assessment and advice
a. Nutrition
b. Healthy behaviour:-e.g. quit smoking and alcoholism
2. General screening
a. Cervical pap smear
b. MCV for thalassemia
c. Rubella immunity
3. Control of pre-existing chronic diseases
a. Diabetes mellitus, thyroid disorders, valvular heart diseases are common in female at reproductive age.
b. Poor control of these diseases would definite causes significant maternal and foetal morbidities
4. Adjustment of medical therapies

a. Medical therapy of these disorders may cause foetal complication, for example, anti-convulsants are associated with
neural tube defects. Discontinuation of the drugs may be considered if there is no recurrence for a long period of time
b. Diabetic patients being treated with oral hypoglycemic agents would be advised to change to insulin before pregnancy, as
insulin has better control of the disease and dosage is more easy to adjust
5. Genetic counselling and prevention
a. Counselling on any possibility of congenital malformation and genetic disorders, particular if there is positive family
history (see genetic counselling)
b. Patients with previous babies suffered from neural tube defects will be benefited from folate supplement for 6 weeks
before getting pregnant.
Discussion/Something to Consider
You are a medical officer of the Family Planning Association.
1. A healthy couple has just married and come for pre-pregnancy advice. History and examination are unremarkable. What
screening tests would you perform for them?
2. Supposed the complete blood pictures of both of the couple show microcystic picture but otherwise normal result. How would
you counsel them and what further tests would you do?
3. The female partner of the couple has negative rubella antibody test. What advice would you give her?
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Antepartum care
Definition
A planned programme of observation, education, and medical management of pregnant women directed towards making
pregnancy and delivery safe and satisfying experiences
Elements
1. Screening of Risk factors
a. To regularly look for any risk factors which adversely affect the health of mother and baby
b. This is achieved through regular history taking, examination, and screening tests.
2. Counselling To advise on the nature and extent of any perceived risks, and how to minimize or eradicate them
3. Monitoring To monitor the maternal and foetal well-being in high risk cases
4. Treatment To treat any medical condition which might affect or be affected by the pregnancy (see maternal medicine)
5. Management of minor disorders See minor disorders of pregnancy
6. Education To provide advice, reassurance and support for the woman and her family, such as:-
a. Advice on wearing seat-belt
b. Instructions to admit to hospital when significant symptoms occur such as fever, vaginal bleeding or discharge,
abdominal pain, etc
Antepartum care consists of booking assessment; and continuing antenatal care.
Booking assessment
1. Timing
a. Optimally takes place at 8 to 10 weeks and should not later than 16 weeks
b. Important for dating of pregnancy:-to look for any date problem and confirm the estimated date of confinement (EDC)
c. Check for any pre-existing risk factors by history taking (Obs), examination (Obs) and screening tests
2. Initial screening tests should include:

a. Haematological
i. Haemoglobin to screen for anaemia
ii. MCV to screen for thalassemia
iii. Blood group and Rhesus type
b. Microbiological
i. Rubella antibodies
ii. Hepatitis B surface antigen
iii. VDRL for syphilis
c. Biochemical Urinalysis for protein and glucose
d. Radiological
i. Dating scan before 16 weeks
ii. Morphology scan around 20 weeks
3. Additional screening tests such as the followings may be required if additional risk markers are present:
a. Urine culture
b. Screening for sexually transmitted diseases
c. Oral glucose tolerance test
d. Biochemical screening for neural tube defects and Down syndrome
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Subsequent assessment
1. When and where to be seen
a. Uncomplicated (low risk) pregnancy
i. Women should be seen every 4 weeks for the first 28 weeks of pregnancy, then every 2 weeks until 36 weeks, and
weekly until delivery
ii. Can be seen in maternal child health centre, by midwives or general practitioners
b. High risk pregnancy
i. Women with medical or obstetric problems require close surveillance at an interval determined by the nature and
severity of the problem.
ii. Under care of a specialist
Routine maternal assessment

- Weight and notation of any change
- Blood pressure with notation of any change
- Urine glucose and protein
- Periphera oedema
- Presence of any symptoms
Routine foetal assessment

- Foetal activity (from history)
- Foetal size:-both the actual size and the growth rate; assessed with fundal height measurement
- Foetal presentation and engagement (in late pregnancy)
- Amount of amniotic fluid
- Foetal heart rate, by auscultation with Pinard stethoscope or a hand-held Doppler apparatus (Doptone)
- Please refer to history taking (Obs) and examination (Obs) for detail
1. A patient at 34 weeks of gestation is found to have weight gain of 2 kg over the last 1 week. Is it normal? What are the
possible causes? How would you assess her condition?
2. A patient asks you in the antenatal clinic whether it is dangerous to wear seat-belt during traveling in a car. How would you
advise her?
Pregnancy test
It is a simple bedside dipstick test for presence of human chorionic gonadotropin in urine. It is highly specific and sensitive
(detection limit of around 25-50IU/L), and produces a result in 1 to 2 minutes. The test can produce to positive result as early as
14 days post-fertilisation.
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Dating of pregnancy
Introduction
Dating is one of the most important tasks in antenatal care. 20% of pregnant women will have date problems because:-
1. Last menstrual period is forgotten or uncertain
2. Menstrual cycles are irregular
Some definitions
1. Last menstrual period (LMP) date of the first day of last menstrual flow
2. Estimated date of confinement (EDC):
a. The mean duration of pregnancy
b. About 40% of women will deliver within 5 days of EDC and 66% within 10 days
c. It is 280 days from the LMP provided that ovulation occurs at day 14 of the menstrual cycle
d. It is 266 days from the date of ovulation
How to calculate EDC (Nagele's rule)

1. By LMP: It is calculated by using LMP by adding 280 days (40 weeks) to it. It is assumed that ovulation occurs at or day
14 of LMP, in a normal regular 28 days cycles. To the first day of LMP add 7 days, then subtract 3 months, and then add
1 year. e.g.:-LMP:-10/10/2009 EDC:17/07/2010
2. By First positive pregnancy test (5-6 weeks of amenorrhoea)
3. By Ultrasound dating.
Some important facts:-menstrual cycles, ovulation and fertilization

- In a normal regular 28-day cycle, ovulation occurs 14 days after the LMP
- Ovulation may be delayed when the usual duration of menstrual cycles is longer. For example, ovulation may occur at day
21 if the menstrual cycles are 35 days
- Fertilization occurs within 2 days of ovulation
- Implantation occurs 7 days after ovulation, and completes 14 days after ovulation
- Foetal life starts at about 14 to 15 days after LMP (if the cycles are 28 days) or even later if the menstrual cycles are longer
- HCG is produced after implantation, and is detectable in the serum 1 week after implantation
- HCG is detectable in urine (positive pregnancy test) since 2 weeks after fertilization (4 week after LMP, or later if ovulation
occurred later)
- Therefore, if a patient has used to have long menstrual cycles, and had a negative pregnancy test at 5 week of amenorrhea,
but positive test at 6 week. Then most probably she had a date problem of 1 to 2 weeks.
Some important facts:-symptoms and signs of pregnancy

Features Week of pregnancy
Morning sickness 4 to 13
Breast changes start from 6 week
Bladder symptoms 6 to 13 week
Cervical softening start from 6 week
Quickening (primigravida) start from 18 week
Quickening (multipara) start from 16 week
Audible foetal heart sound with pinard start from 24 week
Abdominally palpable pregnant uterus start from 12 week
Hegar's sign 8 to 13 week
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Figure 18 Symptoms, signs and tests of pregnancy
Some important facts:-ultrasound dating

1. First trimester Crown-rump length (CRL):-accuracy of EDC estimation:- 4.7 days
2. Second trimester Biparietal diameter (BPD) or femur length (FL):-accuracy of EDC estimation:-7 to 10 days
3. Third trimester Dating at this time is not very helpful in predicting the EDC. The accuracy is only 3 weeks
Determination of EDC
1. As a rule, when an early USG prediction disagrees with an EDC assigned by the LMP by more than 1 week, the USG dates
are assigned.
2. If the scan and the LMP agree to within a week, the EDC based on the LMP is used. This may not always be straightforward
because femur length may or may not agree with the estimated gestational age based on the BPD
1. What is the EDC of a pregnancy which is resulted from in vitro fertilization with the LMP on 01/01/2009, and oocytes
retrieval on 17/01/2009 and embryo transfer on 19/01/2009?
2. Why CRL cannot be used continuously for dating in the second trimester?
3. A teenager presents to the A&E department complaining of acute abdominal pain. She used to have 28-day regular cycles
until Feb 2009. She claims she had menstrual bleeding on 01/02/2009 and the last menstrual bleeding came late for a week,
on 08/03/2009. Today (15/03/2009) she is found to have a positive pregnancy test. How can you account for this history and
finding?
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Antepartum haemorrhage (APH)
Definition
Bleeding from the genital tract occurs after 24 weeks of gestation and before the birth of the baby, including the first and second
stages of labour
Causes
- Placental
Placenta praevia
Abruptio placentae
Vasa praevia:-very rare
- Lesion of the lower genital tract:-cervix or vagina
- APH of unknown origin:-the most common cause
Incidence
Incidence: 2.0% 3-5% of pregnancies
What is your assessment for a woman presents with painless unprovoked vaginal bleeding of 10ml at 28 weeks of gestation?
Placenta praevia
Definition
It is defined as a low-lying placenta, when the placenta encroaches onto the lower segment.
Classification
Figure 19 Classification of placenta praevia

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1. Classification with aids of Ultrasound, with the use of modern ultrasonography, the placental position can now be defined
more accurately antenatally.
Type I low-lying placenta positioned closed to the os (within 5cm).
Type II marginal placenta praevia located at the margin of the os.
Type III partial placenta praevia partially covering the internal os.
Type IV total placenta praeviacompletely covering the os.
2. Old classification (by Dewhurst), based on clinical examination findings or findings at the time of caesarean section:-
Grade I placenta extends on to the lower segment but does not reach the os.
Grade II placenta extends to the os.
Grade III placenta covers the os eccentrically.
Grade IV placenta covers the os centrally.
3. Simplest Classification
Minor placenta encroaches on the lower segment but does not cover internal os (type I and II)
Major placenta covers internal os (type III and IV)
Incidence
0.6% of pregnancies
Risk factors
1. Maternal factors:
a. Multiparity scarring of the endometrium due to repeated pregnancies
b. Advanced maternal age >35 defective vascularization of the decidua due to atrophic changes or inflammation, thus
decrease the blood supply to the endometrium and require a greater surface area for placental attachment to provide
adequate maternal blood flow
c. Previous C/S or surgeries Altered blood supply to the endometrium and changes in the quality of the endometrium,
due to previous incision in the lower segment
2. Foetal factors
Multiple pregnancies Decreased surface area of placental implantation, in multiple pregnancies
Clinical presentation
1. Painless vaginal bleeding
a. Most characteristic sign of placenta praevia
b. Can occur suddenly without warning, during rest or activity, or after coitus or pelvic examination
c. Bleeding usually occurs for the first time early in the third trimester, when the lower segment begins to form.
d. Bleeding is caused by the tearing of the placental attachments at or near the internal os as the cervix changes
e. The bleeding cannot stop spontaneously because the stretched fibres of the lower uterine segment are unable to contract
and compress the torn vessels
2. Present as malpresentation
3. Incidental finding on routine ultrasound scan
Diagnosis
1. Should always be suspected in the presence of vaginal bleeding in the third trimester
2. The index of suspicion is heightened if there is co-existing malpresentation or multiple pregnancy
3. Ultrasonic examination
It is a valuable tool in confirming the diagnosis of placenta praevia Transabdominal scan (TAS) is usually adequate in
assessing the relation between the low-lying placenta and the internal os. In borderline cases or in case of posterior placenta,
transvaginal scan (TVS) is more accurate than TAS
- 36 -
TVS showing a posterior placenta preavia type II (reaching os)
Protocol, as of 19 November 2004

1. Principle
a. The risk of placenta praevia is the massive bleeding that may require immediate delivery of foetus and placenta in
order to control the bleeding. It implies the risk of preterm delivery when massive bleeding occurs in preterm gestation.
b. The principle of management is therefore to tolerate minor bleeding in order to avoid complications of prematurity,
until the pregnancy reaches a safe maturity (at least 34 weeks), but to deliver in case of severe bleeding.
2. General Advise
a. Avoidance of coitus which may provoke bleeding.
b. Admission if vaginal bleeding occurs.
3. Ultrasound surveillance on placenta site for those ASYMPTOMATIC placenta previa <34 weeks.
4. ASYMPTOMATIC placenta previa at gestation 34 weeks
Discuss with patient individually regarding the option of in-patient and outpatient management. Criteria that are
suitable for outpatient management include all types of previa without antepartum haemorrhage and patient is living
within 30 minutes reach of the hospital with means of rapid transportation
5. SYMPTOMATIC placenta previa / low-lying placenta 24 weeks
a. Hospitalize patient until delivery regardless of the type of placenta praevia, the severity and number of bleeding
episodes, unless subsequent USG confirms that placenta is no longer low-lying.
b. If there are uterine contractions accompanying APH. the use of tocolysis before 34 weeks to allow time for steroids is
justified in selected cases:-No continuous bleeding, stable vital signs and No evidence of abruptio placentae
6. Expectant management
a. To monitor severity of bleeding
b. Keep patient in hospital
c. Give one course glucocorticord therapy to enhance foetal lung maturity
d. Regular cross-matching of blood
7. Mode of Delivery
Caesarean section for all grade of placenta praevia except those cases with placental edges more than 2cm away from
internal cervical os under transvaginal scan examination, and the foetal head is well engaged. In that situation, the
chance of antepartum haemorrhage is much less while the chance of successful vaginal delivery is acceptably good.
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Abruptio placentae
Definition
It is also called 'accidental haemorrhage. It is defined as uterine bleeding resulted from a normally implanted placenta that
prematurely detaches from the uterus, after 24 weeks of gestation and before the delivery of the foetus.
Incidence 0.20.8% of all pregnancies, half of the cases occur preterm
Risk factors
1. Maternal
a. Multiparity
b. Previous history of abruption placentae
c. Pre-eclampsia or hypertension
d. Cigarette smoking, cocaine abuse
e. Sudden decompression of the uterus (e.g. traffic accident, rupture of membranes, ECV)
2. Foetal
a. Polyhydramnios
b. Multiple pregnancy
Pathology
There are two types of placental detachment, with different clinical presentation:-
1. Revealed type
a. Peripheral detachment
b. Bleeding from cervical os
2. Concealed type
a. Less common
b. Central detachment
c. Blood is trapped behind the placenta and does not escape
3. Detachment of the placenta results in disruption of uteroplacental transfer of oxygen, leading to foetal hypoxia and death.
Clinical presentations
1. Vaginal bleeding:-
a. A common presentation
b. May be absent, or present very late in the concealed type
c. May be massive and the patient presents with shock
2. Uterine pain:-
a. Uterine pain and tenderness are more severe in the concealed type
b. Uterine irritability, present with irregular but frequent activities in cardiotocogram
c. Uterine contractions, of high frequency low amplitude, may be tonic in Couvelaire uterus
3. Other features:
Foetal distress, presents with decreased foetal movement, abnormal cardiotocogram, or foetal death at presentation.
Rarely, retroplacental clots may be seen between the uterine wall and placenta under USG in severe concealed type.
However, clinical condition would be obvious for making the diagnosis of abruptio rather than relying on USG features.
- 38 -
Complications
1. Maternal
a. Massive haemorrhage and shock
b. Disseminated intravascular coagulopathy due to release of placental thromboplastin and other clotting factors
c. Postpartum haemorrhage due to uterine atony
d. High risk of caesarean section
2. Foetal
a. Intrauterine foetal hypoxia (distress) and death
b. Preterm delivery
Protocol, as of 22 June 2002

1. Transfer to labour ward
2. Assess maternal well-being and perform resuscitation for hypovolaemic shock if necessary
3. Intravenous access with large-bore catheters
4. Monitor vital signs closely:-BP, pulse, urine output
5. Monitor foetal well-being by continuous foetal heart monitoring
6. Check CBP, RFT, Clotting profile and crossmatch, make correction if necessary.
7. Decide mode and time of delivery with midwives, by caesarean section unless the cervix is already fully dilated, or
the foetus has already died
8. Consider steroid if <34 weeks
9. Look for retroplacental clot of the placenta after delivery
10. Clear documentation of events
What are the differences between the management of abruptio placentae and that of placenta praevia, when each of them presents
at 30 weeks of gestation?
Couvelaire uterus
Uterine apoplexy, occurs with severe concealed type of abruptio placentae. The uterus is purple due to haemorrhage within its
musculature with retention of blood and cord. It is a phenomenon wherein the retroplacental blood may penetrate through the
thickness of the uterine wall into the peritoneal cavity. Clinically the uterus is hard and tender.
Velamentous Insertion of the Cord
The placenta has developed some distance away from the attachment of the cord and the vessels divide in the membranes. If they
cross the lower pole of the chorion a condition arises called vasa praevia. Rupture of the membranes will then precipitate
haemorrhage which will exsanguinate the fetus.
Vasa praevia
It the placenta is developed some distance away from the attachment of cord, the connecting vessels run under the membrane. In
case a branch of the umbilical vessels passes over the internal os of the cervix, and therefore becomes the presenting part (vasa
praevia). The vessel may rupture spontaneously or during amniotomy resulting in foetal bleeding. It is a rare cause of antepartum
haemorrhage. The USG film with color-doppler below shows a vessel (colored) running over the internal os.
- 39 -
APH of unknown origin
Definition
Antepartum haemorrhage (APH) from the upper genital tract with no evidence of placenta praevia and abruption placentae
Incidence
1.2% 3% of all pregnancy, is a common cause of antepartum haemorrhage
Causes
The cause by it name is unknown. However, it is thought to be a minor abruptio placentae that cannot be confirmed clinically.
Risk
1. It is associated with preterm labour.
2. In the past, it was thought to be associated with an increased risk of IUGR and perinatal mortality because of foetal
compromise. However the evidence was not convincing. It is clear that the increased perinatal mortality is mainly due to
prematurity.
Clinical presentation and diagnosis

1. Vaginal bleeding, usually of small amount and is unprovoked
2. May associate with uterine contractions
3. No signs of foetal distress or uterine tenderness (when these occur, abruptio placentae must be suspected)
4. It is diagnosed by exclusion of other causes of antepartum haemorrhage

1. Look for causes:-placenta praevia, abruptio placentae, genital tract lesions; Look for symptoms and signs of preterm labour.
2. Document the amount of bleeding by history and speculum examination.
3. Perform CTG if 26 weeks, and consider induction of labour or caesarean delivery if CTG is abnormal.
4. Discharge if no more vaginal bleeding or abdominal pain for 3 days.
5. Gestation below 34 weeks:
a. Glucocorticoid therapy to enhance foetal lung maturity because of high risk of preterm delivery
b. The use of tocolytics when preterm labour occurs is controversial. It is thought that the relaxation of uterus may
cause further bleeding, and some tocolytics (e.g. beta-adrenergic agonists and calcium channel blockers) may
exacerbate the haemodynamic status in case of severe bleeding.
6. Gestation above 34 weeks:
a. Conservative management
b. Consider induction of labour at term when patients have repeated episodes of APH or currently suffered from
significant bleeding
7. Weekly CTG assessment and Induction of labour for history of APH of unknown origin is NOT a routine.
- 40 -
4. Malpresenation
Malpresentation
Definition
Any presentation other than vertex. They are:-
1. Breech presentation:-4.2% 3%
2. Cord presentation:- 1/1000 1/400
3. Face presentation:- 1/2500 1/500
4. Brow presentation:-1/10000 1/2000
5. Shoulder presentation, foetus usually in transverse lie
Medical students should know the most common malpresentation:-breech presentation
Breech presentation
Incidence
- The most common type of malpresentation
- Incidence deceases with maturity.
25-30% at 28 weeks.
3.3-4.2% of all term deliveries.
Due to spontaneous version.
- Up to one third are undiagnosed before labour
Types
1. Complete (10%):-both legs flexed at hip and knee
2. Frank (65-70%):-both legs extended at the knee and flexed at the hip
3. Footling or incomplete (20-25%):-one or both feet tucked underneath the buttock
Causes
1. The majority occurs by chance
2. Maternal
a. Uterine anomalies:-e.g. bicornuate uterus
b. Obstruction at lower pole:- Fibroids, placenta
3. Foetal
a. Multiple pregnancy
b. Preterm
c. Foetal anomalies:-e.g. hydrocephalus
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Foetal risk
1. Foetal risk related to the underlying causes
a. Foetal anomaly
b. Prematurity
2. Foetal risk related to vaginal breech delivery
a. Premature rupture of membranes
b. Cord prolapse:-risk is lowest in frank breech presentation but highest in footling
c. Birth injury:-e.g.:-Intracranial haemorrhage, rupture of viscus, dislocation of joints, fractures of long bones, peripheral
nerve injury
d. Birth asphyxia:-as a result of delayed delivery
Maternal risk
1. Maternal risk related to the underlying causes. e.g. Placenta praevia
2. Maternal risk related to breech delivery:- Higher caesarean section rate and Birth canal injury
Investigations
1. Ultrasound
a. Define the type of breech, assess foetal growth and estimate of foetal weight, and liquor volume
b. Look for any underlying causes like foetal anomalies, placenta praevia and uterine abnormalities
2. CT pelvimetry
a. Ensure adequate pelvis before allowing vaginal breech delivery
b. Rarely indicated now as vaginal breech delivery is not recommended
Decision of mode of delivery

1. External cephalic version (ECV)
2. Elective caesarean section
3. Vaginal breech delivery
Guideline
The mode of term breech delivery is controversial until recently when a large randomized controlled study comparing elective
caesarean section and vaginal breech delivery has shown that the former is associated with significantly lower perinatal mortality
and morbidity. The implication is that patients should be counselled for either elective section or ECV only. Patient who strongly
request vaginal breech delivery must fulfil the strict selection criteria (see vaginal breech delivery).
Other determining factors:

1. Gestation If occurred before 36 weeks, conservative management as spontaneous version may take place
2. Foetal malformations:-
a. Lethal foetal abnormalities:-vaginal delivery
b. Potential salvageable foetal abnormalities:-caesarean section
3. Foetal well-being Caesarean section if there are signs of foetal compromise such as oligohydramnios, or abnormal
cardiotocogram, etc.
4. Number of foetuses,
a. Twin pregnancy:-
i. Presenting twin is breech presenting:-caesarean section
ii. Non-presenting twin is breech:-can try vaginal delivery
b. Triplet or higher order pregnancy:-caesarean section
5. Uterine abnormalities Caesarean section in case of uterine anomalies, placenta praevia or other pelvic obstructions
- 42 -
Protocol, as of 27 July 2002

1. Diagnosed before labour
a. Counsel for ECV unless patient refuses or with contraindication
i. Arrange ECV via computer CMS system(2 cases per week)
ii. If requires batch-in, contact ECV team(Dr.A Fok or LW Chan or TY Leung)
iii. Admit patient on day of ECV, fast after light breakfast
b. If the patient is not for ECV, arrange elective Caesarean section at 38-39 weeks gestation
c. If the patient insists on vaginal breech delivery, inform FHKAM for further counselling
2. Undiagnosed before labour
a. Arrange emergency Caesarean section as soon as possible
b. If patient refuses Caesarean section, inform Mid call-1 and 2 for further counselling.
3. Imminent vaginal delivery (when delivery is judged to be quicker than C/S)
Inform Mid call-1, Mid call-2 and Paediatrician.
Reference data
1. Success rate of ECV in PWH 70-80% (Territory-wide 55%)
2. Perinatal /neonatal mortality
a. All breech (even delivered by C/S) 0.3%
b. Vaginal breech delivery 1.3%
3. Serious neonatal morbidity
a. All breech (even delivered by C/S) 1.4%
b. Vaginal breech delivery 3.8%
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External Cephalic Version (ECV)
Definition
External cephalic version is an operative procedure to turn the mal-presented foetus to cephalic presentation, by applying forces
over the maternal abdomen
Indication
1. Breech presentation at term
2. Transverse lie and unstable lie:-ECV followed by induction of labour
3. Occasionally to rotate a non-cephalic presenting second twin into cephalic presentation during second stage of labour
Contraindications
1. Maternal
a. Obesity
b. Pelvic abnormalities, e.g. placenta or fibroid at the lower pole, ovarian cysts, uterine anomalies or uterine scar
c. Pre-eclampsia
2. Feoetal
b. IUGR
c. Cord round neck
d. Polyhydramnios or oligohydramnios
e. Foetal compromise
3. Obstetrical factors
a. Rupture of membranes
b. Established labour
Prerequisites
1. No contraindications
2. Gestation at least 36 week
3. Normal foetal morphology and well-being
4. Facilities for rapid progression to caesarean section, if necessary
5. Rh-D negative women must be given anti-D immunoglobulin
Advantages of ECV
1. High success rate
2. Low complication rate
3. Mother still has choice of caesarean section after failure
Disadvantages of ECV
Chance of caesarean section after success is still higher than normal population
Procedure
1. USG to exclude any contraindications such as placenta praevia and foetal anomalies
2. CTG, USG for growth and liquor to exclude foetal compromise
3. Ask patient to empty the urinary bladder
4. Give tocolytic to relax the uterus
5. Disengage the breech
6. Grasp the foetal poles and turn in either forward or backward direction
7. Follow up for complications of ECV
- 44 -
Figure 20 External Cephalic Version.

Complications
1. Transient foetal bradycardia:
a. Most common 3-10%
b. Last for seconds to few minutes
c. No long term sequelae, only 0.4% needs further investigation for persistent episodes.
2. Acute foetal distress that requires immediate delivery
3. Reversion 3%
4. Rare:
a. Antepartum haemorrhage or abruptio placentae
b. Uterine rupture
c. Rupture of membranes

1. Let the ECV team know either by booking patient via computer CMS system or inform directly before labour
2. Adequate counselling and obtain consent
3. Ascertain gestation
4. Assess foetal well-being by CTG
5. Ascertain adequate fasting
6. Perform ultrasound examination to look for any contraindications
7. Secure intravenous access; keep NPO, X-match.
8. After the procedure
a. Perform CTG
b. Counsel on the mode of delivery if ECV fails
c. Arrange follow up to ascertain presentation if success
9. PWH Data
a. 150-200 breech per year
b. 1/3 ECV, 1/3 Contraindicated and 1/3 Refused
10. Territory wide
a. 1400-1700 breech per year; 180 (10%) ECV; Sucessful rate 55%.
b. Vaginal breech delivery 200 (1999) 60 (2004)
- 45 -
Cord prolapse
Definition
1. Occult: intact membrane with cord alongside the presenting part but not palpable.
2. Cord presentation a loop of cord lies below the presenting part and the membranes is intact
3. Cord prolapse a loop of cord prolapsed out from the cervix with the membranes ruptured
Figure 21 Presentation of the cord (Left) ; Occult presentation of the cord (Right) Figure 22 Prolapsed cord
Pathology
1. This may occur if the presenting part of the baby does not fit well into the pelvic brim, and a sudden gush of amniotic fluid
when the membranes rupture.
2. As the baby descends, it presses upon the cord. More important is that the umbilical cord blood vessels undergo an
irreversible vasoconstriction when they become cooled.
Risk factors
1. Unengaged foetus:
2. Breech presentation
3. Prematurity
4. Cephalo-pelvic disproportion
5. Polyhydramnios
Complication
Sudden foetal hypoxia and death because of umbilical cord compression or cord vessels constriction
Diagnosis
1. Cord seen at vulva, or felt on vaginal examination
2. Acute foetal distress immediately after rupture of membranes
Management
1. Avoid cord compression and vasoconstriction. Put any visible cord back in the vagina as:-
a. Cool air will make the cord go into spasm, and
b. The vagina will keep it warm and moist and prevent spasm
c. Hold presenting part away from the cord and maintain this until delivery to prevent cord compression
d. Tilt bed head down
2. Immediate delivery if foetus is still alive
a. If cervix is not fully dilated:-emergency caesarean section
b. If cervix is fully dilated:-instrumental delivery
- 46 -
5. Preterm labour and PPROM
Preterm labour
Definition
Onset of labour after 24 completed weeks but before 37 completed week of gestation. The incidence is about 5% (4.7-5.1%), but
prematurity accounts for 70% (67.2-73.8%) of all perinatal deaths.
Risk factors for preterm labour

1. Aetiology of preterm labour is largely unknown. It is believed to be multifactorial.
2. Maternal
a. Dermographic Teenage pregnancy, smoking, socially deprived, malnutrition and low body weight
b. History Primigravida, previous history of preterm labour (Recurrent risk after once:-35%; after two or more:-70%)
c. Local
i. Congenital uterine anomaly
ii. Over distension of uterus, e.g. Polyhydramnios, fibroids
iii. Cervical incompetence
iv. Infection, of genitor-urinary tract, amnion, or appendicitis.
3. Foetal multiple pregnancy, rupture of membrane.
Prediction and prevention

1. No scoring system yet devised has proven itself superior to clinical judgment
2. The strongest association is with previous pre-term delivery
3. Among the measures suggested for prediction of high risk and possible prevention and for which no evidence of benefit exists
are:-
a. Routine cervical examination
b. Home monitoring of uterine activity
c. Prophylactic beta-sympathomimetics
d. Routine screening for bacterial vaginosis
e. Prophylactic antibiotics
Diagnosis
Onset of labour is suspected if there are painful uterine contractions of 1 in 10 minutes, which may be associated with any of the
following:
1. Cervical effacement
2. Progressive cervical dilatation
3. Rupture of membranes
4. Show of mucus
Management
Management depends on 5 main factors:
1. State of membranes labour should not be suppressed if membranes have ruptured as there is high risk of intrauterine
infection
2. Dilatation of cervix Labour is likely to progress if the cervix is or more than 4cm dilated
3. Gestational age The earlier the gestation, the more strenuous attempts to inhibit labour must be. Usually labour is not to be
suppressed after 34 weeks.
4. The cause of pre-term labour Delivery is indicated if foetal well-being is prejudiced, such as in intrauterine infection, or
abruption placentae
5. The availability of neonatal intensive care facilities If all cots are full or facilities are inadequate, consider transfer of the
patient to an unit with better facilities
- 47 -
Protocol, as of 7 May 2001

1. Initial assessment
a. Inform on-call Medical Officer
b. Look for causes of preterm labour e.g. abruptio placentae, chorioamnionitis, polyhrydramnios and foetal anomaly
c. If rupture of membranes
i. Look for chorioamnionitis
ii. Discuss with Mid-call 2 before tocolytic agentis decided for steroid cover
d. Perform HVS, MSU
e. Allow delivery if gestation 34 weeks
2. Management of threatened preterm labour and preterm labour if gestation < 34 weeks
a. Inform Mid-call 1, and consultant if < 26 week
b. To labour ward, NPO, X-match, IV access
c. Administer Dexamethasone for enhancement of foetal lung maturity if immediate delivery is not required.
d. Commence tocolytic agents (Beta-adrenergic agonists and sulindac, a kind of NSAID) unless contraindicated.
e. Foetal monitoring:-CFHM when gestation 26 week, if gestation <26 week should be decided by mid-call 2 or more
senior doctors
Braxton Hicks contractions

Spontaneous painless uterine contractions usually occur in the 3rd trimester. They are us ually irregular in frequency and
inconsistent in intensity, and do not result in cervical dilatation. This normal phenomenon should be differentiated from preterm
labour when it occurs before 37 weeks.
Preterm delivery
Definition
Delivery at a gestational age of less than 37 weeks
Incidence
The incidence is 6% (5.7-6.7%), with 2.5% (2.4-2.7%) before 34 week
Clinical significance
- Significant foetal morbidity and mortality
- Account for 75% of all perinatal death
Causes of preterm delivery

1. Preterm labour, or
2. Iatrogenic preterm delivery
Sometimes a preterm pregnancy has to be discontinued because the risk of continuing the pregnancy is higher than that of
preterm delivery. For example, in severe pre-eclampsia, abruptio placentae, foetal growth retardation (IUGR) and foetal
distress, there is a high risk of intrauterine death or maternal morbidity and mortality when the foetus is not delivered on time.
Modes of preterm delivery

1. If the foetus is viable it must be delivered by the route least likely to cause trauma or hypoxia
2. In general, aims for vaginal delivery if gestation < 26 weeks, as caesarean section at early gestation, and with infants under
1000g, can be hazardous for the mother and are not necessarily safer for the baby
3. The indications for caesarean section are stronger but not absolute in twin pregnancy and breech presentation
4. Pre-term labour is unpredictable and the woman may become fully dilated quickly and silently
5. Aims to have the presence of an experienced neonatal paediatrician at delivery
- 48 -
Rupture of membranes
Definition
1. Premature/Prelabour rupture of membranes (ROM):-ROM before onset of labour
2. Preterm rupture of membranes:-ROM before 37 week
3. Prolonged rupture of membranes:-ROM for more than 24 hours
Incidence
2% (3.7-5.7%) of all pregnancies, 33% of all preterm deliveries
Risk factors for premature rupture of membranes

1. Polyhydramnios
2. Infection of genital tract
3. Cervical incompetence
4. Breech presentation
Diagnosis of rupture of membranes

1. Typical history a sudden gush of clear watery fluid passed vaginally
2. Examination watery fluid in vagina; oozing of fluid from cervical os after coughing
3. Other diagnostic tests (Usually are not required unless the diagnosis is inconclusive from the history and examination):-
a. Amniostrix (Nitrazine paper)
i. The orange colour of amniostrix changes to blue with contact with liquor
ii. May have false positive if the fluid is alkaline (such as mucus, blood)
b. Fern pattern
i. A swab dipped in fluid is used to make a slide and is allowed to dry thoroughly.
ii. Under microscopic examination, a characteristic fern pattern is noted, due to salt content in liquor
iii. False positive from cervical mucus
c. Ultrasonography may reveal decreased liquor volume after ROM. However, if the volume of leaking is not much, the
amniotic fluid volume would still appear normal under USG
Risk after rupture of membranes

1. Cord prolapse
2. Intrauterine infection
3. Preterm labour and delivery

1. Investigation High vaginal swab to exclude infection
2. Decide mode and time of delivery, Depending on gestation and presence of infection
a. Gestation of 24-34 weeks:-
i. Aim to prolong pregnancy beyond 34 week to minimise foetal complications from preterm delivery
ii. Steroid to enhance foetal lung maturity in absence of infection
iii. Monitor any maternal or foetal signs of infection such as maternal fever, tachycardia. uterine
tenderness, keep pads to inspect for foul vaginal discharge or MSL, and foetal tachycardia, and prompt
delivery if infection occurs. Monitor foetal growth with USG.
iv. Avoid vaginal examination unless indicated, and should be done under aseptic technique.
v. Start dexamethasone and antibiotics for 10 days, or till delivery, whichever occurs earlier.
- Erythromycin 250 mg qid po; Treat accordingly for +ve HVS result.
- If carrier ampicillin 2g load IV + amoxicillin 250 po tid;or clindamycin 900 mg IV + above.
b. Gestation between 34-37 weeks, Induction of labour if there is good neonatal support., Otherwise conservative
management till 37 weeks, when induction of labour is indicated if still not in labour after 24 hours of ROM.
(1) If re-sealing of membranes is diagnosed for >=1 week, patient can be discharged.
(2) If continuous leaking of liquor, keep patient in hospital and plan delivery at 34 weeks.
(3) If preterm labour occurs <24hrs of commencement steroid, consider tocolytic agent in the absence of intrauterine infection.
- 49 -
Amniostrix
Amniostrix is made of nitrazine paper which turns from orange to blue when contacting with alkaline fluid. As amniotic fluid is
alkaline, it can be used as a test of rupture of membranes. It is not specific as other fluid such as blood, cervical mucus or urine
may give a false positive result.
Chorioamnionitis
Definition
It is an acute inflammatory process involving the chorion, its foetal blood vessels, the umbilical cord, and the amnion (by local
extension of the inflammation, as the amnion itself has no blood supply). This inflammatory process is potentially fatal to both the
mother and the foetus.
Causes
1. It is often a result of ascending infection, and prolonged rupture of membranes is a major risk factor. The common
micro-organisms are:
a. Group B streptococcus
b. Gram negative rods from bowel contamination
c. Sexually transmitted disease
d. Bacterial vaginosis e.g. Gardnerella vaginalis, E coli, enterococci
e. Others ureaplasma urealyticum, mycoplasma hominis
2. Risk factors
a. Preterm / premature rupture of membranes > 24 hours
b. Preterm labour rupture of membranes
c. Group B Streptococcus carrier
Clinical features
1. Maternal intrapartum fever (>37.8 oC)
2. Maternal tachycardia without other focus of infection identified, particularly if membranes have been ruptured
3. Uterine tenderness
4. Foul smelling discharge from the cervix
5. Maternal leukocystosis
6. Foetal tachycardia without other focus of infection identified.
7. Abnormal CTG, especially ones with decreased variability and lack of accelerations
Diagnosis
1. The diagnosis is mainly relied on the clinical features. Microscopic examination and culture of amniotic fluid are difficult and
inaccurate before delivery, and are not very helpful in an acute setting.
2. Careful clerking and examination are essential to rule out other causes of maternal fever, such as urinary tract or respiratory
tract infections
- 50 -

1. Delivery of pregnancy
a. Foetus is at high risk of intrauterine death, or neonatal sepsis if there is a delay of delivery.
b. Therefore delivery should be immediate regardless of maturity (the risk chorioamnionitis is high than that of
prematurity).
c. Delivery is by Caesarean section when labour is not yet established. If labour has been established,
augmentation of labour may be considered to hasten delivery.
d. Aim for delivery within 2 hours
e. Inform paediatrician before delivery
2. Take HVS, placental swab for culture and sensitivity
3. Send placenta for section
4. Antibiotic treatment
a. Multiple antibiotics to cover gram positive cocci, gram negative rods and anaerobes:-penicillin group,
cephalosporins, metronidazole.
b. Intrapartum:-Ampicillin 2g IV q6h + Gentamycin 1.5mg/kg (in 50ml NS, infusion over 30min) q8h, both till delivery.
i. Caution with gentamycin if patient has severe renal impairment.
ii. In most cases, Ampicillin and Gentamycin will be given as a single dose, since delivery will have been completed
before the second dose of drug is due. Monitoring of Gentamycin concentration in blood is therefore not necessary.
c. Post-delivery:-after clamping the umbilical cord, give Augmentin 1.2g IV q8h
i. Continue IV Augmentin until day 2 post-delivery, or until maternal fever subsides, followed by oral Augmentin
375mg tds to complete a 7-day course.
ii. If allergic to penicillin, replace Augmentin with Metronidazole 500mg IV Q8H + Clindamycin 900mg IV (diluted
in 100ml NS infusion over 30min) Q8H. Change to metronidazole 400mg po tds, and erythromycin 250mg po qid
when fever subsided.
5. Discussion
a. Foetal morbidity and mortality in chorioamniontitis
i. This is caused mainly by Group B streptococcus and Enterobacteriaceae.
ii. High dose Ampicillin given intrapartumaims to treat the neonate by having adequate dosage of ampicillin crossing
the placenta.
iii. High dose Gentamycin has synergistic effects with ampicillin and enhances the effect of Ampicillin.
iv. This combination of Ampicillin and Gentamycin is the most common antibiotics used worldwide to treat
intrapartum chorioamnionitis. It has been shown to reduce the rate of neonatal sepsis effectively.
b. Maternal morbidity and mortality
i. The choice of Augmentin post-delivery was made after consultation with microbiologist in our hospital.
ii. Augmentin has good coverage for Group B strep, most G-negative oragnisms, most anaerobes and also
Staph.aureus (methicillin-sensitive), which are the most common organisms that cause postpartumsepsis,
endometritis and Caesarean section wound infection.
iii. Sensitivity of these organisms e.g. Staph. aureus to Augmentin is not always tested in our laboratory
iv. If in doubt of the sensitivity of the cultured organism to Augmentin, please consult microbiologist before changing
the already-started antibiotic regimen
- 51 -
Cervical incompetence
Definition
Cervical incompetence means cervical dilatation in the absence of uterine contractions in second trimester or early third trimester.
Classically it is defined as a clinical syndrome characterized by painless dilatation of cervix, resulting in recurrent spontaneous
midtrimester abortions or preterm delivery (vaginal), in the absence of any associated uterine activity.
Causes
1. Previous traumatic events:
a. Mechanical cervical dilation
b. Second-trimester abortion
c. Cervical amputation, conization or laceration
2. Congenital:-rare
a. In utero diethylstilbestrol exposure
b. Spontaneous occurrence
Diagnosis
1. History
a. Typical history of painless mid-trimester cervical dilation resulting in expulsion of a nonviable foetus; or premature
labour in early third trimester
b. History of any traumatic events involving the cervix
2. Examination presence of cervical dilation may be accompanied by bulging forewater, without uterine contractions.
3. Ultrasound shows Hour glass appearance and shortened cervix.
4. Diagnostic tests in non-pregnant state, a number of methods for assessing cervical incompetence before pregnancy have been
suggested but none are reliable. These include:
a. Passage of 8mm Hegar dilator through the cervix:-no resistance suggests incompetence
b. Hysterosalpingogram:-dilation of cervix with leaking of dye under X-ray

1. Cervical cerclage placement of a circumferential cervical suture that externally supports the internal os
2. Elective cervical cerclage:
a. Performed when the cervix is not yet dilated, in patients with history of cervical incompetence
b. Performed at around 13 weeks after foetal viability is confirmed
3. Emergency cervical cerclage:
a. Performed when the cervix already dilated
b. Success rate is lower
c. Risk of rupture of membranes, infection, abortion or preterm delivery because the membranes are usually
bulging out after the cervix has dilated
d. Consider waiting for 12-24 hours before deciding cerclage, to observe for signs of preterm labour, to permit uterine
quiescence to facilitate the reduction of herniated membranes and decrease risks of rupture during cerclage placement.
4. Special considerations
a. If chorioamnionitis is diagnosed, for removal of cerclage and delivery
b. If no evidence of chorioamnionitis,
i. 34 weeks / at 37 week for removal of cerclage and induction of labour in labour ward.
ii. 28 weeks to 34 weeks
- Start steroid to enhance foetal lung maturity
- Observe for spontaneous onset of labour
iii. <28 weeks
- Start steroid to enhance foetal lung maturity
- Decision by consultant concerning the removal of cerclage and delivery
5. Mirselene Tape: 5 mm thick, 400 mm long non-absorbable suture for cerclage
When a woman presents to you with a history of recurrent abortions, what information do you want to ask to diagnose a case of
cervical incompetence?
- 52 -
6. Postpartum
Postpartum care
Aims
1. To ensure normal recovery from pregnancy and childbirth during puerperium
2. To follow up any antenatal problems and provide appropriate referral, counselling and management
3. To look for any problems in childcare and feeding
4. To advise on contraception and family planning
Routine care in early postpartum period

1. Look for any complications such as:
a. Postpartum haemorrhage
b. Anaemia
c. Postpartum fever
2. Provide adequate analgesia for wound pain
3. Prophylactic measures such as:
a. Encourage early mobilization to prevent thrombosis
b. Anti-D immunoglobulin for non-sensitized rhesus negative mothers
c. Rubella vaccine for non-immune mothers
4. Counselling, support and education
a. Advise on childcare
b. Encourage maternal-infant bonding
c. Promote and teach breast-feeding
d. Advise contraception and family planning
Postpartum visit at the end of puerperium

1. Usually is arranged at the end of puerperium (6 weeks post-delivery)
2. Examine for blood pressure elevations, breast masses or tenderness, uterine size, anaemia and healing of wound
3. Search for any problem in childcare, resumption of coitus and work, and any adjustment difficulty
4. Advise on contraception
5. Obtain pap smear if not screened before
6. Follow up any remaining problems such as:-
a. Screen for diabetes if previously diagnosed to have gestational diabetes
b. Refer to physicians if persistent proteinuria after pre-eclampsia
7. Continue to encourage healthy habits
What medical students should know?

Three major postpartum complications:
1. Postpartum haemorrhage
2. Postpartum fever
3. Postpartum depression
- 53 -
Postpartum fever
Definition
Body temperature of 38 degree or higher on two occasions beyond the first hours and within the next 9 days postpartum
Incidence
5 to 10% (0.6-1.7%) of all pregnancies
Causes
1. Infectious causes
a. Intrauterine infection High risk after prolonged ruptured membranes and prolonged labour
b. Urinary tract infection High risk when multiple urinary catheterizations are performed during labour
c. Wound infection caesarean wound or episiotomy wound
d. Breast infection
i. Higher risk in breastfeeding mothers, usually cause by staphylococcus aureus
ii. Need to differentiate from breast engorgement of breasts and chemical mastitis
iii. Treat with antibiotic; may require incision and drainage
2. Non infectious causes
a. Haematoma vulval haematoma or pelvic haematoma
b. Lung atelectasis (Day 1-3)
c. Deep vein thrombosis (Day 7-10)
d. Breast problems
i. Engorgement of breasts
ii. Non-infectious mastitis
How to differentiate breast engorgement and infectious mastitis clinically?
Postpartum haemorrhage
Definition
1. Primary PPH Blood loss more than 500ml during the third stage of labour or 800ml during a caesarean section, and for
within 24 hours afterwards
2. Secondary PPH Any abnormal vaginal bleeding after the first day of delivery till the completion of the puerperium
Incidence
2.6%
Causes of primary PPH

1. Bleeding from uterus
a. Uterine atony (63.2-73.0%)
i. The most common cause
ii. May be secondary to retained placental tissue
b. Retained placenta (5.6-11.4%), may result from morbid adhesion of placenta to the uterine wall
c. Inversion of uterus, very rare (0.2-0.3%)
d. Uterine rupture or tear (0.1-0.3%)
2. Bleeding from lower genital tract injuries
a. Cervical tear (2.4-2.9%)
b. Vaginal tear (3.0-6.8%)
c. Vulval tear or haematoma (1.9-3.5%)
3. Secondary to systemic causes disseminated intravascular coagulopathy (0.8%)
Causes of secondary PPH

1. Common causes are Endometritis and retained placental tissue
2. Rare causes are delayed uterine rupture, uterine arterial-venous malformation and DIC.
- 54 -
Complications
1. Shock and death
2. Sheehans syndrome (very rare)
3. Puerperial anaemia
Management of primary PPH
1. Assess the patients haemodynamic status with resuscitation by fluid and oxygen
a. Monitor blood pressure and pulse
b. Place patient in head down position
c. Assess the amount of blood loss
d. Set up large bore ivaccess with colloid or crystalloid fluid replacement
e. CBP, cross match, +/- clotting profile
f. Transfuse blood/ platelets/ FFP if inappropriate
2. Identify the cause and treat the cause
a. Examine placenta for completeness
b. Examine uterine tone
c. Examine lower genital tract for any tear and origin of bleeding
d. Examine signs of internal bleeding
e. Examination under anaesthesia and exploration of uterus may be required if retained placenta is suspected
3. Specific treatment
a. Manual removal of placenta for retained placenta
b. Oxytocic for uterine atony
c. Surgical repair and haemostatsis for genital tract injury
d. Incision and drainage for vulval haematoma
e. Hysterectomy for non-repairable uterine injury, uncontrolled bleeding, morbid adherence of placenta
4. Inform mid-call 1 if persistent bleeding or OT required
Uterine atony
Definition
It means failure of the uterus to contract post delivery. It is a common condition immediately after delivery in which the uterus
become hypotonic and loses it contractility that is the most important mechanism to control blood loss after delivery of the baby
and placenta. It is the most common cause of postpartum haemorrhage.
Risk factors
1. Uterine atony is also caused by retained placental tissue which should be ruled out first when uterine atony occurs.
2. Uterine atony is more common in:
a. High parity
b. Over-distended uterus such as multiple pregnancy, polyhydramnios
c. Abruptio placentae, placenta praevia
d. Prolonged labour, or prolonged stimulation with syntocino
e. Sepsis
Prevention of uterine atony

1. All women should be given syntometrine or syntocinon immediately after the delivery of their babies.
2. High risk cases should also be given additional syntocinon infusion to maintain the uterine tone.

1. Rule out retained placental tissue
2. Resuscitation with fluid or blood replacement
3. Control blood loss with oxytocics which include syntocinon, or other prostaglandins. 40 units syntocinon infusion in
500ml Hartmanns solution/normal saline solution to run over 4 hours. Additional units may be necessary.
4. Bimanual compression of the uterus and massage with the abdominal hand
5. If still fails to control bleeding, inform midcall 1 before giving Hemabate.
6. Inform Midcall 2 if the above measures fail and arrange for EUA laparotomy hysterectomy
- 55 -
Uterine rupture
Definition
1. Complete uterine rupture:- uterine cavity directly communicate with peritoneal cavity
2. Incomplete uterine rupture:- uterine and peritoneal cavities separated by visceral peritoneum
3. Uterine dehiscence:- foetal membranes are not yet ruptured
Incidence 0.01%
Causes
Uterine rupture can occur spontaneously or after traumatic events. A scarred uterus is vulnerable to rupture, but rupture can
occasionally occur in an unscarred uterus. It is not common and usually occurs because of scar from previous operations.
1. Maternal factors
a. Congenital anomaly:-undeveloped uterine horn
b. High parity
c. Previous surgery:- ECV, instrumental delivery, MROP, caesarean section, hysterotomy, myomectomy, metroplasty
d. Previous trauma:-curette, sharp or blunt trauma
2. Foetal factors Foetal anomalies distending lower segment such as hydrocephalus
3. Obstetrics factors
a. Obstructed labour
b. Uterine hyperstimulation
c. Morbid adherence of placenta
Figure 23 Causes of uterine rupture. (Left to right) Spontaneous; Classical C/S; and Lower Segment C/S.
Pathology
1. Rupture of unscarred uterus
a. Longitudinal or lateral
b. Vascular with torn vessels and heavy bleeding
c. 85% are not repairable and require hysterectomy
d. High maternal and foetal mortalities and morbidities
2. Rupture of scarred uterus
a. Rupture along old scar
b. Wound relatively avascular
c. Two-third of the ruptures are amendable
d. Lower maternal and foetal mortalities and morbidities when compared with unscarred uterine rupture
3. Rupture of uterus with previous caesarean section scar
Type of scar Classical Lower Segment

Incidence 2.5% 0.5%
Timing 1/3 before labour rarely before labour
Maternal mortality 5% 0%
Foetal mortality 75% 12%
- 56 -
Clinical features
1. Sudden abdominal pain
2. Vaginal or intra-abdominal bleeding
3. Uterine contractions may cease
4. Foetal distress and misplacement
Diagnosis
1. High suspicion if patient with a scared uterus presented with acute abdominal pain and bleeding with abnormal CTG
2. Some cases of uterine rupture are not diagnosed until during caesarean section
3. Differential diagnosis:
a. Abruptio placentae:- also present with acute pain and bleeding, and foetal distress
b. Uterine hyperstimulation:- also present with sudden foetal distress
c. Amniotic fluid embolism:- present with sudden shook and foetal distress
Management
1. Resuscitation
2. Immediate delivery:-by caesarean section
3. Repair of uterine rupture and hysterectomy, depends on
a. Type and extent of rupture
b. Severity of bleeding
c. Patient's past obstetric history and wish of fertility
4. Patients must be counselled for elective section next pregnancy, if the uterus is repaired and conserved
Prevention
1. Reduce prevalence of scared uterus in the population by avoiding unnecessary caesarean section
2. Avoid overstimulation of uterus by oxytocic during labour
Uterine inversion
Definition
It is a very rare complication of the third stage of labour in which the fundus is inverted into the uterine cavity.
Incidence
1 in 10000 deliveries (0.3% locally)
Classification
1. First degree / incomplete fundus at external os
2. Second degree / complete fundus into vagina
3. Third degree fundus out of vagina
Causes
1. Lax uterus
2. Morbid adherence of placenta
3. Inappropriate cord traction to deliver the placenta:
a. No counter pressure (controlled cord traction) to prevent fundal descent.
b. Premature traction before evidence of placental separation
c. Too vigorous fundal pressure
Clinical Presentation
1. Uterine fundus is protruding out from the cervix (in complete inversion)
2. Severe postpartum haemorrhage
3. Severe abdominal pain
4. Shock
5. Fundus is not palpable on abdominal examination and PV exam will reveal a hard mass.
- 57 -
Figure 24 Uterine inversion. (Left to right) First, second and third degree
Figure 25 Manual reduction by Taxis (Left and Centre); and by laprotomy (Right)

1. Resuscitation and management of haemorrhage and shock
2. Reposition of the uterus
a. Manual replacement by Taxis
i. While the adherent placenta is left undelivered, the fundus is pushed back manually vaginally.
ii. Uterine relaxants such as hexoprenaline 10mcg may be required.
iii. Once the uterus is in position, the attendant's hands should remain in endometrial cavity until a firm contraction
occurs (oxytocic may be required). Then the placenta can carefully be removed .
b. Replacement with hydrostatic pressure by OSullivan
Warm saline (up to 10L) is infused into posterior fornix of vagina, to distend the vagina and uterus so as to push
the fundus of the uterus back.
c. Laparotomy is rarely required. The uterus is cut open to release the constriction and the fundus is reverted.
3. Manual Removal of Placenta
Sheehan syndrome
This is a rare complication of postpartum haemorrhage. Severe blood loss and vascular shock at or after delivery lead to a
reduction of blood flow through the pituitary-hypothalamic circulation, resulting in thrombosis, and necrosis of the pituitary gland
with loss of its function. Patients exhibit hypogonadotropic hypogonadism (fi rst sign:-no return of menstruation after delivery) as
well as evidence of thyroid and adrenal cortex impairment. Replacement of deficient hormones is required.
- 58 -
Puerperium
Definition
In Latin puer means child and parere means to bear. It is the period during which the reproductive organs return to their
pre-pregnant condition and are usually regarded as an interval of 6 weeks after delivery.
Normal physiological changes during puerperium

1. Involutionof uterus
2. Lochia
3. Lactation
Involution
Involution of uterus
Uterus regains its usual nonpregnant size within 5 to 6 weeks, shrinking from 1000g immediately postpartum to 100g. The rapid
atrophy is due to the marked decrease in size of the muscle cells rather than the decrease in their total number. Breast-feeding
accelerates involution because stimulation of nipples releases oxytocin from the neurohypophysis, and the resulting contractions
of the myometrium facilitate the involution process. In primparous women, the uterus tends to remain contracted tonically,
whereas in multiparous, the uterus contracts vigorously at interval. The uterine contraction pain that produced throughout the
period of involution is called afterpain, and is more common in multiparous women and nursing mothers.
Lochia
It is the uterine discharge that follows delivery and lasts for 3 to 4 weeks puerperium. The discharge undergoes changes during the
first few weeks:
Lochia rubia is blood-stained fluid that lasts for the first few days
Lochia serosa appears 3 to 4 days after delivery, it is paler than lochia rubra because it is admixed with serum
Lochia alba occurs after the tenth day, because of an admixture with leukocytes, the lochia assumes a white or yellow-white color.
Foul smelling lochia suggests infection. Look for signs of endometritis such as fever, tachycardia and poor involution.
Engorgement of breasts
It is a normal phenomenon with the breasts become full, red, hard and sore due to increased blood flow before milk secretion
commences. It usually occurs in the first few days post-delivery, and may cause fever. It must be differentiated from mastitis
which is usually unilateral. Other cause of postpartum fever should also be looked for before attributing the fever to breast
engorgement.
Mastitis
If infective cause is found, treat by antibiotics accordingly. Otherwise, it is usually due to the blockage off ducts. Better
positioning can be suggested so that milk can be drained with expression of milk. Analgesics may be prescribed. Its complication
is abscess.
How is engorgement of breasts differentiated from mastitis clinically?
Colostrum
Yellowish fluid expressed from the breasts during late pregnancy and before the onset of true lactation. Compared with mature
breast milk, it contains more minerals and protein, much of which is globulin, but less sugar and fat. It also contains some immune
cells. The immunoglobulin A and other host resistance factors such as complement, macrophages, lymphocytes, lactoferrin in
colostrum provide protection for the newborn against enteric pathogens. The colostrum gradually converts to mature milk a few
days after delivery.
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Lactation
Growth of mammary glands
1. Early in pregnancy, HCG, chorionic somatotropin, prolactin causes a marked increase in ductular sprouting and branching
2. Estradiol and progesterone cause the mammary gland to become richly arboized
3. Serum growth factor and insulin cause cell proliferation at the end of the ducts, which under the influence of prolactin and
corticosteroids, differentiate to form alveoli
4. Placental lactogen and prolactin stimulate the secretion of colostrum
Lactation
1. The withdrawal of oestrogen after the delivery of the placenta allows lactation to begin
2. Lactation is in large part sustained by the stimulus of nursing that causes a transient increase in prolactin and oxytocin, the
former hormone is responsible for alveoli synthesis of milk, while the latter is responsible for ejection of milk from the
alveoli into ductules
Breast-feeding
Advantages to mothers
1. Increases bonding
2. Promotes uterine involution
3. Effective post-partum contraception
4. Economical Save money on formula feeding
Contraindications
1. HIV positive (unless formula feeding confers greater risk through contaminated water supply, especially in the Third World)
2. Drug abusers
Measures to promote breast-feeding

1. Baby-friendly hospital:- promote breast-feeding since antenatal period
2. Nurse specialists to help tackle problems or misunderstanding
3. Never provide formula feeding unless really indicated
Tips
1. Early start
2. Proper positioning - baby's mouth covers the whole nipple and areola
3. Feed on demand
4. Healthy lifestyle
5. No supplements
6. No worry about engorgement - analgesics, tight bra and frequent feed
Breast milk
1. Natural and the best nutrition for babies
2. Not able to be duplicated by formula milk
3. Advantages to babies
a. Just the right amount of nutrition for babys needs
b. Antibodies and cells such as macrophages help to prevent infection
c. Increases bonding
d. Always sterile, which decrease the risk of diarrhoea from contaminated bottle feeding
e. Decreases risk of allergy
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Postpartum depression
Epidemiology
- 12% of Hong Kong Chinese women
- Usually occurs in women with previous depressive disorders or other life situations predisposing them to depression
Clinical features
Depressive symptoms:
- Low mood, tearfulness, not her normal self
- Irritability, bad temper
- Guilt, self-blame, low self-esteem
- Forgetfulness, poor concentration
- Sleep disturbance, especially early morning
- Loss of appetite
- Suicidal ideas or attempt
- Distressed by the inability to have affection towards the baby
- Lack of confidence in child care
- Excessive anxiety about baby's health
- Obsessive fear of harming the baby
Treatment
- Psychoeducation
- Pharmacotherapy:-tricyclic anti-depressant
- Psychotherapy:-discuss childcare and interpersonal problems
Prognosis
- Untreated 1/3 continued to be depressed by one year, 1/10 by 2nd year
- Treated Good and prompt response to treatment
- Persistent stressors and personality tend to associate with poor prognosis
Future pregnancy
1/6-1/2 risk of relapse
Postpartum blue
It affects up to 70% of all mothers, and occurs during the first 2 weeks after delivery, usually 48 and 72 hours postpartum. It is
manifested by tearfulness, anxiety, mood lability, irritability, insomnia and depression. It is said to be related to physiological
changes in hormone levels after delivery, often resolves spontaneously and require no treatment. It should be differentiated from
postpartum depression.
Postpartum psychosis
Or puerperal psychosis usually occurs 2 to 3 months post-delivery. Most show symptoms of manic-depressive type, with
confusion and disorientation; delusional thoughts or expressions of suicide. It should be differentiated from postpartum
depression.
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7. Obstetric statistics
Includes maternal mortality rate, perinatal mortality rate, stillbirth rate, and neonatal death rate
Maternal mortality
Definition
Deaths of women during pregnancy or within 42 days of termination of pregnancy, from any cause related to (direct) or
aggravated by (indirect) the pregnancy or its management, but not from accidental or incidental (fortuitous) causes.
Direct
Deaths resulting from obstetric complications of the pregnant state (pregnancy, labour and puerperium), from interventions,
omission, incorrect treatment, or from a chain of events resulting from any of the above.
Indirect
Deaths resulting from previous existing disease, or disease that developed during pregnancy and which was not due to direct
obstetric causes, but was aggravated by the physiological changes in pregnancy.
Fortuitous
Deaths from unrelated causes which happen to occur in pregnancy or the puerperium
Late
Deaths occurring between 42 days and 1 year after abortion, miscarriage or delivery that are due to Direct or Indirect maternal
causes
Maternal mortality in Hong Kong

Hong Kong has the one of the lowest maternal mortality rate of the world, around 10 (6.1-11.8) per 100000 pregnant women. The
most common causes of maternal death are pulmonary embolism (30%) and suicide secondary (20%) to postpartum depression.
Perinatal mortality
It includes all stillbirth and (early) neonatal death. The perinatal mortality rate is:-number of stillbirth + (early) neonatal death per
1000 total birth (all stillbirth + livebirth). It is about 4.7/1000 in Hong Kong.
Stillbirth
Definition
It is the birth of a dead foetus at or after 24 weeks of gestation. Stillbirth rate is the number of stillbirth per 1000 births (stillbirth +
livebirth). It is about 3-4/1000 (2.4-3.4) in Hong Kong.
Causes
About 50% of cases are unexplained stillbirth. The following are identifiable causes:
1. Foetal complications:
a. Chromosomal abnormalities (32.8%)
b. Complications of twins such as twin-twin transfusion syndrome
c. Intrauterine growth retardation (IUGR)
d. Congenital infections
2. Maternal complications:
a. Abruptio placentae
b. Hypertension (8.2%), Pre-eclampsia
c. Poorly controlled diabetes mellitus (6.6%)
d. Other poorly controlled maternal diseases such as hypothyroidism, SLE, antiphospholipid syndrome
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Intrauterine death
1. Diagnosis and Investigation
a. Confirm diagnosis with USG.
b. Perform the following tests if the cause of IUD is not obvious:
i. Autoimmune tests:-APTT, ACA, ANA
ii. Microbiological screening:
- HVS
- VDRL for syphilis
- Parvovirus serology:-maternal IgM
- Rubella serology if rubella antibody was negative previously:-Maternal IgM
iii. Maternal disease:-intrahepatic cholestasis LFT
c. The following tests should be performed only if suspected as a cause of IUD
i. Toxoplasma serology
ii. Cytomegalovirus serology
iii. Fasting glucose
2. Management of delivery
a. If patient agrees for IOL, induce labour with:
i. <28 weeks - misoprostol or cervagem
ii. 28 weeks - PGE2 vaginal pessary followed by syntocinon infusion if the cervix is favourable
b. Avoid rupture of membranes unless in active labour
c. Provide adequate pain relief
d. Monitor patient preferably in a single room with husbands accompany
e. Manage accordingly for chorioamnionitis and abruptio placentae
3. Management after delivery
a. Record the following information by on-call medical officer with photos for documentation:
i. Body weight
ii. Maceration
iii. Congenital anomalies
iv. Umbilical cord and placental anomalies, placental weight and any retroplacental clots
v. Liquor characteristics
b. Send:
i. Dead body for post-mortem examination if patient agrees
ii. Placenta for histological examination
iii. Placental swab for microbiological examination
c. Perform the following tests only if indicated:
i. Swabs from babys throat, conjunctiva and rectum for viral study
ii. Cord blood (in heparin bottle)/foetal skin/deep placental tissue for chromosomal study if had not been performed
previously (contact Clinical Genetic Labarotary, Cheung Sha Wan 27253773 )
iii. X-ray of whole baby for skeletal abnormality
d. Complete Death documentation forms by on-call Medical officer (to be sent to the Death Certificate Clerk). Discuss
burial/ cremation
e. Maternal Care:
i. Encourage the couple to see the baby photo
ii. Consult Grief Counselling Team
iii. Transfer to Gynae ward side room
iv. Arrange postnatal follow up in LKS clinic
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Neonatal death
Definition
- Early neonatal death are all neonatal deaths within 7 days of delivery
- Late neonatal death are all neonatal deaths after first 7 days but within 28 days of delivery
- The neonatal death rate is the number of early neonatal death per 1000 livebirth. It is about 1.4(1.2-2.8)/1000 in Hong Kong
- Post-neonatal death are all neonatal deaths after 28 days but within 1 year of age
Causes
- Over 80% of cases are due to prematurity (50% <28 weeks)
- Other causes include congenital abnormalities, severe birth asphyxia
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8. Miscellaneous topics in General Obstetrics
Advanced maternal age
It is arbitrarily defined as 35 years old or above on the estimated date of confinement (EDC). In Hong Kong, 24.2% (18) of all
pregnant women, and 16.7% (9%) of all primiparous women are in advanced maternal age. It is epidemiologically associated
with various foetal and maternal risks. However, it is better to consider it as a risk indicator, rather than a risk factor. Apart from
Down syndrome, the associations with other risks are confounded with other socio-medical factors such as parity, smoking,
general health and reproductive health.
Foetal risks
1. There is an exponential increase in risk of Down syndrome with maternal age.
2. Abortion
3. Preterm delivery
4. Higher perinatal mortality
Maternal risks
1. Gestational diabetes
2. Pre-eclampsia
3. Prolonged labour
4. Placenta praevia
Protocol, as of 17 March 2004

1. Discuss in general antenatal clinic the following options of prenatal screening and diagnosis for e.g. Downs syndrome:-
a. Combined first trimester screening with nuchal translucency, free-beta hCG and PAPP-A. Performed at 11-14 weeks.
b. Second trimester biochemical screening with hCG and AFP:-usually performed at 16-20 weeks.
c. Chorionic villi sampling:-Usually performed at 11-13 weeks. Procedure-related foetal loss:-1%
d. Amniocentesis:-Usually performed at 16-18 weeks, but could be up to 21 weeks. Procedure-related foetal loss:-1%
e. Cordocentesis:-only performed at 21-23 weeks when it is too late for amniocentesis. Procedure-related foetal loss:-2%.
2. Arrange morphology scan:
a. Timing:-preferably between 18 and 20 weeks, but not later than 23 weeks. Beyond 24 weeks, morphology scan for the
sole indication of advanced maternal age is not necessary.
b. No need for patients undergoing amniocentesis or cordocentesis as morphology scan will be done at the same session,
c. USGP or USGX for low-risk cases, USG9 for high-risk cases (contact Foetal Medicine Team for any query)
3. Arrange OGTT at 26-28 weeks.
Fecundity
A measure of the ability to produce offspring. This declines markedly with advancing maternal age, especially after 35 year old.
The fecundability rate is the monthly probability of pregnancy when the opportunity for conception exists.
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Postterm
Definition
1. Post-term pregnancy Pregnancy lasting 41/42 completed weeks (294 days) or more (WHO)
2. Post-maturity syndrome clinical syndrome with the neonate manifesting signs of:
a. Long and thin in body girth and underweight from loss of subcutaneous tissues
b. Patchy areas of desquamation and skin is stained with meconium, although rarely the latter feature may be absent
c. The ventral surfaces of the hands and feet are wrinkled and the nails are long and stained with meconium
Incidence
1.4% Varies from 3 to 10%, depending the accuracy of the dating of pregnancy
Causes
1. Most are by chance
2. Rarely it is associated with foetal abnormalities(0.1-1%):-anencephaly, foetal adrenal hypoplasia, absence of foetal pituitary,
placental sulfatase deficiency. The deficiencies of hormones in the above conditions are thought to cause the failure of
initiation of labour.
Risk of post-term pregnancy

1. Maternal risk
a. Maternal anxiety
b. Higher caesarean section rate (17.6-25.8%) resulting from macrosomia, failure of induction of labour, and foetal distress
c. Birth canal injury resulting from difficult delivery of macrosomic baby
2. Foetal risk
a. Post-maturity syndrome
b. Macrosomia (10%) and associated birth injury (0.5%) such as shoulder dystocia
c. Intrauterine growth retardation
d. Foetal compromise
e. High chance of meconium stained liquor (MSL) and therefore meconium aspiration syndrome
f. Overall 2-fold increase in perinatal mortality rate when compared to term gestation
Diagnosis
Accurate dating of pregnancy from menstrual history, early ultrasound assessment, landmarks of foetal development:-quickening,
foetal heart sound, uterine size.

1. Ensure the EDC is well defined.
2. Arrange follow-up in MCH meanwhile.
3. On the day of admission at 41 weeks, perform routine examination and CTG by midwives.
4. If patient declines IOL at 41 weeks, rearrange IOL no later than 42 weeks.
What are the assessments that should be done before induction of labour for postterm?
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Gravid
Means pregnant, irrespective of outcome. A primigravida is a woman pregnant for the first time.
Grand multipara
A woman with parity 4 or more. She is likely to have powerful and coordinated uterine contractions. The labour progress is
usually quite fast. However, the chances of birth before arrival to hospital, uterine rupture and postpartum haemorrhage due to
uterine atony are higher. In addition, their babies may tend to be bigger, causing an unexpected obstructed labour or shoulder
dystocia.
How to prevent uterine rupture and postpartum haemorrhage in this group of patient?
Trimester
- A period of 3 months (about 13 to 14 weeks) in pregnancy:
- First trimester:-up to 14 weeks
- Second trimester:-14 to 28 weeks
- Third trimester:-28 weeks to delivery
Placenta
Structure of a placenta
- Cotyledons Membranes:-see chorioamnionicity
- Umbilical cord
Disorders of placenta
- Placenta praevia
- Abruptio placentae
- Retained placenta
- Morbid adherence of placenta
- Placenta insufficiency
- Placenta tumour:-chorioangioma
- Chorioamnionitis
Obstetric surgery
Operative delivery
1. Caesarean section
2. Instrumental delivery
3. Episiotomy
4. Manual removal of placenta
5. Postpartum hysterectomy
6. Repair of tear of lower genital tract
Prenatal diagnosis and therapy
1. Chorionic villus sampling
2. Amniocentesis
3. Cordocentesis
Obstetric emergency
- Eclampsia
- Shoulder dystocia
- Cord prolapse
- Amniotic fluid embolism
- Pulmonary embolism
- Massive haemorrhage, due to placenta praevia or any causes of postpartum haemorrhage
- Uterine inversion
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Birth trauma
Types of birth trauma
Incidence: 0.4-0.6%
1. Skeletal injury
a. Long bone fractures
b. Skull bone fractures
2. Bleeding
a. Cephalhaematoma
b. Subaponeurotic haematoma
3. Nerve injury
a. Brachial plexus injury (Erb palsy)
b. Facial nerve injury
Subaponeurotic haematoma
Or subgaleal haematoma is a result of birth trauma. The subaponeurotic space is a potential and expansible space between the
skull bone and the scalp, with vessels run through it. Bleeding inside it can be huge resulting in shock and high mortality (20%). It
is extremely uncommon after normal vaginal delivery, but occurs in 6/1000 vacuum extraction. The main clinical feature is a
boggy swelling of the scalp that crosses suture lines, with or without shock. It should be differentiated from other scalp swelling
such as caput succedaneum and cephalhaematoma. Early recognition is crucial in preventing complications and mortality.
Cerebral palsy
Definition
A non-progressive disorder of the brain resulting in impairment of motor function, usually of spastic rigidity type. Other types
includes dyskinetic, ataxic and mixed.
Pathology
Hypoxic ischemic injury of a developing brain, mainly of the white matter
Causes
Causes can be divided into prenatal, perinatal and postnatal. Birth asphyxia was being blamed as the major cause of cerebral palsy
until recent decades. Now it is clear that only 10% of the cases are related to intrapartum events or birth asphyxia. Majority is due
to complications of prematurity, of which the neonate are prone to intraventricular haemorrhage and hypoxic brain injury. Other
causes are chronic antepartum hypoxia, congenital brain malformations, and postpartum insults (20%) such as meningitis
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Jehovahs witness
The patient may refuse whole blood or any blood products including immunoglobulins. If refusal is expressed, counselling should
be given by an obstetric doctor as well as an obstetric anaesthetist for the patient to understand the consequence of refusal of blood
products including death. Patient should sign a standard refusal form (Form A) and her wish clearly documented in the notes.
In emergency situations such as when the patient is unconsious and requires blood products, if there is no doubt that she has
previously clearly expressed a refusal to receive blood transfusion, blood transfusion cannot be given. A standard form B should
be signed by the person providing the information and the next of kin.If doubt exists whether the patient has expressed refusal of
blood products, an FHKAM should be involved in the decision of blood transfusion. All details must be recorded in the notes.
Consanguinity
A relationship by descend from the same ancestor, or having a blood relationship. It is important for genetic counselling when
there is a positive family history of genetic disorder, and a couple has blood relationship.
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Foetal Medicine
0. Foetal medicine
What is foetal medicine?
1. A subspecialty in Obstetrics.
2. Deals with high risk pregnancy with foetal diseases and complications (see below).
3. Carry out prenatal diagnosis and counselling, and foetal therapy.
4. Multi-disciplinary care involving obstetricians, paediatricians, geneticists, and paediatric surgeons.
What are the foetal diseases and complications?

1. Congenital abnormalities such as:
a. Chromosomal abnormalities
b. Genetic disorders
c. Foetal infections
d. Multifactorial malformations
2. Growth disorders:-intrauterine growth retardation (IUGR)
3. Multiple pregnancy
What are the commonly used diagnostic tools

1. Ultrasonography (see USG (Obstetrics))
2. Chorionic villus sampling
3. Amniocentesis
4. Cordocentesis
What are the possible therapeutic tools?

1. Transplacental medication
2. Transumbilical medication and transfusion
3. Foetal surgery
4. Termination of pregnancy
Foetal diseases medical students should know

Please refer to the following individual topics:
1. Congenital abnormalities:-chromosomal abnormalities, genetic disorders, foetal infections, multifactorial malformations
2. Growth disorders:-intrauterine growth retardation (IUGR)
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1. Chromosomal disorders
Chromosomal abnormalities
Introduction
1. Affect 7% of all conceptions, and 6 per 1000 livebirths
2. 95% of gametes with chromosomal abnormalities are not viable
3. 60% of all first trimester spontaneous abortions, 5% of all second trimester abortions, and 5% of stillbirths
4. Most are trisomies
Types of chromosomal abnormalities

1. Numerical aberrations
a. Aneuploidy
i. The number of chromosomes is not the multiple of the haploid; it can be trisomy (47) or monosomy (45)
ii. Autosomal chromosomes involved:-trisomy 21 (Down syndrome); trisomy 18 (Edward syndrome), trisomy 13 (Patau
syndrome)
iii. Sex chromosomes involved:-XO (Turner syndrome), XXY, XXX, XYY
b. Polyploidy The number of chromosomes is an exact multiple of the haploid, but greater than the diploid number (2n),
e.g. Triploidy (3n, 69XXY), or tetraploidy (4n)
2. Structural aberrations
a. Rearrangement of chromosomal structure due to chromosome breakage and inappropriate rejoining of the broken ends.
i. Translocation
ii. Deletion
iii. Duplication
iv. Inversion
v. Isochromosome
- Genetic material may be lost (unbalanced) or maintained (balanced) after a rearrangement
- Balanced rearrangements:- Individuals with balanced rearrangement are phenotypically normal. However, they
have an increased risk of producing unbalanced gametes, leading to reproductive loss or abnormal children
3. Other aberrations
a. Mosaic an individual with two or more cell lines derived from a single zygotes
b. Chimaera two cell lines are derived from two separate zygotes
What should medical students know?

Down syndrome, Turner syndrome, translocation
Translocation
1. Translocations of fragments between chromosomes can be:
a. Reciprocal
b. Robertsonian
c. Insertional
2. Balanced translocation:
a. Exist when the gemone contains the correct amount of genetic matter
b. Usually have no outward manifestation
c. Parental karyotyping is essential
d. If one parent has a balanced translocation, the theoretical outlook for any offspring is 1:-4 having the same balanced
translocation; 1:4 having a normal karyotype; and 1:2 having an unbalanced translocation. However, the actual risk of
having unbalanced translocation is 1:10 as most of them will abort.
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Biochemical screening
What is biochemical screening?
Biochemical screening is a screening test for Down syndrome performed at around 16 to 20 weeks of gestation. It consists of
measurement of maternal plasma level of several markers, including alpha-feto protein (AFP), human chorionic gonadotropin
(HCG) and unconjugated estriol (uE3). It is also called triple test when all three markers are tested, or dual test when only AFP
and HCG are assessed. In public hospitals of Hong Kong, dual tests are offered to pregnant women at or above 35 years old for
cost-effectiveness.
Test aFP hCG uE3 Inhibin-A PAPP-A NT Remarks
Double Test Y Y Early second trimester
Triple Test Y Y Y
Quadruple Test Y Y Y Y
Combined Test Y Y Y Late first trimester; Maternal age.
Integrated Test Y Y Y Y Y Y
Serum Y Y Y Y Y Y A variant of integrated test using
Integrated Test serum markers only
Aim of biochemical screening

The aim is to screen women for increased risk of having a Down fetus. The test itself is not diagnostic, but it selects the high risk
cases for diagnostic amniocentesis which is an invasive procedure. Compared with screening by age alone, biochemical screening
has a higher detection rate and a lower false positive rate so that the number of subjects requiring amniocentesis is reduced.
Mechanism of biochemical screening

Compared with normal pregnancies, women with pregnancy complicated with Down syndrome have lower plasma levels of AFP
and uE3, and a higher level of HCG. (Note that in different chromosomal disorders the biochemical markers may rise or fall)
Although the differences are not very distinctive (otherwise these biochemical tests would be diagnostic), they can be used to
estimate the chance of having a Down fetus. Given the same false-positive rate, by incorporating more markers, the detection rate
can be increased at the expense of higher cost.
OSCAR
In CUHK, One-Stop-Clinic for Assessment of Risk is carried out at 11-13 weeks if the pregnant woman requested. It is a
combined test for detection of Downs syndrome and other chromosomal abnormalities. If high risk is found, women are offered
prenatal diagnosis.
Alpha-feto protein
What is alpha-feto protein (AFP)?
It is an alpha-globulin which is similar in molecular weight to albumin. It is normally synthesized during pregnancy in the yolk
sac and foetal liver. Maternal serum AFP levels rise rapidly in pregnancy as a result of the passage of foetal AFP into maternal
circulation via the placenta. AFP is present in foetal serum and cerebrospinal fluid at a concentration of about 30000 times greater
than that in maternal serum and 150 times greater than that in amniotic fluid It is also increased in non-pregnant patients with liver
diseases such as primary hepatocellular carcinoma, and malignant yolk sac tumour of ovary.
Alpha-feto protein in obstetrics

- Maternal serum AFP is increased in several foetal malformations including open neural tube defects, gastroschisis and
ophalmocele. It is used in some Caucasian countries as a screening test of neural tube defects.
- Maternal serum AFP is decreased in pregnancy with Down syndrome. It is used in combination with human chorionic
gonadotropin or unconjugated estriol as a biochemical screening test for Down syndrome.
- Increased maternal serum AFP is also reported to be associated with poor foetal outcome such as IUGR.
Alpha-feto protein in gynaecology

Serum AFP is secreted from ovarian tumours like yolk sac tumours, and other germ cell tumours. It is a very sensitive and specific
tumour marker for yolk sac tumours, and can be used for diagnosis, monitoring and detection of recurrence.
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Human chorionic gonadotropin
What is human chorionic gonadotropin?
1. Human chorionic gonadotropin (HCG) is a placental-derived glycoprotein, and is almost exclusively produced by the
placenta, with extremely small quantities are produced by the pituitary gland. Similar to other pituitary glycoprotein
hormones, it is composed of two subunits, alpha and beta. While the structure of alpha subunit is the same as the other
glycoproteins, HCG has a specific structure of the beta subunit. Some radioimmunoassays for the measurement of the level of
HCG are based on the detection of the beta subunit.
2. The natural role of HCG is to maintain the corpus luteum for the first seven weeks of gestation, which secretes progesterone
essential for the continuation of the pregnancy.
3. The half-life of HCG ranges from 6 to 24 hours. Serum HCG is measurable as early as 7 days post-ovulation (detection limit
around 0.1-0.3iu/L). During the first few weeks of pregnancy, the maternal serum level of HCG doubles every 2 days, and
rises to peak at 9 to 11 weeks. Subnormal rise or even a drop in the HCG level may suggest ectopic pregnancy or abortion
respectively.
Clinical use of HCG

1. In pregnancy testing
2. In assisting diagnosis of ectopic pregnancy and abortion
3. As a tumour marker of gestational trophoblastic diseases and ovarian choriocarcinoma
4. In ovulation induction program:-
a. To simulate LH surge; and
b. As luteal phase support
5. Association with hyperemesis gravidarum and transient hyperthyroidism during early pregnancy
Nuchal translucency
It is the subcutaneous edema over the back of the foetal neck. Normally it is less than 3mm in the first trimester. It is associated
with chromosomal abnormalities when the nuchal translucency is abnormally high. It has been suggested as a screening test for
Down syndrome. The sensitivity is around 60%, and 5% of population would be screened positive. Its screening power is
therefore similar to that of biochemical screening, but it allows an earlier screening in the first trimester. The limitation of the test
is the technical difficulty in measuring the parameter and therefore a poor reproducibility. Because of that, it is still not a standard
screening test in Hong Kong. A first trimester USG would show an abnormally increased nuchal translucency.
Trisomy
This is a condition of having three copies of a given chromosome in each somatic cell rather than the normal number of two. In
majority of cases, it is resulted from non-disjunction during meiosis. The most common type is trisomy 21(Down syndrome),
trisomy X, trisomy 18 (Edward syndrome) and trisomy 13 (Patau syndrome).
Non-dysjunction
A mistake during meiosis which causes some resulting haploid cells to have only 22 chromosomes and others 24 chromosomes,
instead of the normal 23. If a gamete with 22 chromosomes fuses with one with the normal 23, a zygote with 45 chromosomes
results (monosomy). If a gamete with 24 chromosomes fuses with one with the 23, a zygote with 47 chromosomes results
(trisomy). Non-dysjunction occurs more commonly during ooytes development in women of advanced maternal age.
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Down syndrome
Definition
- Trisomy 21
- Presence of extra chromosome 21 or its material
Incidence
- 1 in 850 of all livebirths
- The most common type of chromosomal abnormalities
- Incidence rises markly with maternal age, with 1 in 1000 at 30 years old, to 1 in 300 at 35 and 1 in 100 at 40
Aetiology
Extra chromosome is resulted from:
1. Non-dysjunction
a. Accounts for 95% of all down syndrome
b. Arises in the stage of meiosis of the ovum before fertilisation
c. Karyotype:-47XX, + 21 or 47XY, + 21
2. Unbalanced translocation
b. One of the parental karyotypes consists of a translocation with the long arm of a Chromosome 21 to the other
Chromosome (e.g. Chr 14)
c. The translocated segment is then inherited to the offspring so that the offspring would have a long arm of Chr 21 in
addition to one pair of Chr 21 (unbalanced)
d. Karyotype:-46, XX, der (14;21) or 46, XY, der (14;21)
3. Mosaicism
b. Results from mitotic non-disjunction during the early stage of embryogenesis. These patients have cells with a normal
Chromosome number and some that are aneuploid.
c. Karyotype:-46, XX / 47, XX, +21 or 46, XY / 47, XY, +21
d. Mosaic patients may exhibit variable or milder symptoms, depending on the proportion of abnormal cells.
Clinical features of Down syndrome

1. Mental retardation
a. Mean IQ is 40% of normal population
b. Only 20% has no or mild mental retardation
2. Malformation
a. Congenital heart defects (40%)
b. Malformations of the gastrointestinal tract, e.g. Duodenal atresia (10%)
c. Head and face:-Brachycephaly / microcephaly; epicanthic folds and flat facial profile;
d. Limbs:-Simian crease; gap between first and second toe
3. Other complications
a. Alzheimer's disease
b. Subfertility
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Prenatal screening
1. Maternal age Using cut-off of 35 years old at time of EDC
a. 18% of pregnant women will be screened positive
b. Only sensitive for 20% of down syndrome, as majority of down (80%) are come from mothers below 35 years old
c. Safe and inexpensive screening tool
2. Biochemical screening
a. Using serum AFP, HCG with or without unconjugated estriol
b. 5% of pregnant women are screened positive
c. Sensitivity of 60%, i.e. Pick up more down than screened by maternal age alone, and less false positive so that few
pregnant women require an invasive diagnostic procedure
d. Disadvantage is that it can only be done in 2nd trimester
3. Nuchal translucency in 1st trimester using cut-off of 3mm
a. 5% of pregnant women are screened positive
b. Sensitivity varies from 33% to 60%
c. Potential benefit of early screening followed by CVS
d. Problem of reproducibility, and further studies required to define its clinical usefulness
4. Screening by USG of Down features in 2nd trimester
a. Shortened femur length, shortened humeral length, thickened nuchal skinfold, short ear length, foetal pyelectasis, choroid
plexus cyst, duodenal atresia, congenital heart defects, abnormalities of the fifth digit, trisomy hands
b. Sensitivity 33% only
Prenatal diagnosis
1. Foetal karyotyping by chorionic villus sampling
2. Foetal karyotyping by amniocentesis
Management of pregnancy with Down syndrome

1. Counselling and support:- Discuss the prognosis and long term complications of Down syndrome, social and health support
available for Down children in the society
2. Options of continuing pregnancy and termination of pregnancy:
a. Termination of pregnancy is legal when before 24 week of gestation
b. Medical and surgical procedures of termination, and their complications.
You are seeing a patient of age 38 at 8 week of gestation of her first pregnancy in the clinic. She was anxious about Down
syndrome. How would you counsel the patient, and which investigation would you suggest?
Edward syndrome
- Trisomy 18
- Multiple foetal abnormalities.
- One of the lethal chromosomal abnormality
- Related to advanced maternal age
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Patau syndrome
Definition
1. Trisomy 13, or presence of extra chromosome 13 or its material
2. Karyotypes
a. Trisomy 13 type:-47, XX, +13
b. Translocation type:-46, XX, t13
c. Mosaic type:-46, XX / 47, XX, +13
Incidence
1 in 15,000 births
Clinical features
- Mental retardation
- Cardiac defects (80%)
- Renal defects (30%)
- Holoprosencephaly, failure of the prosencephalon (the forebrain of the embryo) to develop
- Cleft lip and palate
- Eye defects such as microphthalmia, anophthalmia and coloboma
- Polydactyly
- Umbilical hernia
Prognosis
It is a lethal chromosomal abnormality, second trimester abortion, stillbirth or early death after birth.
Klinefelter syndrome
Definition
A chromosomal disorder of a male with an extra X chromosome (47 XXY), usually resulted from nondisjunction during meiosis.
Incidence
1 in 1000 males
Pathology
1. The most common karyotype is 47 XXY; about 15% of cases show mosaicism
2. Male hypogonadism develops as there are two X chromosomes
Clinical features
- Taller and thinner than average
- Eunuchoid features, female fat distribution
- Reduced facial and body hair
- Gynaecomastia
- Testicular atrophy
- Sterility due to impaired or absent spermatogenesis
- Mild degree of mental retardation (severity is correlated with the number of extra X chromosomes), some may have normal
intelligence
- Mosaics show milder symptoms
Investigation
1. High FSH and LH levels
2. Low testosterone
3. Semen analysis shows azoospermia
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Turner syndrome
Definition
Monosomy X with karyotyping 45XO
Incidence
1/3000 female births
Aetiology
- Non-disjunction in approximately 55% of cases
- The remaining 45% of patients are either mosaics (30%) or have structural abnormalities of the X chromosome (15%)
- The karyotypic heterogeneity is responsible for significant variations in the phenotype.
Clinical features
- Short stature
- Normal intelligence
- Webbed neck
- Low posterior hairline
- Broad chest and widely spaced nipples
- Aortic coarctation
- Diffuse pigmented nevi
- Cubitus valgus
- Peripheral lymphoedema at birth
- Renal anomalies such as horseshoe kidney
- Primary amenorrhea, streak ovaries, infertility, low oestrogens with elevated gonadotropin
- Poor secondary sexual characteristics
- Mosaics can present with oligomenorrhea and some secondary sex characteristics
Prenatal screening
- Unlike Down syndrome, there is no screening program for turner syndrome.
- Turner syndrome should be suspected if routine scan shows presence of cystic hygroma or other characteristic abnormalities
Prenatal diagnosis
1. USG would show characteristic features:
a. Cystic hygroma
b. Renal anomalies
2. Karyotyping with chorionic villus sampling or amniocentesis
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2. Congenital abnormalities
Neural tube defect
What is a neural tube defect (NTD)?
It is a group of congenital malformations of the brain, spinal cord, skull bones and spine that occur during the development of the
neural tube. It includes anencephaly, encephalocele, spina bifida with or without meningocele. It is called a closed NTD when the
lesion is completely covered by skin or thick opaque membrane. Otherwise, it is called opened NTD. Anencephaly is invariably
an open lesion.
Causes of neural tube defect

Multifactorial. It is associated with folate deficiency.
Incidence of neural tube defect

The incidence is about 4 per 1000 birth in Caucasian countries and is higher than in Asian. It is approximately equal for
anencephaly and spina bifida (without anencephaly). Encephalocele is rare, accounting for 5% of all NTDs.
Prognosis of NTDs
1. Anencephaly is not compatible with life.
2. Open spina bifida has a poor survival (5-year:-33%) and tends to be handicapped (90%).
3. Closed spina bifida has a 5-year survival rate of 60%, and 2-third are handicapped.
Screening and diagnosis

1. Maternal serum alpha-feto protein screening (MSAFP) at 16 to 18 weeks. MSAFP is higher in pregnancies with an open NTD.
Pregnancies screened positive should be followed with a morphology scan. However, closed NTDs are likely to be missed.
2. Screening with USG. Nowadays with improved quality in USG imaging, NTD can be screened more accurately with a
morphology scan at around 18 to 20 weeks. Foetal malformations other than NTD can also be examined. However, small
closed NTD can still be missed with USG.
Prenatal management of NTDs

Patients should be counselled the prognosis of the defect, and discussed with different management options including termination
of pregnancy.
Prevention of NTDs
Folic supplement is advised to high risk group. It should be taken at least 8 weeks before pregnancy, and continued till first
trimester. It has been showed to decrease the incidence of NTD by 2-third.
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Gastroschisis
It is a kind of multifactorial congenital abnormalities with an incidence of 1 in 3000 birth. Unlike omphalocele, it is rarely related
to chromosomal abnormalities, and is usually isolated, although cardiac and other structural abnormalities co-exist in 20% of
cases. It is a total anterior abdominal wall defect (often on the right side) resulting in protrusion of abdominal viscera (usually
small bowel) into the amniotic cavity. Unlike omphalocele, the abdominal viscera is not covered by the peritoneum, and is
therefore prone to chemical irritation from amniotic fluid (which usually occurs after 30 weeks of gestation, said to be related to
changes of chemical constituents from that time onwards). This leads to bowel inflammation, ischemia, and dilatation which make
postnatal repair difficult. Besides the risk of bowel injury, there is also increased risk of intrauterine growth retardation,
intrauterine death, intrapartum foetal distress. Management should include close antepartum surveillance and elective caesarean
delivery. The recurrence risk is less than 1%.
Omphalocele
Also called exomphalos, is the extra-embryonic herniation of abdominal viscera due to failure of the gut to return to the
abdominal cavity at 8 weeks of gestation (physiological hernia), resulting in a defect of the abdominal wall. The peritoneal sac is
intact. The incidence is 1 in 5000 delivery, and 30% cases have chromosomal abnormalities, and another 20% have co-existing
malformations (usually involving the heart and kidneys).
Presentation
The defect is detectable with USG after 12 week of gestation by when physiological herniation should have been reduced.
Multiple malformations, growth retardation and polyhydramnios are common associated features. An elevation of maternal serum
alpha-feto protein may be found on biochemical screening.
Management
1. Prenatal
a. Differentiate between omphalocele and gastroschisis:
i. Presence of peritoneal sac in omphalocele
ii. Midline defect in omphalocele but lateral defect in gastroschisis
iii. Herniation of liver occurs in 40% of omphalocele but is very rare in gastroschisis
b. Rule out chromosomal abnormalities and other anomalies which are crucial prognostic factors
c. Counseling
i. Prognosis is good for neonates with surgery, without chromosomal and other structural abnormalities
ii. Survival is well in excess of 75-80%
2. Delivery Can allow vaginal delivery when it is cephalic presenting
3. Postnatal
a. Prevent heat and fluid loss and infection before surgical repair
b. Surgical repair when foetal condition is stable
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Hydrops foetalis
Hydrops foetalis is defined as a foetus with generalised edema plus collection of fluid in at least one of the body cavities (ascites,
hydrothorax, or pericardial effusion). Traditionally in the western countries, it is classified into immune and non-immune hydrops.
The former is due to rhesus isoimmunisation which is more common in the Caucasian population. Actually, the causes of hydrops
are very diverse, including foetal anaemia, primary cardiac abnormalities, extra-cardiac structural abnormalities, and
chromosomal abnormalities. The common end-point is foetal heart failure. The prognosis depends on the underlying cause. Even
the foetus is born, the cardiomegaly will cause pulmonary hypoplasia and the neonate dies soon after birth.
Causes of Hydrops foetalis

1. Foetal anaemia due to:-
a. Alpha-thalassemia (Haemoglobin Bart disease)
i. The most common cause of hydrops in our locality.
ii. A lethal condition in which termination of pregnancy should be considered.
b. Rhesus isoimmunisation Can be treated with repeated intrauterine transfusion or early delivery of the foetus. The
prognosis is much better nowadays.
c. Parvovirus infection The prognosis is good with repeated intrauterine transfusion until the anaemia resolved in a few
weeks time.
2. Chorioangioma
a. A rare placental tumour causing high-output heart failure due to foetal haemolysis and arterio-venous shunting
b. The prognosis is variable, depends on the size of the tumour
c. Other vascular malformation includes vascular teratoma and intracranial arterio-venous malformation.
3. Primary cardiac abnormalities
a. Arrhythmia
i. Heart block, supraventricular tachycardia
ii. Can be treated with transplacental anti-arrhythmic agents
b. Major structural abnormalities of heart
4. Extra-cardiac abnormalities
Some structural abnormalities may compress on the foetal heart or obstruct its outflow resulting poor cardiac function,
like chylothorax, diaphragmatic hernia, primary pleural effusion and Congenital cystic adenomatoid malformation of the
lung (CCAML).
Diagnosis
1. Early sign is cardiomegaly by USG at week 16. If it is normal, the chance of hydrop fetalis will be low.
2. Concommitent features e.g. MCA peak systolic flow and placenta size.
Complication
1. Severe pre-eclampsia due to formation of a large placenta.
2. Birth injury due to big baby.
3. Early diagnosis is important for sake of the mother as this condition is untreatable.
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Renal agenesis
Definition
Bilateral absence of the kidneys, usually associated with the oligohydramnios sequence.
Synonyms
Potter syndrome (no longer used).
Incidence
1-2:10,000
Etiology
Usually sporadic occurrence but 20-36% of bilateral renal agenesis (BRA) present a familial recurrence (possibly autosomal
dominant with incomplete penetrance and variable expression).
Pathogenesis
Results from a lack of induction of the metanephric blastema by the ureteral bud. The absence of kidney results in the absence of
amniotic fluid after 12-13 weeks (before fluid is an exsudate or an extension of the intercellular fluid of the foetus). The
oligohydramnios causes the pulmonary hypoplasia. In rare cases of monozygotic twin discordant for the renal agenesis, the
pulmonary hypoplasia does not occur.
Diagnosis
The diagnosis is first suggested by the absence of amniotic fluid then by the absence of the bladder and the lack of kidneys.
Colour Doppler has been found useful in those difficult exams to identify the lack of renal arteries. Before a final diagnosis is
made one should think and if possible exclude the possibility of pelvic or ectopic kidneys that could compress the bladder and
exclude the possibility of ectopic ureter that could explain the absence of bladder.
Genetic anomalies
Unknown.
Differential diagnosis
Bilateral renal medullary cystic dysplasia and bilateral renal hypoplasia may appear as BRA. Further normal but non-functioning
kidneys anormal placental implantation (on a uterine septum for instance) can lead to the same presentation of severe
oligohydramnios. This information is important to convey during patient's counseling:-The concern is not only the renal agenesis
(which may be absent) but the oligohydramnios that will lead to pulmonary hypoplasia.
Associated anomalies
Since this is a common anomaly, many different associations have been described (Vacterl, Meckel, chromosome 22
malformations#). In practice most of these are difficult to identify by ultrasound because of the oligohydramnios.
Prognosis
Lethal.
Management
Many authors have suggested the use of amnioinfusion or even intraabdominal infusion of saline in order to better visualize the
anatomy. Although there might be indications for such aggressive approach in a non-viable foetuses, these are quite uncommon,
and not justified in the majority of cases. Termination of pregnancy can be offered before viability. Standard prenatal care is not
altered when continuation the pregnancy is opted for. Confirmation of diagnosis after birth is important for genetic counseling.
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Potter syndrome
Several entities use the eponym Potter:
1. Potter syndrome, now renamed either oligohydramnios sequence or bilateral renal agenesis (BRA) depending on whether the
cause of the syndrome (BRA) or the mechanism is referred to.
2. Potter syndrome Type I is now referred to as Autosomal recessive polycystic kidney disease
3. Potter syndrome Type II is now referred to as Renal dysplasia
4. Potter syndrome Type III is now referred to as Autosomal dominant polycystic kidney disease
Teratogen
Definition
It is an agent extrinsic to the embryo or foetus that causes an increased risk of the following:
- Malformation-physical malformation
- Carcinogenesis- increased risk of cancer
- Mutagenesis-increased risk of genetic disease
- Altered function (e.g. Mental retardation)
- Growth deficiency (intrauterine growth retardation)
- Pregnancy wastage (i.e. Abortion or stillbirth)
- Teratogens may produce no effect at all in exposed pregnancies; only the most potent human teratogens typically affect 20 to
70% of exposed foetuses
Classes of teratogenic agents

1. Microbiological
a. Virus:-rubella
b. Bacteria:-syphilis
c. Parasites:-toxoplasmosis
2. Chemical drugs, smoking, alcohol
3. Physical Irradiation
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3. Genetic disorders
Genetic disorder
Introduction
There are more than 1000 known Mendelian disorders, which may be either dominant or recessive and may involve either
autosomal or sex chromosomes
Autosomal disorders
Both sex are equally affected
1. Dominant
a. Expression may be variable from one individual to another (expressivity).
b. Affected individual will produce offspring who are either normal or affected, in a 1:1 ratio
c. Affected individual either has an affected parent or represents a new mutation
d. Obstetric presentation-these disorders confront the obstetrician in several ways:
i. Affected parent:-50% risk
ii. Previously affected child born to unaffected parents means that the child represents a new mutation:-no increase in
recurrent risk
e. Examples:-Achondroplasia, Osteogenesis Imperfecta (type I, II, IV,V), Marfan syndrome, Neurofibromatosis (Type I),
Huntingtons disease, Polycystic Kidneys
2. Recessive
a. Both parents of affected infant must be carriers
b. Offspring of carrier parents will be normal, carriers, or affected in 1:2:1 ratio
c. Siblings may be affected, but other affected relatives are uncommon unless there is consanguinity in the pedigree
d. Example:-thalassemia, sickle cell disease, cystic fibrosis.
X-linked disorders
No father-to-son transmission
1. Dominant
a. Males and females may both be affected
b. An affected male will have all normal sons and all daughters will be affected
c. Offspring of an affected female will be normal or affected, in a 1:1 ratio
d. Examples:-Vitamin D-resistant rickets
2. Recessive
a. Only males are affected (there is the possibility of a rare homozygous female)
b. An affected male will have all normal sons, and all his daughters will be carriers
c. Examples:-G6PD deficiency, Haemophilia, Duchenne's muscular dystrophy, Fragile X syndrome.
Haemophilia
Introduction
- A group of X-linked recessive hereditary disorder of blood coagulation
- Subdivided into Haemophilia A and Haemophilia B
Pathology
1. Haemophilia A
a. Caused by a reduced amount or activity of factor VIII
b. Two-thirds of the cases are inherited as a X-linked recessive condition, and the remaining cases are resulted from
spontaneous mutations and hence do not have a family history
c. The gene for factor VIII is located at Xq2.8
d. Genetic defects include deletions and point mutations (CGA to TGA)
2. Haemophilia B (Christmas diseae)
a. Low Factor IX
b. Inheritance and clinical features are same as Hemophilia A
c. The gene for factor IX is located at Xq2.6
d. Incidence is one-fifth that of Hemophilia A (1:10000 for Haemophilia A and 1:50000 for Haemophilia B)
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Carrier detection
1. Haemophilia A
a. By positive family history
b. Laboratory tests:
i. Factor VIII < 50%
ii. Factor VIIIc/VWF < 0.7
c. Genetic analysis:-gene tracking or identification of direct genetic lesions, e.g. RFLP
2. Haemophilia B
a. By positive family history
b. Genetic analysis:-RFLP
Prenatal diagnosis
1. Sex determination
a. Haemophilia is ruled out if foetus is a female
b. By ultrasound (USG) examination of foetal genitalia
c. Foetal sex may not be identified by USG until in second trimester
2. Genetic study
a. Foetal cells are obtained by chorionic villous sampling (CVS) in first trimester or amniocentesis in second trimester
b. Gene tracking by RFLP or VNTR with extended family members
c. Direct probing for known genetic lesions by PCR, SB techniques, etc. (mutations or deletions)
3. Clotting factor assay More than 18 weeks' gestation, foetal blood can be obtained by cordocentesis can for factor VIII assay.
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4. Foetal Haemolytic Diseases
Thalassemia
Definition
In Greek thal means sea; assemia is an abbreviated term for anaemia. It is a heterogeneous group of genetic disorders of the
synthesis of haemoglobin chains, resulting in imbalance of number of different globin chains. The result is (1) impaired formation
of normal Hb A (which is a tetramer of 2 alpha and 2 beta globin chains), and (2) formation of abnormal tetramers. There are two
major forms:-Alpha-thalassemia and Beta-thalassemia.
Incidence
- Alpha-thalassemia occurs largely in South East Asia; 5% of Hong Kong people are carriers.
- Beta-thalassemia occurs worldwide, particularly in the Mediterranean and the Middle East; 3% of Hong Kong people are
carriers
Pathophysiology
1. Alpha-thalassemia
a. A normal human has 2 pairs of alpha genes. Alpha-thalaessemia is mainly due to gene deletions (a minority is due to
mutation).
b. Alpha haemoglobin gene defects lead to impaired synthesis of the alpha globin chains, with a relative excess of beta and
gamma chains, which form insoluble tetramers, Hb Bart's (gamma 4) and HbH (beta 4) within red cells. The insoluble
tetramers reduce cell plasticity. Consequently, the red cells are more susceptible to premature destruction, leading to
ineffective erythropoiesis and haemolysis.
c. Depends on the number of gene deletion, four degrees of alpha-thalassemia are possible.
Number of gene deletion genotype features

1 +-thalassaemia Asymptomatic with low or near normal MCV
2 0-thalassaemia Asymptomatic with low MCV
-SEA
-thalassaemia
3 Hb H (4) Anaemiabut viable, low MCV
4 Hb Bart's (4) Hydrops foetalis, non-viable
d. Depends on the pattern and number of gene deletion of parents, the newborn has a chance of acquiring major
(homozygous) alpha-thalassemia ranging from zero to 25%.
e. In Hong Kong, the -SEA carrier rate is 4.5%. The chance of getting Hb Barts is 25% for an - couple.
2. Beta-thalassemia
a. 3.4% are carriers in Hong Kong.
b. A normal human has 1 pairs of beta genes. Beta-thalaessemia is due to gene mutation, which results in absence (0) or
reduced beta globin chain synthesis (+), with a relative excess of alpha chains. The end result is haemolysis similar to
that in alpha-thalassemia.
c. Heterozygous carriers are asymptomatic with low MCV and increased HBA2, while homozygous patients suffer from
anaemia requiring regular blood transfusions.
d. If both parents are carriers of beta-thalassemia, the newborn has a 1 in 4 chance of acquiring major (homozygous)
beta-thalassemia.
e. As foetal haemoglobin synthesis does not require beta component, the disease does not reveal until about 6th month of
neonatal life when haemoglobin synthesis switches from gamma chain to beta chain
Parental screening and diagnosis

1. Both alpha and beta thalassemia carriers are screened by MCV (<80). Iron deficiency has to be ruled out in this case first.
2. Husbands CBP and Hb have to be checked.
3. Diagnosis is made by haemoglobin electrophoresis (haemoglobin pattern analysis)
a. Low MCV, with or without HBH inclusion
b. Low MCV, with increased HbF and HBA2
4. Genetic study is required to identify the pattern of -gene deletion, and type of mutation of -gene
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Prenatal diagnosis
1. Alpha-thalassemia
Hb Bart's disease can be diagnosed by following ways:-
a. Ultrasound
i. Look for signs of hydrops foetalis including thickened placenta, cardiomegaly, hydrothorax, ascites and skin edema
ii. The advantages are non-invasive and sensitive
iii. Disadvantage is that the onset of hydrops varies and may not be diagnosed until in second trimester
b. Genetic study
i. Look for presence of alpha gene in foetal cells
ii. Foetal cells are obtained by chorionic villus sampling (CVS) or amniocentesis
iii. The advantages are accurate and early diagnosis is possible with CVS
iv. The disadvantage is invasive and risk of foetal loss
c. Haemoglobin study
i. Look for foetal anaemia and haemoglobin pattern in foetal red blood cells
ii. Foetal red blood cells are obtained by cordocentesis
iii. Advantages are that the diagnosis is accurate and quick
iv. Disadvantages are that cordocentesis is invasive and difficult to perform before 16 weeks
v. It is usually reserved for confirmation of diagnosis when hydrops foetalis has already been present, in which case
quick result is required to guide the subsequent management
2. Beta-thalassemia` As beta-thalassemia is not revealed during foetal life, the only method of diagnosis is by genetic study
3. In conclusion,
a. - couple CVS, amniocentesis and serial USG
b. - couple DNA studies of couple DNA
c. - couple Study partner for mutation as 7% of them may have trait. Manage as - couple if present.
Other Antepartum Management

Women who are carriers of thalassemia should be given folate 5mg once daily and obimin 1 Tab once daily as the demand of the
vitamin is increased during pregnancy. Consider transfusion if Hb < 8g/dL.
If on haemoglobin pattern analysis, one of the couple is found to be an alpha-thalassemia carrier while the other is a beta carrier,
what would be the prenatal counselling and diagnosis?
Rhesus
Rhesus blood group system consists of C, D, E antigens. The genes coded for these antigens are inherited as autosomal dominance,
i.e. the phenotype of DD and Dd is D positive, while dd is D negative. Among thee three rhesus antigens, rhesus D
iso-immunisation is the most common and also most severe type. 99% of Hong Kong Chinese are Rhesus D positive while 85%
Caucasian are D positive.
Rhesus D iso-immunisation
Introduction
Rhesus D iso-immunisation was a common foetal haemolytic disease in the Caucasian population resulting in high foetal morbidy
and mortality. It has now been under control with effective prophylactic therapy.
Pathogenesis
When the mother is rhesus D negative but the foetus is rhesus D positive, the mother may be sensitized when the foetal red cells
enter the maternal circulation. This can occur during labour, abortion, antepartum haemorrhage, or some obstetric procedures such
as chorionic villus sampling. The sensitized mother will then develop IgM against the rhesus antigen. Subsequent sensitisation
will trigger the synthesis of IgG. While the IgM molecules are too big to cross the placenta, IgG can do so, and attack the foetal
red cells, resulting in foetal haemolytic anaemia. In severe case, hydrops foetalis develops.
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Screening and prevention
Every pregnant woman should have the rhesus blood group checked. If the woman is rhesus D negative, rhesus antibody should
then be checked to see if iso-immunisation had been occurred. Prevention of iso-immunisation is now effectively achieved by
giving rhesus antibodies after delivery or any sensitizing events. The incidence has been reduced to 0.3%. With routine
antepartum prophylaxis (at 26 and 34 weeks of gestation), the incidence decreases further to 0.06%. However, this preventive
measure is useless when iso-immunisation has already been occurred.
Diagnosis of foetal haemolytic disease

Once the mother has been sensitized, there is risk of hydrops foetalis. The foetal should be monitored with USG for any early
signs of hydrops such as cardiomegaly. Skin oedema, ascites, and pleural effusion are late signs. The alternative method to
monitor severity of foetal anaemia is by regular amniocentesis. The bilirubin level in the amniotic fluid reflects the severity of
haemolysis.
Management of foetal haemolytic disease

When there is evidence of hydrops or significant increase in amniotic bilirubin level, severe haemolytic anaemia is likely.
Delivery should be considered when the foetus has reached 34 weeks of maturity. Otherwise, the foetus should be treated with
intrauterine blood transfusion and glucocorticord therapy to enhance lung maturity.
Protocol, as of 31 October2002
1. Indications:- non-sensitised Rhesus D negative mothers.
2. Give anti-D immunoglobulin prophylaxis in the following situations:
a. Routinely at 28 weeks and 34 weeks of gestation
b. After delivery
c. After any potential sensitizing events:
i. Termination of pregnancy at any gestation by either surgical and medical method
ii. Ectopic pregnancy at any gestation
iii. Spontaneous abortion after 12 weeks of gestation
iv. Threatened abortion after 12 week sof gestation
v. Antepartum haemorrhage
vi. Invasive prenatal procedures eg:-amniocentesis, chorionic villi sampling, cordocentesis
vii. External cephalic version
viii. Closed abdominal injury
ix. Intrauterine death
3. Regimen
a. 250ug (1250IU) IMI
b. Should be given as soon as possible after the event and always within 72 hours. Beyond that, anti-D Ig should still be
given within 10 days of the event
c. No need for routine Kleihauer test after a sensitizing event
d. No need to repeat anti-D Ig injection if it has been given within prior 4 weeks for another sensitizing event.
4. Checking of anti-D Ig in Rhesus negative mother

a. Check once at first visit, then
b. Recheck just before giving antepartum anti-D prophylaxis at 28 weeks, or before any events required anti-D
prophylaxis (except when the test has been done in the prior 4 weeks).
c. Once anti-D prophylaxis is given, no need to check the anti-D Ig titre as the result will not be accurate
Can you explain why rhesus D iso-immunisation is more commonly affect the subsequent pregnancies than the first one?
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5. Foetal diagnosis and therapy
Amniocentesis
Definition
It is a common procedure which a needle is inserted transabdominally into the amniotic sac to obtain amniotic fluid for prenatal
diagnosis. Amniocytes (desquamated foetal cells in amniotic fluid) obtained are cultured for foetal karyotyping.
What are the indications of amniocentesis?

- Foetal karyotyping (the most common)
- Foetal gene studies in thalassemia, and some other genetic disorders
- Assessment of amniotic fluid bilirubin level as an indicator of severity of foetal haemolytic anaemia secondary to rhesus
isoimmunisation
- Assessment of lung maturity by lecithin:springomyelin ratio (rarely necessary nowadays)
How is amniocentesis performed?

1. Timing:-usually performed around 15 to 20 weeks of gestation (for foetal karyotyping)
2. Under ultrasound guidance
3. 20ml of amniotic fluid is aspirated
4. Anaesthesia or analgesia is rarely required, foetal trauma is rare.
Advantages:
1. Accurate and sensitive
2. Has lower complication rate when compared with CVS
3. Reflects true karyotype of the foetus
Disadvantages:
1. Performed in second trimester
2. Creates anxiety as minor chromosomal abnormalities are also picked up
Risk of amniocentesis
Foetal loss rate of 1% excess over background loss rate
What would be the practical difficulties in performing amniocentesis for foetal karyotyping in twin pregnancy?
Chorionic villus sampling (CVS)

What is chorionic villus sampling?
It is an invasive procedure by which chorionic villi are obtained through needle insertion transabdominally (or less commonly
transcervically). The procedure is performed between 10 and 13 week of gestation. Chorionic villi are excellent source of DNA
that may allow sufficient amount for most molecular genetic studies without prior culture. Time for result to become available is
shorter than with amniocentesis. However, mosaicism occurs more commonly in chorionic villi (1%). The mosaicism is usually
confined to chorionic villi and does not affect the foetus.
Indications
1. Foetal karyotyping CVS allows earlier diagnosis of chromosomal abnormalities when comparing with amniocentesis. It is
advisable to high risk group such as increased foetal nuchal translucency detected in the first trimester.
2. Genetic studies The commonest genetic indication in Hong Kong is diagnosis of thalassemia. In particular, beta-thalassemia
can only be diagnosed with genetic studies in antenatal period.
Complicaions
1. 1% risk of foetal loss which is slightly higher when compared with amniocentesis
2. Previous report of association with foetal limb reduction is not confirmed with recent studies.
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Advantages
1. Accurate and sensitive
2. Can be done in the first trimester (10 to 13 weeks) so that intervention such as termination of pregnancy for abnormal cases
can be performed earlier during when the operative risk is lower
3. Results can be obtained in shorter time.
Disadvantages
1. Foetal loss rate is slightly higher when compared to amniocentesis
2. Rate of mosaicism is slightly higher among trophoblastic cells, and the karyotype of trophoblasts may not reflect the actual
karyotype of the foetus
Cordocentesis
What is cordocentesis?
It is an invasive procedure in which the umbilical cord is punctured in utero. It is indicated when foetal blood sampling is required
for foetal diagnosis, or transfusion of blood and drugs are required for foetal therapy.
Indications
1. Diagnostic purpose:-
a. Foetal white cells for karyotyping
It is a much quicker method for foetal karyotyping than amniocentesis and chorionic villi sampling. A quick diagnosis is
particularly required in highly suspected cases, or if time to decide for termination of pregnancy is limited before 24
week of gestation.
b. Foetal haemoglobin and haemoglobin pattern To assess foetal anaemia, and confirm Haemoglobin Bart's disease
(alpha-thalassemia major)
c. Foetal blood for other genetic diagnosis
d. Assessment of foetal well-being To assess blood gas value (rarely done)
2. Therapeutic purpose:-
For blood transfusion, which is the most common therapeutic indication. Foetal anaemia resulted from Rhesus
iso-immunisation, parvovirus infection
Risk
It is associated with 2% foetal loss rate. It may cause foetal bleeding, tamponade of umbilical cord due to haematoma formation.
For all of the above procedures, Rhesus status must be known and anti-D prophylaxis is indicated if mother is Rhesus
negative while the foetus is Rhesus positive.
Genetic counselling
Definition
The process whereby patients or relatives at risk of a disorder that may be hereditary are advised of:-
1. The consequences of the disorder,
2. The probability of developing and transmitting it, and
3. The ways in which this may be prevented or ameliorated.
The risks of having a child with a genetic disorder or congenital malformations are estimated, and the parents are assisted in
making a decision regarding contraception, sterilization, adoption, artificial insemination, carrier detection, referrals to agencies
concerned with handicapped children, prenatal diagnosis and options regarding pregnancy termination.
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Ultrasound (Obstetrics)
Two ways to perform obstetric USG
1. Transabdominal (TAS)
2. Transvaginal (TVS)
Advantages of TVS over TAS

1. As TVS probe is closer to pelvic organs, requirement for penetration is lower, allowing higher frequency of ultrasound wave
to be used. The result is a better resolution of images
2. Full bladder is not required during TVS
Advantages of TAS over TVS

1. Because of the limited penetration of TVS, TVS may not be able to detect organs that are beyond the pelvis, such as
pregnancy beyond 1st trimester, and a large pelvic tumour which has been displaced up to the lower abdominal cavity
2. Some patients may feel discomfort towards vaginal examination
Three Targets in obstetric USG

1. Foetus
a. Viability:-see viable
b. Number of foetus
c. Identify multiple pregnancy and determine chorioamnionicity
d. Dating of pregnancySize and growth
e. Common foetal USG parameters are crown-rump length, biparietal diameter, femur length, and abdominal
circumference
f. Morphology
g. Well-being monitoring assessed by Doppler studies of foetal arterial blood flow, biophysical profile and amniotic
fluid volume
2. Placenta and amniotic fluid placenta praevia, placental tumour, amniotic fluid volume etc
3. Uterus and adnexa co-existing fibroids, uterine anomaly, ovarian tumour
Four uses of USG in obstetric

1. Screening such as:
a. Screening of Down syndrome with nuchal translucency during first trimester
b. Routine dating scan
c. Routine morphology scan
2. Diagnosis of abortion, ectopic pregnancy, multiple pregnancy, foetal malformations, placenta praevia etc.
3. Monitoring foetal growth, foetal well-being
4. Assisting other invasive procedures such as chorionic villi sampling, amniocentesis and cordocentesis
Role of USG in modern obstetrics

1. Definite Various diagnostic roles
2. Limited amniotic fluid volume assessment, estimation of foetal weight, diagnosis of IUGR, 1st trimester screening of Down
syndrome
3. Controversial Routine 18-22 week USG scan (see below)
Indications of USG during 1st trimester

1. Confirm viability of pregnancy
2. Date gestational age (by crown-rump length)
3. Confirm the location of pregnancy (exclude ectopic pregnancy)
4. Diagnose multiple pregnancy
5. Diagnose abnormal uterine or ovarian tumour / pathology
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Indications of USG during 2nd and 3rd trimester
- Date gestational age(by Biparietal diameter and others)
- Confirm foetal viability and to diagnose intra-uterine death
- Diagnose multiple pregnancy
- Assess foetal growth (by serial measurement of biometry)
- Assess liquor volume
- Assess placental site (to exclude placenta praevia) and pathology
- Exclude or diagnose foetal structural abnormality
- Assess foetal well-being
Routine 18-22 week USG scan

1. Potential benefit:
a. For dating. USG dating predicts EDC better than by LMP
b. Early detection of foetal abnormality:-early management and better outcome
2. Potential problems:
a. Missed foetal abnormalities - potential medico-legal issue
b. False positive leads to anxiety and unnecessary tests (also implication for costs)
c. Request for termination of pregnancy (because of anxiety induced) for minor abnormality only
d. No evidence so far that routine scan improves foetal outcome
Safety of USG
1. Ultrasound of sufficiently high level can lead to tissue damage by various mechanisms such as heating, streaming, and
cavitation.
2. At the level of energy used for medical diagnostic purposes, no definite adverse effect, in particular effect to foetus, has been
documented so far.
Doppler effect
Doppler Effect and use in medicine
Doppler effect is a physical principle named after Doppler, Christian Johann, an Austrian physicist and mathematician who first
discovered in 1842. It is an 'apparent' change in the frequency of waves, as of light or sound (including ultrasound), occurring
when the source and observer are in motion relative to each other. The frequency increases when the source and observer
approach each other, and decreases when they move apart. It can therefore, be used to estimate the velocity of the moving object
by measuring the changes of frequency of waves. In medicine, human blood flow can be examined by applying ultrasound waves
which are then reflected back by the moving red blood cells in the circulation, and analysed with electronic means. See Doppler
studies for application in Obstetrics.
Doppler studies
Doppler studies of blood flow in medicine
Using the principle of Doppler effect, the blood flow in human circulation can be assessed with ultrasound. The changes in
frequency of reflected waves are analysed and displayed as a pattern of waveforms across time. Various ratios using values at the
systolic and the diastolic phase of blood flow are calculated to reflect the degree of blood flow:-
- A/B ratio (or S/D ratio) = systolic/diastolic
- Pulsatity index
- Resistance index
- Ratios rather than the actual velocity are calculated because the calculation of the later required the knowledge of the angle
between the path of the wave and the path of the moving object, which is not possible in practice. This factor can be
eliminated using the ratios.
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6. Foetal growth and Monitoring
Small-for-gestational-age (SGA)
It is usually defined as foetal weight less than the tenth (or more rigorously the fifth or third) percentile for gestational age. It is
different from intrauterine growth retardation (IUGR). Many infants that are small-for-gestational-age (SGA) are appropriately
grown and healthy. On the other hand, some infants with weight lies above the 10th percentile may have not achieved their full
growth potential and therefore growth-retarded.
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Intrauterine growth restriction (IUGR)
Definition
- Failure to achieve the normal genetic growth potential in utero
- It is not synonymous with small-for-gestational-age (SGA)
Causes
1. Foetal
a. Chromosomal abnormalities
b. Genetic disorders
c. Congenital infections such as syphilis, rubella
d. Multi-factorial foetal abnormalities
2. Maternal
a. Diseases: Systemic Lupus Erythematosus, Renal diseases, etc.
b. Malnutrition
c. Smoking, alcohol, substance abuse
3. Placental insufficiency usually secondary to pre-eclampsia and diabetes mellitus.
Classification
1. Symmetric
a. Uniform slowing or arrest of all foetal parameters.
b. Occurs when the growth potential of the foetus is reduced
c. Usually appears early in pregnancy
d. Affects all organ and therefore 'symmetric'
2. Asymmetric
a. Slowing or arrest of foetal abdominal circumference only
b. Supply of nutrients to the foetus is inadequate to support growth
c. Usually presents in later pregnancy when foetal needs are increasing
d. The vital organs are protected and there is sparing of head growth initially. Therefore it appears 'asymmetric', with the
growth of the abdomen more affected than that of the head
e. Mainly due to maternal causes, e.g. placental insufficiency
3. Remark
a. Differentiation of symmetric and asymmetric growth retardation is not always clear cut
b. Some causes will lead to both symmetric and asymmetric pattern, depending on the onset of problem:-e.g. Maternal
malnutrition may result in symmetric growth retardation if the onset of the problem is in early pregnancy, but may lead to
asymmetric pattern if malnutrition only occurs in the late pregnancy
c. The head growth will eventually be affected in the late stage of asymmetric growth retardation.
d. Some disorders may cause asymmetry of growth but is not actually growth retarded:-e.g. Hypochrondroplasia
Diagnosis
1. Rule out date problem and constitutionally small baby.
2. Clinical suspicion from inappropriate small fundal height.
3. Ultrasound diagnosis with small foetal abdominal circumference (AC) (below 3rd centile), or slowing or arrest growth of AC.
4. The biparietal diameter and femur length may also be small. There may also be signs of foetal compromise such as
oligohydramnios.
- 93 -
Distinguishing SGA and IUGR
It is difficult to distinguish SGA from IUGR as the above are same for both conditions. Hence we rely on more foetal parameter
for diagnosis of IUGR:-
1. CTG:- usually normal, if abnormal, detected late
2. Doppler ultrasound:-
a. Umbilical artery end diastolic flow:- for SGA it is normal; for IUGR, it is either reduced, absent or reversed with the
latter two suggesting pacental insufficiency.
b. Cerebral circulation:- foetus try to reserve blood for brain development hence there will be increased flow in IUGR.
Principle of Management
1. Investigation of underlying causes:-
a. Maternal
i. Systemic Lupus Erythematosus: ANA, ACA, APTT for lups anticoagulant
ii. Smoking, substance abus
iii. Renal Disease, Pre-eclmpsia (check for BP and urine albumin)
b. Foetal
i. Ultrasound for morphology
ii. Foetal karyotyping by aminocentesis or cordocentesis
iii. Viral studies if congenital infections are suspected.
2. Monitor foetal well-being:-
a. Growth scans bi-weekly
b. Cardiotocogram > 28 weeks
c. Amniotic fluid volume assessment weekly
d. Doppler studies of foetal vessels
3. Monitor maternal well-being:- essential if maternal causes of IUGR are identified.
4. Decision of time and mode of delivery
a. Balance the risk of continuation of pregnancy against the risk of discontinuation which are:-
i. Risk of continuation of pregnancy chance of intrauterine death
ii. Chance of deterioration of maternal condition in case of maternal disorder such as pre-eclampsia,SLE and renal
disorders
iii. Risk of discontinuation complications of prematurity, consider dexamethasone if < 24 weeks.
b. Deliver if:-
i. Foetal distress occurs, such as
1. Abnormal CTG; or
2. Persistent reverse r absent end-diastolic flow in umbilical artery.
ii. Severe pre-eclampsia; or eclampsia.
iii. Consider delivery if gestation is beyond 34 weeks.
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Protocol, as of 16 January 2008

1. Antenatal Management
a. Consult Foetal Medicine Team
b. Investigate for the underlying causes:
i. Foetal morphology scan
ii. Foetal karyotyping with amniocentesis or cordocentesis
iii. Other investigation such as microbiological or virological test should be based on clinical suspicion
iv. Autoimmune screening
c. Monitoring maternal well-being, is essential if maternal causes of IUGR are identified, such as
i. Pre-eclampsia
ii. Diabetes mellitus
d. Advise to quit smoking if patient smokes:
e. Foetal surveillance Monitor foetal well-being
i. Tests and frequency depends on severity, gestation and intention to deliver:-
- Growth scan bi-weekly
- Liquor volume and Doppler study
z Weekly if SGA with no sign of foetal compromise
z Twice weekly if severe oligohydramnios (AFI <2cm)
z Daily if UA absent EDF
- CTG continuously when UA reversed EDF/ DV reversed a-wave waiting for delivery
ii. Foetal surveillance may be performed in LKS clinic (USGM)
iii. Steroid to enhance lung maturity when:-
- Between 24 and 34 weeks, and
- presence of significant foetal compromise (UA absent EDF or worse)
iv. Remark:-recruit for DNA/RNA study
2. Intrapartum Management
a. Balance the risk of continuation of pregnancy against the risk of discontinuation which are:
i. Risk of continuation of pregnancy
- Chance of intrauterine death
- Chance of maternal condition deterioration from maternal disorders
ii. Risk of discontinuation Complications of prematurity
iii. Deliver if there is signs of foetal distress
- Abnormal CTG
- Persistent reverse or absent end-diastolic flow in umbilical artery
iv. Deliver if there is deterioration of maternal condition
- Severe pre-eclampsia
- Eclampsia
b. Time of delivery:
i. SGA with or without oligohydramnios:-aim at 37-38 weeks
ii. UA Absent EDF:-aim at 34 weeks
iii. UA Reversed EDF / DV reversed a-wave:-early delivery
c. Mode of delivery:
i. Vaginal delivery IOL can be considered for cases with SGA oligohydramnios, with continous CTG monitoring
ii. CS is indicated for more severe case of foetal compromise
d. Neonatologist stand-by at delivery
e. Umbilical cord blood gas analysis
f. Send placenta for histological examination
A routine USG of a primigravida healthy woman at 22 week of gestation shows that all foetal parameters (AC, BPD, FL) are
below 3rd centile. The morphology and liquor volume otherwise appear normal. What are the differential diagnoses and how
would you verify the diagnosis?
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Macrosomia
Definition
There is no universal definition for macrosomia. Some define it by the body weight at or more than 4.0 kg or 4.2 kg, while some
define it by body weight more than 97% for the gestation.
Incidence
About 3% of newborns in Hong Kong are at or above 4.0 kg
Causes
In majority of cases no specific cause can be identified. It is associated with:
- Postterm
- Maternal diabetes mellitus, gestational or established
- Rarely congenital syndromes
Risks
1. Maternal risks
a. Higher risk of operative delivery including caesarean section and instrumental delivery
b. Higher risk of birth canal injury, such as perineal tear, particularly when shoulder dystocia occurs.
2. Foetal risks
a. Higher risk of shoulder dystocia and related birth injury and birth asphyxia, particularly in diabetic patients
b. Foetal risks associated with postterm and poorly controlled maternal diabetes mellitus
Antepartum management
1. Suspect macrosomia when the uterus is large for date. Ultrasound foetal parameters (biparietal diameter, abdominal
circumference, and femur length) are larger than normal. Foetal weight can be estimated from a formula using the above
parameters.
2. Screen for gestational diabetes mellitus and treat accordingly
3. Counsel for risk of macrosomia and mode of delivery. Consider caesarean section if the estimated foetal weight is 4kg
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Crown-rump length
Definition
Crown-rump length is defined as the distance between the topmost part of the foetal head and the buttock, and is the single most
important parameter of foetal size in the first trimester.
Measuring crown-rump length

- The foetal axis is placed perpendicularly to the USG.
- The midline sagittal plane is visualized.
- The measurement is made from the top of the foetus to the buttock.
Uses of crown-rump length measurement

For dating of pregnancy in the first trimester:-accuracy:- 4 days
Abdominal circumference
Definition
Foetal abdominal circumference (AC) is one of the commonest parameters for size and growth. It reflects the liver size and
volume of subcutaneous fat. It is the most sensitive indicator of intrauterine growth restriction (IUGR).
Measuring abdominal circumference

1. The cross-section of the abdomen with the following landmarks identified:
a. Hepatic vein in the anterior one-third of the abdomen
b. Stomach
c. Adrenal glands
2. The outer edge of the circumference is measured
Uses of AC measurement
- Monitoring of foetal growth
- Estimation of foetal weight
Factors affecting AC
1. Abnormal foetal growth AC is decreased in both symmetric and asymmetric IUGR, and increased in macrosomia.
2. Abdominal wall defects and diaphragmatic hernia AC is difficult to be measured in gastroschisis and omphalocele as the
anatomy of the landmarks is distorted. It is underestimated because of herniation of abdominal content.
3. Foetal ascites Ascitic fluid distends the abdomen, resulting in a large AC.
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Biparietal diameter
Definition
Biparietal diameter (BPD) is the longest distance between the two parietal eminences. It reflects the brain growth, and is one of
the commonest parameters of foetal size and growth. It is also the greatest presenting diameter in vertex presentation. The average
size of BPD in a term foetus is 9.5cm.
Measuring biparietal diameter with USG

1. The foetal head should be in lateral position
2. An accurate plane with the following landmarks is identified:
a. The midline falx
b. The thalami are symmetrically positioned on either side of the falx
c. Visualization of the septum pellucidum at one third of the fronto-occipital distance.
3. The measurement is made between the outer plate of one parietal eminence and the inner plate of the other, and is
perpendicular to the midline falx.
Uses of biparietal diameter measurement

1. For dating in the second trimester
2. For monitoring of foetal growth
3. For estimation of foetal weight
Factors affecting the biparietal diameter

1. Dolicocephaly
a. It is a condition is which the foetal skull is moulded and compressed laterally, so that the fronto-occiputal length is
elongated and the BPD is shortened. However, the head circumference should not be changed.
b. It is a normal condition and is commonly seen in breech presentation and transverse lie.
2. IUGR
BPD is the last parameter to be affected in case of asymmetric IUGR because of brain sparing effect. However, it can be
affected early in symmetric IUGR.
3. Brain abnormalities Hydrocephaly and Microcephaly
4. Skull bone abnormalities Thanatophoric dwarfism
Femur length
Definition
Foetal femur length is one of the commonly used parameters of foetal size and growth. It is defined as the distance between the
ends of metaphysis and can be measured with ultrasound. It reflects the crown-heel length (longitudinal growth).
Measuring femur length

1. The femur image is at an angle of less than 30 degrees to the horizontal.
2. Two blunted ends of the femur are clearly visualised.
3. The extension to the greater trochanter and the head of femur is not included.
Uses of femur length measurement

1. For dating in the second trimester.
2. For monitoring of intrauterine growth.
3. For estimation of foetal weight.
Factors affecting the femur length

1. Intrauterine growth retardation (IUGR) It is affected early in symmetric IUGR but late in asymmetric IUGR.
2. Down syndrome In general foetuses with Down syndrome have a shorter femur. Femur length was once suggested as a
screening test for Down syndrome, but was found to be less effective.
3. Congenital dwarfism n various bone disorders are associated with short long bones including thanatophoric dwarfism.
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7. Amniotic fluid
Amniotic fluid
Definition
Also called 'liquor', is the fluid normally inside the amniotic cavity. It is foetal urine.
Volume
- Normal range varies from 300ml to 1500ml
- Normal range depends on gestation, with the peak at 34 to 36 weeks
Composition
1. Electrolytes
2. pH:-slightly alkaline, changes amniostrix from orange to blue, a test for rupture of membranes
3. Foetal cells:-amniocytes can be collected with amniocentesis and cultured for foetal karyotyping
Production and removal

1. Production
a. Foetal urine
i. The major source of liquor
ii. Urine production starts from 12 week
iii. Anhydramnios in case of absent foetal kidneys or infantile type of polycystic kidneys
b. Foetal lung fluid Constitutes small portion of liquor production as most of the fluid is swallowed by the foetus
2. Removal
a. Foetal swallowing and absorption via GI tract
Polyhydramnios when there is pathology affecting the mechanism such as anencephaly, esophageal atresia and duodenal
atresia.
b. Transmembranous and intramembranous:-account for small percentage of amniotic fluid circulation.
How is amniotic fluid volume measured?

1. Subjective method
Relative amount of echo-free fluid areas are subjectively compared with the space occupied by the foetus and placenta
2. Greatest pocket method
a. The vertical length of the deepest pocket of liquor is measured
b. When it is less than 1cm, oligohydramnios is diagnosed; when more than 8cm, polyhydramnios is diagnosed
3. Amniotic fluid index The most common method used
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Abnormality related to amniotic fluid
1. Oligohydramnios and anhydramnios
2. Polyhydramnios
3. Meconium stained liquor
4. Amniotic fluid embolism
5. Blood stained liquor:-may be a result of abruptio placentae
6. Leaking of amniotic fluid because of rupture of membranes
Procedure related to amniotic fluid

1. Amniocentesis
2. Amnioreduction
3. Amnioinfusion
4. Amniotomy
Amniotic fluid index (AFI)

What is amniotic fluid index (AFI)?
It is a semi-quantitative way in assessing liquor volume. The value of AFI is the summation of the vertical depths of the largest
pocket in each of four equal uterine quadrants. It is said to be more accurate than using just a single pocket (see amniotic fluid).
The normal range varies according to the gestational age:-In general, it is polyhydramnios when AFI is greater than 24cm, and
oligohydramnios when it is less than 8cm. AFI is not applicable to assess the amniotic fluid volume in multiple pregnancy.
How to measure amniotic fluid index

1. Divide the uterine surface into 4 equal quadrants.
2. Set transducer parallel to maternal sagittal plane and perpendicular to maternal coronal plane.
3. Apply constant gentle pressure during measurement.
4. Measure the depth of liquor at the deepest unobstructed, clear pocket of each quadrant.
5. AFI = sum of the depths of the 4 pockets
How good is amniotic fluid index?

1. Measurement error:10 to 15%
2. Correlation with actual amniotic volume 5.8 2.6cm:-250ml ; 14cm:-700ml. AFV = exp(5.19+0.093-AFI)
3. Accuracy of diagnosis:- Oligohydramnios:-50%; Polyhydramnios:-50%
- 100 -
Oligohydramnios
Definition
- Oligohydramnios is an inadequate volume of amniotic fluid
- Anhydramnios is the complete absence of amniotic fluid.
Causes
1. Leaking of amniotic fluid after rupture of membranes
a. The most common cause of oligohydramnios
b. however, the amniotic fluid volume may still appear normal after rupture of membranes if the leaked volume is not much
2. Foetal malformations resulting in decreased production of urine:
a. Bilateral renal agenesis (Potter's syndrome) no functional foetal kidneys and therefore completely no foetal urine
production and anhydramnios
b. Infantile type of polycystic kidneys
i. Dysgenesis of kidneys which become non-functional
ii. Autosomal recessive inheritance
c. Posterior urethral valve
i. Urine production is present but excretion is impaired because of urethral obstruction
ii. Bladder is therefore distended and there is secondary dilated renal pelvis. Renal function may be eventually impaired
3. Foetal compromise resulting in decrease production:
Intrauterine hypoxia or growth retardation (IUGR) Renal blood flow decreases and hence the urine production
Foetal Risks
Depends on underlying causes and time of occurrence:
1. Rupture of membranes:-intrauterine infection, preterm labour, cord prolapse
2. Foetal malformations:-may not be viable such as Potter's syndrome and infantile type of polycystic kidneys
3. Foetal compromise:-intrauterine death
4. Pulmonary hypoplasia, when severe oligohydramnios occurs before 20 weeks of gestation during when development of lung
is critical
5. Postural deformities:-various degree of limbs and facial deformities
Diagnosis
1. Clinically, the uterus small for date and foetal parts can be easily felt
2. Ultrasonical:-Decreased amniotic fluid volume demonstrated e.g. by amniotic fluid index measurement
a. AFI < 8cm or Greatest pocket <2cm
b. Anhydramnios if complete absence of liquor

1. Antenatal Management
a. Investigate for the underlying cause:
i. Rule out rupture of membranes from history and physical examination.
ii. Rule out foetal growth restriction
iii. Morphology scan for abnormalities of foetal kidneys and bladder in case of anhydramnios
iv. Assessment of foetal growth and well-being
b. For isolated primary oligohyramnios:-Monitor foetal growth, liquor volume and umbilical arterial flow bi-weekly
2. Intrapartum Management of isolated oligohydramnios
a. Aim at delivery at 38 weeks
b. Aim at vaginal delivery if there is no other contra-indications
c. Induction of labour with PGE2 can be considered in antenatal ward if there is no other signs of foetal compromise
d. Consider early delivery if case of foetal compromise
3. Treatment depends on the underlying causes:
a. Termination of pregnancy for lethal malformations
b. Amnioinfusion to replenish amniotic fluid to avoid pulmonary hypoplasia and postural deformities.
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Oligohydramnios sequence
The oligohydramnios sequence is a set of related conditions resulting from marked decreased in amniotic fluid. This typically
results from bilateral renal agenesis (34%), or chronic leakage of fluid. Other conditions such as bilateral multicystic renal
dysplasia (34%), unilateral renal agenesis and contralateral multicystic renal dysplasia (9%), renal tubular dysgenesis, autosomal
recessive (infantile) polycystic disease, non-functioning but morphologically normal renal tracts (3%), abherrant placental
implantation (on a uterine septum for instance) can lead to the same set of findings. 50% of these foetuses have anomalies that are
not part of the oligohydramnios sequence. In the oligohydramnios sequence, the decrease of fluid causes lung hypoplasia and
foetal compression. The foetal compression results in abnormal limb positions with dislocations and an abnormal face (flat with
low set ears). After delivery these newborn die of pulmonary insufficiency (via pneumothoraces).
Polyhydramnios
Definition
It is an excess of amniotic fluid, in contrast to oligohydramnios where there is a decrease in amniotic fluid (Norm: 500-1500 ml).
Ultrasound would reveal a Single packet > 8cm or AFI >2 standard deviation on chart.
Causes
It is related to the increase in production or decrease in removal of the amniotic fluid. In one-third of cases the cause is idiopathic,
but some are due to foetal, maternal or placental disorders:
1. Foetal causes
a. Anencephaly
b. Oesophgeal atresia, duodenal atresia
c. Gastroschisis and omphalocele
d. Foetal hydrops
2. Maternal causes poorly controlled diabetes
3. Placental causes rarely due to placental tumour such as choriangioma
Risks
1. Foetal
a. Preterm labour
b. Unstable lie
c. Premature rupture of membranes and cord prolapse
d. Foetal abnormalities leading to polyhydramnios
e. Cord prolapse
2. Maternal
a. Discomforts secondary to pressure effects
b. Dyspnea, indigestion, abdominal pain, edema and varicose veins
c. High risk of operative delivery
Figure 26 Fluid thrill (Left)

Diagnosis
1. Clinical
a. Uterus large for date
b. Foetal parts are difficult to feel
c. Unstable lie or malpresentation
d. Fluid thrill may be demonstrated
2. Ultrasonical Single pocket of liquor > 8cm or AFI> 2SD on AFI chart
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1. Investigation of underlying causes
a. Ultrasound for foetal morphology
b. OGTT test for diabetes mellitus
2. Treatment
a. Treat underlying cause:-e.g. control DM
b. Conservative treatment:-
i. For patients have mild symptoms, especially idiopathic polyhydramnios which usually resolve spontaneously
ii. Regular follow up in clinic with USG to monitor liquor volume
c. For symptomatic patients:-
i. Admission.
ii. Give dexamethasone if high risk for preterm labour (<34 wks)
iii. Amnioreductionif patients have severe symptoms, to reduce the liquor volume, to be decided by specialist
iv. Delivery.
v. NSAID has no clinical use
3. Prevention of cord prolapse
a. Precaution in performing amniotomy when patient goes into labour.
b. Avoid amniotomy when there is cord presentation
c. High water amniotomy
d. Sit up patient to encourage descend of foetal head before amniotomy
e. Control the rate of flow of liquor
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Meconium stained liquor (MSL)
Meconium stained liquor (MSL)
Meconium is a dark green fecal material that accumulates in the foetal intestines and is discharged at or near the time of birth.
When the foetus passes meconium before or during labour, the meconium mixes with the amniotic fluid, and depending on the
relative amount of meconium and amniotic fluid, it is classified into thin, moderated and thick MSL.
Significance of MSL
It was thought in the past that MSL is a sign of foetal distress. Nowadays it is clear that foetuses pass meconium very often when
they undergo stress, as a normal parasympathetic response. MSL does not necessarily imply distress, and is commonly seen in
postterm pregnancies. However, thick MSL may imply that the actual amniotic fluid is reduced (oligohydramnios) which itself is
a sign of foetal compromise. When foetuses aspirate thick meconium to the airway or lung during labour, the meconium will
induce a chemical pneumonitis which is called meconium aspiration syndrome. It is a severe disease and potentially fatal. MSL is
uncommon in preterm pregnancy. When it occurs, it is associated with listeriosis and is associated with high foetal morbidity and
mortality.

1. Plan of delivery:
a. Allow vaginal delivery if no sign of foetal distress
i. For induction of labour if no onset yet
ii. Start amnioinfusion in case of moderate and thick MSL.
iii. IV access, X-match
iv. Continuous foetal monitoring with CTG
b. For Caesarean section if foetal distress or malpresentation.
2. On delivery:
a. Inform paediatrician upon delivery.
b. Suck babys oral cavity and nasal cavity upon delivery of foetal head.
c. No need for tracheal aspiration unless intubation is required.
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Amnioinfusion
What is amnioinfusion?
Amnioinfusion is a procedure by which normal saline is infused into the amniotic cavity. It can be done transcervically using an
intrauterine catheter during intrapartum period, or abdominally during antepartum period.
Indication
1. Intrapartum:
a. Meconium stained liquor (MSL)
Heavily meconium stained liquor increases the risk of meconium aspiration syndrome. The aim of amnioinfusion is to
dilute the MSL and hence reduce the risk.
b. Umbilical cord compression
Cord compression may occur during labour. It may result in variable decelerations of foetal heart rate, particularly
when the liquor volume is reduced. It has been suggested that amnioinfusion may help to prevent the event. However,
no control trials have yet proven its role in preventing intrapartum foetal distress.
2. Antepartum - Severe oligohydramnios
a. For diagnostic purpose, Ultrasound images are suboptimal as transmission of ultrasound wave is poor in case of
oligohydramnios. Replenishment of liquor helps to improve ultrasound imaging and allow better assessment of foetal
morphology that may be abnormal in case of severe oligohydramnios
b. For therapeutic purpose, Replenishment of liquor may help to reduce the complications of oligohydramnios such as
postural deformities or pulmonary hypoplasia. In order to prevent pulmonary hypoplasia, the procedure must be
performed before mid-gestation because it is the critical period of bronchial and alveolar differentiation.

1. Insert intrauterine catheter under aseptic technique.
2. Infuse 1L of normal saline at room temperature (rate:-10-15 ml per minute).
3. Repeat every 4 hours until the second stage of labour.
Amnioreduction
What is amnioreduction?
It is a procedure by which excessive amniotic fluid is drained, usually via a needle inserted abdominally.
What are the indications?

1. Severe polyhydramnios
When the uterus is over distended, there may be maternal discomfort and an increased risk of preterm labour and cord
prolapse. Amnioreduction would be required to relieve pressure symptoms. To avoid cord prolapsed during rupture of
membranes in a case with severe polyhydramnios going into labour; reduction of the liquor volume abdominally beforehand
is also suggested. The role of amnioreduction in prevention of preterm labour is not well-defined.
2. Twin-twin transfusion syndrome
As the recipient twin is polyhydramnic, repeated amnioreduction on the recipient may help to improve the prognosis of the
disease and prolong the pregnancy.
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8. Foetal well-being
Foetal well-being
Definition
1. Foetal compromise:
a. Poorly defined
b. Usually means conditions in which the normal growth and neurological development are not optimal
c. Points to a relatively chronic problem, distinguished from foetal distress
2. Foetal distress:
a. Also poorly defined
b. Usually means a acute hypoxic state of foetus that may result in foetal damage or death if it is not reversed or the foetus
is not delivered urgently
3. Ultimately, foetal compromise can lead to distress
Physiological changes associated with foetal compromise

Sequential changes occur when the foetus is undergoing chronic hypoxia and conservation of oxygen and energy for foetal brain
will occur in expense of peripheral organs.
1. Redistribution of blood flow Increase cerebral blood flow and decrease peripheral blood flow
2. Growth discrimination
a. Depletion of storage of liver glycogen, reflected by slowing down of growth of abdominal circumference
b. Slowing down of growth of femur
c. Growth of brain, reflected by the biparietal diameter maintained until at the very late stage
3. Further decrease in peripheral blood flow Decrease in renal blood flow, resulting in reduction of foetal urine, and hence
liquor volume (oligohydramnios)
4. Conservation of energy and oxygen
a. Foetal movements decrease
b. Foetal breathing movements decrease
c. Foetal tones decrease
5. Anaerobic metabolism
a. Metabolic acidosis, resulting in abnormal cardiac function
b. Abnormal heart rate regulation:-decreased baseline variability, late decelerations and bradycardia, as shown in
cardiotocogram
6. Ultimate outcome if not treated Foetal death
How to assess foetal well-being

1. Foetal movements
2. Non-stress test or contraction stress test using cardiotocogram
3. Liquor volume assessment (see amniotic fluid and amniotic fluid index)
4. Biophysical profile
5. Doppler studies of foetal blood flow
The most commonly used are cardiotocogram, amniotic fluid index, Doppler studies
Management
1. Aim is to maximize the chance of survival of the foetus
2. Balance the risk of continuing pregnancy and risk of termination of pregnancy which would usually mean a preterm delivery
3. Decide the time and mode of delivery, determining factors are
a. Degree of foetal compromise
b. Gestation age
i. When there are signs of foetal distress such as abnormal non-stress test:-immediate delivery
ii. When there are signs of foetal compromise but the foetus is not in acute danger, and the foetus is immature:-close
monitoring of foetal well-being
iii. When there are signs of foetal compromise and the foetus is mature, delivery.
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Biophysical profile
It is one of the methods to assess foetal well-being during antepartum period, using the combination of ultrasound and electronic
foetal heart monitoring. It consists of 5 parameters:
Parameters Assessment
Heart reactivity 2 accelerations of 15bpm for 15s in 40 min
Amniotic fluid volume A pocket 1cm in 2 perpendicular planes
Tone 1 episode of limb movement from flexion to extension then back to flexion
Movement 3 gross body movements in 30 min
Breathing movements Sustained foetal breathing movements 30s in 30 min
1. The last four parameters are assessed under USG in 30 minutes

a. A score of 2 is given for each normal parameter (Total mark is 10)
b. A score more than 7 is definitely normal, while a score of 4 or less is definite abnormal. A score in between is equivocal.
c. It was originally designed to supplement foetal heart monitoring in assessment of foetal well-being. However, there is no
good evidence to suggesting that the use of biophysical profile can improve foetal outcome. It is found that among the 5
parameters, foetal heart rate and amniotic fluid volume are the 2 most important factors.
2. Assessment of other parameters with USG is rather time consuming. Furthermore, Doppler studies of foetal circulation has
become a more popular and accurate method in modern obstetrics, and biophysical profile is gradually out of interest.
Foetal movement
Counting of foetal movements
1. A daily count of perceived foetal movements from 28 weeks' gestation is a simple and inexpensive routine screening device
for monitoring of foetal well-being
2. Advice should be sought if fewer than 10 movements are perceived within 12 hours or if the mother feels that the baby is not
moving
3. Other tests of foetal welfare such as foetal cardiotocogram can then be applied
Advantages
1. Simple, safe and inexpensive
2. Can be initiated by mother herself at home
3. No sophisticated equipment is required
Limitations
1. A large number of foetal movements may not be perceived
2. There are great variations in the number of foetal movements from day to day in individual women and from woman to
woman
3. The sensitivity and specificity of the method are low
4. One randomized trial suggests a clear benefit, but another does not
5. Less than 1/1000 women might benefit from formal foetal movement counting, using later foetal death as an outcome
6. Formal counting provokes anxiety in about 25% of women. Another 50% are reassured by it.
Contraction stress test

It is a kind of assessment of foetal well-being but is rarely indicated nowadays. In this test, the foetal heart rate pattern is
examined with cardiotocogram in the presence of uterine contractions which are artificially induced by using syntocinon or nipple
stimulation. The rationale of the test is that a compromised foetus may not show an abnormal foetal heart rate pattern until it is put
under a labour-like condition. It is supposed to be more sensitive than a non-stress test in detecting a compromised foetus. The
disadvantages of the test are that it is time consuming (it takes at least 30 minutes), requires intravenous infusion, and the result is
sometimes difficult to interpret. There is a risk of uterine hyperstimulation, foetal distress, and precipitation of preterm labour. As
less invasive tests such as Doppler studies of foetal circulation are now available, contraction stress test has become obsolete.
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Multiple pregnancy
Incidence
- 1% of all pregnancies
- Most are twin pregnancy (10-15/1000 incidence for twin; 1-4/1000 incidence for triplet)

For medical students, they should know twin pregnancy. They will not be examined on higher order pregnancy except twin, but
they should understand and apply the principles of twin pregnancy in the management of other multiple pregnancy.
Twin pregnancy
Types of twin pregnancy
Twin pregnancyis classified according to:
1. Zygosity Monozygotic and Dizygotic. (M:D = 1:3)
a. Monozygotic: 20% of twin pregnancy (3-4/1000), constant across whole world.
b. Dizygotic: 80% of twin pregnancy, varies among different races. (West African > Japan)
2. Chorioamnionicity
a. All dizygotic twins are dichorionic diamniotic
b. Depends on the time of cleavage, monozygotic twins may be dichorionic diamniotic, monochorionic diamniotic,
monochorionic monoamniotic
Incidence
1% of all pregnancies incidence increases with positive family history, use of ovulation induction, or assisted reproductive
technology (ART). Thus in Hong Kong, the rate of multiple pregnancy increased recently.
Diagnosis of multiple pregnancies

1. History Multiple pregnancy must be suspected if the pregnancy is resulted from ovulation induction or assisted reproductive
technology
2. Physical Examination
a. Uterus large for date
b. More than 2 foetal poles palpable (late)
c. Foetal heart pulsations, which are of different rate (at least 15bpm), are heard simultaneously
3. Ultrasound
a. The only reliable method.
b. Confirm twin pregnancy
c. Also assess the zygosity and chorioamnionicity
Figure 27 The uterus is large-for-date. Figure 28 More than 2 foetal poles are palpable.
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Risks of twin pregnancy
1. In general, risk are higher when it is:
a. Monozygotic
b. Monochorionic
c. Monoamniotic
2. Maternal Risks
a. Anepartum
i. Higher chance of placenta praevia (1.3% vs 0.6%)
ii. Pre-eclampsia:-increase 4 folds (9.9% vs 2.5%)
iii. Nutrition anaemia:-due to increased foetal demand (5.8% vs 4.0%)
iv. Gestational diabetes:-due to increased levels of diabetogenic placental hormones (11.0% vs 6.3%)
v. Increased severity of the minor disorders of pregnancy like hyperemesis gravidarum, backaches, constipation etc.
b. Intrapartum: Higher risk of caesarean section:-50% (57.2%-78.6%) require caesarean delivery
c. Postpartum: Higher chance of postpartum haemorrhage because of over-distension of uterus (3.9% vs. 2.6%)
3. Foetal Risks
a. Antepartum
i. Preterm labour and preterm delivery (50% delivered before 37 weeks)
ii. Foetal malformations:-various kinds of malformations including conjoint twin
iii. Twin-twin transfusionsyndrome (5-10%)
iv. Intrauterine growth retardation (IUGR)
v. Intrauterine death:-6-7 times higher mortality rate than that of singleton pregnancy
b. Intrapartum Risks
i. Vaginal delivery of second twins
ii. Second twin breech presentation.
iii. Locked twins (or twin entrapment).
iv. Cord entanglement:-in monochorionic monoamniotic twins pregnancy where no membranes septum to separate
the cords.
v. Cord prolapse.
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Antepartum management
1. Frequent visits:- from booking to week 28 once monthly; from week 28-36 biweekly.
2. Determination of chorioamnionicity It is best assessed with USG in the first or early second trimester as soon as possible.
3. Close maternal surveillances:-
a. Regular monitoring of blood pressure and urine protein to detect early pre-eclampsia
b. OGTT at 26 to 28 week to exclude gestational diabetes
4. Close foetal surveillances:-
a. Regular monitoring of foetal growth and liquor by USG, as fundal height cannot reflect the growth of individual twins.
b. It is important to detect discordant growth and liquor volume in monochorionic twins which is a sign of twin-twin
transfusion syndrome
c. Morphology scan at 20 week
5. Nutrition supplement Iron, folate and vitamins to prevent nutritional anaemia
6. Prevention of preterm labour At present no effective preventive measure
7. Time of delivery:-
a. Studies have shown that the foetal risks are higher when twin go beyond 38 week of gestation. This may relate to the
accelerated aging of placenta when compared to singleton pregnancy
b. Therefore, twin pregnancy should have induction of labour, or caesarean at 38 week
8. Mode of delivery:-
a. Vaginal delivery if the presenting twin is in cephalic presentation, otherwise for elective caesarean section
b. Caesarean section should also be performed (at 34 week or not later than 37 week) for monochorionic monoamniotic
twins pregnancy to avoid cord entanglement in late pregnancy or during labour
Intrapartum management
1. Foetal monitoring
During labour, both foetuses should be monitored with continuous cardiotogram. The first twin is monitored with a foetal
scalp electrode and the second one with external Doppler apparatus.
2. Pain relief epidural anaglesia is recommended.
3. Delivery of the second twin
a. After vaginal delivery of the first twin, the presentation of the second twin may remain high or altered; uterine
contractions are diminished (uterine inertia); cervix may begin to close. There may also be cord prolapse, diminished
placental function, abruptio placentae resulting in hypoxic injury.
b. USG may be helpful to assess the presentation; if not, perform ECV.
c. Oxytocin augmentation should be considered when uterine inertia occurs.
d. Membranes of the second twin should not be ruptured until the foetal head is well engaged.
e. When foetus remains high in presentation after 30 minutes or when there is foetal distress, operative delivery (including
caesarean section) should be considered.
4. Third stage
a. Give syntometine.
b. Oxytocvin infusion to prevent atony.
c. Check placenta and membranes for chorioamnionicity.
Postpartum management
Prophylactic oxytocic to prevent postpartum haemorrhage. This includes a single bolus of oxytocin or syntometrine followed
by oxytocin infusion.
1. Ultrasound shows a discordant growth of a twin pregnancy at 20 week of gestation, what are the possible diagnoses and how
can we differentiate them?
2. A woman of age 37 has a twin pregnancy. She is at 10 weeks of gestation asking for prenatal diagnosis of Down syndrome.
How would you counsel her?
3. A woman with a twin pregnancy is found to have a twin died in utero at 28 week of gestation. How would you manage her?
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Protocol, as of 26 February 2004
Management for triple pregnancy
1. Perform USG for dating and chorionicity as soon as possible.
2. Follow-up in general clinic every 4 weeks till 24 weeks.
3. Perform USG for fetal growth every 4 weeks.
4. Perform morphology scan between 18 and 20 week.
5. Give folate and obimin supplement.
6. Keep patients in hospital from 24 weeks till delivery
a. Inform paediatrician once admitted
b. Monitor BP/P twice daily, temperature once daily, and urine for albumin weekly
c. Twice weekly USG to confirm fetal viability (no need for daily doptone).
d. OGTT between 26 and 28 weeks, CBP at 26-28 weeks (with OGTT) and at 34 weeks (Pre-Caesarean section)
e. NO need for routine CBP, RFT, LFT, urate, PT/APTT, CTG or Dexamethasone
7. Arrange elective Caesarean section 34-35 weeks.
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Chorioamnionicity
1. Singleton pregnancy must be monochorionic monoamniotic (MCMA). However, chorioamnionicity may be multiple in case
of multiple pregnancy, depends on the zygosity and the time of division of the embryo. Take twin pregnancy as an example,
dizygotic twins must be dichorionic diamniotic (DCDA). Monozygotictwins may be DCDA, MCDA or MCMA depends on
the timing of cleavage as follow:
Time of Cleavage Stage of embryo Chorioamnionicity

Day 0 to 3 Morula DCDA
Day 4 to 8 Embryonic disk MCDA
Day 9 to 12 Blasticyst MCMA
After day 12 Foetus Conjoint twin
2. Determination of chorioamnionicity is very important in management of twin pregnancy because the lower the chorionicity
and amnionicity, the higher is the foetal and maternal risks. Chorioamnionicity is most easily and accurately determined by
USG in the first trimester:
a. DCDA:-the twins are separated by a thick chorionic septum between the gestation sac.
b. MCDA:-each of the twins is contained inside a thin amniotic sac, which in turn, is contained in the same chorionic
membrane.
c. MCMA:-no membranes are seen between the twins
3. During the second trimester, chorioamnionicity can also be accurately assessed:-

a. If they are of different sex, it must be dizygotic. The external genitalia can be determined with USG since early second
trimester
b. If the membrane septum is thick or there is lamda sign, it is DCDA, and the pregnancy can be dizygotic or monozygotic.
c. If there is no membrane septum between the twins, placenta must be MCMA, and the pregnancy must be monozygotic
d. If the membrane septum is thin or there is absence of lamda sign, it is MCDA, and the pregnancy must be monozygotic
Figure 29 Chorioamnionicity.
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Conjoint twin
Conjoint twins are a rare form of monochorionic monoamniotic twin pregnancy (see chorioamnionicity), resulted when the
splitting of the embryonic mass after day 12 of fertilisation. Conjoint twins are classified according to the dominant site of
interfoetal body part connection, into five major types:-
1. Thoracopagus (thorax, 30-40%)
2. Omphalopagus (abdomen, 25-30%)
3. Pygopagus (sacrum, 10-20%)
4. Ischiopagus (pelvis, 6-20%)
5. Craniopagus (head, 2-16%)
The prognosis of conjoint twins is in general poor, and depends on the site and extent of conjoining. Half of them are intrauterine
deaths and one-third of the remaining livebirths have severe defects for which surgery is not possible. Conjoint twins are
suspected under ultrasound, when both foetuses are always facing to each other with the same lie and presentation, with no
membranes separating them. Detail ultrasonic examination will identify the site of conjoining.
Twin-twin transfusion
What is Twin-twin transfusion?
Twin-twin transfusion is a disorder specific to monochorionic twin pregnancy. Normally there are vascular channels between the
twins through the placenta, and the blood flow between the twins is balanced. However, for some reasons that are still uncertain,
unbalanced blood flow sometimes occurs. Consequently, one twin becomes the donor while the other becomes the recipient of
blood.
The donor becomes anaemic, hypoxic and malnutrited, resulting in growth retardation and oligohydramnios. On the other hand,
the recipient becomes volume overload and with hyperviscosity of blood (increase in haematocrit). High-output heart failure
develops, and the foetus becomes hydropic with polyhdyramnios. This condition usually occurs during the second trimester. The
mortality is high without any intervention.
Prenatal diagnosis
Prenatal ultrasonography plays an important role in diagnosing twin-twin transfusion. There is discordance of growth and
oligohydramnios in the growth-deficient twin (donor twin) and polyhydramnios in the other (recipient twin). The bladder of the
donor twin may not been seen at all. Sometimes, the donar twin become a "struck twin" when he has no liquor at all and is
compressed against the uterine wall by the gestation sac of the recipient. The recipient twin may show features of hydrops foetalis
in the latter stage.
Treatment
The most popular treatments are repeated amnioreduction, and devascularisation of the anastomosis with laser.
The prognosis improves to 50 to 70%.
Lamda sign
It is an ultrasonic feature used to diagnose the chorioamnionicity of a twin pregnancy. The presence of a lamda sign suggests a
dichorionic diamniotic (DCDA) placenta. In a DCDA twin pregnancy, there is a thick septum consisting of two layers of amnion
and two layers of chorion between the gestational sacs. After 9 weeks of gestation, this septum becomes progressive thinner, but
remains thick at the base as a triangular tissue projection, which is called lamda sign.
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Maternal Medicine
1. Changes in pregnancy
Physiological changes in pregnancy
Why do we need to study the physiological changes?

1. Understand how human adapt to pregnancy
2. Some medical diseases may become worse during pregnancy, for examples:-
a. Valvular heart diseases, and
b. Diabetes mellitus.
3. Some physiological changes may mimic symptoms and signs of medical disorders, for examples:-
a. Palpitations, ejection murmur are common in normal pregnancy that may mimic heart disorders
b. Pregnant women often have physiological goitre
4. Some normal ranges may alter in pregnancy, for example, mild proteinuria of <0.3g per day is normal in pregnancy (<0.1g
per day in non-pregnant adult)
5. Some changes may alter the pharmacokinetics of drugs
What are the important physiological changes?

The changes are mediated by increased production of progesterone, oestrogens, hCG and hPL.
1. Cardiovascular system
a. Cardiac size increases by 12%
b. Stroke volume increases by 25 to 30%, reaches its maximum at 12 to 24 weeks of gestation
c. Cardiac output increases by 40% and reaches maximum at 20 to 24 weeks
d. Decrease in blood pressure and peripheral vascular resistance
e. Ejection systolic murmur
f. Normal S3 gallop
g. Reversible changes in the ST, T or Q waves in ECG due to the left and upward displacement of the heart
2. Respiratory system
a. Incfease in respiratory rate due to progesterone production.
b. Functional residual capacity, residual volume, and expiratory reserve volume all decrease by 20%
c. Dead space and tidal volume increase by 30 to 50%
d. Marked increase in alveolar ventilation by 65%
e. Minute ventilation increases by 50%
f.Oxygen consumption increases by 15 to 20%
g. Alveolar CO2 decreases due to increased respiratory rate
3. Glucose metabolism
a. During pregnancy, the production of various diabetogenic hormones including human placental lactogen, progesterone,
prolactin and cortisol are increased.
b. Their actions on glucose metabolism are counterbalanced by an increase in insulin concentrations which reaches almost
twice of non-pregnant levels.
c. The vast majority of pregnant women (96-98%) manage to maintain their blood glucose within normal limits, but the rest
of them fail to do so and become hyperglycemic (gestational diabetes).
4. Thyroid gland
a. During the first trimester, human chorionic gonadotropin (which structurally mimics TSH) produced from the placenta
stimulates the secretion of thyroxine from the thyroid glands. The TSH level decreases. There may also be a transient
increase in free T4 level. These changes are associated with hyperemesis gravidarum
b. As the pregnancy goes on, the TSH and free T4 levels return to normal.
c. Total T4 increases as the level of thyroxine binding protein increases because of oestrogen stimulating effect on the liver
production of the binding protein.
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5. Haematologic system
a. Increase in plasma volume up to 50% by term
b. Increase in blood volume up to 50% by term
c. Increase in RBC volume by 30% by term
d. Increase in WBC, mainly polymorphonuclear cells
e. Increase in platelet production
f. Increase in production of clotting factors, particularly factor I (fibrinogen) and III due to oestrogen stimulation.
g. Pegnant women are therefore more prone to develop thromboembolic diseases.
6. Renal system
a. GFR increases by 50% and renal plasma flow increases by 25% to 50%
b. Relative decrease in serum creatinine due to:-
i. increased GFR
ii. Dila;tation of ureters from 10 weeks onward
iii. Secondary to progesterone effect, and
iv. Pressure effect, by uterine compression (right > left)
A liver function and a renal function test are performed in a pregnant woman. Is the result normal? why?
Result Normal range
Na 140mmol/L 134-145mmol/L
K 3.5mmol/L 3.5-5.1mmol/L
Urea 2.5mmol/L 3.4-8.9mmol/L
Creatinine 40umol/L 44-107umol/L
Albumin 28g/L 36-48g/L
Bilirubin 3umol/L 0-15umol/L
ALT 30IU/L <58IU/L
ALP 200IU/L 30-90IU/L
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Pharmacology in pregnancy
Effect of pregnancy on pharmacokinetic
1. Drug absorption form GI tract
a. reduction in gastrointestinal motility may increase absorption of some poorly soluble drugs such as digoxin, or decrease
absorption of some drugs that undergo metabolism in gut wall, such as chlorpromazine
b. vomiting in early pregnancy may reduce absorption of orally administrated drugs
2. Drug distribution
a. Increase of plasma volume and extracellular fluid volume may decrease the steady state concentration of drugs with a
small volume of distribution
b. Decrease in albumin concentration may alter the free fraction of protein-bound drugs
3. Drug elimination
a. increase renal blood flow and GFR increase renal excretion of polar drugs
b. increase in hepatic microsomal oxidase system induced by pregnancy increase the metabolism of certain drugs
particularly anticonvulsants
Effect of drug on foetus

1. Fertilisation and implantation
Mifepristone (RU486), an anti-progesterone that antagonize the endogenous progesterone effects on endometrium, is used as
an abortive agent
2. Organogenesis
a. Diethylstilboestrol (DES):-adenocarcinoma of vagina in teenage years
b. Androgens:-virilization, limb reduction, esophageal anomalies, cardiac defects
c. Tetracyclines:-inhibition of bone growth, discoloration of teeth
d. Anticonvulsants:-neural tube defects
e. Warfarin
3. Growth, development and physiology
a. Anti-thyroid drugs cross placenta and may result in foetal and neonatal hypothyroidism
b. Prostaglandin synthetase inhibitors can cause premature closure or the ductus arteriosus
c. CNS depressants such as opiates cause neonatal respiratory depression
d. Drugs with dependence potential such as opiates taken regularly during pregnancy can result in withdrawal symptoms
in the neonate
Drugs in breastfeeding
1. Most drugs enter breast milk to a greater or lesser extent but, because the concentration has been greatly reduced by
distribution throughout the mother's body, the amount of drug actually received by the breast-fed baby is usually clinical
insignificant
2. Drugs that can safely be given to breast-feeding mothers include:
a. Penicillins, cephalosporins
b. Theophylline, salbutamol by inhaler, prednisolone
c. Valproate, carbamazepine, phenytoin
d. Beta blockers, methyldopa, hydralazine
e. Warfarin, heparin
f. Tricyclic antidepressants
g. Haloperidol, chlorpromazine
3. Certain drugs achieve sufficient concentration in breast milk, and they are sufficiently potent that their use in breast feeding
mothers should be avoided
a. Sulphonamides, chloramphenical, isoniazid, tetracyclines
b. Narcotic analgesics
c. Benzodiazepines
d. Lithium
e. Phenindione
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Maternal medicine
What is maternal medicine
1. Also called medical Obstetrics, is a subspecialty in Obstetrics.
2. Study of physiological changes in pregnancy.
3. Deals with medical diseases and complications of the mothers during pregnancy.
4. Also handles other high risk pregnancies e.g. Surgical diseases.
5. Team-care multi disciplinary approach (obstetricians, midwives, nurse specialists, paediatricians, physicians, surgeons,
anaesthetists, intensive care specialists.) Is important.
Three kinds of medical diseases

1. Medical diseases present before pregnancy (pre-existing) e.g. heart diseases, epilepsy
2. Medical diseases caused by pregnancy (pregnancy specific) e.g. pre-eclampsia, gestational diabetes mellitus
3. Medical diseases occurring for the first time in pregnancy which may be the predisposing factor (co-incidental).
How to study maternal medicine

1. Firstly, understand how a disease and its therapy (which are usually medication) affects the pregnancy (both the mother and
the baby), e.g. poorly controlled diabetes mellitus increases risks of foetal macrosomia, intrauterine death
2. Secondly, understand how a therapy (which are usually medication) affects the pregnancy (both the mother and the baby), e.g.
anti-convulsants increase foetal risk of neural tube defects
3. Conversely, how the pregnancy affects the disease, e.g. pregnancy is diabetogenic and control of diabetes mellitus may
require adjustment of insulin therapy. It is important to understand the physiological changes in pregnancy
4. Finally, how the pregnancy affects the treatment
Which medical diseases a medical student should know

1. Hypertensionin pregnancy
2. Diabetes mellitus
3. Heart diseases in pregnancy
4. Thromboembolic diseases
5. Thyroid disorders
6. Epilepsy
7. Appendicitis
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2. Diabetes mellitus
Diabetes mellitus
Introduction
Diabetes mellitus is one of the most common medical disorders in pregnancy. Pregnant women may have diabetes before
pregnancy (pre-existing), or develop glucose intolerance during pregnancy (gestational diabetes). In both conditions, the glucose
intolerance may be so severe that insulin control is required (insulin-dependent diabetes). During pregnancy, women require more
energy intake. On the other hand, as pregnancy is diabetogenic (see physiological changes in pregnancy), glucose control becomes
more difficult. Poor control of glucose level may result in various maternal and foetal complications. Nephropathy and retinopathy
is more severe during pregnancy.
Foetal Complications
1. Macrosomia
Hyperinsulinemia and hyperglycemia not only result in excessive growth but also an increase in fat deposition over
shoulder, resulting in high risk of shoulder dystocia, birth injuries and operative deliveries
2. Intrauterine growth retardation
IUGR is uncommon but can occur in severe chronic cases of diabetes with vasculopathy. Uteroplacental blood flow is
affected resulting in foetal growth restriction.
3. Foetal malformations
a. CVS-the most common system involved; VSD, ASD, TGA, situs inversus, hypolastic left ventricle
b. CNS:-anencephaly, encephalocele, holoprosencephaly
c. Others:-caudal regression syndrome, bowel atresia, etc
d. Teratogenicity is associated with poorly controlled diabetes during embryogenesis (first trimester).
e. The exact mechanism is unknown, maternal hyperglycemia, hyperketonemia and hypoglycemia have been suggested.
4. Intrauterine death
Sudden intrauterine death can be resulted from poor control of hyperglycemia, or secondary to IUGR. It was the major
cause of perinatal mortality in diabetic patients in the past, before the use of insulin.
Neonatal complications:
1. Hypoglycemia:-poor maternal glucose control can result in foetal beta-cell hyperplasia, leading to exaggerated insulin release
following delivery.
2. Respiratory distress syndrome:-hyperglycemia and hyperinsulinemia affect biosynthesis of pulmonary surfactant.
Maternal complications
1. Pre-eclampsia
2. High risk of operative deliveries
3. Pre-existing nephropathy and retinopathy may be worsen during pregnancy
Principles of management
1. Prepregnancy Pre-conception counselling is very important. Tight glucose control is emphasized to miminize risk of
teratogenicity. Complications such as nephropathy and retinopathy should be looked for.
2. Antenatal
a. Refer to dietitian for diet adjustment (30kcal/kg body weight) to provide adequate energy during pregnancy.
b. Hypoglycemic agents should be changed to insulin for better control.
c. Regular glucose monitoring H'trix (Fasting, Post-breakfast, lunch, supper), blood sugar series, multistix and HbA1c
d. Monitoring of maternal complications Blood pressure, urine albumin/creatinine ratio, RFT, refer to ophthalmologist.
e. Monitoring of foetal condition
i. Morphological assessment at around 20 weeks
ii. USG for growth and liquor volume when uterus is large for date every 4 weeks.
3. Intrapartum
a. Time of delivery While the pregnancies of well controlled cases can be continued till 40-41 weeks, poorly controlled
cases should have induction of labour earlier in 37 weeks to prevent sudden intrauterine death
b. Mode of delivery Pregnancy with macrosomic babies should be counselled for elective caesarean section
4. Postpartum Change to pre-pregnant diet and drug regime and discuss contraception
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Gestational diabetes
Definition
- It is defined as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.
- The definition does not differentiate those pre-existing diabetes mellitus which are not picked up until the patient becomes
pregnant, from those genuine gestational in origin (due to exaggerated physiological changes in glucose metabolism).
- The definition applies irrespective of whether or not insulin is used for treatment or the condition persists after pregnancy.
There have been controversies for long time in the subjects of gestational diabetes on the best method for screening, the diagnostic
criteria and the management of identified gestational diabetes.
Incidence
Total incidence 6.3% - (IGT 4.6%; GDM 1.5%; Pre-existing DM 0.2%)
Antenatal screening
1. Gestational glucose intolerance can be screened by various ways:
a. Presence of clinical risk factors:
i. In previous pregnancies:- history of gestational diabetes, macrosomia, unexplained stillbirth
ii. In current pregnancy:- persistent or significant glycosuria, macrosomia, maternal obesity, advanced maternal age
iii. Other risk factor:- positive family history of diabetes in first-degree relatives
b. Biochemical:- spot glucose level, fasting glucose level
3. A positive screening result should be followed by a diagnostic oral glucose tolerance test
Diagnosis
Oral glucose tolerance test
- It is usually performed around 26 to 28 weeks of gestation when the pregnancy-induced diabetogenic effects are most
prominent. It may be performed earlier when there is clinical suspicion.
- It is the only diagnostic test of gestational diabetes. However, the glucose load and the cut-off levels vary among centres. In
PWH, 50g glucose load is used. The fasting plasma level of more than 5.5mmol level, or the second hour level of more than
8 is diagnostic.
Complications
1. Foetal complications
a. Macrosomia, neonatal hypoglycemia, polycythaemia, hyperbilirubinaemia
b. Risk of congenital malformation is not increased unless the onset of gestational diabetes is at the first trimester
2. Maternal complications Increased risk of pre-eclampsia, operative deliveries (46.4%), and increased chance of development
of diabetes mellitus in future.
Management
The antenatal and intrapartum management is similar to that of pre-existing diabetes mellitus:
1. Maternal diabetes control
a. Refer DM nurse for education
b. Refer dietitian for diet control
c. Admit for blood sugar series after diet control for 3 days (admit soon if FG>7 or 2 hour >11, suspect pre-existing DM)
d. Insulin if poor control
2. Fetal Monitoring
Serial USG for fetal growth parameters and liquor volume
3. Post-Partum
a. Resume normal diet
b. Check Hstix at fasting and postprandial for 1 day
c. A 75g oral glucose tolerance test (WHO criteria) should be repeated 6 weeks postpartum to rule out pre-existing disease.
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ANTENATAL MANAGEMENT OF DIABETES MELLITUS

Protocol, as of 11 October 2007
1. Initial management of pre-existing IGT/DM

a. In patient management is preferred
b. Early admission to start diet control and hstix monitoring
c. Stop any oral hypoglycaemic drug and change to insulin
d. Check HbA1c and investigate for diabetic complications
e. Arrange morphology scan at second trimester
f. Refer to ophthalmologist for retinal assessment
2. Initial management of newly diagnosed GDM

a. Mild (fasting glucose < 6.1mmol/l or 2nd hour < 11.1 mmol/l)
i. Outpatient management is preferred for most GDM
ii. Refer DM education class to see dietitian for DM diet and DM education
iii. Start outpatient Hstix monitoring
iv. Follow up in Thursday medical obstetric clinic
v. Routine growth scan is not necessary
b. Severe (fasting glucose >= 6.1mmol/l and/or 2nd hour glucose >=11.1 mmol/l)
i. Early admission to start diet control and hstix monitoring
ii. Check HbA1c and investigate for diabetic complications
iii. Fetal growth scan
iv. Start insulin as indicated
Diet control:
Pregnancy 1st trimester 2nd trimester
Singleton 1500kcal/day 1800kcal/day
Multiple 1500kcal/day 2000kcal/day
Reference for glycaemic control

H'stix Normal Borderline Abnormal
Fasting (mmol/L) <= 5 > 5 - 5.5 > 5.5
Postprandial (mmol/L) <= 7 > 7 - 7.5 > 7.5
3. Subsequent Outpatient management for DM/GDM

a. GDM/DM on diet control
i. H'stix monitoring one to two days per week (4 times/day: Fasting, Post-Breakfast, Post-Lunch, Post-Supper)
ii. Check compliance and revise dietary plan if glycaemic control is borderline
iii. Admit to consider insulin if glycaemic control is persistently borderline or abnormal
iv. Uncomplicated GDM not requiring insulin can be followed up by midwives diabetic clinic (MCDM) on
Thursday morning
b. GDM/DM on insulin
i. H'stix monitoring two to five days per week (4 times/day: Fasting, PB, PL, PS)
ii. Adjust insulin dosage if persistently borderline or abnormal glycaemic control
iii. Admit if glycaemic control is difficult
iv. Growth scan every 4 weeks
v. CTG weekly from 36 weeks for GDM/DM on insulin
4. Indications for blood sugar series

a. Routine blood sugar series is not necessary for all GDM cases
b. Blood sugar series would be used as a reference for the commencement of insulin, the final insulin dosage for
individual cases and when the hstix result is in doubt
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5. Timing of delivery
a. GDM on diet with good control: await spontaneous labour and induction at 41 weeks gestation
b. GDM requiring insulin or pre-existing DM/IGT with normal H'sitx: consider induction at 40 weeks
c. GDM or pre-existing DM/IGT with poor glycaemic control and/or any complication: consider induction at 38 weeks or
earlier if indicated
6. Mode of delivery
a. Discuss elective caesarean delivery if the EFW > 4 kg
b. Take precaution of shoulder dystocia if mother with a macrosomic fetus (AC > 97 centile) undergoes vaginal delivery:
c. Doctor standby at foetal head delivery
d. Mid-call doctor assess before instrumental delivery

ORAL GLUCOSE TOLERANCE TEST
1. Indication of Antenatal OGTT
a. Perform OGTT at 26-28 weeks in patients with following risk factors:
i. Diabetes mellitus in first degree relative
ii. Advanced maternal age (35 at EDC)
iii. Obesity (BMI 27 at booking)
iv. Previous unexplained stillbirth, neonatal death or second trimester abortion; or previous macrosomic baby (4kg)
v. Multiple pregnancy
b. Patients with previous history of GDM, PCOS or long-term oral steroid:
Perform OGTT at booking, and if normal, repeat OGTT at 26- 28 weeks
c. Patients with foetal macrosomia (AC 97th centile) or polyhydraminos not yet accountable by any causes:
Perform OGTT at the time of diagnosis unless it was performed within 2 weeks.
d. Patients with glycosuria on two or more urine samples:
Perform OGTT at the time of diagnosis unless it has been performed within 2 weeks.
2. Postnatal OGTT
a. Indication:-Macrosomia (4 kg) not explanable by other risk factors such as maternal obesity, post-term pregnancy
b. Timing:-3 days after normal diet (unrestricted, carbohydrate rich diet)
c. In case OGTT cannot be performed before discharge, arrange OGTT as day case, or refer to private sector for OGTT,
with memo to the patient stating postnatal OGTT 3 days after resuming normal diet to screen for GDM.
3. Reference range of 75g OGTT
Fasting plasma level < 5.5mmol/L; 2h plasma level < 8mmol/L
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INTRAPARTUM MANAGEMENT OF DIABETES MELLITUS
1. Insulin dependent DM/GDM

a. Management in antenatal ward during latent phase or phase of cervical ripening for induction of labour:
i. No need to fast patient
ii. Give usual dose of insulin
b. Management in labour ward:
i. Inform on call medial officer
ii. Check blood glucose and RFT Q4H, X-match
iii. Check H'stix Q1H
iv. Check urine ketone after voiding
v. Give insulin infusion using syringe pump, and crystalloid solution according to sliding scale
vi. Use syringe pump for oxytocin infusion
c. Elective Caesarean section
i. Check blood glucose, RFT, X-match on day of admission
ii. Fast after midnight
iii. Omit morning dose of insulin
iv. Check H'stix before operation, and then Q1H
v. Give insulin infusion using syringe pump, and crystalloid solution according to sliding scale
2. Insulin sliding scale for DM/GDM patients:
Histx (mmol/L) Actrapid (unit/hr) Fluid (500ml Q4H) Action

<4.0 0 5%-Dextrose /
4.0-7.0 0 Hartmann's /
7.1-9.0 1 Hartmann's /
9.1-11.0 2 Hartmann's /
11.1-17.0 3 Hartmann's Inform MO & consult endocrinologist
17.1-28.0 4 Hartmann's Inform MO & midcall 1,consult endocrinologist
>=28.1 6 Hartmann's Inform MO & midcall 1,consult endocrinologist
Remark:
a. Insulin should be given through a syringe pump.
b. Actrapid should be used and diluted with isomolar Haemaccel/gelofusin to a concentration of 1U per ml (49.5 ml
isomolar Haemaccel/gelofusin + 0.5 ml Actrapid).
3. Non-insulin treated DM/GDM

a. Management in labour ward:
i. Same as insulin dependent DM/GDM except:-
(1) Check Hstix Q4H and
(2) No need to check RFT unless insulin infusion is required
b. Give insulin according to sliding scale
c. Elective Caesarean section same as insulin dependent DM/GDM except that no need to check RFT, unless insulin
infusion is required.
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POSTPARTUM MANAGEMENT OF DIABETES MELLITUS
1. Insulin dependent DM/GDM
a. When diet is not resumed continue insulin and crystalloid infusion according to the sliding scale.
b. When diet is resumed
i. Stop insulin, dextrose or Hartmann infusion.
ii. For GDM patients:
- Allow normal diet.
- Check Hstix at fasting and postprandial for 1 day
- Advise for 75g OGTT at 6 week postpartum
iii. For EDM patients:
- Give pre-pregnant DM diet.
- Resume pre-pregnant dosage of insulin or oral hypoglycemic agents, and consult endocrinologist for fine
adjustment and follow up.
- Check Hstix at fasting and postprandial
2. Non-insulin treated DM/GDM
a. When diet is not resumed:-
i. Stop insulin infusion and sliding scale, if any.
ii. Check Hstix Q4H
iii. Give Hartmanns solution (or 5%dextrose if H"stix <4mmol/L) 500ml Q4H.
b. When diet is resumed:-
i. Stop crystalloid infusion, and insulin, if any.
ii. For GDM patients:
- Allow normal diet. No need for Hstix monitoring.
- Advise for 75g OGTT at 6 week postpartum
iii. For EDM patients:
- Give pre-pregnant DM diet and check Hstix at fasting and postprandial for 1 day.
- Refer to endocrinologist.
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3. Preeclampsia
Hypertension in pregnancy
Definition of hypertension in pregnancy
1. Arterial diastolic pressure:
a. 110mmHg on any occasion, or
b. 90mmHg on 2 or more occasions at least 4 hours apart
2. Definition of proteinuria in pregnancy
a. Daily urine protein output of 300mg, or
b. Spot urine protein/creatine ratio of > 30mg/mmol
c. 2 clean-catch mid-stream or catheter specimens of urine collected at least 4 hours apart with
i. 1g albumin/l or2+ on reagent strip, or
ii. 0.3g albumin/l or >= 1+ on reagent strip if urine pH is <8 or specific gravity is < 1.030
Causes of hypertension during pregnancy

1. Transient elevation:- also called white-coat hypertension, related to stress and anxiety
2. Pregnancy induced hypertensive disorders:
a. It can be pregnancy induced hypertension, pre-eclampsia or eclampsia
b. This group of disorders may be superimposed with pre-existing hypertension
c. Hypertension induced by pregnancy almost always occurs after 20 week, except in rare cases such as molar pregnancy.
3. Pre-existing hypertension:
a. Also called chronic hypertension
b. Most are primary (or essential) but occasionally it may be secondary to:
i. Renal disorders such as lupus glomerunephritis
ii. Endocrine disorders such as phaemochromocytoma or cushing syndrome
iii. Vascular disorders such as co-arctation of aorta
c. the diagnosis of pre-existing hypertension is made usually because there is history before pregnancy, or the hypertension
is noted at the first in pregnancy, but before 20 week when pre-eclampsia is unlikely
4. Unclassified hypertension:
a. In some situation it may be difficult to differentiate whether the hypertension is due to pre-existing disease or induced by
pregnancy, therefore it is said to be unclassified
b. For example, when a patient comes to the first booking at 25 week of gestation, and is noted to have hypertension, we are
not certain whether it is pre-existing or pregnancy induced, as there is no record of the preceding blood pressure. It is
then belonged to unclassified group
c. Management of this group of patient depends on the clinical symptoms and signs, and may be treated as pre-eclampsia if
it progresses
1. How to differentiate transient hypertension from pre-eclampsia clinically?
2. When a patient comes to you at 28 weeks of gestation for the booking visit, and is noted to have blood pressure of 150/95.
What is your management?
Protocol, as of March 2006

1. Diagnostic criteria for hypertension in pregnancy
SBP 140 mm Hg or DBP 90 mm Hg on 2 occasions at 4 hours apart, or
SBP 160 mm Hg or DBP 110 mm Hg at any occasion
2. Diagnostic criteria for significant proteinuria in pregnancy
a. Urine protein 0.3 g/d (24-hour urine collection should always be used for the diagnosis of significant proteinuria unless
the clinical urgency dictates immediate delivery)
b. Spot urine Protein to creatinine ratio 30 mg/mmol which usually equivalent to > to 0.3 g proteinuria / 24 hours can be
used as an alternative
c. Urine albustix 2+ usually suggest significant proteinuria but should always be confirmed by 24 hour urine or spot urine
protein to creatinine ratio
d. Urinary tract infection should be excluded by MSU
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Blood pressure measurement
Equipment
1. Sphygmomanometer
2. DINAMAP (stands for 'Device for Indirect Noninvasive Automatic Mean Arterial Pressure')
Method of blood pressure measurement in obstetric patients

a. Use a correct size of cuff for each patient
b. Hypertension in obese patients is over-diagnosed if the cuff is too small in relation to the arm circumference:-
Arm circumference (cm) Appropriate cuff size (cm2)
<33 Regular cuff (12x23)
33-41 Larger cuff (15x33)
>41 Thigh cuff (18x36)
c. Correct positioning of the patient during measurement
i. Should be measured with the cuff at the level of the heart, with the patient either
ii. Sitting position, or lying on a bed or couch on the right side at 30 degrees of lateral tilt
d. Use of the correct phase of the Korotkoff sounds in measuring diastolic pressure:- either use Korotkoff sound IV (the
sounds become muffled) or Korotkoff sound V (the sounds disappear) to define the diastolic pressure.
Preeclampsia
Introduction
It is a common disorder, peculiar to pregnancy, characterized by hypertension and proteinuria (see hypertension in pregnancy for
definition of hypertension and proteinuria). It is a multisystem disorder involving CNS, hepatorenal system, and coagulation. It
invariably progresses as pregnancy advances, and can only be cured by delivery.
Definition
1. Gestation onset after 20 weeks; and
2. Arterial pressure
a. 170/110 mmHg or more on any 1 occasion; or
b. 140/90 mmHg or more on 2 occasions at least 4 hours apart; and
3. Proteinuria
a. 300 mg or more in 24 hours; or
b. Spot urine protein/creatinine ratio 30mg/mmol or more.
Incidence
- 6% in Caucasian
- 2% in Hong Kong Chinese
Risk factors (RR:-relative risk)

1. Pre-existing medical diseases
a. Renal diseases (RR 20:1)
b. Chronic hypertension (RR 10:1)
c. Antiphospholipid syndrome (RR 10:1)
d. Diabetes mellitus (RR 2:1)
2. History of
a. Previous pre-eclampsia
b. Pre-eclampsia in family (RR 5:1)
3. Pregnancy associated
a. Twin pregnancy (RR 4:1)
b. Nulliparity (RR 3:1)
c. Maternal age < 15 or > 40 years
d. Hydrop foetalis (Rhesus iso-immunisation, alpha-thalassaemia major)
e. Pregnancy by a new partner
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Pathophysiology
The exact mechanism is unknown. It is characterized by:-
1. Generalized vasoconstriction, leading to hypertension and reduction in blood volume.
2. Widespread endothelial damage, leading to:-
a. Capillary leaking of protein and proteinuria
b. leaking of fluid to extravascular space resulting in peripheral edema and pulmonary edema, and reduction in
intravascular volume
These pathological changes probably start in the early second trimester as follow:
1. Stage 1:-starts before 20 weeks and causes no symptoms
a. Failure of trophoblastic invasion of spiral arterioles which normally results to vasodilatation of vessels walls
b. Placenta is perfused under high pressure because of the vasoconstriction effect
c. Local endothelial damage causes aggregation of platelets, fibrin and lipid-laden macrophages (acute atherosis) and
microthrombi formation. Spiral arterioles become further occluded
2. Stage 2:-Manifestation of disease
a. Ischaemic placenta releases an unknown but apparently blood-borne substance, which leads to widespread endothelial
cell damage, causing generalised vasoconstriction, increased vascular permeability, and clotting dysfunction
b. Because of the high resistance, the uteroplacental blood flow decreases, resulting in malnutrition and hypoxia of foetus
Clinical manifestation
1. Onset
a. At any time after 20 week, but most commonly in the third trimester near term.
b. In practice it seldom occurs before week 24.
2. Symptoms
a. Usually asymptomatic with detection of high blood pressure and proteinuria on routine check up
b. Minority would present with symptoms of impending eclampsia
c. Occasionally present with complications of PET such as convulsion and abruptio placentae
Symptoms of impending eclampsia Comlications of PET

1. Hypertension: arterial pressure 160 mmHg systolic or Maternal
110 mmHg diastolic on two occasions at least 6 hours 1. DIC / HELLP syndrome (10-20%)
apart with the patient at bed rest 2. Pulmonary edema / aspiration (2-5%)
2. Proteinuria: 5g in 24 hour urine collection or 3+ on 3. Liver failure or haemorrhage (<1%)
dipstick in at least two random clean catch samples at 4. Acute renal failure (1-5%)
least 4 hours apart 5. Eclampsia (<1%)
3. Oliguria (500 ml in 24 hours) Foetal
4. Cerebral signs: headache, papilloedema, blurred vision 1. IUGR
or altered consciousness 2. Preterm delivery
5. Hyper-reflexia and sustained ankle clonus 3. Abruptio placentae
6. Epigastric pain due to subcapsular haemorrhage
7. Pulmonary oedema or cyanosis
8. Thrombocytopenia
9. Impaired liver function
10. Intrauterine growth restriction or fetal growth restriction
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Management
1. Principles
a. The disease can only be cured by delivery.
b. Aims to minimise risk of prematurity, and avoid maternal and foetal complications of pre-eclampsia
c. Depends on severity of disease and maturity of the pregnancy:
i. If the pregnancy is >34 weeks, deliver the pregnancy to prevent progression of the disease
ii. If the pregnancy is premature and disease is mild, try to prolong the pregnancy to reduce the risk of preterm delivery
iii. If maternal and foetal complications already occur, should consider delivery regardless of maturity, or it will end up
with maternal or foetal mortalities.
Maturity Mild Severe
< 34 - Steroid to enhance fetal lung maturity - X match for blood, platelet, FFP
weeks - Close monitoring of BP in hospital - Correct the coagulopathy: platelet transfusion, FFP
- Monitoring of albuminuria and Input/output chart - Control BP: IV antihypertensive
- Monitoring of biochemistry and haematological - Magnesium sulphate: prophylactic for eclampsia
parameters : CBP, RFT, LFT, PT/APTT (twice - Monitor CTG for fetal well being
weekly) - Arrange emergency CS when the mother is
- USG for foetal growth (every 2 weeks) and liquor stabilized
volume (weekly)
- Monitor CTG for fetal well being (twice weekly)
- Cross-match
- Delivery if maternal deterioration or foetal
compromise
>34 - Assess cervical status for induction of labour - Give MgSO4 and arrange emergency CS as soon as
weeks - Investigation: CBP, RFT, LFT, PT/APTT possible
- CTG monitoring for fetal well being
- Cross match
2. Surveillance
a. Aim to look for any deterioration of maternal or foetal condition that may require prompt delivery
b. Maternal surveillance
i. Blood pressure
ii. Urine protein
iii. Liver and renal function
iv. Clotting profile
c. Foetal surveillance
i. Foetal growth with USG
ii. Foetal well-being with CTG, Doppler studies and liquor volume
3. Control of blood pressure
a. Aim
i. To control blood pressure to prevent CVA
ii. Would not alter the progress of disease
b. Drugs
i. Hydralazine
ii. Methyldopa
4. Control of convulsion
a. Aim To prevent and recurrence of convulsion and stop acute convulsion
b. Drugs
i. Magnesium sulphate
ii. Diazepam
5. Fluid management
a. To maintain adequate intravascular volume and perfusion pressure
b. To prevent fluid overload which would result in pulmonary edema, and under-replacement would result in renal failure.
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1. General Peripartum management
a. Manage patient in the labour ward.
b. NPO. IV Fluid: Hartmann solution at 80 ml/hr. (1 pint Q6H).
c. Check CBP, platelet count, urate, renal and liver function tests, X-match (clotting profile is not required routinely if
platelet count is normal).
d. Maternal Monitoring: BP every 15 minutes, U/O hourly and manage oliguria accordingly (see below)
e. Foetal Monitoring: CTG.
f. Advise epidural aneasthesia for pain relief if no contraindication
g. Give anti-hypertensive or anti-convulsant according to clinical condition (see below).
h. Use syntocinon instead of syntometrine or ergometrine in third stage of labour. Use infusion pump for syntocinon
infusion and adjust maintenance fluid accordingly.
2. Diagnostic criteria of severe pre-eclampsia
a. Severe hypertension (SBP 170 mmHg or DBP 110mmHg on 2 or more occasions) with significant proteinuria, or
b. Moderate hypertension and significant proteinuria, with any symptom or sign of impending eclampsia, such as
i. Neurological:-ankle clonus, severe headache, persistent visual disturbances, papilloedema
ii. Hepatological:-epigastric pain +/- vomiting, liver tenderness, impaired liver function (ALT > 70)
iii. Haematological:-thrombocytopenia < 100, disseminated intravascular coagulation; haemolysis
c. Other clinical features which also indicate the severity of the clinical condition and may be an indication of earlier
delivery
i. Renal insufficiency plasma creatinine 90 mol/l or oliguria (< 500 ml/24 h)
ii. Foetal growth restriction or features of utero-placental insufficiency
d. In case the clinical conditions warrant delivery in a case of severe pre-eclampsia, MgSO4 is indicated for the
prophylaxis of eclampsia
3. Management of oliguria (U/O < 20 ml/hr for 2 hours):
a. Fluid challenge with 250 ml of Hartmanns solution over 1 hour, if no evidence of pulmonary edema or heart failure.
b. Avoid rapid fluid loading unless in hypovolaemic shock. Discuss with mid-call 1 for further fluid challenge. Discuss
with anaethetist to insert CVP line if oliguria does not improve in the next hour after fluid challenge.
c. Give IV furosemide 20-40 mg if there is pulmonary oedema.
d. Inform senior call if pulmonary edema or heart failure occurs.
e. Stop any MgSO4.
4. Indications for anticonvulsant prophylaxis
a. SBP 170 mmHg, or DBP 110 mmHg, MAP 125mmHg
b. Proteinuria 3 gm/24hr (or 3+ dipstix test)
c. Symptoms and signs of impending eclampsia
d. Complications such as oliguria, pulmonary oedema, DIC
e. Elevated bilirubin/transaminases or thrombocytopenia < 100x109/l
5. Indications of anti-hypertensive treatment
a. Indicated when SBP 160 mmHg or DBP 100 mmHg or at a lower threshold if there symptom and sign of
impending eclampsia, or serious condition like HELLP syndrome
b. IV Labetalol
i. First line for intrapartum BP control
ii. Stop labetalol if maternal heart rate falls below 70/min
iii. Avoid in the presence of pulmonary edema, heart failure or with asthma
c. IV Hydralazine
i. Second line for intrapartum BP control if labetalol fails or is contraindicated
ii. Consider other alternative antihypertensive if hydrallazine fails to control BP or causes maternal side effects (e.g.
tachycardia >120/min)
iii. Caution:-Maternal hypotension may occur with bolus or infusion regimen
d. PO Nifedipine Should only be given as oral and preferably used in postpartum
e. PO labetalol For BP control in postpartum
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6. Postpartum management for pre-eclampsia
a. Investigate for underlying cause if the case is an early onset pre-eclampsia
b. BP control:
i. Use Adalatretard: 20 mg - 40 mg bd and/or labetalol 200 mg bd - 400 mg tid
ii. Avoid methyldopa as it may increase the risk of postpartum depression
iii. Consult physician for refractory case
iv. At discharge from postnatal ward, anti-hypertensive drugs can be tailed off gradually over 2-4 weeks with dose
revision at weekly to biweekly interval with BP monitored at ward follow up.
c. Postnatal follow up in General clinic at 6 weeks to review blood pressure and proteinuria by urine albustix
v. Renal function and 24 hour urine collection are not required routinely except renal impairment at the diagnosis
of pre-eclampsia or persistent positive albustix at postnatal follow up
vi. CBP and LFT at 1 week before follow up as indicated in case of HELLP syndrome
d. Refer patient to physician if hypertension or proteinuria (according to 24 hour urine result) still persists after
puerperium
e. Recheck CBP / LFT / RFT / 24 hour urine collection 1 week before FU only when previous results showed impairment
f. When hypertension or proteinuria persist at Postnatal FU, check 24hr urine for protein and creatinine clearance and
refer to medical
1. You have a patient who is just diagnosed to have pre-eclampsia with BP 150/95 and 1+ proteinuria at 32 weeks of gestation.
What is your assessment and plan of management?
2. Supposed the above patient has been stable for a week (now at 34 weeks of gestation). She suddenly complains of vaginal
bleeding and uterine contraction pain. What is the possible diagnosis and how would you manage her?
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Eclampsia
Definition
Presence of convulsions in addition to pre-eclampsia, probably resulted from cerebrovascular vasospasm, or cerebral oedema.
Incidence
About 0.1% of all pregnancies
1. Onset:
a. In vast majority of cases it is preceded by several days and often weeks of clinically evident PET
b. In a very few cases an unheralded fulminant onset occurs
c. 50% occur antepartum, 25% intrapartum, 25% postpartum
d. Most of the postpartum convulsions occur within 1 day of delivery but seldom beyond 3 weeks
2. Symptoms:
a. Prior to convulsions, patients usually have restlessness, tremulousness and facial twitching
b. Grand mal seizures with loss of consciousness
3. Signs: Prior to convulsions, there may be hyper-reflexia and sustained clonus, with Papilloedema
Differential diagnoses of convulsions during pregnancy

- Pre-existing epilepsy
- Cerebral lupus
- Meningitis
- Space occupying lesions
1. General measure
a. Call for help, inform medical officer, mid-call, senior call and anaesthetist.
b. Lie patient in left lateral position, Maintain airway and give 100% O2
c. Documentation of the event and duration of convulsion
2. Anti-convulsants
a. Diazepam is used to terminate any ongoing convulsion. Regimen: 5-10 mg slow IV bolus (given over about 1 min.)
b. MgSO4 is used to prevent further recurrent convulsion
i. If eclampsia occurs before commencement of MgSO4, start loading dose infusion over 5 min
ii. If eclampsia occurs during initial loading dose, complete the loading dose over 5 min
iii. If eclampsia occurs during MgSO4 maintenance infusion, additional 2 gram bolus of MgSO4 (4 ml of 50%
MgSO4 diluted with normal saline into 10 ml) given over 5 minutes
c. Recurrent eclampsia can be managed with a further 2 gram bolus of MgSO4 but alternative anti-convulsant or
intubation should be considered if a total 10 gram of bolus has been given
3. A consultant or specialist in maternal medicine should be involved in case of eclampsia
4. Investigate for underlying cause if the case is an early onset pre-eclampsia
5. Oral antihypertensive can be used as to control BP if indicated
a. Use Adalat Retard: 20 mg - 40 mg bd and/or labetalol 200 mg bd - 400 mg tid
b. Avoid methyldopa as it may increase the risk of postpartum depression. Consult physician for refractory case
6. At discharge from postnatal ward, antihypertensive drugs can be tailed off gradually over 2-4 weeks with dose revision at
weekly to biweekly interval with BP monitored at ward follow up.
7. Postnatal follow up in General clinic at 6 to 8 weeks to review blood pressure and proteinuria by urine albustix
a. Renal function and 24 hour urine collection are not required routinely except renal impairment at the diagnosis of
pre-eclampsia or persistent positive albustix at postnatal follow up
b. CBP and LFT at 1 week before follow up as indicated in case of HELLP syndrome
8. Refer patient to physician if hypertension or proteinuria still persists after puerperium
9. Delivery
Baby should be delivered immediately after stabilisation of the mother. Caesarean section is usually the choice, unless
the second stage of labour is reached and instrumental delivery can be attempted.
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1. How to differentiate eclampsia from epilepsy clinically?
2. You are the junior on-call obstetrician and are informed that a 24 years old lady at 30 week of gestation was brought to the
A&E Department by her husband. She was noticed by her husband at home that she suddenly collapsed and convulsed for 2
minutes. The patient is now awake. What are you going to do?
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HELLP syndrome
Definition
It is an acronym formed from Haemolysis, Elevated Liver enzymes, and Low Platelets (thrombocytopenia). It is a disorder
specific to pregnancy, and is thought to be one of the complications or variants of pre-eclampsia.
Clinical features
1. Features of pre-eclampsia
2. Features of HELLP:
a. Complete blood picture
i. Anaemia
ii. Thrombocytopenia
b. Liver function test
i. Elevated bilirubin
ii. Elevated ALT
3. Other features Impaired clotting profile
Management
1. Immediate delivery of pregnancy
2. See management of pre-eclampsia
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4. Other maternal medical diseases
Heart disease
Introduction
Heart diseases are a common medical disorder affecting 1% of all pregnancies.
Types of heart diseases in pregnancy

1. Common
a. Rheumatic heart diseases
i. Relatively common in young female, especially immigrants from Mainland China
ii. Can be complicated with heart failure, arrhythmia, endocarditis and thromboembolism
b. Mitral valve prolapse
i. The commonest heart disease in young female
ii. Usually does not cause major problems such as heart failure
iii. But may present with palpitation, and increase risk of endocarditis if the valve is damaged
c. Arrhythmia
i. Atrial and ventricular ectopic beats are more frequent in pregnancy. They are benign and require no treatment
ii. Superventricular tachycardia is also common and requires treatment
iii. Atrial fibrillation may complicate rheumatic heart diseases (especially mitral stenosis)
2. Uncommon
a. Congenital heart diseases
b. Ischemic heart diseases
Maternal risks
1. Heart failure
2. Infectious endocarditis
3. Thromboembolism
4. Arrhythmia
Assessment
Cardiac function (according to New York Heart Association Functional Classification)
- Class I:-symptoms free
- Class II:-distressed on moderate exertion
- Class III:-distressed on slight exertion
- Class IV:-distressed at rest (cardiac failure)
What should medical students know

Rheumatic heart disease with mitral stenosis. This is a very good example to illustrate how pregnancy is affected with heart
disease, with all maternal risks mentioned above are possible to occur during pregnancy and labour.
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Mitral stenosis
This is a good example to illustrate the various ways how a heart disease can affect a pregnancy.
Effect of pregnancy on the disease
1. Left atrial outflow obstruction results in:
a. Reduction in ventricular filling and hence reduction in cardiac output (risk of heart failure).
b. Elevation of left atrial, pulmonary venous and pulmonary capillary wedge pressure (risk of pulmonary oedema).
c. Abnormally increase in left atrial size which may affect the atrial condition (risk of atrial fibrillation).
d. The risk is higher during pregnancy because:
i. During antepartum:-there is an increase in cardiac demand; the increase in heart rate further impairs ventricular filling;
increase in blood volume further exaggerates pulmonary oedema.
ii. During intrapartum:-cardiac demand further increases because of pain and pushing in second stage.
iii. During postpartum:-about 500ml of blood volume returns from the uterus to the circulation as the uterine volume
shrinks after delivery (autotransfusion).
2. In addition, the damaged mitral valve or the replaced valve is associated with increased risk of endocarditis.
3. There is also an increased risk of thromboembolism secondary to atrial fibrillation and a mechanic valve replacement.
Effect of disease on pregnancy

1. Patient with significant disease will have increased risk of intrauterine growth restriction.
2. It can cause atrial fibrillation, with increased risk of DVT / PE especially during pregnancy.
Pre-conceptional counselling
- Patient should be assessed for the physical and physiological fitness of bearing a pregnancy, and counselled on the risk of
undergoing pregnancy.
- The functional class status is assessed with symptoms and signs of cardiac failure and atrial fibrillation.
- Echocardiogram to determine the severity of the disease, ventricular function and diameter of mitral valve.
- Patient with severe disease may become suitable for pregnancy after valvotomy or valvular replacement.
Management during pregnancy

- Monitor maternal cardiac status by the functional class, cardiac symptoms, and echocardiogram assessment.
- Monitor foetal growth and foetal well-being by serial ultrasound scan for growth parameters and liquor volume, and CTG.
Management in labour
- Antibiotic cover at the onset of labour or rupture of membranes in order to prevent bacterial endocarditis.
- Close monitoring of maternal vital sign, fluid input and output. Severe cases will require arterial line (monitor systemic
blood pressure), CVP line (monitor the central venous pressure) or even Swan Ganz catheter (monitor the pulmonary
pressure).
- Continuous monitoring of foetal heart tracing with CTG.
- Avoid fluid overload.
- Prophylactic instrumental delivery to avoid strenuous effort during the bear down.
- Avoid syntometrine as the drug will increase the afterload; slow intravenous syntocinon at third stage (too rapid injection
will lead to a drop in the systemic blood pressure and hence reduce the venous return).
- IV diuretics (frusemide) at the third stage to reduce fluid overload from autotransfusion of blood from the uterine circulation
after the delivery.
- Continue to monitor input and output after the delivery as the patient will be at risk of pulmonary oedema within 48 hours
postdelivery.
Other Management
- Adjust the dosage of anti-coagulants to prevent thromboembolism
- Anti-arrhythmic agents to control atrial fibrillation.
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Anaemia
Common types of maternal anaemia during pregnancy
1. Physiological anaemia
a. Low haemoglobin due to dilution effect in pregnancy, because the increase in plasma volume is relatively higher than the
increase in red cell volume (see physiological changes in pregnancy)
b. Haemoglobin level is usually not less than 10g/dL
2. Nutritional anaemia
a. Synthesis of haemoglobin is inadequate because of nutritional deficiency in iron, folate, and vitamin B12
b. Increase risk in multiple pregnancy, maternal malnutrition
3. Inherited anaemia
Deficient synthesis of haemoglobin because of inherited diseases such as thalassemia and sickle cell anaemia
4. Post-haemorrhagic anaemia
It is common to have anaemia after heavy postpartum haemorrhage or antepartum haemorrhage

1. Investigations
a. Check peripheral blood smear and Fe / TIBC
b. If MCV >100 fL, refer to Macrocytosis
c. If MCV <= 80 fL, check Hb pattern, husband"s CBP and Hb pattern
2. Refer to Thalassemia, Iron deficiency, or Macrocytosis for specific treatment.
3. Give iron supplement for NCMC anaemia of unknown cause, unless there is known history of iron overload.
4. If Hb 8 g/dL:
a. Follow up in midwife clinic 4 weeks after supplement with CBP taken 1 day before the appointment
b. Discharge patient to MCHC if Hb > 10 g/dL and continue supplement
c. Refer back to doctor if Hb does not rise despite supplement
5. If Hb < 8 g/dL:
a. Consider transfusion if symptomatic
b. Admit as soon as possible for investigation and treatment if Hb < 6g/dL
c. Follow up in medical obstetrics clinic 2 weeks after treatment with CBP taken 1 day before the appointment
Macrocytosis
1. Investigations
a. Mild macrocytosis (MCV between 100 fL and 110 fL)
i. Check peripheral blood smear
ii. No need for further investigation unless
- Smear show features of megaloblastic anaemia
e.g. hypersegmented neutrophils and oval macrocytes on the blood film, then check Vit B12 and folate status.
- Clinically suspicious of thyroid or hepatic disorder, then check TFT or LFT.
b. Moderate to severe macrocytosis (MCV > 110 fL)
i. Check peripheral blood smear, serum vitamin B12, serum and red blood cell folate
ii. Check TFT or LFT according to clinical suspicion
2. Diagnosis
a. Vitamin B12 deficiency:
Serum vitamin B12 level below the laboratory normal range in the presence of hypersegmented neutrophils and oval
macrocytes.
b. Folate deficiency:
RBC folate level below the laboratory normal range in presence of hypersegmented neutrophils and oval macrocytes.
c. Serum vitamin B12 or RBC folate slightly below the laboratory reference range in the absence of hypersegmented
neutrophils and oval macrocytes should not be regarded as genuine deficiency.
3. Treatment Admit patients under medical obstetrics team and consult haematologist. Vitamin B12 supplement should only
be commenced after haematologists assessment.
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Iron deficiency
1. Diagnosis
a. Low serum iron and high TIBC, or
b. Low serum ferritin
2. Investigation
a. No need to check faecal occult blood or parasite unless clinically suspicious
b. Admit patient and consult physician immediately if patient complains melena
3. Treatment FeSO4 200mg tds or fortifer 1 tab qd if intolerant to FeSO4
Asymptomatic bacteriuria
It is bacterial growth in a concentration of 10,000 or more per ml of urine without symptoms. This is present in about 8% of
pregnant women, and about half of them will develop signs of urinary tract infection during pregnancy if untreated.
Disseminated intravascular coagulopathy (DIC)

Obstetric and gynaecological causes of DIC
1. Septic abortion
2. Abruptio placentae
3. Pre-eclampsia
4. Massive haemorrhage such as uncontrolled postpartum haemorrhage
Investigation results
1. Low platelet
2. Increased INR and APTT
3. Increased D-dimmer
4. Increased fibrin-degradation products
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Thrombocytopenia
Definition:-Low platelet count

1. Classification
a. Gestational thrombocytopenia
b. Idiopathic thrombocytopenic purpura (ITP)
c. Thromboctyopenia due to other autoimmune disease
d. Thrombocytopenia due to HELLP, pre-eclampsia and acute fatty liver of pregnancy
2. Diagnostic criteria for gestational thrombocytopenia and ITP
a. Gestational thrombocytopenia
i. Platelet 100*109/L, and
ii. in the absence of underlying pre-eclampsia or HELLP, autoimmune diseases, or history of thrombocytopenia
outside pregnancy
b. Idiopathic thrombocytopenia purpura
i. Platelet < 100 *10E9/L, or
ii. Known history of thrombocytopenia before pregnancy, and
iii. In the absence of underlying pre-eclampsia or HELLP and autoimmune diseases
c. Remarks:
i. No need to screen for auto-immune diseases unless clinically suspicious
ii. Definite diagnosis of gestational thrombocytopenia and ITP can only be made retrospectively after pregnancy.
3. Out-patient management for gestational thrombocytopenia
No need for monitoring platelet count if there is no bleeding tendency and initial platelet >=100*10E9/L,
4. Out-patient management for ITP
a. Mild thrombocytopenia (Plt = 100-140*109/L) Monitor Plt at 28 and 36 weeks in general obstetric clinic
b. Moderate thrombocytopenia (plt = 50-100*109/L) Monitor Plt every 4 weeks in general obstetric clinic
c. Severe thrombocytopenia (plt < 50*109/L)
i. Admit patient and consult haematologist.
ii. Discharge to medical obstetrics clinic when Plt >= 50*10E9/L after treatment.
iii. Monitor Plt every 2 weeks in medical obstetrics clinic.
iv. Arrange anaesthetic consultation
5. Intrapartum management for all thrombocytopenic patients
a. Check CBP on admission
b. Notify anaesthetist early in labour ward if Plt <100*109/L
c. Intramuscular injection is contraindicated if Plt <80*109/L (Consider intravenous pethidine vs. IMI pethidine)
d. Reserve platelet concentrate if platelet < 50*109/L
e. Give hydrocortisone cover if patient has been on long term steroid.
6. Postpartum management
a. For gestational thrombocytopenia
i. Check platelet at 6 weeks after delivery in postnatal ward
ii. Follow up in midwife clinic at 8 weeks to review platelet result while routine postnatal care should be in MCH
iii. Refer to haematologist clinic if platelet still <140*10E9/L
b. For idiopathic thrombocytopenia Arrange follow up with haematologist
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Thromboembolism
Epidemiology:
Less common in Chinese than in Caucasian, incidence around 1 in 300 in PWH, majority in postnatal period, predominantly calf
vein DVT, above knee DVT less than 1 in 1000 pregnancy.
Risk factors of deep vein thrombosis:

Constitutional factors:
- Advanced age (>40)
- Gross obesity
- Smoker
- Previous history of DVT
Charcots Triad
- Stasis:- Caesarean section, Immobilisation (for > 4 days)
- Endothelial injury:- antiphospholipid syndrome, pre-eclampsia.
- Hypercoagulability:- pregnancy itself (due to oestrogen), Thrombophilia (protein C/S deficiency, anti-thrombin deficiency)
Clinical features:
- Calf and leg swelling, pain
- Leg swelling
- Homans' sign may be present (active or passive dorsiflexion of the foot associated with pain incomplete dorsiflexion or
flexion of the knee to release tension. This sign may be absent in about 50% of cases of DVT
- Dyspnoea, respiratory distress, desaturation and chest pain are features of pulmonary embolism
Diagnosis:
High index of suspicion when a pregnant woman complains of unilateral calf pain and swelling, in particular within a few days
after caesarean section.
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Management:
1. Medical treatment - current treatment is either subcutaneous low molecular weight heparin (predominantly used in
antenatal DVT) or warfarin (predominantly used in puerperium)
a. Enoxaparin till post-delivery
b. Start warfarin at day 3 post-delivery (provided that there is no excess bleeding)
c. Then stop Enoxaparin when INR is between 2 to 2.5
2. General management
a. Above knee DVT - Slightly elevate the legs and bed rest for 1 or 2 days until calf pain resolves after medical
treatment, then encourage mobilisation, apply elastic stocking
b. Below knee DVT- Encourage mobilisation and elastic stocking.
3. Follow up
a. Patient can be discharged when she has been on the same dose of warfarin for 2 consecutive days.
b. It has been agreed with haematologist that patient will be seen in 1 weeks time in warfarin clinic
c. Follow up in medical obstetric clinic at 6 weeks postpartum
Prophylaxis
Protocol, as in 22 June 2002
1. Indicated in patients with previous history of
a. DVT, PE or thrombophilia;
b. Anti-phospholipid syndrome
c. Mitral stenosis with atrial fibrillation
d. Peripartum cardiomyopathy
e. Immobilisation such as observation in labour ward for a long period and after long operation
2. Physical measures:-elastic stocking, intermittent pneumatic compression during labour, caesarean section and early
puerperium
3. Medical:-subcutaneous low molecular weight heparin (Enoxaparin and Fraxiparine)
Pulmonary embolism
Embolism involving pulmonary vasculature with high mortality and needs intensive care support
Clinical Features
- Asymptomatic
- Dyspnoea, respiratory distress.
- Haemoptysis
- Desaturation and chest pain
- Loss of consciousness.
Investigations
- D-dimer
- Doppler USG
- V/Q Scan
- Venography
Treatment
- Urgent open embolectomy may be needed to clear the blood clots. Usually associated with deep vein thrombosis, especially
bilaterally
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Amniotic fluid embolism
It is a very rare but serious and unpredictable condition in which amniotic fluid enters the maternal circulation, resulting in acute
cardiorespiratory compromise and coagulation derangement.
Incidence
About 1 in 30000 pregnancies.
Risk factors
- Rupture of membranes
- Rapid labou
- Caesarean section
- Use of oxytocin
Mechanism
Amniotic fluid accesses directly into the maternal circulation through a defect somewhere near the placental site at a higher than
usual intrauterine pressure. The biochemical constituents of the amniotic fluid activate the coagulation cascade, and the foetal
squames may also plug into the pulmonary circulation resulting in failure of gaseous exchange.
Clinical features
The patient has a sudden onset of severe chest pain and difficulty in breathing, followed shortly by cyanosis and cardiorespiratory
collapse. Coagulation failure may present with postpartum haemorrhage or spontaneous bleeding from the puncture sites. 30% of
patients will die in the first hour, and the overall mortality is > 90%.
Diagnosis
- The diagnosis is mainly on clinical basis. It should be differentiated from other acute causes of cardiorespiratory arrest such
as acute myocardial infarction and pulmonary embolism, and causes of coagulation failure such as acute fatty liver and
abruptio placentae.
- The diagnosis may be confirmed by demonstration of amniotic debris and trophoblasts in pulmonary vasculature, by
aspirating blood from the pulmonary artery (via a Swan-Ganz catheter), or during postmortem examination.
Management
1. Cardiopulmonary resuscitation with circulatory support and artificial ventilation
2. Correction of coagulopathy
3. Correction of acidosis
4. Delivery of baby:
The foetus is unlikely to survive such a major insult, but immediate delivery by caesarean section carries a high maternal risk.
Therefore delivery should be undertaken after stabilization of the mother, and vaginal delivery is preferable.
Systemic Lupus Erythematosus (SLE)

1. Anti-cardiolipin antibodies: Higher rates of miscarriage and preterm labour.
2. Anti-Lo, anti-Ro: Congenital complete heart block.
3. Management:
a. Low dose aspirin for anti-cardiolipin
b. Low dose heparin for previous thromboembolism.
c. Prednisolone if flare up.
d. Monitor foetal growth and morphology.
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Antiphospholipid syndrome
Definition
Antiphospholipid syndrome (APS) is an uncommon autoimmune disorder characterised by:
1. Presence of one or both of the following auto-antibodies:-anticardiolipin antibodies (aCL) and lupus anticoagulant (LA), and
2. Presence of thromboembolic disorders, recurrent pregnancy loss, thrombocytopenia, or haemolytic anaemia; and
3. Less commonly, systemic or pulmonary hypertension.
Diagnosis
The diagnostic criteria include:
1. Two positive readings for LA and / or aCL at least 3 months apart, plus
2. At least one of the clinical criteria
3. The presence of auto-antibodies alone without clinical complications may not require treatment. Antiphospholipid syndrome
should also be differentiated from systemic lupus erythematosus (SLE), although they both have aCL and similar clinical
features.
Management
1. High-dose steroid and immunosuppression used for treating SLE are not recommended in APS.
2. Positive history of thromboembolism:- Patients are at high risk of recurrence of thromboembolism during pregnancy and
should be given heparin prophylaxis
3. Positive history of recurrent pregnancy loss alone:- Combination of low-dose aspirin and heparin (low molecular weight)
decreases the risk of recurrent loss.
Epilepsy
Introduction
Epilepsy affects 0.5% of women of child-bearing age and is the most common chronic neurological disorder complicating
pregnancy. The cause of majority of epilepsy is primary, but some are secondary to previous medical events like cranial surgery or
meningitis. The important points in obstetrics are:
1. Epilepsy should be differentiated from other pregnancy-related causes of convulsions such as eclampsia
2. Anti-convulsants are potentially teratogenic
3. It may be difficult to control the disease during pregnancy because:
a. The physioloigical changes during pregnancy may affect the pharmacokinetic of anti-convulsants
b. Patients may be fear of the foetal side effects and not compliant to treatment
Effect of pregnancy on epilepsy

Risk of relapse of convulsions
1. While half of the pregnant women have no changes in the frequency of convulsion, one-quarter of women have increased
frequency of convulsions, due to the reasons mentioned above.
2. Those women who have been fit-free for many years are unlikely to fit in pregnancy unless she discontinues her medication.
Effect of epilepsy on pregnancy

1. There is no direct effect on pregnancy in epileptics.
2. Indirect effects include:
a. Acute convulsions may result in physical trauma;
b. Status epilepticus may lead to hypoxic damage of both the mother and the foetus.
c. The baby has risk of developing epilepsy:
i. 4% when either parents has primary epilepsy
ii. 10% when there is a previously affected sibling
iii. 20% when both parents have epilepsy
d. Teratogenicity of anti-convulsants
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1. Pre-conception counselling
a. Because of teratogenic risk of anti-convulsants, patients on treatment should be given folic acid (5mg daily) for
at least 12 weeks prior to conception reduce risk of folic deficiency and neural tube defects.
b. Evaluate and optimize antiepileptic medication in conjunction with neurologist.
c. Monotherapy at the lowest effective dose is preferable.
d. Counsel on the importance of seizure control, drug compliance and teratogenic risk
2. Antentatal management
a. May consider discontinuation of the anti-epileptics if seizure-free for 2 years
b. Monotherapy, of phenytoin, carbamazepine or valpoate if needed, depends on the type of seizure, and there is little
difference between individual drug.
c. There is no need to change the type and dosage of anticonvulsants, or measure drug level provided that the
disease is under control.
d. Prenatal screening at around 20 weeks for congenital abnormalities, particularly neural tube defects and
cardiac defects should be provided
e. Because of possible hepatic enzyme-induction by anti-convulsants, vitamin K-dependent clotting factors may be
reduced. Vitamin K (10 mg PO daily) should be given in the last 4 weeks of pregnancy as prophylaxis against
haemorrhagic disease of newborn.
f. The four commonly used drugs:-Carbamazepine, Phenobarbitone, Phenytoin, Valpoic acid all cross the placenta and
have potential teratogenic effect
g. Neural tube defect is around 1%. Figures on other teratogenic effects such as Hydantoin syndrome, limb abnoramlity,
growth deficiency and mental deficiency are more variable.
h. In general, balancing the risks and benefits of anti-convulsant therapy favours continuation of the drugs.
i. Give Folic acid 5mg daily throughout pregnancy
3. Intrapartum management
a. Continue anti-epileptics, if any.
b. Time and mode of delivery not affected, manage as normal labour and delivery
c. Inform paediatrician for assessment at delivery
d. Vitamin K1 intramuscular injection to neonate as routine
e. If require anti-convulsant for prevention of eclampsia, consult neurologist if patient is on anti-convulsant already. In
general, the guidelines for pre-eclamptic anti-convulsants still apply.
4. Postnatal management
a. The neonate should be given vitamin K prophylaxis.
b. There is no contraindication to breast-feeding, caution if mother is on diazepam or high-dose phenobarbitone
c. When patients want hormonal contraception, higher dose of combined oral contraceptive or progestogen-only
pills should be advised.
d. Educate about safe child care in the context of possibility of fitting episode e.g. during bathing of baby
e. Consult neurologist for adjustment of anticonvulsant dosage after delivery if dosage has been increased during
pregnancy, otherwise early out-patient follow up would be adequate.
f. Advise on contraception:-efficacy of OCP may be reduced. High dose (50mcg E2) preparations should be
recommended if used.
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Acute fatty liver
This is a very rare but serious hepatic disorder specific to pregnancy. The incidence is about 1 in 10000 pregnancies. Similar to
pre-eclampsia, the aetiology and pathogenesis are unknown, but it occurs more commonly in primiparous women, in the third
trimester. As its name implies, the clinical occurrence is acute, and histologically, there is perilobular fatty infiltration of the liver
cells. This is different from that of the fatty changes due to obesity or alcoholism.
Clinical features
The presenting symptoms are of acute or subacute onset of epigastric pain, headache, nausea and vomiting which are shortly
followed by progressive jaundice, liver failure, coagulopathy, encephalopathy and renal failure. It is associated with high maternal
and foetal mortality.
Diagnosis
The diagnosis relies on the clinical features with deranged liver function and clotting profile. It should be differentiated from
HELLP syndrome, pre-eclampsia, and acute viral hepatitis. Liver biopsy is dangerous because of bleeding tendency.
Management
The mainstay of treatment is immediate delivery, supportive treatment including blood transfusion, and correction of clotting
disorders.
Appendicitis
Incidence
It is a common acute surgical condition during pregnancy:-1:1500 to 1:2000
Clinical features
1. It is more frequent in the first two trimesters
2. It is more difficult to diagnose as the clinical symptoms and signs are more vague than in non-pregnant women.
3. Delayed diagnosis and treatment are not uncommon in pregnancy and account for the high maternal and foetal morbidities
and mortalities.
4. Patients usually present with fever, nausea and vomiting, right-sided abdominal pain and tenderness. The site of the pain
changes with the position of the appendix which is pushed upwards by the gravid uterus. Signs of peritonitis may be masked
by the gravid uterus. White cells count is usually raised.
Complications
1. Maternal Peritonitis and maternal death (potentially fatal if delay in diagnosis)
2. Foetal Preterm labour, foetal distress, intrauterine death
Differential diagnoses
1. Related to genital organs:
a. Ectopic pregnancy (during the first trimester)
b. Torsion ovarian cyst
c. Red degeneration of fibroid
d. Abruptio placentae
e. Chorioamnionitis
2. Other surgical diseases:- Acute cholecystitis, pancreatitis
Management
1. Appendicectomy
2. Antibiotics
3. Monitor foetal well-being and maternal vital sign during the peri-operative period.
A 29-year-old lady at 30 weeks of gestation presented with one-day history of severe right lower quadrant pain preceded by
epigastric pain. It was associated with nausea, vomiting and fever. What are the differential diagnosis and how to make diagnosis?
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Thyroid disorder
Introduction
Thyroid disorders are common endocrine disorders affecting women at reproductive age. It may complicate pregnancy or cause
various gynaecological disorders.
Thyroid disorders in gynaecology

1. Hypothyroidism
a. Menorrhagia
b. Infertility
2. Hyperthyroidism
a. Amenorrhea
b. Infertility
Thyroid disorders in obstetrics

1. Hyperthyroidism
a. Causes
i. Due to the effect of human chorionic gonadotropin, there is usually transient hyperthyroidism during the first
trimester (see physiological changes in pregnancy). It is usually self-limiting but may be associated with hyperemesis
gravidarum.
ii. The most common cause of hyperthyroidism during pregnancy is Graves disease (95%), in which auto-immune TSH
receptor-stimulating antibodies (an IgG) can cross the placenta leading to foetal hyperthyroidism.
b. Complications
i. Uncontrolled hyperthyroidism results in various foetal complications:-abortion, IUGR, preterm labour, foetal
thyrotoxicosis (in Graves disease only). Rarely a foetal gotire may cause hypertension of the foetal neck, leading to
malpresentation.
ii. Maternal complications are thyroid storm, tracheal obstruction due to a retrosternal gotire.
c. Treatment
i. The mainstay of treatment is by antithyroid agents such as propylthiouracil and carbimazole.
ii. Beta-blockers may be required to control the cardiac symptoms before the hyperthyroidism is under controlled.
iii. Carbimazole is not used as the drug crosses placenta and may cause fetal hypothyroidism.
1. Newly diagnosed hyperthyroidism
a. Admit patient for endocrinologist's assessment
b. Propylthiouracil (PTU) is the preferred antithyroid drug
c. Check:
i. ATG antithyroglobulin antibody
ii. AMC antimicrosomal antibody
iii. If suspected transient gestational hyperthyroidism:-check red cell zinc
2. Transient gestational hyperthyroidism
a. Diagnosis (1) No feature of Graves' disease, (2) Normal red cell zinc; and (3) Clinically euthyroid
b. Monitoring Check TFT every 4 weeks in general obstetrics clinic until result returns to normal
3. Hyperthyroidism in remission
a. Check TSH, ATG and AMC (only if not checked in recent years) to predict postpartum thyroid dysfunction
b. If raised antibody, make sure patient has a follow up with the endocrinologist post delivery
c. If normal TSH, routine antenatal care
4. Hyperthyroidism on treatment
a. Review fT4 result and current treatment
b. Regular FU in medical obstetrics clinic (every 4 weeks if stable) and general obstetrics clinic
c. Monitor fT4 every 4-8 weeks during pregnancy, no need to check TSH unless suspicious of over-treatment.
5. If inadequate treatment
a. Admit to ward to consult endocrinologist
b. USG for foetal growth and CTG are recommended for uncontrolled hyperthyroidism
c. Inform paediatrician post delivery for neonatal assessment
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2. Hypothyroidism
a. Causes
Hypothyroidism can be resulted from iodine deficiency in endemic area, thyroiditis or post-surgical or radiation therapy
for previous hyperthyroidism.
b. Complications
Abortion, IUGR decreased intelligence quotient of the offspirngs.
c. Treatment
The treatment is by thyroxine replacement which does not cross the placenta.

1. Newly diagnosed hypothyroidism
a. Admit patient for endocrinologist's assessment
b. Check:
i. ATG antithyroglobulin antibody
ii. AMC antimicrosomal antibody
2. Hypothyroidism in remission
a. Check:
i. TSH instead of fT4 (a normal fT4 does not exclude subclinical hypothyroidism)
- Once if not on thyroxine replacement
- Every 4-8 weeks if on thyroxine replacement
- If normal TSH, routine antenatal care
- If raised TSH, admit to ward to consult endocrinologist
ii. ATG and AMC (only if not checked in recent years)
- To predict postpartum thyroid dysfunction
- If raised antibody, make sure patient has a follow up with the endocrinologist post delivery
3. Hypothyroidism on treatment
a. Review TSH result and current treatment
b. Regular FU in medical obs clinic (every 4 weeks if stable) and general obs clinic
c. Monitor TSH every 4-8 weeks
4. If inadequate treatment
a. Admit to ward to consult endocrinologist
b. Patients on thyroxine replacement usually requires an increment dose of 25-50% during first or second trimester of
pregnancy
c. USG for foetal growth and CTG are recommended for uncontrolled hypothyroidism
d. Inform paediatrician post delivery for neonatal assessment
Postpartum thyroiditis
1. It is now found to be a common complication of pregnancy (5-10%), although majority of the are subclinical. It is a kind of
autoimmune destructive lymphocytic inflammation, thought to represent an activation of a previously subclinical thyroiditis,
caused by rebound in levels of antimicrosomal antibodies as the immunosuppressive effects of pregnancy are reversed.
2. As a result of destruction, thyroxine is released from the gland in the initial phase of the disease. Afterwards, there may be
hypothyroidism when the thyroid reserve is depleted. Presentation is usually between 3 to 4 months It results in
hyperhyroidism in 40% cases, hypothyroidism in another 40%, and biphasic (initial hyperthyroidism followed by
hypothyroidism) in 20%.
3. Postpartum thyroiditis is also a common pregnancy-specific complication.
What are the signs of foetal thyrotoxicosis? and what is the most effective way to look for foetal thyrotoxicosis in a woman known
to have Graves disease? Which antithyroid agent, propylthiouracil or carbimazole is preferred during pregnancy?
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Labour Management
Intrapartum management is one of the most important area in Obstetrics. The aims are to ensure that the foetus is delivered in the
most optimal condition for gestation, while the potential hazards of childbirth and any underlying pathology to the mother are
minimised. It consists of the following aspects:
1. Maternal monitoring:-to ensure maternal well-being during labour and delivery, relief stress and anxiety.
2. Labour pain relief:-provides adequate and safe analgesia to the mother.
3. Intrapartum foetal monitoring:-to ensure foetal well-being during labour and delivery.
4. Monitoring the progress of labour:-to ensure the progress of labour is normal, look for any obstruction of labour and take
prompt actions.
5. Decision of mode of delivery:-to decide the most optimal time and the safest way of delivery which may involve instrumental
delivery or caesarean section.
6. All the above monitoring can be summarised in a partogram that facilitate the intrapartum management.
Management of first and second stage of labour

1. General Nursing
a. Nurse patient in semi-recumbent position during first stage, and prop-up during second stage of labour, unless
condition allows ambulation.
b. Keep nil by mouth unless specified by medical officer.
c. No need for routine cross-matching for all patients.
d. Provide adequate analgesia.
e. Record intrapartum monitoring on partogram.
f. Routine intrapartum monitoring
2. Progress of labour:
a. Vaginal examination(V.E.)
i. Q4H in the latent phase
ii. Q2H in the active phase
b. Inform medical officer if
iii. Cervical dilatation less than 1cm/h in the active phase
iv. Prolonged second stage (1 hour for nullipara, 30min for multipara)
3. Maternal well being:

a. BP/P Q1H, temp Q2H
b. Fluid balance chart
c. Urine for albumin (and ketone in EDM patients) after passing urine, or Q2H if foley catheter is inserted.
d. Adequacy of pain relief by Entonox, Pethidine or Epidural anaesthesia.
4. Fetal well being

a. Continuous fetal heart rate monitoring unless otherwise specified by medical officer
b. Meconium or blood stained liquor
c. Inform medical officer if CTG is abnormal
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Partogram
The partogram is a graphic display of progress in labour, with complete collection of information on the cervical dilatation,
presentation, station (descend) and position of the presenting part. There are also recordings of the intrapartum monitoring of the
maternal and foetal well-being, and administration of any drugs. The partogram facilitates the monitoring of the progress of labour,
diagnosis of dystocia, and continuation of intrapartum management and decision making.
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1. Normal Labour
Labour
Definition of labour
Onset of regular painful uterine contractions accompanied by
1. Effacement of the cervis
2. Dilatation of the cervix
3. Show.
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Initiation of labour
- It is not fully understood
- The main trigger is probably foetal rather than maternal
- It may involve foetal cortisol, and prostaglandins
- Once initiated, labour appears to be self-perpetuating
Three stages of labour

The labour process is divided into three stages:
1. First stage
a. It starts from the diagnosis of labour until the cervix is fully dilated (10cm for term pregnancy)
b. The foetal head engages, descends gradually into the pelvis and rotates
c. The cervix often dilates slowly for the first 3cm and is called the latent phase
d. Thereafter, average cervical dilatation is at the rate of 1cm/hour in nulliparous, and about 2cm/hour in multiparous
e. It normally would not last longer than 12 hours
2. Second stage
a. It starts from full dilatation of the cervix to the delivery of the foetus
b. Descent, flexion, and internal rotation of the foetal head are completed
c. Followed by extension and restitution (external rotation)
d. Maternal pushing is essential
e. It usually takes 40 minutes for nulliparous and 20 minute for multiparous.
3. Third stage
a. It starts from delivery of the foetus to delivery of the placenta
b. It normally lasts about 15 minutes
c. Normal blood loss is up to 500ml
Mechanism of vaginal cepahlic delivery

1. Engagement
The ovoid-shaped head normally enters the pelvis in the occipito-transverse position, because the transverse diameter of
the inlet is greater than the antero-posterior diameter
2. Descend
a. The foetal head descends further into the birth canal.
b. The degree of descent is measured by station.
c. During the descend, the foetal skull may change shape to adapt the maternal pelvis (moulding). Caput succedaneum is
usually formed by compression.
3. Flexion
The head also flexes as it descends further, so that the its vertex becomes the presenting part
4. Rotation (internal rotation)
a. The foetal head rotates 90 degree so that the face is facing the sacrum; the occiput is anterior, below the symphysis pubis
b. This enables it to pass through the pelvic outlet which has a wider antero-posterior than transverse diameter
c. In 5% of cases, the head rotates to occipito-posterior position
5. Extension
The foetal head extends and distends the perineum (crowning), and finally is delivered
6. Restitution (external rotation)
The foetal head then rotates 90 degree back to the same position in which it enters the inlet, facing either right or left, to
enable delivery of the shoulders
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Second stage of labour
Definition
The second stage of labour starts from time when the cervix is fully dilated, to end of the delivery of the baby.
Delivery of the foetal head

1. The presenting part (which is usually the foetal head) continues to descend and finally passes through the pelvic outlet. The
foetal head usually rotates to occiputo-anterior and extends round the pubis (crowning). It distends theperineum during
crowning.
2. Episiotomy is routinely indicated during crowning to prevent perineal tear in primigravida and if necessary in parous women.
Maternal pushing during the whole process is essential for success.
3. After the foetal head is delivered, it rotates to the natural position relative to the shoulder (restitution).
4. Difficulty may be encountered at this stage. The foetal heads may fail to descend further (prolonged second stage). It may be
due to inadequate maternal effort, occipito-posterior position or cephalopelvic disproportion. Careful assessment should be
taken before performing instrumental delivery.
Delivery of the foetal shoulder and rest of the body

The anterior shoulder is usually delivered by downward traction and the posterior shoulder follows spontaneously.
Sometimes difficulty (shoulder dystocia) may be encountered at this stage. The rest of the trunk is often delivered without
difficulty, except in rare situations such as foetal ascites or meconium peritonitis, the distended foetal abdomen results in
abdominal dystocia.
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The late second stage is presented as follow:
Beginning of crowning. The foetal head is distending the

perineum
Local anaesthesia is injected to the perineum before episiotomy
A mediolateral episiotomy is performed
Crowning of foetal head. The greatest diameter of the presenting

part is passing through the outlet. Control of the speed of
crowning and guarding of the perineum is necessary to avoid
perineal tear
The foetal head is delivered and restitution occurs. Suction of

airway is then performed.
Delivery of the anterior shoulder by downward traction. Shoulder

dystocia may be encountered at this stage
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Delivery of the posterior shoulder
Delivery of the rest of the body
Clamping of the umbilical cord
Drinking during labour

Protocol, 22 April 2005
1. Drinking during labour is allowed only in low risk women with:
a. Full term gestation (37 weeks or above)
b. Singleton fetus with cephalic presentation
c. Normal liquor
d. Reassuring intrapartum CTG
e. Afebrile
f. No history of previous caesarean section
g. No history of difficult intubation
h. Remark: induction of labour or regional anaglesia is not a contraindication provided that the above criteria are
fulfilled
2. Withhold drinking when
a. Narcotic drug is given for pain relief
b. Labour become complicated e.g. slow progress, change of liquor status, CTG become non-reassuring
c. Remain in latent phase after 8 hour of induction of labour
d. At the discretion of obstetrician and anaesthetist
3. Types and amount of fluid allowed
a. Water and isotonic fluid e.g. Lucozade Sport (still)
b. No more than 80 ml per hour
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Caput succedaneum
Foetal scalp edema resulted from obstructed venous return caused by pressure of the head against the rim of the cervix during
labour. While it is quite common during a normal labour, severe edema may signify an obstructed labour. On vaginal examination,
the edema also makes the foetal head felt at a lower station. However, the foetal head is actually high in the birth canal, and
difficulty may be encountered when instrumental delivery is wrongly attempted.
Figure 30 Caput Succedaneum

Moulding
The alternation in shape and diameters of the foetal skull during labour. The fontanelles and sutures permit the force of
contractions to compress the head against the bony pelvis and adapt its shape to that of the birth canal. Moulding is divided into 3
degrees:
1. First degree closure of the suture lines
2. Second degree reducible overlapping of the skull bones over suture lines
3. Third degree Irreducible overlapping of the skull bones over suture lines
While moulding is a normal phenomenon during labour, severe moulding signifies obstructed labour.
Engage
A term applied when the greatest diameter of the baby's presenting part has passed through the pelvic inlet of themother. The
greatest diameter is biparietal diameter in cephalic presentation, and bi-iliac diameter for breech presentation. Engagement is
particularly important when the mother has a platypoid pelvis, as when the head is engaged, the rest of the labour should present
no difficulty. As disproportion becomes less of a problem nowadays, engagement becomes less important. The descent of the head,
as measured by the number of fifths of the head still palpableabdominally, becomes more important.
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Station
Definition
It denotes the level of descent of the presenting part as assessed on vaginal examination, similar to engagement which is assessed
abdominally. Station is defined by the distance in centimeters between the leading portion of the foetal presenting part, and the
plane of the maternal ischial spines (which is arbitrarily set as zero level). For example, it is S+2 if the leading bony portion of the
foetal skull is 2cm below the ischial spines but is S-1 if it is 1cm above them.
Clinical importance
When the presenting part reaches the ischial spines (station 0), it is often engaged. Station is one of the five parameters making up
the bishop score. It is also used to define the level of instrumental delivery. Station may be incorrectly assessed when there is
significant caput succedaneum which gives a wrong impression that the presenting part is low.
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Third stage of labour
It starts from delivery of the foetus to delivery of the placenta. Normally it lasts not more than 30 minutes and blood loss is up to
250-500ml. Retained placenta (prolonged third stage), and postpartum haemorrhage are the major risks at this stage.

Admininster oxytocic agent prophylaxis on delivery of baby
1. Give prophylactic syntometrine 1 ampoule IM; or syntocinon 5units IV bolus injection over 1-2 (up to 5) minutes (or 10
units IM) immediately after the delivery of the baby.
2. Give second dose of oxytocic if uterus is atonic.
3. Infusion of syntocinon 40unit in 500ml crystalloid Q4H; or Carbetoicin 100 mcg IM if:-
a. Placenta praevia d. Multiple pregnancy
b. Abruptio placentae e. Co-existing fibroid
c. Parity 4 f. Polyhydramnios
Delivery of Placenta
4. Look for signs of separation of placenta:-
a. Lengthening of cord
b. Uterine contractions with rising of its fundus to umbilical level, and
c. Gush of blood coming out from vagina.
5. Empty urinary bladder if placenta is separated but retained.
6. Deliver the placenta by controlled cord traction. Do not apply fundal pressure and cord traction at the same time as uterine
inversion may occur.
7. Examine the placenta for any missing membranes, cotyledons or succentiate lobes.
Remainders
8. Examine the perineum, vagina and the cervix for any tear.
9. Repair episiotomy, perineal tear or other kinds of tears.
10. Take cord blood for blood gas assay (arterial and venous), thyroid function and G6PD.
Difficulties
11. Inform Medical Officer if prolonged 3rd stage (retained placenta) or postpartum haemorrhage.
12. If the placenta is retained, perform manual removal of placenta (MROP) under general or regional anaesthesia. There is a
possibility of morbid adherence of placenta.
13. If the is excessive bleeding from inside of uterus, repeat the oxytocic injection, or give a syntocinon infusion, or
prostaglandin F2a (a stronger oxytocic) to correct any uterine atony. Exploration of uterus under anaesthesia may be
required.
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Neonatal Resuscitation
1. Take cord blood for blood gas assay (arterial and venous), thyroid function and G6PD.
2. Give newborns injection:
a. Vitamin K1 to all newborns.
b. Hyperhep(hepatitis immunoglobulin) to newborns of hepatitis B carrier mother.
3. Routine Resuscitation
a. Apply gentle suction confining to the oral cavity, oropharynx, and the nasal cavity.
b. Dry the baby thoroughly and wrap in a warm blanket.
c. Stimulate the baby by flicking the feet or by rubbing the skin with towel if the baby is not active.
d. Record Apgar score, cord arterial and venous blood gases results.
4. Use of Nalaxone
a. Give naloxone intramuscular injection to the baby if and only if
i. The mother has received narcotic injection within 6 hours of delivery, and
ii. The baby shows evidence of respiratory depression at birth.
b. The baby should be reassessed by neonatologist before being discharged from the labour ward.
c. If the baby does not respond to naloxone, inform neonatologist.
5. Resuscitation of Extremely Preterm Delivery
a. Before delivery, arrange neonatalogical consultation for counselling of the patient
b. Inform neonatal MO for resuscitation in the following conditions:
i. Preterm deliveries with working gestation >=24 weeks irrespective of birth weight
ii. Cases of working gestation around 22-24 weeks but:
- Baby weight >500g and shows evidence of life at birth, or
- Patient has decided for resuscitation after counselling by neonatologist, or
- Patient has not been counselled by neonatologist
c. Do NOT resuscitate babies from termination of pregnancies irrespective of birth weight.
Controlled cord traction

The standard technique to deliver the placenta in order to shorten the third stage of labour and reduce postpartum haemorrhage,
with precaution to avoid uterine inversion:
1. Place the left hand on the uterus to feel for any contraction.
2. Once a contraction has occurred, move the left hand suprapubically to elevate the fundus with palm facing towards mother.
3. At the same time, the right hand grasps the cord and exert steady traction so that the placenta separate and is delivered gently.
4. Care should be taken to peel off all the membranes, usually with a twisting motion.
5. It is of crucial importance that controlled cord traction is not performed in the absence of a ut erine contraction; otherwise
uterine inversion may occur.
6. After the placenta is delivered, it should be inspected for missing cotyledons or succenturiate lobe.
Figure 31 Controlled cord traction
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Routine management of placenta after delivery
Figure 32 Placenta examined on a flat surface to demonstrate any missing lobes

1. Examine systematically by the midwife or doctor in charge of the mother and delivery:
2. Maternal surface:
a. Cotyledons
b. Infarction
c. Calcification
d. Old blood clot
3. Foetal surface:
a. Course of umbilical vessels
b. Velamentous insertion of the cord
c. Succenturiate lobe - suspect if a vessel runs to the edge of the placenta and the membranes there are ragged or absent
4. Membranes:
a. Number of layers of membranes, especially in multiple pregnancy
b. Completeness
c. Circumvallate placenta
5. Umbilical cord:
a. Number of vessels
b. True or false knots
c. Length of the cord
If retained placenta (partial or complete) is suspected, inform medical officer. Placentae of multiple pregnancies should be
examined by medical officer. Send the placenta for the following investigations accordingly. Otherwise dispose placenta for
incineration.
1. For microbiological study:-

a. Maternal pyrexia
b. Foul smelling liquor
c. Preterm labour or PPROM
d. Other suspicion of chorioamnionitis
e. The placental swab should be taken from the chorion as soon as possible after delivery to avoid contamination.
2. For pathological examination:-
b. Abnormal looking placenta
c. Abnormal baby
d. Pre-eclampsia
e. Intrauterine death
f. Hydrops foetalis
g. chorioamnionitis
h. Preterm labour or PPROM
3. For Cytogenetic study:- intrauterine death with abnormal morphology (when cord blood is unavailable)
- 157 -
Retained placenta
It is a condition in which the whole placenta or part of it is retained inside the uterine cavity after the delivery of the baby. It may
be due to morbid adherence of placenta to the myometrium. Complications include:
2. Uterine inversion when excessive cord traction is attempted to deliver the placenta
It is managed by manual removal of placenta (MROP).

1. Inform the intern and obstetric call medical officer.
2. Assess and treat postpartum haemorrhage
3. Set drip, CBP and X-match.
Morbid adherence of placenta

Definition
It is an implantational disorder in which the placental villi reach the myometrium lacking a normal decidual layer in between. It is
classified into:-
1. Placentaacreta the placenta reaches the myometrium.
2. Placenta increta the placenta invades the myometrium.
3. Placenta percreta the placenta reaches the serosa of the uterus and may even perforate it.
Incidence
About 1 in 7000 deliveries
Causes
The deficiency of the decidual layer is usually a consequence of previous multiple or excessive uterine curettage, previous
endometritis or uterine scarring. Rarely pregnancy may follow an incomplete endometrial ablation, and the placenta is at high risk
of morbid adherence.
Complications
- Placenta praevia - 50% cases of morbid adherence of placenta also have placenta praevia, due to deficiency of decidua in the
lower segment following repeated caesarean section.
- Retained placenta
- Uterine inversion - as a result of excessive traction to deliver the adherent placenta.
- Postpartum haemorrhage - as a result of retained placenta, uterine inversion and uterine atony.
- Uterine perforation rarely occurs in case of percreta
As above
Management
1. Resuscitation for postpartum haemorrhage
2. If the patient wants to preserve uterus for fertility, attempt manual removal of placenta (MROP); otherwise
3. Hysterectomy
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Manual removal of placenta (MROP)
Definition
It is a operation in which the operator inserts his/her hands into the uterine cavity, identifies the placental site, separates the
placenta from the uterine wall and removes it.
Indications
Retained placenta (partial or complete)
Procedure

1. It is performed under general or regional anaesthesia, with prophylactic augmentin cover
2. The cervical os is dilated gradually to admit the whole fist
3. The forearm of the operator is inserted into the uterine cavity
4. The placenta is separated and removed
5. The uterine cavity is checked empty
Commence syntocinon infusion (40 units syntocinon in 500 ml of Hartmanns solution over 4 hours) after removal.
If the placenta is morbidly adherent to the uterus (especially in patients with uterine scar), inform the mid-call as hysterectomy
may be needed.
Complications
- Introduction of infection into the uterine cavity
- Perforation of the uterus by the operator's hands
- Postpartum haemorrhage
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Neonatological consultation

1. Conditions requiring neonatal medical officer to stand-by at delivery
a. Antenatal conditions
i. Preterm delivery (gestation< 37 completed week)
ii. Estimated foetal weight < 2kg or significant intrauterine growth retardation
iii. Multiple pregnancies
iv. Oligohydramnois
b. Perinatal conditions
i. Suspected foetal distress
ii. Meconium stained liquor
iii. Babies with known or suspected malformations that may require immediate medical attention at birth.
c. Placental conditions
i. Suspected chorioamnionitis
ii. Prolapsed cord
iii. Abrutpio placentae
iv. Placenta praevia
d. Difficult deliveries
i. All Caesarean deliveries
ii. Vaginal breech deliveries
iii. Difficult deliveries e.g. shoulder dystocia
e. Other conditions in which the obstetricians anticipate adverse neonatal outcome.
2. Conditions required neonatal medical officers assessment after delivery

a. Foetal conditions
i. Congenital malformations
ii. Respiratory depression at birth
b. Maternal disorders:
i. Endocrine diseases, e.g. diabetes mellitus, thyrotoxicosis
ii. Autoimmune diseases, e.g. systemic lupus erythematosus, myasthenia gravis, immune thrombocytopenic purpura
iii. Infectious risk e.g. syphilis, Group B streptococcus carrier
iv. Medical diseases on drugs that may affect the baby, e.g. anti-epileptic, anti-psychotic
v. Substance abuse
c. Unattended delivery
d. Other conditions as instructed by obstetricians
3. Conditions requiring notification of NNU upon admission to labour ward

a. Gestation of 35 weeks or less
b. Severe IUGR or severe oligohydramnios
c. Major congenital disorders which may require special neonatal care or immediate surgery
d. Multiple pregnancy
e. Other conditions as instructed by obstetricians
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Postnatal discharge
1. Time of discharge
Usual length of stay after term delivery (calculated from the time of birth of the baby):
a. Uncomplicated labour and vaginal delivery (included instrumental):
i. 3 days for parity 1 patients,
ii. 2 days for patients of parity 2 or above
b. Complicated labour and vaginal delivery:-3 days or more.
c. Caesarean section:-4 days or more
2. Patient's request for early discharge within 48 hours after birth
a. Early discharge is allowed only if the following criteria are fulfilled:
i. Uncomplicated vaginal delivery
ii. Patient should have been observed for at least 24 hours after birth
iii. Midwife has assessed the following:
- Patient is mobile with adequate pain control.
- Bladder and bowel functions are adequate.
- No problem in feeding baby.
- Stable emotion.
- Advice on perineal care has been given.
- Advice on postnatal follow-up and health check for both the mother and the baby has been given.
- Patient is accessible to medical and social support including MCH, postnatal ward hotline, postnatal clinic at
Li Ka Shing Outpatient Clinic, community nursing service, medical social worker when needed.
- Patient can be contacted for follow-up.
iv. Doctor or intern has assessed the following:
- Perineal wound is normal.
- No postpartum haemorrhage or ongoing bleeding.
- No fever (> 38 degrees for two or more readings of at least one hour apart) within 24 hours before discharge.
- Rh immunoglobulin has been given if indicated.
- No intrapartum or postpartum complications that require inpatient medical treatment or observation.
- Follow up plan has been drawn for any antepartum, intrapartum or postpartum problems or complications.
- Contraceptive advice has been given.
b. For cases not fulfilling the above criteria:
i. Decision should be made by a medical officer on individual basis (or agreed by a medical officer after assessment
by an intern).
ii. If patient insists early discharge against medical advice, she should sign the "Discharge with acknowledgement of
medical advice" (DAMA).
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2. Inducation of Labour and Failure to Progress
Induction of labour
Definition
It is an obstetric procedure designed to pre-empt the natural process of labour by initiating its onset artificially before this occurs
spontaneously.
Indications
1. Foetal indications
a. Postterm pregnancy:-the most common indication (23.9-30.0%)
b. Prolonged rupture of membranes:-the second most common indication (29.0-31.0%)
c. Foetal compromise that may risk intrauterine death if pregnancy is continued:-IUGR (2.7%), oligohydramnios
d. Lethal foetal abnormalities requiring termination of pregnancy (0.2%):-such as Edward syndrome, Patau syndrome,
anencephaly, thanatophoric dwarfism
e. Stillbirth (0.6%)
2. Maternal indications
Presence of medical diseases that may deteriorate or is poorly controlled as pregnancy continues:-such as pre-eclampsia
(3.6%), poorly controlled diabetes mellitus (4.7%)
Contraindications
- Malpresentation:-foetuses may better be delivered by caesarean section or external cephalic version (ECV) before induction.
- Date problems:-may need to unnecessary induction for postterm, iatrogenic preterm delivery
- Presence of indications of caesarean section:-such as placenta praevia, classical caesarean section
- Severe foetal compromise that is likely to fail to sustain the stress of labour:-better to deliver by caesarean section
- Poor maternal condition such as severe pre-eclampsia:-better to deliver by caesarean section
Methods
1. Cervical ripening
a. With vaginal insertion of prostaglandin E2
b. Required if the cervix is unfavourable, with bishop score less than 6
2. Initiation of uterine contractions
a. With amniotomy (artificial rupture of membranes) and syntocinon intravenous infusion
b. Syntocinon infusion rate should be titrated with frequency and strength of uterine contractions (aim at 4 uterine
contactions in 10 minutes) to avoid hyperstimulation.
Complications
1. Maternal complications
a. Uterine rupture
b. Risk of caesarean section secondary to failure of induction
2. Foetal complications
a. Acute foetal distress resulted from uterine hyperstimulation or uterine rupture
b. Intrauterine infection secondary to prolonged induction and labour
1. Unfavourable cervix (Bishops score <6)
a. Rule out any contraindications of prostaglandins, like asthma, allergy, cardiac disease and raised intraocular pressure.
b. Perform 20-minute CTG. If reactive, insert one 3 mg prostaglandin E2 (PGE2) pessary into the posterior fornix.
c. Repeat another 20-minute CTG 1 hour after insertion or when uterine contractions occur.
d. Reassess 4 to 6 hours later, and give second PGE2 pessary if Bishop Score still < 6.
2. Favourable cervix (Bishops score 6 )
a. Transfer patient to labour ward.
b. X-match and insert IV line.
c. Perform artificial rupture of the membranes (ARM).
d. Start syntocinon infusion and titrate the infusion rate until regular uterine contractions of 1 in 3-4 minutes is achieved.
e. Avoid uterine hyperstimulation.
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Bishop score
The score used to assess the ripening of the cervix for induction of labour. Scores are assigned to each of the five cervical features
and the total score is obtained by summation. With a low score (0-3), there is a higher risk of failed induction, resulting in
caesarean section (over 20%) compared with a score of eight or more, where the failed induction rate is less than 3%. With a high
score the cervix is said to be ripe.
Bishop's score 0 1 2 3
Dilatation (cm) <1 1-2 3-4 >4
Length (cm) 4 2-4 1-2 <1
Consistency firm medium soft /
Position posterior central anterior
Station -3 -2 -1, 0 1
Amniotomy
Amniotomy or artificial rupture of membranes is a common intrapartum procedure, performed with an amnihook (or with a
Drew-Smythe cannula in hindwater amniotomy).
Indication
1. Augmentation of labour in spontaneous rupture of membrane, and Induction of labour. The procedure would stimulate
production of endogenous prostaglandins which brings about uterine contractions as well as cervical softening.
2. Application of foetal scalp electrode or blood sampling;
3. Instrumental delivery.
Risk
1. Compression of foetal head during labour, thus it should be avoided in vaginal delivery of preterm foetuses as the forewater
protects the vulnerable foetal head
2. Cord prolapse, particularly if there is polyhydramnios.
3. In the management of intrauterine death, amniotomy should be avoided until the late stage of labour, in order to prevent
intrauterine infection.
Amnihook
It is a simple instrument with a small hook at the tip for amniotomy. Under aseptic technique, amnihook slides between index and
middle fingers, which are already in contact with membrane. Amnihook is then turned upward to rupture the membranes. Fingers
should withdraw after cord prolapse excluded. If liquor not seen, treat as Meconium Stained Liqour.
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Uterine hyperstimulation
It is an iatrogenic complication due to the excessive use of oxytocics, resulting in too frequent or too strong uterine contractions.
The uteroplacental blood flow is jeopardised, resulting in foetal hypoxia and foetal distress. The cardiotocogram typically shows
frequent uterine contractions (>4 in 10 minutes) and recurrent foetal decelerations or bradycardia. The other risk is uterine rupture.
Prevention
Titrate the rate of infusion of syntocinon and avoid using prostaglandins in multiparous women or when women already in labour.

1. Definition More than 4 painful uterine contractions in 10 minutes induced by prostaglandins or syntocinon
2. Inform Medical Officer.
3. Uterine hyperstimulation with normal foetal heart rate
a. Hyperstimulation induced by PGE2
i. Abandon further PGE2 and remove any residual PGE2 from vagina.
ii. NPO, X-match.
iii. To labour ward for continuous foetal heart monitoring.
iv. For combined induction after hyperstimulation subsides.
b. Hyperstimulation induced by syntocinon Titrate oxytocin to keep contractions less than 4 in 10 minutes.
4. Uterine hyperstimulation with abnormal foetal heart rate
a. Hyperstimulation induced by PGE2
i. NPO, X-match.
ii. Immediate delivery.
b. Hyperstmulation induced by syntocinon
i. Stop syntocinon.
ii. Immediate delivery if no improvement in foetal heart rate.
5. Tocolytic treatment for hyperstimulation
a. Not recommended unless there is persistent bradycardia when arranging emergency Caesarean section.
b. Beware of hypotension particularly if epidural anaesthesia, and beware of uterine atony after delivery.
c. Hexoprenaline is the only choice. Give IV bolus 5 mg. Can only repeat once if no improvement after 2 mins.
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Failure to progress
Definition of failure of progress of labour
It is defined as the labour progress fails to reach an acceptable rate. The criteria are different depending on parity.
1. Prolong latent phase
During latent phase, there is cervical effacement, dilation may not be apparent and appears prolonged. It is common in
primgravida and usually idiopathic. Management is wat and supportive including sufficient pain relief. As cervix may dilate
rapid later, therefore syntocinon is not indicated.
2. Prolonged active phase:
Cervical dilatation:-less than 1.2cm/hr in a primigravida; less than 1.5cm in a multipara
3. Prolonged descend:
Descend of the presenting part:-less than 1.0cm/hr in a primigravida; less than 2.0cm in a multipara
4. Secondary arrest of dilatation:
Cervical dilatation ceases during active phase of labour for 2 or more hours
5. Prolonged second stage:
Second stage last more than 1 hour in a primigravida; 30 minutes in a multipara
6. Failed induction Fail to achieve active phase in 12 hours.
Causes of failure of progress

1. Insufficient power:
a. Incoordinate or inadequate uterine contractions
b. Poor maternal efforts during second stage
2. Obstructed labour due to disproportion of sizes of the passenger and the pathway:
a. True Cephalopelvic disproportion
i. Abnormally large presenting part:-hydrocephaly
ii. Contracted pelvis
b. False: malpresentation or malposition of the head.
Principle of management
1. It is essential to differentiate insufficient power from obstructed labour. The former is managed with syntocinon augmentation
or instrumental delivery in the second stage, while caesarean section should be performed in obstructed labour.
2. Mismanagement of obstructed labour with syntocinon or instrumental delivery causes significant maternal (e.g. uterine
hyperstimulation, uterine rupture) and foetal complications (foetal distress, birth injuries)
3. Mismanagement of insufficient power with caesarean section puts patients to unnecessary risk of operation.
Incoordinate uterine contraction

During normal labour, the contractions begin from the fundus, and progress downwards. Consequently, the baby is pushed
downwards towards the os. In incoordinate uterine contractions, ectopic contractions begin at sites other than the fundus, so the
foetus is not pushed towards the os despite strong contractions. Labour is therefore prolonged. Incoordinateuterine contractions
can usually be diagnosed when the cardiotocogram (CTG) is reviewed. The contractions recorded are typically irregular in
frequency, shape and amplitude. There is also overlapping of the tracing of uterine contractions.
Trial of labour
It implies that the outcome of labour is uncertain because of mechanical difficulty and that particularly vigilant monitoring of
progress and of foetal well-being is required.
Obstructed labour
- Obstructed labour occurs when the the birth canal (pelvis) is relatively small for the presenting part (usually the foetal head)
to pass through. It is usually a 'relative' condition in a pair of normal woman and foetus, but can also be due to an
abnormally contracted pelvis or the presenting part is abnormally large such as hydrocephaly.
- labour presents with failure to progress, with cessation of cervical dilatation or descend of foetal head, and prominent caput
succedaneum and moulding. The station of foetal head may be high or even not engaged.
- The pelvis may appear small on vaginal examination (see pelvimetry). Obstructed labour should be differentiated from
insufficient power when there is failure of progress. The treatment should be caesarean section.
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Deep transverse arrest
Definition
The foetal head is stuck in an occipito-lateral position, in the transverse diameter of the outlet, between the ischial spines.
Transverse arrest may also occur higher in the mid-cavity of the pelvis
Causes
- Deflexion of the foetal head
- Poor uterine contractions
- Inadequate channelling of the foetal head by the pelvic floor (as happens with a relaxed pelvic floor under epidural)
- Cephalopelvic disproportion
Dystocia
From Greeks words dys means (bad) and os means opening. It is a vague term meaning some sorts of difficulty in labour.
Originally it was used to describe obstructed labour when there was disproportion between the size of the presenting part and that
of the birth canal, results in in failure of progress of labour. The causes of dystocia were then classified as due to the passage (birth
canal), the passenger (baby), or power (uterine contractions and maternal effort):
Problems of Passage
Abnormal shape and dimensions of pelvis resulting in obstruction of labour. The pelvis can be assessed with pelvimetry.
Problems of Passenger
1. Malpresentation such as breech presentation
2. Malposition such as Occipito-posterior position
3. Macrosomia
4. Shoulder dystocia
5. Abnormal size of presenting part such as hydrocephaly
Problem of Power
1. Dysfunctional uterine contractions which can be:
a. Too irregular, or
b. Too infrequent, or
c. Incoordinate
d. Too weak (hypotonic)
2. Inadequate maternal effort during second stage of labour which can be due to:
a. Maternal exhaustion
b. Effect of epidural analgesia
c. Maternal paralysis due to pre-existing neurological diseases
d. Incooperative patients
Implication
It is important to differentiate the underlying causes of dystocia. While problems with the passage and passenger would result in
obstructed labour that require caesarean delivery, dysfunctional uterine contractions are treated with syntocinon augmentation, and
inadequate maternal effort can be managed with instrumental delivery.
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Shoulder dystocia
Definition
This is an obstetric emergency and is defined as difficult delivery of shoulders that
(1) Requires additional manoeuvres besides usual downward traction and episiotomy, or
(2) Results in foetal birth asphyxia or trauma such as fractures and neural plexus injuries.
Pathology
The pathology lies in the pelvic inlet. While the foetal head is delivered, one or both shoulders are struck above the inlet. Usually,
the anterior shoulder remains hooked behind the symphysis pubis and fails to rotate into a larger pelvic diameter.
Incidence
The incidence is about 0.2%, and is more common in foetal macrosomia and maternal diabetes.
Risk Factors
1. Antepartum risk factors:
a. Maternal obesity >81kg:-increase 8 fold
b. Maternal diabetes:-increase >2 fold for same birth weight
c. Post-term:-<40 week, 0.7%; .42 week 1.3%
d. Macrosomia:-<4kg incidence 0.3%; >4kg 3-10%; >4.5kg >22%
2. Intrapartum risk factors:
a. Secondary arrest of labour
b. Instrumental delivery
3. Remark 23% of shoulder dystocia do not exhibit any of the classical risk factors
Foetal complications
1. Birth asphyxia
2. Brachial plexus injury
a. Erb's 6- 16%, usually transient and mild
b. Klumpke's, phrenic palsy, rare but serious
3. Skeletal injury fracture of clavicle 15%, humerus 26%
4. Perinatal mortality
Maternal complications
1. Birth canal injury
HELPERR for Shoulder Dystocia

H: Help seeking
E: Episiostomy: Extend or perform a large one.
L: Leg: McRoberts manoeuvre
P: Pressure on suprapubis.
E: Enter the vagina for rotational manoeuvre
R: Remove posterior arm
R: Roll over
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1. Summon for help:-experienced obstetricians, paediatrician, anaesthetist, and prepare operation theatre
2. Make a large mediolateral episiotomy or extend the pre-existing episiotomy.
3. Perform special manoeuvre to deliver the shoulders:
a. Mcrobert's manoeuvre,
i. Lie the patient flat and hyperflex the patients thighs against her abdomen
ii. This helps to rotate the symphysis pubis cephalad and decrease the pelvic angle of inclination.
b. Wood's or Rubin's rotational manoeuvre
i. Insert hand into vagina to reach the shoulder and attempt to rotate the axis of the baby into a more favourable oblique
diameter by adducting the shoulder, and then apply gentle downward traction to deliver the foetal trunk.
ii. This procedure risks fracture of the clavicle
c. Posterior arm extraction
i. If the above procedure fails, insert a hand vaginally behind the posterior shoulder to grasp the arm, which is then
adducted across the foetal chest and delivered out of the vagina first, followed by the rest of the foetal body.
ii. This procedure risks fracture of the foetal arm.
d. Symphysectomy and Zanvanelli's manoeuvre (rarely done)
4. Examine any maternal trauma and birth injury after delivery
5. SHOULD NOT DO Aggressive lateral flexion of the head. Excessive traction; Apply fundal pressure and cleidotomy
Prevention
1. Prevent macrosomia by good control of diabetes and induction of labour at 41 week before the babies are getting too big
2. Counsel for elective caesarean section in case of macrosomia
3. Consider caesarean section instead of instrumental delivery in case of macrosomic baby during a prolonged second stage
4. Have experienced obstetricians to conduct the vaginal delivery in case of macrosomia
Why fundal pressure is contraindicated in case of shoulder dystocia?
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Asynclitism
A sideway tilting of the head, so that the sagittal suture of the foetal skull does not lie midway between the maternal sacral
promontory and pubic symphysis. It is usually due to uneven pressure on the foetal head during its descent through the pelvis.
Asynclitism can occur before the head is engaged, or when the head is in the pelvic cavity.
Occipito-posterior
The foetus with vertex presentation begins labour usually in the occipito-lateral position because its slightly longer anteroposterior
diameter fits best into the slightly longer lateral diameter of the pelvic brim. When labour progresses, the head rotates so the baby
faces the back of the mother, occipito-anterior position. Occipito-posterior position commonly occurs if the maternal pelvis is of
the anthropoid or the android shape. It is associated with dystocia and incoordinate uterine contractions. Occipito-posterior
position usually resolves in one of following three ways:-
1. Most commonly, after a longish and difficult labour, the head rotates to the occipito-anterior position, and the baby delivers
normally.
2. Sometimes, the head stays persistently occipito-posterior (POP), and the head is delivered in this position. The head tends to
act like a battering ram on the perineum, and usually severe trauma to the perineum results. Occasionally a third degree
perineal tears results.
3. Occasionally, during the rotation, the head is held up by the sacrum. The part of the head near the back of the mother fails to
descend while the part near the front continues to descend, and the baby's head therefore tilts sideways (asynclitism). As the
head tilts, it becomes more obstructed, and eventually the head cannot descend anymore. This is called deep transverse arrest.
Usually, a Caesarean section is necessary. However, delivery can sometimes be affected by the use of Kielland's forceps, the
vacuum extraction, or in the old days by manual rotation of the head.
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Vaginal breech delivery
Introduction
Vaginal breech delivery is a high risk procedure. A recent randomized controlled study has showed that it is associated with
higher perinatal mortality and morbidity than elective caesarean section in delivering singleton pregnancy with breech
presentation. Women should be counselled for external cephalic version (ECV) or elective section. Vaginal breech delivery should
only be considered in highly-selected group of pregnancies:
1. Multiparous with previous successful vaginal deliveries
2. Term foetuses of average size (estimated weight between 1.5 to 3.5kg)
3. Foetal neck is not hyperextended
4. Frank or complete breech presentation
5. There is no evidence of foetal compromise
6. Induction and augmentation are not required
Mechanism and technique

1. Delivery of the lower part of the body
a. Vaginal breech delivery begins with its bitrochanteric diameter fitting into the lateral diameter of the maternal pelvis, and
the rotation is therefore sacral anterior or posterior.
b. As the breech descends towards the outlet, it rotates into a sacral lateral position, and the baby presents by the anterior
buttock. During delivery, the baby bends its back laterally, so first the anterior buttock, then the anus, then the posterior
buttock delivers. Episiotomy is made at this stage.
c. The lower limbs and the trunk usually deliver spontaneously. The baby will then be lying with the shoulders in the
transverse diameter.
2. Delivery of the shoulder
a. The arms may extend and abduct over the back of the foetal neck (see nuchal arm below). Rotation of the body by
Loveset maneuver is then necessary to deliver the shoulders:
b. The shoulders are rotated into anterio-posterior diameter, so that the anterior shoulder is adducted. The anterior shoulder
and elbow are then flexed and delivered. The posterior shoulder is then rotated to the anterior position and delivered in a
similar way. The shoulders finally lie in the transverse diameter again.
3. Delivery of the head
The head usually requires assisted delivery. Head entrapment is an dangerous condition (see below). The aim is to
encourage flexion of the neck. This can be done with a pair of Piper forceps, the Burns Marshall maneuver, or the
Mauriceau Smellie Viet maneuver. Refer to your textbooks for these maneuvers.
Potential difficulties in vaginal breech delivery

1. Cord prolapse
In case of footling breech presentation, the foetal buttock is not well fit to the cervix, and is more prone to cord prolapse.
2. Nuchal arm
One or both foetal arms are extended, abducted over the back of the foetal neck. This results in obstruction.
3. Head entrapment
During vaginal delivery, the foetal head is presented to the birth canal with the base of the skull, and there is not adequate
time for moulding. The head may be trapped by the cervix.
In both cases of nuchal arm and head entrapment, the umbilical cord is being compressed and occluded between the cervix and the
head. Prolonged delivery results cause hypoxic damage. Excessive traction to overcome dystocia also causes severe trauma.
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Loveset maneuver
A maneuver originally described to deliver the shoulder in a breech presentation. The principle is that the pelvic canal is curved,
so that its anterior wall (pubic symphysis) is much shorter than the posterior wall (the sacrum). It is most likely therefore when the
foetal part is obstructed anteriorly by the pubic symphysis, the posterior part is already below the sacral promontory. Given that
the baby is held firmly by pelvic tissue, a rotation of the baby will cause the posterior part of the baby to come to the front, and as
this is already below the inlet, the baby descends. In other words, the pelvis acts like a screw, and any rotation of the baby will
bring it lower. The maneuver is very useful to deliver the shoulders of the baby after the breech is delivered. The principle is also
used when there is shoulder dystocia after cephalic delivery. Sometimes, if the baby can be rotated, the shoulder will slip under
the pelvic inlet and can be delivered.
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3. Pain relief and maternal monitoring
Obstetric anaesthesia
Types of anaesthesia
1. General anaesthesia
2. Regional anaesethesia Spinal anaesethesia; Epidural anaesethesia
3. Local anaesethesia Pudendal nerve block; Local infiltration
Entonox
Entonox is a gas mixture of oxygen and nitrous oxide with 50% each. It is an inhalational analgesic commonly used for labour
pain relief. It can be self-administered, is fasting acting, and has minimal maternal and foetal side effects. The effect is peak at
20-30 seconds, and offset in 1 minute. The efficacy is variable, and 85% of women find it helpful. In order to get maximal
analgesic effect, patients should be instructed to inhale when uterus is starting to contract, and continue inhalation until the
contraction begins to subside. Side effects are hypocarpia, dizziness, tetany and foetal hypoxia after prolonged use. Midwives can
prescribe Entonox to parturiting patients according to departmental standing order. Patients should be advised with other forms of
analgesia when labour is expected to be long, in order to avoid side effects of Entonox.
Narcotic analgesia
The most commonly used narcotic analgesic is pethidine. It is often used for labour pain relief, and post-operative analgesia. It can
be administered intramuscularly or intravenously. The former route is contraindicated in patients with clotting disorders or
thrombocytopenia. The intravenous route can be used for patient-control-analgesia. For labour pain relief, its efficacy is variable
with 50% reported good analgesic effect. The maternal side effects are vomiting and drowsiness. Since it can cross the placenta,
the major foetal risk is neonatal respiratory depression which is readily reversible with naloxone.
Pethidine
It is indicated for labour and postoperative pain relief, in the regimen of 75mg (body weight <80kg) or 100mg (body weight
80kg) Q4H prn IMI. Never give IV >25 mg at any one time. Midwives can administer the first pethidine injection for and only
for labour pain control. Doctors should be consulted when repeated injections are required. Pethidine is not contraindicated in
advanced first stage of labour. Maxolon may also be given to relieve GI upset caused by pethidine.
Epidural anaesthesia
Contraindications
1. Bleeding disorder, thrombocytopenia or on anticoagulants
2. Infection in area of epidural injection
The Pros of Epidural:

1. Excellent labour pain relief
2. Allows time for rest
3. Reduces hyperventilation and serum catecholamines
4. Great for PIH (pregnancy induced hypertension) and Caesarean sections
The Cons:-(possible spin-off problems)

1. Major
a. Hypotension (requires IV fluids)
b. Nerve injuries
2. Mild
a. May hamper 'push-ability' and increase need for vacuum/forceps extraction for prolonged second stage
b. Headache after accidental dural puncture (1/100); Backache; Fever
c. Postpartum urinary retention;
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4. Intrapartum foetal monitoring
Intrapartum foetal monitoring
Aim
To detect intrapartum foetal distress, or hypoxia on time so that perinatal mortality and permanent hypoxic insult can be
prevented.
Physiological changes in response to foetal hypoxia

- Foetal hypoxia triggers anaerobic glycolysis resulting in an accumulation of lactic and metabolic acidosis.
- Foetal PCO2 rises as a buffer effect, causing a respiratory acidosis.
- Normally the excess CO2 and lactic acids can be driven out from the foetus via the placenta, but this mechanism may be
affected by an underlying pathology.
- The effects of hypoxia depend on the foetal glycogen reserves. A growth-retarded foetus will therefore be affected earlier
and more severely than a well-nourished foetus.
- Blood pH falls as there is accumulation of CO2 and lactic acids.
- Foetal heart rate patterns change during hypoxia and acidosis, resulting in decelerations or bradycardia.
Methods of foetal monitoring

1. Intermittent auscultation
a. Record foetal heart rate using a Pinard stethoscope between contractions to obtain a baseline rate, and during and
immediately after contractions to detect accelerations or decelerations.
b. Apply only to low-risk patients with no obstetric complications.
c. More intensive monitoring should be used if any risk factors are present
2. Continuous foetal heart monitoring (CFHM)
a. Both foetal heart rate pattern and uterine activity are recorded using cardiotocogram.
b. See foetal heart rate pattern for the interpretation of cardiotogram.
c. This is a screening technique which facilitates the detection of foetal hypoxic stress. It is not often diagnostic.
d. Limitations of CTG are:
i. High false-positive rate
ii. Even when the most ominous pattern is present only 50% of the babies have a low Apgar score at birth.
iii. The use of continuous FHR monitoring should therefore be backed up by measurement of foetal blood ph through
foetal scalp blood sampling.
iv. Difficulty in interpretation during the second stage of labour, as brief profound decelerations is not uncommon at
that stage. Prolonged bradycardia however must not be ignored.
v. Recording problems in cases of foetal arrhythmia
3. Foetal Electrocardiogram (ECG)
a. Foetal ECG can be detected with a foetal scalp electrode.
b. The following adverse features have been suggested:
i. T/QRS ratio > 0.25
ii. A negative T wave
iii. ST depression with T elevation
c. Its main benefit is to provide reassurance in the presence of an abnormal CTG and perhaps reduce the rate of unnecessary
caesarean sections. It may also be helpful in case of foetal arrhythmias.
4. Foetal scalp blood sampling
a. FHR monitoring and scalp pH measurement are complementary
b. The former without the latter increases the caesarean section rate unnecessarily because of false-positive diagnoses
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Intermittent auscultation
It is a basic method of intrapartum foetal monitoring that has been used for a long period of time before the introduction of
cardiotocogram. It is still being used in many centres. During labour, the foetal heart rate is listened with Pinard stethoscope or a
Doppler apparatus (doptone) immediately after a contraction for 1 minute in a 15-minute interval. Any changes in foetal heart rate
such as decelerations are examined. Intermittent auscultation has often been compared with routine continuous foetal heart
monitoring with cardiotocogram, which has become the standard in many centres (including our unit). The former method is
simple and requires no sophisticated machines and equipments, and is less expensive. Its potential disadvantage is that it may not
be as sensitive as cardiotocogram in detecting foetal hypoxia. The latter has been shown to reduce the incidence of neonatal
seizures. However, it also has a high false-positive rate, leading to unnecessary intervention (high operative delivery rate).
Cardiotocogram (CTG)
Definition
It is an electronic monitoring method which presents graphically the status of the foetal heart rate pattern (cardio), and the uterine
activities (toco). Foetal movements can also be recorded.
Mechanism
The foetal heart rate is picked up with an external detector using Doppler effect, or during labour, with a foetal scalp electrode.
The uterine activities are usually picked up with a transducer applied on the maternal abdomen. The transducer cannot pick up the
exact intrauterine pressure, but it detects the changes of contour of the abdominal wall, which can reflect the frequency and
duration of the uterine contractions. If absolute intrauterine pressure monitoring is required during labour, an intrauterine catheter
can be inserted to the uterine cavity and connected to a transducer.
Function
Cardiotocogram is a valuable method of assessment of foetal well-being during antenatal period, as well as intrapartum period, in
modern obstetrics. It is also called non-stress test when used for antenatal monitoring. When it is used under artificial induction of
uterine contractions, it is called a contraction stress test. Contraction stress test is seldom used nowadays because of foetal risk and
inaccuracy of the test.
Mechanism
1. External cardiography
a. Doppler effect to detect cardiac movements
b. Heart rate is computed using the interval between each cardiac contraction
c. Can also detect maternal pulses
d. Auto-correlation to filter noises
2. Fetal Scalp Electrodes
a. Detect the fetal ECG
b. Heart rate is computed using the RR interval
c. Can also detect maternal ECG
d. Require rupture of membranes
Interpretation of CTG
Always remember the 3 components
1. Uterine Contractions
2. Fetal movements
3. Fetal Heart Rate Tracing
a. Baseline heart rate
b. Baseline variability
c. Accelerations
d. Decelerations
A maternal heart tracing can be added by attaching the mother to pulse oximeter to distinguish fetal bradycardia and maternal
heart rate
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Foetal heart rate pattern
Baseline Heart rate
1. Normal value is 110 160 bpm, higher in premature foetuses
2. It is determined over a period of 5-10min by drawing a line through the midpoint of the tracing which represents the most
common rate having excluded accelerations and decelerations
3. Bradycardia:
a. Baseline <110bpm for at least 15 minutes
b. Causes: hypoxia, congenital heart block, drug induced
4. Tachycardia:
a. Baseline > 150 pm for at least 15 minutes
b. Causes: active phase, drugs (ritodrine), infection, hypoxia
Variability
1. It is the degree to which the baseline varies within a particular bandwidth excluding accelerations and decelerations
2. It is determined by drawing a horizontal line at the level of the highest point of the peaks and the lowest point of the troughs
of the tracing in a 1 cm segment
3. Normal amplitude of baseline variability is 5-25 bpm.
4. Cases of reduced variability is sleep phase, prematurity, hypoxia, drugs (sedatives, anaesthetics), congenital malformations
(CNS or CVS)
Accelerations
1. Increase in heart rate of >15 bpm for >15 minutes.
2. Normally there should be presence of two or more accelerations during a 10-minute period.
3. Absence of acceleration for more than 40 minutes is suspicious.
Deceleration
1. Decrease in heart rate of >15 bpm for >15 minutes.
2. Early decelerations
a. Onset, nadir and recovery of decelerations synchronous with contractions
b. Associated with foetal head compression that causes a rise in intracranial pressure and results in vagal stimulation.
Usually observed in late first stage to second stage of labour and is usually benign.
3. Late decelerations
a. Onset, nadir and recovery are out of phase with contractions for >30 sec delay.
b. It is associated with hypoxia or placenta insufficiency:- when uterus contracts, blood flow is decreased.
Chemoreceptor-vagal response causes direct myocardial depression and decelerations. The lag period reflects the time
necessary for the foetal pO2 to fall below a critical level during a contraction. This is usually pathological.
4. Variable decelerations
a. Variable decelerations decelerations vary in shape and timing with respect to each other
b. It is associated with umbilical cord compression, but may or may not indicate hypoxia.
5. Sinusoidal pattern
a. A typical pathological sinusoidal pattern: Stable baseline rate with regular oscillations having an amplitude of 5-15
bpm; amplitude above and below are equal
b. It is associated with fetal anaemia
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Figure 33 Early onset. These may be normal in late labour but should not be ignored if persistent or severe.
Figure 34 Late onset. These may indicate hypoxia.
Figure 35 Variable onset. These are thought to be due to cord compression. They are quite common and may be related to the
mother's position. They should not however be ignored if persistent or associated with other adverse features.
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Royal College of Obstetricians and Gynaecologists (RCOG) Categorisation of Foetal Heart Rate features
1. Normal: All features fall into the reassuring category.
2. Suspicious: 1 feature falls into the non-reassuring category.
3. Pathological: 2 or more features fall into the non-reassuring category; OR 1 or more features fall into abnormal category.
Features Baseline Variability Decelerations Accelerations

Reassuring 110-160 5 None Present
Non-reassuring 100-109 <5 for 40-90 mins 1. Early Absence for >40 mins.
deceleration The absence of
2. Variable acceleration with an
deceleration otherwise normal CTG
3. Single is of uncertain
prolonged significance
deceleration
up to 3 mins
Abnormal 1. <100 <5 for >90 mins 1. Atypical
2. >180 variable
3. Sinusoidal decelerations.
pattern > 10 2. Late
mins decelerations
3. Single
prolonged
deceleration
for > 3 mins
Uterine contractions
1. It is recorded by external tocography: a strain gauge device detecting forward movement and change in the abdominal wall
contour on account of the contractions. It cannot measure the actual intrauterine pressure and hence not accurate. Note that
Itis also not accurate in obese or restless patients.
2. Intrauterine pressure catheter can measure the actual intrauterine pressure with risk of infection and trauma and hence
limited clinical use.
Optimal hypertonus
Frequency 3-4/10 min >4 /10 min
Duration 40-90 sec > 90 sec
Peak 50-75 mmHg >80mmHg
Basel tone 8-12 mmHg >15mmHg
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Foetal bradycardia
1. Foetal bradycardia for 1 minute and not yet recovered
a. Inform medical officer
b. Look for any possible causes and manage accordingly:-
i. Uterine hyperstimulation: stop any oxytocic administer hexoprenaline
ii. Hypotension due to regional anaesthesia:-
- Fluid replacement
- Inform anaesthetist
- Prepare vasopression which may be needed by anaesthetist
iii. Hypotension due to aorto-caval compression: lateral tilting of patient
iv. Placental abruption, uterine rutpure, cord prolapse: immediate delivery
c. If 'bradycardia' is suspected to be maternal pulse, rule out the possibility either by maternal oxymetry, USG Foetal
heart or Foetal scalp electrode
d. Take blood for cross-matching / set-up IV line if not yet done
e. Enquiry of time of last food / fluid intake if not yet done
2. Foetal bradycardia persists for 3 minutes and not yet recovered
a. Start preparing operation theatre for caesarean section
b. Inform anaesthetist to stand-by
c. Inform health care assistant to stand-by
d. Check cervical status if vaginal delivery is feasible
e. Prepare patient by explaining the following:-
i. The current foetal condition
ii. If foetal bradycardia persists, immediate delivery (caearean or instrumental) may be required
iii. Possible complications of operative delivery
3. Foetal bradycardia persists for 5 minutes and not yet recovered
a. Decide caesarean section and get consent from patient immediately
b. Aim at decision-to-delivery interval of less than 15 minutes
c. Transfer to theatre as quick as possible, perform urinary bladder catheterisation and stripping of pubic hair in the
theatre
d. Put the patient under anaesthesia whichever way is the fastest (which is general anaesthesia in most of the cases)
e. Foetal heart rate would not be monitored in the theatre unless requested by the doctors
4. Foetal bradycardia recovers before decision of caesarean Depends on the foetal condition and the underlying cause of
bradycardia, foetal scalp blood sampling or early delivery may be indicated
5. Remark Decision for delivery could be made earlier depending on the actual situation and presence of any other risk
factors
Foetal scalp electrode

It is an electrode anchored to the foetal scalp to monitor the foetal heart rate during intrapartum period. Unlike the abdominal
detector which uses Doppler effect to detect the foetal heart rate, the scalp electrode can pick up the ECG. The heart rate is
computed by analyzing the PP interval. The ECG waveform analysis is a method of intrapartum foetal monitoring.
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Foetal scalp blood sampling
It is a method of intrapartum foetal monitoring. Blood from the foetal scalp is aspirated with amnioscope and the blood pH, partial
pressure of carbon dioxide (pCO2), base excess are analysed.
1. A foetal scalp pH of 7 or less is strongly associated with a poor outcome
2. A pH of 7.20 or less suggests the need to deliver immediately
3. A base deficit of > 9mmol/L is also abnormal
pH Action
=<7.20 Delivery indicated
7.21-7.24 Repeat FBS within 30 minutes or consider delivery if rapid fall since last sample
>=7.25 FBS should be repeated if the CTG abnormality persists
Procedure
a. Need rupture of membrane
b. Underseptic techniquie, insert amnioscope
c. Scalp is dried with sponge or swab on long sponge-holders
d. Scalp sprayed with ethyl chloride to induce hyperaemia and the area is covered with a think layer of paraffin jelly so that the
blood will not run down along the scalp
e. A blade is used to make a small incision
f. The blob of blood is touched with capillary tube
Protocol, as of 23 February 2004.

1. Preferably perform with patient in left lateral position.
2. Should not perform if breech presentation.
3. Repeat procedure (within 30-60 min of the first sample) if:
a. Initial scalp pH 7.20-7.25 or
b. persistent CTG abnormality
c. Inform Midcall-1 if repeated sampling is considered
Amnioscope
This is a set of instruments for performing foetal scalp blood sampling. It includes:-
1. Hollow tube that is put into the vagina for the examiner to see through and perform the procedure.
2. A blade on a long handle to make a small incision on the foetal scalp.
3. A light source.
4. A capillary tube to aspirate blood from the foetal scalp.
Foetal distress
Definition
This is a clinical diagnosis made antenatally or intrapartumly signifying an adverse foetal condition that requires an immediate
delivery, otherwise foetal hypoxic damage or birth asphyxia may follow.
Diagnosis
The clinical suspicion of foetal distress is usually based on foetal heart rate pattern on the cardiotocogram (CTG). Although CTG
is sensitive, it is not specific for foetal hypoxia and acidosis. Correct interpretation of CTG is very important in making the
diagnosis, and foetal scalp blood sampling should be performed whenever possible to assess the foetal blood pH. Finding of
acidosis (less than 7.2 during labour) confirms the diagnosis and the foetus should then be delivered immediately by caesarean
section or by instrumental delivery.
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Apgar score
Introduction
A numerical scoring system for neonatal assessment usually applied at 1 and 5 minutes after birth to evaluate the condition of the
baby, based on heart rate, respiration, muscle tone, reflexes and colour:
Sign/Score 0 1 2
Heart rate per minute Absent <100 >100
Respiratory effort Absent Weak Strong
Muscle tone Limp Some flexion Well flexed
Reflex response None Weak Strong
Colour Blue or pale Body pink, extremities blue Pink
Use of Apgar score

Previously low Apgar score was thought to be predictive to neonatal outcome. A lower score implied birth asphyxia and predicted
the development of cerebral palsy and mental retardation in future. However, it is now clear that the correlation between low
Apgar score and low cord pH (which reflects foetal hypoxia) is very poor. There are many causes of low Apgar score other than
birth asphyxia, including neonatal depression by maternal transfer of narcotic analgesic. The Apgar score is now mainly used as
an indicator for the need of neonatal resuscitation.
Birth asphyxia
Asphyxos in Greek means without pulse. Birth asphyxia is a poorly defined term. Originally it means depression at birth, which is
assessed by Apgar scoreIn the past, depression at birth was always assumed to be associated with hypoxia and acidosis. However,
it is now clear that depression at birth can be due to various causes, such as congenital abnormalities, drugs or trauma. Therefore,
it has been proposed that birth asphyxia should be defined biochemically as the presence of hypoxia, hypercarbia and acidosis, by
blood gas analysis using umbilical arterial blood.
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5. Operative delivery
Episiotomy
Definition and aim of episiotomy
It is a surgical incision of the perineum and vagina in order to prevent perineal tear during vaginal delivery.
Types of episiotomy
1. Posterolateral incision
It is the most common method. The incision starts from the posterior forchette of vagina and then goes postero-laterally, at 45
degrees from the midline. The main advantage is that it provides the best protection against anal sphincter damage. However,
it is more difficult to repair as the edges may retract unequally.
2. Median incision
It is a midline incision from the posterior forchette downwards. It may cause anal sphincter damage, although it is relatively
easier to repair (provided that there is no anal tear).
3. J-shaped incision
The incision starts from posterior forchette, initially in downward direction and then goes laterally. It is a theoretical
compromise of the above two.
Indications of episiotomy
1. The usual practice in Hong Kong is routine episiotomy. All nulliparous and almost all primiparous women would have an
episiotomy at delivery. Selective episiotomy is advocated in many Western countries. It is argued that episiotomy is not
necessary in majority of pregnant women, and the incision may even result in more perineal tear. The experience in Chinese
favours a routine episiotomy.
2. Episiotomy should be performed in instrumental delivery, delivery of macrosomic babies, vaginal breech delivery, and
delivery in occipito-posterior position.
3. In the vaginal delivery of a premature foetus, episiotomy may be needed to protect the foetal head from being forced
repeatedly against an unyielding perineum.
4. Other indications include shoulder dystocia, previous third degree perineal tear and any other conditions when considered
necessary by the attendant.
Procedures of episiotomy repair

1. Examine for any vaginal and cervical tear before repair.
2. Apply adequate local anaesthetics (10ml of 1% ligocaine infitration).
3. Repair with absorbable stitch such as 2-0 Dexon or Vircyl.
4. Repair vaginal wound with continuous stitch.
5. Repair perineal wound with interrupted stitches, followed by a superficial continuous subcuticular stitch.
6. At the end of the repair:
a. Perform digital vaginal examination to ensure an adequate vaginal opening.
b. Perform digital rectal examination to exclude any suture penetrated through the anorectal mucosa.
c. Remove any gauze packed inside the vagina.
Complications of improper episiotomy repair

- Ano-vaginal fistula
- Vaginal and vulval haematoma
- Wound infection and dehiscence
- Dyspareunia
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Cervical Tear
Cervical lacerations up to 2 cm are common and do not require suturing if there is no active bleeding.
Deep cervical laceration should be repaired or supervised by Mid-call-1. This may require general or regional anaesthesia,
especially when there is extension into the vaginal vault
Perineal tear
Classification
1. First degree tear, when only skin and mucosa are involved.
2. Second degree tear, when the muscles and the perineal body are involved.
3. Third degree tear, when the anal sphincter or rectum is involved.
Figure 36 Different degrees of perineal tear. (Left to Right) First, second and third.
Complications
2. Anal sphincter damage resulting in faecal incontinence
3. Poor healing of the wound resulting in ano-vaginal fistula

First and second degree:-Similar to repair of episiotomy.
Third degree:-The repair must be under general or regional anaesthesia. After the repair, the patient should be put on low
residue diet for three days, faecal softener (e.g. lactulose 10ml tds) and antibiotics (e.g. Augmentin 375mg tds)
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Operative delivery
1. Caesarean section (30.4%)
2. Vacuum extraction (9.7%)
3. Forceps delivery (0.9%)
Instrumental delivery
What is instrumental delivery?
There are two types of instrument delivery:
1. Vacuum extraction
2. Forceps delivery
These allow the use of traction if delivery needs to be expedited in the second stage of labour. The overall instrumental delivery
rate is around 10.6% 15% in PWH
Level of instrumental delivery

Outlet The foetal head is at or on the perineum
Scalp is visible at the introitus without separating the labia
Foetal skull has reached the pelvic floor
Sagittal suture is in anteroposterior diameter or right or left occiput anterior or posterior position
Rotation does not exceed 45
Low-cavity The leading point of the foetal skull is at station +2 cm, but not on the pelvic floor rotation 45 (left or right
occiput anterior to occiput anterior, or left or right occiput posterior to occiput posterior rotation > 45
Mid-cavity Station < +2cm but the head is engaged
High-cavity Not included in classification and any instrumental delivery for level higher than mid-cavity should be
abandoned because of significant risk
Level Head Descend Head position

Outlet Foetal head reaches pelvic floor and at Sagittal suture is in anteroposterior
the perineum. diameter.
Direct OA or OP.
Low Below S+2 cm Direct OA or OP
Mid Engaged Rotation > 45o
S to S+2 cm OT position
High Unengaged head Any position
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Indications
1. Maternal indications
a. Maternal exhaustion
b. Neurological disorder where voluntary efforts are contraindicated or impossible.
c. Avoid maternal exertion which may be dangerous to the mother, such as:
i. Severe cardiac diseases
ii. Hypertensive disorders, pre-eclampsia
iii. Liver cirrhosis with oesophageal varices:-risk of bleeding
2. Foetal indication
a. Foetal distress
i. Abnormal heart rate pattern
ii. Abnormal scalp pH
iii. Meconium stained Liqour
b. Cord prolapse
c. Vaginal breech delivery (use piper forceps only for after coming head)
Prerequisites for instrumental delivery

1. Maturity 34 weeks
2. Foetal head must not be palpable abdominally (Head 0/5 or at most 1/5 palpable abdominally)
3. Foetal head must be at or below the level of the ischial spines (Station of at least S+1)
4. Vertex presentation (except for forceps delivery)
5. Cervix must be fully dilated
6. Ruptured membranes
7. Position of the head must be known
8. There must be adequate analgesia
9. Bladder should be empty
10. Procedure must be conducted by experienced operator
Trial of instrumental delivery

Attempts of vaginal instrumental delivery with the full knowledge that a certain degree of cephalopelvic disproportion at the
mid-pelvis or outlet may make the procedure incompatible with safety for the foetus. The operating room should be both equipped
and staffed for immediate caesarean section. If there is no descend after good application of the instrument and traction, the
procedure should be abandoned and caesarean section should be performed.
Protocol, as of 24 February 2004

1. Abandon instrumental delivery if:-
a. No descent with each pull
b. Head not crowned after 3 pulls
c. Delivery not completed after 5 pulls or within 15 minutes from first pull
d. Slipped cup in the absence of apparatus failure
2. Minimum analgesia required
a. Ventouse extraction perineal infiltration
b. Non-rotational forceps pudendal block
3. Special conditions:
a. Gestation < 34 weeks
i. Should be performed or supervised by MRCOG
ii. Forceps is preferred
b. Mid cavity forceps delivery Should be performed or supervised by MRCOG
c. Rotational forceps delivery experienced FHKAM should be present
d. Trial of instrumental delivery
i. Should be performed or supervised by MRCOG
ii. Operation theatre should be ready for immediate caesarean section.
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Forceps
What are Forceps?
It is a pair of instrument designed for vaginal instrumental delivery. A forceps is divided into following parts:
1. Handle Is to produce a compression force on the impacted head and to facilitate traction
2. Lock Is where the pair articulates to each other. There are three types of lock:-sliding (in Kielland's forcep), crossover (in
most of the forceps), and fixed pivot.
3. Shank forceps with long shank is designed for delivery of foetal head at higher station (such as in mid and low-cavity).
Forceps with short shank (Wrigley's forceps) are used in outlet instrumentation. The longer shank increases maternal
discomfort and risk of soft tissue trauma.
4. Blade consists of a cephalic curve which is ovoid in shape designed for a moulded foetal head, and a pelvic curve to fit the
maternal pelvis
5. The axis of the blades and that of the handles can be parallel (in Kielland), or angled (in most of other forceps)
6. The variation in the design of the different parts are made for use in different situation:
a. Kielland's forceps are designed for rotation of head in mid to high-cavity instrumental delivery. Besides a long shank, the
pelvic curves are reduced to facilitate rotation inside the pelvic cavity. They have a sliding lock that facilitates correction
of asynclitism.
b. Wrigley's forceps are used for outlet delivery, and have a short shank and handle
c. Piper's forceps are designed for delivery of after-coming head in vaginal breech delivery. It has a long shank as well as an
angle between the axis of the blades and that of the shank.
Indications and prerequisites

See instrumental delivery
Figure 37 Wrigley's Forceps
Figure 38 Anderson's / Simpsons forceps
Figure 39 Kielland's Forceps
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How to perform assess & prepare
1. Explain the indication, risk
2. Consent
3. Abdominal palpation of the fetal size and head engagement
4. Position the patient
5. Clean and drape
6. Catheterisation of the bladder
7. Confirm fully dilated cervix & membranes ruptured
8. Examine the position and station, look for caput, moulding, assess the size of the pelvis
9. Analgesics: (pudendal block, or epidural in case of forceps)
10. Documentation
11. Left hand Left blade left side of mother
Complications
1. Foetal Trauma
a. Intracranial haemorrhage.
b. Cephalic haematoma.
c. Facial / Brachial palsy.
d. Injury to the soft tissues of face & forehead.
e. Skull fracture
2. Maternal
a. Genital tract injury
b. Post partum haemorrhage Due to trauma, atonic uterus or anaesthesia.
c. Shock Due to blood loss, dehydration or prolonged labour.
d. Sepsis Due to improper asepsis or devitalisation of local tissues.
e. Anaesthetic hazards
f. Delayed or long-term sequel - Genital prolapse & stress incontinence
When use forceps instead of vacuum?

1. Prematurity increase risk of intracranial bleeding
2. Face presentation
3. After-coming head in breech presentation.
4. Maternal ITP (risk of fetal thrombocytopenia or bleeding tendency)
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Complications
1. Foetal injury
a. Facial bruising
b. Facial nerve palsy
c. Depression fracture of foetal skull
2. Maternal injury
a. Perineal, vaginal and cervical tears
b. Postpartum haemorrhage Complication rate is higher with higher-cavity forceps delivery and malposition of the forceps.
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Vacuum extraction
What is vacuum extraction?
It is a form of instrumental delivery and the instrument consists of the following parts:
1. Cup:-to be applied over the vertex area of the foetal head. It can be made of metal, or silastic material
2. Vacuum pump:-a electric pump to create a vacuum pressure
3. Rubber tubing connecting the vacuum pump and the cup
Figure 40 (Left to right) Vacuum cups for OA and OP position respectively; vacuum tubing; and vacuum machine.
Indications and prerequisites

See instrumental delivery
Procedure
1. Informed consent
2. Anaesthesia by local infiltration.
3. Insertion of the vacuum cup and apply it to the vertex.
4. Apply negative pressure to 60 cmH2O.
5. Apply traction synchronise to maternal effort.
6. Adequate episiostomy.
Complications
1. Foetal injury
a. Cephalhaematoma
b. subaponeurotic haematoma
2. Maternal injury
a. Tear of lower genital tract
b. Postpartum haemorrhage
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Caesarean section
Definition
A surgical procedure that involves the delivery of the foetus through an abdominal incision. It accounts for about 20% of all
births.
Classification
1. Lower segment CS (99.6%)
a. It is a transverse incision over the lower segment of the uterus
b. It is the most common incision used nowadays
c. Compared with classical incision, it is associated with less operative blood loss, more ease to repair, and the scar is less
likely to rupture (0.5%, see uterine rupture).
2. Classical CS (0.4%)
a. It is a midline longitudinal incision over the anterior wall starting from the fundus
b. It allows larger space for delivery
c. It is an old type of incision but is still used in modern obstetrics in some situations:-
i. In preterm delivery when lower segment has not been formed yet
ii. In placenta praevia where lower segment is covered with placenta and delivery may be difficult or cause severe
bleeding
iii. In transverse lie
iv. In delivery of conjoint twins
Indications
1. When vaginal delivery is not possible or at high risk because of mechanical factors:
a. Contracted pelvis
b. Cephalo-pelvic disproportion
c. Failure to progress of labour
d. Failed induction of labour
e. Failed instrumental delivery
f. Macrosomia
g. Malpresentation such as:
i. Breech presentation, in particular footling breech
ii. Transverse lie
h. Placenta praevia
2. When immediate or early delivery is required before cervix is fully dilated:
a. Foetal distress
b. Maternal distress or complications such as pre-eclampsia, eclampsia
c. Intrauterine infection
3. When the labour progress is associated with foetal or maternal risk
a. IUGR foetus:-may be in distress when undergoing the stress of labour
b. Previous uterine scar or injury
i. Risk of uterine rupture during labour
ii. High risk in classical scar, myomectomy scar and previous history of uterine tear
Procedure
1. Epidural anaesthesia.
2. Abdominal incision:-usually Pfannenstiel incision is performed
3. Dissection of urinary bladder to expose the lower segment of uterus
4. Incision of the lower segment
5. Delivery of the baby; followed by delivery of the placenta
6. Repair of the lower segment, usually in two layers, with haemostasis
7. Closure of the abdominal wall (parietal peritoneum, rectus sheath, skin). Usually a rediac drain is inserted into the subrectus
space to prevent haematoma formation.
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- 190 -
Maternal Complications
- Excessive bleeding
- Infection:-endometritis, wound infection
- Uterine injury:-uterine tear
- Visceral injury:-most common:-bladder
- Complications related to anaesthesia
- Deep vein thrombosis and thromboembolism
- The maternal death rate is three times higher than with natural delivery
Management of wound dehescience and infection

1. Initial assessment
a. Inform medical officer and Midcall-1 in charge of the case and the principal surgeon for the operation.
b. Initial wound assessment should be performed by a senior midwife, an intern and the medical officer in charge.
c. Record the size and depth of the wound, the presence or absence of haematoma/pus/necrotic tissue/cavity and
surrounding cellulitis.
d. Take a wound swab for culture and sensitivity.
2. Care of the wound
a. Irrigate wound with normal saline and dress the wound one to three times daily. Frequency of dressing is to be decided
by Medical officer in charge. Usually once daily dressing would reduce disturbance of the wound and promote healing.
b. Liaise with midwife for the best type of dressing.
a. Empirical treatment of Augmentin 375mg tds should be started while awaiting for swab culture result.
b. Patients allergic to penicillin should use erythromycin 500mg qid.
c. Augmentin has good coverage for Group B strep, most G-negative oragnisms, most anaerobes and also Staph. aureus
(methicillin-sensitive), although sensitivity of these organisms to Augmentin is not always tested e.g. Staph. aureus
d. If in doubt of the sensitivity of the cultured organism to Augmentin, please consult microbiologist before changing the
already-started antibiotic regimen.
e. Antibiotics should continue for at least 7-10 days.
4. Resuturing of the wound
a. Time of resuturing is to be decided by the Medical Officer in charge
b. General anaesthesia is preferred to resuture the wound, unless the patient prefers local anaesthesia
c. Re-suturing should be performed either in the main Gynaecological operation theatre (under GA) or the ward treatment
room under aseptic technique (under LA). Surgeons should be properly gowned up.
d. Removal of the new sutures should be performed at least 7-10 days after re-suturing. Patient can be managed as
out-patient after re-suturing and followed up in the ward for the removal of sutures.
e. In case of a second wound dehiscence, Midcall 1 is to be involved to take personal care of this complicated patient.
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Trial of scar
Incidence: 17.2% of patients with one previous uterine scar.
1. All patients with previous caesarean section are strongly encouraged to have trial of scar (TOS) unless:
a. More than 1 previous sections;
b. Previous classical Caesarean section;
c. Previous major uterine tear in which TOS was not recommended by the attending obstetricians;
d. Previous myomectomy with entry into endometrial cavity;
e. Previous hysterotomy;
f. Other obstetric indications for Caesarean section.
2. Antepartum Management
a. During the first antenatal clinic, counsel patient for TOS. Arrange admission at 41 weeks for uncomplicated
pregnancy (see postdate pregnancy).
b. For those cases that require a repeat Caesarean section, arrange elective Caesarean section at 37-38 weeks.
c. Meanwhile, arrange follow up in MCH.
d. There is no need for radiological pelvimetry.
e. If a written documentation of the nature of the scar is not available, the mode of delivery should be determined by
MRCOG.
f. If the patient strongly refuses TOS despite explanation despite counselling by MRCOG, arrange elective Caesarean
section at 37-38 weeks.
3. Intrapartum Management
a. Inform MRCOG if vaginal PGE2 or syntocinon is needed for induction or augmentation of labour.
b. To labour ward once there are regular contractions or the cervix is effaced.
c. X-match and insert iv line
d. Monitor progress, maternal and fetal well-being
e. Intrauterine pressure monitoring is NOT mandatory
f. Epidural analgesia is not contraindicated.
g. Suspect scar rupture if abnormal fetal heart rate, abnormal abdominal pain, vaginal bleeding or high presenting parts.
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General Gynaecology
0. Gynaecology
Gynae means women. Gynaecology is a branch of medicine dealing with the diagnosis and treatment of disorders affecting the
female reproductive organs. It is subdivided into:
1. General gynaecology
2. Gynae-oncology
3. Reproductive medicine and Endocrinology
4. Urogynaecology
General gynaecology
1. Menstrual disorders
2. Menopause and Hormone replament therapy
3. Birth control (contraception and sterilisation)
4. Early pregnancy complications
5. Benign tumours of ovaries and uterus
6. Endometriosis and adenomyosis
7. Infections
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1. Menstrual problems
Menstrual disorders
Type of menstrual disorders

1. Abnormal onset and cessation
a. Menarche starts too early:-precocious puberty
b. Menarche does not occur:-primary amenorrhea
c. Menopause occurs too early:-premature menopause
2. Abnormal volume
a. Too much:-Menorrhagia (Polymenorrhea)
b. Too little:-Hypomenorrhea
3. Abnormal regularity
a. Too infrequent:-oligomenorrhea
b. Stopped for 6 months / 3 consecutive cycles: after menarche- Secondary amenorrhea
4. Pain and discomfort
a. Dysmenorrhea
b. Premenstrual syndrome
5. Remark postcoital bleeding, postmenopausal bleeding are not 'menstrual' disorders.
Menstrual cycle
Menstruation resulted from the changes in endometrium in response to sex hormones which are under the regulation of the
hypothalamic-pituitary-ovarian axis. During the first half of the cycle, oestrogenic effect is dominant and causes proliferation of
the endometrial glands (proliferative phase). After ovulation, progestogenic effect becomes dominant, inhibits proliferative
changes and stimulates the secretary function of the endometrial glands (secretary phase). Decidualisation is irreversible. When
serum concentrations of these hormones decline, endometrial shedding is initiated and the menstrual loss consists of endometrial
glands and secretions as well as blood. The first day of the onset of the menstruation of the preceding cycle is defined as the last
menstrual period (LMP).
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Amenorrhea
Definition
1. Primary amenorrhea
a. No menstruation by the age of 14 accompanied by failure to grow properly or develop secondary sexual
characteristics, or
b. No menstruation by the age of 16 when growth and sexual development are normal
2. Secondary amenorrhea
Absence of menses in a woman who has menses before for:-
(1) 6 months, or
(2) 3 consecutive cycles,.
3. Oligomenorrhea
Occurrence of menses of:-
(1) 5 or less occasions per year, or
(2) more than 6 weeks in most of the cycles
Causes
To have normal cyclic menstruation, one must have:
1. An intact hypothalamus-pituitary-ovarian axis producing normal ovarian cycles
2. A normal endometrium that respond to ovarian hormones
3. A normal outflow tract:-cervix, vagina and vulva
Therefore amenorrhea occurs when there are:

1. Physiological:- Pregnancy, lactation, menopause.
2. Failure of hypothalamus-pituitary-ovarian axis: (WHO Type II)
a. Hypothalamus:-anorexia nervosa, Kallman syndrome, etc
b. Pituitary:- Stress, Anorexia nervosa, antipsychotics, prolactinoma
c. Ovary:-
i. Ovarian failure (WHO Type III) [Hypergonadotrophic amenorrhoea]:- Turner syndrome, Testicular feminisation
syndrome, ovarian dysgenesis, resistant ovarian syndrome, premature menopause
ii. Ovarian hormone dysfunction (WHO Type I)[Normogonadotropic amenorrhoea]:- Polycystic ovarian disease
3. Absence of normal endometrium:
a. Uterine agenesis, Mullerian tract abnormality, androgen insensitivity syndrome
b. Asherman syndrome, TB endometritis.
4. Obstruction of outflow tract:
a. Vaginal:-transverse vaginal septum, vaginal agenesis or hypoplasia
b. Vulval:-Imperforate hymen
5. Other endocrinopathy
a. Hyperthyroidism
b. Cushings syndrome
Remarks
1. Endocrinopathologies usually cause secondary amenorrhea except primary ovarian failure such as Turner Syndrome and
ovarian dysgenesis.
2. Structural abnormalities of uterus and outflow tract often result in primary amenorrhea except in Asherman syndrome.
3. Pregnancy and natural menopause are two physiological causes of amenorrhea that should be considered in women at
reproductive age and perimenopausal age respectively.
4. Amenorrhoea is related to a spectrum of pathologies, and it is not the only but one of the different manifestations. Patients can
present with absent secondary sexual maturation, infertility or long term compications, e.g. endometrial cancer, osteroporosis,
cardiovascular diseases, etc.
Clinical evaluation
1. General examination
2. Body weight, height and growth
3. Secondary sexual characteristic, breasts and body hair
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Investigations
Depends on the clinical suspicion, the following investigations are required:
1. Karyotyping:-Turner syndrome, testicular feminisation syndrome
2. Hormonal profile:-FSH for ovarian failure, LH/FSH ratio for PCOD, prolactin for hyperprolactinemia
3. Radiological examination for structural abnormalities of genital tract such as uterine agenesis.
4. Radiological examination of urinary tract may also be required in case of abnormal genital tract as both systems are related in
embryonic development
Primary amenorrhoea Secondary amenorrhoea

More focus on growth and development More focus on endocrine pathologies
History History
- Family history of menarche - Menstrual History
- Growth and sexual development - Medical & Drug History
- Medical and Drug history - Symptoms related to aetiology:
Physical Examination - Stress, weight loss, exercise
- Height, weight, body form (? Turner syndrome), growth - Galactorrhea, headache, visual disturbances
- Secondary sexual characteristics: (Breast beware of AIS, - Hirsutism, hotflush
axillary and pubic hair, external genetalia ? signs of Physical Examination
virilism) - BMI
- Stigmata of other endocrine diseases
- Goiter
- Galactorrhea, bitemporal hemianopia
- Hirsutism, virilism
- Stigmata of hypo-estrogenism
- Atrophic genetalia
* Fertility wishes
1. Karotyping: 46XX = Pure Gonadal Dysgenesis; 46X = Turner Syndrome; 46XY = AIS
2. Hormone assay: FSH, LH, E2, PRL, TFT, androgens; mid-luteal progesterone (confirm ovulation); hCG
3. Radiological examination
4. USG Pelvis (presence of uterus / other structural abnormalities), Ovary (PCO),
5. MRI pituatary
6. Others:
- Hysteroscopy: Asherman, TB
- Laparoscopy and EUA: for Gonad, Uterine abnormalities, Vaginal or vulval abnormalities
- Autoimmune (premature ovarian failure)
Treatment
1. Treat underlying causes if possible
2. Restore fertility:
a. Endocrinopathologies are always associated with anovulation and infertility, and may require ovulation induction or in
vitro fertilisation.
b. Patients with ovarian failure or absence of uterus or normal endometrium, are infertile. Oocyte donation and surrogacy
are the alternatives.
3. Restore sexual function Vaginal malformations (septum, hypoplasia, agenesis) require surgical correction
4. Restore growth and development Patients with Turner syndrome are short and with poor breasts development. Early
hormonal replacement therapy is required.
5. Protect against any long-term complication
a. WHO Type I Protect against chronic unopposed E2 stimulation (CA Breast, CA endometrium) by OCP.
b. WHO Type II & III Protect agains hypoestrogenism (Osteoporosis and cardiovascular disease) by HRT.
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1. Criteria for evaluation
a. Primary amenorrhoea
i. Absence of menses at the age of 16
ii. Absence of menses at the age of 14 if there are no secondary sexual characteristics
b. Secondary amenorrhoea
i. Absence of menstruation for more than 6 months in a woman who has previously menstruated
2. Work up
a. At the first visit
i. Exclude pregnancy
ii. Check serum FSH, LH, E2, prolactin & TFT
iii. Progestagen withdrawal test (PWT):-Give Norethisterone 5mg tds oral for 1 week & check for any
vaginal bleeding after progestagen withdrawal
b. At the second visit
i. Classification of the etiologic groups of amenorrhoea & further work up
Etiologic groups FSH & LH E2 Prolactin PWT Further work up
Hyperprolactinaemic Low Normal Low High +ve MRI pituitary
Normal (>1000IU/L)
Normogonadotrophic Normal Normal Normal +ve USG pelvis to exclude
PCOS
Hypergonadotrophic High Low Normal -ve Karyotyping
(>20IU/L)
Hypogonadotrophic Low Low Normal -ve ---
Anatomical Normal Normal Normal -ve CEPWT ve & USG
pelvis
ii. CEPWT (combined estrogen & progestagen withdrawal test)
- Give three cycles of Nordette & check for any bleeding after withdrawal
- Absence of withdrawal bleeding suggests an abnormal genital tract or a non-functional endometrium
3. Management
a. For hyperprolactinaemic amenorrhoea Follow the protocol Hyperprolactinaemia
b. For normogonadotrophic amenorrhoea
i. Follow the protocol PCOS if the diagnosis of PCOS is established
ii. Give Nordette if not planning for pregnancy
c. For hypergonadotrophic amenorrhoea
i. Establish the diagnosis based on the karyotyping result
- Karyotype:-45XO Diagnosis:-Turners syndrome
- Karyotype:-46XY
z Diagnosis:-Pure gonadal dysgenesis
z Advise gonadectomy because of risk of malignant transformation
- Karyotype:-46XX
z Diagnosis:-Idiopathic ovarian failure
z Check ANA & sTSH
z If ANA positive, check anti-dsDNA
z If anti-dsDNA positive or sTSH are abnormal, refer to combined gynae-endocrinology
clinic
z Counseling by FHKAM
z No curative treatment
z Implication of infertility
z Implication of long term hypoestrogenism
z Benefits and risk of long term HRT and refer to HRT clinic
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d. For hypogonadotrophic amenorrhoea
i. Reversible causes (e.g. stress, excessive weight loss) are common & should be corrected
ii. If anorexia nervosa is suspected:- Refer to psychiatry clinic
iii. If organic cause is suspected (e.g. with other pituitary insufficiency):-Refer to combined
gynae-endocrinology clinic
iv. Give OC pills or HRT to prevent hypoestrogenism
- Give Nordette if:-
z Contraception is needed or
z Body height or breast development is suboptimal
- Otherwise, give combined cyclical HRT
- Review the treatment if the reversible cause is corrected
e. For anatomical amenorrhoea
i. Delineate the nature of anatomical anomalies by physical examination (e.g. imperforate hymen, transverse
vaginal septum) and pelvic ultrasound (to look for uterine anomalies)
ii. If the anomalies are due to Mullerian dysgenesis, arrange USG kidney to look for any associated renal
abnormalities
iii. Treatment, if any, is directed to the anatomical anomalies & to be decided by FHKAM
iv. Counseling on the implication of sexual function and fertility potential
v. No need for HRT
Oligomenorrhea
Defined as in Amenorrhea. It is common among teenagers as well as perimenopausal women, and is usually associated with
anovulation as a result of underlying endocrine disorders such as polycystic ovarian disease (PCOD) and hyperprolactinemia.
Cryptomenorrhea
Cryptomenorrhea means hidden menstruation. This occurs when endometrial shedding takes place but the menstrual loss cannot
escape due to blockage of parts of the lower genital tract, usually as a result of congenital malformations:-e.g. In vaginal atresia,
transverse vaginal septum, and imperforate hymen. The uterus or vagina is distended with menstrual blood. Patients present with
primary amenorrhea, cyclic lower abdominal pain, and abdominal distension, and urinary retention (due to distended uterus).
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Polycystic Ovarian Disease (PCOD)
What is Polycystic ovarian disease
A condition characterized by chronic anovulation with hyperandrogenemia, raised LH secretion with alternation of the normal
relationship between LH and FSH leading to raised LH to FSH ratio. No specific underlying diseases of the adrenal or pituitary
glands can be demonstrated.
Epidemiology
It affects:-
1. 2% of women in reproductive age
2. 30% of women with amenorrhea
3. 80% of women with oligomenorrhea
4. 80% of women with anovulatory infertility
5. 70% of women with hirsutism
Pathology of ovaries
1. Macroscopic:-bilateral enlarged and lobular ovaries
2. Microscopic:-multiple atretic follicles (represent the polycystic features), theca cell hyperplasia and generalised increase in
stroma
Figure 41 Macroscopic (Left) and microscopic (Right) appearance of polycystic ovaries.

Pathogenesis
1. There is evidence of autosomal dominant mode of inheritance, with variable expression
2. The exact mechanism of endocrinopathology is unknown. It can be reside within the ovaries or secondary to extra-ovarian
disturbances (from adrenal glands or fatty tissue). However, once it is initiated, it is self-perpetuating.
a. Elevated oestrogen level (resulted from conversion of androgens in fatty tissue and ovaries).
b. High oestrogen environment feedback on pituitary gland gonadotropin secretion leading to a relative excess of LH
secretion compared to that of FSH.
c. Consequently, there is failure of ovulation as the developing Graafian follicle depends upon stimulation of FSH.
d. FSH stimulates the conversion of androgen to oestrogen by inducing ovarian aromatase, is also impaired.
e. Androgen production is also enhanced by LH.
f. Increase in adrenal glands androgens (androstenedione DHEA and testosterone)
Clinical features
1. The four typical features are:
a. Oligo-amenorrhea
b. Infertility
c. Obesity
d. Hirsutism
2. Remark:-Not all patients have all the four features. Some features are more dominant while others may be less obvious or
absent.
3. Onset of symptoms:-usually gradual
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Complications
1. Reproductive disorders
a. Infertility
b. Recurrent abortion
c. High risk of ovarian hyperstimulation syndrome (OHSS) when undergoing
ovulation induction
2. Metabolic disorders Risk of insulin resistance, hypertension.
3. Long term risk of cancer Risk of endometrial hyperplasia and endometrial carcinoma
Biochemical features
1. Increased LH levels
2. Elevated (early follicular) LH/FSH ratio > 3
3. Increased sex-hormone-binding-protein
4. Increased androgen secretion
5. Associations with hyperprolactinemia and hyperinsulinemia
Ultrasound features
1. Bilateral enlarged ovaries
2. Multiple (>10 each side) small cysts of size 1-5mm arranged at the periphery of the ovaries (necklace appearance)
3. Thickened stroma
Diagnosis
1. Biochemical:-
a. More specific
b. High LH to FSH ratio >3
2. Ultrasonic:-
a. Less specific as it may occur in other endocrinopathologies that result in anovulation
b. Features as described above
Management
1. General measures
a. Weight reduction
b. Counsel for the risk of diabetes, endometrial carcinoma
c. OGTT, endometrial sampling may be indicated
2. Treatment of menstrual problems
a. Aim to regulate cycles as well as to protect against endometrial hyperplasia
b. Can use combined oral contraceptives or progestogen if pregnancy is not wished
c. Can use clomiphene citrate if pregnancy is wished
3. Treatment of infertility See ovulation induction
4. Treatment of hirsutism See hirsutism
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1. Diagnosis
a. At least 2 out of the 3 criteria listed below:-
i. Anovulation or menstrual disturbance (oligomenorrhoea / amenorrhoea)
ii. Clinical signs of hyperandrogenism (hirsutism or acne) and/or hyperandrogenemia, with other causes of
hyperandrogenemia excluded
iii. Ultrasound features of polycystic ovaries
b. Other supportive features:-
i. Elevated early follicular phase (LH >10 IU/L) whilst FSH normal
ii. Elevated LH/FSH ratio (>2.5)
iii. Obesity (BMI > 25) / Insulin resistance
2. Investigations
a. For patients with oligomenorrhoea / amenorrhoea
i. Exclude pregnancy
ii. Check early follicular phase FSH, LH, E2, prolactin & TFT
b. For patients with oligomenorrhoea / amenorrhoea together with hirsutism
i. Follow previous work-up for oligomenorrhoea / amenorrhoea
ii. additional tests include:
- Check serum testerosterone
z Mildly elevated testerosterone suggestive of PCOS
z If testosterone >2.5 nmol/l, need to exclude other etiologies
- Arrange ultrasound scan of pelvis, preferably transvaginal scan, to look for polycystic ovary
- If causes other than PCOS are suspected, refer to COMBINED gynae-endocrinology clinic
c. For patients with chronic anovulation with irregular bleeding (e.g. prolonged menstrual flow, heavy flow) Arrange
Vabra aspiration to exclude endometrial hyperplasia / carcinoma
d. For patients with the clinical diagnosis of PCOS Check serum testerosterone and fasting glucose & lipid profile
(or metabolic profile in 9F)
3. Management
a. General advice
i. Educate patient about the clinical features and health implications of PCOS
- Endocrinological disturbance: menstrual disturbance, hirsutism or acne
- Reproductive disturbance: anovulation, infertility, pregnancy loss
- Metabolic disturbance: DM, hyperlipidemia, cardiovascular disease
- Others: risk of endometrial hyperplasia and endometrial cancer
ii. Advise weight reduction if BMI > 25 kg/m2
- Refer to dietitian for low-calorie diet
- Emphasize the importance of weight reduction Even a mild degree of weight reduction will result in a
significant improvement in most clinical features of PCOS
b. Specific treatment according to presenting symptoms
i. Menstrual disturbance and fertility not wanted
- Nordette as first line treatment
- If Nordette is contraindicated, give Norethisterone 5mg tds PO day 5-25
ii. Hirsutism / acne
- Simple cosmetic measures
- Medical treatment with Diane
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iii. Infertility
- Refer to infertility clinic
- Check metabolic profile in 9F (OGTT, fasting glucose/insulin & lipid)
- Exclude other co-existing infertility problem
- Medical ovulation induction if confirm anovulation
z 1st line treatment: clomiphene citrate
z 2nd line treatment: metformin, ovulation induction by gonadotropins, laparoscopic ovarian
drilling
iv. Co-existing metabolic syndrome (glucose intolerance, hyperlipidaemia etc Refer to COMBINED
gynae-endocrinology clinic
v. With evidence of endometrial hyperplasia,
- Correct endometrial hyperplasia before any plan for pregnancy
- Follow protocol Endometrial hyperplasia for the management
Kallman syndrome
1. It is a rare congenital disease with two main features:
a. Failure of migration of GnRH producing neurons, resulting in absence of hypothalamic GnRH secretion, and hence
hypogonadotropic hypogonadism. Female patients therefore present with delayed puberty, absence of breast
development, primary amenorrhea and anovulation.
b. Absence of olfactory bulb resulting in anosmia (loss of sense of smell)
2. Treatment:
a. Low doses of estradiol to encourage breast development, followed by
b. Cyclic hormonal replacement therapy consisting of oestrogen and progestogen
c. Ovulation induction when patients want pregnancy. Pulsatile GnRH or gonadotropin is the treatment of choice.
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Anorexia nervosa
Introduction
Anorexia nervosa is one of the underlying causes of secondary amenorrhea in young women. Because of significant weight
reduction, the hypothalamus-pituitary-ovarian axis is suppressed, resulting in hypogonadotropic hypogonadism. It is a potentially
fatal disorder if not treated.
Epidemiology
1. 1% of young females
2. Predominant age group:-10-20+ years old
3. Male to female ratio:-at least 1:10
Subtypes restrictive and bulimic.
Clinical features
1. History
a. Marked weight loss (of more than 15% of standard weight or BMI less than 16.5kg/m2), in the absence of any
primary medical disorder
b. Food refusal attributed to fat-phobia, stomach bloating, no hunger, no appetite, fear of food.
c. Weight controlling behaviour:-dieting, exercise, use of anorectics, laxatives or diuretics
d. Self-induced or spontaneous vomiting, especially in fat-phobia
e. Delusion of self body image
f. Stunted growth (pre-pubertal)
g. Amenorrhea
2. Physical signs
a. Hypotension
b. Bradycardia
c. Lanugo
d. Hypothermia
e. Varying degrees of dysphoria, obsessionality, perfectionism or low self-esteem
f. Biochemical disturbances
Aetiology
- Personal:-personality
- Family:-enmeshed or conflicting
- Environment:-stress, peers, relationships, losses
- Socio-cultural:-media publicity, gender role conflict, disempowerment
- Biological:-genetics? Neuroendocrine?
Management
Multi-disciplinary approach.
1. Assessment:
a. Physical condition, e.g., degree of weight loss
b. Psychosocial factors:- Suicidal risk and co-morbid psychiatric disorders
2. Treatment:
a. Nutritional counselling, gradual weight gain, treat any physical condition if needed
b. Psychological treatment:- Individual motivation enhancement therapy and family therapy
c. No medication is proven to be effective
Poor prognostic factors

1. Significant weight loss
2. Chronicity
3. Presence of purging or bulimia
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Prolactin
A hormone secreted from the anterior pituitary gland, responsible for glandular proliferation of breasts and establishment of
lactation. It can also reduce gonadal activity by decreasing the pulsatile secretion of gonadotropin releasing hormone from the
hypothalamus, and blocks the action of luteinising hormone on the ovary. Normally the secretion of prolactin is under the
inhibition of dopamine secretion from the hypothalamus. Physiological hyperprolactinemia occurs during pregnancy, after
childbirth and continuation of lactation, and during stress. Pathological hyperprolactinemia can be resulted from prolactinoma,
other pituitary gland tumours that block the dopaminergic tract from the hypothalamus, anti-dopaminergic agents such as
anti-psychotic agents. Prolactin level may also rise in case of polyscytic ovarian disease and hypothyroidism. Hyperprolactinemia
results in amenorrhea, anovulation, and galactorrhea.
Hyperprolactinaemia
Causes of hyperprolactinemia
1. Physiological
a. Prolactin levels are influenced by the time of day when blood is collected, and are also increased by stress
b. Transient rises can occur at ovulation
c. During pregnancy and lactation
2. Pathological
a. Prolactinoma or other pituitary gland tumour
b. Other pituitary gland tumours that block the dopaminergic inhibitory tract from the hypothalamus
c. Drug induced:-anti-dopamingeric
d. Association with polycystic ovarian disease (PCOD)
- Oligo-amenorrhea
- Galactorrhea
Further investigation
- Mild hyperprolactinemia can be a transient `physiological change (see above) and may require no further investigation, or a
repetition of the test.
- Significant hyperprolactinemia requires radiological investigation to rule out prolactinoma or other pituitary gland tumours.
Principle of treatment
- Dopaminergic agent:-bromocriptine
- Surgery for macro-prolactinoma or other pituitary gland tumours

1. Work up
a. Detailed drug history To exclude drug-induced hyperprolactinaemia (e.g. anti-psychotics)
b. Pregnancy test To exclude pregnancy
c. sTSH To exclude hypothyroidism
d. Repeat prolactin if prolactin < 1000 IU/L
e. Arrange MRI pituitary to look for pituitary adenoma or space-occupying lesion if
i. Patient is symptomatic (e.g. menstrual disturbance, galactorrhoea & infertility) and there is persistent
hyperprolactinemia (regardless to the level of prolactin)
ii. Prolactin > 1000 IU/L, regardless of symptoms
iii. There is evidence of pituitary insufficiency (e.g. hypogonadism, hypothyroidism, delayed puberty or growth
failure), even with modest elevations of prolactin. Non-functioning pituitary tumor may present with only
mildly elevated prolactin level due to the compression of the hypothalamus-pituitary stalk.
iv. There are neurological symptoms
f. Screening for macroprolactinaemia
i. Automatically performed in our hospital if hyperprolactinaemia is detected
ii. If positive, the test will automatically be repeated with a more specific assay
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2. Treatment
a. If repeat prolactin confirmed hyperprolactinaemia but < 1000 IU/L and
i. Patient is asymptomatic (no galactorrhoea / menstrual disturbance)
- Discharge from gynae-endocrinology clinic
- Refer to medical endocrine clinic for assessment of persistent hyperprolactinaemia
ii. Patient is symptomatic (galactorrhoea / menstrual disturbance)
- Give bromocriptine (Follow the protocol Bromocriptine)
- Arrange MRI pituitary
b. If MRI result is not available and prolactin 1000 IU/L, give bromocriptine regardless of symptoms
c. If MRI shows pituitary microadenoma (<10mm), in the presence of hyperprolactinemia, give bromocriptine
regardless of the symptoms
d. If MRI shows pituitary macroadenoma (10mm) or other CNS tumours
i. Give bromocriptine regardless of symptoms
ii. Urgent referral to neurosurgery clinic and medical endocrine clinic
e. If hypothyroidism (elevated sTSH) is detected, refer to combined gynae-endocrinology clinic for treatment plan
3. Long term management
a. If the main problem is infertility, work up for other infertility cause and refer to infertility clinic
b. Otherwise
i. Follow up in gynae-endocrinology clinic
ii. Review symptoms and prolactin level (check PRL two weeks before follow up)
4. When gynaecological symptoms have resolved and PRL has been normalized with bromocriptine,
5. If MRI has shown pituitary microadenoma,
6. Refer to combined gynae-endocrinology clinic for decision on long term management as long term treatment is anticipated,
refer out to Integrated Family Medicine clinic for continuation of bromocriptine therapy will be considered.
7. If MRI has shown no pituitary adenoma, stop bromocriptine and follow-up for symptoms and prolactin level
a. If symptoms or hyperprolactinaemia recur
i. Resume bromocriptine
ii. Refer to combined gynae-endocrinology clinic for decision on long term management
b. If asymptomatic and prolactin remains normal after treatment stopped
i. Discharge from clinic
ii. Advise self surveillance with regular monitoring of prolactin
8. If drug-induced hyperprolactinaemia (e.g. anti-psychotics) is suspected, follow the protocol Antipsychotic
Antipsychotic-induced hyperprolactinaemia
1. Pituitary adenoma has not yet been ruled out work up for other causes of hyperprolactinaemia and start treatment as
described in the protocol hyperprolactinaemia.
2. If MRI shows no evidence of pituitary adenoma and
a. Patient is asymptomatic
i. Stop bromocriptine
ii. Reassure and discharge from clinic
iii. Advise to attend if symptoms (galactorrhoea / menstrual disturbance) occur
b. Patient is symptomatic
i. Consult psychiatrists for dose reduction or change of the antipsychotic drugs if applicable
ii. Treatment is based on symptoms
- Menstrual disturbance change from bromocriptine to Nordette
- Galactorrhoea / infertility continue bromocriptine
iii. # Nordette is not contraindicated once pituitary adenoma has been excluded
3. If MRI shows pituitary adenoma Refer to combined gynae-endocrinology clinic for decision on long term management
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Galactorrhoea
It is the spontaneous milk secretion from breasts not associated with childbirth or the lactation. It is associated with
hyperprolactinemia.
1. Exclude pregnancy, exclude local causes, check prolactin level.
2. If prolactin level is elevated Follow the protocol hyperprolactinaemia
3. If prolactin level is normal, reassurance if symptoms are not disturbing
a. Give bromocriptine if symptoms are disturbing
b. Step-up dosing as described in the protocol Bromocriptine Titrate the dose according to the amount of galactorrhoea.
Tail off bromocriptine (stepwise reduction of the dosage by 50%) if symptoms resolve
Bromocriptine
1. Initial treatment
a. Step-up dosing
i. 1.25 mg nocte for 1 week then
ii. 2.5 mg nocte for 9 weeks
b. Follow up in Intern Clinic 10 weeks & Gynae-endocrinology Clinic as routine
i. Check prolactin level two weeks before each follow up
ii. See follow-up plan on next session
iii. # The intern should consult doctors in gynae-endocrinology clinic on the same day if dose adjustment for
bromocriptine is necessary
2. Follow up treatment
a. Review side effects (e.g. drowiness), symptoms improvement and prolactin level to adjust the dose accordingly:-
b. If symptoms resolved, prolactin normalized and no side effect from drug maintain bromocriptine at 2.5mg nocte till
next FU
c. If symptoms resolved, prolactin normalized but side effects from drug
i. Bromocriptine can be reduced to the lowest maintenance dose of 1.25mg daily
ii. Follow up 10 weeks in gynae-endocrinology clinic after dose adjustment (check prolactin two weeks before FU)
d. If symptoms and/or hyperprolactinemia persist or recur,
i. Increase the dosage
ii. Follow up 10 weeks in gynae-endocrinology clinic after dose adjustment (check prolactin two weeks before FU)
e. If patient is refractory to bromocriptine (total daily dose of 10mg) or cannot tolerate it,
i. Change from bromocriptine to cabergoline (0.5mg once/week for the first week & then twice/week)
ii. Follow up 10 weeks in combined gynae-endocrinology clinic (check prolactin two weeks before FU)
iii. Adjust the dosage according to symptoms and prolactin
Testicular feminisation syndrome

- End-organ resistance to androgens by absence of 5-alpha reductase or functional defect.
- Male genotype (46XY) but female phenotype.
- Undesecended Testis anywhere along the normal course of descent.
- Normal or large breasts with small nipples.
- Lack of uterus, female external genetalia with blind vagina.
- Raised up as a girl.
- Until full growth is achieved no treatment should be attempted.
Asherman syndrome
The partial or complete obliteration of the uterine cavity by adhesions (synechiae) caused by endometrial infection (such as
tuberculosis), or over-vigorous curettage after miscarriage or abortion. Depending on the severity of adhesions, amenorrhea,
hypomenorrhea, spontaneous abortion or infertility may occur. Endometrial ablation is a surgical procedure aiming at reduction or
complete cessation of menstrual flow by iatrogenically inducing Asherman syndrome, through electrical cauterization of the
endometrial cavity.
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Menorrhagia
Definition
1. Subjective complaint of excessive cyclical menstrual bleeding
2. Objective measurement
a. Defined as >80 ml of menstrual loss.
b. The mean menstrual blood loss per menstruation in a healthy woman ranges between 37-43ml.
i. Menstrual blood loss of more than 80ml is regarded as excessive, and this occurs in 9-14% of women. However,
it is very difficult to document the volume of blood loss clinically
ii. Only about 50% of women presenting with menorrhagia actually have a loss outside the normal range (>80ml).
iii. About 60% of these women would become anaemic.
iv. There is also a poor correlation between subjective and objective assessment of blood loss.
Incidence
Hong Kong incidence 3.2% in 2004.
Causes
1. Primary:- Dysfunctional uterine bleeding (DUB)
a. It is the most common cause of menorrhagia
b. By the name implies, there is no underlying organic cause
c. The diagnosis is made on clinical basis, after excluding other possible organic causes (see below)
2. Local:-
a. Uterine cavity:- IUCD
b. Endometrium:- Endometritis, polyp, hyperplasia and carcinoma
c. Myometrium:- Uterine fibroid (epsically submucosal), adenomyosis
3. Systemic:-
a. Endocrine:- Hypothyroidism, Cushings disease, Exogenous steroids
b. Bleeding tendency:-Von Willebrand's disease, idiopathic thrombocytopenia, anticoagulants.
Assessment
1. History taking
a. Routine gynaecological history, especially focus on menstrual history
b. When does the menstrual problem start
c. Volume of loss each period
i. How many and how frequent does the patient change pad each day
ii. Any flooding of blood clots
iii. How long does each period last
d. Any anemic symptoms and sign
e. How is the social life affected
2. Physical Examination
a. General: pallor, goitre, tachycardia
b. CVS: tachycardia
c. Abdominal: pelvic masses
d. Pelvic for polyp, inspection of cervix, etc.
3. Investigations
a. Blood: CBC, Fe profile; Other if suspected
b. Radiological: USG only indicated if any abnormalities detected or fail medical treatment
c. Endometrial assessment / Hysteroscopy for Age > 40; Long standing symptoms; Irregular bleeding or No response to
previous medical treatment
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Treatment
Depends on the cause of menorrhagia, age of patients, and wish of patients to preserve fertility:
1. Medical Treamtments:-
a. General (Fertility desired)
i. Mefenamic acid (Ponstan): 30% decrease, for dysmenorrhea
ii. Tranexamic acid (Transamin): 40-50% decrease, commenced during bleeding
b. Hormonal (Fertility not desired)
i. Combined oral contraceptives: effective, for irregular cycles
ii. Levo-norgestrel IUCD (LNG-IUS, Mirena)
iii. Danazol (A mild testosterone.)
iv. Cyclical Progestogens: No contraceptive effects
v. GnRH Analogues
2. Surgical Treatments:-
a. Endometrial ablation
b. Myomectomy
c. Hysterectomy
3. Remarks
a. In general, medical therapy should be attempted for DUB. Surgical treatment is considered if medical treatment is
failed, or in severe case of DUB.
b. Medical treatment is less useful for fibroids and adenomyosis1
c. Myomectomy is only for treatment of fibroids if patients want to conserve uterus, otherwise fibroids and adenomyosis
are better dealt with hysterectomy.
d. Complex atypical endometrial hyperplasia and endometrial carcinoma should be treated with hysterectomy1
Do you know any methods to estimate the menstrual blood loss clinically?
Metropathia haemorrhagia
A term to describe a very heavy menstruation after several weeks of amenorrhea which is associated with anovulation cycles.
Follicular development occurs and continues as ovulation fails to take place. This results in high circulating oestrogen levels
which continue to stimulate endometrial development in the absence of antagonism of progesterone. The consequence is cystic
glandular endometrial hyperplasia. Eventually, after several weeks the endometrium breaks down and prolonged heavy bleeding
occurs.
Dysfunctional uterine bleeding

What is dysfunctional uterine bleeding (DUB)?
It is a common disease diagnosed by exclusion. It is defined as heavy and / or irregular menses in the absence of recognisable
pelvic pathology, pregnancy or generalized bleeding disorder. It is the most common cause of menorrhagia (60%) in reproductive
women, especially at the extreme of reproductive age. The diagnosis should be made after excluding any organic causes.
Pathophysiology of dysfunctional uterine bleeding (DUB)

The exact pathophysiology is not known but generally two patterns of DUB are recognised:
1. Anovulatory pattern:
Anovulation is common among teenagers who have just started menarche, and perimenopausal women who are approaching
menopause. The endometrial glands continuously proliferate under unopposed stimulation of estrogen (lack of progesterone),
and result in irregular and heavy menstrual flow.
2. Ovulatory pattern:
Some women ovulate with regular cycles but still have menorrhagia. The mechanism is unknown. It may be related to the
inadequate production of progesterone from corpus luteum, or a shift in endometrial conversion of endoperoxide from the
vasoconstrictor prostaglandin F2&alpha to vasodilator prostaglandin E2.
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Treatment of dysfunctional uterine bleeding (DUB)
1. Medical therapy
a. Tranexamic acid from day 1 of mense to the end of the heaviest days
b. Non-steroidal anti-inflammatory agents (NSAID) e.g. Mefenamic acid from Day 1 to end of the heaviest days
c. Combined oral contraceptives
d. Progestogens - cyclical
e. Levonorgestrel intra-uterine system (Mirena)
2. Surgical therapy
b. Hysterectomy

First visit
1. Routine investigation
a. Complete blood picture; Fe & TIBC
b. Pictorial chart
c. Cervical smear if due
d. TFTs only when there are symptoms or signs of thyroid disorder
e. No need for routine ultrasound scan
2. Perform endometrial biopsy if:-
a. Irregular bleeding (not irregular menstrual cycles) or persistent intermenstrual bleeding at age 40
b. Presence of risk factors for endometrial hyperplasia or carcinoma
i. Obesity, polycystic ovarian syndrome or chronic anovulation, unopposed oestrogen therapy, tamoxifen
therapy
ii. Vabra aspiration can be arranged in outpatient hysteroscopy session (for patients in PWH) if patient is
menstruating during visit or endometrial sampling with pipelle failed due to positioning.
3. Refer for outpatient diagnostic hysteroscopy (OPH) if:-
a. Suspected intrauterine pathology
b. Failed endometrial sampling
4. Medical management (first-line) in the absence of specific contraindications:-
a. Cyclical menstruation with heavy flow:-
i. Tranexamic acid (500 mg to 1 g qid) for days of heavy flow
ii. Mefenamic acid (500 mg tds) from day 1, or just before, until heavy blood loss has stopped (after food or with
Gelusil to prevent ulcer pain)
iii. Combined oral contraceptives (COC) if contraception desired
b. Irregular menstruation:-
i. COC especially if contraception is also desired
ii. Norethisterone 10 mg daily to bd D5 to D25
iii. Offer option of Levonorgestrel IUCD, arrange OPH to rule out intrauterine pathology before insertion
c. Prescribe iron supplement to patient who is known or suspected to have anaemia
5. Review in routine follow-up appointment Consider checking CBP Fe/TIBC one week before follow-up to review
treatment response
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Follow up visit
1. Responded to first-line medical treatment
a. If no anaemia Discharge from clinic with medication
b. If iron deficiency anaemia
i. Optimise medical treatment
ii. Prescribe iron sulphate 300 mg tds for 4-6 weeks
iii. Follow up in routine appointment, recheck CBP 1 week before appointment
2. Failed first-line medical treatment
a. Arrange USG, preferrably transvaginal, to assess for structural intrauterine lesion, like submucosal fibroid or
endometrial polyp
b. If high suspicion of structural intrauterine pathology, refer for OPH directly
c. Discuss with patient about second-line management
i. If patient needs to preserve fertility Levonorgestrel IUCD
ii. If fertility is not desired Consider Levonorgestrel IUCD or endometrial ablation
d. Levonorgestrel IUCD (Mirena)
i. This is particularly preferred for those aged less than 40
ii. This should be considered if patient is dependent on oral Norethisterone
iii. Pre-insertion OPH to rule out intrauterine structural lesion is preferable
e. Advise surgery especially if anaemia persists:-
i. Endometrial ablation if absence of large uterine fibroid or co-existing symptomatic adenomyosis or
endometriosis Refer to guidelines on booking of second generation endometrial ablation
ii. Hysterectomy if presence of large or multiple uterine fibroid, or co-existing symptomatic adenomyosis or
endometriosis
iii. Hysteroscopic surgery
- If endometrial polyp or submucosal fibroid is confirmed on OPH, consider arranging endometrial
ablation at the time of hysteroscopic surgery if the patient aged > 40 and had complete family,
especially for those with documented anaemia.
- For submucosal fibroid > 3 cm, consider giving preoperative GnRHa for 3 months to shrink it before
operation.
- GnRHa should be given 6 to 8 weeks before operation if concurrent endometrial ablation is to be
performed.
Discharge
In general, patient can be discharged from clinic if there is no active management which can only be offered in gynaecology
specialists clinic. Patient can be discharged from clinic if she has no active menstrual problem, even on first visit. Patient can
be discharged from clinic if the response to procedure for menorrhagia is satisfactory. Patient can be referred back to their
family doctor if her menstrual problem has been solved by simple medication.
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Postcoital bleeding
It is a vaginal bleeding after coitus. An acute onset can be due to trauma secondary to intercourse. Tear of hymen is common after
the first coitus, and tear of vagina sometimes occurs after a vigorous intercourse. Postcoital bleeding is also a symptom of cervical
lesions such as cervical cancer, cervical polyps, cervicitis, or occasionally endometrial polyps.
Postmenopausal bleeding
It is any vaginal bleeding occurs after menopause. It is always abnormal and investigation should not be delayed. There are many
possible causes and genital malignancies should be ruled out in the menopausal age group of patients.
Causes
1. Uterine pathology:
a. Atrophic endometritis It is the most common cause and the diagnosis is made after excluding other pathologies
b. Endometrial polyp
c. Endometrial carcinoma
d. Uterine sarcoma:-rare
e. Endometrial glands activation following hormonal replacement therapy or stimulation by endogenous oestrogen from
ovarian stromal tumours
2. Cervical pathology:
a. Cervical polyp
b. Cervical cancer
c. Cervicitis
3. Fallopian tube pathology: Fallopian tube cancer. Very rare but postmenopausal bleeding may be the sole symptom
4. Vaginal pathology:
a. Vaginal cancer
b. Vaginal infection and ulcer:-particularly decubitus ulcer following genital prolapse
5. Vulval pathology:
a. Vulval cancer
b. Vulval infection and ulcer
Assessment
1. Any lower genital tract pathologies are usually picked up by speculum and digital examination.
2. Diagnosis of endometrial pathologies requires a hysteroscopy or endometrial sampling.
Remark
Sometimes per rectal bleeding or haematuria may be mistaken as vaginal bleeding. Clinical assessment should be able to
differentiate these conditions.
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Dysmenorrhoea
Definition
1. Primary (idiopathic) dysmenorrhoea Painful periods for which no organic or psychological cause can be found
2. Secondary dysmenorrhoea ainful periods for which an organic or psychosexual cause can be demonstrated
3. Remark The uses of the terms 'primary' and 'secondary' are different from that in infertility
Causes of primary dysmenorrhea

1. Primary dysmenorrhoea
a. The cause is unknown but there is a familial tendency, with a strong likelihood that the attitude of the mother may
influence the response of the daughter
b. It occurs in ovulatory cycles during when prostaglandins production may cause vasoconstriction or myometrial
contraction, resulting in pain.
2. Secondary dysmenorrhea
a. Endometriosis, Chronic pelvic inflammatory disease
b. Adenomyosis, Submucosal fibroid
c. Uterine cavity and outflow tract: Ashermans syndrome
Clinical features of primary dysmenorrhea

1. Usually develops within the first 2 years of menarche
2. Cramping, sometimes intense, and can be crippling and disturb social activity
3. Site:-over lower abdomen, radiates down the anterior aspects of thighs
4. Onset on the day of menses or a day before menstruation, and last for 2 to 3 days
5. Often associated with vomiting and diarrhea
6. Pain often disappears or improves after the birth of the first child
7. No abnormal finding on physical examination
Clinical features of secondary dysmenorrhea

1. Usually develops later in reproductive age, can develop after childbirth
2. Dull, congestive pain
3. Site:-over lower abdomen, radiate to back
4. Onset usually on the day of menstruation, but can be few days before that. Can last as long as the menstruation, or even
persist after menstruation
5. Organic pathology is identified on physical or ultrasound examination
Treatment of primary dysmenorrhea

NSAID or combined oral contraceptives
Treatment of secondary dysmenorrhea

Refer to individual pages for treatment of underlying causes
Mittelschmerz
It means pain in the middle. It is the lower abdominal pain in women which occurs at the mid-menstrual cycle and is generally
assumed to be related to ovulation. It is suggested that the pain is due to peritoneal irritation by follicular fluid and blood
following rupture of the follicle. However, the relation of the pain to the exact time of ovulation and to the side on which
ovulation has occurred is variable.
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Premenstrual syndrome
Definition
1. Primary premenstrual syndrome (primary PMS)
a. A disorder of non-specific somatic, psychological or behavioural symptoms that recur in the premenstrual phase of the
menstrual cycle, but resolve completely by the end of menstruation, leaving a symptom-free period. The symptoms
are of sufficient severity to produce social, familial, or occupational disruption.
b. Symptoms must have occurred in at least four of the six previous menstrual cycles.
2. Secondary premenstrual syndrome (secondary PMS)
Similar to primary premenstrual syndrome except that the symptoms do not completely resolve when the menstruation
ceases (i.e. Not symptom-free period), but does significantly improve for at least 1 week after menstruation.
3. Remark:
The implication of these definitions is that in secondary PMS there is an underlying psychological disorder whose
aetiology is similar to that of common psychiatric disorders such as depression or anxiety. Both primary PMS and the
cyclical component of secondary PMS are presumed to be related to the endocrine changes of the ovarian cycle.
Clinical features
1. Common somatic symptoms:-Breast pain, pelvic pain, abdominal bloatedness, lethargy and tiredness
2. Common psychological symptoms:-Depressive mood, decreased libido, anorexia, insomnia
3. Common behavioural symptoms:-Loss of self-control, loss of judgment, impulsive behaviour
Aetiology
Unknown. It may be due to variations in sex steoid levels and low serotonin levels.
Diagnosis
1. Many women will have some forms of discomfort during or before menstruation. To make a diagnosis of PMS, the symptoms
must fulfill the definition of PMS:-occur cyclically; be severe enough to cause disruption of women daily living, and occur
for at least 4 out of 6 cycles.
2. Rule out underlying psychiatric disorder such as depression, anxiety and psychosexual problems, and endocrine causes such
as menopause, hyperthyroidism, and organic causes such as endometriosis, pelvic inflammatory disease.
3. There is no specific test to confirm PMS. In difficult case, GnRHa depot for 3 months may be indicated to suppress
menstruation. Total cessation of the symptoms after the menstruation has suppressed is a support of the diagnosis of PMS.
Treatment
1. There are various forms of medications proposed but none of them are well proven to be effective with randomized controlled
trials.
2. Oral contraceptive pills, progestogens, vitamin B6 may be tried. Danazol and GnRHa can effectively suppress menstruation
but also have side-effects. In severe cases refractory to medical treatment, oophorectomy is the last resort.
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2. Birth control
Contraception
Methods of contraception
1. Natural methods
a. Periodic abstinence (rhythm or calendar method)
i. It means the avoidance of intercourse during the fertile period of the cycle.
ii. There are different methods to predict the fertile period, such as calendar method, mucus method or by basal
body temperature
b. Coitus interruptus
i. It means the withdrawal of the penis in time, before ejaculation, ensuring that all sperms are deposited outside
the vagina. However, there are few sperms in the pre-ejaculate.
ii. The failure rate is high (Pearl index = 10/100 women yr), mainly due to conscious rule breaking
c. Lactational amenorrhoea
i. 3 criteria must be met: (1) Within 6 months postpartum; (2) Exclusive breastfeeding; and (3) Amenorrhoeic.
ii. 98% effective.
2. Barrier methods
a. The method failure rate is low (4%) but the user failure rate is high (Pearl index = 10/100 women yr), mainly due to
inconsistent or improper use. It is sometimes used together with spermaticides to increase the effectiveness.
b. It consists of Male condom, Female condom, Diaphragm and Cervical cap with or without spermicides.
3. Hormonal methods
a. Combined oral contraceptives (COC)
b. Progestogen-only pills (mini pills)
c. Progestogen injectable
4. Intrauterine contraceptive devices (IUCD)
a. Non-medicated / Inert IUCD
b. Copper-containing IUCD
c. Hormone-containing IUCD
Factors in choosing different kinds of contraception

1. Failure rate:
a. Can be due to method failure and user failure
b. Assessed in term of Pearl index or life table analysis
2. Reversibility How fast and how effective of recovery of fertility after stopping use of the contraceptive method
3. Side effects:
a. Sexual satisfaction
b. Menstrual disturbance
4. Non-contraceptive benefits:
a. COC can also treat dysmenorrhea and menorrhagia
b. Condoms can also prevent sexually transmitted diseases
5. Patient's past medical history:
a. COC is contraindicated in case of history of thromboembolism
b. Patient's acceptability and compliance
c. Progestogen injectable requiring 4 injections a year while COC has to be taken every day.
Postcoital contraception
See postcoital contraception
Pearl index
It is a measurement of the effectiveness of a method of contraception. It is defined as number of failure per 100 women years of
exposure. The denominator is the total months (or menstrual cycles) exposed from onset of method until completion of study or an
unintended pregnancy, or discontinuation of the method by the users. The nominator is the number of unintended pregnancy. It
measures method and user failure.
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Life table analysis
It is a calculation of failure rate per month, and its cumulative failure rate is used to compare among different methods.
Effectiveness Method % of women experiencing an unintended pregnancy
group within the first year of use
Typical Lowest expected
Always very effective Norplant 0.05 0.05

Male sterilisation 0.15 0.1
Female sterilisation 0.5 0.5
Monthly injectable (Lunelle) 3 0.05
Depo-provera injection 3 0.3
Copper T IUCD (ParaGuard) 0.8 0.6
LNG-IUS 0.1 0.1
Effective as commonly used. Combined oral contraceptives 8 0.3

Very effective when used Evra Patch 8 0.3
correctly & consistently. NuvaRing 8 0.3
Progesterone only pills 8 0.3
Male condom alone 15 2

Female condom alone 21 5
Only somewhat effective as Coitus interruptus 27 4
commonly used. Diaphragm and spermicides 16 6
Effective when used Natural methods 25 1-9
correctly & consistently. Sponge - nulliparous 16 9
- parous 32 20
Cervical cap - nulliparous 16 9
- parous 32 26
No method 85 85
Typical means user effectiveness was taken into account while Lowest rules out user factor by highly motivated subjects and
medical support.
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Calendar method
It is a way of contraception by means of periodic abstinence from coitus. It is based on the fact that :-
1. Viability of sperms in female reproductive tract is about 2 to 7 days,;
2. Lifespan of an ovum is only 1 day; and
3. Ovulation occurs at day 14
Therefore, the fertile period starts from 7 days before ovulation, and ends 1 day after ovulation. In a normal regular 28-day cycle
(ovulation at day 14), the fertile period starts at day 7 and ends at day 15.
If there is a variation of menstrual cycle length in a woman, then

1. The beginning of the fertile period should be calculated by subtracting 21 (14+7) days from the length of the shortest cycle;
2. The end should be calculated by subtracting 13 (14-1) days from the longest cycle.
Couples are advised to avoid coitus within the estimated fertile period. This method has a high failure rate (Pearl index 40 per 100
women year). It is not suitable for women with irregular cycles, need of frequent sex, and forgettable women.
Other methods to predict ovulation includes:-

1. Basal body temperature
2. Cervical mucus:- becomes clear, thin, stretchy and slippery around the time of ovulation
3. Syptothermal:- combination of the above two
4. Over the counter LH kits (to detect for the LH surge in ovulation)
5. Microscopic examination of saliva for ferning.
Figure 42 Basal body temperature (left) and cervical mucus (right) method
Condom
Male condom
It is a latex (rubber) sleeve that fits snugly over the penis for contraception. It is also effective against sexually transmitted
diseases such as AIDS, hepatitis and chlamydia. It is the most popular contraceptive method in Hong Kong. The advantages are:
1. Cheap 5. Free from medical risks
2. Widely available 6. No medical supervision needed
3. Convenient and only use when needed. 7. Protection against sexually transmitted diseases
4. Highly effective if used consistently and correctly 8. Possible protection against cervical neoplasia
Figure 43 Condom (Left two); Diaphragm (Right three) and Cervical Cap (Below)
Female condom, Diaphragm and Cervical cap
It is not popular in Hong Kong because:
1. Low patients' acceptance due to the need of handling her own genitalia
2. Need fitting by trained personnel and training in use
3. Less effective than other female contraception like hormonal methods or IUCD
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Combined oral contraceptives
Mode of action
The primary mode of action is the inhibition of ovulation due to negative feedback of oestrogen on the hypothalamo-pituitary-
ovarian axis. The secondary effect is the progestogen effect on cervical mucus and endometrium
Nature
Pills consist of combination of synthetic oestrogen and progestogen, taken for 21 days per cycle.
Synthetic oestrogen
The only synthetic oestrogen used is ethinyloestradiol, with dose ranging from:
1. 20-30 mcg (low dose; e.g. Nordette):-most commonly used
2. 50 mcg (median dose; e.g. Duoluton)
3. 75-100 mcg (high dose):-seldom used now because of side effects
Synthetic progestogen
4 generations of synthetic progestogen including:
1. 1st generation:-norethisterone 5mg:-low potency, seldom used now
2. 2nd generation:-levonorgestrel 150-250 mcg:
3. 3rd generation:-desogestrel 150 mcg; gestodene, highly specific progestogenic effect.
a. Advantages:- less androgenic and so less adverse effect on serum lipids.
b. Disadvantages:- is shown in some studies to be associated with a higher risk of non-fatal venous thromboembolic
disease
th
4. 4 genereation:- clamed to have spirolactone-like effect, thus can maintain slimness.
Types of COC
1. Everyday COC:-
a. Each package consists of 21 pills of COC and 7 pills of placebo.
b. Advantage of reduction in risk that user will forget to restart her next packet on time a potent cause of pill failure.
2. Non-everyday COC
a. Each package consists of 21 pills of COC without placebo
b. With or without phasic changes of hormones content
3. Monophasic every pill of COC consists of same amount of oestrogen and progestogen
4. Biphasic or triphasic
a. Pills consist of different amount of oestrogen and progestogen in different phase of the cycle
b. Designed to minimize the dose of progestogen and hence its side effect
c. The clinical benefits are modest and are replaced by monophasic COC with 3rd generation of progestogen/
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Prinicple of prescribing COC
1. Assessment before prescription rule out any contraindications by history and examination.
2. When to start
a. Best within 5 days of menstrual cycle, preferably day 1.
b. Immediate after abortion or termination of pregnancy.
c. Post-coitus or emergency contraception.
3. How to take the pills:
a. Start a pack on the same day of the week.
b. Advise patient to take the pill every day at the same time
c. Advise patient to consult doctors if no withdrawal bleeding during pill-free period
Efficacy
1. Median dose COC:-Pearl index:-<1/100 women year
2. Low dose COC:-Pearl index:-3/100 women year
Non-contraceptive benefits of COC

1. Control of dysmenorrhea and menorrhagia and regulate cycles.
2. Reduced risk of endometrial carcinoma (0.34-0.46 RR) and ovarian cancer (0.49-0.60 RR) by at least 50%.
3. Reduced risk of pelvic inflammatory disease, ectopic pregnancy, fibroid and benign breast diseases
4. Positive effects on bone mass and reduce vasomotor symptoms.
Side effects
1. Cardiovascular (Mainly associated with first generatiob. For second generation onwards, risk does not increase in young
ladies without cardiovascular risk factors.
a. Venous thrombosis
i. Risk 1st Gen> 3rd Gen (25/100,000)> 2nd Gen (15/100,000) > non-user (10/100,000).
ii. Risk decreases as duration of taking increases.
iii. Note other risk factors also increase the risk (e.g. smoking)
b. Thrombotic stroke (1-4/10000 women year)
c. Haemorrhagic stroke (1.5-2 RR)
d. Hypertension (2 RR) Reversible by stopping COC
e. Myocardial infarction Relative risk of 3-5
2. Metabolic effects
a. Increase LD to HD ratio, and insulin resistance
b. Effects are modest with low dose COC and are not clinically significant
3. Minor side effects
a. Breast tenderness, nausea, vomiting, weight gain and mood changes
b. Uncommon with low dose COC
4. Cancer of breast it possibly increases thr risk of breast carcinoma slightly. (1.02-1.73 RR, decreases with age.)
Absolute contraindications of COC

1. Pregnancy
2. Exclusive breastfeeding < 6 weeks postpartum.
3. Multiple risk factors for arterial cardiovascular diseses.
a. Current or history of myocardial infarction, stroke, venous thromboembolism.
b. Complicated valvular heart diseases, with pulmonary hypertension, atrial fibrillation, subacute bacterial endocarditis.
c. Known hypertension > 160/90 mmHg or with vascular complications.
d. Diabetes mellitus, long standing for >20 years or with complications.
e. Heavy smoker (>15 cig/day) aged >35 years
f. Major surgery with prolonged immobilisation.
4. Current oestrogen dependent neoplasms. (e.g. breast cancer)
5. Migraine, common (> 35 years) and classical (any age)
6. Deranged liver function including any neoplasm; systemic lupus erythematosus.
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Seven-day rule
It is an easily remembered rule to guide the prescription of combined oral contraceptives:-
1. Ovulation is successfully suppressed after taking COC for 7 days continuously
2. Up to seven pills can be omitted without ovulation, as indeed is regularly the case in the pill-free week
3. More than seven pills missed in total risks ovulation
Progestogen-only pill
Nature
Also called mini-pill. Consist of daily low dose synthetic progestogen, e.g.:
1. Norethisterone 350 microgram
2. Levonorgestrel 30 microgram
Mode of action
To antagonize the endogenous oestrogenic effect on cervical mucus, making it thick, hostile and impermeable to sperms, and also
causes endometrial atrophy. Disordered luteal phase in 40 to 50% of cycles
Efficacy
1. Pearl index of 3/100
2. Increased efficacy when combined with breastfeeding
Remark
1. Similar to COC but not coagulation side effects
2. Does not protect against endometrial and ovarian cancer.
Side effects
Irregular menstrual cycles, unpredictable bleeding, amenorrhea and spotting
Advantages
- No increased risk of ectopic pregnancy
- No metabolic effects
- No coagulation effects
Use in special groups

- Lactating women
- Age> 40
- Smoker, history of thomboembolism
Progestogen injectable
It is one form of contraception consisting of progestogen (e.g. depomedroxyprogesterone acetate 150mg) given intramuscularly
every 12 weeks. It acts by inhibiting the ovulation.
1. The advantages are:
a. Highly effective (Pearl index= 1/100)
b. Highly convenient
c. Low reliance on compliance, need only 4 injections per year.
d. Reversible though with some delay in fertility
2. Side effects:
a. Menstrual disturbance (After one year use, 40% of user a amenorrhea, 40% scanty infrequent period, 20% prolonged
irregular bleeding)
b. Weight gain
c. Delay in resumption of fertility
d. Possible reduction in bone mineral density osteoporosis in users with long term amenorrhea
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Intrauterine contraceptive device (IUCD)
Types of intrauterine contraceptive device (IUCD)
1. Non-medicated / Inert IUCD
a. Rarely used now, except in China
b. Usually a metalic ring
2. Copper-containing IUCD
a. Different preparation has different copper content
b. Latest designs are smaller with higher copper content.
c. Need to change every 4-10 years as the effect of copper declines with time
3. Progestogen-containing IUCD (Mirena)
a. Levonorgestrel releasing IUCD.
b. Need to change every 5 years as the effect of progestogen declines with time.
Mode of action
1. Induce foreign body reaction which is hostile to gametes and embryo, and affect implantation
2. Copper ions affect tubal fluid, sperm transport and oocytes, and induce metabolic changes of endometrium
3. Progestogen make cervical mucus hostile and endometrium thin
Efficacy
Pearl index of less than 1/100 woman year for latest IUCD
Time of insertion
1. Anytime that pregnancy is ruled out.
2. Intermenstrual
a. From the end of menstruation through until mid cycle
b. The best time is towards the end of menstruation as it is certain that patient is not pregnant, and insertion is easier due
to natural dilatation of cervix at menstruation
c. However, fitting can take place at any point in the cycle if necessary
3. Post-termination of pregnancy or miscarriage
Risk is minimal immediately after first trimester termination or abortion, but risk of expulsion is higher in second
trimester.
4. Post-delivery
High expulsion rate during the first week of puerperium, best time is 6-8 week after delivery. If inserted too early, it
may be expelled with lochia.
5. Post-coitus
As emergency contraception, should be within 5 days post-coitus, and copper-IUCD only.
Method of insertion
1. Aims to achieve correct fundal placement allowing the IUCD to open to its pre-insertion shape, with minimal pain and
discomfort.
2. Careful explanation of procedure to patient.
3. Careful bimanual pelvic examination of uterus with sounding of the cavity to determine its length and direction, and rule out
acute genital infection.
4. Aseptic and careful technique to ensure fundal placement
5. Leave the thread of IUCD outside the cervix
6. Ask patient to check IUCD regularly and report if IUCD is expulsed
Missing Thread
1. Differential diagnoses:- Expulsion; Intrauterine displacement; Perforation.
2. Investigations:- USG to search in uterus; X-ray to serach in abdominal cavity.
3. If both investigations are unremarkable, the IUCD is possibly expelled.
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Figure 44 Procedure of IUD/IUCD insertion.

Removal of IUCD
During the menstrual period or any time if the woman had no unprotected coitus in the past 5 days.
Side effects of IUCD

1. Menorrhagia and dysmenorrhoea are common in the first 6 months of use. (Treat by ponstan and iron supplement.)
2. Vaginal discharge because of foreign body reaction, but infection has to be ruled out first.
3. Infection (Pelvic inflammatory disease, actinomycosis) risk is greatest in the first 20 days after insertion due to traumatisation
and increased susceptibility to infection by endogenous cervico-vaginal flora.
4. Expulsion (5% within the first year of use, highest in first 3 months) may be unnoticed and result in contraceptive failure
5. Uterine perforation (1-4/1000 insertion)
6. Ectopic pregnancy:-the overall incidence of ectopic is decreased, but when pregnancy occurs, the likelihood of ectopic is
higher
Non-contraceptive benefits of IUCD

90% of ladies can control menorrhagia with latest progestogen-containing IUCD (Mirena)
Contraindications of IUCD
1. Known or suspected pregnancy (Spontaneous miscarriage rate 40-50% vs. 20%; 4-fold increase in preterm; risk of infection.)
2. Infection:- Current pelvic / cervical infection; or sepsis; or immediately post-septic abortion.
3. Uterine deformity:- such as fibroid and congenital malformations (e.g. uterine septum)
4. Undiagnosed abnormal vaginal bleeding.
5. High risk of pelvic inflammatory diseases and ectopic pregnancy:- Past history of sexually transmitted diseases, pelvic
inflammatory diseases or ectopic pregnancy; Multiple sexual partners.
6. All cervical or endometrial cancer awaiting treatment; malignant gestational trophoblastic disease; (For Mirena) breast cancer
7. Wilson's disease (for copper-IUCD)
When a patient asks for removal of IUCD, what is your assessment and when and how do you remove it?
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Levonorgestrel intra-uterine system
Intrauterine contraceptive device containing levonorgestrel
Contraception
Not recommended as an emergency contraception.
Areas of use
1. Decrease menstrual flow
2. Treat endometrial hyperplasia
3. Protect uterus from endometrial carcinoma because of unopposed oestrogen in hormone replacement therapy
Other Information
1. It releases levonorgestrel daily and has localized effect to render endometrium atrophic, hence very effective to reduce
menstrual flow (95%) or achieve amenorrhoea.
2. Minimal systemic side effects, only same as progesterone.
3. Irregular vaginal spotting in initial three months of use. Patients may abandon the device at this stage causing wastage of
money ($1000).
4. It has to be changed every 5 years.
Emergency contraception / Postcoital contraception

Definition
A contraceptive method to prevent conception after unprotected coitus. There are 2 types of emergency contraception:-Hormonal
and IUCD
Hormonal therapy
Should be given within 72 hours after an unprotected coitus
1. Yuzpe regimen:
a. This is also called the morning-after pills
b. Ethinylestradiol 100 microgram + Levonorgestrel 500 microgram for 2 doses 12 hours apart
c. Side effects are nausea (50%), vomiting (20%) because of the high dose oestrogen
2. Levonorgestrel only regimen:
a. Levonorgestrel pills 1.5 mg given once; or 0.75 mg for 2 doses 12 hours apart, within 72 hours of unprotected coitus.
b. Less side effects of nausea (25%) and vomiting (5%) than the Yuzpe regimen
Copper-containing IUCD
Should be given within 5 days after an unprotected coitus. It can be removed after menstruation returns in the next cycle, or be
kept as a long-term contraception.
Mechanisms
1. The precise mechanism of post-coital contraception is uncertain. It may act by blocking the implantation.
2. Yuzpe action is likely to be multifocal:-
a. At ovarian level:- when given before ovulation, it may delay ovulation; when given after ovulation, it is luteolytic.
b. At endometrial level:- cause de-synchronisation of endometrium and prevent implantation.
c. Levonorgestrel inhibits ovulation.
3. Intrauterine Contraceptive Device
a. Causes local changes in the endometrium which prevent implantation.
b. Neither pills nor IUCD act as abortifacient.
Efficacy and Failure rates
1. Yuzpe:- Reduce chance of pregnancy by 70%; failure rate 1-5%, depending on the exposure time of the menstrual cycle.
2. Levonorgestrel:- Reduce chance of pregnancy by 85%.
3. Background risk of unplanned pregnancy by unprotected coitus is <35%; for those who take EC pills <2% will get pregnant.
4. IUCD:- Failure rate 1-2 /1000cycles; <1% will get pregnant.
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Sterilisation
It is a long term irreversible contraception by which the fallopian tubes are excised or ligated (female sterilisation), or the vas
deferens are excised (vasectomy in male sterilisation)
Female sterilisation
Methods
1. Route:-Via laparotomy (e.g. in the same session of Caesarean section), mini-laparotomy or laparoscopy
2. Method:-By ligation, Falope rings or clips
3. Time:-In the post-partum period or interval period
Assessment before the decision

1. Age of patients
2. Number, ages and health of her children
3. Previous and current contraception, in particular any problems with them
4. Reason for the request of sterilization
5. Stability of marriage
6. Gynaecological, obstetric & medical history
Counseling after the assessment

1. Irreversibility
2. Regret rate
3. Failure rate (1%)
4. Risk of ectopic pregnancy if failure
5. Operative procedure and risks, such as bleeding, infection and visceral injury
6. Alternative contraceptive methods including male sterilisation
Male sterilisation
See vasectomy.
Vasectomy
It is the excision of a small piece of the vas deferens and is a kind of male sterilisation. It is performed under local anaesthesia on
an out-patient basis. Since sperm are produced 72 days prior to ejaculation and stored in the proximal collecting ducts, a
vasectomy is not immediately effective. Azoospermia should be confirmed with semen analysis before a couple relies on a
vasectomy for contraception. The failure rate is 0.15%. Complications are uncommon, including bleeding, infection and
haematoma. Sometimes the patients may develop anti-sperm antibodies following the operation, and this accounts for the male
infertility even after anastomosis of the vas deferens.
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3. Disorders of early pregnancy
Viable
Viability means 'the ability to survive'. Foetuses with maturity at or more than 24 weeks are regarded as potentially viable, and
therefore maturity of 24 weeks gestation is set as the cut off of abortion. However, the term 'viable foetus' is also commonly
misused when patients present with threatened abortion, to describe a life foetus, while 'non-viable' is used for missed abortion.
Termination of pregnancy
What is termination of pregnancy
It is also called induced abortion, is a procedure to discontinue a life pregnancy by evacuation of the uterus before 24 weeks of
gestation. It should only be performed under the Abortion Act, and patients should be counselled properly before the procedure.
Abortion Act (1967)

Abortion can be performed if 2 registered medical practitioners agree that the pregnancy should be terminated on the one or more
of the following grounds:-
1. Risks of continuance of pregnancy to the life of the pregnant woman are greater than that of termination of pregnancy
2. Risks of continuance of pregnancy to the physical or mental health of the pregnant woman or her existing children are
greater than that of termination of pregnancy AND the pregnancy is less than 24 weeks
3. There is a substantial risk that if the child were born it would be seriously handicapped
Pre-abortion counselling
- Why is the pregnancy unwanted?
- Whether the woman is absolutely certain about her decision?
- Has the woman think about the other options like continuing the pregnancy and adoption?
- Methods and risks of abortion
- Future contraceptive plans
Methods of abortion The choice of the method of termination depends on gestational age:
1. Early first trimester (up to 9 weeks)
a. Medical:-anti-progesterone mifepristone (but it is not licensed in Hong Kong)
b. Surgical:-vacuum (or suction) evacuation of uterus
Figure 45 Medical abortion for early first trimester.
Figure 46 Vacuum suction evacuation of the uterus.

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2. Late first trimester (9 -14 weeks)
Surgical:-vacuum evacuation of uterus, may need cervical priming by prostaglandin analogue to reduce the risk of
haemorrhage and genital tract trauma
3. Mid-trimester
a. Medical:
i. First line treatment at this gestation
ii. By vaginal gemeprost (a prostaglandin analogue)
b. Surgical:-by dilatation and evacuation
i. High risk of haemorrhage, uterine perforation and incomplete evacuation
ii. Need expertise
Figure 47 Dilation and evacuation.

Complications of termination of pregnancy
- Haemorrhage
- Post-abortion infection
- Uterine perforation
- Cervical trauma
- Failed abortion
- Psychological sequalae
Follow up
- Exclude complications like infection or incomplete abortion or even failed abortion
- Advise contraception and emphasize the importance of compliance
Early pregnancy complications

A group of disorders commonly occurs during the first trimester of pregnancy, including:-
1. Threatened and true abortions
2. Ectopic pregnancy
3. Gestational trophoblastic diseases
4. Hyperemesis gravidarum
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Abortion
Definition of abortion
- In Hong Kong and the United Kingdom, abortion is defined as a pregnancy loss occurring before 24 completed weeks of
gestation.
- The WHO definition is 'the loss of a foetus or embryo weighing 500g or less which corresponds to a gestation age of 20-22
weeks, the irreducible age for foetal well-being'.
Threatened abortion
A very common condition (15%) in early pregnancy, presents with painless vaginal bleeding. The cervical os is closed and the
intrauterine pregnancy is viable.
Figure 48 Different types of abortion.

Missed abortion
A spontaneous abortion in which the embryo dies but the gestational sac is retained in the uterus, and there is no symptom such as
vaginal bleeding or abdominal pain. Therefore, the abortion is 'missed' by the patient. However, features of pregnancy such as
nausea, vomiting and breast bloating subside. On examination, the uterus is small for date and foetal pulsation is absent.
Evacuation of products of gestation is required (see evacuation of uterus below).

1. The diagnosis of missed abortion can be made when:-
a. A gestational sac of mean diameter greater than 20 mm with no evidence of an embryo or yolk sac.
b. The embryo of CRL greater than 10 mm with no evidence of fetal heart movement.
2. If the mean diameter of the gestational sac is less than 20 mm or CRL is less than 10 mm in the absence of fetal heart
movement, ultrasound examination should be repeated 1-2 weeks later to assess the growth of sac and embryo and any
evidence of fetal heart activity.
3. If the gestational sac is smaller than expected for gestational age, the possibility of incorrect dates should be considered. A
repeated ultrasound scan should be arranged after 1-2 weeks.
4. Whenever there is uncertainty, even slightly doubt, the ultrasound examination should be repeated 1-2 weeks later to
monitor the growth of gestational sac or the appearance of fetal cardiac activity.
5. When the diagnosis of early pregnancy failure is made, the findings should be confirmed by a staff with FHKAM or HA
ultrasound certificate before any intervention.
Blighted ovum / anembryonic pregnancy

They are both misnomers of missed abortion, with no foetal pole found in an empty gestational sac on ultrasound scan.
Complete abortion
A complete abortion is one in which all the products of conception have been expelled. Pain and bleeding usually subside. The
cervix closes again. The uterus is smaller for date. Transvaginal ultrasound scan is usually done to confirm that the uterus is empty.
An intrauterine heteroechogenic dimension of less than 5cm2 in both transverse and sagittal planes is considered as complete
abortion. No further treatment is generally needed.
Incomplete abortion
Only part of the products of gestation has been passed. There may be considerable pain and bleeding. The cervix is dilated.
Evacuation of products of gestation is required (see evacuation of uterus below).
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Inevitable abortion
The product of gestation has not been passed out yet, but there is increasing contraction pain and vaginal bleeding, and the
cervical os is dilating. The products of gestation may sometimes be felt through the open internal os.
Remark
The above terms were defined clinically in the old days when ultrasound (USG) was not in use. The use of these terms has
changed slightly with the introduction of USG. For example, the diagnosis of missed abortion is now commonly referred to
pregnant women present with vaginal bleeding and has identified a 'non-viable' foetus. Complete abortion is diagnosed according
to ultrasound finding as described above.
Septic abortion
Septic abortion is an infected abortion. It is associated with high maternal morbidity and mortality when treatment is delayed. It is
often due to illegal abortion under unsterilized condition.
Recurrent abortion
Also called habitual abortion, recurrent abortion is defined as three or more consecutive losses of pregnancy. The incidence is 1%
which is higher than when it occurs by chance. Therefore investigations for the underlying cause are needed.
Management of abortion
1. Principles
a. Rule out other causes of vaginal bleeding or pain complicating early pregnancy such as ectopic pregnancy
b. Confirm foetal viability (see viable) with USG
c. Counselling and evacuation of uterus when required
d. The diagnosis and management is often easy nowadays with USG, but history and examination are still essential,
particularly when the USG finding is inconclusive
2. Counselling
a. Explain the cause of abortion, the chance of abortion and successful pregnancy next time.
b. Investigate further in case of recurrent abortion, or second trimester abortion.
Evacuation of uterus
1. Owing to the advances in ultrasound and medicine, treatment of abortion has been changed in the recent decades.
2. In the past, almost all women with abortion required surgical treatment to ascertain complete evacuation. With the improved
resolution with transvaginal scan, uterine cavity is much more accurately assessed. Women with diagnosis of complete
abortion by USG can then be managed conservatively. Secondly, prostaglandin analogues, such as misoprostol, have effect of
cervical softening and oxytocic effects. When misoprostol is taken orally, it causes a complete evacuation of uterus in 70% of
cases in 24 hours. It has the advantages of minimizing operative complications such as perforation of uterus and introduction
of intrauterine infection. The side effects are mild and well tolerated, including diarrhea, vomiting and abdominal pain.
Occasionally, it may cause severe vaginal bleeding which requires an emergency surgical evacuation.
3. Therefore, options of surgical and medical treatment should be offered to patients with abortion.
How would you counsel a patient who is diagnosed to have threatened abortion at 6 week of gestation? How would you explain
the treatment of uterine evacuation to a patient with incomplete abortion?
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Recurrent abortion
Definition
Recurrent abortion or habitual abortion is defined as 3 or more consecutive abortion.
Incidence
The incidence is about 1% of all women and is greater than the rate expected by chance alone, suggesting that there is a specific
underlying cause in many cases.
Figure 49 Anatomical factors:-Fibroid (Left) and arcuate uterus with septum (Right).
Causes
In majority of cases, the causes are unknown. The following pathologies are identified causes:-
1. Chromosomal abnormalities
One of the couple may have some forms of chromosomal abnormalities that may be transmissable, resulting in
recurrent abortion. They themselves, however, may be phenotypically normal. A typical example is translocation
(reciprocal or robertsonian). The abortion usually present with absent foetal heart in-utero, in the first or sometimes
second trimester. Structural abnormalities may be present.
2. Uterine anomalies
a. Congenital anomalies of uterus are associated with recurrent abortions. Implantation to the site of underdeveloped
uterine body, or hypoplastic and hypovascular area of uterus may result in restriction of foetal growth and abortion.
b. Cervical incompetence typically presents with painless mid-trimester miscarriage
3. Endocrine disorders
a. Poorly controlled diabetes is associated with early pregnancy failure. However, well-controlled DM, asymptomatic or
mild glucose intolerance are unlikely to cause pregnancy failure. OGTT to rule out occult diabetes in case of recurrent
abortion is therefore not necessary.
b. Similarly clinical hypothyroidism is also a risk factor for recurrent abortion but subclinical disease is not. Screening of
thyroid disease is again not indicated.
c. Hypersecretion of luteinizing hormone:-It has been showed that polycystic ovarian disease (PCOD) with high LH
level is associated with recurrent pregnancy loss, usually in the first trimester.
4. Immunological disorders Autoimmune diseases such as antiphospholipid syndrome and systemic lupus erythematosus are
associated with foetal loss.
5. Other risk factors
a. Environmental factors such as heavy alcohol consumption and smoking may contribute to recurrent pregnancy loss.
b. Congenital infections Congenital infections are unlikely to cause recurrent foetal loss, although they can result in
sporadic loss. Patients can develop immunity after primary infection such as in rubella, chickenpox.
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Investigations for underlying causes of recurrent abortion
1. History
History provides the most important information to look for the underlying aetiology, and guide the investigation.
Information such as when and how the abortions occurred, and whether there are abnormal foetal morphology,
presence of positive past medical history (DM, thyroid disease, PCOD) and social history (smoking and alcoholism)
are essential (see above).
2. Investigation tests
a. Parental karyotyping
b. Screening of autoimmune disorders:-autoimmune disorders are suspected if there are positive symptoms and signs, or
thrombocytopenia and derangement of clotting profile.
c. Investigation of uterine anomalies and cervical incompetence should only be performed on clinical suspicion.
d. OGTT and thyroid function, screening of congenital infections are not necessary
Management
1. Counselling
Patients should be counselled that the underlying causes cannot be identified in majority of cases. There is still a 60%
chance that they will have a successful pregnancy in the future.
2. Treatment of underlying causes:
a. Abnormal parental karyotyping
i. Couples should be counselled the risk of transmission of chromosomal abnormalities in future pregnancy.
ii. Prenatal diagnosis should be advised.
b. Uterine abnormalities
Various types of metroplasty may be indicated for congenital anomalies, and cervical cerclage is indicated for
cervical incompetence
c. Control of medical disorders
Medical treatment is indicated for autoimmune diseases and endocrine disorders. Patients should also be advised
to quit smoking and alcohol.
Protocol, as of 25 September 2008

1. Investigation
a. History and examination is important for diagnosis of cervical incompetence
b. Blood tests:-platelet count, clotting profile, ANA, AC
i. If ANA is positive, check anti-dsDNA
ii. If AC is positive, repeat it 6 weeks later
iii. If anti-ds DNA or repeated AC is positive, refer rheumatology clinic
iv. We screen lupus anticoagulant (LA) by clotting profile because it is rare for APTT to be normal with a +ve
LA. If there is raised AC or strong suspicion of APL, phone contact with haematologist to arrange LA assay.
c. Refer both partners to clinical geneticists:- peripheral blood karyotyping.
d. Pelvic ultrasound scan:- to look for polycystic ovaries and uterine anomalies
e. If at least one of the miscarriages occurred in the second trimester,
i. Hysterosalpingogram (HSG) to look for uterine anomalies
ii. Send fetus and placenta for section to look for evidence of chorioamnionitis
iii. Take high vaginal swab (HVS) for culture
f. Remarks:-It is not necessary to send foetal tissue for chromosomal studies.
i. Although fetal chromosome abnormalities are the commonest cause of sporadic miscarriage, they are less
frequent in women with recurrent miscarriage.
ii. It has to be done in TYH and the result seldom influences clinical management
2. Follow up
a. In 4-6 months time
b. Review investigation results
c. Formation of management plan for further pregnancies
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3. Management plan for further pregnancies

a. Treatment with unproven value should be discouraged. They include progestagen support in early pregnancy, HCG
support in early pregnancy, and immnotherapy such as paternal leukocyte immunization
b. Treatment is directed to the cause and decided by doctor at FHKAM level
i. Cervical incompetence
- Elective cervical cerclage in early second trimester of future pregnancies
- If the diagnosis is in doubt, consider serial ultrasound scan for the monitoring of cervical length in
future pregnancies
ii. Antiphospholipid syndrome (either positive LA or raised AC on two occasions)
- Refer to medical rheumatolgoy clinic
- Aspirin 80mg daily PO (once pregnancy test is positive) and Enoxaparin 40 mg daily SC (since fetal
viability is confirmed) in future pregnancies
iii. Chromosome anomalies Refer to clinical geneticists for genetic counseling
iv. PCOS
- Check fasting glucose to screen for diabetes mellitus
- Consider ovarian drilling or metformin, to be decided by gynae-endocrinology team
v. Uterine pathology Consider hysteroscopic metroplasty for septate uterus or hysteroscopic myomectomy for
submucosal fibroid
vi. Chorioamnionitis or positive HVS culture Antibiotics as indicated
vii. Idiopathic Counseling
- 50% of patients with recurrent miscarriage have no cause identified.
- The cause is most likely due to repeated sporadic fetal chromosomal anomalies occurring by chance,
especially with increasing maternal age
- If 3 miscarriages, still 70% chance that the next pregnancy will be successful. (The chance is reduced by
20% for each additional miscarriage)
- Continued psychological support in future pregnancies
Septic abortion
Definition
It is a condition in which the abortion is associated with an ascending intrauterine infection.
Causes
It can be a result of surgical evacuation of uterus under inadequate aseptic technique. It commonly occurs in the setting of illegal
termination of pregnancy where sterilisation of instruments is poor. Septic abortion can also follow incomplete abortion or
prolonged rupture of membranes before 24 weeks of gestation.
Clinical features
- Fever and tachycardia
- Pelvic pain and tenderness
- Vaginal bleeding or pusty discharge
- Cervical os may be opened
- There may be evidence of retained product of gestation (POG) under USG
Complications
- Septic shock
- Disseminated intravascular coagulopathy (DIC)
Management
- Antibiotics
- Evacuation of uterus if there is evidence of retained POG
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Ectopic pregnancy
Definition
A pregnancy with implantation outside the normal uterine cavity. The ectopic site can be:
- Fallopian tubes:-the most common site
- Ovary:-uncommon
- Cornus of uterus:-uncommon
- Cervix of uterus:-uncommon
- Peritoneal or omental surface:-very rare
Figure 50 Fallopian tube (left) and uterine cornus (right) implantation.
Figure 51 Ovarian (left) and cervical (right) implantation

Incidence
1.13-2.14% of all maternalities (Hong Kong rate)
Causes
- By chance, migration of ovum.
- Previous tubal surgery or injury such as sterilisation, pelvic inflammatory disease
- Intrauterine devices
- After assisted reproductive procedures (see ART)
Presentation
1. Symptomatic
The typical presentation is acute pelvic pain after amenorrhea. Vaginal bleeding may occur but is usually of small amount.
There may be signs of internal bleeding such as abdominal distension, tenderness and guarding, with hypotension,
tachycardia and pallor. Pregnancy test is positive
2. Asymptomatic
With the use of transvaginal ultrasound and HCG monitoring, ectopic pregnancy can now be diagnosed at an earlier gestation
when patients are asymptomatic or with only mild symptoms. Ectopic pregnancy is diagnosed or suspected with USG which
is done as a routine in early pregnancy, or for investigation of vaginal bleeding complicating pregnancy
Figure 52 Rupture into the tube (left) and peritoneum (right).
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Ultrasound features of ectopic pregnancy
1. Gestational sac and foetal pole are seen outside the uterus
a. These features can be seen in only 10% of cases, when the pregnancy is already big but not yet ruptured
b. A definite diagnosis of ectopic pregnancy can be made in this situation
2. Adnexal mass and free fluid in Pouch of Douglas
a. It is the most common presentation
b. The adnexal mass represents the tubal ectopic pregnancy surrounded by blood clots. The free fluid is the bleeding
from the ectopic pregnancy
c. Ectopic pregnancy is highly suspected in this situation. The differential diagnosis is a bleeding corpus luteal cyst
3. Absence of features of intra- or extra-uterine pregnancy
a. Sometimes pregnancy test is positive, but there is no intrauterine gestational sac, neither is there any positive
ultrasonic feature of ectopic pregnancy as mentioned above
b. The possibilities include:
i. An early intrauterine pregnancy which is still not visualised by USG;
ii. An abortion of an intrauterine pregnancy has just occurred
iii. An early ectopic pregnancy that is still small and has not bled or ruptured yet
c. In this situation, measuring serum HCG level will be helpful in making a diagnosis (see below).
4. Sometimes an ectopic pregnancy may present with a pseudo-gestational sac that mimics a true intrauterine sac.
Serum HCG levels in ectopic pregnancy
1. During the first trimester of a normal pregnancy, the serum HCG levels should be double in 2 days.
2. An intrauterine gestational sac is usually visible when the HCG level reaches 1500iu/L. Therefore,
a. When there is a suboptimal rise in the HCG levels (which are taken 2 days apart), or when it have been above 1500iu
but yet no intrauterine gestational sac is identified, ectopic pregnancy should be suspected;
b. When the HCG level is decreasing, abortion is more likely and it should be decided if the abortion is complete or not;
c. When the HCG level is rising normally, repeat USG to confirm a viable intrauterine pregnancy;
Diagnosis
Diagnostic laparoscopy is the definite diagnostic tool for ectopic pregnancy and should be done if clinical suspicion of ectopic,
positive ultrasound features, or abnormal HCG result.
Figure 53 Diagnosis (Left) and Treatment (Right) of tubal pregnancy.

Treatment
1. Surgical Treatment It is the mainstay of treatment of ectopic pregnancy. In the radical surgical treatment, the whole ectopic
pregnancy including the products of gestation (POG) and the site (e.g. Tubes) are excised together. In the conservative
approach, only the POG is removed. The surgery can be performed with laparotomy or laparoscopy approach.
2. Radical surgery It ensures a complete removal of POG. The disadvantage is part of the genital tract (e.g. Tube) is excised.
3. Conservative surgery
a. Aims to preserve genital structure for fertility, e.g. In salpingotomy, the tube is cut open and POG is removed.
b. Indications:- Patients want to preserve the tube, particularly the other tube has already been damaged or excised
c. Contraindications:
i. The ectopic pregnancy is too big that complete removal is unlikely
ii. The ectopic pregnancy has already ruptured
iii. There has been previous tubal damage
iv. Patients have already required in vitro fertilisation
v. Patients have completed family
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d. Disadvantages:
i. Persistent ectopic pregnancy because of incomplete removal of POG:-5%
ii. Risk of recurrence of ectopic at the same site in subsequent pregnancy:-5%
4. Medical Treatment
a. Consists of systemic injection of methrotrexate which is a cytotoxic agent that kills the proliferating foetal and
trophoblastic tissue. Direct injection of methrotrexate or KCl into the site of ectopic pregnancy is not shown to be
effective.
b. Success of treatment is confirmed by gradual reduction and disappearance of serum HCG.
c. Medical treatment is rarely used in Hong Kong and is only indicated when:-
i. Cervical ectopic pregnancy where surgical excision is difficult and associated with heavy bleeding.
ii. There is persistent ectopic pregnancy after conservative surgical treatment
iii. There is persistently detectable HCG but the site of ectopic is unknown
iv. Patient refuses surgery
5. Chance of success is low when the initial HCG level is high, or the ectopic pregnancy is big.
6. Complications of medical treatment are those of side effects of cytotoxic:-nausea, vomiting, liver function derangement, etc.
Which kinds of patients are contraindications for conservative surgery for tubal pregnancy?
Protocol, as of 21 April 2008

1. Use of methotrexate
a. Not for primary treatment of tubal ectopic pregnancy
b. Usage need to be endorsed by FHKAM
i. Ectopic pregnancy with hCG > 5,000iu/L, ectopic mass over 3cm, cardiac activity documented
ii. Patient unlikely to comply with follow up and repeated hCG assay
iii. Deranged LFT, RFT or neutropenia or thrombocytopenia
c. Advice to patients
i. Refrain from use of alcohol, vitamins with folic acid
ii. Refrain from sexual intercourse until hCG return to normal
iii. Avoid pregnancy for 6 months from last injection
d. Dosage regime, follow up and monitoring
i. Single dose:-50mg/m2 SA IM Check hCG on D4 and D7, repeat same dose if D7 decline < 15% of D4
ii. Multiple doses may be used:-1mg/kg IM on alternate day; folinic acid 0.1mg/kg IM on other days Check
hCG on D1, 3, 5 and 7 every 48 hours, stop further dose if 4 doses given or until hCG decline by > 15% on 2
consecutive readings
e. Consent from patient needed
2. Operative treatment
a. Laparoscopic approach preferred, laparotomy acceptable if patient hemodynamic status not stable or surgical
expertise not available
b. Milking or aspiration of ectopic content as treatment is not recommended
c. Salpingostomy:-
i. Contra-indicated if:-
- Ectopic site over 4cm, cardiac activity documented, tube ruptured already
- Patient not reliable for monitoring and follow up or not acceptable to secondary treatment
ii. Not recommended if:-
- Family completed
- Diseased tube
iii. Check hCG on D1, give single dose of MTX if <50% drop in hCG level.
iv. Repeat hCG weekly till normal.
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Pseudo gestational sac
A pseudo gestational sac (or pseudosac) is an ultrasonic feature of ectopic pregnancy that may mimic a true gestational sac. In
case of ectopic pregnancy, the endometrium will still undergo a decidual reaction because of hormonal effects. The secretion from
the decidua is collected inside the uterine cavity, and appears as a cystic structure under ultrasound. It may be mistaken as an
intrauterine gestational sac, and the diagnosis of ectopic pregnancy may therefore be missed. The pseudo gestational sac can be
differentiated from a true gestational sac. The former is centrally located, without an hyperechoic rim or foetal pole, while the
latter is eccentrially located, with hyperechoic rim (the trophobastic layer), and may have a foetal pole or a yolk sac.
Corpus luteal cyst

It is a common physiological ovarian cyst. Sometimes a corpus luteum becomes cystic, enlarged and persists, particularly if the
patient is pregnant. It usually regresses spontaneously after the first trimester, but may rupture or bleed causing acute pelvic pain.
When these occur during pregnancy, the clinical picture may be confused with ectopic pregnancy. Ultrasound features are same as
described in follicular cyst.
Hyperemesis gravidarum
Definition
Excessive vomiting during early pregnancy, to the extent of dehydration, weight loss, electrolyte imbalance and acid-base
disturbance.
Causes and pathophysiology

1. Vomiting is one of the commonest early pregnancy complications, and is thought to be related to the production of HCG
which stimulates the chemoreceptor in the hypothalamus. The risk is higher in:
b. Gestational trophoblastic disease
c. Hyperthyroidism
d. Urinary tract infection
2. The symptoms usually subside after the first trimester when the HCG level starts to decrease from the peak.
3. Remark:-Vomiting can be due to co-existing pathology of other systems, such as GI and CNS system. Careful clerking and
examination are very important not to miss the diagnosis.
Complications
- Hypokalemia
- Malnutrition
- Wernicke syndrome (due to deficiency of thiamine)
- Mallory-Weiss syndrome
Clinical features
1. Onset of symptoms:-in the first trimester, around 6 to 8 weeks
2. Common features:
a. Nausea and vomiting
b. Loss of appetite
c. Weight loss
d. Signs of dehydrations
Investigation
1. To assess severity:
a. Renal and liver function tests
b. complete blood picture
2. To rule out underlying causes:
a. USG to look for multiple pregnancy and gestational trophoblastic disease
b. Thyroid function test
c. Mid-stream urine for culture
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Treatment
1. Regular monitoring
a. Blood pressure and pulse
b. Fluid input and urine output
c. Urine ketone
d. Body weight
2. Fluid electrolytes correction
a. Rehydration with intravenous fluid
b. Potassium supplement
3. Nutrition support
a. Dry food
b. Vitamin supplement
4. Antiemetics Metroclopramide
Minor disorders of pregnancy

1. Although they seldom cause any dangers to the mother and foetus, they are common and often cause discomforts to the
mother and sometimes annoying.
2. The symptoms may also mimic those of severe disorders.
3. Medical students are required to know how to explain, advise and manage these minor disorders for pregnant women, and to
differentiate them from major disorders.
Nausea and vomiting

1. Most common symptom and is due to high HCG level
2. Need to rule out multiple pregnancy and molar pregnancy when severe
3. Usually improve after first trimester
4. Avoid greasy or highly spiced foods; frequent small meals
5. in severe form hyperemesis gravidarum, admit and rehydrate patients with intravenous fluid supplement and give antiemetics
Heartburn
1. Resulted from gastric reflux due to relaxation of the lower oesophageal sphincter and pressure from the enlarging uterus later
in pregnancy
2. Advise frequent, light bland meals; avoiding a late meal; raising the head of the bed; and use of antacid
Constipation
1. Due to decreased bowel motility because of high levels of progesterone
2. Increase dietary fibre and fluid intake
3. Bulk laxative if necessary
Haemorrhoids
Due to progesterone-induced venodilatation, obstruction of venous return from the lower body by the enlarged uterus, and
increased bearing down because of constipation or at delivery
Epistaxis
Result of increased peripheral vascularity. Usually self-limiting
Varicose veins
1. Occur mostly in the legs but also in the vulva.
2. Cause aching and tiredness
3. May be complicated with thrombophlebitis and deep vein thrombosis
4. Treat with combination of elevation an use of full-length support tights
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Backache
1. A common symptom and results from increased joint laxity in the lumbar spine and the exaggerated lordosis which occurs in
pregnancy.
2. Management is conservative, with rest, analgesia, and improvement in posture
Breast soreness
1. Commonest in early pregnancy as the breasts increase in size.
2. Reassurance and symptomatic relief with a brassiere that provides adequate support are all that is needed
Peripheral paraesthesiae
1. Numbness and tingling occur due to compression of peripheral nerves because of fluid retention, most commonly the median
nerve (carpal tunnel syndrome)
2. No treatment is usually required when the cause has been explained to the patient
Headache
1. Usually a typical tension headache and is best treated by rest and mild analgesia
2. Migraine often improves but may deteriorate, stay the same or occur de novo, in pregnancy
Postural hypotension
1. More likely to occur in pregnancy because of venous pooling in the lower limbs
2. It is best prevented by avoiding precipitating factors:-standing up quickly, hot bath, standing in hot weather for long time
Pruritus
1. Generalized
a. Generalized itching (pruritus gravidarum) usually begins in the third trimester and may be associated with cholestasis
in pregnancy
b. Treat with topical antipruritus
2. Pruritus vulva
a. Usually due to candidiasis
b. Treat with topical anti-fungal agent
Frequency of micturition
1. Symptoms of early pregnancy when it may be due to increased renal filtration
2. Also in late pregnancy when it is due to pressure from the enlarged uterus
3. Urinary tract infection has to be excluded when there is also dysuria or urgency
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4. Endometriosis and Adenomyosis
Endometriosis
Definition
- Presence of tissue outside the uterus that is histological similar to that of endometrium.
- Adenomyosis does not belong to the group of endometriosis by this definition
Incidence
- A very common gynaecological disease with incidence of 10 to 15%.
- Presents in 20 to 40% of patients with infertility, and 17% of patients with chronic pelvic pain.
- Inpatient incidence remained about 700 (1%) per year throughout 1994-2004. Total incidence was thought to be increased
possibly due to environmental factors or increased use of laparoscopy.
Pathogenesis
- Retrograde menstruation and implantation (Sampson's theory)
- Lymphatic and haematogenous dissemination
- Transformation of coelomic epithelium
- Immunological and genetic factors
- The above mechanisms are not mutually exclusive
- Growth of endometriosis is oestrogen dependent
- The ectopic endometriotic tissue induces inflammation, fibrosis and adhesions that cause complications
Histology:- Simulate endometrial tissue with glands, stroma, and evidence of menstrual cyclicity:-i.e. haemorrhage or
haemosiderin- laden macrophages. It shows proliferative and secretary changes
Histological subtype Componnts Hormonal response
Free Surface epithelium, glands and stroma Proliferative, secretory and menstrual changes
Enclosed (by peritoneum) Glands and stroma Proliferative, variable secretory changes. No menstruation.
Healed / Fibrotic Glands only No response.
Sites:
1. Most common in pelvic peritoneum and ovaries as there are high estrogen concentration
2. Peritoneal deposits:-
a. Lesions of a few mm in size
b. Endometriotic tissue appears as red or bluish spots
c. Brownish spots represent haemosiderin
d. Whitish scarring resulted from inflammation and fibrosis
3. Ovary:-
a. Superficial: hemorrhagic lesions
b. Endometriomas (endometriotic cysts):
i. Formation by inverted superficial deposits when proliferating.
ii. Also called chocolate cysts, as they are filled with chocolate-coloured liquid, representing debris from cyclical
menstruation within the cyst walls.
iii. Arise only from ovaries.
iv. In long standing cases they results in scarring and firbrosis.
4. Adhesions:-
a. Endometriotic deposits, also leakage from chocolate cysts, induce pelvic inflammation and adhesion formation
between ovaries, fallopian tubes, posterior uterus, and sometimes bowel.
b. Adhesion is sometimes very dense and obliterates the pouch of Douglas, causing bowel or ureteric obstruction.
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Clinical features
1. Subclinical
a. Some women are asymptomatic and the diagnoses are made incidentally on routine examination or during surgery for
other reasons
b. Signs and symptoms are caused by:-
i. Proliferation,inflammation and bleeding at different sites;
ii. Adhesions at different sites.
2. Pelvic pain
a. Dysmenorrhea, dyspareunia, chronic pelvic pain that may be progressive, and not relieved by simple analgesics
b. Pain arises because of:-
i. Prostaglandins production
ii. Local inflammation
iii. Adhesion and scarring
iv. Stretching of nerves after scarring
c. Remark:-severity of endometriosis is not correlated to the degree of pain
3. Infertility
Possible mechanisms of infertility in endometriosis include:-
Problem area Mechanism

Ovarian function Anovulation, luteolysis
Coital function Dyspareunia causing reduced penetration and coital frequency
Tubal function Altered tubal and cilial motility, impaired fimbrial oocytes pick-up
Sperm function Inactivation or destruction by inflammative changes
Endometrium Luteal phase deficiency, endometrial interference
Early pregnancy failure Increased abortion
4. Endometrioma
a. Presents with acute abdominal pain related to rupture or haemorrhage, or
b. Presents with pelvic mass under physical or ultrasonic examination
5. Others
a. Gastreointestinal system:- dyschezia, cyclical GI bleed, intestinal obstruction and tenesmus
b. Urinary system:- cyclical dysuria and haematuria
c. Lung: cyclical haemoptysis, haemopneumothorax
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Diagnosis
1. Diagnostic laparoscopy
a. Gold stsandard in diagnosis but may miss lesions because of difficulty in visualising the whole pelvis and there are
variable appearances of deposits.
b. Indications:
i. Patients with chronic pelvic pain, secondary dysmenorrhea or dyspareunia not responsive to simple analgesic
ii. Patients with infertility with above symptoms
c. Look for peritoneal deposits, endometrioma and pelvic adhesions (features as mentioned above)
2. Ultrasound
a. While endometrioma can be picked up by USG, peritoneal deposits are not visible by USG
b. USG features of endometrioma
i. Variable with homogenous or heterogeneous echogenic content
ii. Usually around 3 to 7cm in diameter
iii. Can be bilateral
iv. No papillary growth
3. Biopsy
a. Seldom required to diagnose peritoneal deposits as the gross features are obvious
b. May be needed to confirm diagnosis when the endometriosis is found in atypical sites such as in bladder or skin
Management
Principle
1. Endometriosis is a chronic disease that is difficult to be eradicated, without radical surgery
2. The disease may present without causing significant symptoms
3. High recurrent rate after medical or conservative surgical treatment
4. Choices of treatment depends on the severity and type of symptoms, and desire of fertility, and are introduced as follows.
Expectant management
- Indications:-asymptomatic or mildly symptomatic
- NSAID prn for pain relief
Hormonal treatment
1. Indications severe pain, want to preserve fertility
2. Mechanisms suppress oestrogen that stimulates the proliferation of endometirum.
3. Choices:
a. Gonadotropin releasing hormone analogue (GnRHa)
i. Mechanism:-suppresses ovarian function and hence endogenous oestrogen production which supports the
growth of endometriosis
ii. Advantages:-effective pain relief (90%), no androgenic effects compared with danazol
iii. Disadvantages:-side effects of hypoestrogenism, delay fertility
b. Danazol
i. Mechanism:-Androgen that suppresses hypothalamic-pituitary-ovarian axis and therefore decreases endogenous
oestrogen production
ii. Advantages:-effective pain relief (90%), no hypoestrogenic effects compared with GnRHa
iii. Disadvantages:-androgenic side effects; delay fertility
Conservative surgery
- Aims at pain relief and restoration of fertility
- Choices vary from cystectomy (for endometrioma), adhesiolysis, ablation of endometriotic spots
Radical surgery
- Consists of bilateral salpingo-oophorectomy and total hysterectomy
- Aims at pain relief and complete eradication of the disease
- Fertility is not preserved
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Adenomyosis
Definition
The presence of tissue resembling endometrial glands and stroma within the myometrium of the uterus
Pathology
1. Macroscopic
a. Grossly enlargement of uterus, usually globally
b. Spongy appearance with no cleavage plane
2. Microscopic
a. Endometrial glands and stroma embedded in the myometrium
b. Focally or uniformly
Clinical features
1. History
a. Asymptomatic
b. Menorrhagia
c. Secondary dysmenorrhea
d. Deep dyspareunia
2. Examination Enlarged tender uterus, especially during perimenstrual period
Diagnosis
1. Can only be confirmed by histology
2. Ultrasound to rule out fibroids
3. Endometrial biopsy to rule out other causes of menorrhagia
Treatment
Hysterectomy if symptomatic
What are the similarities and differences between the clinical presentation and management of adenomyosis and that of fibroid?
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5. Benign gynaecological tumours
Benign ovarian tumour
Introduction
It is a heterogeneous group of benign ovarian pathologies that is very common in women in reproductive age. They are classified
as below:
1. Physiological cysts:-follicular cyst and corpus luteal cyst
2. Endometriotic cysts (see endometriosis)
3. Epithelial neoplasms (cystadenoma)
4. Germ cell neoplasms:-benign teratoma (or dermoid cyst)
They usually have similar clinical features. The majority of them are small in size (less than 5cm in diameter). The patients are
usually asymptomatic, or present with non-specific abdominal discomfort, and the tumours are picked up incidentally with
ultrasound. Sometimes the tumours may enlarge resulting in abdominal distension, and pressure or space occupying effect. Some
patients may present with acute complications such as rupture, haemorrhage and torsion. Endometriotic cysts may associate with
dysmenorrhea and dyspareunia. As their clinical features are quite similar, they are usually differentiated by ultrasound, which
also help to distinguish them from malignant ovarian tumours.
Physiological cysts
See follicular cyst.
Follicular cyst
It is a common physiological ovarian cyst. Sometimes a developing follicle may not ovulate and become persistent. It is
associated with the use of progestogen contraceptive and ovulation induction agents. It has a thin wall and clear content under
ultrasound and often less than 5cm in diameter. Majority of them are asymptomatic but in few occasions they present with acute
lower abdominal pain as a result of haemorrhage or rupture.
Ovarian cystadenoma
The two most common types are serous cystadenoma and mucinous cystadenoma. The former tends to be unilateral and unicystic,
while the later is more likely to be bilateral and multicystic.
Figure 54 Gross appearance of mucinous cystadenoma.
Mucinous cystadenoma The surface of the cyst is completely smooth and round but maybe slightly nodular due to projecting
loculi. The cut surface of the cyst is multilocular and has a mosaic pattern
Serous cystadenoma may take any one of the following three forms:-
(1) A simple cystic form with smooth surface and smooth lining.
(2) A cystic structure with intracystic papillary formations, which may be sessile buttons or pedunculated frond like projections.
(3) An adenomatous form where many of the loculi are small and papillary structures are solid and complex.
Sometimes they can be very large with diameter more than 10cm. USG features are similar with thin wall and clear content. They
are different from their malignant counterparts as they do not have solid element or papillary growth, and there is no ascites.
Treatment is cystectomy or oophorectomy, by laparoscopy or laparotomy method.
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Dermoid cyst
It is a benign teratoma which consists of mainly skin tissue, with sebaceous material and hair, and is the reason for its name.
Sometimes it may contain teeth or bone tissues. Rarely, active thyroid tissue (stromal ovarii) may be present. It is one of the
commonest benign ovarian tumours occurring in in reproductive age. It is often bilateral (10%), with size ranged from a few
centimetres to up to 10 cm. It is ovoid and unilocular in shape. The wall consists of dense fibrous tissue lined by stratified
squamous epithelium. The eminence may contain sebaceous glands, teeth, hair, nervous tissues, cartilage, bone, respiratory and
intestinal epithelium and thyroid gland tissue. Thick yellow sebaceous material fills the cyst. It is very mobile and therefore
commonly presents with torsion. Patients usually present with on and off colicky lower abdominal pain signifying a process of
intermittent torsion. They then suddenly experience acute colicky abdominal pain that changes to constant sharp pain, signifying
an acute torsion with ischemic necrosis and peritoneal inflammation. On physical examination, peritoneal signs with pelvic mass
and tenderness can be found. Under USG, a dermoid cyst is well-circumscribed with homogenous content. A hyperechogenic
shadow signifies a bone or a tooth. The treatment is cystectomy or oophorectomy which can be done under laparoscopy or
laparotomy.
Figure 55 The macroscopic (left) and microscopic (right) appearance of dermoid cyst.
Teratoma
Ovarian teratoma is one of the commonest germ cell tumours. It develops from a totipotential germ cell (a primaryoocyte) of the
ovary, and therefore can give rise to all kinds of cells and tissues. The commonest tissue types are skin with hair follicles and
sebaceous glands, bone, teeth, and neural tissues. Depending on the maturity of the neural component, teratoma is divided into
mature (benign) and immature (malignant) type.
1. For mature teratoma,
a. The tissues of a mature teratoma are well differentiated. It is also often called dermoid cyst as it contains skin tissue,
hair and sebaceous material.
b. Uncommonly a benign tetratoma may contain functional thyroid gland tissue (stromal ovarii) that secrets thyroxine,
resulting in hyperthyroidism.
2. For imature teratoma,
a. 2% of teratoma consist of immature or undifferentiated tissue, and is called immature teratoma, or malignant teratoma.
As in other germ cell tumours, the treatment of malignant teratoma is surgery followed by chemotherapy.
b. Unilateral oophorectomy is adequate provided that the other ovary is not involved. Fertility can be preserved.
Hysterectomy and bilateral oophorectomy is suggested if patients have completed family.
Nabothian cyst
It is a small cyst beneath the epithelium of the uterine cervix of no clinical significance. It can be multiple and the size is not more
than 10mm. See transformation zone for the formation of Nabothian cyst.
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Fibroid
Definition
fibre:-connective tissue; oid:-like. It is actually a benign smooth muscle tumour (leiomyoma) of uterus.
Incidence
20-25% of women in reproductive age
Pathology
1. Sites:
a. Intramural most common site
b. Submucosal
i. 5% of all fibroids
ii. Most commonly cause symptoms
c. Subserosal pedunculated may sometimes undergo torsion
d. Cervical
i. Uncommon but can cause urinary problems such as urinary retention and ureteric obstruction, and
ii. Surgical difficulty because of close proximity to ureters and accessibility
e. Within broad ligament extremely rare but can cause diagnostic and surgical difficulties
2. Histology:
a. Benign smooth muscle fibres

b. No true capsule
c. Various degenerative changes:
i. Hyaline degeneration
ii. Calcification
iii. Fatty changes
3. Remark:
a. Growth is hormone dependent
b. Sarcomatous change is rare (0.1%)
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1. Clinical presentation depends on sites and size of fibroids, 50% of women are asymptomatic
2. Menorrhagia
a. Menorrhagia is more common with submucosal and intramural fibroids
b. Mechanism:
i. Increases total surface area of the uterine cavity
ii. Disordered uterine motility
iii. Ulceration and haemorrhage overlying submucosal fibroids
iv. Disordered prostaglandin synthesis
3. Pressure symptoms
a. Abdominal distension and discomfort, especially with rapid growing fibroids
b. Symptoms of urinary retention, especially with cervical fibroids
4. Pain
a. Uterine camping:-attempted expulsion of submucosal fibroids
b. Acute torsion of pedunculated fibroids
c. Red degeneration (usually during pregnancy)
5. Sub-fertility
a. An uncommon presentation, accounts for only 3% of all infertile women
b. Possible mechanisms:
i. Mechanical cornual occlusion
ii. Distortion of uterine cavity resulting in failure of implantation
iii. Alternation of local blood flow
6. Sarcomatous change very rare:-0.1%
7. Specific complications during pregnancy
a. Red degeneration of fibroid
i. Presents as acute localised uterine pain, usually in the second or third trimester
ii. Occasionally there is fever and leucocytosis
iii. Treatment is conservative with adequate anaglesia
b. Malpresentation occurs when a large fibroid occupying the cervical or lower pole of the uterus
Diagnosis
1. Diagnosis is usually obvious on physical examination
a. Enlarged uterus, usually of irregular shape
b. Submucosal fibroid protruding out from cervix
2. Ultrasound
a. Is usually not required unless clinical examination is not definite
b. Identifies the sites and number of fibroids that may help to plan of management
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Management
1. Principle
a. Choice of treatment depends on degree of symptoms, desire to preserve fertility, and site and size of fibroids
b. Expetect management
c. Medical treatment
i. Only for temporary symptomatic relief, during waiting for surgery, and correction of anaemia
ii. Symptoms usually return and fibroid re-grow after stopping medication
d. Myomectomy
i. Only for symptomatic women who want to preserve fertility
ii. Can be performed via laparotomy, laparoscopy, or hysteroscopy, depends on the site of fibroids
iii. Recurrence of fibroids and symptoms:-15%; 10% require re-operation
iv. Risk of unplanned hysterectomy (for large intramural fibroids) because of uncontrolled bleeding
v. Post-operative pelvic adhesions that may affect tubal patency, if posterior uterine wall is cut
e. Hysterectomy definite treatment for symptomatic women who do not want to preserve fertility
A 30 year-old single woman is referred to you because of incidental finding of a 3cm diameter intramural fibroid on routine
check-up. How would you manage her?

1. Antenatal management
a. Counsel the patient:-
i. It is a bengin lesion and would not cause any risk to the mother and the fetus in most of the cases
ii. Small chance of red degeneration that may lead to abdominal pain
iii. May cause fetal malpresentation if the fibroid is situated at the lower pole of the uterus
b. No need to arrange serial ultrasound examination routinely throughout the antenatal period, unless there is difficulty
in monitoring fetal growth by fundal height measurement.
c. For fibroid locating at the lower pole of the uterus, arrange follow-up at 37 weeks of gestation (+/- USG) to assess
the fetal presentation and engagement and decide mode of delivery:
d. Allow vaginal delivery unless the uterine fibroid is situating at the lower segment AND affect engagment of fetal
head or cause malpresentation.
a. If Caesaerean section is indicated for any reason, DO NOT perform myomectomy at the same time.
b. After delivery, no need for routine prophylactic syntocinon infusion unless the uterine fibroid larger than 5 cm. Give
syntocinon infusion (40 units in 500 ml of cystalloid solution over 4 hours) if it is required.
3. Postnatal follow up
a. For patients who are asymptomatic before the pregnancy (no menorrhagia or pressure symptoms):-
i. It is not necessary to give gynaecology follow-up after delivery
ii. Advise patient to seek medical advice when she has symptoms
b. For patients who has symptoms before the pregnancy:-
i. Arrange a follow-up appointment at Pelvic Mass Clinic in 6 months with pictorial chart given to patient to
document the menstrual pattern
ii. It may be necessary to postpone the follow-up appointment if the patient would have long period of breast
feeding and remains amenorrhoea.
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6. Gynaecological infection
Pelvic inflammatory disease
Definition
- The strict definition of pelvic inflammatory disease (PID) is the clinical syndrome attributed to the ascending spread of
microorganisms (unrelated to abdominal surgery or pregnancy) from the vagina and cervix to the endometrium, fallopian
tube and / or the contiguous structures.
- It implies sexual transmission as the main source of infection, or secondary to some procedures such as uterine curetting. It
is distinguished from pelvic infections resulted from other sources such as appendicitis, diverticulitis, and pelvic
tuberculosis from haematological spread.
- It is a clinical diagnosis and does not specify the exact location of infection. An anatomical terminology such as
endometritis, salpingitis, parametritis, or tub-ovarian abscess is more specific and preferred if the site of infection can be
identified via laparoscopy.
- It is subdivided into acute and chronic PID
Acute PID
Pathogenesis
- Ascending infection:-common organisms are gonorrhea and chlamydia
- Secondary anaerobic invasion after the genital tract is infected and damaged
Clinical features
- Acute or subacute pelvic pain, usually bilateral
- Purulent vaginal discharge
- Fever
- History of recent coitus
- Cervical excitation pain
- Acute appendicitis is the most common differential diagnosis
Complications of acute PID

- Tubo-ovarian abscess
- Septicemia
- Long term
Tubal damage and infertility
Increase risk of ectopic pregnancy
Chronic PID and pelvic pain
Diagnosis
- Clinical diagnosis of PID and empirical treatment with antibiotic is the mainstay of management
- CBC will show raised white cell count
- Pelvic ultrasound may reveal fluid in the pouch of Douglas or tubo-ovarian abscess formation
- In case of doubt, or if patient does not respond to antibiotics, diagnostic laparoscopy is performed to confirm the diagnosis,
and to rule out other pathology such appendicitis
- Microbiological investigation:-such as endocervical swabs for cultures
Treatment
a. Penicillin group to cover Gonorrhoea
b. Tetracycline group to cover Chlamydia
c. Metronidazole to cover anaerobes
2. Surgical treatment
a. Indicated when patients do not respond to medical treatment, or tubo-ovarian abscesses are formed
b. Laparoscopic drainage of abscess and pus in pelvic cavity
3. Counselling for screening of other sexually transmitted diseases and contact tracing
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Chronic PID
Recurrent or chronic symptoms of pelvic pain resulted from chronic pelvic inflammatory changes, fibrosis and adhesion which are
consequences of previously partially treated acute PID
Clinical features
- Chronic pelvic pain
- Dysmenorrhea
- Acute exacerbation may superimpose on a chronic PID
- There is usually but not always a history of acute PID because sometimes a diagnosis of acute PID may have been missed in
the past
- Differential diagnosis is endometriosis
Diagnosis
Diagnostic laparoscopy
Treatment
1. No curative treatment as damage has already occurred
2. Aim to relief symptoms or treat infertility
3. Pain relief By NSAID; and hysterectomy in case of intractable pain and fertility is not required
4. Fertility tubal surgery or assisted reproductive procedure
1. How to differentiate acute PID and acute appendicitis when a young women presents to the A&E department complaining of
acute lower abdominal pain?
2. Are there any differences between the clinical presentations of acute PID caused by gonorrhea and that of chlamydia?
1. Diagnosis
a. Minimal criteria:-
i. Uterine/adnexal tenderness or
ii. Cervical motion tenderness
b. Additional criteria (to enhance specficity):-
i. Oral temperature > 38.3oC (tympanic > 38.8 oC)
ii. Abnormal cervical or vaginal mucopurulent discharge
iii. Elevated erythrocyte sedimentation rate (ESR)
iv. Laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis
v. Elevated C-reactive protein (C-RP)
vi. Presence of abundant numbers of WBCs on saline microscopy of vaginal secretions
c. Specific criteria:-
i. Endometrial biopsy with histopathologic evidence of endometritis
ii. Transvaginal sonography or magnetic resonance imaging techniques showing thickened, fluid-filled tubes
with or without free pelvic fluid or tubo-ovarian complex
iii. Laparoscopic abnormalities consistent with PID
2. Investigation
a. HVS, ECS for N. gonorrhoeae or C. trachomatis
b. CBC with differential count
c. ESR, C-RP (for patients who are clinically suspicious of having PID, but having normal white cell count)
d. VDRL and HIV testing
e. Pregnancy test
f. TVS
g. Endometrial biopsy (warranted in woman who has undergone laparoscopy, but no visual evidence of salpingitis)
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3. Treatment
a. Outpatient care For mild to moderate PID not requiring hospitalisation
b. Antibiotic regime:-
i. Ceftibuten 400mg orally for single dose (to cover gonorrhea) AND
ii. Metronidazole 400mg TDS orally for two weeks (to cover anaerobes) AND
iii. Doxycycline 100mg BD orally for two weeks (to cover chlamydia)
iv. Patients should be reviewed at 72 hours for assessment of clinical response. If there is no clinical
improvement, patient should be hospitalised and evaluated on the diagnosis and the need for laparoscopy. The
antibiotics should then be changed to parental regime.
c. Alternative antibiotic regime for patient with beta-lactam allergy or tetracycline allergy
i. Low risk for sexually transmitted disease (STD)
- Ciprofloxacin 500mg BD for one week AND
- Metronidazole (Flagyl) 400mg TDS orally for two weeks
ii. High risk for STD
- Azithromycin 2g orally for single dose AND
- Metronidazole (Flagyl) 400mg TDS orally for two weeks
4. In-patient care
a. Indications
i. Surgical emergencies (eg appendicitis / ectopic pregnancy) cannot be excluded.
ii. Pregnant women
iii. Unreliable patients
iv. No response, severe symptoms, or not tolerating out-patient treatment
v. Increased risk of anaerobic infection as suggested by prior IU instrumentation, IUCD in-situ, suspected
tubo-ovarian abscess
b. Antibiotic regimes (from local hospital data)
i. Cefuroxime (Zinacef) 750mg Q8H IV AND 500mg BD orally (one week in total) AND
ii. Metronidazole (Flagyl) 500mg Q8H IV AND 400mg TDS orally (two weeks in total) AND
iii. Doxycycline 100mg BD orally 100mg BO orally (two weeks in total)
c. Alternative regimefor patient with beta-lactam allergy, tetracycline allergy, or high operative risk
i. Gentamicin 2 mg/kg of body weight i.v. or i.m. as loading dose, followed by 1.5 mg/kg of body weight Q8H
i.v. or i.m. as maintenance dose, until 24 hours after clinical improvement (The response rate is higher when
Gentamicin is included.) AND
ii. Clindamycin 900mg Q8H i.v. (can be switched to 450mg QID orally when there is adequate clinical response
for over 24 hours, for a total of 2 weeks)
5. Operative management
a. Indicated for:-
i. Exclusion of other surgical emergencies
ii. Tubo-ovarian abscess with no response (review in 24 hours for decision on operation)
iii. Failed medical treatment (review in 24-48 hours for decision on operation)
b. Laparoscopy preferable.
c. Procedure:- Lysis of adhesion when limiting access to tubo-ovarian complex / abscess or which tether bowel.
Salpingotomy for drainage of pyosalpinges. Dissect and drain loculations of pus. Irrigate pelvic and abdominal
cavity liberally. Avoid blunt dissection OR excision of tubo-ovarian mass. Insertion of wide bore drain after
drainage of tubo-ovarian abscess
6. IUCD
No evidence suggests that IUCD should be removed in women diagnosed with acute PID, however, close clinical
follow-up is mandatory if the IUCD remains in place. The rate of treatment failure and recurrent PID in women
continuing to use an IUCD is unknown. IUCD may be left in situ in women with clinically mild PID. In severe PID,
IUCD shall be removed shortly after commencement of antibiotics
7. Male sex partners
Refer to Social Hygiene Clinic all the sexual partners with sexual contact occurred within 60 days preceding the patient's
onset of symptoms. If last sexual contact beyond 60 days, refer the last sexual partner to Social Hygiene Clinic.
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Bartholins Gland
Figure 56 (Left to Right) Bartholin's cyst and its differential diagnoses, sebaceous cyst, and lipoma.
Bartholin's gland is a pea-sized mucus-secreting gland situated in the lower part of each labium majus. It is connected to the
vaginal entrance by a duct. Its secretion contributes to vaginal lubrication. Obstruction of the duct causes a Bartholin cyst.
Inflammation may lead to abscess formation (Bartholin abscess). The treatment is marsupialisation. It should be differentiated
from other lesions of the perineum, such as sebaceous cysts, lipoma, as the treatment is different.
Pyometra
It is a collection of pus inside endometrial cavity. It is usually due to outflow obstruction such as cervical stenosis secondary to
menopause, previous surgery, or cervical cancers. The obstruction results in stasis of endometrial secretion and secondary
infection. It may be asymptomatic, or presents with purulent vaginal discharge, or symptoms of primary causes such as
postmenopausal bleeding in case of cervical cancers. Pyometra should be drained with Vabra aspiration and the collection should
be sent for histological and microbiological examination. Hysteroscopy is contraindicated as it may spread the infection.
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7. Growth and Development
Adolescence
It encompasses physiological, social and cognitive changes leading to the development of an adult identity. It is different from
puberty.
Puberty
Definition
It encompasses physiological changes leading to the development of adult reproductive capacity. It is different from adolescence.
Normal puberty
A normal puberty consists of following stages:
1. Adrenache the beginning of pubic hair development
2. Thearche the beginning of breast development
3. Menarche the beginning of first menstrual period
Abnormal puberty
Precocious puberty
Precocious puberty
Definition
Features of puberty develop too early with:
1. Breast development before 8 years of age; or
2. Menarche before 10 years (or more than 2 standard deviations before the mean ages of onset).
It is further classified according to the underlying pathophysiology:
1. True or central due to gonadotrophin production driving the ovaries
2. False or peripheral due to autonomous adrenal or ovary production of sex hormones
Tanner staging
Tanner staging of breast development at puberty:
Stage 1 Infantile stage

Stage 2 Bud stage:-
The breasts and papillae are elevated as a small mound and there is an increase in the diameter of the areola
Stage 3 Small adult breast:-
The breasts and areola are further enlarged with a continuous round contour
Stage 4 Secondary mound:-
The areola and papilla enlarge to form a secondary mound projecting above the contour of the remainder of the breast
Stage 5 Typical adult breast:-
The secondary mound disappear so that the breasts have smooth rounded contour
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Hirsutism
Figure 57 Hirsutism (Left) and Virilism (Right).

Definition
Excessive facial and body hair in otherwise femine women. It is different from virilism.
Causes
1. Idiopathic:-most common, there may be racial or familial element.
2. Endogenous endocrine disorders:-polycystic ovarian disease (PCOD), congenital adrenal hyperplasia, Cushing syndrome
3. Androgen secreting tumours of adrenal gland or ovary:-very rare
4. Drug induced:-danazol, phenytoin, anabolic steroid, androgens
Investigations
Depend on clinical suspicion:
1. Hormone profile
2. Radiological investigation if tumour is suspected
Management
Treat underlying causes accordingly; e.g. Surgical removal of adrenal tumour
Treatment of excessive body hair

1. Cosmetic treatment
a. e.g. Waxing, shaving, electrolysis, depilatory creams, bleaching
b. Takes 3-6 months for the effect to be apparent, and often needs a year for an acceptable improvement.
Therefore, it is important to forewarn patients of this so that cosmetic measures are continued during this time.
2. Medical treatment:
a. Combined oral contraceptives
With less androgenic progestogen (e.g. Third generation progestagen), or with anti-androgen component (e.g.
Cyproterone in Dianette)
b. Anti-androgens
i. Cyproterone:-first choice; either prescribed on its own (need additional contraceptive measures) or
ii. With COC (e.g. Dianette)
iii. Spironolactone:-less effective
c. Glucocorticoids
Only useful for those with hirsutism due to an underlying adrenal cause, e.g. Late onset congenital adrenal
hyperplasia. Dexamethasone to suppress excessive adrenal androgens
Virilism
It is the presence of one or more of the following:-clitoral hypertrophy, breast atrophy, male-type baldness and deepening of voice.
It is different from hirsutism. It is invariably due to excessive endogenous androgen production, such as congenital adrenal
hyperplasia and androgen-secreting ovarian stromal cell tumour.
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8. Menopause and HRT
Menopause
Definition
- In Greek meno means month and pauo means to stop.
- It is the permanent cessation of menstruation due to loss of ovarian follicular activity. Usually it is defined after one year of
amenorrhea.
- It is different from the term 'climacteric' which is an extended period of gradually declining ovarian function often
beginning years before and lasting years after menopause itself
- Premature menopause is defined as menopause occurred before 40 years old.
Epidemiology
- In Hong Kong the mean age of menopause is 50 years old.
Causes
- Natural menopause
- Iatrogenic:-oophorectomy, post-chemotherapy, post-radiotherapy
- Infection:-post-mump infection, tuberculosis
- Autoimmune diseases
Health Issues of menopause

Acute Intermediate Long term
Physical Physical - Asymptomatic
- Hotflushes, night sweating (due - Urinary:- - Osteoporosis
to loweing of set-point of Frequency - Cardiovascular disesaes
temperature control). Urgency
Psychological Incontinence
- Mood disturbances, anxiety, - Reproductive:-
irritability Vaginal Dryness
- Difficult to concentrate Dyspareunia
- Insomnia Atrophic vaginitis
Discharge
Climacteric
1. In Greek 'klimakter' means the rung of a ladder. It is a 'critical' period of time around menopause when ovarian function is
gradually compromised.
2. This is a time of decreasing fertility, decreasing oestrogen level and the appearance of the typical symptoms of menopausal
syndrome, although the menstrual periods will still be present.
3. The earliest endocrine change at the climacteric period is hypothalamic-pituitary hyperactivity due to lack of negative
feedback by follicular hormone. Therefore, elevated FSH is a early endocrine marker of climacteric period.
4. The menopausal symptoms include:
a. Vasomotor symptoms:-hot flushes, palpitation, 80% of patients
b. Psychological symptoms; anxiety, depression, irritability, liability of mood, lack of concentration; in 30% of patients
c. Atrophic symptoms:-vaginal dryness, urgency and frequency of micturition.
Osteoporosis
Bone disease characterised by low bone mass, micro-architectural deterioration of bone tissue leading to enhancement of bone
fragility and a consequent increase in fracture risk. It is different from osteomalacia. Women after menopause or with chronic
hypoestrogenemia are at risk of development of osteoporosis. Bone fractures secondary to osteoporosis causes significant
morbidity and mortality in this group of patients, as well as medical cost of the society. Hormonal replacement therapy effectively
prevents bone loss in these high risk patients. A T-score of BMD >-1 = normal; -1 to -2.5 = osteopenia; and <-2.5 = osteoporosis.
Women are more prone to osteoporosis because they have a lower pealk bone mass, a longer life, and they are easier to fall.
Treamtment would incluie hormonal replacement therapy, biphosphonates, vitamin D, Calcitonin, SERM and Tibolone.
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Oestrogens and Progesterone
Oestrogen s
1. Female reproductive / sexual functions
a. Development of secondary sexual characteristics
b. Trophic for tube, endometrium, vaginal wall, cervix (facilitate sperm penetration), vulva, breast and other pelvic
structures.
2. Systemic
a. Cardiovascular system:- Lower cholesterol, increases Nitric Oxide production
b. Haematological:- increases coagulability
c. Hepatological:- increases production of SHBG, TBG
d. Renal:- salt and fluid retention to increase blood pressure
e. Musculoskeletal:- Antagonise bone resorption
f. Oxidant of subintimal lipoproteins.
Progesterone
1. Female reproduction
a. Inhibits myometrium activity
b. Decidualisation of endometrium
c. Cervix:- lower penetration of sperm
d. Breast:- secretory development
e. With oestrogen:- inhibit pituitary FSH and LH production
2. Systemic
a. Increases body temperature
b. Respiratory:- increases breathing rate
c. Renal:- antagonise aldosterone action.
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Hormonalreplacementtherapy
Definition
Replacement of natural oestrogen (with or without progestogen) to patients with deficiency of endogenous oestrogen due to
ovarian failure in order to minimize the risk of lack of oestrogen such as osteoporosis and atherosclerotic heart diseases
Type of natural oestrogen

1. Estradiol
2. Estradiol valerate
3. Equilin
Different preparation of oestrogen

1. Oral oestrogens
a. First pass effect of liver leads to conversion of 1/3 of oestrogen to weak estrone glucoronide which is excreted quickly
b. Estrone to estradiol of 2:1 instead of natural ratio of 1:2
c. Also cause increase in sex hormone binding globulin, cortisol binding globulin, rennin substrate and HD and a
depressant effect on anti-thrombin III, and therefore theoretically contraindicated in women with a history of clotting
disorders or hypertension
2. Vaginal oestrogen cream for local treatment as well a systemic treatment
3. Percutaneous oestrogen cream
a. Consists of 3mg estradiol in each daily 5g applicator of cream
b. Bypasses liver and achieves a 1:2 estrone to estradiol ratio
4. Transdermal patches
a. Consist of a thin multi-layered unit containing a drug reservoir, a rate-controlled ,membrane and an adhesive layer
b. Patches have surface area of 5 to 20cm2 and administer estradiol at a controlled rate of 25 to 100mcg/day in vivo
c. Need to change twice weekly
d. Troublesome skin reactions ranging from hyperaemia to blistering, now little since new patches are used.
5. Subcutaneous implants
a. Consist of 50mg estradiol pellet implanted subcutaneously in lower abdomen
b. Estradiol level peaks at 2 to 3 months and declines to pretreatment level after 6 months
Progestogen
1. Is used with oestrogen in case of intact uterus
2. Aims to oppose oestrogen stimulation on endometrium and hence prevents endometrial cancer
3. On its own it is not a good HRT to control climacteric symptoms or prevent osteoporosis and atherosclerotic heart disease
4. Side effects:- mastalgia, bloating, pre-menstrual syndrome like symptoms.
Different forms of combination of oestrogen and progestogen

1. Unopposed (without progestogen) For those without uterus
2. Opposed (with progestogen)
a. Cyclic:-for those with uterus and want regular withdrawal bleeding
b. Continuous:-for those with uterus and want complete amenorrhea
Indications of HRT
1. Prolonged hypoestrogenism
2. Physiological menopause
3. Surgical menopause
4. Premature ovarian failure
5. Hypogonadotrophic hypogonadism
6. Symptomatic relief of climacteric discomforts
7. Prophylaxis against osteoporosis
8. Prophylaxis against atherosclerotic cardiovascular diseases
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Contra-indications of HRT
1. Absolute
a. Oestrogen dependent cancers:- Endometrial cancer, Breast cancer
b. Venous thromboembolism
c. Active liver disease
d. Undiagnosed abnormal vaginal bleeding
2. Relative
a. Past history of thromboembolism
b. Chronic liver diseases
c. Hypertension and diabetes are not contraindications for HRT, provided that they are under good control.
Side effects
1. Most are mild and well-tolerated:
a. Breast bloating and tenderness
b. Weight gain
c. Breakthrough bleeding:-need to rule out underlying endometrial pathology when abnormal vaginal bleeding occurs
2. Risk of breast cancer no firm evidence of increased risk. Possible long term (>5 years) risk.
1. Should all menopausal women be given hormonal replacement therapy routinely?
2. A postmenopausal woman of age 55 who has been put on opposed HRT for 3 years, presents to you with persistent vaginal
bleeding for 2 week. What is your management and counselling?

1. Regimens
a. Estrogen only therapy
i. For women with no uterus
ii. Oral regimens
- Progynova 1 mg daily PO (low dose regime)
- Premarin 0.625 mg daily PO
- Premarin 0.3 mg daily PO (low dose regime)
iii. Non-oral regimens
- Estreva (topical gel 0.5 mg / dose) 3 doses daily LA
- Estraderm (transdermal patch 50 mcg / 24 hour) 1 piece once, 2 days /week LA
b. Combined estrogen + progestin therapy
i. For women with intact uterus
ii. Continuous regimens:-No withdrawal bleeding
- Kliogest 1 tab daily PO
- Premelle 1 tab daily PO
- Activelle 1 tab daily PO (low dose regime)
iii. Cyclical regimens:-With monthly withdrawal bleeding
iv. (For women with premature ovarian failure or recent menopause < 2 year)
- Femoston 1 tab daily PO
- Premelle cycle 1 tab daily PO
c. Second line postmenopausal hormone therapy
Consult FHKAM for initial commencement (Prescriptions need authorization)
- Evista (Raloxifene) 60 mg daily PO
- Livial (Tibolone) 2.5 mg daily PO
2. Follow up (FU) Plan 6 months intern clinic & FU 12 months HRT clinic
a. Assess side effects (e.g. irregular vaginal bleeding, breast discomfort)
b. Assess drug compliance
c. Assess efficacy of HRT (e.g. relief of menopausal symptoms)
d. Review benefit-risk profile & justification of HRT use every year
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9. Gynaecological surgery & investigations
Gynaecological surgery
Route of surgery
1. Conventional
a. Via laparotomy
b. Via vaginal route
2. Minimal invasive surgery
a. Via laparoscopy
b. Via hysteroscopy
Aim of surgery
1. Excision of pathology hysterectomy, myomectomy, ovarian cystectomy, oophorectomy, salpingectomy
2. Destruction of pathology Endometrial ablation
3. Reconstruction of functioning organs
a. Metroplasty:-reconstruction of uterus for congenital uterine anomaly
b. Salpingostomy:-reconstruction of a fallopian opening for transfer of oocytes
c. Pelvic floor repair:-reconstruction of the pelvic floor to treat vaginal prolapse
d. Vaginoplasty:-reconstruction of vagina for sexual functioning
Special surgery
1. Oncological surgery
a. Radical hysterectomy
b. Exenteration
c. Pelvic or para-aortic lymphadenectomy
2. Urogynaecological surgery For treatment of genuine stress incontinence:
a. Colposuspension
b. Urethral sling
c. Urethral injection of collagen
3. Fertility surgery tubal anastomosis, salpingostomy
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Curettage
Definition
Uterine curettage is a minor gynaecological surgery in which part of the endometrial lining of the uterus is removed by means of a
hollow spoon-shaped instrument (curette). Dilatation of the cervix is required to admit all but the smallest curette.
Figure 58 Dilation and curettage

Indications
This operation is a diagnostic procedure to study hormonal or other changes (inflammatory, neoplastic) in the endometerial cells,
or a therapeutic procedure for the removal of retained products of conception (treatment of incomplete abortion) or uterine polyps.
Admissions
On average there are 25000 admissions for D&C per year.
Complications
- Perforation of uterus, after which the bowel may also be injured by the curette
- Introduction of infection to the uterus
- Bleeding
Figure 59 Trauma to the cervix and uterus.
Hysterotomy
It is a gynaecological surgery for termination of pregnancy in the early second trimester. The uterus is cut open longitudinally and
the products of gestation are removed. The procedure is essentially the same as that of a classical caesarean section which is for
delivery of babies after 24 weeks of gestation. Hysterotomy is rarely done nowadays because of very effective and much safer
medical methods of termination of pregnancy (with prostaglandins). The risks of hysterotomy are haemorrhage, and uterine
rupture in subsequent pregnancy.
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Endometrial ablation
It is a relative minor gynaecological operation in which the endometrial lining down to the basal layer is destroyed, so that no
more or only minimal endometrial glands will be responsive to oestrogen. It is used to treat dysfunctional uterine bleeding (DUB).
Incidence
Endoscopic endometrial ablation:- 176 admissions in 2004.
Hysteroscopic endometrial ablation:- 187 admissions in 2004.
Methods of ablation
There are various ways of ablating the endometrium including microwave, thermal balloon, and electrocautery via hysteroscopy.
The former two methods can be performed under local anaesthesia in an out-patient setting.
Efficacy
About75-90% of patient will become amenorrhea after the treatment, 15% will still have menstruation but the flow is much
reduced, 5% have no improvement and require further treatment.
Advantages
Endometrial ablation has advantages over medical therapy of DUB:
- No hormonal side-effects
- No problem of drug compliance
- Avoids the need of hysterectomy and subsequent morbidity and mortality. It can be done as a minor surgery in a day-case
setting, allowing quick recovery.
Disadvantages
- It cannot treat dysmenorrhoea.
- Long term effects for DUB is not satisfactory. Many patient may need repeat ablation or hysterectomy.
- Contraception is not guaranteed - patients have to continue practising contraception
- High risk of miscarriage, intrauterine growth restriction, abnormal placental adherence (e.g. Placenta accreta) if pregnancy
occurs.
Protocol, as of 1 December 2008

1. Novasure endometrial ablation is available within NTEC:-
2. The Second generation endometrial ablation can be offered to the following women:-
a. DUB or menorrhagia refractory to medical treatment
b. No fertility wish
c. Women > 40 years old
3. If you want to book the Novasure endometrial ablation, please make sure the followings is available:-
a. A recent normal endometrial sampling
b. A recent normal cervical smear
c. Relatively normal endometrial cavity, without the presence of the followings:-
i. Congenital uterine abnormalities, such as bicornuate uterus, uterine septum
ii. Submucosal fibroid or intramural fibroid that severely distorting the endometrial cavity
iii. Large endometrial polyp
iv. The assessment of the endometrial cavity can be done by TVS or OPH
d. Uterine size less than 12 weeks, preferably with uterine length 4-12cm. (due to the limitation of device, the ablation
cannot be performed if uterine length less than 4cm and more than 12 cm)
4. Advise contraception till the date of the operation
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Myomectomy
What is myomectomy?
It is the excision of uterine fibroids. It is indicated when the fibroids become symptomatic or too large, and the patient Wants to
preserve the uterus for fertility. Otherwise, hysterectomy is the preferred choice. Depends on the site of the Fibroids, it can be
performed via laparotomy (for intramural fibroids), laparoscopy (for pedunculated fibroids), or hysteroscopy (for submucosal
fibroids).
Open myomectomy (via laparotomy) (65%)

The uterus is cut over the greatest diameter of the fibroid which is then enucleated. The uterine wound is finally repaired with the
dead space closed. The complications are excessive bleeding from the wound, and adhesion formation. Pre-operative GnRHa or
danazol may be used to decrease the size and vascularity of the fibroid.
Laparoscopic myomectomy (15%)

It is for pedunculated fibroids. The stalk of the fibroid is ligated or diathermized and cut. The fibroid is the morcelated and
removed in pieces via the small laparoscopic wound.
Hysteroscopic myomectomy (20%)

It is for small submucosal fibroid. A loop diathermy is used to cut the stalk, or the fibroid into pieces which are the removed
vaginally.
Outcome of myomectomy
- Recurrence of fibroids (10%)
- Recurrence of symptoms (10%)
- Improvement of fertility in patient having fibroids as the sole cause of infertility (30%)
You are the house officer going to obtain the consent of a 26 years old patient with a 6cm intramural fibroid causing menorrhagia.
What would you explain to the patient about the operation?
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Hysterectomy
What is hysterectomy?
Excision of uterus. It can be divided into:-
1. Total (or simple) hysterectomy (95%)
a. Both the corpus and cervix of the uterus are excised
b. It is the most common form of hysterectomy for benign uterine lesion
2. Subtotal hysterectomy (1.5%)
a. Only the corpus uterus is removed. Uncommon in Hong Kong
b. Cervix is sometimes preserved for the following reasons:-
i. Patient's wish because of the belief of the role of cervix in sexual satisfaction
ii. Surgical difficulty in case of dense adhesion around the cervix
iii. Potential advantage in reducing ureteric and bladder injury
iv. Potential advantage in maintaining pelvic floor support
3. Extended hysterectomy (0.5%)
a. The whole uterus together with the upper vagina are excised
b. It is indicated when the pathology involves the vagina such as VAIN
4. Radical hysterectomy (3%)
a. Choice for treatment of cervical cancer and uterine cancer with secondary involvement of the cervix.
b. The whole uterus, upper vagina, together with the parametrium are excised.
c. It is extensive and operative morbidity and mortality is higher when compared to other forms of hysterectomy.
Methods of hysterectomy
1. Laparotomy
a. The traditional method of both benign and malignant lesions
b. In general operative mortality is low but various morbidities are common (8%)
2. Vaginal hysterectomy
a. Method of choice for treatment of uterine prolapse
b. Operative morbidity and mortality are generally lower compared to laparotomy (7%) because:
i. Abdominal wound is avoided
ii. Technically easier as patient selected for vaginal hysterectomy usually has a small, atrophic, prolapsed uterus
and less pelvic adhesion
c. The drawback is that other pelvic pathology such as ovarian lesion may not be assessed in vaginal hysterectomy
3. Laparoscopic method
a. Aims to minimise the operative complications of laparotomy by converting it to a vaginal hysterectomy (LAVH), or
take the corpus uterus out via laparoscopic wound after morcelation (LASH)
b. Two common types:
i. Laparoscopic assisted vaginal hysterectomy (LAVH)
ii. Laparoscopic assisted subtotal hysterectomy (LASH)
c. Case selection:
i. Benign uterine pathologies
ii. Vaginal hysterectomy alone is not feasible
iii. Uterine size less than 14 week
iv. No severe pelvic adhesion
Complications of hysterectomy
1. General complications
a. Febrile morbidity
b. Haemorrhage
c. Infection
2. Visceral injury
a. Ureteric and bladder injury
b. Bowel injury
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TOTAL HYSTECTOMY BY LAPROTOMY
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SUBTOTAL HYSTERECTOMY
VAGINAL HYSTECTOMY
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Hysteroscopy
What is hysteroscopy?
It is a kind of minimal invasive gynaecological operation in which an instrument (hysteroscope) with lumination is inserted
through the cervix to allow have direct visualization of the uterine cavity, which should be distended with CO2, normal saline or
glycine. It allows visual diagnosis of any endometrial pathologies, guides biopsy, and other surgical procedures.
Indications
1. Diagnostic:-can be performed as a day-case under no anaesthesia or paracervical block
a. Abnormal vaginal bleeding such as
b. Intermenstrual bleeding and menorrhagia refractory to medical therapy which may be due to endometrialPolyps or
submucosal fibroid)
c. Postmenopausal bleeding (to rule out endometrial carcinoma)
d. Suspected congenital uterine abnormality such as septated uterus
2. Therapeutic:
b. Resection of submucosal fiborids or endometrial polyps
Contraindication
Pyometra (risk of spreading infection to peritoneal cavity)
Complications
1. Infection
2. Haemorrhage
3. Uterine perforation
4. Cervical laceration
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Cryotherapy
Cryotherapy is also called cryocautery and cryosurgery, and is commonly used to treat CIN. It involves the use of a metal probe
cooled through isotropic expansion of a compressed gas released from a tank through a small orifice under pressure. The gases
mostly used are nitrous oxide and CO2. This allows destruction of affected tissue to a depth of 3 mm. It is quick and sufficiently
painless to be used in the conscious patient. The destructive effect in the tissue depends on the rapid lowering of the temperature,
resulting in crystallization of cell water and disruption of cell membranes and organelles. The success rate of the treatment is
80-90%.
Figure 60 Cryotherapy Figure 61 Electrocautery

Electrocautery
It is also called electrocoagulation, hot cautery or diathermy. It is commonly used to treat CIN, and for haemostasis during
operation. The device consisted of a heating instrument of high resistance similar to the soldering iron heated to a dull red. The
device delivers electric current from the generators. The procedure is very painful and usually requires general anaesthesia. It will
destroy tissue to a depth of 7-8 mm
Cold coagulation
It is commonly used method to treat CIN. The apparatus generates a probe temperature of 100 to 120 degree Celsius which is
'cold' in comparison to electrocautery or electrocoagulation diathermy, hence the name "cold coagulation". The heat is conveyed
to the tissues via thermosounds, which are held against the lesion in several overlapping applications, each lasting 20 to 30
seconds.
Marsupialisation
It is a surgical procedure in which a cyst is everted rather than excised. This is particularly used in the treatment of Bartholin's
cysts and makes the operation quicker and more bloodless than excision of the gland. It also reduces the incidence of recurrence.
The cyst or abscess is widely opened within the labium minus and drained and its walls sutured to the skin leaving a large orifice
which it is hoped will form a new duct orifice and allow conservation of the gland. A ribbon-gauze pack is inserted for 48 hours
by some operators.
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Endometrial sampling
Indications
It is the biopsy of the endometrial tissue for histological examination. It is mainly indicated for investigation of abnormal uterine
bleeding, in which case endometrial hyperplasia or endometrial carcinoma is suspected. Occasionally it is indicated for
investigation of infertility. It may help to diagnose ovulation and luteal phase insufficiency by the presence of secretary phase
changes. Endometrial tuberculosis can be diagnosed by the presence of caseous granuloma or culture of the tissue.
Methods
1. Uterine curetting
a. It is the traditional method that has to be performed under general anaesthesia, and is therefore much replaced by the
following methods nowadays.
b. It is supposed that it provides the greatest yield of tissue
2. Aspiration technique, with endometrial sampler or Vabra aspirator
A rapid and simple out-patient procedure, and provides a reasonable good yield of tissue for histological examination.
3. Hysteroscopically directed biopsy
The endometrial cavity is also examined at the same time via hysteroscopy. Localised suspicious lesions can be
targeted. The yield however is very limited due to because of the small-sized biopsy forceps.
In general, sampling by both uterine curetting and aspiration methods provide comparative good sensitivity for histological
diagnosis of endometrial pathologies. Hysteroscopic assessment allows visualisation of structural abnormalities such as
submucosal fibroids or endometrial polyps that can be missed by the other two methods. However, it has to be supplemented with
endometrial sampling by other methods.
Complications
1. Perforation of uterus
2. Introduction of infection
Endometrial sampler
A simple narrow plastic tube inserted into the uterine cavity for endometrial sampling. It provides reasonable good yield of tissue
for histological assessment.
1. Pipelle de Cornier
The Pipelle is inserted into the uterine cavity and the plunger withdrawn to produce a vacuum. The endometrium is thereby
sucked into the tube and subsequently expelled into fixative. This procedure is better tolerated than the Vabra curette but does
not always produce sufficient tissue to evaluate histologically.
2. Vabra Curettage
This method of obtaining material for histological examination can be done in the out-patient clinic. Adequate specimens can
be obtained, but the procedure is painful. If out-patient methods of examining endometrium do not provide reliable
information, conventional curettage must be carried out.
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Hysterosalpingogram
What is Hysterosalpingogram?
Hysterosalpingogram (HSG) is an X-ray examination of the genital tract after contrast injection into the uterine cavity, by which
contour of the uterine cavity, fallopian tubes and endocervical canal are visualized. It is normally performed within the first ten
days of menstruation in order to avoid inadvertent exposure of the early embryo to irradiation
-
This is a normal salpingogram. Note:
1: The antevered uterus is foreshortened.
2: The long thin tubal outline.
3: The ill-defined shadow of peritoneal spill.
4: Cervico-vaginal leakage
Indications
Investigations of the following:
1. Patency of fallopian tubes (to investigate infertility)
HSG is less invasive when compared with laparoscopy and chromotubation for the investigation of the tubal patency.
However, it has false positive result as the injected contrast may cause tubal spasm that transiently blocks the tubes. In
addition, laparoscopy allows assessment of any pelvic pathology such as endometriosis, chronic pelvic inflammatory
disease, and pelvic adhesion, which is not possible with HSG.
2. Structural abnormalities of uterus:-congenital uterine anomalies such as bicornuate uterus and septate
Sometimes submucosal fibroids and endometrial polyps can be identified incidentally with HSG but HSG is not the
primary diagnostic method of these lesions
3. Cervical incompetence
Leaking of contrast from the internal os the cervix may be seen in case of cervical incompetence. However, the
diagnostic accuracy is still limited. See cervical incompetence for detail.
Contra-indications
- Allergy reaction to contrast
- Active pelvic inflammatory disease
- Pregnancy
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10. Miscellaneous topics in gynaecology
Retroversion of uterus
Uterus rotates backwards in relation to the vagina. A mobile retroversion is a variant of normal occurring in over 25% of women.
It is usually asymptomatic although many gynaecological symptoms including pelvic pain and infertility have been attributed to it
in the past. A fixed retroversion, however, results from adhesion formation secondary to pelvic inflammatory disease or
endometriosis. Both are common causes of pelvic pain, dyspareunia and infertility. Very rarely, a gradually enlarging retroverted
uterus may be eventually impacted inside the pelvic cavity, resulting in incarceration. One more importance concerning
retroversion is that when it is misdiagnosed as anteversion during performing uterine curetting, the uterus would be perforated.
Chronic pelvic pain

Introduction
Chronic pelvic pain is one of the most common symptoms of women. Most of the time the symptom is nonspecific, and no
organic causes can be identified.
Possible causes
- Endometriosis
- Chronic pelvic inflammatory disease
Imperforate hymen
It is a congenital disorder in which the hymen membrane remains intact. When patients start menarche, menstrual blood flow is
blocked and the blood accumulates and distends the vagina. Usually patients present at early teenage with amenorrhea
(cryptomenorrhea), cyclic abdominal pain, abdominal distension and urinary retention. On examination, the hymen membrane is
bulging out and appears blue because of the blood collection behind the membrane. Ultrasound shows a distended vagina beneath
the bladder. The treatment is excision and drainage.
Figure 62 Complications of imperforate hymen.
Figure 63 Examination (Left) and Treatment (Right) of imperforate hymen.
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A mild bulging intact hymen membrane. A Foley catheter is

inserted because of urinary retention
The angle of the hymen membrane is lifted up before incision
The hymen membrane is cut open. Chocolate material (old blood)

is drained
The hymen membrane is excised
The wound is repaired
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Reproductive medicine
0. Reproductive medicine and Endocrinology
Introduction
It is a branch of gynaecology dealing with various kinds of hormonal disorders directly or indirectly involving the hypothalamic-
pituitary-ovarian axis, resulting in anovulation, infertility or ovarian failure (menopause), or sometimes disorders of puberty. The
management of these kinds of disorders is usually medical therapy, with ovulation induction, or hormonal replacement therapy. It
may also involve sophisticated bio-technicology when assisted reproductive technology (ART) is used to treat infertility.
What medical students should know

Common disorders:
1. Polycystic ovarian disease (PCOD)
2. Hyperprolactinemia
3. Various causes of infertility and the investigations
4. Problems associated with menopause
Common treatments:
1. Ovulation induction
2. Hormonal replacement therapy
3. Some ideas about ART
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1. Anovulation and endocrinopathy
Infertility
Definition
Infertility is defined as failure of a heterosexual couple to conceive after one year of unprotected intercourse. This definition is
based on certain empiric statistical observation of conception rate as follow:
After 3 months: 30%
After 6 months: 50%-60%
After 24 months: 95%
Infertility is further defined as follow:

1. Primary infertility Failure to conceive in a couple who have never achieved a pregnancy.
2. Secondary infertility Failure to conceive after 1 or more pregnancies, regardless of the outcome of those pregnancies.
3. Unexplained infertility Infertility with all standard clinical investigations (usually include:-semen analysis, assessment of
ovulation, demonstration of tubal patency, some may include postcoital test) yield normal results
Incidence
As defined, it affects 10 to 20% of couples
Causes
1. Female infertility, account for 40% of cases, due to:-
a. Anovulation:-20%
b. Endometriosis:-6%
c. Tubal blockage:-14%
2. Male infertility:
a. Accounts for 30% of cases
b. Due to poor quality or quantity of sperms
3. Sexual dysfunction:-6%
4. Unexplained:-30%
5. Remark:-there may be multiple causes of infertility
Evaluation
1. Interview both female and male partners
2. Complete history of both partners including:
a. General medical health especially sexually transmitted diseases, mump, pelvic surgery (female)
b. Occupational history:-environmental and occupational exposure to heavy metals, toxins, etc
c. Social history:-especially heavy smoking or alcoholism
d. Sexual history:-coital frequency and difficulty
3. Look for evidence of anovulation:
a. Irregular long menstrual cycles or amenorrhea
b. Features of polycystic ovarian disease (PCOD), hyperprolactinemia, hypogonaditropic hypogonadism
c. Confirm with hormonal studies
4. Look for evidence of endometriosis:
a. Dysmenorrhea, dyspareunia, chronic pelvic pain
b. Endometriotic cyst from past history, physical examination or ultrasound
c. Confirm with laparoscopy
5. Look for hints of tubal blockage which are often secondary to pelvic inflammatory disease:
a. Dysmenorrhea, dyspareunia, chronic pelvic pain
b. History of pelvic inflammatory disease, pelvic surgery
c. Confirm with hysterosalpingogram or laparoscopy plus chromotubation
6. Screen for male infertility:- By semen analysis
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Treatment
1. Principle:
a. Correct underlying causes if possible
b. Try appropriate method with the least risk first
2. Treatment modalities include:
a. Ovulation induction (OI)
b. In utero insemination (IUI) with or without ovulation induction
c. Assisted reproductive procedure
i. In vitro fertilisation (IVF)
ii. In vitro fertilisation with intracytoplasmic sperm injection (ICSI)
d. Besides medical treatment, adoption should also be discussed
Treatment of anovulation
Treat with ovulation induction
1. Clomid is the first line
2. HMG or FSH if clomid is failed or contraindicated
3. Ovarian drilling only for PCOD
Treatment of endometriosis
1. Risk of infertility increases with severity of endometriosis
2. Medical treatments relieve pelvic pain but not improve fertility
3. Surgical treatments including cystectomy, ablation of endometriosis improve chance of fertility
4. IVF should be considered if surgical treatment failed, or in case of severe endometriosis which is not easily treated by surgery
Treatment of tubal blockage

Can be treated with tubal surgery or with in vitro fertilisation (IVF):
1. Tubal reanastomosis for previous sterilisation
2. Salpingostomy for simple and small hydrosalpinges
3. Severe tubal blockage is managed with IVF
Treatment of male infertility

1. In utero insemination for mild impairment of semen quality
2. In vitro fertilisation with ICSI for severe impairment
3. Sperm donation:-insemination of donor sperm
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Anovulation
Definition
It means absence of ovulation. Two different conditions occur in anovulation:
1. Defective follicular phase and follicular development that result in hypoestrogenemia
2. Apparently normal follicular phase but defective luteal phase, leading to normal or increased level of oestrogens, but deficient
progesterone. It may result in endometrial hyperplasia
Causes
1. Endocrine disorders involving the hypothalamo-pituitary-ovarian axis
a. Ovary:-
i. Polycystic ovarian disease (PCOD), the most common cause
ii. Turner syndrome
b. Pituitary:-
i. Congenital absence of FSH or LH-secreting cells
ii. Sheehan syndrome
iii. Damage by surgery or radiotherapy
iv. Hyperprolactinaemia
c. Hypothalamus:-
i. Anorexia neurosa
ii. Weight and stress related causes of hypogonadotropism
iii. Kallman syndrome:-rare
iv. Compression or destruction by intracranial tumour:-uncommon
d. Other endocrine disorders that indirectly affect the hypothalamo-pituitary-ovarian axis:-
i. Hyper or hypothyroidism
ii. Hyperandrogenaemia
iii. Cushing disease,
iv. Menopause
2. Most of the causes (except PCOD) result in hypoestrogenic type of anovulation
Clinical features
1. Features of anovulation:
a. Oligomenorrhea or amenorrhea
b. Infertility
c. Absence of biphasic changes of basal body temperature, etc
2. Features of underlying causes:-Features of Turner syndrome, PCOD, menopause, thyroid disorders etc
Investigation
Confirm anovulation:-
1. Low progesterone at the middle of the supposed luteal phase (i.e. Day 21 of 28-day menstrual cycle)
2. Look for underlying causes, such as:
3. FSH and LHtaken at the follicular phase
a. LH:-FSH ratio >3 or high LH level is diagnostic of PCOD
b. High FSH suggests menopause
4. Prolactin levels, etc
Management
1. Treat underlying causes
2. Treat infertility with ovulation induction
3. Prevent endometrial hyperplasia which is a complication of chronic anovulation associated with hyperestrogenemia
4. Prevent complications of hypoestrogenemia, usually with hormonal replacement therapy
How do different causes of anovulation affect the choice of ovulation induction?
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Ovulation
Definition
Ovulation is the process during which a Graafian follicle ruptures to release a mature oocyte with its surrounding cumulus
oophorus. This is initiated by a luteinizng hormone (LH) surge (a brief rise in LH started 36 to 38 hours before ovulation), which
precipitates the final changes in the follicular wall, follicular fluid volume and the oocytes which are the necessary precursors to
ovulation. The first meiotic division is completed at this stage and half of the chromosome complement discarded as the first polar
body.
How can we know the timing of ovulation?

1. It is sometimes necessary to know the time of ovulation for purpose of conception, treatment of fertility (such as correct
timing of artificial insemination or the transfer of previously frozen embryos.) and as well as contraception (rhythmic
method)
2. Clinical
a. Ovulation usually occurs 14 days before the next expected menstruation (i.e. around day 14 in a 28 day cycle).
b. In longer cycles, ovulation occurs later.
c. Ovulation may be associated with temporary discomfort or pain (see Mittelschmerz).
d. Soon after its occurrence there is a rise in the basal body temperature due to progesterone production.
e. There are changes in cervical mucous before ovulation (spinnbarkeit sign and ferning)
3. USG monitoring:- serial ultrasound scans to monitor the growth of ovarian follicles and rupture
4. Measuring the LH:- The onset of the LH surge can be determined by measuring LH concentrations in blood and urine.
5. Measuring the progesterone:- Blood taken at the expected mid-luteal phase (i.e. day 21 in a normal 28-day cycle) shows a rise
in progesterone level.
Ovulation Induction
1. Some women fail to ovulate (see anovulation) and become infertile, because of various endocrinopathologies.
2. Ovulation induction is required
3. l In assisted reproductive technology (ART), the administration of hCG is used to trigger ovulation and time oocyte collection
(to simulate a LH Surge), particularly if spontaneous LH surges are suppressed by GnRHa.
Spinnbarkeit
The ability of cervical mucus to be drawn into threads. This is maximal a day or so before ovulation due to the oestrogen surge for
the Graafian follicle. After ovulation this quality is lost and cervical mucus becomes thick (tacky) due to the effect of progesterone.
It is one of a bedside method to assess timing of ovulation
.
Ferning
Ferning of cervical mucus
When cervical mucus obtained just before ovulation is dried and allowed to crystallize, a pattern resembling fern leaves can be
observed under microscope. This property of cervical mucus is resulted from the influence of estrogens which makes the mucus
more profuse and fluid just before ovulation. This is a favourable sign in the assessment of quality of cervical mucus.
Ferning of amniotic fluid

A ferning pattern can also be observed under microscope after drying and crystallization of amniotic fluid. It can be used as a test
to confirm rupture of membranes when a specimen of fluid is obtained from the vagina (not from the cervix). However, it is not
very practical and is seldom applied clinically now.
Fertilisation
The process by which the male and female gametes unite to form a zygote. This begins when the spermatozoon first contacts the
oolemma (the oocyte surface membrane) and lasts until the genetic material of sperm and oocyte have mixed and reduplicated as
the zygote initiates its first division into two cells. In vivo, fertilisation occurs in the fallopian tube, usually within one day of
ovulation, and is completed in approximately 24 hours.
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Conception
The process from fusion of the gametes through the early development of the conceptus, to implantation of the blastocyst. The
intervention of conception in order to prevent pregnancy to occur is called contraception.
Luteal phase
A phase of an ovarian cycle starting from ovulation to the next menstruation. It usually lasts 14 days. During this period, the
corpus luteum secrets progesterone which turns the endometrium into secretary state, becomes thicker, more vascular and
receptive to a blastocyst. The cervical mucus also becomes thicker and impenetrable to spermatozoa. Luteal phase insufficiency
may occur resulting in failure of a blastocyst to implant.
Luteal phase insufficiency

A condition proposed as a cause of infertility. There is ovulation but the luteal phase is short (< 10 days), with a low luteal phase
progesterone level. The endometrial glands do not show normal secretary phase changes. The diagnostic criteria of this condition,
however, are not well defined.
Follicular phase
The period of development of the dominant follicle (with its oocyte and theca and granulosa cells) to become a fully formed
Graafian follicle, which will be responsive to the pre-ovulatory LH surge. The follicular phase usually lasts for 14 days.
Basal body temperature
A normal BBT Chart. (97.2 F = 36.2 C; 98.3 F = 36.8 C. )
Ovulation leads to an increase in blood progesterone concentration which is associated with a small rise in body temperature. A
woman can therefore assess herself whether and when ovulation occurs simply by monitoring her basal body temperature. The
temperature must be recorded daily under standard conditions, before rising in the morning, and before eating or drinking.
The woman also marks on the chart the days when intercourse has occurred. A lower temperature during menstruation and in the
follicular phase of the cycle, followed by an increase of approximately 0.5 degree Celsius throughout the second half of the cycle
(biphasic changes) indicates that ovulation has occurred. The temperature remains elevated if pregnancy has occurred.
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Postcoital test
What is a postcoital test (PCT)?
It assesses the quality of the cervical mucus which may be one of the causes of infertility. Inflammation of cervix, presence of
antisperm antibodies in the cervical mucus may cause death or inactivation of sperm.
How to perform postcoital test

- Timing:-6 to 12 hours after a normal unprotected intercourse, performed just before the estimated date of ovulation.
- Procedure:-After passage of a speculum, a small amount of cervical mucus is aspirated and immediately examined
microscopically. The viability and mobility of sperms are assessed.
- Assessment:-
The test is considered adequate if 5 to 10 freely mobile sperms are seen per high power field.
Their motility is assessed:-it may vary from highly active progressive movement to sluggish, or no, motility.
Clumping, shaking or agglutination (head to head or taito tail) may suggest the presence of antisperm antibodies.
How to interpret postcoital test result

- A good PCT indicates that intercourse is adequate, the male is likely to be fertile and the woman is normal up to the level or
the cervix. The prognosis for conception is good in the presence of good PCT.
- On the other hand, a single unsatisfactory test may not be of any significance as most commonly, the poor cervical mucus is
due to inappropriate timing of the test. When performed too early, it may not be fully oestrogenic; when performed too late,
it may have become highly viscous under the influence of progesterone.
- The test may need to be repeated.
- A gross deficiency of mucus (dry cervix) may result from amputation of the cervix and certain other operations which
destroy cervical glands. The presence of white blood cells may indicate inflammatory condition, prejudicial to conception.
- If sperms are not present in repeated PCT despite a normasemen analysis, a coital problem should be suspected.
- It is still controversial whether post-coital test should be a routine investigation in the management of infertile couple. Due
to the poor reproducibility and diagnostic and prognostic performance of postcoital test, it is not routinely performed in
PWH.
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2. Assisted reproductive procedures
Assisted Reproductive Technology (ART)
Assisted reproductive technology (ART) is a part of reproductive medicine which deals with means of conception other than
normal coitus. ART frequently involves the handling of gametes or embryos, and includes one or more of the followings:-ovarian
stimulation; oocyte collection; sperm preparation; in vitro fertilisation; embryo transfer; intra-uterine insemination; donor
insemination; micro manipulation such as intracytoplasmic sperm injection (ICSI); cryopreservation and other related procedures.
Oocyte collection (above) and embryo transfer (below).
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Ovulation induction
What is ovulation induction?
It is a procedure or treatment to induce ovulation artificially for patients suffering from infertility due to anovulation.
Methods of induction
1. Medical
a. Clomiphene citrate:- as an anti-oestrogen to raise LH and FSH level, therefore promotes follicular development.
b. Gonadotropin therapy:- for WHO type I and II.
c. Pulsatile gonadotropin releasing hormone (GnRH):- for WHO type I and II.
d. Dopamine agonists:-bromocriptine (only for hyperprolactinemia)
2. Surgical
a. For medical therapy resistant PCOS
b. Beneficial for ovulation than hirsutism
c. Different surgical approach:- Wedge resection, laparoscopic ovarian drilling.
3. No remedy for WHO Type III hypergonadotropic hypoonadism (primary ovarian failure), consider donor oocyte and
adoption.
Two main complications of ovulation induction

2. Ovarian hyperstimulation syndrome (OHSS)
Confirmation of ovulation
1. Biphasic BBT
2. Elevated Luteal phase progesterone (Measure 7 days before menstruation)
3. Others: LH surge, serial ultrasound

Figure 64 Progesterone level, highest at day 21 (7 days before menstruation).
Figure 65 Serial ultrasound of ovaries.
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Clomiphene
Nature
1. An oranon-steroidaanti-estrogen
2. Racemic mixture of its 2 sterochemical isomers zuclomiphene (weak oestrogen) &enclomiphene citrate (potent antiestrogen)
Mechanism of action
1. Its anti-estrogenic activities diminish the negative feedback and increase the release of endogenousgonadotropin.
2. An intact hypothalamic-pituitary axis and presence of endogenous oestrogen are essential for its effectiveness
Regime
1. Start with a daily dose of 50mg, taken for 5 days from day 2 to 6 of the menstruacycle (some may start from day 5)
2. Confirm ovulation by basabody temperature chart or mid luteaprogesterone
3. Adjust the dosage according to the ovulation response. The maximum dose is 200mg daily
4. The couple is advised to have intercourse on alternate days for 1 week around the time of ovulation
Efficacy
1. Ovulation rate:- 40-60% per cycle
2. Conception rate:-15-20% per ovulatory cycle
3. Cumulative 6-month conception rate:-60-75%
4. Remark:-alternative method of ovulation induction should be consider if the patient is anovulatory even on maximum dose of
clomid or fail to conceive after 6 to 12 ovulatory cycles
Complications
1. Usually safe with mild side effects
2. Vasomotor flushes (10%), abdominal bloating (5%), breast discomfort (2%), headache (1%), visual symptoms
3. Multiple pregnancy rate:-5% (mostly twin); higher multiple pregnancies rare
4. Ovarian hyperstimulation is very rare
Advantages
1. Simple, safe and cheap
2. Orally active
3. Worth trying as the first line agent in those cases with intact hypothalamic-pituitary-ovarian axis
Protocol, as of10 May 2003

1. Usual starting dose of clomid is 50mg daily from D2 to D6 each cycle
2. Increase the dose by a monthly increment of 50 mg daily until ovulation occurs or a maximum dose of 200 mg daily has
reached
3. Check response by BBT
4. Confirm ovulation by mid-luteal (D21 in 28-days-cycle) progesterone
5. If remained anovulatory on maximum dose of clomid, refer for OI (with gonadotropins) after confirmation of tubal
patency
6. If failed to conceive after 12 cycles of successful clomid treatment with confirmation of ovulation, refer for further
assessment infertility clinic
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In vitro fertilisation(IVF)
What is in vitro fertilisation?
1. It is a 4-stage assisted reproductive procedure which includes:
a. Controlled ovarian hyperstimulation,
b. Oocyte retrieval under transvaginal ultrasound guidance,
c. Fertilization with sperm in vitro, and
d. Embryo replacement into the uterus.
2. Main indications
a. Tubal infertility
b. Moderate-to-severe endometriosis
c. Male infertility
d. Failure of other infertility treatments.
3. Efficacy
a. Conception rate:-10-30% per cycle (success rate decreases with increasing female age)
b. Cumulative conception rate:-40-60% after five cycles (success rate decreases with increasing female age)
4. Complication
a. Multiple pregnancy rate:-20-30%
b. Ovarian hyperstimulation syndrome (1% risk of severe OHSS)
c. Potential risks during oocyte retrieval. E.g. Haemorrhage, infection, visceral injuries to vessels, bowels etc.
d. Recent studies have suggested that it may be associated with a higher risk of carcinoma of ovary. This has not be
confirmed yet
Insemination
Intra-uterine insemination is an assisted reproduction technique (ART) in which a prepared specimen of semen is injected by
means of a cannula through the cervical canal, directly into the uterine cavity. The semen can be prepared from husband or from
donor if it is a case of male infertility. The insemination is performed at the time of ovulation as determined by ultrasound or
hormone measurements, and is usually preceded by ovarian stimulation.
Complications of insemination itself are very low but ovarian hyperstimulation and multiple pregnancy may be resulted from
concurrent ovarian stimulation. Intra-uterine insemination is particularly useful in women with deficient cervical mucus. It is
widely used for unexplained infertility and mild endometriosis before resorting to in vitro fertilisation (IVF). Success in men with
impaired sperm concentration or motility and those with antisperm antibodies is doubtful. The technique is simpler and cheaper
than IVF and less objectionable in those who, on religious or personal grounds, may not wish to undergo IVF.
Intra-cytoplasmic sperm injection (ICSI)
Intra-cytoplasmic sperm injection (ICSI) is one of the ART procedures to treat male infertility. A single spermatozoon is injected
into the cytoplasm of the oocyte using a microinjection pipette. It overcomes the problem of severe oligospermia because only a
few sperms are required, as compared to millions in conventional in vitro fertilisation. It also helps in sperm dysfunction such as
immotility and penetration failure, since the sperm is injected directly into the oocyte. Provided that the injected sperm is viable,
the chance of fertilisation is good. The risk of the treatment is that as severe oligospermia or azospermia is associated with
chromosomal abnormalities, there is a higher chance of transmission of abnormal karyotype to the offsprings.
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Ovarian Hyperstimulation Syndrome (OHSS)
What is Ovarian hyperstimulation syndrome
Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic condition arising from over-stimulation of the ovaries by ovulation
induction agents.
Pathophysiology
The basic pathophysiology is fluid shift from the int ravascular compartment to the third space (mainly the peritoneal cavity). The
exact mechanism is unclear but may be related to ovarian endocrine, paracrine and autocrine factors. Hypovolaemia and
haemoconcentration is resulted. In severe case there are ascites, pleural effusion, hypovolaemic shock, renal and liver dysfunction,
and electrolyte disturbances. There is also an increased risk of thromboembolism secondary to haemoconcentration.
Risk factors
OHSS is more likely to occur in:-
1. Ovulation induction with gonadotropin
2. Patients with PCOD
3. Development of high oestrogen level and numerous small to medium sized follicles during the ovulation induction procedure
4. Use of human chorionic gonadortropin (hCG)
Clinical features
Clinically, there are abdominal distension, nausea, vomiting, and diarrhea, dyspnea, oligouria.
Treatment
1. For mild cases, treatment is conservative:
a. Monitoring of haemodynamic status, urine output, weight gain, electrolytes
b. Fluid support which may consist of albumin or other kinds of colloid infusion
c. Prevent deep vein thrombosis with elastic stocking
2. For severe cases, surgical intervention may be required:
a. Pleural effusion:-pleural drainage
b. Massive ascites:-paracentesis
c. Laparotomy or laparoscopy for ruptured or bleeding ovarian cysts
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3. Male infertility
Spermatogenesis
- Formation of spermatozoa inside testes.
- Needs further maturation process through the epididymis.
- Impaired spermatogenesis occurs in chromosomal abnormality (e.g. Klinefelter's syndrome)
Male infertility
Male factor accounts of 30% of all cases of infertility. There are two major mechanisms for male infertility:
1. Abnormalities in spermatogenesis
2. Abnormalities in the delivery system of semen:
a. Blockage at vas deferens
b. Retrograde ejaculation
Abnormalities in spermatogenesis
1. Spermatogenesis can be affected by:
a. General environmental factors:- Such as chronic smoking, alcoholism, toxin or heavy metal, hot environment
b. Primary testicular failure resulted from:
i. Chromosomal abnormalities such as Klinefelter syndrome
ii. Irradiation, chemotherapy, surgery, tuberculosis and mump infections
c. Endocrine disorders such as:
i. Deficiency of hormones of pituitary gland and hypothalamus such as in Kallman syndrome
ii. Hyperprolactinemia
d. Miscellaneous:
i. Y-chromosome microdeletion is found in 10% of severe male infertility
ii. Varicoele which may result in a higher testicular temperature, is said to be associated with poor spermatogenesis
Diagnosis of male infertility

Male infertility is screened with semen analysis. More sophisticated tests for sperm functions are not very useful clinically.
Treatment of male infertility

1. General measures Improvement of general health including stopping smoking and alcohol intake may improve semen
quality in patients with mild impairment of semen quality
2. Hormones Only for correction of endocrine disorders
3. Intrauterine insemination For mild impairment of semen analysis
4. In vitro fertilisation and ICSI For severe impairment of semen quality
5. Surgery For correction of blocking, retrograde ejaculation, and varicocele
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Semen analysis
What is semen analysis (SA)
A laboratory test of seminal fluid carried out to investigate male fertility or the effectiveness of vasectomy. The technique and
range of normal values have been standardized by the World Health Organisation (WHO).
How to perform semen analysis

1. Timing:-the male have ejaculated at least once within the week prior to the test but not within the previous 2 days
2. Collection:-all semen samples should be obtained by masturbation into a clean, wide-mouthed nontoxic plastic container and
delivered to the laboratory as soon as possible, preferably within one hour
3. Assessment:-volume and liquefaction time of the semen, sperm count, motility and morphology
WHO criteria for normal semen characteristics:
Parameter Normal value

Volume 2ml or more
Concentration 20 million/ml
Motility 50% or more sperms have progressive motility
Morphology 30% or more sperms have normal form
Liquefication Complete in 30 min
White Blood Cell <1 x 106/L
Diagnosis
The diagnosis is made when two or semen analysis on separated occasion at least 3 months apart is abnormal.
How to interpret a SA report

1. The most common reason for abnormal SA is the inaccurate collection of the specimen, or history of recent illness (in 3
months) that may affect the production of sperm. Therefore, it is advisable to repeat the SA after a 3-month interval
2. If the SA is grossly abnormal, further investigation should be taken to look for the underlying causes.
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4. Sexual dysfunction
Sexual dysfunction
Sexual functioning involves a unique combination of physical, psychological and social expression. It allows a couple to
reproduce, bond and enjoy each other. Sexual dysfunction accounts for 5% of all cases of infertility. Both male and female can be
affected.
Female sexual dysfunction

- Vaginismus
- Dyspareunia
Male sexual dysfunction

- Erectile or ejaculatory dysfunction
Libido
Sexual drive or desire. The intensity of libido varies from person to person, and may also vary in women in relation to the
menstrual cycle, pregnancy or menopause. Libido generally decreases in both sexes with advancing age. The term must not be
confused with orgasm.
Vaginismus
It is a kind of sexual dysfunction. It is involuntary painful spasm of the pubococcygeus muscle (see levator ani) leading to closure
of the vaginal introitus, preventing penetration. It is different from dyspareunia. The cause is psychological rather than organic.
Treatment is by gradual desensitization.
Dyspareunia
It means painful sexual intercourse. Pain on penetration may be superficial or deep. Deep dyspareunia often has underlying
pathologies such as pelvic endometriosis and chronic pelvic inflammatory disease. Superficial dyspareunia usually has a
psychological element and lack of lubrication during intercourse. Sometimes superficial dyspareunia of acute onset is related to
local pathologies such as vaginitis, vulval herpes and ulcer.
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Oncology
0. Gynae-oncology
Introduction
It is a subspecialty of gynaecology deals with malignant and pre-malignant lesion of the genital tract
Female genital cancer in Hong Kong

Hospital Authority 2006 Report:-
Cancer Incidence Death
Ca Cervix 459 (9.6, 5th) 133 (2.4, 9th)
Ca Ovary 450 (9.7, 6th) 136 (2.6, 8th)
Ca Corpus 570 (11.7, 4th) 49 (1.0, 15th)
Cervical cancers and ovarian cancers are the 4th and 10th most common cancers in female population in Hong Kong
Topics
1. Premalignant lesion of genital tract
a. Cervical intraepithelial neoplasm (CIN)
b. Vaginal intraepithelial neoplasm (VAIN)
c. Vulval intraepithelial neoplasm (VIN)
d. Endometrial hyperplasia
2. Cervical cancers
a. Majority is squamous cell carcinoma
b. Rarely adenocarcinoma
3. Ovarian cancers
a. Majority is epithelial cancer
b. The rest is non-epithelial cancer including:-germ cell tumours and stromal cell tumours
4. Cancers of corpus uterus
a. Most are endometrial carcinoma
b. Rarely sarcoma arise from the smooth muscle tissue
5. Vaginal cancers
a. Most are squamous cell cancer
b. Very rarely adenocarcinoma related to in utero exposure to DES
6. Vulval cancers Most are squamous cell cancer and rarely melanoma
7. Gestational trophoblastic diseases more common in Asian than in Caucasian
Modalities of treatment
1. Surgery mainstay of curative treatment for epithelial type of cancers:-endometrial, ovarian, and cervical cancer
2. Chemotherapy mainstay of treatment for trophoblastic disease and germ cell ovarian tumours
3. Radiotherapy
a. Mainstay of treatment for cervical cancer
b. Adjuvant therapy for high-stage endometrial cancer
What should medical students know?

Students should know cervical cancer, endometrial carcinoma, ovarian cancer, gestational trophoblastic disease and premalignant
lesions:-CIN and endometrial hyperplasia as they are relatively common.
Sarcoma, vaginal and vulval premalignant lesions and cancers are very uncommon.
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1. Malignant neoplasms of vagina and vulva
Staging of CA vagina
Staging CA vagina FIGO 1995 5-year survival rate
0 Intraepithelial neoplasia Curable.
I Invasive carcinoma confined to vagina mucosa. 75-90%
II Subvaginal infiltration not extending to the pelvic wall. 45%
III Extends to pelvic wall. 30-40%
IVa Involves mucosa of bladder or rectum >20%
IVb Spread beyond the pelvis <20%
Incidence
Primary growths of the vagina are rare and the average gynaecologist will see only one such tumour for 30 of the cervix.
Pre-invasive lesions (VAIN) are now more frequently diagnosed. They may proceed to cancer. There is little evidence for
radiotherapy as a cause and intrauterine exposure to di-ethyl stilboestrol (DES) in fact carried a very low risk of causing vaginal
cancer as opposed to vaginal adenosis. Secondary growths are more common, especially extension from cervical cancer, and
metastatic deposits may appear from disease elsewhere in the body.
Histology
85% are squamous carcinomas, occurring in women over 60. The remainder include melanoma, sarcoma, adenocarcinoma and
clear cell carcinoma, all of which tend to be associated with middle-aged or even young women
Clinical Features
The patient is usually menopausal and most commonly complains of bleeding (60%). Discharge (15%) and pelvic pain (<10%)
may be present. If the bladder is involved, she will experience pain and dysuria. The tumour is not at first painful and unless it
appears in a woman who is still sexually active, it is not likely to present until it has penetrated the vaginal wall and caused
bleeding. Old women often believe or affect to believe that all bleeding is from haemorrhoids.
Diagnosis
An early tumour can easily be missed if it is obscured by the blade of a metal
speculum. The whole vagina should always be inspected, and cytological smears
taken from any lesion at all unusual. Colposcopy, cystoscopy and
proctosigmoidoscopy are indicated to detect spread.
Site and Spread

Tumours of the lower third (25-30% of cases) have a much poorer prognosis than those of the upper and middle thirds, partly
because spread to the inguinal nodes is quicker and because of the danger to the bladder. Prognosis depends on the stage, which
depends on when the patient goes to her doctor, and on the position in the vagina. The lower third with its much quicker lymphatic
spread is the least favourable.
Treatment
In stage 0 growths, good results have been obtained with local application of 5-fluorouracil cream, but for stage I onwards,
radiotherapy is the usual treatment.
1. It can be applied at any stage.
2. It is more readily available than skilled radical surgery.
3. The patients are often elderly and poor surgical risks.
Radical surgery (radical hysterectomy, vaginectomy, lymphadenectomy) is claimed to give good results in experienced hands, and
a cure rate of over 80% has been achieved for stage I. In stage IV where radiotherapy is only palliative, surgery which includes
some form of exenteration is the better treatment if the patient is fit and the gynaecologist has the necessary experience. Vaginal
melanoma is almost always fatal, with poor results from radiotherapy and no appropriate chemotherapy available. Sarcoma
botrioides is a rare tumour of young children, presenting as grape-like masses with bleeding. Chemotherapy with vincristine,
actinomycin D and cyclophosphamide gives good results.
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1. Preoperative Investigations
a. Haematological Investigations:
i. CBP
ii. RFT and LFT
iii. TA4
iv. CA125
v. Serum for blood grouping and cross match
b. ECG
c. Imaging
i. Chest X-ray
ii. Abdominal and pelvic ultrasound scan to look for distant metastasis especially over the lymphatic areas of the
groin and pelvis
iii. IVU, CT and MRI To be performed as clinically indicated
d. Staging procedure (EUA + Cystoscopy) proctosigmoidoscopy is indicated if rectal wall involvement is suspected
e. Tumour tissue and blood collection for molecular biology researches
i. 10 ml clotted blood
ii. 10 ml heparinized blood
iii. 20 ml citrate blood for molecular biology study
2. Management by Stage
a. Stage I and II
i. Radical Hysterectomy and Pelvic Lymphadenectomy
- Lesions less than 2 cm in the upper third of the vagina may be treated by radical hysterectomy, removal
of upper half of the vagina and pelvic lymphadenectomy.
- Postoperative pelvic radiotherapy should be given to patients with positive pelvic nodes
ii. Exenteration Surgically low risk patients with rectal or bladder involvement alone are suitable for anterior,
posterior or total exenteration provided there is no evidence of pelvic or aortic nodal metastasis.
iii. Radiotherapy Intracavity radiation and external irradiation is generally used as the primary form of
treatment in most cases
b. Stage III and IV
i. Radiotherapy Intracavity radiation and external irradiatin is generally used as the primary form of treatment
in most cases
ii. Combination Therapy An option of giving three courses of PVB prior to combined external pelvic and
intracavitary irradiation can be considered
3. Follow up
a. Schedule
i. For patients with low risk for recurrence, the followed up plan is:-
- 4 monthly in the first 2 years
- 6 monthly thereafter
ii. Patients should be encouraged to advance their appointment if PV bleeding occurs.
b. Physical Examination
c. Routine Investigations
i. Serial monitoring of the TA4 and/or CA125 are carried out in the first 2 years if they are elevated before the
primary treatment
ii. Pap smear is not a routine in the follow up
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Staging of CA vulva
Staging CA vulva FIGO 2009
Stage I Tumor confined to the vulva
Stage II Tumor of any size with extension to adjacent perineal structures (1/3 lower urethra, 1/3 lower vagina, anus) with
negative nodes
Stage III Tumor of any size with or without extension to adjacent perineal structures with positive inguino-femoral lymph
nodes
Stage IV Tumor invades other regional (2/3 upper urethra, 2/3 upper vagina), or distant structures
Incidence:-3 per 100 000 (UK); 1.3 per 100 000 (HK) per year
Aetiology
The aetiology of vulval cancer is unknown. Some vulval cancers contain viral antigens
(e.g. HSV 2), but the importance of these in the aetiology of the disease is uncertain.
Histology
Squamous carcinoma:-85%
Melanoma:-5%
Clinical features
The majority of patients with vulval cancer are over 60. The presenting features include vulval irritation and pruritus (70%), a
vulval mass (60%) and bleeding (30%). The diagnosis is often delayed, partly due to the patient's reluctance to seek medical help,
and partly due to delay in performing a clinical examination once the patient presents. Any lump on the vulva must be examined
and biopsied. The inguinal lymph nodes may be enlarged, but absence of enlargement does not guarantee absence of lymphatic
spread.
Protocol of this disease is too lengthly and unnecessary to be included.
Surgical treatment
1. Radical vulvectomy is the optimum treatment for vulval cancer. The conventional operation is radical vulvectomy with
dissection of the superficial and deep inguinal glands and the external iliac glands. Such surgery has increased the five year
survival for the disease which is now 75%. The whole vulva, skin and subcutaneous tissue are excised down to the
periosteum. The wound should be closed completely if possible, undercutting and mobilizing skin if necessary. Radical
vulvectomy with en bloc dissection and removal of the inguinal and iliac lymph glands is associated with significant
morbidity. The following variations in technique have been introduced to reduce morbidity.
2. In vuval cancer, lymphatic metastases develop initially by embolisation. In early disease there is no need to remove the
lymphatic channels between the tumour and the groin nodes. Therefore, three separate incisions can be used to remove the
tumour and the nodes on each side. Such an approach is associated with lower morbidity than conventional surgery.
3. If the primary tumour is small, and confined to one area, a more limited operation may be as effective as radical vulvectomy.
In modified radical vulvectomy, the lesion and surrounding area is removed, leaving the reminder of the perineum intact. A
2-3 cm margin of healthy tissue should be removed along with the tumour.
Figure 66 Conventional radical vulvectomy (Leftmost two), Separate groin incision(third) and modified radical vulvetomy(right).
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2. Malignant neoplasms of ovary
Ovarian cancer
Primary ovarian cancer
In general, primary ovarian cancer is divided into two types:
1. Ovarian epithelial carcinoma which is subclassified into:
a. Serous 40%
b. Mucinous 10%
c. Endometrioid 20%
d. Clear cell 5%
e. Brenner
f. Mixed
2. Non-epithelial cancer which include:-
a. Germ cell tumours
b. Stromal cell tumours
3. They are different not only in pathology, but also in epidemiology, clinical presentation and treatment. Please refer to
individual topics for detail.
Secondary ovarian cancer

Metastasis from other sites such as bowel, stomach, and breast can occur. A characteristic secondary cancer is called Krukenberg
tumour.
Incidence
9.0 in 100, 000 (Hong Kong 1998-2007)
1. FIGO Staging for Carcinoma of Ovary (1996)
Stage 1 Growth limited to the ovaries
1a Growth limited to 1 ovary; no tumour on the external surface; capsule intact; no ascites
1b Growth is limited to both ovaries; no tumour on the external surface; capsule intact; no ascites
1c Tumour either Stage 1a or 1b, but with tumour on surface of one or both ovaries; or with capsule ruptured; or with ascites
present containing malignant cells; or with positive peritoneal washings
Stage 2 Growth involves 1 or both ovaries with pelvic extension

2a Extension and/or metastasis to the uterus and/or tubes
2b Extension to other pelvic tissues
2c Tumour either Stage 2a or 2b but with tumour on the surface of 1 or both ovaries; or with capsule(s) ruptured; or with
ascite present containing malignant cells; or with positive peritoneal washings
To assess the impact prognosis of the different criteria for alloting cases to stage 1c or stage 2c it would be of value to know
whether the source of malignant cells was (i) peritoneal washing or (ii) ascites, and whether rupture of the capsule was
spontaneous or caused by the surgeon.
Stage 3 Tumour involving one or both ovaries with peritoneal implants outside the pelvis and/or positive retroperitoneal
LN or inguinal lymph nodes; superficaial liver metastasis equals stage 3; tumour limited to the true pelvis but with
histologically proven malignant extension to small bowel or omentum
3a Tumour grossly limited to the true pelvis with negative nodes but with histologically confirme microscopic seeding of
abdominal peritoneal surfaces
3b Tumour involving one or both ovaries with histologically confirmed implants of abdominal peritoneal surfaces none
exceeding 2cm in daimeter; nodes are negative
3c Abdominal implants >2cm in diameter and/or positive retroperitoneal or inguinal nodes
Stage 4 Growth involving one or both ovaries with distant metastasis. If pleural effusion present, there must be positive
positive cytology to allot a case to stage 4; parenchymal liver metastasis equals stage 4
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2. Preoperative Investigations
a. Haematological Investigations:
i. CBP
ii. RFT and LFT
iii. Tumour markers
- AFP, BHCG, CEA for suspected germ cell tumours
- CA125 for suspected epithelial cell carcinoma
iv. Serum for blood grouping and cross match
b. ECG
c. Chest X-ray
d. Abdominal and pelvic ultrasound scans to look for distant metastasis especially over the lymphatic areas of the
groin and pelvis
e. CT and MRI To be performed as clinically indicated
f. Pleural or peritoneal tapping
i. This is performed for symptomatic relief
ii. Fluid would be sent for cytology to look for malignant cells
g. Sigmoidoscopy/colonoscopy For patients with bowel symptoms or raised CEA
3. Preoperative Preparation
a. Inform the possibility of losing reproductive function if the patient has not completed her family
b. Bowel preparation
i. Fluid diet for 48 hours before OT
ii. Phosposoda 24 hours before OT
Borderline malignancy of ovary

These are ovarian tumours with histological features that are intermediate between those of clearly benign and unquestionably
malignant tumours of a similar cell type. They have some, but not all, of the morphological features of malignancy:-such as
stratification of epithelial cells, apparent detachment of cellular clusters from their sites of origin, mitotic activity and nuclear
abnormality, but lack invasion to adjacent stroma. Metastasis can occur in borderline malignancy (WHO).
Germ cell tumour

Ovarian germ cell tumours, together with stromal cell tumours, are usually classified as non-epithelial carcinoma of the ovary, as
they are very different from ovarian epithelial carcinoma. Compared to epithelial type, germ cell tumours are rare, and occur in
younger age group of patients. They are in general more sensitive to chemotherapy. They also have a specific and sensitive
tumour marker. They are usually unilateral and solid. They arise from the germ cell line of the ovary and are subclassified into:
1. Teratoma
2. Dysgerminoma
3. Yolk sac tumour
4. Choriocarcinoma
In general, the treatment consists of unilateral oophorectomy (lesion side) followed by chemotherapy. Radical surgery is not
required and fertility can be preserved. Bilateral oophorectomy and hysterectomy is advised for patients who have completed
family.
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Dysgerminoma
It is the most common malignant germ cell tumours of the ovary, and also account for 2-5% of all primary ovarian cancers. It
mainly affects the young women (< 30 year old). It is similar to seminoma of men. It is solid, loculated, moderate in size, and
usually has a long ovarian pedicle which is at risk of torsion. It is bilateral in 10% of cases, and is spread through lymphatic
channels to para-aortic, mediastinal and supraclavicular lymph nodes. It does not produce hormones, but may contain elements of
yolk sac tumour and choriocarcinoma, and their presence may make the prognosis worse. Therefore, testing for serum level of
alpha-feto protein and human chorionic gonadotropin are important. Dysgeminoma is very sensitive to both chemotherapy and
radiotherapy. Treatment is usually oophorectomy followed by chemotherapy. The contralateral ovary and uterus can be preserved
for fertility.
As dysgeminoma is also radiosensitive, what is the reason that chemotherapy is preferably to radiotheray as a post-surgical
adjuvant treatment?
Yolk sac tumour

Also called endodermal sinus tumour, is the second most common malignant germ cell tumour of the ovary. It usually affect
children or young aged women. It is a rapid-growing solid tumour, and usually presents as an acute abdomen due to rupture,
necrosis and haemorrhage. The tumour secrets alpha-feto protein which acts as a sensitive tumour marker and is useful for
monitoring of the disease. The tumour is very chemosensitive but not radiosensitive. Treatment is oophorectomy followed by
chemotherapy. As chemotherapy is very effective, the contralateral ovary and the uterus can be preserved if they are not involved.
Krukenberg tumour
It is a secondary ovarian cancer with characteristic histological picture of mucin-ladin, signet-ring cells infiltrating a hypoplastic
ovarian stroma of spindle shaped cells, and is usually metastasized from stomach, colon, breast, pancreas. It is usually bilateral,
and most are lobulated, of moderate size, rapid growing, and retained the normal shape of ovary.
Figure 67 Gross and microscopic appearance of Krukenberg tumour.
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3. Malignant neoplasms of uterine cervix
Transformation zone
Formation of transformation zone
1. Normally the endocervix is covered with columnar
epithelium while the ectocervix with squamous
epithelium. The boundary is called squamo-columar
junction (SCJ)
2. During reproductive age when the cervix is under the
influence of oestrogen effects, it tends to evert leading
to the exposure of the columnar epithelium on the
ectocervix. The thin columnar epithelium appears red
and the result is so often erroneously referred to as a
cervical erosion or ectropian.
3. The exposed part of columnar epithelium on the ectocervix is gradually replaced by a process of squamous metaplasia
spreading from the SCJ towards the cervical canal. The end result of this transformation is the replacement of the ectopic
columnar epithelium with mature squamous epithelium.
4. If the squamous epithelium covers the entrance to a cervical crypt and the columnar cells continue to secrete mucus in the
crypt, a nabothian cyst results.
5. The region of cervix in which the process of metaplasia take place
6. In some women the transformation zone may extend on to the vaginal walls
Clinical significance of transformation zone

1. Cervical intraepithelial neoplasia (CIN) results from a disruption of the metaplastic process, with the possible involvement of
human papillomavirus (HPV)
2. The transformation zone and the CIN lesion are visible under colposcopy
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Cervical intraepithelial neoplasm (CIN)
Definition
1. Cervical intraepithelial neoplasm (CIN) describes the histopathological condition where part or whole of the thickness of the
cervical squamous epithelium is replaced by cells showing varying degrees of dysplasia.
2. It is graded as CIN I, II, or III according to the differentiation of basal, intermediate and superficial thirds of the epithelium
respectively, but the conditions are recognized as being part of a continuous process.
3. When the whole thickness is involved (without invasion to underlying stroma) it is called carcinoma-in-situ
4. It is a premalignant lesion that if left untreated, can progress to invasive cervical cancer
Cause
Associated with infection by human papillomavirus (type 16 and 18), which alters the normal squamous metaplastic changes in
the transformation zone of cervix
Progression
- CIN I:-46% regress and 26%progress to CIN III over 2 years
- CIN III:-18% progress to invasive cancer in years, and 36% in 20 years

1. Is screened regularly by pap smear
2. Is diagnosed with colposcopy and guided biopsy
3. Features of ciunder colposcopic examination:
a. Usually has distinct acetowhite lesion with clear margins
b. Shows a mosaic vascular pattern
c. Punctation (where a vessel rums perpendicular to the surface)
d. In general, the high grade of ciwill be when:-
i. The more quickly and strongly the acetowhite changes develop,
ii. The clearer and more regular the margins of the lesion, and
iii. The more pronounced the mosaic or punctation
Treatment
The following options of surgical treatments are guided by colposcopy:
1. Ablative methods
a. Cryotherapy
b. Electrocautery
Figure 68 Cone excision by knife.
c. Laser vaporisation
d. In general, ablative methods are quick, cheap and easy to peform. The main disadvantage is lack of histology for
review. About 1% of cases of CIN II may have invasive carcinoma that may be missed after ablative treatment.
2. Excisional methods
a. Loop electrodiathermy excision procedure (LEEP)
b. Cone excision using laser or knife.
i. Knife excision requires general anaesthesia with high risk of haemorrhage and cervical stenosis or incompetence
in a subsequent pregnancy.
ii. Laser excision requires more technique.
c. Hysterectomy:-for patients who have complete family. The advantage is no risk of recurrence
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Pap smear
Definition
It is a cytological investigation of the cervical cells designed for screening of cervical intraepithelial neoplasia (CIN), as a
preventive measure against cervical cancer.
Who should be screened?

All women aged 20 to 64 who are or ever have been sexually active.
When should be screening stopped

- At age 65
- However, women aged 65 or above should be encouraged to have a smear if they have not been screened previously
How often should smears be taken?

1. Every 3 to 5 years
2. in HK, yearly in the first 2 years, then every 3 years
Frequency of screening Reduction in risk of developing invasive diseases
Every 5 year 84%
Every 3 year 93%
Every year 95%
3. As there is only 2% reduction of risk of invasive cancer by yearly screening when compared to 3-yearly screening, the later is
more cost-effective
How to take a Pap smear

1. Patient relaxes in the dorsal position. Perform speculum examination to visualise the whole cervix.
2. Use a small amount of water-based lubricant so that it would not affect the smear. Swab away any blood or discharge.
3. If the squamo-columar junction can be seen, take a smear from the transformation zone by 360 degree firm surface sweep
with a suitable spatula
4. If the squamo-columar junction is sited within the endocervical canal then take a smear by rotating a cytobrush in the canal.
5. Spread the smear evenly over a labelled glass slide. Fix it rapidly with ethanol to avoid drying artifact.
How to examine a pap smear under microscope

1. The cytological features of individual cervical cells are examined. The degree of dyskaryosis depends on the nuclear features
and nuclear to cytoplasmic ratio, and is classified to mild, moderate and severe. Koilocytosis, a feature of human
papillomavirus infection may also be picked up.
2. Because of the difficulties in differentiate the grading; an alternative classification system called Bethesda is also commonly
used. In the Bethesda system, CIN II and III are combined into high grade squamous intraepithelial lesion (HGSIL), while
CIN I and koilocyotosis are combined into low grade SIL. The Bethesda system also includes 'atypical squamous cells of
unknown origin' (ASCUS) of which cervical cells show mild dyskaryosis but do not fit in low grade SIL. They are usually
due to reactive changes toward inflammation.
3. Besides, lower genital tract infection may sometimes be picked up from a smear:-trichomonas vaginalis, candidiasis, clue
cells of bacterial vaginosis.
How good is a Pap smear?

False negative rate of 15% in detection of histologically confirmed CIN.
Management of abnormal pap smear

1. For HGSI(CIN II and III):-Refer to colposcopy with early appointment
2. For LGSI(CIN I and koilocyotosis):-Refer to colposcopy
3. For ASCUS:-Repeat smear after 6 months
1. What features of cervical cancer and Pap smear fit the WHO criteria of screening?
2. Which factors account for the false negative of a Pap smear?
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A. Pap smear screening programme
1. All women with sexual activities should have PS annually for the initial 2 years, followed by PS every 3 years till the age of
65 if the previous PS results are normal for those without high risk factors for cervical cancer
2. PS annually till the age of 65 if the previous PS results are normal for those with high risk factors for cervical cancer
B. Management for abnormal results
1. Colposcopy
a. For LSIL or ASCUS x 2 - within 12 weeks
b. For HSIL, AGUS, AGC, AIS, ASC-H - within 6 weeks +/- Biopsy
c. Carcinoma is suspected on PS or clinically - within 1 week +/-biopsy
2. Normal or HPV - Perform PS 6-monthly
a. If there are 2 normal PS results, return to normal screening programme
b. If there are episodic ASC-US or LSIL, perform colposcopy at 2-year
c. If there is HSIL, perform colposcopy
3. CIN I
a. LEEP is indicated if:-
i. Lesion occupies more of cervix
ii. Patient prefers operation
iii. Patient may not return for follow-up
b. Otherwise, perform PS 6-monthly:-
i. If there are 3 normal PS results, return to normal screening programme
ii. If there are episodic ASC-US or LSIL, perform colposcopy at 2-year
iii. LEEP is indicated if CIN I persists or HSIL is present.
4. CIN II or CIN III LEEP
5. Carcinoma Admit for workup
C. Management of glandular cells abnormalities
1. Perform endometrial sampling if the origin of AGC is endometrial
2. Perform colposcopy (and endometrial sampling for patients older than 35 years old or with abnormal uterine bleeding) if:-
a. The origin of AGC is endocervical; or
b. Not specified; or
c. AGC favour neoplasia; or
d. Endocervical AIS
3. If slide review does not confirm AGUS, manage according to PS result
4. If slide review is not available or concurs with AGUS, perform cone biopsy and endocervical curettage followed by PS
6-monthly till 4 consecutive normal results
5. If endometrial hyperplasia / carcinoma or cervical carcinoma is revealed, manage according to the corresponding protocol
D. Management of cancer cells on PS
1. Squamous cells - Colposcopy to take directed biopsy if cervical pathology is found. Otherwise, perform LEEP.
2. Glandular cells - Endometrial Sampling and Colposcopy. If endometrial hyperplasia / carcinoma is revealed, manage
according to the protocol. Take directed biopsy if cervical pathology is found. Otherwise, perform cone biopsy
Spatula
An implantment with a broad, flat, blunt blade, used especially for mixing or spreading. The Aryes spaula is designed to take a
Pap smear from the cervical os. For postmenopausal women who usually have a tight stenotic cervical cos, it would be more
appropriate to use a cytobrush.
Cyutobrush
An instryument designed to take Pap smear from a stenotic os which is more commonly encountered in postmenopausal women.
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Bethesda
What is Bethesda system?
It is a reporting system for Pap smear result as follows:
1. Adequacy of the specimen 5. General Categorization (optional)
2. Satisfactory for evaluation 6. Within normal limits
3. Satisfactory for evaluation but limited by... (specific 7. Benign cellular changes:-See Descriptive Diagnosis
reason) 8. Epithelial cell abnormality:-See Descriptive Diagnosis
4. Unsatisfactory for evaluation (specific reason)
Descriptive Diagnoses
1. Benign cellular changes
a. Infection
i. Trichomonas vaginalis
ii. Fungal organisms morphologically consistent with Candida spp
iii. Predominance of coccobacilli consistent with shift in vaginal flora
iv. Bacteria morphologically consistent with Actinomyces spp
v. Cellular changes associated with Herpes simplex virus
vi. Others
b. Reactive changes
i. Reactive cellular changes associated with:
ii. Inflammation (includes typical repair)
iii. Atrophy with inflammation ("atrophic vaginitis")
iv. Radiation
v. Intrauterine contraceptive device
vi. Others
2. Epithelial cell abnormalities
a. Squamous cell
i. Atypical squamous cells of undetermined significance (ASCUS):-Qualify*
ii. Low-grade squamous intraepithelial lesion encompassing:- HPV** mild dysplasia/ CIN 1
iii. High-grade squamous intraepithelial lesion encompassing:- Moderate and severe dysplasia. CIS/CIN I & II
iv. Squamous cell carcinoma
b. Glandular cell
i. Endometrial cells, cytologically benign, in postmenopausal women
ii. Atypical glandular cells of undetermined significance (ASGUS):-Qualify*
iii. Endocervical adenocarcinoma
iv. Endometrial adenocarcinoma
v. Extrauterine adenocarcinoma
vi. Adenocarcinoma, NOS (not otherwise specify)
c. Other malignant neoplasms:-Specify
d. Hormonal
i. Hormonal evaluation (applies to vaginal smears only)
ii. Hormonal pattern compatible with age and history
iii. Hormonal pattern incompatible with age and history:-Specify
iv. Hormonal pattern not possible due to:-Specify
3. Remark:
a. *Atypical squamous or glandular cells of undetermined significance should be further qualified as to whether a
reactive or a premalignant/malignant process is favoured.
b. **Cellular changes of human papillomavirus (HPV), previously termed koilocytosis, koilocytotic atypia, or
condylomatous atypia, are included in the category of low-grade squamous intraepithelial lesion.
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Colposcopy
Definition
Colpo:-vagina; scopy:-view. A detail examination of the female lower genital tract with the aids of low-power (magnification of 5
to 20 times) illuminated binocular microscope.
Indications
1. Diagnostic:- To examine and guide biopsy when there are abnormal pap smears or lesions of lower genital tract suspicious of
intraepithelial neoplasms (such as CIN, viand VAIN)
2. Therapeutic:- To excise or destroy benign or premalignant lesions by means of loop electrosurgical excisional procedure
(LEEP), cryotherapy, electrocautery or laser therapy
How to perform colposcopy

1. Bimanual examination and taking pap smear (if indicated):
a. Essential to aid detection of frank invasive disease of cervix, an uterine or an ovarian mass
b. Deferring the smear until after colposcopic inspection may provide a less satisfactory sample for cytological
examination
c. After that, the cervix is examined under a microscope.
2. Examination with saline:-
a. Remove any discharge with normal saline
b. Look for any leukoplakia, viral condyloma and any evidence of invasive disease such as ulcerated or rrregular surface,
and atypical vessels.
3. Examination with acetic acid:
a. Apply 5% acetic acid
b. Acetic acid causes tissue to swell, especially abnormal epithelium, which has a higher nuclear density, high protein
concentration. This results in change of refraction of light, and therefore the abnormal epithelial tissue appears white
(acetowhite lesion)
c. Identify the squamo-columnar junction (SCJ) which is defined by the lower limit of normal columnar epithelium.
Failure to identify the SCJ correctly is one of the main pitfalls in colposcopy.
d. Determine the nature of the lesion by assessing the colour, the margins and vascular markings of the lesions:
i. CIN lesions are acetowhite with distinct margin. They often show a mosaic vascular pattern with patches of
acetowhite separated by red vessels. Punctations are vessels running perpendicular to the surface. In general, the
more quickly and strongly the acetowhite changes develop, the clearer and more regular the margins of the
lesion, and the more pronounced the mosaic or punctation, the more severe is the CIN lesion is.
ii. Flat warts usually present as acetowhite lesions of faint and very irregular margins. There are usually isolated,
satellite lesions.
iii. See acetowhite for other causes of acetowhite changes.
iv. Invasive lesions have very marked mosaic pattern or coarse punctation. There are atypical vessels which run a
bizarre course and are often corkscrew or comma-shaped, with large diameter, abruptly appearing on and
disappearing from the surface, and do not branch dichotomously like normal vessels.
4. Examination with Lugol solution (Schiller test):- Normal squamous epithelium (which contains glycogen) stains dark brown
by Lugol solution (iodine and potassium iodine). Whereas columnar or abnormal squamous epithelium do not.
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Dyskaryosis
A cytological term used to describe cells compatible with origin from epithelium with dysplasia. In cervical intraepithelial
neoplasia, dyskaryosis is classified as mild, moderate, or severe according to appearances suggesting origin from CIN I, II, or III.
The distinction between changes compatible with human papillomavirus (HPV) infection or CIn I is particularly difficult to make.
Cytological grading correlates poorly with subsequent histological diagnosis. This correlation can be substantially improved if the
three cytological grades are merged to two. Bethesda system divides abnormal smears into those showing high and low grade
squamous intraepithelial lesions (HGSIL and LGSIL)
Koilocyte
It represents the diagnostic cytopathic effect of human papillomavirus (HPV). Koilcytes are HPV-infected epithelial cells with
enlarged, wrinkled and sometimes hyperchromatic nuclei, which are surrounded by a clear space or halo. Koilocytes are usually
seen in the intermediate and superficial layers of the epithelium.
Acetowhite
It is a term used during colposcopy to describe any lesion that changes to white in colour after being treated with acetic acid.
Lesions that typically show acetowhite change include cervical intraepithelial neoplasm (CIN) and wart (human papillomavirus
infection). The intracellular protein content is high in these lesions and therefore the abnormal cells swell after being treated with
acetic acid. This results in change of refraction of light and hence the lesion appears white.
Sometimes normal columnar epithelium will also blanch briefly after exposure to acetic acid. It can be identified by its villous or
furrowed surface. Squamous metaplasia has a glassy white appearance but it is hard to distinguish from CIN I. Subepithelial
fibrosis secondary to previous cervical excision or destruction surgery may also appear white. This can be recognised by the radial
arrangement of lines of fine punctations.
Loop electrosurgical excisional procedure (LEEP)

Loop electrosurgical excisional procedure, also called large loop excision of transformation zone (LLETZ), is performed under
guidance of colposcopy. It utilises electricity through a cutting loop to provide excision. It is performed as a day-case without
anaesthesia and requires simple equipment, and therefore has become the most popular method to treat cilesions. The major
disadvantage is that it is not easy to tailor the excision to the exact area of the abnormality. In consequence, there is a risk of
incomplete excision. Common complications are infection and haemorrhage. Patients are advised to avoid coitus for two weeks
after the procedure.
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Cervical cancer
Introduction
1. Squamous cell carcinoma is the most common type of cervical cancer. Only 5% belong to adenocarcinoma.
2. Medical students are not required to know the detail of adenocarcinoma except the following:-
a. Adenocarcinoma is different from squamous cell type in the following aspects:
i. It affects women of younger age
ii. It is difficult to be screened or diagnosed as it arises in the endocervical canal
b. Adenocarcinoma is similar to squamous cell type in that there is a premalignant stage, and spread, staging and
treatment are the same.
3. The rest of the content refers to squamous cell carcinoma.
Epidemiology
1. Second most common gynaecological cancer in Hong Kong. Incidence in 2007 is 400.
2. Median age of onset:
a. CIN:-35-40
b. Cancer:-45-50
c. Trends toward younger age group
3. Drastic reduction of mortality by pap smear screening (24.7 in 1983; 7.7 in 2007)
Aetiology and pathogenesis

Abnormal squamous metaplasia of the cervical epithelium in the transformation zone associated with human papillomavirus 16
and 18, resulting in cervical intraepithelial neoplasia (CIN) which progresses to carcinoma.
Risk factors
- Lower social class
- Cigarette smoking (more than 20 cigarettes/ day)
- Coitus at young age
- Compromised immune status
- Multiple sexual partners , Prostitution
- Multipara, age at first pregnancy
- Sexually transmitted diseases especially HPV type 16 and 18
- Male partner with STD, penile CA
- History of cervical dysplasia (CIN)
Clinical features
1. Asymptomatic in some patients Screened by smear
2. Present with local symptoms:
a. Abnormal vaginal bleeding:-Postcoital bleeding, Intermenstrual bleeding
b. Vaginal discharge:-blood-stained, unpleasant smell
3. Rarely with symptoms associated with advanced disease Bowel or urinary symptoms, bone pain, cachexia, weakness, SOB
4. Local signs:
a. Hard, friable, irregular, enlarged, fixed, contact bleeding
b. Vaginal and parametrial involvement, pelvic side wall involvement
5. Systemic signs are uncommon:
a. Anaemia
b. Inguinal lymphadenopathy
c. Pulmonary involvement, hydronephosis, hepatomegaly, ascites
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Spread
Figure 69 Direct spread (Leftmost two) and lymphatic spread.

- Mainly direct spread:-upper and lower vagina, parametrium, pelvic side wall
- Lymphatic:-obturator, hypogastric, external iliac, common iliac, para-aortic, rarely retrograde to inguinal
- Rarely through blood to:-liver, lung, bone, brain
Staging
Staging of CA cervix remains on clinical assessment (see staging of CA cervix)
Diagnosis
Confirmed with cervical biopsy, which can be assisted with colposcopy. Pap smear is not a diagnostic tool.
Staging procedure
1. Plan for option of treatment
2. Provide information of prognosis
a. Cystoscopy and examination under general anaesthesia
b. USG, CT scan or MRI:-assess liver, kidneys, lymph nodes involvement
c. Proctoscopy, Barium enema:-if rectal involvement is suspected
d. IVU:-look for urinary tract involvement, replaced with good USG
e. Lymphangiography:-limited role because of inaccuracy in assessing lymph node involvement
Protocol, Preoperative Investigations, as of 16 April 2004

1. Haematological Investigations:
a. CBP
b. RFT and LFT
c. TA4 for squamous cell carcinoma
d. CA125 for adenocarcinoma
e. Serum for blood grouping and cross match
2. ECG
3. Chest X-ray
4. Abdominal and pelvic ultrasound scan to look for distant metastasis especially over the lymphatic areas of the groin and.
pelvis
5. CT and MRI to be performed as clinically indicated
6. Examination under Anaesthesia and Cystoscopy
a. Can be omitted if satisfactory assessment can be accomplished without anaesthesia or when the patients medical
condition is poor
b. If there is a difference in opinion, the lower stage should be awarded
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Treatment
1. Principle
a. Radical surgery and radiotherapy are the mainstay of treatment
b. Choice of treatment depends on staging, age, and medical fitness of patients
2. Stage vs Treatment
a. Ia1 Simple hysterectomy
b. Ia2-IIa Radical hysterectomy and bilateral pelvic lymhadenectomy or RT
(Both achieve similar good cure rate but have advantages and disadvantages compared to each others)
c. IIb-IV Radiotherapy
3. Advantages of radical surgery :

a. Preservation of ovarian steroidogenesis
b. Better coital function
c. Avoid long term complications of RT
d. Accurate surgical staging & evaluation of aortic, pelvic LN
e. Psychological effect of extirpation of primary tumour
4. Disadvantages of radical surgery :
a. Immediate morbidity especially bladder and ureteric injury, excessive blood loss
b. Fistula formation
c. Bladder denervation
d. Lymphocyst
e. Obturator nerve damage
f. DVT/ paralytic ileus/ sexual dysfunction
5. Disadvantages of radiotherapy :
a. Bowel irritation (nausea, vomiting, diarrhoea)
b. Bowel ulceration (ischaemic change)
c. Subacute bowel obstruction
d. Chronic haemorrhagic proctitis
e. Rectovaginal fistula
Figure 70 Radiotherapy for cervical cancer.
f. Haemorrhagic cystitis / haematuria
Figure 71 Radical hysterectomy.

Postoperative pelvic irradiation
Some patients would require adjuvant radiotherapy after a radical hysterectomy because of:
1. Surgical specimen margin involvement
2. Positive pelvic LN
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Treatment of recurrent disease
1. Local recurrence:
a. Radiation
b. Pelvic exenteration
i. Extensive operation involves removal of bladder, rectum, uterus and vagina
ii. Require colostomy and ileal conduit
2. Distant recurrence:
a. Radiotherapy
b. Chemotherapy
Protocol, Follow up, as of 16 April 2004
Schedule
1. For patients with low risk for recurrence, the followed up plan is:-
a. 4 monthly in the first 2 years
b. 6 monthly thereafter from 3rd to 5th year
c. yearly follow up can be offered to patients with squamous cell carcinoma but not to patients with adenocarcinoma
2. More intensive follow up is offered to patients with high risk factors such as:-
a. large primary tumour
b. deep tumour invasion; parametrial involvement; lymphovascular invasion; positive lymph nodes
c. close resection margins
3. Patients are advised to return promptly if vaginal bleeding occurs.
Clinical Assessment
1. History taking and physical examination are conducted in every visit
2. Attentions should be given to the psychosexual dysfunction
Routine Investigations
1. Serial monitoring of the TA4 and/or CA125 are carried out in the first two years if they are elevated before the primary
treatment
2. Imaging studies is not routine practice but should be arranged as indicated clinically
3. Vault smear is not a routine
Prognosis
Stage 5-year survival
I 80%
II 50%
III 20%
IV 7%
Overall57%
Prevention
Routine Pap smear effectively reduces the incidence and mortality. Patients with abnormal smear result shouldbe referred for
colposcopy examination.
1. Why does the staging of cervical cancer still remain on clinical level?
2. Why is surgery not an effective treatment for stage IIB or beyond?
3. Which treatment, radical surgery or radiotherapy, would you advise to a young woman with stage Ia CA cervix but otherwise
healthy? And why?
4. In what way would the urinary tract get involved in CA cervix?
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Exenteration
It is an ultra major gynaecological surgery in which the midline pelvic organs including the uterus, rectum, and bladder are
excised. Urinary diversion and colostomy are required after exenteration. It is subclassified into:
1. Anterior exenteration radical hysterectomy together with total cystectomy
2. Posterior exenteration radical hysterectomy plus excision of rectum and rectosigmoid
3. Total exenteration anterior and posterior exenteration
It is indicated in and only in advanced primary or recurrent malignancy of the uterine cervix (or rarely uterine corpus) that has
invaded the bladder and/or rectum, but still confined to the pelvis, so that excision of these major pelvic organs may result in cure.
It is of high operative morbidity and mortality and patient selection for this surgery is very important.
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Staging of CA cervix
The carcinoma is strictly confined to the cervix
I
(extension to the corpus would be disregarded)
Invasive carcinoma which can be diagnosed only by microscopy, with deepest
Ia
invasion <5 mm and largest extension >7 mm
Ia1 Measured stromal invasion of <3.0 mm in depth and extension of <7.0 mm
Ia2 Measured stromal invasion of >3.0 mm and <5.0 mm with extension of <7.0 mm
Clinically visible lesions limited to the cervix uteri or pre-clinical cancers greater
Ib
than stage IA
Ib1 Clinically visible lesion <4.0 cm in greatest dimension
Ib2 Clinically visible lesion >4.0 cm in greatest dimension
Cervical carcinoma invades beyond the uterus, but not to the pelvic wall or to the
II
lower third of the vagina
IIa Without parametrial invasion
IIa1 Clinically visible lesion <4.0 cm in greatest dimension
IIa2 Clinically visible lesion >4.0 cm in greatest dimension
IIb With obvious parametrial invasion
The tumour extends to the pelvic wall and/or involves lower third of the vagina
III
and/or causes hydronephrosis or non-functioning kidney
IIIa Tumor involves lower third of the vagina, with no extension to the pelvic wall
IIIb Extension to the pelvic wall and/or hydronephrosis or non-functioning kidney
The carcinoma has extended beyond the true pelvis or has involved (biopsy
IV
proven) the mucosa of the bladder or rectum.
IVa Spread of the growth to adjacent organs
IVb Spread to distant organs
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4. Malignant neoplasms of uterine corpus
Endometrial hyperplasia
Classification
It is classified into four groups:
1. Simple (cystic) endometrial hyperplasia without atypia
a. Glands with single layer of glandular cells and dilated in a cystic pattern
b. Less than 1% chance of developing endometrial carcinoma
2. Simple endometrial hyperplasia with atypia
a. Glandular structure as above but individual cells nuclei are abnormal
b. About 5% chance of developing endometrial carcinoma
3. Complex endometrial hyperplasia without atypia
a. Glands are closely packed together with more than one layer. Cells nuclei are still normal
b. About 5% chance of developing endometrial carcinoma
4. Complex endometrial hyperplasia with atypia
a. Glands are closely packed together with more than one layer. Dyskaryotic cells are present
b. 10 to 15% chance of developing endometrial carcinoma
Causes
It is mainly secondary to chronic unopposed oestrogenic stimulation. Following patients are particularly at risk:-
1. Polycystic ovarian disease (PCOD)
2. Unopposed oestrogen due to hormonal replacement therapy in patients with intact uterus
Presentation
Menorrhagia, irregular menstrual bleeding
Diagnosis
By endometrial sampling:
1. Endometrial sampler
2. Vabra aspiration
3. Uterine curettage
Treatment
Patients with complex atypical hyperplasia should be advised to have hysterectomy. High dose progestogen therapy may be tried
if patients are very keen to keep uterus for pregnancy. Other types of hyperplasia can be managed with hormonal treatment.
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1. Simple hyperplasia without atypia

a. Give Norethisterone 5mg tds PO day 5-25
b. Repeat Vabra aspiration every 6 months until the endometrium shows normal tissue on two consecutive occasions.
i. If persistent simple hyperplasia without atypia, continue Norethisterone with adjusted dosage and monitor
with Vabra aspiration every 6 months
ii. If hyperplasia resolves with at least 2 consecutive normal Vabra results and fertility is wanted, refer to
infertility clinic for medical ovulation induction
2. Complex hyperplasia without atypia
a. If fertility is unwanted, counsel by FHKAM and advise hysterectomy because of risk of endometrial carcinoma
b. If fertility is wanted,
i. Give Megace: starting dose is 40 mg daily PO (can increase up to 160 mg/day)
ii. Repeat Vabra aspiration every 3 months until the endometrium shows normal tissue on two consecutive
occasions. If persistent hyperplasia without atypia, continue Magace with adjusted dosage and monitor with
Vabra aspiration every 3 months
iii. If hyperplasia resolves with at least 2 consecutive normal Vabra results and fertility is wanted, refer to
infertility clinic for medical ovulation induction
3. Hyperplasia with atypia
a. Counsel by FHKAM and advise hysterectomy because of risk of endometrial carcinoma
b. If hysterectomy is refused,
i. Give Megace: starting dose is 40 mg daily PO (can increase up to 160 mg/day)
ii. Repeat Vabra aspiration every 3 months until the endometrium shows normal tissue on two consecutive
occasions.
- If persistent hyperplasia without atypia, continue Magace with adjusted dosage and monitor with Vabra
aspiration every 3 months
- If persistent hyperplasia with atypia, counsel by FHKAM again and strongly advise for hysterectomy.
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Endometrial carcinoma
Incidence
1. Most common gynaecological malignancy in USA and Hong Kong, which is higher than cervical cancer. .
2. 600 new cases in Hong Kong, with an average rate of 11.8 in 100,000 in 2007.
3. Median age of onset:-55
Risk factors
Mainly related to chronic exposure of endogenous or exogenous oestrogen:-
- Early menarche and late menopause
- Nulliparity and infertility
- Exogenous oestrogens Oestrogen used alone without progestogen:-increases risk of CA endometrium by 4-9 time
- Polycystic ovary disease (PCOD) Chronic anovulation develops CA endometrium at an earlier age, accounts for most of
cases diagnosed before age 40
- Obesity Conversion of androstenedione to oestrone by fat cells, with subsequent conversion to oestradiol
- Hypertension
- DM 20% incidence of DM in patients with CA endometrium
Protective factors
- Pregnancy
- Oral contraceptive pills
Pathology
1. Histology type:
a. Majority (60%) is endometrioid adenocarcinoma which is the least aggressive type
b. Other types are papillary, clear cell adenocarcinoma, adenosquamous and squamous type which are in general more
aggressive
Figure 72 (Left to Right) Adenoacanthoma (Grade I); Adenosquamous carcinoma (Grade II); Clear cell carcinoma.
2. Grade:- Good correlation between grade and prognosis
Grade 1 well differentiated. Gland Grade 2 patchy differentiation. Gland Grade 3 This type consists of solid
forms are conspicuous. Mitotic figures forms are much less prominent and many masses of malignant cells of varying
are moderately numerous. deposits consist of infiltrating single cell sizes and shapes with little or no stroma.
columns or solid masses. Mitoses are numerous.
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Spread
1. Local Myometrium, Cervix and Adnexa
2. Lymphatic Pelvic and Para-aortic lymph nodes
3. Distant:-rare, to lungs.
Clinical features
1. Most cases present with abnormal vaginal bleeding:-Postmenopausal bleed, irregular short menstrual periods, menorrhagia
2. Rarely present with secondary symptoms:-Urinary or bowel symptoms
3. Physical examination:-Local signs are uncommon until it metastasis to cervix or beyond. Uterus may be enlarged
Diagnosis
Confirm with endometrial biopsy which can be obtained by:
1. Endometrial sampler
2. Vabra aspiration
3. Dilatation and curettage
Staging procedure
1. Surgical staging is used. Following preoperative assessments provide some ideas about the extent of the tumour:
a. USG, CT scan, or MRI of abdomen for liver, pelvic and paraaortic Lenlargement
b. Hysteroscopy to assess any cervical involvement; it replaces the old fashion method:-fractional curettage
c. Grading from histological examination
d. Cystoscopy, proctoscopy and examination under general anaesthesia if local spread is suspected
2. Surgical staging procedure:
a. Peritoneal cytology
b. LN Biopsy
c. Cut open the uterus after hysterectomy to look for the depth of myometrial invasion and the cervical invasion
d. See Staging of CA endometrium
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Management
1. Stage I Grade 1
a. TAHBSO
b. No need for lymhadenectomy (only 2 % involvement in stage I grade 1 disease)
c. Myometrial involvement >1/2, whole pelvic RT
2. Stage I Grade 2, 3
a. TAHBSO + LN sampling
i. 10% of LN involvement in grade 2
ii. 25-30% LN involvement in grade 3
- If pelvic LN +ve, need whole pelvic irradiation
- If para-aortic LN +ve, need progestogen or chemotherapy
b. If peritoneal cytology + ve
i. At risk of peritoneal recurrence
ii. Progestational agent
iii. Chemotherapy
iv. Intraperitoneal P32
3. Stage II
a. Radical hysterectomy; or
b. Whole pelvic irradiation followed by intracavity Cesium, followed by TAHBSO
4. Stage III and IV TAHBSO pre-op RT
Recurrence
Treat by progestational agents (effective in 1/3 recurrence) or chemotherapy
Prognostic factors
1. Histologic grading
2. Staging
3. Depth of myometrial invasion
4. Metastasis of lymph nodes
5. Peritoneal cytology
6. Cervical involvement
7. Adnexal involvement
8. (Uterine size is not a significant prognostic factor)
Prognosis
Stage 5-year survival
I 75%
II 50%
III 25%
IV 5%
Why the surgical treatment of early stage CA endometrium is is different from that of CA cervix?
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Staging of CA endometrium
Staging CA Endometrium FIGO 2006
I Tumour confined to the corpus uteri

Ia Invasion < half of the myometrium (denoted as a and b)
Ib Invasion > half of the myometrium (denoted as c)
II Tumour invades cervical stroma, but does not extend beyond the uterus
III Local and/or regional spread of the tumor

IIIa Tumor invades the serosa of the corpus uteri and/or adnexae
IIIb Vaginal and/or parametrial involvement
IIIc Metastases to pelvic and/or para-aortic lymph nodes
IIIc1 Positive pelvic nodes
IIIc2 Positive para-aortic lymph nodes with or without positive pelvic lymph
nodes
IV Tumour invades bladder and/or bowel mucosa, and/or distant metastases

IVa Tumor invasion of bladder and/or bowel mucosa
IVb Distant metastases, including intra-abdominal metastases and/or inguinal
lymph nodes
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5. Trophoblastic diseases
Gestational trophoblastic disease (Molar Pregnancy)
This is a group of disorders involving benign and malignant growth of trophoblastic tissue, and
is classified into:
- Hydatiform mole which is subclassifed into complete and partial
- Invasive mole
- Choriocarcinoma:-a rare but severe disease
- Placentasite tumour:-very rare
- Residual trophoblastic disease may follow a mole
Hydatiform mole
Also called molar pregnancy, is one form of gestational trophoblastic diseases and is further
subclassified into complete and partial mole.
Complete mole
- It is an abnormaconception without an embryo or foetus, but solely cytotrophoblastic and syncytotrophoblastic hyperplasia,
with loss of villous vascularity, causing gross hydropic swelling and centracistern formation.
- The karyotyping of the conception is usually 46XX
Incomplete mole
- It is an abnormaconception with presence of embryonic or foetaelement, and a mixture of normaappearing villi and
focavillous swelling and trophoblastic hyperplasia.
- The karyotyping of the conception is usually 69XXY or 69XXX, as a result of fertilisation of an ovum by two sperms or a
sperm that has duplicated chromosomes.
Epidemiology
- Common in Asian:-Asian to West ratio:-8:1
- 1 in 350 (HK); 1 in 82 (Taiwan); 1 in 1500 (USA)
- Higher risk < 20 and > 40 years of age
- Usually present between 8 and 24 weeks of gestation with peak at 14 weeks
- Vaginal bleeding (occurs between 6-16 weeks, 95%)
- Passed vesicular tissue vaginally
- Uterus large for date (50%)
- Hyperemesis gravidarum (30%)
- Bilateral thecal-luteacyst (15%)
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Complications
- Anaemia (due to massive haemorrhage)
- Uterine perforation (due to invasion or surgicaevacuation)
- Pelvic sepsis
- Clinical hyperthyroidism (10%, related to high HCG level)
- Residuatrophoblastic disease
- Pre-eclampsia
- Disseminated intravascular coagulopathy (DIC)
- Trophoblastic pulmonary embolisation (rare)
Remark:-clinical presentation is less severe and complications are less common in case of partial mole
Diagnosis
1. USG A complete mole has typical intrauterine vesicular features without foetal element. The differential diagnosis would
be cystic degeneration of an abortion. A partial mole may be difficult to detect under USG.
2. Biochemical There is a very high serum level of HCG in complete mole. The elevation of HCG level in partial mole is less.
Management
The mainstay of treatment is suction evacuation of uterus. The HCG level should be monitored post-operatively until it returns to
normal because of the risk of residual trophoblastic disease. Chemotherapy may be required if there is a persistent elevation of
HCG.
1. Classification of Trophoblastic Diseases

a. Non-invasive Mole
i. Partial Mole
ii. Complete Mole
b. Invasive Mole
c. Gestational Trophoblastic Tumour
i. Choriocarcinma
ii. Placental site trophoblastic tumour
2. Preoperative Investigations for patients with molar pregnancy
a. Plasma
i. beta Human Chorionic Gonadotrophin (HCG)
ii. CBP
iii. R/LFT
iv. Cross-match of blood
v. Thyroid Function Test
b. Abdominal and pelvic USG
c. CXR
3. Treatment
a. Suction evacuation of uterus
i. Obtain consent for hysterectomy from the patient before the procedure because uncontrollable haemorrhage
may occur during the procedure or as a result of uterine perforation
ii. Give syntocinon IV 10 mg after the suction curettage has been put inside the uterus
b. Second uterine curettage is not routinely performed. The procedure may be considered for patients with persistent
vaginal bleeding or suboptimal fall in beta HCG level
c. Emptying the uterus with oxytocic such as porstaglandins or oxytocin is contraindicated because the increased risk of
embolization of trophoblast
d. Hysterectomy may be contemplated in the following circumstances:
i. the patient has completed her family and has co-existing gynaecological problems that warrant a hysterectomy
ii. women with complications such as uterine perforation, uncontrollable haemorrhage
iii. residual trophoblastic disease found in the uterus
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4. Follow Up
a. Serial monitoring of plasma beta HCG is used to detect any residual trophoblastic disease
b. The follow up plan is as follow:
i. Weekly beta HCG is measured until the level has returned to normal.
ii. For those patients who have suboptimal fall in HCG, HCG would be checked weekly
iii. Monthly follow up is carried out in the first 12 months after evacuation of uterus
iv. Oral contraception is not recommended until beta HCG levels has returned to normal
v. Practice contraception for 1 year after the beta HCG has returned to normal is required to ensure complete cure.
vi. Beta HCG needed to be measured 6 weeks after any future delivery or abortion
5. Indications for Systemic Treatment in GTD
a. Histological evidence of choriocarcinoma
b. An abnormal regression pattern of HCG in terms of rising of by >10% or plateauing for three consecutive times
c. HCG level > 20,000 IU/ml noticed > 4 weeks after the evacuation
d. Persistently elevated HCG 6 onths after evacuation
e. Rising HCG in the absence of another pregnancy
f. Evidence of metastases
A histological diagnosis of GTD is not required for chemotherapy treatment.
6. Pre-Chemotherapy Work Up
a. Serum
i. CBP
ii. LFT
iii. RFT
iv. Beta HCG
b. Chest X ray
c. Ultrasound of the abdomen and pelvis
d. Lumbar puncture to collect cerebral spinal fluid for beta HCG, culture and sensitivity test, microscopy and biochemical
study. A CSF to serum level beta-HCG ratio exceeds 1:60 indicates CNS involvement
7. Subsequent Monitoring
While on chemotherapy, patients need weekly plasma beta HCG, CBP, LFT and RFT
8. Scoring of Risk Factors
a. Patients are classified as low, medium or high risk using the WHO Scoring system
b. Multiple agents chemotherapy is used for patients at medium or high risk
Prognosis
1. Complete mole (malignant:-15-20%)
2. Partial mole (smaller risk)
Invasive mole (Destructive mole, Villous choriocarcinoma)
Invasive mole is one kind of gestational trophoblastic diseases and is

always preceded by hydatiform mole. The abnormal trophoblasts
invade the myometrium and therefore it is much less readily removed
by evacuation. It may also metastasize to any part of the body such has
lung, liver, brain and vagina. Invasive mole usually presents as residual
trophoblastic disease with persistent vaginal bleeding and a high serum
human chorionic gonadotropin (HCG) level after evacuation of uterus.
Occasionally it presents with perforation of uterus as a result of
invasion. The diagnosis of invasive mole can only be confirmed by
histological examination of the uterus after hysterectomy, which is
rarely required nowadays, unless there is uncontrolled bleeding or
perforation. Therefore, invasive mole is usually managed as residual
trophoblastic disease with chemotherapy.
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Choriocarcinoma
This is a rare but highly malignant tumour and can arise from:-
- Product of gestation:-gestational choriocarcinoma, a kind of gestational trophoblastic disease)
- Ovaries (a kind of germ cell tumour of ovary)
Gestational choriocarcinoma
Incidence
1. 1 in 40,000 in the West and 1 in 13000 in the East
2. 50% arise from complete mole; 25% from abortion/ tubal pregnancy; and 25% from term gestation
Pathology
1. Highly malignant with invasion and necrosis of uterine wall

2. Predominantly vascular spread with pulmonary metastasis in 70% of cases
3. Secret HCG which can be used as a tumour marker for monitoring of the disease as well as a prognostic factor.
Treatment
Chemotherapy
Residual trophoblastic disease

It is a clinical diagnosis made when after evacuation of uterus for hydatiform mole, there is still evidence of persistent molar tissue
inside the body (e.g. Persistent high HCG). Residual trophoblastic disease can be due to invasive mole, or metastasis of the molar
tissue. Normally after the initial treatment of hydatiform mole, the HCG level will drop to pre-pregnant level gradually within a
few weeks. In some situation, however, the HCG level may stop to drop after reaching a plateau, or may even rise again.
Investigations including chest X-ray, lumbar puncture for HCG assay, and USG of liver should be performed to look for any
evidence of metastasis. Treatment is chemotherapy (choice according to Bagshawe score) which is often effective. The serum
HCG level should be checked to monitor the chemoresponse.
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Bagshawe score
The Bagshawe score is designed to classify patients with gestational trophoblastic diseases into low risk, medium and high risk
according to the prognostic factors. Each prognostic factor is assumed to act as an independent variable and the effects of the
factors are additive. It helps to guide the clinical management:
1. Low risk:-methrotrexate
2. Medium risk:-etoposide or actinomyocin D
3. High risk:-EMA/CO regimen
Prognostic factors score 0 score 1 score 2 score 4

Age (years) <39 >39 / /
Antecedent pregnancy Mole Abortion Term /
Interval between end of antecedent pregnancy
and start of chemotherapy (months) 4 4-6 7-12 12
HCG (iu/L) <103 103-104 104-105 >105
ABO group (female X male) / O X A or A X O B or AB /
Largest tumour / 3-5cm >5cm /
Site of metastases / Spleen, kidney GI tract, liver Brain
Number of metastases identified / 1-4 4-8 >8
Previous use of chemotherapy / / single drug 2 or more
The total score for a patient is obtained by adding the individual scores for each prognostic factor.
Total score:-<4=low risk; 5-7= medium risk; >8= high risk
Staging of GTD
FIGO staging of gestational trophoblastic diseases
Stage Disease development
0 Molar pregnancy
I Persistently elevated HCG titres (i.e. 6 months or more after evacuation) and tumour confined to body of uterus
II Pelvic and / or vaginal metastasis
III Pulmonary metastasis
IV All other distance metastases
Remark:-This staging system is not used by most major centres for trophoblastic diseases as it does not help in treatment planning.
The Bagshawe score which guides the use of chemotherapy is used more often.
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6. Disease monitoring and treatment in gynae-oncology
Tumour marker
A tumour marker is a biochemical substance that can indicate the presence of some kinds of neoplasic disease. It may be a product
or a component of cancer cells from where the tumour marker is secreted into the circulation. Measurement of the blood level of
the marker may be used as (1) a diagnostic test, (2) a screening test, or (3) for monitoring of the neoplastic disease and
effectiveness of treatment. An ideal tumour marker for a particular neoplasic disease should be:
1. Produced by and solely by that particular tumour (specific).
2. Always produced by that particular tumour (sensitive).
3. That the blood level of the marker is proportional to the volume of the tumour.
Examples of tumour marker in gynae-oncology:-
1. Alpha-feto protein for yolk sac tumour of ovary
2. Human chorionic gonadotropin for gestational trophoblastic diseases and choriocarcinoma
3. CA125 for ovarian epithelial carcinomas
CA125
It is a kind of tumour-associated antigens, uses as a tumour marker for ovarian epithelial carcinoma. It has several limitations:-
1. Although its level is elevated in 90% of advanced stage, it is only elevated in 50% of stage I disease and therefore is not a
good screening test for early disease.
2. It is also found in many benign gynaecological conditions such as endometriosis, uterine fibroid, adenomyosis, as well as
other malignant lesions of endometrium, endocervix, fallopian tube, pancreas. Therefore it is not specific.
3. It is not sensitive for mucinous type and borderline ovarian epithelial cancer.
4. The clinical use of CA125 is therefore mainly as a monitoring of the disease and effectiveness of treatment. The decline of
the level after chemotherapy implies good chemo-response, while an increase in level suggests recurrence of the disease.
Chemotherapy
Chemotherapy plays a major role in treatment of various gynaecological malignancies especially gestational trophoblastic disease,
ovarian germ cell tumour and ovarian epithelial carcinoma. It may also used to treat some cases of ectopic pregnancy (such as
cervical or residual ectopic pregnancy). The following discussion will concentrate on the role of chemotherapy in gynae-oncology.
Role of Chemotherapy
1. Curative role
a. Gestational trophoblastic diseases
i. Chemotherapy is the primary treatment in residual gestational trophoblastic diseases. The rapidly growing
trophoblastic cells are very sensitive to chemotherapy.
ii. The advantages over surgical treatment are:-
- Surgical morbidities are avoided. In particular, haemorrhage as the uterus would be very vascular.
- Distant spread of the disease can also be controlled with chemotherapy
- Uterus is preserved for future fertility.
iii. Usually a single cytotoxic agent, methrotrexate is used. It is very effective and has less side-effects. Other
cytotoxic drugs may be used depending on the Bagshawe score.
b. Ovarian germ cell tumours Ovarian germ cell tumours, such as dysgerminoma, malignant teratoma, yolk sac tumour
are very aggressive. However, because of good responses to chemotherapy, these kinds of tumours can be treated with
unilateral oophorectomy followed by chemotherapy. The remaining ovary can be preserved if not involved.
Dysgeminoma are sensitive to radiotherapy, yet chemotherapy is still the preferred choice because of less side-effects.
c. Other gynaecological tumours Cervical cancers, endometrial cancers, vulval and vaginal cancers are NOT
chemosensitive.
2. Adjuvant role Ovarian epithelial cancers are less chemosensitive to the germ cells counterparts. Chemotherapy is used as an
adjuvant treatment to surgical excision.
3. Palliative role Chemotherapy is seldom use for palliative treatment in gynae-oncology. Tamoxifen or progestogens may be
used for advanced stage of endometrial cancers.
4. Commonly used cytotoxic agents are Methrotrexate for gestational trophoblastic disease and platinum group for ovarian
epithelial carcinoma
- 315 -
Radiotherapy
Radiotherapy plays critical therapeutic role in gynae-oncology, especially squamous cell carcinoma of cervix. It is applied in two
major ways:-internal (bradytherapy) and external (teletherapy).
1. Bradytherapy:-
a. Radioactive substances are inserted into vagina, targeting at the cervix, parametrium, and vagina. It is used to treat
carcinoma of the lower genital tract
b. Complications are local skin effects, vaginal stenosis, cystitis and proctitis
2. Teletherapy:-
a. External beam of irradiation targeting at the pelvic and aortic lymph nodes where bradytherapy cannot reach
b. Complications are damages from small bowel and ovarian irradiation,
It is used as a primary curative treatment, adjuvant or palliative therapy, and can be either used alone or integrated with surgery
and cytotoxic chemotherapy:
1. Curative:- As a primary treatment for cancinomas of cervix, vagina and vulva.
2. Adjuvant:- After radical surgical treatment for cervical cancers (when risk of distant metastasis is high) and endometrial
carcinoma (beyond stage I)
3. Palliative:- For bone metastasis and pain control
Palliative
Palliative treatment in malignant diseases does not aim to cure but to improve a problem or condition such as symptomatic relief.
For example, radiotherapy or narcotic injection to relieve bone pain due to metastasis.
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Urogynaecology
0. Urogynaecology
Introduction
Urogynaecology is a subspecialty of gynaecology dealing with disorders of pelvic floor that result in two major problems:-genital
prolapse and urinary incontinence. It also deals with other lower urinary tract problems such as voiding disorder The diagnosis of
urinary disorders usually requires urodynamic study.

4. The physical examination and management of various types of genital prolapse which are usually vaginal hysterectomy with
pelvic floor repair (colporrhaphy), or conservatively with ring pessary.
5. The two main causes of urinary incontinence in female:-genuine stress incontinence and detrusor instability, and how to
differentiate them clinically and with urodynamic study.
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1. Genital prolapse
Genital prolapse
Definition
It is a group of disorders caused by weakness of the pelvic floor resulting in abnormal descend of various pelvic structures through
the vagina. These include:
1. Cystocele Backward descend of the urinary bladder into the vagina and beyond. It appears as a protrusion of the anterior
vaginal wall
2. Urethrocele Backward descend of the urethra into the vagina and beyond. It appears as a small protrusion of the distal end
of anterior vaginal wall
3. Rectocele Forward descend of the rectum into the posterior vagina. It appears a protrusion of the posterior vaginal wall into
the vagina and beyond
4. Enterocele Herniation of the pouch of Douglas which often contains loops of small bowel, through the upper part of the
posterior vagina.
5. Uterine prolapse
a. Downward displacement of the uterus towards or through the introitus
b. Divided into three degrees:
i. 1st degree:-descend of the cervix within the vagina and not through the introitus
ii. 2nd degree:-descend of the cervix, but not the whole uterus, through the introitus
iii. 3rd degree (or procidentia):-descend of the cervix and the whole uterus through the introitus, usually bringing
with it the cystocoele, enterocele and rectocele
6. Vault prolapse Prolapse of the vaginal cuff in the hysterectomized patient.
Incidence
Genital prolapse usually occurs after middle age, and affects 10% of multiparous women, and is very rare among nulliparous.
Aetiology
- The above pelvic organs are normally supported by the pelvic floor, which consists of levator ani and pelvic fascia. Its
weakness results in genital prolapse. The main factors leading to the deficiency are trauma (often as a result of childbirth),
and ageing (collagen lack of oestrogen support).
- Failure to support the vaginal vault by plicating it to the cardinal ligaments during hysterectomy may precipitate vault
prolapse subsequently, and colposuspension may also lead to enterocele or rectocele.
- Rarely, some genetic disorders associated with congenital weakness of collagen may contribute in a minority of patients.
Clinical features
All kinds of genital prolapse may present with a mass protruding out of the vagina spontaneously, or after coughing or straining. It
is usually reducible. The protruded mass causes dragging pain, discomfort during walking or standing, and may bleed secondary
to rubbing or laceration. Depends on the site and degree of prolapse, urinary, bowel or sexual problems may result:-
1. Cystocele and urethrole:
a. Stress incontinence, frequency of micturition, voiding difficulty
b. Rarely in severe case of cystocele, there are kinking at the ureterovesical junction, leading to bilateral hydronephrosis
2. Rectocele:- difficulty on defaecation
3. Uterine prolapse, vault prolapse:- discomfort during coitus, dyspareunia
4. Enterocele:- usually asymptomatic but rarely the enterocele may be performated leading to exposure of prolapsed small
bowel and consequently bowel injury
History
1. Assess the degree of prolapse and severity of symptoms
2. Look for any precipitating factors:-childbirth history and birth injury; chronic cough, etc
3. Ask for any medical illness and assess the physical fitness of patients
- 318 -
Physical examination
1. General examination and examination after other systems:-important as majority of patients are old and have some form of
medical illness. It help to assess whether patients are fit for surgery
2. Examination of genital prolapse
Diagnosis and Investigations

1. Investigate with urodynamic study when there are multiple urinary symptoms
2. Investigate for fitness if patients also have medical disorders
3. Decide the mode of treatment according to the type of prolapse, physical fitness and wish of patients
Treatment
1. Definite surgical correction is the mainstay of treatment which include:
a. Vaginal hysterectomy (for uterine prolapse)
b. Colporrhaphy (pelvic floor repair):-anterior colporrhaphy for cystocele & urethrocele; posterior colporrhaphy for
rectocele
c. Repair of enterocele
d. Sacrocolpopexy for vault prolapse
2. Conservative management with vaginal ring pessary may be considered when:
a. Patients are physically unfit for surgery
b. Patients refuse surgery
c. Temporary relief while patients are waiting for surgery
d. Patients are pregnant or want to preserve uterus for fertility (rare)
- 319 -
Cystocele
Figure 73 Cystocele
Urethrocele
Figure 74 Urethrocele
Rectocele
Figure 75 Rectocele
- 320 -
Enterocele
Figure 76 Enterocele
Uterine prolapse
Vault prolapse
See genital prolapse for detail
- 321 -
Examination of genital prolapse
Aim
To assess pelvic floor weakness, types and degree of genital prolapse and any urinary incontinence
Procedure
1. In lithotomy position:
a. Inspect the external genitalia, look for any prolapse or protrusion
b. Ask the patient to cough and look for any descend and stress incontinence
c. If a there is already a huge prolapse, confirm if it is a third degree by palpating the fundus (get above the prolapsed
mass), and then examine the vaginal wall and cervix for any ulcer or laceration
d. If there is no obvious prolapse or just a mild degree, proceed to the Sim speculum examination
2. In Sims position:
a. Ask the patient to lie on her left, with the buttock at the right edge of the coach, and the right hip and knee flexed. Ask
the patient to hold up the right buttock with her right hand will provide a better exposure of the genitalia
b. Insert a Sim speculum with adequate lubrication to the vagina, and retract the posterior vaginal wall. This would
facilitate the examination of the anterior wall. Cystocele and urethrocele appear to bulge backwards. Sometimes a
cystocele may obscure the view of the cervix
c. Inert a pair of sponge-holding forceps to retract the anterior wall. This would help to expose the cervix.
d. With the sponge-holding forceps retracting anteriorly, slowly withdraw the sim speculum. Enterocele will appears as a
bulge from the upper posterior vaginal wall, and the rectocele from the lower vaginal wall.
3. Digital examination
a. Perform a bimanual pelvic examination
b. Assess the size and mobility of the uterus if vaginal removal is feasible
c. Look for any ovarian masses, presence of which may affect the choice of surgery
d. Assess the space of the pelvis is enough for vaginal surgery
e. Assess the distance between the posterior fornix and symphysis pubis in case a ring pessary is required
Finally a rectal examination may be necessary to differentiate rectocele from a enterocele, and to assess the anal tone If the genital
prolapse cannot be demonstrated at that moment, ask the patient to walk around for a while and re-examine later.
Sims speculum
- 322 -
Pad test
Pad test is a simple bedside assessment to verify and quantify urine loss. The patient wears a preweighed sanitary towel, drinks
500ml of water and rests for 15 minutes. After a series of defined manoeuvers the pad is reweighed. A urine loss of more than 1g
is considered significant.

1. The pad test (test) is performed when the patient has a full bladder, which is usually at the end of the filling cystometry
(after filling up the bladder with normal saline).
2. The patient should not be menstruating or having excessive vaginal secretion.
3. Test duration normally lasts for 10 minutes.
4. The test is performed in a separate room outside the urodynamics room.
5. The same electronic weighing machine should be used throughout the test.
6. Two gynae pads (pads) and one square white linen (linen) are to be used for the test.
7. Weigh pads and linen before test. Record the total weight in grammes (g).
8. Give the pads to the patient to put inside her underpants / panties, and the pads should be secured against the perineum.
9. Perform standardised exercise in area covered by pre-weighed linen:
a. Walk for 50 metres on level ground at usual pace. This can be done by asking the patient to walk a 5-metre distance
to-and-fro 10 times.
b. Climb 5 steps.
c. Cough for 5 times.
d. Perform heel-bounce for 5 times.
e. Perform sit-and-stand for 5 times.
f. Place hands in running tap water at comfortable temperature for 1 minute.
10. Pads and linen (if soiling occurs during test) are weighed at completion of the test. Record the total weight in grammes (g).
Ring pessary
A device made of silicon or plastic used as a conservative management for genital prolapse. It is put into the vagina so that it rests
in the posterior fornix and sits over the symphysis pubis. It is indicated when the patients are unfit or refuse surgical treatment,
want to preserve fertility, or as a temporary relief while waiting for surgery. However, it is ineffective in severe degree of genital
prolapse. There are various sizes of ring pessaries in reference the diameter of the ring in minimetre. The size should fit the patient,
as it would fall out when it is too small, or cause voiding difficulty, laceration or pressure necrosis, and infection of vagina when it
is too big. The appropriate size is the one with a diameter equal to the distance between the posterior fornix and the symphysis
pubis (can be assess by digital vaginal examination). After it is inserted, the patient should be asked to walk around and void to
see if any discomfort. The patient should also be followed every 6 months for changing the pessaries, and look for any
complications.
Figure 77 Ring pessary
- 323 -
Colporrhaphy
It is the vaginal surgical repair of the pelvic floor as the treatment of genital prolapse. It is often performed together with vaginal
hysterectomy.
Anterior colporrhaphy is the plication of the pubocervical fascia (a part of the pelvic fascia between the bladder and the vagina) so
that the descended bladder (cystocele) is elevated with the support of the fascia. It is however not a effective treatment for genuine
stress incontinence (50% success rate). The risk of the operation is perforation of the bladder.
Posterior colporrhaphy is the plication of the part of levator ani muscle between the posterior vaginal wall and the anterior rectal
wall, so that the herniated rectum (rectocele) is reduced by the reinforced muscle. It is often performed together with the repair of
the perineum (perinorrhaphy). The risks of the procedure are perforation of rectum, dyspareunia secondary to tight vaginal
opening after repair.
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1. Opening up the anterior vaginal wall. 2. Mobilising cystocele from vaginal walls.
3. Mobilising cystocele from cervix. 4. Placing the tightening sutures as far laterally as possible.
6. Removing redundant vaginal wall.This is followed by closure

5. Obliteration of the cystocele completed with interrupted absorbable sutures
ANTERIOR COLPORRHAPHY
- 325 -
POSTERIOR COLPOPERINEORRHAPHY
- 326 -
REPAIRMENT OF ENTEROCELE
- 327 -

Definition of Pelvic Organ Prolapse
1. Symptoms Associated with Pelvic Organ Prolapse
The feeling of a lump (something coming down), low backache, heaviness, dragging sensation, or the need to digitally
replace the prolapse in order to defaecate or micturate, are amongst the symptoms women may describe who have a
prolapse.
2. Pelvic Organ Prolapse
Pelvic organ prolapse is defined as the descent of one or more of: the anterior vaginal wall, the posterior vaginal wall, and
the apex of the vagina (cervix / uterus) or vault (cuff) after hysterectomy. Absence of prolapse is defined as stage 0 support;
prolapse can be staged from stage I to stage IV.
3. Anterior Vaginal Wall Prolapse (AVWP)
a. Anterior vaginal wall prolapse is defined as descent of the anter ior vagina so that the urethrovesical junction (a point 3
cm proximal to the external urinary meatus) or any anterior point proximal to this is less than 3 cm above the plane of
the hymen.
b. This term should replace the term cystocoele.
4. Prolapse of the Apical Segment of the Vagina (PASV)
a. Prolapse of the apical segment of the vagina is defined as any descent of the vaginal cuff scar (after hysterectomy) or
cervix, below a point which is 2 cm less than the total vaginal length above the plane of the hymen.
b. This term should replace the terms uterine prolapse and vaginal vault prolapse.
5. Posterior Vaginal Wall Prolapse (PVWP)
a. Posterior vaginal wall prolapse is defined as any descent of the posterior vaginal wall so that a midline point on the
posterior vaginal wall 3 cm above the level of the hymen or any posterior point proximal to this, less than 3 cm above
the plane of the hymen.
b. This term should replace the term rectocoele.

Outpatient Management Protocol
1. First degree uterine prolapse other prolapse(s)
a. There is no need to insert ring pessary immediately.
b. Refer to Urogynaecology Clinic if the patient has one or more of the following problems:
i. Concurrent urinary symptoms.
ii. Large symptomatic cystocoele and/or rectocoele.
iii. Patient worries.
2. Second or third degree uterine prolapse other prolapse(s)
a. No ulceration
i. Insert ring pessary.
ii. Prescribe Dienoestrol cream once per week.
iii. Refer Urogynaecology Clinic for further assessment.
b. Ulceration but no bleeding
i. Prescribe Dienoestrol cream once daily.
ii. Refer Urogynaecology Clinic (within 2 weeks) for further assessment.
c. Ulceration with bleeding
i. Admit.
ii. Consult Urogynaecology Team.
iii. Take HVS for culture
iv. Check fasting blood sugar.
v. Insert obstetric tampon soaked with Dienoestrol cream.
vi. Reassess lower genital tract condition within 48 hours.
vii. If bleeding stops and ulceration starts to heal, insert ring pessary and discharge patient.
viii. Prescribe Dienoestrol cream once daily.
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2. Urinary incontinence
Urgency
Urgency is the complaint of a sudden compelling desire to pass urine which is difficult to defer. Motor urgency is associated with
uninhibited detrusor contractions. The most common cause is detrusor instability. Sensory urgency is due to irritable lesions such
as cystitis, calculus in which the detrusor is stable.
Incontinence
See urinary incontinence
Urinary incontinence
Introduction
Urinary incontinence is defined as an involuntary loss of urine which is objectively demonstrable and cause a social or hygienic
problem (definition of International Continence Society). It is reported to be very common in reproductive aged women and
postmenopausal women (20%). It is subdivided into various types (see below). Majority are belonging to stress incontinence and
urge incontinence.
Types of urinary incontinence

1. Stress incontinence Involuntary loss of urine when the intra-abdominal pressure is increased, such as during exercise,
coughing, and sneezing. It is most commonly due to genuine stress incontinence. Sometimes detrusor instability may present
as stress incontinence, and urodynamic study may be required to differentiate them.
2. Urge incontinence Inability to withhold the passage of urine with a sudden strong desire to micturate (urgency), due to
hyperexcitability of the bladder detrusor muscle. Hyperexcitability can be primary or secondary to infection or irritation of
the bladder wall.
3. Overflow incontinence Involuntary loss of urine due to when the intravesical pressure exceeds maximum urethral pressure
due to bladder distension and in the absence of detrusor activity. It is secondary to bladder outflow obstruction.
4. True incontinence Involuntary loss of urine due to a defect in the anatomical integrity of the urinary tract, such as
vesicovaginal fistula
What medical students should know

- Definitions of various urinary symptoms
- Genuine stress incontinence and detrusor instability, and how to differentiate them clinically and with urodynamic study.
- Principles of treatment of the above diseases
Stress incontinence
Involuntary loss of urine when the intra-abdominal pressure is increased, such as during exercise, coughing, and sneezing. It is
most commonly due to genuine stress incontinence or detrusor instability. See urinary incontinence for detail.
Urodynamic Stress Incontinence (USI)

Urodynamic stress incontinence is noted during filling cystometry and
is defined as the involuntary leakage of urine during increased
abdominal pressure, in the absence of a detrusor contraction. This
term should replace the term Genuine Stress Incontinence (GSI).
Genuine stress incontinence

Genuine stress incontinence is the involuntary loss of urine resulted
from an increase in intra-abdominal pressure, which is transmitted to
the bladder, and to an extent that exceeds the maximum urethral
pressure. The detrusor muscles remain quiescent (do not contract) and
do not contribute to the increase of the intracystic pressure.
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Urge incontinence
Overflow incontinence
The involuntary loss of urine when the intravesical pressure exceeds maximum urethral pressure due to bladder distension and in
the absence of detrusor activity.
True incontinence
Reflex incontinence
The involuntary loss of urine due to abnormal spinal reflex activity in the absence of the sensation to micturate.
Colposuspension
Colpo means vagina. Each side of the vaginal vault are 'suspended' by stitching it to the ipsilateral iliopectineal ligament. The
bladder neck is therefore elevated. It is one of the most effective continence surgery (90%). The surgical complications are de
novo detrusor instability (5%), voiding disorder (5%), development of enterocele or rectocele.
Urethropexy
The bladder neck is approached through a suprapubic incision and elevated by suturing
the paraurethral tissues to adjacent structures such as the rectus sheath or the
ilio-pectinealligament. These operations are more difficult than vaginal urethroplasty,
especially in obese women. Some operators employ a laparoscopic technique
Urethral Sling Operations

A sling of synthetic material,sutures or tendon is passed under the urethra and attached to
the rectus muscles or adjacent ligaments. This requires a combined vaginalsuprapubic
approach and is the most difficult of the 3 methods.
Figure 78 Burch's colposuspension

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Definitions of urinary symptoms
Urinary Incontinence is the complaint of any involuntary leakage of urine.
Stress Incontinence / Stress Urinary Incontinence (SUI) is the complaint of involuntary leakage on effort or exertion, or on
sneezing or coughing.
Urge Incontinence / Urge Urinary Incontinence (UUI) is the complaint of involuntary leakage accompanied by or
immediately preceded by urgency.
Mixed Urinary Incontinence (MUI) is the complaint of involuntary leakage associated with urgency and also with exertion,
effort, sneezing or coughing.
Urgency is the complaint of a sudden compelling desire to pass urine which is difficult to defer.
Nocturia is the complaint that the individual has to wake at night one or more times to void.
Frequency is the complaint by the patient who considers that the patient voids too often by day.
Nocturnal Enuresis is the complaint of loss of urine occurring during sleep.
Slow Stream is reported by the individual as his or her perception of reduced urine flow, usually compared to previous
performance or in comparison to others.
Intermittent Stream (Intermittency) is the term used when the individual describes urine flow which stops and starts, on one
or more occasions, during micturition.
Hesitancy is the term used when an individual describes difficulty in initiating micturition resulting in a delay in the onset of
voiding after the individual is ready to pass urine.
Straining Straining to void describes the muscular effort used to either initiate, maintain or improve the urinary stream.
Suprapubic pressure may be used to initiate or maintain urine flow.
Incomplete Emptying is a self-explanatory term for a feeling experienced by the individual after passing urine.
Post micturition dribble is the term used when an individual describes the involuntary loss of urine immediately after the
patient has finished passing urine, usually after after rising from the toilet.
Polyuria is defined as the measured production of more than 2.8 litres of urine in 24 hours in adults.
Nocturnal polyuria is present when an increased proportion of the 24-hour output occurs at night (normally during the 8 hours
whilst the patient is in bed).
Acute Retention of Urine (AROU) is defined as a painful, palpable or percussable bladder, when the patient is unable to pass
any urine.
Chronic Retention of Urine (CROU) is defined as a non-painful bladder, which remains palpable or percussable after the
patient has passed urine. Such patients may be incontinent.
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Non-surgical Treatment Modalities of Urinary Incontinence
1. Lower Urinary Tract Rehabilitation
a. is defined as non-surgical, non-pharmacological treatment for lower urinary tract function and includes:
b. Pelvic floor training defined as repetitive selective voluntary contraction and relaxation of specific pelvic floor
muscles.
c. Biofeedback the technique by which information about a normally unconscious physiological process is presented
to the patient and/or the therapist as a visual, auditory or tactile signal.
d. Behavioural modification
i. Defined as the analysis and alteration of the relationship between the patients symptoms and his or her
environment for the treatment of maladaptive voiding patterns.
ii. May be achieved by modification of the behaviour and / or environment of the patient.
2. Electrical Stimulation
a. Electrical Stimulation is the application of electrical current to stimulate the pelvic viscera or their nerve supply.
b. The aim of electrical stimulation may be to directly induce a therapeutic response or to modulate lower urinary tract,
bowel or sexual dysfunction.
3. Catheterisation Catheterisation is a technique for bladder emptying employing a catheter to drain the bladder or a urinary
reservoir.
4. Intermittent Catheterisation Intermittent (in/out) Catheterisation is defined as drainage or aspiration of the bladder or a
urinary reservoir with subsequent removal of the catheter.
5. Indwelling Catheterisation Indwelling catheterisation: an indwelling catheter remains in the bladder, urinary reservoir or
urinary conduit for a period of time longer than one emptying.
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3. Other topics in urogynaecology
Frequency of micturition
It is voiding more than 7 times a day, or being woken twice or more for voiding at night whilst asleep (nocturia). It can be due to:
1. Bladder irritation
a. Cystitis
b. Bladder stone
c. Detrusor instability
2. Decrease of functional volume of bladder
a. Cystocele
b. Bladder outflow obstruction and retention of urine
3. Increase of urine production Diabetes mellitus
Nocturia
Being woken twice or more for voiding at night whilst asleep. See also frequency of micturition for causes of nocturia and
frequency.
Dysuria
Pain during micturition. It is a symptom of urethritis or cystitis.
Interstitial cystitis
A chronic condition which presents with severe frequency of micturition, urgency, lower abdominal pain, dysuria and haematuria
in the absence of bacterial cystitis. At cystoscopy, ulcers with a granulomatous base and surrounding hyperaemia are found.
Biopsy of the lesion shows chronic non-specific ulceration.
Voiding disorder
Causes
- Urinary voiding disorder is less common in female than in male. It is either due to outflow obstruction, or inadequate
detrusor contractions. Sometimes it may be too painful to void in situations such as post-vaginal surgery, or urethritis.
- The causes of obstruction in female include:-large fibroids, or other pelvic masses, severe cystocele.
- Inadequate detrusor pressure can be due to various kinds of neurological disorders involving the central nervous system, or
the sacral plexus (neuropathic bladder). After regional anaesthesia, patients may also lose the sensation of bladder filling as
well as the motor function.
Clinical features
Patient with chronic voiding difficulty usually complain of hesitancy, frequency of micturition, nocturia, poor stream of urine,
incomplete emptying, straining to void. Acute urinary retention may develop. On examination during acute episode, a full bladder
is demonstrated, and a large volume of residual urine is drained on catheterization. There are also complications such as recurrent
urinary tract infection.
Investigation
Uroflowmetry would show a low peak flow rate with a prolonged voiding time. There is also residual urine.
Detrusor Overactivity (DO)

Detrusor overactivity is an urodynamic observation characterised by involuntary detrusor contractions during the filling phase
which may be spontaneous or provoked. There is no lower limit for the amplitude of an involuntary detrusor contraction but
confident interpretation of low pressure waves (amplitude smaller than 5 cm of H2O) depends on high quality urodynamic
technique. This term should replace the term Detrusor Instability (DI).
Detrusor Overactivity Incontinence (DOI)

Detrusor overactivity incontinence is incontinence due to an involuntary detrusor contraction. This term should replace the term
Urethral Sphincter Incompetence + Detrusor Instability (USI + DI).
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Detrusor instability
Definition
Abnormal contractions of the bladder muscle (detrusor) occur spontaneously or in response to a stimulus (e.g. Filling of bladder,
coughing, sound of running water, etc), when the individual is attempting to inhibit micturition.
Aetiology
It can either be primary (idiopathic) or secondary to cystitis, urinary stones, atrophy, neuropathy, or post-surgery (de novo DI).
Clinical features
Urinary symptoms including:-urgency, frequency of micturition, urge incontinence, stress incontinence.
Diagnosis
Cystometry is diagnostic. It shows detrusor activities on provocation during the filling phase of the cystometry. Other features
are:-gradually increased of baseline deterusor pressure during filling. Early occurrence of the first sensation of urgency. It is
essential to differentiate detrusor instability from genuine stress incontinence because the treatments are different from each other.
Incorrect diagnosis and consequently wrong treatment will even make the problem worse.
Treatment
1. Bladder retraining, biofeedback, hypnotherapy:-successful in 60% of cases
2. Medicine
a. Anti-cholinergices (oxybutynin)
b. Amitriptylline (imipramine)
3. Surgery (Last resort)
As both detrusor instability and genuine stress incontinence can present with stress incontinence. Are there any differences
between the two in term of symptomatology?
Urodynamic study
The two most commonly performed urodynamic studies are: (1) Cystometry; and (2) Uroflowmetry. Occasionally video
cystourethrography or urethral pressure profilometry may be indicated.
Uroflowmetry
It is a simple non-invasive urodynamic study in urogynaecology, used to investigate voiding disorder. It is usually performed
together with cystometry. The patient is asked to void to a toilet which is sensitive to the change of volume over time, from which
the urine flow rate is estimated. The peak flow rate should be more than 15ml/s, and the normal flow curve is bell-shaped and
duration of voiding. should not be prolonged. The urine volume should be at least 150ml as flow rates with a small volume are not
reliable. Low peak flow rate, prolonged flow indicates a voiding disorder, which can be due to obstruction, or a neuropathic
bladder.
Cystoscopy
An endoscope is inserted via the urethra into the urinary bladder allowing examination of the interior wall. Biopsy and excision
surgery can be performed during cystocopy. It is indicated for:
1. Multiple irritable bladder symptoms such as urgency, dysuria, frequency of micturition, haematuria, in which case chronic
cystitis (e.g. Interstitial cystitis), bladder stones are suspected
2. Investigation of urinary fistula
3. Staging of cervical cancer
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Cystometry
It is one of the most commonly performed urodynamic study in urogynaecology, in which the detrusor activity during filling of
the bladder and a series of provocation is assessed. The detrusor pressure (the pressure generated by the detrusor contractions)
cannot be measured directly but is calculated by subtracting intraabdominal pressure from intracystic pressure. It is mainly used to
differentiate detrusor instability from genuine stress incontinence. The indications are:-
1. Multiple urinary symptoms:- urge incontinence, urgency, frequency of micturition, stress incontinence are suggestive of
detrusor instability and cystometry is indicated to confirm the diagnosis. Isolated stress incontinence is almost always due to
genuine stress incontinence and cystometry is not essential.
2. Previous unsuccessful continence surgery:- to assess the severity of residual urinary problem and diagnosis of de novo
detrusor instability
3. Pre-continence surgery assessment:- Occasionally cystometry may be indicated before corrective surgery for genuine stress
incontinence to detect any subclinical pre-existing detrusor instability and voiding disorder which may get worse after surgery
4. Other conditions:-voiding disorder, neuropathic bladder
How to perform cystometry

1. Setting
a. Ask the patient to empty the bladder. Usually the patient voids on the flowmeter as uroflowmetry is usually performed
at the same setting.
b. Catheter the bladder. The residual urine volume is recorded
c. Insert a smaller fluid-filled catheter into the bladder via the urinary catheter. It is connected to an external pressure
transducer for measurement of the intracystic pressure
d. Insert another catheter into the rectum for measurement of the intraadbominal pressure
2. Filling phase
a. The bladder is then filled up with normal saline at room temperature gradually at a rate of 10 to 100ml/min
b. During filling, the following information are recorded over time:
c. The changes in the volume, the intracystic pressure and intraabdominal pressure
d. The time and volume at which the patient has the first and maximal desire to void
e. Provocative tests are performed, with the following methods:
f. Coughing, change of position
g. Fast filling of bladder
h. Running water
3. Voiding phase
a. After the maximal filling capacity of the bladder is reached, the patient is asked to stand up and cough. Any leaking of
urine is documented
b. The patient is finally ask to void on the uroflowmeter again
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Normal results and interpretation
1. First desire to void:-150-200ml
2. Maximal capacity:-400-600ml
3. Detrusor pressure rise during filling phase:-< 15cmH2O (abnormal high pressure indicates poor compliance of the bladder)
4. Absence of systolic detrusor contractions during filling and on provocation (Presence is diagnostic of detrusor instability)
5. No leakage on coughing (leaking in the absence of systolic detrusor contractions indicate genuine stress incontinence)
6. Voiding detrusor pressure rise:-< 70cmH2O with a peak flow rate of > 15ml/s for a volume over 150ml
7. Residual urine volume:-< 50ml
Can you explain why the detrusor pressure is equal the difference between the intracystic pressure and the intraabdominal
pressure?
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Definition of Urodynamic Studies
Urodynamic Studies (UDS)

Urodynamic studies involve the assessment of the function and dysfunction of the urinary tract by any appropriate method.
Aspects of urinary tract morphology, physiology, biochemistry and hydrodynamics affect urine transport and storage. Other
methods of investigation such as the radiographic visualisation of the lower urinary tract is a useful adjunct to conventional
urodynamics.
Conventional Urodynamic Studies

Conventional urodynamic studies normally take place in the urodynamic laboratory and usually involve artificial bladder filling.
Filling Cystometry
Filling cystometry is the method by which the pressure/volume relationship of the bladder is measured during bladder filling.
Intravesical Pressure
Intravesical pressure is the pressure within the bladder.
Abdominal Pressure
Abdominal pressure is taken to be the pressure surrounding the bladder. In current practice it is estimated from rectal, vaginal
or, less commonly, from extraperitoneal pressure or a bowel stoma. The simultaneous measurement of abdominal pressure is
essential for the interpretation of the intravesical pressure trace.
Detrusor Pressure
Detrusor pressure is that component of intravesical pressure that is created by forces in the bladder wall (passive and active). It
is estimated by subtracting abdominal pressure from intravesical pressure.
Post Void Residual (PVR)

Post void residual is defined as the volume of urine left in the bladder at the end of micturition. This term can be used
interchangeably with Residual Volume (RU) or Post Void Residual Bladder Volume (PVRBV).
Normal Detrusor Function

Normal detrusor function: allows bladder filling with little or no change in pressure. No involuntary phasic contractions occur
despite provocation.
Detrusor Sphincter Dyssynergia (DSD)

Detrusor sphincter dyssynergia is definec as a detrusor contraction concurrent with an involuntary contraction of the urethral
and/or periurethral striated muscle. Occasionally, flow may be prevented altogether. Although acute retention is usually thought
of as painful, in certain circumstances pain may not be a presenting feature, for example when due to prolapsed intervertebral
disc, post partum, or after regional anaesthesia such as an epidural anaesthetic. The retention volume should be significantly
greater than the expected normal bladder capacity. In patients after surgery, due to bandaging of the lower abdomen or
abdominal wall pain, it may be difficult to detect a painful, palpable or percussable bladder.
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Drugs
0. Drugs
The following groups of drugs are commonly used in O&G:
1. Oxytocics
2. Tocolytics
3. Anti-hypertensives
4. Anti-convulsants
5. Steroid and Hormonal replacement therapy
6. Antibiotics
7. Anticoagulants
The followings drugs are discussed in previous chapers.

1. Analgesics during labour
2. Insulin
3. Contraceptives
a. Combined oral contraceptives
b. Rogestogen-only pills (mini pills)
c. Progestogen injectable
4. Ovulation induction agents clomiphene citrate
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1. Oxytocics
Definition
1. From Greek:-oxys:-sharp, quick; tokos:-childbirth (from tiktein:-to bear); meaning hastening labour.
2. It is a group of agents that are able to stimulate myometrial contractions.
3. Common oxytocics include:
a. Oxytocin or syntocinon
b. Prostaglandins and their analogue
c. Ergometrine
Indication of oxytocics
1. In Obstetrics
a. Induction of labour and augmentation of labour
b. Prophylaxis and treatment of uterine atony
2. In Gynaecology:- Evacuation of uterus in abortion, and termination of pregnancy
Complications of oxytocics
1. Uterine hyperstimulation, resulting in uterine rupture and severe bleeding
2. Water intoxication with oxytocin
3. Gastrointestinal and cardiorespiratory complications with prostaglandins
4. Hypertension with ergometrine
Oxytocin
What is oxytocin
It is a peptide hormone secreted from the hypothalamus and transported to the posterior lobe of the pituitary where it is eventually
released.
What are the effects of oxytocin

It has two major actions in human:-
1. Firstly, it stimulates smooth muscle contraction in uterus (oxytocic)
a. It is essential for the initiation and progression of labour
b. It binds to oxytocin receptors of myometrial cells and activate the contractile protein
c. The number of oxytocin receptors increases gradually as pregnancy go on, and exponentially before onset of labour.
The production of receptors is stimulated by prostaglandins
d. A positive feedback loop acts on the pituitary secretion of oxytocin. More oxytocin is secreted as uterine contractions
are stimulated and continued
2. Secondly, it stimulates contractions of myoepithelial cells of mammary glands. It facilitates lactation
3. Besides, as its biochemical structure is similar to that of vasopressin (antidiuretic hormone also secreted from the posterior
pituitary gland), it also has weak antidiruetic effect.
How is oxytocin metabolised

The peptide is rapidly broken down into amnio acid by oxytocinase in blood. The half-life of oxytocin is therefore 3-4 minutes.
What are the clinical uses of oxytocin

See syntocinon for clinical uses.
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Syntocinon
Syntocinon is a synthetic oxytocin, and has the same biochemical structure, pharmacokinetic and pharmacodynamic
characteristics as oxytocin. It is given intravenously, as a bolus injection or infusion.
Clinical use of syntocinon

1. Intrapartum use:-
a. For induction of labour and augmentation of labour. Syntocinon is given as intravenous infusion. The rate of infusion
is titrated against the frequency of uterine contractions. The optimal frequency is 3 to 4 contractions in 10 minutes.
Care must be taken to avoid uterine hyperstimulation.
b. To overcome uterine inertia in the second stage delivery of twin pregnancy. Uterine contractions may diminish after
the first twin is delivered, and the second twin may not descend. Augmentation is required to hasten the delivery of
the second twin
2. Postpartum use:-
a. As an alternative of routine syntometrine in the third stage of labour against uterine atony. It is given as a bolus
injection.
b. As a prevention or maintenance treatment against uterine atony in high risk cases such as placenta praevia, abruptio
placentae, twin pregnancy. It is given by continuous infusion
3. Other uses:-
a. As an adjuvant agent for evacuation of uterus in treatment of abortions
b. As an oxytocic in a stress test:- Syntocinon was used to stimulate uterine contractions in a stress test for foetal
well-being. This test is rarely required nowadays as less invasive tests for foetal well-being are now available.

1. Regimen
a. For induction and augmentation of labour:
i. Start infusion using either infusion drip set or syringe pump (see table 1), and titrate the infusion rate accordingly.
ii. Maintain the infusion rate if adequate contractions (3 to 4 contractions per 10 minutes) are achieved, till the next
cervical assessment.
iii. Inform medical officer if more than 20 mu/min of oxytocin is required to achieve optimal uterine contractions.
b. For intrapartum managment third stage of labour:
i. IV bolus 5 units over 1-2 minutes, or
ii. IM bolus 10 units if no IV access available and in absolute emergency (unlicensed route). Patients with cardiac
disease or those particularly at risk of hypotension should have the IV bolus 5 units given slower i.e. over 5
minutes
iii. iv infusion 40 units in 500ml crystalloid solution Q4H once
2. Midwives can administer syntocinon bolus injection at third stage of labour according to departmental standing order.
Risks of syntocinon
The major risk is uterine hyperstimulation, which would result in foetal distress and uterine rupture. The other risks are less
common and mild, and include hypotension (related to direct peripheral vasodilatation), water intoxication (related to anti-diuretic
effect).
Syntometrine
It is a combined drug consisting of 5 mg of syntocinon and 0.5mg of ergometrine. It is commonly given intramuscularly during
the third stage of labour routinely as a prophylaxis against uterine atony and postpartum haemorrhage. It is given as a regimen of 1
ampoule IMI. The syntocinon component acts quickly in 2 minutes and produces clonic uterine contractions while the ergometrine
component stimulates sustained tonic contractions. It is contraindicated in cardiac diseases, hypertension and asthma because of
vasocontrictive effects of ergometrine. Midwives can administer routine syntometrine injection at third stage of labour according
to standing order.
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Ergometrine
A compound oxytocic consisting of syntocinon and ergometrine used for prophylaxis or treatment of uterine atony in the third
stage of labour. It is given intramuscularly. It has the advantages of both syntocinon and ergometrine. It is contraindicated in
hypertension because of vasoconstrictive effect of ergometrine.
Prostaglandin
What are Prostaglandins
They are groups of compounds derived from unsaturated 20 carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase
pathway. It was thought to be come from the prostate gland from which its name originated. It is now well known that
prostaglandins are found in many organs with diverse physiological effects in human. The most important groups of
prostaglandins in obstetrics and gynaecology are prostaglandin E (PGE) and prostaglandin F (PGF). They are involved in the
process of ovulation, initiation of labour, and pathogenesis of dysmenorrhea and menorrhagia. Synthetic PGE and PGF are also
used in various obstetric situation including cervical ripening for induction of labour, treatment of uterine atony, and in
gynaecological conditions such as termination of pregnancy and treatment of abortion.
Misoprostol
Introduction
- A prostaglandin E1 analogue. Originally used for prevention and treatment of gastric ulcers associated with the use of
nonsteroidal anti-inflammatory drugs.
- Has become an important drug in obstetrics and gynaecology because of its uterotonic and cervical ripening actions.
Pharmacology
1. Administration and absorption:-
a. Can be given orally or vaginally.
b. After oral administration, misoprostol is rapidly absorbed and converted to its pharmacologically active metabolite,
misoprostol acid. Plasma concentrations of misoprostol acid peak in 30 minutes and decline rapidly thereafter.
c. After vaginal administration, plasma concentrations peak in 1 to 2 hours and then decline slowly, resulting in slower
increases and lower peak plasma levels, but overall exposure to the drug is increased.
d. Uterine contractility becomes plateaued 1 hour after oral administration. When given vaginally, uterine contractility
increases continuously for 4 hours and reaches a maximum level higher than that when given orally.
2. Metabolism and excretion:- It is primarily metabolised in the liver and less than 1% of it is excreted in urine.
Side effects
1. Side effects are dose-dependent and less severe when the drug is administered vaginally.
2. Fever, chills and shivering.
3. Gastrointestinal upset:-Nausea, vomiting, diarrhea, abdominal pain.
4. Unlike prostaglandin E2 and F2, it would not cause bronchospasm or myocardial infarction.
5. Teratogenicity:-limbs defects, ring-shaped constrictions of the extremities, arthrogryposis, hydrocephalus, holoprosencephaly,
Mobius syndrome (congenital facial paralysis) are reported.
Obstetric and gynaecological Indications

1. Medical termination of pregnancy
a. When combined with mifepristone, can be used for termination of pregnancy at a gestation less than 9 weeks.
i. Oral mifepristone 600mg followed 48 hours by oral misoprostol 400mcg, or
ii. Oral mifepristone 200mg followed 48 hours by oral misoprostol 600mcg
b. Efficacy:
i. 95% complete abortion rate when used before 7 completed weeks
ii. 90% complete abortion rate when used between 8 to 9 completed weeks
2. Treatment of miscarriage
3. Cervical ripening before surgical abortion
4. Induction of labour
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Misoprostol (Cytotec)
1. Nature A PGE-1 analogue of the prostaglandin group
2. Indications
First line treatment for:-
a. First and second trimester miscarriages to evacuate the uterus
b. Second trimester medical induced abortion
c. Cervical ripening prior to mechanical cervical dilatation for first trimester suction termination of pregnancy
3. Caution Patients with high risk for uterine rupture, hypersensitivity, severe cardiac disease.
4. Adverse reactions Uterine rupture
5. Side effects GI upset, vomiting, diarrhoea, pyrexia
6. Route of administration Oral or vaginal
7. Regimen
a. For medical evacuation of the uterus for first trimester miscarriage, 400micrograms every 4 hours for 3 doses orally.
b. For medical evacuation of the uterus for second trimester abortion (spontaneous or induced), 400micrograms every 3
hours vaginally for 5 doses. May repeat the course if necessary. If 2 courses fail, consider change to gemeprost.
c. For cervical ripening prior to mechanical cervical dilatation for first trimester suction termination of pregnancy,
200micrograms single dose vaginally 3 hours before the procedure
8. Discussion / Justification
a. Vaginal Misoprostol is more effective than Gemeprost in second trimester TOP.
b. Vaginal route of Misoprostol is more effective than oral Misoprostol in second trimester induced abortion
c. For cervical priming, oral Misoprostol is better than vaginal Gemeprost with greater baseline cervical dilatation and
easier dilatation.
d. For cervical priming, 200mcg vaginally is as effective as 400mcg vaginally
e. For cervical priming, vaginal Misoprostol is more effective if given 2-4hrs prior to surgery than oral Misoprostol given
8-12 hrs prior to surgery.
Gemeprost (Cervagem)
1. Nature PGE-1 analogue of the prostaglandin group
2. Indications
a. Second line treatment for second trimester induced or spontaneous abortion
b. Second line treatment for cervical ripening prior to first trimester suction termination of pregnancy
3. Cautions Cardiovascular disease, hypersensitivity
4. Adverse reactions Uterine rupture
5. Side effects Vaginal bleeding, uterine pain, GI upset, vomiting, headache, flushing, pyrexia
6. Route of administration Vaginal pessary inserted high into the posterior vaginal fornix
7. Regimen
a. 1 pessary 3 hours before surgery if used for cervical ripening
b. 1 pessary at 3-hourly interval to a maximum of 5 administrations if used for medical evacuation of uterus. Treatment
should be continued for the full course unless complete abortion occurs earlier.
c. If abortion is not established after 5 pessaries, a second course of treatment may be instituted starting 24 hours after the
initial commencement of treatment.
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Prostaglandin E2 (Dinoprostone)
1. Nature A PGE-2 analogue of the prostaglandin group
2. Indications
a. Induction of labour
b. Softening and dilatation of cervix before induction of labour
3. Caution Patients with high risk for uiterine rupture, hypersensitivity
4. Adverse reactions Uterine hyperstimulation, foetal distress, uterine rupture
5. Side effects GI upset, vomiting, pyrexia
6. Route of administration Vaginal pessary inserted high into the posterior vaginal fornix
7. Regimen -
a. 1 tablet every 4-6 hours
b. Maximum dosage 3 tablets
Sulprostone
1. Nature A PGE2-analogue (c.f. dinoprostone)
2. Indication for induction of abortion or induction of labour after intra-uterine death when other treatment has failed
3. Contraindications
a. Asthma
b. Cardiac disease
c. Hepatic or renal failure
4. Regimen
a. Add 500mcg to 250ml of NS for infusion
b. Infuse at 100mcg per hour
c. May infuse continuously for 10 hours
d. Never exceed infusion rate of 500mcg per hour
e. Maximum total dosage of 1500mcg
5. Side effects:- Nausea, vomiting, diarrhoea, headache, fever
Hemabate (Carboprost)
1. Nature Carboprost tromethamine (PGF2-alpha)
2. Indication Severe postpartum haemorrhage due to uterine atony
3. Regimen
a. 250 ug imi. NOT for IVI.
b. Same dose may be repeated after 15 minutes, for at most 8 doses.
4. Side effects
a. Common side effects include diarrhea, vomiting, fever, and hypertension.
b. Serious side effects such as asthma and pulmonary oedema are rare.
a. Heart failure or severe heart diseases
b. Chronic lung disease with respiratory failure
c. Renal or liver impairment
d. Hypersensitivity to Hemabate
6. Monitoring Continuous SaO2 monitoring
7. Remark
a. Hemabate is stored in the freezer compartment of the fridge in labour ward.
b. Concurrent administration of Maxolon is advised to relief GI upset.
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2. Tocolytic
Definition
In Greek toco means labour; lysis means dissolve; It is a group of agents that cause relaxation of uterine muscle and hence
dissolution of labour. It is opposite to oxytocic
Common tocolytic agents

1. Beta-sympathomimetic
a. Ritodrine
i. It is administered by continuous intravenous infusion, usually indicated for suppression of preterm labour.
ii. The rate of infusion is titrated against the frequency of uterine contractions.
iii. Maternal side effects are:
- Tachycardia and hypotension
- Heart failure and pulmonary edema
- Hypokalemia and hyerglycemia
iv. Foetal side effects are:
- Foetal tachycardia
- Foetal distress secondary to maternal hypotension
b. Hexoprenaline
i. It is usually given in bolus intravenous injection
ii. It is a short acting agent used mainly for uterine relaxation during external cephalic version (ECV) and relief of
uterine hyperstimulation
iii. Types of side effects are similar to ritodrine but severity is much less because it is short-acting, and often
adminstered in a single bolus rather than by continuous infusion
2. Prostaglandin inhibitors Sulindac
a. It is a kind of non-steroidal anti-inflammatory drugs (NSAID) that inhibit cyclooxygenase in the synthesis of
prostaglandin from arachidonic acid.
b. It is administered orally
c. Maternal side effects are not pronounced; foetal side effects not common but include oligohydramnios, patent ductus
arteriosus
3. Calcium channel blocker Nifedipine
a. It is administered orally
b. Maternal side effects are headache, flushing, hypotension and tachycardia
Indications of tocolytics
1. Preterm labour
a. The main aim of tocolytics is to allow more time for glucocortiocord to effect on lung maturation, in order to prevent
neonatal respiratory disease (RDS) and other complications of prematurity
b. The first line treatment has been ritodrine until recently nifedipine has been proven to be as effective but less side
effects than ritodrine
2. External cephalic version Short-acting agents like hexoprenaline improve the chance of success by relaxing the uterus
3. Uterine hyperstimulation Short-acting hexoprenaline may also help to relax the uterus rapidly and relieve foetal distress
during uterine hyperstimulation
Contraindications
1. When continuation of pregnancy is of higher risk than inhibition of labour:
a. Chorioamnionitis
b. Abruptio placentae
2. When the pregnancy has reached a maturity of low neonatal mortality or morbidity:- at 34 or more weeks of gestation
3. When there are co-existing maternal disorders that may be worsen with the tocolytics:-
a. Beta-sympathomimetic are contraindicated in thyrotoxicosis and major heart diseases
b. Prostaglandin inhibitors are contraindicated in thrombocytopenia and peptic ulcer diseases
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General Guideline
1. Types
a. Calcium channel blockers:-nifidepine
b. Beta-adrenergic agonists:-salbutamol, ritodrine, hexoprenaline
c. Oxytocin antagonists:-atosiban
d. Prostaglandin antagonists:-sulindac
2. Indications
a. Suppression of preterm labour before 34 weeks Nifidepine > Ritodrine > Sulindac
b. Prophylaxis against preterm labour eg. after laparotomy, cervical cerclage Nifidepine
c. Prior to external cephalic version Hexoprenaline
d. Uterine hyperstimulation Hexoprenaline
e. Uterine inversion Hexoprenaline
a. Obstetric complications:- Antepartum haemorrhage, abruptio placentae, chorioamnionitis
b. Maternal complications:- Pre-eclampsia
c. Foetal complications:-IUGR, foetal compromise
d. Medical diseases of which the condition may be exacerbated by side effects of certain tocolytics:
i. Beta-adrenergic agonists:- (Ritodrine and Hexoprenaline)
- Severe cardiac diseases (e.g.heart failure, aortic stenosis or arrhythmia)
- Poorly controlled hyperthyroidism or taking beta-blocker for control of tachycardia
- Poorly controlled diabetes mellitus
ii. Prostaglandin antagonists:- (Sulindac)
- Asthma
- Drug allergy
- Thrombocytopenia
- Renal, cardiac, hepatic impairment
- Peptic ulcer
4. Special precautions
Discuss with Mid-call 2 if tocolytics are used in:
a. Rupture of membranes
b. Cervical dilatation of > 4 cm
c. Multiple pregnancy
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Nifedipine (as tocolytics)
1. First episode of preterm labour <34 weeks
a. First line treatment
i. Initial dosage
- Adalat sublingual 10mg capsule
- Repeat the same dosage every 15 minutes until contractions cease
- Total maximum dosage 40mg
ii. Maintenance dosage:
- Oral Adalat 20mg q8h for 3 days
- Start 6 hours after the initial sublingual dose
- Titrate against response and side-effects
- Can increase dosage, firstly to 20mg q6h then up to 40 mg q6h on the first day
- From day 4 onwards, give oral Adalat GITS (extended release) 60mg tablet once daily until 34 weeks
- Withhold maintenance treatment after completion of antenatal steroids (48h) if there is rupture of membranes
2. Recurrent preterm labour (labour suppressed in previous episode)
a. Sublingual Nifedipine of initial dosage as above
b. Withhold maintenance regime i.e. adalat GITS while sublingual regime is being given
c. Once labour is suppressed, restart maintenance regimen i.e.oral Adalat retard followed by Adalat GTS
3. Nursing Orders
a. BP/P Q15 mins for 12 hours, then Q1H for 24 hours if stable, then QID/Q4H if stable. Inform if BP <90/60 or P>140
b. RR Q1H for 12 hours, off if stable.
c. Continuous foetal heart monitoring. Inform if >180.
d. Monitor symptoms:- flushing, nausea, vomiting, palpitations, chest pain, dyspnoea, hypotension, inform if severe.
e. Maintenance fluid:-Hartmanns solution 500 ml q6h
f. Input/ output chart
g. No need to take blood for electrolytes, haemoglucostix, glucose
4. Change of tocolytic agent if:
a. Failure of Nifedipine declared, due to any of the following:
i. Persistent uterine contractions 2 hours after initiation of nifedipine
ii. Progress in cervical dilatation
b. Intolerable maternal side effects
i. Flushing or headache, change to Salbutamol
ii. Significant hypotension, maternal tachycardia, change to Sulindac
c. Foetal side effect Foetal tachycardia, change to Sulindac
Sulindac
1. Nature NSAID.
2. Indication
As third line treatment of preterm labour when both Nifedipineand Ritodrine are contraindicated
3. Regimen
200mg po Q12H for 4 doses
a. Asthma
b. Drug allergy
c. Renal, cardiac, hepatic impairment
d. Peptic ulcer
e. Thrombocytopenia
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Atosiban
1. Nature oxytocin and vasopressin antagonist
2. Introduction
a. Competitive antagonist for oxytocin receptors
b. Peak plasma concentration 2-8mins after IV injection
c. Half-life 16mins
3. Indication
a. As a second line tocolytic for threatened preterm labour / preterm labour before 34 weeks.
b. Indicated if nifedipine, the first line tocolytic, fails despite maximal dose, or has to be ceased due to side effects.
a. Allergy to Atosiban
b. Contraindication for tocolysis
5. Administration
a. Loading bolus dose:-7.5mg/ml solution (as in original ampoule), give 0.9ml ivi over 1 minute.
b. High dose loading infusion:
i. Start after loading bolus dose completed
ii. 7.5mg/ml solution x 10 ml (2 x 5ml vials in brown box) diluted to 100ml with normal saline
iii. Infusion rate 24ml/hour (18mg/hour or 300mcg/min)
iv. Total duration 3 hours
c. Low dose infusion:
i. Start at 3 hours after initial bolus
ii. 7.5mg/ml solution x 10 ml (2 x 5ml vials in brown box) diluted to 100ml with normal saline
iii. Infusion rate 8ml/hour (6mg/hour or 100mcg/min)
iv. Maximum duration:-till 48 hours after initial bolus dose
5. Possible side effects
a. Nausea and vomiting - for maxalon injection
b. Dizziness and hot flushes
c. Tachycardia and hypotension
d. Hyperglycaemia
e. Injection site reaction
6. Monitoring during Atosiban therapy
a. Check BP / pulse:-Q15mins for the initial 3 hours, then Q1H if stable
b. Continuous foetal heart monitoring
c. Monitor maternal symptoms of nausea, vomiting, palpitations, dizziness
d. Monitor for hyperglycaemia and hypokalaemia by checking plasma glucose and RFT at 12h, 24h, and 48h after initial
loading dose
e. Monitor fluid input/ output (give maintenance fluid Hartmann's solution 500ml q6h)
7. Change to other tocolytic agents if
a. Failure of Atosiban declared:
i. Persistent painful uterine contractions
ii. Progress in cervical dilatation
iii. Change to Salbutamol unless contraindicated
b. Intolerable maternal side effects:
i. Significant hyperglycaemia
ii. Hypokalaemia < 2.8
iii. Maternal tachycardia > 140/min
iv. Foetal tachycardia > 180/min
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Salbutamol
Protocol, as of 1 August 2002
1. Indication
Beta-agonist as second line treatment of preterm labour.
2. Regimen
a. Prepare infusion solution of 50 microgram/ml by adding 25 mg of salbutamol solution into 500 ml NS
b. If fluid restriction is necessary, can give higher concentration at 200 ug/ml by adding 10mg of salbutamol into 40 ml
NS and administer through syringe driver
c. Start infusion rate at 10 ug/min.
d. Increment at 15 minute-interval by 5ug/min until:-
i. Uterine contractions are suppressed
ii. Maximun dosage attained (45ug/min)
iii. Complications arise
3. Caution
a. Stop or reduce infusion if:-
i. Maternal pulse >140 bpm or BP<90/60mmHg
ii. Hypokalemia (serum level< 2.8mmol/L)
iii. Foetal tachycardia > 180 bpm
iv. Remark:-mild degree of hyperglycemia can be tolerated. Consult medical obstetrics team for any problem of
glucose control.
b. Stop infusion and inform mid-call 2 if pulmonary oedema
c. Maintain dosage for 1 hour after uterine contractions have subsided, then reduce by 50% decrements at six-hourly
interval. Aim to give Salbutamol for steroid to work
d. Consider third line tocolytic agent with midcall-1 if:
i. The above complications arise, or intolerable side effects
ii. Contractions not suppressed despite maximum dosage of ssalbutamol
4. Monitoring in labour ward
a. NPO
b. Intravenous fluid add up to 83ml/hr
c. BP/pulse Q15min
d. Respiratory rate Q1H
e. Haemoglucostix/serum glucose/electrolytes Q4H (Q1H in case of DM requiring insulin treatment)
f. I/O chart
g. SaO2 as required
h. Continuous foetal heart monitoring
i. Note adverse effects:-palpitations, chest pain, dyspnoea, hypotension, pulmonary oedema
a. See general contradindications for tocolytic agent
b. Severe cardiac diseases and arrhythmia
c. Poorly controlled hyperthyroidism or taking beta-blocker for control of tachycardia
d. Poorly controlled diabetes mellitus
e. Consult medical obstetrics team for concern in the use of ritodrine in patients with the above medical disease.
Hexoprenaline
1. Indications
a. Uterine relaxation for ECV
b. Uterine relaxation in uterine hyperstimulation
c. Uterine relaxation in uterine inversion
2. Regimen
a. In ECV or uterine inversion IV bolus 10ug given in 3 equally divided doses every 2 minutes.
b. In uterine hyperstimulation IV bolus 5ug. Can only repeat once if no improvement after 2 minutes.
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Ritodrine
1. Indication
Beta-agonist as second line treatment of preterm labour.
2. Regimen
a. Effective dosage:-150-350ug/min.
b. Start with 50ug/min, increment at 15 minute-interval by 50ug/min until:-
i. Uterine contractions are suppressed, or
ii. Maximun dosage attained (350ug/min), or
iii. Complications arise
3. Caution
a. Stop or reduce infusion if:
i. Maternal pulse >140 bpm or BP<90/60mmHg
ii. Hypokalemia (serum level< 2.8mmol/L)
iii. Foetal tachycardia > 180 bpm
iv. Remark:-mild degree of hyperglycemia can be tolerated. consult medical obstetrics team for any problem of glucose
control.
b. Stop infusion and inform mid-call 2 if pulmonary oedema
c. Maintain infusion rate for at least 6 hours after contractions have ceased, and up to 24 hours for steroid to work
d. Consider third line tocolytic agent with midcall-1 if:
i. The above complications arise, or intolerable side effects
ii. Contractions not suppressed despite maximum dosage of ritodrine
4. Monitoring in labour ward
a. NPO
b. Intravenous fluid add up to 83ml/hr
c. BP/P Q15min
d. Respiratory rate Q1H
e. Haemoglucostix/serum glucose/electrolytes Q4H (Q1H in case of DM requiring insulin treatment)
f. I/O chart
g. SaO2 as required
h. Continuous foetal heart monitoring
i. Note adverse effects:-palpitations, chest pain, dyspnoea, hypotension, pulmonary oedema
a. See general contraindications for tocolytic agent
b. Severe cardiac diseases and arrhythmia
c. Poorly controlled hyperthyroidism or taking beta-blocker for control of tachycardia
d. Poorly controlled diabetes mellitus
e. Consult medical obstetrics team for concern in the use of ritodrine in patients with the above medical disease.
1. Can you explain why prenatal use of NSAID is associated with oligohydramnios and neonatal patent ductus arteriosus?
2. Can you explain why ritodrine is associated with hypokalemia and hyperglycemia?
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3. Anti-hypertensives
The role of anti-hypertensives in obstetrics is to prevent complications of hypertension such as stroke. It is indicated In patients
with pre-existing hypertension, or severe pre-eclampsia. However, it cannot alter the progress of pre-eclampsia, which would only
be resolved after delivery. The commonly used anti-hypertensives in obstetrics are:
Methyldopa
It is a centrally acting agent that causes peripheral vasodilatation given orally, and requiring a high loading dose because of long
half life, therefore not for acute control. It is very safe in pregnancy, and is therefore the first choice for long term treatment during
antenatal period. Side effects include depression, nightmares and postural hypotension.
Hydralazine
It is a potent direct smooth muscle relaxant leading to vasodilatation, usually given in bolus intravenously for acute control, and
also for maintenance therapy when given as infusion. Side effects include headache, nausea and palpitation
1. Indication
a. As second-line treatment for intrapartum anti-hypertensive treatment in pre-eclampsia
b. May be used in postpartum
2. Regimen
a. Bolus
i. 5 mg IV slowly in 1 min.
ii. Observe for effect over 20 minutes. Repeat if BP remains high (i.e. SBP > 160 or DBP > 100) after 20 minutes
iii. Consider giving pre-load crystalloid fluid such as 250ml Hartmann solution over 30 minutes if repeated doses of
hydralazine are given, particularly if there is haemoconcentration.
iv. If fail to control the BP with 2 bolus doses, for infusion regime.
b. Infusion:-
i. Consult medical obstetrics team before starting hydralazine infusion
ii. Start with 5 mg/h (i.e. 5 ml/h ) (Dilute 100 mg of hydrallazine into 100 ml with normal saline).
iii. Titrate against BP with an increment of 5 mg/h every 20 minutes.
3. Caution:- Action of IV hydralazine peaks at 20 minutes, therefore less than 20 minute interval of increment or repeated
dosage is not recommended
Nifedipine
Acts quickly when given orally or sublingually, effective for acute control. Slow releasing form is effective as maintenance. The
main side effect is headache
1. For postpartum use only.
a. Oral Adalat 5 mg as an alternative to IV hydralazine if SBP> 160 or DBP > 100.
b. Repeat after 15 minutes if blood pressure is not controlled
2. Adalat Retard (slow release):- Start with 20mg bd, can increase up to 40mg bd
3. Caution if used with MgSO4, as interaction may cause severe hypotension.
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Labetolol
It is an alpha and beta-adrenergic blocker that causes peripheral vasodilatation. It is mainly used postnatally because of the risk of
IUGR after long term use. It can be given orally for maintenance, or intravenously for acute control. It is contraindicated in heart
failure.
1. Nature Alpha and Beta-blocker
2. Indications
a. For intrapartum blood pressure control, if hydralazine causes maternal tachycardia >120, or other significant side
effects.
b. For postpartum blood pressure control as first line if being given MgSO4. (Since Nifedipine cannot be given.)
3. Regimen:
a. Infusion:
i. Start with 20 mg/h (i.e. 20 ml/h) (Dilute 100 mg of labetalol into 100 ml with normal saline).
ii. Titrate against the BP with an increment or reduction by 5-10 mg/h (i.e. 5-10 ml/h) at 15-30 min interval.
iii. Maximum rate should not exceed 100 mg/h.
iv. Stop infusion if maternal heart rate < 70/min, and restart at a lower infusion rate when heart rate > 70/min.
b. Bolus regime:
i. Only used for malignant hypertension.
ii. Instruction to be given by consultant or anaesthetist.
c. Oral regime:
i. For postpartum use only, as first-line if MgSO4 is being used.
ii. Start with 200 mg bd.
iii. Should not be used in the presence of pulmonary edema and heart failure.
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4. Anticonvulsants
1. Indications
a. Prophylaxis in pre-eclampsia and eclampsia
b. Treatment of eclampsia and epilepsy.
2. Drugs used in pre-eclampsia and eclampsia
a. Magnesium sulphate MgSO4
b. Diazepam
c. Phenytoin for patients with epilepsy who has been on long-term phenytoin
d. Thiopentone to be prescribed by anaesthetist
3. Drugs used in epilepsy should be decide by physician/ neurologist
4. Antenatal patients should receive oral vitamin K 10mg once daily from 36 weeks onwards
Diazepam
Diazepam is used as an anticonvulsant to stop acute seizure in eclampsic patients. It is given as an intravenous bolus. It may also
be used as a prophylactic agent but it would require continuous intravenous infusion. It is less effective than MgSO4 as a
prophylaxis, and sedation of mother and neonatal depression are the concerns.
Protocol, as of 22 December 2007
1. Indications
a. As immediate treatment for the convulsing eclamptic patient
b. As second-line anticonvulsant prophylaxis in severe pre-eclampsia and eclampsia if MgSO4 is contraindicated or fails
to control convulsions, or causes significant toxicity.
2. Regimen for the convulsing patient:
a. 5-10 mg slow IV bolus injection over 1 minute.
b. Total bolus dose preferably does not exceed 30 mg before delivery.
3. Prophylaxis regimen:
a. Loading dose:
IV bolus of 10 mg over 2 min (if diazepam has just been given to stop convulsion, decrease the loading dose by the
amount that was given)
b. Maintenance dose:
i. Start at 3 mg/h (18 ml/h, 80 mg of diazepam into 500 ml with 5% dextrose).
ii. Titrate at hourly interval so that patient is sedated but arousable, by increment of 2 mg/h until maximum rate of 10
mg/h (62 ml/h) is reached.
iii. Maximum daily dose is 3 mg/kg/ 24h.
iv. Continue till 24 hours after delivery or 24 hours after the last convulsion, whichever occurs later.
4. Monitoring and management of toxicity:
Conscious state and respiratory rate hourly.
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Phenytoin
1. Indications
a. As prophylaxis for eclampsia in severe pre-eclamptic patients in circumstances where phenytoin is decided by midcall
2 and neurologist to be the preferred agent
b. As treatment for epilepsy as prescribed by neurologist
2. Remarks
a. Should liase with neurologist and decide by midcall 2 before commencement
b. Generally, MgSO4 is still the first line prophylactic and treatment drug for severe PET/eclampsia in epileptic patients.
3. Regimen as prophylaxis for PET patients
a. Loading dose
i. At time 0 hour, give 10mg/kg made up to 50ml with Hartmann"s solution as intravenous infusion over 20 minutes
ii. At time 2 hours, give 5mg/kg made up to 50ml with Hartmann"s solution as intravenous infusion over 20 minutes
b. Maintenance dose At time 12 hours and every 8 hours thereafter for 4 days, given as 200mg i.v. or oral
4. Monitoring
a. Phenytoin level should be checked on day 1-2 before the morning dose (day of delivery counts as day 0) to avoid
toxicity
b. Inadequate phenytoin level without convulsion does not necessarily require increase in dosage
c. Cardiac monitoring if patient has cardiac disease
Magnesium Sulphate
Indication of Magnesium sulphate
It is an anticonvulsant for prophylaxis against development of eclampsia, or prevention of recurrent convulsions. It has been
shown to be more effective than diazepam in preventing recurrence of convulsions. It does not have side effect of neonatal
depression.
Administration of Magnesium sulphate

It is administered by bolus injection intramuscularly, followed by intravenous infusion for maintenance.
Side effects of Magnesium sulphate

Magnesium sulphate antagonizes calcium in the muscle contractility and nerve conduction. The side effects are therefore muscle
paralysis and cardiac arrest. The therapeutic range is narrow:-
Plasma level (mmol/l) Effect

2-4 Therapeutic
>5 Loss of patella reflex
>6 Prolonged AV conduction
>7.5 Respiratory arrest
>12 Cardiac arrest
Therefore, it is important to monitor the reflex, respiration, ECG for sign of toxicity during administration of MgSO4. As
magnesium is excreted via the renal system, the dosage have to be decreased when the urine output is diminished.
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1. Indication:
a. First-line anti-convulsant for prophylaxis in severe pre-eclampsia
b. Prevention of recurrence in eclampsia.
2. Regimen:
a. Loading dose:
IV bolus infusion of 4g (8ml of 50% MgSO4 diluted with normal saline to 20ml)
- Over 20min for severe pre-clampsia, or
- Over 5min for eclampsia.
b. Maintenance dose:
IV infusion at 1g/hr till 24 h after delivery or the last convulsion, whichever occurs later.
(20ml of 50% MgSO4 diluted with normal saline to 50ml infuse at rate of 5ml/h).
c. Caution: MgSO4 should be used with caution in patient with renal impairment, neuromuscular disease or respiratory
depression Decrease the infusion rate of maintenance dose to 0.5g/hr
3. Patient convulses while giving MgSO4:
a. If convulsion occurs / recurs during loading infusion, complete the loading over 5min.
b. If convulsion occurs during maintenance infusion, add IV bolus of 2g over 5min (4ml of 50% MgSO4 diluted with
normal saline to 10 ml).
c. Caution: recurrent eclampsia can be managed with a further 2g bolus of MgSO4 but alternative anti-convulsant or
intubation should be considered if a total 10g of bolus has been given
4. Monitoring while on MgSO4:
a. Output hourly
b. Deep tenon reflex hourly(e.g. Patellar reflex, or biceps reflex if patient is / has been on regional anaesthesia)
c. Respiratory rate hourly.
d. SaO2 continuously.
e. Mg level monitoring
i. Routine serum is not necessary, but
ii. In patient with renal impairment, it should be monitored every 6 hourly.
5. Management of MgSO4 toxicity
a. Signs of MgSO4 toxicity:
i. Slurred speech, double vision, absent deep tendon reflexes and respiratory depression may be symptoms and signs
of toxicity.
ii. Absence of deep tendon reflexes:
b. Stop MgSO4
c. Monitor:
i. Check respiratory depression
ii. Continue cardiac monitoring
iii. Check urgent serum Mg level
d. Give IV 1g (10ml of 10%) Ca gluconate over 10min
6. Respiratory depression (respiratory rate <10/min):
As for Absence of deep tendon reflexes, plus
a. Give O2 via mask to maintain SaO2 >95%
b. Consult anaesthetist for need of respiratory support
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5. Steroids and Hormonal Replacement Therapy
Dexamethasone
Benefit of Glucocorticoid therapy for preterm pregnancy
Glucocorticoid therapy has been showed to reduce various neonatal complications of prematurity such as respiratory distress,
intraventricular haemorrhage, necrotizing enterocolitis.
Indications of Glucocorticoid therapy

1. Patients undergoing preterm labour
2. High risk of preterm delivery
a. After an episode of antepartum haemorrhage due to placenta praevia or of unknown origin
b. Foetal complications that may require preterm delivery such as severe IUGR
c. Maternal complications such as pre-eclampsia that may require preterm delivery
Complications of Glucocorticoid therapy

Side effects of steroid therapy are uncommon and mild. Repeated course of steroid however may result in foetal complications
such as adrenal suppression.

1. Indication Give at 24-34 week for foetal lung maturation
2. Regimen 6mg im/iv Q12H for 4 doses
3. Contraindications:-
a. Chorioamnionitis
b. Active TB
4. Special precautions Poorly controlled diabetes mellitus
5. Weekly dexamethasone
a. Decision of the treatment should be made by FHKAM, and the need of continuation of the treatment should be
reviewed regularly.
b. Should not be given unless the risk of preterm delivery is high and persistent such as:
i. PPROM
ii. Triplet pregnancy or other higher-order multiple pregnancies
iii. Twin-twin transfusion syndrome
iv. IUGR or severe polyhydramnios
v. Pre-eclampsia
vi. Placenta praevia with antepartum haemorrhage
vii. Vasa praevia
c. Not mandatory in the following conditions:-
i. APH of unknown origin, single episode
ii. Preterm labour suppressed by tocolytic therapy in the current pregnancy
iii. Cervical incompetence treated with elective cerclage
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Steroid Cover
1. Indications for steroid cover during labour, delivery and surgery
a. Patients on long-term oral corticosteroids > 10 mg prednisolone daily (or equivalent) or have received this dose in the
last three months.
b. Dosage of various kinds of steroid that is equivalent to 10mg prednisolone:-
i. Dexamethasone or Betamethasone 1.5mg
ii. Methylprednisolone 8mg
iii. Hydrocortisone 40mg
iv. Cortisone acetate 50mg
2. Steroid cover is not indicated when:-
a. Oral daily prednisolone intake is 10mg or less or the last dose of steroid is more than 3 months ago.
b. Short course of steroids for 1 - 2 week.
3. Regimen
a. Labour and intrapartum caesarean section
i. Give usual dose of steroid before labour
ii. Give 25mg IV hydrocortisone Q6H at onset of labour till delivery
iii. Resume usual steroid dose post-delivery
iv. In case of complicated instrumental delivery or emergency caesarean section, continue IV hydrocortisone 25 mg
Q6H till 24 hour after delivery or longer till oral intake is resumed
b. Minor surgery
i. For example: cervical cerclage, fetoscopic surgery, first trimester surgical TOP, operation for ectopic pregnancy.
ii. Give usual dose of steroid pre-operatively
iii. Give stat 25mg IV hydrocortisone on-call to OT
iv. After uneventful surgery, resume usual steroid dose on resumption of oral intake
c. Intermediate surgery
i. For example: elective or pre-labour emergency caesarean section, appendicectomy, cholecystectomy, ovarian
cystectomy complicating pregnancy
ii. Give usual dose of steroid pre-operatively
iii. Give stat 25mg IV hydrocortisone on-call to OT, then
iv. 25mg IV hydrocortisone Q6H for 24 hours post-operatively or longer till oral intake is resumed
v. After uneventful surgery, resume usual steroid dose on resumption of oral intake
d. Major surgery or complications
i. For example: internal iliac artery ligation, uterine artery embolization or caesarean hysterectomy; septicaemia; DIC
ii. Increase to IV hydrocortisone dose to 50 mg Q6H and gradually wean off at 48-72 hrs post-op/post-delivery
iii. Maintain this regimen until light diet started and usual steroid dose is resumed.
Tibolone
It is a synthetic steroid which exhibits all oestrogenic, progestogenic and androgenic activity. It is used as a kind of hormonal
replacement therapy and is effective in suppressing climacteric symptoms as well as preventing bone loss. The side effects are
mainly androgenic, and is usually mild and well-tolerated.
Danazol
It is a synthetic androgen frequently prescribed in gynaecology. The pharmacodynamic effect is the suppression of the
hypothalamic-pituitary-ovarian axis, resulting in hypoestrogenemia. It is used to control symptoms of endometriosis, menorrhagia
due to dysfunctional uterine bleeding, and as a pre-myomectomy treatment to reduce size and vascularity of fibroids. It is as
effective as GnRHa, but the androgenic side effects (deepening of voice, acnes, weight gain and cramping) may not be as
acceptable as that of GnRHa to women. Some of these changes may not be reversible. Prolonged use may also result in
osteoporosis, so that the use of the drug is limited to 6 months.
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GnRHa
What is Gonadotropin releasing hormone analogue (GnRHa)
GnRHa are synthetic substances in which one or more of the amino acids in GnRH are substituted by a different amino acid, so
that the activity and binding ability to receptors are altered. Their affinity to GnRH receptors is usually higher than that of GnRH,
and is more resistant to metabolism. Therefore, they produce a down-regulatory effect on the pituitary glands. In long term use, it
will result in hypogonadotropic hypogonadism. This mechanism accounts for its therapeutic effects as well as its side effects.
What are the clinical uses of GnRHa

1. Treatment of endometriosis:- Hypogonadotropic hypogonadism leads to the lack of endogenous oestrogen stimulation on
the growth of endometriosis. The progress of the disease is arrested and symptoms are relieved.
2. Treatment of fibroids and menorrhagia:- The size of fibroids is decreased because of lack of oestrogen stimulation. Menstrual
flow is stopped or diminished. It is however cannot be used as a definite treatment of fibroids or menorrhagia because the
problems often recur after stopping the treatment. It can be used before hysterectomy or myomectomy, as a temporary relief
of symptoms, or to shrink the size of the fibroids in order to facilitate surgery.
3. Use in assisted reproductive technology:- GnRHa is used as a pre-treatment before ovarian stimulation. The ovaries are first
suppressed with GnRHa before undergoing stimulation. This helps to synchronize the growth of oocytes. The endogenous
premature surge of LH is also suppressed.
Side effects of GnRHa

They are mainly related to hypoestrogenism and therefore patients will experience discomforts similar to that of climacteric.
Osteoporosis is the major long term complication. The duration of GnRHa should not exceed 6 months.

1. Management of Endometriosis
a. Aims
i. To reduce or alleviate severe symptoms pelvic pain, dyspareunia
ii. To eradicate any remaining disease and reduce recurrence
iii. To preserve fertility
b. Indications (For asymptomatic women who have completed their family, treatment is generally not necessary)
i. Women with severe symptoms
ii. Women with visible residual or spillage at operation, especially if fertility is a concern
c. Duration of treatment 6 months
d. Alternatives Danazol 200 mg tds; Nordette; Depo-povera 150 mg IMI 3 monthly; and Provera 100mg QD
2. Management of Fibroid
a. Indications
In general, GnRHa is not necessary for management of uterine fibroids. The role of GnRHa in the
management of fibroid is mainly of facilitate surgery or to avoid surgery in special circumstance. The decision
must be made or approved by specialists. The followings are possible indications:-
i. Large fibroid for myomectomy
ii. Large cervical fibroid for hysterectomy
iii. Symptomatic fibroid in patients with high surgical risk
b. Duration of treatment
i. For pre-operative shrinkage of fibroid no more than 3 months
ii. For temporary relief of symptoms and await menopause generally no more than 6-12 months. If the drug
needs to be used for longer period of time, consult doctors with specialist qualification.
3. Preparation for endometrial ablation
a. Aims To cuase atrophy of endometrium so as to shorten reduce operative time, reduce complication and
subsequent recurrence.
b. Regime Decapeptydul 3.75 mg SC
c. Arrange operation 6-8 weeks after starting treatment
d. Alternative Danazol 200mg tds for 6-8 weeks
4. Precocious Puberty Discuss with doctors with specialist qualification and liaise with Paediactricians
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GnRH
Gonadotropin releasing hormone (GnRH) is a peptide hormone secreted from the hypothalamus in a pulsatile Manner. It
stimulates pituitary gonadotropins secretion, and its secretion is inhibited by oestrogen. They form the hypothalamus-
pituitary-ovarian axis for the control mechanism of ovulation. The beginning of pulsatile GnRH secretion in teenage initiates the
development of puberty. Psychological stress, Excessive exercise, significant weight reduction such as in anorexia neurosa result
in suppression of GnRH secretion. Synthetic GnRH can be used as a ovulation induction when given in a pulsatile manner. GnRH
analogue (GnRHa), having a similar chemical structure, are used to treat various gynaecological disorders.
Gonadotropin
There are two kinds of pituitary gonadotropins:-follicular stimulating hormone (FSH) and luteinizing hormone (LH). They are
glycoprotein hormones secreted from the anterior pituitary glands, under the stimulation of gonadotropin releasing hormone
(GnRH, which is secreted from the hypothalamus). They form the hypothalamus-pituitary-ovarian system that controls the
mechanism of folliculogenesis and ovulation. Absence of gonadotropins results in anovulation or failure to reach puberty such as
in Kallman syndrome. On the other hand, premature secretion results in precocious puberty. Another gonadotropin is human
chorionic gonadotropin secreted from the placenta. Gonadotropins can be extracted from human (e.g Human menopausal
gonadotropin (HMG), highly-purified urinary follicular stimulating hormone (hpFSH)) or synthesized by genetic engineering
technology (Recombinant FSH) They are powerful agents for ovulation induction. See gonadotropin therapy
Gonadotropin therapy
Nature
Gonadotropins are extracted from human or synthesized, and used as very effective ovulation induction agents:-
- Human menopausal gonadotropin (HMG)
- Highly-purified urinary follicular stimulating hormone (FSH)
- Recombinant FSH
Mechanism of action
Act directly on ovaries to stimulate folliculogenesis
Efficacy
- Ovulation rate:->95% per cycle
- Conception rate:-20% per ovulatory cycle
- Cumulative conception rate (6-month):-90%
Complications
- Multiple pregnancy rate 10-30%, higher order pregnancy:-5%
- Ovarian hyperstimulation syndrome (OHSS)
- Remark:-Intensive monitoring in specialist clinic is necessary because of the higher risk of multiple pregnancies and OHSS
Advantages Most powerful
Disadvantages
- Narrow therapeutic range, intensive monitoring necessary
- High risks of multiple pregnancy and ovarian hyperstimulation syndrome (OHSS)
- Expensive
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6. Antibiotics
Augmentin is useful in those organisms resistant to penicillin. E. coli is one of the most common organism causing urinary tract
infection and now over half of them is resistant to penicillin, but not Augmentin. It also covers the anaerobes. It is used as
prophylactic antibiotics in emergency Caesarean section Prophylactic antibiotics in vaginal surgery (e.g. Vaginal hysterectomy)
Antibiotics Prophylaxis (Heart Disease)

1. Antibiotic prophylaxis is indicated in:
a. High risk category:
i. Prosthetic valves
ii. Previous infective endocarditis
iii. Complex cyanotic congenital heart diseases
iv. Surgically constructed systemic-pulmonary shunts or conduits
b. Moderate risk category:
i. Most other congenital heart diseases
ii. Acquired valvular dysfunction eg. chronic rheumatic heart disease
iii. Hypertrophic obstructive cardiomyopathy
iv. Mitral valve prolapse with any regurgitation and/or thickened leaflets
2. Antibiotic prophylaxis is not indicated in:
Negligible risk category:
i. Previous rheumatic fever or Kawasaki disease without valvular dysfunction
ii. Mitral valve prolapse without valvular regurgitation or thickened leaflets
iii. Mild mitral regurgitation without MVP, mild tricuspid regurgitation, pulmonary regurgitation without pulmonary
hypertension
iv. Isolated secundum ASD
v. Six months or more after repair of VSD, ASD and ligation of PDA without residual lesions
vi. Previous coronary artery bypass graft surgery, implantation of pacemakers or defibrillators
3. Antibiotic Regimen
Period High Risk Moderate Risk
At onset of labour, rupture of Ampicillin 2.0g + Ampicillin 2.0g
membranes or 30 min before elective Gentamicin 1.5mg/kg IV infusion
caesarean section
Intrapartum Ampicillin 500mg ivi Q6H + Ampicillin 500mg IVI Q6H
Gentamicin 1.5mg/kg IV infusion Q8H
Postpartum/post-caesarean section Ampicillin 1.0g IVI 6 hour after delivery Not required
If patient is allergic to ampicillin, replace ampicillin (any dosage) with Vancomycin 1.0g IV infusion and have the infusion
completed 30 minutes before elective caesarean section. For postpartum/post-CS, no antibiotics are administered.
4. Remark
a. Gentamicin infusion
i. Dilute in 50 ml NS, infuse over 30 min
ii. Dose not exceed 120 mg
b. Vancomycin infusion
i. Reconstitute in 20 ml water, and dilute with 200 ml NS
ii. Infuse over at least 100 min
c. If both ampicillin and vancomycin are contraindicated, consult physician for opinion
d. In case of renal impairment, consult physician for gentamicin and vancomycin dosage
5. Drug removal
a. Gentamycin has replaced netromycin which is no longer available.
b. Parenteral Erythromycin is no longer available.
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Antibiotics Prophylaxis (Caesarean Section)
1. Emergency Caesarean section
After clamping the umbilical cord, give
a. Augmentin 1.2g iv; or
b. Metronidazole 500mg IV if allergic to penicillin.
2. Special conditions
a. For patients with cardiac disease:-
i. Give antibiotics as per antibiotic for heart diseases
ii. Add Augmentin 1.2g IV after clamping umbilical cord, or metronidazole 500mg IV if allergic to penicillin
b. For group B streptococcus carrier:-
i. Give antibiotics as per Gp B streptococcus
ii. Add Augmentin 1.2g IV after clamping umbilical cord, or metronidazole 500mg IV if allergic to penicillin
c. For suspected cases of chorioamnionitis:-
i. Refer to protocol of chorioamnionitis
ii. Give Augmentin for a total of 7 days:-1.2g IV Q8H; change to 375mg po tds when fever subsides
iii. Omit further Ampicillin in cases of cardiac diseases or group B streptococcus carrier.
iv. If allergic to penicillin, replace Augmentin with combination of metronidazole and clindamycin:-
- Metronidazole 500mg IV Q8H, clindaymycin 900mg IV (diluted in 100ml NS infusion over 30 min) q8h
- Change to metronidazole 400mg po tds, and erythromycin 500mg po qid when fever subsided
3. Elective Caesarean section
No need for routine antibiotic cover.
4. Discussion / Justification
Non-oral erythromycin is no longer available
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7. Anticoagulants
1. Subcutaneous injection
a. Enoxaparin:-first choice
b. Fraxiparine:-alternative
2. Oral tablets:-Warfarin
3. There is inadequate experience in the use of Tinzaparin in obstetrics patient and is therefore not recommended.
Enoxaparin
1. Nature
Low molecular weight heparin
2. Indication
a. Prophylaxis and treatment of thrombo-embolism
b. First-line drug for obstetrics patients
3. Route of administration Subcutaneous injection
4. Regimen
a. Prophylaxis 40mg daily SC
b. Treatment 1mg/kg body weight q12H SC
Fraxiparine (Nadroparin)
1. Nature
Low molecular weight heparin
2. Indication
a. Prophylaxis and treatment of thrombo-embolism
b. Second line drug, used when enoxaparin is not available
3. Route of administration Subcutaneous injection
4. Regimen
a. Prophylaxis regimen
i. 75 kg 0.4 ml daily SC
ii. >75 kg 0.5 ml daily SC
b. Treatment regimen
i. 75 kg 0.4 ml Q12h SC
ii. > 75 kg 0.5 ml Q12h SC
Warfarin
1. Indication INR Warfarin dosage
Treatment and prophylaxis of: <=1.5 5 mg
a. Deep vein thrombosis > 1.5 - 2.0 4 mg
b. Thromboemobism related to heart diseases > 2.0 - 2.5 3 mg
c. Pulmonary thromboembolism > 2.5 - 3.0 2 mg
2. Regimen > 3.0 - 3.5 1.5 mg
a. At least one baseline INR result should be available before starting > 3.5 0 mg
b. Day 1 and day 2:-Oral Warfarin 5 mg in the evening daily.
c. Day 3 onwards:-Warfarin dosage (which is given in the afternoon) titrated according to INR which should be checked
every morning.
3. Remarks:
The warfarin sliding scale is just a guideline and it varies with individual patients. Medical officers should not adjust the
dosage or discharge patient without discussion with seniors. Patient can be discharged when she has been on the same dose of
warfarin for 2 consecutive days. Arrange warfarin clinic 1 week
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8. Others
HyperHep (Hepatitis B Immune Globulin)
1. Nature Human hepatitis B immunoglobin
2. Indication Prophylaxis for newborns whose mothers are HBsAg carriers
3. Regimen 0.5ml imi once after delivery
4. Remark Hyperhep can be administered by midwives according to departmental standing order.
Naloxone
1. Indication Treatment of neonatal respiratory depression resulted from narcotic overdose.
2. Regimen 0.3mg imi
3. Remark Midwives can administer naloxone injection according to departmental standing order, while waiting for
paediatricians resuscitation.
Vitamin K
1. Indications
a. Neonatal prophylaxis against haemorrhagic disorders
b. For mothers who are on anti-epileptic drugs
2. Regimen for neonatal prophylaxis against haemorrhagic disorders
a. Mothers who agree for neonatal IMI vitamin K1 1 mg IMI at birth
b. If mothers refuse IMI vitamin K1 for the baby, give vitamin K orally to the baby:
i. 500ug PO at birth by midwife
ii. 500ug PO at 4 weeks by mother
3. Remark
a. Vitamin K oral preparation is different from Vitamin K1
b. Vitamin K1 can be administered by midwives according to departmental standing order.
4. Regimen for mothers who are on anti-epileptic drugs Oral vitamin K daily from 36 weeks of gestation till delivery.
Methrotrexate
Anti-metabolites used as a chemotherapuetic agent for residual trophoblastic disease or ectopic pregnancy
Can be used alone or in combination with other agents
Side effects
- Alopeccia
- Nausea and vomiting
- Myelosuppression
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Miscellaneous
1. English usage
English usage
1. Parity O Nullipartiy is commonly said to be parity 'O'. It should be more correct to say parity 'zero'.
2. Sure LMP It is common to say 'LMP is sure', or 'She has a sure LMP'. The correct way is 'She is sure of her LMP'.
3. Rupture of membranes It should be in plural form as there are two membranous layers:-amnion and chorion.
4. Large > date We use symbols '<' or '>' in the medical notes to denote whether the uterine size is normal for date for
convenience. However, we should not say 'uterus is larger than date' or 'smaller than date', as 'size' and 'date' are two different
parameters and are not comparable. It is correct to say 'uterus is large (small) for date', or 'uterus is larger (smaller) than
expected (from date)'
Acronym
A word formed from the initial letters of a name, or by combining initial letters or parts of a series of words, such as:
1. HELLP for Haemolysis, Elevated Liver enzymes, Low Platelets
2. TORCH for Toxoplasmosis, Rubella, Cytomegalovirus, and Herpes
3. OHSS for Ovarian Hyper-Stimulation Syndrome
Eponym
Epi means on or upon, onyma means name. An eponym is one for whom or which something is named or supposed named, for
example, Down syndrome named after Down; Apgar score named after Virginia Apgar (1909-1974), anaesthesiologist.
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2. Basic clinical skills
History taking (Obstetrics)
Past medical history
To identify any pre-existing diseases that may affect the pregnancy, or may get worse during pregnancy. Common diseases are
hypertension, diabetes mellitus, thyroid disorders, epilepsy and psychiatric disorders
Past obstetric history

- To look for any foetal or maternal complications in past pregnancies that may recur in current pregnancy, e.g. preterm
labour, pre-eclampsia, gestational diabetes
- To review mode of deliveries of past pregnancies that may affect the management of current pregnancy. The number,
indications and mode (Classical or Lower Segment) of C/S affect the management of subsequent modes of delivery.
Present obstetric history

1. To confirm the gestation
a. Date of last menstrual period:-
b. Cycle length and regularity of menstrual period
c. Date of pregnancy test, with both positive and negative results
d. Result of any dating scan
2. To look for any teratogenic agents:-
a. Any rash and fever during pregnancy
b. Any drug taken during pregnancy
3. To look for any symptoms related to the pregnancy:- such as nausea, vomiting (see minor disorders of pregnancy)
Family history
- To look for any risk of having hereditary diseases, such as thalassemia, haemophilia
- To check consanguinity (particularly for Indian and Parkistian)
- To look for any risk of having gestational maternal diseases, such as gestational diabetes, pre-eclampsia or hypertension
Social history
Drug abuses, smoking and alcohol intake
Family planning and childcare

Plan of breast-feeding, childcare, and contraception.
In an antenatal clinic, you are seeing a patient who has an emergency caesarean section 4 years ago in China. What question
concerning that delivery would you want to ask your patient?
Symptomatology (Obstetrics)
Vaginal bleeding
During pregnancy, any vaginal bleeding occurred after 24 weeks is defined as antepartum haemorrhage. Any bleeding comes from
the upper genital tract before that period is diagnosed as threatened abortion.
Abdominal pain
1. Uterine origin Uterine contraction pain
a. It is usually related to the onset of labour.
b. Sometimes it may just be a false labour or Braxton Hicks contractions
c. Abruptio placentae, chorioamnionitis, uterine rupture give rise to constant severe pain
d. Other causes:-red degeneration of fibroids
2. Ovarian origin:- Co-existing ovarian pathologies such as tumour or cysts may bleed, rupture or undergo torsion resulting in
acute abdominal pain.
3. Non-gynaecological origin:- Various kinds of surgical disorders such as appendicitis, cholecystitis, peptic ulcer diseases,
pancreatitis, etc.
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Examination (Obstetrics)
On every antenatal visit
The following examination should be performed:
1. Check for anaemia
2. Maternal weight
3. Blood pressure measurement
4. Urinalysis (urine protein and sugar)
5. Abdominal examination (see obstetric abdominal exam)
On first booking
In addition to above, the following examinations should be performed at the booking visit:-
1. Measurement of maternal height
2. Examination of thyroid glands and signs of thyroid disorders
3. Examination of breasts
4. Examination of heart
5. Examination of perineum and lower genital tract (with speculum) for any pre-existing lesions. The cervix should be examined
for:-
a. Warts, polyps and tumours
b. Length and dilatation (the cervix is dilated and shortened in case of cervical incompetence)
c. Pap smear to screen for cervical intra-epithelial neoplasia (CIN)
Digital vaginal examination

1. Digital examination is performed in the following conditions:-
a. Before induction of labour, assess the bishop score for the favourability (ripening) of cervix
b. During labour, assess the cervical dilatation and effacement, station and position of the foetal presenting part
c. Assess the size of the pelvis (see clinical pelvimetry).
Discussion/something to consider
1. You may notice in the antenatal clinic that the obstetricians often do a bimanual examination of the pelvis when pregnant
women come at the first trimester of pregnancy, but they seldom do so when the their patients come at a later gestation. Do
you know why?
2. You have found a 2cm cervical wart in a woman at her booking visit at 12 weeks. What are your management and advice?
Obstetric abdominal exam

Positioning of patient
1. Patient should lie as flat as possible
2. Discrete exposure from just below the breasts to the symphysis pubis
Inspection
1. Inspect for signs of pregnancy:
a. Abdominal distension
b. Pigmented and flattened umbilicus
c. Linear nigra
i. Pigmented linea alba
ii. May persist after the first pregnancy
d. Striae gravidarum
i. Recent striae are purplish red while old striae from previous pregnancy are silvery white
ii. Striae follow the lines of stress in the skin of the abdominal wall and may also occur on the lateral aspect of the
thighs and the breasts
2. Inspect for foetal movements:- observable after 24 weeks
3. Inspect for any surgical scar:- caesarean section is usually performed with pfannenstiel incision
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Palpation of uterus
1. Palpate the outline and contour of the uterus
2. Irregular if there are fibroids or uterine anomalies
3. Palpate for any uterine tenderness tender if abruptio placentae or intrauterine infection
4. Assess the size of the uterus
a. 12 week:-just palpable over the abdomen
b. 14 week:-a quarter-way from symphysis to umbilicus
c. 16 week:-midway between the symphysis and umbilicus
d. 18 week:-three-quarter-way from symphysis to umbilicus
e. 20 week:-uterus fundus at the umbilical level
5. Measurement of symphysial-fundal height
a. Search for the fundus by palpating from above downward with the left hand
b. Locate the fundus with the ulnar border of the left hand
c. Put one end of the measure tape at the fundus
d. Locate the pubic symphysis with the right hand by sliding downward along the uterine body until the upper border of
the pubis bone is felt
e. Measure the distance between the fundus and the symphysis pubis
f. After 20 week, the fundal height in centimetre correlates to gestation in week:-e.g. The fundal height at 30 week
should be around 30 2cm
6. Palpation of foetus
a. Number of foetus:- suspect multiple pregnancy if more than two foetal poles are identified
b. Foetal lie:-
i. Search for the foetal poles at the fundus and over the suprapubic region. If present, then it is longitudinal lie;
ii. Otherwise, search carefully at the frank region (transverse lie) or iliac fossa (oblique lie)
c. Foetal presentation:
i. Cephalic:-hard round well-defined border
ii. Breech:-soft, bulky
d. Engagement:- some degree of engagement is common when gestation is near term. High floating presenting part
should lead to the suspicion of pelvic inlet obstruction or placenta praevia
e. Foetal back:- if it is longitudinal lie, push the foetus to the other size of the uterus and feel the foetus with the other
hand, and vice versa. The back is round and soft while the limbs are irregular, and moving
f. Liquor volume:
i. Foetal parts are difficult to define when there is significant polyhydramnios. The fundal height is large for date.
Fluid thrill may also be demonstrated.
ii. In oligohydramnios, the foetal parts are easily felt and prominent. The fundal height is also small for date.
g. Foetal parts are usually not palpable before 24 week
Auscultation of foetal heart sound

1. Site:-
a. Best heard over the shoulder (back) of the foetus
b. In cephalic presentation, it is at the level midway between the maternal umbilicus and the anterior superior spine of
the ilium
c. In breech presentation, it is at or slightly above the level of the umbilicus
2. Instruments:- use a pinard stethoscope or a doptone
3. Foetal heart sounds are usually not audiable with a pinard stethoscope before 24 week
Discussion/something to consider
1. A patient comes at 30 week of gestation is found to have a fundal height of 35cm. Is it normal? What are the possibilities
accounts for the finding? How would you assess the case further?
2. A patient comes at 34 week of gestation is found to have a fundal height of 30cm. Is it normal? What are the possibilities
accounts for the finding? How would you assess the case further?
3. You have picked up a pulsative sound of rate 120bpm over the abdomen of a pregnant patient during an antenatal clinic. Is it
normal for foetal heart rate? Can it be maternal origin? How can you differentiate a maternal pulse from a foetal pulse?
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(Left)The presenting part is fixed. (Right) The presenting part is mobile.
OBSTETRICS PALPATION
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Fundal height
Full name is symphysial-fundal height. It is the distance between the top of the uterus and the upper border of the pubic symphysis
at the midline. It is an objective method of monitoring uterine size which in term reflects foetal growth. The fundal height in
centimetre is correlated with gestation age in week, starting from 20 week of maturity. For example, at 30 week, the fundal height
is around 302cm. After 37 week, the fundal height may decrease, due to the engagement of the foetus, as well as the reduction of
amniotic fluid.
Figure 79 Fundal height (Left) and Doptone (Right)

Doptone
It is a hand-held electrical apparatus used for detection of foetal heart pulsation by Doppler effect.
It has several advantages over the Pinard stethoscope:-
1. The foetal heart sounds are audible as early as 12 weeks of gestation
2. It is more sensitive in picking up heart sounds, even though it is not placed exactly over the foetal back
3. The mother can also hear the heart sounds at the same time
The disadvantages are:-
1. It requires battery to work
2. Interference may occur when more than one doptone are used at the same time for multiple pregnancies
3. Maternal pulse can be picked up easily and may be mistaken as the foetal pulse
What are the advantages and disadvantages of using a doptone when compared to a Pinard stethoscope?
Pinard stethoscope
The pinard stethoscope is a simple instrument designed for auscultation of low-pitch foetal heart sounds transabdominally. It is
pressed firmly over the site of the maternal abdomen where the back of the foetus is supposed to be. The foetal heart sound is
usually audible with the pinard stethoscope after 24 weeks of gestation.
What are the advantages and disadvantages of using a doptone when compared to a Pinard stethoscope?
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History taking (Gynaecology)
Gynaecological symptoms
1. See symptomatology (Gyn) for various kinds of symptoms
2. Ask for the development of the symptoms in chronological order
3. Qualify and quantity the severity of symptoms, e.g. Number and type of pads for menorrhagia
4. Note how the patient reacts to the symptoms, e.g. Urinary incontinence may be so severe that makes the patient home-bound
5. Ask for any relevant treatments or investigation results:- Many patients before coming to see a gynaecologist may have been
managed by a general practitioners. e.g. A patient may have been given many medications for dysfunctional uterine bleeding.
Sexual history
- Sexual practice:- number of sexual partners, frequency of coitus, sexual dysfunction, etc
- Contraceptive practice:- methods of contraception
Past obstetric history

It is important in cases such as infertility, ectopic pregnancy and recurrent abortions
Past medical history

- Risk factors to the development of present problem:- e.g. Past history of sexually transmitted diseases:-related to pelvic
inflammatory disease, ectopic pregnancy, ciand cervical cancer
- General health of the patient which may affect your management:- History of diabetes, heart disease, hypertension may
affect surgical and anaesthetic management
Social history
Alcohol intake, smoking, drug abuse, occupation etc.
Symptomatology (Gynaecology)
Menstrual symptoms
1. It is the most common group of symptoms in gynaecology.
2. It may be abnormal in volume of flow, regularity, onset and cessation, or with associated pain and discomforts.
Abnormal vaginal bleeding

1. Related to menstruation (see menstrual disorders for details)
2. In early pregnancy:-various kinds of abortions and ectopic pregnancy
3. Benign tumours or cancers of the genital tract, presented with:-
a. Postcoital bleeding
b. Postmenopausal bleeding
Vaginal discharges
1. Abnormal in colour and odour
2. Usually due to infections, occasionally related to fistula formation between the urinary tract and genital tract
Abdominal and pelvic pain

1. Pain related to menstruation (see menstrual disorders)
2. Pain related to coitus:-dyspareunia
3. Acute pelvic pain
4. Chronic pelvic pain
Urinary symptoms
1. Urinary incontinence:- stress incontinence, urge incontinence, overflow incontinence, etc
2. Abnormal frequency
3. Frequency of micturition, nocturia
4. Discomfort
5. Dysuria, urgency
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Examination (Gynaecology)
Attitude
Be gentle, considerate and courteous.
Pre-requisites
1. Good light
2. Chaperone
3. Full exposure
4. Empty bladder immediately prior to examination
5. Gloves
Positioning of patient
1. Lithotomy position Supine + knees drawn up & fall apart + heels together
2. Sim position For examination of genital prolapse
Procedure
1. Inspection of external genitalia
2. Speculum (bivalve) examination
3. Bimanual palpation
4. Rectal examination
Examination of external genitalia

1. Pubic hair:-presence, distribution and hygiene
2. Labia majora and labia minora:-swelling, mass, ulcer
3. Urethra
4. Anus
5. Remark:-good exposure by separating the labia
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Bivalve speculum examination
1. For inspection of:- Cervix, Fornix and Vaginal wall
2. Remark:
a. Use lubrication
b. Do not turn and lock speculum
c. Take pap smear if not been done recently
d. Gently close speculum on withdrawal
Bimanual examination
To palpate pelvic organs between both hands
1. Use lubrication
2. Insert the right index and middle fingers into vagina, with the thumb upwards and away from the urethral orifice
3. Place the left hand over suprapubic region and press downwards, while the right index and middle fingers and press upwards
4. Palpate the uterus and bilateral adnexae between both hands
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Assess:
1. Cervix:- size, consistency, tenderness (cervical excitation)
2. Uterus:- size, position (anteversion or retroversion of uterus), shape, mobility, consistency
3. Adnexal region:- mass:-size, shape, consistency, mobility, tenderness
4. Pouch of Douglas:- mass, tenderness
Examination of genital prolapse

See Examination of genital prolapse
1. How to differentiate the origin of a pelvic mass, whether it is from uterus or from ovary on examination?
2. As we have high resolution ultrasound scanning which can visualise the pelvic organs clearly, what is the value of clinical
examination?
3. How to differentiate rectocoele from enterocoele, and what is the clinical importance of differentiation between these two
lesions?
Lithotomy
A term derived from one of the oldest known surgical operations, i.e. cutting for (bladder) stone (lith means stone, tomy means
cut). It is now used to refer to the position of the patient on the operating table used for many gynaecological procedures. The
patient is placed on the operating table on their back; the hips are flexed with the thighs opened outwards and the legs supported
by strrups attached to poles on the operating table, so that the operator has easy access to the genital tract.
Speculum
Figure 80 Speculums, made of (Left) steel and (Right) perspex.

An instrument for dilating certain passages of the body, and throwing light within them, thus facilitating examination or surgical
operations. In Gynaecology, the bi-valve speculum and the sim speculum are commonly used for vaginal examination and for
carrying out gynaecological surgery. Using the bi-valve speculum, the anterior and posterior walls of the vagina are retracted apart,
providing a good exposure of the cervix and vaginal cavity. The sim speculum is mainly used for examination of genital prolapse
and vaginal surgery. One side of the vagina is retracted by the speculum so that examination or procedure can be performed on the
opposite side.
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3. Infections
Foetal infection
Introduction
Foetus can acquire infection in the following ways:-
1. Placental transmission
2. Ascending infection from lower genital tract
3. Majority is sexually transmitted diseases
4. Infection acquired during labour when the foetus passing through the birth canal
Micro-organisms
The followings are common or important micro-organisms:
- Viral:- rubella, herpes-varicella (chickenpox), HIV. Hepatitis B
- Bacterial:- syphilis, group B streptococcus, gonorrhea, chlamydia
- Protozal:- Toxoplasmosis
Foetal complications resulted from infection

Foetus can be damaged by infections in the following ways:
1. Congenital infection:-
a. Infection can be teratogenic and cause multiple malformations
b. High risk when infection is acquired in the first trimester
c. Examples are Rubella and Syphilis infection
2. Neonatal infection:-
a. Infection is acquired around the time of labour or delivery, often from the lower genital tract
b. Causes localised neonatal infections
c. Examples are
i. Gonorrhea and chlamydia cause neonatal eye infection
ii. Group B streptococcus causes neonatal pneumonia or meningitis
iii. Chickenpox infection through placental transmission causes neonatal pneumonia
3. Neonates become the carriers of the disease:
a. Foetus acquires the micro-organism and becomes a carrier
b. The micro-organism does not cause any harm to the foetus or neonate immediately, but will cause significant health
problems in the later life.
c. Examples are
i. Hepatitis B:-the child has high chance of developing CA liver in their later life
ii. Indirect foetal complications
iii. Foetal health is also affected indirectly because of preterm labour and delivery secondary to intrauterine
infection or preterm rupture of membranes. Organisms such as group B streptococcus, chlamydia are associated
with preterm delivery
Common foetal infections that medical students should know

The following are chosen because they are relatively common, cause significant foetal morbidity and mortality, and illustrate
various ways how foetus or neonate are affected
1. Rubella
2. Herpes-zoster (chickenpox)
3. Syphilis
4. Gonorrhea and chlamydia
5. Group B streptococcus
6. Listeriosis
7. Hepatitis B
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Hepatitis
Viral hepatitis
- Hepatitis A
- Hepatitis B
- Hepatitis C
Hepatitis B
Introduction
Hepatitis B infection is an important topic in Obstetrics because:-
1. Acute hepatitis may mimic liver disorder specific to pregnancy, such as acute fatty liver and HELLP syndrome. The
differentiation of these diseases is important in the obstetric management.
2. Vertical transmission is the main cause of endemicity in Hong Kong and perinatal infection is the major predisposing factor
of primary hepatocellular carcinoma. Neonatal prophylactic programme has been implemented.
Epidemiology
- In Hong Kong, 10% adults are HBV carriers
- Vertical transmission results in >90% chronic carriage
Virology
1. Double-stranded DNA virus (circular DNA with single stranded regions)
2. Family:-Hepadnaviridae; genus:-Hepadnavirus
3. Transmission via:
a. Blood:-transfusions, sharing of needles or razors, tattooing acupuncture, renal dialysis or organ donation
b. Sexual intercourse
c. Close personal contact in horizontal transmission in children within families
d. Vertical transmission:-perinatal infection at delivery, or rarely transplacental
Complications
1. Acute hepatitis
2. Fulminant hepatitis (rare; 1%)
3. Persistent infection (5%):-chronic persistent hepatitis or chronic active hepatitis
4. Risk of hepatocellular carcinoma in chronic carrier in future:-in Hong Kong, 80% of hepatocellular carcinoma cases are
caused by HBV infection
Perinatal infection
1. Vertical transmission usually occurs at delivery from maternal blood or body fluids, and transplacental transmission is very
rare
2. Vertical transmission rate depends on the level of maternal viraemia. For HBsAg positive mothers, perinatal infection occurs
in 10-20%. For women who are positive for both HBsAg and hbeag, the transmission rate is 90%.
3. Acute maternal infection during the first or second trimesters rarely leads to vertical transmission, while maternal infections
during the third trimester or chronic carriers increase the risk of vertical transmission.
4. Effect on neonates
a. Neonates would become hepatitis B carriers. Over 90% of chronic carriers are a result of vertical transmission.
b. Some of the infected neonates may develop hepatitis which is often mild. Rarely, fulminant hepatitis may occur.
c. Teratogenic effects have not been reported.
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Prevention of perinatal infection
1. Every pregnant woman should be screened with HBsAg.
2. Neonates of carriers should be given prophylactic Hepatitis B immunoglobulin immediately after delivery (within 12 hours
after birth) to prevent perinatal infection. The efficacy of treatment decreases if delayed.
3. All neonates should receive Hepatitis B vaccination during postnatal period:
a. The first dose must be administered within the first week, the second dose at 1 month of age, and the third at 3-4
months.
b. The efficacy is >90%. The child is tested after 1 year as 10% of neonates born to seropositive mothers become chronic
HBV carriers despite prophylaxis is given.
Management of acute hepatitis B infection during pregnancy

1. Principle:- It should be differentiated from other causes of hepatic dysfunction such as HELLP syndrome and acute fatty liver,
and other causes of hepatitis
2. Diagnosis:- Serology
3. Treatment
a. Supportive care, control of symptoms like nausea and vomiting
b. Dietary advice, e.g. Hydration
c. Monitoring of:-
i. Liver function
ii. Foetal growth and health
iii. Uterine activity
d. Infection control measures
e. Contact tracing, testing and vaccination if necessary
f. Follow-up for evidence of resolution or chronic carriage
g. Counselling of family members of HBsAg-positive women and infants
Hepatitis C
Epidemiology
- In Hong Kong, <0.5% of the general population are HCV carriers.
- Vertical transmission rate depends on the level of viraemia and the overall risk appears to be 5-10% and increased to 36% if
the woman is co-infected with HIV.
- No effective way of preventing vertical transmission of HCV.
Virology
- Single-stranded (+ve) RNA virus
- Family:-Flaviviridae; genus:-Hepacavirus
- Enveloped
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HIV
Virology
1. Single-stranded(+ve) RNA virus:-retroviridae
2. Several types; type 1 is the most common and type 2 is similar to type 1, which is confined to West Africa and Less virulent
Epidemiology
1. Worldwide distribution; Africa is the most prevalent area.
2. In the USA and Europe, AIDS is mainly caused by HIV-1; HIV-2 is responsible for a proportion of infections in Africa.
3. Hong Kong (in July 1999):-1255 HIV positive cases have been reported, the male-to-female ratio of new cases is around 6:1
with an increasing trend for females, 9 cases of vertical transmission were found.
4. Parenteral transmission through blood and body fluids, sexual intercourse or from mother to the child.
5. Risk factors of infection:
a. Multiple sexual partners
b. Bisexual activity
c. Sexually transmitted diseases (previous or current)
d. IV drug addicts
e. Transfusion of blood or blood productsz
f. Originating from an endemic area.
Maternal infection
1. Asymptomatic in early stage
2. Some women may have early diseases like vulvovaginal candidiasis, pelvic inflammatory disease (PID) and cervical
dysplasia
3. Anaemia, thrombocytopenia or neutropenia may occur
4. Women with thrombocytopenia may have epistaxis, petechiae and menorrhagia
5. Some may have non-specific symptoms like fever, arthralgias, myalgias and fatigue
6. Advanced cases:-at increased risk of opportunistic infections, such as Pneumocystis carinii pneumonia, toxoplasmosis,
lymphoma, cryptococcal meningitis
Perinatal infection
1. The transmission rate of HIV-1 to foetus was estimated to be 15-35%. Infections occur either in utero (13-33%) or at
delivery.
2. The rate of transmission to infants by infected mothers increases with the clinical severity of maternal disease and is inversely
proportional to the maternal CD4+ T-lymphocyte count.
3. The progress of the disease in these infants varies directly with the disease severity in the mother at the time of delivery.
4. Antenatal and intrapartum antiviral therapy decreases the transmission by 60-70%.
5. Breast-feeding is associated with an additional 14% risk of transmission.
Clinical features
1. No added risk of malformation
2. Most infected infants develop symptoms within the first 2 years of life.
3. Common clinical manifestations include bacterial infections, chronic parotitis, fever, lymphadenopathy, hepatosplenomegaly,
chronic or recurrent diarrhea, failure to thrive, and recurrent or persistent candidiasis.
Screening
Serological screening of HIV status should be considered in high risk patients (see above). Consent is required
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Diagnosis
1. Maternal diagnosis
a. PCR assays for HIV cDNA in serum
b. Virus isolation (expensive and slow)
2. Neonatal diagnosis of perinatal infection
a. Conventional serological assays are difficult to interpret as passively transferred maternal antibodies may take up 18
months to disappear
b. Other diagnostic tests include:-
i. PCR assays for HIV cdna
ii. p24 antigen detection (ELISA)
iii. Virus isolation
iv. IgA class-specific antibody detection (EIA)
v. Early diagnosis allows prophylaxis against opportunistic infections
Management of for HIV-positive carriers

1. Pre-conception counselling:
a. Counselling of risks and prognosis of the child.
b. Consider avoiding pregnancy.
2. Antenatal:
a. Monitoring of CD4+ counts.
b. Extensive and ongoing counselling.
c. Zidovudine (azidothymidine, AZT) treatment is offered to the mother during pregnancy, labour and delivery, and to
the newborn. This reduces the risk of perinatal transmission.
d. Looking for any development of opportunistic infections or AIDS.
3. Intrapartum:- Elective caesarean section may reduce the risk of perinatal transmission.
4. Postnatal:-
a. The newborn's skin should be cleansed of all maternal secretions before being punctured by a needle.
b. Breast-feeding is avoided if possible.
c. Prevent the baby from contacting with maternal secretions.
Pre-test counselling and testing

1. Antenatal Clinic
a. Post posters
b. Patients attending first visit :
i. Give information pamphlets
ii. Show a video.
iii. Counseling:- By midwife HIV co-ordinators; to enquire about patient"s objections; and further individual
counselling by midwife HIV co-ordinators, if patients are undecided,wish to opt-out or have questions
iv. Verbal consent before blood taking for HIV testing and other routine antenatal blood tests.
v. If patient is still undecided, refer to AN general / MC-General / MC clinics and enquire for decision in the next
clinic follow up. Other antenatal routine blood tests should be taken first.
c. Repeat HIV test after 3 months if patients have high risk behaviour
d. Inform patients of the result of HIV testing in the next clinic visit.
e. If refer to MCHC for shared antenatal care, patients will be called back if result is abnormal.
2. Antenatal / Labour / Postnatal wards
a. Post posters
b. For non-booked cases with no prior testing
i. Arrange HIV testing and/or other antenatal routine blood tests
ii. If patient is in labour or condition not allows for HIV counselling, delay testing till condition allows or till after
delivery in postnatal wards
iii. Perform other antenatal routine blood tests as indicated
c. Trace results if tests done elsewhere.
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3. Gynaecological wards
a. Antenatal routine blood testing including HIV is NOT a routine.
b. HIV testing can be performed during antenatal care in the clinics
4. Booked courtesy / private obstetric patients
a. Video and pamphlets will be shown before doctor"s consultation.
b. Counselling and blood testing will be performed during consultation.
5. Sending blood specimens
a. Same blood sample used for hbsag / Rubella Ab testing.
b. Order test through the CMS laboratory request system.
6. Documentation of testing status / results
a. Enter status of HIV testing into CMS:
i. HIV test done with result : + or - or indeterminate
ii. Repeat test result : +, -, indeterminate
iii. Opt-out
iv. Undecided
b. Enter HIV testing status in a separate Record Book by designated midwifery staff.
c. HIV results should be tracked for, if still not available by 2 weeks after the tests are requested, by contacting Dr. Paul
Chan, virologist of PWH.
d. The Obstetrics SCIS can be entered with these results
7. Reporting of HIV results
a. Currently under liaison, through the CMS if agreed by the Department of Microbiology
b. Before reporting via CMS is implemented, test results are reported under the existing mechanism :
i. Negative results sent via sealed envelopes in batches to the designated midwifery co-ordinator of the clinical
areas from where the blood specimens are sent.
ii. Positive / Indeterminate results
Laboratory staff will inform the doctor requesting the test by phone and to arrange for repeat testing from the
patient
If positive result is confirmed, laboratory staff will inform the requesting doctor by phone, followed by a formal
report in a sealed envelope.
The requesting doctor should inform the Obstetrics HIV co-ordinator or deputy (Dr. C Y Li / Prof W H Tam) of
all positive and indeterminate results and seek advice for further management.
c. Central reporting A monthly return on the numbers of cases screened, opt-out, and positive / indeterminate cases
will be prepared and sent to Dr. H K Wong, the central HIV co-ordinator.
8. Management of HIV positive cases
a. For cases first referred to the antenatal clinic / on-call obstetric medical staff, the Obstetrics HIV co-ordinator or
deputy should be notified for advice on subsequent arrangement
b. Early antenatal clinic appointment or admission to antenatal ward for post-test counselling of the patient
c. Confidentiality maintained
d. Obstetrics care in PWH by medical obstetrics team
e. Patients will be referred to SMS (QEH) or SPP (DH) for medical care of HIV infection
f. Paediatrician will be informed for paediatric counselling and stocking of anti-retroviral drugs for neonatal treatment.
g. Pharmacy staff will be notified for stocking of anti-retroviral drugs for antenatal / intrapartum / postnatal use.
h. Anti-retroviral drugs will also be stocked in the labour ward for emergency use for unanticipated HIV positive
nonbooked cases admitted in labour.For the drugs regimen, please refer to HIV-antenatal screening at AHNH/NDH.
9. Tracing of HIV positive patients who default follow up
a. For MCHC referred cases who fail to turn up in the first antenatal clinic / admission appointment in PWH, MCH HIV
co-ordinator will be informed for tracing.
b. For cases first diagnosed in the postnatal period, discharged patients will be called back for joint post-test counselling
with paediatrician. Patients will be referred to DH / QEH for long term medical follow up while their babies will be
referred to the paediatrician for assessment.
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Antepartum management of HIV positive patients
1. If newly diagnosed, notify and liaise with QEH (SMS) or DH (SPP)for joint care
2. If <24 weeks, discuss termination of pregnancy
3. Take cervical smear, HVS, ECS for gonorrhoea, chlamydia and herpes
4. Serum screening for VDRL
5. Watch out for related opportunistic infections
6. Follow up Medical Obstetric clinic every 2 weeks then weekly from 36 weeks onwards
7. Offer Zidovudine from 14 weeks onwards
8. The exact anti-retroviral therapy should be individualised and finalized after discussion with QEH or DH.
9. Liaise with QEH (SMS) or DH (SPP) for screening for toxoplasmosis, CMV and herpes, and for monitoring of CD4
lymphocyte count +/- pneumocystis carinii prophylaxis
10. Avoid invasive antenatal diagnostic/therapeutic procedure
11. Arrange elective Caesarean section at 38 weeks of gestation if patient agrees
Intrapartum management of HIV positive patients

1. Inform anaesthetist and paediatrician
2. For booked cases with HIV-positive status already known during antenatal care
a. Exact anti-retroviral regimen is to be pre-decided by QEH or DH
b. Arrange Caesarean section if labour is not established and membranes have not ruptured.
3. For unanticipated nonbooked cases admitted in labour
a. Inform FHKAM on-call
b. Give ORAL anti-retroviral therapy
i. Loading dose
Zidovudine 300mg and
Lamivudine 150mg bd
ii. Maintenance dose till delivery
Zidovudine 300mg q3h and
Lamivudine 150mg bd
4. If labour has already been firmly established +/- spontaneous rupture of membranes
a. Allow to labour
b. Follow anti-retroviral regimen as appropriate
c. Avoid ARM
d. Augment labour with oxytocin
e. Avoid invasive procedures eg. Fetal scalp electrode, fetal scalp blood sampling, amnioinfusion
f. Avoid episiotomy
g. Repair genital tract trauma by MO or above
h. Perform instrumental delivery by MO or above
i. If appropriate, forceps delivery is preferable to ventouse extraction
j. Use disposable instruments
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Lamivudine therapy
1. Nature A nucleoside reverse transcriptase inhibitor of retrovirus including HIV.
2. Indication
a. To reduce the risk of vertical transmission of HIV from HIV-positive mothers who have not received antenatal
Zidovudine therapy.
b. Not routinely given, but individualized treatment.
3. Regimen
a. Intrapartum maternal therapy
i. Orally 150mg every 12 hours till delivery
ii. Combined with oral Zidovudine
b. Neonatal therapy by paediatrician
Nevirapine
1. Nature A non-nucleoside reverse transcriptase inhibitor of HIV-1.
2. Indication
a. To reduce the risk of vertical transmission of HIV from HIV-positive mothers to their babies.
b. Not routinely given, but individualized treatment.
3. Regimen
a. Intrapartum maternal therapy:- 200mg po single dose 1 hour prior to Caesarean section or at the onset of labour
b. Neonatal therapy:- To be decided by paediatrician.
4. Contra-indication Hypersensitivity
5. Toxicity
a. Rash
b. Deranged liver function (reported with multiple doses in non-pregnant patients)
Zidovudine
1. Nature A nucleoside reverse transcriptase inhibitor of retrovirus including HIV.
2. Indication To reduce the risk of vertical transmission of HIV from HIV-positive mothers to their babies
3. Regimen
a. Antenatal maternal therapy:
i. 300mg b.d. orally
ii. Specialist from QEH(SMS)/DH(SPP) may give the dosage differently in order to improve compliance
b. Intrapartum maternal therapy
i. If patient had antenatal Zidovudine therapy
2mg/kg iv loading dose over 30-60min, then 1mg/kg per hour iv till clamping of cord
ii. If patient had not received antenatal Zidovudine therapy
300mg oral therapy for loading following by 300mg q3h till delivery
Combined with Lamivudine
c. Neonatal therapy
i. Give Zidovudine syrup 2mg/kg po 4 doses/day for 6 weeks
ii. or if not tolerate orally,give iv 1.5mg/kg over 30min Q6H
iii. start therapy within 8 to 12 hours of birth
iv. if no intrapartum therapy was given, start therapy immediately after delivery
4. Monitoring of Zidovudine therapy
a. To be performed by specialist from QEH(SMS)/DH(SPP)
b. baseline CBP, LFT, CPK then
c. CBP Q2weeks for 1 month, then Q4 weeks
d. LFT, CPK Q4 weeks
e. Consider discontinuation if:- Hb<8g/dl; Platelet<100x109/L; WCC<75x109/L
f. ALT/AST >5X normal
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Group B streptococcus
Organism
Group B streptococcus (GBS); Gram positive aerobic coccus
Epidemiology
1. In UK, 15-20% of women carry GBS in the vagina at delivery
2. 40-70% of infants of mothers colonised antenatally with GBS are themselves colonised, but only 1% develop evidence of
infection affected by it
3. Nevertheless GBS infections are one of the commonest infective causes of neonatal morbidity and mortality in the developed
world with an incidence of 1-4/1000 birth
4. The mortality rate for perinatal infection can be as high as 80% despite early recognition and prompt treatment
Foetal Risk
- Neonatal pneumonia
- Neonatal meningitis
- Preterm rupture of membranes, preterm labour and delivery
Maternal Risk
- Patients are usually carriers and asymptomatic
- May cause vaginitis, and intrauterine infection after rupture of membranes
Screening and prevention

1. Routine screening for maternal colonisation and treatment
2. Controversial
3. GBS is only temporarily eradicated by short-term antibiotic therapy during pregnancy
4. If treatment is based on a positive culture at 28 week up to 50% will be negative at delivery, and up to 15% of
culture-negative women at 28 weeks will be culture-positive by delivery. Thus some women would be overtreated while
others would be undertreated.
Management
Intrapartum antibiotic (ampicillin) prophylaxis to prevent perinatal infection

1. At onset of labour, ROM or induction of labour, give:-
a. Ampicillin 2g IV bolus then 1g Q6h till delivery; or
b. Clindamycin 900mg IV (diluted in 100ml NS infusion over 90min) q8h till delivery, if allergic to penicillin.
c. Request bacterial sensitivity to clindamycin whenever possible. If bacteria is resistant to clindamycin, give other
antibiotics according to sensitivity, or vancomycin 1g q12h (reconstitute in 20 ml of water and dilute with 200ml
normal saline, infusion over at least 100mins)
2. It is not necessary to give antibiotics for group B streptococcus if patient is going to have elective Caesarean section
without rupture of membranes.
3. Post-delivery
a. Inform neonatologist the result at delivery or whenever a positive result is available.
b. If the positive result is available during the postnatal period and the patient remains asymptomatic, it is not necessary to
give antibiotics to the patient.
c. Inform patient that she is a carrier and intrapartum antibiotic prophylaxis is required in future pregnancy.
d. Give a memo to the patient stating the result of positive group B streptococcus on discharge.
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Rubella
Virology
1. Family:-Togaviridae; genus:-Rubivirus 4. Infects only humans
2. Single-stranded RNA virus 5. Spread by droplets infection
3. With haemagglutinin antigens 6. Incubation period:-14 to 21 days
Clinical features
1. 25% are subclinical
2. Usually present with mild febrile illness with macular rash and lymphadenopathy which lasts for 5 to 7 days
3. Macular rash first appears on the face and behind the ears before spreading down the trunk and the limbs.
4. The contagious period (i.e. Viral shedding) extends from 8 days before to 8 days after the onset of the rash.
5. Rubella antibodies are present by the time rash appears.
Foetal Risk of Congenital rubella syndrome

1. Chance
Gestation at infection Chance of infection Abnormalities
< 8 week up to 85% All infected foetuses will develop complications
< 12 week 50 - 80% 65 - 85% of infected foetuses have clinical defects
13 - 16 week 30% 30% will suffer sensorineural deafness
16 week 10% Clinical manifestation rare
2. Features of congenital rubella syndrome
a. Bilateral cataracts, microphthalmia
b. Sensorineural deafness
c. Congenital heart disease especially patent ductus arteriosus
d. Mental retardation
e. Intrauterine growth retardation
f. Abortion, intrauterine death
Diagnosis of maternal rubella

1. As 25% are subclinical, diagnosis should not be based on clinical presentation alone
2. Serologic confirmation is essential:
a. Four-fold rise in IgG titres
b. Rubella-specific IgM antibody (false positive occurs with rheumatic factor)
Diagnosis of congenital rubella after delivery

- Virus isolated from infant's pharynx, urine and cerebrospinal fluid in the first three months of life
- Igm rubella-specific antibody present in cord blood
- Persistence of rubella antibodies after 6 months
Screening
- Immunity is screened with rubella antibody (IgG) at booking, or before pregnancy
- IgG ELISA test, latex agglutination test and radial immune haemolysis test can be used
Prevention
1. Vaccination before pregnancy. This is a live attenuated virus vaccine
2. Contraception is advised for 3 months post-vaccination although the chance of congenital rubella infection caused by the live
vaccine is very rare.
1. During the booking visit at 9 weeks of gestation, a patient tells you that her child got a rubella rash 2 weeks ago. How would
you manage this case?
2. A subsequent test confirmed that she had recent rubella infection. How would you counsel and manage this pregnancy?
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1. Incubation period 14-21 days
2. Infectious period 7 days before to 4 days after the onset of rash (c.f. 8 days before to 8 days after the onset of rash)
3. Clinical features:-
a. Fever
b. Erythematous maculopapular rash spreading from face to trunk and extremities.
c. Arthritis and arthralgia
d. Lymphadenopathy esp. postauricular, suboccipital glands.
e. 25% of infections are subclinical
4. Diagnosis
a. Serologic confirmation is essential.
b. Rubella specific IgM antibody.
c. A 4-fold rise in Rubella IG antibody titre.
d. Seek opinion from Virologist and ensure rapid testing.
5. Management of confirmed maternal Rubella infection
a. Notify the Department of Health
b. Maternal risk is low, rare complications include encephalitis, bleeding diathesis.
6. Congenital Rubella nfection
a. There is neither reliable antenatal diagnostic tool nor effective treatment for congenital infection.
b. Discuss the option of termination of pregnancy if confirmed maternal infection before 16 weeks of gestation
c. Diagnosis of congenital rubella infection after delivery:
i. Virus isolated from infants pharynx, urine and CSF in the first 3 months of life
ii. IgM rubella-specific antibody present in cord blood
iii. Persistence of rubella antibodies after 6 months
7. Rubella accine
a. A live attenuated vaccine.
b. Should be given to all potentially child-bearing women who are susceptible to infection, with advice on
contraception.
c. Should avoid pregnancy within 3 months after vaccination.
d. The risk of vaccination causing congenital rubella infection in pregnancy is a THEORETICAL one. There is as yet no
evidence of teratogenic risk of the Rubella vaccine.
e. If pregnancy occurs within 3 months of vaccination, there is no ground to advise termination of pregnancy. Patient
should be reassured that the risk of teratogenic effect is negligible.
f. If an antenatal patient is found not immune to rubella during antenatal care, postnatal vaccination should be advised
and possibly given in the postnatal ward.
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Chickenpox
Virology
1. Herpes varicella-zoster causes chickenpox in a primary infection, and shingles on reactivation.
2. Incubation period:-10 - 21 days after initial contact (delayed up to 28 days if vzig immunization is given)
3. Infectious period:-2 days before onset of skin rash until cropping have ceased and crusted over (usually takes about 5 days)
Varicella-zoster virus
1. Epidemiology
a. Primary infection (chicken pox) is common in childhood
b. In Hong Kong, >90% of adults are seropositive, reactivation (herpes zoster) does not usually cause problem in
pregnancy as the foetus is protected by maternal antibodies
2. Virology
a. Double-stranded DNA virus
b. Family:-Herpesviridae; genera:-alphaherpesvirinae; HHV-3
c. Cubic, icosahedral symmetry
d. Morphology:-monomorphic, enveloped
3. Clinical features of primary infection (chickenpox)
a. Symptoms like fever, malaise and a vesicular rash develop 10-20 days after exposure
b. The rash usually begins on the face and scalp which then spreads to the trunk
c. Contagious period from 2 days before the appearance of rash to all ruptured vesicles become crusted
d. Highly infectious but mild in children
e. More severe in adults and may associated with complications like encephalitis, myocarditis, pericarditis, pneumonia,
superinfection of skin lesions and adrenal insufficiency
f. In pregnant women, the disease is more severe, pulmonary complications with initial symptoms such as cough,
tachypnoea, dyspnoea and chest pain. Gradually, the disease becomes disseminated, oral lesions and higher fever
develop, and finally respiratory insufficiency, pneumothorax, pulmonary parenchymal fibrosis and bacterial
superinfection may occur and lead to death.
Chickenpox
1. The name was meant to distinguish this weak form of the pox from smallpox (chicken being used, as in chickenhearted, to
mean weak or timid).
2. It is a febrile disease with generalised skin rash, starts as an eruption of red papules (bumps) which become vesicles (blisters)
than pustules. Other symptoms include malaise, weakness, sore throat, cough and fever.
3. Maternal risk Complications including pneumonia and encephalitis are uncommon but can be severe in adults.
4. Foetal risk
a. When infected during pregnancy, there is a risk of congenital varicella syndrome:
i. 1% risk before 12 week of gestation
ii. 2% between 13 and 20 week
iii. Minimal after 20 week
iv. Syndrome consists of:-mental retardation, microcephaly, neurological and visual deficit, IUGR and deformity
b. When infected during perinatal period, there is a risk of neonatal varicella
i. Risk is 20 to 30% when mothers develop chickenpox within 5 days before and 2 days after delivery
ii. Neonatal mortality is 30%
Diagnosis
Unlike rubella infection, chickenpox is always symptomatic, and diagnosis can often be made based on clinical features. Serology
is not required to confirm the diagnosis
Treatment of active chickenpox infection during pregnancy

1. Give acyclovir to reduce severity and duration of disease.
2. Varicella-zoster immunoglobulin is not useful for established infection.
3. Delay delivery, whenever practical, until at least 5 days after onset of skin rash, to allow passive placental transfer of maternal
antibodies.
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Management of susceptible pregnant women who have contact with chickenpox
Susceptible pregnant women (non-immune) should be given varicella-zoster immunoglobulin within 10 days of significant contact
with chickenpox
Gestation Abnormalities
1. <20 weeks (the earlier the gestational age, the more severe the foetal damage)
2. Foetal transmission in 25% and congenital defects in about 3% of cases
3. Congenital varicella syndrome:
a. Specific features:-Cutaneous scarring, Hypoplasia of limbs, Muscular atrophy/limb paralysis, rudimentary digits
b. Brain:-Psychomotor retardation, Convulsions, Microcephaly, Cerebral cortical atrophy
c. Eye:-Chorioretinitis, Cataracts, Chorioretinal scarring Optic disc hypoplasia
d. Others:-Horner's syndrome
4. Second and third trimester
a. Subtle findings only
b. A week before to a week after deliviery. Fatal disseminated disease in neonates due to acquisition of virus with no
transplacentally acquired maternal antibodies (30% of cases)Rash in mother beginning from 4 days before to 2 days
after delivery has the highest risk.
c. If systemic symptoms are severe, premature uterine activity may occur and lead to premature delivery
d. Babies infected in utero may develop zoster in early infancy
Reactivation (herpes zoster; shingles)

1. Dormant virus reactivates in times of stress
2. Presents with patches of painful and pruritic vesicles with a erythematous base along the course of a cutaneous nerve in a
dermatomal pattern
3. Rarely involves viscera except in immunosuppressed patients
4. Has no effect on the foetus
Diagnosis
1. Clinical presentation is reliable in most cases
2. Laboratory confirmation:
a. IgM detection
b. Viral antigen detection
c. Virus isolation from vesicle/scraping
Management
1. Prenatal
a. Counseling
b. Monitoring of uterine activity
2. Postnatal
a. Infection control measures for congenitally infected infants
b. Pediatric follow-up
Prophylaxis
Varicella-zoster immunoglobulin (VZIG) post-exposure prophylaxis is recommended for:-
1. VZ antibody negative pregnant women exposed at any stage of pregnancy
2. Infants whose mother develops chicken pox in the period 7 days before to 28 days after delivery VZIG does not prevent
infection but can attenuate disease
- 385 -

Basic Information
1. Incubation period:-10 -21 days after initial contact (delayed up to 28 days if VZIg immunization is given)
2. Infectious period:-2 days before the onset of skin rash until cropping has ceased and crusted over (usually takes about 5
days)
3. Congenital varicella syndrome
a. Risk:
i. 1% risk before 12 weeks of gestation
ii. 2% between 13 and 20 weeks
iii. Minimal after 20 weeks
b. Mental retardation, microcephaly, neurological and visual deficit, IUGR and limb deformity
4. Neonatal varicella
a. 20 to 30% risk if mother develops chickenpox within 5 days before and 2 days after delivery
b. 30% mortality
Isolation
1. When infectious patient presents to out-patient clinic
a. Refer immediately to A&E Dept for assessment by Gynae on call MO
b. DO NOT admit patients to O&G wards
c. Arrange transfer to PMH if in-patient care is required
2. When infectious patient has already been admitted
a. Isolate patient immediately
b. Arrange transfer to PMH (including patients baby) unless patient is medically not fit
3. Administration
a. Earmark patients file
b. Contact tracing. See Chickenpox-significant contact and manage them accordingly
c. Notify PWH Infectious Control Unit and Dept of Health
4. Medical and obstetrical management
a. Diagnosis
i. Should be made clinically.
ii. Serological confirmation of the diagnosis is not required unless for equivocal cases.
b. Treatment
i. Give acyclovir to reduce severity and duration of disease if patient is seen within 24 hours after development of the
rash; or has varicella pneumonia.
- No evidence of pneumonia:-800mg po 5 times a day for 1 week
- For vaicella pneumonia:-10mg/kg IV Q8H for 1 week
ii. VZIg administration is not useful for established infection.
iii. Arrange foetal morphology scan at 18 to 22 weeks of gestation for patients infected before 20 weeks of gestation.
(The USG should be performed at least 5 weeks after the infection).
c. Delivery
i. Delay delivery, whenever practical, until at least 5 days after the onset of skin rash, to allow passive placental
transfer of maternal antibodies.
ii. During intrapartum period, isolate patient in a single room.
iii. Inform paediatricians.
5. Susceptible staff should stay away from patients with active chickenpox infection, or patients who had contact with chicken
pox and are within the infectious period.
- 386 -
Significant contact
1. Definition of significant contact with Chickenpox
a. Time of exposure
i. Chickenpox/ disseminated zoster:-2 days before onset of rash till cropping has crusted
ii. Localised zoster:-day of onset of rash till crusting
b. Closeness /duration of contact
i. Continuous home contact
ii. In the same room for 15min
iii. Face to face contact e.g. conversation
iv. Large and open wards
c. Susceptible patients are potentially infectious from 10 days after the first contact, to 21 days after the last contact (or to
28 days after the last contact if VZIg is given).
2. Management of susceptible patients with significant contact
When patient is identified in out-patient
a. Refer patient to A&E Dept for obstetric follow-up by Gynae on call medical officer, until
i. Infection is excluded, or
ii. Infectious period has passed, or
iii. Patient is confirmed immune.
b. Advise patient to avoid further contact with index cases until the latter becomes non-infectious
c. Earmark patients file
d. Check patients immune status by VZIgG test
e. Ward Manager of the antenatal clinic should:
i. Liaise with A&E staff and virologist for the urgent serology test
ii. Keep track of the test result and inform Rm1 doctor when result is available
f.Manage according to VZIgG test result
3. Interpretation of and VZIgG test result and Management
a. First VZIg titre taken within 10 days of first exposure
i. Negative/ Equivocal:-treat as susceptible
- If patient is asymptomatic, give chickenpox-VZIg immunoglobulin in A&E Dept as soon as possible
- No need to check second titre.
ii. Positive:-treat as immune
b. First VZIg titre taken after 10 days of first exposure
i. Negative/ Equivocal:-
- Treat as susceptible
- Check second titre at least 3 days after incubation period has passed
- Not for chickenpox-VZIg immunoglobulin
ii. Positive:-
- Likely to be due to past infection
- observe for symptoms and check second titre to exclude recent infection at least 3 days after incubation period
has passed
- no change in titre in paired samples implies immunity; slight rise may occur in immune patients after contact;
consult virologist if in doubt
4. Admission of patients during potentially infectious period
a. Do NOT admit patient to O&G wards whenever possible.
b. Decision should be made by FHKAM
c. Alert antenatal ward staff before admission by nursing staff in clinic
d. Isolate the patient
e. Check her immune status and give chickenpox-VZIg immunoglobulin if appropriate
5. Susceptible staff should stay away from patients with active chickenpox infection, or patients who had contact with chicken
pox and are within the infectious period.
- 387 -
Varitect (Varicella-Zoster Immunoglobulin)

1. Indications
a. Susceptible pregnant women within 10 days of significant contact with chickenpox. See definition of
chickenpox-significant contact
b. Babies born to mothers who develop chickenpox within 5 days before and 2 days after delivery
a. Patients intolerant of homologous immunoglobulins, especially in very rare cases of IgA deficiency, when the patient
has antibodies aganist IgA.
b. Patients with signs of chickenpox-active infection
3. Administration
For prophylaxis in susceptible women:
a. Administer as soon as possible and preferably within 96 hours of exposure
b. dosage:-0.2ml(5iu) per kg body weight, higher dose of up to 1ml(25iu)/kg if repeated exposure
c. IV infusion at rate not faster than 1ml per minute
4. Side effects
a. Anaphylactic reaction
b. Fever, chills, headache and GI upset
c. Symptoms of aseptic meningitis
5. Precautions
a. Closely observe patient for at least 20 minutes after administration for any adverse reaction
b. The rate of infusion must be followed strictly
c. Do not mix VZIg with other solution other than Normal saline as the Immunoglubulin may be denatured
d. Patients with renal impairment, or history of migraine
e. VZIg may impair the efficacy of other live attenuated virus vaccines such as MMR or varicella for 6 weeks to 3 months
6. Remark
a. Liaise with Pharmacy on status of availability of VZIg. If demand is greater than supply, the priority will be those
patients with <20 weeks gestation, followed by those with > 37 weeks of gestation.
b. The incubation period and hence the potential infectious period can be prolonged after VZIg administration to 28 days
after exposure
Toxoplasmosis
A systemic infection caused by the protozoon Toxoplasma gondii. It is either asymptomatic or confused with 'flu' or other
pregnancy symptoms
Incidence
It is extremely uncommon in Hong Kong. The best estimate of the incidence in pregnant women in the UK is about 2/1000.
Congenital toxoplasmosis
Toxoplasma gondii can cause significant congenital abnormality of foetus:-
1. During the first trimester, transmission to the foetus occurs in about 10% of maternal infection. Foetal death or severe
sequelae are likely.
2. During the second trimester, transmission is frequent with a high risk of congenital infection.
3. During the third trimester, transmission is very frequent but the risk of problems at birth is low. However, as many as 80% of
children may develop chorioretinitis in later years.
Prevention
The best policy is prevention by avoiding undercooked meat, unpasterurised milk, and contact with cat litter; washing all garden
produce well and washing hands after gardening.
- 388 -
Cytomegalovirus
Virology
Double-stranded DNA virus belongs to Herpesviridae
Epidemiology of CMV infection

1. Common; worldwide distribution
2. Most infections occur subclinically in childhood
3. In Hong Kong, about 95% of women at their childbearing age are seropositive
4. In some European countries like the UK, 40% of adults are susceptible
5. Seropositivity depends on age, socioeconomic class and country
6. Congenital infection has a high incidence:-0.2-2.2% of live births
Pathogenesis
1. Transmission via close contact with CMV-infected secretions (blood/marrow transfusion, sexual contact, close contact in
institutions)
2. A replication in the nucleus of infected cells producing the characteristic nuclear inclusions
3. Viraemia results in risk of transplacental transmission to the foetus
Clinical features
1. Primary CMV infection
a. Usually asymptomatic except in immunosuppressed patients, but glandular fever-like illness may occur.
b. During pregnancy, primary infection carries a foetal infection rate of 40%. The chance of foetal infection is not
affected by the gestational age, but the severity is higher in the first half of the pregnancy.
2. Reactivation of latent CMV infection
a. Common in pregnancy
b. Almost always asymptomatic
c. CMV may also be transmitted to the foetus, but the maternal antibodies can reduce the severity of foetal infection
when it occurs
3. Congenital CMV infection
a. Resulted from transplacental transmission
b. 5-10% of the infected infants are symptomatic at birth, of which 15% have classic cytomegalic inclusion syndrome
(CID)
c. 15-20% of symptomatic infants die and 90% of survivors have sequelae like hearing loss and mental retardation
d. 5-15% of asymptomatic newborns also develop sequelae
e. The prognosis of infants who are symptomatic at birth is poor
Cytomegalic inclusion syndrome (CID)

1. Congenital infection
a. Intrauterine growth retardation (IUGR)
b. Central nervous system:-microcephaly, intracerebral calcifications, encephalitis, chorioretinitis
c. Hematological:-anemia, thrombocytopenia, petechial hemorrhage
d. Hepatic hepatosplenomegaly, elevated liver enzymes, jaundice
2. Perinatal infection
a. Resulted from transmission via maternal secretions
b. Common in infancy but does not harm the infant
- 389 -
Diagnosis
1. Screening of primary infection using serologic testing, e.g. ELISA
a. CMV-specific IgM can only be detected in around 60% of primary infection
b. CMV-specific IgM may reappear in about 20% of cases of reactivation
c. Confirmatory results:-seroconversion/igg is negative and igm is positive when first tested with a subsequent
seroconversion in IgG
2. Foetal
a. Ultrasound examination
b. Virus isolation from amniotic fluid
c. Pathologic examination of the aborted tissue
3. Postnatal
a. Congenitally infected infants may excrete virus for up to 5-7 years
b. Congenital infection can be confirmed by virus isolation from urine and saliva taken within 3 weeks after birth
Management
1. Pre-pregnancy Discuss risks for women working in high-risk environment (e.g. Nurseries, institutions)
2. Prenatal
a. No treatment for acute maternal infection
b. Counseling about foetal risks
c. Monitoring of the foetus
d. Termination of pregnancy is considered at early gestational age
3. At delivery Infection control
4. Postnatal
a. Confirm the diagnosis
b. Pediatric follow-up if infection is confirmed
Parvovirus
Virology
- Single-stranded DNA virus
- Family:-Parvoviridae; genera:-Parvovirus
- Infects only humans
- Transmission via respiratory route (aerosolized droplets)
- Viraemia develops 7-8 days after inoculation and ends when rash appears
- The contagious period lasts from inoculation to eruption of rash, and is increased during the 1-4 days of mild fever and
myalgias which precede the rash in up to 60% of patients.
Infection
Parvovirus causes erythema infectiosum or fifth disease which is a common viral infection among children. 25% of adult
infections are asymptomatic. Patients usually have rash or/and acute symmetrical peripheral polyarthralgia that usually resolves
within 2 weeks. Occasionally it may cause bone marrow suppression, anaemia and thrombocytopenia. When a pregnant woman
acquires the infection (B19), the foetus may be infected transplacentally (33%), resulting in foetal anaemia and hydrops foetalis.
Prenatal diagnosis and management

1. Any pregnant woman who has been exposed to B19 infection or develops symptoms suggestive of B19 infection should be
investigated serologically. The presence of igm confirms recent primary infection (appears >14 days after inoculation and is
present for 3-4 months) IgG appears in the third week and persists life-long, conferring immunity
2. If the mother is found to be infected, the foetus should be monitored by ultrasonography. Hydropic changes may manifest
4-12 weeks after maternal infection
3. When signs of hydrops develop, foetal anaemia should be confirmed by cordocentesis. The presence of viral infection can be
confirmed with detection of B19 antigen or nucleic acid in foetal blood, or viral detection using electron microscopy.
4. Treatment is repeated intrauterine blood transfusion until the foetus is recovered from the viral infection. The prognosis is
good provided that prompt treatment is given.
- 390 -
Listeriosis
Epidemiology
- About 1 in 10000 birth in the UK
- About 25% of cases are pregnancy-related
Bacteriology
Listeria monocytogenes
1. Gram-positive aerobic
2. Non-spore forming bacilli
3. Grows well at 4C (Can grow in refrigerated food)
4. An animal pathogen which is widely distributed in nature:-present in faeces of infected animals, soil, water or sewage
5. Pasteurisation may not eradicate the organism
6. Human acquire the bacteria through:-
a. direct contact with infected animal
b. handling raw meat
c. outbreaks may occur by ingestion of diary products made from unpasturized milk or drinking infected milk
Clinical features
1. Maternal:-
a. Asymptomatic or flu-like illness and fever in healthy individuals
b. Can result in preterm labour and meconium-stained amniotic fluid (MSL)
c. Septicemia, pyrexia of unknown origin (PUO), pneumonia or meningitis in immunosuppressed patients
d. Haematogenous spread of Listeria may result in intrauterine infection of foetus
2. Foetal:-
a. Infections in early in pregnancy:-abortion
b. Infections later in pregnancy:-multi-organ morbidity, e.g., intraventricular hemorrhage, pneumonia, hepatitis,
neurological handicap and intrauterine death
c. Foetal mortality may exceed 75%
3. Neonatal:-
a. Early-onset manifestations due to transplacental transmission:-premature, congenital granulomatous pneumonia or
respiratory distress
b. Late-onset manifestations due to infection at delivery:-meningitis
Maternal diagnosis
1. Pregnant women who have flu-like illness, pyrexia, uterine irritability and bloody vaginal discharge should be investigated
2. Blood, vaginal and amniotic fluid cultures
3. Demonstration of Listeria confirms the diagnosis
Management
1. A combination of ampicillin and gentamicin (or tobramycin) for 3-6 weeks
2. Gentamicin should be avoided in the absence of foetal infection since it has potential foetal ototoxicity
- 391 -
Sexually transmitted disease
Sexually transmitted diseases (STD) are a diverse group of infective diseases that are mainly transmitted via sexually activity.
Some of them confine to local cervical or vaginal infection (e.g. Trichomonas vaginalis, human papillomavirus). Some may
ascend to upper genital tract and spread to pelvic cavity (e.g. Gonorrhea, chlamydia). A few of them may cause systemic infection
and complications such as syphilis and HIV. They are one of the major areas in obstetrics and gynaecology.
STD in gynaecology
- They are the major cause of pelvic inflammatory disease, which is associated with infertility and chronic pelvic pain
- One of the organisms, human papillomavirus is associated with cervical cancer
STD in obstetrics
- They are associated with increased risk of preterm labour and preterm rupture of membranes
- Congenital infection causes foetal malformations:-e.g. Syphilis
- They can be acquired from birth canal during labour causing neonatal infection:-e.g. Gonorrhea and Chlamydia cause
neonatal eye infection, herpes simplex causes neonatal encephalitis
Principles of management of STD

- Treat the primary organism
- Screen for other STD
- Contact tracing
- Advise on protection against further STD e.g. Use of condom
Gonorrhea
Organism
Neisseria gonorrheae, a gram-negative diplococci
Gonococcal infection in gynaecology

1. Acute cervicitis usually asymmptomtic in women (80%)
2. Pelvic inflammatory disease
3. Pharyngitis (oral sex)
4. Disseminated gonococcal infection consists of a bacteremic phase associated with malaise, fever, and a pustular
haemorrhagic rash, and a secondary septic arthritis stage with asymmetric involvement of the knees, wrists or ankles.
Gonococcal infection in obstetrics

1. It is associated with premature rupture of membranes, preterm labour, chorioamnionitis
2. Neonates may acquire the bacteria during labour and result in eye infection (gonococcal ophthalmia neonatorum).
Diagnosis
Microscopy (intracellular gram-negative diplococci) and culture from swab of the endocervix, oral pharynx or pelvic cavity.
Treatment
Penicillin group of antibiotics
- 392 -
Syphilis
Bacteriology
Treponema pallidium (a spirchaete)
1. Slender, tightly coiled, helical cells, 6-14 fine spirals, often flexed in centre
2. Cannot grow in vitro
3. Requires special stains, silver, immunofluorescence or dark ground illumination to visualize it
4. Transmission by:
a. Sexual contact
b. Intrauterine infection
c. Transfusion of infected blood or blood products
d. Direct inoculation
Incidence
0.05% of all pregnancies in PWH
Pathology and incubation period

1. Enters body through skin abrasion
2. Produces granulomas and necrotizing vasculitis
3. Primary:
a. 10-100 days
b. Painless ulcer (primary chancre) at the site of sexual contact
4. Secondary:
a. 4 -12 weeks after chancre
b. Fever, malaise, lymphadenopathy, rash, patchy alopecia, condylomata lata, snail track ulcer on palate and lip
5. Tertiary:
a. Follows period of 2 - 20 years (latent period) after secondary syphilis
b. Gumma (noninfectious granulomatous lesion) in skin, bones, viscera, aorta, brain
c. General paralysis of insane (GPI)
d. Leading to dementia and psychiatric symptoms
e. Fatal if not treated
f. Tabes doralis
g. Posterior column of spinal cord leading to ataxia, numbness, lightening limb pain, gastric crisis, absent tendon
reflexes, Charcot's joints
6. Congenital
a. Hutchinson's triad (developmental damage):-notched teeth, nerve deafness, keratitis of sclera and cornea
b. Secondary syphilis after birth and tertiary syphilis in adolescence
- 393 -
1. VDRL test
a. Use as a screening test in antenatal care, sensitive
b. False positive:-due to pregnancy, autoimmune diseases, tuberculosis
2. FTA-ABS
a. Diagnostic test
b. Very specific
Treatment
- Procaine penicillin 2g/24 hours im for 21 days
- Erythromycin 500mg/ 6 hours po for 15 days
A patient is found to be VDRL positive on routine antenatal screening. How would you counsel the patient and what further
management would you do?
Trichomonas vaginalis
Trichomonas vaginalis is a motile protozoa with four unipolar flagellae. It is one of the common sexually transmitted diseases.
Clinical features:
1. Foul smelling mucopurulent vaginal discharge
2. Dysuria
3. Vulval soreness
4. Physical examination often reveals severe vulvovaginitis, with perivulval intertrigo and petechial hemorrhage on the vaginal
wall and ectocervix ('strawberry cervix')
Diagnosis:
A wet film will demonstrate the motile organisms, but the diagnosis may be confirmed by culture.
Treatment:
1. Antibiotic - Metronidazole (Flagyl)
2. STD screening
3. Contact tracing
Bacterial vaginosis
It is also known as non-specific vaginitis, Gardnerella vaginitis and anaerobic vaginosis as a mixture of these kinds of bacteria is
usually identified. Gardnerella vaginalis is an anaerobic gram-negative rod anaerobe normally found in the vagina. During
infection, the number of the bacteria increases enormously to produce the characteristic grey vaginal discharge with a fishy odour.
True itching does not occur but there may be vulval soreness. It is one of the commonest causes of vaginal discharge in sexually
active women. Diagnosis is usually made clinically, with typical discharge, raised vaginal pH, and positive KOH amine ("sniff")
test. Examination of a stained vaginal smear shows the presence of 'clue cells' and culture on human blood agar shows
beta-haemolysis by Gardnerella vaginalis. The treatment is oral metronidazole or clindamycin vaginal cream. Recent data
suggests that the infection may be associated with preterm delivery.
Human papillomavirus (HPV)

It belongs to the papovaviridae group (a small double-stranded DNA virus) that causes proliferation of the epithelium. It is one
kind of sexually transmitted disease and causes a soft wart-like growth on the genitalia. Today more than 100 different subtypes
have been identified, approximately 40 occur predominantly or exclusively in the genital tract. The subtype 16 and 18 are
associated with the development of cervical epithelial neoplasia (CIN) and risk of cervical cancer. They are present in
approximately 70% of cervical cancer.
- 394 -
Chlamydia
It is a kind of atypical bacteria that replicate in cytoplasmic vacuoles within susceptible eukaryotic cells. Chlamydia trachomatis
is one of the commonest sexually transmitted diseases that causes many complications in Obstetrics and Gynaecology.
Chlamydial infection in gynaecology

- Urethritis
- Cervicitis
- Pelvic inflammatory disease
Chlamydial infection in obstetrics

- Is associated with preterm labour and preterm rupture of membranes
- Causes neonatal conjunctivitis acquired from the birth canal during vaginal delivery
Diagnosis
1. Immunofluorescence test for Chlamydial antigen
2. Uses smear from endocervix, urethra, conjunctivae, rectum and pus from pelvic cavity. etc
3. Fast and sensitive test
4. Tissue culture special transport medium and prompt delivery are required
5. Serology not useful clinically
Treatment
A 2-week course of antibiotic
- Tetracycline group:-is the first line but is contraindicated in pregnancy because of tetratogenic effect
- Erythromycin:-second line when tetracycline is contraindicated
- 395 -
Index
A Breast-feeding ............................................................................... 60
Abdominal circumference ............................................................ 97 Breech presentation....................................................................... 41
Abortion ..................................................................................... 226 Bromocriptine ............................................................................. 206
Abruptio placentae........................................................................ 38 Brow presentation ......................................................................... 20
Acetowhite.................................................................................. 297 C
Acronym ..................................................................................... 363 CA125 ......................................................................................... 315
Acute fatty liver .......................................................................... 143 Caesarean section ........................................................................ 189
Adenomyosis .............................................................................. 240 Calendar method ......................................................................... 216
Advanced maternal age ................................................................ 65 Caput succedaneum .................................................................... 153
AFP (Alpha-feto protein).............................................................. 72 Carboprost................................................................................... 343
Alpha-feto protein (AFP).............................................................. 72 Cardiotocogram (CTG) ............................................................... 174
Amenorrhea ................................................................................ 195 Cephalopelvic disproportion ......................................................... 28
Amniocentesis .............................................................................. 88 Cerebral palsy ............................................................................... 68
Amnioinfusion ............................................................................ 105 Cervagem .................................................................................... 342
Amnioreduction .......................................................................... 105 Cervical cancer ........................................................................... 298
Amnioscope ................................................................................ 179 Cervical incompetence .................................................................. 52
Amniostrix .................................................................................... 50 Cervical intraepithelial neoplasm ................................................ 292
Amniotic fluid .............................................................................. 99 Cervical Tear .............................................................................. 182
Amniotic fluid embolism ............................................................ 140 Chemotherapy ............................................................................. 315
Amniotic fluid index................................................................... 100 Chickenpox ................................................................................. 384
Amniotomy ................................................................................. 163 Chlamydia ................................................................................... 395
Anaemia ..................................................................................... 135 Chorioamnionicity ...................................................................... 112
Android......................................................................................... 27 Chorioamnionitis .......................................................................... 50
Anorexia nervosa ........................................................................ 203 Choriocarcinoma ......................................................................... 313
Anovulation ................................................................................ 272 Chorionic villus sampling (CVS) .................................................. 88
Antepartum ................................................................................... 30 Chromosomal abnormalities ......................................................... 71
Antepartum care ..................................................................... 18, 31 Chronic pelvic pain ..................................................................... 267
Antepartum haemorrhage (APH) .................................................. 35 CIN (Carcinoma-in-situ) ............................................................. 292
Anthropoid.................................................................................... 26 Climacteric.................................................................................. 252
Antibiotics .................................................................................. 359 Clomiphene ................................................................................. 278
Anticoagulants ............................................................................ 361 Cold coagulation ......................................................................... 264
Anticonvulsants .......................................................................... 352 Colostrum ..................................................................................... 59
Anti-hypertensives ...................................................................... 350 Colporrhaphy .............................................................................. 324
Antiphospholipid syndrome........................................................ 141 Colposcopy ................................................................................. 296
Apgar score................................................................................. 180 Colposuspension ......................................................................... 330
APH of unknown origin ............................................................... 40 Combined oral contraceptives ..................................................... 217
Appendicitis................................................................................ 143 Conception .................................................................................. 274
ART (Assisted Reproductive Technology) ................................. 276 Condom ...................................................................................... 216
Asherman syndrome ................................................................... 206 Congenital abnormalities .............................................................. 78
Assisted Reproductive Technology (ART) ................................. 276 Conjoint twin .............................................................................. 113
Asymptomatic bacteriuria........................................................... 136 Consanguinity ............................................................................... 69
Asynclitism................................................................................. 169 Contraception .............................................................................. 214
Atosiban ..................................................................................... 347 Contracted pelvis .......................................................................... 28
B Contraction stress test ................................................................. 107
Bacterial vaginosis...................................................................... 394 Controlled cord traction .............................................................. 156
Bagshawe score .......................................................................... 314 Cord prolapse ................................................................................ 46
Bartholins Gland ....................................................................... 249 Cordocentesis ................................................................................ 89
Basal body temperature .............................................................. 274 Corpus luteal cyst........................................................................ 234
Benign ovarian tumour ............................................................... 241 Couvelaire uterus .......................................................................... 39
Bethesda ..................................................................................... 295 Crown-rump length ....................................................................... 97
Biochemical screening .................................................................. 72 Cryotherapy ................................................................................ 264
Biparietal diameter ....................................................................... 98 Cryptomenorrhea ........................................................................ 198
Birth asphyxia............................................................................. 180 CTG (Cardiotocogram) ............................................................... 174
Birth trauma .................................................................................. 68 Curettage ..................................................................................... 257
Bishop score ............................................................................... 163 CVS (Chorionic villus sampling) .................................................. 88
Blood pressure measurement ...................................................... 125 Cystocele..................................................................................... 320
Braxton Hicks contractions........................................................... 48 Cystometry .................................................................................. 335
Breast milk ................................................................................... 60 Cystoscopy .................................................................................. 334
- 396 -
Cytomegalovirus......................................................................... 389 Examination (Gynaecology) ....................................................... 370
Cytotec ....................................................................................... 342 Examination (Obstetrics) ............................................................ 365
Cyutobrush ................................................................................. 294 Examination of genital prolapse.................................................. 322
D Exenteration ................................................................................ 302
Danazol....................................................................................... 356 Exomphalos .................................................................................. 79
Dating of pregnancy ..................................................................... 33 Extension .................................................................................... 149
Deep transverse arrest ................................................................. 166 External Cephalic Version (ECV) ................................................. 44
Denominator ................................................................................. 20 F
Dermoid cyst .............................................................................. 242 Failure to progress ...................................................................... 165
Descend ...................................................................................... 149 Fecundity ...................................................................................... 65
Destructive mole ......................................................................... 312 Femur length ................................................................................. 98
Detrusor instability ..................................................................... 334 Ferning ........................................................................................ 273
Detrusor Overactivity ................................................................. 333 Fertilisation ................................................................................. 273
Detrusor Overactivity Incontinence ............................................ 333 Fibroid ........................................................................................ 243
Dexamethasone........................................................................... 355 Flexion ........................................................................................ 149
Dextrorotation of uterus................................................................ 29 Foetal anatomy.............................................................................. 19
Diabetes mellitus ........................................................................ 118 Foetal bradycardia....................................................................... 178
Diazepam .................................................................................... 352 Foetal diagnosis and therapy ......................................................... 88
Dinoprostone .............................................................................. 343 Foetal distress ............................................................................. 179
Disorders of early pregnancy ...................................................... 224 Foetal growth ................................................................................ 92
Disseminated intravascular coagulopathy................................... 136 Foetal heart rate pattern .............................................................. 175
Doppler effect ............................................................................... 91 Foetal infection ........................................................................... 373
Doppler studies ............................................................................. 91 Foetal medicine ............................................................................. 70
Doptone ...................................................................................... 368 Foetal Medicine ............................................................................ 70
Down syndrome............................................................................ 74 Foetal movement......................................................................... 107
Drinking during labour ............................................................... 152 Foetal scalp blood sampling ........................................................ 179
Dysfunctional uterine bleeding ................................................... 208 Foetal scalp electrode .................................................................. 178
Dysgerminoma ........................................................................... 290 Foetal skull.................................................................................... 19
Dyskaryosis ................................................................................ 297 Follicular cyst ............................................................................. 241
Dysmenorrhoea........................................................................... 212 Follicular phase ........................................................................... 274
Dyspareunia ................................................................................ 283 Fontanelle ..................................................................................... 19
Dystocia ...................................................................................... 166 Forceps........................................................................................ 185
Dysuria ....................................................................................... 333 Fraxiparine .................................................................................. 361
E Frequency of micturition............................................................. 333
Early pregnancy complications................................................... 225 Fundal height .............................................................................. 368
Eclampsia ................................................................................... 130 Funnel pelvis ................................................................................. 27
Ectopic pregnancy ...................................................................... 231 G
ECV (External Cephalic Version) ................................................ 44 Gastroschisis ................................................................................. 79
Edward syndrome ......................................................................... 75 GBS(Group B streptococcus)..................................................... 381
Electrocautery ............................................................................. 264 Gemeprost ................................................................................... 342
Emergency contraception ........................................................... 222 Genetic counselling....................................................................... 89
Endometrial ablation................................................................... 258 Genetic disorder ............................................................................ 83
Endometrial carcinoma ............................................................... 306 Genital prolapse .......................................................................... 318
Endometrial hyperplasia ............................................................. 304 Genuine stress incontinence ........................................................ 329
Endometrial sampler ................................................................... 265 Germ cell tumour ........................................................................ 289
Endometrial sampling ................................................................. 265 Gestational diabetes .................................................................... 119
Endometriosis ............................................................................. 237 Gestational trophoblastic disease ................................................ 310
Engage ........................................................................................ 153 GnRH (Gonadotropin releasing hormone) .................................. 358
Engagement ........................................................................ 149, 153 GnRHa (Gonadotropin releasing hormone analogue) ................. 357
English usage .............................................................................. 363 Gonadotropin .............................................................................. 358
Engorgement of breasts ................................................................ 59 Gonadotropin releasing hormone (GnRH) ................................. 358
Enoxaparin.................................................................................. 361 Gonadotropin releasing hormone analogue (GnRHa) ................ 357
Enterocele ................................................................................... 321 Gonadotropin therapy ................................................................. 358
Entonox ...................................................................................... 172 Gonorrhea ................................................................................... 392
Epidural anaesthesia ................................................................... 172 Grand multipara ............................................................................ 67
Epilepsy ...................................................................................... 141 Gravid ........................................................................................... 67
Episiotomy.................................................................................. 181 Group B streptococcus ................................................................ 381
Eponym ...................................................................................... 363 Gynaecoid ..................................................................................... 26
Ergometrine ................................................................................ 341 Gynaecological surgery .............................................................. 256
- 397 -
H J
Haemophilia ................................................................................. 83 Jehovahs witness ......................................................................... 69
Haemophilia A ............................................................................. 83 K
Haemophilia B .............................................................................. 83 Kallman syndrome ...................................................................... 202
HCG (Human chorionic gonadotropin) ........................................ 73 Klinefelter syndrome .................................................................... 76
HELLP syndrome ....................................................................... 132 Koilocyte..................................................................................... 297
Hemabate .................................................................................... 343 Krukenberg tumour ..................................................................... 290
Hepatitis ..................................................................................... 374 L
Hepatitis B .................................................................................. 374 Labetolol ..................................................................................... 351
Hepatitis B Immune Globulin ..................................................... 362 Labour ......................................................................................... 148
Hepatitis C .................................................................................. 375 Lactation ....................................................................................... 60
Hexoprenaline ............................................................................ 348 Lamda sign.................................................................................. 113
History taking (Gynaecology) .................................................... 369 LEEP (Loop electrosurgical excisional procedure) ..................... 297
History taking (Obstetrics) ......................................................... 364 Levator ani .................................................................................... 24
HIV (Human Immunodeficiency Virus) ..................................... 376 Levonorgestrel intra-uterine system ............................................ 222
Hormonal replacement therapy (HRT) ....................................... 254 Lie ................................................................................................. 19
HPV (Human papillomavirus) .................................................... 394 Life table analysis ....................................................................... 215
HRT (Hormone Replacement Therapy) .................................... 254 Listeriosis.................................................................................... 391
Human chorionic gonadotropin (HCG) ........................................ 73 Lithotomy ................................................................................... 372
Human Immunodeficiency Virus (HIV) ..................................... 376 Lochia ........................................................................................... 59
Human papillomavirus (HPV) .................................................... 394 Loop electrosurgical excisional procedure (LEEP) ..................... 297
Hydatiform mole ........................................................................ 310 Lordosis ........................................................................................ 28
Hydralazine ................................................................................ 350 Loveset maneuver ....................................................................... 171
Hydrops foetalis............................................................................ 80 Lower segment.............................................................................. 29
Hyperemesis gravidarum ............................................................ 234 Luteal phase ................................................................................ 274
Hyperhep .................................................................................... 362 Luteal phase insufficiency .......................................................... 274
Hyperprolactinaemia .................................................................. 204 M
Hypertension .............................................................................. 124 Macrosomia .................................................................................. 96
Hysterectomy.............................................................................. 260 Magnesium Sulphate (MgSO4)................................................... 353
Hysterosalpingogram .................................................................. 266 Malignant neoplasms of ovary .................................................... 288
Hysteroscopy .............................................................................. 263 Malignant neoplasms of uterine cervix ....................................... 291
Hysterotomy ............................................................................... 257 Malignant neoplasms of uterine corpus ...................................... 304
I Malignant neoplasms of vagina and vulva .................................. 285
ICSI (Intra-cytoplasmic sperm injection) ................................... 279 Malpresenation.............................................................................. 41
Imperforate hymen ..................................................................... 267 Manual removal of placenta (MROP) ......................................... 159
In vitro fertilisation (IVF) ........................................................... 279 Marsupialisation.......................................................................... 264
Incontinence ............................................................................... 329 Maternal anatomy ......................................................................... 24
Induction of labour (IOL) ........................................................... 162 Maternal medicine ...................................................................... 117
Infertility..................................................................................... 270 Maternal mortality ........................................................................ 62
Inlet .............................................................................................. 24 Meconium stained liquor (MSL)................................................. 104
Insemination ............................................................................... 279 Menopause .................................................................................. 252
Instrumental delivery .................................................................. 183 Menorrhagia ................................................................................ 207
Intermittent auscultation ............................................................. 174 Menstrual cycle ........................................................................... 194
Interstitial cystitis ....................................................................... 333 Menstrual disorders..................................................................... 194
Intertuberous diameter .................................................................. 25 Methrotrexate .............................................................................. 362
Intra-cytoplasmic sperm injection (ICSI) ................................... 279 Methyldopa ................................................................................. 350
Intrapartum care............................................................................ 18 Metropathia haemorrhagia .......................................................... 208
Intrapartum foetal monitoring..................................................... 173 MgSO4 (Magnesium Sulphate)................................................... 353
Intrauterine contraceptive device (IUCD)................................... 220 Minor disorders of pregnancy ..................................................... 235
Intrauterine growth restriction (IUGR) ......................................... 93 Misoprostol ................................................................................. 341
Intrauterine system ..................................................................... 222 Mitral stenosis ............................................................................. 134
Invasive mole ............................................................................. 312 Mittelschmerz ............................................................................. 212
Involution ..................................................................................... 59 Molar pregnancy ......................................................................... 310
IOL ............................................................................................. 162 Morbid adherence of placenta ..................................................... 158
Ischial spine .................................................................................. 25 Moulding .................................................................................... 153
IUCD (Intrauterine contraceptive device)................................... 220 MROP (Manual removal of placenta) ......................................... 159
IUGR (Intrauterine growth restriction) ................................... 48, 93 MSL(Meconium stained liquor).................................................. 104
IVF (In-vitro fertilisation)........................................................... 279 Multiple pregnancy ..................................................................... 108
Myomectomy .............................................................................. 259
- 398 -
N Placenta increta ........................................................................... 158
Nadroparin .................................................................................. 361 Placenta percreta ......................................................................... 158
Nagele's rule ................................................................................. 33 Placenta praevia ............................................................................ 35
Naloxone .................................................................................... 362 Placentaacreta ............................................................................. 158
Narcotic analgesia ...................................................................... 172 Platypoid ....................................................................................... 27
Neonatal death .............................................................................. 64 Polycystic Ovarian Disease / Syndrome (PCOD/PCOS) ............ 199
Neonatal resuscitation................................................................. 156 Polyhydramnios .......................................................................... 102
Neonatological consultation ....................................................... 160 Position ......................................................................................... 20
Neural tube defect......................................................................... 78 Postcoital bleeding ...................................................................... 211
Nifedipine ........................................................................... 346, 350 Postcoital contraception .............................................................. 222
Nocturia ...................................................................................... 333 Postcoital test .............................................................................. 275
Non-dysjunction ........................................................................... 73 Postmenopausal bleeding ............................................................ 211
Nuchal translucency ..................................................................... 73 Postnatal discharge ..................................................................... 161
O Postpartum blue ............................................................................ 61
Obstetric abdominal exam .......................................................... 365 Postpartum care....................................................................... 18, 53
Obstetric anaesthesia .................................................................. 172 Postpartum depression .................................................................. 61
Obstetric emergency ..................................................................... 67 Postpartum fever ........................................................................... 54
Obstetric statistics ......................................................................... 62 Postpartum haemorrhage .............................................................. 54
Obstetric surgery .......................................................................... 67 Postpartum psychosis .................................................................... 61
Obstetrics ...................................................................................... 18 Postterm ........................................................................................ 66
Obstructed labour ....................................................................... 165 Potter syndrome ............................................................................ 82
Occipito-posterior ....................................................................... 169 PPROM (Premature Prelabour Rupture of Membranes) ............... 49
OHSS (Ovarian Hyperstimulation Syndrome) ........................... 280 Pre-conception counselling ........................................................... 30
Oligohydramnios ........................................................................ 101 Preeclampsia ....................................................................... 124, 125
Oligohydramnios sequence......................................................... 102 Pregnancy test ............................................................................... 32
Oligomenorrhea .......................................................................... 198 Premature Prelabour Rupture of Membranes (PPROM) ............. 49
Omphalocele ................................................................................. 79 Premenstrual syndrome ............................................................... 213
Operative delivery .............................................................. 181, 183 Presentation................................................................................... 20
Os ................................................................................................ 29 Preterm delivery ............................................................................ 48
Osteoporosis ............................................................................... 252 Preterm labour............................................................................... 47
Outlet ...................................................................................... 24, 28 Progestogen injectable ................................................................ 219
Ovarian cancer ............................................................................ 288 Progestogen-only pill .................................................................. 219
Ovarian cystadenoma ................................................................. 241 Prolactin ...................................................................................... 204
Ovarian Hyperstimulation Syndrome (OHSS) ........................... 280 Prostaglandin .............................................................................. 341
Overflow incontinence ............................................................... 330 Prostaglandin E2 ......................................................................... 343
Ovulation .................................................................................... 273 Pseudo gestational sac................................................................. 234
Ovulation induction .................................................................... 277 Pubic symphysis ........................................................................... 25
Oxytocics .................................................................................... 339 Puerperium.................................................................................... 59
Oxytocin ..................................................................................... 339 Pulmonary embolism .................................................................. 139
P Pyometra ..................................................................................... 249
Pad test ....................................................................................... 323 R
Palliative ..................................................................................... 316 Radiotherapy ............................................................................... 316
Pap smear ................................................................................... 293 Rectocele..................................................................................... 320
Partogram ................................................................................... 147 Recurrent abortion ...................................................................... 228
Parvovirus................................................................................... 390 Reflex incontinence .................................................................... 330
Patau syndrome ............................................................................ 76 Renal agenesis............................................................................... 81
PCOD/PCOS (Polycystic Ovarian Disease/Syndrome) .............. 199 Residual trophoblastic disease .................................................... 313
Pearl index .................................................................................. 214 Restitution ................................................................................... 149
Pelvic inflammatory disease ....................................................... 246 Retained placenta ........................................................................ 158
Pelvimetry .................................................................................... 28 Retroversion of uterus ................................................................. 267
Pelvis ............................................................................................ 24 Rhesus ........................................................................................... 86
Perinatal mortality ........................................................................ 62 Rhesus D iso-immunisation .......................................................... 86
Perineal tear ................................................................................ 182 Rickets .......................................................................................... 28
Pethidine ..................................................................................... 172 Ring pessary................................................................................ 323
Phenytoin .................................................................................... 353 Ritodrine ..................................................................................... 349
Physiological cysts ..................................................................... 241 Rotation ...................................................................................... 149
Pinard stethoscope ...................................................................... 368 ROM (Rupture of membranes) ................................................... 49
Pipelle de Cornier ...................................................................... 265 Rubella ........................................................................................ 382
Placenta ........................................................................................ 67 Rupture of membranes (ROM) ..................................................... 49
- 399 -
S Tocolytic ..................................................................................... 344
Sagittal suture ............................................................................... 19 TOS (Trial of Scar) ..................................................................... 192
Salbutamol .................................................................................. 348 Toxoplasmosis ............................................................................ 388
Second stage of labour ................................................................ 150 Transformation zone ................................................................... 291
Semen analysis ............................................................................. 76 Trial of labour ............................................................................. 165
Septic abortion ............................................................................ 230 Trial of scar (TOS) ...................................................................... 192
Seven-day rule ............................................................................ 219 Trichomonas vaginalis ................................................................ 394
Sexually transmitted disease (STD) ............................................ 392 Trimester ....................................................................................... 67
SGA (Small-for-gestational-age) ................................................ 92 Trisomy ......................................................................................... 73
Sheehan syndrome ........................................................................ 58 Trophoblastic diseases ................................................................ 310
Shoulder dystocia ............................................................... 151, 167 True incontinence ....................................................................... 330
Sinciput......................................................................................... 19 TTTS (Twin-twin transfusion syndrome) ................................. 113
Sling Operations ........................................................................ 330 Tumour marker ........................................................................... 315
Small-for-gestational-age (SGA) .................................................. 92 Turner syndrome ........................................................................... 77
Spatula ........................................................................................ 294 Twin pregnancy .......................................................................... 108
Speculum .................................................................................... 372 Twin-twin transfusion syndrome (TTTS) ................................... 113
Spinnbarkeit................................................................................ 273 U
Staging of CA cervix .................................................................. 303 Urethral Sling Operations .......................................................... 330
Staging of CA endometrium ....................................................... 309 Urethrocele ................................................................................. 320
Staging of CA vagina ................................................................. 285 Urethropexy ............................................................................... 330
Staging of CA vulva ................................................................... 287 Urge incontinence ....................................................................... 330
Staging of GTD .......................................................................... 314 Urgency ...................................................................................... 329
Station......................................................................................... 154 Urinary incontinence................................................................... 329
STD (Sexually transmitted disease) ........................................... 392 Urodynamic Stress Incontinence (USI)....................................... 329
Sterilisation................................................................................. 223 Urodynamic study ....................................................................... 334
Steroid Cover .............................................................................. 356 Uroflowmetry ............................................................................. 334
Steroids ....................................................................................... 355 Urogenital diaphragm ................................................................... 24
Stillbirth ........................................................................................ 62 Urogynaecology .......................................................................... 317
Stress incontinence ..................................................................... 329 Uterine atony ................................................................................ 55
Subaponeurotic haematoma .......................................................... 68 Uterine hyperstimulation............................................................. 164
Subgaleal haematoma ................................................................... 68 Uterine inversion........................................................................... 57
Subpubic arch ............................................................................... 25 Uterine prolapse .......................................................................... 321
Sulindac ...................................................................................... 346 Uterine rupture .............................................................................. 56
Sulprostone ................................................................................. 343 V
Symphysial-fundal height .......................................................... 368 Vabra Curettage ......................................................................... 265
Symptomatology (Gynaecology) ................................................ 369 Vacuum extraction ...................................................................... 188
Symptomatology (Obstetrics) ..................................................... 364 Vaginal breech delivery .............................................................. 170
Syntocinon .................................................................................. 340 Vasa praevia.................................................................................. 39
Syntometrine .............................................................................. 340 Vasectomy .................................................................................. 223
Syphilis ....................................................................................... 393 Vault prolapse ............................................................................. 321
T Velamentous Insertion of the Cord ............................................... 39
Teratogen ...................................................................................... 82 Vertex ........................................................................................... 19
Teratoma..................................................................................... 242 Viable.......................................................................................... 224
Termination of pregnancy........................................................... 224 Villous choriocarcinoma ............................................................. 312
Testicular feminisation syndrome ............................................... 206 Vitamin K ................................................................................... 362
Thalassemia .................................................................................. 85 Voiding disorder ......................................................................... 333
Third stage of labour................................................................... 155 W
Thrombocytopenia ...................................................................... 137 Warfarin ...................................................................................... 361
Thromboembolism ..................................................................... 138 Y
Thyroid disorder ......................................................................... 144 Yolk sac tumour .......................................................................... 290
Tibolone ..................................................................................... 356
- 400 -
Figure Legend
Figure 1 Attitude ............................................................................................................................................................................... 21
Figure 2 Lie....................................................................................................................................................................................... 21
Figure 3 Position ............................................................................................................................................................................... 21
Figure 4 Breech and Cephalic Presentation ...................................................................................................................................... 21
Figure 5 Brow Presentation .............................................................................................................................................................. 21
Figure 6 Shoulder Presentation ......................................................................................................................................................... 21
Figure 7 Vertex Presentation ............................................................................................................................................................. 21
Figure 8 Face Presentaton ................................................................................................................................................................. 21
Figure 9 Foetal Skull......................................................................................................................................................................... 22
Figure 10 Measurements of Foetal Skull .......................................................................................................................................... 22
Figure 11 Sutures .............................................................................................................................................................................. 23
Figure 12 Circumferences ................................................................................................................................................................. 23
Figure 13 Levator Ani (Perineum) .................................................................................................................................................... 25
Figure 14 Pelvic Floor ...................................................................................................................................................................... 25
Figure 15 Pelvic Brim; Pelvic Inlet................................................................................................................................................... 26
Figure 16 Gynaecoid (Left) and Anthropoid (Right) ........................................................................................................................ 27
Figure 17 Android (Left) and Platypoid (Right) ............................................................................................................................... 27
Figure 18 Symptoms, Signs and Tests of Pregnancy ........................................................................................................................ 34
Figure 19 Classification of Placenta Praevia .................................................................................................................................... 35
Figure 20 External Cephalic Version. ............................................................................................................................................... 45
Figure 21 Presentation of the Cord (Left) ; Occult Presentation of the Cord (Right) ....................................................................... 46
Figure 22 Prolapsed Cord ................................................................................................................................................................. 46
Figure 23 Causes of Uterine Rupture. (Left To Right) Spontaneous; Classical C/S; and Lower Segment C/S. ............................... 56
Figure 24 Uterine Inversion. (Left To Right) First, Second and Third Degree ................................................................................. 58
Figure 25 Manual Reduction by Taxis (Left and Centre); and by Laprotomy (Right) ...................................................................... 58
Figure 26 Fluid Thrill (Left) ........................................................................................................................................................... 102
Figure 27 Uterus Large-for-Date. ................................................................................................................................................... 108
Figure 28 More than 2 Foetal Poles are Palpable............................................................................................................................ 108
Figure 29 Chorioamnionicity. ......................................................................................................................................................... 112
Figure 30 Caput Succedaneum ....................................................................................................................................................... 153
Figure 31 Controlled Cord Traction ................................................................................................................................................ 156
Figure 32 Placenta Examined ......................................................................................................................................................... 157
Figure 33 Early Onset.. ................................................................................................................................................................... 176
Figure 34 Late Onset....................................................................................................................................................................... 176
Figure 35 Variable Onset................................................................................................................................................................. 176
Figure 36 Different Degrees of Perineal Tear. (Left To Right) First, Second and Third. ................................................................ 182
Figure 37 Wrigley's Forceps ........................................................................................................................................................... 185
Figure 38 Anderson's / Simpsons Forceps ..................................................................................................................................... 185
Figure 39 Kielland's Forceps .......................................................................................................................................................... 185
Figure 40 (Left To Right) Vacuum Cups for OA and OP Position respectively; Vacuum Tubing; and Vacuum Machine. ............. 188
Figure 41 Macroscopic (Left) and Microscopic (Right) Appearance of Polycystic Ovaries. ......................................................... 199
Figure 42 Basal Body Temperature (Left) and Cervical Mucus (Right) Method ............................................................................ 216
Figure 43 Condom (Left Two); Diaphragm (Right Three) and Cervical Cap (Below) ................................................................... 216
Figure 44 Procedure of IUCD Insertion. ......................................................................................................................................... 221
Figure 45 Medical Abortion for Early First Trimester. ................................................................................................................... 224
Figure 46 Vacuum Suction Evacuation of the Uterus. .................................................................................................................... 224
Figure 47 Dilation and Evacuation. ................................................................................................................................................ 225
Figure 48 Different Types of Abortion. ........................................................................................................................................... 226
Figure 49 Anatomical Factors:-Fibroid (Left) and Arcuate Uterus With Septum (Right). .............................................................. 228
Figure 50 Fallopian Tube (Left) and Uterine Cornus (Right) Implantation. ................................................................................... 231
- 401 -
Figure 51 Ovarian (Left) and Cervical (Right) Implantation .......................................................................................................... 231
Figure 52 Rupture Into the Tube (Left) and Peritoneum (Right). ................................................................................................... 231
Figure 53 Diagnosis (Left) and Treatment (Right) of Tubal Pregnancy. ......................................................................................... 232
Figure 54 Gross Appearance of Mucinous Cystadenoma. .............................................................................................................. 241
Figure 55 The Macroscopic (Left) and Microscopic (Right) Appearance of Dermoid Cyst. .......................................................... 242
Figure 56 (Left To Right) Bartholin's Cyst and its Differential Diagnoses, Sebaceous Cyst, and Lipoma. .................................... 249
Figure 57 Hirsutism (Left) and Virilism (Right). ............................................................................................................................ 251
Figure 58 Dilation and Curettage .................................................................................................................................................... 257
Figure 59 Trauma To the Cervix and Uterus. .................................................................................................................................. 257
Figure 60 Cryotherapy .................................................................................................................................................................... 264
Figure 61 Electrocautery ................................................................................................................................................................. 264
Figure 62 Complications of Imperforate Hymen. ........................................................................................................................... 267
Figure 63 Examination (Left) and Treatment (Right) of Imperforate Hymen. ............................................................................... 267
Figure 64 Progesterone Level, Highest At Day 21 (7 Days Before Menstruation). ........................................................................ 277
Figure 65 Serial Ultrasound of Ovaries. ......................................................................................................................................... 277
Figure 66 Conventional Radical Vulvectomy (Leftmost Two), Separate Groin Incision(Third) and Modified Radical
Vulvetomy(Right).................................................................................................................................................................. 287
Figure 67 Gross and Microscopic Appearance of Krukenberg Tumour. ......................................................................................... 290
Figure 68 Cone Excision By Knife. ................................................................................................................................................ 292
Figure 69 Direct Spread (Leftmost Two) and Lymphatic Spread. .................................................................................................. 299
Figure 71 Radical Hysterectomy. .................................................................................................................................................... 300
Figure 70 Radiotherapy For Cervical Cancer.................................................................................................................................. 300
Figure 72 (Left To Right) Adenoacanthoma (Grade I); Adenosquamous Carcinoma (Grade Ii); Clear Cell Carcinoma. .............. 306
Figure 74 Cystocele ........................................................................................................................................................................ 320
Figure 75 Urethrocele ..................................................................................................................................................................... 320
Figure 76 Rectocele ........................................................................................................................................................................ 320
Figure 77 Enterocele ....................................................................................................................................................................... 321
Figure 73 Ring Pessary ................................................................................................................................................................... 323
Figure 78 Burch's Colposuspension ................................................................................................................................................ 330
Figure 79 Fundal Height (Left) and Doptone (Right) ..................................................................................................................... 368
Figure 80 Speculums, Made of (Left) Steel and (Right) Perspex. .................................................................................................. 372
1 January 2004 Dr. Edward Chu

1 November 2009 Anonymous collegues in Class 2011
1 March 2010 RTHL
- 402 -

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THE CHINESE UNIVERSITY OF HONG KONG MEDICAL YEAR IV

OBSTETRICS & GYNAECOLOGY MODULE

(1) Obstetrics Illustrated (6th Ed.) by Hanretty, K.P. in 2003;

NOTICE FOR FIRST DRAFT EDITION

NOTICE FOR SECOND DRAFT EDITION

For ladies, wives, mothers, and our future generations.

Aims of obstetric care

There are three phases of obstetric care:

Other important topics in general obstetrics

Different types of presentation

Figure 1 Attitude Figure 2 Lie

Figure 3 Position Figure 4 Breech and Cephalic Presentation

The presenting diameters of the skull

Figure 9 Foetal Skull

Figure 10 Measurements of foetal skull

The exact origins of the muscles are:-

Clinical role of levator ani

Figure 13 Levator Ani (Perineum)

Figure 14 Pelvic Floor

Figure 15 Pelvic Brim; Pelvic Inlet

Android pelvis can be diagnosed by pelvimetry, with the following features:-

Figure 16 Gynaecoid (Left) and Anthropoid (Right)

Figure 17 Android (Left) and Platypoid (Right)

4. Adjustment of medical therapies

Antepartum care consists of booking assessment; and continuing antenatal care.

2. Initial screening tests should include:

Routine maternal assessment

Routine foetal assessment

How to calculate EDC (Nagele's rule)

Some important facts:-menstrual cycles, ovulation and fertilization

Some important facts:-symptoms and signs of pregnancy

Figure 18 Symptoms, signs and tests of pregnancy

Some important facts:-ultrasound dating

Figure 19 Classification of placenta praevia

TVS showing a posterior placenta preavia type II (reaching os)

Protocol, as of 19 November 2004

Incidence 0.20.8% of all pregnancies, half of the cases occur preterm

Protocol, as of 22 June 2002

Velamentous Insertion of the Cord

Clinical presentation and diagnosis

Protocol, as of 22 June 2002

Decision of mode of delivery

Other determining factors:

Protocol, as of 27 July 2002

Figure 20 External Cephalic Version.

Protocol, as of 27 July 2002

Risk factors for preterm labour

Prediction and prevention

Protocol, as of 7 May 2001

Braxton Hicks contractions

Causes of preterm delivery

Modes of preterm delivery

Risk factors for premature rupture of membranes

Diagnosis of rupture of membranes

Risk after rupture of membranes

Protocol, as of 5 November 2002

Protocol, as of 6 November 2002

Protocol, as of 22 June 2002

Routine care in early postpartum period

Postpartum visit at the end of puerperium

What medical students should know?

Causes of primary PPH

Causes of secondary PPH