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Hwees

Obstetrics &
Gynaecology

Tan Hwee Leong Yong Loo Lin School of Medicine Class of 2009-2014

Sources:
Hacker and Moores Essentials of Obstetrics and Gynaecology 5th Edition
Oxford Handbook of Clinical Specialties 8th Edition
NUS Department of O&G Lecture Slides 2012/2013
KKH Lecture Slides 2012/2013
SGH A/Prof Tay Sun Kuies Gynaecologic Oncology Lecture Slides
CONTENTS

Obstetrics Gynaecology
Antenatal Care 1 Benign Gynaecologic Conditions 70
Introduction to Antenatal Care 1 Benign Conditions of the Vulva 70
1st Trimester Antenatal Care 1 Benign Conditions of the Vagina 71
2nd Trimester Antenatal Care 4 Benign Conditions of the Cervix 72
3rd Trimester Antenatal Care 5 Benign Conditions of the Uterine Corpus 73
Prenatal Screening & Diagnosis 8 Uterine Leiomyoma (Fibroid) 73
Maternal Ailments in Pregnancy 10 Endometrial Conditions 75
Endometriosis 76
Labour & Puerperium 11 Benign Conditions of the Fallopian Tube 79
Anatomic Considerations in Labour 11 Benign Conditions of the Ovary 79
Normal Labour 14
Induction of Labour 20 Gynaecologic Bleeding & Pain 80
Abnormal Labour Progress 21 Normal Menstrual Cycle 80
Malpresentation 22 Amenorrhea & Oligomenorrhea 82
Assisted (Instrumental) Delivery 24 Abnormal Uterine Bleeding 86
Caesarian Delivery 26 Post-Coital & Post-Menopausal Bleeding 87
Obstetric Emergencies 27 Dysmenorrhea 88
Shoulder Dystocia 27 Pelvic Pain 89
Cord Prolapse 29
Amniotic Fluid Embolism 29 Reproductive Tract Infections 90
Puerperium 30
Vulvovaginitis 90
Sexually Transmitted Infections 91
Obstetric Complications 34 Pelvic Inflammatory Disease 94
Preterm Labour 34
Premature Rupture of Membranes 37 Family Planning 96
Intrauterine Growth Restriction 40
Principles of Contraception 96
Post-Term Pregnancy 41
Hormonal Contraception 97
Intrauterine Fetal Demise 41
Non Hormonal Contraception 101
Emergency Contraception 103
Hypertensive Disorders of Pregnancy 42 Termination of Pregnancy 104
Preeclampsia & Eclampsia 42
Chronic Hypertension in Pregnancy 45 Infertility 107
Approach to Infertility 107
Obstetric Hemorrhage 46 Etiologic Factors of Infertility 108
Bleeding in Early Pregnancy 46 Assisted Reproductive Techniques 110
Miscarriage (Spontaneous Abortion) 46
Ectopic Pregnancy 49
Gynaecologic Oncology 113
Antepartum Hemorrhage 52
Cervical Dysplasia & Cancer 113
Placenta Praevia 53
Ovarian Neoplasms 118
Abruptio Placentae 55
Types of Ovarian Neoplasms 118
Vasa Praevia 57
Clinical Approach to Ovarian Cancer 120
Approach to Ovarian Masses/Cysts 123
Miscellaneous Conditions in Pregnancy 58 Uterine Corpus Cancer 127
Endocrine Disorders 58 Endometrial Cancer 127
Diabetes Mellitus in Pregnancy 58 Uterine Sarcomas 130
Thyroid Disorders in Pregnancy 60 Gestational Trophoblastic Neoplasia 131
Cardiovascular Disorders 61 Vulvar & Vaginal Cancers 135
Heart Disease in Pregnancy 61
Anemia in Pregnancy 62
Menopause 136
Venous Thromboembolism in Pregnancy 62
Changes in Menopause 136
Autoimmune Disorders 63
Management of Menopausal Women 137
Seizure Disorders 63
Pharmacological Therapy for Menopause 140
Infectious Diseases in Pregnancy 64

CONTENTS

ANTENATAL CARE
Introduction to Antenatal Care 1st Trimester Antenatal Care
Goals of Antenatal Care Confirmation of Pregnancy & Viability
- Detect maternal disease & ameliorate discomforts of Regardless of reason for initial presentation, a formal diagnosis of
pregnancy pregnancy followed by a determination of its viability are essential before
- Monitor & promote fetal well-being progressing on to the other aspects of antenatal assessment or care
- Early & continued risk assessment to identify high-risk
pregnancies Symptoms of Pregnancy
- Prepare mother for labour - Amenorrhea (commonest presentation)
- Urinary frequency
Overall Chronology of Routine Antenatal Care Note that acute urinary retention may occur at times
- Pre-Conception Care with a growing gravid uterus especially in the
Ideally, prenatal care should begin before pregnancy context of a retroverted uterus
as modifiable maternal factors often have the - Breast engorgement &/or tenderness
greatest impact on the early events following - Nausea/vomiting
conception - Easy fatigability
- Implantation occurs 7 days after conception
- Placental development then follows Signs of Pregnancy
- Organogenesis occurs before 1st trimester ends - Presumptive signs of pregnancy (skin, mucous membrane)
Hence by the time most pregnant women have their Dark discolouration of the vulva & vaginal walls
first antenatal visit, it is often too late to prevent (Chadwick sign)
certain birth defects or defective placental Pigmentation of the skin & abdominal striae
development - Linea nigra (pigmented midline running from
- 1st Trimester Antenatal Care umbilicus to pubic region)
(4-weekly visits) - Chloasma aka melasma (facial skin
Confirm pregnancy & determine viability pigmentation, commonly under the eyes & over the
Confirm gestational age & expected date of delivery nose bridge)
with dating & viability scan (6-11 weeks) - Probable signs of pregnancy (uterus)
Comprehensive history & physical examination Globular uterus (as early uterine enlargement tends
Routine antenatal screening blood tests to occur in the anteroposterior diameter)
Identification of high-risk pregnancies (from above) Disproportionate enlargement of 1 cornua of the
Preliminary maternal counseling uterus due to asymmetrical implantation of the
Management of maternal well-being ovum (Piskacek sign)
Offer 1st trimester prenatal screening Palpable/compressible junction between the uterine
- 2nd Trimester Antenatal Care corpus & cervix due to softening of the uterine
(4-weekly visits) consistency (Hegar sign)
Clinical fetal monitoring Softening of the cervix
Continued maternal counseling - Positive signs of pregnancy
Continued management of maternal well-being Detection of fetal heartbeat
Offer 2nd trimester prenatal screening (in the event - May be detected as early as 9 weeks with
that patient presents only in the 2nd trimester) modern Doppler techniques, but usually only
Detect possible problems with pregnancy with fetal detected by 12 weeks transabdominally as that
screening (anomaly) ultrasound scan (20-22 weeks): is when the uterus becomes clinically palpable
- Fetal anomalies through the abdominal wall
- Abnormal placentation - Fetal heart tones can usually be detected with
- Multiple pregnancies a stethoscope by 16-20 weeks
- Uterine abnormalities, pelvic tumours Recognition of fetal movements
- Uterine blood flow waveform assessment - Primigravida usually by 18-20 weeks
- 3rd Trimester Antenatal Care - Multiparous usually by 15-17 weeks
(2-weekly visits up till 35 weeks; weekly thereafter)
Clinical fetal monitoring
Continued maternal counseling
Continued management of maternal well-being
Assess fetal growth & well-being with fetal
ultrasound growth scan (32 weeks):
- Growth parameters
- Amniotic fluid index
- Doppler assessment Linea nigra Chloasma aka melasma
- Cardiotocography
Preparation for labour, delivery & puerperium
Close fetal well-being supervision for post-date
gestations (from 40 weeks)

ANTENATAL CARE

1
Investigations for Confirmation of Pregnancy Confirmation of Gestational Age & Expected Date
- Pregnancy test of Delivery (EDD)
Detects human chorionic gonadotropin (hCG) in
Gestational age confirmation is of paramount importance at the first
either the serum or urine, using the First antenatal visit as multiple decisions & assessments made at subsequent
International Reference Preparation (1st IRP) antenatal visits will depend on it
Maternal serum hCG levels in early pregnancy:
- 1st secreted ~7days after conception Determination via Menstrual History (Naegeles Rule)
- Doubles every 2.2 days for the first 30 days - Expected date of delivery:
- Reaches ~100IU/L by the time of the expected Last menstrual period (LMP) + 9 months & 7 days
menses Note: LMP = 1st day of last menses
Pregnancy test result interpretation (for serum hCG): - Gestational age is approximated by number of weeks of
- hCG < 5IU/L = negative amenorrhea (i.e. from LMP till present)
- hCG >25IU/L = positive - Assumptions of Naegeles Rule:
- hCG 6-24IU/L = equivocal, retest in 2 days Assumes a 28-day menstrual cycle with ovulation
(hence most women presenting at the time of the 1st occurring on day 14
missed period would give a positive pregnancy test if
EDD calculated corresponds to 40 weeks gestation
they are truly pregnant)
- Hence inaccurate if cycles are not 28-day long or cycles
Possible false-positives:
are irregular
- Ectopic pregnancy
Can modify if cycles are not 28 days long (works on
- Molar pregnancy the basis that luteal phase is usually a constant of 14 days
- hCG-secreting tumour whereas follicular phase is the main factor accounting for
- Transvaginal ultrasound variability in cycle lengths between women):
Useful for excluding ectopic pregnancy & - If cycles <28 days, subtract the difference from
determining viability of the gestation: the calculated EDD
- If cycles are >28 days, add the difference to the
Normal Ultrasound Findings in Early Gestation calculated EDD
Gestational age U/S Finding Mean hCG level Even then, probably still inaccurate (even with
5 weeks Gestational sac 1500IU/L regular 28-day cycles, calculated dates still wrong in
6 weeks Fetal pole 5200IU/L ~15% of cases)
7 weeks Fetal cardiac motion 17500IU/L
Determination via Dating Ultrasound Scan
Indications of probable embryonic demise (i.e. non- (most accurate estimations of gestational age are obtained via 1st
viable pregnancy): trimester ultrasound dating scans, hence recommended routinely for
- Presence of gestational sac of 8mm without a patients presenting early enough; for patients presenting later, other
demonstrable yolk sac ultrasound parameters can still be used, but with significantly less
- Presence of gestational sac of 16mm without a accuracy)
demonstrable embryo - 1st trimester dating ultrasound scan estimates gestational
- Crown-rump length >5mm without any age using crown-rump length measurement
demonstrable fetal cardiac motion Usually done between 6-11 weeks
Accuracy of dating up to 3-4 days
- 2nd trimester ultrasound scan estimates gestational age
using multiple measurements:
Biparietal diameter, head & abdominal
circumference, femur length
Accuracy of dating up to 1-2 weeks

ANTENATAL CARE

2
The First Antenatal Visit Routine 1st Trimester Screening (Baseline Investigations)
Alongside confirmation of pregnancy, determining viability & - Full blood count
confirmation of gestational age & EDD, a whole host of other history, Assess baseline haemoglobin levels
physical examinations & investigations are essential at the first Preliminary screen for thalassemia (see Anemia in
antenatal visit to establish a comprehensive maternal profile, which Pregnancy for more details)
allows stratification of pregnancy risk which will determine whether the - Blood group & antibodies
mother will be managed routinely or in a high-risk pregnancy clinic To assess need for management of possible rhesus
alloimmunization
Important History to Elicit - Hepatitis B screening (test for HBsAg)
- Obstetric history - HIV screening
Gynae code (age/number of years married/number of - Syphilis screening (using VDRL)
previous pregnancies/number of children) - Urine protein & glucose
Menstrual history (last menstrual period, age of Assess baseline absence/presence to guide
menarche, length of periods, regularity of periods, any interpretation of results from every other subsequent
menorrhagia) antenatal visit
Details of each previous pregnancy:
- Gestational age at birth Other Routine 1st Trimester Care Issues
- Mode of delivery
- Perinatal complications & events Manage Common Maternal Ailments (see below)
- Antenatal issues & problems (any obstetric
condition diagnosed? any interventions or treatment
1st Trimester Counseling
administered?)
- Nutrition (standard eat well & healthily advice; increase caloric
Check pap smear status (last one done when? results?)
intake by about 300kcal; avoid raw meats to prevent
- Past medical & surgical history
toxoplasmosis infection; give folic acid supplementation
Any past medical conditions (chronic hypertension,
5mg/day if not already on it)
diabetes mellitus, heart disease, anemia etc)
- Lifestyle adjustments (can continue to work; can engage in
Any past surgeries (previous caesarian section, uterine
mild exercise, avoiding strenuous physical activity or activities
surgery etc)
with a significant risk of falls)
Drug history (current active medications, drug allergies)
- Travel advice (avoid long-haul flights)
- Family history
- Coital advice (can continue to engage in coitus; one thing to
Any family history of medical conditions (e.g. first
avoid is stimulation of the nipples as it induces a surge in serum
degree relatives with diabetes mellitus, thromboembolic
oxytocin levels)
disease)
Any family history of obstetric conditions (e.g.
Offer 1st Trimester Prenatal Screening (see below)
maternal history of pre-eclampsia)
- Social history
Complications in 1st Trimester
Smoking, alcohol & recreational drug use
- Ectopic pregnancy
Occupation, financial issues
- Miscarriage (occurs in 10-15% of all pregnancies)
Get a profile of the spouse as well
- Hyperemesis gravidarum
Physical Examination on the 1st Antenatal Visit
- General examination
Obtain a baseline height, weight & blood pressure
Look for pallor & edema
Do targeted systemic examinations:
- Oral cavity, thyroid
- Breast (anticipate breastfeeding difficulties e.g. due
to inverted nipples)
- Heart, lung
- Fundoscopy if hypertensive/diabetic
- Abdominal examination
Inspect for cutaneous signs of pregnancy (linea nigra,
striae gravidarum) & surgical scars
Palpate abdomen (gravid uterus usually not palpable
until ~12 weeks gestation)
- Pelvic examination
Baseline assessment of the external genitalia, vaginal
walls & cervix

ANTENATAL CARE

3
2nd Trimester Antenatal Care 2nd Trimester Screening (Anomaly) Scan
Usually done between 20-22 weeks; ~2% of fetuses have malformations

Clinical Fetal Monitoring Recognition of Fetal Anomalies


Beginning from the 2nd trimester, the gravid uterus becomes palpable - Importance of detecting fetal anomalies:
through the abdomen, which allows for various parameters & Certain abnormalities not compatible with life (option
characteristics to be assessed for at each antenatal visit; pointers here of termination of pregnancy)
apply not only to 2nd trimester care but to any antenatal visit following Certain abnormalities are associated with an
the initial first (booking) antenatal visit underlying chromosomal abnormality (e.g. if AVSD
detected, high likelihood of Downs syndrome)
Routine Antenatal History Taking Advance anticipation of need for perinatal &/or
- Enquire about general well-being & any symptoms since
multidisciplinary care
the previous visit
- Anomaly ultrasound scan is better at detecting externally
- Ask about fetal movements
impinging structural abnormalities than internal ones:
Can consider starting patient on fetal movement
External: anencephaly, spina bifida
chart from 30 weeks onwards, utilizing Cardiff
Internal: structural heart defects, diaphragmatic hernia
count to ten method (count 10 fetal movements
- Can also detect soft signs of underlying abnormalities
beginning from a specific time each day; report if the fetus
(markers of aneuploidy):
takes longer than usual to achieve the 10 movements, or if
Nuchal thickening: trisomy 21
there are fewer than 10 movements in 12 hours)
Choroid plexus cysts: trisomies 18 & 21
Fetal movements in theory help monitor fetal well-
Echogenic bowel: trisomy 21 & cystic fibrosis
being, decrease in which may signal fetal
- Overall sensitivity ~60-70%, hence a negative scan does
compromise
not effectively exclude the presence of fetal anomalies
Not proved by randomized controlled trials to
- Prenatal diagnostic test (see below) to detect possible
reduce perinatal morbidity & mortality however
chromosomal abnormality offered if:
Major fetal anomaly detected (cleft lip, congenital heart
Routine Antenatal Physical Examination
disease, exomphalos etc)
- General examination
2 markers of aneuploidy detected
Obtain current weight & blood pressure
- Abdominal examination
Detection of Other Abnormalities
Can inspect for visible fetal movements
- Detect low-lying placenta
Measure symphysial fundal height (SFH), which
Present in ~28% of pregnancies at 24 weeks
can in turn help determine:
With lower uterine segment development, only ~3%
- Appropriateness of size for gestational age
remaining at term (placenta praevia)
(another clinical method of gauging fetal growth as a
- Diagnosis of multiple pregnancies
surrogate measure of fetal well-being; not proven by
- Detection of uterine abnormalities or pelvic tumours
randomized controlled trials to reduce perinatal
- Uterine artery waveform assessment
morbidity & mortality however):
Can be used to predict risk of developing pre-
Gestational age (weeks) = SFH (cm) 2-3cm
eclampsia, intrauterine growth restriction (IUGR) &
- Clinical estimation of fetal weight using placental abruption
Johnson formula (not routinely done anymore):
Features increasing risk include:
Birth weight (g) = [SFH (cm) 13] x 155 - High pulsatility index ([peak systolic flow
Palpate gravid uterus to determine (usually only after end-diastolic flow]/mean flow) which is a
28 weeks, i.e. 3rd trimester onwards): surrogate measure of vascular resistance
- Number of fetuses (singleton or multiple?) - Early diastolic notch in the waveform (only
- Fetal orientation (lie, presentation, back) bilateral uterine artery notching is significant)
- Liquor volume Aspirin 75mg/day can be offered if uterine artery
- Degree of engagement waveform abnormalities found to improve outcome
Auscultate fetal heart (best heard over anterior shoulder
of the fetus, using stethoscope or DopTone)
Other Routine 2nd Trimester Care Issues
Routine Antenatal Investigations
Manage Common Maternal Ailments (see below)
- Urine protein & glucose
- Consider testing for diabetes mellitus with oral glucose
2nd Trimester Counseling
tolerance test (OGTT) in patients with risk factors (if done,
- As per 1st trimester, plus:
usually performed between 24-28 weeks):
- Breastfeeding advice
Previous gestational diabetes mellitus
- Antenatal classes
Body mass index >30
Personal history of chronic hypertension
Offer 2nd Trimester Prenatal Screening (see below)
Previous baby with birth weight >4.5kg
- This is in the case where the patients first antenatal visit
Previous malformed or stillborn child
occurs after the 1st trimester & hence no longer eligible for
1st degree relative with diabetes mellitus
the 1st trimester prenatal screening

ANTENATAL CARE

4
3rd Trimester Antenatal Care 3rd Trimester Growth Scan
Usually done at around 32 weeks; sonographic parameters assessed are
(i) growth parameters (ii) amniotic fluid index (iii) Doppler assessment;
Clinical Fetal Monitoring additionally, a cardiotocogram may also be done; application of these 4
As per described for 2nd trimester care, except with increased frequency parameters extend beyond the 3rd trimester growth scan, being used in
of follow-up visits; a few additional things to note on antenatal visits in various obstetric scenarios such as routine monitoring of high-risk
the 3rd trimester are stated below pregnancies or acute assessment of fetal well-being in obstetric
emergencies (e.g. pre-eclampsia)
Additional Considerations at 36 Weeks
- Pelvic assessment on top of usual abdominal examination Growth Parameters
(used to be for performing clinical pelvimetry to detect possible - Fetal measurements (used to estimate fetal weight):
cephalopelvic disproportion; not routinely done anymore) Biparietal diameter (BPD)
- Consider reviewing haemoglobin levels Head circumference
In anticipation of blood loss during delivery Abdominal circumference
Safe options of managing iron-deficiency anemia Femoral length
such as iron pills take time to bring up Hb, hence Head:abdominal ratio (calculated from head &
review should be done early enough ahead of EDD abdominal circumference)
- Consider high vaginal swab (HVS) to test for Group B - Possible growth assessment results:
Streptococcus (GBS) colonization Appropriate for gestational age
If positive, offer intrapartum antibiotic prophylaxis Large for gestational age (LGA) = >90th percentile
(usually IV penicillin or ampicillin) Small for gestational age (SGA) = <10th percentile
- Evaluation of SGA detected on growth scan:
Management of Post-Date Pregnancy First step is to reconsider if dates are correct
(post-date pregnancy = >40 weeks; post-term = 42 weeks) - Check how gestational age was determined in
- Weekly monitoring of: the first place (1st trimester dating scans are the
Amniotic fluid index (to assess liquor volume) most reliable compared to 2nd trimester dating scans
Umbilical artery Doppler assessment or calculations based on LMP)
Cardiotocography - If LMP was used to calculate, check patients
menstrual history (if irregular, non-28 day cycle,
Other Routine 3rd Trimester Care Issues makes it even less reliable)
If dates are reliable (i.e. fetus is truly SGA), consider
Manage Common Maternal Ailments (see below) the 3 possibilities of SGA:
(i) Constitutional (20%, normal healthy fetuses
3rd Trimester Counseling who are small because their parents & siblings also
- As per 2nd trimester, plus: tend to be on the small side)
- Counsel patient with regards to delivery: (ii) Intrinsically small fetuses (40%, usually due
Timing & mode of delivery to 1st trimester intrauterine insult such as
How to recognize onset of labour & what to do when chromosomal abnormalities, intrauterine infections
labour begins (come to A&E, will be sent to labour ward) or exposure to teratogens)
Labour process & choice of anesthesia (iii) Growth-restricted fetuses (40%, usually due
Reinforce benefits of breastfeeding to mid & late trimester uteroplacental insufficiency
due to conditions such as pre-eclampsia, chronic
Complications in 3rd Trimester placental abruption, maternal thrombophilia etc)
- Antepartum hemorrhage Determining pattern of intrauterine growth
- Pregnancy-induced hypertension, pre-eclampsia restriction (IUGR) can help assess the likely cause:
- Gestational diabetes mellitus - Symmetrical IUGR = head & abdominal
circumference both at the same low centile
(likely to be constitutional or intrinsically small
fetuses)
- Asymmetrical IUGR = head circumference
relatively normal with abdominal
circumference at low centile (likely to be growth-
restricted fetuses; occurs due to preferential
redistribution of blood to fetal head when
uteroplacental insufficiency sets in)
- Evaluation of LGA detected on growth scan:
First step is to check if dates are correct, as above
If dates are reliable (i.e. fetus is truly LGA), consider
the 3 possibilities of LGA:
(i) Constitutional
(ii) Fetal syndromes
(iii) Gestational diabetes mellitus (consider an
OGTT to test for it)

ANTENATAL CARE

5
Amniotic Fluid Index (AFI) Doppler Assessment
- Assesses liquor volume (assesses placental sufficiency, useful in high-risk pregnancies; note
- AFI = sum of the linear measurements (in cm) of the that Doppler assessment is the only measure in antenatal monitoring
largest amniotic fluid pockets noted on ultrasound of fetal growth & well-being that has been proven by meta-analysis to
inspection of each of the 4 quadrants of the gestational sac reduce perinatal morbidity & mortality)
4 quadrants of abdomen divided based on umbilicus
Transducer placed vertically in each quadrant, Vessel Assessed Indicator of Placental Insufficiency
perpendicular to the floor Uterine artery High pulsatility index, early-diastolic notch
Largest vertical pool of liquor seen in each quadrant Umbilical artery Absent or reverse end-diastolic waveform
is measured & summed to give AFI Increased end-diastolic flow velocity (due to
Middle cerebral
- Interpretation of AFI: preferential shunting of blood to the head in
artery
Oligohydramnios = AFI < 8; suggests fetal compromise placental insufficiency)
& placental insufficiency (preferential redistribution of Ductus venosus Reverse a wave
fetal blood to head reduces renal perfusion, hence lowering Umbilical vein Venous double pulsation
glomerular filtration & fetal urine production)
Polyhydramnios = AFI > 18; may indicate fetal
anomaly (e.g. GIT malformation causing decreased fetal
ingestion of amniotic fluid) or poor control in a diabetic
pregnancy (fetal hyperglycemia causing osmotic diuresis)

Uterine artery Umbilical artery Middle cerebral artery


Above: normal Above: normal Above: normal
Below: early-diastolic Below: reverse end- Below: increased end-
notch diastolic waveform diastolic flow velocity

Calculation of AFI using vertical measurements in the 4 quadrants

ANTENATAL CARE

6
Cardiotocography
(assesses fetal well-being, useful in high-risk pregnancies & fetal
monitoring during labour)
- Assessment of fetal heart rate patterns with concomitant
monitoring of uterine contractions
Fetal heart rate can be monitored transabdominally
using external transducers or internally using fetal
scalp electrodes (applicable only during intrapartum
monitoring)
Uterine contractions can be monitored
transabdominally using external transducers or
internally using a transcervical placement of a plastic Normal CTG trace; top trace: fetal heart rate; bottom trace: uterine contractions
catheter (applicable only during intrapartum monitoring)
- Interpretation of fetal heart rate patterns (4 main
parameters monitored):
Baseline heart rate
- Normal: 110-160 beats per minute
- Baseline tachycardia: maternal fever, -agonist
use, chorioamnionitis, acute/subacute fetal hypoxia, Reduced baseline variability (<5 bpm)
fetal tachyarrhythmias (in which case FHR >
200bpm)
- Baseline bradycardia: fetal heart block, cord
compression (late sign), fetal hypoxia (late sign)
Baseline variability
- Normal: amplitude >5 beats per minute
- Loss of baseline variability (i.e. flat trace):
acute/subacute fetal hypoxia, preterm infant who is
asleep, drugs (benzodiazepines, morphine,
phenothiazine), chorioamnionitis
Accelerations
- Normal: 2 accelerations of amplitude 15 beats
per minute (each lasting >15 seconds) over a 20 Accelerations
minute period (indicates intact fetal sympathetic
activity)
Decelerations
(usually indicates fetal compromise; can be categorized
into various subtypes if temporal relationship between
FHR & uterine contractions is observed)
- Early decelerations: only form of deceleration
which can be considered normal; deceleration
corresponds to simultaneous uterine contraction; can
be observed during labour following engagement of
the fetal head; due to head compression by uterine Early decelerations (coincides with uterine contractions)
contractions, causing increased intracranial pressure
which elicits vagally-mediated reflex bradycardia
- Late decelerations: deceleration occurs following
uterine contraction; indicates uteroplacental
insufficiency; due to decreased placental perfusion
during uterine contractions, which in a background
of underlying uteroplacental insufficiency
exacerbates fetal hypoxia, resulting in preferential
shunting of fetal circulation to the head via
vasoconstriction of systemic vessels, in turn
increases systemic arterial pressure which elicits
vagally-mediated reflex slowing of fetal heart rate Late decelerations (occurs after each uterine contraction)
- Variable decelerations: decelerations with
variable time of onset & form (classically M
shaped or described as shouldering), may be non-
repetitive; due to cord compression
- Format for reporting a CTG (DR BRaVADO):
Determine Risk
Baseline Rate
Variability
Accelerations
Decelerations
Overall plan
Variable decelerations

ANTENATAL CARE

7
Prenatal Screening & Diagnosis Prenatal Diagnostic Tests
3 main modalities: (i) CVS (ii) amniocentesis (iii) fetal blood sampling;
Involves screening tests to assess the risk of genetic diseases in the fetus
Definitive diagnostic tests to detect fetal genetic conditions;
as well as follow-up diagnostic procedures to confirm it where the risk is
Usually as a follow up to screening tests (not only chromosomal but
assessed to be high
others such as thalassemia screening) where risk of fetal condition is
determined to be high (>1:300); there are several other uses for these
Prenatal Screening procedures as delineated below
Prenatal screening here mainly covers the standard screening tests for
chromosomal disorders (specifically trisomies 13, 18 & 21) routinely Chorionic Villus Sampling (CVS)
offered to pregnant women during antenatal care; screening for other - Ultrasound-guided sampling of chorionic villi, can be
genetic conditions (e.g. thalassemia) are not discussed here performed transabdominally or transcervically
Tissue culture yields cytogenetic results in 6-8 days
1st Trimester Screen For Chromosomal Abnormalities Direct visualization of dividing villi cells allows for
(note: detection rates & false positive rates reported here are with detection of chromosomal abnormalities in 3 days
respect to the detection of trisomy 21 specifically) - Can be performed from 10 weeks onwards
- Maternal age Hence advantage over amniocentesis is that it can be
Table charting gestational age of fetus against performed earlier
maternal age depicting risk of Downs syndrome - Utility of test:
Ballpark risk figures of Downs syndrome at birth: Karyotype for chromosomal abnormalities
- Maternal age of 35 years 1:350
Identify single gene mutations (e.g. thalassemia)
- Maternal age of 40 years 1:100
- Complications:
Risk based on maternal age (background risk) is
Fetal loss rate = 1%
further augmented if there is a history of previous
Culture failure rate = 0.5% (i.e. no results can be
chromosomal abnormalities:
determined after procedure is performed)
- Previous trisomy 13, 18 or 21 background risk +
Mosaicism rate = 1% (i.e. >1 cell population which differ
0.75%
in genetic makeup present in chorionic villi, resulting in
- Previous 45XO, 47XXY/XXX or triploidy no
sampling error; however, the presence of mosaicism is
increase to background risk
almost always detectable during analysis of the sample,
Detection rate = 30%, false positive rate = 5%
hence the main implication of this is that a follow-up
- Nuchal translucency (NT)
amniocentesis may be required for definite diagnosis)
Ultrasound measurement of subcutaneous space
Transplacental hemorrhage (hence need to give anti-D
between fetal skin & cervical spine in the mid-
to rhesus-negative mothers after procedure)
sagittal view
Risk is calculated with respect to maternal age
Detection rate = 80%, false positive rate = 5%
- Combined test
NT + pregnancy-associated plasma protein A
(PAPPA) + -hCG (w.r.t. maternal age)
Detection rate = 90%, false positive rate = 5%
Best screening test offered locally, hence the one
routinely recommended for all patients eligible for it

2nd Trimester Screen For Chromosomal Abnormalities


- Triple test
-fetoprotein + -hCG + estriol (w.r.t. maternal age)
Detection rate = 70%, false positive rate = 5%
Not as good as combined test, but the only
alternative that can be offered to patients presenting
in the 2nd trimester
- Quadruple test
-fetoprotein + -hCG + estriol + inhibin A (w.r.t.
maternal age)
Detection rate = 81%, false positive rate = 5%
Better than triple test, but not offered locally as assay
for inhibin A is not available locally

ANTENATAL CARE

8
Amniocentesis Fetal Blood Sampling
- Ultrasound-guided aspiration of amniotic fluid sample - Ultrasound-guided percutaneous sampling of fetal blood;
using a 22G needle transabdominally various sources of fetal blood possible (umbilical vein aka
Amniocytes in sample are cultured, requiring 1-2 cordocentesis, intrahepatic blood sampling, cardiocentesis):
weeks before final chromosomal analysis is possible Fetal leukocytes are cultured, requiring as little as 3
Fluorescent in-situ hybridization (FISH) can be used days for chromosomal analysis results
using chromosome-specific probes (e.g. for trisomy Hence main indication is for rapid karyotyping (as
13, 18 & 21) can give preliminary results in 3 days fetal leukocytes can be cultured more rapidly than
Amniotic fluid itself can be tested for various amniocytes)
substances depending on the indication for the test - Can be performed from 20-23 weeks onwards
- Can be performed from 16 weeks onwards - Utility of test:
- Utility of test: Karyotype for chromosomal abnormalities
Karyotype for chromosomal abnormalities Identify single gene mutations (e.g. thalassemia)
Identify single gene mutations (e.g. thalassemia) Assessment of fetal anemia (historically in the setting
Test for perinatal infections: of rhesus isoimmunization; not necessary anymore with
- Detect intrauterine infections (TORCH, VZV, the advent of middle cerebral artery Doppler as an effective
parvovirus B19) if maternal exposure has occurred indicator of fetal anemia)
with ultrasonographic features suggestive of fetal Therapeutic in-utero blood transfusion (e.g. for
infection (fetal hydrops, echogenic bowel, parvovirus B19 infection, Barts hydrops)
ventriculomegaly, intracranial calcification) - Complications:
- Analysis of amniotic fluid to diagnosis preterm Fetal loss rate = 2-5%
chorioamnionitis (gram stain, white cell count, Cord hematoma, hemorrhage
glucose level, culture)
Biochemical tests for fetal structural abnormalities:
- AFP: elevated levels in neural tube (e.g. spina
bifida) & ventral abdominal wall defects (e.g.
gastrochisis, omphalocele)
- Acetylcholinesterase: presence indicates open
neural tube defect
Test for fetal pulmonary maturity:
- Test for amniotic phospholipids to calculate
lecithin:sphingomyelin (L/S) ratio; L/S ratio >2
is associated with low risk for respiratory distress in
the neonate (not done anymore with advent of
routine corticosteroid injections in threatened
preterms to mature fetal lungs)
Therapeutic amniocentesis for:
- Polyhydramnios
- Twin-twin transfusion syndrome (uses serial
amniocentesis to remove excessive amniotic fluid
from sac of recipient twin)
- Complications:
Fetal loss rate = 0.5%
Culture failure rate = 0.5%
Mosaicism rate = almost zero
Transplacental hemorrhage (hence need to give anti-D
to rhesus-negative mothers after procedure)

ANTENATAL CARE

9
Maternal Ailments in Pregnancy Constipation
- Due to progesterones effect on smooth muscle relaxation,
decreasing colonic motility
Nausea & Vomiting - Non-pharmacological management:
- Occurs in up to 70% of pregnancies, usually worst during Dietary modification (increase fibre & water intake)
the 1st trimester - Pharmacological management:
- Non-pharmacological management: Stool softeners in combination with bulk laxatives
Eat small, frequent meals
Avoid greasy & spicy food Hemorrhoids & Varicosities
Acupressure using sea-sickness arm bands - Due to increased venous pressure with the gravid uterus
- Pharmacological management: compressing pelvic veins
Vitamin B6 (pyridoxine) - Management:
Antihistamines Increased rest with elevation of legs
Avoid constipation
Hyperemesis Gravidarum
- Severe persistent vomiting + significant weight loss (>5% Leg Cramps
of pre-pregnancy weight) + ketosis - Experienced by almost 50% of all pregnant women,
Usually affects primips particularly at night & in the later half of pregnancy
Postulated to be due to high levels of hCG, hence can - Management:
also be seen in special conditions associated with Massage & stretching exercises
high maternal hCG levels (hence need to exclude): Calcium & sodium chloride may help
- Molar pregnancy
- Multiple gestation Back Aches
- Management: - Management:
Exclude secondary causes of severe vomiting (e.g. Avoid excessive weight gain during pregnancy
pre-eclampsia, pyelonephritis etc) Exercise
Ensure adequate hydration & correction of Analgesia (e.g. paracetamol)
hyponatremia & hypokalemia that may result (admit
for IV fluids if necessary)
Consider giving thiamine to prevent Wernickes
encephalopathy
Consider venous thromboembolism prophylaxis
Symptomatic treatment:
- 1st line: antihistamines (e.g. cyclizine)
- 2nd line: corticosteroids

Heartburn
- Occurs in about 2/3 of pregnancies
- Due to progesterones effect on smooth muscle relaxation,
hence lowering lower esophageal sphincter tone,
predisposing to gastroesophageal reflux
- Non-pharmacological management:
Eat small, frequent meals
Avoid greasy & spicy food
Avoid recumbent position immediately after meals
Raise head of bed while sleeping
- Pharmacological management:
Antacids

ANTENATAL CARE

10
LABOUR & PUERPERIUM
Anatomic Considerations in Labour Diameters of the Fetal Head
- Anteroposterior diameters
Fetal Head Anatomy (relevant when fetus is exiting the pelvic outlet)
The head is the largest & least compressible part of the fetus, hence it is
the most important part from an obstetric viewpoint regardless of
Diameter Length Presentation
whether the presentation is cephalic or breech
Suboccipitobregmatic 9.5cm Cephalic (well flexed)
Fetal Head Structure Occipitofrontal 11-12.5cm Cephalic (deflexed)
- Fetal skull comprises the base & the vault (cranium) Supraoccipitomental
Base of skull comprises large, ossified, firmly united 13.5cm Brow
(aka Mentovertical)
& non-compressible bones to protect the brainstem
Submentobregmatic 9.5cm Face
Cranium comprises occipital bone posteriorly, 2
parietal bones bilaterally & 2 frontal & temporal
bones anteriorly; these bones are thin, weakly - Transverse diameters
ossified, compressible & interconnected only by (relevant when fetus is entering the pelvic inlet)
membrane at birth, hence able to overlap under Biparietal (9.5cm): largest transverse diameter
external pressure to change the shape of the cranium Bitemporal (8cm): smallest transverse diameter
to conform to the maternal pelvis (moulding)
- Sutures refer to the membrane-occupied space between
the cranial bones:
Frontal suture: lies between the frontal bones, extending
from the glabella to the bregma
Coronal suture: extends laterally from the bregma,
separating the frontal & parietal bones
Sagittal suture: lies between the parietal bones, extending
from the bregma to the lambda
Lambdoid suture: extends laterally from the lambda,
separating the parietal & occipital bones A: suboccipitobregmatic, B: occipitofrontal, C: mentovertical, D: submentobregmatic
- Fontanelles refer to the membrane-filled spaces at the
points where the sutures intersect: Maternal Pelvic Anatomy
Anterior fontanelle (bregma): diamond-shaped space
found at the intersection of the frontal, coronal & sagittal Bony Pelvis
sutures; measures about 2x3cm; closes after birth at about - Bony pelvis comprises 4 bones:
18 months of age Sacrum: comprises 5 fused sacral vertebrae, with the
Posterior fontanelle (lambda): Y-shaped space found at anterior-superior edge of S1 (the promontory) protruding
the intersection of the sagittal & lambdoid sutures; much slightly into the pelvic cavity; the sacrum has a concave
smaller than the bregma; closes after birth at about 6-8 anterior surface; it articulates with the ilium at its upper
weeks of age segment, with the coccyx at its lower segment & with the
sacrospinous & sacrotuberous ligaments laterally
Coccyx: comprises 3-5 fused rudimentary vertebrae;
articulates with the sacrum at the sacrococcygeal joint
Innominate bone (x2): comprises the ilium, ischium &
pubis which fuse at puberty following the ossification of
the tri-radiate cartilage
- The pelvis is anatomically divided into the false pelvis
superiorly & the true pelvis inferiorly by the linea
terminalis:
False pelvis: bounded by lumbar vertebrae posteriorly,
iliac fossae bilaterally, abdominal wall anteriorly
True pelvis: bounded by sacrum & coccyx posteriorly,
ischium & pubis laterally & anteriorly; essentially a bony
Landmarks canal with relatively immobile internal borders
(important landmarks of the fetal skull often used in the naming of
diameters & fetal positioning during labour)
- Chin (mentum): anterior prominence of the mandible
- Glabella: elevated area between the orbital ridges
- Brow (sinciput): area between the glabella inferiorly & the
bregma superiorly
- Anterior fontanelle (bregma)
- Vertex: area between the fontanelles, bounded laterally by the
parietal eminences
- Posterior fontanelle (lambda)
- Occiput: area posteroinferior to the lambda & lambdoid sutures

LABOUR & PUERPERIUM

11
Pelvic Planes
- The true pelvis is divided into 4 pelvic planes for
descriptive purposes, each constituting a flat surface
extending across the pelvis at a different level:

Boundaries
Pelvic Plane
Anterior Lateral Posterior
Superior edge of pubic Linea Sacral
Pelvic inlet
symphysis terminalis promontory
Upper part of
Posterior surface of
Zone of cavity the obturator S2/S3
midpoint of pubis
foramina
Posterior surface of
Mid-pelvis Ischial spines S4/S5
lower edge of pubis
Sacrotuberous Sacrococcygeal
Pelvic outlet Subpubic arch
ligaments joint

Pelvic inlet: uppermost plane; fetus in labour is said to be


engaged when the largest diameter of the presenting
part crosses this plane; fetus enters pelvis through this
during labour in the transverse position
Zone of cavity: the plane of greatest diameter; the fetal
head begins internal rotation into the anteroposterior
position in this plane during labour
Mid-pelvis: the plane of least diameter; most arrests of
descent during labour occur at this level
Pelvic outlet: lowermost plane; fetus exits the birth canal Pelvic Shapes
& is born through this plane during labour in the (4 types of pelvises described based on the general bony architecture)
anteroposterior position
- Each plane in turn has a set of pelvic diameters which Pelvis Type
describes measurements made at the level of the plane in Feature
different directions (not very important nowadays since Gynecoid Android Anthropoid Platypelloid
clinical pelvimetry is no longer performed); understanding the Oval; AP > Oval; AP <
Inlet Round Triangular
differences in at least the AP & transverse diameters at transverse transverse
each plane however helps appreciation of the occurrence Side walls Straight Convergent Straight
Straight or
of rotation during labour: divergent
Far apart
Close to
Ischial spines Average Prominent from each
Anteroposterior Transverse each other
Pelvic Plane other
Diameter Diameter
Sacrospinous Long & Long &
Pelvic inlet 11.5cm 13.5cm Large Small
notches narrow small
Zone of cavity 12.5cm 13.5cm Posterior
Mid-pelvis 12.5cm 12.5cm Well- Shallow Posterior
Sacrum inclination,
Pelvic outlet 13.5cm 11.5cm curved curve inclination
flat
Narrow,
Subpubic Wide
AP diameter increases while transverse diameter Narrow outwardly Wide
arch (90o)
decreases with descent of the fetal head through the shaped
true pelvis during labour
The AP diameters of the fetal head are greater than - Gynecoid pelvis
that of the greatest transverse diameter of the fetal Classical female type of pelvis (50% of women)
head, which will result in the alignment of the AP Overall cylindrical shape that is spacious throughout
diameter of the fetal head with the larger of the 2 Fetal head tends to rotate into the occipitoanterior
diameters of the true pelvis along the descent at any position during descent
point in time - Android pelvis
Hence the fetal head enters the pelvic inlet in the Typical male type of pelvis (<30% of women)
transverse position (AP diameter of fetal head aligned Funneling effect down the pelvis
with transverse diameter of pelvic inlet), rotates Fetal head tends to rotate into the occipitoposterior
internally as it descends, & eventually exits the position to conform to the narrow anterior pelvis;
pelvic outlet in the anteroposterior position (AP arrest of descent is common at the mid-pelvis
diameter of fetal head aligned with AP diameter of pelvic - Anthropoid pelvis
outlet) Resembles that of anthropoid apes (20% of women)
Fetus enters pelvic inlet in the anteroposterior
position instead of the typical transverse position
(usually occipitoposterior as there is more space in
the posterior pelvis)
- Platypelloid pelvis
A flattened gynecoid pelvis (3% of women)

LABOUR & PUERPERIUM



12
Anatomic Terminology Relating to Labour

Lie = relation of the long axis of the fetus to the long axis of the
mother
- Longitudinal lie
- Transverse lie

Presentation = designation of the fetal part over the pelvic inlet


- Cephalic/vertex presentation
- Breech presentation (buttocks)
- Transverse/shoulder presentation
- Compound (multiple parts)
- Face presentation
- Brow presentation

Attitude = posture assumed by the fetus


- Flexion
- Extension (associated with larger presenting diameters &
malpositions)

Position = relation of an arbitrarily chosen potion of the


presenting part (the denominator) to the maternal pelvis
- For cephalic presentations, denominator is occiput
Occipitoanterior = occiput of fetal head facing the
front of the maternal pelvis (hence in lithotomy position
during labour, fetus is delivered facing the floor)
Occipitoposterior = occiput of fetal head facing the
back of the maternal pelvis (hence in lithotomy position
during labour, fetus is delivered facing the ceiling)
Occipitotransverse = occiput of fetal head facing the
side of the maternal pelvis
Note: right & left can be put in front of the above descriptors Station = relation (in cm) of the bones of the presenting part to
to further specify if the occiput is slightly deflected to the the level of the ischial spines during labour; used to denote
right/left (for OA & OP) fetal descent during labour
- For face or brow presentations, denominator is mentum - Station of 0 at level of ischial spines
Mentoanterior = mentum of fetal head facing the - Station of -5 at level of pelvic inlet
front of the maternal pelvis (hence in lithotomy position - Station of +2 to +3 at level of perineal floor
during labour, fetus is delivered facing the ceiling)
Mentoposterior = occiput of fetal head facing the
back of the maternal pelvis (hence in lithotomy position
during labour, fetus is delivered facing the floor cannot
actually occur in reality due to reasons specified later)
- For breech presentations, denominator is sacrum
Sacroanterior
Sacroposterior

LABOUR & PUERPERIUM

13
Engagement = descent of the largest diameter of the presenting
part (that is lying in the anteroposterior diameter of the pelvic
Normal Labour
inlet) past the pelvic inlet
- Depends on presentation: Overview of Normal Labour
For cephalic presentations, occurs when the
biparietal diameter crosses the pelvic inlet Definition of Labour
For breech presentations, occurs when the bi-ischial - Labour = presence of contractions of sufficient frequency,
diameter crosses the pelvic inlet strength & duration to cause cervical effacement &
- Clinically assessed via abdominal palpation & using the dilatation
method of fifths palpable (engagement said to have Cervical effacement = the shortening of the length of
occurred when only 2/5s palpable or less): the cervix (from ~3-4cm normally until it is
completely indistinguishable from the uterine wall)
at the onset of labour; occurs with concomitant
softening of the cervix due to increased water
content & collagen lysis
Cervical dilatation = the widening of the cervical os;
progresses from closed 3-4cm (roughly coincides
with complete cervical effacement, marks the onset of
active phase of 1st stage of labour) 10cm (complete
cervical dilatation, marks the beginning of 2nd stage of
labour)
Show = small amount of blood-tinged mucous
passed per vaginally (due to release of the mucous plug
normally occupying the endocervical canal when cervical
effacement & dilatation occur)
- Diagnosis of labour
Patient presents with:
- Regular painful contractions
Synclitism vs Asynclitism
- Show
- During engagement, in the context of a normal descent of
- Leaking liquor (may be reported as a sudden
the fetal head through the pelvic inlet in a transverse
gush of fluid per-vaginally; ask for colour & presence
position (hence with the biparietal diameter in line with
of foul-smelling odour)
the AP diameter of the pelvic inlet):
Vaginal examination reveals:
If the biparietal diameter is parallel to the pelvic inlet
- Cervical effacement & dilatation
plane (hence sagittal suture runs midway between the
- Pooling of liquor in the fornices
anterior & posterior halves of the pelvic inlet plane), the
- Differential diagnoses of labour
head position is considered to be synclitic
Braxton-Hicks contractions
Otherwise, the head position is considered to be
- Sporadic contractions which usually begin in
asynclitic (usually deflected such that the sagittal sutures
the last 4-8 weeks of pregnancy, typically of
lie closer to the sacrum than the pubic symphysis)
mild intensity
- Relevance of this lies in that the presenting diameter is
- Differentiation from true labour: no cervical
smaller in an asynclitic position than a synclitic position
changes
(which is essentially the biparietal diameter); hence
Antepartum hemorrhage
asynclitism present helps permit a larger head to enter the - Differentiation from true labour: no cervical
pelvis than would be possible in a synclitic position changes, no contractions
Abruptio placentae
- Usually presents with acute onset of sudden
abdominal pain per-vaginal bleed; palpation
reveals a woody-hard uterus
- Differentiation from true labour: no cervical
changes, pain is usually constant rather than
intermittent as for contractions
Premature rupture of membranes (PROM)
- Usually present with a sudden gush of fluid
per-vaginally
- Differentiation from true labour: no cervical
changes, no contractions

LABOUR & PUERPERIUM

14
Stages of Labour - Flexion
- 1st stage of labour Partial flexion is normally present even before labour
Begins with the onset of true labour, ends with the due to the resting muscle tone of the fetus
complete dilatation of the cervix During descent, resistance from the cervix, pelvic
Further subdivided into 2 phases: walls & pelvic floor cause further flexion of the fetal
- Latent phase (initial cervical effacement & cervical spine, bringing the chin closer to the chest
dilatation, variable duration 6-18 hours in Effect on the presenting part:
primiparous, 2-10 hours in multiparous ends when - For occipitoanterior position, this changes the
cervical dilatation is 3-4cm) presenting diameter from occipitofrontal
- Active phase (cervix is fully effaced, cervical (deflexed) to suboccipitobregmatic (well-flexed)
dilatation continues to progress at a rate of which has a smaller diameter
1cm/hour; if progress is slower than this, assessment - For occipitoposterior position, complete
for abnormal labour progress is performed) flexion may not occur (as natural tilt of the
- 2nd stage of labour maternal pelvis counteracts flexion with the natural
Begins with the complete dilatation of the cervix, tendency to extend at the cervical spine as the fetal
ends with the delivery of the fetus head descends), resulting in a larger presenting
Lasts 30 minutes to 3 hours in primiparous, 5-30 diameter which can contribute to longer labour
minutes in multiparous - Rotation (internal rotation)
- 3rd stage of labour Rotation of the fetal head within the pelvic cavity as
Begins with the delivery of the fetus, ends with it descends against the pelvic floor muscles
delivery of the placenta, cord & membranes Usually rotates the fetal head from the original
Lasts 0-30 minutes in both primi- multiparous transverse position (for it to pass through the pelvic
inlet) to an eventual anteroposterior position (either
occipitoanterior or occipitoposterior)
- Extension
As the fetal head continues descent, it has to exit via
extension (as the vaginal outlet is directed up & forward)
- Crowning occurs when the largest diameter of
Fetal Events During Labour the fetal head is encircled by the vulvar ring
(events here are for cephalic presentations; events occurring during (clinically defined when head retraction no longer
other presentations will be discussed in Malpresentations below) occurs in between uterine contractions)
- Engagement - An episiotomy may be made at this stage to
Passage of the greatest diameter of the presenting aid in reducing perineal resistance
part through the pelvic inlet (see above) Birth of the fetal head depend on the position:
Assessed clinically via abdominal palpation using - Occipitoanterior: head is born via rapid
the method of fifths palpable (engagement occurs extension as the occiput, brow, nose, mouth &
when only two-fifths palpable) chin (in succession) pass over the perineum
May occur before or after rupture of the membranes - Occipitoposterior: head is born via a
takes place during labour (if engagement does not combination of flexion & extension; at the time
happen before rupture of membranes however, there is a of crowning, the pelvic floor promotes further
risk of cord prolapse as the gush of liquor carries the cord flexion, with the brow & occiput born as the
out through the vagina with it; this risk is especially fetal chin approaches the chest; subsequently,
significant for non-cephalic presentations which doesnt the occiput falls back & the nose, mouth & chin
have the large head to tamponade the flow of liquor
are born via extension
following rupture of membranes) - Restitution (external rotation)
- Descent
Following birth of the head, the head rotates back to
Progress of presenting part through the birth canal
its original position at the point of engagement to
brought about by the force of uterine contractions,
align itself with the fetal back & shoulders
maternal bearing down (Valsalva maneuver) &
Further rotation of the fetal head may occur (in
gravity (if mother is standing up)
accordance with the shoulders) as the fetal shoulders
Clinically assessed via periodic vaginal examination
undergo internal rotation to align themselves
to determine the station of the presenting part
anteroposteriorly within the pelvis
Fetal head changes during descent: - Expulsion
- Moulding (overriding of fetal cranial bones due to Following birth of the fetal head, the shoulders are
external pressure; helps head conform to birth canal) born with the anterior shoulder delivered under the
- Caput succedaneum (localized edematous pubic symphysis & the posterior shoulder delivered
swelling of the scalp superficial to the cranial
over perineal body; rest of the fetus then delivered
periosteum due to pressure of the cervix on the head)

LABOUR & PUERPERIUM

15
Management of Normal Labour Management of the 1st Stage
- Parameters monitored (recorded on a partogram)
Basic Principles in Management of Normal Labour Vaginal examination every 4 hours to:
- Siting of care - Assess cervical effacement
There is no evidence to suggest that childbirth in a - Assess cervical dilatation (once 3-4cm, i.e. active
hospital (with obstetricians in attendance) improves phase has begun, should expect 1cm/hour dilation
perinatal outcomes as compared to childbirth at subsequently)
home (with midwives in attendance) for normal - Assess amniotic fluid colour (if membranes have
labour already ruptured)
Either way, a one-to-one trained care-to-mother ratio - Assess station of presenting part
is recommended - For cephalic presentations, presence of caput
In Singapore, most births usually occur in hospitals & moulding should also be noted
- Monitoring of progress Abdominal examination every 30 minutes to:
A variety of methods for monitoring are employed to - Assess uterine contractions via palpation
monitor the progress of labour as well as fetal & (frequency of about 4 in 10 minutes is appropriate;
maternal well-being throughout the process at higher rates, uterus contracts inefficiently,
Findings are plotted on a partogram causing poor labour progress & also increases the
If thresholds for abnormal labour progress are risk of fetal hypoxia as fetus has less time in between
reached, interventions are introduced for labour contractions to recover)
augmentation (see below) - Assess engagement of fetal head
- Terminology for interventions pertaining to labour Maternal well-being:
Induction of labour = intervention to promote the - Blood pressure (every 4 hours)
onset of labour when it has not occurred - Pulse rate (every 30 minutes)
Augmentation of labour = intervention to speed up - Pain score
the progress of labour when labour has already been Fetal well-being assessment depends on technique:
established - Intermittent auscultation (fetal heart rate
Stimulation of labour = intervention to promote the assessed every 15 minutes for 1st stage)
onset of labour when rupture of membranes have - Cardiotocography (continuous monitoring of
occurred (in which case it is termed pre-labour fetal heart rate, usually done in Singapore)
rupture of membranes) - Maternal position
- Miscellaneous issues Mother may ambulate
Analgesia provided as requested If in bed, lateral recumbent position is encouraged to
Regular bladder emptying is encouraged to avoid ensure perfusion of the uteroplacental unit
over-distension of the bladder for prolonged periods - Management
of time as labour progresses IV fluids (IV line also provides route of
Perineal shaving not recommended (shown to increase administration of drugs for augmentation of labour if
rates of colonization with gram negative bacteria) subsequently required)
Bowel preparation with enemas not recommended Adequate analgesia
Keep nil-by-mouth in case of the need for emergency Baseline investigations (sent off at presentation after
caesarean with general anaesthesia diagnosis of labour is made):
- Full blood count (check haemoglobin level)
- Group & cross match (in case of the need for
transfusion with excessive peripartum blood loss)
- Urine analysis (check for presence of protein &
glucose)
- Maternal blood group, rhesus type & antibody
screen (if not already known, as it determines need
for maternal anti-D administration post-partum)
- Hepatitis B & HIV status (if not already known,
as they affect post-natal management of the child)
- High vaginal swab for Group B Streptococcus
colonization (if not already known, as it affects
decision to give intrapartum antibiotics to prevent
neonatal sepsis)

LABOUR & PUERPERIUM

16
Management of the 2nd Stage - Management
- Parameters monitored Episiotomy
Fetal descent - Done when crowning occurs to decrease
- Can be monitored by using fetal head station perineal resistance to birth
vaginally (every 30 minutes) & number of fifths - 2 main types: mediolateral (cut from 6 o clock
palpable abdominally position obliquely left or right 45 degrees) &
- Moulding & excessive caput formation can midline/median (cut from 6 o clock position down
affect the accuracy of the assessment of fetal towards direction of anus)
head station, hence the importance of also - Controversial; liberal use vs restrictive use
considering number of fifths palpable - Pros of episiotomies: creates a controlled perineal
abdominally especially in difficult labours tear which is easier to repair
Fetal well-being assessment depends on technique: - Cons of episiotomies: higher incidence of 3rd
- Intermittent auscultation (fetal heart rate degree tears, creation of a tear larger than required
assessed every 5 minutes for 2nd stage of labour) Delivery of fetal head using Ritgen maneuver
- Cardiotocography (continuous monitoring of (applies to the typical occipitoanterior position)
fetal heart rate, usually done in Singapore) - Right hand draped with a towel exerts
- Maternal position upward pressure through the perineal body
Mother can assume any position she prefers: onto the fetal supraorbital ridges (&
- Upright or lateral positions are associated with subsequently chin) to facilitate extension
a reduction in pain & assisted deliveries but - Left hand counteracts by exerting downward
with an increase in tears & blood loss >500ml pressure on the fetal occiput to prevent overtly
Mother should be encouraged to push/bear down rapid extension of the fetal head
once they have got a pressure sensation/urge to Delivery of rest of fetus
push (usually occurs once cervix is fully dilated with the - Mother is told to give only small pushes or just
onset of the 2nd stage of labour) pant once the head has been delivered
- Maternal pushing efforts should be synced - Anterior shoulder is delivered via gentle
with the occurrence of uterine contractions downward traction on the externally rotated
- Note that the sensation to push may be fetal head
decreased with the use of epidurals, hence the - Posterior shoulder is delivered via elevation of
need for encouragement by the healthcare staff the fetal head
in attendance to push with contractions - Rest of fetal body delivered via gentle traction
on the shoulders
Cord clamping
- Umbilical cord is usually clamped & cut
within 15-20 seconds
- Prolonged holding of the newborn below the
level of the maternal introitus with a patent
cord will promote infusion of the newborn with
blood from the placenta (can contribute to
neonatal hyperbilirubinemia; may be used
therapeutically for premature babies to decrease need
for respiratory support post-natally)
- Cord blood sample taken for G6PD & TSH
umbilical artery pH for high-risk cases
Initial management of neonate
- APGAR score, resuscitate where needed
- Examine for birth injuries
- Vitamin K where indicated (premature,
complicated &/or instrumental delivery)

Ritgen maneuver Episiotomy incisions

LABOUR & PUERPERIUM

17
Management of the 3rd Stage Pain Relief Options in Labour
- Repair of perineal tears (including episiotomy if made) - Non-pharmacological measures:
Classification of perineal tears Acupuncture
- 1st degree = involves vaginal epithelium or Hypnosis
perineal skin only (doesnt need repair) Back massage
- 2nd degree = involves perineal muscles Transcutaneous electrical nerve stimulation (TENS)
- 3rd degree = laceration involving the anal - Inhalational analgesia
sphincter (3a: <50% of the external anal sphincter, Entonox (1:1 mixture of O2 & NO2)
3b: >50% of the external anal sphincter, 3c: involves Short acting, works for as long as the patient inhales
internal anal sphincter) Side-effects: nausea & vomiting, giddiness
- 4th degree: involves rectal mucosa - Parenteral narcotics
Episiotomy repair Pethidine, morphine, fentanyl
- Pre-repair to-do: take informed consent, sterilize Easy to administer
& drape, VE to assess for other tears, PR to assess Side effects: nausea & vomiting, neonatal respiratory
for anal mucosal involvement, ensure adequate depression (especially if used within 1-3 hours of
analgesia delivery; reverse by administrating naloxone to neonate)
- Repair is done using Vicryl rapid sutures - Local infiltrations
- 1st repair done beginning from ~0.5cm above Perineal/pudendal nerve blocks
the apex of the vaginal incision (to ensure that Useful when performing episiotomy, repairs &
any retracted incised vessel is caught within the instrumental deliveries
repair), done with a continuous interlocking - Epidural analgesia/anaesthesia
stitch until the mucocutaneous junction is Bupivacaine, 16-20 gauge needle, injected into
reached epidural space at L2-L5
- 2nd repair done involves apposition of perineal Very good pain relief, useful for both vaginal &
muscles with interrupted or continuous stitches caesarian deliveries
- 3rd repair done involves repair of perineal skin However, associated with increased risk for
using a subcuticular stitch or interrupted instrumental delivery (due to decreased maternal
stitches sensation of urge to push during 2nd stage of labour) &
- If anal sphincter torn, repair using PDS sutures slight risk of headaches (<1%)
- Post-repair to-do: ensure no more bleeding, PR - Spinal analgesia/anaesthesia
again to see if any suture went too deep through the Bupivacaine/lignocaine, 24-27 gauge needle, injected
anal mucosa, dispose of equipment appropriate, into subarachnoid space at L2-L5)
observe patients pad chart thereafter Easy & fast when compared to epidural, mainly
- Delivery of the placenta employed for caesarian deliveries
Separation of the placenta generally occurs 2-10 However, limited time span of use (2 hours) &
minutes after the end of the 2nd stage of labour higher risk (1-2%) of post-dural puncture headache
Signs of placental separation: (a severe positional headache)
- Cord elongation outside the vagina
- Fresh short gush of blood
- Uterus becomes smaller, firm & globular
Active management of placental delivery:
- Controlled cord traction (with abdominal
massage of the uterus to stimulate contraction)
- IM syntometrine administration (ergometrine +
oxytocin, helps decrease blood loss)

1st degree tear 2nd degree tear 3rd degree tear 4th degree tear

Mediolateral incision Mediolateral episiotomy repair

LABOUR & PUERPERIUM



18
Fetal Surveillance & Intervention Umbilical cord conditions
This section gives a more in-depth discussion on the aspect on fetal - Vasa praevia
surveillance during labour which has been briefly mentioned earlier in - Umbilical cord compression
the management of the different stages of labour as well as the strategies - Umbilical cord prolapse
for intervention when fetal distress is detected - Umbilical cord hematoma (e.g. iatrogenic after
cordocentesis)
Techniques for Fetal Surveillance During Labour Fetal conditions
- Intermittent auscultation - Fetal anemia
Manual auscultation of fetal heart rate using a - Intrauterine infections
stethoscope or DopTone at regular intervals: - Donor twin in twin-twin transfusion
- Every 15 minutes for 1st stage of labour - Signs of fetal distress:
- Every 5 minutes in 2nd stage of labour Changes in fetal heart rate pattern on CTG:
Not routinely done in Singapore - Earliest sign is decelerations (variable decels
- Cardiotocography typical for cord compression, late decels typical for
(refer to Cardiotocography in the chapter on Antenatal uteroplacental insufficiency)
Care for more details on interpretation of CTG patterns) - Baseline tachycardia sets in next as
Continuous monitoring of fetal heart rate using compensatory response to prolonged fetal
external transducers (or where applicable, internally hypoxia to improve circulation
monitored using fetal scalp electrodes) with - Loss of baseline variability follows with
simultaneous monitoring of uterine contractions further hypoxia due to blunted autonomic
- Indications for use of fetal scalp electrode function with prolonged brain hypoxia
monitoring: multiple gestations, obese mother - Baseline bradycardia is a late sign
Useful for assessing both fetal well-being as well as Meconium passage
frequency & amplitude of uterine contractions Fetal acidosis (detected on fetal blood sampling)
Good negative predictive value (i.e. if CTG is
reassuring, fetus is most likely well) but poor positive Strategies for Intervention
predictive value (i.e. if CTG is pathological, fetus may - Managing non-reassuring fetus status on CTG in labour
often still be well) Give 100% oxygen via face mask to mother
- Fetal blood sampling Change maternal position to left recumbent position
Can be done from fetal scalp (during 2nd stage of - Helps relieve fetal compression of umbilical cord in
labour) or umbilical artery (after fetus is delivered) variable decelerations
Done to assess fetal blood pH to detect fetal acidosis, - Helps relieve gravid uterus compression of vena
which has a good accuracy for predicting neonatal cava & aorta in late decelerations
outcome (sensitivity 90%, specificity 92%) Assess maternal vitals to exclude correctable causes
- Umbilical artery blood pH <7.0 is associated of poor uteroplacental perfusion (e.g. maternal
with cerebral palsy hypotension as a side effect of epidural anesthesia)
Indicated when fetal distress is suspected during Vaginal examination to exclude cord prolapse (if
labour (non-reassuring CTG, meconium staining) diagnosed, see Obstetric Emergencies)
Technique for fetal scalp blood sampling: Discontinue oxytocin infusion if present (be it for
- Amnioscope is placed transvaginally against scalp induction or augmentation of labour initially)
- Cotton swabs are used to remove cervical mucus, Consider administering IV tocolytic (e.g. terbutaline
before silicone grease is applied to the scalp to 0.25mg or magnesium sulphate 2.0g)
facilitate blood bead formation If abnormal CTG pattern persists, consider fetal scalp
- 2x2mm lancet is used to make a stab incision on the blood sampling:
fetal scalp, before aspirating a drop of blood into a - pH 7.25 = observe, repeat blood sampling
long heparinized capillary tube - pH 7.20 = consider immediate delivery
Complications of fetal scalp blood sampling: Consider amnioinfusion if in 2nd stage (replacement of
-Scalp abscess amniotic fluid with normal saline infused through a
transcervical intrauterine pressure catheter)
Fetal Distress Consider assisted (instrumental) delivery if in 2nd
- Implications of fetal distress: stage & fetal station permits
Fetal distress fundamentally signifies fetal hypoxia Last resort: emergency caesarian delivery
Prolonged or repeated fetal hypoxia will result in - Managing meconium passage in labour
fetal acidosis, which can result in perinatal fetal As above to manage/exclude poor uteroplacental
morbidity & mortality perfusion
- Causes of fetal distress (both during labour & before): Amnioinfusion may be considered for its dilutional
Maternal conditions effect (reported to reduce incidence of meconium-related
- Maternal hypertension, pre-eclampsia fetal respiratory complications)
- Maternal hypotension, obstetric shock After successful delivery, nasal suction of newborn
- Severe maternal anemia should be avoided to prevent reflex gasping which
- Maternal cardiac & respiratory disease may drive meconium further into lungs
- Maternal seizures (both eclamptic & otherwise) Neonatal resuscitation of meconium aspiration
Uteroplacental conditions requires swift intubation, endotracheal suction of
- Uterine tetany/hyperstimulation meconium from airways & assisted ventilation (do
- Placental abruption not bag & mask as per normal neonatal resuscitation
- Post-mature placenta (>42 weeks gestation) protocol as this would drive meconium further down the
respiratory tree)

LABOUR & PUERPERIUM

19
Induction of Labour - Success of induction of labour depends on:
Gestational age (the closer to EDD, the better)
Induction of labour refers specifically to the intentional triggering of the Parity (previous normal vaginal delivery better)
onset of true labour in a pregnant woman who is not already in State of cervix/cervical ripeness
established labour & has not had her membranes ruptured yet - Scoring system for assessment of cervical ripeness:

Indications for Induction of Labour


Modified Bishops Score (Cervical Score)
- Maternal indications
Parameter 0 1 2
Intrauterine fetal death (IUFD)
Cervical dilatation 0cm 1-2cm 3-4cm
Polyhydramnios
Cervical length (effacement) >2cm 1-2cm <1cm
Social reasons (horoscope induction) Cervical direction Posterior Axial Anterior
- Fetal indications Cervical consistency Firm Medium Soft
Evidence of fetal compromise Station of presenting part -3 -2 -1
Intrauterine growth restriction (IUGR)
Score of >5 is favourable, surgical induction can be done
Oligohydramnios If score 5, medical induction is used instead
Post-date pregnancy (especially after 41 weeks)
Maternal diabetes mellitus (both pre-existing & GDM)
Induction of Labour in Special Circumstances
Fetal abnormalities requiring earlier delivery
- Previous caesarian section
- Indications pertaining to both mother & fetus
Previous CS is a relative contraindication, but where
Hypertensive disorders, pre-eclampsia
vaginal delivery is desired by mother & indications
Placental abruption
for induction of labour is present, still possible
Medical disorders (e.g. SLE, chronic renal disease)
If modified Bishops score is favourable, surgical
Premature rupture of membranes (PROM)
induction of labour can be carried out
Chorioamnionitis
Cervical priming with prostaglandin analogues
associated with a higher risk of uterine rupture with
Contraindications to Induction of Labour
previous CS
- Maternal contraindications
- Twin pregnancy
Contracted pelvis (assumed cephalopelvic disproportion)
Possible only if the 1st twin is in cephalic presentation
Prior uterine surgery
Previous caesarian delivery (risk of uterine rupture)
- Fetal contraindications Risks & Complications of Induction of Labour
Preterm fetus without lung maturity - Iatrogenic prematurity (dates may be inaccurate)
Acute fetal distress - Failed induction/abnormal labour progress
Malpresentation (breech, transverse) Higher rates of need for assisted (instrumental)
Placenta praevia major delivery & caesarian delivery for induced labours vs
Vasa praevia spontaneous labours
- Risks & complications of amniotomy:
Umbilical cord prolapse
Principles of Induction of Labour
Chorioamnionitis
- Two main types of labour induction:
- Risks & complications of oxytocin infusion:
Surgical induction of labour
Uterine hyperstimulation (especially if >7 contractions
- Involves amniotomy/artificial rupture of
every 10 minutes resulting in fetal hypoxia)
membranes (ARM) (stimulates endogenous
Uterine rupture (especially if previous caesarian section)
prostaglandin production) used in conjunction
Water intoxication (especially if oxytocin infusion is
with IV oxytocin infusion
prolonged, as oxytocin has anti-diuretic physiological
- Used only if modified Bishops score is
effect, leading to hyponatremia)
favourable
Uterine atony post-partum (hence higher risk of post-
Medical induction of labour
partum hemorrhage)
- Involves use of vaginal prostaglandins (pessary
preparations of PGE1 analogues like misoprostol aka
Cytotec; PGE2 analogues like dinoprostone aka
Prostin)
- Usually used if modified Bishops score is
unfavourable (helps with cervical priming)
- A disadvantage is that this method is not very
titratable (vs oxytocin infusion for surgical
induction which can be titrated)

LABOUR & PUERPERIUM

20
Abnormal Labour Progress - Management of prolonged active phase (of 1st stage)
Artificial rupture of membranes (ARM, amniotomy)
- If rupture of membranes has not occurred
Approach to Poor Labour Progress - Works by stimulating endogenous release of
prostaglandins by encouraging application of
Types of Poor Labour Progress presenting part to the cervix
- Primary dysfunctional labour Augmentation with IV oxytocin (syntocin)
Considered when labour progresses at a rate slower - 1st-line management
than expected - Risks: uterine hyperstimulation, uterine rupture
- 1st stage: prolonged latent or active phase of labour - Common mistake: note that syntometrine &
- 2nd stage: prolonged descent prostaglandins are not used in the augmentation of
Suspect when: labour; syntometrine is only used after delivery of
- 1st stage (latent phase): >20 hours (nulliparous) the fetus as part of managing the 3rd stage to reduce
or >14 hours (multiparous) blood loss; prostaglandins are only used in the
- 1st stage (active phase): <0.5-1cm/hour of cervical induction of labour
dilatation after 3-4cm dilatation has been attained Caesarian section
- 2nd stage: <1cm/hour (nulliparous) or <2cm/hour - 2nd line management
(multiparous) of presenting part descent or >2 hours - Done if adequate uterine activity has been
in nullip (>3 hours if regional anesthesia used) or >1 achieved for at least 2-4 hours without
hour in multip (>2 hours if regional anesthesia used) improvement in rate of cervical dilatation
Usually a problem of poor uterine contractility (presumed cephalopelvic disproportion present)
- Secondary arrest of labour - Management of prolonged descent (2nd stage)
Considered when labour progresses normally at an Augmentation with IV oxytocin (syntocin)
expected rate initially before abruptly stopping or - Used if uterine contractility is inadequate
slows down very significantly Assisted delivery (see Assisted Delivery)
- 1st stage: arrest of dilatation - Used if uterine contractility is adequate
- 2nd stage: arrest of descent - Management of arrested labour
Suspect when: (depends on underlying etiology)
- 1st stage: when cervical dilatation rate falls Cephalopelvic disproportion
significantly or ceases to dilate - Absolute indication for caesarian section
- 2nd stage: when fetal station ceases to progress Shoulder dystocia
- Large caput succedaneum (see Obstetric Emergencies)
- Excessive moulding Malpositions
- Edematous cervix & vulva - Persistent occipitotransverse position (arrest of
Usually due to cephalopelvic disproportion descent usually occurs at the level of the mid-pelvis;
managed by manual rotation or midforceps rotation
Assessing Poor Labour Progress The 3 Ps using a Kielland forceps)
(when dealing with poor labour progress, fall back on the 3 Ps to - Persistent occipitoposterior position (course of
evaluate the possible etiology) labour in OT positions usually normal except for
- Power tendency to be prolonged; can consider vacuum
Poor uterine contractility (normally has frequency of 4 extraction mediolateral episiotomy)
times in 10 minutes & amplitude of >50mmHg) Malpresentations (see below)
Accounts of 90% of poor labour progress
Risk factors: older age, obesity, primips Complications of Abnormal Labour Progress
- Passage - Obstructed (neglected) labour
Inadequate maternal pelvic anatomy/dimensions to Occurs when arrested labour progresses without
accommodate passage of fetus medical intervention
- Passenger Maternal consequences:
Big baby (macrosomia, leading to shoulder dystocia, - Maternal tachycardia
defined as difficult delivery of the shoulders) - Edematous cervical lips
Abnormal baby (large abdomen, hydrocephalus) - Distended lower segment
Malpositions - Inadequate uterine relaxation
- Persistent occipitotransverse position - Haematuria (prolonged bladder compression
- Persistent occipitoposterior position leading to bladder wall necrosis; long term sequelae:
Malpresentations vesico-vaginal fistula)
- Brow presentations Fetal consequences:
- Face presentations - Significant caput & excessive moulding
- Transverse/shoulder presentations - Fetal hypoxia
- Uterine rupture
Management of Poor Labour Progress - Erbs palsy
- Management of prolonged latent phase (of 1st stage) Specifically in the setting of shoulder dystocia
Give analgesia Upper brachial plexus injury due to excessive fetal
- Pain increases sympathetic activity which neck lateral flexion to the contralateral side
decreases uterine smooth muscle contractility Erbs palsy on the anterior shoulder is often due to
(mediated via 2-adrenergic receptors) excessive traction by the delivery attendant
Erbs palsy on the posterior shoulder is most likely
caused by abnormalities of the sacral promontory
applying on the brachial plexus before delivery

LABOUR & PUERPERIUM

21
Malpresentation - Management of breech presentations:
Refers to any presentation other than cephalic (vertex) Consider excluding fetal & uterine abnormalities
- If breech presentation after 34 weeks
- Look out for any Mllerian abnormalities,
uterine fibroids or fetal structural abnormalities
External cephalic version (ECV)
- Done at 37 weeks of gestation (in case of need
for emergency caesarian if complications arise)
- Under ultrasound guidance by an experienced
obstetrician, extra-uterine manipulation is done
to convert the breech fetus to a cephalic one;
tocolytics helps facilitate procedure; CTG done
before & after procedure; anti-D Ig given after
procedure where indicated
Breech Presentation
- Complications: abruptio, cord compression,
- Breech presentation = fetal buttocks or feet present into
premature rupture of membranes (with cord
the maternal pelvis
prolapse), uterine rupture, fetomaternal hemorrhage
Incidence is 1 in 25 deliveries (4%)
- Hence needs to be done in a hospital with the
About 25% of all fetuses before 28 weeks gestation
facilities for emergency caesarian with the
are in breech presentation, but eventually rotates to
patient prepped for the operation if needed (nil-
assume a vertex presentation as they grow & occupy
by-mouth, establish IV access)
more of the uterus (hence breech isnt much of an issue
- Immediate success rate = 35-76%
except in the context of preterm labour or persistent breech
- Contraindications to ECV: evidence of placental
presentation after 34 weeks gestation)
insufficiency, placenta praevia, hypertension, IUGR,
- Etiologies & associations:
oligohydramnios, history of previous uterine surgery
Prematurity (major predisposing factor)
Multiple gestation
Fetal structural abnormality (e.g. hydrocephalus)
Placenta praevia
Polyhydramnios
Uterine abnormalities (e.g. bicornuate uterus)
Contracted maternal pelvis
Pelvic tumours obstructing birth canal
- Classification of breech presentations: Caesarian section
Frank breech 65% (thighs flexed, knees extended) - Where ECV is not an option (contraindicated or
Complete breech 25% (thighs & knees flexed) patients refusal to do it), caesarian section is the
Footling (incomplete) breech 10% (one or both thighs current standard of care for the delivery of
extended with one or both knees/feet lying below the level breeches
of the buttocks) - Term breech trial (year 2000) demonstrated
significant reduction in perinatal morbidity &
mortality when elective caesarian was
performed for breeches instead of normal
vaginal delivery (1.6% vs 5.0%, p<0.0001)
Assisted breech delivery
- Assisted vaginal delivery of breeches may still
be performed in certain situations (no facilities
for caesarian, mothers wish to deliver vaginally,
delivery of a breech 2nd twin)
Frank breech Complete breech (Single) Footling breech - Fetus is allowed to descend naturally until the
level of the umbilicus is reached
- Issues pertaining to breech deliveries: - In frank breeches, delivery of the feet can be
High risk of cord prolapse facilitated by the use of Pinard maneuver
Risk of head entrapment (when fetal body passes pressure on the popliteal fossa of the fetal lower limb
through a relatively undilated cervix with the head to cause flexion of the knee, thereby bringing the foot
trapped subsequently; especially so an issue with very down to the level of the vagina
preterm babies with a larger head-to-body ratio)
Birth trauma (e.g. Erbs palsy)
Perinatal mortality 2.5% vs 1.2-1.6% for non-breech
- Diagnosis of breech presentations:
Can be made antenatally by abdominal palpation &
ultrasound scan

Pinard maneuver

LABOUR & PUERPERIUM

22
- The delivery attendants hands grasped on the Face Presentation
fetal pelvis (to avoid injury to abdominal viscera), - Face presentation = fetal face (between the chin & orbits) is
gentle traction is employed until the scapulae the presenting part as a result of hyperextension of the
appear at the introitus fetal neck
- The shoulders are then delivered by sweeping Incidence is about 1 in 500 deliveries
each arm in turn across the fetal chest; however, Presenting diameter is submentobregmatic (9.5cm,
if the arms are stretched above the head (nuchal similar to suboccipitobregmatic in typical occipitoanterior
arms), may need to employ Lovset maneuver: cephalic presentations)
- Etiology & associations:
In most cases, no underlying cause is found
Extreme prematurity
High maternal parity
Polyhydramnios
Placenta praevia
Fetal goitre (causes fetal neck extension)
Anencephaly (anencephalic fetuses present uniformly
face-first, hence need to exclude this if face presentation is
Lovset maneuver suspected)
- Issues pertaining to face presentations:
- Delivery of the fetal head can proceed in 3 Possible cause of abnormal labour progress
ways: (i) Burns Marshall maneuver hang fetus Fetal face injuries during birth
from the introitus until the hair at the back of his Perineal trauma during birth
head can be seen, then grasp both legs & rotate the Perinatal morbidity & mortality similar to that for
body of the fetus through an arc to bring him cephalic presentations
towards the mothers abdomen (ii) Mauriceau- - Diagnosis of face presentations:
Smellie-Veit maneuver one hand is placed into Usually diagnosed intra-partum when the soft
the vagina with the palm facing the fetal face, with tissues of the fetal mouth & nose are noted adjacent
the index & ring fingers applying pressure on the to the malar bones & orbital ridges on vaginal
fetal maxilla & middle finger in the fetal mouth (or examination
alternatively on the fetal chin) to produce downward 60% are mentoanterior, 25% mentoposterior, 15%
flexion of the neck; other hand is placed over the back
mentotransverse at the time of diagnosis
of the fetal skull to provide flexion at the base of the
- Management of face presentations:
skull (iii) Outlet forceps books describe a special
Vaginal delivery
Piper forceps for this purpose; locally, a Wrigley
- Viable option for mentoanterior (as fetal chin
forceps is used
can rotate under pubic symphysis with fetal neck
flexion, allowing vaginal delivery to occur)
- Can be assisted with low forceps (but not
vacuum) if required
- Mentoposterior positions cannot deliver
vaginally due to inability for further neck
extension to allow delivery to be completed;
mentotransverse positions usually experience
arrest of descent as well
- However, about 50% of mentoposterior &
mentotransverse spontaneously rotate to
mentoanterior after a significant period of
maternal pushing, hence can manage
Burns Marshall maneuver expectantly initially
- Use of oxytocin for augmentation of labour
controversial
Caesarian section
- Reserved for persistent mentoposterior &
mentotransverse positions which do not
spontaneously rotate to mentoanterior

Mauriceau-Smellie-Veit maneuver Outlet forceps

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23
Brow Presentation Assisted (Instrumental) Delivery
- Brow presentation = fetal brow (between orbits & bregma) is
the presenting part as a result of extension of the fetal Forceps Delivery
neck midway between hyperextension (face presentation) & - Obstetric forceps = instruments designed to provide
flexion (cephalic presentation) traction & rotation of the fetal head when the expulsive
Incidence is 1 in 1400 deliveries efforts of the mother are insufficient to accomplish safe
Presenting diameter is mentovertical (13.5cm, the deliver of the fetus
largest anteroposterior diameter of the fetal head possible) - Parts of a forceps:
- Etiologies & associations:
Similar to those for face presentations
- Issues pertaining to brow presentations:
Possible cause of abnormal labour progress
Perinatal morbidity & mortality similar to that for
cephalic presentations
- Diagnosis of brow presentations:
Head does not engage due to large presenting
diameter, possibly with a sulcus that is palpable
between the fetal occiput & back
On vaginal examination, anterior fontanelle &
supraorbital ridges may be felt
Diagnosis often made late in labour
- Management of brow presentations:
Expectant treatment
- May be indicated as the brow presentation is
an unstable one (50-70% will convert to a face or
cephalic presentation)
Caesarian section
- Indicated for a persistent brow presentation Cephalic curve = the curve on the inner aspect of the
blades (giving the blades a cupped surface) to fit the
Transverse Lie Shoulder & Compound Presentations fetal head
- Compound presentation = fetal extremity (usually the Pelvic curve = the curve along the lower margin of
hand) prolapses alongside the presenting part (the head) & the blade (hence when you put a locked forceps flat on a
both parts enter the maternal pelvis at the same time; if table the tips of the blades curve upwards) to fit the birth
the complete extremity prolapses = shoulder presentation canal
Incidence is 1 in 700 deliveries - Types of forceps:
Spontaneous version occurs in 80-85% of cases (many different types; 3 main ones used locally described here)
- Etiologies & associations: Wrigley forceps
Prematurity - Has pelvic & cephalic curves
Multiple pregnancy - Used for outlet (lift-out) forceps procedures
Polyhydramnios Neville-Barnes forceps
Placental praevia - Classic/standard forceps
Multiparity - Has pelvic & cephalic curves
Uterine abnormalities (e.g. arcuate/septate uterus) - Has a detachable attachment for better traction
- Issues pertaining to transverse lie: Kielland forceps
High risk of cord prolapse - Reduced pelvic curve, hence suitable for rotation
- Diagnosis of transverse lie: - Sliding lock mechanism which allows adjustment of
Antenatally, uterus is felt to be ovoid in shape wider the blades even after both blades are locked, allowing
at the sides, with an empty lower pole & the fetal for accommodating asynclitic presentations
head felt in one flank - Not routinely used nowadays (need training, high
Symphysial fundal height less than expected risk of birth trauma)
Confirmed with ultrasound
- Management of transverse lie:
External cephalic version
- Admission at 37 weeks gestation for ECV may
be attempted, followed by stabilizing induction
of labour & controlled amniotomy
Caesarian section
- Indicated for persistent malpresentation

Wrigley forceps Neville-Barnes forceps Kielland forceps

LABOUR & PUERPERIUM

24
- Types of forceps operations:
Outlet forceps (lift-out) = scalp is visible at introitus
without separating the labia, fetal head at perineum, fetal
skull at pelvic floor, sagittal suture is anteroposterior &
rotation of fetal head <45 degrees
Low forceps = leading part of fetal skull is at station
+2cm or more
Mid forceps = fetal head is engaged but leading point of
skull is above station +2cm
- Indications for forceps delivery:
Prolonged 2nd stage of labour
Suspected immediate/impending fetal compromise
To stabilize aftercoming head during breech delivery
To shorten 2nd stage of labour for maternal benefit: Applying traction in sync with contractions Episiotomy
- Maternal conditions (hypertension, cardiac
disorders, pulmonary disease) in which strenuous Vacuum Extraction
pushing in 2nd stage of labour is hazardous - Vacuum extractor = instrument which uses a suction cup
- Prerequisites for forceps delivery: that is applied to the fetal head
Cervix must be fully dilated - Types of vacuum extractors:
Membranes must be ruptured
Fetal head must be engaged into the pelvis
Clinical assessment performed to determine level of
presenting part, exact position of head, estimation of
fetal size & adequacy of maternal pelvis
Bladder must be emptied
Adequate anesthesia:
- Local infiltration (e.g. pudendal nerve block) for
outlet forceps
- Regional anesthesia for other procedures
- Forceps technique:
Forceps blades are inserted sequentially into the Kiwi cup Ventouse (silc cup)
vagina such that the sagittal suture of the fetal head
is directly between & perpendicular to the shanks - Indications for vacuum extraction:
Left blade is inserted before the right (as the locking Largely similar to those for forceps delivery (in fact,
mechanism is such that the shank of the right blade needs vacuum extraction is usually preferred due to relative ease
to be above the left blade) of use) except in the following cases where forceps
Guiding toe of the blade along the natural pelvic use is indicated over vacuum extraction:
curve of the birth canal helps avoid damage to - Preterm delivery (preterm head & scalp more
maternal tissues prone to injury from suction cup)
Forceps are locked &, timed in sync with - Certain malpresentations (breech, face)
contractions, traction is applied - Prerequisites for vacuum extraction:
Pajot maneuver: direction of pull should be parallel Same as those for forceps delivery
to the axis of the birth canal at that level, such that Must be cephalic presentation
typically there is a downward traction initially, - Vacuum extraction technique:
followed by an ever-increasing upward traction as Suction cup is placed with its edge 3cm posterior to
delivery of the fetal head occurs the anterior fontanelle squarely over the sagittal
Episiotomy may be done when the crowning occurs suture to maintain flexion of the fetal head
- For occipitoanterior position, this involves placing
If progress of fetal head is not obtained with
the cup right onto the presenting part
appropriate traction (i.e. failed forceps), procedure is
- For occipitoposterior position, this requires sliding
abandoned in favour of a caesarian delivery
the cup along the back of the fetal head as far as
- Forceps complications:
possible to place it (hence only kiwi cup can be used)
Failure rate = 7%
Suction is created:
Maternal: birth canal injuries (higher risk than with
- For kiwi cup, hand pump attached is pumped until
vacuum extraction)
the pressure indicator reaches the green zone
Fetal: facial bruising, injury to CN7 & brachial plexus
- For ventouse, foot pump is usually attached
Traction is provided in sync with contractions
parallel to the axis of the birth canal (as for forceps)
Detachment of the cup from the fetal head = pop-off
If progress of fetal head is not obtained with
appropriate traction of if 2 pop-offs occur, procedure
is abandoned in favour of a caesarian delivery
- Vacuum extraction complications:
Failure rate = 12%
Maternal: birth canal injuries (less risk than with forceps)
Introducing left blade Introducing right blade Forceps blades locked Fetal: chignon, cephalohematoma, subgaleal hematoma,
fetal retinal hemorrhages (overall more fetal morbidity
than with forceps)

LABOUR & PUERPERIUM

25
Caesarian Delivery

Indications for Caesarian Delivery


- Abnormal labour progress
- Malpresentation
Breech presentation (not absolute indication, but
standard of care as support by term breech trial)
Persistent brow presentation
Persistent mentoposterior or mentotransverse face
presentation
Persistent transverse lie
- Repeat caesarian Complications & Risks of Caesarian Delivery
- Intra-operative risks:
Not absolute indication for previous lower segment
Anesthesia risk
caesarian section (LSCS)
Bleeding requiring transfusion or even hysterectomy
Recommended for previous classical CS
Injury to bladder, bowel, ureters
- Fetal distress
Amniotic fluid embolism
- Previous full-thickness non-transverse incision through
- Post-operative risks:
the myometrium
Post-partum hemorrhage
E.g. myomectomy for fibroids
Infection (wound, endometritis, other infections)
Due to high risk of uterine rupture with NVD
Longer hospital stay & recovery (vs NVD)
- Placenta praevia
- Long-term complications:
Placenta praevia major is an absolute indication
Post-operative adhesions (future pelvic surgeries or
(placenta blocking cervical os)
repeat CS may be more difficult & complicated)
Placenta praevia minor is a relative indication
Uterine rupture (in future pregnancies)
(normal vaginal delivery still possible is edge of placenta is
Increased risk of placentation problems in future
at least 2cm away from cervical os)
pregnancies (placenta accreta, placenta praevia)
Types of Caesarian Deliveries
Pre-Operative Management for Caesarian Deliveries
- Classical caesarian section
- Take informed consent from mother for procedure
Vertical incision made in the upper segment of the
- Establish large bore IV access, catheterize bladder
uterus through the myometrium of the uterus
- Pre-operative bloods & investigations:
- Note that this refers only to the uterine incision;
Take bloods for FBC, PT/PTT, GXM (4-6 units of
skin incision could still be a transverse suprapubic
(pfannenstiel) incision blood), urea/creatinine
Indications: Consider ECG & chest x-ray
- Preterm breech (lower segment undeveloped) - Measures to decrease risk of aspiration pneumonia in
pregnancy if GA is used (Mendelson syndrome):
- Transverse back-down fetal position (as no fetal
For elective CS: nil-by-mouth + H2-antagonists (e.g.
part to grasp after performing an LSCS)
ranitidine to neutralize gastric contents)
- Poor access to lower segment due to fibroids
For emergency CS: sodium citrate (for immediate
or adhesions
neutralization of gastric contents) + metoclopramide
- Some cases of anterior placenta praevia with
(promote gastric emptying)
high risk of massive hemorrhage if an LSCS is
Intubation: cricoid pressure, cuffed endotracheal tube,
done instead
rapid-sequence induction, pre-extubation gastric emptying
- Planned caesarian hysterectomy
- Thromboprophylaxis
Implications of a classical caesarian section:
Low-risk: early mobilization, hydration
- Higher risk of post-partum hemorrhage,
Moderate-risk: IV heparin + TED stockings
infections & thromboembolism (vs NVD)
High-risk: IV heparin continued till 5-days post-op +
- Risk of uterine rupture in future pregnancies
TED stockings
(4-7%; increased if induction of labour) - Antibiotic prophylaxis
- Hence patients with classical caesarian section IV cefazolin, given after fetus is delivered & cord is
are destined to have repeat caesarian deliveries clamped (to prevent crossing over of drug)
for all subsequent pregnancies Reduces incidence of wound infection, endometritis
- Lower segment caesarian section (LSCS) & urinary tract infection post-op
Transverse incision (Joel Cohen incision )made in the
lower uterine segment after establishing a bladder
Vaginal Birth After Caesarian (VBAC)
flap
- A trial of labour offered to women in subsequent
Indications:
pregnancies if one or two previous LSCSs were
- As per for indications for caesarian deliveries
performed, with the uterine incision not extending into
other than the circumstances in which classical
the cervix or upper uterine segment
caesarian is indicated
- Benefits of VBAC vs repeat caesarian section:
Implications of a LSCS:
Shorter hospital stay & recovery period
- Higher risk of post-partum hemorrhage,
Lower rates of neonatal RDS
infections & thromboembolism (vs normal
Successful VBAC increases likelihood of future
vaginal delivery)
successful VBACs
- Risk of uterine rupture in future pregnancies
- Overall success rate of VBAC ~70%
(<1%; increased if induction of labour)
- Increased incidence of placenta praevia &
placenta accreta

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26
Obstetric Emergencies Intrapartum Management of Shoulder Dystocia (HELPERR)
- Help
Emergency situations which require immediate intervention to avoid Call for immediate help (senior obstetrician,
maternal &/or fetal demise neonatologist, operating theatre, anesthetist, midwives)
Ideally need at least 4 assistants for managing
Shoulder Dystocia shoulder dystocia
A delivery requiring additional obstetric maneuvers to release the Get someone to continually watch the time &
shoulders after gentle downward traction has failed regularly report the amount of time elapsed since
shoulder dystocia was diagnosed
Risk Factors for Shoulder Dystocia - Very narrow window period for intervention
- Past pregnancy factors: to maximize fetal outcomes
Previous delivery complicated by shoulder dystocia - Time is of the essence when deciding to
Previous macrosomic baby escalate interventions
- Maternal factors: - Evaluate for need for episiotomy
Short maternal stature This is typically done at the point before enter
Maternal obesity vagina, primarily to allow easier entry of hands into
- Current antenatal factors: the vagina to perform the maneuvers described
Maternal diabetes Note that an episiotomy does not intrinsically help
Postdates pregnancy shoulder dystocia because shoulder dystocia
Fetal macrosomia involves a bony obstruction while episiotomies only
High pregnancy weight & weight gain relieve soft tissue obstructions
- Note: despite these theoretical risk factors, a large number of - Legs up
shoulder dystocias still occur in patients without risk factors McRobert maneuver
- Get patient into knee-chest position
Diagnosis of Shoulder Dystocia (hyperflexion of both hips) using the help of 2
- Diagnosis is made clinically intra-partum with the assistants, each holding up 1 lower limb
observation of the following signs: - Reduces lumbar lordosis & the angle between
Abnormal labour progress the lumbar spine & the sacrum
- Prolonged or arrest of labour at 1st or 2nd stage - Does not change the pelvic inlet diameter, but
- Need for oxytocin augmentation of labour rather, rotates the pubic symphysis more
- Need for assisted instrumental delivery cephalad such that the plane of the pelvic inlet
Head-bobbing in 2nd stage of labour (significant head becomes more perpendicular to the direction of
retractions occurring in between uterine contractions) maternal expulsive efforts, which helps delivery
Turtle-necking (following delivery of fetal head, fetal of the shoulders
head retracts back against the maternal perineum, causing
fetal cheeks to bulge, resembling a turtle retracting its
head back into its shell)
Poor restitution following delivery of the fetal head

Complications of Shoulder Dystocia


- Maternal complications:
Uterine rupture
Perineal tears & anal sphincter damage
Post-partum hemorrhage
Symphysial separation
- Fetal complications:
Brachial plexus injuries (Erbs palsy)
Clavicular & humeral fractures McRobert maneuver
Birth asphyxia, fetal acidosis, hypoxic brain injury
- Fetal cord pH drops at 0.4 per minute once - Pressure (suprapubic)
shoulder dystocia is established Get an assistant to apply suprapubic pressure (using
- Studies have shown that cord pH < 7.0 is 2 hands in a CPR-like position), ideally directed in an
highly associated with cerebral palsy oblique manner such that the pressure is applied
- Hence, assuming an average cord pH of 7.2 at onto the posterior aspect of the fetus anterior
the time of shoulder dystocia establishment, shoulder
there is only a short window period of 5 Helps dislodge the anterior shoulder from the pubic
minutes to get the fetus delivered to avoid long- symphysis
term hypoxic brain injury sequelae

Suprapubic pressure

LABOUR & PUERPERIUM

27
- Enter vagina (to attempt the following maneuvers) - Roll patient over (Gaskin maneuver)
Rubin II maneuver Roll patient over onto all fours
- Use 2 fingers to locate & press on the posterior Uses gravity & an increased sacral hollow to help
aspect of the anterior shoulder with delivery of the shoulders
- Apply a rotational force to turn the fetus to an
oblique diameter to help deliver the anterior
shoulder
Woods corkscrew maneuver
- Using both hands, place one on the posterior
aspect of the anterior shoulder & the other on
the anterior aspect of the posterior shoulder
- Apply pressure with both hands to rotate fetus
Reverse Woods corkscrew maneuver
- Using both hands, place one on the anterior
aspect of the anterior shoulder & the other on
the posterior aspect of the posterior shoulder
- Apply pressure with both hands to rotate fetus Gaskin maneuver

- If everything above fails, may need to resort to the


following heroic measures:
Fracture fetal clavicles
- Intentional fracture of the fetal clavicles to
decrease the diameter of the shoulders
Zanavelli maneuver
- Manual replacement of fetal head into the
Woods corkscrew maneuver vagina by steady upward pressure (reverse
restitution, manually flex fetal head)
- Send for emergency caesarian section
Symphysiotomy
- Not performed locally due to significant
maternal morbidity & easy accessibility to
caesarian section following Zanavelli maneuver
as a last resort
- Stiff silicon catheter placed into mothers
bladder to allow palpation of the urethra using
Rubin II maneuver Reverse Woods corkscrew maneuver
a hand placed in the vagina
- Urethra is manually deflected away from the
- Remove posterior arm
midline before a scalpel is used to incise the
Use your hand corresponding to the direction of the
pubic symphysis
fetal back (right hand if fetal back facing maternal right,
- Creates an iatrogenic open-book fracture of the
left hand if fetal back facing maternal left)
pelvis, resulting in an increased pelvic inlet
Grasp the posterior arm of the fetus & move it into a
diameter to allow the delivery of the fetal
flexed position at the elbow
shoulders
Sweep the posterior arm across the fetal chest to
deliver it, thereby helping reduce the shoulder
diameter by 20% to help deliver the anterior Postpartum Management of Shoulder Dystocia
shoulder - Management of mother:
Inspect for perineal tears & repair them
Anticipate & manage post-partum hemorrhage
- Management of fetus:
Resuscitate accordingly
Assess for fetal injuries (Erbs palsy, fractures etc)
Test cord pH
- Record the following clearly in notes:
Direction fetal head faced after restitution
- Determines which shoulder was anterior &
which was posterior
- Important medicolegal implications as only
brachial plexus injuries of the anterior shoulder
are considered iatrogenic, whereas posterior
shoulder brachial plexus injuries are usually
attributed to excessive traction resulting from
Remove posterior arm
impaction against the sacral promontory
occurring naturally
Time of delivery of head & body respectively
Baby APGAR score
Umbilical cord blood acid-base measurement

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28
Cord Prolapse Amniotic Fluid Embolism
Descent of the umbilical cord through the cervix alongside (occult) or Obstetric emergency resulting from entry of fetal cells into maternal
past the presenting part (overt) in the presence of ruptured membranes; circulation, leading to sudden maternal &/or fetal deterioration
occurs in approximately 0.2% of all births
Risk Factors for Amniotic Fluid Embolism
Risk Factors for Cord Prolapse - Medical induction of labour (especially in the presence of
- Fetal factors: uterine tetany; doubles risk, but absolute excess risk is low)
Small fetus (low birth weight, prematurity) - Invasive obstetric procedures:
Unengaged fetal presenting part Amniocentesis
Malpresentation (breech, transverse lie) Termination of pregnancy
Second twin Caesarian section
- Uterine factors:
Multiparity Diagnosis of Amniotic Fluid Embolism
Polyhydramnios - Symptoms:
- Placental & umbilical cord factors: Shortness of breath
Long umbilical cord Chest pain
Placenta praevia Altered mental state (light-headedness, restlessness,
- Procedure-related risk factors: distress, panic)
Artificial rupture of membranes Nausea & vomiting
Vaginal fetal manipulation in the presence of Frank maternal collapse
ruptured membranes - Signs:
External cephalic version (if rupture of membranes Cardiovascular instability (hypotension, cardiac arrest)
occurs during procedure) Hypoxia (dyspnea, cyanosis, respiratory arrest)
Signs of coagulopathy
Diagnosis of Cord Prolapse Seizures
- When to suspect cord prolapse: - Supportive investigations:
Fetal heart rate pattern abnormalities detected on ECG, chest x-ray
CTG (e.g. variable decelerations, bradycardia), especially FBC, DIVC screen, group & cross match
if such changes occur soon after ROM Other investigations depending on differentials
- Diagnosis of cord prolapse:
Vaginal examination (either speculum or digital Complications of Amniotic Fluid Embolism
whichever is applicable depending on the stage of labour) - Maternal morbidity, multi-organ failure & mortality
to detect presence of umbilical cord alongside or - Fetal morbidity & mortality
ahead of the presenting part
Management of Amniotic Fluid Embolism
Complications of Cord Prolapse - Initial management is as per for an undifferentiated
- Birth asphyxia, fetal acidosis, hypoxic brain injury (due to obstetric shock/maternal collapse:
cord compression between presenting part & bony pelvic inlet) ABCs, resuscitation with oxygen & fluids
Inotropic support & vasopressors
Management of Cord Prolapse Ventilatory support
Close (invasive) monitoring (central venous line,
Diagnosed cord prolapse arterial line, pulmonary wedge catheter, urinary catheter)
Treat coagulopathy (whole blood, packed cells, fresh
- Call for help (senior obstetrician, midwives, neonatologist, OT, anesthetist) frozen plasma, cryoprecipitate)
- Avoid manipulating loops of cord lying outside vagina (prevent vasospasm) - No specific treatment for amniotic fluid embolism is
- Assess fetal heart rate (FHR) pattern using CTG validated (supportive treatment + transfusion is mainstay)

FHR pattern normal FHR pattern abnormal In-utero death

Consider expectant Relieve cord compression: Allow vaginal


treatment if extreme - Maternal knee-chest or delivery to proceed
prematurity trendelenberg (tilted towards as per normal
left lateral) position
- Bladder instillation with 500ml
normal saline
- Manual elevation of
presenting part with 2 fingers
- Consider tocolysis

Assess imminence of vaginal delivery

Vaginal delivery Vaginal delivery


imminent (2nd stage) not imminent

Allow normal vaginal Emergency


delivery to proceed; consider caesarian section
use of instrumental delivery

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29
Puerperium Support breastfeeding (counsel patient appropriately to
support them through the initial establishment of
The puerperium is defined as the 6-week period following delivery breastfeeding which is often the toughest)
during which various changes that occurred during pregnancy revert to Contraception (talk to patient about when they intend to
the non-pregnant state have the next child, if at all; educate on contraceptive
options to promote good family planning)
Normal Puerperal Changes & Monitoring - Other miscellaneous issues:
Anti-D (within 72 hours of delivery where indicated)
Puerperal Anatomical & Physiological Changes Check rubella status (if previously unknown, so that
- Involution of the uterus vaccine can be administered before next pregnancy)
After delivery of the placenta, the uterus is Check relevant parameters at 6 weeks post-delivery
approximately a 20-week size (level of umbilicus); for retrospective diagnosis:
subsequent reduction in size occurs at a rate of 1 - Oral glucose tolerance test (gestational diabetes
finger breadth/day such that it cannot be palpable should have resolved; if not, patient is determined to
through the abdomen anymore after 2 weeks have diabetes mellitus)
Uterine weight decreases from 1kg at delivery to 200- - Blood pressure & urine protein (pre-eclampsia
300g at 3 weeks post-delivery should have resolved; if not, patient is determined to
By the end of the puerperium, the uterus is only have chronic hypertension)
slightly larger than before pregnancy
- Cervical changes Puerperal Complications
Cervix regains firmness by the 3rd day
Internal os closes within 3 days, while the external os Common Puerperal Problems
closes within 3 weeks - Perineal injury
- Vagina & perineal changes Perineal tears & episiotomies would still be painful
After delivery: vaginal wall is initially swollen, in the immediate post-partum period
bluish & pouting; perineal edema present Infection may occur (note that episiotomy wound
Pelvic floor gradually regains former tone by 6 infections are actually quite uncommon, possibly due to
weeks (may never return to the pre-pregnant state) the high vascularity in the area which promotes good
Kegel exercises (intermittent tightening of the wound healing & immune defense against infection)
perineal muscles) can help Management: exclude wound site infection, give
- Lochia (per-vaginal discharge of endometrial slough with red & analgesia, rubber ring for sitting on
white blood cells) - Bladder function
Lochia rubra (red): for first 3 days Voluntary bladder emptying may be difficult in the
Lochia serosa (yellow): transition from red to white over first 24 hours, especially if epidural was used;
a 10-day period (sloughing of eschar at placental site at requiring catheterization
day 7-14 post-delivery may cause transient PV bleeding) Urinary incontinence (usually stress incontinence)
Lochia alba (white): discharged up to 6 weeks may occur due to excessive pelvic floor stretch
- Cardiovascular changes during labour; usually resolves by a few weeks,
Marked increased in peripheral resistance helped by Kegel exercises
immediately after delivery due to removal of the More rarely, urinary fistulas may form (e.g. between
low-pressure uteroplacental shunt bladder & vagina) as a complication of anterior
Cardiac output & plasma volume gradually returns vaginal wall injuries or obstructed labour, resulting
to normal over the first 2 weeks, resulting in dieresis in complete incontinence; requires surgical repair
& marked weight loss - Bowel function
- Return of menstruation & ovulation Constipation may persist for a short while; stool
Without breastfeeding, menses returns by 6-8 weeks softeners are useful
With exclusive breastfeeding, lactational amenorrhea Hemorrhoids may appear for the 1st time after labour
may occur up to 6 months, following which or become more painful if already present previously
menstrual flow returns (by 36 weeks post-delivery) - Mastitis
May be due to failure to express milk from one part
Management & Assessment in Early Puerperium of the breast; can be further complicated by infection
- Regular monitoring of maternal parameters with Staphylococcus aureus & breast abscess formation
Temperature (to detect puerperal sepsis) Management: ensure all milk is expressed, use of
Blood pressure (to detect concealed PPH) cold compress, flucloxacillin (for S. aureus infection),
- Regular physical examination incision & drainage (for breast abscess)
Breasts (look out for complications of breastfeeding such - Backache
as mastitis & breast abscess) May persist after delivery, affects 25% of women
Fundal height (to detect possible retained products of Pain may be considerable & last for several months
conception suggested by failure of uterine involution) - Postnatal blues
Lochia (check normal progression of lochia changes; Usually occurs on days 3-5, when 50-70% of women
persistent lochia rubra suggests retained products of become temporarily sad & emotional
conception; foul-smelling lochia suggests endometritis) About 10% develop postnatal depression which can
Lower limbs (check for signs of DVT) present anytime within the 1st year after delivery
Assess for urinary function (may have self-limiting Postulated to be due to hormonal changes, reaction
overflow incontinence for ~24 hours after epidural use) to excitement of childbirth & doubts by the mother
- Patient education, support & counseling about her ability to care for the child
Teach Kegel exercises to help regain pelvic floor tone Management: counsel mother

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30
Post-Partum Hemorrhage (PPH) If retained products of conception is the cause:
- Classification of PPH: - Always check completeness of placenta after
Primary PPH = loss of >500ml (>1000ml if caesarian) of 3rd stage of labour to ensure all cotyledons are
blood within the first 24 hours after delivery present
Secondary PPH = abnormal bleeding after 24 hours post- - If delivery of placenta cannot occur via the
delivery up until 6 weeks normal way, manual removal under general
- Causes of PPH anesthesia may be required
Typical causes of primary PPH: If genital tract injuries is the cause:
- Uterine atony (accounts for 80% of cases; - Always ensure 1st suture in repair of vaginal
increased risk in conditions where excessive uterine lacerations is placed well above apex of tear to
stretch/contraction occurred multiple gestation, ensure any retracted vessel is caught
polyhrdramnios, use of oxytocin for - Repair any tears seen
induction/augmentation of labour use of halothane - Hematomas require urgent surgical
anesthesia, uterine fibroids & placental abruption) management (evacuation of clots, ligation of
- Retained products of conception (RPOC) bleeding vessel, bilateral hypogastric artery ligation)
- Low placental implantation (as lower uterine If uterine inversion is the cause:
segment contracts less well than the rest of the - Usually a result of uncontrolled cord traction
uterus, hence less able to constrict spiral arteries in the 3rd stage of labour; patient quickly goes
following placental separation) into shock as profound vasovagal response
- Genital tract injury (may be concealed e.g. poor causes systemic vasodilation which promotes
repair of perineal tears, forming a hematoma which heavy bleeding & extravasation of fluid
is exquisitely painful; patient can exsanguinate as - After stabilizing patient, attempt to replace
bleed continues tracking into ischiorectal fossae) uterus by placing a cupped hand around the
- Uterine inversion, uterine rupture fundus & elevating it in the long axis of the
- Coagulopathy (may be pre-existing or due to vagina
complications such as placental abruption or - If unsuccessful, further attempt made after use
amniotic fluid embolism) of nitroglycerin general anesthesia to relax the
Typical causes of secondary PPH: uterine muscle
- Poor epithelialization of placental site (accounts - Once replaced, oxytocin administered to
for 80% of cases) contract the uterus before removing the
- Retained products of conception intrauterine hand
- Endometritis - Rarely, if uterus cannot be replaced from
- Management of PPH & obstetric shock below, surgery required (vertical incision down
Initial management: cervix to incise the constriction ring to allow
- Resuscitate patient if necessary replacement of the fundus before suturing the
- Establish intravenous access & catheterize cervical incision)
- Monitor patients vitals closely If coagulopathy is the cause:
- Group & cross match blood + FBC + PT/PTT - Correct coagulopathy with relevant
if not already done before delivery transfusions
- Palpate uterus (detect uterine atony) - Amniotic fluid embolus often requires
- Speculum examination (exclude genital tract intensive supportive measures (e.g. CPR,
injuries, uterine inversion & pelvic hematoma; open mechanical ventilation, inotropes etc)
os suggests RPOC) Managing poor epithelialization of placental site:
If uterine atony is determined to be the cause: - Ergometrine + antibiotics
- Massage uterus through abdomen - Curettage necessary if bleeding persists
- Administer uterotonic agents; options include:
(i) IV oxytocin infusion 40-80U in 1L saline
(ii) IM ergonovine maleate or methylergonovine
0.2mg (ergot drugs may precipitate myocardial
infarction & stroke; contraindicated in pre-
eclampsia, severe hypertension, severe heart disease
& familial hypercholesterolemia)
(iii) Per rectal misoprostol
(iv) IM carboprost aka Hemabate 0.25mg every
15min up to max of 3 doses (PGF2 analogue; can
also be given straight into the myometrium which
has a much faster onset of action: 4min vs 20min)
- If pharmacological measures fail, tamponade
bleed using bimanual compression or uterine
packing or balloon catheter (e.g. Sengstaken-
Blackmore tube or obstetric-specific Bakri balloon)
or external pressure on abdominal aorta
- Uterine artery embolization (enlist help of
interventional radiology) can be considered B-lynch suture
- Surgical measures as a last resort include use
of B-lynch suture (preferable option as it preserves
fertility) or stepwise arterial ligation (uterine,
ovarian, internal iliac) or hysterectomy

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31
Puerperal Sepsis Thromboembolism
- Puerperal pyrexia = temperate of 38oC during the first 14 - Risk factors:
days after delivery Maternal (obesity, >35 years old)
- Etiology of puerperal sepsis Caesarian delivery
Usually due to anaerobic Streptococci which normally - Clinical features:
inhabit the vagina (Peptostreptococcus, Peptococcus etc) Deep vein thrombosis: low-grade fever, tachycardia,
Other common organisms include Bacteroides fragilis, painful swollen calf
Escherichia coli & enterococci Pulmonary embolism: dyspnea, pleuritic chest pain,
Ascending infections initially infect the placental bed tachycardia
& endometrium (endometritis), before spreading into - Management of thromboembolism:
the fallopian tubes & parametrium (parametritis) Confirm diagnosis:
- Clinical features of puerperal sepsis - Doppler ultrasound of lower limbs to confirm
Classically presents with fever on the postpartum diagnosis of DVT
day 2 or 3 with increasing uterine tenderness - CT pulmonary angiogram or ventilation-
Lochia may be foul-smelling; cessation of lochial perfusion scan to confirm diagnosis of PE
flow may suggest occlusion of cervical os by slough Definitive treatment with IV heparin
material which itself predisposes to endometritis - Prevention of thromboembolism:
Complicated cases with parametritis & pelvic Encourage early ambulation after delivery
peritonitis may had added features of fluctuating Ensure adequate hydration
temperature, chills & rigors Use of thromboembolic deterrent (TED) stockings
- Differential diagnoses for puerperal pyrexia intermittent pneumatic calf compression
Atelectasis
- Usually presents with day 1 fever (hence fevers Postnatal Psychosis
on the 1st day post partum are usually managed - Affects 1-3/1000 women
expectantly without investigations or interventions) - Clinical features:
- Self-resolving Usually begins abruptly at days 5-15 initially with
Wound site infection confusion, anxiety, restlessness & sadness
- Usually first presents on day 2 or 3 Followed by rapid development of delusions &
- Exclude by inspecting wound hallucinations (e.g. baby died or deformed) with
Urinary tract infection deepening melancholy
- Usually presents after day 2 - Management:
- Ask for symptoms of flank pain, hematuria & Manage inpatient, preferably with baby also
lower urinary tract symptoms admitted with patient
- Consider urine analysis & culture to exclude Use of 1 or more drugs from the antidepressant,
Pneumonia mood stabilizing or neuroleptic groups of drugs
- May be nosocomial or aspiration (especially if
general anesthesia was used for caesarian delivery) Breastfeeding
- Ask for symptoms of pleuritic chest pain,
productive cough & shortness of breath Recommendations on Breastfeeding
- Examine lungs - It is the obligation of every healthcare professional to
- Consider chest x-ray to exclude encourage & support exclusive breastfeeding
Mastitis - Current recommendations:
- Examine breasts to exclude Exclusive breastfeeding for 6 months
Pelvic thrombophlebitis (non-infective) Continued breastfeeding (with introduction of solid
- Usually presents on days 7-10 with a feeds starting from 6 months) up till 1-2 years of age
persistent spiking fever If mother is willing, can breastfeed well beyond 2
- Managed using low molecular weight heparin years of age by all means
Thromboembolism (see below)
- Management of puerperal sepsis Benefits of Breastfeeding
History & thorough physical examination to exclude - Maternal benefits decreased risk of:
aforementioned causes Type 2 diabetes mellitus by 12% for each year of
Aerobic & anaerobic cultures to be sent before breastfeeding
administration of antibiotics: Ovarian cancer by 21%
- Blood sample Breast cancer by 28% in those whose lifetime
- Endocervical & uterine cavity samples duration of breastfeeding was 12 months or longer
- Urine sample - Baby benefits decreased risk of:
Start IV broad spectrum antibiotics: Acute otitis media
- Ampicillin or cephalosporin + aminoglycoside Nonspecific gastroenteritis
- Clindamycin can be considered as well (in Severe lower respiratory tract infections
penicillin allergy or cases with Bacteroides fragilis) Atopic dermatitis, asthma
Pelvic abscess suspected if it does not respond to Obesity
treatment: Type 1 & 2 diabetes mellitus
- Confirm with pelvic ultrasound or CT scan Childhood leukemia
- Requires surgical drainage Sudden infant death syndrome
Necrotizing enterocolitis
- Benefits to both mother & baby:
Promotes mother-baby bonding

LABOUR & PUERPERIUM

32
Breast Milk Content Contraception Post-Delivery
- Anti-bacterial & anti-viral properties
Secretory IgA Conception After Delivery
Bifidus factor (support growth of probiotic - Contraception is not required in the 21 days after
Lactobacillus bifidus in infant gut) childbirth (earliest that ovulation can occur is day 27 after
Lysozymes, lactoferrin (binds iron) delivery in the absence of breastfeeding)
Interferons, macrophages & lymphocytes - Subsequently, contraception should be employed if
- Nutritional properties pregnancy in the short-term is not desired
High whey:casein ratio
Lipid quality promotes digestibility & absorption Options for Post-Delivery Contraception
High lactose content with a small amount of - Lactational amenorrhea
oligosaccharides which act as prebiotics Useful only if exclusive breastfeeding & complete
Hypoallergenic amenorrhea is present, up to 6 months post-delivery
Lower mineral content (more suited to immature Not reliable after 6 months
capacity of infants for renal excretion) Barrier contraception should still be encouraged as
Calcium:phosphate ratio of 2:1 (promotes gut an added precaution
absorption of calcium) - Intrauterine devices (IUD)
Iron (high bioavailability) Useful option
Vitamins (rich in vitamins A C E, low in D K; all Levonorgestrel-releasing IUD (Mirena) especially
breastfeeding mothers need K supplementation, D useful if patient also has history of menorrhagia
supplementation if child does not get sun exposure, Should only be inserted 2-3 weeks after delivery
B supplementation if mother is vegetarian) (earlier insertion has higher incidence of spontaneous
expulsion of IUD)
Correct Breastfeeding Technique - Progestogen-only pill (POP)
- Mothers position: any comfortable position - Etonogestrel implant (Implanon)
- Babys position: - Injectable progesterone contraceptives
Baby held close to mothers body - Post-partum sterilization (PPS)
Infant faces breast with head & body in straight line Interval tubal ligation (done 2-3 weeks after delivery)
Upper lip opposite nipple recommended as failure rates are higher for
Baby can reach breast easily immediate ligation after delivery (due to swollen tubes
Move baby to breast, not breast to baby which are less easily occluded)
- Preparing for latch: Exception is when elective caesarian is done, during
Stimulate rooting reflex with nipple which concomitant tubal ligation can be done so as
Wait for baby to open mouth wide to combined both procedures in one setting
Babys bottom lip touches base of areola Remember that vasectomy is also an option
Help baby take sufficient areola into mouth - Combined oral contraceptives (COCs)
- Correct latch (CLAMS) The only contraception method which interferes with
Chin touching lip breastfeeding (hence not recommended for breastfeeding
Bottom Lip curling back mothers)
Areola more visible above top than below bottom lip
Mouth wide open with a big mouthful of breast
Sucking pattern change from short sucks to long
deep sucks with pauses

Measures to Support Breastfeeding


- Give adequate patient education & counseling (should be
done both antenatally & continued post-delivery)
- Address common concerns of breastfeeding mothers:
Concerns about child not getting enough milk (may
be due to perception of too little milk expressed or because
child seems to be hungry all the time)
- Tell mother that so long as child is happy,
growing well & has adequate urine & bowel
output, child is definitely getting enough
- In fact, breastfeeding may help prevent
overfeeding babies because babies feed as much
as they want to each time, without mothers
feeling a need to finish feeding a whole bottle in
the case of formula feeding
Maternal fatigue
- Tell mother to get support at home to help out
with household chores etc so that she can
concentrate on breastfeeding the baby & resting
- Alternatively, can express breast milk & get
someone else to help bottle feed at times
- Ask about breastfeeding at every subsequent postnatal
visit & continue encouraging/counseling/educating

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33
OBSTETRIC COMPLICATIONS
Preterm Labour - Placental-vascular pathway:
Process of implantation occurring early in pregnancy
Defined as the occurrence of regular painful contractions associated with involves important changes at the placental-
cervical changes between the gestational ages of 24 (after onset of decidual-myometrial interface:
viability) & 36+6 weeks (before term) inclusive - Immunological switch from TH1 immunity to
TH2 immunity; prevents embryo rejection
Epidemiology & Associations - Trophoblastic invasion of the spiral arteries in
- Leading cause of fetal morbidity & mortality both the decidual & myometrial portions to
- Incidence of preterm delivery:
establish dilated vascular channels with low
6% of all singleton pregnancies
resistance
46% of all twin pregnancies
Disruptions to these early changes play a
79% of all triplet or higher order pregnancies
pathophysiological role in poor fetal growth (itself an
- Risk factors for preterm delivery:
important cause of preterm delivery, both
Low socioeconomic status, single mothers, stress
spontaneous & elective) & pre-eclampsia
Smoking & alcohol
- Stress-strain pathway:
Extremes of reproductive age (<20 or >35 years)
Stress response increases release of cortisol &
Untreated genital tract infections:
catecholamines:
- Bacterial vaginosis
- Cortisol initiates early corticotrophin-releasing
- Trichomoniasis
hormone (CRH) gene expression in the fetus
- Chlamydial infection
which results in elevated CRH levels known to
- Gonorrhea
initiate labour at term
Previous preterm labour:
- Catecholamines affects perfusion of the
- 1 previous RR 3.9
uteroplacental unit & induces uterine
- 2 previous RR 6.5
contractions (norepinephrine specifically)
Previous spontaneous abortions:
Sources of maternal stress:
- Any 2nd trimester spontaneous abortion
- Emotional/work stress
- Repeated 1st trimester spontaneous abortions
- Poor nutrition
- Uterine stretch pathway:
Causes of Preterm Delivery
Involved in normal initiation of labour with
- 40% unknown (spontaneous preterm labour)
increased uterine stretch with fetal growth
- 25% due to elective preterm delivery
Excessive uterine stretch before term may predispose
- 10% due to multiple gestations
to labour initiation, seen in several conditions:
- 25% due to other causes:
- Multiple gestations
Preterm premature rupture of membranes (PPROM)
- Polyhydramnios
Pregnancy-associated hypertension
Structural abnormalities of the reproductive tract
Complications of Preterm Labour
(cervical incompetence, uterine anomalies)
- Intrapartum complications:
Antepartum hemorrhage
Fetal distress (fetal acidosis, asphyxia, meconium)
Intrauterine growth restriction
Cord prolapse following rupture of membranes
Polyhydramnios
Malpresentation (higher incidence of breech in preterm
Urinary tract infections
labour, in which case cervical entrapment of the
aftercoming fetal head can occur as the head is
Pathophysiology of Preterm Labour proportionally larger than the body before term)
- Infection-cervical pathway: - Post-partum complications:
Genital tract infections have been shown to be an Respiratory distress syndrome
independent risk factor for preterm labour: Periventricular leukomalacia (PVL) &
- Treating bacterial vaginosis decreases intraventricular hemorrhage (IVH) with subsequent
incidence of preterm labour risk of cerebral palsy
- Treating women in preterm labour with Necrotizing enterocolitis
antibiotics significantly prolongs the time from Hyperbilirubinemia
onset of treatment to delivery compared to that Hypoglycemia, hypothermia, hypomagnesemia
in patients without antibiotic treatment Patent ductus arteriosis
Vaginal & cervical infections have also been shown
to be associated with progressive changes in cervical
Diagnosis of Preterm Labour
length, which is in turn related to preterm labour - Similar to the diagnosis of labour at term, just that it is
with the following relative risks: diagnosed before term (37 weeks):
- Cervical length 3.5cm (50th centile) RR 2.4 Regular painful contractions (usually 4 in 20 min)
- Cervical length 2.5cm (10th centile) RR 6.2 Cervical changes (effacement, dilatation)
bloody show, leaking liquor

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34
Adjuncts for Diagnosis of Preterm Labour Management of Preterm Labour
- Actim partus - Initial management:
Rapid screening test to determine the likelihood of Admit mother to labour ward
patient going into preterm labour Vaginal examination to determine:
Test detects phosphorylated insulin-like growth (provided membranes not ruptured & no other
factor binding protein-1 (phIGFBP-1) which is a contraindications to VE such as placenta praevia)
major protein found in the decidua, which is - Cervical effacement & dilatation
detectable when the decidua & chorion begin to - Nature of presenting part & station
separate following cervical maturity Rest mother in lateral decubitus position
Not present in semen or urine, hence highly accurate Monitor maternal vitals
Test procedure: CTG monitoring of fetus
- Sterile cotton swab used to sample cervical os - Initial investigations:
- Swab is then placed into the specimen Routine bloods: FBC, GXM, PT/PTT, renal panel
extraction solution & swirled vigorously for 10s Urine FEME & culture (detect urinary tract infection)
- Yellow front of the dipstick is then placed into High vaginal swab for microscopic examination &
the specimen extraction solution & held there culture
until the liquid front reaches the result area Vaginal swab for group B streptococcus
- Negative (confirmed in 5min) = 1 blue line Ultrasound: estimate fetal weight, confirm presentation,
- Positive (as soon as it appears) = 2 blue lines detect possible etiology (e.g. multiple gestation,
- Best used to rule out preterm labour (negative polyhydramnios, uterine anomalies)
predictive value 99%; i.e. if results negative, patient
is extremely unlikely to go into preterm labour in the in 20-50% of cases, contractions cease spontaneously with
next 7 days) initial management (bed rest, hydration, treat underlying
- Other biochemical tests: infections); further management needs to be instituted for cases
Fetal fibronectin (fFN) likely to persist to delivery
Corticotrophin releasing hormone (CRH)
Salivary estriol - Subsequent management:
Metalloproteinases (MMP) Antibiotic prophylaxis:
Interleukins (e.g. IL-6) - Advocated by several studies due to
- Sonographic measurement of cervical changes association of preterm labour with subclinical
Most commonly used parameter is cervical length chorioamnionitis (but not locally practiced)
- Usual threshold used: 25mm - Helps prolong interval to eventual delivery &
Methods of measuring cervical length: possibly prevents progression of a subclinical
- Transvaginal ultrasound (provides most reliable infection to clinical amnionitis
and consistent results) - Options: ampicillin &/or erythromycin;
- Translabial/transperineal (cervical length may clindamycin is an alternative for penicillin allergy
be unmeasurable in up to 20% of cases)
- Transabdominal (unmeasurable in up to 40-50% Consider tocolysis:
of cases; requires a full bladder which falsely (see PPROM below for more details)
increases cervical length) - Tocolysis in preterm labour is controversial
Applications of sonographic cervical length: (association with subclinical infection suggests that
- Diagnosis of preterm labour attempts to prolong gestation may result in
- Prognostic tool for cerclage cases progression of infection; furthermore, studies have
- Screening tool for risk of preterm labour in failed to show the efficacy of tocolysis at decreasing
high-risk pregnancies: risk of preterm labour preterm births on the whole)
before 32 weeks is 78% if 5mm, 4% if 15mm, 1.1% if - Tocolysis however still has a role for certain
25mm purposes: prolong gestation sufficiently to allow
corticosteroids to work maximally or allow in-utero
transfer of fetus to a tertiary hospital
- Options: nifedipine (aka Adalat), atosiban
(oxytocin receptor antagonist), salbutamol,
terbutaline, GTN patch, magnesium sulphate,
indomethacin)
- Contraindications to tocolysis: chorioamnionitis,
fetal death or lethal abnormalities, maternal or fetal
condition requiring immediate delivery (severe pre-
eclampsia, abruptio, IUGR), severe hemorrhage from
placenta praevia
- Tocolysis unlikely to be successful in cases
with infection, ruptured membranes or
significantly dilated cervix (>4cm)

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35
Corticosteroids for fetal lung maturation: Prevention of Preterm Labour In Subsequent Pregnancies
- Antenatal corticosteroid therapy for fetal lung - Progesterone therapy
maturity achieves several benefits: decreased fetal Can be offered to women with previous spontaneous
mortality, incidence of respiratory distress syndrome preterm delivery at <34 weeks gestation
( RDS by 40-50%), intraventricular hemorrhage & Shown to decrease risk of preterm delivery in
necrotizing enterocolitis subsequent pregnancies
- Indicated for gestational ages of 24-34 weeks Start at 16-20 weeks gestation & continue through to
(between 34 & 36+6 weeks, benefits are still present 36 weeks gestation
but number needed to treat is much higher than Options:
before 34 weeks, hence not recommended on grounds - IM 17-hydroxyprogesterone weekly
of overall healthcare economic feasibility; however, in - Vaginal progesterone pessary daily
many cases, steroids are still given for gestational - Screening for infections
ages within this range anyway) Bacterial vaginosis, candidiasis, trichomoniasis,
- Dosing regimens: IM dexamethasone 6mg x 4 asymptomatic bacteriuria
doses 12 hours apart or IM betamethasone 12mg x 2 Treat as appropriate if detected
doses 24 hours apart (SGH is the only hospital in - Cervical cerclage
Singapore to use this regime; studies have shown it Offered in cases of cervical incompetence
to be associated with lower incidence of necrotizing Types of cervical cerclage:
enterocolitis than dexamethasone) - Primary cerclage (in cases where history is
- Optimal benefit begins 24 hours after initiation suggestive of cervical incompetence; offered electively
of the 1st dose, lasting for 7 days, but significant in 2nd trimester)
benefits still accrue even before 24 hours (hence - Secondary cerclage (in cases where history is
steroids should still be given even if labour is unclear for cervical incompetence; serial ultrasound
expected to occur within <24 hours) cervical length monitoring; cerclage offered when
significant shortening is detected)
- Delivery of the preterm infant: - Tertiary/emergency cerclage (in cases where
For vertex presentations: cervical dilatation 2cm occurs in the absence of
- Vaginal delivery is preferred regardless of regular painful uterine contractions, where
gestational age, provided fetal acidosis & membranes may be bulging or prolapsing through
trauma are avoided cervical opening)
- Use of outlet forceps & episiotomy to shorten Surgical options for cervical cerclage:
the 2nd stage of labour are advocated - McDonalds stitch: a transvaginal procedure
- Some reports recommend caesarian delivery entailing placement of a monofilament pursestring
of very-low-birth-weight fetuses (<1500g) suture near the cervicovaginal junction
For breech presentations: - Shirodkar stitch: a transvaginal procedure
- High incidence in preterm deliveries (23% entailing incision through the vaginal mucosa,
fetuses are breech at 28 weeks gestation) dissection of the bladder & rectum off the cervix,
- Significant risk of cord prolapse & cervical placement of the cerclage as close to the internal os as
entrapment of aftercoming head possible, before replacing the vaginal mucosa over
- However, no landmark studies to date have the knot
evaluated the definite benefit of caesarian - Transabdominal cervicoisthmic cerclage:
delivery of breech preterms (term breech trial performed through an abdominal incision, involving
studies breech deliveries of babies at term) dissection of the bladder from the lower uterine
- Caesarian delivery improves neonatal segment, after which a stitch at the isthmus is placed
outcome for very-low-birth-weight breech
fetuses (<1500g)

McDonalds stitch Shirodkar stitch Transabdominal cerclage

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36
Premature Rupture of Membranes Diagnosis of PROM & PPROM
(diagnosis for both is similar, just that PPROM is the diagnosis made
PROM; also known as prelabour rupture of membranes; defined as the if PROM occurs before term)
spontaneous rupture of membranes (amniorrhexis) before the onset of - History for suspected PROM:
labour; note that premature in PROM is a misnomer in that it does Nature of per vaginal fluid discharge (sudden
not denote prematurity; preterm premature rupture of membranes unprovoked gush is typical for PROM; dribbling may
(PPROM) refers to the subset of PROM occurring before term (before suggest urine leakage)
37 weeks gestation)
Duration of per vaginal fluid discharge
Characteristics of discharge: colour, odour, any
Epidemiology & Associations
presence of blood (foul smelling fluid suggests
- PPROM affects 2% of all pregnancies
chorioamnionitis; dark green fluid suggests meconium)
- PROM is seen in 8% of all term pregnancies
Other associated symptoms:
- Associations/risk factors:
- Any pain or contractions (PROM is usually
Vaginal & cervical infections
painless; constant lower abdominal pain may be
Abnormal membrane physiology present in chorioamnionitis; intermittent regular
Cervical incompetence crampy pain may suggest preterm labour)
Nutritional deficiencies - Any other vaginal discharge (infection)
- Any fever (infection)
Complications of PROM & PPROM Fetal movements (assess for fetal well being; may be
- Complications of PPROM compromised if infection, cord prolapse &/or abruption
Oligohydramnios, with sequelae of pulmonary complicates the PROM)
hypoplasia & positional skeletal deformities (e.g. - Physical examination for suspected PROM:
talipes equinovarus) if it occurs early (<24 weeks) General examination:
Infection (loss of membranes & amniotic fluid as natural - Assess patients vitals
barrier; predisposes to chorioamnionitis & fetal infections) - General condition (well? toxic looking?)
Preterm labour Abdominal examination:
Cord prolapse (especially in PPROM as fetus is usually - Inspect for fetal movements
much smaller & more likely to not be in cephalic - Symphysial fundal height (may be small for
presentation at the time of rupture of membranes) dates if significant liquor loss has occurred)
- Complications of PROM - Palpate uterus for tenderness/irritability
Cord prolapse - Assess fetal lie, presentation & engagement
Infection (more so with prolonged rupture of membranes - Assess liquor volume (fetal parts become more
at term: >18 hours) easily palpable in significant liquor losses)
Placental abruption (especially in cases with pre-existing Sterile speculum examination:
polyhydramnios; resulting from rapid decompression of
- Visualize cervical os (closed unless preterm
the amniotic cavity)
labour supervenes)
- Rule out cord prolapse
- Look for pool of liquor in the posterior fornix
(test if it is truly amniotic fluid using tests below)
- Ask patient to cough (spurt of liquor from
cervical os is diagnostic of PROM if present)
Vaginal examination is contraindicated to prevent
infection & stimulation of preterm labour in the case
of PPROM; only done in certain circumstances:
- Regular painful contractions present (suspect
preterm labour, need VE to assess cervical changes)
- Non-reassuring CTG status (to rule out occult
cord prolapse not visible on speculum examination)

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37
- Investigations for confirmation of PROM: Management of PROM (i.e. 37 weeks gestation onwards)
Tests to confirm amniotic fluid: - Active management of PROM is associated with
- Nitrazine paper or Amnicator test (detects pH decreased maternal infective morbidity without
changes; normal vaginal pH is acidic; turns dark increasing rates of caesarian section or operative vaginal
blue/black when it contacts amniotic fluid due to deliveries
alkaline pH; false positive rate of 17%: blood, semen, - However, up to 24 hours of expectant management of
urine, lower tract infections) PROM can be done based on the clinicians discretion if
the following criteria are met:
Fixed cephalic presentation
Group B Streptococcus negative
No signs of infection (uterine tenderness, fever,
maternal tachycardia)
Reassuring CTG status
No history of digital vaginal examination or cervical
suture in place
4-hourly monitoring of maternal parameters
- Expectant management of PROM:
- Examine for ferning using microscopy (place Admit patient
sample of fluid on microscopic slide, air-dry it then Regular monitoring of parameters:
examine it for ferning pattern which is diagnostic of - Maternal temperature & vitals
amniotic fluid) - Pad chart
- CTG for fetal monitoring
Consider prophylactic antibiotics:
- Penicillin G for GBS-positive cases
- Erythromycin prophylaxis given 12 hours after
onset of PROM
Await spontaneous labour onset:
- Follows PROM within 24 hours in 70%
- Follows PROM within 48 hours in 85%
- Follows PROM within 96 hours in 95%
Ferning pattern of amniotic fluid under microscopy - Induction (stimulation) of labour in PROM:
(technically speaking, promoting the onset of labour after
- Actim PROM (dipstick test detecting insulin-like membranes have already ruptured without the spontaneous
growth factor binding protein-1 IGFBP-1 present in onset of labour is termed stimulation of labour, but most
amniotic fluid; highly sensitive able to detect as people would refer to it as induction anyway)
little as 0.5 l & specific no false positives with Indicated after 24 hours of expectant management of
semen, urine or blood; test procedure is similar to PROM without spontaneous labour onset or earlier
that for Actim Partus, just that vaginal fluid is based on clinicians discretion
sampled instead of the cervical os) - Risk of maternal and neonatal infection
increases significantly 24 hours after PROM
Options for induction of labour in PROM:
Actim PROM dipstick - Prostin vaginal pessary (associated with higher
After vaginal fluid is sampled with swab & swirled into the specimen extraction rates of chorioamnionitis & neonatal infections when
solution, the yellow portion of this dipstick (left-most region) is dipped into the used in PROM)
solution; the fluid front progresses from left to right & eventually reaches the
results area where either 1 or 2 blue lines will appear (2 blue lines indicating a
- Oral misoprostol
positive result for PROM in this picture) - IV oxytocin infusion (may not be feasible if the
cervix is extremely unfavourable at the time of
Ultrasound to assess liquor volume: induction of labour)
- Decreased liquor volume/AFI supports
diagnosis of PROM
- Amount of liquor present also has prognostic
value in determining outcomes of pregnancy

Other Initial Investigations for PROM & PPROM


- Routine blood tests:
Full blood count, PT/PTT, GXM
Urea/electrolytes
CRP (monitor for signs of infection)
- Tests for infection:
Urine FEME & culture (for UTI)
Amniotic fluid microscopy & culture (for underlying
infections)
Vaginal swab (for underlying infections & group B
streptococcus carriage)

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38
Management of PPROM - Corticosteroids for fetal lung maturation:
(essentially involves concomitant management of both the issues of Same considerations, options & administration
premature rupture of membranes and possibility of preterm delivery) regimen as that for preterm labour
- Admit & monitor patient closely: - Watch out for & treat chorioamnionitis:
Establish large bore IV access for blood taking & IV Monitor for signs of chorioamnionitis 12-hourly:
fluids where required - Maternal pyrexia (>37.8oC)
Maternal vitals, pad chart - Maternal tachycardia
CTG daily for fetal monitoring - Uterine tenderness
PPROM charting: - Offensive vaginal discharge
- FBC every other day - Fetal tachycardia on CTG monitoring
- CRP every other day - Maternal leukocytosis
- Ultrasound every other day for liquor volume Treatment of clinical chorioamnionitis:
- High vaginal swab for culture once a week - Empirical: rocephine + flagyl while awaiting
Complete rest in bed + thromboprophylaxis culture & sensitivity results to be back
- Empirical antibiotics: - Delivery in PPROM:
Erythromycin 250mg orally 6-hourly x 10 days Indications for delivery at any point in time: clinical
- Given as prophylactic antibiotics for all chorioamnionitis, fetal distress
PPROM patients Otherwise, delivery planned at 34 weeks gestation
- Shown to decrease risk of chorioamnionitis (i.e. for borderline PPROM cases presenting at 34 weeks
(RR 0.57), prolong time to delivery & decrease to 36+6 weeks gestation, can manage as per for term
risk of neonatal infection (RR 0.68) PROM, with the additional consideration of inducing
- Recommended over previous use of labour after fetal lung maturation with corticosteroids)
Augmentin (ORACLE trial demonstrated increased Mode of delivery determined by presentation &
risk of necrotizing enterocolitis vs placebo with use progress of labour
of Augmentin especially in very premature neonates
<32 weeks gestation)
Penicillin G 5mu loading dose, 2.5mu every 4-hourly
- Given in addition to erythromycin in cases of
Group B Streptococcus carriage
- Consider tocolysis:
Routine tocolysis for patients with PPROM without
uterine activity is not recommended (no proven
decrease in preterm delivery or improvement in perinatal
outcomes demonstrated)
Tocolysis should be reserved for patients with
PPROM & uterine activity in these situations:
- Antenatal corticosteroids
- In-utero transfer to a tertiary hospital
Options for tocolysis:
Nifedipine (Adalat)
- Calcium channel blocker
(PO loading dose
- Effective & cheap tocolytic agent
10mg q 15-30min x 4
- First-line tocolytic agent
up to 40mg/h;
- Side effects: headache, flushing, hypotension,
maintenance dose up
tachycardia
to 20mg/6h)
- Oxytocin receptor blocker
Atosiban
- Approved for use in Europe; not in USA
(IV)
- Expensive, not routinely used in Singapore
- -agonist
- Side effects: maternal tachycardia & palpitations,
Salbutamol
fluid overload, pulmonary edema, hypokalemia,
(IV)
tachyphylaxis (requiring increasing doses of
salbutamol to remain effective)
Terbutaline - -agonist
(IV or SQ) - Quick & short-acting; for short requirements
Nitroglycerin (GTN) - Smooth muscle relaxant via production of
(transdermal patch) nitrous oxide
- Competes with calcium for cellular entry at
the time of depolarization
Magnesium sulphate
- Side effects: warmth & flushing shortly after
(IV)
administration, respiratory depression, cardiac
arrhythmias; accumulates in renal impairment
- Cyclo-oxygenase inhibitor which blocks
synthesis of prostaglandins
Indomethacin - Side effects limited if restricted to use not
(PO 25mg TDS or PR exceeding 48-72 hours
100mg) - Side effects: oligohydramnios, closure of ductus
arteriosus leading to pulmonary hypertension &
cardiac failure in the fetus

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39
Intrauterine Growth Restriction - Ultrasound assessment
Fetal measurements
Refers to the situation where a fetus is unable to achieve its genetically- - Parameters used: biparietal diameter (BPD), head
determined potential for physical growth circumference, abdominal circumference, head-to-
abdominal circumference ratio, femoral length,
Causes of IUGR estimated fetal weight
- Maternal causes: - In symmetrical IUGR, both head & abdominal
Maternal hypertension circumferences will be at or below 10th
Cyanotic heart disease & chronic pulmonary disease percentile, with a normal head-to-abdominal
Thrombophilia, SLE, antiphospholipid syndrome circumference ratio
Maternal smoking, alcoholism, drugs, malnutrition - In asymmetrical IUGR, head circumference
- Placental causes: will remain normal while abdominal
Maternal conditions causing placental insufficiency circumference will be at or below 10th
(chronic hypertension, chronic renal disease, percentile, with a high head-to-abdominal
pregnancy-induced hypertension) circumference ratio
Placental &/or cord abnormalities - In both cases, estimated fetal weight would be
- Fetal causes: at or below 10th percentile for gestational age
Chromosomal anomalies, congenital syndromes Ultrasound Doppler
Intrauterine infections - Uterine artery Doppler: bilateral notching
Multiple gestation predicts higher risk of developing IUGR
- Umbilical artery Doppler: absent or reversed
Clinical Features of IUGR diastolic waveform indicates uteroplacental
- IUGR is usually defined as an estimated fetal weight (or insufficiency
neonatal weight) at or below the 10th percentile for - Middle cerebral artery Doppler: increased end-
gestational age diastolic flow velocity indicates preferential shunting
- IUGR can further be subtyped based on the distribution of of blood to the fetal head (as seen in asymmetrical
the growth restriction: IUGR)
Symmetrical IUGR = both head & abdominal Amniotic fluid volume
circumferences are at or below the 10th percentile for - IUGR may be accompanied by abnormalities
gestational age in amniotic fluid volume depending on the
- Usually due to intrauterine insults in the 1st underlying etiology (e.g. oligohydramnios in
trimester (chromosomal anomalies, congenital uteroplacental insufficiency, polyhydramnios in
syndromes, early intrauterine infections) congenital abnormalities with congenital GI tract
Asymmetrical IUGR = abdominal circumference is atresia)
at or below the 10th percentile for gestational age
with sparing of head circumference Management of IUGR
- Usually due to insults at a later stage of - Pre-conception management
pregnancy resulting in uteroplacental (applies to women with pre-existing risk factors for IUGR)
insufficiency (e.g. pre-eclampsia) Lifestyle medications (improve nutrition, quit smoking,
- Asymmetry of head vs truncal growth is due drinking & drug use)
to preferential shunting of blood flow to the Low-dose aspirin for antiphospholipid syndrome
head in uteroplacental insufficiency Low-dose heparin low-dose aspirin for hereditary
thrombophilias
Diagnosis of IUGR - Antepartum management
- History & physical examination (once a fetus has been identified to have IUGR)
Comprehensive history-taking & physical Lifestyle modifications
examination at the booking visit may highlight Close follow-up & monitoring of fetal well-being
characteristics indicative of a pregnancy at-risk of Eventual objective is to expedite delivery of the fetus
IUGR before occurrence of fetal compromise but after fetal
- Maternal past medical history (hypertension, lung maturation has been achieved
cyanotic heart disease, chronic lung disease, SLE) - Delivery of IUGR fetuses
- Past obstetric history (past IUGR, pre-eclampsia) Close monitoring during labour due to lower
- Maternal alcohol, tobacco & drug use capacity of IUGR infants to tolerate asphyxia
Serial uterine symphysial fundal height (SFH) Management issues following delivery:
measurements made at each routine antenatal visit - Examination to look for congenital anomalies
serves as primary screening tool for IUGR - Higher incidence of hypoglycemia,
- If SFH lags >2-3cm behind a well-established hypothermia & respiratory distress requiring
gestational age of the pregnancy, further close monitoring & prompt management
sonographic assessment may be indicated
Prognosis of IUGR
- Depends on the underlying etiology
Chromosomal abnormalities & early intrauterine
infections may have poorer prognoses
IUGR also confers a greater risk on future
development of adult-onset disease such as
hypertension, diabetes mellitus & atherosclerosis in
the IUGR infant

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40
Post-Term Pregnancy Intrauterine Fetal Demise
Defined as a pregnancy persisting to 42 weeks or beyond from the onset Fetal death occurring after 20 weeks gestation but before onset of labour;
of the last menstrual period fetal death occurring before gestational age of viability (ranges from 20-
24 weeks depending on which country youre in) is termed a miscarriage
Relevant Terminology
- Preterm = before 37 weeks (i.e. up to 36+6 weeks) Causes of IUFD
- Term = 37 to 41+6 weeks - Idiopathic (up to 50% of cases)
- Post-dates = after estimated date of delivery (EDD, 40 weeks) - Maternal conditions
- Post-term = 42 weeks and after Hypertensive diseases of pregnancy
Diabetes mellitus
Causes of Post-Term Pregnancy Hereditary thrombophilias
- Idiopathic (most cases) Antiphospholipid syndrome
- Anencephaly - Uteroplacental conditions
- Placental sulfatase deficiency Fetomaternal hemorrhage
- Extra-uterine pregnancy Umbilical cord accidents
- Fetal conditions
Complications of Post-Term Pregnancy Congenital anomalies
- Post-maturity (dysmaturity) syndrome Intrauterine infections
Seen in 20-30% of post-term pregnancies Erythroblastosis fetalis (rhesus isoimmunization)
Results from aging and infarction of the placenta
with resultant placental insufficiency Diagnosis of IUFD
Physical features of dysmaturity syndrome: - Clinical suspicion:
- Meconium staining of umbilical cord, fetal Mother reports absence of fetal movements
membranes, skin & nails Uterus is small for date
- Loss of subcutaneous fat Fetal heart tone not heard with DopTone
- Long fingernails, abundant hair Note: after IUFD, placenta may continue to produce hCG,
- Dry, peeling skin hence a positive pregnancy test does not exclude IUFD
Associated with an increased risk of intrauterine fetal - Diagnostic confirmation by ultrasound:
demise & stillbirths Absence of fetal cardiac activity
- Macrosomia Lack of fetal movement
Seen in a proportion of the remaining post-term
fetuses not affected by dysmaturity syndrome Management of IUFD
Defined as a birth weight of >4000g - Watchful expectancy:
Complications of macrosomia: About 80% of patients with IUFD will experience
- Shoulder dystocia spontaneous onset of labour within 2-3 weeks of fetal
- Birth trauma demise
- Increased incidence of caesarian delivery Problems with approach of watchful waiting:
- Patients personal feeling of guilt & loss
Management of Post-Term Pregnancy - Risk of chorioamnionitis
- Begin close follow-up & screening (weekly) in post-date - Risk of disseminated intravascular coagulation
pregnancies (i.e. after 40 weeks gestational age): (10% risk if dead fetus is retained for >5 weeks)
Amniotic fluid volume Monitoring for coagulopathy:
Umbilical arterial Doppler flow - Indicated for as long as expectant
Fetal heart rate tracing (CTG) management is carried out in IUFD
- Indications for induction of labour: - Weekly platelet count, PT, aPTT, d-dimer,
Any evidence of uteroplacental insufficiency fibrinogen levels
(oligohydramnios, absent or reversed umbilical arterial - Induction of labour:
Doppler flow, non-reassuring fetal CTG status) Similar regime as for medical induction of labour in
Clinicians discretion (locally, many clinicians would normal pregnancies (vaginal pessary of prostaglandin
opt to induce labour once 41 weeks gestation is reached analogues such as misoprostol or dinoprostone)
without spontaneous onset of labour) - Follow-up after IUFD:
Investigate for possible cause of IUFD:
- Investigation for intrauterine infections
(TORCH, parvovirus B19, Listeria etc)
- Testing for maternal antiphospholipid
antibodies hereditary thrombophilias
- Consider fetal autopsy & fetal chromosomal
studies
- Kleihauer-Betke test to detect fetomaternal
hemorrhage
Psychological/emotional support for parents
Subsequent pregnancies should be managed as high-
risk cases

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41
HYPERTENSIVE DISORDERS OF PREGNANCY
Overview Preeclampsia & Eclampsia
Definition of Hypertension in Pregnancy Etiology & Associations
- Systolic blood pressure 140mHg &/or - Disease of theories has multiple proposed etiologies
Diastolic blood pressure 90mmHg Genetic, immunologic, hormonal, environmental
At least 2 blood pressure measurements should - Risk factors for developing preeclampsia:
fulfill this criteria, taken at least 4-6 hours apart Primigravidity
Primipaternity (i.e. in a woman who has had a previous
Classification of Hypertensive Disorders of Pregnancy pregnancy, the first pregnancy she has with a new male
- Chronic hypertension partner thereafter is at greater risk of preeclampsia)
Criteria (any of the following): Mothers >35 years old
(i) Known hypertension before pregnancy History of pregnancy-induced hypertension (either
(ii) Development of hypertension during personally or patients mother)
pregnancy before 20 weeks gestation Pre-existing maternal conditions (renal disease, chronic
(iii) Development of hypertension during hypertension, diabetes mellitus, obesity, autoimmune)
pregnancy after 20 weeks gestation, with Multiple gestation
persistence beyond 12 weeks post-partum Molar pregnancy (***note: in molar pregnancies,
Causes of chronic hypertension: especially complete moles, may present with atypical
- Essential hypertension (most cases) early-onset pre-eclampsia, i.e. before 20 weeks gestation)
- Secondary hypertension (renal, endocrine, aortic Smoking is protective against preeclampsia
coarcation etc) - Complications 5-7% of all pregnancies
- Preeclampsia
Criteria (all of the following): Pathophysiology of Preeclampsia
(i) Development of hypertension during - Pathogenesis of preeclampsia:
pregnancy after 20 weeks gestation Multifactorial initial etiology (?immunogenetic)
(ii) Development of new-onset proteinuria results in inadequate trophoblastic invasion
( 0.3g/24 hour urine collection) during - Cytotrophoblasts normally invades the uterine
pregnancy after 20 weeks gestation spiral arteries to establish a low-resistance
Subtypes of preeclampsia: uteroplacental circulation
- Mild preeclampsia - Failure to do so results in subsequent
- Severe preeclampsia impairment of uteroplacental perfusion
- HELLP syndrome (hemolysis, elevated liver Placental ischemia then results in oxidative stress &
enzymes, low platelets) production of toxins which enters the circulation:
- Eclampsia - Widespread inflammation
Criteria (all of the following): - Endothelial injury & dysfunction, leading to
(i) Criteria for preeclampsia met altered permeability & vasospasm
(ii) Presence of generalized tonic-clonic seizures - Inappropriate activation of coagulation system
which cannot be attributed to other causes Net effect of the above processes results in:
- Chronic hypertension with superimposed preeclampsia - Widespread vasoconstriction resulting in
Criteria (any of the following): systemic hypertension & ischemic damage in
(i) Known hypertension before pregnancy, with various vascular beds
development of proteinuria ( 0.3g/24 hour - Extravasation of fluid from intravascular space
urine collection) during pregnancy after 20 - Intravascular coagulation with progressive
weeks gestation consumptive coagulopathy
(ii) Known hypertension & proteinuria before - Pathology of preeclampsia:
pregnancy, with significant increases in blood Lack of decidualization of myometrial segments of
pressure &/or proteinuria during pregnancy the spiral arteries
(not a definite diagnosis per se, needs to be evaluated - Normally, invasion of the spiral arteries by
at the clinicians discretion in accordance with other trophoblastic tissue results in the replacement
warning signs & symptoms of preeclampsia) of the muscular & elastic layers of the spiral
Carries a worse prognosis than either chronic arteries by fibrinoid & fibrous tissue, resulting
hypertension or preeclampsia does alone in large, tortuous & low-resistance channels that
- Gestational (transient) hypertension extend through the myometrium
Criteria (all of the following): - In preeclampsia, such changes are mostly
(i) Development of hypertension during limited to the decidual segments of the vessels
pregnancy after 20 weeks gestation or within - As such, the myometrial segments of the
48-72hours after delivery vessels may have a 60% reduction in diameter
(ii) No development of proteinuria compared to that in a normal placenta
(iii) Resolution of hypertension by 12 weeks Glomerular capillary endotheliosis
post-partum - Marked swelling of the glomerular capillary
Difficult to differentiate from early-stage endothelium with deposits of fibrinoid material
preeclampsia; a diagnosis made in retrospect in & beneath the endothelial cells
Ischemia, hemorrhage & necrosis in multiple organs

HYPERTENSIVE DISORDERS OF PREGNANCY

42
Clinical Features Important History & Physical Examination in Preeclampsia
- Maternal manifestations: - History:
Weight gain & edema Age, P_G_
- One of the earliest signs of preeclampsia Presenting complaints
- Due to extravasation of fluid secondary to - Weight gain, edema
increased capillary permeability - Headache, blurred vision
- May also manifest as increased hematocrit due - Epigastric/right upper quadrant pain
to hemoconcentration - Shortness of breath
- While preeclamptic patients have an increase - Oliguria
in total body fluid volume, they are relatively - Hemorrhagic manifestations
intravascularly volume-depleted due to the - Per-vaginal bleed (abruption)
extravasation of fluid - Fetal movements (assess fetal well being)
Systemic hypertension Antenatal history
- Due to widespread vasoconstriction - Routine blood pressure & urine dipstick
- Diastolic pressure is particularly affected as it - Results of ultrasound scans so far (fetal growth,
more closely reflects a rise in peripheral any abnormalities noted)
vascular resistance Past obstetric history
Renal impairment - Previous pregnancy-induced hypertension
- Glomerular arteriolar vasoconstriction results - Previous preeclampsia
in decreased glomerular filtration rate, Past medical history
manifesting as oliguria or even anuria - Pre-existing hypertension, diabetes mellitus
- Altered glomerular capillary permeability - Chronic renal disease, autoimmune disease
results in proteinuria Family history
Coagulopathy - Preeclampsia in patients mother
- Due to thrombocytopenia most commonly - Physical examination:
- Disseminated intravascular coagulation may General examination
occur as well, especially in the context of - Vitals (BP, HR, RR, SpO2)
placental abruption complicating preeclampsia - Weight (note trend if available)
Liver impairment - Pallor, petechiae, edema
- Systemic vasoconstriction results in ischemic Chest examination
damage to the liver, with resultant focal - Lungs (crepitations in pulmonary edema)
hemorrhages & infarctions Abdominal examination
- May present as right upper quadrant or Epigastric or right upper quadrant tenderness
epigastric pain Neurological examination
- In rare instances, hepatic rupture may occur - Hyperreflexia, clonus
Neurological impairment - Visual field testing
- Visual field disturbances Obstetric examination
- New-onset headache - Symphysial fundal height (small for dates?)
- Hyperreflexia, clonus - Palpate for fetal lie & presentation (important to
- Seizures (in which case it becomes eclampsia) note if emergent induction of labour is required)
Cardiopulmonary impairment - Palpate for uterine tenderness (if tender &
- Pulmonary edema woody-hard, may indicate abruption)
- Fetoplacental manifestations: - Estimate liquor volume (fetal parts very well felt
Intrauterine growth restriction (usually asymmetrical) in oligohydramnios)
Intrauterine fetal demise - DopTone for fetal heart sounds
Oligohydramnios
Abruptio placentae Investigations
- Maternal hematological investigations
Grades of Severity in Preeclampsia Full blood count
- Mild preeclampsia - Anemia (due to hemolysis in HELLP syndrome)
Does not fulfill criteria for severe preeclampsia - Thrombocytopenia
- Severe preeclampsia Renal panel + serum uric acid
(any of the following present makes it severe preeclampsia) - Raised serum creatinine & urea
Severe hypertension ( 160/110mmHg) - Raised serum uric acid levels is the earliest
Heavy proteinuria ( 3g/24 hour urine collection) change in renal impairment in preeclampsia
Oliguria (<500ml/24 hour) 24-hour urinary total protein
Cerebral &/or visual disturbances - Needed for formal diagnosis of preeclampsia
Pulmonary edema or cyanosis - May indicate severe preeclampsia if heavy
Epigastric or right upper quadrant pain proteinuria is present
Impaired liver function (elevated liver enzymes) Liver function test
Thrombocytopenia - Raised AST & ALT levels
Fetal growth restriction - Unconjugated hyperbilirubinemia (hemolysis)
- HELLP syndrome Coagulation profile
A variant of severe preeclampsia with particularly - PT & aPTT d-dimers & fibrinogen (for DIVC)
high morbidity & mortality - Fetal ultrasound
Entails a combination of hemolysis, elevated liver Estimated fetal weight, fetal lie & presentation,
enzymes & low platelets liquor volume, umbilical artery Doppler flow

HYPERTENSIVE DISORDERS OF PREGNANCY

43
Management of Preeclampsia (iii) Seizure prophylaxis & management
(the only definitive treatment for preeclampsia is delivery of the fetus; Agent of choice = IV magnesium sulphate
as such, the decision on when to deliver needs to take into account - Validated by the Magpie trial (Magnesium
maximizing gestational age for fetal growth & pulmonary maturity Sulphate for Prophylaxis of Eclampsia)
alongside managing the maternal effects of preeclampsia) - Shown to reduce recurrent seizures (50%
reduction), reduce maternal mortality &
- Admission for further work-up & monitoring morbidity, as well as to improve neonatal
All newly-diagnosed preeclamptic patients need to outcome
be admitted - Superior to valium & phenytoin
Perform relevant investigations to determine severity Indications for magnesium sulphate treatment:
of preeclampsia (mild vs severe) - Severe preeclampsia
Put patient on preeclampsia charting: - Signs & symptoms of imminent eclampsia
- BP, HR, weight, edema (hyperreflexia, clonus, severe headaches)
- Urinary protein - Eclampsia (in which case MgSO4 is as treatment)
- Input & output Pritchard Regime for MgSO4 administration:
- Fetal movement, fetal heart rate - Intramuscular regimen: 4g IV loading dose
Consider the 3 main aspects of pre-delivery followed immediately by 10g IM, then 5g IM every 4
management of preeclampsia: hours in alternating buttocks
(i) Blood pressure control - Intravenous regimen: 4g IV loading dose,
(ii) Fluid management followed by maintenance infusion of 1-2g/h by a
(iii) Seizure prophylaxis & management controlled infusion pump
Monitoring for MgSO4 toxicity:
(i) Blood pressure control - Narrow therapeutic range (2-4mmol/L)
Antihypertensive agents: - Progressive symptoms & signs of increasing
- Labetalol serum magnesium levels: loss of patellar reflexes,
- Hydralazine warmth & flushing, somnolence, slurring of speech,
- Nifedipine (Adalat) paralysis & respiratory difficulties, cardiac arrest
- Methyldopa - Hence patient needs to be regularly assessed
Choice of agent & administration route depends on for tendon reflexes, pulse oximetry & urine
clinical evaluation of severity of preeclampsia: output (as magnesium is renally excreted)
- Mild preeclampsia: oral methyldopa, nifedipine - Resuscitation equipment + calcium gluconate
or labetalol (antidote for magnesium toxicity; IV 10ml of a 10%
- Severe preeclampsia with blood pressure solution) should be on standby
160/110mmHg: IV labetalol or hydralazine
(beware precipitous drop in BP especially with - Delivery
hydralazine which may worsen placental perfusion; Remains the only cure for preeclampsia
ensure fluid preloading & close fetal CTG Timing of delivery is dictated by the clinical state of
monitoring) the mother & fetus (but maternal interests are of
paramount importance)
(ii) Fluid management Concept of temporizing management
Fluid replacement to treat intravascular depletion in - Symptomatic management of mother to buy
preeclampsia as well as to minimize risk of time for fetal pulmonary maturity & growth
precipitous drop in blood pressure following - Administer corticosteroid where indicated to
administration of antihypertensive agents accelerate fetal pulmonary maturation
Precautions to avoid iatrogenic pulmonary edema: - Plan for induction of labour at 34 weeks
- Auscultate to ensure clear lungs gestation if no overriding indication for
- Chart input & output, consider urinary induction occurs prior to that
catheterization to accurately chart output Indications for emergent induction of labour:
- Consider invasive monitoring where deemed - Severe preeclampsia with maternal
necessary (CVP, pulmonary artery wedge pressure) complications refractory to medical
Fluid replacement regime: management (refractory hypotension, pulmonary
- Start with 1L Hartman solution (500ml over edema, oliguria, HELLP, impending eclampsia)
30min followed by 500ml over 4h) - Severe IUGR, signs of fetal compromise,
- If urine output is satisfactory (>30ml/h), suspected placental abruption
infuse another 1L Hartman solution over 12h
- If urine output remains inadequate (<30ml/h),
proceed with judicious volume loading
diuretics; consider invasive monitoring

HYPERTENSIVE DISORDERS OF PREGNANCY

44
Management of Eclampsia
(eclampsia is a true obstetric emergency)
Chronic Hypertension in Pregnancy
- Initial resuscitation & stabilization
Airway, breathing, circulation Main Goals of Management
- Position patient in left lateral position - Control hypertension
- Clear & protect airway - Detect development of superimposed preeclampsia
- Supplemental oxygen by face mask - Detect IUGR in fetus
- Establish large bore IV access
Place patient on close monitoring (BP, HR, pulse Baseline Evaluation
oximetry, ECG, urinary catheter) - Review records to determine cause of hypertension
Consider & exclude other possible causes of seizures (essential hypertension vs secondary hypertension)
- Pre-existing epilepsy If no prior evaluations done, may consider
- Hypertensive encephalopathy investigations to rule out some of the more common
- Metabolic derangements (hypoglycemia, endocrine, renal or cardiovascular causes
hyponatremia) - Other baseline investigations are similar to that for
- Intracranial hemorrhage or infection normal pregnancies
- Pharmacologic stabilization Baseline blood pressure & presence of proteinuria
Seizure management with magnesium sulphate: especially important to aid detection of development
- Loading dose of 6g IV (higher than that used for of superimposed preeclampsia later on
4 g, 1g/h for 24 h seizure prophylaxis in preeclampsia) followed by Additional baseline assessment of end-organ
maintenance infusion of 2g/h changes from chronic hypertension:
- Monitor tendon reflexes, pulse oximetry & - Fundoscopy for hypertensive retinopathy
urine output - Renal panel
- May consider adding on diazepam for - ECG for hypertensive heart disease
refractory seizures (monitor for respiratory
depression & be prepared to intubate) Pharmacological Management of Hypertension
Blood pressure control: - Principles of antihypertensive use in pregnancy:
- IV labetalol or hydralazine Use safest possible antihypertensive at lowest
- Ensure adequate fluid preloading & watch for possible dose
precipitous drop in BP Keep blood pressure at about 130/80mmHg to
- Delivery 140/90mmHg
Delivery should only be attempted after stabilization - Little evidence that lowering blood pressure
of maternal condition as induction of labour or too much benefits the pregnancy
caesarian section during the acute phase may - Lowering blood pressure too much may
aggravate the course of the disease compromise uteroplacental perfusion & result
Expedite delivery once maternal condition is in fetal compromise
stabilized, preferable by the vaginal route - In many cases, blood pressures will decrease
to normal in the 2nd trimester, during which
Sequelae & Outcome of Preeclampsia antihypertensives can be taken off
- Post-natal follow-up of preeclamptic patient: - Antihypertensive options:
Monitor for resolution of hypertension & proteinuria Methyldopa (safest antihypertensive in pregnancy)
Persistence beyond 12 weeks postpartum Nifedipine
necessitates physician referral for further Labetalol
investigations - Antihypertensives not recommended in pregnancy:
- Prognosis (maternal): ACE-inhibitors & angiotensin II receptor blockers (to
Mild preeclampsia has no long-term maternal be avoided in all stages of pregnancy due to potential fetal
sequelae toxicity)
Severe preeclampsia increases risk of: Beta-blockers (to be used with caution as it can result in
- Cardiovascular disease in later life fetal growth restriction)
- Recurrent preeclampsia risk (up to 40%) Diuretics
- Prognosis (fetal):
Depends on impact of preeclampsia on fetal growth Antenatal Care
If IUGR occurred, child may be at increased risk of - Consider early & serial ultrasound monitoring
adult-onset diseases (hypertension, diabetes etc) To detect signs of IUGR early
- Monitor routine BP & urine dipstick closely
Significant increase in blood pressure &/or
worsening of pre-existing proteinuria are likely signs
of superimposed preeclampsia (15-25% incidence)

HYPERTENSIVE DISORDERS OF PREGNANCY



45
OBSTETRIC HEMORRHAGE
Overview of Obstetric Hemorrhage Causes of Miscarriages
- Fetal abnormalities
Most common cause of miscarriages (>50%)
Types of Obstetric Hemorrhage Often due to chromosomal abnormalities (trisomy,
- Bleeding in early pregnancy monosomy, triploidy etc)
Bleeding in pregnancy before 24 weeks gestation Usually sporadic (occurring by chance in the particular
- No minimum bleeding volume required conceptus), but may occasionally be due to
Differential diagnosis: chromosomal aberrations in one or both parents:
- Miscarriage (spontaneous abortion) - Germline mosaicism
- Ectopic pregnancy - Balanced (Robertsonian) translocations
- Gestational trophoblastic disease - Local maternal factors
(refer to Gynaecologic Oncology) Congenital uterine abnormalities
- Lower genital tract pathology - Septate uterus, bicornuate uterus etc
- Antepartum hemorrhage (APH) Acquired uterine abnormalities
Bleeding in pregnancy at or after 24 weeks gestation - Submucous fibroids
(i.e. after gestational age of viability) - Endometrial polyps
- No minimum bleeding volume required - Intrauterine adhesions (synechiae)
- Underlying etiological agents may be similar - Ashermans syndrome (obliteration of most of
to that for miscarriage, but clinical distinction is the uterine cavity with extensive synechiae)
made because fetus is considered salvageable Cervical incompetence
after 24 weeks gestation - May be congenital or acquired (e.g. after cone
Differential diagnosis: biopsy of cervix)
- Placenta praevia - Tends to present with 2nd trimester abortions
- Abruptio placentae - General maternal factors
- Vasa praevia Advance maternal age
- Lower genital tract pathology (cervicitis, - If a live fetus is demonstrated with ultrasound
cervical polyps, cervical cancer etc) at 8 weeks gestation, <2% will abort
- Systemic coagulopathy spontaneously if the mother is <30 years old,
- (Preterm) labour but risk increases to >10% if >40 years old & up
- Postpartum hemorrhage (PPH) to 50% at 45 years old
Bleeding after delivery - Probably due to increased incidence of
- Primary PPH = loss of >500ml (or >1000ml if chromosomally abnormal conceptus in older
caesarian delivery) of blood within the 1st 24 hours mothers
post-partum Maternal medical conditions
- Secondary PPH = abnormal bleeding after 24 - Diabetes mellitus
hours postpartum up until 6 weeks
- Hypothyroidism, hyperthyroidism
(Refer to Labour & Puerperium)
- Chronic renal disease
- Systemic lupus erythematosus
Bleeding in Early Pregnancy - Antiphospholipid syndrome
Maternal infections
- TORCH infections (toxoplasmosis, rubella,
Miscarriage (Spontaneous Abortion)
cytomegalovirus, herpes simplex virus)
Defined as fetal loss between the time of conception & the time of fetal
- Mycoplasma, Ureaplasma infections
viability (at 24 weeks gestation); may alternatively also include cases
- Listeria, Brucella, syphilis
with expulsion of a fetus or embryo weighing 500g; fetal loss after the
time of fetal viability (of 24 weeks) is termed intrauterine fetal demise Maternal substance use
(IUFD; see Obstetric Complications) - Alcohol, smoking, drug abuse
Immunological factors
Epidemiology of Miscarriages - Abnormal alloimmune response resulting in
- Miscarriage occurs in approximately 10-20% of all failure to accept the fetus for the duration of a
clinically-recognizable pregnancies normal pregnancy
Many conceptions may never reach clinical
recognition (e.g. biochemical pregnancies)
Biochemical pregnancy = presence of hCG in
maternal serum 7-10 days post-ovulation in whom
menstruation occurs as expected; indicative of
conception that occurred but subsequently lost
without prolongation of the menstrual cycle
If one were to consider both clinically-recognized
pregnancies & biochemical pregnancies, total
miscarriage rate would be even higher (some studies
suggest over 50%, mostly occurring within the 14 days
following conception)

OBSTETRIC HEMORRHAGE

46
Types & Clinical Features of Miscarriages - Complete miscarriage/abortion
Salient features: PV bleed with completed process of fetal
- Threatened miscarriage/abortion loss; uterus reverts back to pre-pregnant conditions
Salient features: PV bleed without any impending fetal History findings:
loss, fetus remains viable - Per-vaginal bleed (history of gush of blood
History findings: possibly with greyish tissues passed together with it;
- Per-vaginal bleed (usually small amount) bleeding usually of small amount at the time of
- With or without abdominal pain presentation)
- Symptoms of pregnancy (e.g. nausea) present - Abdominal pain would have been experienced
Physical examination findings: during prior gush of blood, may not be
- Uterus is appropriate for dates present at the time of presentation
- Cervical os closed - Symptoms of pregnancy (e.g. nausea) absent
Investigation findings: Physical examination findings:
- Ultrasound reveals a viable (fetal cardiac - Uterus smaller than expected for dates
activity present) intrauterine pregnancy - Cervical os closed
Investigations findings:
- Inevitable miscarriage/abortion - Ultrasound reveals an empty uterus with
Salient features: PV bleed with open cervical os with no normal endometrial lining
loss of fetus yet; will invariably lead on to an incomplete
or complete abortion with fetal loss - Missed miscarriage/abortion
History findings: Salient features: fetal death or failure of development of
- Per-vaginal bleed (usually large amount) fetal tissue to start with, with no extrusion of products of
- Abdominal pain likely to be present conception
Physical examination findings: History findings:
- May have signs of acute blood loss (pallor, - Per-vaginal bleed is usually absent
tachycardia, hypotension) - Abdominal pain is usually absent
- Uterus is appropriate for dates - Pregnancy symptoms may be absent or less
- Cervical os open without products of intense (placenta can still produce hCG)
conception seen at cervical os Physical examination findings:
Investigations findings: - Uterus smaller than expected for dates
- Ultrasound reveals an intrauterine pregnancy - Cervical os closed
which may or may not be viable Investigations findings:
- Ultrasound reveals a non-viable (absent fetal
- Incomplete miscarriage/abortion cardiac activity despite a crown-rump length of
Salient features: PV bleed with fetal loss in progress >7mm) intrauterine pregnancy
History findings: - In the case of an anembryonic pregnancy (aka
- Per-vaginal bleed (usually large amount) blighted ovum, where conception occurs with the
- Abdominal pain likely to be present development of a gestational sac with no subsequent
Physical examination findings: normal development of an embryo), ultrasound
- May have signs of acute blood loss (pallor, would reveal a gestational sac >25mm in size
tachycardia, hypotension) but with no fetal pole
- Uterus may be smaller than expected for dates - Note that pregnancy test at this point can still
- Cervical os open with products of conception be positive as placenta can continue to produce
seen at the cervical os hCG even after fetal death
Investigations findings:
- Ultrasound reveals non-viable (absent fetal - Septic miscarriage/abortion
cardiac activity) intrauterine pregnancy, thick Salient findings: similar to an incomplete abortion but
endometrial lining & retained products of complicated by infection
conception within uterus & at the cervical os History findings:
(note that ultrasound is not required to diagnose an - Per-vaginal bleed discharge
incomplete abortion; pelvic examination would - Abdominal pain usually present
suffice) - May have prior history of instrumentation of
uterus (e.g. amniocentesis)
Physical examination findings:
- Uterus may be smaller than expected for dates
- Cervical os open with products of conception
seen at cervical os
- Cervical motion tenderness
- Adnexal tenderness
Investigations findings:
- Ultrasound reveals non-viable (absent fetal
cardiac activity) intrauterine pregnancy, thick
endometrial lining & retained products of
conception within uterus & at the cervical os

- Recurrent miscarriage/abortion
Salient features: defined as 3 consecutive miscarriages

OBSTETRIC HEMORRHAGE

47
Management of Miscarriages - Management of missed miscarriage
If in doubt of diagnosis (e.g. very early on in the
- Management of threatened miscarriage pregnancy where the case is borderline for the thresholds
Reassure patient & continue routine antenatal used to diagnose a non-viable pregnancy), repeat
follow-up visits ultrasound scan after 7-14 days
Consider progesterone therapy (some evidence that it Arrange for evacuation of uterus (similar
reduces the risk of miscarriage & preterm labour) considerations as for inevitable/incomplete abortion)
Expectant management is an option if patient is
- Management of inevitable, incomplete & septic stable & non-febrile:
miscarriages - Patient may subsequently spontaneously expel
Stabilize & resuscitate patient dead fetus & products of conception or reabsorb
- Airway, breathing, circulation trophoblastic tissue with no bleeding
- Establish IV access & start fluid infusion - Need to arrange close follow-up visits (risk of
- Draw bloods for preliminary investigations DIVC in mother with retained dead fetus)
(full blood count, group & cross match) - Tell patient to return immediately if excessive
- Start empirical IV antibiotics in cases of septic bleeding or fever develops
miscarriage Other general management considerations:
Remove any products of conception at cervical os - Anti-D immunoglobulin if rhesus negative
- Use sponge forceps (can be done even if the - Psychological support & counselling
primary care setting before considering need to send - Follow-up to convey findings of pathological
patient to a hospital) report (if tissue sample was obtained & sent) &
- In certain cases, cervical os may close reassure about chances of future reproductive
following removal of products of conception at success where appropriate
cervical os (if no POC is left), with subsequent
cessation of per-vaginal bleeding - Management of recurrent miscarriage
Arrange for evacuation of uterus Offer investigations to determine possible cause(s):
- Surgical evacuation via vacuum aspiration - Rule out maternal medical conditions (diabetes
after cervical priming with 400 g misoprostol mellitus, thyroid disease, renal disease, SLE)
PV 3 hours prior (indicated if patient is bleeding - Rule out maternal infections
profusely, septic or requires tissue for analysis such - Rule out uterine & cervical abnormalities
as in the context of recurrent miscarriage) (pelvic ultrasound, hysterography, hysteroscopy)
- Medical evacuation via misoprostol (+ Treat any causes identified appropriately:
mifepristone if available) PV (indicated if patient is - Medical management of maternal conditions
unfit for anaesthesia or has retained fetal parts >14 - Treat underlying infections
weeks gestation in size which may render surgical - Surgical &/or hysteroscopic management of
evacuation unsafe) uterine abnormalities
Other general management considerations: - Cervical cerclage for cervical incompetence
- Anti-D immunoglobulin if rhesus negative (see Obstetric Complications)
- Psychological support & counselling
- Follow-up to convey findings of pathological
report (if tissue sample was obtained & sent) &
reassure about chances of future reproductive
success where appropriate

- Management of complete miscarriage


No specific treatment required if patient is stable
Other general management considerations:
- Anti-D immunoglobulin if rhesus negative
- Psychological support & counselling

OBSTETRIC HEMORRHAGE

48
Ectopic Pregnancy Clinical Features of Ectopic Pregnancy
Gestation that implants outside the endometrial cavity; estimated to - History:
occur in 1 in every 80 spontaneously conceived pregnancies Classical triad of symptoms in ectopic pregnancy:
prior missed menses + PV bleed + lower abdominal pain
Etiology & Associations - PV bleed can originate from bleeding from a
- Risk factors for ectopic pregnancy: tubal ectopic pregnancy or from shed
History of tubal inflammation endometrial lining due to insufficient
- Pelvic inflammatory disease pregnancy hormones provided by an ectopic
- Endometriosis pregnancy to support the endometrium
History of tubal surgery May have additional features of an acute abdomen
- Previous tubal reconstructive surgery (diffuse abdominal pain, ipsilateral shoulder pain from
- Previous tubal sterilization in past 1-2 years phrenic nerve irritation due to blood in the upper
(especially if cauterization was used) abdomen, dizziness from acute blood loss) in the setting
Use of intrauterine contraceptive devices of a ruptured ectopic pregnancy
(if a pregnancy occurs while an IUCD is in place, higher Enquire about risk factors for ectopic pregnancies
risk of ectopic pregnancy; but given that IUCD vastly - Physical examination:
decreases the chance of a pregnancy, the overall rate of General examination:
ectopic pregnancy with an IUCD vs without is still lower) - Assess vitals for signs of hypovolemia & acute
Use of assisted reproductive technologies blood loss
- Associated with a higher risk for development Abdominal examination:
of heterotropic implantation (simultaneous - Assess for tenderness
intrauterine pregnancy & ectopic pregnancy) - Guarding & rebound tenderness if ruptured
Previous ectopic pregnancy Pelvic examination:
- Risk of recurrence after 1 previous = 15% - Per-vaginal bleeding
- Risk of recurrence after 2 previous = 30% - Cervical motion tenderness
Subfertility due to tubal factors - Tender adnexal mass
Smoking (relative risk of 1.26) - Slightly enlarged, globular uterus

Sites of Ectopic Pregnancy Differential Diagnosis:


- Gynaecologic differentials:
Threatened, inevitable or incomplete abortion
Ruptured corpus luteal cyst
Adnexal accidents (e.g. ovarian cyst torsion)
Acute pelvic inflammatory disease
Red degeneration of fibroid (not uncommonly seen in
pregnancy with pre-existing fibroids of significant size)
- Non-gynaecologic differentials:
Acute appendicitis, diverticulitis
Pyelonephritis, ureteric colic
Acute pancreatitis
Perforated peptic ulcer

Diagnosis & Evaluation


- Diagnose pregnancy:
- Extra-uterine sites Urine pregnancy test
Tubal (98%) Serum hCG quantification
- Isthmic (12%) - Helps to (i) diagnose pregnancy (ii) aid in
- Ampullary (75-80%) management algorithm in the event that pelvic
- Infundibular & fimbrial (6-11%) ultrasound is non-diagnostic (see below)
Ovarian (0.5%) Pelvic ultrasound
Abdominal & intraligamentous (0.1%) - Empty uterus + free fluid in the pouch of
- Intra-uterine sites
Douglas coupled with a positive urine
Cervical (0.4%)
pregnancy test is diagnostic
Cornual/interstitial (1%)
- May occasionally be able to visualize a non-
ruptured tubal ectopic pregnancy as a double
Natural History of Tubal Ectopic Pregnancy ring sign
- Tubal rupture
- Visualization of intrauterine pregnancy does
- Tubal abortion into peritoneal cavity
not rule out possibility of concomitant ectopic
- Spontaneous resolution/resorption of pregnancy
pregnancy (heterotropic implantation)
- Investigations to aid management:
Investigations to rule out differentials
Full blood count, PT, aPTT, group & cross match

OBSTETRIC HEMORRHAGE

49
Management of Ectopic Pregnancy Surgical Management
Surgical approaches:
- Management of a ruptured ectopic pregnancy - Laparotomy (indicated in patients who are
Ruptured ectopic pregnancy would present with a hemodynamically unstable as rapid access to the
clinical acute abdomen bleeding site is critical)
Initial resuscitation, stabilization & investigations: - Laparoscopy (gold standard for hemodynamically
- ABCs stable patients with advantages of less postop pain,
- Large bore IV access, infuse fluids shorter postop length of stay & quicker recovery)
- Take essential bloods (FBC, PT aPTT, GXM), Surgical options:
do urine pregnancy test pelvic ultrasound - Salpingectomy = removal of entire fallopian tube
Emergent surgical intervention - Partial salpingectomy = removal of a portion of
- Emergency laparotomy usually indicated with the fallopian tube; remnants of the tube may be
a clinical picture of an acute abdomen reapproximated in the future
- In stable cases, an exploratory laparoscopy - Salpingotomy = operative identification of
first may be appropriate to determine etiology ectopic pregnancy site in tube injection of
- Procedure of choice in ruptured ectopic is vasoconstrictive agents incision made parallel to
usually salpingectomy the axis of the tube along its antimesenteric border
over the site of implantation gentle removal of
- Management of a non-ruptured ectopic pregnancy products of conception using hydrodissection
(various management options available for a confirmed ectopic primary closure of incision
pregnancy in a non-emergency setting) - Salpingostomy = similar procedure as
salpingotomy, except that incision is left open at the
Medical Management end of the procedure
Using methotrexate IM 50mg/m2 in divided doses - Salpingocentesis = at the time of laparoscopy,
(usually half the dose in each buttock) injection of methotrexate, prostaglandins or
Patient returns on days 4 & 7 for repeat hCG hyperosmolar glucose into the amniotic sac of the
measurements: ectopic pregnancy; currently still experimental
- If hCG falls 15% between days 4 & 7, Factors affecting choice of surgical option:
continue follow up on a weekly interval to - 10-20% risk of residual trophoblastic tissue
ensure 15% fall every 7 days until hCG titres with salpingotomy or salpingostomy (need to
are undetectable (may take 1-3 months) repeat hCG titres 3-7 days postop to confirm decline
in hCG; if it fails to decline appropriately,
- If hCG titres plateau or fall too slowly (<15%
methotrexate therapy can be started)
every 7 days), give another dose of MTX
- Trend towards higher risk of recurrence of
- If patient becomes more symptomatic or if
ectopic pregnancy in salpingotomy vs
hCG titres rise (failure rate 15-25%), surgical
salpingectomy with no significant different in
treatment is indicated
rates of subsequent intrauterine pregnancy
- Patient to avoid foods & vitamins containing
(hence in the presence of a normal healthy
folic acid, NSAIDs & alcohol during treatment
contralateral fallopian tube, no evidence that
period; offer effective contraception for at least
salpingotomy should be used in preference to
3 months after treatment to allow wash out
salpingectomy)
(methotrexate is teratogenic)
- Partial salpingectomy reserved for cases where
Advantages of medical treatment:
implantation is at the mid-ampullary portion
- Avoids surgical risks
with a possibility of 6cm of function tube left
- Preserves future fertility
after resection
Criteria to meet for methotrexate treatment:
(i) hCG levels <5000IU/L
Expectant Management
(ii) Ultrasound reveals absence of yolk sac &
A possible option in a select group of patients:
fetus, adnexal mass 3.5cm in its greatest
- hCG 200mIU/mL
diameter, no free fluid in the pouch of Douglas
- Hemodynamically stable
(iii) Good understanding & compliance
- No signs of impending or ongoing rupture
(iv) Hemodynamically stable
(e.g. persistent abdominal pain or >300ml free
(v) No contraindications to methotrexate
peritoneal fluid outside the pelvic cavity)
(breastfeeding, immunodeficiency, peptic ulcer
- Compliant to follow-up
disease, active pulmonary disease, renal or hepatic
Risk of rupture with hCG <1000mIU/mL is 20%
insufficiency, coexisting viable intrauterine
Requires close follow-up monitoring of hCG
pregnancy, allergy to methotrexate)
- Every 48 hours initially to confirm declining
Side-effects of methotrexate therapy:
trend in hCG
- Pain within 1st week of receiving treatment
- Weekly thereafter until hCG titre becomes
due to tubal abortion or tubal distension from
undetectable
hematoma formation (common; can be controlled
- If hCG levels plateau, offer methotrexate
with paracetamol)
- If hCG levels rise or patient becomes more
- Conjunctivitis, dermatitis, alopecia
symptomatic, surgical intervention indicated
- Stomatitis, gastritis, enteritis
- Pneumonitis
- Elevated liver enzymes
- Bone marrow suppression

OBSTETRIC HEMORRHAGE

50
Patient presents with suspected ectopic pregnancy

Emergency laparotomy Emergency laparotomy


not indicated indicated

Pelvic ultrasound Emergency laparotomy

Salpingectomy Partial Salpingectomy Intrauterine Ectopic Abnormal Non-diagnostic


pregnancy (IUP) pregnancy IUP

Antenatal care Treat ectopic Dilation & Serum hCG


curettage (D&C)

hCG > discriminatory zone hCG < discriminatory zone

Serial serum hCG

Abnormal Normal rise Normal fall


rise or fall
Salpingotomy/Salpingostomy
Repeat pelvic Failing pregnancy;
Evaluation of uterine ultrasound no treatment needed
- Management if initial investigations are non-diagnostic contents with repeat when hCG >
Use of serum hCG levels to guide further pelvic ultrasound + discriminatory
management D&C if scan remains zone
Dynamics of serum hCG during pregnancy: non-diagnostic
- Rapidly dividing fertilized egg begins to
produce hCG, but communication with
No chorionic villi Chorionic villi
maternal circulation to allow detection of hCG
begins with implantation
Ectopic pregnancy; Abnormal IUP;
- Normally in the 1st trimester, hCG levels
treat ectopic D&C would have been therapeutic
increase exponentially, with a doubling time
varying from 1.2 days shortly after implantation
to 3.5 days at 2 months amenorrhea Outcomes & Sequelae of Ectopic Pregnancy
- Most pregnancies demonstrate doubling time - Patients with ectopic pregnancy have:
of 48 hours in the first few weeks of pregnancy, Decreased fertility
with the slowest rise being 53% within 2 days - No difference however between patients
accepted as being normal managed expectantly vs patients managed via
- Also, following spontaneous loss of a normal surgical management
pregnancy, the minimal decline in hCG levels is Increased risk of subsequent ectopic pregnancy
21-35% within 2 days - 15% after 1 previous ectopic pregnancy
- Also, there exists the idea of a discriminatory - 30% after 2 previous ectopic pregnancies
zone, defined as the hCG titre at which an - Hence proper counselling on risks of future ectopic
intrauterine sac should be reliably seen with pregnancies is indicated after an episode of ectopic
transvaginal ultrasonography in a normal pregnancy
pregnancy (this value differs between institutions;
locally taken as 1500IU/L)
As such, the following situations would suggest an
ectopic pregnancy or abnormal intrauterine
pregnancy (i.e. molar pregnancy):
- Rise in hCG <53% in 2 days
- Fall in hCG <20% in 2 days
- hCG level >1500IU/L with no intrauterine
gestational sac seen on transvaginal ultrasound
Differentiation between ectopic & abnormal
intrauterine pregnancy would require evaluation of
uterine contents to look for presence of chorionic villi
(via repeat ultrasound + dilation & curettage if
ultrasound remains non-diagnostic)

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51
Antepartum Hemorrhage Physical Examination
- General examination:
Per-vaginal bleeding occurring during pregnancy from the time of fetal Maternal vitals (BP, HR, RR, SpO2)
viability (24 weeks gestation) to before delivery Assess for pallor & signs of coagulopathy
- Obstetric examination:
Approach to Antepartum Hemorrhage Palpate for tenderness (abdominal &/or uterine),
uterine consistency (woody hard uterus in abruption) &
History fetal lie + presentation
- Characterize per-vaginal bleed: DopTone to look for fetal heartbeat
Onset, duration, number of episodes, amount - Pelvic examination:
Any precipitating factor(s) (done only after ultrasound is performed to rule out placenta
- Blunt abdominal trauma abruptio praevia in which case a pelvic examination is contraindicated)
- Rupture of membranes abruptio or vasa praevia Rule out lower genital tract pathology
- Associated symptoms: Assess for cervical dilatation/effacement (indicates
Pain vs painless preterm delivery which can occur as a result of other
- Abruptio usually painful causes of antepartum hemorrhage as well)
- Placenta praevia & vasa praevia usually painless
Uterine contractions Investigations
- Abruptio placentae usually associated with strong - Pelvic ultrasound
uterine contractions Helps clinch diagnosis in certain cases
- Placenta praevia & vasa praevia usually not - Placenta praevia
associated with uterine contractions - Retroplacental hematoma may be seen in abruptio
- Regular uterine contractions may indicate onset of - Vasa praevia may be visualized
(preterm) labour Assesses for signs of fetal compromise
Fetal movements - IUGR, oligohydramnios, absent or reversed end-
- Antenatal history: diastolic umbilical arterial Doppler flow
Results of investigations & scans done so far Assess fetal lie & presentation to guide mode of
- Placental &/or umbilical cord abnormalities noted delivery
(e.g. low-lying placenta, aberrant cord insertion) - Hematological investigations:
- Any preeclampsia (increases risk of abruptio) Full blood count
Use of assisted reproductive technologies PT, aPTT DIVC screen (fibrinogen, d-dimers)
- Increased risk of placenta praevia
Group & cross-match (4-6 units of blood)
- Increased risk of vasa praevia (multiple gestations)
- Fetal cardiotocography
- Obstetric history:
Any previous antepartum hemorrhage & diagnosis
Principles of Management
Any previous caesarian section or uterine surgery
- Initial resuscitation & investigations:
- Increased risk of placenta praevia
ABCs, establish IV access
- Past medical, surgical, social history
Establish close monitoring of maternal parameters &
Any known lower genital tract pathology
fetal CTG
- Cervicitis, cervical polyps, cervical cancer etc
Investigate accordingly to determine cause(s) of
- Last Pap smear & results
antepartum hemorrhage
Any pre-existing hypertension or thrombophilia
- Decide between expectant vs emergent management:
- Increased risk of abruptio
Balance to be struck between maternal well-being &
Any known coagulopathy
fetal maturity
Smoking & drug use
- Mode of delivery:
- Increased risk of placenta praevia & abruptio
Vaginal delivery general preferred unless clear
indications for caesarian are present (e.g. placenta
praevia, previous classical caesarian, rapid bleed control)
- Other general considerations:
Anti-D immunoglobulin for rhesus negative mother
Post-partum hemorrhage management (conditions
leading to antepartum hemorrhage can predispose to post-
partum hemorrhage)

OBSTETRIC HEMORRHAGE

52
Placenta Praevia Classification of Placenta Praevia
The most common type of abnormal placentation (incidence 0.5%); - Complete placenta praevia (praevia major)
defined as a placenta that is partially or completely located in the lower Placenta covers internal cervical os completely
uterine segment (hence lies over or proximate to the internal cervical os) Central placenta praevia is a subtype in which the
internal cervical os is approximately equidistant
Etiology & Associations between the anterior & posterior edges of the
- Risk factors for placenta praevia: placenta (20-30% of complete placenta praevia)
Maternal factors: - Partial placenta praevia (praevia major)
- Advanced maternal age Placenta covers internal cervical os partially
- Multiparity - Marginal placenta praevia
- Smoking or cocaine use Placental edge is adjacent to/at the edge of the
Previous procedure which may have resulted in internal cervical os without covering it
uterine scar tissue &/or endometrial damage: - Low-lying placenta (praevia minor)
- Previous caesarian delivery Placenta is partially or completely in the lower
- Previous intrauterine surgical procedures uterine segment, with the placental edge >0cm but
- Previous abortion <2cm away from the internal cervical os
Prior placenta praevia (4-8% subsequent risk) Low-lying placenta is also used to describe a
Multiple gestation placenta found to be in the lower portion of the
Use of assisted reproductive technologies uterus (including those partially or completely covering
- May be associated with other forms of abnormal the internal cervical os) in the 2nd trimester
placental implantation such as placenta accreta: - By definition, lower uterine segment only
Abnormal attachment of placenta through the develops in the 3rd trimester, hence strictly put,
uterine myometrium as a result of defective decidual a placenta praevia cannot be diagnosed until
formation: the 3rd trimester
- Decidua basalis is the decidual layer - Most low-lying placentas discovered in the 2nd
(endometrium lining) directly beneath the site trimester eventually migrate superiorly due to
of implantation, which gives rise to the basal growth & development of the lower uterine
plate of the placenta segment in the 3rd trimester such that at term,
- As implantation progresses, trophoblastic they are in normal position
giant cells invade the decidua basalis - A minority of low-lying placentas discovered
extensively, establishing the placenta in 2nd trimester however persists to become
- Where the invading trophoblastic tissue meets placenta praevia in the 3rd trimester (especially
the decidua basalis normally appears a zone of those already found to be covering the internal os)
fibrinoid degeneration (Nitabuchs layer)
- Absence of the Nitabuchs layer is seen in
placenta accreta, as the trophoblastic invasion
extends beyond the decidual layer into the
uterine myometrium
Types of placenta accreta:
- Placenta accreta = abnormal attachment of
placenta to myometrium is superficial
Complete Partial Marginal Low-lying
- Placenta increta = abnormal attachment of
placenta to myometrium extends into myometrium
partially
- Placenta percreta = abnormal attachment of
placenta to myometrium extends through the whole
myometrium to the serosal surface

OBSTETRIC HEMORRHAGE

53
Complications of Placenta Praevia Management of Placenta Praevia
- Maternal complications: - Initial resuscitation & assessment:
Uncontrolled hemorrhage Assess ABCs
- Antenatally Establish large bore IV access & begin fluid infusion
- Postpartum (as lower uterine segment does not Put patient on close monitoring:
contract well following delivery, hence placentation - BP, HR, RR, SpO2
in the lower uterine segment increases risk of PPH; - Catheterize for urine output
risk is further heightened if there is a concomitant Initial investigations:
placenta accreta associated with the praevia) - FBC, PT, aPTT, GXM (4-6 units of blood)
Abruptio placentae - Urgent ultrasound (confirm diagnosis, confirm
Disseminated intravascular coagulation (especially exact placental location, assess for fetal well-being,
with heavy bleeding & abruptio placentae) determine fetal lie & position)
- Fetal complications: - Fetal CTG
Fetal malpresentation (due to mass effect & distortion of Decide on expectant vs emergent management
the lower uterine segment) depending on:
Preterm delivery - Maternal status (maternal compromise, e.g.
Premature rupture of membranes uncontrolled bleeding, is indication for emergent
IUGR, IUFD management)
- Fetal status (fetal compromise, e.g. non-reassuring
Diagnosis of Placenta Praevia CTG status, is indication for emergent management)
- Clinical presentation: - Gestational age (low threshold for emergent
Per-vaginal bleeding management if already past 34 weeks gestation)
- Painless in majority of cases (70-80%); - Presence of concomitant conditions
associated with contractions in remaining cases (concomitant preterm labour, PROM, abruptio etc
- 1st episode of bleed occurs prior to 30 weeks would require additional relevant management plans
gestation in one-third, between 30 & 36 weeks as indicated)
in one-third, & after 36 weeks in most of the - Expectant management:
remaining patients Hospitalize patient & manage conservatively:
- 10% reach term without any PV bleed episode - Regular maternal parameters monitoring
- Investigations: (vitals, FBC, pad chart)
Ultrasound - Regular fetal CTG assessment
- Confirms placental site, establishing firm - Corticosteroids to accelerate fetal pulmonary
diagnosis of placenta praevia (should ideally maturation (in case of precipitous bleed)
precede digital vaginal examination in cases of Consider discharge & outpatient management if
antepartum hemorrhage to exclude placenta praevia patient is stable, no longer bleeding & compliant
because inadvertent palpation of the placenta in with follow-up
placenta praevia can lead to severe hemorrhage) - Educate on condition prior to discharge
- Transabdominal ultrasound is 1st-line; - Tell patient to return immediately if further
transvaginal ultrasound used if diagnosis episodes occur
remains uncertain after transabdominal scan - Advise to avoid sexual intercourse
Plan for elective delivery at term (37-38 weeks):
- Usually via caesarian unless placental margin
is >2cm from internal os (in which case vaginal
delivery can be considered)
- May require classical caesarian instead of
LSCS (e.g. in anterior placenta praevia where
placenta is directly under the site of the incision
made for a LSCS)
- Low threshold for immediate delivery once
>34 weeks gestation if patient has further
episodes of PV bleed
- Emergent management:
Stabilize patient
Expedite delivery (usually via caesarian section as for
elective delivery mentioned above)
- Other general considerations (for both expectant &
emergent management plans):
Give anti-D immunoglobulin after each episode of
PV bleed antenatally if mother is rhesus-negative
Manage post-partum hemorrhage following delivery
- Higher risk of PPH in placenta praevia
(refer to Labour & Puerperium)

OBSTETRIC HEMORRHAGE

54
Abruptio Placentae - Severity of clinical consequences depend on source of
Retroplacental bleeding (i.e. bleeding occurring at the decidual-placental retroplacental bleed:
interface) resulting in placental separation (specifically separation of the Arterial bleed (usually in central area of placenta)
decidua from the basal plate); occurs in 1 in 120 pregnancies (0.4-1.3%) - Rapid development of potentially life-
threatening clinical manifestations (acute onset of
Etiology & Associations maternal hemodynamic instability & fetal
- Risk factors for abruptio placentae: compromise)
Maternal risk factors: Venous bleed (usually in periphery of placenta)
- Maternal medical conditions (hypertension, - More likely to present with clinical
thrombophilias) manifestations which occur over time (light
- Maternal tobacco & cocaine use intermittent PV bleed, oligohydramnios, IUGR)
- Uterine abnormalities (bicornuate uterus, large - Thrombin plays a key role in clinical consequences of
submucous fibroids) abruptio placentae:
Pregnancy-related factors: Decidual bleeding results in production of thrombin
- Previous abruptio placentae (5-15% risk after 1, via various pathways (directly induction of tissue factor
20-25% risk after 2 previous abruptions) release from injured decidual cells which initiates cascade
- Preeclampsia in the current pregnancy to activate thrombin; hypoxia-induced production of
- Rupture of membranes (PROM, iatrogenic in VEGF which in turn induces aberrant production of
context of surgical induction of labour) tissue factor & thereafter, thrombin)
- Intrauterine infections Thrombin in turn causes:
- Short umbilical cord - Direct uterotonic effect inducing uterine
Mechanical factors: contractions
- Maternal abdominal trauma - Enhanced expression of matrix
- Rapid decompression of amniotic sac (e.g. metalloproteinases
rupture of membranes in the setting of - Induced expression of inflammatory cytokines
polyhydramnios) (IL-8) leading to tissue necrosis
Hence thrombin production results in further
Pathophysiology of Abruptio Placentae vascular disruption & tissue damage, initiating a
- Initiating event is usually the rupture of a maternal vessel vicious cycle, often leading to initiation of labour &
in the decidua basalis (rarely due to bleeding from a fetal- rupture of membranes
placental vessel rupture): Furthermore, large amounts of activated thrombin
Results in hemorrhage into the decidua basalis entering maternal circulation can induce widespread
Splits the decidua, separating a thin layer of decidua activation of the coagulation cascade, leading to
with its placental attachment from the basal plate maternal DIVC
Depending on the extent of continued hemorrhage,
the bleed may continue to dissect through the
placental-decidual interface
Detached portion of placenta becomes non-
functional
If retroplacental hemorrhage dissects downwards
towards the cervix, an external (revealed)
hemorrhage results (vs a concealed hemorrhage if the
retroplacental hematoma does not reach the cervix)
- Initial bleed from maternal vessels in the decidua basalis
could be caused by various factors:
Mechanical (trauma, rapid uterine decompression)
- Causes shearing of the inelastic placenta
Vasoconstrictive (smoking, cocaine) Complications of Abruptio Placentae
- Causes local areas of ischemia, reflex - Maternal consequences:
vasodilatation & disruption of vascular Excessive maternal hemorrhage (may lead to
integrity permanent end-organ damage e.g. Sheehans syndrome)
Abnormal placentation (uterine abnormalities) Disseminated intravascular coagulation
- Causes inadequate placentation & - Fetal consequences:
decidualization which may predispose to IUGR, IUFD
vascular disruption with relatively minor Preterm labour, PROM
mechanical forces

OBSTETRIC HEMORRHAGE

55
Diagnosis of Abruptio Placentae - Expectant management:
- Clinical presentation: Usually reserved for minor abruptions with stable
Patient usually presents with: maternal & fetal condition before 34 weeks gestation
- Acute onset of PV bleed (unless concealed Hospitalize patient & manage conservatively:
abruption occurs) - Regular maternal parameters monitoring
- Mild to moderate abdominal &/or back pain (vitals, FBC, pad chart)
- Uterine contractions - Regular fetal CTG assessment
Physical examination findings: - Corticosteroids to accelerate fetal pulmonary
- Signs of acute hemorrhage (pallor, tachycardia, maturation (in case of precipitous bleed)
hypotension) Plan for elective delivery at term (37-38 weeks):
- Abdominal tenderness - Via vaginal route unless indications for
- Woody-hard uterus (classically described) caesarian delivery is present (e.g. concomitant
- Investigations: placenta praevia, rapid control of heavy bleed)
Ultrasound - Low threshold for immediate delivery if >34
- Identification of retroplacental hematoma is weeks gestation in cases of recurrent bleed or
the classical ultrasound finding confirming worsening of maternal &/or fetal condition
presence of placental abruption - Emergent management:
- Other suggestive findings: subchorionic fluid Indicated if:
collections, echogenic debris in amniotic fluid, - Maternal &/or fetal compromise requiring
thickened placenta which shimmers with maternal immediate delivery
movement (Jello sign) - Fetal demise (in which case there is no need to
- Sensitivity for diagnosis of abruption is only weigh benefits of immediate delivery against risks of
25-50% (i.e. if negative, does not confidently rule neonatal prematurity)
out presence of placental abruption) Correct coagulopathy prior to delivery:
- Hence need to correlate with clinical findings - Many experts recommend that operative
& assessment of maternal & fetal well-being to intervention should not begin until
decide on management plan in many cases coagulopathy is corrected, which is desirable
but not always possible
Management of Abruptio Placentae - Monitor coagulation status & treat DIVC with
- Initial resuscitation & investigations: necessary transfusions (packed cells, platelets,
Assess ABCs fresh frozen plasma, cryoprecipitate etc) to achieve:
Establish large bore IV access & begin fluid infusion (i) platelet count 50000
Put patient on close monitoring: (ii) fibrinogen 100mg/dL
- BP, HR, RR, SpO2 (iii) PT & aPTT < 1.5x control
- Catheterize for urine output (iv) hematocrit 25-30%
Initial investigations: Mode of delivery:
- FBC, PT, aPTT, GXM (4-6 units of blood) - Vaginal delivery is generally preferable (as
- Consider DIVC screen patient is usually contracting vigorously in
- Urgent ultrasound (confirm diagnosis, confirm abruptio, an amniotomy may be all that is required
exact placental location to exclude concomitant to expedite delivery oxytocin augmentation)
placenta praevia, assess for fetal well-being, - Caesarian delivery is indicated if (i) rapid
determine fetal lie & position) control of bleeding required (ii) obstetric
- Fetal CTG contraindications to vaginal birth (e.g.
Decide on management options based on: concomitant placenta praevia, previous classical
- Maternal status (maternal compromise, e.g. caesarian, certain malpresentations)
uncontrolled bleeding or DIVC, is indication for - Other general considerations (for both expectant &
emergent management) emergent management plans):
- Fetal status (fetal compromise, e.g. non-reassuring Give anti-D immunoglobulin if mother is rhesus-
CTG status, is indication for emergent management; negative
fetus being alive vs dead also changes management Manage post-partum hemorrhage following
considerations) delivery; higher risk of PPH especially if:
- Gestational age (low threshold for emergent - Couvelaire uterus (blood extravasated into
management if already past 34 weeks gestation) myometrium which renders uterus atonic), which
- Presence of concomitant conditions has a higher incidence of requiring a post-
(concomitant preterm labour, PROM, placenta partum hysterectomy
praevia etc would require additional relevant - DIVC complicating abruption
management plans as indicated) (refer to Labour & Puerperium)

Couvelaire uterus (internal view) Couvelaire uterus (external view)

OBSTETRIC HEMORRHAGE

56
Vasa Praevia
A unique condition which may arise in cases of velamentous insertion of
the cord involving passage of unprotected umbilical vessels over the
internal cervical os

Pathophysiology of Vasa Praevia


- Velamentous cord insertion = insertion of vessels of the
umbilical cord between the amnion & chorion at a point
away from the placental site (i.e. the vessels will have a
segment which courses between the amnion & chorion before
reaching the placenta)
Occurs in 1% of singleton pregnancies, 10% in twin
pregnancies & 50% in triplets
In itself increases the risk of vessel rupture, resulting
in fetal hemorrhage
- Vasa praevia = velamentous cord insertion with the
unprotected umbilical vessels coursing over the internal
cervical os
Occurs in 1 in 5000 pregnancies
Accentuates risk of vessel rupture compared to
velamentous cord insertion without vasa praevia
50% perinatal fetal mortality rate (75% if membranes
rupture)
- Note that unlike other causes of antepartum
hemorrhage in which blood loss is maternal in
origin, bleeding from vasa praevia is fetal in
origin

Vasa praevia Velamentous cord insertion

Diagnosis of Vasa Praevia


- Clinical presentation:
Painless per-vaginal bleeding (patient is otherwise very
well as it involves fetal rather than maternal
exsanguination)
May present for the first time following rupture of
membranes which ruptures the vessels crossing the
internal cervical os
- Investigations:
Ultrasound can possibly diagnose via visualization
of umbilical vessels crossing internal cervical os
(especially with Doppler flow)

Management of Vasa Praevia


- Immediate delivery via caesarian section indicated if
antepartum hemorrhage is suspected to be from vasa
praevia

OBSTETRIC HEMORRHAGE

57
MISC. CONDITIONS IN PREGNANCY
Endocrine Disorders In cases of gestational DM:
- Polyhydramnios (with its attendant risks of
preterm labour, PROM, cord prolapse)
Diabetes Mellitus in Pregnancy - Macrosomia (with its attendant risks of birth
trauma, shoulder dystocia)
Definitions & Terminology - Intrauterine fetal demise (especially in the
- Pre-existing diabetes mellitus setting of poor DM control)
Existing type 1 or type 2 diabetes mellitus in an - Neonatal hypoglycemia, hypocalcemia,
individual prior to pregnancy hypomagnesemia, hyperbilirubinemia &
- Gestational diabetes mellitus (GDM) respiratory distress syndrome
Glucose intolerance with onset during pregnancy &
eventual resolution within 6 weeks post-partum Screening & Diagnosis
- Screening for diabetes mellitus during pregnancy:
Pathophysiology of Diabetes Mellitus in Pregnancy Pre-existing DM:
- Gestational diabetes mellitus occurs due to hormonal - History & previous investigations done are
alterations in pregnancy: reviewed at booking visit to identify known
Production of human placental lactogen, pre-existing DM cases
progesterone, prolactin & cortisol - Urine dipstick test at booking visit may reveal
Results in increased peripheral insulin resistance glycosuria in an undiagnosed pre-existing DM,
- Maternal hyperglycemia results in fetal hyperglycemia (as prompting further testing for diagnosis
glucose crosses the placental barrier easily) & thereafter, Gestational DM:
secondary fetal hyperinsulinism - Universal screening vs targeted screening
- Fetal hyperglycemia has various fetal effects: (Singapore practices targeted screening based on risk
Teratogenic during embryogenesis (hence pre-existing factors for GDM)
DM is associated with birth defects while GDM is not) - Risk factors for GDM:
Fetal osmotic diuresis & polyuria, leading to Advance maternal age (>35 years old)
polyhydramnios Maternal obesity
- Fetal hyperinsulinism has various fetal effects: 1st-degree relative with DM
Fetal overgrowth, leading to macrosomia Obstetric history (previous GDM, fetal
Neonatal hypoglycemia following delivery macrosomia, stillbirth, fetal anomaly or
- Vascular complications of pre-existing DM can further polyhydramnios)
augment the effect of DM on pregnancy due to increased - Women with any risk factors identified will
risk of uteroplacental insufficiency, resulting in: undergo diagnostic oral glucose tolerance test
Early pregnancy loss (75g 2-hour OGTT) at 28 weeks gestation (or
Increased risk of pre-eclampsia earlier where clinically indicated; e.g. persistent
Intrauterine growth restriction glycosuria detected in early antenatal visits)
Oligohydramnios - Diagnosis of diabetes mellitus during pregnancy:
Pre-existing DM:
Clinical Features - Fasting blood glucose 7.0mmol/L
- Maternal risks: - Random blood glucose 11.1mmol/L
In cases of pre-existing DM: - 75g 2-hour OGTT 11.1mmol/L
- Accelerated retinopathy & nephropathy ***DM diagnosis needs (i) 2 positive tests on 2
- Increased risk of diabetic ketoacidosis different occasions if patient is asymptomatic or (ii)
- Increased risk of preeclampsia 1 positive test if patient is symptomatic or (iii) first
- Increased risk of infections (e.g. UTI) presentation with a diabetic emergency (e.g. DKA)
- Hypoglycemia (due to overly tight control) Gestational DM:
In cases of gestational DM: - Fasting blood glucose 7.0mmol/L
- Perineal trauma during birth secondary to - Random blood glucose 11.1mmol/L
fetal macrosomia - 75g 2-hour OGTT 7.8mmol/L
- Hypoglycemia (due to overly tight control) ***in pregnancy, impaired oral glucose tolerance
- Fetal risks: (OGTT 7.8mmol/L is regarded as GDM)
In cases of pre-existing DM: Note that if a patient presents for booking visit late, it
- Early pregnancy loss (miscarriage, may be a may be difficult to determine if a positive test for DM
cause of recurrent miscarriages) indicates undiagnosed pre-existing or gestational
- Congenital defects (cardiac, neural tube, caudal DM; possible differentiating factors include:
regression syndrome very rare but very unique to - Presence of vascular complications of DM
pre-existing DM in pregnancy) (retinopathy, nephropathy, neuropathy etc) is
- Intrauterine growth restriction suggestive of pre-existing DM
- Oligohydramnios - Fetal anomalies, IUGR & oligohydramnios are
- Intrauterine fetal demise (especially in the suggestive of pre-existing DM
setting of poor DM control) - Polyhydramnios & fetal macrosomia are
- Neonatal hypoglycemia, hypocalcemia, suggestive of GDM
hypomagnesemia, hyperbilirubinemia &
respiratory distress syndrome

MISC. CONDITIONS IN PREGNANCY

58
Antenatal Management - Planned delivery:
- Principles of antenatal management of DM in pregnancy: Gestational age at which delivery is planned
DM renders a pregnancy a high-risk pregnancy depends on type of treatment & adequacy of control:
- Needs to be followed-up antenatally in a high- - Well-controlled on diet alone allow to go up
risk clinic/joint clinic with endocrinology to EDD (40 weeks)
- Multidisciplinary management (obstetrician, - Poorly-controlled on diet alone indication for
endocrinologists, diabetic nurse clinician, dietician) adding on insulin, after which adequacy of controlled
- Monitoring for fetal abnormalities & IUGR reassessed to determine planned delivery date
Pre-existing DM requires baseline tests for assessing - Well controlled on diet + insulin 38 weeks
complications: - Poorly-controlled on diet + insulin may
- Renal panel (assess renal function) require earlier delivery, based on severity, but
- Ophthalmology review (assess retinopathy) generally always after 34 weeks
- Neurological testing (assess neuropathy) Mode of delivery is preferably vaginal in the absence
- Cardiac testing (ECG, echocardiogram) of contraindications
Tight blood sugar control is required to decrease
incidence of congenital anomalies & perinatal Intrapartum Management
morbidity & mortality - Tight blood sugar control
Regular blood sugar monitoring to determine level Establish insulin infusion using sliding scale (starting
of glycemic control, which influences: at 1unit/hour) + dextrose drip
- Treatment option (diet alone or + insulin) Hourly assessment of blood sugar level to guide
- Planned delivery date insulin infusion titration:
Delivery is planned at different gestational ages - BSL <4mmol/L stop insulin infusion
depending on the degree of glycemic control during - BSL 4-7mmol/L continue insulin 1U/hour
pregnancy in order to achieve a balance between - BSL >7mmol/L up insulin to 2U/hour
maximizing gestational age of fetus & minimizing - If elective LSCS is arranged:
risk of antenatal obstetric complications Arrange as 1st case of the day (to avoid prolonged pre-
- Blood sugar control: op fasting which increases risk of hypoglycemia)
Dietary control
- Remains the cornerstone Postnatal Management
- Caloric control (1800kcal/day or 30kcal/kg/day) - Blood sugar management:
- + moderate intensity exercise (insulin requirements drop drastically following delivery of the
- Insulin is added on top of dietary control if placenta as this source of the hormonal antagonists of insulin
DM is not adequately controlled with diet alone activity is removed)
Insulin Pre-existing DM previously on insulin:
- Most commonly used dosing regime is the - Revert to previous insulin regime
basal-bolus regime (4 injections daily) Pre-existing DM previously on oral hypoglycemic:
- 1 injection of intermediate-acting insulin - Consider continuing on lower doses of
before bedtime (10pm) + 1 injection of short- subcutaneous insulin for time the being (as oral
acting insulin before each of the 3 main meals hypoglycemic agents cross into breast milk & can
Oral hypoglycemic agents cause neonatal hypoglycemia in breastfeeding
- Not conventionally used in DM treatment mothers)
during pregnancy due to concerns of Gestational DM:
teratogenicity - Frequently able to stop insulin immediately
- Metformin has recently been used however in - Gestational DM follow-up:
certain instances, but still not routine Perform OGTT at 6 weeks post partum to ensure that
- Blood sugar monitoring: results revert back to normal
Home blood sugar monitoring: Counsel patients with GDM regarding risk of long-
- 7-point blood sugar profile (once before & once term metabolic sequelae (30% of GDM patients develop
after each of the 3 main meals + once before diabetes mellitus subsequently; should maintain healthy
bedtime/10pm) diet & exercise level to minimize risk)
- Ideal pre-meal level: 4.5-5.5mmol/L - Other general considerations:
- Ideal post-meal level: 5.5-6.6mmol/L Give contraception advice
- 7-point BSP done daily initially, can be For pre-existing DM, advise to return early for
reduced to weekly BSP if well-controlled assessment & adequate control of blood sugar when
Clinic HbA1c monitoring: planning the next child in order to optimize
- Test at baseline when DM is diagnosed & pregnancy outcomes
thereafter at 3-monthly intervals
- Ideal HbA1c: 6.0%
- Antenatal fetal monitoring:
For pre-existing DM:
- Early fetal anomaly scan (16-18 weeks)
- Detailed fetal anomaly scan at 20-22 weeks as
per for normal pregnancies
- Serial growth scans after 28 weeks
For gestational DM:
- Detailed fetal anomaly scan at 20-22 weeks as
per for normal pregnancies
- Serial growth scans after 28 weeks

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59
Thyroid Disorders in Pregnancy Hyperthyroidism in Pregnancy
- Etiology & associations:
Thyroid Physiology in Pregnancy Incidence of maternal thyrotoxicosis = 1 in 500
- Maternal thyroid function: Causes of maternal hyperthyroidism:
Increase in glomerular filtration rate results in - Graves disease (most common, even though most
increase in renal iodine excretion, with plasma cases of Graves experience transient remission
inorganic iodine levels nearly halved during pregnancy, postulated to be due to the
- Goitre from iodine insufficiency unlikely so increased immunological tolerance in pregnancy)
long as plasma inorganic levels >0.08 g/dL - Toxic multinodular goitre
- Inorganic iodine supplementation up to - Hydatidiform mole (as hCG, which is produced
250 g/day is sufficient to prevent goitre in high levels, is structurally analogous to TSH)
formation during pregnancy - Clinical features:
Pregnancy increases hepatic production of serum Maternal features:
proteins which bind circulating thyroid hormone - Signs & symptoms of a hyperdynamic
(albumin, thyroid-binding globulin) circulation (may be difficult to differentiate from the
- Total T3 & T4 levels may be increased during normal changes that occur in pregnancy)
pregnancy despite euthyroidism - Signs & symptoms supporting diagnosis of
- Free T4 levels remain normal hyperthyroidism vs normal pregnancy changes:
- Fetal thyroid function: thyroid eye signs, weight loss, heat intolerance
Fetal thyroid gland does not contain organic iodine - Thyroid storm is the major maternal risk of
before 10 weeks gestation hyperthyroidism in pregnancy with >25%
Able to produce iodothyronines & T4 by weeks 11-12 mortality; may be precipitated by: infection,
Able to concentrate iodine by weeks 12-14 labour, caesarian delivery or non-compliance with
- Placental barrier in thyroid physiology: thyroid medications
Placenta allows free transfer of iodide, TRH & Fetal features:
thyroid stimulating antibodies, limited transfer of T4 - Increased risk of preterm labour, IUGR,
& no transfer of TSH preeclampsia & intrauterine fetal demise
- Transfer of maternal T4 to fetal circulation is - 1% of maternal Graves results in neonatal
vital in the 1st trimester while fetal thyroid thyrotoxicosis due to transplacental transfer of
function is absent for proper neural thyroid stimulating antibodies (transient & lasts
development for <2-3 months but associated with mortality rate of
- Transfer of maternal TRH to fetal circulation 16%); may be suspected by persistent fetal
has minimal effect due to low levels present in tachycardia & visualization of fetal goitre on
maternal systemic circulation ultrasound
- Transfers of maternal thyroid stimulating - Diagnosis & evaluation:
antibodies can cause fetal thyrotoxicosis Thyroid function test (TSH, free T4, thyroid stimulating
Thyroid drugs with smaller molecular weights antibody)
(propylthiouracil, methimazole) can also cross the - Management:
placenta, causing fetal hypothyroidism Antithyroid medications:
- Thioamides remains mainstay of treatment
- Drugs: propylthiouracil, carbimazole, methimazole
Hypothyroidism in Pregnancy
- Etiology & associations: - No conclusive evidence that they result in fetal
Incidence of neonatal congenital hypothyroidism = 1 anomalies & cretinism, although 1-5% of fetus
in 4000 exposed in-utero may develop a goitre
Causes of congenital hypothyroidism: - PTU is minimally excreted in breastmilk,
- Insufficient maternal iodine ingestion hence can be safely continued in the
- Maternal goitrogen ingestion postpartum period in breastfeeding mothers
- Thyroid dysgenesis/agenesis Radioactive iodine is contraindicated in pregnancy
- Inborn-errors of metabolism pertaining to Surgical treatment:
thyroid hormones (dyshormonogenesis) - Reserved for cases refractory to medical
- Clinical features: treatment, preferably performed in the 2nd
Maternal features: trimester as per for most elective surgeries
- Similar to hypothyroidism in normal patients during pregnancy
Fetal features:
- Increased risk of miscarriage, preeclampsia,
intrauterine fetal demise, low birth weight &
lower intelligence
- Fetal hypothyroidism affecting neural
development in the 1st trimester can result in
cretinism
- Diagnosis & evaluation:
Thyroid function test (TSH, free T4)
- Management:
Thyroxine replacement

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60
Cardiovascular Disorders Risk Stratification of Heart Disease in Pregnancy
- New York Heart Association (NYHA) classification:
NYHA class specifications:
Heart Disease in Pregnancy - Class I = no signs or symptoms of cardiac
decompensation
Cardiovascular Physiology in Pregnancy - Class II = No symptoms at rest, minor limitation
- Circulatory changes: of physical activity
Both plasma volume & red blood cell count increases - Class III = No symptoms at rest, marked limitation
during pregnancy, with a disproportionately higher of physical activity
increase in plasma volume - Class IV = Symptoms present at rest
- Results in hemodilution & physiological In general:
anemia of pregnancy - Class I & II are low risk
- Results in increased cardiac output which - Class III & IV are high risk
places greater strain on the heart - Other factors augmenting risk:
Blood pressure generally decreases during the early Type of valve defect (stenotic worse than regurgitant)
half of pregnancy Presence of pulmonary hypertension
- Diastolic pressure decreases more than systolic Poor left-ventricular ejection fraction (<40%)
(due to decrease in systemic resistance) Marfans syndrome
- Blood pressure begins increasing in the 2nd Presence of prosthetic valves
trimester & progresses back to normal towards History of cardiac event or arrhythmia
term
- Mechanical effects of the gravid uterus: Management of Heart Disease in Pregnancy
Supine hypotensive syndrome - Prenatal management:
- Gravid uterus compresses iliac veins & Ideally, patients should be assessed & worked up
inferior vena cava, especially when patient is in thoroughly & counseled on the risks of pregnancy
supine position before conception
- Causes decrease in venous return which may - Antenatal management:
in turn result in decreased cardiac output & Multidisciplinary management (including cardiologist)
maternal hypotension with frequent antenatal visits admissions
Pelvic vein compression General measures:
- Gravid uterus compresses pelvic veins - Avoid excessive weight gain & edema (low salt
- Results in venous stasis & impaired venous diet, regular left-lateral decubitus position for >1
drainage of pelvic structures & lower limbs hour each day to promote venous return from lower
- May manifest as lower limb edema, varicose extremities & subsequent diuresis)
veins, hemorrhoids - Avoid strenuous activity
- Predisposes to venous thromboembolism - Avoid anemia
Poseiro effect Pharmacological management:
- Gravid uterus compresses abdominal aorta & - Loop diuretics -blockers if sodium
its branches, especially when patient is in restriction is inadequate in preventing excessive
supine position fluid retention
- Typically occurs during late pregnancy if at all - Patients requiring anticoagulation should be
- Can result in compromised uteroplacental on full anticoagulation using heparin, with
perfusion & subsequent fetal distress warfarin reinstituted post-partum
- Intrapartum management:
Risks of Heart Disease in Pregnancy Vaginal delivery is preferable unless indications for
- Maternal risks: caesarian delivery are present
Decompensation of existing heart disease General considerations:
- Stenotic valvular lesions do not tolerate - Patient should be placed in left lateral position
decrease in afterload well due to an impaired to minimize compression of major vessels by
ability to increase cardiac output adequately, the gravid uterus
resulting in congestive cardiac failure, cardiac - Adequate analgesia should be ensured to
arrhythmias (e.g. atrial fibrillation) & pulmonary minimize excessive strain on cardiac function
edema brought on by pain
- Pulmonary hypertension may also - Pushing should be avoided in the 2nd stage of
decompensate with the increase in intravascular labour (consider assisted vaginal delivery)
volume during pregnancy - Ergometrine should be avoided in the 3rd stage
- Shunt reversals may also be precipitated by of labour due to its side effect of raised BP
the drop in left-sided afterload (Eisenmenger) - Antibiotic prophylaxis is not indicated for
Peripartum cardiomyopathy delivery alone, but should be given if patient is
Infective endocarditis high-risk (prosthetic valves, unrepaired or
- Fetal risks: incompletely repaired congenital heart defects) &
Early pregnancy loss, intrauterine fetal demise bacteremia is suspected (e.g. chorioamnionitis)
Intrauterine growth restriction Acute decompensation of heart failure:
- Managed as a medical emergency
- Medical therapy instituted (oxygen, morphine,
vasodilators [nitroglycerin, hydralazine], inotropic
support [dopamine, dobutamine])

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61
Anemia in Pregnancy Management of Anemia
- Management of anemia in pregnancy is etiology-specific
Relevance of Anemia in Pregnancy Remember that anemia is not a diagnosis in itself, &
- Physiological anemia occurs during pregnancy due to an underlying cause has to be sought
hemodilution from greater increase in plasma volume - Options for management of iron-deficiency anemia:
than in red blood cell mass Haematinics (oral supplementation)
Normal Hb levels during pregnancy ~ 12-16g/dL - Iron gluconate (Sangobion), iron fumarate
Lower levels (<11g/dL) suggests an underlying - 1st-line option for prophylaxis against anemia
pathological cause of anemia requiring work-up & for treatment of mild, stable cases
- Untreated anemia can have adverse pregnancy outcomes: - Side-effect: constipation, black stools
Maternal risks: Parenteral iron
- High-output cardiac failure - IV iron dextrin, IM iron sorbitol
Fetal risks: - Quicker onset of therapeutic action than oral
- Uteroplacental insufficiency, leading to IUGR, iron, doesnt require patient compliance
intrauterine fetal demise, preterm labour etc - Reserved for more serious cases of anemia
- Maternal anemia may be due to a hereditary cause, with requiring more urgent normalization of
implications for the fetus hemoglobin levels (e.g. planned caesarian soon)
Locally, thalassemia is of the greatest relevance - Side-effect: pain, skin discolouration, anaphylaxis
Blood transfusion
Screening for Anemia - Last-resort for serious cases requiring
- Booking visit: normalization of hemoglobin levels quickly
Baseline FBC is performed as a basic screening tool (Hb<7g/dL, symptomatic anemia etc)
for previously undetected anemia
If anemia is detected, further investigations are Venous Thromboembolism in Pregnancy
required to determine the cause of the anemia & to
determine if there is undiagnosed thalassemia in the Superficial Thrombophlebitis
mother (has implications for genetic testing; see below) - Clinical features:
- During episodes of antepartum hemorrhage: Usually seen in patients with varicose veins, obesity
FBC done at presentation to screen for anemia as a &/or limited physical activity
possible complication of antepartum hemorrhage Usually affects the calf area:
- Peripartum: - Swelling, erythema, warmth, tenderness
FBC can be done to screen for anemia, especially in - Palpable cord
cases where blood loss is expected to be excessive - Management:
(caesarian deliveries, maternal anticoagulation, placenta Symptomatic (bed rest, pain medications)
praevia, placental abruption etc) Wear support hose to prevent recurrences

Thalassemia Work-up Deep Vein Thrombosis & Pulmonary Embolism


(if anemia is picked up at booking visit, thalassemia work-up is - Clinical features:
indicated to determine risk of thalassemia in the child) Some cases may be asymptomatic
- Maternal blood investigations: Symptomatic presentations:
Full blood count (Hb, MCV) - DVT: dull ache, tightness, pain; Homans sign
- Can use Mentzer index (MCV/RBC count) to (pain on passive dorsiflexion of the ankle)
help differentiate between iron-deficiency - PE: SOB, cough, chest pain, tachycardia
anemia & thalassemia (<13 suggests thalassemia) - Diagnosis & evaluation:
Iron panel (iron, ferritin, transferrin, TIBC) Deep vein thrombosis:
Peripheral blood film - Compression ultrasonography with Doppler
- Microcytic hypochromic RBCs, target cells flow studies is primary investigation of choice
(these findings are seen in thal but are not specific) - MRI may be considered in cases where iliac
- HbH inclusion bodies (seen using Brilliant vein thrombosis is suspected
Cresyl Blue stain) are indicative of -thal Pulmonary embolism:
Hb electrophoresis - Baseline investigations (chest x-ray, ECG)
- Much higher yield for -thal (decreased HbA, - Diagnostic investigations (CTPA, ventilation-
increased HbA2 & HbF) perfusion scan, pulmonary angiography)
Genetic testing - Management:
- Definitive diagnosis can be made Anticoagulation using unfractionated heparin or low
- Paternal screening: molecular weight heparin
Indicated if mother is found to have thalassemia to - Continued until at least 6 weeks post-partum
determine if father has thalassemia as well (affects - Monitor aPTT if heparin is used; no
risk of fetus having serious forms of thalassemia such as monitoring required for LMWH (factor Xa is
thal-major, HbH disease or Barts hydrops) used for monitoring but not practical)
- Prenatal diagnosis: - Side-effects: heparin-induced thrombocytopenia
Decision to perform prenatal diagnosis depends on: (monitor platelet count), osteoporosis (consider
- Calculated risk based on results from maternal calcium & vitamin D)
& paternal screening for thalassemia Switch to warfarin if need for long-term
- Whether knowledge makes a difference to the anticoagulation is determined post-partum
couple (decision to abort or make plans in advance) Consider prophylactic anticoagulation (with UFH or
Options: chorionic villus sampling, amniocentesis LMWH) in future pregnancies

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62
Autoimmune Disorders Seizure Disorders
Rheumatoid Arthritis Effect of Pregnancy on Seizure Disorders
- Effect of pregnancy on RA: - Pregnancy itself does not usually alter seizure frequency
RA usually improves during pregnancy - Pregnancy-related factors may affect plasma levels of
- Effect of RA on pregnancy: antiepileptic drugs (AED), resulting in breakthrough
No significant effects on both mother & fetus seizures & increased seizure frequency:
Some medications for RA have teratogenic effects Nausea & vomiting affecting GI absorption of AED
- Transplacental transfer of antibodies: Increased intravascular volume resulting in larger
None volume of distribution of AED
Induction of hepatic enzymes metabolizing AED
Idiopathic Thrombocytopenic Purpura Increased glomerular filtration rate increasing renal
- Effect of pregnancy on ITP: excretion of AED
No significant effect
- Effect of ITP on pregnancy: Risks of Seizures in Pregnancy
Increases risk of maternal antepartum, intrapartum - Obstetric events & complications (due to seizures):
& postpartum hemorrhage Preeclampsia
- Treatment not initiated unless plt <40000 Abruptio placentae
- Options: steroids, IVIG, splenectomy IUGR or intrauterine fetal demise
Neonatal thrombocytopenia may occur, leading to - Fetal congenital anomalies (due to AED use):
neonatal intracranial hemorrhage in rare cases Neural tube defects are especially associated with
- Monitor neonatal platelet counts AED use in pregnancy; requires higher-dose folic
- Transplacental transfer of antibodies: acid supplementation than normal pregnancies
Anti-platelet antibodies Overall risk for major malformations with AED use
in pregnancy is 4-6% (higher than women without
Graves Disease epilepsy & women with epilepsy not on AED)
- Effect of pregnancy on Graves disease:
Graves disease usually improves during pregnancy Management of Seizure Disorders in Pregnancy
May experience postpartum exacerbation - Anti-epileptic drug treatment:
- Effect of Graves disease on pregnancy: If no seizure activity for 2 years, can consider
If thyrotoxicosis is not well-controlled, may have stopping AED before conception
increased risk of preterm labour, IUGR, For patients requiring AED maintenance:
preeclampsia, intrauterine fetal demise - Stick with existing AED if it has been effective
1% risk of neonatal thyrotoxicosis - Aim for monotherapy with lowest possible
- Transplacental transfer of antibodies: dose needed
Thyroid stimulating immunoglobulins - No ideal AED as all are teratogenic to varying
extents (but valproate is especially teratogenic &
Myasthenia Gravis should be avoided where possible)
- Effect of pregnancy on myasthenia gravis: - Should be maintained throughout pregnancy,
Pregnancy has variable effects on myasthenia gravis intrapartum & postpartum
Moderate exacerbation postpartum - Supplementation:
- Effect of myasthenia gravis on pregnancy: Folic acid supplementation
May have transient neonatal myasthenia - Indicated for use of all AEDs
- Transplacental transfer of antibodies: - To minimize risk of neural tube defects
Acetylcholine receptor antibodies - Dosage: 1mg/day if on most AEDs; 4mg/day if on
carbamazepine or valproate
Systemic Lupus Erythematosus Vitamin K supplementation
- Effect of pregnancy on SLE: - Indicated for use of enzyme-inducing AEDs
1/3 improves, 1/3 same, 1/3 worsens in pregnancy (carbamazepine, phenytoin, phenobarbitone,
- Effect of SLE on pregnancy: topiramate, oxcarbazepine)
Increased risk of miscarriage, preterm labour, IUGR, - Dosage: 10mg/day in the last month of pregnancy
preeclampsia, intrauterine fetal demise Vitamin D supplementation
10% risk of neonatal lupus (skin lesions, hematologic - Indicated for use of AEDs which interfere with
manifestations, congenital heart block, endomyocardial intestinal absorption of calcium (phenytoin,
fibrosis) phenobarbitone, primidone)
- Transplacental transfer of antibodies: - Begin taking from 34 weeks gestation
Anti-Ro (SS-A) - Status epilepticus management:
Anti-La (SS-B) Resuscitate & stabilize
IV diazepam or lorazepam phenytoin infusion
phenobarbitone
Check plasma AED levels
Monitoring fetal well-being
Admit patient

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63
Infectious Diseases in Pregnancy Management
- Antiretroviral therapy:
Antenatal antiretroviral therapy shown to decrease
Human Immunodeficiency Virus (HIV) the rates of vertical transmission significantly:
- Pediatric AIDs Clinical Trial 079 in 1994
Etiology & Transmission demonstrated that use of zidovudine to mother
- Caused by the human immunodeficiency virus (HIV) antenatally & to infant for 6 weeks postpartum
Retrovirus, RNA genome reduced maternal transmission of HIV from
Infects & replicates within T4 helper lymphocytes, 25.5% to 8.3%
macrophages & other cells in the hematopoietic - More potent antiretroviral therapies currently
system & central nervous system have been shown to reduce risk to 1-2%
Viral antigens: Principles of antiretroviral therapy in pregnancy:
- Surface proteins gp120, gp41 - Multiple agents to minimize risk of resistance
- Core proteins p24, p18 - All regimes should include zidovudine unless
- Transmission: it is contraindicated
Sexual contact, blood Classes of antiretroviral drugs:
Vertical transmission: - Nucleoside reverse transcriptase inhibitors
- Risk of transmission is 20-30% (NRTIs): zidovudine, lamivudine
- 50% of transmission occurs peripartum - Non-nucleoside reverse transcriptase
- Antenatal transmission risk may theoretically inhibitors (NNRTIs): efavirenz, nevirapine
be increased by invasive procedures (e.g. - Protease inhibitors (PIs): saquinavir, indinavir,
amniocentesis) but exact risk is unknown lopinavir, ritonavir
- Postpartum transmission by breastfeeding has Monitoring while on antiretroviral drugs:
risk of 10-20% - NRTIs & NNRTIs: liver enzymes, renal function
- PIs: OGTT at 28 weeks to screen for GDM
Clinical Features - Monitor maternal plasma HIV RNA
- Maternal features: concentration to determine effectiveness of
Chronic progressive course of disease after infection treatment (target <1000 copies/mm)
- Seroconversion usually occurs 3-14 weeks - Antibiotic prophylaxis:
after exposure, but may take up to 6 months; Offered when mother is significantly
this phase is marked by a mononucleosis-like immunocompromised (CD4 T-cell <200/ L)
syndrome (flu, cervical lymphadenopathy, rash) Organisms to target include:
- An asymptomatic period then follows, during - Pneumocystis carinii
which T-cell count gradually drops - Mycobacterium avium complex
- Eventually, more generalized symptoms set in - Intrapartum management:
(generalized lymphadenopathy, constitutional Mode of delivery:
symptoms) - Offer elective caesarian at 38 weeks if maternal
- Opportunistic infections gradually set in plasma HIV RNA >1000 copies/mm
- Average duration interval from initial - Offer normal vaginal delivery if maternal
infection to full-blown AIDS is 10 years in plasma HIV RNA <1000 copies/mm
untreated cases (transmission risk is very low, 1-2%)
Pregnancy does not affect the course of HIV Avoid intrapartum measures which increase the risk
HIV in pregnancy increases the risk of infections of HIV transmission to the fetus:
during pregnancy - Artificial rupture of membranes
- Fetal features: - Fetal scalp electrodes
HIV has no significant antenatal effects - Fetal scalp blood sampling
Disease progression in children after birth is much - Assisted vaginal delivery
faster than in adults - Episiotomy
- 50% develop full blown AIDS within 1st year For vaginal delivery, once membranes have
of life, 80% by 3rd year of life ruptured, augment with oxytocin to reduce the
- Average survival time for diagnosis = 3 years interval between membrane rupture & delivery
- Postpartum management:
Diagnosis & Evaluation Neonate should continue to receive antiretroviral
- Screening for HIV in pregnancy: treatment for the first few weeks of life
Offered to all women presenting at booking visit Avoid breastfeeding to mitigate transmission risk
- Diagnostic tests for maternal infection: Confirmation of HIV status in neonate:
Enzyme-linked immunosorbent assay (ELISA) - Done using Western blot, PCR or culture
- Detects HIV antibodies or p24 antigen (serological methods not accurate initially due to
- 93-99% sensitive; 99% specific false positive results from maternal antibodies)
Western blot - At least 2 positive results using 2 different
- Detects HIV core & surface antigens tests should be obtained before confirming
- 99% sensitive, 98.5 specific neonatal HIV infection
HIV PCR, HIV tissue culture - At least 2 negative results, at least 1 done after
6 months of life, should be obtained to predict
absence of neonatal HIV infection (confirmation
is by demonstrating absence of HIV antibodies at 15
months of age)

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64
Rubella (German Measles) Cytomegalovirus (CMV)

Etiology & Transmission Etiology & Transmission


- Caused by the Rubella virus: - Caused by cytomegalovirus
Togavirus, RNA genome Herpesvirus family (HHV5), DNA genome
- Transmission: Extremely prevalent within the population
Respiratory route - Transmission:
Vertical transmission: Blood, sexual contact, urine, saliva
- Risk of congenital rubella syndrome is Vertical transmission:
primarily dependent on the time of pregnancy - May be transmitted transplacentally or at
during which maternal infection occurs delivery via direct contact
- 80% risk if infection occurred in the 1st - 40-50% transmission rate if mother has an
trimester, drops to 30-50% thereafter acute infection during pregnancy
- Congenital rubella syndrome rarely occurs if - 0.15-1% transmission rate if mother has a
infection occurs after 20 weeks gestation reactivation of CMV infection during pregnancy

Clinical Features Clinical Features


- Maternal features: - Maternal features:
Incubation period of 14-21 days Commonly asymptomatic
Prodromal flu-like illness Symptomatic presentation resembles a
Maculopapular rash mononucleosis-like illness
- Fetal features: Virus usually establishes latency after acute infection
Fetus may be entirely unaffected by rubella & may reactivate years later
Affected fetuses manifest the congenital rubella - Fetal features:
syndrome to varying extents: May be symptomatic at birth (10-15%)
- Symmetrical IUGR - Non-immune hydrops
- Congenital deafness - Symmetrical IUGR
- Cataracts, retinopathy, microphthalmia - Chorioretinitis
- PDA, pulmonary artery hypoplasia - Hepatosplenomegaly
- Hepatosplenomegaly - Microcephaly, cerebral calcifications,
- Microcephaly, panencephalitis, intra-cranial hydrocephalus
calcifications May only manifest features later in life (80-90%)
- Thrombocytopenic purpura (classical blueberry - Visual impairment
muffin rash) - Progressive hearing loss
- Delayed psychomotor development
Diagnosis & Evaluation - Mental retardation
- Screening for rubella in pregnancy:
Rubella screening is not routinely performed locally Diagnosis & Evaluation
(as rubella vaccination as part of MMR is part of the - Screening for CMV in pregnancy:
national immunization schedule) Not routinely performed
For patients unsure of immune status (e.g. foreign), - Diagnostic tests for maternal infection:
can offer to test for rubella IgG antibodies to Serologic testing:
determine immune status at booking visit - Demonstrate CMV IgM antibody (peaks at 3-6
- Diagnostic tests for maternal infection: months after infection, resolves by 1-2 years;
Serologic testing: prolonged elevation of IgM levels makes delineation
- Demonstrate presence of rubella IgM antibody of timing of infection difficult)
- Demonstrate 4-fold rise in paired titres of Culture (from urine or other bodily secretions)
rubella antibodies taken 2 weeks apart - Diagnostic tests for fetal infection:
Culture & isolation Ultrasound
- Look for associated fetal anomalies
Management CMV PCR
- No specific treatment for rubella available: - Done on amniocentesis sample
Rubella in the adult (in the mother in this case) is - Offered if ultrasound is inconclusive &
usually a transient illness without significant definitive diagnosis is desired (affects choice of
complications or long-term sequelae management option)
- Rubella immunization
Offered to non-immune mother post-partum (live- Management
attenuated viral vaccine, hence cannot be given during - If ultrasound shows signs of fetal abnormalities or CMV
pregnancy) PCR for CMV is positive:
Can offer hyperimmune anti-CMV globulin
Advise patient on option of termination of
pregnancy

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65
Varicella-Zoster Virus (VZV) Diagnosis & Evaluation
- Diagnostic tests for maternal infection:
Etiology & Transmission Serologic testing:
- Caused by varicella-zoster virus - Demonstrate VZV IgM antibody
Herpesvirus family (HHV3), DNA genome - Demonstrate rise in paired VZV IgG titres
Acute infection causes varicella (chickenpox) taken 2 weeks apart
whereas reactivation causes zoster (shingles) Culture (from vesicular fluid)
- Zoster does not pose significant risks to
mother or child, hence will not be discussed Management
- Transmission: - Management of mother:
Direct contact with vesicular fluid, respiratory route Symptomatic management in uncomplicated cases
Vertical transmission: Chest x-ray should be done to rule out varicella
- Transplacental transmission of varicella results Pneumonitis (if suspected, need admission for close
in one of two possible fetal/neonatal outcomes monitoring& antiviral therapy)
if at all: (i) congenital varicella syndrome (ii) - Management of fetus/neonate:
neonatal varicella Decision to treat depends on:
- Risk of congenital varicella syndrome if: - Immunity of mother after exposure (if immune
<13 weeks gestation = 0.4% status unknown, offer IgG testing; if mother has
13-20 gestation weeks = 2% acute varicella, confirms lack of immunity)
>20 weeks gestation = extremely rare - Time of exposure/infection
Immune mother with exposure at any time:
Clinical Features - No treatment required
- Maternal features: Non-immune mother with exposure/infection
Incubation period of 10-21 days occurring between 13 & 20 weeks gestation:
Primary feature of varicella is a systemic rash: - Offer IV VZIG to patient (best given within 6
- Polymorphous in nature (maculopapular days of exposure)
vesicular crusted), with rashes of different - Role of antiviral treatment is not established
stages seen at the same time - Can do serial ultrasounds to monitor for signs
- Usually affects the trunk > extremities of fetal anomaly (but no reliable method of prenatal
Complications of varicella (more commonly seen in diagnosis for congenital varicella syndrome is
adults than children) currently available) & counsel on option of
- Encephalitis, aseptic meningitis termination of pregnancy where indicated
- Pneumonitis (complicates 16% of cases, with a Non-immune mother with exposure/infection
mortality rate of up to 40%) occurring before 13 weeks or after 20 weeks:
- Fetal features: - Counsel mother on the extremely small risk of
Congenital varicella syndrome the fetus being affected
- Symmetrical IUGR - IV VZIG can still be offered to patient if
- Limb hypoplasia patient still decides to have it
- Cutaneous scars Non-immune mother with exposure/infection
- Chorioretinitis, cataracts occurring between 5 & 21 days prior to delivery:
- Cortical atrophy, microcephaly - Counsel mother that neonate is immune due
Neonatal varicella to transplacental transfer of maternal
- Mild illness if maternal infection occurred 5 to antibodies, hence no need for treatment
21 days prior to delivery (transplacental transfer Non-immune mother with exposure/infection
of maternal antibodies would have occurred, which occurring between 5 days prior to delivery & 2 days
confers effective protection for the neonate) after delivery:
- Fulminant varicella infection if maternal - Administer IV VZIG to neonate
infection occurred between 5 days prior to - Place neonate in contact isolation
delivery & 2 days after delivery (transplacental
transfer of maternal antibodies would not have
occurred)

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66
Herpes Simplex Virus (HSV) Hepatitis B Virus (HBV)

Etiology & Transmission Etiology & Transmission


- Caused by herpes simplex virus - Caused by hepatitis B virus
Herpesvirus family (HHV1 & 2), DNA genome Hepadnavirus, DNA genome
2 serotypes (HSV-1 & HSV-2) - Transmission:
- Transmission: Blood, sexual contact
Intimate mucocutaneous contact Vertical transmission:
Vertical transmission: - Mostly occurs peripartum (hence effectiveness of
- No congenital syndrome due to vertical postpartum passive & active immunization of
transmission of herpes described neonate remains very high)
- Neonatal herpes can occur due to intrauterine
(5%), peripartum (85%) or postnatal (10%) Clinical Features
transmission - Maternal features:
Chronic asymptomatic carrier state
Clinical Features Chronic hepatitis B
- Maternal features: Hepatitis B cirrhosis
Primary genital herpes - Fetal features:
Recurrent genital herpes Effects on pregnancy depends on maternal condition:
See Reproductive Tract Infections - Chronic carriage has no effect on pregnancy
- Fetal features: - Chronic hepatitis B is associated with an
Maternal primary genital herpes is associated with increased risk of preterm labour, low birth
an increased risk of miscarriage, IUGR & preterm weight & neonatal death
labour (minimal risk for recurrent genital herpes) - Hepatitis B cirrhosis carries very poor
Neonatal herpes prognosis for both mother & pregnancy
- Especially high risk if active genital herpetic Acute hepatitis B at birth
lesions (either primary or recurrent) are present - 10% risk if mother is only HBsAg+; 70-90%
during normal vaginal delivery risk if mother if HBsAg+ & HBeAg+
- Symptoms usually present on day 2-3 of life - Acute hepatitis B in the neonate may be
- 3 main manifestations: fulminant & lethal
(i) Disseminated disease Chronic asymptomatic carriage
(ii) CNS disease with encephalitis - Can occur without clinical acute infection or
(iii) Skin, eye or mouth infection with following acute hepatitis B at birth
localized involvement - Much higher risk of chronic carriage in vertical
- Even with treatment, 30-50% of disseminated transmission as compared to adults who are
disease die; 2/3 of survivors have long-term infected by hepatitis B virus
neurologic sequelae (microcephaly, mental
retardation, seizures, microphthalmos) Diagnosis & Evaluation
- Screening for hepatitis B in pregnancy:
Management Offered to all women at booking visit
- Antenatal treatment: - Test for HBsAg & anti-HBS antibody
Antenatal prophylactic antiviral therapy (acyclovir,
valacyclovir) from 36 weeks gestation until delivery Management
- Decreases asymptomatic shedding of virus - For non-immune & uninfected mother:
- Decreases herpes outbreak at delivery Offer vaccination (vaccine is safe for use in pregnancy)
- Decreases need for caesarian delivery - For chronic infection in mother:
For patients with active genital herpetic lesions at the Perform liver function tests & complete hepatitis
time of labour, should be delivered via caesarian panel (including HBeAg level determination)
section Following delivery, administer hepatitis B
- Treatment of neonates with suspected neonatal herpes: immunization to neonate:
IV acyclovir - Passive immunization (HBIG)
- Active immunization (hepatitis B vaccine at 0,
1 & 6 months)
Test for hepatitis B immune status of child at 9
months:
- If immune, no further action
- If not immune but not carrier, readminister
full dose of vaccination (0, 1 & 6 months)
- If not immune but carrier, refer for long-term
follow-up with gastroenterology

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67
Group B Streptococcus (GBS) Syphilis

Etiology & Transmission Etiology & Transmission


- Caused by group B streptococcus - Caused by Treponema pallidum
Gram positive cocci, -hemolytic streptococcus Spirochaete bacteria
Considered part of the normal flora of humans - Transmission:
- Gastrointestinal tract is the major reservoir Sexually-transmitted infection
- Can also be found in vagina, cervix, throat, Vertical transmission
skin, urethra & urine of healthy individuals - Occurs transplacentally at any gestational age
- Transmission: - Risk of transmission is 50-80%
Faecal contamination or sexual transmission from a
colonized partner Clinical Features
Vertical transmission: - Maternal features:
- Occurs during delivery in women with GBS Primary syphilis
colonization in the lower reproductive tract Secondary syphilis
- In absence of preventive efforts, 50% of Tertiary syphilis
neonates born to GBS-colonized mothers will (see Reproductive Tract Infections)
develop GBS carriage as well, of which 2% will - Fetal features:
develop invasive disease (see below) Early congenital syphilis (presents at birth)
- Nonimmune hydrops
Clinical Features - Hepatosplenomegaly, hepatitis
- Maternal features: - Profound anemia, thrombocytopenia
Typically asymptomatic - Skin lesions
Colonization can be episodic/intermittent in nature, - Osteitis, periostitis
hence early & mid trimester cultures are inaccurate - Pneumonia
predictors of GBS carriage at term - 50% perinatal mortality rate
- Fetal features: Late congenital syphilis (presents after 1-2 years)
GBS is the most common cause of early-onset (<72 - Hutchinsons teeth, mulberry molars
hours postpartum) neonatal sepsis: - Sabre shins
- Neonatal sepsis - Saddle nose deformity
- Neonatal meningitis - Interstitial keratitis
- Neonatal pneumonia - Eighth nerve deafness
- Failure to thrive
Diagnosis & Evaluation
- Screening for GBS colonization in pregnancy: Diagnosis & Evaluation
Done using vaginal swab & culture - Screening for syphilis in pregnancy:
Screening for GBS carriage can be offered near term Offered to all women at booking visit
(35-37 weeks gestation) 1st-line screening test would be a non-treponemal
specific test (e.g. VDRL)
Management - Has a false-positive rate of 0.5-14%
- Intrapartum antibiotic prophylaxis (IAP) - Hence diagnostic treponemal specific test is
IV antibiotic (penicillin or ampicillin) given during performed if screening test is positive
intrapartum period for cases with positive GBS - Diagnostic investigations for maternal infection:
carriage diagnosed or high risk cases Non-treponemal specific tests:
High risk cases: - Venereal disease research laboratory (VDRL)
- Preterm labour - Rapid plasma regain (RPR)
- Prolonged rupture of membranes (>18 hours) Treponemal-specific tests:
- Maternal intrapartum fever (>38.0oC) - Fluorescent treponemal antibody absorption
- Previous child with invasive GBS disease test (FTA-Abs)
- GBS bacteriuria in this current pregnancy
IAP is not indicated if: Management
- Planned caesarian delivery without ruptured - Antibiotic treatment:
membranes Penicillin G is treatment of choice
- Risk factors present but GBS culture negative - 2.4 million units IM single dose for primary,
secondary or latent syphilis of <12 months
duration
- Cases with >12 months duration require
weekly IM penicillin G for 3 weeks
- Neurosyphilis requires admission for
prolonged IV penicillin therapy
Monitoring for effectiveness of treatment:
- Monthly VDRL or RPR titres to observe a
downward trend which would indicate
successful treatment
- FTA-Abs will remain positive for life after
infection & hence cannot be used to monitor
response to treatment

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68
Toxoplasmosis

Etiology & Transmission


- Caused by Toxoplasma gondii
Protozoa
- Transmission:
Ingestion of uncooked meat, drinking contaminated
water, exposure to contaminated cat faeces, blood
transfusion containing tachyzoites (rarely)
Vertical transmission:
- Risk of vertical transmission increases with
increasing gestational age:
1st trimester risk = 15%
2nd trimester risk = 25%
3rd trimester risk = 65%
- However, severity of fetal infection decreases
with increasing gestational age (congenital
defects rarely seen if infected after 20 weeks)

Clinical Features
- Maternal features:
Most infections are asymptomatic
Symptomatic cases present as an infectious
mononucleosis-like illness
- Fetal features:
Early congenital toxoplasmosis (presents at birth)
- Chorioretinitis, microphthalmia
- Hydrocephalus, cerebral calcifications,
microcephaly
- Delayed mental development, convulsions
- Rash, lymphadenopathy
- Anemia
- Pneumonia
Late congenital toxoplasmosis (presents later on)
- Visual impairment
- Hearing loss
- Delayed psychomotor development
- Seizure disorders
- Spasticity, palsies
- Mental retardation

Diagnosis & Evaluation


- Screening for toxoplasmosis in pregnancy:
Not routinely performed locally
- Diagnostic investigations for maternal infection:
Serologic tests:
- Demonstrate toxoplasma IgM
- Diagnostic investigations for fetal infection:
Toxoplasma PCR
- Done using amniocentesis sample
- Offered to women with a confirmed diagnosis
of primary toxoplasmosis at 18-20 weeks
gestation

Management
- Treatment of toxoplasmosis:
Toxoplasmosis is usually a self-limiting illness in
adults, hence primary indication for treatment is to
reduce fetal infection risk
Drug options:
- Spiramycin (given to diagnosed maternal
infections without confirmed fetal infection)
- Pyrimethamine + sulphadiazine + folinic acid
(given in cases of confirmed fetal infection)
Treatment of infected infants for 1st year of life is also
recommended as many infected infants may appear
asymptomatic at birth but develop morbidity later

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69
BENIGN GYNAECOLOGIC CONDITIONS
Benign Conditions of the Vulva Lumps & Bumps of the Vulva

Fox-Fordyce Disease
Congenital Anomalies of the Vulva - Series of pruritic, raised, yellowish retention cysts; often
inflamed; resulting from keratin-plugged apocrine glands
Ambiguous Genitalia - Can occur in the labia, mons or axilla
- Possible presentations of ambiguous genitalia:
Clitoromegaly; bifid clitoris Galactocele
Midline fusion of the labioscrotal folds - Milk-containing cysts which can form anywhere along the
- Causes of ambiguous genitalia in females: milk line which extends from the axilla to the vulva
Genetic mosaicism
- Usually seen in pregnant & post-partum women
- Genetic mosaicism, with 2 or more cell
populations present in an individual with
Vulvar Varicosity
different genetic make-up, specifically with
- Dilated vulvar veins; can enlarge & become clinically
respect to the sex chromosomes in this context
apparent (e.g. in pregnancy)
- Commonly 45XO/46XY
- Causes discomfort & carries risk of rupture or thrombosis
- Results in varying degrees of virilization &
Mllerian development
Urethral Caruncle
- Gonads are dysgenetic & should be located &
- Small fleshy red painful growths at distal edge of urethra
surgically removed prophylactically due to
- Seen in extremes of age:
significant risk of eventual neoplastic
Children: spontaneous prolapse of urethral epithelium
transformation (gonadoblastoma, dysgerminoma)
Post-menopausal women: due to hypoestrogenic
Partial androgen insensitivity syndrome
vaginal epithelium contracting; everts urethral epithelium
- An incomplete form of the androgen
insensitivity syndrome, in which a genotypic
Vulvar Vestibulitis (Vulvar Adenitis)
male (46XY) is phenotypically female due to a
- Multiple small (1-4mm) erythematous dots in the
genetic deficiency (usually X-linked recessive)
vestibule which are exceedingly tender when touched
in the androgen receptors
- Due to non-infectious inflammation of the minor
- In the complete form, testes are usually
vestibular glands
undescended, the external genitalia is
- Clinically: severe introital dyspareunia & vulvar pain
phenotypically normal female due to lack of
- Management options:
testosterone effect & no internal genitalia is
Topical estrogen cream
present (Mllerian inhibiting factor secreted
Topical corticosteroids
normally causing Mllerian duct involution; lack of
Surgical excision of affected glandular area
testosterone effect causes Wolffian duct involution)
- In the partial form, varying degrees of
Other Common Cutaneous Lumps & Bumps
responsiveness to testosterone results in
- Sebaceous cyst, lipoma, fibroma, neurofibroma
incomplete virilization of the external genitalia
- In either case, testes should be located &
removed due to significant risk of malignant Traumatic Lesions of the Vulva
transformation in undescended testes
Congenital adrenal hyperplasia (CAH) Blunt Trauma to the Vulva
- A group of autosomal recessive disorders - Commonly results from saddle injuries, motor vehicle
involving enzyme deficiencies in the production accidents or sexual assault
of steroidal hormones (cortisol & aldosterone) - Results in vulvar bruising, lacerations or hematomas
- Most common: 21-hydroxylase - Hematomas should be monitored closely & managed with
- Others: 11-hydroxylase, 17 -hydroxylase, surgical exploration & drainage (as blood loss can be
aldosterone synthetase, 20,22-desmolase extensive, tracking deep into large potential spaces such as the
- Different mutations in the same gene can ischiorectal fossae)
result in a spectrum of phenotypes clinically
unapparent, mild form which only presents in Female Genital Mutilation (Female Circumcision)
adolescence or adulthood (late-onset CAH) or - Continues to be a common practice in certain countries
severe disease that results in adrenal - WHO classification of female genital mutilation (2008):
insufficiency in infancy Type I: partial or total removal of the clitoris &/or
- Enzyme deficiencies can cause build-up of prepuce (clitoridectomy)
upstream intermediate precursors of cortisol Type II: partial or total removal of the clitoris & labia
&/or aldosterone which then get shunted minora, with or without excision of the labia majora
towards the production of adrenal androgens Type III: narrowing of the vaginal orifice with creation of
- Hyperandrogenism in turn causes virilization a covering seal by cutting & appositioning the labia
of the external genitalia (severe forms present at minora &/or the labia majora, with or without excision of
birth; mild forms may cause signs & symptoms of the clitoris (infibulation)
virilization in adolescence & adulthood) Type IV: all other harmful procedures to the female
Androgen-producing tumour; exogenous androgen genitalia for nonmedical purposes

BENIGN GYNAECOLOGIC CONDITIONS

70
Epithelial Conditions of the Vulva Benign Conditions of the Vagina
Lichen Simplex Chronicus
- Squamous cell hyperplasia which results from a Congenital Anomalies of the Vagina
prolonged itch-scratch cycle
- Clinically: pruritus & pain; examination reveals a white or Canalization Defects of the Vagina
reddish, thickened, leathery & raised surface - Imperforate hymen
- Histologically: thick keratin layer (hyperkeratosis) with Occurs at the site where the vaginal plate contacts
deepened rete ridges & a dense infiltrate of chronic the urogenital sinus
inflammatory cells in the superficial dermis Presents with primary amenorrhea associated with
- Treatment: cyclical pelvic pain (due to menstrual blood pooling up
Moderate-strength steroid ointments proximal to the imperforate hymen)
Anti-pruritic agents Hematocolpos results (old blood within vagina)
Treatment: cruciate incision of hymen
Lichen Sclerosis - Transverse vaginal septum
- Idiopathic epithelial condition more commonly Similar anomaly as imperforate hymen
presenting in the elderly; can involve any body part, but Usually found at the junction between the upper &
usually found on the vulva of the menopausal woman middle thirds of the vagina
- Clinically: intense pruritus, burning pain & dyspareunia; - Vaginal atresia
examination reveals skin that is thin, inelastic, white & crinkled Represents a more substantial lack of canalization at
(tissue paper appearance) either the cranial or caudal end of the vaginal plate
- Histologically: thin epithelium with loss of rete ridges & Cranially-placed vaginal atresia usually also have an
inflammatory cells lining the basement membrane absent cervix but with normal uterus & fallopian
- Long-term sequelae if left untreated: tubes present
Labia minora lost, labia majora flattened, introitus - Double vagina (longitudinal vaginal septum)
severely constricted, clitoris inverted & trapped Many variants:
Development of vulvar intraepithelial neoplasia - Septum may be partially present at various
(VIN) & eventual vulvar cancer levels in the upper & middle vagina or
- Treatment: throughout
Potent topical steroids (0.05% clobetasol) - Septum may be midline or deviated to a side
Topical emollients - Septum may deviate & attach to the lateral
vaginal wall, creating a blind vaginal pouch
Vulvar Involvement in Other Systemic Disorders May be associated with duplication anomalies of the
- Lichen planus upper tract
Presents as purplish polygonal papules that may
appear in erosive forms Vaginal Agenesis
May involve vulva, vagina & mouth (vulvar- - Most extreme form of congenital vaginal anomalies
vaginal-gingival syndrome) Total absence of the vagina except for the most distal
- Psoriasis portion that is embryologically derived from the
Appears velvety on the vulva, often without the urogenital sinus
usual scaly patches seen in other affected areas - May occur in isolation (rare) or in association with
- Pemphigus congenital absence of the uterus & underdevelopment of
Autoimmune blistering condition that can involve the fallopian tubes Mllerian agenesis (Rokitansky-
the vulvovaginal & conjunctival areas Kster-Hauser syndrome)
- Behets disease
Classically involves ulcers of the genitalia & oral Adenosis of the Vaginal Wall
cavity with superficial ocular lesions - Islands of columnar epithelium in the normal squamous
- Crohn disease epithelium of the vagina
Vulvar ulcers can occur as an extra-gastrointestinal - Often in the upper third
manifestation of Crohn disease - One of many associations of in-utero exposure to
Draining sinuses to the rectum may also occur diethylstilbestrol (DES):
Vaginal adenosis
Structural anomalies of the cervix & vagina
- Transverse vaginal septum
- Cervical collar
- Cockscomb (raised ridge on anterior cervix)
- Cervical hypoplasia
Structural anomalies of the uterus
- T-shaped uterus with small uterine cavity
Clear cell adenocarcinoma of the vagina

Gartners Duct Cyst


- Most common dysontogenic cyst of the vagina (thick-
walled soft cysts resulting from embryonic remnants)
- Arises from remnant of the mesonephros (Wolffian duct)
- 1-5cm in size, found in the anterolateral walls of the upper
vagina & more laterally in the lower vagina

BENIGN GYNAECOLOGIC CONDITIONS

71
Lumps & Bumps of the Vagina Benign Conditions of the Cervix
Urethral Diverticula
- Small (0.3-3cm) sac-like projections found in the anterior Structural Conditions of the Cervix
vagina along the course of the urethra
- Clinically: recurrent urinary tract infections, dysuria, Nabothian Cysts
dyspareunia, urinary dribbling - Common condition resulting from squamous metaplasia:
- Treatment: A layer of superficial squamous epithelium entraps
Urethral dilation an invagination of columnar cells beneath it
Surgical excision Underlying columnar cells continue to secrete
mucus, hence a mucous retention cyst is formed
Vaginal Inclusion Cysts
- Common lesions resulting from the infolding of vaginal Cervical Ectropion (Cervical Erosion)
epithelium, usually located in the posterior or lateral wall - Normal developmental changes in cervical appearance:
of the lower third of the vagina At birth, the cervix comprises columnar epithelium
- Most commonly associated with lacerations from (lining the endocervical canal) & squamous epithelium
childbirth or gynaecologic surgery (lining the ectocervix)
At puberty, under the influence of estrogen, the
Bartholins Cyst endocervical canal undergoes a degree of eversion,
- Cyst arising from the Bartholins glands of the vagina exposing the lower part of the columnar epithelium
- Clinical presentation: Acidification of the vagina at puberty squamous
Asymptomatic swelling seen in the posterolateral metaplasia of the exposed columnar epithelium
aspect of the introitus Hence cervical ectropion represents an area of
If infected, may become a large painful inflammatory columnar epithelium that has yet to undergo
mass squamous metaplasia
- Treatment: - Clinical features:
Small asymptomatic cysts can be left alone Increased vaginal secretions
Large symptomatic non-infected cysts can be Post-coital spotting/bleeding
marsupialized - Treatment:
Infected cysts can be treated by inserted an inflatable None needed once other etiologies (especially
cervical neoplasia) ruled out with Pap smear
bulb-tipped catheter (Word catheter) through a small
stab incision into the mass & left in place for 4-6
weeks to form an epithelialized fistula tract which Cervical Polyps
will remain open for drainage - Types of cervical polyps:
Endocervical polyps (beefy red, arise from endocervical
In women >40 years old, careful examination of the
canal on a long pedunculated stalk)
base of the cyst needed to exclude an underlying
Ectocervical polyps (less common, pale, arise from the
Bartholins gland carcinoma
ectocervix to form a broad-based protrusion)
- Clinical features:
Endometriosis
Asymptomatic
- Endometriotic deposits on the vagina (usually upper
Symptomatic polyps: menorrhagia, post-coital bleeding
third) appear as steel-gray or black cysts that may bleed
- Management:
slightly at the time of menstruation
Narrow based polyps: twist polyp off its base
Broad based polyps: excised with electrocautery
Pelvic Organ Prolapse
All specimens should be sent for histological
(see Urogynaecology for more details)
examination to rule out cancer
- Anterior vaginal prolapse (cystocele)
- Posterior vaginal prolapse (rectocele, enterocele)
- Apical vaginal & uterine prolapse Functional Conditions of the Cervix

Cervical Stenosis
- Causes of cervical stenosis:
Trauma (dilatation & curettage, LLETZ, cone biopsy)
Hypoestrogenism (menopause, prolonged DMPA)
- Clinical features & consequences:
Hematometra (as blood is unable to escape)
Subfertility (as sperm is unable to pass through cervix)
Cervical dystocia (difficult labour due to stenosed cervix)

Cervical Incompetence
- Causes of cervical incompetence:
Intrinsic (poor ground substance in cervix)
In-utero diethylstilbestrol exposure leading to
cervical hypoplasia
Cervical surgery (LLETZ, cone biopsy)
- Clinical features & consequences:
Increased risk of early pregnancy loss
Increased risk of premature labour

BENIGN GYNAECOLOGIC CONDITIONS

72
Benign Conditions of the Uterine Corpus Uterine Leiomyoma (Fibroid)

Pathophysiology of Fibroids
Congenital Anomalies of the Uterus & Cervix - Pathology of fibroids:
In the absence of Mllerian inhibiting factor without a Y chromosome, Benign proliferation of a single clone of smooth
the Mllerian ducts develop; Mllerian ducts first appear at 6 weeks muscle cells within the myometrium of the uterus
gestation lateral to the cranial pole of the Wolffian ducts & expand Grossly: spherical, well-circumscribed, white, firm lesions
caudally; by 9-10 weeks, they fuse in the midline at the urogenital with a whorled appearance on cut surface
septum to form the uterovaginal primordium; subsequent dissolution of Compressed smooth muscle cells on the tumours
the septum leads to the development of a single uterus & cervix
periphery forms a pseudocapsule
Few blood vessels traverse the pseudocapsule, hence
Incomplete Fusion of the Mllerian Ducts
degenerative changes occur as the tumour enlarges:
- Uterus didelphys
- Hyaline acellularity (replacement of fibrous &
Complete failure of fusion of Mllerian ducts
smooth muscle tissues with hyaline tissue)
2 separate uterine bodies, each with its own cervix &
- Cystic degenerations (breakdown of hyaline
attached fallopian tube & vagina
substance with further reduction in blood supply)
- Bicornuate uterus with rudimentary horn
- Calcification of degenerated fibroids may
2 cornua present, but fusion failure results in 1 of
occur (particularly after menopause)
them remaining underdeveloped
- Fatty degeneration (uncommon)
- Bicornuate uterus
- Red degeneration (painful condition resulting
Single uterine cavity fused at the caudal end but
from hemorrhage into the tumour, usually occurring
incompletely fused at cranial end
during pregnancy)
May be with a single or double cervix
- Hormonal influence on fibroids:
Fibroids have increased numbers of estrogen &
Incomplete Dissolution of Midline Fusion of the Ducts
progesterone receptors compared to normal smooth
- Septate uterus
muscle cells of the uterus:
Complete fusion of Mllerian ducts but incomplete
- Estrogen stimulates smooth muscle cell
dissolution of the septum to a varying extent
proliferation
- Progesterone induces increased production of
Failure of Formation
cellular proteins which interfere with apoptosis
- Unicornuate uterus
Fibroid growth hence reflects hormonal changes in a
Failure of formation & development of 1 of the 2
womans reproductive life:
Mllerian ducts
- Usually only appear after menarche
- Mllerian agenesis (Rokitansky-Kster-Hauser syndrome)
- Ceases to enlarge & tends to decrease in size
Failure of complete development of both Mllerian
after menopause
ducts, resulting in incomplete fallopian tube
- Rapid increase in size may occur in pregnancy,
development with absent uterus, cervix & most of
& use of clomiphene, which may be
the vagina
complicated by red degeneration
- Classification of fibroids by location:
Diethylstilbestrol (DES) Associated Anomalies
Intramural fibroids
- T-shaped uterus
Submucosal fibroids
- Cervical collar deformity
- Beneath the endometrial surface
- If pedunculated, can abort through the
endocervical canal, causing cramping pain
- Distortion of endometrial surface may cause
abnormal uterine bleeding
Subserosal fibroids
- Beneath the serosal surface of the uterus
Uterus didelphys Bicornuate uterus with Bicornuate uterus
- If pedunculated, can be complicated by torsion
rudimentary horn with single cervix
Parasitic fibroids
- Rare situation where a pedunculated
subserosal fibroid attaches to the vascular
supply of omentum or bowel mesentery &
subsequently loses its uterine connection

Septate uterus Unicornuate uterus T-shaped uterus

Mllerian agenesis Cervical collar deformity

BENIGN GYNAECOLOGIC CONDITIONS

73
Clinical Features Investigations
- Asymptomatic (investigations are usually tailored according to the presentation;
Most fibroids are asymptomatic being benign & usually asymptomatic, differentials for each
May be incidentally picked up on imaging presentation need to be ruled out first before it is appropriate to
- Mass effect presume that any fibroid(s) found is responsible for the symptoms)
Bloating, early satiety - Pelvic ultrasound
Sense of heaviness in the lower abdomen Most useful modality for visualizing fibroid(s),
Dull back ache/pain determining their location & size
Urinary symptoms: frequency; rarely if fibroid is big Also useful for diagnosing common differentials for
enough, may cause urinary retention & even a abdominopelvic or pelvic mass:
hydronephrosis - Adenomyosis/adenomyoma
- Abnormal uterine bleeding (AUB) - Ovarian cysts/adnexal masses
Usually occurs in cases of submucosal & large
intramural fibroids which distort the endometrium Management of Fibroids
Any abnormal uterine bleeding that results is usually (incidentally detected asymptomatic fibroids do not need treatment;
heavy (menorrhagia) or prolonged, which may be treatment of symptomatic fibroids should be tailored according to the
accompanied by symptoms of anemia if prolonged presentation as well as the specific patients context e.g. desire for
Irregularity of cycles & intermenstrual bleeding do future fertility)
not classically occur - Medical management of fibroids
Note: bleeding cause by fibroids is dependent on the 1st line management for AUB due to fibroids
presence of menstruation, hence fibroids are not classically Options available:
considered a cause of post-menopausal bleed - Tranexamic acid (anti-fibrinolytic)
- Acute abdominal/pelvic pain - Mefenamic acid aka Ponstan (NSAID)
Fibroids are usually not painful - Hormonal (combined oral contraceptive pill,
Acute pain can arise from fibroids in certain progestin-only therapies like POPs or Mirena)
uncommon situations: - GnRH agonists (helps halt endometrial
- Red degeneration (usually during pregnancy) proliferation & can sometimes even reduce fibroid
- Torsion of pedunculated subserosal fibroid size; not routinely used due to high costs &
- Effects on fertility & pregnancy deleterious effects on bone mineral density &
Negative effects usually due to submucosal or large vasomotor symptoms)
intramural fibroids which distorts the uterine cavity: - Surgical management of fibroids
- Subfertility (due to placentation challenges posed) (for failed medical treatment of AUB or for mass symptoms)
- Early pregnancy loss Myomectomy
- Malpresentation (fibroid mass in the lower uterus - Surgical excision of fibroid
may hinder cephalic presentation) - Can be done via laparoscopy, laparotomy or
even hysteroscopy (for submucosal fibroids)
Physical Examination - Pros: good option for patients desiring uterine
- General examination preservation or desiring future fertility (but if
Assess patients vitals & look for pallor endometrial cavity is entered during the time of
Look for signs of malignancy (uterine & ovarian myomectomy, future deliveries need to be via elective
malignancies are potential differentials): caesarian due to significant risk of uterine rupture)
- Supraclavicular lymphadenopathy - Cons: fibroids can recur in myometrium
- Pleural effusion Uterine artery embolization
- Abdominal examination - Interventional radiology procedure where
Palpate for any abdominopelvic mass (large fibroid uterine artery is accessed & embolized via a
resulting in a uterus bigger than a 12-week size may be transcutaneous femoral approach
palpable in the lower abdomen) - Occludes blood supply of fibroids, causing
Look for signs of malignancy (uterine & ovarian them to shrink by 40-60% in size (uterus still
malignancies are potential differentials): receives sufficient blood supply from collaterals)
- Hepatomegaly, ascites - Pros: good option for patients desiring uterine
- Pelvic examination preservation or desiring future fertility
Speculum examination: - Cons: future pregnancies may be at higher risk
- Visualize cervix & take a Pap smear to rule out Endometrial ablation
cervical pathology - Hysteroscopic procedure where endometrial
Digital vaginal examination: lining is destroyed, thereby treating abnormal
- Test for cervical excitation (if present, may be uterine bleeding (~70% effective)
indicative of PID with a tubo-ovarian abscess as a - Option for patients desiring uterine
differential in this context) preservation but not fertility
Bimanual palpation: Hysterectomy
- Assess uterine size & surface (may be enlarged - Provides definitive treatment for fibroids (no
with bosselated protrusions if fibroids are intramural more abnormal uterine bleeding, no risk of
or subserosal) recurrence of fibroids)
- Assess mobility of any uterine or adnexal mass - Transvaginal or transabdominal can be done
felt while simultaneously assessing whether (but latter needed if subtotal hysterectomy desired)
cervix moves (if both move together, mass is - Concomitant bilateral salpingo-oophorectomy
attached to uterus; if not, may still be a fibroid which can be offered for post-menopausal women
is pedunculated) (negates risk for future development of ovarian CA)

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74
Endometrial Conditions Adenomyosis
- Condition defined by the extension of endometrial glands
Endometrial Polyps & stroma into the uterine musculature (myometrium)
- Benign condition where polyps arising from the >2.5mm beneath the basalis layer of the endometrium
endometrium protrude into the uterine cavity - Pathology of adenomyosis:
- Clinical features: Grossly: diffuse uterine enlargement (globular uterus)
Asymptomatic with accompanying thickened myometrium containing
Abnormal uterine bleeding (menorrhagia, prolonged glandular irregularities with implants containing
menstruation) endometrial tissue
- Investigations & management: Histologically: normal endometrial glands & stroma
Pelvic ultrasound (visualizes endometrial polyps as a extending into the myometrium
focal thickening of the endometrial stripe) In some cases, the adenomyosis may be more
Biopsy of polyp via endometrial sampling or pronounced in a focal region of the myometrium,
dilatation & curettage (may miss polyp though if they forming an adenomyoma (resembling a fibroid)
are too large to be aspirated through the sampling orifice - Clinical features:
or are flexible enough to fold out of the path of the curette) Abnormal uterine bleeding (usually menorrhagia;
Hysteroscopy may be indicated to visualize the should not cause post-menopausal bleeding as it usually
polyp & allow an excision of the polyp for regresses after menopause)
histological assessment (curative + allows exclusion of Secondary dysmenorrhea (usually severe)
underlying malignancy) Deep-thrust dyspareunia (especially during
premenstrual period)
Endometrial Hyperplasia Physical examination findings:
- Overabundant growth & proliferation of the - Diffusely enlarged uterus
endometrium resulting from prolonged unopposed - Adenomyoma may cause asymmetrical
estrogen stimulation: enlargement of the uterus, making it difficult to
Extremes of reproductive age where anovulation is differentiate from fibroids (but significant feature
common (initial post-menarche; peri-menopausal) of severe dysmenorrhea usually makes adenomyosis
Polycystic ovary syndrome (chronic anovulation) more likely as fibroids are classically painless)
Obesity (increased extra-ovarian aromatization of - Investigations
circulating adrenal androstenedione into estrone) Pelvic ultrasound
Granulosa-theca cell tumours (estrogen-producing) - Reveals a poorly defined endomyometrial
Prolonged use of estrogen-only hormonal therapy junction with thickened myometrium featuring
Chronic tamoxifen use (selective estrogen modulator a heterogeneous echotexture
that is agonistic on endometrial tissue) - Adenomyomata may appear similar to
- Clinical features: fibroids on ultrasound
Asymptomatic MRI pelvis
Abnormal uterine bleeding (menorrhagia, prolonged - Greater sensitivity in definitive diagnosis of an
menstruation; any associated menstrual irregularity is adenomyomata
usually due to the underlying cause) Endometrial biopsy
- Investigations: - May be indicated in the setting of a clinical
Pelvic ultrasound presentation of abnormal uterine bleeding in
- Used to measure the endometrial thickness older women to rule out endometrial
- >5mm is considered suspicious for hyperplasia &/or cancer
endometrial hyperplasia or even cancer (most - Management of adenomyosis:
useful post-menopausally; pre-menopausally, it may Medical management:
be confounded by the time of the menstrual cycle the - Tranexamic acid (anti-fibrinolytic)
women was in at the time of ultrasound, hence - Mefenamic acid aka Ponstan (NSAID; helps
biopsy is usually only indicated if woman is older) with both the bleeding & the dysmenorrhea)
Endometrial biopsy - Hormonal (combined oral contraceptive pill,
- Can be done via endometrial sampling &/or progestin-only therapies)
dilatation & curettage hysteroscopy Surgical management:
- Indicated as a follow-up to pelvic ultrasound (indicated when refractory to medical management)
finding suspicious of endometrial hyperplasia - Endometrial ablation
to rule out any underlying dysplasia or cancer - Hysterectomy
(see Endometrial Cancer for algorithm for
endometrial evaluation)
- Possible results: normal endometrium; simple
hyperplasia; complex hyperplasia without atypia;
complex hyperplasia with atypia; endometrial cancer
- Management of endometrial hyperplasia:
Simple hyperplasia: progestins (10d/month x3 months)
Complex hyperplasia without atypia: evaluate with
D&C to rule out underlying malignancy; treat with
progestins (daily for 3-6 months)
Complex hyperplasia with atypia: evaluate with D&C
to rule out underlying malignancy; consider hysterectomy
to negate future risk of malignancy Adenomyosis

BENIGN GYNAECOLOGIC CONDITIONS

75
Asherman Syndrome Developmental Stages of Endometriosis
- Condition in which the endometrium is denuded with the - Vesicular stage
uterine cavity filled with adhesions (synechiae) 1st stage, where endometriotic implant appears as a
- Causes of Asherman syndrome: discrete vesicle
Endometrial curettage (especially in high-risk settings Mean age = 21.5 years
such as treatment of post-partum hemorrhage or septic - Red nodular stage
abortion) 2nd stage, where endometriotic implant appears red
Endometrial ablation (endometrial denudation in this due to accumulation of hemosiderin from cycles of
case is intended) bleeding during menstruation
- Clinical features: Mean age = 26.3 years
Oligomenorrhea or amenorrhea - Blue nodular stage
Subfertility 3rd stage, where endometriotic implant appears
dusky & bluish due to old blood seen through a layer
Endometriosis of fibrosis
Benign condition in which endometrial glands & stroma are present Mean age = 29.5 years
outside the uterine cavity & walls - Fibrotic stage
Final stage, where dense fibrosis predominates at site
Epidemiology & Associations of original endometriotic implant
- About 1 in 6 women have clinical endometriosis (probably Mean age = 31.9 years
more have subclinical endometriosis which may be incidentally
found on gynaecologic laparotomies) Sites of Occurrence of Endometriosis
- Proportion of endometriosis is higher in women with
chronic gynaecologic conditions:
One third of women with chronic pelvic pain
Half of women with subfertility

Pathophysiology of Endometriosis
(3 main hypotheses for its pathogenesis present)
- Retrograde menstruation theory (Sampson)
Proposes that fragments of endometrial tissue is
transported through the fallopian tubes at the time of
menstruation which subsequently implant & grow
on various intra-abdominal sites; hematogenous
spread further accounts for deposits found in extra-
abdominal sites
Features supporting this theory:
- Endometriotic implants tends to be in gravity - Ovarian involvement is the most common (2 in 3)
dependent sites in the pelvis (e.g. pouch of Endometriotic implants initially on the mesothelial
Douglas) surface of the ovary
- High prevalence of endometriosis in patients Subsequently invaginates into stroma of ovary
with congenital genital outflow tract facilitated by cyclical bleeding
obstructions (e.g. transverse vaginal septum) Forms endometriotic cysts (chocolate cysts)
- Studies have demonstrated an association with - Peripheral sites not mentioned in above diagram:
uterotubal hypotonia (possibly leading to lack of Laparotomy scars (especially after caesarian delivery or
effective tubal opening occlusion during myomectomy where the endometrial cavity is entered;
menstruation, allowing endometrial fragments to probably due to seeding of endometrial tissue in the
enter the tubes & be propagated into the peritoneal surgical incision)
cavity) Distant sites (e.g. lungs can present with cyclical
Further augmentations to this theory (attempts to hemoptysis)
explain why endometriosis does not occur in every woman
with retrograde menstruation):
- Differences in chemical & biologic pathways
(reduced apoptosis, altered cell polarization &
adhesion, increased angiogenesis, altered oncogene
expression)
- Differences in immunologic responses in the
pelvis (altered macrophage function, decreased T-
killer cell & natural killer cell function)
- Mllerian metaplasia theory (Meyer)
Proposes that metaplastic transformation of the
peritoneal mesothelium into endometrium occurs
under the influence of certain generally unidentified
stimuli
- Lymphatic spread theory (Halban)
Proposes that endometrial tissues can be taken by
lymphatics draining the uterus & subsequently
transported to various pelvic & extra-pelvic sites

BENIGN GYNAECOLOGIC CONDITIONS

76
Clinical Features of Endometriosis Classification System for Endometriosis
- Asymptomatic
- Dysmenorrhea
Initially cyclical, beginning 1-2 days before
menstruation & lasting till the end of the menses (due
to intense inflammatory reaction induced by the
premenstrual swelling & subsequent extravasation of
blood & debris when endometriotic implants shed)
Over time, chronic pelvic pain may predominate (due
to chronic inflammation established), with exacerbations
at the time of menstruation each month
- Dyspareunia
Usually deep-thrust dyspareunia, occurring when
the uterosacral ligaments, pouch of Douglas &
posterior vaginal fornix are involved
- Dyschezia
Pain occurring during defaecation
Occurs with uterosacral ligament, pouch of Douglas
& rectosigmoid colon involvement
- Other presentations:
Cyclical bleeding from organ involved (menstrual
hematuria, hematochezia, hemoptysis etc)
Subfertility (due to distortion of pelvic structures from
extensive fibrosis)
Abnormal uterine bleeding (e.g. menorrhagia) does
not usually occur in endometriosis as the bleeding
from the ectopic endometrial tissue occurs in extra-
uterine sites
- Physical examination findings:
Tender pelvic nodules
- Uterosacral nodules
- Pouch of Douglas nodules
- Tender nodule/mulberry-like spot may be
seen in the posterior fornix of the vagina
Adnexal mass, which may be fixed & tender (due to
endometriotic cyst/endometriomas of the ovary or
endometrial implants on the other adnexal structures)

Investigations
(endometriosis is generally presumptively diagnosed on clinical
grounds with a history & physical examination findings suggestive of
it; any investigation performed is limited for its confirmation but - 4 stages (I to IV) of endometriosis based on sites involved
should be done to rule out important differentials) & extent of visualized disease
- Non-radiological investigations: - However, there is poor clinical correlation between this
Urine pregnancy test (to rule out ectopic pregnancy) staging system & the actual manifestation of
Serum CA-125 (levels are usually raised in endometriosis in the patient (in terms of fertility & pain),
endometriosis, typically in the range of 50-100 U/ml; hence this staging system is not routinely used
positive predictive value is poor however & hence should
not be used for the diagnosis of endometriosis)
- Pelvic ultrasound
Only diagnostic of endometriosis when an
endometriotic cyst of the ovary is present
Useful for ruling out other pelvic differentials of
endometriosis:
- Ectopic pregnancy
- Tubo-ovarian abscess in chronic PID
- Hemorrhagic corpus luteum
- Other ovarian cysts/masses

BENIGN GYNAECOLOGIC CONDITIONS

77
Management of Endometriosis Dienogest (Visanne)
- Basic principles in managing endometriosis: - Orally-active semi-synthetic progestin; differs
Choice of management options depends on: from conventional progestins in that it has anti-
- Certainty of the diagnosis on clinical grounds androgenic effects
- Severity of the symptoms - Studies have shown that it is as effective as
- Extent of the disease GnRH agonists for treating endometriosis, but
- Patients age & desire for future fertility without the hypoestrogenic side effects of
All three main approaches (medical treatment alone, GnRH agonists
surgical treatment alone & medical + surgical treatment) - Hence currently the 2nd-line treatment of
have been shown to be superior to placebo in choice (over Danazol & GnRH agonists)
treating endometriosis, with no difference in pain - Side effects (similar to those for most
scores at 6 months between the three approaches progestins except that it has no androgenic side-
Hence choice of which method to employ depends effects): nausea, weight gain, increased blood
largely on the treatment objectives & patients pressure
unique circumstances: - Surgical management of endometriosis:
- Medical management generally 1st-line (within Fertility-preserving surgery (ablative + excisional)
which there are 1st & 2nd line agents to be tried) - Can be done via laparoscopy or laparotomy
- Surgical management indicated if symptoms - Removal of all adhesions & destruction of all
refractory to medical treatment visible implants
- Surgery (fertility-preserving procedures - Endometriomas >3cm should be excised
specifically) may also be beneficial if (occasionally, adhesions surrounded endometrioma
endometriosis is suspected to be a contributing may preclude feasible cystectomy, hence
factor to subfertility oophorectomy may be required)
- Medical management of endometriosis: Total hysterectomy + bilateral salpingo-
NSAIDs (e.g. mefenamic acid aka Ponstan) oophorectomy (THBSO)
- 1st-line treatment alongside hormonal therapy - Definitive surgical treatment for
options for relief of pain in endometriosis endometriosis, usually done in combination
Hormonal therapy with concomitant ablative procedures of all
- Oral contraceptives & low-dose progestins are visible implants & adhesions
useful 1st-line treatment for pain in - Complications: bowel & urinary system injury;
endometriosis, helping induce a variable abrupt menopausal effects if patient is pre-
amount of regression in the disease (curious menopausal (severe hot flushes, loss of libido,
feature of endometriosis in that it grows with decreased bone mineral density)
cyclical physiologic hormonal exposure but tends to - Need for hormone replacement therapy with
regress with continuous hormonal exposure, estrogen-only therapy if patient is pre-
especially in higher doses) menopausal
- High dose progestins can be used as 2nd-line - There is still a 20% recurrence rate of
treatment as well endometriosis with this procedure, usually
- Mirena (Levonorgestrel-releasing intrauterine involving the bowel
system) is also a good long-term option Adjunctive medical therapy:
Danazol (17-ethinyl testosterone) - Pre-operative medical therapy (e.g. with
- Derivative of ethisterone (a synthetically GnRH agonists) for 3-6 months can improve
modified testosterone) surgical success (helps induce some regression of
- 1st drug specifically licensed in 1970s for the the disease to make surgical intervention easier)
treatment of endometriosis; currently a 2nd-line - Post-operative long-term hormonal therapy
option alongside GnRH agonists for treatment (e.g. Depo-Provera, continuous oral contraceptives,
of endometriosis refractory to 1st-line therapy Mirena) helps reduce risk of post-surgical
- Physiologically induces a pseudomenopause, recurrence of endometriosis
suppressing menstruation & hence helping
suppress the growth & symptoms of
endometriosis as well
- Side effects: hirsutism, acne
GnRH agonist (+ estrogen add-back)
- Options: leuprolide, goserelin
- 2nd-line treatment for endometriosis
- Mechanism of action: continuous steady levels of
GnRH initially causes surge in gonadotropins (flare
effect); subsequently leads to desensitization due to Ruptured endometrioma
internalization of pituitary GnRH receptors, in turn
resulting in decreased gonadotropin production,
causing a temporary medically-induced menopausal
state which relieves pain & brings about regression
of endometriosis
- Side effects: hot flushes, decreased bone mineral
density, worsened lipid profile (+ very expensive)
- Low-dose estrogen & progestin add-back
helps mitigate some of the side-effects, thereby Implant on uterosacral ligament Endometriosis in right paracolic gutter
permitting longer use of GnRH agonists

BENIGN GYNAECOLOGIC CONDITIONS

78
Benign Conditions of the Fallopian Tube Benign Conditions of the Ovary
Congenital Anomalies of the Fallopian Tube Congenital Anomalies of the Ovary

Sporadic Anomalies of the Fallopian Tubes Non-Chromosomal-Related Anomalies


- Aplasia or atresia (usually of the distal ampullary segment) - Congenital duplication of ovaries
- Duplication (complete duplication rare; distal duplication or - Congenital absence (agenesis) of ovaries
accessory ostia relatively common) - Ectopic ovaries
- Ovotestis (occurs when bipotentiality noted in embryological
Diethylstilbestrol (DES) Associated Anomalies development progresses without the usual regression of one
- Shortened fallopian tubes system)
- Distorted fallopian tubes
- Clubbed fallopian tubes Chromosomal-Related Anomalies
- Turner syndrome (45XO)
Structural Conditions of the Fallopian Tube Rudimentary streaked ovaries
Women with turner syndrome usually still progress
Hydrosalpinx & Pyosalpinx through puberty & develop secondary sexual
- Enlarged fallopian tube secondary to blockage of the characteristics but subsequently enter menopause
fimbrial end of the tube due to tubal inflammation shortly thereafter
Hydrosalpinx = fluid filled
Pyosalpinx = pus-filled Benign Ovarian Cysts
- Sequelae of pelvic inflammatory disease; common causes:
Chlamydia trachomatis Non-Neoplastic Ovarian Cysts
Neisseria gonorrheae - Cysts of mesothelial origin
- Actinomycosis of the fallopian tubes: Germinal inclusion cysts
Filamentous branched clubbed organism - Formed by the invagination of ovarian surface
Gram positive, non-acid fast mesothelium into the cortex or stroma of the ovary
Associated with intrauterine device use (36%) - Cystic enlargement occurs from accumulation of
serous fluid secreted by the mesothelium
- No association with epithelial ovarian cancer
- Cysts of follicular origin (functional cysts)
Follicular cysts
- Develop from partially-developed follicles that
undergo atresia
- Mostly physiological; extremely common
- Usually undergoes spontaneous regression
Corpus luteal cysts
- Develops after corpus luteal hematoma is formed
Salpingitis Isthmica Nodosa following ovulation
- Idiopathic condition usually seen in young women - Lined by luteinized granulosa cells with a deeper
- Diverticulae of the fallopian tube which communicate layer of theca cells
with the lumen results in nodular swellings of the tube - Persistence leads to continued secretion of
- Bilateral in 80% of cases progesterone which clinically results in delayed
- Clinical consequences: subfertility, ectopic pregnancy menstruation
- May rarely rupture; if it does, classically
associated with massive intraperitoneal hemorrhage
Theca lutein cysts
- Formed as a result of intensely luteinized theca
interna cells occurring when the corpus luteum
comes under the influence of high levels of hCG
- Usually small, but may be large & multiple as well
- Associated with multiple gestations, molar
pregnancies & patients on gonadotropin treatment
(ovarian hyperstimulation syndrome)
Polycystic ovary syndrome
- Multiple eccentrically-placed follicular cysts within
Benign Neoplasms of the Fallopian Tube the ovary, as a result of chronic anovulation
(relatively rare compared to the other parts of the female genital tract) - See Polycystic Ovary Syndrome
- Tubal neoplasms - Cysts of inflammatory conditions
Epithelial adenomas/polyps Tubo-ovarian abscess
Myomas - Abscess resulting from pelvic inflammatory disease
Angiomas Endometriotic cysts (endometrioma; chocolate cysts)
Inclusion cysts (from mesothelium) - Ovarian cysts enclosing stale/old blood
- Paratubal (paraovarian) neoplasms - Result from endometriotic implant on ovary
Hydatids of Morgagni (paratubal cysts derived from (initially on surface; subsequently invaginates into
remnants of the Mllerian duct) stroma with repeated cyclical bleeding)
Neoplasms derived from Wolffian remnants

BENIGN GYNAECOLOGIC CONDITIONS

79
GYNAECOLOGIC BLEEDING & PAIN
Normal Menstrual Cycle - Ovary
Ovaries contain a finite number of follicles, each
containing an oocyte, from birth:
Hypothalamic-Pituitary-Ovarian (HPO) Axis - At 8-10 weeks of fetal development, oocytes
- Hypothalamus get surrounded by precursor granulosa cells
Gonadotropin-releasing hormone (GnRH) is a which in turn are separated from the
decapeptide synthesized primarily within the surrounding ovarian stroma by a basal lamina;
arcuate nucleus this forms the primordial follicles
GnRH release from the hypothalamus occurs in a - Between 20-24 weeks gestation, in response to
pulsatile manner throughout the menstrual cycle: gonadotropins & ovarian steroids with further
- Increases from once every 90 min in the early fetal development, the granulosa cells become
follicular phase to once every 60-70 min in the more cuboidal & the surrounding stromal cells
immediate pre-ovulatory phase become more prominent, forming primary
- Luteal phase pulse frequency is lower but with follicles
greater amplitude - With further proliferation of granulosa cells, a
Release of GnRH by the hypothalamus is influenced clear gelatinous material surrounds the oocyte,
by various factors (both hormonal & from higher forming the zona pellucida; this forms the
centres in the brain): secondary follicles, which remain dormant in
- Stress, emotional factors the ovary from birth until puberty
- Nutritional status From the onset of puberty, with the beginning of
- Level of physical activity/exercise each menstrual cycle, increasing FSH secretion from
GnRH is carried from the hypothalamus to the the anterior pituitary recruits a cohort of follicles for
anterior pituitary via the hypophyseal venous development:
plexus, where it acts on the gonadotrophs - Follicular growth & development occurs with
- Pituitary increasing levels of estrogen & inhibin
Anterior pituitary (adenohypophysis) comprises produced by the follicular cells
various cell populations, each producing a different - Inhibin elicits negative feedback on FSH
anterior pituitary hormone secretion, limiting the FSH rise
Gonadotrophs release 2 types of gonadotropins in - With low FSH levels, only 1 follicle (dominant
response to GnRH from the hypothalamus: follicle) will be able to continue responding &
- Follicle-stimulating hormone (FSH) developing as it has the highest number of FSH
- Luteinizing hormone (LH) & LH receptors, aromatase enzyme &
- Note: the -subunit of FSH, LH, thyroid- intrafollicular estrogen
stimulating hormone (TSH) & human chorionic - Other hormonal factors involved in enhancing
gonadotropin (hCG) is identical; each has its own responsiveness of follicles to FSH include
distinct -subunit insulin, insulin-like growth factor-1 (IGF-1) &
Gonadotrophs physiologically respond to pulsatile epidermal growth factor (EGF)
GnRH release; if GnRH exposure is continuous - Remaining follicles of the recruited cohort
instead, there would be a desensitization of undergo atresia induced by high local androgen
gonadotrophs to GnRH via down-regulation of levels (these follicles can be rescued from atresia
GnRH receptors via exogenous administration of gonadotropins, an
- This effect is used therapeutically via effect used therapeutically in assisted reproductive
exogenous GnRH administration in situations techniques)
where it is desirable to shut down the Various structural changes occur in the dominant
endogenous ovarian hormonal cycle (e.g. follicle as it continues to grow in the lead-up to
endometriosis, fibroids, precocious puberty etc) ovulation:
FSH effects on the ovary: - Dominant follicle develops from a secondary
- Recruit follicles at the beginning of each follicle into a graafian follicle where the
menstrual cycle, stimulating their growth & innermost 3-4 layers of rapidly multiplying
development granulosa cells become adherent to the oocyte
- Induces aromatization of testosterone within (forms the cumulus oophorus) with
granulosa cells to produce estrogen concomitant formation of a fluid-filled antrum
LH effects on the ovary: among the granulosa cells
- Induces testosterone production by theca cells - Continued accumulation of antral fluid causes
which acts as the substrate for estrogen the central located oocyte to migrate
production by granulosa cells eccentrically to the wall of the follicle;
- Increases proteolytic enzymes & prostaglandin innermost layer of the cumulus oophorus
F2 production in the follicles which results in become elongated & forms the corona radiata,
eventual rupture of the follicle at the point of which is released with the oocyte at the point of
ovulation (induced by a LH surge) ovulation
- Luteinizes the granulosa cells, resulting in the
production of progesterone during the luteal
phase of the menstrual cycle

GYNAECOLOGIC BLEEDING & PAIN

80
Following ovulation, the corpus luteum forms:
- After ovulation, under the influence of LH, the
granulosa cells of the ruptured follicle undergo
luteinization
- These luteinized cells then produce
progesterone & estrogen
- The corpus luteum is programmed to have a
functional life span of 9-10 days, after which
time it regresses & becomes an avascular scar
known as corpus albicans

Menstrual Cycle
- Menstrual phase
1st phase of the menstrual cycle, usually occurring
from day 1 to day 5 of the menstrual cycle
Histological changes:
- Disruption & disintegration of the endometrial
glands & stroma (functionalis layer sloughs while
retaining the basalis layer of the endometrium)
- Leukocyte infiltration & red cell extravasation
Corresponds to the immediate period following the
complete regression of the corpus luteum in the
ovary which results in a drastic fall in serum ovarian
hormone levels (estrogen & progesterone)
- Proliferative phase
Follows the menstrual phase up to ovulation
Histological changes:
- Endometrial proliferation under the influence
of increasing serum estrogen levels
- Cellular proliferation is accompanied by
growth of the basal arteries (in the basalis layer)
Key Features of a Normal Menstrual Cycle
to form spiral arteries extending into the new
- Length of menstrual cycle
developing functionalis layer Defined as the interval between the 1st day of one
- Resultant endometrial glands formed are menses to the 1st day of the next menses
straight with narrow lumens Normal length = 21-35 days (28 days 1 week)
- Secretory phase - Duration of menstruation
Follows ovulation with the change in the circulating Normal duration = 3-7 days
ovarian hormone profile - Amount of menstrual bleeding
Histological changes: Normal volume of menstrual bleeding = 20-80ml (but
- Progesterone secreted by the corpus luteum difficult to quantify clinically)
stimulates glandular cells to secrete glycogen, Usually heaviest on the first 1-3 days
mucus & other substances Surrogate assessment of amount of menstrual bleed:
- Glands also become tortuous with dilated - 4 pads a day
lumens filled with the secreted substances - No excessive blood clots
- Stroma becomes edematous - No flooding
- Spiral arteries continue to extend into the - Intermenstrual bleeding
functionalis layer & become convoluted Small amount of intermenstrual bleeding can be
- If implantation does not occur by day 23, the physiological & normal (sudden drop in estrogen levels
corpus luteum begins to regress, with the following ovulation may result in some degree of
resultant decreasing ovarian hormonal levels endometrial sloughing)
inducing endometrial involution - Pain
- In the immediate period before the menstrual Some discomfort & cramps is normal during menses,
phase, the spiral arteries undergo marked & should not affect day-to-day activities
constriction, causing ischemia of the
functionalis layer

GYNAECOLOGIC BLEEDING & PAIN

81
Amenorrhea & Oligomenorrhea Approach to Primary Amenorrhea
- History:
Amenorrhea = absence of menstruation Pubertal status: any thelarche/pubarche yet? (e.g.
Primary amenorrhea = failure of occurrence of menarche before 16 years hyperprolactinemia can present with primary amenorrhea
Secondary amenorrhea = cessation of menses for 6 months despite thelarche & pubarche having occurred)
Oligomenorrhea = infrequent menstruation with >35 days length Hypothalamic: family history of delayed puberty, chronic
illness, stress, exercise, diet, headache, visual field
Primary Amenorrhea disturbance, sense of smell
Defined as failure of occurrence of menarche before 16 years of age; Pituitary: headache, visual field disturbance, hypothyroid
however, work-up should be done earlier in girls with failure of symptoms, drug use
occurrence of thelarche before 14 years of age or failure of occurrence of Ovarian: usually asymptomatic
menarche within 2 years after thelarche Anatomic: cyclical pelvic pain, bulge at introitus
- Physical examination:
Causes of Primary Amenorrhea General: pubertal assessment (Tanner staging), blood
- Hypothalamic pathology pressure, height/weight/nutritional status, dysmorphism
Constitutional delay of puberty Systemic: sense of smell, visual fields, fundoscopy,
- Delay in normal onset of puberty thyroid examination, breast examination
- Attributable to undefined hereditary factors Pelvic examination: inspect obstructive abnormalities; if
(history of delayed puberty in family members) vagina only rudimentarily present as a dimple, assess
- Diagnosis of exclusion presence of uterus via rectal examination
Systemic stresses: - Investigations & work-up:
- Significant weight loss (e.g. anorexia nervosa) Amenorrhea panel (FSH, LH, E2, T, prolactin TSH)
- Excessive physical activity/exercise - Low FSH, LH & E2 in hypothalamic &
- Severe emotional distress pituitary causes (hypogonadotropic hypogonadism)
- Chronic illness - High FSH & LH + low E2 in primary ovarian
Kallmann syndrome causes (hypergonadotropic hypogonadism)
- Congenital syndrome due to failure of - Normal FSH, LH & E2 in anatomical causes
developmental neuronal migration (however note that some ovarian causes may also be
- Clinically manifests as primary amenorrhea associated with reproductive tract anomalies)
(due to failure of GnRH secretion) + anosmia or Chromosomal & genetic studies
hyposmia (no or impaired of sense of smell) - Karyotype for chromosomal anomalies
Destructive lesions of the hypothalamus - Genetic testing for suspected genetic causes
- Neoplasms/space-occupying lesions (e.g. Pelvic ultrasound
craniopharyngioma, which can compress on - Assess uterine size (onset of puberty is suggested
pituitary stalk) by a uterine corpus:cervix ratio of 2:1)
- Previous encephalitis - Detect structural abnormalities of the
- Pituitary pathology reproductive tract & presence of gonads
Hyperprolactinemia Intravenous pyelogram
- Pituitary adenoma - Indicated in cases of reproductive tract
- Primary hypothyroidism abnormalities to rule out concomitant urinary
- Drugs tract structural abnormalities
Destructive lesions of the pituitary MRI brain
- Neoplasms/space occupying lesions - Assess for hypothalamic & pituitary pathology
- Ovarian pathology
Developmentally abnormal gonads Management of Primary Amenorrhea
- Pure gonadal dysgenesis (46XX & 46XY) - Management of hypothalamic pathology:
- Pseudohermaphroditism (androgen insensitivity Reassurance & follow-up constitutional delay
syndrome, testicular regression syndrome, Leydig Lifestyle modifications
cell agenesis) Exogenous estrogen to induce breast development
- Chromosomal defects affecting gonadal for untreatable hypogonadotropic causes
development (Turner syndrome, mosaicism with or Surgical resection of tumours
without Y chromosome) - Management of pituitary pathology:
Enzymatic defects Dopamine agonists for hyperprolactinemia
- Rare defects in enzymes involved in androgen (bromocriptine, cabergoline)
& estrogen production Thyroxine replacement for hypothyroidism
- e.g. 17-hydroxylase deficiency (results in lack of Exogenous estrogen to induce breast development
sex hormone production, with precursors shunted to for untreatable hypogonadotropic causes
aldosterone production, which may result in Surgical resection of tumours
hypokalemia & secondary hypertension) - Management of ovarian pathology:
- Anatomic abnormalities of the reproductive tract Exogenous estrogen to induce breast development
Congenital obstructive reproductive tract anomalies for untreatable hypogonadism
- Imperforate hymen Surgical removal of gonads if dysgenetic gonads
- Transverse vaginal septum diagnosed to prevent malignant transformation
- Cervical agenesis - Management of anatomical causes:
Congenital uterine abnormalities Surgical treatment for obstructive causes (e.g. cruciate
- e.g. Mllerian agenesis (Rokitansky-Kster- incision for imperforate hymen)
Hauser syndrome) Neovagina creation (Frank method of vagina dilation,
McIndoe vaginoplasty)

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Secondary Amenorrhea/Oligomenorrhea - Investigations & work-up:
Secondary amenorrhea = cessation of menses for 6 months
Oligomenorrhea = infrequent menstruation with >35 days length Secondary amenorrhea/oligomenorrhea

Causes of Secondary Amenorrhea/Oligomenorrhea Urine pregnancy test


(always rule out pregnancy first)
- Hypothalamic dysfunction (35%) Negative Positive
Systemic stresses:
- Significant weight loss (e.g. anorexia nervosa) Assess for signs of significant
- Excessive physical activity/exercise hyperandrogenism
- Severe emotional distress
- Chronic illness Present Absent
Destructive lesions of the hypothalamus:
- Neoplasms/space-occupying lesions (e.g. Test serum testosterone, DHEA-S Do amenorrhea panel
craniopharyngioma, which can compress on (dihydroepiandrosterone-sulphate) (serum FSH, LH, prolactin,
pituitary stalk) & 17-hydroxyprogesterone estradiol, testosterone TSH)
- Sarcoidosis
- Previous encephalitis Mild hyperandrogenism of Low FSH/LH & E2
- Pituitary dysfunction (20%) adrenal origin ( DHEA-S) &/or high prolactin
Hyperprolactinemia (15%)
- Pituitary adenoma - Cushing syndrome (confirm with 24- - Hypothalamic/pituitary cause &/or
- Drugs (anti-psychotics, metoclopramide, hour urinary free cortisol & low-dose hyperprolactinemia (MRI brain &
butyrophenones & phenothiazines) dexamethasone-suppression test) other necessary work-ups)
- Breast-feeding or breast stimulation - Late-onset congenital adrenal
- Primary hypothyroidism (leads to secondary hyperplasia ( 17-hydroxyprogesterone)
High FSH/LH, low E2
elevation of TRH which has stimulatory effect on
prolactin secretion) Mild hyperandrogenism of - Premature ovarian failure
- Chronic renal failure (decreased clearance of ovarian origin ( testosterone) (karyotype if <30years old; screen for
prolactin leading to its accumulation in serum) other endocrinopathies if no cause found
Destructive lesions of the pituitary (5%) - Polycystic ovary syndrome as autoimmune ovarian failure has no
(confirm with pelvic ultrasound) diagnostic test + can be associated with
- Neoplasms/space-occupying lesions other endocrine failure)
- Sarcoidosis
- Sheehan syndrome Severe hyperandrogenism Normal FSH elevated LH
- Iatrogenic (previous transphenoidal resection of (testosterone >5nmol/L)
pituitary tumours or cranial radiation) Cyclical estrogen/progesterone test
- Ovarian dysfunction (40%) - Androgen secreting tumour
Premature ovarian failure (ultrasound ovaries &
CT scan adrenals) Withdrawal bleed Withdrawal bleed
- Dysgenetic gonads (e.g. Turners) present absent
- Autoimmune premature ovarian failure
- Infections (e.g. mumps) - ?PCOS - Anatomical cause
- Iatrogenic (pelvic radiation, chemotherapy) (consider ultrasound &
Hyperandrogenic disorders hysterosalpingogram)
- Ovarian disorders: PCOS, HAIR-AN
(hyperandrogenic insulin resistance & acanthosis
Urine pregnancy test
nigricans) syndrome, virilizing tumours
- Always important to rule out pregnancy in
(arrhenoblastoma, lipid cell tumour)
women of reproductive age presenting with
- Adrenal disorders: late-onset CAH, Cushing
syndrome, androgen-secreting adrenal tumour amenorrhea
- Anatomic abnormalities of the reproductive tract (5%) Serum LH/FSH
Asherman syndrome (past terminations of pregnancy, - Low in states of decreased gonadotropin
dilatation & curettage) production (hypothalamic & pituitary dysfunction)
- Very high FSH is suggestive of a menopausal
state (premature ovarian failure)
Approach to Secondary Amenorrhea/Oligomenorrhea
- History: - Normal FSH is present in PCOS & anatomical
Hypothalamic: chronic illness, stress, exercise, diet, causes of amenorrhea
headache, visual field disturbance - Reversed LH:FSH ratio (normal is 1:1; ratios
Pituitary: headache, visual field disturbance, hypothyroid 3:1 may be present in PCOS
symptoms, drug use, galactorrhea Serum prolactin & TSH
Ovarian: perimenopausal vasomotor symptoms, - Diagnoses hyperprolactinemia
hirsutism, virilizing changes, history of pelvic radiation or - Extremely high prolactin (>1000) is suggestive
chemotherapy of a pituitary adenoma
Anatomic: any past TOPs or dilatation & curettage - High TSH suggests a primary hypothyroidism
- Physical examination: cause of hyperprolactinemia
General: body habitus/BMI, signs of virilization, Serum estradiol
cutaneous signs (acanthosis nigricans), secondary sexual - Low in hypothalamic/pituitary dysfunction &
characteristics, dysmorphism premature ovarian failure
Systemic: visual fields, fundoscopy, thyroid examination,
breast examination, pelvic examination

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Serum testosterone Polycystic Ovary Syndrome (PCOS)
- Elevated in PCOS Syndrome of chronic anovulation/oligo-ovulation with clinical or
- Very high testosterone (>5nmol/L) is laboratory evidence of hyperandrogenism after excluding any other
suggestive of an androgen producing tumour underlying condition (a diagnosis of exclusion)
Serum dihydroepiandrosterone-sulphate (DHEA-S)
- Elevated in adrenal hyperandrogenic Epidemiology & Associations
disorders (Cushings, late onset CAH) - 6-10% of pre-menopausal women have some form of
Serum 17-hydroxyprogesterone PCOS
- Elevated in late onset CAH - Associations:
Cyclical estrogen/progesterone test Peripheral insulin resistance, hyperinsulinemia
- Tests for withdrawal bleed which if present, Diabetes mellitus (type 2), obesity, dyslipidemia,
indicates an normal responsive endometrial hypertension (metabolic syndrome)
lining (hence ruling out anatomical causes) Hirsutism
Pelvic ultrasound - Stein-Leventhal syndrome characterizes the subset of
- Assess for possible ovarian tumours women with PCOS demonstrating all the combined
- Assess for PCOS features of obesity, hirsutism & polycystic ovaries
- Assess for anatomical abnormalities
MRI brain Pathophysiology of Polycystic Ovary Syndrome
- Assess for hypothalamic & pituitary pathology - Exact etiology & pathogenesis in unknown; however, the
CT abdomen following pathophysiological features are noted:
- Assess for adrenal tumours Hereditary component (1st degree relative affected
increases risk of PCOS)
Reference Ranges for Amenorrhea Panel Peripheral insulin resistance
FSH LH Estradiol Testosterone Prolactin - Hormonal changes in PCOS:
Phase
(IU/L) (IU/L) (pmol/L) (nmol/L) (mIU/L) Increased serum LH levels, which in turn promotes
Follicular 3.5-12.5 2.4-12.6 90-716 increased amount of ovarian androgen (testosterone,
Ovulating 4.7-21.5 14.0-45.6 243-1509 androstenedione) secretion
0.22-2.90 70-510
Luteal 1.7-7.7 1.0-11.4 147-958
- High androgen levels induces atresia of ovarian
Menopause 25.8-134.8 7.7-58.5 <50-145
follicles, interfering with normal follicular
development leading up to ovulation
Management of Secondary Amenorrhea/Oligomenorrhea
- High androgen levels also results in increased
- Management of hypothalamic dysfunction:
peripheral aromatization of androgens into estrogen,
Lifestyle modifications (improve nutrition, cut down on
resulting in tonically elevated estrogen levels which
excessive exercise, psychosocial help) suppresses FSH secretion
Combined oral contraceptives (to help prevent - Lack of normal estrogen rise results in lack of LH
osteoporosis & maintain normal breast & vagina tissue) surge, with resultant anovulation
Surgical resection of tumours Peripheral insulin resistance often found
- Management of pituitary dysfunction: concomitantly results in secondary hyperinsulinemia
Dopamine agonists for hyperprolactinemia - High insulin levels stimulate further ovarian
(bromocriptine, cabergoline) androgen production
Thyroxine replacement for hypothyroidism - High insulin levels combined with elevated
Combined oral contraceptives (to help prevent androgens also suppresses hepatic secretion of sex-
osteoporosis & maintain normal breast & vagina tissue) hormone binding proteins, resulting in an increased
Surgical resection of tumours serum unbound fraction of androgens
- Management of premature ovarian failure:
Hormonal replacement therapy (combined estrogen Clinical Consequences of Polycystic Ovary Syndrome
+ progestin) to prevent osteoporosis - Gynaecological consequences:
Surgical removal of gonads if dysgenetic gonads Oligomenorrhea, amenorrhea
diagnosed to prevent risk of malignant Increased risk of endometrial hyperplasia & cancer
transformation due to chronic anovulation leading to prolonged
- Management of hyperandrogenism: unopposed estrogenic stimulation of endometrium
Androgen blockers for hirsutism (spironolactone, Subfertility
cyproterone acetate, flutamide) Increased risk of GDM during pregnancy
Progestin therapy for chronic anovulation e.g. in - Hyperandrogenic consequences:
PCOS to protect against endometrial hyperplasia & Hirsutism (can be scored using Ferriman Gallwey score)
endometrial cancer Balding, oily skin, acne
Combined oral contraceptives (to regulate menstrual - Complications related to metabolic syndrome:
cycle & suppress gonadotropin stimulation of excess Hypertension, diabetes mellitus, dyslipidemia
ovarian androgen production in PCOS) Atherosclerotic diseases
Surgical resection of tumours Obstructive sleep apnea
- Management of anatomical causes:
Hysteroscopic excision of synechiae for Ashermans

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Rotterdam Criteria (2003) for the Diagnosis of PCOS Management of Polycystic Ovary Syndrome
(European Society of Human Reproduction & Embryology/American - Conservative management:
Society for Reproductive Medicine (ESHRE/ASRM) sponsored Lifestyle modifications (exercise, dietary modifications,
workshop on PCOS in 2003; requires 2 out of the following 3 quit smoking)
criteria met + exclusion of other possible etiologies) - Can have dramatic effect on normalizing
1. Evidence of oligo- &/or anovulation menstrual cycles & improving insulin resistance
<8 menstrual cycles per year - Medical management:
2. Evidence of hyperandrogenism Combined oral contraceptives
Clinical evidence: Ferriman Gallwey score &/or - Helps regulate menstrual cycle
Biochemical evidence: serum total testosterone - Protects against unopposed estrogen
3. Evidence of polycystic ovaries stimulation of endometrium in long run
Presence of 12 follicles 2-9mm in diameter &/or - Has also been shown to suppress excess
Increased ovarian volume (>10ml) ovarian androgen production & increase
Note: only 1 ovary fitting this criteria is sufficient hepatic synthesis of serum sex-hormone
- Following differentials should be ruled out: binding globulin
Late onset CAH Progestin therapy
Androgen-secreting tumours - Used to induce withdrawal bleed every month
Cushing syndrome - Useful in patients in whom exogenous
estrogen is risky or contraindicated
- Protects against unopposed estrogen
stimulation of endometrium in long run
Metformin
- Used to improve insulin sensitivity which can
result in menstrual regularity & ovulatory
function
- Used as adjunctive treatment to clomiphene in
women with PCOS trying to conceive
Androgen blockers
Ultrasound of polycystic ovary - Spironolactone, cyproterone acetate, flutamide
- Used to treat hirsutism
Other Adjunctive Investigations - Pregnancy should be avoided due to
- Amenorrhea panel: teratogenic effects of these drugs
May be performed in the initial work-up for a Clomiphene
presenting complain of oligo-/amenorrhea - Selective estrogen receptor modulator with
Typical profile seen in PCOS: antagonistic effect on pituitary estrogen
- Normal FSH LH receptors (blocks negative feedback, hence
- Reversed LH:FSH ratio (~3:1) stimulating gonadotropin release, which induces
- Normal/slightly elevated estradiol follicular development in the ovaries)
- Elevated testosterone - 1st-line treatment for women with PCOS trying
- Prolactin may be elevated to conceive
- Hyperandrogenism panel: - Risks: multiple pregnancies, epithelial ovarian
Elevated testosterone cancers, ovarian hyperstimulation
Normal 17-hydroxyprogesterone (rules out late onset Medical treatment of other co-morbidities (diabetes
congenital adrenal hyperplasia) mellitus, hypertension, dyslipidemia)
- 24-hour urinary free cortisol & low dose dexamethasone - Surgical management:
suppression test Ovarian drilling
Rules out Cushing syndrome - Creation of holes in ovaries using laser or
- Radiological investigations: diathermy with the intent of reducing steroid
CT abdomen (excludes androgen secreting tumour of the hormone production
adrenals) - 2nd-line treatment for women with PCOS
- Screening for co-morbidities: trying to conceive after failed clomiphene
Test for diabetes with OGTT treatment
Test fasting lipids to detect dyslipidemia Assisted reproductive techniques (IVF)
Measure blood pressure

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Abnormal Uterine Bleeding Approach to Abnormal Uterine Bleeding
- History:
Uterine bleeding which is excessive in amount, duration &/or frequency Menstrual history (current & past):
occurring in reproductive years (i.e. pre-menopausal) - Last menstrual period
- Regularity & length of cycles
Types of Abnormal Uterine Bleeding (AUB) - Duration & amount of menses
- Menorrhagia - Any intermenstrual &/or post-coital bleeding
Excessive (>80ml) &/or prolonged menses (>7 days) Any pain or dysmenorrhea
occurring at normal intervals (i.e. regularity normal - Dysmenorrhea may suggest adenomyosis or
- Polymenorrhea chronic pelvic inflammatory disease
Abnormally frequent menses (length <21 days)
- Lower abdominal pain may be present in
- Metrorrhagia
infections of the reproductive tract or
Irregular episodes of uterine bleeding of normal
pregnancy complications
amount (normal regularity completely disrupted)
Per-vaginal discharge
- Metromenorrhagia
- Foul-smelling coloured discharge may indicate
Uterine bleeding that is excessive & irregular
infection of reproductive tract
- Intermenstrual bleed (IMB)
- Greyish tissues passed may suggest products
Scant bleeding occurring between 2 consecutive
of conception in an incomplete abortion
menses (usually at ovulation, lasting 1-2days)
Systemic screen
- Constitutional symptoms (fever, LOA, LOW)
Causes of Abnormal Uterine Bleeding
- Symptoms of anemia (to assess severity)
- Dysfunctional uterine bleeding
- Thyroid symptoms (lethargy, cold intolerance,
Abnormal uterine bleeding for which no organic
constipation)
cause is found (diagnosis of exclusion)
- Urinary symptoms (hematuria may occur in
2 main types:
locally invasive neoplasms; frequency or obstructive
- Ovulatory DUB: corpus luteal deficiency with
symptoms may be present due to mass effect of local
resultant insufficiency of progesterone secretion
pathology)
during luteal phase, causing shortened menstrual
- Changes in bowel habits
cycles & pre-menstrual spotting
- Any other sources of bleeding
- Anovulatory DUB: failure of achieving ovulation
Past medical/surgical/gynaecological history
with no resultant corpus luteum or progesterone
secretion, hence unopposed estrogen continues - Any current medications
stimulating endometrial proliferation; however, lack - Any contraceptives currently used
of progesterone which is required for inducing - Last Pap smear & mammogram (+ results)
adequate vascular growth to support further Family history
endometrial growth results in eventual breakdown & Social history
sloughing of endometrium; this sloughing tends to - Smoking, drinking
be heavy, prolonged & irregular due to the thickened - Sexual history (especially if STD suspected)
endometrial lining & lack of clear hormonal events to - Desire for future fertility; desire for menses or
induce a thorough sloughing (unlike in normal amenorrhea (affects management)
cycles where regression of corpus luteum results in a - Physical examination:
sharp fall in hormones) General examination
Anovulatory DUB is most commonly seen in - Assess patients vitals & look for pallor
extremes of reproductive life: - Assess for supraclavicular lymphadenopathy
- Post-menarche: HPO-axis may not be fully - Neck examination for goitre
sensitized & functional initially - Breast examination
- Pre-menopausal: diminishing population of - Chest & lungs for pleural effusion
follicles left in the ovaries Abdominal examination
- Pregnancy complications: - Inspect for distension, past surgical scars
Miscarriage (threatened, incomplete, complete) - Palpate for organomegaly & abdominopelvic
Ectopic pregnancy, molar pregnancy masses
- Pelvic pathology: - Palpate for any lower abdominal tenderness
Uterine fibroids - Percuss for shifting dullness
Adenomyosis Pelvic examination
Endometrial pathology (polyps, hyperplasia, cancer) - Inspect for any vulvar lesions
Cervical pathology (polyps, cancer) - Speculum examination to inspect cervix (any
Lower tract neoplasms lesions, os open? products of conception seen?) &
Infection (endometritis, cervicitis, lower tract infection) vaginal walls
Trauma/lacerations - Take a Pap smear & swabs where indicated
- Systemic causes: during speculum examination
Coagulopathy/blood dyscrasias - Digital vaginal examination to elicit cervical
Thyroid disease (usually hypothyroidism) excitation & feel for uterosacral & pouch of
Liver disease (may cause coagulopathy & increased Douglas masses
levels of serum estrogen due to decreased metabolism) - Bimanual palpation to assess uterine size,
- Iatrogenic causes: define any abdominopelvic mass felt
Anti-platelets & anti-coagulants - Rectal examination where indicated to assess
Exogenous hormones local invasion where malignancy is suspected
Copper IUCD

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86
- Investigations & work-up: Endometrial ablation
Urine pregnancy test - Reserved for older patients who do not desire
Blood tests fertility but wish to retain uterus with bleeding
- Full blood count (assess for anemia & platelets) refractory to medical treatment
- PT/PTT (rule out coagulopathy) - Best done for uterus <10 weeks size
- Thyroid function test (rule out hypothyroidism) - Modalities: transcervical resection of the
Tests for sexually-transmitted diseases endometrium (TCRE), roller ball diathermy,
- Urine PCR for Chlamydia antigen microwave endometrial ablation, novasure
- Endocervical & high vaginal swab (HVS) for - 60-70% success rate, can decrease heavy
gonococcal culture bleeding by 40%
- Workup for bacterial vaginosis, Trichomonas - Not definitive however, recurrence would
& Candida where indicated require repeat ablation
- Consider HIV, VDRL & hepatitis B screening Hysterectomy
Pelvic ultrasound - Definitive treatment for bleeding refractory to
- Assess for uterine pathology medical treatment
- Assess for viability & site of pregnancy - Option in older patients with no desire for
Endometrial biopsy uterus preservation or future fertility
- Done where endometrial hyperplasia or cancer
is suspected (see Algorithm for Endometrial
Evaluation in Gynaecologic Oncology)
Post-Coital & Post-Menopausal Bleeding
Post-coital bleed (PCB) = per-vaginal bleeding after intercourse
Post-menopausal bleed (PMB) = per-vaginal bleeding after menopause
Management of Abnormal Uterine Bleeding
Both are assumed pathological until proven otherwise
- Non-hormonal medical treatment:
Tranexamic acid
Causes of PCB & PMB
- Decreases heavy flow by 50%
- Causes of post-coital bleeding:
NSAIDS (e.g. mefenamic acid aka Ponstan)
Vaginal causes (rare)
- Decreases heavy flow by 30%
- Vaginal trauma/lacerations
- Helps relieve dysmenorrhea as well
- Vaginal growths/neoplasms
- Hormonal medical treatment:
Combined oral contraceptive pills Cervical causes
- Decreases heavy flow by 43% - Cervical trauma/lacerations
- Helps relieve dysmenorrhea as well - Cervical ectropion
- Protects against risk of endometrial cancer in - Cervical polyps
anovulatory DUB - Cervical cancer
Progestin therapy - Causes of post-menopausal bleeding:
- Progestin-only pills aka POP (norethisterone, Vulvar causes (rare)
medroxyprogesterone acetate) decreases heavy Vaginal causes
flow by 80% - Atrophic vaginitis (most common)
- Depot progestin injections (Depo-Provera) - Vaginal growths/neoplasms
decreases heavy flow by 70-90% Cervical causes
- Subcutaneous implantable Etonogestrel - Cervical growths/neoplasms
(Implanon) decreases heavy flow by 70-90% Uterine causes
- Levonorgestrel-releasing intra-uterine system - Endometrial growths/neoplasms
(Mirena) decreases heavy flow by 70-90%; also
helps with dysmenorrhea in adenomyosis Evaluation of PCB & PMB
For patients with DUB desiring fertility: - Evaluation of post-coital bleeding:
- Luteal phase progesterone (e.g. Duphaston aka Requires evaluation of the entire lower genital tract
dydrogesterone) for ovulatory DUB Direct examination under good light to look for
- Ovulation induction for anovulatory DUB visible lesions of the lower genital tract
GnRH agonists Assessment of cervix:
- Induces pseudo-menopause to achieve (refer to Cervical Screening (Pap Smear) Algorithm in
amenorrhea Gynaecologic Oncology)
- Option for heavy symptomatic abnormal - Visible lesion biopsy
uterine bleeding refractory to other medical - No visible lesion Pap smear
treatments to allow for patient to restore a - Evaluation of post-menopausal bleeding:
normal haemoglobin level + buy time to plan Requires evaluation of the entire lower genital tract +
definitive treatment evaluation of the endometrium
- Adverse effect on bone mineral density; use Direct examination under good light to look for
limited to 6 months at most visible lesions of the lower genital tract
- Surgical treatment: Assessment of cervix (as for post-coital bleeding)
Dilatation & curettage + hysteroscopy Transvaginal ultrasound to assess endometrial
- Does not offer a permanent cure thickness & determine need for follow-up
- Therapeutic for bleeding in short term + investigations:
diagnostic (provides better sample for endometrial (refer to Algorithm for Endometrial Evaluation in
histological assessment than endometrial sampling) Gynaecologic Oncology)
- Therapeutic measures can be undertaken for - <5mm observe
certain pathologies visualized (e.g. resection of - >5mm endometrial biopsy
polyps & submucosal fibroids)

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Dysmenorrhea Secondary Dysmenorrhea
Painful menstruation; may be primary (no readily identifiable cause) or
Causes of Secondary Dysmenorrhea
secondary (results from underlying organic pelvic disease)
- Endometriosis
Pain tends to extend to pre- & post-menstrual phases
Primary Dysmenorrhea or may even be continuous
Other symptoms: deep dyspareunia
Pathophysiology of Primary Dysmenorrhea Signs: uterosacral tender nodules, pouch of Douglas
- Occurs during ovulatory cycles, typically appearing nodularity, visible tender nodules in posterior fornix,
within 6-12 months from menarche palpable adnexal mass (endometrioma)
- Etiology attributed to uterine contractions with ischemia - Adenomyosis (occasionally fibroids)
& production of prostaglandins Other symptoms: menorrhagia
- Evidence supporting involvement of prostaglandins in Signs: enlarged bulky uterus which may be mildly tender
primary dysmenorrhea: - Pelvic inflammatory disease
Menstrual fluid from women with primary Pain may extend into pre-menstrual phase
dysmenorrhea contain higher than normal levels of Other symptoms: deep dyspareunia, intermenstrual
prostaglandin bleeding, vaginal discharge
NSAIDs are effective treatment modalities Signs: pelvic tenderness, may have adnexal mass (tubo-
Anovulatory cycles often have painless menses ovarian abscess, hydrosalpinx)
(secretory endometrium under the influence of - Ovarian cysts (especially luteal & endometriotic cysts)
progesterone have much higher levels of prostaglandin Other symptoms: may have mass symptoms if large
than proliferative endometrium) Signs: palpable adnexal mass
- Pelvic congestion
Clinical Features of Primary Dysmenorrhea Dull ill-defined pelvic ache worse premenstrually,
- Cramping lower abdominal pain: relieved by menses
Often begins a few hours before onset of menses History of sexual problems usually present
May persist for hours or days (usually 48-72 hours)
May radiate to thighs & lower back
- Associated symptoms:
Nausea/vomiting
Fatigue, dizziness, headache
Altered bowel habits (diarrhea)
- Pelvic examination should be normal

Management of Primary Dysmenorrhea


- Conservative management:
Reassurance & explanation
- Medical management:
Paracetamol
NSAIDs (ibuprofen, naproxen, mefenamic acid)
Combined oral contraceptive pills
High-dose continuous progestins (dydrogesterone,
medroxyprogesterone acetate)
Smooth muscle anti-spasmodics (alverine, hyoscine)
- Alternative management:
Transcutaneous nerve stimulation
Acupuncture
Psychotherapy, hypnotherapy
- Dysmenorrhea refractory to NSAIDs & hormonal therapy:
Should re-assess patient to look harder for possible
underlying organic pelvic disease
Ultrasound, exploratory laparoscopy, hysteroscopy
are all modalities to be considered for a more
thorough workup

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88
Pelvic Pain Evaluation of Chronic Pelvic Pain
- History:
Take a thorough pain history (+ relation to menstrual
Acute Pelvic Pain cycle)
Menstrual history
Gynaecologic Causes of Acute Pelvic Pain Screen symptoms of other systems (bowel, urinary,
- Physiological: musculoskeletal)
Mittelschmerz (midcycle pain resulting from ovulation) Past medical, surgery, obstetric & gynaecologic
- Adnexal accidents: history
Ovarian cyst torsion - Physical examination:
Ovarian cyst rupture Abdominal examination
Intra-cystic hemorrhage - Palpate for masses
- Acute infections: - Examine abdominal wall for myofascial
Acute pelvic inflammatory disease trigger points & for nerve entrapment pain in
Endometritis corresponding dermatomes (T12, L1, L2)
- Pregnancy complications: Pelvic examination
Ruptured ectopic pregnancy - Assess uterine size & version (fixed retroverted
Incomplete/complete miscarriage uterus may suggest endometriosis)
- Feel for uterosacral & pouch of Douglas
Non-Gynaecologic Causes of Acute Pelvic Pain nodularity & tenderness
- Gastrointestinal causes: - Palpate for adnexal masses
Acute appendicitis - Investigations & work-up:
Diverticulitis Pelvic ultrasound
Intestinal obstruction CT abdomen, GI endoscopy, cystoscopy & CT
- Urinary system causes: urogram are useful modalities for assessment of
Acute cystitis gastrointestinal & urinary system differentials
Ureteral stones Diagnostic laparoscopy
Urethral syndrome
- Other causes: Management of Chronic Pelvic Pain
Pelvic thrombophlebitis - Treat any treatable underlying pathology identified
Acute porphyria - For no pathology or pathology not amenable to treatment
Mesenteric adenitis identified:
Multidisciplinary team care
Chronic Pelvic Pain Medical treatment:
Defined as pelvic pain of >6 months duration that has a significant - Hormonal treatment
impact on the daily function & quality of life of a patient - NSAIDs
- Tricyclic antidepressants
Causes of Chronic Pelvic Pain - Serotonin-norepinephrine reuptake inhibitors
- Gynaecologic causes: - Anti-convulsants
Endometriosis Anesthesia
Chronic pelvic inflammatory disease - Nerve blocks
Ovarian pain (e.g. in ovarian remnant syndrome where - Trigger point injections of local anesthetic
an ovary or a remnant of it becomes retroperitoneal Surgical treatment
secondary to inflammation or previous surgery; cyst - Presacral neurectomy
formation in these circumstances causes chronic pain) - Adhesiolysis
Adenomyosis - Unilateral adnexectomy
Uterine fibroids (typically painless; however, large - Hysterectomy
degenerating fibroids or those compression pelvic nerves
may cause chronic pain)
Pelvic congestion syndrome (clinical entity seen in
multiparous women with pelvic vein varicosities &
congested pelvic organs; pain is worse premenstrually,
upon standing & during sexual intercourse)
- Gastrointestinal causes:
Irritable bowel syndrome (most common)
Inflammatory bowel disease
Hernia
Locally invasive GI malignancies
- Urinary system causes:
Urinary retention
Urethral syndrome
Trigonitis
Interstitial cystitis
- Neuromuscular causes:
Fibromyalgia
Nerve entrapments (iliohypogastric, ilioinguinal,
pudendal)

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REPRODUCTIVE TRACT INFECTIONS
Vulvovaginitis Vulvovaginal Candidiasis
2nd most common cause of vulvovaginal-related symptoms; up to 75% of
women acquire vulvovaginal candidiasis at some point in time
Bacterial Vaginosis
Most common cause of vaginal discharge Microbiology & Pathophysiology
- Caused by fungal pathogens:
Microbiology & Pathophysiology Candida albicans (most common)
- Involves disruption of normal healthy vaginal microflora Candida glabrata
(e.g. Lactobacillus jensenii, Lactobacillus crispatus) by a - Risk factors & associations for developing candidiasis:
characteristic set of BV-complex microorganisms: Highly-estrogenized vaginal epithelium:
Gardnerella vaginalis - High-dose oral contraceptives
Genital mycoplasmas (Mycoplasma hominis, - Pregnancy
Ureaplasma urealyticum) - After menarche, before menopause
Vaginal anaerobic bacteria (Prevotella, Bacteroides, Immunosuppresion:
Mobiluncus) - Diabetes mellitus
- Risk factors & associations for developing BV: - Long-term steroid use
New sexual partner - HIV
Smoking Disruption of normal vaginal flora:
Use of intrauterine device - Frequent douching
Frequent douching - Antibiotic use

Clinical Features Clinical Features


- Asymptomatic - Symptomatic presentation:
- Symptomatic presentation: Vaginal itching, burning sensation, irritation
Vaginal odour Vaginal discharge (odourless, white, thick & curdy with
Vaginal discharge (profuse, milky, non-adherent) appearance of cottage cheese)
- Complications: Dysuria may also be present
For non-pregnant women, increases risk of: Vaginal speculum examination often reveals
- Pelvic inflammatory disease vulvovaginal erythema with evidence of acute on
- Postoperative infections (e.g. after hysterectomy, chronic excoriation
termination of pregnancy) - Recurrent vulvovaginal candidiasis:
- HIV transmission Defined as 4 episodes within 1 year (5% of cases)
For pregnant women, increases risk of:
- 2nd trimester miscarriage Diagnosis & Evaluation
- Preterm labour - Microscopy of wet mount preparation
Reveals budding yeast cells, pseudohyphae or
Diagnosis & Evaluation mycelial tangles (in 50-70% of cases)
- Amsel criteria (requires 3 of 4 features) - Fungal culture
Characteristic vaginal discharge (homogeneous, May be considered in cases with suggestive clinical
watery, white/grey coloured, thin) findings but absent wet-prep microscopy evidence
Whiff test positive (fishy odour after alkalinizing
vaginal discharge with a drop of 10% potassium
hydroxide)
Presence of >20% clue cells (vaginal epithelial cells with
edges blurred by bacteria) on microscopy of wet mount
preparation
Vaginal pH >4.5

Wet-prep microscopy findings for Candida

Management
- Antimicrobial therapy:
Management Clotrimazole 500mg (as vaginal pessary or cream)
- Antimicrobial therapy: Fluconazole PO 150mg single dose
Metronidazole PO 500mg twice daily x 7 days - Partner screening:
Clindamycin cream 2% with one applicator (5g) Can be considered & treatment instituted where
intravaginally at bedtime x 7 days appropriate even though vulvovaginal candidiasis is
- Partner screening: not thought to be sexually transmitted in most cases
Generally not recommended for BV

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Trichomoniasis Sexually Transmitted Infections
Microbiology & Pathophysiology
- Caused by protozoan Trichomonas vaginalis Genital Herpes

Clinical Features Microbiology & Pathophysiology


- Asymptomatic (up to 50% of cases) - Caused by Herpes Simplex Virus (HSV); 2 serotypes:
- Symptomatic presentation: HSV 1 (most commonly associated with oral lesions/cold
Vaginal odour (musty) sores; contributes to about 30% of primary genital herpes)
Vaginal discharge (green-yellow, frothy) HSV 2 (causes 70% of primary genital herpes & 95% of
May have vaginal irritation, dyspareunia, dysuria recurrent genital herpes)
Vaginal speculum examination may reveal a cervix - Transmitted through intimate oral, genital or anal contact
with punctate hemorrhages (strawberry cervix) Virus enters body through microabrasions in the skin
- Complications: or mucosa, thereafter travelling along sensory nerves
For non-pregnant women, increases risk of: to end up in the dorsal root ganglion where it
- Pelvic inflammatory disease remains dormant until reactivation occurs
- Postoperative infections (e.g. after hysterectomy, Infected mother can transmit herpes to her neonate
termination of pregnancy) during delivery
- HIV transmission
For pregnant women, increases risk of: Clinical Features
- 2nd trimester miscarriage - Acute genital herpes
- Preterm labour Anogenital vesicles
- Multiple, bilateral & painful
- Erythematous base
- Heal spontaneously within 2-3 weeks without
residual scarring
Systemic signs & symptoms
- Fever, headache, malaise
- Lymphadenopathy
Acute cervicitis may also be present
- Recurrent genital herpes
Frothy discharge in trichomoniasis Strawberry cervix
Lesions are usually fewer, unilateral & less painful
- Heal spontaneously within 5-7 days in
immunocompetent individuals
Diagnosis & Evaluation
- Microscopy of wet mount preparation: Systemic signs & symptoms less likely to be present
Reveals motile trichomonads
- Culture: Diagnosis & Evaluation
Using Fineberg Whittington medium - Diagnostic tests:
Viral culture
- Requires live cells from swab taken from the
herpetic lesion
- Expensive, time-consuming & relatively low-
sensitivity (50-80%)
Viral PCR
- Expensive but highly accurate
- Typically used for testing cerebrospinal fluid
in suspected herpes simplex encephalitis, not
routinely done for genital herpes
Type-specific serology tests for antibodies

Wet-prep microscopy findings for Trichomoniasis Management


- Pharmacological therapy:
Management Symptomatic relief of pain with analgesics
- Antimicrobial therapy: - Topical lignocaine gel
Metronidazole PO 2g single dose Antiviral agents
Tinidazole PO 2g single dose (for cases resistant to - Acyclovir (200mg 5 times daily x 7-10 days for 1st
metronidazole) acute episode of genital herpes; 400mg twice daily for
- Partner screening: long-term suppression in cases of recurrent herpes)
Indicated in trichomoniasis (along with appropriate - Famciclovir, valacyclovir
treatment) so as to prevent reinfection - Other considerations:
Do urine pregnancy test
Offer testing for other sexually transmitted diseases
Advice on barrier contraception

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Human Papillomavirus Chlamydia

Microbiology & Pathophysiology Microbiology & Pathophysiology


- Human papillomavirus; many serotypes (about 200): - Caused by Chlamydia trachomatis
Serotypes 6 & 11 commonly associated with genital Obligate intracellular bacteria
warts Infects columnar epithelial cells of the endocervix,
Serotypes 16 & 18 commonly associated with cervical urethra, endometrium, fallopian tubes & rectum
cancer & penile cancer No effective immunity conferred even though
- Transmitted via close contact antibodies are produced after 1 episode of infection,
Occurs even when no visible lesions are present hence multiple reinfections are possible
Mother-to-infant transmission is rare - Several serotypes exist:
Oculogenital biovars A, B, Ba, C
Clinical Features - Conjunctivitis
- Genital warts (condylomata acuminata) - Trachoma
Can be found on the vulva, vagina, cervix, urethra & Oculogenital biovars D to K
perianal region - Paratrachoma
May bleed due to mechanical abrasion (e.g. post-coital - Genital infections
bleed in the setting of cervical or vaginal warts) - Non-gonococcal urethritis
Differential diagnoses: - Ophthalmia neonatorum
- Condylomata lata (caused by syphilis; should be LGV biovars L1, L2 & L3
considered if lesions look atypical or fail to respond - Lymphogranuloma venereum
to treatment for HPV)
- Malignancy (consider if lesions look atypical or Clinical Features
remain persistent despite treatment) - Asymptomatic
- Cervical cancer Asymptomatic carriage in 70% of infected females &
(see Gynaecologic Oncology) 50% of infected males
- Symptomatic Chlamydia infection:
Diagnosis & Evaluation Non-gonococcal urethritis
- Diagnosis is usually made on clinical grounds Mucopurulent cervicitis (30% of untreated cases
progress further to more severe upper tract infections)
Management Acute salpingitis
- Pharmacological therapy: Pelvic inflammatory disease
Provider-applied topical therapy: Fitz-Hugh-Curtis syndrome (perihepatitis)
- Podophyllin resin 10-25% Proctitis
- Trichloroacetic acid - Pregnancy-related complications & sequelae:
- Bichloracetic acid 80-90% Subfertility
Patient-applied topical therapy: Ectopic pregnancy
- Podofilox 0.5% solution or gel Preterm labour
- Imiquimod 5% cream Chorioamnionitis
- Surgical treatment: Post-partum endometritis
Cryotherapy Ophthalmia neonatorum & neonatal pneumonia
Surgical excision from intrapartum transmission
Electrocautery
Laser vaporization Diagnosis & Evaluation
Intralesional interferon - Diagnostic investigations:
- Vaccination: Tissue culture
Gardasil - Requires live cells, expensive
- Quadrivalent vaccine (protects against HPV - Not routinely done
serotypes 6, 11, 16 & 18) manufactured by Merck Urine antigen test
- Approved for use between 9 & 26 years of age PCR
Cervarix - Done using urine or endocervical swab sample
- Bivalent vaccine (protects against HPV serotypes
16 & 18) manufactured by GlaxoSmithKline Management
- Approved for use between 9 & 45 years of age - Pharmacological therapy:
- Other considerations: Doxycycline 100mg twice daily x 7 days
Do urine pregnancy test Azithromycin 1g single dose (safe in pregnancy)
Offer testing for other sexually transmitted diseases Ofloxacin 400mg once daily x 7 days
Advice on barrier contraception Erythromycin 500mg twice daily x 14 days (safe in
pregnancy)
- Other considerations:
Do urine pregnancy test
Offer testing for other sexually transmitted diseases
Advice on barrier contraception
Contact tracing
Abstain from sexual contact within 7 days after last
sexual partner starts on treatment to minimize risk of
reinfection

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Gonorrhea Other Sexually Transmitted Infections

Microbiology & Pathophysiology Syphilis


- Caused by Neisseria gonnorhoeae - Caused by Treponema pallidum
Gram negative diplococci Spirochete bacteria
Infects the same columnar epithelial cells as - Clinical features:
Chlamydia trachomatis, additionally able to infect the Primary syphilis
pharynx in about 10%, establishing throat carriage - Chancre (painless genital ulcer)
No effective immunity conferred even though - Regional lymphadenopathy (inguinal)
antibodies are produced after 1 episode of infection, Secondary syphilis
hence multiple reinfections are possible - Systemic rash (usually involves palms & soles)
- Generalized lymphadenopathy
Clinical Features - Condylomata lata (warts in anogenital areas)
(mostly similar to Chlamydia) - Mucous patches (lesions on mucous membranes,
- Asymptomatic e.g. snail patch ulcers in mouth)
Asymptomatic carriage in most infected females & Tertiary syphilis
only 5% of infected males - Neurosyphilis (general paresis of the insane, tabes
- Symptomatic gonococcal infection: dorsalis, Argyll Robertson pupils)
Gonococcal urethritis - Gummatous syphilis (granulomatous lesions
Mucopurulent cervicitis (15% of untreated cases progressing on to necrosis, leaving gumma ulcers,
progress further to more severe upper tract infections) perforations - on skin, mucous membranes & bone)
Acute salpingitis - Syphilitic aortitis (vasculitis of the thoracic aorta
Pelvic inflammatory disease leading to aortic regurgitation, ascending aortic
Fitz-Hugh-Curtis syndrome (perihepatitis) aneurysms, coronary artery ostia narrowing)
Proctitis Congenital syphilis (vertical transmission)
- Pregnancy-related complications & sequelae: - Hutchinsons triad (interstitial keratitis, 8th nerve
Subfertility deafness, Hutchinsons teeth notched incisors)
Ectopic pregnancy - Neonatal bullous rash (may go on to develop
Preterm labour lesions resembling secondary syphilis, gumma &
Chorioamnionitis neurosyphilis)
Post-partum endometritis - Treatment:
Ophthalmia neonatorum & neonatal pneumonia IM benzathine penicillin G
from intrapartum transmission
Chancroid
Diagnosis & Evaluation - Caused by Haemophilus ducreyi
- Diagnostic investigations: - Clinical features:
Gram stain of discharge or endocervical swab Chancroid (aka soft chancres; painful genital lesions)
- Visualization of gram negative diplococci in Usually accompanied by regional lymphadenopathy
polymorphonuclear cells (neutrophils) - Treatment:
- Highly sensitive for diagnosis of gonorrhea in Azithromycin PO 1g single dose
men, but only 50% sensitive in women Ceftriaxone IM 250mg single dose
Bacterial culture
- Gonococcus is fastidious & requires culture on Granuloma inguinale (donovanosis)
chocolate agar (Thayer-Martin or Transgrow - Caused by Klebsiella granulomatis (used to be named
media culture) Calymmatobacterium granulomatis)
- Takes longer while but has good sensitivity - Clinical features:
(90%) and specificity (97%) Subcutaneous red raised nodules which break down
PCR to form painless ulcers that subsequently enlarge
- Done using urine or endocervical swab sample with prominent granulation tissue formation, tissue
loss & scarring
Management Spread to inguinal region causes periadenitis
- Pharmacological therapy: (pseudobubo formation) and pelvic fibrosis
Ceftriaxone IM 250mg single dose - Treatment:
Ciprofloxacin PO 500mg single dose Doxycycline PO 100mg twice daily x 3 weeks
Amoxicillin PO 1g single dose + probenecid 2g
- Concomitant treatment of Chlamydia empirically: Molluscum contagiosum
Recommended as 20-40% of gonococcal cervical - Caused by Molluscum contagiosum, a poxvirus
infections have concomitant Chlamydia infection - Clinical features: waxy papules
Azithromycin PO 1g single dose - Treatment: cryotherapy, topical imiquimod
- Other considerations:
Do urine pregnancy test Pediculosis pubis
Offer testing for other sexually transmitted diseases - Caused by Phthirus pediculosis, a crab louse
Advice on barrier contraception - Treatment: permethrin 1% cream rinse
Contact tracing
Abstain from sexual contact within 7 days after last Scabies
sexual partner starts on treatment to minimize risk of - Caused by Sarcoptes scabiei, a mite
reinfection - Treatment: permethrin 5% cream, ivermectin

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Pelvic Inflammatory Disease Clinical Features of PID
(the following delineates typical features of symptomatic PID; many
Infection of the female upper reproductive tract (endocervix, uterine cases of PID can be asymptomatic, which may come to clinical
cavity & endometrium, fallopian tubes, intraperitoneally) attention as a result of associated sequelae)
- History:
Etiology & Associations Presenting symptoms:
- Causative organisms: - Local symptoms (vaginal discharge, abnormal
Chlamydia trachomatis uterine bleeding, pelvic pain, dyspareunia, dysuria,
Neisseria gonnorhoeae abdominal pain)
Genital mycoplasmas: - Systemic symptoms (fever, nausea/vomiting)
- Mycoplasma hominis - Last menstrual period
- Ureaplasma urealyticum
Past gynaecological & obstetric history:
- Mycoplasma genitalium
- Previous episodes of PID
Other endogenous lower reproductive tract &/or
- History of reproductive tract instrumentation
gastrointestinal tract organisms (often isolated from
(recent uterine procedures, TOP, IUD insertion)
pelvic abscesses complicating PID):
- Previous ectopic pregnancies
- Escherichia coli
- History of subfertility
- Anaerobes (Bacteroides, Prevotella, anaerobic
- Previous obstetric events (miscarriage, preterm
Streptococci)
labour, chorioamnionitis, post-partum endometritis)
- Gardnerella vaginalis
- Last Pap smear & results
- Risk factors for PID:
Past medical, surgical & drug history:
Sexual behavior-related risk factors:
Sexual history:
- Young age (highest rates amongst sexually active
- Number of sexual partners
adolescents & young adults)
- Use of (barrier) contraception
- Multiple sexual partners
- Physical examination:
- Recent new partner (within previous 3 months)
General examination:
- Past history of sexually transmitted infections
- Vitals (temperature, HR, BP, RR, SpO2)
Uterine instrumentation:
- Assess for pallor & general well-being
- Termination of pregnancy
Abdominal examination:
- Insertion of intrauterine device (IUD-insertion
- Palpate for abdominal tenderness, rebound
related infections usually occur within the first 3
tenderness & guarding
weeks following insertion)
- Palpate for pelviabdominal masses
- Hysterosalpingography
- Percuss for shifting dullness
- In-vitro fertilization, intrauterine insemination
Pelvic examination:
- Inspect external genitalia for evidence of lower
Pathophysiology of PID
tract sexually-transmitted infections
- PID-causing organism usually gains entry via the lower
- Speculum examination to visualize cervix &
reproductive tract as a result of sexual intercourse or
vaginal canal (take relevant swabs for gram stain &
uterine instrumentation
culture; do Pap smear where applicable)
Acute cervicitis caused by Chlamydia or gonococcus
- Digital vaginal exam/bimanual exam to assess
can lead on to PID in 30% & 15% of untreated cases
for uterine size, adnexal masses & cervical
respectively
motion tenderness (tenderness elicited upon digital
- Ascending infection subsequently involves more
deflection of cervix to one side, felt on the side
structures & regions:
ipsilateral to the side of deflection; due to stretching
Endometrium
of inflamed broad ligament & adnexa)
- Not usually a problem in non-pregnant
women as the endometrium is shed regularly
Diagnosis & Evaluation
- In pregnancy, infection of endometrium can
- Urine pregnancy test (to exclude ectopic pregnancy)
result in miscarriage, preterm labour,
- Routine haematological tests:
chorioamnionitis & post-partum endometritis
Full blood count (anemia, leukocytosis)
Fallopian tubes
CRP & ESR
- Results in acute salpingitis
- Microbiological investigations:
Pelvic intraperitoneal cavity
Endocervical & high vaginal swabs for gram stain &
- Results in pelvic & tuboovarian abscesses
cultures (including chocolate agar)
Abdominal intraperitoneal cavity
Urine FEME & urine culture
- Distant abscesses, peritonitis (e.g. in the setting
Urine Chlamydia antigen test
of tuboovarian abscess rupture)
Offer other STI screening (HIV, hep B, VDRL)
- Fitz-Hugh-Curtis syndrome (perihepatic - Pelvic ultrasound:
inflammation & adhesions as a result of PID;
Visualize any adnexal masses suggestive of
classically can visualize violin-string adhesions
tuboovarian abscesses & fluid in the pouch of
when mobilizing the liver intraoperatively)
Douglas
- Scarring of infected areas as a result of PID can lead to
long-term sequelae even after resolution of the acute
episode of infection:
Chronic pelvic pain
Ectopic pregnancy (6x more likely)
Subfertility (14 times more likely)

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94
Management of PID

- Initial resuscitation & stabilization:


ABCs, establish IV access, do necessary initial
investigations, establish monitoring of vitals
Other initial considerations:
- Analgesia
- Remove IUCD if present & send it for culture
Admission for inpatient management if:
- Diagnostic uncertainty exists
- Severe symptoms & signs
- Presence of tuboovarian abscess &/or sepsis
- Inability to tolerate or failure to respond to
oral antibiotic therapy
- Pregnancy

- Antimicrobial therapy:
Inpatient empirical antibiotic regime: (i) + (ii) + (iii)
(i) Cefoxitin IV 2g 4 times daily or ceftriaxone
IV/IM 1g once daily
(ii) Doxycycline IV 100mg twice daily
(iii) Metronidazole IV 500mg twice daily
until patient condition improves, then continue
on oral therapy with:
(iv) Doxycycline PO 100mg twice daily +
metronidazole PO 500mg twice daily x 14 days
Outpatient empirical antibiotic regime (i) + (ii) + (iii):
(i) Ceftriaxone IM 250mg single dose or
cefoxitin IM 2g single dose with oral probenecid
(ii) Doxycycline PO 100mg twice daily x 14 days
(iii) Metronidazole PO 500mg twice daily x 14
days
***Note: review at 72 hours is recommended to
assess improvement on outpatient treatment

- Surgical intervention:
Indications for surgery in PID:
- Drainage of tuboovarian abscess
- Adnexal mass of uncertain diagnosis
- Treatment for other sequelae of PID (e.g.
salpingectomy for ectopic, hysterectomy for
refractory chronic pelvic pain, adhesiolysis for
intestinal obstruction from adhesions)

- Other general considerations:


Contact tracing, partner screening & treatment
- Avoid sexual intercourse until both parties
have completed treatment
Contraceptive counselling:
- Barrier contraceptives advisable to reduce risk
of STI transmission
- IUD not advisable due to heightened risk of
infection and ectopic pregnancy
- Consider hormonal contraception
Counsel on long-term sequelae:
- Risk of subfertility correlates with duration of
untreated illness & number of episodes of PID
(1st episode prompt treatment usually have well-
preserved fertility; impaired fertility risk doubles
with each subsequent episode)
- Chronic pelvic pain affects 30% of women
following PID to varying extents
- Increased risk of ectopic pregnancy in
subsequent pregnancies, hence early booking
visit to ascertain viable intrauterine pregnancy
via ultrasound is advisable

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95
FAMILY PLANNING
Principles of Contraception Risk of Contraceptive Failure During 1st Year of Use
Technically speaking, contraception refers to the prevention of Contraceptive Method Theoretical % Typical %
fertilization, whereas interception refers to the prevention of No contraceptive method 85 85
implantation (but both are broadly considered under contraception); Male sterilization 0.1 0.15
Female sterilization 0.5 0.5
Importance of Contraception Copper IUCD 0.6 0.8
Mirena 0.1 0.1
- Maternal benefits:
Norplant 0.2 0.2
Allows for a satisfying & safe sex life with the
Depot medroxyprogesterone acetate 0.3 6.7
freedom to decide if, when & how often to reproduce
Combined oral contraceptive pill 0.3 8.7
Prevents unplanned pregnancies which carry with it Progestin-only pill 0.5 8.7
a whole host of unnecessary maternal complications: Diaphragm with spermicide 6.0 16.0
- Risks involved with abortions Male condom 2.0 17.4
- Obstetric complications Nulliparous 9.0 16.0
Cervical cap
- Peripartum complications Multiparous 26.0 32.0
Barrier methods protect against sexually-transmitted Spermicide alone 15.0 29.0
diseases Rhythm method 19.0 25.3
- Fetal benefits: Coitus interruptus - 18.4
Allows optimization of fetal outcomes with proper
pre-conception care permitted when timing of Overview on Contraceptive Options
pregnancy can be controlled - Hormonal contraception
Planned pregnancies can also have earlier antenatal Oral contraceptives
care instituted to optimize care & allow for early - Combined oral contraceptives (COCs)
detection of pregnancy complications & fetal - Progestin-only pills (POPs)
anomalies Progestin depot injections
- Public health benefits: - Depot medroxyprogesterone acetate (aka
Decreases pregnancy-related maternal & fetal DMPA, Depo-Provera)
morbidity & mortality Progestin implants
Improves reproductive health of the population as a - Norplant
whole (physical, mental & social well-being) - Implanon
Barrier methods help prevent transmission of Levonorgestrel-releasing intrauterine system
sexually-transmitted diseases - Non-hormonal contraception
Copper intrauterine contraceptive device
The Ideal Contraceptive Male barrier contraception
- 100% effective - Male condoms
- Acts only on the genital tract (no systemic side effects) Female barrier contraception
- Removed from the act of coitus - Female condoms
- No short term or long term side effects - Cervical caps
- Immediate return of fertility when stopped - Diaphragms
- Simple, cheap & freely available Spermicides (usually used together with above
- Requires minimal motivation, maintenance & supervision mentioned barrier methods)
- Behavioral contraception
Assessment of Contraceptive Efficacy Rhythm method
- Pearl Index Coitus interruptus
Defined as the number of failures per 100 woman - Surgical sterilization
years (HWY) of exposure: Male sterilization (vasectomy)
Female sterilization (tubal ligation)
Total no. of accidental pregnancies x 12 x 100
Rate per HWY =
Total no. of months of use Factors to be Considered In Choosing Contraceptive Options
- Patient factors:
Limitation of this statistical analysis is the Reproductive factors
assumption that the rate of failures for each - Future reproductive intention
contraceptive method remains constant over a given Social factors:
period of time - Sexual habits (multiple partners?)
- Life table analysis - Motivation & compliance
Calculates a failure rate for a specified period - Education & socioeconomic factors
Eliminates the time-related biases present with the Medical factors:
Pearl Index, for example: - Age of patient
- Fertile couples getting pregnant & dropping - Existing medical/surgical/gynae conditions
out of the study early - Non-patient factors:
- Couples becoming more skilled at using a Methods available
form of contraceptive over time Government policies

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96
Hormonal Contraception - Types of administration:
21-day pack: 21 combined E + P pills
- To be taken from day 5 to day 26 of cycle,
Combined Oral Contraceptive Pills followed by a 7-day pill-free interval
- Menstruation occurs during the 7-day pill free
Composition of COCs period (withdrawal bleed), allows woman to
- Combination of synthetic estrogens & progestins experience normal menses & be sure that she is
- Synthetic estrogen options: not pregnant
Ethinyl estradiol (EE) 28-day pack: 21 combined E + P pills with 7 sugar pills
Mestranol - Uninterrupted pill-taking continuously with
- Progestin options: the 7-day sugar pill interval substituting the 7-
1st generation progestins day pill-free period of the 21-day pack
(estrane family) - Easier for woman to keep track of pills (dont
- Megestrol need to remember & count number of pill-free days
- Chlormadinone before starting on the next pack)
- Medroxyprogesterone acetate (Provera)
- Ethynodiol
- Norethisterone (aka norethindrone)
- Norethynodrel
2nd generation progestins
(gonane family; varying degrees of androgenic &
estrogenic activity as well)
- Levonorgestrel (LNG) 21-day pack 28-day pack
- Norgestrel
3rd generation progestins - Missed pills what to do?
(gonane family; minimal androgenic activity) Single active pill missed:
- Desogestrel - Take the pill as soon as remembered
- Norgestimate - Take the next pill at the usual time (e.g. if pill
- Gestodene taken at 8am every morning but forgotten until 5pm
4th generation progestins when it was taken, the next pill should still be taken
(minimal androgenic activity) at 8am again the following day)
- Drospirenone 2 active pills missed:
- Dienogest (Visanne) - At least 7 days of continuous pill-taking is
needed to effectively suppress endogenous FSH
Mode of Action of COCs production
- Inhibition of ovulation - After 2 active pills are missed, FSH starts
Hormones (especially estrogen) administered effect rising & recruiting follicles, necessitating a new
negative feedback inhibition of pituitary round of 7 continuous days of pill-taking before
gonadotropin production full contraceptive efficacy is restored
Blocks LH surge, hence inhibiting ovulation - If 7 active pills left in the pack: continue taking
- Affects tubular transport of ovum the rest of the pills + barrier contraception for at
- Thickens cervical mucus least 7 days in the meantime
Effect of progestin - If <7 active pills left in the pack: discard pack &
Blocks sperm penetration begin on a new pack + barrier contraception for at
- Induces endometrial thinning & atrophy least 7 days in the meantime
Effect of progestin - Efficacy of COCs:
Inhibits implantation Highly efficacious (0.1-3.0% failure rate)
Most failures are due to non-compliance, hence need
Administration of COCs for careful instructions & reinforcement of routine
- 2 different types of dosing regimen:
Monophasic: fixed dose of estrogen + progestin
throughout the cycle
- Microgynon 30: 30 g EE + 150 g LNG
- Nordiol: 50 g EE + 150 g LNG
- Yasmin: 30 g EE + 3mg drospirenone
Multiphasic: bi-/triphasic dose variations of estrogen +
progestin throughout the cycle to mimic normal cycle &
reduce the total hormonal dose per cycle of administration
(no proven advantage over monophasic however)
- Triquilar: EE + LNG
- Trinordiol: EE + LNG
- Qlaira: estradiol valerate + dienogest

FAMILY PLANNING

97
Benefits of COCs - Other systemic side effects:
- Contraceptive benefits: Carbohydrate metabolism:
Highly effective in pregnancy prevention, with - Impairs glucose tolerance & induces
regular withdrawal bleeding providing reassurance peripheral insulin resistance (progestin effect)
Decreased incidence of ectopic pregnancy - Cautious use in latent diabetes; can be used
Removed from the act of coitus with drug/dietary modifications in young
Readily reversible, with speedy return of fertility diabetes; avoid use in advanced or long-
- Non-contraceptive benefits: standing diabetics
Menstrual benefits: - Long term use does not in itself cause diabetes
- Regulates menses Lipid metabolism:
- Reduces menstrual loss (any long-term progestin - 19-norsteroids increase LDL & decrease HDL
thins the endometrial lining) - However, estrogens counteract this effect
- Relieves dysmenorrhea (anovulatory cycles tend Vitamin levels:
to have less dysmenorrhea) - Decreases vitamins B2, B6, B12 & folic acid
Cancer benefits: - Increases iron levels
- Decreases incidence of epithelial ovarian Pregnancy outcomes
cancer (reduced ovulation reduces repeated damage - No increase in spontaneous abortion or fetal
to the ovarian epithelium) abnormalities in former users of COCs
- Decreases incidence of endometrial cancer - No proven teratogenic potential (if pregnancy
(reduces number of cycles a woman might experience occurs during use of COCs)
with unopposed estrogen action on endometrium)
Other gynaecologic benefits: Drug Interactions of COCs
- Decreases incidence of benign breast diseases - Drugs which reduce COC efficacy:
- Possibly protective against benign ovarian Anticonvulsants: phenytoin, phenobarbitone
cysts, fibroids, endometriosis & osteoporosis Antibiotics: rifampicin, griseofulvin
Sedatives: chlordiazepoxide
Side Effects of COCs - Drugs requiring dose adjustment if COC is taken:
- Minor side effects: Anticoagulants (needs increased dose)
Estrogen-related: nausea, vomiting, headache, giddiness Tricyclic antidepressants (needs increased dose as COCs
Progestin-related: weight gain, acne, facial pigmentation can aggravate depression)
E&P-related: breast fullness & tenderness Insulin & oral hypoglycemic (needs increased dose)
Others: breakthrough bleeding, loss of libido, depression Corticosteroids (needs decreased dose)
- Major side effects:
Effects on circulatory system: Contraindications to Use of COCs:
- Venous thromboembolism, coronary arterial - Absolute contraindications:
disease & stroke (both hemorrhagic & ischemic) Circulatory disorders (thrombotic disorders, coronary
- Primarily related to estrogen dose ( clotting artery disease, stroke)
factors, anti-coagulants, platelet aggregation) Hepatic disorders (impaired liver function, existing
- Risk is much more significant for the high- hepatic adenoma)
dose (50 g) estrogen pills vs the lower dose Estrogen-dependent malignancies (breast cancer,
estrogen pills (30 g) existing endometrial cancer)
- VTE: OR 3.25 for non-Europeans, 4.15 for Pregnancy or breast-feeding (interferes with lactation)
Europeans; applies only to current users; unrelated Any undiagnosed abnormal uterine bleeding
to duration of use; COCs should hence be stopped 4 - Relative contraindications:
weeks prior to major surgery Smokers >35 years old
- Coronary arterial disease: RR 1.8 (4.2 for high- Metabolic diseases (diabetes, hypertension, obesity)
dose pills), applies to current users; young women Migraine
have non-significant increased risk (RR 1.1), Gallbladder disease
especially in the absence of risk factors Cardiac disease
- Stroke: lower-dose COC (<50 g EE) does not Planned elective surgery
increase risk of hemorrhagic stroke in women <35,
small increase for women >35; ischemic stroke risk Combined Patches
has overall small increased risk (OR<3.0) but lower - Ortho Evra
in the women <35 age group (norelgestromin/ethinyl estradiol transdermal system)
Effects on liver disease: Applied once weekly x 3 weeks (usually on buttock)
- 19-norsteroids alter liver function & cause Start on day 1 or within 1st week of menses
cholestasis, hence best avoided in women with Similar side-effect profile & efficacy as COCs
active hepatitis or history of cholestatic jaundice
or symptomatic gallstone disease
- Long term COC use also increases risk of
developing benign hepatic adenomas (10-20x)
Effects on breast cancer:
- Current users: slight increased risk (RR 1.24)
- <10 after stopping: small increased risk of
having breast cancer diagnosed
- 10 years after stopping: no increased risk
- Women starting COCs before 20 years old:
higher risk (RR 1.59)

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Progestin-Only Pills Contraindications to use of POPs
- Breast cancer
Composition of POPs - Liver disease
- Estrogen-free oral contraceptive pills containing low-dose - Undiagnosed abnormal uterine bleeding
progestin (aka progestogen aka synthetic progesterone) - Previous ectopic pregnancy
- Progestin options (see Combined Oral Contraceptive Pills)
Progestin Depot Injections
Mode of Action of POPs
- Thickens cervical mucus Mode of Action of Progestin Depot Injections
Blocks sperm penetration - Similar to progestin-only pills
- Induces endometrial thinning & atrophy
Inhibits implantation Administration of Progestin Depot Injections
- Inhibits ovulation (in 50% of cases) - Administration:
Depot medroxyprogesterone acetate (Depo-Provera)
Administration of POPs - Intramuscular injection
- Administration: - Continuous release occurs over 12 weeks
Taken daily at the same time each day throughout - 150-300mg every 3 months
cycle Norethisterone enanthate (Noristerat)
- Missed pills what to do? - Intramuscular injection
Missed for <3 hours - Continuous release occurs over 8 weeks
- Take the pill as soon as remembered - 200mg every 2 months
- Take the next pill at the usual time the
following day
- No need for barrier contraception
Missed for >3 hours
- Take 1 pill as soon as remembered (even if >1
pill have been missed)
- Take the next pill at the usual time the
following day
- Use barrier contraception for at least 2 days
- Efficacy of POPs:
Less efficacious than COCs (0.5-10.0 per HWY) - Efficacy of Progestin Depot Injections
Highly effective (failure rate of 0.1-0.6% in 1st year)
Benefits of POPs
- Contraceptive benefits: Benefits of Progestin Depot Injections
Immediately effectively (<24 hours) - Contraceptive benefits:
Decreased incidence of ectopic pregnancy Similar to progestin-only pills plus:
Removed from the act of coitus Less need for patient compliance (vs taking pills)
Readily reversible, with speedy return of fertility BUT return of fertility is delayed (median time of 10
Does not affect lactation months)
Suitable for patients with medical contraindications - Non-contraceptive benefits:
to exogenous estrogens Similar to progestin-only pills plus:
- Non-contraceptive benefits:
Menstrual benefits: Side-effects of Progestin Depot Injections
- Reduces menstrual loss (any long-term progestin - Menstrual irregularities:
thins the endometrial lining) Irregular menstrual spotting (60-70%)
- Relieves dysmenorrhea Eventual amenorrhea (50-80%)
Cancer benefits: - Weight gain
- Decreases incidence of endometrial cancer - Delay in return of fertility (median time of 10 months)
(reduces number of cycles a woman might experience - Possible bone loss for long term use
with unopposed estrogen action on endometrium)
Contraindications to use of Progestin Depot Injections
Side Effects of POPs - Breast cancer
- Menstrual problems: - Suspected pregnancy
Increased menstrual irregularity (biggest side-effect of - Undiagnosed abnormal uterine bleeding
any progestin-only contraceptive)
- Progestogenic side-effects:
Breast engorgement & tenderness
Headache, nausea
- Androgenic side-effects
Acne, hirsutism
More so with the 19-nortestosterone derivatives
(norethisterone, Levonorgestrel etc)
Newer progestins actually have anti-androgenic
properties & are licensed for even the use of acne
treatment (Dienogest, drospirenone)

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Progestin Implants Levonorgestrel-Releasing Intrauterine System
(Mirena)
Mode of Action of Progestin Implants
- Similar to progestin-only pills Mode of Action of Mirena
- Thickens cervical mucus
Administration of Progestin Implants Blocks sperm penetration
- Administration: - Induces endometrial thinning & atrophy
Levonorgestrel implant (Norplant) Inhibits implantation
- 6 rods placed subdermally in arm - Inhibits sperm motility & function inside the uterus &
- Sustained release of Levonorgestrel fallopian tubes
- Change every 5 years Inhibits fertilization
- Removed using a forceps through a small skin - Does not affect ovarian function in most women
incision made in the arm
Etonogestrel implant (Implanon) Administration of Mirena
- 1 rod placed subdermally in arm - Composition of Mirena:
- Sustained release of Etonogestrel Silastic rod impregnated with 52mg of levonorgestrel
- Change every 3 years Slow release at 20 g/day for 5 years
- Removed using a forceps through a small skin - Administration:
incision made in the arm Insertion should be done when sure that patient is
not pregnant:
- Anytime when patient is very sure she has no
possibility of being pregnant
- Days 1-7 of menses
- Post-abortion
- Post-partum not recommended due to very high
expulsion rates (wait till 6 weeks post-partum)
Outpatient office procedure without anesthesia
Speculum is used to visualize cervix
Norplant Implanon Vulsellum forceps is used to grasp cervix
Under transabdominal ultrasound guidance, uterine
- Efficacy of Progestin Implants: sound inserted through the cervix to gauge the depth
Highly efficacious (failure rate 0.2/100 users in 1st year) of the uterine cavity (6mm required for use of Mirena)
Almost similar efficacy as sterilization in 1st 3 years Mirena applicator is then inserted through the cervix
& Mirena is placed within the uterine cavity
Benefits of Progestin Implants Removed after 5 years (just pull on attached thread)
- Contraceptive benefits:
Similar to progestin-only pills plus:
Less need for patient compliance (vs taking pills)
- Non-contraceptive benefits:
Similar to progestin-only pills plus:
No significant effect on liver, kidney, thyroid, lipid
metabolism & hemostasis
- Efficacy of Mirena:
Side Effects of Progestin Implants Highly efficacious (0-0.2% in 1st year)
- Menstrual irregularities: Unsurpassed efficacy
Prolonged spotting Provides fertility control comparable to female
Breakthrough bleeding sterilization
Amenorrhea
- Minor side-effects: Benefits of Mirena
Headache, dizziness, nausea - Contraceptive benefits:
Weight gain, acne Similar to progestin-only pills plus:
- Insertion & removal requires minor surgical procedure Less need for patient compliance (vs taking pills)
Lowest plasma concentration of hormone amongst
Contraindications to use of Progestin Implants all the hormonal methods of concentration
- Breast cancer - Non-contraceptive benefits:
- Suspected pregnancy Menstrual benefits:
- Undiagnosed abnormal uterine bleeding - Reduction in menstrual flow (reduces
menorrhagia by 97% after 1 year of use)
- Effective relieve of dysmenorrhea (used in
adenomyosis, endometriosis)
- Treats endometrial hyperplasia
Other gynaecologic benefits:
- Decreases growth & incidence of fibroids
- Decreases incidence of PID
- Decreases incidence of ectopic pregnancy
No significant effect on carbohydrate metabolism,
coagulation, liver enzymes or lipid levels

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Side-Effects & Complications of Mirena
- Menstrual irregularities:
Non Hormonal Contraception
Prolonged spotting
Breakthrough bleeding Copper Intrauterine Contraceptive Device
Amenorrhea
- Minor side-effects: Mode of Action of Copper IUCD
Headache, dizziness, nausea - Interferes with sperm transport
Weight gain, acne - Spermicidal
- Insertion requires minor procedure: - Interferes with embryo implantation
Crampy discomfort may be experienced
Risk of bleeding & uterine perforation Administration
Risk of infection (if at all, usually occurs in 1st 3 weeks) - Types of IUCDs:
- Expulsion (drop out) rate = 0.5% Many types available (different in shapes, size, material)
Main type used now is the Copper T-380
Contraindications to use of Mirena
- Breast cancer
- Suspected pregnancy
- Undiagnosed abnormal uterine bleeding
- Active pelvic inflammatory disease
- High risk of PID (e.g. multiple sexual partners)
- Abnormal uterine cavity (large fibroids, congenital
abnormalities)

Management of Intrauterine Device Problems


- Missing thread
Patients should be advised to check monthly for the Types of intrauterine devices Copper T-380
thread to ensure that device in still in place
If suspected to be missing: - Administration of Copper IUCD:
- Speculum examine to look for thread Similar to that for Mirena
- Pelvic ultrasound to look for device - Efficacy of Copper IUCD:
- X-ray may be required if pelvic ultrasound Highly effective
cannot locate device
- Bleeding Benefits of Copper IUCD
Observe & follow-up - Contraceptive benefits:
Remove device if patient cannot stand it Highly & immediately effective
If persistent following removal, investigation as per Minimal patient compliance required
for abnormal uterine bleeding Removed from the act of coitus
- Infection Readily reversible, with speedy return of fertility
Remove device Does not affect lactation
Antibiotics Suitable for patients with medical contraindications
to hormonal contraceptives

Side Effects & Complications of Copper IUCD


- Menstrual problems:
Increased menstrual bleeding
Increased menstrual cramps
- Other gynaecologic side-effects:
Increased risk of PID
If pregnancy occurs, more likely to be ectopic
- Insertion requires minor procedure:
Crampy discomfort may be experienced
Risk of bleeding & uterine perforation
Risk of infection (if at all, usually occurs in 1st 3 weeks)
- Expulsion of IUCD can occur

Contraindications to use of Copper IUCD


- Suspected pregnancy
- Undiagnosed abnormal uterine bleeding
- Active pelvic inflammatory disease
- High risk of PID (e.g. multiple sexual partners)
- Abnormal uterine cavity (large fibroids, congenital
abnormalities)

Management of Intrauterine Device Problems


- Similar to that for Mirena

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Barrier Methods Behavioral Methods

Types of Barrier Methods Types of Behavioral Methods


- Male condoms - Calendar method
Worn over the penis before intercourse occurs Requires regular cycles
- Female condoms Monitor for at least 6 cycles first
Placed into the vagina before intercourse occurs Fertile period is from:
- Cervical caps & diaphragms [shortest cycle 18] to [longest cycle 11]
Needs to be fitted in place before intercourse occurs - Basal body temperature method
Removed 6 hours after intercourse is over - Cervical mucus (Billings technique)
- Spermicide
Usually used in conjunction with above mentioned Mode of Action of Behavioral Methods
barrier methods - Avoid intercourse during calculated fertile period
Comes in various forms (tablets, cream, aerosols)
Advantages of Behavioral Methods
- Free, no side effects

Disadvantages of Behavioral Methods


- Not very effective
- Requires willingness to abstain during fertile period
- Needs motivation & record keeping

Left: female condom Placement of female condom


Right: male condom

Diaphragm & cervical cap Placement of diaphragm & cervical cap

Mode of Action of Barrier Methods


- Prevents sperm from reaching upper genital tract
- Spermicides causes sperm cell membrane lysis

Advantages of Barrier Methods


- Contraceptive benefits:
Immediately effective
Easily available & used
Does not affect fertility or lactation
No systemic side effects
Protects against sexually-transmitted diseases

Disadvantages of Barrier Methods


- Problem with patient compliance:
Interferes with coital act, decreased sexual pleasure
Needs consistency in usage
Needs both partners to agree to its use
Cervical caps & diaphragms need pre-fitting &
removal only after 6 hours post-intercourse
- Possible allergy (to latex or spermicide)

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Surgical Sterilization Emergency Contraception
Male Sterilization
Indications for Emergency Contraception
- Vasectomy
- No contraception used before intercourse occurred
Interruption of the vas deferens
- Contraceptive accident
- Techniques:
- Victim of sexual assault
No-scalpel vasectomy (under local anesthesia in office)
Outpatient surgical procedure
Approach to Patient Presenting for Emergency Contraception
- Essential history to elicit:
Last menstrual period
Cycle length
Timing of 1st act of unprotected intercourse (patient
may have had multiple episodes of unprotected intercourse
before presentation)
Relevant medical & surgical history (to assess for
contraindications to the options for emergency
contraception):
- Drug allergies
- Metabolic diseases (DM, hypertension, lipids)
Conventional vasectomy No-scalpel vasectomy
- Cardiovascular disease, stroke
- Venous thromboembolic disease
- Efficacy:
- Liver disease
Highly effective (more so than female sterilization)
- Any undiagnosed abnormal uterine bleeding
Need to wait for 3 months after procedure before
- Any malignancies (especially breast)
sterility sets in completely (should use barrier
Relevant social history:
contraception in the meantime)
- Advantages: - Sexual habits (may be at risk of STDs, offer tests)
Similar to that for female sterilization - Sexual assault requires counselling & police
- Disadvantages: - Essential patient counselling:
Anti-sperm antibodies may develop, resulting in Possibility of failure (especially if multiple episodes of
intercourse have already occurred outside the protective
persistent infertility despite reversal of vasectomy
period of the emergency contraception used)
should the male choose to down the road
Possible side effects & complications involved
Importance of regular contraception
Female Sterilization
Importance of follow-up if delayed menses occurs
- Tubal ligation
Interruption of the fallopian tubes
Performed when sure that woman not pregnant: Options for Emergency Contraception
- Woman is sure she is not pregnant - Combined hormonal pill
Known as the Yuzpe regime
- Follicular phase of menstrual cycle
Requirement:
- Postpartum sterilization (PPS)
- Patient presents within 72 hours of intercourse
- Post-abortion
- Techniques: 2 tablets of 50 g EE + 500 g norgestrel (or 250 g
Abdominal approach levonorgestrel) given at presentation; repeated again
- Via mini-laparotomy or laparoscopy 12 hours later
- Pomeroy technique (ligation & division of tubes) Failure rate = 2%
- Filshie clips (clips used to clamp tubes) Side effects: nausea, vomiting, breast tenderness
- Falope ring (ring placed around tubes) - Progestin-only pill
Uses Postinor
Hysteroscopic approach
Requirement:
- Tubal plugs anchored in the proximal portions
- Patient presents within 48 hours of intercourse
of the tube to incite fibrosis
750 g levonorgestrel given at presentation; repeated
again 12 hours later
Failure rate = 3%
Side effects: similar to above but less
- Copper intrauterine contraceptive device
Pomeroy Filshie clip Falope ring Tubal plug Requirement:
- Patients presents within 5 days of intercourse
- Efficacy: Copper IUCD inserted at presentation
Highly effective & immediate effect Failure rate < 1%
- Advantages: Side effects: as per for copper IUCD
No side-effects
Does not interfere with coital act or breast-feeding
Permanent contraception
- Disadvantages:
Irreversible (success of reversal of sterilization varies)
Surgical procedure (pain, bleeding, anesthesia risk)
Small risk of failure (0.1-0.4%)
May regret later in life

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Termination of Pregnancy Indications for Induced Abortion
- Maternal indications:
Abortion refers to the disruption of an established pregnancy, which Cardiac disease
may be spontaneous (a miscarriage) or induced (termination of Malignancy
pregnancy) via medical &/or surgical interventions Renal disease
Psychotic state
Abortion Legislation in Singapore - Fetal indications:
- Induced abortion = termination of pregnancy before 24 Genetic/chromosomal anomalies
weeks gestation (i.e. before fetal viability) Fetal anomalies
- Evolution of abortion legislation in Singapore: - Social indications:
Before 1967: Unwanted pregnancy
- Legal abortion restricted only to cases in
which maternal life was endangered Pre-Abortion Assessment
1967: Abortion Authorization Board set up - Confirm pregnancy viability & site
- Abortion extended to those with fetal Exclude ectopic pregnancy
malformations, mothers who were victims of Assess if fetus is viable (if non-viable, patient is
sex crimes or intercourse with a mentally insane technically experiencing a missed miscarriage, in which
person case evacuation of the uterus can be offered as a
1968: First Abortion Bill management option; this would technically not be an
- Law liberalized to allow abortion for family, induced abortion, hence all the legislations requiring pre-
social & economic reasons abortion counselling would not apply)
1974: New Abortion Act - Determine gestational age
- Abortion could be performed at the request of If too early to confirm viability of pregnancy, may
any female up to 24 weeks of pregnancy by a need to follow-up patient with a repeat scan
registered doctor with prescribed qualification Gestational age important to determine the method
in an approved institution of induced abortion used (see below)
- This is regardless of age Gestational age >24 weeks is legally not allowed for
- Does not require consent of anyone (including an induced abortion except in special circumstances
parental consent even in the case of minors) (e.g. late detection of fetal anomaly which is not
1986: Abortion Counselling Introduced compatible with extra-uterine life)
- Mandatory pre-abortion counselling - Determine parity
- Consent for abortion procedure can only be Nulliparous women tend to require cervical priming
given 48 hours after counselling is completed before surgical termination of pregnancy
- Impact of legislations on legalized abortions in Singapore Nulliparous women also tend to have higher risk of
Total number of legalized abortion per year rose cervical injury during surgical termination of
from 1913 (year 1970) to 23512 (year 1986) with pregnancy with sequelae of cervical incompetence
increasingly liberal abortion laws - Determine maternal rhesus status
Following introduction of abortion counselling, total Give anti-D Ig after abortion if rhesus negative &
number of legalized abortions per year fell gradually antibody negative to prevent isoimmunization
until it reached a stable rate of ~12000 from year 2004 - Mandatory pre-abortion counselling
onwards Involves watching a abortion counselling video
However, when fertility rates are taken into account, Consent for abortion can only be taken 48 hours later
the falling fertility rates over time meant that the so patient has to return if she still wishes to proceed
proportion of pregnancies abortion did not change
despite the introduction of mandatory pre-abortion
counselling (still about 1 in every 4 pregnancies)

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Methods for Induced Abortion - Second trimester termination of pregnancy
- First trimester termination of pregnancy Medical abortion
Medical abortion - Options include: misoprostol + mifepristone
- Can be used up to 8 weeks gestation (aka RU 486, an anti-progesterone; not available
- Options include: misoprostol + mifepristone locally) or misoprostol alone
(aka RU 486, an anti-progesterone; not available - Essential induces a mini-labour
locally) or misoprostol alone - Route of administration: vaginal pessary
- Route of administration: vaginal pessary Surgical abortion
- Dosage of misoprostol for medical abortion: - Cervical preparation
loading dose of 800 g followed by 3 doses of 400 g - Dilatation & evacuation
given 3-hourly
- Success rate = 96%
Surgical abortion
- Can be used anytime in 1st trimester
- Done via vacuum aspiration
- Pre-aspiration cervical priming using
misoprostol may be needed especially in cases
where difficulty of cervical dilatation is
expected (e.g. nulliparous)
- Route of administration: vaginal pessary
- Dosage of misoprostol for cervical priming:
400 g given 3 hours before surgical abortion
- Alternative method of cervical priming is the
use of laminaria tents (osmotic dilators which
gradually dilate the cervix as they enlarge in
diameter through absorbing bodily fluid)
- Success rate >99%

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Complications of Induced Abortion
(in general, 1st trimester abortions carry much lower risk of
complications as compared to 2nd trimester abortions)
- Complications of medical induced abortions:
Bleeding
Retained products of conception
- Complications of surgical induced abortions:
Immediate:
- Bleeding, infection, anesthesia risk
- Cervical injury
- Uterine perforation
- Bladder &/or bowel injury
- Retained products of conception (much less
likely as compared to medical induced abortions)
Long-term:
- Cervical incompetence
- Uterine rupture in subsequent pregnancy
- Placenta accreta
- Subfertility (Asherman syndrome, tubal blockage)
- Chronic pelvic inflammatory disease
- Rhesus isoimmunization
- Psychological

Follow-up After Induced Abortion


- Immediate follow-up (1-2 weeks after abortion):
Assess for retained products of conception
- Any persistent per-vaginal bleeding?
- Speculum examination for signs of RPOC
(opened os, visualized products of conception)
Assess for infection
- Any fever, lower abdominal pain, discharge?
- Abdominal & pelvic examination for
tenderness & discharge
Psychological support
Advice on contraception
- Delayed follow-up (6-8 weeks after abortion):
Assess for return of normal menses
Psychological support
Advice on contraception

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INFERTILITY
Approach to Infertility Physical Examination
- General examination:
Height, weight, BMI (overweight? underweight?)
Definitions Signs of virilization & hirsutism
- Infertility = inability to conceive following 1 year of Signs of thyroid disease
unprotected intercourse Visual field testing for bitemporal hemianopia
Primary infertility = when infertility occurs without - Breast examination:
any prior pregnancy Nipple discharge (hyperprolactinemia)
Secondary infertility = when infertility occurs after a - Abdominal examination:
previous conception Palpable masses, tenderness
- Average time required for conception in couples who will Scars from previous surgeries
eventually attain pregnancy: - Pelvic examination:
After 3 months of exposure 57% Assess uterine size, version & mobility, presence of
After 6 months of exposure 72% adnexal masses, tenderness & thickened uterosacrals
After 1 year of exposure 85%
After 2 years of exposure 93% Range of Investigations for Infertility
- Hormonal investigations:
Incidence of Different Causes of Infertility Female: day 2-3 FSH, LH, estradiol, testosterone & TSH
- Male coital factor (40%) + mid-luteal (day 20-22) prolactin & progesterone
- Female factor (30%) Male: FSH, prolactin & TSH
Ovulatory factor - Infection screen:
Tuboperitoneal factor To assess for PID in female
Uterine factor - Imaging studies:
Cervical factor Pelvic ultrasound
- Both male & female factors (23%) - Assesses uterine size & pathology (fibroids,
- Unexplained infertility (7%) endometrial polyps, congenital anomaly)
- Assesses adnexal masses (endometrioma,
History polycystic ovaries)
- Conception attempts: Hysterosalpingography
Age (especially womans age, as age itself is related to - Assesses uterine cavity
decreasing fertility) - Assesses tubal patency
Duration couple has tried conceiving so far Saline sonography
Any previous successful conceptions - Assesses uterine cavity
- Menstrual history: - Assesses tubal patency
Age of menarche, last menstrual period - Diagnostic laparoscopy:
Regularity & length of cycles Can aid in diagnosis for cases of infertility remaining
- Existing symptoms: unexplained despite more conservative
Pelvic symptoms (pelvic pain, dysmenorrhea, investigations
dyspareunia, abnormal uterine bleeding, vaginal Can assess for:
discharge) - Pelvic adhesions
Symptoms related to systemic causes (galactorrhea, - Signs of endometriosis
visual disturbances) - Tubal patency
- Past medical, surgical & gynaecologic history: - Semen analysis:
Previous infections (STDs, PID, mumps) Baseline investigation to assess possible male factor
Known gynaecologic conditions (PCOS, uterine infertility
fibroids, endometriosis etc) - Other tests:
Past gynaecologic procedures (pelvic surgery, tubal Basal body temperature monitoring
surgery, uterine instrumentation) Post-coital test
Past exposure to radiation or chemotherapy (husband
as well) Prioritizing Investigations in Infertility
Drug history - 1st-line investigations:
- Social history: Hormonal tests + pelvic ultrasound + semen analysis
Smoking & alcohol habits (of husband as well) infection screen
Occupation (of husband as well) Convenient, non-invasive procedures which can
- Coital history: guide the need for further evaluation (e.g. abnormal
Frequency of sexual intercourse semen analysis may require urologist referral)
Any coital difficulties (dyspareunia, ejaculatory - 2nd-line investigations:
problems) Hysterosalpingography or saline sonography
More invasive procedures with attendant risks
Assesses uterine cavity & tubal patency
- 3rd-line investigations:
Diagnostic laparoscopy
Surgical procedures with attendant risks

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107
Etiologic Factors of Infertility Relevant terminology of semen analysis:
- Aspermia = no ejaculate
- Azoospermia = no measurable sperm in semen
Male Coital Factor - Oligospermia = low sperm concentration/count
- Asthenospermia = poor sperm motility
Contributory Etiologies - Teratospermia = abnormal sperm morphology
- Problems with sperm production:
Congenital abnormalities (undescended testes, gonadal - Endocrine evaluation:
dysgenesis, congenital absence of vas deferens) (may be useful in men with abnormal semen analysis findings
Varicocele to elucidate possible underlying causes)
Genital tract infections (prostatitis, orchitis) Thyroid function test (for hypothyroidism)
Endocrine causes (hypothalamic-pituitary dysfunction, Prolactin (for hyperprolactinemia)
hypothyroidism, hyperprolactinemia) Follicle-stimulating hormone (FSH)
Allergic reactions, anti-sperm antibodies - Elevated FSH levels in a male generally
Surgery or trauma to genitalia or inguinal region (e.g. indicates substantial testicular parenchymal
previous inguinal hernia repair) damage (as the hormone inhibin normally produced
Exposure to radiation by the Sertoli cells of the testes provides the principle
Exposure to toxins: excessive alcohol & smoking, negative feedback control of FSH secretion by the
heavy metals (lead, cadmium) or chemotherapeutic anterior pituitary)
agents (e.g. cyclophosphamide) - Elevated FSH thus predicts a high likelihood
Excessive genital exposure to environmental heat of failure of most forms of treatment targeted at
(sauna, hot tubs, tight underwear, occupational exposure) improving male fertility, but does not predict
- Problems with sperm deposition: the likelihood of sperm recovery from testicular
Abnormal location of urethral meatus sperm extraction for assisted reproductive
Ejaculatory problems (e.g. premature ejaculation) techniques
Erectile dysfunction (idiopathic, alcoholism, diabetes,
hyperprolactinemia etc) Management
- Problems with sperm function: - Conservative management:
Use of lubricants toxic to sperm function Coital advice:
Poor intrinsic sperm function: low motility &/or - Scheduled sexual intercourse (once every 1-2
abnormal morphology (can be idiopathic or due to days during periovulatory period days 12 to 16 of a
similar causes as for problems with sperm production) 28-day cycle)
- Avoid use of toxic lubricants
History & Physical Examination - Woman to lie on her back for at least 15
- History: minutes after coitus to prevent rapid loss of
Check if patient has ever fathered a child before semen from the vagina
Assess for possible causes of infertility Avoid environmental exposures:
- Physical examination: - Cut down on alcohol & smoking
(usually done by urologist upon referral after an abnormal - Avoid excessive genital heat exposure
semen analysis report) - Treatment of underlying causes:
Check location of urethral meatus Impaired sperm production due to hypothalamic-
Assess testicular size pituitary dysfunction or unknown cause:
Assess for presence of varicocele - Clomiphene
- Gonadotropins (e.g. hCG or hMG - human
Diagnosis & Evaluation menopausal gonadotropin)
- Semen analysis: - Testosterone, mesterolone
Important considerations: Hyperprolactinemia:
- Semen analysis sample should be collected - Dopamine agonists (bromocriptine, cabergoline)
after a 2-4 day period of abstinence from sex - Surgical resection of pituitary adenoma
- Entire ejaculate should be collected in a clean Infection:
non-toxic container - Treat infection
- Semen quality varies greatly between samples, Varicocele:
hence an accurate appraisal of abnormal semen - Venous plexus ligation
requires at least 3 analyses - Assisted reproductive techniques:
Reference values for semen analysis report: (indicated if infertility is refractory or not amenable to
Characteristic Reference Value treatment by other modalities)
WHO Semen Analysis Guidelines 2009 Intrauterine insemination (IUI) with own or donor
Semen volume 1.5ml sperm
Sperm concentration 15 million/ml In-vitro fertilization (IVF) intracytoplasmic sperm
Total sperm number 39 million per ejaculate injection (ICSI)
Total motility (PR + NP) 40%
Sperm motility
Progressive motility (PR) 32%
Sperm morphology 4% normal forms (by strict criteria)
Other Parameters not in WHO Guidelines 2009
White blood cells <1 million/ml
Immunobead test <20% spermatozoa with adherent particles
SpermMar test <10% spermatozoa with adherent particles

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108
Female Ovulatory Factor Female Tuboperitoneal Factor

Contributory Etiologies Contributory Etiologies


- Hypothalamic dysfunction: - Congenital tubal obstruction
Systemic stresses (poor nutrition, significant weight - Inflammatory causes:
loss, excessive physical activity, severe emotional distress, Endometriosis
chronic medical illness) Pelvic inflammatory disease
Structural abnormalities (congenital hypothalamic Previous ruptured appendiceal abscess
abnormalities, acquired space-occupying lesions or - Iatrogenic causes
destructive lesions of the hypothalamus) Previous pelvic surgery (causes adhesions & scarring)
- Pituitary gland dysfunction: Previous tubal surgery (e.g. salpingectomy)
Hyperprolactinemia (pituitary adenoma, drugs, primary
hypothyroidism, chronic renal failure) Diagnosis & Evaluation
Destructive lesions of the pituitary (space-occupying - Pelvic ultrasound:
lesions, Sheehan syndrome) Can visualize signs of tubal blockage (hydrosalpinx)
- Ovarian dysfunction: - Hysterosalpingography (HSG):
Premature ovarian failure (dysgenetic gonads, mumps Can assess tubal patency
infection, post-radiation or chemotherapy, autoimmune) - Note: even if only 1 tube fills with dye during
Hyperandrogenic disorders HSG, it may still be normal due to the dye following
- Polycystic ovarian syndrome (PCOS) the path of least resistance
- Virilizing adrenal or ovarian tumours Procedure:
- Congenital adrenal hyperplasia - Anesthesia is generally not required
- Occlusive cannula placed in the cervix
Diagnosis & Evaluation - Radiopaque water-soluble dye is then instilled
- Test hormonal levels: to preliminarily assess tubal patency
FSH, LH, estradiol, testosterone & TSH (taken on days (sequestration of oil-based dye within a blocked tube
3-5 of cycle) has adverse effects)
Prolactin & progesterone (taken in mid luteal phase - Fluoroscopy used for image intensification
days 20-22 of cycle) - If tubal patency is confirmed, a further
- Progesterone >5-10ng/ml indicates that instillation of an oil-based dye is carried out
ovulation has occurred this cycle (demonstrated to have significant therapeutic effect
- Pelvic ultrasound for women with unexplained infertility)
Assess ovaries for PCOS Risks of procedure:
- Other adjunctive evaluations: - Discomfort during procedure
Tanner staging (for virilization) - Infection (hence need a normal pelvic examination
Basal body temperature charting beforehand to rule out overt signs of lower tract
- 0.3oC rise in basal body temperature is infection + prophylactic doxycycline)
significant and indicates ovulation has occurred - Saline sonography:
(temperature is higher in the luteal phase) An alternative to HSG whereby saline is infused into
the uterine cavity under ultrasound monitoring
Management - Diagnostic laparoscopy:
- Treatment for systemic stresses: Can assess for pelvic adhesions, stigmata of chronic
Put on weight if underweight endometriosis & tubal patency
Moderate level of physical activity
- Treatment for hyperprolactinemia: Management
Dopamine agonists (bromocriptine, cabergoline) - Expectant treatment:
Surgical resection of pituitary adenoma For unilateral tubal blockage (pregnancy possible still)
- Treatment for PCOS: - Surgical treatment:
Conservative measures: Tubal surgery:
- Lose weight - Surgical options:
Pharmacological measures: (i) Selective catheterization (1st-line for
- Clomiphene proximal tubal occlusions)
- Metformin (useful adjunct to clomiphene) (ii) Microsurgical tuboplasty (surgery for
Surgical measures: reversal of previous tubal ligation)
- Laparoscopic ovarian drilling (iii) Neosalpingostomy (option for fimbrial
- Assisted reproductive techniques: occlusion by creating a new tubal opening)
(indicated if infertility is refractory or not amenable to (iv) Tubal reimplantation (option for
treatment by other modalities) occlusions of the intramural portion of the tube)
IVF ICSI with own or donor oocyte - Risk of ectopic pregnancy after tubal surgery:
Repair of diseased tubes: at least 10% risk
Anastomosis of healthy tubes: 3-5% risk
Adjunctive surgical procedures:
- Adhesiolysis
- Ablation of endometriotic deposits
- Resection of endometriomas (cystectomy)
- Assisted reproductive techniques:
IVF ICSI

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Female Uterine Factor Assisted Reproductive Techniques
Contributory Etiologies
- Congenital uterine abnormalities In-Vitro Fertilization (IVF) &
- Structural uterine abnormalities Intracytoplasmic Sperm Injection (ICSI)
Submucous large intramural fibroids
Endometrial polyps Indications for IVF ICSI
Uterine synechiae, Asherman syndrome - IVF ICSI essentially serves as a last resort treatment for
many of the causes of infertility
Diagnosis & Evaluation Involves obtaining oocyte & sperm before carrying
- Pelvic ultrasound out fertilization of the oocyte in-vitro, with
- Hysterosalpingography (HSG): subsequent transfer of a successfully developed
- Hysteroscopy embryo into the uterine cavity for implantation
Donor sperm &/or oocyte may be used if either is
Management not obtainable from the couple
- Surgical treatment: - ICSI is additionally useful for cases with poor sperm
Myomectomy for fibroids production &/or function:
Hysteroscopic excision of synechiae, endometrial Involves direct injection of a single selected good
polyps & submucous fibroids quality sperm into the harvested oocyte

Female Cervical Factor Phases of IVF ICSI

Contributory Etiologies i. Baseline investigations:


- Structural cervical abnormalities: Investigations for infertility:
Congenital cervical incompetence - Semen analysis
Acquired cervical incompetence (e.g. after cone biopsy) - Hormonal blood tests
- Poor cervical mucus quality: - Pelvic ultrasound
A profuse watery cervical mucus (spinnbarkeit) - HSG or saline sonogram
exudes out of the cervix during the few days prior to Screening blood tests (for both husband & wife):
ovulation which comes into contact with seminal - HIV, Hepatitis B, Hepatitis C, VDRL
ejaculate - Mandatory by MOH guidelines
- Serves to protect sperm from the natural acidic - Results are only valid for 6 months
pH & enzymatic activity of vaginal secretions
Alterations to the constitution of this cervical mucus ii. Ovarian stimulation:
can impair sperm function & survival: Aim of this phase is to assume exogenous control of
- Chronic cervicitis & stimulate multiple follicular development
- Cervical infections Procedure:
- Begin in the mid-luteal phase (day 21)
Diagnosis & Evaluation - Begin administering a GnRH agonist to shut
- Evaluation of spinnbarkeit: down the endogenous hypothalamus-pituitary-
Tested during the immediate pre-ovulatory phase ovary axis (as a non-pulsatile GnRH exposure
(days 12-14 of a 28-cycle) inhibits gonadotropin production by the pituitary,
Parameters assessed: contrary to an endogenous pulsatile exposure which
- Amount of cervical mucus stimulates gonadotropin secretion)
- pH of cervical mucus (normally 6.5) - On day 2-3 of the subsequent cycle, begin
- When litmus paper is used to touch mucus & administering a gonadotropin (FSH &/or hMG)
lifted vertically, the mucus should extend in a to induce ovarian follicular development
thread to 6cm in length - Monitor follicular development with serial
- Post-coital test (Sims Huhner test): serum estradiol levels & pelvic ultrasounds
Performed 2-12 hours after intercourse (follicular diameter 18mm considered mature)
Assesses number & fertility of spermatozoa that have - Once mean follicular size is 18mm, administer
entered the cervical canal an injection of hCG (usually 10000U) to induce
Poor correlation with fertility, poor predictive value completion of oocyte maturation
Risks of ovarian stimulation:
Management - Ovarian hyperstimulation syndrome (OHSS):
- Treatment of underlying cause: bloatedness, nausea/vomiting, shortness of
Treat cervical infection (e.g. doxycycline) breath, fluid retention (may need hospitalization)
Cryotherapy for chronic cervicitis refractory to - Failed stimulation (in 5% of cases, in which case
medical treatment procedure is cancelled)
- Assisted reproductive techniques:
Intrauterine insemination (IUI)
- Useful as it helps bypass poor cervical mucus

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iii. Oocyte pick-up (OPU): vi. Embryo transfer & embryo freezing:
Performed 35 hours after the hCG injection Normal embryos that have formed successfully from
Procedure: in-vitro fertilization can then be transferred to the
- May be performed under conscious sedation uterine cavity 2-3 days after insemination
- Transvaginal ultrasound guidance is used to Procedure:
direct aspiration of the multiple follicles in both - Can usually be done without sedation
ovaries - Under transabdominal ultrasound guidance,
- Harvested oocytes are then prepared & the embryos loaded in a soft catheter are
selected for subsequent fertilization introduced into the uterine cavity through the
Risks of oocyte pick-up: vagina & cervix
- Risks of sedation (respiratory depression) Risks of embryo transfer:
- Bleeding from ovaries, uterus or adjacent - Bleeding
blood vessels - Infection
- Injury to bowel & bladder - Failed transfer requiring use of sedation or
- Infection postponement of procedure
Determining number of embryos transferred:
iv. Sperm collection & preparation: - Up to 2 embryos are allowed to be transferred
Fresh semen sample is collected on the same day as in most cases
for oocyte pick-up - Up to 3 embryos are allowed to be transferred
Semen sample is then assessed, washed & prepared if all 3 of the following criteria are met:
for fertilization (i) all children conceived as a result of the
procedure will be delivered & cared for in a
v. In-vitro fertilization: hospital which has Level 3 neonatal
(2 main methods used for fertilization of harvested oocyte) intensive care facilities
2 main methods: (ii) patient is 37 years old
- Conventional IVF: thousands of sperm are (iii) patient has undergone 1 previous
incubated overnight with selected oocytes for stimulated assisted reproduction cycle
fertilization to occur by itself which was unsuccessful or if there is no
- Intracytoplasmic sperm injection (ICSI): a good quality embryo available
single good quality sperm is selected by the Remaining good quality normal embryos not
embryologist & injected into the oocyte transferred will be frozen:
Not all the oocytes harvested have to be fertilized; of - Can be kept & used for thawed embryo
oocytes not used, 2 options for patient: transfer in a subsequent menstrual cycle in the
- Disposed of immediately event of failure of the current attempt or for
- Made available for research future additional pregnancies desired
Fertilized oocytes are then cultured & monitored for - Survival rate of frozen embryos is 83%
2-3 days: - Storage of frozen embryos is limited to 10
- Successful fertilization can be identified by years from the date of fertilization, subjected to
visualization of 2 pronuclei occurring 14-18 an annual storage fee
hours after insemination - Patient & spouse are to indicate from the onset
- Additional procedures following successful a joint decision on what to do with their frozen
fertilization may be recommended based on embryos in the event that the marriage is
individual circumstances (Blastocyst culture, terminated or patient becomes uncontactable
Laser Assisted Hatching) (either disposed of or made available for research)
Not all the embryos derived after fertilization will be
usable; for abnormal embryos, 2 options for patient: vii. Luteal support:
- Observed until they cease development, Luteal support essential involves progesterone
following which they will be disposed of supplementation to maintain the endometrial lining
- Disposed of immediately