O&G Terminology

2004 Revised Version

General Obstetrics ................................................................................ 2

Fetal Medicine ..................................................................................... 33
Maternal Medicine ............................................................................... 63
Labour Management ........................................................................... 78
General Gynaecology.......................................................................... 96
Oncology ........................................................................................... 136
Reproductive Medicine ...................................................................... 152
Urogynaecology ................................................................................ 160
Miscellaneous.................................................................................... 167
Index ................................................................................................. 198

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General Obstetrics

Obstetrics
What is Obstetrics
In Latin obstre means to stand opposite to (oba: opposite to; stre: stand). It originally pertained to a midwife standing
opposite to a parturiting woman and assisting in delivery. Now Obstetrics does not just concern of delivery, but a
branch of medicine that deals with pregnancy, labour and puerperium. In general, it has been subdivided into
general obstetrics, maternal medicine and fetal medicine. Topics of general obstetrics are highlighted below.
Aims of obstetric care
To minimize maternal and fetal morbidities and mortalities (see maternal mortality and perinatal mortality) by early
identification of problems, actual and potential, and instituting appropriate management.
To prepare, psychologically and mentally, the mother and her husband (or partner) for pregnancy, labour and
parenting, by providing them with support and education about pregnancy and childbirth and childcare.
There are three phases of obstetric care:
Antepartum care
l To detect and monitor any risk factors and manage it accordingly.
n Majority of women are healthy. However, they may carry some risk factors that may affect the pregnancy.
Common examples are carrier of thalassemia genes; maternal obesity and family history of diabetes are
associated with gestational diabetes.
n In addition, some women may have subclinical diseases that may not reveal until during pregnancy. For
example, an asymptomatic valvular heart disease may deteriorate because of increased cardiac demand
during pregnancy.
n Many antenatal disorders are not predictable or preventable, but their complications can be reduced by
early recognition, through regular monitoring. For example, regular blood pressure measurement and
urinalysis during every antenatal visit can pick up the evolution phase of pre-eclampsia.
l To decide the optimal time and mode of delivery.
n The normal time and mode of delivery is spontaneous labour at term (37 to 41 weeks of gestation)
followed by vaginal cephalic delivery. However, maternal or fetal complications may arise and preterm
delivery, either by induction of labour or caesarean section is required. The risks of continuation
pregnancy to both the mother and fetus should always be balanced against the risks of early delivery.
Intrapartum management
l To ensure maternal and fetal well-being during labour and delivery.
l To provide adequate labour pain relief.
l To deliver the baby in the safest way for both the mother and the baby. Sometimes operative delivery may be
required.
Postpartum care
l To ensure normal recovery from pregnancy and childbirth.
n Common early complications are postpartum haemorrhage and postpartum fever.
n One of the important late complication is postpartum depression.
l To look for any problems in childcare and feeding.
l To advise on contraception and family planning.
l To follow up any antenatal problems and provide appropriate referral, counselling and management.
In addition to the above three parts, some couples will also be benefited from pre-conception counselling,
particularly those who have pre-existing chronic diseases, or family history of genetic disorders.
Other important topics in general obstetrics
l Antepartum haemorrhage, postterm;
l Besides, it is important to understand the physiological changes in pregnancy, the anatomy of the maternal
pelvis and the fetal skull.

1. Fetal anatomy

Lie
This defines how the axis of the baby is aligned with that of the mother.
l Longitudinal lie is when the baby is up and down, so the baby is in either cephalic or breech presentation. It is
the normal lie as the uterine cavity is longitudinal in shape.
l Transverse lie is when the fetal poles are on the sides of the mother's abdomen. Causes are those that distort
the shape of uterine cavity: lower segment fibroid, placenta praevia.
l Oblique lie is when one of the fetal poles is over one of the iliac fossae. The causes are similar to that of
transverse lie
l Unstable lie: the fetal lies change frequently from and to longitudinal, transverse or oblique. It implies that there

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 is too much room for the baby, such as in polyhydramnios, or the mother has a very lax abdomen (such as in
grand multipara); or in pelvic inlet contraction where the fetal poles fail to engage.

Position
The relationship of a defined area on the presenting part called the denominator, to the maternal pelvis. The most
common presenting position in cephalic presentation is occipto-anterior. Occipito-posterior position occurs in
one-third of the cases.

Denominator
It is a defined area of the fetal presenting part, used to describe the position of the fetal presenting part in relation to
the maternal pelvis.
Presentation Denominator
Vertex Occiput
Face Mentus
Breech Sacrum

Presentation
Definition
This is the part of the baby most easily felt by vaginal examination during labour.
Different types of presentation
Cephalic presentation
l It is when the fetal head presents first.
l It is an imprecise term as it does not specify which part of the head is presenting, and is usually used after
abdominal palpation.
Vertex presentation
l Vertex is the normal one, and occurs when the head is well flexed.
l Anterior fontanelle presentation is also normal, especially in early labour before the head is fully flexed. It is
also common in occipital posterior position. Presentations other than this are malpresentations.
Brow presentation
l It occurs when the head is extended. This sometimes occurs naturally, especially in multipara where the baby
is not fixed in position. More commonly it is associated with an obstruction in the birth canal such as
disproportion, fibroid, ovarian cyst, or placenta praevia. Unless the baby is very small, brow presentation
makes the fetal diameters too large to deliver vaginally. The head usually cannot enter the pelvic brim, so that
when the membranes rupture, there is a high risk of cord prolapse.
Face presentation
l It is when the head is fully extended, and this occurs in very small babies, when the head enters the pelvis as a
brow, but extends into a face at the outlet and delivers. Although it can occur spontaneously, more commonly it
is associated with many loops of cords around the neck, or with a thyroid gotire so the baby is forced into an
extended position. Face presentation can deliver vaginally if the head is rotated to a mentum anterior position.
If rotation is to mentum posterior, then the baby cannot bend its neck any further to fit the curvature of the
pelvic canal, and so obstructed labour results.
Breech presentation
l Breech presentation is when the baby's bottom comes out first. This can be a frank breech, where the baby's
buttocks and perineum present, with the legs fully extended. If the feet comes out first then a footling
presentation occurs.
Other types of presentation
l If the baby is in the transverse lie, then the presentation would be either the shoulder, elbow, or the hand. If the
baby is floating free, sometimes the umbilical cord is the presentation.

Fetal skull
Anatomy
The fetal skull is made up of the vault, face and the base. The vault are formed from parts of the frontal, occiputal
and the pair of temporal bones and parietal bones. Between these bones there are four membranous sutures:
sagittal, frontal, coronal and lambdoidal sutures.
Fontanelles are the junction of the various sutures. The anterior fontanelle or bregma (diamond shaped) is at the
junction of the sagittal, frontal and coronal sutures. The posterior fontanelle (triangular shaped) lies at the junction of
the sagittal sutured and the lambdoidakl sutures between the two parietal bones and the occioital bone.
These sutures and fontanelles allow moulding during labour, and facilitate in assessment of the position of the fetal
head during vaginal examination in labour.
The diameters of the skull
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Depends on the degree of flexion of the fetal head, it may present to the birth canal (maternal pelvis) in different
longitudinal diameters and presentation:
Fetal neck Longitudinal diameter (cm) Presentation
fully-flexed suboccipito-bregmatic (9.5) vertex
semi-flexed suboccipitao-frontal (10) vertex, usually with OP position
mildly-extended occipito-frontal (11.5) vertex, usually with OP position
moderately-extended mento-vertical (13) brow
fully-extended submento-bregmatic (9.5) face
Remark:
l OP: occiputo-posterior
l suboccipito-bregmatic: from the suboccipital region to the centre of the anterior fontanelle
l suboccipitao-frontal: from the suboccipital region to the prominence of the forehead
l occipito-frontal: from the posterior fantanelle to the root of the nose
l mento-vertical: from the chin to the furthest point of the vertex
l submento-bregmatic: from below the chin to the anterior fontanelle

Fontanelle
The fetal skull consists of a number of bones, and there are two fontanelles on the head, each being where a
number of bones meet.
The anterior fontanelle is where the two parietal and two frontal bones meet. This is a large space, and can be
identified because 4 sutures run from it. The anterior fontanelle is in the center of the head, and is the presentation
when the head is in the military of deflexed position. When the head undergoes flexion, the presentation is the
vertex.
The posterior fontanelle is where the two parietal and the single occipital bone meet. Usually it cannot be felt as a
space, rather where 3 sutures meet.
The two fontanelles define the anterior and posterior limits of the vertex.

Sagittal suture
This is the suture on the fetal skull where the two parietal bones meet, and is between the anterior and posterior
fontanelles.

Sinciput
The part of the fetal head in front of the anterior fontanelle. It is subdivided into the brow and the face.

Vertex
A well-defined area of the fetal skull, bounded by the anterior and posterior fontanelles, and the two parietal
eminences. The vertex presentation is the normal and the most common one. It occurs once the head has
undergone flexion, when the fetal head will present with the smallest diameter to the birth canal.

2. Maternal anatomy

Anatomy
Maternal pelvis
Fetal skull
Pelvic floor
Pudendal nerve

Levator ani
Anatomy
Levator ani muscles is a pair of broad flat muscles, each arises from the inner surface of the anterio-lateral pelvis,
passes downwards and inwards, from the lateral sides and meet each other at the midline. The muscles together
constitute the pelvic diaphragm. Each muscle is also divided into two parts: puibococcygeus anteriorly and
iliococcygeus posteriorly. The nerve supply is by the pudendal nerve (S2-4) on each side.
The exact origins of the muscles are:
l the lower part of the body of the os pubis
l the tendinous arch of the parietal pelvic fascia (white line)

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l the pelvic surface of the ischial spine,
and the site of midline insertions are:
l the pre-anal raphe and the central point of the perineum where one muscle meets the other on the opposite
side
l the wall of the anal canal, where the fibres blend with the deep exernal sphincter muscle
l the postanal or anococcygeal raphe, where again one muscle meets the other on the opposite side
l the lower part of the coccyx
Clinical role of levator ani
l The pubococcygeus muscles support the pelvic and abdominal viscera, including the bladder. Weakness of
the support results in genital prolapse.
l The medial edge passes beneath the bladder and runs laterally to the urethra, into which some of its fibres are
inserted. Together with fibres from the opposite muscle they form a loop which maintains the angle between
the posterior aspect of the urethra and the bladder base. During micturition this loop relaxes to allow the
bladder neck and upper urethra to open and descend. Failure to maintain the angle results in urinary stress
incontinence.
l The medial borders of the pubococcygeus muscles pass on either side from the pubic bone to the prenal raphe.
They thus embrace the vagina, and on contraction have some sphincteric action. Spasm of the muscle results
in vaginismus.

Urogenital diaphragm
It is a triangular-shaped ligament lying below the levator ani muscles, and filling the gap between the descending
pubic rami. It consists of two layers of pelvic fascia, with the deep transverse perineal muscle (compressor urethrae)
lying between the layers. The diaphragm is pierced by the urethra and the vagina.

Pelvis
Anatomy
l It is composed of a pair of iliac bones, a pair of ischial bones, a pair of pubic bones and a sacrum. Together
with the pelvic ligaments, they form the birth canal, with an inlet, cavity and an outlet.
Inlet
l The inlet of the pelvis is bounded by the sacral promontory and alae posteriorly, laterally by the upper edges of
iliac bones, and anteriorly by the horizontal rami of the pubic bones and pubic symphysis.
Cavity
l The walls of the pelvis are partly bony and partly ligamentous. The posterior boundary is the anterior surface of
the sacrum, and the lateral limits are formed by the inner surface of the ischial bones and sacrosciatic notches
and ligaments. In front the pelvis is bounded by the pubic bones, the ascending superior rami of the ischial
bones and the obturator foramina.
Outlet
l The outlet is bounded by the pubic symphysis in the front, the lower edges of the pubic rami, limited laterally by
the ischial tuberosities, and posteriorly by the coccyx.
The pelvis is classified according to different pelvic shapes and the size is assessed by clinical pelvimetry.
A normal pelvis
l The brim is round, and the sacral promontory is not prominent
l The angle of inclination is about 55 degree to the horizontal
l The cavity is shallow with straight, non-converging walls
l The sacrum is smoothly curved
l In the outlet the sacro-sciatic notches are wide and shallow
l The sacrum does not project forwards
l The ischial spines are not prominent
l The pubic arch is wide and domed
l The sub-pubic angle is about 90 degree
l The inter-tuberous diameter is wide
Pelvic shapes
Four major pelvic shapes have been described:
l Gynaecoid
l Anthropoid
l Android
l Platypoid

Pelvimetry
Definition
Measurement of the size of the pelvis, either clinically or radiographically.
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Clinical pelvimetry
Clinical method is as follow:
Inlet assessment:
l assess the diagonal conjugate diameter by inserting the index and middle fingers to reach the sacral
promontory. If the sacral promontory can be reached, it means the inlet is small (usual length of the index
finger is 10cm).
Mid cavity assessment:
l assess the sacral curvature by digital examination.
l assess the ischial spines.
Outlet assessment:
l assess the intertuberous diameter. It should be as wide as a normal fist (9cm)
l assess the subpubic arch which is normally 90 degree.
Clinical assessment of pelvic size and shape is only likely to be of benefit if the pelvis is severely contracted
Radiological pelvimetry
l By X-ray, CT, MRI
l CT is the most common way as it has less radiation and more accurate when compared with X-ray, but
cheaper and more available than MRI
l Criteria for normality have not yet been set
l Pelvimetry is of no reliable evidence of benefit for the traditional indications of primigravid breech presentation,
or after caesarean section for suspected disproportion

Ischial spine
The sharp posterior-medical protrusion from the ischial bone. It is halfway between the pelvic inlet and outlet. The
ischial spines are of great obstetrical importance because the distance between them represents the shortest
diameter of the pelvic cavity. They are readily felt vaginally or rectally and therefore serve as valuable landmarks in
assessing the station of the presenting part. It is also a landmark to identify the site of pudendal nerve during
pudendal anaesthesia.

Intertuberous diameter
The distance between the tuberosity of the ischial bones. It is the transverse diameter of the pelvic outlet and
normally measured 9cm. It can be assessed clinically by putting a fist to the perineum. The intertuberous diameter is
normal when it can accommodate 4 knuckles of fingers.

Brim
Also known as the pelvic inlet, the upper limit of the true pelvis. It consists of the pubic symphysis in front, the upper
edge of the pubic bones and the iliac bones on both sides, and in the back the sacrum (usually the S1).
The normal diameters of the brim are said to be 11cm anteroposteriorly, and 12cm laterally. An AP diameter of 10 cm
is usually considered to be narrowed, and 9cm would be diagnosed to be a contracted pelvis.

Inlet
Also known as the pelvic brim, the upper limit of the true pelvis. It consists of the pubic symphysis in front, the upper
edge of the pubic bones and the iliac bones on both sides, and in the back the sacrum (usually the S1). The normal
diameters of the brim are said to be 11cm anteroposteriorly, and 12cm laterally. An AP diameter of 10 cm is usually
considered to be narrowed, and 9cm would be diagnosed to be a contracted pelvis.

Outlet
The lower end of the bony birth canal. Marked by the pubic symphysis in the front, the lower edges of the pubic rami,
limited laterally by the ischial tuberosities, and posteriorly by the coccyx. In women with android pelvis, the pelvic
outlet is narrowed from side to side, and this sometimes prevents the baby from being delivered in the second stage,
resulting in a failed instrumental delivery.

Subpubic arch
This is formed by the inferior borders of the pubic rami, ending at the ischial tuberosities. Normally this has an angle
of 90 degrees. The shape of this arch is important in that it determines whether the fetal head has difficulty in coming
out of the pelvic outlet. As the baby's head is more or less round, a narrowed arch will force the baby's head
backwards, so that the available antero-posterior diameter is much less than as measured in the pelvimetry. The
unavailable part of this AP diameter is called the waste space of Morris. A good way to envisage this is to draw the
pubic arch, and try to put a circle 9.5cm inside it. The distance between the circumference and the apex of the arch

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is the waste space.
The pubic arch is best assessed clinically, by feeling for the arch and estimating its angle. Also, the distance
between the ischial tuberosities should be about 10cm, which is usually the width of the doctor's knuckles.
A narrowed pubic arch will lead to difficulty in the second stage, and is a common cause of failed instrumental
delivery.

Pubic symphysis
Where the two pubic rami join in the front. It forms the anterior border of the pelvic canal.

Gynaecoid
This is the normal and most common type of pelvis. The brim is oval in shape, with the lateral diameter larger than
the antero-posterior diameter. The sacrum is well curved, and tilted in such a manner as to render the
antero-posterior diameter of the outlet slightly larger than the inlet. The midcavity is wide, the anteroposterior
diameter being generous because of a good sacral curve, and the lateral diameters are also good, with a good
distance of 3-4 cm between the ischial spines and the sacrum. The outlet has an antero-posterior diameter larger
than the lateral diameter, and the subpubic arch is more than 80 degrees. Such a pelvis fits naturally into the
diameters of fetal skull with a normal vertex presentation.

Anthropoid
This is a variant of the normal pelvis. Its shape is very similar to that of the gynaecoid pelvis, except that the inlet is
ovoid shape, with a long antero-posterior diameter, and the lateral diameter near the back is slightly larger than that
in front. Such a shape tends to encourage occipito-posterior position.

Android
It is a male-like pelvic shape which tends to have a triangular inlet with beaking near the front. This encourages an
occipital posterior position. It is also a funnel pelvis, where the outlet is smaller than the inlet, and a side to side
narrowing of the pelvic canal. The outlet has a narrow subpubic arch. Typically women with android pelvis may have
other android features, such as having broad shoulders, are muscular, and sometimes hirsute.
Android pelvis can be diagnosed by pelvimetry, with the following features:
l The antero-posterior diameter at the outlet is smaller than that at the inlet
l A narrowing of the distance between the ischial spines
l A narrowed sacrosciatic notch
For this type of pelvis, the fetus tends to present with occipital posterior position, and the head has difficulty in
rotating to the anterior position as the pelvic canal is narrowed. The funnel shaped pelvis also results in obstructed
labour. As the narrowest part is at the outlet, the worst situation is the arrest at the second stage of labour. This
would lead to a failed instrumental delivery with all its disastrous consequences.

Platypoid
One of the pelvic shapes. 'Plat' is derived from a Greek word meaning flat. This type of pelvis is a result of clinical or
subclinical rickets. The pelvic brim is narrowed from front to back, so appearing flat, and this sometimes is
associated with an exaggerated lumbar lordosis. The combination of these causes the pelvic inlet to be small, and
this contracted pelvis makes it difficult for the fetal head to enter the pelvis. This is classically the situation of
cephalopelvic disproportion.
The softening of the bones caused by rickets also leads to a splaying of the subpubic arch, so that the pelvis is
usually only narrowed at the brim while the rest presents no difficulty. This is responsible for the old obstetric adage
that if the head will go in the brim it will come out the outlet.
Sometimes the head will angle sideways in an attempt to enter the pelvis, and this is called asynclitism.

Contracted pelvis
This denotes a pelvis which is smaller than normal, to the extent that it may cause difficulties in labour. Contraction
may occur at the inlet, and this is usually associated with a platypoid pelvis. Contraction can also occur at the outlet,
and this is usually associated with the android pelvis. The android pelvis may also be contracted in midpelvis, with a
side to side narrowing of the pelvis, which can be seen as a narrowed sacral sciatic notch on pelvimetry, or as a
narrowed distance between the ischial spines.

Cephalopelvic disproportion
This describes the situation where the fetal head is too big for the birth canal. Before World War II, when nutrition
was poor, many women had rickets and so developed platypoid pelvis. These lead to inlet disproportion.
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Women who have android features however may have an adequate pelvic inlet, but a narrow outlet. They tend to
have difficulty in delivering the baby at the second stage, and are said to have outlet disproportion.

Funnel pelvis
This describes a pelvis where the outlet diameter is smaller than the inlet, especially the antero-posterior diameters
as seen on the pelvimetry. Funnel pelvis occurs in the android pelvis. Women with funnel pelvis have difficult labours,
because the birth canal gets tighter as labour progresses, and the smallest part of the pelvis is only encountered at
the second stage of labour.

Os
Greek word meaning opening. In obstetrics means where the cervical canal is. The internal os is the end of the
cervical canal at the uterine end, and external os the vaginal end.

Lower segment
The thin expanded lower portion of the uterus which forms from the isthmus during the last trimester of pregnancy. It
is located between the attachment of the peritoneum of the uterovescial pouch superiorly and the level of the internal
os inferiorly. It provides the usual method of approach to the baby in the operation of caesarean section. When
abdominal delivery is necessary in a preterm pregnancy when the lower segment is not yet formed, a classical
caesarean section is then the method of approach. The lower segment is less contractile as there are fewer muscle
fibres. When the placenta is located there (placenta praevia), bleeding from the placental bed is more difficult to
control.

Dextrorotation of uterus
The pregnant uterus is usually rotated towards the right side, due to the presence of the rectum and sigmoid colon
on the left side. This is relevant that to avoid injury to uterine vessels during lower segment caesarean section, the
operation table should be tilted towards the left side.

3. Antepartum

Antepartum care
Definition
A planned programme of observation, education, and medical management of pregnant women directed towards
making pregnancy and delivery safe and satisfying experiences
Elements
Screening of Risk factors
l To regularly look for any risk factors which adversely affect the health of mother and baby
l This is achieved through regular history taking, examination, and screening tests.
Counselling
l To advise on the nature and extent of any perceived risks, and how to minimize or eradicate them
Monitoring
l To monitor the maternal and fetal well-being in high risk cases
Treatment
l To treat any medical condition which might affect or be affected by the pregnancy (see maternal medicine)
Management of minor disorders
l See minor disorders of pregnancy
Education
l To provide advice, reassurance and support for the woman and her family, such as:
n advice on wearing seat-belt
n instructions to admit to hospital when significant symptoms occur such as fever, vaginal bleeding or
discharge, abdominal pain, etc
Antepartum care consists of:
l Booking assessment; and
l Continuing antenatal care
Booking assessment
Timing
l Optimally takes place at 8 to 10 weeks and should not later than 16 weeks
l Important for dating of pregnancy: to look for any date problem and confirm the estimated date of confinement
(EDC)
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l Check for any pre-existing risk factors by history taking (Obs), examination (Obs) and screening tests
Initial screening tests should include:
l Haematological
n Haemoglobin to screen for anaemia
n MCV to screen for thalassemia
n Blood group and Rhesus type
l Microbiological
n Rubella antibodies
n Hepatitis B surface antigen
n VDRL for syphilis
l Biochemical
n Urinalysis for protein and glucose
l Radiological
n Dating scan before 16 weeks
n Morphology scan around 20 weeks
Additional screening tests such as the followings may be required if additional risk markers are present:
l Urine culture
l Screening for sexually transmitted diseases
l Oral glucose tolerance test
l Biochemical screening for neural tube defects and Down syndrome
Subsequent assessment
When and where to be seen
l Uncomplicated (low risk) pregnancy
n Women should be seen every 4 weeks for the first 28 weeks of pregnancy, then every 2 weeks until 36
weeks, and weekly until delivery
can be seen in maternal child health centre, by midwives or general practitioners
l High risk pregnancy
n Women with medical or obstetric problems require close surveillance at an interval determined by the
nature and severity of the problem.
n Under care of a specialist
Routine maternal assessment
l Weight and notation of any change
l Blood pressure with notation of any change
l Urine glucose and protein
l Peripheral edema
l Presence of any symptoms
Routine fetal assessment
l Fetal activity (from history)
l Fetal size: both the actual size and the growth rate; assessed with fundal height measurement
l Fetal presentation and engagement (in late pregnancy)
l Amount of amniotic fluid
l Fetal heart rate, by auscultation with Pinard stethoscope or a hand-held Doppler apparatus (Doptone)
l Please refer to history taking (Obs) and examination (Obs) for detail
Discussion/Something to Consider
A patient at 34 weeks of gestation is found to have weight gain of 2 kg over the last 1 week. Is it normal? What are
the possible causes? How would you assess her condition?
A patient asks you in the antenatal clinic whether it is dangerous to wear seat-belt during traveling in a car. How
would you advise her?

Pre-conception counselling
Aim
l To ensure women are in good and healthy condition before being pregnant
l It is important as the most critical phase of fetal development is complete by the time of the first antenatal clinic
attendance, and adverse factors may have already begun to produce their effects
Elements
General health assessment and advice
l Nutrition
l Healthy behaviour: e.g. quit smoking and alcoholism
General screening
l Cervical pap smear
l MCV for thalassemia
l Rubella immunity

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Control of pre-existing chronic diseases
l Diabetes mellitus, thyroid disorders, valvular heart diseases are common in female at reproductive age. Poor
control of these diseases would definite causes significant maternal and fetal morbidities
Adjustment of medical therapies
l Medical therapy of these disorders may cause fetal complication, for example, anti-convulsants are associated
with neural tube defects. Discontinuation of the drugs may be considered if there is no recurrence for a long
period of time
l Diabetic patients being treated with oral hypoglycemic agents would be advised to change to insulin before
pregnancy, as insulin has better control of the disease and dosage is more easy to adjust
Genetic counselling and prevention
l Counselling on any possibility of congenital malformation and genetic disorders, particular if there is positive
family history (see genetic counselling)
l Patients with previous babies suffered from neural tube defects will be benefited from folate supplement for 6
weeks before getting pregnant.
Discussion/Something to Consider
You are a medical officer of the Family Planning Association. A healthy couple has just married and come for
pre-pregnancy advice. History and examination are unremarkable.
What screening tests would you perform for them?
Supposed the complete blood pictures of both of the couple show microcystic picture but otherwise normal result.
How would you counsel them and what further tests would you do?
The female partner of the couple has negative rubella antibody test. What advice would you give her?

Dating of pregnancy
Introduction
Dating is one of the most important tasks in antenatal care.
20% of pregnant women will have date problems because:
l Last menstrual period is forgotten or uncertain
l menstrual cycles are irregular
Some definitions
Last menstrual period (LMP):
l date of the first day of last menstrual flow
Estimated date of confinement (EDC):
l the mean duration of pregnancy
l about 40% of women will deliver within 5 days of EDC and 66% within 10 days
l it is 280 days from the LMP provided that ovulation occurs at day 14 of the menstrual cycle
l it is 266 days from the date of ovulation
How to calculate EDC
l it is calculated by using LMP:
l adding 280 days (40 weeks) to the LMP
l it is assumed that ovulation occurs at or day 14 of LMP, in a normal regular 28 days cycles
l Nagele's rule to calculate EDC:
l to the first day of LMP add 7 days, then subtract 3 months, and then add 1 year. e.g.: LMP: 10/10/2000
EDC:17/07/2001
Some important facts: menstrual cycles, ovulation and fertilization
l In a normal regular 28-day cycle, ovulation occurs 14 days after the LMP
l Ovulation may be delayed when the usual duration of menstrual cycles is longer. For example, ovulation may
occur at day 21 if the menstrual cycles are 35 days
l Fertilization occurs within 2 days of ovulation
l Implantation occurs 7 days after ovulation, and completes 14 days after ovulation
l Fetal life therefore starts at about 14 to 15 days after LMP (if the cycles are 28 days) or even later if the
menstrual cycles are longer
l HCG is produced after implantation, and is detectable in the serum 1 week after implantation
l HCG is detectable in urine (positive pregnancy test) since 2 weeks after fertilization (4 week after LMP, or later
if ovulation occurred later)
l Therefore, if a patient has used to have long menstrual cycles, and had a negative pregnancy test at 5 week of
amenorrhea, but positive test at 6 week. Then most probably she had a date problem of 1 to 2 weeks.
Some important facts: symptoms and signs of pregnancy
Features Week of pregnancy
morning sickness 4 to 13
breast changes start from 6 week
bladder symptoms 6 to 13 week
cervical softening start from 6 week
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 quickening (primigravida) start from 18 week
quickening (multipara) start from 16 week
audible fetal heart sound with Pinard start from 24 week
abdominally palpable pregnant uterus start from 12 week
hegar's sign 8 to 13 week
Some important facts: ultrasound dating
First trimester
l Crown-rump length (CRL): accuracy of EDC estimation: +/- 4.7 days
Second trimester
l Biparietal diameter (BPD) or femur length (FL): accuracy of EDC estimation: +/- 7 to 10 days
Third trimester
l Dating at this time is not ve ry helpful in predicting the EDC. The accuracy is only +/- 3 weeks
Determination of EDC
l As a rule, when an early USG prediction disagrees with an EDC assigned by the LMP by more than 1 week,
the USG dates are assigned.
l If the scan and the LMP agree to within a week, the EDC based on the LMP is used. This may not always be
straightforward because femur length may or may not agree with the estimated gestational age based on the
BPD
Discussion/Something to Consider
What is the EDC of a pregnancy which is resulted from in vitro fertilization with the LMP on 01/01/2000, and oocytes
retrieval on 17/01/2000 and embryo transfer on 19/01/2000?
Why CRL cannot be used continuously for dating in the second trimester?
A teenager presents to the A&E department complaining of acute abdominal pain. She used to have 28-day regular
cycles until Feb 2000. She claims she had menstrual bleeding on 01/02/2000 and the last menstrual bleeding came
late for a week, on 08/03/2000. Today (15/03/2000) she is found to have a positive pregnancy test. How can you
account for this history and finding?

Antepartum haemorrhage
Definition
l Bleeding from the genital tract occurs after 24 weeks of gestation and before the birth of the baby, including the
first and second stages of labour
Causes
l Placenta praevia
l Abruptio placentae
l APH of unknown origin: the most common cause
l Lesion of the lower genital tract: cervix or vagina
l Vasa praevia: very rare
Incidence
l 3-5% of pregnancies
Discussion/Something to Consider
What is your assessment for a woman presents with painless unprovoked vaginal bleeding of 10ml at 28 weeks of
gestation?

Placenta praevia
Definition
It is when the placenta encroaches onto the lower segment.
Classification
Old classification (by Dewhurst):
l based on clinical examination findings or findings at the time of caesarean section:
n Grade I- placenta extends on to the lower segment but does not reach the os.
n Grade II- placenta extends to the os.
n Grade III- placenta covers the os eccentrically.
n Grade IV- placenta covers the os centrally.
Classification with aids of Ultrasound
l With the use of modern ultrasonography, the placental position can now be defined more accurately
antenatally.
n Type I- low-lying placenta positioned closed to the os (within 5cm).
n Type II- marginal placenta praevia located at the margin of the os.
n Type III- partial placenta praevia partially covering the internal os.
n Type IV- total placenta praevia completely covering the os.

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Simplest Classification
l Minor- placenta encroaches on the lower segment but does not cover internal os (type I and II)
l Major- placenta covers internal os (type III and IV)
Incidence
0.4% of pregnancies
Risk factors
Maternal factors:
l Multiparity
l Advanced maternal age >35
Factors related to abnormal placentation:
l Defective vascularization of the decidua due to atrophic changes or inflammation
l Scarring of the endometrium due to repeated pregnancies due to repeated pregnancies
l Vessel changes at the placental site that decrease the blood supply to the endometrium and require a greater
surface area for placental attachment to provide adequate maternal blood flow
Decreased surface area of placental implantation
l in multiple pregnancies
Altered blood supply to the endometrium and changes in the quality of the endometrium
l due to previous incision in the lower segment
Clinical presentation
Painless vaginal bleeding
l Most characteristic sign of placenta praevia
l Can occur suddenly without warning, during rest or activity, or after coitus or pelvic examination
l Bleeding usually occurs for the first time early in the third trimester, when the lower segment begins to change,
causing the cervix to efface and dilate
l Bleeding is caused by the tearing of the placental attachments at or near the internal os as the cervix changes
l The bleeding continues because the stretched fibres of the lower uterine segment are unable to contract and
compress the torn vessels
Present as malpresentation
Incidental finding on routine ultrasound scan
Diagnosis
l Should always be suspected in the presence of vaginal bleeding in the third trimester
l The index of suspicion is heightened if there is co-existing malpresentation or multiple pregnancy
l Ultrasonic examination
n It is a valuable tool in confirming the diagnosis of placenta praevia. Transabdominal scan (TAS) is usually
adequate in assessing the relation between the low-lying placenta and the internal os. In borderline case
or in case of posterior placenta, transvaginal scan (TVS) is more accurate than TAS

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

Management
Principle
l The risk of placenta praevia is the massive bleeding that may require immediate delivery of fetus and placenta
in order to control the bleeding. It implies the risk of preterm delivery when massive bleeding occurs in preterm
gestation.
l The principle of management is therefore to tolerate minor bleeding in order to avoid complications of
prematurity, until the pregnancy reaches a safe maturity (at least 34 weeks), but to deliver in case of severe
bleeding.
Expectant management
l to monitor severity of bleeding and
l keep patient in hospital

Page 12
l glucocorticord therapy to enhance fetal lung maturity
l regular cross-matching of blood
Mode of Delivery
l Caesarean section for all grade of placenta praevia except those cases with placental edges more than 2cm
away from internal cervical os under transvaginal scan examination, and the fetal head is well engaged. In that
situation, the chance of antepartum haemorrhage is much less while the chance of successful vaginal delivery
is acceptably good.

Abruptio placentae
Definition
l It is also called 'accidental haemorrhage'.
l It is defined as uterine bleeding resulted from a normally implanted placenta that prematurely detaches from
the uterus, after 24 weeks of gestation and before the delivery of the fetus.
Incidence
l 0.8% of all pregnancies
l Half of the cases occur preterm
Risk factors
l Pre-eclampsia
l Sudden decompression of the uterus (such as in traffic accident, rupture of membranes, ECV)
l Cigarette smoking
l Cocaine abuse
l previous history of abruption
Pathology
l There are two types of placental detachment, with different clinical presentation:
Revealed type
l Peripheral detachment
l Bleeding from cervical os
Concealed type
l Less common
l Central detachment
l Blood is trapped behind the placenta and does not escape
Detachment of the placenta results in disruption of the uteroplacental transfer of oxygen, leading to fetal hypoxia and
death.
Release of placental thromboplastin and other clotting factors initiate coagulopathy (DIC)
Complications
Maternal
l Massive bleeding and shock
l DIC
l Postpartum haemorrhage
l High risk of caesarean section
Fetal
l Intrauterine fetal hypoxia and death
l Preterm delivery
Clinical presentations
Vaginal bleeding:
l a common presentation
l may be absent, or present very late in the concealed type
l may be massive and the patient presents with shock
Uterine pain:
l Uterine pain and tenderness are more severe in the concealed type
l Uterine contractions, may be tonic in Couvelaire uterus
Other features:
l Fetal distress, presents with decreased fetal movement, abnormal cardiotocogram. In severe case, the fetus
may have died already at presentation in severe case
l Uterine irritability, present with irregular but frequent activities in cardiotocogram
l Rarely, retroplacental clots may be seen between the uterine wall and placenta under USG in severe
concealed type. However, the clinical condition would be obvious for making the diagnosis of abruption rather
than replying on the USG features.
Management
Principles
l Resuscitation for hypovolemic shock
l Immediate delivery after stabilisation
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 n usually by caesarean section unless the cervix is already fully dilated, or the fetus has already died
l Look for coagulopathy and make correction
Discussion/Something to Consider
What are the differences between the management of abruptio placentae and that of placenta praevia, when each of
them presents at 30 weeks of gestation?

Couvelaire uterus
Uterine apoplexy. Occurs with severe concealed type of abruptio placentae. The uterus is purple due to
haemorrhage within its musculature. Clinically the uterus is hard and tender.

Vasa praevia
It is a rare condition in which a branch of the umbilical vessels passes over the internal os of the cervix, and
therefore becomes the presenting part (vasa praevia). The vessel may rupture spontaneously or during amniotomy
resulting in fetal bleeding. It is a rare cause of antepartum haemorrhage. The USG film with color-doppler below
shows a vessel (colored) running over the internal os.

APH of unknown origin

Definition
Antepartum haemorrhage (APH) from the upper genital tract with no evidence of placenta praevia and abruptio
placentae
Incidence
l 3% of all pregnancy
l a common cause of antepartum haemorrhage
Causes
l The cause by it name is unknown
l However, it is thought to be a minor abruptio placentae that cannot be confirmed clinically
Risk
l It is associated with preterm labour.
l In the past, it was thought to be associated with an increased risk of intrauterine growth restriction (IUGR) and
perinatal mortality because of fetal compromise. However the evidences was not convincing. It is clear that the
increased perinatal mortality is mainly due to prematurity.
Clinical presentation and diagnosis
l Vaginal bleeding, usually of small amount and is unprovoked
l May associate uterine contractions
l No signs of fetal distress or uterine tenderness (when these occur, abruptio placentae must be suspected)
l It is diagnosed by exclusion of other causes of antepartum haemorrhage
Management
Gestation below 34 weeks:
l Glucocorticoid therapy to enhance fetal lung maturity because of high risk of preterm delivery
l The use of tocolytics when preterm labour occurs is controversial. It is thought that the relaxation of uterus may
cause further bleeding, and some tocolytics (e.g. beta-adrenergic agonists and calcium channel blockers) may
exacerbate the haemodynamic status in case of severe bleeding.
Gestation above 34 weeks:
l Conservative management
Consider induction of labour at term when patients have repeated episodes of APH or currently suffered from
significant bleeding

4. Malpresenation

Malpresentation
Definition
Any presentation other than vertex. They are:
Breech presentation: 3%
Cord presentation: 1/400
Face presentation: 1/500
Brow presentation: 1/2000
Shoulder presentation, fetus usually in transverse lie

Page 14
What medical students should know
Medical students should know the most common malpresentation: breech presentation

Breech presentation
Incidence
l 2 to 3% of all deliveries
l Incidence is relatively higher before term
l Up to one third are undiagnosed before labour
l The most common type of malpresentation
Types
l Frank (65%): both legs extended at the knee and flexed at the hip
l Complete (10%): both legs flexed at hip and knee
l Footling or incomplete (25%): one or both feet tucked underneath the buttock
Causes
l The majority occurs by chance
l Preterm
l Uterine anomalies: e.g. bicornuate uterus
l Fetal anomalies: e.g. hydrocephalus
l Obstruction: placenta praevia, fibroids at lower pole of uterus
l Multiple pregnancy
Fetal risk
Fetal risk related to the underlying causes
l Fetal anomaly
l Prematurity
Fetal risk related to vaginal breech delivery
l Premature rupture of membranes and cord prolapse: risk is lowest in frank breech presentation but highest in
footling
l Birth injury: e.g.: Intracranial haemorrhage, rupture of viscus, dislocation of joints, fractures of long bones,
peripheral nerve injury
l Birth asphyxia: as a result of delayed delivery
Maternal risk
Maternal risk related to the underlying causes:
l e.g. Placenta praevia
Maternal risk related to breech delivery
l Higher caesarean section rate
l Birth canal injury
Investigations
Ultrasound
l Define the type of breech, assess fetal growth and estimate of fetal weight, and liquor volume
l Look for any underlying causes like fetal anomalies, placenta praevia, and uterine abnormalities
CT pelvimetry
l Ensure adequate pelvis before allowing vaginal breech delivery
l rarely indicated now as vaginal breech delivery is not recommended
Decision of mode of delivery
Options:
l Vaginal breech delivery
l External cephalic version (ECV)
l Elective caesarean section
Guideline
The mode of term breech delivery is controversial until recently when a large randomized controlled study
comparing elective caesarean section and vaginal breech delivery has shown that the former is associated with
significantly lower perinatal mortality and morbidity. The implication is that patients should be counselled for either
elective section or ECV only. Patient who strongly request vaginal breech delivery must fulfill the strict selection
criteria (see vaginal breech delivery).
Other determining factors:
l Gestation:
n Before 36 weeks: conservative management as spontaneous version may take place
l Fetal malformations:
n Lethal fetal abnormalities: vaginal delivery
n Potential salvageable fetal abnormalities: caesarean section
l Fetal well-being:
Page 15
 n Caesarean section if there are signs of fetal compromise such as oligohydramnios, abnormal
cardiotocogram
l Number of fetuses:
n Twin pregnancy:
u Presenting twin is breech presenting: caesarean section
u Non-presenting twin is breech: can try vaginal delivery
u Triplet or higher order pregnancy: caesarean section
l Uterine abnormalities
n Caesarean section in case of uterine anomalies, placenta praevia or other pelvic obstructions

Cord prolapse
Definition
Cord presentation:
l a loop of cord lies below the presenting part and the membranes is intact
Cord prolapse:
l a loop of cord prolapsed out from the cervix with the membranes ruptured
Pathology
l This may occur if the presenting part of the baby does not fit well into the pelvic brim, and a sudden gush of
amniotic fluid when the membranes rupture.
l As the baby descends, it presses upon the cord. More important is that the umbilical cord blood vessels
undergo an irreversible vasoconstriction when they become cooled.
Risk factors
Unengaged fetus:
l Breech presentation
l Prematurity
l Cephalo-pelvic disproportion
l Polyhydramnios
Complication
Sudden fetal hypoxia and death because of umbilical cord compression or cord vessels constriction
Diagnosis
l Cord seen at vulva, or felt on vaginal examination
l acute fetal distress immediately after rupture of membranes
Management
Avoid cord compression and vasoconstriction:
l Put any visible cord back in the vagina as
n cool air will make the cord go into spasm, and
n the vagina will keep it warm and moist and prevent spasm
n Hold presenting part away from the cord and maintain this until delivery to prevent cord compression
n Tilt bed head down
Immediate delivery if fetus is still alive
l If cervix is not fully dilated: emergency caesarean section
l If cervix is fully dilated: instrumental delivery

ECV
Definition
External cephalic version is an operative procedure to turn the mal-presented fetus to cephalic presentation, by
applying forces over the maternal abdomen
Indication
l Breech presentation at term
l Transverse lie and unstable lie: ECV followed by induction of labour
Contraindications
Pre-existing factors that require caesarean section any way, or are associated with high chance of section:
l placenta praevia, uterine scar
Pre-existing risk that causes high risk of the procedure:
l IUGR, fetal compromise
Pre-existing factors that make ECV not possible technically
l Obesity, uterine anomaly
Prerequisites
l no contraindications
l gestation at least 36 week
Page 16
l normal fetal morphology and well-being
l facilities for rapid progression to caesarean section, if necessary
l Rh-D negative women must be given anti-D immunoglobulin
Advantages of ECV
l High success rate
l Low complication rate
l Mother still has choice of caesarean section after failure
Disadvantages of ECV
l Chance of caesarean section after success is still higher than normal population
Procedure
l USG to exclude any contraindications such as placenta praevia and fetal anomalies
l CTG, USG for growth and liquor to exclude fetal compromise
l Ask patient to empty the urinary bladder
l Give tocolytic to relax the uterus
l Disengage the breech
l Grasp the fetal poles and turn in either forward or backward direction

Complications
l Transient fetal bradycardia:
n most common 3-10%
n last for seconds to few minutes
n no long term sequelae
l Acute fetal distress that requires immediate delivery
l Antepartum haemorrhage or abruptio placentae: rare
l uterine rupture: rare
l rupture of membranes: rare

Page 17
5. Preterm labour and PPROM

Preterm labour
Definition
Onset of labour after 24 completed weeks but before 37 completed week of gestation.
The incidence is about 5 to 10%, but prematurity accounts for 70 to 80% of all perinatal deaths.
Risk factors for preterm labour
Maternal demographic factors
l Smoking, malnutrition, primigravida, teenage pregnancy
Past reproductive history
l Recurrent risk after one Previous preterm labour: 35%; after two or more: 70%
Over distension of uterus
l Multiple pregnancy
l Polyhydramnios
Uterine abnormality
l Congenital uterine anomaly
l Cervical incompetence
Concurrent obstetric complications
l Antepartum haemorrhage
l Rupture of membranes
l Genital tract infection
l Amnionitis
Co-existing maternal diseases, such as
l Pyelonephritis
l appendicitis
Prediction and prevention
l No scoring system yet devised has proven itself superior to clinical judgment
l The strongest association is with previous pre-term delivery
l Among the measures suggested for prediction of high risk and possible prevention and for which no evidence
of benefit exists are
n Routine cervical examination
n Home monitoring of uterine activity
n Prophylactic beta-sympathomimetics
n Routine screening for bacterial vaginosis
n Prophylactic antibiotics
Management
Management depends on 5 main factors:
l State of membranes
n labour should not be suppressed if membranes have ruptured as there is high risk of intrauterine infection
l Dilatation of cervix
n Labour is likely to progress if the cervix is or more than 4cm dilated
l Gestational age
n The earlier the gestation, the more strenuous attempts to inhibit labour must be. Usually labour is not to
be suppressed after 34 weeks
l The cause of pre-term labour
n Delivery is indicated if fetal well-being is prejudiced, such as in intrauterine infection, or abruptio
placentae
l The availability of neonatal intensive care facilities
n If all cots are full or facilities are inadequate, consider transfer of the patient to an unit with better facilities
Principle of management
l Enhancement of fetal lung maturity
n by Glucocorticoid therapy
l Inhibition of pre-term labour with tocolytic:
n Beta-adrenergic agonists
n sulindac (a kind of NSAID)
l Modes of delivery of pre-term pregnancy
n If the fetus is viable it must be delivered by the route least likely to cause trauma or hypoxia
n In general, aims for vaginal delivery if gestation < 26 weeks, as caesarean section at early gestation, and
with infants under 1000g, can be hazardous for the mother and are not necessarily safer for the baby
n The indications for caesarean section are stronger but not absolute in twin pregnancy and breech
presentation
n Pre-term labour is unpredictable and the woman may become fully dilated quickly and silently

Page 18
 n Aims to have the presence of an experienced neonatal paediatrician at delivery

Preterm delivery
Definition
Delivery at a gestational age of less than 37 weeks
Incidence
The incidence in PWH is 7%, with 2% before 34 week
Clinical significance
Significant fetal morbidity and mortality
Account for 80% of all perinatal death
Causes of preterm delivery
Preterm delivery is resulted from
l preterm labour, or
l iatrogenic preterm delivery
n Sometimes a preterm pregnancy has to be discontinued because the risk of continuing the pregnancy is
higher than that of preterm delivery. For example, in severe pre-eclampsia, abruptio placentae, fetal
growth retardation (IUGR) and fetal distress, there is a high risk of intrauterine death or maternal
morbidity and mortality when the fetus is not delivered on time.

Cervical incompetence
Definition
Classically it is defined as a clinical syndrome characterized by painless dilatation of cervix, resulting in recurrent
spontaneous midtrimester abortions or preterm delivery (vaginal), in the absence of any associated uterine activity.
Causes
Previous traumatic events:
l mechanical cervical dilation
l second-trimester abortion
l cervical amputation, conization or laceration
Congenital: rare
l in utero diethylstilbestrol exposure
l spontaneous occurrence
Diagnosis
History
l typical history of painless midtrimester cervical dilation resulting in expulsion of a nonviable fetus
l history of any traumatic events involving the cervix
Examination
l presence of cervical dilation with or without bulging forewater
Diagnostic tests in non-pregnant state
l A number of methods for assessing cervical incompetence before pregnancy have been suggested but none
are reliable. These include:
n Passage of 8mm Hegar dilator through the cervix: no resistance suggests incompetence
n Hysterosalpingogram: dilation of cervix with leaking of dye under X-ray
Management
Cervical cerclage
l placement of a circumferential cervical suture that externally supports the internal os
Elective cervical cerclage:
l performed when the cervix is not yet dilated, in patients with history of cervical incompetence
l performed at around 13 weeks after fetal viability is confirmed
Emergency cervical cerclage:
l performed when the cervix already dilated
l success rate is lower
l risk of rupture of membranes, infection, abortion or preterm delivery because the membranes are usually
bulging out after the cervix has dilated
Discussion/Something to Consider
When a woman presents to you with a history of recurrent abortions, what information do you want to ask to
diagnose a case of cervical incompetence?

Page 19
Rupture of membranes
Definition
l Premature rupture of membranes (ROM): ROM before onset of labour
l Preterm rupture of membranes: ROM before 37 week
l Prolonged rupture of membranes: ROM for more than 24 hours
Incidence
l 2% of all pregnancies
l 33% of all preterm deliveries
Risk factors for premature rupture of membranes
l Polyhydramnios
l Infection of genital tract
l Cervical incompetence
Diagnosis of rupture of membranes
Typical history
l a sudden gush of clear watery fluid passed vaginally
Examination
l watery fluid in vagina; oozing of fluid from cervical os after coughing
Other diagnostic tests
l Usually are not required unless the diagnosis is inconclusive from the history and examination:
l Amniostrix (Nitrazine paper)
n The orange colour of amniostrix changes to blue with contact with liquor
n may have false positive if the fluid is alkaline (such as mucus, blood)
l Fern pattern
n A swab dipped in fluid is used to make a slide. The slide is allowed to dry thoroughly. Under microscopic
examination, a characteristic fern pattern is noted, due to salt content in liquor
n false positive from cervical mucus
l USG
n may revealed decreased liquor volume after ROM. However, if the volume of leaking is not much, the
amniotic fluid volume would still appear normal under USG
Risk after rupture of membranes
l Cord prolapse
l Intrauterine infection
l Preterm labour and delivery
Management
Investigation
l High vaginal swab to exclude infection
Decide mode and time of delivery
l Depending on gestation and presence of infection
n Gestation after 37 weeks:
u induction of labour is still not in labour after 24 hours of ROM
l Gestation before 34 weeks:
n aim to prolong pregnancy beyond 34 week to minimise fetal complications from preterm delivery
n steroid to enhance fetal lung maturity in absence of infection
n monitor any maternal or fetal signs of infection such as maternal fever, tachycardia. uterine tenderness,
foul vaginal discharge, and fetal tachycardia, and prompt delivery if infection occurs
l Gestation between 34 and 37 weeks:
n induction of labour if there is good neonatal support.
n otherwise conservative management till 37 weeks

6. Postpartum

Postpartum care
Aims
l To ensure normal recovery from pregnancy and childbirth during puerperium
l To follow up any antenatal problems and provide appropriate referral, counselling and management
l To look for any problems in childcare and feeding
l To advise on contraception and family planning
Routine care in early postpartum period
l Look for any complications such as:
n Postpartum haemorrhage

Page 20
 n anaemia
n postpartum fever
l Provide adequate analgesia for wound pain
l Prophylactic measures such as:
n Encourage early mobilization to prevent thrombosis
n Anti-D immunoglobulin for non-sensitized rhesus negative mothers
n Rubella vaccine for non-immune mothers
l Counselling, support and education
n advise on childcare
n encourage maternal-infant bonding
n promote and teach breast-feeding
n advise contraception and family planning
Postpartum visit at the end of puerperium
l usually is arranged at the end of puerperium (6 weeks post-delivery)
l examine for blood pressure elevations, breast masses or tenderness, uterine size, anaemia and healing of
wound
l search for any problem in childcare, resumption of coitus and work, and any adjustment difficulty
l advise on contraception
l obtain pap smear if not screened before
l follow up any remaining problems such as:
n screen for diabetes if previously diagnosed to have gestational diabetes
n refer to physicians if persistent proteinuria after pre-eclampsia
l continue to encourage healthy habits
What medical students should know
Three major postpartum complications:
l postpartum haemorrhage
l postpartum fever
l postpartum depression

Postpartum fever
Definition
Body temperature of 38 degree or higher on two occasions beyond the first hours and within the next 9 days
postpartum
Incidence
5 to 10% of all pregnancies
Causes
Infectious causes
l Intrauterine infection
n High risk after prolonged ruptured membranes and prolonged labour
l Urinary tract infection
n High risk when multiple urinary catheterizations are performed during labour
l Wound infection
n caesarean wound or episiotomy wound
l Breast infection
n higher risk in breastfeeding mothers
n usually cause by Staphylococcus aureus
n need to differentiate from breast engorgement of breasts and chemical mastitis
n treat with antibiotic; may require incision and drainage
Non infectious causes
l Haematoma
n vulval haematoma or pelvic haematoma
l Deep vein thrombosis
l Lung atelectasis
l Breast problems
n engorgement of breasts
n Noninfectious mastitis
Discussion/Something to Consider
How to differentiate breast engorgement and infectious mastitis clinically?

Page 21
Postpartum haemorrhage
Definition
Primary PPH
l Blood loss more than 500ml during the third stage of labour or 800ml during a caesarean section, and for 24
hours afterwards
Secondary PPH
l Any abnormal vaginal bleeding after the first day of delivery till the completion of the puerperium
Causes of primary PPH
Bleeding from uterus
l Uterine atony
n the most common cause
n may be secondary to retained placental tissue
l Retained placenta, may result from morbid adhesion of placenta to the uterine wall
l Uterine rupture or tear
l inversion of uterus, very rare
Bleeding from lower genital tract
l Cervical tear
l vaginal tear
l Vulval tear or haematoma
Secondary to systemic causes
l disseminated intravascular coagulopathy (DIC)
Causes of secondary PPH
Common causes are
l Endometritis
l retained placental tissue
l Rare causes are
l delayed uterine rupture
l uterine arterial-venous malformation
l disseminated intravascular coagulopathy (DIC)
Management of primary PPH
Resuscitation
l fluid support
l oxygen support
Assessment and diagnosis
l examine placenta for completeness
l examine lower genital tract for any tear and origin of bleeding
l examine uterine tone
l examine signs of internal bleeding
l examination under anaesthesia and exploration of uterus may be required if retained placenta is suspected
Specific treatment
l manual removal of placenta for retained placenta
l oxytocic for uterine atony
l surgical repair and haemostatsis for genital tract injury
l incision and drainage for vulval haematoma
l hysterectomy for non-repairable uterine injury, uncontrolled bleeding, morbid adherence of placenta

Uterine atony
What is uterine atony
It is a common condition immediately after delivery in which the uterus become hypotonic and loses it contractility
that is the most important mechanism to control blood loss after delivery of the baby and placenta. It is the most
common cause of postpartum haemorrhage.
What are the risk factor and causes of uterine atony
Uterine atony is more common in:
l overdistended uterus such as multiple pregnancy, polyhydramnios
l abruptio placentae, placenta praevia
l prolonged labour, or prolonged stimulation with syntocinon
Uterine atony is also caused by retained placental tissue which should be ruled out first when uterine atony occurs.
Prevention of uterine atony
l All women should be given syntometrine or syntocinon immediately after the delivery of their babies.
l High risk cases should also be given additional syntocinon infusion to maintain the uterine tone.
Management of uterine atony

Page 22
l rule out retained placental tissue
l resuscitation with fluid or blood replacement
l control blood loss with oxytocics which include syntocinon, or other prostaglandins

Uterine rupture
Definition
Complete uterine rupture:
l uterine cavity directly communicate with peritoneal cavity
Incomplete uterine rupture:
l uterine and peritoneal cavities separated by visceral peritoneum
Uterine dehiscence:
l fetal membranes are not yet ruptured
Causes
Uterine rupture can occurred spontaneously or after traumatic events. A scarred uterus is vulnerable to rupture, but
rupture can occasionally occur in an unscarred uterus.
l Spontaneous rupture: risk increases in:
n high parity
n obstructed labour
n morbid adherence of placenta
n uterine hyperstimulation
n fetal anomalies distending lower segment such as hydrocephalus
n previous surgery: caesarean section, hysterotomy, myomectomy, metroplasty previous trauma: curette,
sharp or blunt trauma
congenital anomaly: undeveloped uterine horn
l Traumatic rupture, after:
n blunt or sharp trauma
n operative procedures: ECV, instrumental delivery, MROP
Pathology
Rupture of unscarred uterus
l longitudinal or lateral
l vascular with torn vessels and heavy bleeding
l 85% are not repairable and require hysterectomy
l high maternal and fetal mortalities and morbidities
Rupture of scarred uterus
l rupture along old scar
l wound relatively avascular
l two-third of the ruptures are amendable
l lower maternal and fetal mortalities and morbidities when compared with unscarred uterine rupture
Rupture of uterus with previous caesarean section scar
Type of scar classical lower segment
Incidence 2.5% 0.5%
Timing 1/3 before labour rarely before labour
maternal mortality 5% 0%
fetal mortality 75% 12%
Clinical features
l sudden abdominal pain
l vaginal or intra-abdominal bleeding
l uterine contractions may cease
l fetal distress
l fetal misplacement
Diagnosis
l high suspicion if patient with a scared uterus presented with acute abdominal pain and bleeding with abnormal
CTG
l some cases of uterine rupture are not diagnosed until during caesarean section
Differential diagnosis:
l abruptio placentae: also present with acute pain and bleeding, and fetal distress
l uterine hyperstimulation: also present with sudden fetal distress
l amniotic fluid embolism: present with sudden shook and fetal distress
Management
l Resuscitation
l Immediate delivery: by caesarean section
l Repair of uterine rupture and hysterectomy, depends on
Page 23
 n type and extent of rupture
n severity of bleeding
n patient's past obstetric history and wish of fertility
l patients must be counselled for elective section next pregnancy, if the uterus is repaired and conserved
Prevention
l reduce prevalence of scared uterus in the population by avoiding unnecessary caesarean section
l avoid overstimulation of uterus by oxytocic during labour

Uterine inversion
Definition
It is a very rare complication of the third stage of labour in which the fundus is inverted into the uterine cavity. It is
complete when the fundus has passed completely through the cervix, or incomplete where the fundus is still above
the cervix.
Incidence
l 1 in 10000 deliveries
Causes
l It is often a result of inappropriate cord traction to deliver the placenta:
n no counter pressure (controlled cord traction) to prevent fundal descent.
n premature traction before evidence of placental separation
n too vigorous fundal pressure
l The risk of inversion is higher when the uterus is very lax, or there is morbid adherence of placenta.
Clinical Presentation
l Uterine fundus is protruding out from the cervix (in complete inversion)
l Severe postpartum haemorrhage
l Severe abdominal pain
l Shock
Management
Resuscitation and management of haemorrhage and shock
Reposition of the uterus
l Manual replacement
n While the adherent placenta is left undelivered, the fundus is pushed back manually vaginally. Uterine
relaxants may be required. Once the uterus is in position, the attendant's hands should remain in
endometrial cavity until a firm contraction occurs (oxytocic may be required). Then the placenta can
carefully be removed.
l Replacement with hydrostatic pressure
n Warm saline is infused into posterior fornix of vagina, to distend the vagina and uterus so as to push the
fundus of the uterus back.
l Laparotomy
n It is rarely required. The uterus is cut open to release the constriction and the fundus is reverted.

Sheehan syndrome
This is a rare complication of postpartum haemorrhage. Severe blood loss and vascular shock at or after delivery
lead to a reduction of blood flow through the pituitary-hypothalamic circulation, resulting in thrombosis, and necrosis
of the pituitary gland with loss of its function. Patients exhibit hypogonadotropic hypogonadism (fi rst sign: no return
of menstruation after delivery) as well as evidence of thyroid and adrenal cortex impairment. Replacement of
deficient hormones is required.

Puerperium
Definition
l In Latin puer means child and parere means to bear
l The period during which the reproductive organs return to their pre-pregnant condition and are usually
regarded as an interval of 6 weeks after delivery.
Normal physiological changes during puerperium
Involution of uterus
l Uterus regains its usual non-pregnant size within 5 to 6 weeks, shrinking from 1000g immediately postpartum
to 100g
l Uterine fundus at umbilicus shortly after delivery, at symphysis by 2 weeks and nonpregnant size by 6 weeks
l Rapid atrophy is due to the marked decrease in size of the muscle cells rather than the decrease in their total
number

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l Breast-feeding accelerates involution because stimulation of nipples releases oxytocin from the
neurohypophysis, and the resulting contractions of the myometrium facilitate the involution process
l Afterpain: the uterus contracts throughout the period of involution, which produces afterpain, especially in
multiparous women and nursing mothers. In primparous women, the uterus tends to remain contracted
tonically, whereas in multiparous, the uterus contracts vigorously at interval
Lochia
l It is the uterine discharge that follows delivery and last for 3 to 4 weeks.
l Lochia rubia is blood-stained fluid that lasts for the first few days
l Lochia serosa appears 3 to 4 days after delivery, it is paler than
l lochia rubra because it is admixed with serum
l Lochia alba occurs after the tenth day, because of an admixture with leukocytes, the lochia assumes a white or
yellow-white color.
l Foul smelling lochia suggests infection.
Lactation
l see lactation

Involution
Involution of uterus
Uterus regains its usual nonpregnant size within 5 to 6 weeks, shrinking from 1000g immediately postpartum to
100g. The rapid atrophy is due to the marked decrease in size of the muscle cells rather than the decrease in their
total number. Breast-feeding accelerates involution because stimulation of nipples releases oxytocin from the
neurohypophysis, and the resulting contractions of the myometrium facilitate the involution process. In primparous
women, the uterus tends to remain contracted tonically, whereas in multiparous, the uterus contracts vigorously at
interval. The uterine contraction pain that produced throughout the period of involution is called afterpain, and is
more common in multiparous women and nursing mothers.

Lochia
It is the uterine discharge that follows delivery and lasts for 3 to 4 weeks puerperium. The discharge undergoes
changes during the first few weeks:
l Lochia rubia is blood-stained fluid that lasts for the first few days.
l Lochia serosa appears 3 to 4 days after delivery, it is paler than lochia rubra because it is admixed with serum.
l Lochia alba after the tenth day, because of an admixture with leukocytes, the lochia assumes a white or
yellow-white color.
l Foul smelling lochia suggests infection.

Engorgement of breasts
It is a normal phenomenon with the breasts become full, red, hard and sore due to increased blood flow before milk
secretion commences. It usually occurs in the first few days post-delivery, and may cause fever. It must be
differentiated from mastitis which is usually unilateral. Other cause of postpartum fever should also be looked for
before attributing the fever to breast engorgement.
Discussion/Something to Consider
How is engorgement of breasts differentiated from mastitis clinically?

Lactation
Growth of mammary glands
l early in pregnancy, HCG, chorionic somatotropin, prolactin causes a marked increase in ductular sprouting and
branching
l estradiol and progesterone cause the mammary gland to become richly arboized
l serum growth factor and insulin cause cell proliferation at the end of the ducts, which under the influence of
prolactin and corticosteroids, differentiate to form alveoli
l Placental lactogen and prolactin stimulate the secretion of colostrum
Lactation
l The withdrawal of estrogen after the delivery of the placenta allows lactation to begin
l lactation is in large part sustained by the stimulus of nursing that causes a transient increase in prolactin and
oxytocin, the former hormone is responsible for alveoli synthesis of milk, while the latter is responsible for
ejection of milk from the alveoli into ductules

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Breast-feeding
Advantages to mothers
l Increases bonding
l Promotes uterine involution
l Effective post-partum contraception
l Economical - Save money on formula feeding
Contraindications
l HIV +ve (unless formula feeding confers greater risk through contaminated water supply, especially in Third
World countries)
l Drug abusers
Measures to promote breast-feeding
l "Baby-friendly hospital": promote breast-feeding since antenatal period
l Nurse specialists to help tackle problems or misunderstanding
l Never provide formula feeding unless really indicated
Tips
l Early start
l Proper positioning - baby's mouth covers the whole nipple and areola
l Feed on demand
l Healthy lifestyle
l No supplements
l Don't worry about engorgement - analgesics, tight bra and frequent feed

Breast milk
l Natural and the best nutrition for babies
l Not able to be duplicated by formula milk
l Advantages to babies
n Just the right amount of nutrition for babys' needs
n Antibodies and cells such as macrophages help to prevent infection
n Increases bonding
n Always sterile --> Decrease risk of diarrhoea from contaminated bottle feeding
n Decreases risk of allergy

Colostrum
Yellowish fluid expressed from the breasts during late pregnancy and before the onset of true lactation. Compared
with mature breast milk, it contains more minerals and protein, much of which is globulin, but less sugar and fat. It
also contains some immune cells. The immunoglobulin A and other host resistance factors such as complement,
macrophages, lymphocytes, lactoferrin in colostrum provide protection for the newborn against enteric pathogens.
The colostrum gradually converts to mature milk a few days after delivery.

Postpartum depression
Epidemiology
l 12% of Hong Kong Chinese women
l usually occurs in women with previous depressive disorders or other life situations predisposing them to
depression
Clinical features
Depressive symptoms:
l Low mood, tearfulness, not her normal self
l Irritability, bad temper
l Guilt, self-blame, low self-esteem
l Forgetfulness, poor concentration
l Sleep disturbance, especially early morning
l Loss of appetite
l Suicidal ideas or attempt
l Distressed by the inability to have affection towards the baby
l Lack of confidence in child care
l Excessive anxiety about baby's health
l Obsessional fear of harming the baby
Treatment
l Psychoeducation

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l Pharmacotherapy: tricyclic anti-depressant
l Psychotherapy: discuss childcare and interpersonal problems
Prognosis
Untreated
l 1/3 continued to be depressed by one year, 1/10 by 2nd year
Treated
l Good and prompt response to treatment
Persistent stressors and personality tend to associate with poor prognosis
Future pregnancy
l 1/6-1/2 risk of relapse

Postpartum blue
It affects up to 70% of all mothers, and occurs during the first 2 weeks after delivery, usually 48 and 72 hours
postpartum. It is manifested by tearfulness, anxiety, mood lability, irritability, insomnia and depression. It is said to be
related to physiological changes in hormone levels after delivery, often resolves spontaneously and require no
treatment. It should be differentiated from postpartum depression.

Postpartum psychosis
Or puerperal psychosis, usually occurs 2 to 3 months post-delivery. Most show symptoms of manic-depressive type,
with confusion and disorientation; delusional thoughts or expressions of suicide. It should be differentiated from
postpartum depression.

7. Miscellaneous topics in General Obstetrics

Advanced maternal age

It is arbitrarily defined as 35 years old or above on the estimated date of confinement (EDC). In Hong Kong, 18% of
all pregnant women, and 9% of all primiparous women are in advanced maternal age. It is epidemiologically
associated with various fetal and maternal risks. However, it is better to consider it as a risk indicator, rather than a
risk factor. Apart from Down syndrome, the associations with other risks are confounded with other socio-medical
factors such as parity, smoking, general health and reproductive health.

Fetal risks
l There is an exponential increase in risk of Down syndrome with maternal age.
l Abortion
l Preterm delivery
l Higher perinatal mortality

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Maternal risks
l Gestational diabetes
l Pre-eclampsia
l Prolonged labour
l Placenta praevia
Management of pregnant women with advanced maternal age
l Counselling for prenatal diagnosis or screening of Down syndrome
l Oral glucose tolerance test at around 26 to 28 week of gestation

Rhesus
Rhesus blood group system consists of C, D, E antigens. The genes coded for these antigens are inherited as
autosomal dominance, i.e. the phenotype of DD and Dd is D positive, while dd is D negative. Among thee three
rhesus antigens, rhesus D iso-immunisation is the most common and also most severe type.
99% of Hong Kong Chinese are Rhesus D positive while 85% Caucasian are D positive.

Rhesus D iso-immunisation
Introduction
Rhesus D iso-immunisation was a common fetal haemolytic disease in the Caucasian population resulting in high
fetal morbidy and mortality. It has now been under control with effective prophylactic therapy.
Pathogenesis
When the mother is rhesus D negative but the fetus is rhesus D positive, the mother may be sensitized when the
fetal red cells enter the maternal circulation. This can occur during labour, abortion, antepartum haemorrhage, or
some obstetric procedures such as chorionic villus sampling.
The sensitized mother will then develop IgM against the rhesus antigen. Subsequent sensitisation will trigger the
synthesis of IgG. While the IgM molecules are too big to cross the placenta, IgG can do so, and attack the fetal red
cells, resulting in fetal haemolytic anaemia.
In severe case, hydrops fetalis develops.
Screening and prevention
Every pregnant woman should have the rhesus blood group checked. If the woman is rhesus D negative, rhesus
antibody should then be checked to see if iso-immunisation had been occurred.
Prevention of iso-immunisation is now effectively achieved by giving rhesus antibodies after delivery or any
sensitizing events. The incidence has been reduced to 0.3%. With routine antepartum prophylaxis (at 26 and 34
weeks of gestation), the incidence decreases further to 0.06%.
However, this preventive measure is useless when iso-immunisation has already been occurred.
Diagnosis of fetal haemolytic disease
Once the mother has been sensitized, there is risk of hydrops fetalis. The fetal should be monitored with USG for
any early signs of hydrops such as cardiomegaly. Skin edema, ascites, pleural effusion are late signs.
The alternative methods to monitor severity of fetal anaemia is by regular amniocentesis. The bilirubin level in the
amniotic fluid reflects the severity of haemolysis.
Management of fetal haemolytic disease
When there is evidence of hydrops or significant increase in amniotic bilirubin level, severe haemolytic anaemia is
likely. Delivery should be considered when the fetus has reached 34 weeks of maturity. Otherwise, the fetus should
be treated with intrauterine blood transfusion and glucocorticord therapy to enhance lung maturity.
Discussion/Something to Consider
Can you explain why rhesus D iso-immunisation is more commonly affect the subsequent pregnancies than the first
one?

Postterm
Definition
Post-term pregnancy
l Pregnancy lasting 42 completed weeks (294 days) or more (WHO)
Post-maturity syndrome
l clinical syndrome with the neonate manifesting signs of:
n long and thin in body girth and underweight from loss of subcutaneous tissues
n patchy areas of desquamation and skin is stained with meconium, although rarely the latter feature may
be absent
n the ventral surfaces of the hands and feet are wrinkled and the nails are long and stained with meconium
Incidence
Varies from 3 to 10%, depending the accuracy of the dating of pregnancy

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Causes
l Most are by chance
l Rarely it is associated with fetal abnormalities: anencephaly, fetal adrenal hypoplasia, absence of fetal pituitary,
placental sulfatase deficiency. The deficiencies of hormones in the above conditions are thought to cause the
failure of initiation of labour
Risk of post-term pregnancy
Maternal risk
l Maternal anxiety
l Higher caesarean section rate resulting from macrosomia, failure of induction of labour, and fetal distress
l Birth canal injury resulting from difficult delivery of macrosomic baby
Fetal risk
l 2-fold increase in perinatal mortality rate when compared to term gestation
l intrauterine growth retardation
l fetal compromise
l macrosomia and associated birth injury such as shoulder dystocia
l post-maturity syndrome
l high chance of meconium stained liquor (MSL) and therefore meconium aspiration syndrome
Diagnosis
l Accurate dating of pregnancy from menstrual history, early ultrasound assessment, landmarks of fetal
development: quickening, fetal heart sound, uterine size
Management
Induction of labour at 41 week
Discussion/Something to Consider
What are the assessments that should be done before induction of labour for postterm?

Braxton Hicks contractions

Spontaneous painless uterine contractions usually occur in the 3rd trimester. They are us ually irregular in frequency
and inconsistent in intensity, and do not result in cervical dilatation. This normal phenomenon should be
differentiated from preterm labour when it occurs before 37 weeks.

Cerebral palsy
Definition
l A non-progressive disorder of the brain resulting in impairment of motor function, usually of spastic rigidity type.
Pathology
l hypoxic ischemic injury of a developing brain, mainly of the white matter
Causes
l Birth asphyxia was being blamed as the major cause of cerebral palsy until recent decades. Now it is clear that
only 10% of the cases are related to intrapartum events or birth asphyxia. Majority is due to complications of
prematurity, of which the neonate are prone to intraventricular haemorrhage and hypoxic brain injury. Other
causes are chronic antepartum hypoxia, congenital brain malformations, and postpartum insults (20%) such as
meningitis

Chorioamnionitis
Definition
It is an acute inflammatory process involving the chorion, its fetal blood vessels, the umbilical cord, and the amnion
(by local extension of the inflammation, as the amnion itself has no blood supply). This inflammatory process is
potentially fatal to both the mother and the fetus.
Causes
It is often a result of ascending infection, and prolonged rupture of membranes is a major risk factor. The common
micro-organisms are:
l Group B streptococcus
l Gram negative rods from bowel contamination
l those of sexually transmitted diseases
Clinical features
l Maternal fever and tachycardia
l Uterine tenderness
l Fetal tachycardia
l Foul smelling discharge from the cervix
l Maternal leukocystosis
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Diagnosis
l The diagnosis is mainly relied on the clinical features. Microscopic examination and culture of amniotic fluid are
difficult and inaccurate before delivery, and are not very helpful in an acute setting.
l Careful clerking and examination are essential to rule out other causes of maternal fever, such as urinary tract
or respiratory tract infections
Management
Delivery of pregnancy
l Fetus is at high risk of intrauterine death, or neonatal sepsis if there is a delay of delivery.
l Therefore delivery should be immediate regardless of maturity (the risk chorioamnionitis is high than that of
prematurity).
l Delivery is by Caesarean section when labour is not yet established. If labour has been established,
augmentation of labour may be considered to hasten delivery.
Antibiotics
l Multiple antibiotics to cover gram positive cocci, gram negative rods and anaerobes: penicillin group,
cephalosporins, metronidazole.

Gravid
Means pregnant. A primigravida is a woman pregnant for the first time.

Grand multipara
A woman with parity 4 or more. She is likely to have powerful and coordinated uterine contractions. The labour
progress is usually quite. However, the chances of birth before arrival to hospital, uterine rupture and postpartum
haemorrhage due to uterine atony are higher. In addition, their babies may tend to be bigger, causing an unexpected
obstructed labour or shoulder dystocia.
Discussion/Something to Consider
How to prevent uterine rupture and postpartum haemorrhage in this group of patient?

Obstetric statistics
l Maternal mortality rate
l Perinatal mortality rate
l Stillbirth rate
l Neonatal death rate

Maternal mortality
Definition
l Deaths of women during pregnancy or within 42 days of termination of pregnancy, from any cause related to
(direct) or aggravated by (indirect) the pregnancy or its management, but not from accidental or incidental
(fortuitous) causes.
Direct
l deaths resulting from obstetric complications of the pregnant state (pregnancy, labour and puerperium), from
interventions, omission, incorrect treatment, or from a chain of events resulting from any of the above.
Indirect
l deaths resulting from previous existing disease, or disease that developed during pregnancy and which was
not due to direct obstetric causes, but which was aggravated by the physiological changes in pregnancy
Fortuitous
l deaths from unrelated causes which happen to occur in pregnancy or the puerperium
Late
l deaths occurring between 42 days and 1 year after abortion, miscarriage or delivery that are due to Direct or
Indirect maternal causes
Maternal mortality in Hong Kong
l Hong Kong has the one of the lowest maternal mortality rate of the world, around 1 per 10000 pregnant women.
The most common causes of maternal death are pulmonary embolism and suicide secondary to postpartum
depression.

Perinatal mortality
It includes all stillbirth and (early) neonatal death. The perinatal mortality rate is: number of stillbirth + (early)
neonatal death per 1000 total birth (all stillbirth + livebirth). It is about 4.7/1000 in Hong Kong.

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Stillbirth
Definition
It is the birth of a dead fetus at or after 24 weeks of gestation. Stillbirth rate is the number of stillbirth per 1000 birth
(stillbirth + livebirth). It is about 3 to 4/1000 in Hong Kong.
Causes
About 50% of cases are unexplained stillbirth. The following are identifiable causes:
Fetal complications:
l chromosomal abnormalities
l complications of twins such as twin-twin transfusion syndrome
l intrauterine growth retardation (IUGR)
l congenital infections
Maternal complications:
l abruptio placentae
l poorly controlled diabetes mellitus
l pre-eclampsia
l other poorly controlled maternal diseases such as hypothyroidism, SLE, antiphospholipid syndrome

Neonatal death
Definition
l Early neonatal death are all neonatal deaths within 7 days of delivery
l Late neonatal death are all neonatal deaths after first 7 days but within 28 days of delivery
l The neonatal death rate is the number of early neonatal death per 1000 livebirth. It is about 1.4/1000 in Hong
Kong
l Post-neonatal death are all neonatal deaths after 28 days but within 1 year of age
Causes
l Over 80% of cases are due to prematurity
l Other causes include congenital abnormalities, severe birth asphyxia

Trimester
A period of 3 months (about 13 to 14 weeks) in pregnancy:
l first trimester: up to 14 weeks
l second trimester: 14 to 28 weeks
l third trimester: 28 weeks to delivery

Placenta
Structure of a placenta
l Cotyledons Membranes: see chorioamnionicity
l Umbilical cord
Disorders of placenta
l Placenta praevia
l Abruptio placentae
l Retained placenta
l Morbid adherence of placenta
l Placental insufficiency
l Placental tumour: chorioangioma
l Chorioamnionitis

Obstetric surgery
Operative delivery
l Caesarean section
l Instrumental delivery
l Episiotomy
l Manual removal of placenta
l Postpartum hysterectomy
l Repair of tear of lower genital tract
Prenatal diagnosis and therapy
l Chorionic villus sampling
l Amniocentesis
l Cordocentesis
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Obstetric emergency
l Eclampsia
l Shoulder dystocia
l Cord prolapse
l Amniotic fluid embolism
l Pulmonary embolism
l Massive haemorrhage, due to placenta praevia or any causes of postpartum haemorrhage
l Uterine inversion

Birth trauma
Types of birth trauma
Skeletal injury
l long bone fractures
l skull bone fractures
Bleeding
l cephalhaematoma
l subaponeurotic haematoma
Nerve injury
l Brachial plexus injury (Erb palsy)
l Facial nerve injury

Subaponeurotic haematoma
Or subgaleal haematoma, is a result of birth trauma. The subaponeurotic space is a potential and expansible space
between the skull bone and the scalp, with vessels run through it. Bleeding inside it can be huge resulting in shock
and high mortality (20%). It is extremely uncommon after normal vaginal delivery, but occurs in 6/1000 vacuum
extraction. The main clinical feature is a boggy swelling of the scalp that crosses suture lines, with or without shock.
It should be differentiated from other scalp swelling such as caput succedaneum and cephalhaematoma. Early
recognition is crucial in preventing complications and mortality.

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Fetal Medicine

Fetal medicine
What is fetal medicine
l a subspecialty in Obstetrics.
l deal with high risk pregnancy with fetal diseases and complications (see below).
l carry out prenatal diagnosis and counselling, and fetal therapy.
l multi-disciplinary care involving obstetricians, paediatricians, geneticists, and paediatric surgeons.
What are the fetal diseases and complications
l Congenital abnormalities, such as:
n chromosomal abnormalities
n genetic disorders
n fetal infections
n multifactorial malformations
l Growth disorders: intrauterine growth retardation (IUGR)
l Multiple pregnancy
l Preterm labour and delivery
What are the commonly used diagnostic tools
l Ultrasonography (see USG (Obstetrics))
l Chorionic villus sampling
l Amniocentesis
l Cordocentesis
What are the possible therapeutic tools
l Transplacental medication
l Transumbilical medication and transfusion
l Fetal surgery
l Termination of pregnancy
Fetal diseases medical students should know
Please refer to the following individual topics:
l Congenital abnormalities: chromosomal abnormalities, genetic disorders, fetal infections, multifactorial
malformations
l Growth disorders: intrauterine growth retardation (IUGR)
l Multiple pregnancy
l Preterm labour and delivery

1. Chromosomal disorders

Chromosomal abnormalities
Introduction
l affect 7% of all conceptions, and 6 per 1000 livebirths
l 95% of gametes with chromosomal abnormalities are not viable
l 60% of all first trimester spontaneous abortions, 5% of all second trimester abortions, and 5% of stillbirths
l most are trisomies
Types of chromosomal abnormalities
Numerical aberrations
l Aneuploidy
n The number of chromosomes is not the multiple of the haploid; it can be trisomy (47) or monosomy (45)
n autosomal chromosomes involved: trisomy 21 (Down syndrome); trisomy 18 (Edward syndrome), trisomy
13 (Patau syndrome)
n sex chromosomes involved: XO (Turner syndrome), XXY, XXX, XYY
l Polyploidy
n The number of chromosomes is an exact multiple of the haploid, but greater than the diploid number (2n),
e.g. Triploidy (3n, 69XXY), or tetraploidy (4n)
Structural aberrations
l Rearrangement of chromosomal structure due to chromosome breakage and inappropriate rejoining of the
broken ends. They are:
n translocation
n deletion
n duplication

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 n inversion
n isochromosome
u genetic material may be lost (unbalanced) or maintained (balanced) after a rearrangement
u balanced rearrangements:
u individuals with balanced rearrangement are phenotypically normal
u However, they have an increased risk of producing unbalanced gametes, leading to reproductive
loss or abnormal children
Other aberrations
l mosaic
n an individual with two or more cell lines derived from a single zygotes
l chimaera
n two cell lines are derived from two separate zygotes
What should medical students know:
l Down syndrome, Turner syndrome, translocation
Translocation
Translocations of fragments between chromosomes can be:
l Reciprocal
l Robertsonian
l Insertional
Balanced translocation:
l exist when the gemone contains the correct amount of genetic matter
l usually have no outward manifestation
l parental karyotyping is essential
l if one parent has a balanced translocation, the theoretical outlook for any offspring is 1: 4 having the same
balanced translocation; 1:4 having a normal karyotype; and 1:2 having an unbalanced translocation. However,
the actual risk of having unbalanced translocation is 1:10 as most of them will abort.

Biochemical screening
What is biochemical screening
Biochemical screening is a screening test for Down syndrome performed at around 16 to 20 weeks of gestation. It
consists of measurement of maternal plasma level of several markers, including alpha-feto protein (AFP), human
chorionic gonadotropin (HCG) and unconjugated estriol (uE3). It is also called triple test when all three markers are
tested, or dual test when only AFP and HCG are assessed. In public hospitals of Hong Kong, dual tests are offered
to pregnant women at or above 35 years old for cost-effectiveness (see below).
What is the aim of biochemical screening
The aim is to screen women for increased risk of having a Down fetus. The test itself is not diagnostic, but it selects
the high risk cases for diagnostic amniocentesis which is an invasive procedure. Compared with screening by age
alone, biochemical screening has a higher detection rate and a lower false positive rate (see below) so that the
number of subjects requiring amniocentesis is reduced.
How does biochemical screening work
Compared with normal pregnancies, women with pregnancy complicated with Down syndrome have lower plasma
levels of AFP and uE3, and a higher level of HCG. Although the differences are not very distinctive (otherwise these
biochemical tests would be diagnostic), they can be used to estimate the chance of having a Down fetus. For
example, when the AFP level is at 0.7MoM (multiple of the median level), 998 out of 1000 women would have a
normal pregnancy while 2 have a Down fetus. The chance is 0.2%. When it is at 0.3MoM, 10 out of 1000 are
abnormal. The chance is therefore 1%. Similarly, the overall chance of having a Down fetus can be computed by
combining the chances estimated using different markers.
How good is biochemical screening
When applied to all pregnant women, biochemical screening has a sensitivity of 60%. Five percent of the population
would be screened positive. For example, if there were 10 Down cases in a population of 1000 (prevalence=1%).
Fifty cases would be screened positive. Among these 50 cases, 6 of them would be true Down fetuses (sensitivity of
60%). The other 44 cases would be false positive (false positive rate= 44/50).

Trisomy
This is a condition of having three copies of a given chromosome in each somatic cell rather than the normal number
of two. In majority of cases, it is resulted from non-disjunction during meiosis. The most common type is trisomy 21
(Down syndrome), trisomy X, trisomy 18 (Edward syndrome) and trisomy 13 (Patau syndrome).

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Non-dysjunction
A mistake during meiosis which causes some resulting haploid cells to have only 22 chromosomes and others 24
chromosomes, instead of the normal 23. If a gamete with 22 chromosomes fuses with one with the normal 23, a
zygote with 45 chromosomes results (monosomy). If a gamete with 24 chromosomes fuses with one with the 23, a
zygote with 47 chromosomes results (trisomy). Non-dysjunction occurs more commonly during ooytes development
in women of advanced maternal age.

Down syndrome
Definition
l Trisomy 21
l Presence of extra chromosome 21 or its material
Incidence
l 1 in 850 of all livebirths
l the most common type of chromosomal abnormalities
l incidence rises markly with maternal age, with 1 in 1000 at 30 years old, to 1 in 300 at 35 and 1 in 100 at 40
Aetiology
Extra chromosome is resulted from:
l non-dysjunction
n accounts for 95% of all Down syndrome
n arises in the stage of meiosis of the ovum before fertilisation
n karyotype: 47XX, + 21 or 47XY, + 21
l unbalanced translocation
n accounts for 4% of all Down syndrome
n one of the parental karyotypes consists of a translocation with the long arm of a chromosome 21 to the
other chromosome (e.g. chr 14)
n The translocated segment is then inherited to the offspring so that the offspring would have a long arm of
chr 21 in addition to one pair of chr 21 (unbalanced)
n karyotype: 46, XX, der (14;21) or 46, XY, der (14;21)
l Mosaicism
n accounts for 1% of all Down syndrome
n results from mitotic non-disjunction during the early stage of embryogenesis. These patients have cells
with a normal chromosome number and some that are aneuploid.
n karyotype: 46, XX / 47, XX, +21 or 46, XY / 47, XY, +21
n mosaic patients may exhibit variable or milder symptoms, depending on the proportion of abnormal cells.
Clinical features of Down syndrome
Mental retardation
l mean IQ is 40% of normal population
l Only 20% has no or mild mental retardation
Malformation
l Congenital heart defects (40%)
l Malformations of the gastrointestinal tract, e.g. duodenal atresia (10%)
l Head and face: Brachycephaly / microcephaly; epicanthic folds and flat facial profile;
l Limbs: Simian crease; gap between first and second toe
Other complications
l Alzheimer's disease
l Subfertility
Prenatal screening
Maternal age
l Using cut-off of 35 years old at time of EDC
n 18% of pregnant women will be screened positive
n only sensitive for 20% of Down syndrome, as majority of Down (80%) are come from mothers below 35
years old
n safe and inexpensive screening tool
Biochemical screening
l Using serum AFP, HCG with or without unconjugated estriol
l 5% of pregnant women are screened positive
l sensitivity of 60%
l i.e. pick up more Down than screened by maternal age alone, and less false positive so that few pregnant
women require an invasive diagnostic procedure
l disadvantage is that it can only be done in 2nd trimester
Nuchal translucency in 1st trimester
l Using cut-off of 3mm
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 n 5% of pregnant women are screened positive
n sensitivity varies from 33% to 60%
n potential benefit of early screening followed by CVS
n problem of reproducibility
n further studies required to define its clinical usefulness
Screening by USG of Down features in 2nd trimester
l Ultrasound marker for Down syndrome:
n Shortened femur length, shortened humeral length, thickened nuchal skinfold, short ear length, fetal
pyelectasis, choroid plexus cyst, duodenal atresia, congenital heart defects, abnormalities of the fifth digit,
trisomy hands
n sensitivity 33% only
Prenatal diagnosis
Fetal karyotyping by chorionic villus sampling
advantages:
l is accurate and sensitive
l can be done in the first trimester (10 to 13 weeks) so that intervention such as termination of pregnancy for
abnormal cases can be performed earlier during when the operative risk is lower
disadvantages:
l fetal loss rate is slightly higher when compared to amniocentesis
l rate of mosaicism is slightly higher among trophoblastic cells, and the karyotype of trophoblasts may not reflect
the actual karyotype of the fetus
l creates anxiety as minor chromosomal abnormalities are also picked up
Fetal karyotyping by amniocentesis
advantages:
l is accurate and sensitive
l has lower complication rate when compared with CVS
l reflects true karyotype of the fetus
disadvantages:
l is performed in second trimester
l creates anxiety as minor chromosomal abnormalities are also picked up
Management of pregnancy with Down syndrome
Counselling and support:
l discuss the prognosis and long term complications of Down syndrome, social and health support available for
Down children in the society
Options of continuing pregnancy and termination of pregnancy:
l termination of pregnancy is legal when before 24 week of gestation
l medical and surgical procedures of termination, and their complications.
Discussion/Something to Consider
You are seeing a patient of age 38 at 8 week of gestation of her first pregnancy in the clinic. She was anxious about
Down syndrome. How would you counsel the patient, and which investigation would you suggest?

Patau syndrome
Definition
l Trisomy 13
l Presence of extra chromosome 13 or its material
Karyotypes
l Trisomy 13 type: 47, XX, +13
l Translocation type: 46, XX, t13
l Mosaic type: 46, XX / 47, XX, +13
Incidence
l 1 in 15,000 births
Clinical features
l Cardiac defects (80%)
l Renal defects (30%)
l Holoprosencephaly
l Cleft lip and palate
l Eye defects such as microphthalmia, anophthalmia and coloboma
l Polydactyly
l Umbilical hernia
l Mental retardation
Prognosis

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l Lethal chromosomal abnormality
l second trimester abortion, stillbirth or early death after birth

Edward syndrome
l Trisomy 18
l Multiple fetal abnormalities.
l One of the lethal chromosomal abnormality
l Related to advanced maternal age

Turner syndrome
Definition
l Monosomy X with karyotyping 45XO
Incidence
l 1/3000 female births
Aetiology
l non-disjunction in approximately 55% of cases
l The remaining 45% of patients are either mosaics(30%) or have structural abnormalities of the X
chromosome(15%)
l The karyotypic heterogeneity is responsible for significant variations in the phenotype.
Clinical features
l Short stature
l Webbed neck
l Low posterior hairline
l Cubitus valgus
l Broad chest and widely spaced nipples
l Diffuse pigmented nevi
l Peripheral lymphoedema at birth
l Renal anomalies such as horseshoe kidney
l Aortic coarctation
l Poor secondary sexual characteristics
l Normal intelligence
l Primary amenorrhea, streak ovaries, infertility, low estrogens with elevated gonadotropin
l Mosaics can present with oligomenorrhea and some secondary sex characteristics
Prenatal screening
l Unlike Down syndrome, there is no screening program for Turner syndrome
l Turner syndrome should be suspected if routine scan shows presence of cystic hygroma or other characteristic
abnormalities
Prenatal diagnosis
USG would show characteristic features:
l cystic hygroma
l renal anomalies
Karyotyping with chorionic villus sampling or amniocentesis

Klinefelter syndrome
Definition
A chromosomal disorder of a male with an extra X chromosome (47 XXY), usually resulted from nondisjunction
during meiosis.
Incidence
1 in 1000 males
Pathology
l The most common karyotype is 47 XXY; about 15% of cases show mosaicism
l Male hypogonadism develops as there are two X chromosomes
Clinical features
l Taller and thinner than average
l Eunuchoid features, female fat distribution
l Reduced facial and body hair
l Gynaecomastia
l Testicular atrophy
l Sterility due to impaired or absent spermatogenesis
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l Mild degree of mental retardation (severity is correlated with the number of extra X chromosomes), some may
have normal intelligence
l Mosaics show milder symptoms
Investigation
l High FSH and LH levels
l Low testosterone
l Semen analysis shows azoospermia

Nuchal translucency
What is nuchal translucency
It is the subcutaneous edema over the back of the fetal neck. Normally it is less than 3mm in the first trimester. It is
associated with chromosomal abnormalities when the nuchal translucency is abnormally high. It has been
suggested as a screening test for Down syndrome. The sensitivity is around 60%, and 5% of population would be
screened positive. Its screening power is therefore similar to that of biochemical screening, but it allows an earlier
screening in the first trimester. The limitation of the test is the technical difficulty in measuring the parameter and
therefore a poor reproducibility. Because of that, it is still not a standard screening test in Hong Kong.

A first trimester USG showing an abnormally increased nuchal translucency

2. Congenital abnormalities

Neural tube defect

What is a neural tube defect (NTD)
It is a group of congenital malformations of the brain, spinal cord, skull bones and spine that occur during the
development of the neural tube. It includes anencephaly, encephalocele, spina bifida with or without meningocele. It
is called a closed NTD when the lesion is completely covered by skin or thick opaque membrane. Otherwise, it is
called opened NTD. Anencephaly is invariably an open lesion.
Causes of neural tube defect
Multifactorial. It is associated with folate deficiency.
Incidence of neural tube defect
The incidence is about 4 per 1000 birth in Caucasian countries and is higher than in Asian. It is approximately equal
for anencephaly and spina bifida (without anencephaly). Encephalocele is rare, accounting for 5% of all NTDs.
Prognosis of NTDs
l Anencephaly is not compatible with life.
l Open spina bifida has a poor survival (5-year: 33%) and tends to be handicapped (90%).
l Closed spina bifida has a 5-year survival rate of 60%, and 2-third are handicapped.
Screening and diagnosis
l Maternal serum alpha-feto protein screening (MSAFP) at 16 to 18 weeks. MSAFP is higher in pregnancies with
an open NTD. Pregnancies screened positive should be followed with a morphology scan. However, closed
NTDs are likely to be missed.
l Screening with USG. Nowadays with improved quality in USG imaging, NTD can be screened more accurately
with a morphology scan at around 18 to 20 weeks. Fetal malformations other than NTD can also be examined.
However, small closed NTD can still be missed with USG.
Prenatal management of NTDs
l Patients should be counselled the prognosis of the defect, and discussed with different management options
including termination of pregnancy.
Prevention of NTDs
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Folic supplement is advised to high risk group. It should be taken at least 8 weeks before pregnancy, and continued
till first trimester. It has been showed to decrease the incidence of NTD by 2-third.

Gastroschisis
It is a kind of multifactorial congenital abnormalities with an incidence of 1 in 3000 birth. Unlike omphalocele, it is
rarely related to chromosomal abnormalities, and is usually isolated, although cardiac and other structural
abnormalities co-exist in 20% of cases.
It is a total anterior abdominal wall defect (often on the right side) resulting in protrusion of abdominal viscera
(usually small bowel) into the amniotic cavity. Unlike omphalocele, the abdominal viscera is not covered by the
peritoneum, and is therefore prone to chemical irritation from amniotic fluid (which usually occurs after 30 weeks of
gestation, said to be related to changes of chemical constituents from that time onwards). This leads to bowel
inflammation, ischemia, dilatation which make postnatal repair difficult.
Besides the risk of bowel injury, there are also increased risks intrauterine growth retardation, intrauterine death,
intrapartum fetal distress. Management should include close antepartum surveillance and elective caesarean
delivery. The recurrence risk is less than 1%.

Omphalocele
Also called exomphalos, is the extra-embryonic herniation of abdominal viscera due to failure of the gut to return to
the abdominal cavity at 8 weeks of gestation (physiological hernia), resulting in a defect of the abdominal wall. The
peritoneal sac is intact. The incidence is 1 in 5000 delivery, and 30% cases have chromosomal abnormalities, and
another 20% have co-existing malformations (usually involving the heart and kidneys).
Presentation
The defect is detectable with USG after 12 week of gestation by when physiological herniation should have been
reduced. Multiple malformations, growth retardation and polyhydramnios are common associated features. An
elevation of maternal serum alpha-feto protein may be found on biochemical screening.
Management
Prenatal
l Differentiate between omphalocele and gastroschisis:
n Presence of peritoneal sac in omphalocele
n Midline defect in omphalocele but lateral defect in gastroschisis
n Herniation of liver occurs in 40% of omphalocele but is very rare in gastroschisis
l Rule out chromosomal abnormalities and other anomalies which are crucial prognostic factors
l Counseling
n Prognosis is good for neonates with surgery, without chromosomal and other structural abnormalities
n Survival is well in excess of 75-80%
Delivery
l Can allow vaginal delivery when it is cephalic presenting
Postnatal
l Prevent heat and fluid loss and infection before surgical repair
l Surgical repair when fetal condition is stable

Hydrops fetalis
Hydrops fetalis is defined as a fetus with generalised edema plus collection of fluid in at least one of the body
cavities (ascites, hydrothorax, or pericardial effusion). Traditionally in the western countries, it is classified into
immune and non-immune hydrops. The former is due to rhesus isoimmunisation which is more common in the
Caucasian population. Actually, the causes of hydrops are very diverse, including fetal anaemia, primary cardiac
abnormalities, extra-cardiac structural abnormalities, and chromosomal abnormalities The common end-point is
fetal heart failure. The prognosis depends on the underlying cause.
Causes of Hydrops fetalis
Fetal anaemia due to:
l Alpha-thalassemia (Haemoglobin Bart disease)
n The most common cause of hydrops in our locality
n A lethal condition in which termination of pregnancy should be considered
l Rhesus isoimmunisation
n Can be treated with repeated intrauterine transfusion or early delivery of the fetus. The prognosis is much
better nowadays
l Parvovirus infection
n The prognosis is good with repeated intrauterine transfusion until the anaemia resolved in a few weeks
time
l Chorioangioma
n A rare placental tumour causing high-output heart failure because of fetal hemolysis and arterio-venous
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 shunting
n The prognosis is variable, depends on the size of the tumour
Primary cardiac abnormalities
l Arrhythmia
n Heart block, supraventricular tachycardia
n can be treated with transplacental anti-arrhythmic agents
l Major structural abnormalities of heart
Extra-cardiac abnormalities
l Some structural abnormalities may compress on the fetal heart or obstruct its outflow resulting poor cardiac
function:
n Chylothorax
n Diaphragmatic hernia

Renal agenesis
Philippe Jeanty, MD, PhD & Sandra R Silva, MD
Definition
Bilateral absence of the kidneys, usually associated with the oligohydramnios sequence.
Synonyms
Potter syndrome (no longer used).
Incidence
1-2:10,000
Etiology
Usually sporadic occurrence but 20-36% of bilateral renal agenesis (BRA) present a familial recurrence (possibly
autosomal dominant with incomplete penetrance and variable expression).
Pathogenesis
result from a lack of induction of the metanephric blastema by the ureteral bud. The absence of kidney results in the
absence of amniotic fluid after 12-13 weeks (before fluid is an exsudate or an extension of the intercellular fluid of
the fetus). The oligohydramnios causes the pulmonary hypoplasia. In rare cases of monozygotic twin discordant for
the renal agenesis, the pulmonary hypoplasia does not occur.
Diagnosis
The diagnosis is first suggested by the absence of amniotic fluid then by the absence of the bladder and the lack of
kidneys. Color Doppler has been found useful in those difficult exam to identify the lack of renal arteries. Before a
final diagnosis is made one should think and if possible exclude the possibility of pelvic or ectopic kidneys that could
compress the bladder and exclude the possibility of ectopic ureter that could explain the absence of bladder.
Genetic anomalies
Unknown.
Differential diagnosis
Bilateral renal medullary cystic dysplasia and bilateral renal hypoplasia may appear as BRA. Further normal but
non-functioning kidneys anormal placental implantation (on a uterine septum for instance) can lead to the same
presentation of severe oligohydramnios. This information is important to convey during patient's counseling: The
concern is not only the renal agenesis (which may be absent) but the oligohydramnios that will lead to pulmonary
hypoplasia.
Associated anomalies
Since this is a common anomaly, many different associations have been described (Vacterl, Meckel, chromosome
22 malformations#). In practice most of these are difficult to identify by ultrasound because of the oligohydramnios.
Prognosis
Lethal.
Management
Many authors have suggested the use of amnioinfusion or even intraabdominal infusion of saline in order to better
visualize the anatomy. Although there might be indications for such aggressive approach in a non-viable fetuses,
these are quite uncommon, and not justified in the majority of cases. Termination of pregnancy can be offered before
viability. Standard prenatal care is not altered when continuation the pregnancy is opted for. Confirmation of
diagnosis after birth is important for genetic counseling.

Potter syndrome
Philippe Jeanty, MD, PhD & Sandra R Silva, MD
Several entities use the eponym Potter:
Potter syndrome, now renamed either oligohydramnios sequence or bilateral renal agenesis (BRA) depending on
whether the cause of the syndrome (BRA) or the mechanism is referred to.
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Potter syndrome Type I is now referred to as Autosomal recessive polycystic kidney disease
Potter syndrome Type II is now referred to as Renal dysplasia
Potter syndrome Type III is now referred to as Autosomal dominant polycystic kidney disease

Teratogen
Definition
l It is an agent extrinsic to the embryo or fetus that causes an increased risk of the following:
l malformation-physical malformation
l carcinogenesis- increased risk of cancer
l mutagenesis-increased risk of genetic disease
l altered function (e.g. mental retardation)
l growth deficiency (intrauterine growth retardation)
l pregnancy wastage (i.e. abortion or stillbirth)
Teratogens may produce no effect at all in exposed pregnancies; only the most potent human teratogens typically
affect 20 to 70% of exposed fetuses
Classes of teratogenic agents
Microbiological
l virus: rubella
l bacteria: syphilis
l parasites: toxoplasmosis
Chemical
l drugs, smoking, alcohol
Physical
l Irradiation

3. Fetal diagnosis and therapy

Amniocentesis
What is amniocentesis
It is a procedure by which a needle is inserted transabdominally into the amniotic sac to obtain amniotic fluid.
It is a commonly performed for prenatal diagnosis. Amniocytes (desquamated fetal cells in amniotic fluid) obtained
are cultured for fetal karyotyping.
What are the indications of amniocentesis
fetal karyotyping (the most common)
fetal gene studies in thalassemia, and some other genetic disorders
assessment of amniotic fluid bilirubin level as an indicator of severity of fetal haemolytic anaemia secondary to
rhesus isoimmunisation
assessment of lung maturity by lecithin:springomyelin ratio (rarely necessary nowadays)
How is amniocentesis performed
Timing: usually performed around 16 to 20 weeks of gestation (for fetal karyotyping)
Under ultrasound guidance
20ml of amniotic fluid is aspirated
anaesthesia or analgesia is rarely required
Risk of amniocentesis
Fetal loss rate of 0.5% over background loss rate of 2%
Discussion/Something to Consider
What would be the practical difficulties in performing amniocentesis for fetal karyotyping in twin pregnancy?

Chorionic villus sampling

What is chorionic villus sampling
It is an invasive procedure by which chorionic villi are obtained through needle insertion transabdominally (or less
commonly transcervically). The procedure is performed between 10 and 13 week of gestation. Chorionic villi are
excellent source of DNA that may allow sufficient amount for most molecular genetic studies without prior culture.
Time for result to become available is shorter than with amniocentesis. However, mosaicism occurs more commonly
in chorionic villi (1%). The mosaicism is usually confined to chorionic villi and does not affect the fetus.
What are the indications of CVS
Fetal karyotyping
l CVS allows earlier diagnosis of chromosomal abnormalities when comparing with amniocentesis. It is
advisable to high risk group such as increased fetal nuchal translucency detected in the first trimester.

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Genetic studies
l The commonest genetic indication in Hong Kong is diagnosis of thalassemia. In particular, beta-thalassemia
can only be diagnosed with genetic studies in antenatal period.
What are the complications of CVS
l 1% risk of fetal loss which is slightly higher when compared with amniocentesis
l previous report of association with fetal limb reduction is not confirmed with recent studies.

Cordocentesis
What is cordocentesis
It is an invasive procedure in which the umbilical cord is punctured in utero. It is indicated when fetal blood sampling
is required for fetal diagnosis, or transfusion of blood and drugs are required for fetal therapy.
What are the indications of cordocentesis
Diagnostic purpose:
l Fetal white cells for karyotyping
n It is a much quicker method for fetal karyotyping than amniocentesis and chorionic villi sampling. A quick
diagnosis is particularly required in highly suspected cases, or if time to decide for termination of
pregnancy is limited before 24 week of gestation.
l Fetal haemoglobin and haemoglobin pattern
n To assess fetal anaemia, and confirm Haemoglobin Bart's disease (alpha-thalassemia major)
l Fetal blood for other genetic diagnosis
l Assessment of fetal well-being
n To assess blood gas value (rarely done)
Therapeutic purpose:
l Blood transfusion
n It is the most common therapeutic indication. Fetal anaemia resulted from Rhesus isoimmunisation,
parvovirus infection
What are the risks of cordocentesis
It is associated with 2% fetal loss rate. It may cause fetal bleeding, tamponade of umbilical cord due to haematoma
formation.

Genetic counselling
Definition
The process whereby patients or relatives at risk of a disorder that may be hereditary are advised of:
l the consequences of the disorder,
l the probability of developing and transmitting it, and
l the ways in which this may be prevented or ameliorated.
The risks of having a child with a genetic disorder or congenital malformations are estimated, and the parents are
assisted in making a decision regarding contraception, sterilization, adoption, artificial insemination, carrier detection,
referrals to agencies concerned with handicapped children, prenatal diagnosis and options regarding pregnancy
termination.

USG (Obstetrics)
Two ways to perform obstetric USG
l Transabdominal (TAS)
l Transvaginal (TVS)
l Advantages of TVS over TAS:
n As TVS probe is closer to pelvic organs, requirement for penetration is lower, allowing higher frequency
of ultrasound wave to be used. The result is a better resolution of images
n Full bladder is not required during TVS
l Advantages of TAS over TVS:
n Because of the limited penetration of TVS, TVS may not be able to detect organs that are beyond the
pelvis, such as pregnancy beyond 1st trimester, and a large pelvic tumour which has been displaced up
to the lower abdominal cavity
n Some patients may feel discomfort towards vaginal examination
Three Targets in obstetric USG
l Fetus
n Viability: see viable
n Number of fetus
n identify multiple pregnancy and determine chorioamnionicity
n Dating of pregnancy

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 n Size and growth
n Common fetal USG parameters are crown-rump length, biparietal diameter, femur length, and abdominal
circumference
n Morphology
n Well-being monitoring
n Fetal well-being is assessed by Doppler studies of fetal arterial blood flow, biophysical profile and
amniotic fluid volume
l Placenta and amniotic fluid
n placenta praevia, placental tumour, amniotic fluid volume etc
l Uterus and adnexa
n co-existing fibroids, uterine anomaly, ovarian tumour
Four uses of USG in obstetric
l Screening such as:
n screening of Down syndrome with nuchal translucency during first trimester
n routine dating scan
n routine morphology scan
l Diagnosis
n abortion, ectopic pregnancy, multiple pregnancy, fetal malformations, placenta praevia etc.
l Monitoring
n fetal growth, fetal well-being
l Assisting other invasive procedures such as
n chorionic villi sampling, amniocentesis and cordocentesis
Role of USG in modern obstetrics
l Definite
n Various diagnostic role
l Limited
n amniotic fluid volume assessment, estimation of fetal weight, diagnosis of IUGR, 1st trimester screening
of Down syndrome
l Controversial
n Routine 18-22 week USG scan (see below)
Indications of USG during 1st trimester
l confirm viability of pregnancy
l date gestational age (by crown-rump length)
l confirm the location of pregnancy (exclude ectopic pregnancy)
l diagnose multiple pregnancy
l diagnose abnormal uterine or ovarian tumour / pathology
Indications of USG during 2nd and 3rd trimester
l date gestational age(by Biparietal diameter and others)
l confirm fetal viability and to diagnose intra-uterine death
l diagnose multiple pregnancy
l assess fetal growth (by serial measurement of biometry)
l Assess liquor volume
l Assess placental site (to exclude placenta praevia) and pathology
l exclude or diagnose fetal structural abnormality
l assess fetal well-being
Routine 18-22 week USG scan
Potential benefit:
l For dating. USG dating predicts EDC better than by LMP
l Early detection of fetal abnormality: early management and better outcome
Potential problems:
l Missed fetal abnormalities - potential medico-legal issue
l False positive leads to anxiety and unnecessary tests (also implication for costs)
l Request for termination of pregnancy (because of anxiety induced) for minor abnormality only
l No evidence so far that routine scan improves fetal outcome
Safety of USG
l Ultrasound of sufficiently high level can lead to tissue damage by various mechanisms such as heating,
streaming, and cavitation.
l At the level of energy used for medical diagnostic purposes, no definite adverse effect, in particular effect to
fetus, has been documented so far.

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Amnioinfusion
What is amnioinfusion
Amnioinfusion is a procedure by which normal saline is infused into the amniotic cavity. It can be done
transcervically using an intrauterine catheter during intrapartum period, or abdominally during antepartum period.
What are the indications
Intrapartum:
l Meconium stained liquor (MSL)
n Heavily meconium stained liquor increases the risk of meconium aspiration syndrome. The aim of
amnioinfusion is to dilute the MSL and hence reduce the risk.
l Umbilical cord compression
n Cord compression may occur during labour. It may result in variable decelerations of fetal heart rate,
particularly when the liquor volume is reduced. It has been suggested that amnioinfusion may help to
prevent the event. However, no control trials have yet proven its role in preventing intrapartum fetal
distress.
Antepartum:
l Severe oligohydramnios
n For diagnostic purpose:
u Ultrasound images are suboptimal as transmission of ultrasound wave is poor in case of
oligohydramnios. Replenishment of liquor helps to improve ultrasound imaging and allow better
assessment of fetal morphology that may be abnormal in case of severe oligohydramnios
n For therapeutic purpose:
u Replenishment of liquor may help to reduce the complications of oligohydramnios such as postural
deformities or pulmonary hypoplasia. In order to prevent pulmonary hypoplasia, the procedure must
be performed before mid-gestation because it is the critical period of bronchial and alveolar
differentiation.

Amnioreduction
What is amnioreduction
It is a procedure by which excessive amniotic fluid is drained, usually via a needle inserted abdominally.
What are the indications
Severe polyhydramnios
l When the uterus is overdistended, there may be maternal discomfort and an increased risk of preterm labour
and cord prolapse. Amnioreduction would be required to relieve pressure symptoms. To avoid cord prolapse
during rupture of membranes in a case with severe polyhydramnios going into labour, reduction of the liquor
volume abdominally beforehand is also suggested. The role of amnioreduction in prevention of preterm labour
is not well-defined.
Twin-twin transfusion syndrome
l As the recipient twin is polyhydramnic, repeated amnioreduction on the recipient may help to improve the
prognosis of the disease and prolong the pregnancy.

4. Fetal growth and liquor volume

Small-for-gestational-age
It is usually defined as fetal weight less than the tenth (or more rigorously the fifth or third) percentile for gestational
age. It is different from intrauterine growth retardation (IUGR). Many infants that are small-for-gestational-age (SGA)
are appropriately grown and healthy. On the other hand, some infants with weight lies above the 10th percentile may
have not achieved their full growth potential and therefore growth-retarded.

IUGR
Definition of intrauterine growth retardation (IUGR)
l Failure to achieve the normal genetic growth potential in utero
l It is not synonymous with small-for-gestational-age (SGA)
Classification and causes
Symmetric
l occurs when the growth potential of the fetus is reduced
l usually appears early in pregnancy
l affects all organ and therefore 'symmetric'
l Causes
n chromosomal abnormalities

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 n genetic disorders
n congenital infections such as syphilis, rubella
n multifactorial fetal abnormalities
n maternal smoking etc
n maternal malnutrition
Asymmetric
l supply of nutrients to the fetus is inadequate to support growth
l usually presents in later pregnancy when fetal needs are increasing
l the vital organs are protected and there is sparing of head growth initially. Therefore it appears 'asymmetric',
with the growth of the abdomen more affected than that of the head
l Causes
n Placental insufficiency usually secondary to maternal diseases such as pre-eclampsia, autoimmune
diseases, renal disorders
n maternal malnutriton in later half of pregnancy
Remark
l Differentiation of symmetric and asymmetric growth retardation is not always clear cut
l Some causes will lead to both symmetric and asymmetric pattern, depending on the onset of problem: e.g.
maternal malnutrition may result in symmetric growth retardation if the onset of the problem is in early
pregnancy, but may lead to asymmetric pattern if malnutrition only occurs in the late pregnancy
l The head growth will eventually affected in the late stage of asymmetric growth retardation.
l Some disorders may cause asymmetry of growth but is not actually growth retarded: e.g. hypochrondroplasia
Diagnosis
l Clinical suspicion from inappropriate small fundal height
l Ultrasound diagnosis with small fetal abdominal circumference (AC) (below 3rd centile), or slowing or arrest
growth of AC. The biparietal diameter and femur length may also be small. There may also be signs of fetal
compromise such as oligohydramnios
Management
Investigation of underlying causes
l Ultrasound for morphology
l Fetal karyotyping with amniocentesis or cordocentesis
l Viral studies if congenital infection is suspected
Monitoring fetal well-being
l Cardiotocogram (CTG)
l Amniotic fluid volume assessment
l Doppler studies of fetal vessels
Monitoring fetal growth
l Serial scan every 2 weeks
Monitoring maternal well-being
l essential if maternal causes of IUGR are identified, such as
n pre-eclampsia
n diabetes mellitus
Decision of time and mode of delivery
Principles:
l Balance the risk of continuation of pregnancy against the risk of discontinuation which are:
l Risk of continuation of pregnancy:
n Chance of intrauterine death
n Chance of deterioration of maternal condition in case of maternal disorders such as pre-eclampsia, SLE,
renal disorders
l risk of discontinuation:
n complications of prematurity
l deliver if there is signs of fetal distress
n abnormal CTG
n persistent reverse or absent end-diastolic flow in umbilical artery
l deliver if there is deterioration of maternal condition
n severe pre-eclampsia
n eclampsia
l consider delivery if gestation beyond 34 weeks
Discussion/Something to Consider
A routine USG of a primigravida healthy woman at 22 week of gestation shows that all fetal parameters (AC, BPD,
FL) are below 3ed centile. The morphology and liquor volume otherwise appear normal. What are the differential
diagnosis and how would you verify the diagnosis?

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Macrosomia
Definition
l There is no universal definition for macrosomia. Some define it by the body weight at or more than 4kg or 4.2kg,
while some define it by body weight more than 97% for the gestation.
Incidence
l About 3% of newborns in Hong Kong are at or above 4kg
Causes
In majority of cases no specific cause can be identified. It is associated with:
l postterm
l maternal diabetes mellitus, gestational or established
l rarely congenital syndromes
Risks
Maternal risks
l higher risk of operative delivery including caesarean section and instrumental delivery
l higher risk of birth canal injury, such as perineal tear, particularly when shoulder dystocia occurs.
Fetal risks
l Higher risk of shoulder dystocia and related birth injury and birth asphyxia, particularly in diabetic patients
l fetal risks associated with postterm and poorly controlled maternal diabetes mellitus
Antepartum management
l Suspect macrosomia when the uterus is large for date. Ultrasound fetal parameters (biparietal diameter,
abdominal circumference, and femur length) are larger than normal. Fetal weight can be estimated from a
formula using the above parameters.
l Screen for gestational diabetes mellitus and treat accordingly
l Counsel for risk of macrosomia and mode of delivery. Consider caesarean section if the estimated fetal weight
is >=4kg

Amniotic fluid
Definition
l Also called 'liquor', is the fluid normally inside the amniotic cavity.
Volume
l Normal range varies from 300ml to 1500ml
l Normal range depends on gestation, with the peak at 34 to 36 weeks

Composition
l Electrolytes
l pH: slightly alkaline, changes amniostrix from orange to blue, a test for rupture of membranes
l Fetal cells: amniocytes can be collected with amniocentesis and cultured for fetal karyotyping
Production and removal
Production
l Fetal urine
n the major source of liquor
n urine production starts from 12 week
n anhydramnios in case of absent fetal kidneys or infantile type of polycystic kidneys
l Fetal lung fluid
n constitutes small portion of liquor production as most of the fluid is swallowed by the fetus
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Removal
l Fetal swallowing and absorption via GI tract
n polyhydramnios when there is pathology affecting the mechanism such as anencephaly, esophageal
atresia and duodenal atresia
l Transmembranous and intramembranous: account for small percentage of amniotic fluid circulation
How is amniotic fluid volume measured
Subjective method
l Relative amount of echo-free fluid areas are subjectively compared with the space occupied by the fetus and
placenta
Greatest pocket method
l The vertical length of the deepest pocket of liquor is measured
l When it is less than 1cm, oligohydramnios is diagnosed; when more than 8cm, polyhydramnios is diagnosed
Amniotic fluid index
l The most common method used
l See amniotic fluid index
Abnormality related to amniotic fluid
l Oligohydramnios and anhydramnios
l Polyhydramnios
l Meconium stained liquor (see MSL)
l Amniotic fluid embolism
l Blood stained liquor: may be a result of abruptio placentae
l Leaking of amniotic fluid because of rupture of membranes
Procedure related to amniotic fluid
l Amniocentesis
l Amnioreduction
l Amnioinfusion
l Amniotomy

Amniotic fluid index

What is amniotic fluid index (AFI)

It is a semi-quantitative way in assessing liquor volume. The value of AFI is the summation of the vertical depths of
the largest pocket in each of four equal uterine quadrants. It is said to be more accurate than using just a single
pocket (see amniotic fluid). The normal range varies according to the gestational age:
In general, it is polyhydramnios when AFI is greater than 24cm, and oligohydramnios when it is less than 8cm.
How to measure amniotic fluid index
l Divide the uterine surface into 4 equal quadrants.
l Set transducer parallel to maternal sagittal plane and perpendicular to maternal coronal plane.
l Apply constant gentle pressure during measurement.
l Measure the depth of liquor at the deepest unobstructed, clear pocket of each quadrant.
l AFI= sum of the depths of the 4 pockets

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How good is amniotic fluid index
l Measurement error:10 to 15%
l Correlation with actual amniotic volume:
n 5.8cm+/-2.6cm: 250ml
n 14cm: 700ml
n AFV=exp(5.19+0.093-AFI)
l Accuracy of diagnosis:
n Oligohydramnios: 50%
n Polyhydramnios: 50%
AFI is not applicable to assess the amniotic fluid volume in multiple pregnancy.

Oligohydramnios
Definition
l Oligohydramnios is an inadequate volume of amniotic fluid
l Anhydramnios is the complete absence of amniotic fluid.
Causes
Leaking of amniotic fluid after rupture of membranes
l the most common cause of oligohydramnios
l however, the amniotic fluid volume may still appear normal after rupture of membranes if the leaked volume is
not much
Fetal malformations resulting in decreased production of urine:
l bilateral renal agenesis (Potter's syndrome)
n no functional fetal kidneys and therefore completely no fetal urine production and anhydramnios
l Infantile type of polycystic kidneys
n dysgenesis of kidneys which become nonfunctional
n autosomal recessive inheritance
l Posterior urethral valve
n urine production is present but excretion is impaired because of urethral obstruction
n bladder is therefore distended and there is secondary dilated renal pelvis. Renal function may be
eventually impaired
Fetal compromise resulting in decrease production:
l Intrauterine hypoxia or growth retardation (IUGR)
n Renal blood flow decreases and hence the urine production
Fetal Risks
Depends on underlying causes and time of occurrence:
l Rupture of membranes: intrauterine infection, preterm labour, cord prolapse
l Fetal malformations: may not be viable such as Potter's syndrome and infantile type of polycystic kidneys
l Fetal compromise: intrauterine death
l Pulmonary hypoplasia when severe oligohydramnios occurs before 20 weeks of gestation during when lung
development is critical
l Postural deformities: various degree of limbs and facial deformities
Diagnosis
Clinical:
l Uterus small for date
l Fetal parts are easily felt
Ultrasonical:
l Decreased amniotic fluid volume demonstrated e.g. by amniotic fluid index measurement
Management
Investigation of underlying cause:

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l Rule out rupture of membranes from history and examination
l Morphology scan (can be difficult if there is minimal liquor)
l Assessment of fetal growth
l Assessment of fetal well-being
Treatment:
l Depends on the underlying causes:
n See rupture of membranes
n Termination of pregnancy for lethal malformations
n Consider early delivery if case of fetal compromise
n Amnioinfusion to replenish amniotic fluid to avoid pulmonary hypoplasia and postural deformities.

Oligohydramnios sequence
Philippe Jeanty, MD, PhD & Sandra R Silva, MD
The oligohydramnios sequence is a set of related conditions resulting from marked decreased in amniotic fluid. This
typically results from bilateral renal agenesis (34%) (fig. 1), or chronic leakage of fluid. Other conditions such as
bilateral multicystic renal dysplasia (34%), unilateral renal agenesis and contralateral multicystic renal dysplasia
(9%), renal tubular dysgenesis, autosomal recessive (infantile) polycystic disease, non-functioning but
morphologically normal renal tracts (3%), abherrant placental implantation (on a uterine septum for instance) # can
lead to the same set of findings Ref1.
50% of these fetuses have anomalies that are not part of the oligohydramnios sequence (Vacterl, Meckel,
Smith-Lemli-Opitz).
In the oligohydramnios sequence, the decreas e of fluid causes lung hypoplasia and fetal compression. The fetal
compression results in abnormal limb positions with dislocations and an abnormal face (flat with low set ears). After
delivery these newborn die of pulmonary insufficiency (via pneumothoraces).
References
Ref1 Newbould MJ, Lendon M, Barson AJ: Oligohydramnios sequence: the spectrum of renal malformations. Br J
Obstet Gynaecol 1994 Jul;101(7):598-604

Polyhydramnios
Definition
It is an excess of amniotic fluid, in contrast to oligohydramnios where there is a decrease in amniotic fluid
Causes
It is related to the increase in production or decrease in removal of the amniotic fluid.
In one-third of cases the cause is idiopathic, but some are due to fetal, maternal or placental disorders:
Fetal causes
l anencephaly
l oesophgeal atresia, duodenal atresia
l gastroschisis and omphalocele
l fetal hydrops
Maternal causes
l poorly controlled diabetes
Placental causes
l rarely due to placental tumour such as choriangioma
Risks
Fetal
l preterm labour
l unstable lie
l premature rupture of membranes and cord prolapse
l fetal abnormalities leading to polyhydramnios
Maternal
l Discomforts secondary to pressure effects
l dyspnea, indigestion, abdominal pain, edema and varicose veins
l high risk of operative delivery
Diagnosis
Clinical
l Uterus large for date
l fetal parts are difficult to feel
l unstable lie or malpresentation
l Fluid thrill may be demonstrated
Ultrasonical
l increase in amniotic fluid volume e.g. demonstrated by amniotic fluid index measurement
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Management
Investigation of underlying causes
l Ultrasound for fetal morphology
l OGTT test for diabetes mellitus
Treatment
l Treat underlying cause: e.g. control DM
l Conservative if patients have mild symptoms
n in particular, idiopathic polyhydramnios is usually mild and resolve spontaneously
l Amnioreduction if patients have severe symptoms
n to reduce the liquor volume
l NSAID
n no clinical use
Prevention of cord prolapse
l Precaution in performing amniotomy when patient goes into labour.
n Avoid amniotomy when there is cord presentation
n High water amniotomy
n Sit up patient to encourage descend of fetal head before amniotomy
n Control the rate of flow of liquor

MSL
Meconium stained liquor (MSL)
Meconium is a dark green fecal material that accumulates in the fetal intestines and is discharged at or near the time
of birth. When the fetus passes meconium before or during labour, the meconium mixes with the amniotic fluid, and
depending on the relative amount of meconium and amniotic fluid, it is classified into thin, moderated and thick MSL.
What is the significant of MSL
l It was thought in the past that MSL is a sign of fetal distress. Nowadays it is clear that fetuses pass meconium
very often when they undergo stress, as a normal parasympathetic response. MSL does not necessarily imply
distress, and is commonly seen in postterm pregnancies. However, thick MSL may imply that the actual
amniotic fluid is reduced (oligohydramnios) which itself is a sign of fetal compromise.
l When fetuses aspirate thick meconium to the airway or lung during labour, the meconium will induce a
chemical pneumonitis which is called meconium aspiration syndrome. It is a severe disease and potentially
fatal.
l MSL is uncommon in preterm pregnancy. When it occurs, it is associated with listeriosis and is associated with
high fetal morbidity and mortality.

Crown-rump length
Definition
l Crown-rump length is defined as the distance between the topmost part of the fetal head and the buttock, and
is the single most important parameter of fetal size in the first trimester.
Measuring crown-rump length

l The fetal axis is placed perpendicularly to the USG.

l The midline sagittal plane is visualized.
l The measurement is made from the top of the fetus to the buttock.
Uses of crown-rump length measurement
l For dating of pregnancy in the first trimester: accuracy: +/- 4 days

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Abdominal circumference
Definition
l Fetal abdominal circumference (AC) is one of the commonest parameters for size and growth. It reflects the
liver size and volume of subcutaneous fat. It is the most sensitive indicator of intrauterine growth restriction
(IUGR).
Measuring abdominal circumference

l The cross-section of the abdomen with the following landmarks identified:

n hepatic vein in the anterior one-third of the abdomen
n stomach
n adrenal glands
l The outer edge of the circumference is measured
Uses of AC measurement
l Monitoring of fetal growth
l Estimation of fetal weight
Factors affecting AC
l Abnormal fetal growth
n AC is decreased in both symmetric and asymmetric IUGR, and increased in macrosomia
l Abdominal wall defects and diaphragmatic hernia
n AC is difficult to be measured in gastroschisis and omphalocele as the anatomy of the landmarks is
distorted. It is underestimated because of herniation of abdominal content.
l Fetal ascites
n Ascitic fluid distends the abdomen, resulting in a large AC

Biparietal diameter
Definition
Biparietal diameter (BPD) is the longest distance between the two parietal eminences. It reflects the brain growth,
and is one of the commonest parameters of fetal size and growth.
It is also the greatest presenting diameter in vertex presentation. The average size of BPD in a term fetus is 9.5cm.
Measuring biparietal diameter with USG

l The fetal head should be in lateral position

l An accurate plane with the following landmarks is identified:
n The midline falx
n The thalami are symmetrically positioned on either side of the falx
n Visualization of the septum pellucidum at one third of the fronto-occipital distance.

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l the measurement is made between the outer plate of one parietal eminence and the inner plate of the other,
and is perpendicular to the midline falx.
Uses of biparietal diameter measurement
l For dating in the second trimester
l For monitoring of fetal growth
l For estimation of fetal weight
Factors affecting the biparietal diameter
Dolicocephaly
l It is a condition is which the fetal skull is moulded and compressed laterally, so that the fronto-occiputal length
is elongated and the BPD is shortened. However, the head circumference should not be changed.
l It is a normal condition and is commonly seen in breech presentation and transverse lie.
IUGR
l BPD is the last parameter to be affected in case of asymmetric IUGR because of brain sparing effect. However,
it can be affected early in symmetric IUGR
Brain abnormalites
l Hydrocephaly
l Microcephaly
Skull bone abnormalities
l Thanatophoric dwarfism

Femur length
Definition
l Fetal femur length is one of the commonly used parameters of fetal size and growth. It is defined as the
distance between the ends of metaphysis and can be measured with ultrasound. It reflects the crown-heel
length (longitudinal growth).
Measuring femur length

l The femur image is at an angle of less than 30 degrees to the horizontal.

l Two blunted ends of the femur are clearly visualised.
l The extension to the greater trochanter and the head of femur is not included.
Uses of femur length measurement
l For dating in the second trimester.
l For monitoring of intrauterine growth.
l For estimation of fetal weight.
Factors affecting the femur length
l Intrauterine growth retardation (IUGR)
n It is affected early in symmetric IUGR but late in asymmetric IUGR.
l Down syndrome
n In general fetuses with Down syndrome have a shorter femur. Femur length was once suggested as a
screening test for Down syndrome, but was found to be less effective.
l Congenital dwarfism
n various bone disorders are associated with short long bones including thanatophoric dwarfism.

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5. Fetal well-being

Fetal well-being
Definition
Fetal compromise:
l poorly defined
l usually means conditions in which the normal growth and neurological development are not optimal
l points to a relatively chronic problem, distinguished from fetal distress
Fetal distress:
l also poorly defined
l usually means a acute hypoxic state of fetus that may result in fetal damage or death if it is not reversed or the
fetus is not delivered urgently
Ultimately, fetal compromise can lead to distress
Physiological changes associated with fetal compromise
Sequential changes occur when the fetus is undergoing chronic hypoxia:
l Conservation of oxygen and energy for fetal brain in expense of peripheral organs
n Redistribution of blood flow
u Increase cerebral blood flow
u Decrease peripheral blood flow
n Growth discrimination
u Depletion of storage of liver glycogen, reflected by slowing down of growth of abdominal
circumference
u Slowing down of growth of femur
u Growth of brain, reflected by the biparietal diameter maintained until at the very late stage
n Further decrease in peripheral blood flow
u Decrease in renal blood flow, resulting in reduction of fetal urine, and hence liquor volume
(oligohydramnios)
n Conservation of energy and oxygen
u Fetal movements decrease
u Fetal breathing movements decrease
u Fetal tones decrease
n Anaerobic metabolism
u Metabolic acidosis, resulting in abnormal cardiac function
l Abnormal heart rate regulation: decreased baseline variability, late decelerations, and
bradycardia as shown in cardiotocogram
n Ultimate outcome if not treated:
u Fetal death
Remark
l Some differences when the fetus is undergoing acute hypoxia
How to assess fetal well-being
Several methods are available:
l Fetal movements
l non-stress test or contraction stress test using cardiotocogram
l Liquor volume assessment (see amniotic fluid and amniotic fluid index)
l Biophysical profile
l Doppler studies of fetal blood flow
The most commonly used are cardiotocogram, amniotic fluid index, Doppler studies
Management
l Aim is to maximize the chance of survival of the fetus
l Balance the risk of continuing pregnancy and risk of termination of pregnancy which would usually mean a
preterm delivery
l Decide the time and mode of delivery
Determinating factors
l Degree of fetal compromise
l Gestation age
n When there are signs of fetal distress such as abnormal non-stress test: immediate delivery
n When there are signs of fetal compromise but the fetus is not in acute danger, and the fetus is immature:
close monitoring of fetal well-being
n When there are signs of fetal compromise and the fetus is mature, delivery

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Fetal distress
Definition
This is a clinical diagnosis made antenatally or intrapartumly signifying an adverse fetal condition that requires an
immediate delivery, otherwise fetal hypoxic damage or birth asphyxia may follow.
Diagnosis
The clinical suspicion of fetal distress is usually based on fetal heart rate pattern on the cardiotocogram (CTG).
Although CTG is sensitive, it is not specific for fetal hypoxia and acidosis. Correct interpretation of CTG is very
important in making the diagnosis, and fetal scalp blood sampling should be performed whenever possible to assess
the fetal blood pH. Finding of acidosis (less than 7.2 during labour) confirms the diagnosis and the fetus should then
be delivered immediately by caesarean section or by instrumental delivery.

Biophysical profile
It is one of the methods to assess fetal well-being during antepartum period, using the combination of ultrasound
and electronic fetal heart monitoring.
It consists of 5 parameters:
Parameters Assessment
Heart reactivity >=2 accelerations of 15bpm for 15s in 40 min
Amniotic fluid volume A pocket >=1cm in 2 perpendicular planes
Tone 1 episode of limb movement from flexion to extension then back to flexion
Movement >=3 gross body movements in 30 min
Breathing movements Sustained fetal breathing movements >= 30s in 30 min
l The last four parameters are assessed under USG in 30 minutes
l A score of 2 is given for each normal parameter (Total mark is 10)
l A score more than 7 is definitely normal, while a score of 4 or less is definite abnormal. A score between 4 and
7 is equivocal
l It was originally designed to supplement fetal heart monitoring in assessment of fetal well-being. However,
there is no good evidence to suggesting that the use of biophysical profile can improve fetal outcome. It is
found that among the 5 parameters, fetal heart rate and amniotic fluid volume are the 2 most important factors.
Assessment of other parameters with USG is rather time consuming. Furthermore, doppler studies of fetal
circulation has become a more popular and accurate method in modern obstetrics, and biophysical profile is
gradually out of interest.

CTG
See cardiotocogram

Cardiotocogram
What is cardiotocogram
l It is an electronic monitoring method which presents graphically the status of the fetal heart rate pattern
(cardio), and the uterine activities (toco). Fetal movements can also be recorded.
l The fetal heart rate is picked up with an external detector using Doppler effect, or during labour, with a fetal
scalp electrode. The uterine activities are usually picked up with a transducer applied on the maternal
abdomen. The transducer cannot pick up the exact intrauterine pressure, but it detects the changes of contour
of the abdominal wall, which can reflect the frequency and duration of the uterine contractions. If absolute
intrauterine pressure monitoring is required during labour, an intrauterine catheter can be inserted to the
uterine cavity and connected to a transducer.
l Cardiotocogram is a valuable method of assessment of fetal well-being during antenatal period, as well as
intrapartum period, in modern obstetrics.
It is also called non-stress test when used for antenatal monitoring. When it is used under artificial induction of
uterine contractions, it is called a contraction stress test. Contraction stress test is seldom used nowadays because
of fetal risk and inaccuracy of the test.

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 A CTG machine CTG showing a reactive tracing

Fetal heart rate pattern

FIGO Definitions of fetal heart rate pattern
Baseline fetal heart rate
l the mean level of FHR when this is stable, with acceleration and deceleration being absent; it is determined
over a period of 5 to 10 minutes and expressed in beats per minute (bpm)
Bradycardia
l baseline heart rate < 110bpm
Tachycardia
l baseline heart rate > 150bpm
Acceleration
l transient increase in heart rate of 15bpm or more and lasting 15 seconds or more
Deceleration
l transient episode of slowing of the heart rate below the baseline level of more than 10bpm (some use 15bpm)
and lasting 15 seconds or more
Early decelerations
l onset, nadir and recovery of decelerations synchronous with contractions
Late decelerations
l onset, nadir and recovery are out of phase with contractions
Variable decelerations
l decelerations vary in shape and timing with respect to each other
Baseline variability
l the degree to which the baseline varies within a particular band width excluding accelerations and
decelerations
Antepartum CTG interpretation
Normal pattern
l baseline rate 110-150bpm
l amplitude of baseline variability 5-25bpm
l absence of decelerations except for sporadic, mild deceleration of very short duration
l presence of two or more accelerations during a 10-minute period
Suspicious pattern
Any one of the following:
l baseline rate of 150-170bpm or 100-110bpm
l amplitude of variability between 5-10bpm for more than 40 minutes
l increased variability above 25bpm
l absence of accelerations for more than 40 minutes
l Sporadic decelerations of any type unless severe
Pathological
Any of the following:
l baseline heart rate below 100bpm or above 170bpm
l Variability less than 5bpm for more than 40 minutes
l Periodically and non-recurrent severe variable, prolonged or late decelerations
l sporadic and non-recurrent severe variable, prolonged or late decelerations
l A sinusoidal pattern: frequency< 6 cycles/ minute; amplitude >/= 10bpm; duration >/= 20 minutes
Intrapartum CTG interpretation
Normal pattern
l Baseline rate between 110-150bpm
l amplitude of heart rate variability between 5bpm and 25bpm
Suspicious pattern
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l baseline heart rate between 150bpm and 170bpm or between 110bpm and 100bpm
l amplitude of variability between 5bpm and 10bpm for more than 40 minutes
l Increased variability above 25bpm
l Variable decelerations
Pathological pattern
l baseline heart rate below 100bpm or above 170bpm
l variability less than 5bpm for more than 40 minutes
l severe variable decelerations or severe, repetitive early decelerations
l prolonged decelerations
l late decelerations: the most ominous trace is a steady baseline without variability and with small decelerations
after each contraction
l Sinusoidal pattern
Comment
Normal implies that the trace assures fetal well-being
Suspicious indicates that continued observation or additional tests are required to ensure fetal well-being
Pathological warrants some action in the form of additional tests or delivery depending on the clinical picture

Fetal movement
Counting of fetal movements
l A daily count of perceived fetal movements from 28 weeks' gestation is a simple and inexpensive routine
screening device for monitoring of fetal well-being
l Advice should be sought if fewer than 10 movements are perceived within 12 hours or if the mother feels that
the baby is not moving
l Other tests of fetal welfare such as fetal cardiotocogram can then be applied
Advantages
l simple, safe and inexpensive
l can be initiated by mother herself at home
l no sophisticated equipment is required
Limitations
l A large number of fetal movements may not be perceived
l There are great variations in the number of fetal movements from day to day in individual women and from
woman to woman
l the sensitivity and specificity of the method are low
l One randomized trial suggests a clear benefit, but another does not
l Less than 1/1000 women might benefit from formal fetal movement counting, using later fetal death as an
outcome
l Formal counting provokes anxiety in about 25% of women. Another 50% are reassured by it.

Contraction stress test

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

6. Genetic disorders

Genetic disorder
Introduction
There are more than 1000 known Mendelian disorders, which may be either dominant or recessive and may involve
either autosomal or sex chromosomes
Autosomal disorders
l both sex are equally affected
Dominant
l expression may be variable from one individual to another (expressivity).
l affected individual will produce offspring who are either normal or affected, in a 1:1 ratio

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l affected individual either has an affected parent or represents a new mutation
l obstetric presentation-these disorders confront the obstetrician in several ways:
n affected parent: 50% risk
n previously affected child born to unaffected parents means that the child represents a new mutation: no
increase in recurrent risk
l examples: achondroplasia, osteogenesis imperfecta (some types)
Recessive
l both parents of affected infant must be carriers
l offspring of carrier parents will be normal, carriers, or affected in 1:2:1 ratio
l siblings may be affected, but other affected relatives are uncommon unless there is consanguinity in the
pedigree
l example: thalassemia
X-linked disorders
l no father-to-son transmission
Dominant
l males and females may both be affected
l an affected male will have all normal sons and all daughters will be affected
l offspring of an affected female will be normal or carrier, in a 1:1 ratio
l examples: vitamin D-resistant rickets
Recessive
l only males are affected (there is the possibility of a rare homozygous female)
l an affected male will have all normal sons, and all his daughters will be carriers
l examples: haemophilia, Duchenne's muscular dystrophy

Haemophilia
Introduction
l A group of X-linked recessive hereditary disorder of blood coagulation
l Subdivided into Haemophilia A and Haemophilia B
Pathology
Haemophilia A
l Caused by a reduced amount or activity of factor VIII
l Two-thirds of the cases are inherited as a X-linked recessive condition, and the remaining cases are resulted
from spontaneous mutations and hence do not have a family history
l The gene for factor VIII is located at Xq2.8
l Genetic defects include deletions and point mutations (CGA to TGA)
Haemophilia B
l Low Factor IX
l Inheritance and clinical features are same as Hemophilia A
l The gene for factor IX is located at Xq2.6
l Incidence is one-fifth that of Hemophilia A
Carrier detection
Haemophilia A
l by positive family history
l Laboratory tests:
n Factor VIII < 50%
n Factor VIIIc/VWF < 0.7
l Genetic analysis: gene tracking or identification of direct genetic lesions, e.g. RFLP
Haemophilia B
l by positive family history
l Genetic analysis: RFLP
Prenatal diagnosis
Sex determination
l Haemophilia is ruled out if fetus is a female
l by ultrasound (USG) examination of fetal genitalia
l Fetal sex may not be identified by USG until in second trimester
Genetic study
l fetal cells are obtained by chorionic villous sampling (CVS) in first trimester or amniocentesis in second
trimester
l gene tracking by RFLP or VNTR with extended family members
l direct probing for known genetic lesions by PCR, SB techniques, etc. (mutations or deletions)
Clotting factor assay
l More than 18 weeks' gestation, fetal blood obtained by cordocentesis can be done for factor VIII assay

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Thalassemia
Definition
l In Greek thal means sea; assemia is an abbreviated term for anaemia
l It is a heterogeneous group of genetic disorders of the synthesis of haemoglobin chains, resulting in imbalance
of number of different globin chains. The result is (1) impaired formation of normal Hb A (which is a tetramer of
2 alpha and 2 beta globin chains), and (2) formation of abnormal tetramers
l There are two major forms:
n Alpha-thalassemia
n Beta-thalassemia
Incidence
l Alpha-thalassemia occurs largely in South East Asia; 5% of Hong Kong people are carriers
l Beta-thalassemia occurs worldwide, particularly in the Mediterranean and the Middle East; 3% of Hong Kong
people are carriers
Pathophysiology
Alpha-thalassemia
l A normal human has 2 pairs of alpha genes. Alpha-thalaessemia is mainly due to gene deletions (a minority is
due to mutation).
l Alpha haemoglobin gene defects lead to impaired synthesis of the alpha globin chains, with a relative excess
of beta and gamma chains, which form insoluble tetramers, Hb Bart's (gamma 4) and HbH (beta 4) within red
cells. The insoluble tetramers reduce cell plasticity.
l Consequently, the red cells are more susceptible to premature destruction, leading to ineffective erythropoiesis
and haemolysis.
l Depends on the number of gene deletion, four degrees of alpha-thalassemia are possible.
number of gene deletion genotype features
1 a +-thalassemia Asymptomatic with low MCV
2 a 0-thalassemia Asymptomatic with low MCV
3 Hb H (beta 4) anaemia but viable, low MCV
4 Hb Bart's (gamma 4) Hydrops fetalis, non-viable
l Depends on the pattern and number of gene deletion of parents, the newborn has a chance of acquiring major
(homozygous) alpha-thalassemia ranging from zero to 25%.
Beta-thalassemia
l A normal human has 1 pairs of beta genes. Beta-thalaessemia is due to gene mutation
l Mutations result in absence or reduced beta globin chain synthesis, with a relative excess of alpha chains
l The end result is haemolysis similar to that in alpha-thalassemia.
l As fetal haemoglobin synthesis does not require beta component, the disease does not reveal until about 6th
month of neonatal life when haemoglobin synthesis switches from gamma chain to beta chain
l Carriers with one abnormal beta globin gene are asymptomatic with low MCV, while patients with two abnormal
beta genes suffer from anaemia requiring regular blood transfusion
l If both parents are carriers of beta-thalassemia, the newborn has a 1 in 4 chance of acquiring major
(homozygous) beta-thalassemia.
Parental screening and diagnosis
l Both alpha and beta thalassemia carriers are screened by MCV
l Diagnosis is made by haemoglobin electrophoresis (haemoglobin pattern analysis)
l Genetic study is required to identify the pattern of alpha-gene deletion, and type of mutation of beta-gene
Prenatal diagnosis
Alpha-thalassemia
Hb Bart's disease can be diagnosed by following ways:
l Ultrasound
n look for signs of hydrops fetalis including thickened placenta, cardiomegaly, hydrothorax, ascites and skin
edema
n the advantages are non-invasive and sensitive
n disadvantage is that the onset of hydrops varies and may not be diagnosed until in second trimester
l Genetic study
n look for presence of alpha gene in fetal cells
n fetal cells are obtained by chorionic villus sampling (CVS) or amniocentesis
n the advantages are accurate and early diagnosis is possible with CVS
n the disadvantage is invasive and risk of fetal loss
l Haemoglobin study
n look for fetal anaemia and haemoglobin pattern in fetal red blood cells
n fetal red blood cells are obtained by cordocentesis
n advantages are that the diagnosis is accurate and quick
n disadvantages are that cordocentesis is invasive and difficult to perform before 16 weeks

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 n it is usually reserved for confirmation of diagnosis when hydrops fetalis has already been present, in
which case quick result is required to guide the subsequent management
Beta-thalassemia
l As beta-thalassemia is not revealed during fetal life, the only method of diagnosis is by genetic study
Other Antepartum Management
l Women who are carriers of thalassemia should be given folate supplement as the demand of the vitamin is
increased during pregnancy.
Discussion/Something to Consider
If on haemoglobin pattern analysis, one of the couple is found to be an alpha-thalassemia carrier while the other is a
beta carrier, what would be the prenatal counselling and diagnosis?

7. Multiple pregnancy

Multiple pregnancy
Incidence
l 1% of all pregnancies
l Most are twin pregnancy
What medical students should know
For medical students, they should know twin pregnancy
Medical students will not be examined on higher order pregnancy except twin, but they should understand and apply
the principles of twin pregnancy in the management of other multiple pregnancy.

Twin pregnancy
Types of twin pregnancy
Twin pregnancy is classified according to:
l Zygosity
n Monozygotic
n Dizygotic
l Chorioamnionicity
n All dizygotic twins are dichorionic diamniotic
n Depends on the time of cleavage, monozygotic twins may be dichorionic diamniotic, monochorionic
diamniotic, monochorionic monoamniotic
Incidence
1% of all pregnancies
incidence increases with positive family history, use of ovulation induction, or assisted reproductive technology
(ART)
Diagnosis of multiple pregnancy
History
l must suspect multiple pregnancy if the pregnancy is resulted from ovulation induction or assisted reproductive
technology
Examination
l uterus large for date
l more than 2 fetal poles palpable
l 2 fetal heart pulsations, which are of different rate (at least 15bpm), are heard simultaneously
Ultrasound
l Confirm twin pregnancy
l Also assess the zygosity and chorioamnionicity
Risks of twin pregnancy
In general, risk are higher when it is:
l Monozygotic
l Monochorionic
l Monoamniotic
Maternal Risks
l Nutrition anaemia: due to increased fetal demand
l Pre-eclampsia: increase 4 folds
l Gestational diabetes: due to increased levels of diabetogenic placental hormones
l higher chance of placenta praevia
l Increased severity of the minor disorders of pregnancy such as hyperemesis gravidarum, backaches,
constipation etc.

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Fetal Risks
l Fetal malformations: various kinds of malformations including conjoint twin
l Twin-twin transfusion syndrome (5-10%)
l Preterm labour and preterm delivery (50% delivered before 37 weeks)
l Intrauterine growth retardation (IUGR)
l Intrauterine death
l Higher mortality rate: 7 times higher than that of singleton pregnancy
Intrapartum Risks
l Higher risk of caesarean section: 50% require caesarean delivery
l Vaginal delivery of second twins (see intrapartum management below)
l Locked twins (or twin entrapment)
l Cord entanglement: in monochorionic monoamniotic twins pregnancy where no membranes septum to
separate the cords.
l higher chance of postpartum haemorrhage because of overdistension of uterus
Antepartum management
Determination of chorioamnionicity
l It is best assessed with USG in the first trimester or early second trimester
Close maternal surveillances
l Regular monitoring of blood pressure and urine protein to detect early pre-eclampsia
l OGTT at 26 to 28 week to exclude gestational diabetes
Close fetal surveillances
l Regular monitoring of fetal growth and liquor by USG, as fundal height cannot reflect the growth of individual
twins. It is important to detect discordant growth and liquor volume which is a sign of twin-twin transfusion
l Morphology scan at 20 week
Nutrition supplement
l Iron and vitamins to prevent nutritional anaemia
Prevention of preterm labour
l At present no effective preventive measure
Time of delivery
l Studies have shown that the fetal risks are higher when twin go beyond 38 week of gestation. This may relate
to the accelerated aging of placenta when compared to singleton pregnancy
l Therefore, twin pregnancy should have induction of labour, or caesarean at 38 week
Mode of delivery
l Vaginal delivery if the presenting twin is in cephalic presentation, otherwise for elective caesarean section
l Caesarean section should also be performed (at 34 week or not later than 37 week) for monochorionic
monoamniotic twins pregnancy to avoid cord entanglement in late pregnancy or during labour
Intrapartum management
Fetal monitoring
l During labour, both fetuses should be monitored with continuous cardiotogram. The first twin is monitored with
a fetal scalp electrode and the second one with external doppler apparatus.
Pain relief
l epidural anaglesia is recommended
Delivery of the second twin
l After vaginal delivery of the first twin, the presentation of the second twin may remain high or altered; uterine
contractions are diminished (uterine inertia); cervix may begin to close. There may also be cord prolapse,
diminished placental function, abruptio placentae resulting in hypoxic injury.
l USG may be helpful to assess the presentation
l Oxytocin augmentation should be considered when uterine inertia occurs
l Membranes of the second twin should not be ruptured until the fetal head is well engaged
l When fetus remains high in presentation after 30 minutes or when there is fetal distress, operative delivery
(including caesarean section) should be considered
Postpartum management
l Prophylactic oxytocic to prevent postpartum haemorrhage. This includes a single bolus of oxytocin or
syntometrine followed by oxytocin infusion.
Discussion/Something to Consider
Ultrasound shows a discordant growth of a twin pregnancy at 20 week of gestation, what are the possible diagnoses
and how can we differentiate them?
A woman of age 37 has a twin pregnancy. She is at 10 weeks of gestation asking for prenatal diagnosis of Down
syndrome. How would you counsel her?
A woman with a twin pregnancy is found to have a twin died in utero at 28 week of gestation. How would you
manage her?

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Chorioamnionicity
Singleton pregnancy must be monochorionic monoamniotic (MCMA). However, chorioamnionicity may be multiple in
case of multiple pregnancy, depends on the zygosity and the time of division of the embryo. Take twin pregnancy as
an example, dizygotic twins must be dichorionic diamniotic (DCDA). Monozygotic twins may be DCDA, MCDA or
MCMA depends on the timing of cleavage as follow:
Time of Cleavage Stage of embryo chorioamnionicity
Day 0 to 3 Morula DCDA
Day 4 to 8 Embryonic disk MCDA
Day 9 to 12 Blasticyst MCMA
After day 12 Fetus conjoint twin

Determination of chorioamnionicity is very important in management of twin pregnancy because the lower the
chorionicity and amnionicity, the higher is the fetal and maternal risks. Chorioamnionicity is most easily and
accurately determined by USG in the first trimester:
l DCDA: the twins are separated by a thick chorionic septum between the gestation sac.
l MCDA: each of the twins is contained inside a thin amniotic sac, which in turn, is contained in the same
chorionic membrane.
l MCMA: no membranes are seen between the twins
During the second trimester, chorioamnionicity can also be accurately assessed:
l If they are of different sex, it must be dizygotic. The external genitalia can be determined with USG since early
second trimester
l If the membrane septum is thick or there is lamda sign, it is DCDA, and the pregnancy can be dizygotic or
monozygotic.
l If there is no membrane septum between the twins, placenta must be MCMA, and the pregnancy must be
monozygotic
l If the membrane septum is thin or there is absence of lamda sign, it is MCDA, and the pregnancy must be
monozygotic

Conjoint twin
Conjoint twins are a rare form of monochorionic monoamniotic twin pregnancy (see chorioamnionicity), resulted
when the splitting of the embryonic mass after day 12 of fertilisation. Conjoint twins are classified according to the
dominant site of interfetal body part connection, into five major types:
l thoracopagus (thorax, 30-40%)
l omphalopagus (abdomen, 25-30%)
l pygopagus (sacrum, 10-20%)
l ischiopagus (pelvis, 6-20%)
l craniopagus (head, 2-16%)
The prognosis of conjoint twins is in general poor, and depends on the site and extent of conjoining. Half of them are
intrauterine deaths and one-third of the remaining livebirths have severe defects for which surgery is not possible.
Conjoint twins are suspected under ultrasound, when both fetuses are always facing to each other with the same lie
and presentation, with no membranes separating them. Detail ultrasonic examination will identify the site of
conjoining.

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Twin-twin transfusion
What is Twin-twin transfusion
Twin-twin transfusion is a disorder specific to monochorionic twin pregnancy. Normally there are vascular channels
between the twins through the placenta, and the blood flow between the twins are balanced. However, for some
reasons that are still uncertain, unbalanced blood flow sometimes occurs. Consequently, one twin becomes the
donar while the other becomes the recipient of blood. The donar becomes anaemic, hypoxic and malnutrited,
resulting in growth retardation and oligohydramnios. On the other hand, the recipient becomes volume overload and
with hyperviscosity of blood (increase in haematocrit). High-output heart failure develops, and the fetus becomes
hydropic with polyhdyramnios. This condition usually occurs during the second trimester. The mortality is high
without any intervention. The picture shows a pair of twins suffered from twin-twin transfusion syndrome. The twin on
the right side (recipient) is hydropic and polycythemic while the one on the left side (donar) is small and pale.
Diagnosis
Twin-twin transfusion was traditionally diagnosed postnatally when both the neonatal weights and hemoglobin
concentrations were divergent. The scientific basis for this tradition is weak.
Prenatal diagnosis
Prenatal ultrasonography plays an important role in diagnosing twin-twin transfusion. There is discordance of growth
and oligohydramnios in the growth-deficient twin (donor twin) and polyhydramnios in the other (recipient twin). The
bladder of the donor twin may not been seen at all. Sometimes, the donar twin become a "struck twin" when he has
no liquor at all and is compressed against the uterine wall by the gestation sac of the recipient . The recipient twin
may show features of hydrops fetalis in the latter stage. The USG shows discordance of growth.
Treatment
The most popular treatments are repeated amnioreduction, and devascularisation of the anastomosis with laser.
The prognosis improves to 50 to 70%.

Lamda sign
It is an ultrasonic feature used to diagnose the chorioamnionicity of a twin pregnancy. The presence of a lamda sign
suggests a dichorionic diamniotic (DCDA) placenta. In a DCDA twin pregnancy, there is a thick septum consisting of
two layers of amnion and two layers of chorion between the gestational sacs. After 9 weeks of gestation, this septum
becomes progressive thinner, but remains thick at the base as a triangular tissue projection, which is called lamda
sign.

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Maternal Medicine

1. Changes in pregnancy

Physiological changes in pregnancy

Why do we need to study the physiological changes?
Understand how human adapt to pregnancy
Some medical diseases may become worse during pregnancy
l Examples:
n Valvular heart diseases
n Diabetes mellitus
Some physiological changes may mimic symptoms and signs of medical disorders
l Examples:
n Palpitations, ejection murmur are common in normal pregnancy that may mimic heart disorders
n pregnant women often have physiological gotire
Some normal ranges may alter in pregnancy
l Examples:
n mild proteinuria of <0.3g per day is normal in pregnancy (<0.1g per day in non-pregnant adult)
Some changes may alter the pharmacokinetics of drugs
l see pharmacology in pregnancy
What are the important physiological changes?
Cardiovascular system
l Cardiac size increases by 12%
l Stroke volume increases by 25 to 30%, reaches its maximum at 12 to 24 weeks of gestation
l Cardiac output increases by 40% and reaches maximum at 20 to 24 weeks
l Decrease in blood pressure and peripheral vascular resistance
l Ejection systolic murmur
l Normal S3 gallop
l Reversible changes in the ST, T or Q waves in ECG due to the left and upward displacement of the heart
Respiratory system
l Functional residual capacity, residual volume, and expiratory reserve volume all decrease by 20%
l Dead space and tidal volume increase by 30 to 50%
l Marked increase in alveolar ventilation by 65%
l Minute ventilation increases by 50%
l Oxygen consumption increases by 15 to 20%
l Alveolar CO2 decreases due to increased respiratory rate
Glucose metabolism
l During pregnancy, the production of various diabetogenic hormones including human placental lactogen,
progesterone, prolactin and cortisol are increased. Their actions on glucose metabolism are counterbalanced
by an increase in insulin concentrations which reaches almost twice of non-pregnant levels. The vast majority
of pregnant women (96-98%) manage to maintain their blood glucose within normal limits, but the rest of them
fail to do so and become hyperglycemic (gestational diabetes).
Thyroid gland
l During the first trimester, human chorionic gonadotropin (which structurally mimics TSH) produced from the
placenta stimulates the secretion of thyroxine from the thyroid glands. The TSH level decreases. There may
also be a transient increase in free T4 level. These changes are associated with hyperemesis gravidarum
l As the pregnancy goes on, the TSH and free T4 levels return to normal.
l Total T4 increases as the level of thyroxine binding protein increases because of estrogen stimulating effect on
the liver production of the binding protein.
Haematologic system
l Increase in plasma volume up to 50% by term
l Increase in blood volume up to 50% by term
l Increase in RBC volume by 30% by term
l Increase in WBC, mainly polymorphonuclear cells
l Increase in platelet production
l Increase in production of clotting factors, particularly factor I (fibrinogen) and III due to estrogen stimulation.
Pregnant women are therefore more prone to develop thromboembolic diseases.
Renal system
l GFR increases by 50% and renal plasma flow increases by 25% to 50%
l Relative decrease in serum creatinine due to increased GFR
n Dilatation of ureters from 10 weeks onward
n secondary to progesterone effect, and

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l pressure effect, by uterine compression (right > left)
Discussion/Something to Consider
A liver function and a renal function test are performed in a pregnant woman. Is the result normal? why?
Result Normal range
Na 140mmol/L 134-145mmol/L
K 3.5mmol/L 3.5-5.1mmol/L
Urea 2.5mmol/L 3.4-8.9mmol/L
Creatinine 40umol/L 44-107umol/L
Albumin 28g/L 36-48g/L
Bilirubin 3umol/L 0-15umol/L
ALT 30IU/L <58IU/L
ALP 200IU/L 30-90IU/L

Pharmacology in pregnancy
Effect of pregnancy on pharmacokinetic
Drug absorption form GI tract
l reduction in gastrointestinal motility may increase absorption of some poorly soluble drugs such as digoxin, or
decrease absorption of some drugs that undergo metabolism in gut wall, such as chlorpromazine
l vomiting in early pregnancy may reduce absorption of orally administrated drugs
Drug distribution
l increase of plasma volume and extracellular fluid volume may decrease the steady state concentration of
drugs with a small volume of distribution
l decrease in albumin concentration may alter the free fraction of protein-bound drugs
Drug elimination
l increase renal blood flow and GFR increase renal excretion of polar drugs
l increase in hepatic microsomal oxidase system induced by pregnancy increase the metabolism of certain
drugs particularly anticonvulsants
Effect of drug on fetus
Fertilisation and implantation
l mifepristone(RU486), an anti-progesterone that antagonize the endogenous progesterone effects on
endometrium, is used as an abortive agent
Organogenesis
l diethylstilboestrol (DES): adenocarcinoma of vagina in teenage years
l androgens: virilization, limb reduction, esophageal anomalies, cardiac defects
l tetracyclines: inhibition of bone growth, discoloration of teeth
l anticonvulsants: neural tube defects
l warfarin
Growth, development and physiology
l anti-thyroid drugs cross placenta and may result in fetal and neonatal hypothyroidism
l prostaglandin synthetase inhibitors can cause premature closure or the ductus arteriosus
l CNS depressants such as opiates cause neonatal respiratory depression
l drugs with dependence potential such as opiates taken regularly during pregnancy can result in withdrawal
symptoms in the neonate
Drugs in breastfeeding
l most drugs enter breast milk to a greater or lesser extent but, because the concentration has been greatly
reduced by distribution throughout the mother's body, the amount of drug actually received by the breast-fed
baby is usually clinical insignificant
l drugs that can safely be given to breast-feeding mothers include:
n penicillins, cephalosporins
n theophylline, salbutamol by inhaler, prednisolone
n valproate, carbamazepine, phenytoin
n beta blockers, methyldopa, hydralazine
n warfarin, heparin
n tricyclic antidepressants
n haloperidol, chlorpromazine
l certain drugs achieve sufficient concentration in breast milk, and they are sufficiently potent that their use in
breast feeding mothers should be avoided
n sulphonamides, chloramphenical, isoniazid, tetracyclines
n narcotic analgesics
n benzodiazepines
n lithium
n phenindione

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Maternal medicine
What is maternal medicine
l also called medical Obstetrics, is a subspecialty in Obstetrics.
l study of physiological changes in pregnancy.
l deals with medical diseases and complications of the mothers during pregnancy.
l also handles other high risk pregnancies e.g. surgical diseases.
l team-care multi disciplinary approach (obstetricians, midwives, nurse specialists, paediatricians, physicians,
surgeons, anaesthetists, intensive care specialists.) is important.
Three kinds of medical diseases
l Medical diseases present before pregnancy (pre-existing)
l e.g. heart diseases, epilepsy
l Medical diseases caused by pregnancy (pregnancy specific)
l e.g. pre-eclampsia, gestational diabetes mellitus
l Medical diseases occurring for the first time in pregnancy which may be the predisposing factor (co-incidental)
How to study maternal medicine

Principles:
l Firstly, understand how a disease and its therapy (which are usually medication) affects the pregnancy (both
the mother and the baby):
l e.g. poorly controlled diabetes mellitus increases risks of fetal macrosomia, intrauterine death
l Secondly, understand how a therapy (which are usually medication) affects the pregnancy (both the mother
and the baby):
l e.g. anti-convulsants increase fetal risk of neural tube defects
l Conversely, how the pregnancy affects the disease
l e.g. pregnancy is diabetogenic and control of diabetes mellitus may require adjustment of insulin therapy
l It is important to understand the physiological changes in pregnancy
l Finally, how the pregnancy affects the treatment
l see pharmacology in pregnancy for more examples
Which medical diseases a medical student should know
l hypertension in pregnancy
l diabetes mellitus
l heart diseases in pregnancy
l thromboembolic diseases
l thyroid disorders
l epilepsy
l appendicitis

2. Diabetes mellitus

Diabetes mellitus
Introduction
l Diabetes mellitus is one of the most common medical disorders in pregnancy.
l Pregnant women may have diabetes before pregnancy (pre-existing), or develop glucose intolerance during
pregnancy (gestational diabetes). In both conditions, the glucose intolerance may be so severe that insulin
control is required (insulin-dependent diabetes).
l During pregnancy, women require more energy intake. On the other hand, as pregnancy is diabetogenic (see
physiological changes in pregnancy), glucose control becomes more difficult.

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l Poor control of glucose level may result in various maternal and fetal complications.
Fetal Complications
Fetal malformations
l Various malformations are reported:
n CVS: the most common system involved; VSD, ASD, TGA, situs inversus, hypolastic left ventricle
n CNS: anencephaly, encephalocele, holoprosencephaly
n Others: caudal regression syndrome, bowel atresia, etc
l Teratogenicity is associated with poorly controlled diabetes during embryogenesis (first trimester).
l The exact mechanism is unknown, maternal hyperglycemia, hyperketonemia and hypoglycemia have been
suggested.
Macrosomia
l Hyperinsulinemia and hyperglycemia not only result in excessive growth but also an increase in fat deposition
over shoulder, resulting in high risk of shoulder dystocia, birth injuries and operative deliveries
Intrauterine growth retardation
l IUGR is uncommon but can occur in severe chronic cases of diabetes with vasculopathy. Uteroplacental blood
flow is affected resulting in fetal growth restriction.
Intrauterine death
l Sudden intrauterine death can be resulted from poor control of hyperglycemia, or secondary to IUGR. It was
the major cause of perinatal mortality in diabetic patients in the past, before the use of insulin.
Neonatal complications:
l Hypoglycemia: poor maternal glucose control can result in fetal beta-cell hyperplasia, leading to exaggerated
insulin release following delivery.
l Respiratory distress syndrome: hyperglycemia and hyperinsulinemia affect biosynthesis of pulmonary
surfactant.
Maternal complications
l Pre-eclampsia
l High risk of operative deliveries
l Pre-existing nephropathy and retinopathy may be worsen during pregnancy
Principles of management
Prepregnancy
l Pre-conception counselling is very important. Tight glucose control is emphasized to miminize risk of
teratogenicity. Hypoglycemic agents should be changed to insulin for better control. Complications such as
nephropathy and retinopathy should be looked for.
Antenatal
l Diet adjustment (30kcal/kg body weight) to provide adequate energy during pregnancy.
l Insulin control
l Regular glucose monitoring
n H'trix at home
n blood sugar series and HbA1c
l Monitoring of maternal condition
n Blood pressure and urine albumin
l Monitoring of fetal condition
n Morphological assessment at around 20 weeks
n USG for growth and liquor volume when uterus is large for date
n CIG after 37 weeks or earlier in case of poorly controlled cases
Intrapartum
l Time of delivery
n While the pregnancies of well controlled cases can be continued till 41 weeks, poorly controlled cases
should have induction of labour earlier to prevent sudden intrauterine death
l Mode of delivery
n Pregnancy with macrosomic babies should be counselled for elective caesarean section
Postpartum
l Change to pre-pregnant diet and drug regime
l Discuss contraception

Gestational diabetes
Definition
l It is defined as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.
l The definition does not differentiate those pre-existing diabetes mellitus which are not picked up until the
patient becomes pregnant, from those genuine gestational in origin (due to exaggerated physiological changes
in glucose metabolism).
l The definition applies irrespective of whether or not insulin is used for treatment or the condition persists after
pregnancy.
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l There have been controversies for long time in the subjects of gestational diabetes:
l the best method for screening
l the diagnostic criteria
l the management of identified gestational diabetes
Incidence
l 1 to 3%
Antenatal screening
Gestational glucose intolerance can be screened by various ways:
l Presence of clinical risk factors:
n in previous pregnancies: history of gestational diabetes, macrosomia, unexplained stillbirth
n in current pregnancy: persistent or significant glycosuria, macrosomia, maternal obesity, advanced
maternal age
n other risk factor: positive family history of diabetes in first-degree relatives
l Biochemical:
n spot glucose level, fasting glucose level
A positive screening result should be followed by a diagnostic oral glucose tolerance test
Diagnosis
Oral glucose tolerance test
l is usually performed around 26 to 28 weeks of gestation when the pregnancy-induced diabetogenic effects are
most prominent. It may be performed earlier when there is clinical suspicion.
l is the only diagnostic test of gestational diabetes. However, the glucose load and the cut-off levels vary among
centres. In PWH, 50g glucose load is used. The fasting plasma level of more than 5.5mmol level, or the second
hour level of more than 8 is diagnostic.
Complications
Fetal complications
l macrosomia, neonatal hypoglycemia, polycythaemia, hyperbilirubinaemia
l risk of congenital malformation is not increased unless the onset of gestational diabetes is at the first trimester
Maternal complications
l increased risk of pre-eclampsia, operative deliveries, and increased chance of development of diabetes
mellitus in future.
Management
The antenatal and intrapartum management is similar to that of pre-existing diabetes mellitus:
l Tight control of diet, and insulin when dietary control is inadequate.
l Regular monitoring of glucose level, maternal and fetal condition (see management in diabetes mellitus).
A 75g oral glucose tolerance test (using WHO criteria) should be repeated 6 weeks postpartum to rule out
pre-existing disease.

3. Preeclampsia

Hypertension in pregnancy
Definition of hypertension in pregnancy
Arterial diastolic pressure:
l >= 110mmHg on any occasion, or
l >= 90mmHg on 2 or more occasions at least 4 hours apart
Definition of proteinuria in pregnancy
l daily urine protein output of 300mg, or
l 2 clean-catch mid-stream or catheter specimens of urine collected at least 4 hours apart with
n 1g albumin/l or>=2+ on reagent strip, or
n 0.3g albumin/l or >= 1+ on reagent strip if urine pH is <8 or specific gravity is < 1.030
Causes of hypertension during pregnancy
Elevation of blood pressure during pregnancy can be due to:
Transient elevation:
l also called white-coat hypertension
l related to stress and anxiety
Pregnancy induced hypertensive disorders:
l it can be pregnancy induced hypertension, pre-eclampsia or eclampsia
l this group of disorders may be superimposed with pre-existing hypertension
l hypertension induced by pregnancy almost always occurs after 20 week, except in rare situation such as molar
pregnancy.
Pre-existing hypertension:
l also called chronic hypertension
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l most are primary (or essential) but occasionally it may be secondary to:
n renal disorders such as lupus glomerunephritis
n endocrine disorders such as phaemochromocytoma or Cushing syndrome
n vascular disorders such as co-arctation of aorta
l the diagnosis of pre-existing hypertension is made usually because there is history before pregnancy, or the
hypertension is noted at the first in pregnancy, but before 20 week when pre-eclampsia is unlikely
Unclassified hypertension:
l in some situation it may be difficult to differentiate whether the hypertension is due to pre-existing disease or
induced by pregnancy, therefore it is said to be unclassified
l for example, when a patient comes to the first booking at 25 week of gestation, and is noted to have
hypertension, we are not certain whether it is pre-existing or pregnancy induced, as there is no record of the
preceding blood pressure. It is then belonged to unclassified group
l management of this group of patient depends on the clinical symptoms and signs, and may be treated as
pre-eclampsia if it progresses
Classification of hypertension disorder in pregnancy
The classification by International Society for the Study of Hypertension (ISSHP) is as follow:
gestational hypertension and / or proteinuria
hypertension and/ or proteinuria developing during pregnancy, labour or puerperium in a previously normotensive
non-proteinuric woman and subdivided into:
l gestational hypertension or pregnancy induced hypertension( without proteinuria)
l gestational proteinuria (without hypertension)
l gestational proteinuric hypertension (pre-eclampsia)
chronic hypertension and chronic renal disease
hypertension and / or proteinuria in pregnancy in a woman with chronic hypertension or chronic renal disease
diagnosed either before or during or persisting after pregnancy and subdivided into:
l chronic hypertension (without proteinuria)
l chronic renal disease (proteinuria and hypertension)
l chronic hypertension with superimposed pre-eclampsia
unclassified hypertension and / or proteinuria
hypertension and / or proteinuria found either (1) at first 'booking' examination after the 20th week of pregnancy in a
woman without known chronic hypertension or chronic renal disease, or (2) during pregnancy, labour, or the
puerperium where information is insufficient to permit classification is provisionally regarded as unclassified and
subdivided into:
l unclassified hypertension (without proteinuria)
l unclassified proteinuria (without hypertension)
l unclassified proteinuric hypertension (pre-eclampsia)
eclampsia
Eclampsia is the occurrence of generalised convulsions during pregnancy, labour or within 7 days of delivery in the
absence of epilepsy or another condition predisposing to convulsions.
Discussion/Something to Consider
How to differentiate transient hypertension from pre-eclampsia clinically?
When a patient comes to you at 28 weeks of gestation for the booking visit, and is noted to have blood pressure of
150/95. What is your management?

Pre-eclampsia
Introduction
l a common disorder, peculiar to pregnancy
l characterized by hypertension, proteinuria, and edema (see hypertension in pregnancy for definition of
hypertension and proteinuria)
l a multisystem disorder involving CNS, hepatorenal system, and coagulation
l can only be cured by delivery
l second commonest causes of maternal death in UK (94-96) (after thromboembolism)
Pregnancy induced hypertensive disorders
Pre-eclampsia is the most common form of in this group of disorder. It can progress to eclampsia. It is called
pregnancy induced hypertension or gestational hypertension if there is no proteinuria (see hypertension in
pregnancy for detail classification)
Incidence
l 6% in Caucasian
l 2% in Hong Kong Chinese
Risk factors (RR: relative risk)
l Nulliparity (RR 3:1)
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l Pregnancy by a new partner
l Previous history
l Positive family history (RR 5:1)
l Maternal age < 17 or > 40 years
l pre-existing medical disorders
n Chronic hypertension (RR 10:1)
n renal diseases (RR 20:1)
n diabetes (RR 2:1)
n antiphospholipid syndrome (RR 10:1)
n Twin pregnancy (RR 4:1)
n Hydrops fetalis (Rhesus iso-immunisation, alpha-thalassemia major)
Pathophysiology
The exact mechanism is unknown
It is characterized by:
l Generalized vasoconstriction, leading to hypertension and reduction in blood volume
l widespread endothelial damage, leading to
n capillary leaking of protein and proteinuria
n leaking of fluid to extravascular space resulting in peripheral edema and pulmonary edema, and
reduction in intravascular volume
These pathological changes probably start in the early second trimester as follow:
l Stage 1: starts before 20 weeks and causes no symptoms
n Failure of trophoblastic invasion of spiral arterioles which normally results to vasodilatation of vessels
walls
n Placenta is perfused under high pressure because of the vasoconstriction effect
n Local endothelial damage causes aggregation of platelets, fibrin and lipid-laden macrophages (acute
atherosis) and microthrombi formation
n Spiral arterioles become further occluded
l Stage 2: Manifestation of disease
n Ischaemic placenta releases an unknown but apparently blood-borne substance, which leads to
widespread endothelial cell damage, causing generalised vasoconstriction, increased vascular
permeability, and clotting dysfunction
n Because of the high resistance of flow, the uteroplacental blood flow decreases, res ulting in malnutrition
and hypoxia of fetus
Complications
Maternal
Eclampsia
l Renal failure
l Pulmonary edema
l Cerebrovascular haemorrhage
l HELLP syndrome, liver failure
l DIC
l abruptio placentae
Fetal
l IUGR
l Fetal distress secondary to abruptio placentae
l Preterm delivery
l Perinatal death
Clinical manifestation
Onset
l At any time after 20 week, but most commonly in the third trimester near term
Symptoms
l Usually asymptomatic with detection of high blood pressure and proteinuria on routine check up
l Minority would present with symptoms of impending eclampsia
l Headache, drowsiness, visual disturbances, nausea and vomiting or epigastic pain
l Occasionally present with complications of PET such as convulsion and abruptio placentae
Examination
l High blood pressure (see examination)
l Edema, particularly over nondependent area (face and hands)
l Hyper-reflexia
l Sustained ankle clonus
l Proteinuria with urinstix
l Urine output
Screening and prevention
Regular monitoring of blood pressure for high risk cases
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Aspirin has limited role
Management
Principles
l the disease can only be cured by delivery
l aims to minimise risk of prematurity, and avoid maternal and fetal complications of pre-eclampsia
l depends on severity of disease and maturity of the pregnancy:
n if the pregnancy is already at term, deliver the pregnancy to prevent progression of the disease
n if maternal and fetal complications already occur, should consider delivery regardless of maturity, or it will
end up with maternal or fetal mortalities
n if the pregnancy is premature and the disease is mild, try to prolong the pregnancy to reduce the risk of
preterm delivery
Surveillance
l Aim
n to look for any deterioration of maternal or fetal condition that may require prompt delivery
l Maternal surveillance
n blood pressure
n urine protein
n liver and renal function
n clotting profile
l Fetal surveillance
n fetal growth with USG
n fetal well-being with CTG, doppler studies and liquor volume
Control of blood pressure
l Aim
n To control blood pressure to prevent CVA
n Would not alter the progress of disease
l Drugs
n Hydralazine
n methyldopa
Control of convulsion
l Aim
n To prevent eclampsia
n To prevent recurrence of convulsion
n To stop acute convulsion
l Drugs
n Magnesium sulphate
n Diazepam
Fluid management
l Aim
n to maintain adequate intravascular volume and perfusion pressure
n To prevent fluid overload which would result in pulmonary edema, and under-replacement which would
result in renal failure.
Discussion/Something to Consider
You have a patient who is just diagnosed to have pre-eclampsia with BP 150/95 and 1+ proteinuria at 32 weeks of
gestation. What is your assessment and plan of management?
Supposed the above patient has been stable for a week (now at 34 weeks of gestation). She suddenly complains of
vaginal bleeding and uterine contraction pain. What is the possible diagnosis and how would your manage her?

Eclampsia
Definition
l presence of convulsions in addition to pre-eclampsia
Pathophysiology of convulsions
Probably resulted from:
l cerebrovascular vasospasm, or
l cerebral edema
Incidence
l about 0.1% of all pregnancy
Clinical presentation
Onset:
l In vast majority of cases it is preceded by several days and often weeks of clinically evident PET
l In a very few cases an unheralded fulminant onset occurs
l 50% occur antepartum, 25% intrapartum, 25% postpartum

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l Most of the postpartum convulsions occur within 1 day of delivery but seldom beyond 3 weeks
Symptoms:
l Prior to convulsions, patients usually have restlessness, tremulousness and facial twitching
l Grand mal seizures with loss of consciousness
Signs:
l Prior to convulsions, there may be hyper-reflexia and sustained clonus
l Papilloedema
Management
See pre-eclampsia for general management
Management of convulsions
l Lie patient prone to prevent aspiration pneumonia, maintain airway and oxygen supply
l Stop convulsions with diazepam injection if convulsions do not subside spontaneously
l Give magnesium sulphate (MgSO4) as prophylaxis against recurrent convulsions
Delivery
l baby should be delivered immediately after stablisation of the mother. Caesarean section is usually the choice,
unless the second stage of labour is reached and instrumental delivery can be attempted.
Remark
Differential diagnosis of convulsions during pregnancy
l epilepsy
l cerebral lupus
l meningitis
l CNS tumours
l other disorders involving the CNS
Discussion/Something to Consider
How to differentiate eclampsia from epilepsy clinically?
You are the junior on-call obstetrician and are informed that a 24 years old lady at 30 week of gestation was brought
to the A&E Department by her husband. She was noticed by her husband at home that she suddenly collapsed and
convulsed for 2 minutes. The patient is now awake. What are you going to do?

Epilepsy
Introduction
Epilepsy affects 0.5% of women of child-bearing age and is the most common chronic neurological disorder
complicating pregnancy. The cause of majority of epilepsy is primary, but some are secondary to previous medical
events like cranial surgery or meningitis. The important points in obstetrics are:
l Epilepsy should be differentiated from other pregnancy-related causes of convulsions such as eclampsia
l Anti-convulsants are potentially teratogenic
l It may be difficult to control the disease during pregnancy because:
n The physioloigical changes during pregnancy may affect the pharmacokinetic of anti-convulsants
n Patients may be fear of the fetal side effects and not compliant to treatment
Effect of pregnancy on epilepsy
Risk of relapse of convulsions:
l While half of the pregnant women have no changes in the frequency of convulsion, one-quarter of women have
increased frequency of convulsions, due to the reasons mentioned above
l Those women who have been fit-free for many years are unlikely to fit in pregnancy unless she discontinues
her medication.
Effect of epilepsy on pregnancy
l There is no direct effect on pregnancy in epileptics.
l Indirect effects include:
n Acute convulsions may result in physical trauma;
n status epilepticus may lead to hypoxic damage of both the mother and the fetus.
n The baby has risk of developing epilepsy:
n 4% when either parents has primary epilepsy
n 10% when there is a previously affected sibling
n 20% when both parents have epilepsy
n Teratogenicity of anti-convulsants
Management
Pre-conception counselling
l Because of teratogenic risk of anti-convulsants, patients on treatment should be given folic acid (5mg daily) for
at least 12 weeks prior to conception reduce risk of folic deficiency and neural tube defects.
Antentatal management
l may consider discontinuation of the anti-epileptics if seizure-free for 2 years
l monotherapy if needed
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l There is no need to change the type and dosage of anticonvulsants, or measure drug level provided that the
disease is under control.
l Prenatal screening for congenital abnormalities, particularly neural tube defects and cardiac defects should be
provided
l Because of possible hepatic enzyme-induction by anti-convulsants, vitamin K-dependent clotting factors may
be reduced. Vitamin K (10 mg orally) should be given to patients in the last 4 weeks of pregnancy as
prophylaxis against haemorrhagic disease of newborn.
Intrapartum management
l Continue anti-epileptics, if any
l Time and mode of delivery not affected
Postnatal management
l The neonate should be given vitamin K prophylaxis.
l There is no contraindication to breast-feeding.
l When patients want hormonal contraception, higher dose of combined oral contraceptive or progestogen-only
pills should be advised.

HELLP syndrome
Definition
It is an acronym formed from Haemolysis, Elevated Liver enzymes, and Low Platelets (thrombocytopenia). It is a
disorder specific to pregnancy, and is thought to be one of the complications or variants of pre-eclampsia.
Clinical features
Features of pre-eclampsia
Features of HELLP:
l Complete blood picture
l anaemia
l thrombocytopenia
l Liver function test
l elevated bilirubin
l elevated ALT
Other features
l impaired clotting profile
Management
Immediate delivery of pregnancy
See management of pre-eclampsia

4. Other maternal medical diseases

Acute fatty liver

This is a very rare but serious hepatic disorder specific to pregnancy. The incidence is about 1 in 10000 pregnancies.
Similar to pre-eclampsia, the aetiology and pathogenesis are unknown, but it occurs more commonly in primiparous
women, in the third trimester. As its name implies, the clinical occurrence is acute, and histologically, there is
perilobular fatty infiltration of the liver cells. This is different from that of the fatty changes due to obesity or
alcoholism.
Clinical features
The presenting symptoms are of acute or subacute onset of epigastric pain, headache, nausea and vomiting which
are shortly followed by progressive jaundice, liver failure, coagulopathy, encephalopathy and renal failure. It is
associated with high maternal and fetal mortality.
Diagnosis
The diagnosis relies on the clinical features with deranged liver function and clotting profile. It should be
differentiated from HELLP syndrome, pre-eclampsia, and acute viral hepatitis. Liver biopsy is dangerous because of
bleeding tendency.
Management
The mainstay of treatment is immediate delivery, supportive treatment including blood transfusion, and correction of
clotting disorders.

Amniotic fluid embolism

It is a very rare but serious and unpredictable condition in which amniotic fluid enters the maternal circulation,
resulting in acute cardiorespiratory compromise and coagulation derangement. The incidence is about 1 in 30000
pregnancies. The aetiology is unknown but rupture of membranes, rapid labour, caesarean section, use of oxytocin

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increase the risk. The speculated mechanism is that amniotic fluid accesses directly into the maternal circulation
through a defect somewhere near the placental site, at a higher than usual intrauterine pressure. The biochemical
constituents of the amniotic fluid activate the coagulation cascade, and the fetal squames may also plug into the
pulmonary circulation resulting in failure of gaseous exchange.
Clinical features
The patient has a sudden onset of severe chest pain and difficulty in breathing, followed shortly by cyanosis and
cardiorespiratory collapse. Coagulation failure may present with postpartum haemorrhage or spontaneous bleeding
from the puncture sites. 30% of patients will die in the first hour, and the overall mortality is > 90%.
Diagnosis
The diagnosis is mainly on clinical basis. It should be differentiated from other acute causes of cardiorespiratory
arrest such as acute myocardial infarction and pulmonary embolism, and causes of coagulation failure such as
acute fatty liver and abruptio placentae.
The diagnosis may be confirmed by demonstration of amniotic debris and trophoblasts in pulmonary vasculature, by
aspirating blood from the pulmonary artery (via a Swan-Ganz catheter), or during postmortem examination.
Management
Cardiopulmonary resuscitation with circulatory support and artificial ventilation
Correction of coagulopathy
Correction of acidosis
Delivery of baby:
l The fetus is unlikely to survive such a major insult, but immediate delivery by caesarean section carries a high
maternal risk. Therefore delivery should be undertaken after stabilization of the mother, and vaginal delivery is
preferable.

Anaemia
Common types of maternal anaemia during pregnancy
Physiological anaemia
l Low haemoglobin due to dilution effect in pregnancy, because the increase in plasma volume is relatively
higher than the increase in red cell volume (see physiological changes in pregnancy)
l Haemoglobin level is usually not less than 10g/dL
Nutritional anaemia
l Synthesis of haemoglobin is inadequate because of nutritional deficiency in iron, folate, and vitamin B12
l Increase risk in multiple pregnancy, maternal malnutrition
Inherited anaemia
l Deficient synthesis of haemoglobin because of inherited diseases such as thalassemia and sickle cell anaemia
Post-haemorrhagic anaemia
l It is common to have anaemia after heavy postpartum haemorrhage or antepartum haemorrhage

Antiphospholipid syndrome
Definition
l Antiphospholipid syndrome (APS) is an uncommon autoimmune disorder characterised by:
l Presence of either one of both of the following auto-antibodies: anticardiolipin antibodies (aCL) and lupus
anticoagulant (LA), and
l Presence of thromboembolic disorders, recurrent pregnancy loss, thrombocytopenia, or haemolytic anaemia,
and less commonly, systemic or pulmonary hypertension
Diagnosis
The diagnostic criteria include:
l Two positive readings for LA and / or aCL at least 3 months apart, plus
l At least one of the clinical criteria
l The presence of auto-antibodies alone without clinical complications may not require treatment.
Antiphospholipid syndrome should also be differentiated from systemic lupus erythematosus (SLE), although
they both have aCL and similar clinical features.
Management
High-dose steroid and immunosuppression used for treating SLE are not recommended in APS.
Positive history of thromboembolism:
l Patients are at high risk of recurrence of thromboembolism during pregnancy and should be given heparin
prophylaxis
Positive history of recurrent pregnancy loss alone:
l Combination of low-dose aspirin and heparin (low molecular weight) decreases the risk of recurrent loss.

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Appendicitis
Incidence
l It is a common acute surgical condition during pregnancy: 1:1500 to 1:2000
Clinical features
l It is more frequent in the first two trimesters
l It is more difficult to diagnose as the clinical symptoms and signs are more vague than in non-pregnant
women.
l Delayed diagnosis and treatment are not uncommon in pregnancy and account for the high maternal and fetal
morbidities and mortalities.
l Patients usually present with fever, nausea and vomiting, right-sided abdominal pain and tenderness. The site
of the pain changes with the position of the appendix which is pushed upwards by the gravid uterus. Signs of
peritonitis may be masked by the gravid uterus. White cells count is usually raised.
Complications
Maternal
l Peritonitis
l Maternal death (potentially fatal if delay in diagnosis)
Fetal
l Preterm labour, fetal distress, intrauterine death
Differential diagnoses
Related to genital organs:
l Ectopic pregnancy (during the first trimester)
l Torsion ovarian cyst
l Red degeneration of fibroid
l Abruptio placentae
l Chorioamnionitis
Other surgical diseases:
l Acute cholecystitis, pancreatitis
Management
l Appendicectomy
l Antibiotics
l Monitor fetal well-being and maternal vital sign during the peri-operative period.
Discussion/Something to Consider
A 29 year-old woman at 30 weeks of gestation presented with one-day history of severe right lower quadrant pain
preceded by epigastric pain. It was associated with nausea, vomiting and fever. What are the possible differential
diagnosis and how to make the diagnosis?

DIC
Disseminated intravascular coagulopathy
Obstetric and gynaecological causes of DIC
l Septic abortion
l Abruptio placentae
l Pre-eclampsia
l Massive haemorrhage such as uncontrolled postpartum haemorrhage
Investigation results
l Low platelet
l Increased INR and APTT
l Increased D-dimmer
l Increased fibrin-degradation products

Heart disease
Introduction
Heart diseases is a common medical disorder affecting 1% of all pregnancies.
Types of heart diseases in pregnancy
Common
l Rheumatic heart diseases
n relatively common in young female, especially immigrants from Mainland China
n can be complicated with heart failure, arrhythmia, endocarditis and thromboembolism
l Mitral valve prolapse
n the commonest heart disease in young female

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 n usually does not cause major problems such as heart failure
n but may present with palpitation, and increase risk of endocarditis if the valve is damaged
l Arrhythmia
n atrial and ventricular ectopic beats are more frequent in pregnancy. They are benign and require no
treatment
n superventricular tachycardia is also common and requires treatment
n atrial fibrillation may complicate rheumatic heart diseases (especially mitral stenosis)
Uncommon
l Congenital heart diseases
l Ischemic heart diseases
Maternal risks
l Heart failure
l Infectious endocarditis
l Thromboembolism
l Arrhythmia
Assessment
Cardiac function (according to New York Heart Association Functional Classification)
l Class I: symptoms free
l Class II: distressed on moderate exertion
l Class III: distressed on slight exertion
l Class IV: distressed at rest (cardiac failure)
What should medical students know
Rheumatic heart disease with mitral stenosis
This is a very good example to illustrate how pregnancy is affected with heart disease, with all maternal risks
mentioned above are possible to occur during pregnancy and labour.

Mitral stenosis
This is a good example to illustrate the various ways how a heart disease can affect a pregnancy.
Effect of pregnancy on the disease
l Left atrial outflow obstruction results in:
n reduction in ventricular filling and hence reduction in cardiac output (risk of heart failure).
n elevation of left atrial, pulmonary venous and pulmonary capillary wedge pressure (risk of pulmonary
edema).
n abnormally increase in left atrial size which may affect the atrial condition (risk of atrial fibrillation).
n The risk is higher during pregnancy because:
u During antepartum: there is an increase in cardiac demand; the increase in heart rate further
impairs ventricular filling; increase in blood volume further exaggerates pulmonary edema.
u During intrapartum: cardiac demand further increases because of pain and pushing in second
stage.
u During postpartum: about 500ml of blood volume returns from the uterus to the circulation as the
uterine volume shrinks after delivery (autotransfusion).
l In addition, the damaged mitral valve or the replaced valve is associated with increased risk of endocarditis.
l There is also an increased risk of thromboembolism secondary to atrial fibrillation and a mechanic valve
replacement.
Effect of disease on pregnancy
l Patient with significant disease will have increased risk of intrauterine growth restriction (IUGR).
Pre-conceptional counselling
l Patient should be assessed for the physical and physiological fitness of bearing a pregnancy, and counselled
on the risk of undergoing pregnancy.
l The functional class status is assessed with symptoms and signs of cardiac failure and atrial fibrillation.
l Echocardiogram to determine the severity of the disease, ventricular function and diameter of mitral valve.
l Patient with severe disease may become suitable for pregnancy after valvotomy or valvular replacement.
Management during pregnancy
l Monitor maternal cardiac status by the functional class, cardiac symptoms, and echocardiogram assessment.
l Monitor fetal growth and fetal well-being by serial ultrasound scan for growth parameters and liquor volume,
and CTG.
Management in labour
l Antibiotic cover at the onset of labour or rupture of membranes in order to prevent bacterial endocarditis.
l Close monitoring of maternal vital sign, fluid input and output:
n Severe cases will require arterial line (monitor systemic blood pressure), CVP line (monitor the central
venous pressure) or even Swan Ganz catheter (monitor the pulmonary pressure).

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l Continuous monitoring of fetal heart tracing with CTG.
l Avoid fluid overload.
l Prophylactic instrumental delivery to avoid strenuous effort during the bear down.
l Avoid syntometrine as the drug will increase the afterload; slow intravenous syntocinon at third stage (too rapid
injection will lead to a drop in the systemic blood pressure and hence reduce the venous return).
l IV diuretics (frusemide) at the third stage to reduce fluid overload from autotransfusion of blood from the
uterine circulation after the delivery.
l Continue to monitor input and output after the delivery as the patient will be at risk of pulmonary edema within
48 hours postdelivery.
Other Management
l Adjust the dosage of anti-coagulants to prevent thromboembolism
l Anti-arrhythmic agents to control atrial fibrillation.

Pulmonary embolism
l Embolism involving pulmonary vasculature
l High mortality
l Needs intensive care support
l Urgent open embolectomy may be needed to clear the blood clots. Usually associated with deep vein
thrombosis, especially bilaterally

Thrombocytopenia
Definition: Low platelet count

Thromboembolism
Epidemiology:
Less common in Chinese than in Caucasian, incidence around 1 in 300 in PWH, majority in postnatal period,
predominantly calf vein DVT, above knee DVT less than 1 in 1000 pregnancy.
Risk factors of deep vein thrombosis:
l Advanced age (>40)
l Gross obesity
l Smoker
l Caesarean section
l Immobilisation (for > 4 days)
l Previous history of DVT
l Thrombophilia (protein C deficiency
l Protein S deficiency
l Anti-thrombin deficiency
l Antiphospholipid syndrome
Clinical features:
l Calf swelling
l Calf pain
l Leg swelling
l Homans' sign may be present (active or passive dorsiflexion of the foot associated with pain Incomplete
dorsiflexion or flexion of the knee to release tension. This sign may be absent in about 50% of cases of DVT
l Dyspnoea
l Respiratory distress
l Desaturation and chest pain are features of pulmonary embolism
Diagnosis:
l High index of suspicion when a pregnant woman complains of unilateral calf pain and swelling, in particular
within a few days after caesarean section.
Management:
l Medical treatment - current treatment is either subcutaneous low molecular weight heparin (predominantly
used in antenatal DVT) or warfarin (predominantly used in puerperium)
l General management
n Above knee DVT - Slightly elevate the legs and bed rest for 1 or 2 days until calf pain resolves after
medical treatment, then encourage mobilisation, apply elastic stocking
n Below knee DVT- Encourage mobilisation
Prophylaxis:
Patients with previous DVT, known thrombophilia

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l Physical measures: elastic stocking, intermittent pneumatic compression during labour, caesarean section and
early puerperium
l Medical: subcutaneous low molecular weight heparin

Thyroid disorder
Introduction
Thyroid disorders are common endocrine disorders affecting women at reproductive age. It may compicate
pregnancy or cause various gynaecological disorders.
Thyroid disorders in gynaecology
Hypothyroidism
l Menorrhagia
l Infertility
Hyperthyroidism
l Amenorrhea
l Infertility
Thyroid disorders in Obstetrics
Hyperthyroidism
l Causes
n Due to the effect of human chorionic gonadotropin, there is usually transient hyperthyroidism during the
first trimester (see physiological changes in pregnancy). It is usually self-limiting but may be associated
with hyperemesis gravidarum.
n The most common cause of hyperthyroidism during pregnancy is Graves disease (95%), in which
auto-immune TSH receptor-stimulating antibodies (an IgG) can cross the placenta leading to fetal
hyperthyroidism.
l Complications
n Uncontrolled hyperthyroidism results in various fetal complications: abortion, IUGR, preterm labour, fetal
thyrotoxicosis (in Graves disease only). Rarely a fetal gotire may cause hypertension of the fetal neck,
leading to malpresentation.
n Maternal complications are thyroid storm, tracheal obstruction due to a retrosternal gotire.
l Treatment
n The mainstay of treatment is by antithyroid agents such as propylthiouracil and carbimazole.
Beta-blockers may be required to control the cardiac symptoms before the hyperthyroidism is under
controlled.
Hypthyroidism
l Causes
n Hypothyroidism can be resulted from iodine deficiency in endemic area, thyroiditis or post-surgical or
radiation therapy for previous hyperthyroidism.
l Complications
n Abortion, IUGR, decreased intelligence quotient of the offspirngs.
l Treatment
n The treatment is by thyroxine replacement which does not cross the placenta.
Postpartum thyroiditis
l It is now found to be a common complication of pregnancy (5-10%), although majority of the are subclinical. It
is a kind of autoimmune destructive lymphocytic inflammation, thought to represent an activation of a
previously subclinical thyroiditis, caused by rebound in levels of antimicrosomal antibodies as the
immunosuppressive effects of pregnancy are reversed.
l As a result of destruction, thyroxine is released from the gland in the initial phase of the disease. Afterwards,
there may be hypothyroidism when the thyroid reserve is depleted. Presentation is usually between 3 to 4
months It results in hyperhyroidism in 40% cases, hypothyroidism in another 40%, and biphasic (initial
hyperthyroidism followed by hypothyroidism) in 20%.
l Postpartum thyroiditis is also a common pregnancy-specific complication.
Discussion/Something to Consider
What are the signs of fetal thyrotoxicosis? and what is the most effective way to look for fetal thyrotoxicosis in a
woman known to have Graves disease? Which antithyroid agent, propylthiouracil or carbimazole is preferred during
pregnancy?

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Labour Management

Intrapartum management
Intrapartum management is one of the most important area in Obstetrics. The aims are to ensure that the fetus is
delivered in the most optimal condition for gestation, while the potential hazards of childbirth and any underlying
pathology to the mother are minimised. It consists of the following aspects:
l Maternal monitoring: to ensure maternal well-being during labour and delivery, relief stress and anxiety.
l Labour pain relief: provides adequate and safe analgesia to the mother.
l Intrapartum fetal monitoring: to ensure fetal well-being during labour and delivery.
l Monitoring the progress of labour: to ensure the progress of labour is normal, look for any obstruction of labour
and take prompt actions.
l Decision of mode of delivery: to decide the most optimal time and the safest way of delivery which may involve
instrumental delivery or caesarean section.
All the above monitoring can be summarised in a partogram that facilitate the intrapartum management.

1. Induction and progress of labour

Labour
Definition of labour
l Onset of regular painful uterine contractions accompanied by effacement and dilatation of the cervix.
Initiation of labour
l It is not fully understood
l The main trigger is probably fetal rather than maternal
l It may involve fetal cortisol, and prostaglandins
l Once initiated, labour appears to be self-perpetuating
Three stages of labour
The labour process is divided into three stages:
First stage
l It starts from the diagnosis of labour until the cervix is fully dilated (10cm for term pregnancy)
l The fetal head engages, descends gradually into the pelvis and rotates
l The cervix often dilates slowly for the first 3cm and is called the latent phase
l Thereafter, average cervical dilatation is at the rate of 1cm/hour in nulliparous, and about 2cm/hour in
multiparous
l It normally would not last longer than 12 hours
Second stage
l It starts from full dilatation of the cervix to the delivery of the fetus
l Descent, flexion, and internal rotation of the fetal head are completed, followed by extension and restitution
(external rotation)
l Maternal pushing is essential
l It usually takes 40 minutes for nulliparous and 20 minute for multiparous.
l See also the second stage of labour for more detail
Third stage
l It starts from delivery of the fetus to delivery of the placenta
l It normally lasts about 15 minutes
l Normal blood loss is up to 500ml
l See also the third stage of labour for more detail
Mechanism of vaginal cepahlic delivery
Engagement
l the ovoid-shaped head normally enters the pelvis in the occipito-transverse position, because the transverse
diameter of the inlet is greater than the antero-posterior diameter
Descend
l the fetal head descends further into the birth canal.
l the degree of descent is measured by station.
l during the descend, the fetal skull may change shape to adapt the maternal pelvis (moulding). Caput
succedaneum is usually formed by compression.
Flexion
l the head also flexes as it descends further, so that the its vertex becomes the presenting part
Rotation (internal)
l the fetal head rotates 90 degree so that the face is facing the sacrum, and the occiput is anterior, below the
symphysis pubis

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l this enables it to pass through the pelvic outlet which has a wider antero-posterior than transverse diameter
l in 5% of cases, the head rotates to occipito-posterior position
Extension
l the fetal head extends and distends the perineum (crowning), and finally is delivered
Restitution (external rotation)
l the fetal head then rotates 90 degree back to the same position in which it enters the inlet, facing either right or
left, to enable delivery of the shoulders

Second stage of labour

Definition
The second stage of labour starts from time when the cervix is fully dilated, to end of the delivery of the baby.
Process of delivery during the second stage
Delivery of the fetal head
The presenting part (which is usually the fetal head) continues to descend and finally passes through the pelvic
outlet. The fetal head usually rotates to occiputo-anterior and extends round the pubis (crowning). It distends the
perineum during crowning. Episiotomy is indicated during crowning to prevent perineal tear. Maternal pushing during
the whole process is essential for success. After the fetal head is delivered, it rotates to the natural position relative
to the shoulder (restitution). Difficulty may be encountered at this stage. The fetal heads may fail to descend further
(prolonged second stage). It may be due to inadequate maternal effort, occipito-posterior position or cephalopelvic
disproportion. Careful assessment should be taken before performing instrumental delivery.
Delivery of the fetal shoulder and rest of the body
The anterior shoulder is usually delivered by downward traction and the posterior shoulder follows spontaneously.
Sometimes difficulty (shoulder dystocia) may be encountered at this stage. The rest of the trunk is often delivered
without difficulty, except in rare situations such as fetal ascites or meconium peritonitis, the distended fetal abdomen
results in abdominal dystocia.
The late second stage is presented as follow:

Beginning of crowning. The fetal head is distending the

perineum

Local anaesthesia is injected to the perineum before

episiotomy

A mediolateral episiotomy is performed

Crowning of fetal head. The greatest diameter of the

presenting part is passing through the outlet. Control of
the speed of crowning and guarding of the perineum is
necessary to avoid perineal tear

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 The fetal head is delivered and restitution occurs.
Suction of airway is then performed

Delivery of the anterior shoulder by downward traction.

Shoulder dystocia may be encountered at this stage

Delivery of the posterior shoulder

Delivery of the rest of the body

Clamping of the umbilical cord

Third stage of labour

It starts from delivery of the fetus to delivery of the placenta. Normally it lasts not more than 30 minutes and blood
loss is up to 500ml. Retained placenta (prolonged third stage), and postpartum haemorrhage are the major risks at
this stage.
Management of the third stage
l Give prophylactic syntocinon or syntometrine bolus injection immediately after the delivery of the baby. Infusion
of syntocinon may be required.
l Look for signs of separation of placenta: lengthening of cord, uterine contractions, gush of blood coming out
from vagina.
l Deliver the placenta by controlled cord traction.
l Examine the placenta for any missing membranes, cotyledons or succentiate lobes
l Examine the perineum, vagina and the cervix for any tear
l Repair episiotomy, perineal tear or other kinds of tears
l If the placenta is retained, perform manual removal of placenta (MROP) under general or regional anaesthesia.
There is a possibility of morbid adherence of placenta
l If the is excessive bleeding from inside of uterus, repeat the oxytocic injection, or give an syntocinon infusion,

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 or prostaglandin F2a (a stronger oxytocic) to correct any uterine atony. Exploration of uterus under
anaesthesia may be required.

Vaginal breech delivery

Introduction
Vaginal breech delivery is a high risk procedure. A recent randomized controlled study has showed that it is
associated with higher perinatal mortality and morbidity than elective caesarean section in delivering singleton
pregnancy with breech presentation. Women should be counselled for external cephalic version (ECV) or elective
section. Vaginal breech delivery should only be considered in highly-selected group of pregnancies:
l multiparous with previous successful vaginal deliveries
l term fetuses of average size (estimated weight between 1.5 to 3.5kg)
l fetal neck is not hyperextended
l frank or complete breech presentation
l there is no evidence of fetal compromise
l induction and augmentation are not required
Mechanism and technique
Delivery of the lower part of the body
l Vaginal breech delivery begins with its bitrochanteric diameter fitting into the lateral diameter of the maternal
pelvis, and the rotation is therefore sacral anterior or posterior.
l As the breech descends towards the outlet, it rotates into a sacral lateral position, and the baby presents by the
anterior buttock. During delivery, the baby bends its back laterally, so first the anterior buttock, then the anus,
then the posterior buttock delivers. Episiotomy is made at this stage.
l The lower limbs and the trunk usually deliver spontaneously. The baby will then be lying with the shoulders in
the transverse diameter.
Delivery of the shoulder
l The arms may extend and abduct over the back of the fetal neck (see nuchal arm below). Rotation of the body
by Loveset maneuver is then necessary to deliver the shoulders:
l The shoulders are rotated into anterio-posterior diameter, so that the anterior shoulder is adducted. The
anterior shoulder and elbow are then flexed and delivered. The posterior shoulder is then rotated to the
anterior position and delivered in a similar way. The shoulders finally lie in the transverse diameter again.
Delivery of the head
l The head usually requires assisted delivery. Head entrapment is an dangerous condition (see below). The aim
is to encourage flexion of the neck. This can be done with a pair of Piper forceps, the Burns Marshall maneuver,
or the Mauriceau Smellie Viet maneuver. Refer to your textbooks for these maneuvers.
Potential difficulties in vaginal breech delivery
Cord prolapse
l In case of footling breech presentation, the fetal buttock is not well fit to the cervix, and is more prone to cord
prolapse.
Nuchal arm
l One or both fetal arms are extended, abducted over the back of the fetal neck. This results in obstruction.
Head entrapment
l During vaginal delivery, the fetal head is presented to the birth canal with the base of the skull, and there is not
adequate time for moulding. The head may be trapped by the cervix.
In both cases of nuchal arm and head entrapment, the umbilical cord is being compressed and occluded between
the cervix and the head. Prolonged delivery results cause hypoxic damage. Excessive traction to overcome dystocia
also causes severe trauma.

Engage
A term applied when the greatest diameter of the baby's presenting part has passed through the pelvic inlet of the
mother. The greatest diameter is biparietal diameter in cephalic presentation, and bi-iliac diameter for breech
presentation. Engagement is particularly important when the mother has a platypoid pelvis, as when the head is
engaged, the rest of the labour should present no difficulty. As disproportion becomes less of a problem nowadays,
engagement becomes less important. As a failure to progress in labour becomes the important diagnosis regardless
of the cause of this failure, the descent of the head, as measured by the number of fifths of the head still palpable
abdominally, becomes more important.

Station
Definition
It denotes the level of descent of the presenting part as assessed on vaginal examination, similar to engagement
which is assessed abdominally. Station is defined by the distance in centimeters between the leading portion of the
fetal presenting part, and the plane of the maternal ischial spines (which is arbitrarily set as zero level). For example,

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it is S+2 if the leading bony portion of the fetal skull is 2cm below the ischial spines but is S-1 if it is 1cm above the
them.
Clinical importance
When the presenting part reaches the ischial spines (station 0), it is often engaged.
Station is one of the five parameters making up the bishop score.
It is also used to define the level of instrumental delivery.
Station may be incorrectly assessed when there is significant caput succedaneum which gives a wrong impression
that the presenting part is low.

Partogram
The partogram is a graphic display of progress in labour, with complete collection of information on the cervical
dilatation, presentation, station (descend) and position of the presenting part. There are also recordings of the
intrapartum monitoring of the maternal and fetal well-being, and administration of any drugs. The partogram
facilitates the monitoring of the progress of labour, diagnosis of dystocia, and continuation of intrapartum
management and decision making.

A partogram showing normal progress

Occipito-posterior
The fetus with vertex presentation begins labour usually in the occipito-lateral position because its slightly longer
anteroposterior diameter fits best into the slightly longer lateral diameter of the pelvic brim. When labour progresses,
the head rotates so the baby faces the back of the mother, occipito-anterior position.
Occipito-posterior position commonly occurs if the maternal pelvis is of the anthropoid or the android shape. It is
associated with dystocia and incoordinate uterine contractions.
Occipito-posterior position usually resolves in one of following three ways:
l Most commonly, after a longish and difficult labour, the head rotates to the occipito-anterior position, and the
baby delivers normally.
l Sometimes, the head stays persistently occipito-posterior (POP), and the head is delivered in this position. The
head tends to act like a battering ram on the perineum, and usually severe trauma to the perineum results.
Occasionally a third degree perineal tear results.
(*)Occasionally, during the rotation, the head is held up by the sacrum. The part of the head near the back of the
mother fails to descend while the part near the front continues to descend, and the baby's head therefore tilts
sideways (asynclitism). As the head tilts, it becomes more obstructed, and eventually the head cannot descend
anymore. This is called deep transverse arrest. Usually, a Caesarean section is necessary. However, delivery can
sometimes be effected by the use of Kielland's forceps, the vacuum extraction, or in the old days by manual rotation
of the head.

Bishop score
The score used to assess the ripening of the cervix for induction of labour. Scores are assigned to each of the five
cervical features and the total score is obtained by summation. With a low score (0-3), there is a higher risk of failed
induction, resulting in caesarean section (over 20%) compared with a score of eight or more, where the failed
induction rate is less than 3%. With a high score the cervix is said to be ripe.
Bishop's score 0 1 2 3
Dilatation (cm) <1 1-2 3-4 >4
Length (cm) 4 2-4 1-2 <1
Consistency firm medium soft /
Position / posterior central anterior
Station -3 -2 -1, 0 >=1
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Induction of labour
Definition
It is an obstetric procedure designed to pre-empt the natural process of labour by initiating its onset artificially before
this occurs spontaneously.
Indications
Fetal indications
l Postterm pregnancy: the most common indication
l Prolonged rupture of membranes: the second most common indication
l Fetal compromise that may risk intrauterine death if pregnancy is continued: IUGR, oligohydramnios
l Lethal fetal abnormalities requiring termination of pregnancy: such as Edward syndrome, Patau syndrome,
anencephaly, thanatophoric dwarfism
l Stillbirth
Maternal indications
l presence of medical diseases that may deteriorate or is poorly controlled as pregnancy continues: such as
pre-eclampsia, poorly controlled diabetes mellitus
Contraindications
l Malpresentation: fetuses may better be delivered by caesarean section, or external cephalic version (ECV)
before induction
l Date problems: may need to unnecessary induction for postterm, iatrogenic preterm delivery
l Presence of indications of caesarean section: such as placenta praevia, classical caesarean section
l Severe fetal compromise that is likely to fail to sustain the stress of labour: better to deliver by caesarean
section
l Poor maternal condition such as severe pre-eclampsia: better to deliver by caesarean section
Methods
Cervical ripening
l with vaginal insertion of prostaglandin E2
l required if the cervix is unfavourable, with bishop score less than 7
Initiation of uterine contractions
l with amniotomy (artificial rupture of membranes) and syntocinon intravenous infusion
l syntocinon infusion rate should be titrated with frequency and strength of uterine contractions to avoid
hyperstimulation of uterus
Complications
Maternal complications
l uterine rupture
l risk of caesarean section secondary to failure of induction
Fetal complications
l acute fetal distress resulted from uterine hyperstimulation or uterine rupture
l intrauterine infection secondary to prolonged induction and labour

Amniotomy
Amniotomy, or artificial rupture of membranes, is a common intrapartum procedure, performed with an amnihook (or
with a Drew-Smythe cannula in hindwater amniotomy). It is indicated in augmentation or induction of labour. The
procedure would stimulate production of endogenous prostaglandins which brings about uterine contractions as well
as cervical softening. The procedure is also indicated before the application of fetal scalp electrode, fetal scalp blood
sampling, or instrumental delivery. In the management of intrauterine death, amniotomy should be avoided until the
late stage of labour, in order to prevent intrauterine infection. It is also advisable to avoid amniotomy in vaginal
delivery of preterm fetuses as the forewater protects the vulnerable fetal head from excessive compression during
labour. An uncommon complication of amniotomy is cord prolapse, particularly if there is polyhydramnios.

Failure to progress
Definition of failure of progress of labour
It is defined as the labour progress fails to reach an acceptable rate. The criteria is different depending on parity.
l Prolonged active phase:
n cervical dilatation: less than 1.2cm/hr in a primigravida; less than 1.5cm in a multipara
l Prolonged descend:
n descend of the presenting part: less than 1.0cm/hr in a primigravida; less than 2.0cm in a multipara
l Secondary arrest of dilatation:
n cervical dilatation ceases during active phase of labour for 2 or more hours
l Prolonged second stage:
n second stage last more than 1 hour in a primigravida; 30 minutes in a multipara

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Causes of failure of progress
l Insufficient power:
n Incoordinate or inadequate uterine contractions
n Poor maternal efforts during second stage
l Obstructed labour due to disproportion of sizes of the passenger and the pathway:
n Cephalopelvic disproportion
n Abnormally large presenting part: hydrocephaly
n Contracted pelvis
Principle of management
l It is essential to differentiate insufficient power from obstructed labour. The former is managed with syntocinon
augmentation or instrumental delivery in the second stage, while caesarean section should be performed in
obstructed labour.
l Mismanagement of obstructed labour with syntocinon or instrumental delivery causes significant maternal (e.g.
uterine hyperstimulation, uterine rupture) and fetal complications (fetal distress, birth injuries)
l Mismanagement of insufficient power with caesarean section puts patients to unnecessary risk of operation.

Obstructed labour
Obstructed labour occurs when the the birth canal (pelvis) is relatively small for the presenting part (usually the fetal
head) to pass through. It is usually a 'relative' condition in a pair of normal woman and fetus, but can also be due to
an abnormally contracted pelvis or the presenting part is abnormally large such as hydrocephaly. Obstructed labour
presents with failure to progress, with cessation of cervical dilatation or descend of fetal head, and prominent caput
succedaneum and moulding. The station of fetal head may be high or even not engaged. The pelvis may appear
small on vaginal examination (see pelvimetry). Obstructed labour should be differentiated from insufficient power
when there is failure of progress. The treatment should be caesarean section.

Dystocia
From Greeks words dys means (bad) and os means opening. It is a vague term meaning some sorts of difficulty in
labour. Originally it was used to describe obstructed labour when there was disproportion between the size of the
presenting part and that of the birth canal, results in in failure of progress of labour. The causes of dystocia were
then classified as due to the passage (birth canal), the passenger (baby), or power (uterine contractions and
maternal effort):
Problems of Passage
l Abnormal shape and dimensions of pelvis resulting in obstruction of labour. The pelvis can be assessed with
pelvimetry.
Problems of Passenger
l Malpresentation such as breech presentation
l Malposition such as Occipito-posterior position
l Macrosomia
l Shoulder dystocia
l Abnormal size of presenting part such as hydrocephaly
Problem of Power
l Dysfunctional uterine contractions which can be:
n too irregular, or
n too infrequent, or

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 n incoordinate
n too weak (hypotonic)
l Inadequate maternal effort during second stage of labour which can be due to:
n Maternal exhaustion
n Effect of epidural analgesia
n Maternal paralysis due to pre-existing neurological diseases
n Incooperative patients
Implication
It is important to differentiate the underlying causes of dystocia. While problems with the passage and passenger
would result in obstructed labour that require caesarean delivery, dysfunctional uterine contractions are treated with
syntocinon augmentation, and inadequate maternal effort can be managed with instrumental delivery.

Shoulder dystocia
Definition
This is an obstetric emergency and is defined as difficult delivery of shoulders that (1) requires additional
manoeuvres besides usual downward traction and episiotomy, or (2) results in fetal birth asphyxia or trauma such as
fractures and neural plexus injuries.
Pathology
The pathology lies in the pelvic inlet. While the fetal head is delivered, one or both shoulders are struck above the
inlet. Usually, the anterior shoulder remains hooked behind the symphysis pubis and fails to rotate into a larger
pelvic diameter.
Incidence
The incidence is about 0.2%, and is more common in fetal macrosomia and maternal diabetes.
Risk Factors
Antepartum risk factors:
l maternal obesity >81kg: increase 8 fold
l maternal diabetes: increase >2 fold for same birth weight
l postterm: <40 week, 0.7%; .42 week 1.3%
l macrosomia: <4kg incidence 0.3%; >4kg 3-10%; >4.5kg >22%
Intrapartum risk factors:
l secondary arrest of labour
l instrumental delivery
Remark:
l 23% of shoulder dystocia do not exhibit any of the classical risk factors
Fetal complications
l birth asphyxia
l brachial plexus injury
n Erb's 6- 16%, usually transient and mild
n Klumpke's, phrenic palsy, rare but serious
l skeletal injury
n fracture of clavicle 15%, humerus 26%
l perinatal mortality
Maternal complications
l birth canal injury
l postpartum haemorrhage
Management
l Summon for help: experienced obstetricians, paediatrician, anesthetist
l prepare operation threatre
l perform special manoeuver to deliver the shoulders:
n McRobert's manoeuvre
n Wood's or Rubin's rotational manoeuvre
n Delivery of posterior arm
n Symphysectomy (rarely done)
n Zanvanelli's manoeuvre (rarely done)
l examine any maternal trauma and birth injury after delivery
l SHOULD NOT DO:
n excessive traction
n fundal pressure
n cleidotomy
Prevention
l Prevent macrosomia by good control of diabetes and induction of labour at 41 week before the babies are
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 getting too big
l Counsel for elective caesarean section in case of macrosomia
l Consider caesarean section instead of instrumental delivery in case of macrosomic baby undergoing a
prolonged second stage
l have experienced obstetricians to conduct the vaginal delivery in case of macrosomia
Discussion/Something to Consider
Why fundal pressure is contraindicated in case of shoulder dystocia?

Asynclitism
A sideway tilting of the head, so that the sagittal suture of the fetal skull does not lie midway between the maternal
sacral promontory and pubic symphysis. It is usually due to uneven pressure on the fetal head during its descent
through the pelvis. Asynclitism can occur before the head is engaged, or when the head is in the pelvic cavity.

Caput succedaneum
Fetal scalp edema resulted from obstructed venous return caused by pressure of the head against the rim of the
cervix during labour. While it is quite common during a normal labour, severe edema may signify an obstructed
labour. On vaginal examination, the edema also makes the fetal head felt at a lower station. However, the fetal head
is actually high in the birth canal, and difficulty may be encountered when instrumental delivery is wrongly
attempted.

Moulding
The alternation in shape and diameters of the fetal skull during labour. The fontanelles and sutures permit the force
of contractions to compress the head against the bony pelvis and adapt its shape to that of the birth canal. Moulding
is divided into 3 degrees:
First degree
l closure of the suture lines
Second degree
l reducible overlapping of the skull bones over suture lines
Third degree
l irreducible overlapping of the skull bones over suture lines
While moulding is a normal phenomenon during labour, severe moulding signify obstructed labour.

Deep transverse arrest

Definition
The fetal head is stuck in an occipito-lateral position, in the transverse diameter of the outlet, between the ischial
spines. Transverse arrest may also occur higher in the mid-cavity of the pelvis
Causes
l Deflexion of the fetal head
l Poor uterine contractions
l Inadequate channelling of the fetal head by the pelvic floor (as happens with a relaxed pelvic floor under
epidural)
l cephalopelvic disproportion

Incoordinate
Incoordinate uterine contraction
During normal labour, the contractions begin from the fundus, and progress downwards. Consequently, the baby is
pushed downwards towards the os. In incoordinate uterine contractions, ectopic contractions begin at sites other
than the fundus, so the fetus is not pushed towards the os despite strong contractions. Labour is therefore
prolonged. Incoordinate uterine contractions can usually be diagnosed when the cardiotocogram (CTG) is reviewed.
The contractions recorded are typically irregular in frequency, shape and amplitude. There are also overlapping of
the tracing of uterine contractions.

Trial of labour
It implies that the outcome of labour is uncertain because of mechanical difficulty, and that particularly vigilant
monitoring of progress and of fetal well-being are required.

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Uterine hyperstimulation
It is an iatrogenic complication due to the excessive use of oxytocics, resulting in too frequent or too strong uterine
contractions. The uteroplacental blood flow is jeopardised, resulting in fetal hypoxia and fetal distress. The
cardiotocogram typically shows frequent uterine contractions (>4 in 10 minutes) and recurrent fetal decelerations or
bradycardia. The other risk is uterine rupture.

Prevention
l carefully titrate the rate of infusion of syntocinon
l avoid using prostaglandins in multiparous women or when women already in labour
Treatment
l stop infusion of syntocinon immediately
l remove any undissolved prostaglandin pessaries from vagina
l deliver fetus immediately when there is fetal distress
l tocolytics to relax uterus may try in acute fetal distress

2. Intrapartum fetal monitoring

Intrapartum fetal monitoring

Aim of Intrapartum fetal monitoring
l To detect intrapartum fetal distress, or hypoxia on time so that perinatal mortality and permanent hypoxic insult
can be prevented.
Physiological changes in response to fetal hypoxia
l Fetal hypoxia triggers anaerobic glycolysis resulting in an accumulation of lactic and metabolic acidosis.
l Fetal PCO2 rises as a buffer effect, causing a respiratory acidosis.
l Normally the excess CO2 and lactic acids can be driven out from the fetus via the placenta, but this
mechanism may be affected by an underlying pathology.
l The effects of hypoxia depend on the fetal glycogen reserves. A growth-retarded fetus will therefore be affected
earlier and more severely than a well-nourished fetus.
l Blood pH falls as there is accumulation of CO2 and lactic acids.
l Fetal heart rate patterns change during hypoxia and acidosis, resulting in decelerations or bradycardia.
Methods of fetal monitoring
l Intermittent auscultation
n Record fetal heart rate using a Pinard stethoscope between contractions to obtain a baseline rate, and
during and immediately after contractions to detect accelerations or decelerations.
n Apply only to low-risk patients with no obstetric complications.
n More intensive monitoring should be used if any risk factors are present
l Continuous fetal heart monitoring
n Both fetal heart rate pattern and uterine activity are recorded using cardiotocogram.
n See fetal heart rate pattern for the interpretation of cardiotogram.
n This is a screening technique which facilitates the detection of fetal hypoxic stress. It is not often
diagnostic.
n Limitations of CTG are:
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 u High false-positive rate
u Even when the most ominous pattern is present only 50% of the babies have a low Apgar score at
birth.
u The use of continuous FHR monitoring should therefore be backed up by measurement of fetal
blood pH through fetal scalp blood sampling.
u Difficulty in interpretation during the second stage of labour, as brief profound decelerations are not
uncommon at that stage. Prolonged bradycardia however must not be ignored.
u Recording problems in cases of fetal arrhythmia
l Fetal Electrocardiogram (ECG)
n Fetal ECG can be detected with a fetal scalp electrode.
n The following adverse features have been suggested:
u T/QRS ratio > 0.25
u A negative T wave
u ST depression with T elevation
n Its main benefit is to provide reassurance in the presence of an abnormal CTG and perhaps reduce the
rate of unnecessary caesarean sections. It may also be helpful in case of fetal arrhythmias.
l Fetal scalp blood sampling
n FHR monitoring and scalp pH measurement are complementary
n The former without the latter increases the caesarean section rate unnecessarily because of
false-positive diagnoses
n A fetal scalp pH of 7 or less is strongly associated with a poor outcome
n A pH of 7.15 or less suggests the need to deliver
n A base deficit of > 9mmol/L is also abnormal

Intermittent auscultation
It is a basic method of intrapartum fetal monitoring that has been used for a long period of time before the
introduction of cardiotocogram. It is still being used in many centres. During labour, the fetal heart rate is listened
with Pinard stethoscope or a doppler apparatus (doptone) immediately after a contraction for 1 minute in a
15-minute interval. Any changes in fetal heart rate such as decelerations are examined. Intermittent auscultation has
often been compared with routine continuous fetal heart monitoring with cardiotocogram, which has become the
standard in many centres (including our unit). The former method is simple and requires no sophisticated machines
and equipments, and is less expensive. Its potential disadvantage is that it may not be as sensitive as
cardiotocogram in detecting fetal hypoxia. The latter has been shown to reduce the incidence of neonatal seizures.
However, it also has a high false-positive rate, leading to unnecessary intervention (high operative delivery rate).

Fetal scalp blood sampling

It is a method of intrapartum fetal monitoring. Blood from the fetal scalp is aspirated with amnioscope and the blood
pH, partial pressure of carbon dioxide (pCO2), base excess are analysed.
A fetal scalp pH of 7 or less is strongly associated with a poor outcome
A pH of 7.15 or less suggests the need to deliver
A base deficit of > 9mmol/L is also abnormal

Apgar score
What is Apgar score
A numerical scoring system for neonatal assessment usually applied at 1 and 5 minutes after birth to evaluate the
condition of the baby, based on heart rate, respiration, muscle tone, reflexes and colour:
Sign/Score 0 1 2
Heart rate per minute Absent <100 >100
Respiratory effort Absent Weak Strong
Muscle tone Limp Some flexion Well flexed
Reflex response None Weak Strong
Colour Blue or pale Body pink, extremities blue Pink
What is the use of Apgar score
Previously low Apgar score was thought to be predictive to neonatal outcome. A lower score implied birth asphyxia
and predicted the development of cerebral palsy and mental retardation in future. However, it is now clear that the
correlation between low Apgar score and low cord pH (which reflects fetal hypoxia) is very poor. There are many
causes of low Apgar score other than birth asphyxia, including neonatal depression by maternal transfer of narcotic
analgesic. The Apgar score is now mainly used as an indicator for the need of neonatal resuscitation.

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Birth asphyxia
Asphyxos in Greek means without pulse. Birth asphyxia is a poorly defined term. Originally it means depression at
birth, which is assessed by Apgar score. In the past, depression at birth was always assumed to be associated with
hypoxia and acidosis. However, it is now clear that depression at birth can be due to various causes, such as
congenital abnormalities, drugs or trauma. Therefore, it has been proposed that birth asphyxia should be defined
biochemically as the presence of hypoxia, hypercarbia and acidosis, by blood gas analysis using umbilical arterial
blood.

3. Operative delivery

Episiotomy
Definition and aim of episiotomy
It is a surgical incision of the perineum and vagina in order to prevent perineal tear during vaginal delivery.
Types of episiotomy
Posterolateral incision
l It is the most common method. The incision starts from the posterior forchette of vagina and then goes
postero-laterally, at 45 degrees from the midline. The main advantage is that it provides the best protection
against anal sphincter damage. However, it is more difficult to repair as the edges may retract unequally.
Median incision
l It is a midline incision from the posterior forchette downwards. It may cause anal sphincter damage, although it
is relatively easier to repair (provided that there is no anal tear).
J-shaped incision
l The incision starts from posterior forchette, initially in downward direction and then goes laterally. It is a
theoretical compromise of the above two.
Indications of episiotomy
l The usual practice in Hong Kong is routine episiotomy. All nulliparous and almost all primiparous women would
have an episiotomy at delivery. Selective episiotomy is advocated in many Western countries. It is argued that
episiotomy is not necessary in majority of pregnant women, and the incision may even result in more perineal
tear. The experience in Chinese favours a routine episiotomy.
l Episiotomy should be performed in instrumental delivery, delivery of macrosomic babies, vaginal breech
delivery, and delivery in occipito-posterior position.
l In the vaginal delivery of a premature fetus, episiotomy may be needed to protect the fetal head from being
forced repeatedly against an unyielding perineum.
Procedures of episiotomy repair
l Examine for any vaginal and cervical tear before repair.
l Apply adequate local anaesthetics (10ml of 1% ligocaine infitration).
l Repair with absorbable stitch such as 2-0 Dexon or Vircyl.
l Repair vaginal wound with continuous stitch.
l Repair perineal wound with interrupted stitches, followed by a superficial continuous subcuticular stitch.
l At the end of the repair:
n Perform digital vaginal examination to ensure an adequate vaginal opening.
n Perform digital rectal examination to exclude any suture penetrated through the anorectal mucosa.
n Remove any gauze packed inside the vagina.
Complications of improper episiotomy repair
l ano-vaginal fistula
l vaginal and vulval haematoma
l wound infection and dehiscence
l dyspareunia

Perineal tear
Classification
During childbirth, the perineum may be lacerated, and the severity of the trauma is classified as follows:
l First degree tear, when only skin and mucosa are involved.
l Second degree tear, when the muscles and the perineal body are involved.
l Third degree tear, when the anal sphincter or rectum is involved.
Complications
l postpartum haemorrhage
l anal sphincter damage resulting in faecal incontinence
l poor healing of the wound resulting in ano-vaginal fistula

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Loveset maneuver
A maneuver originally described to deliver the shoulder in a breech presentation. The principle is that the pelvic
canal is curved, so that its anterior wall (pubic symphysis) is much shorter than the posterior wall (the sacrum). It is
most likely therefore when the fetal part is obstructed anteriorly by the pubic symphysis, the posterior part is already
below the sacral promontory. Given that the baby is held firmly by pelvic tissue, a rotation of the baby will cause the
posterior part of the baby to come to the front, and as this is already below the inlet, the baby descends. In other
words, the pelvis acts like a screw, and any rotation of the baby will bring it lower.
The maneuver is very useful to deliver the shoulders of the baby after the breech is delivered. The principle is also
used when there is shoulder dystocia after cephalic delivery. Sometimes, if the baby can be rotated, the shoulder will
slip under the pelvic inlet and can be delivered.

Operative delivery
l Caesarean section
l Vacuum extraction
l Forceps delivery

Instrumental delivery
What is instrumental delivery
There are two types of instrument delivery:
l vacuum extraction
l forceps delivery
These allow the use of traction if delivery needs to be expedited in the second stage of labour
The overall instrumental delivery rate is around 15% in PWH
Level of instrumental delivery
outlet The fetal head is at or on the perineum
l Scalp is visible at the introitus without separating
the labia
l Fetal skull has reached the pelvic floor
l Sagittal suture is in anteroposterior diameter or
right or left occiput anterior or posterior position
l Rotation does not exceed 45
low-cavity The leading point of the fetal skull is at station >/= +2
cm, but not on the pelvic floor rotation <=45' (left or right
occiput anterior to occiput anterior, or left or right
occiput posterior to occiput posterior rotation > 45'
mid-cavity station < +2cm but the head is engaged
high-cavity not included in classification and any instrumental
delivery for level higher than mid-cavity should be
abandoned because of significant risk
What are the indications
Maternal indications
l maternal exhaustion
l avoid maternal pushing which may be dangerous to the mother, such as in the following situations:
n severe cardiac diseases
n hypertensive disorders
n liver cirrhosis with esophageal varices: risk of bleeding
Fetal indication
l fetal distress
Obstetrics indications
l prolonged second stage of labour
l vaginal breech delivery (use piper forceps only for after coming head)
Prerequisites for instrumental delivery
l fetal head must not be palpable abdominally
l fetal head must be at or below the level of the ischial spines
l cervix must be fully dilated
l position of the head must be known
l there must be adequate analgesia
l bladder should be empty
l procedure must be conducted by experienced operator

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

Forceps
What are Forceps
It is a pair of instrument designed for vaginal instrumental delivery. A forcep is divided into following parts:
l Handle
n is to produce a compression force on the impacted head and to facilitate traction
l Lock
n is where the pair articulate to each other. There are three types of lock: sliding (in Kielland's forcep),
crossover (in most of the forceps), and fixed pivot.
l Shank
n forceps with long shank is designed for delivery of fetal head at higher station (such as in mid and
low-cavity). Forceps with short shank (Wrigley's forceps) are used in outlet instrumentation. The longer
shank increases maternal discomfort and risk of soft tissue trauma.
l Blade
n consists of a cephalic curve which is ovoid in shape designed for a moulded fetal head, and a pelvic
curve to fit the maternal pelvis
l The axis of the blades and that of the handles can be parallel (in Kielland), or angled (in most of other forceps)
l The variation in the design of the different parts are made for use in different situation:
l Kielland's forceps are designed for rotation of head in mid to high-cavity instrumental delivery. Besides a long
shank, the pelvic curves are reduced to facilitate rotation inside the pelvic cavity. They have a sliding lock that
facilitates correction of asynclitism.
l Wrigley's forceps are used for outlet delivery, and have a short shank and handle
l Piper's forceps are designed for delivery of after-coming head in vaginal breech delivery. It has a long shank as
well as an angle between the axis of the blades and that of the shank.
Indications and prerequisites
see instrumental delivery

Anderson's forceps Fergusson's forceps

Complications
Fetal injury
l facial bruising
l facial nerve palsy
l depression fracture of fetal skull
Maternal injury
l perineal, vaginal and cervical tears
l postpartum haemorrhage Complication rate is higher with higher-cavity forceps delivery, and with malposition
of the forceps.

Vacuum extraction
What is vacuum extraction
It is a form of instrumental delivery and the instrument consists of the following parts:
l Cup: to be applied over the vertex area of the fetal head. It can be made of metal, or silastic material
l Vacuum pump: a electric pump to create a vacuum pressure
l Rubber tubing connecting the vacuum pump and the cup

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 vacuum cup vacuum tubing vacuum machine
Indications and prerequisites
see instrumental delivery
Complications
Fetal injury
l cephalhaematoma
l subaponeurotic haematoma
Maternal injury
l tear of lower genital tract
l postpartum haemorrhage

Caesarean section
What is Caesarean section (CS)
A surgical procedure that involves the delivery of the fetus through an abdominal incision. C-sections account for
about 20% of all births.
There are two types of CS
l Lower segment CS
n It is a transverse incision over the lower segment of the uterus
n It is the most common incision used nowadays
n Compared with classical incision, it is associated with less operative blood loss, more ease to repair, and
the scar is less likely to rupture (0.5%, see uterine rupture).
l Classical CS
n It is a midline longitudinal incision over the anterior wall starting from the fundus
n It allows larger space for delivery
n It is an old type of incision but is still used in modern obstetrics in some situations:
u in preterm delivery when lower segment has not been formed yet
u in placenta praevia where lower segment is covered with placenta and delivery may be difficult or
cause severe bleeding
u in transverse lie
u in delivery of conjoint twins
When is caesarean section needed
When vaginal delivery is not possible or at high risk because of mechanical factors:
l contracted pelvis
l cephalo-pelvic disproportion
l failure to progress of labour
l failed induction of labour
l failed instrumental delivery
l macrosomia
l Malpresentation such as:
n breech presentation, in particular footling breech
n transverse lie
l placenta praevia
When immediate or early delivery is required before cervix is fully dilated:
l fetal distress
l maternal distress or complications such as pre-eclampsia, eclampsia
l intrauterine infection
When the labour progress is associated with fetal or maternal risk
l IUGR fetus: may be in distress when undergoing the stress of labour
l previous uterine scar or injury
n risk of uterine rupture during labour
n high risk in classical scar, myomectomy scar and previous history of uterine tear
How is it performed
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Lower segment CS:
l Abdominal incision: usually Pfannenstiel incision is performed
l Dissection of urinary bladder to expose the lower segment of uterus
l Incision of the lower segment
l Delivery of the baby
l Delivery of the placenta
l Repair of the lower segment, usually in two layers
l haemostasis
l Closure of the abdominal wall(parietal peritoneum, rectus sheath, skin). Usually a rediac drain is inserted into
the subrectus space to prevent haematoma formation
What are the complications
Maternal complications:
l excessive bleeding
l infection: endometritis, wound infection
l uterine injury: uterine tear
l visceral injury: most common: bladder
l complications related to anaesthesia
l deep vein thrombosis and thromboembolism
l The maternal death rate is three times higher than with natural delivery

Retained placenta
It is a condition in which the whole placenta or part of it is retained inside the uterine cavity after the delivery of the
baby. It may be due to morbid adherence of placenta to the myometrium. Complications include:
l Postpartum haemorrhage
l Uterine inversion when excessive cord traction is attempted to deliver the placenta
It is managed by manual removal of placenta (MROP).

Morbid adherence of placenta

Definition
l It is an implantational disorder in which the placental villi reach the myometrium lacking a normal decidual layer
in between.
l It is classified into:
n Placenta acreta
u the placenta reaches the myometrium.
n Placenta increta
u the placenta invades the myometrium.
n Placenta percreta
u the placenta reaches the serosa of the uterus and may even perforate it.
Incidence
l About 1 in 7000 deliveries
Causes
l The deficiency of the decidual layer is usually a consequence of previous multiple or excessive uterine
curettage, previous endometritis or uterine scarring. Rarely pregnancy may follow an incomplete endometrial
ablation, and the placenta is at high risk of morbid adherence.
Complications
l Placenta praevia
n 50% cases of morbid adherence of placenta also have placenta praevia, due to deficiency of decidua in
the lower segment following repeated caesarean section.
l Retained placenta
l Uterine inversion
n as a result of excessive traction to deliver the adherent placenta.
l Postpartum haemorrhage
n as a result of retained placenta, uterine inversion and uterine atony.
l Uterine perforation
n rarely occurs in case of percreta
Clinical presentation
l As above
Management
l Resuscitation for postpartum haemorrhage
l If the patient wants to preserve uterus for fertility, attempt manual removal of placenta (MROP), otherwise
l Hysterectomy
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Controlled cord traction
The standard technique to deliver the placenta in order to shorten the third stage of labour and reduce postpartum
haemorrhage, with precaution to avoid uterine inversion:
l Place the left hand on the uterus to feel for any contraction.
l Once a contraction has occurred, move the left hand suprapubically to elevate the fundus with the palm facing
towards the mother.
l At the same time, the right hand grasps the cord and exert steady traction so that the placenta separate and is
delivered gently. Care should be taken to peel off all the membranes, usually with a twisting motion.
l It is of crucial importance that controlled cord traction is not performed in the absence of a ut erine contraction;
otherwise uterine inversion may occur.
l After the placenta is delivered, it should be inspected for missing cotyledons or succenturiate lobe.

Manual removal of placenta

Definition
It is a operation in which the operator inserts his/her hands into the uterine cavity, identifies the placental site,
separates the placenta from the uterine wall and removes it.
Indications
Retained placenta (partial or complete)
Procedure
l It is performed under general or regional anaesthesia, with antibiotic cover
l The cervical os is dilated gradually to admit the whole fist
l The forearm of the operator is inserted into the uterine cavity
l The placenta is separated and removed
l The uterine cavity is checked empty
Complications
l Introduction of infection into the uterine cavity
l Perforation of the uterus by the operator's hands
l Postpartum haemorrhage

4. Pain relief and maternal monitoring

Labour pain relief

Entonox
Narcotic analgesia
Epidural analgesia (see epidural anaesthesia)

Obstetric anaesthesia
Types of anaesthesia
l General anaesthesia
l Regional anaesethesia
n Spinal anaesethesia
n Epidural anaesethesia
l Local anaesethesia
n Pudendal nerve block
n Local infiltration

Entonox
Entonox is a gas mixture of oxygen and nitrous oxide with 50% each. It is a inhalational analgesic commonly used
for labour pain relief. It can be self-administered, is fasting acting, and has minimal maternal and fetal side effects.
The efficacy is variable.
In order to get maximal analgesic effect, patients should be instructed to inhale when uterus is starting to contract,
and continue inhalation until the contraction begins to subside. Side effects are hypocarpia, dizziness, tetany and
fetal hypoxia after prolonged use.

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Narcotic analgesia
The most commonly used narcotic analgesic is pethidine. It is often used for labour pain relief, and post-operative
analgesia. It can be administered intramuscularly or intravenously. The former route is contraindicated in patients
with clotting disorders or thrombocytopenia. The intravenous route can be used for patient-control-analgesia.
For labour pain relief, its efficacy is variable with 50% reported good analgesic effect. The maternal side effects are
vomiting and drowsiness. The major fetal risk is neonatal respiratory depression which is readily reversible with
naloxone.

Epidural anaesthesia
Contraindications
l Bleeding disorder, thrombocytopenia or on anticoagulants
l Infection in area of epidural injection
The Pros of Epidural:
l Excellent labor pain relief
l Allows time for rest
l Reduces hyperventilation and serum catecholamines
l Great for PIH (pregnancy induced hypertension)
l Great for Caesarean sections
The Cons: (possible spin-off problems)
Mild
l headache after accidental dural puncture (1/100)
l backache
l postpartum urinary retention
l fever
l May hamper 'push-ability' and increase need for vacuum/forceps extraction for prolonged second stage
Major
l Hypotension (requires IV fluids)

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General Gynaecology

Gynaecology
Gynae means women. Gynaecology is a branch of medicine dealing with the diagnosis and treatment of disorders
affecting the female reproductive organs. It is subdivided into:
l General gynaecology
l Gynae-oncology
l Reproductive medicine and Endocrinology
l Urogynaecology
General gynaecology
l Menstrual disorders
l Early pregnancy complications
l Benign ovarian tumours and endometriosis
l Benign uterine growth such as fibroid and adenomyosis
l Birth control (contraception and sterilisation)

1. Benign gynaecological tumours

Benign ovarian tumour

Introduction
It is a heterogeneous group of benign ovarian pathologies that is very common in women in reproductive age.
They are classified as below:
l Physiological cysts: follicular cyst and corpus luteal cyst
l Endometriotic cysts (see endometriosis)
l Epithelial neoplasms (cystadenoma)
l Germ cell neoplasms: benign teratoma (or dermoid cyst)
They usually have similar clinical features. The majority of them are small in size (less than 5cm in diameter). The
patients are usually asymptomatic, or present with non-specific abdominal discomfort, and the tumours are picked
up incidentally with ultrasound. Sometimes the tumours may enlarge resulting in abdominal distension, and pressure
or space occupying effect. Some patients may present with acute complications such as rupture, haemorrhage and
torsion. Endometriotic cysts may associate with dysmenorrhea and dyspareunia.
As their clinical features are quite similar, they are usually differentiated by ultrasound, which also help to distinguish
them from malignant ovarian tumours.

Ovarian cystadenoma
l The two most common types are serous cystadenoma and mucinous cystadenoma
l The former tends to be unilateral and unicystic, while the later is more likely to be bilateral and multicystic.
Sometimes they can be very large with diameter more than 10cm
l USG features are similar with thin wall and clear content. They are different from their malignant counterparts
as they do not have solid element or papillary growth, and there is no ascites.
l Treatment is cystectomy or oophorectomy, by laparoscopy or laparotomy method.

Fibroid
Definition
l fibre: connective tissue; oid: like
l it is actually a benign smooth muscle tumour (leiomyoma) of uterus
Incidence
20% of women in reproductive age
Pathology
Sites:
l intramural
n most common site
l submucosal
n 5% of all fibroids
n most commonly cause symptoms
l subserosal
n pedunculated may sometimes undergo torsion
l cervical
n uncommon but can cause urinary problems such as urinary retention and ureteric obstruction, and
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 n surgical difficulty because of close proximity to ureters and accessibility
l within broad ligament
n extremely rare but can cause diagnostic and surgical difficulties
Histology:
l benign smooth muscle fibres
l no true capsule
l various degenerative changes:
n hyaline degeneration
n calcification
n fatty changes
Remark:
l Growth is hormone dependent
l Sarcomatous change is rare (0.1%)
Clinical presentation
l Clinical presentation depends on sites and size of fibroids
l 50% of women are asymptomatic
Menorrhagia
l menorrhagia is more common with submucosal and intramural fibroids
l mechanism:
n increases total surface area of the uterine cavity
n disordered uterine motility
n ulceration and haemorrhage overlying submucosal fibroids
n disordered prostaglandin synthesis
Pressure symptoms
l abdominal distension and discomfort, especially with rapid growing fibroids
l symptoms of urinary retention, especially with cervical fibroids
Pain
l uterine camping: attempted expulsion of submucosal fibroids
l acute torsion of pedunculated fibroids
l red degeneration (usually during pregnancy)
Subfertility
l an uncommon presentation
l accounts only 3% of all infertile women
l possible mechanisms:
n mechanical cornual occlusion
n distortion of uterine cavity resulting in failure of implantation
n alternation of local blood flow
Sarcomatous change
l very rare: 0.1%
Specific complications during pregnancy
l Red degeneration of fibroid
n presents as acute localised uterine pain, usually in the second or third trimester
n occasionally there is fever and leucocytosis
n treatment is conservative with adequate anaglesia
l Malpresentation
n occurs when a large fibroid occupying the cervical or lower pole of the uterus
Diagnosis
Diagnosis is usually obvious on physical examination
l enlarged uterus, usually of irregular shape
l submucosal fibroid protruding out from cervix
Ultrasound
l is usually not required unless clinical examination is not definite
l identifies the sites and number of fibroids that may help to plan of management
Management
Principle
l choice of treatment depends on degree of symptoms, desire to preserve fertility, and site and size of fibroids
l Choices include:
l expectant management
l Medical treatment
n only for temporary symptomatic relief, during waiting for surgery, and correction of anaemia
n symptoms usually return and fibroid regrow after stopping medication
l Myomectomy
n only for symptomatic women who want to preserve fertility
n can be performed via laparotomy, laparoscopy, or hysteroscopy, depends on the site of fibroids

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 n recurrence of fibroids and symptoms: 15%
n 10% require re-operation
n risk of unplanned hysterectomy (for large intramural fibroids) because of uncontrolled bleeding
n post-operative pelvic adhesions that may affect tubal patency, if posterior uterine wall is cut
l Hysterectomy
n definite treatment for symptomatic women who do not want to preserve fertility

A hysterectomy of a huge uterus with multiple fibroids

Discussion/Something to Consider
A 30 year-old single woman is referred to you because of incidental finding of a 3cm diameter intramural fibroid on
routine check-up. How would you manage her?

Adenomyosis
Definition
l The presence of tissue resembling endometrial glands and stroma within the myometrium of the uterus
Pathology
Macroscopic
l Grossly enlargement of uterus, usually globally
l Spongy appearance with no cleavage plane
Microscopic
l Endometrial glands and stroma embedded in the myometrium
l Focally or uniformly
Clinical features
History
l Menorrhagia
l Secondary dysmenorrhea
l Deep dyspareunia
l May be asymptomatic
Examination
l Enlarged uterus
l Tender uterus, especially during perimenstrual period
Diagnosis
Can only be confirmed by histology
l Ultrasound to rule out fibroids
l Endometrial biopsy to rule out other causes of menorrhagia
Treatment
l Hysterectomy if symptomatic
Discussion/Something to Consider
What are the similarities and differences between the clinical presentation and management of adenomyosis and
that of fibroid?

Dermoid cyst
l It is a benign teratoma which consists of mainly skin tissue, with sebaceous material and hair, and is the
reason for its name. Sometimes it may contain teeth or bone tissues. Rarely, active thyroid tissue (stromal
ovarii) may be present.
l It is one of the commonest benign ovarian tumours occurring in in reproductive age
l It is often bilateral (10%), with size ranged from a few centimetres to up to 10 cm.
l It is very mobile and therefore commonly presents with torsion.

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l Patients usually present with on and off colicky lower abdominal pain signifying a process of intermittent torsion.
They then suddenly experience acute colicky abdominal pain that changes to constant sharp pain, signifying
an acute torsion with ischemic necrosis and peritoneal inflammation. On physical examination, peritoneal signs
with pelvic mass and tenderness can be found.
l Under USG, a dermoid cyst is well-circumscribed with homogenous content. A hyperechogenic shadow
signifies a bone or a tooth.
l The treatment is cystectomy or oophorectomy which can be done under laparoscopy or laparotomy.

Teratoma
Ovarian teratoma is one of the commonest germ cell tumours. It develops from a totipotential germ cell (a primary
oocyte) of the ovary, and therefore can give rise to all kinds of cells and tissues. The commonest tissue types are
skin with hair follicles and sebaceous glands, bone, teeth, and neural tissues. Depending on the maturity of the
neural component, teratoma is divided into mature (benign) and immature (malignant) type.
Mature teratoma
The tissues of a mature teratoma are well differentiated. It is also often called dermoid cyst as it contains skin tissue,
hair and sebaceous material.
Uncommonly a benign tetratoma may contain functional thyroid gland tissue (stromal ovarii) that secrets thyroxine,
resulting in hyperthyroidism.
Imature teratoma
2% of teratoma consist of immature or undifferentiated tissue, and is called immature teratoma, or malignant
teratoma. As in other germ cell tumours, the treatment of malignant teratoma is surgery followed by chemotherapy.
Unilateral oophorectomy is adequate provided that the other ovary is not involved. Fertility can be preserved.
Hysterectomy and bilateral oophorectomy is suggested if patients have completed family.

2. Birth control

Contraception
Methods of contraception
Natural methods
l Periodic abstinence (rhythm or calendar method): it means the avoidance of intercourse during the fertile
period of the cycle.
l There are different methods to predict the fertile period, such as calendar method, mucus method or by basal
body temperature
Coitus interruptus
l It means the withdrawal of the penis in time, before ejaculation, ensuring that all sperms are deposited outside
the vagina. However, there are few sperms in the pre-ejaculate
l The failure rate is high (Pearl index = 10/100 women yr), mainly due to conscious rule breaking
Barrier methods
l The method failure rate is low (4%) but the user failure rate is high (Pearl index = 10/100 women yr), mainly
due to inconsistent or improper use. It is sometimes used together with spermaticides to increase the
effectiveness.
l Male condom
l Female condom
l Diaphragm
Hormonal methods
l combined oral contraceptives (COC)
l progestogen-only pills (mini pills)
l progestogen injectable
Intrauterine contraceptive devices (IUCD)
l non-medicated IUCD
l copper-containing IUCD
l hormone-containing IUCD
Factors in choosing different kinds of contraception
Failure rate:
l can be due to method failure and user failure
l assessed in term of Pearl index or life table analysis
Reversibility:
l how fast and how effective of recovery of fertility after stopping use of the contraceptive method
Side effects:
l sexual satisfaction
l menstrual disturbance
Non-contraceptive benefits:
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l COC can also treat dysmenorrhea and menorrhagia
l Condoms can also prevent sexually transmitted diseases
Patient's past medical history:
l COC is contraindicated in case of history of thromboembolism
Patient's acceptability and compliance
l progestogen injectable requiring 4 injections a year while COC has to be taken every day.
Postcoital contraception
see postcoital contraception

Pearl index
l It is a measurement of the effectiveness of a method of contraception
l It is defined as number of failure per 100 women years of exposure
l The denominator is the total months (or menstrual cycles) exposed from onset of method until completion of
study or an unintended pregnancy, or discontinuation of the method by the users. The nominator is the number
of unintended pregnancy.

Calendar method
It is a way of contraception by means of periodic abstinence from coitus. It is based on the fact that the viability of
sperms in female reproductive tract is about 2 to 7 days, and the lifespan of an ovum is only 1 day. Therefore, the
fertile period starts from 7 days before ovulation, and ends 1 day after ovulation. In a normal regular 28-day cycle
(ovulation at day 14), the fertile period starts at day 7 and ends at day 15. If there is a variation of menstrual cycle
length in a woman, then the beginning of the fertile period should be calculated by subtracting 21 (14+7) days from
the length of the shortest cycle. and the end should be calculated by subtracting 13 (14-1) days from the longest
cycle. Couples are advised to avoid coitus within the estimated fertile period.
This method has a high failure rate (Pearl index 40 per 100 women year). It is not suitable for women with irregular
cycles, need of frequent sex, and forgettable women.

Condom
Male condom
It is a latex (rubber) sleeve that fits snugly over the penis for contraception. It is also effective against sexually
transmitted diseases such as AIDS, hepatitis and chlamydia. It is the most popular contraceptive method in Hong
Kong. The advantages are:
l Cheap
l Widely available
l Highly effective if used consistently and correctly
l Free from medical risks
l No medical supervision needed
l Protection against sexually transmitted diseases
l Possible protection against cervical neoplasia
Female condom

It is not popular in Hong Kong because:

l Low patients' acceptance due to the need of handling her own genitalia
l Need fitting by trained personnel and training in use
l Less effective than other female contraception like hormonal methods or IUCD

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Combined oral contraceptives
Nature
l pills consist of combination of synthetic estrogen and progestogen, taken for 21 days per cycle:
Synthetic estrogen
l the only synthetic estrogen used is ethinyloestradiol, with dose ranging from:
n 20-30 mcg (low dose; e.g. Nordette): most commonly used
n 50 mcg (median dose; e.g. Duoluton)
n 75-100 mcg (high dose): seldom used now because of side effects
Synthetic progestogen
l 3 generations of synthetic progestogen including:
n 1st generation: norethisterone 5mg: low potency, seldom used now
n 2nd generation: levonorgestrel 150-250 mcg:
n 3rd generation: desogestrel 150 mcg; gestodene, highly specific progestogenic effect. Advantage: less
androgenic and so less adverse effect on serum lipids; Disadvantage: is shown in some studies to be
associated with a higher risk of non-fatal venous thromboembolic disease
Types of COC
With or without placebo
Everyday COC:
l each package consists of 21 pills of COC and 7 pills of placebo
l advantage of reduction in risk that user will forget to restart her next packet on time- a potent cause of pill
failure
Non-everyday COC
l each package consists of 21 pills of COC without placebo
l With or without phasic changes of hormones content
Monophasic
l every pill of COC consists of same amount of estrogen and progestogen
Biphasic or triphasic
l pills consist of different amount of estrogen and progestogen in different phase of the cycle
l designed to minimize the dose of progestogen and hence its side effect
l the clinical benefits are modest and are replaced by monophasic COC with 3rd generation of progestogen The
picture shows a package of triphasic COC (with pills of three different colors)
Mode of action
l The primary mode of action is the inhibition of ovulation due to negative feedback of estrogen on the
hypothalamo-pituitary-ovarian axis
l The secondary effect is the progestogen effect on cervical mucus and endometrium
Prinicple of prescribing COC
Assessment before prescription
l rule out any contraindications by history and examination(see below)
When to start:
l best time on day 1 of menstrual cycle
l immediate after abortion or termination of pregnancy
l post-coitus or emergency contraception
How to take the pills:
l See Seven-day rule
l Advise patient to take the pill every day at the same time
l Advise patient to consult doctors if no withdrawal bleeding during pill-free period
Efficacy
l median dose COC: Pearl index: <1/100 women yr
l low dose COC: Pearl index: 3/100 women yr
Non-contraceptive benefits of COC
l Control of dysmenorrhea and menorrhagia and regulate cycles
l Reduced risk of endometrial carcinoma and ovarian cancer by at least 50%
l Reduced risk of pelvic inflammatory disease, ectopic pregnancy, fibroid and benign breast diseases
Side effects
Cardiovascular
l Venous thrombosis
n high dose COC: relative risk >2
n low dose COC: relative risk <2
l Thrombotic stroke
n fatal: 2-4/10000 women yr
n non-fatal: 1/10000 women yr

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l Haemorrhagic stroke
n relative risk of 1.5-2
n higher risk with smoking and hypertension
l Hypertension
n relative risk of 2
n reversible by stopping COC
l Myocardial infarction
n relative risk of 3-5
Metabolic effects
l increase LDL to HDL ratio, and insulin resistance
l effects are modest with low dose COC and are not clinically significant
Minor side effects
l breast tenderness, nausea, vomiting, weight gain and mood changes
l uncommon with low dose COC
Cancer of breast
l it is still controversial whether COC increases risk of CA breast
Absolute contraindications of COC
l Present and past history of circulatory diseases such as arterial and venous thrombosis, ischemic heart
disease, strokes, valvular heart diseases, known abnormalities of coagulation, hyperlipidemia
l Liver diseases
l Undiagnosed genital tract bleeding
l Estrogen-dependent neoplasm
l Pregnancy
l SLE
l smoker at age > 35 yr

Seven-day rule
It is an easily remembered rule to guide the prescription of combined oral contraceptives:
l ovulation is successfully suppressed after taking COC for 7 days continuously
l up to seven pills can be omitted without ovulation, as indeed is regularly the case in the pill-free week
l more than seven pills missed in total risks ovulation

Progestogen-only pill
Nature
l also called mini-pill
l consist of daily low dose synthetic progestogen, e.g.:
n norethisterone 350 microgram
n levonorgestrel 30 microgram
Mode of action
l the main action is to antagonize the endogenous estrogenic effect on cervical mucus, making it hostile and
impermeable to sperms
l disordered luteal phase in 40 to 50% of cycles
Efficacy
l Pearl index of 3/100
l Increased efficacy when combined with breastfeeding
Side effects
l irregular menstrual cycles, unpredictable bleeding, amenorrhea and spotting
Advantages
l no increased risk of ectopic pregnancy
l no metabolic effects
l no coagulation effects
Use in special groups
l lactating women
l age> 40
l smoker, history of thomboembolism

Progestogen injectable
It is one form of contraception consisting of progestogen (e.g. depomedroxyprogesterone acetate 150mg) given
intramuscularly every 12 weeks. It acts by inhibiting the ovulation.

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The advantages are:
l Highly effective (Pearl index= 1/100)
l Highly convenient
l Low reliance on compliance, need only 4 injections per year
l Reversible though with some delay in fertility
Side effects:
l Menstrual disturbance (After one year use, 40% of user a amenorrhea, 40% scanty infrequent period, 20%
prolonged irregular bleeding)
l Weight gain
l Delay in resumption of fertility
l Possible reduction in bone mineral density osteoporosis in users with long term amenorrhea

IUCD
Types of intrauterine contraceptive device (IUCD)
Non-medicated IUCD
l rarely used now, except in China
l usually a metalic ring The USG film shows a ring IUCD inside the uterine cavity
Copper-containing IUCD
l different preparation has different copper content
l latest designs are smaller with higher copper content, with silver too
l need to change every 5 to 7 years as the effect of copper declines with time

Progestogen-containing IUCD
l need to change every 5 to 7 years as the effect of progestogen declines with time
Mode of action
Induce foreign body reaction which is hostile to gametes and embryo, and affect implantation
Copper ions affect tubal fluid, sperm transport and oocytes, and induce metabolic changes of endometrium
Progestogen make cervical mucus hostile and endometrium thin
Efficacy
Pearl index of less than 1/100 woman year for latest IUCD
Time of insertion
Intermenstrual
l From the end of menstruation through until mid cycle
l The best time is towards the end of menstruation as it is certain that patient is not pregnant, and insertion is
easier due to natural dilatation of cervix at menstruation
l However, fitting can take place at any point in the cycle if necessary
Post-termination of pregnancy or miscarriage
l risk is minimal after first trimester termination or abortion, but
l risk of expulsion is higher in second trimester
Post-delivery
l high expulsion rate during the first week of puerperium
l best time is 3 to 4 week after delivery
Post-coitus
l as emergency contraception
l should be within 5 days post-coitus
Method of insertion

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l aims to achieve correct fundal placement allowing the IUCD to open to its pre-insertion shape, with minimal
pain and discomfort
l careful explanation of procedure to patient
l careful bimanual pelvic examination of uterus with sounding of the cavity to determine its length and direction,
and rule out acute genital infection
l aseptic and careful technique to ensure fundal placement
l leave the thread of IUCD outside the cervix
l ask patient to check IUCD regularly and report if IUCD is expulsed
Removal of IUCD
l During the menstrual period or any time if the woman had no unprotected coitus in the past 5 days
Side effects of IUCD
l Abnormal vaginal bleeding and pelvic pain:
l Expulsion: may be unnoticed and result in contraceptive failure
l Ectopic pregnancy: the overall incidence of ectopic is decreased, but when pregnancy occurs, the likelihood of
ectopic is higher
l Pelvic inflammatory disease
l Actinomycosis
l Uterine perforation
Non-contraceptive benefits of IUCD
l control of menorrhagia with latest progestogen-containing IUCD
Contraindications of IUCD
l Pregnancy
l Uterine deformity such as fibroid and congenital malformations
l Endometrial pathology under investigation
l High risk of pelvic inflammatory diseases and ectopic pregnancy
n past history of sexually transmitted diseases, pelvic inflammatory diseases or ectopic pregnancy
n Multiple sexual partners
l Wilson's disease (for copper-IUCD)
Discussion/Something to Consider
When a patient ask for removal of IUCD, what is your assessment and when and how do you remove it?

Levonorgestrel intra-uterine system

Intrauterine contraceptive device containing levonorgestrel
Contraception
l Not recommended as an emergency contraception.
Areas of use
l Decrease menstrual flow
l Treat endometrial hyperplasia
l Protect uterus from endometrial carcinoma because of unopposed estrogen in hormone replacement therapy
Other Information
l Localized effect to render endometrium atrophic
l Minimal systemic side effects
l Irregular vaginal spotting in initial three months of use

Emergency contraception
Definition
A contraceptive method to prevent conception after an unprotected coitus. There are 2 types of emergency
contraception:
l Hormonal
l IUCD
Hormonal therapy
Should be given within 72 hours after an unprotected coitus
Yuzpe regimen:
l Ethinylestradiol 100 microgram + Levonorgestrel 0.5 mg for 2 doses 12 hours apart
l Side effects are nausea (50%), vomiting (20%) because of the high dose estrogen
Levonorgestrel only regimen:
l 0.75 mg for 2 doses 12 hours apart
l less side effects than the Yuzpe regimen
Copper-containing IUCD

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Should be given within 5 days after an unprotected coitus
Can be removed after menstruation returns in the next cycle, or be kept as a long-term contraception.

Postcoital contraception
What is postcoital contraception
It is also called emergency contraception, and is a female contraceptive method administered as soon as possible
after an unprotected intercourse, in order to prevent implantation.
Methods
Yuzpe (hormonal) method
l It is also called 'morning after pill'.
l It should be commenced within 72 hours of a single unprotected intercourse.
l Regime: 100mcg ethinylestradiol and 500mcg levonorgesterol (2 tablets of median dose COC) every 12 hours
for 2 doses
l The precise mechanism of post-coital contraception is uncertain. It may act by blocking the implantation.
l Failure rates vary between 1-5%, depending on the exposure time of the menstrual cycle.
l Risks: same as COC
Insertion of a copper-bearing IUCD
l It should be inserted not more than 5 days from the most probable calculated date of ovulation, even if there
have been several acts of unprotected intercourse.
l It acts mainly by blocking the implantation.
l Failure rate is very low, 1-2 failures/1000cycles
l Risks: same as IUCD

Sterilisation
It is a long term irreversible contraception by which the fallopian tubes are excised or ligated (female sterilisation), or
the vas deferens are excised (vasectomy in male sterilisation)
Female sterilisation
Methods
l Route: Via laparotomy (e.g. in the same session of Caesarean section), mini-laparotomy or laparoscopy
l Method: By ligation, Falope rings or clips
l Time: In the post-partum period or interval period
Assessment before the decision
l Age of patients
l Number, ages and health of her children
l Previous and current contraception, in particular any problems with them
l Reason for the request of sterilization
l Stability of marriage
l Gynaecological, obstetric & medical history
Counseling after the assessment
l Irreversibility
l Regret rate
l Failure rate (1%)
l Risk of ectopic pregnancy if failure
l Operative procedure and risks, such as bleeding, infection and visceral injury
l Alternative contraceptive methods including male sterilisation
Male sterilisation
See vasectomy.

Vasectomy
It is the excision of a small piece of the vas deferens and is a kind of male sterilisation. It is performed under local
anaesthesia on an out-patient basis. Since sperm are produced 72 days prior to ejaculation and stored in the
proximal collecting ducts, a vasectomy is not immediately effective. Azoospermia should be confirmed with semen
analysis before a couple relies on a vasectomy for contraception. The failure rate is 0.15%. Complications are
uncommon, including bleeding, infection and haematoma. Sometimes the patients may develop anti-sperm
antibodies following the operation, and this accounts for the male infertility even after anastomosis of the vas
deferens.

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3. Conplications of early pregnancy

Viable
Viability means 'the ability to survive'. Fetuses with maturity at or more than 24 weeks are regarded as potentially
viable, and therefore maturity of 24 weeks gestation is set as the cut off of abortion. However, the term 'viable fetus'
is also commonly misused when patients present with threatened abortion, to describe a life fetus, while 'non-viable'
is used for missed abortion.

Termination of pregnancy
What is termination of pregnancy
It is also called induced abortion, is a procedure to discontinue a life pregnancy by evacuation of the uterus before
24 weeks of gestation. It should only be performed under the Abortion Act, and patients should be counselled
properly before the procedure.
Abortion Act (1967)
Abortion can be performed if 2 registered medical practitioners agree that the pregnancy should be terminated on
the one or more of the following grounds:
l Risks of continuance of pregnancy to the life of the pregnant woman are greater than that of termination of
pregnancy
l Risks of continuance of pregnancy to the physical or mental health of the pregnant woman or her existing
children are greater than that of termination of pregnancy AND the pregnancy is less than 24 weeks
l There is a substantial risk that if the child were born it would be seriously handicapped
Pre-abortion counselling
Decision making:
l Why is the pregnancy unwanted?
l Whether the woman is absolutely certain about her decision?
l Has the woman think about the other options like continuing the pregnancy and adoption?
Methods and risks of abortion
Future contraceptive plans
Methods of abortion
The choice of the method of termination depends on gestational age:
Early first trimester (up to 9 weeks)
l Medical: anti-progesterone mifepristone (but it is not licensed in Hong Kong)
l Surgical: vacuum (or suction) evacuation of uterus
Late first trimester (9 -14 weeks)
l Surgical: vacuum evacuation of uterus
l may need cervical priming by prostaglandin analogue to reduce the risk of haemorrhage and genital tract
trauma
Mid-trimester
l Medical:
n first line treatment at this gestation
n by vaginal gemeprost (a prostaglandin analogue)
l Surgical: by dilatation and evacuation
n High risk of haemorrhage, uterine perforation and incomplete evacuation
n Need expertise
Complications of termination of pregnancy
l Haemorrhage
l Post-abortion infection
l Uterine perforation
l Cervical trauma
l Failed abortion
l Psychological sequalae
Follow up
l Exclude complications like infection or incomplete abortion or even failed abortion
l Advise contraception and emphasize the importance of compliance

Early pregnancy complications

A group of disorders commonly occurs during the first trimester of pregnancy, including:
l threatened and true abortions
l ectopic pregnancy

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l gestational trophoblastic diseases
l hyperemesis gravidarum

Abortion
Definition of abortion
l In Hong Kong and the United Kingdom, abortion is defined as a pregnancy loss occurring before 24 completed
weeks of gestation.
l The WHO definition is 'the loss of a fetus or embryo weighing 500g or less which corresponds to a gestation
age of 20 to 22 weeks, the irreducible age for fetal well-being'.
Threatened abortion
l A very common condition (15%) in early pregnancy, presents with painless vaginal bleeding. The cervical os is
closed and the intrauterine pregnancy is viable.
Missed abortion
l A spontaneous abortion in which the embryo dies but the gestational sac is retained in the uterus, and there is
no symptom such as vaginal bleeding or abdominal pain. Therefore, the abortion is 'missed' by the patient.
However, features of pregnancy such as nausea, vomiting and breast bloating subside. On examination, the
uterus is small for date and fetal pulsation is absent. Evacuation of products of gestation is required (see
evacuation of uterus below).
Blighted ovum / anembryonic pregnancy
l They are both misnomers of missed abortion, with no fetal pole found in an empty gestational sac on
ultrasound scan.
Complete abortion
l A complete abortion is one in which all the products of conception have been expelled. Pain and bleeding
usually subside. The cervix closes again. The uterus is smaller for date. Transvaginal ultrasound scan is
2
usually done to confi rm that the uterus is empty. An intrauterine heteroechogenic dimension of less than 5cm
in both transverse and sagittal planes is considered as complete abortion. No further treatment is generally
needed.
Incomplete abortion
l Only part of the products of gestation has been passed. There may be considerable pain and bleeding. The
cervix is dilated. Evacuation of products of gestation is required (see evacuation of uterus below).
Inevitable abortion
l The products of gestation has not been passed out yet, but there is increasing contraction pain and vaginal
bleeding, and the cervical os is dilating. The products of gestation may sometimes be felt through the open
internal os.
Remark
l The above terms were defined clinically in the old days when ultrasound (USG) was not in use. The use of
these terms has changed slightly with the introduction of USG. For example, the diagnosis of missed abortion
is now commonly referred to pregnant women present with vaginal bleeding and has identified a 'non-viable'
fetus. Complete abortion is diagnosed according to ultrasound finding as described above.
Septic abortion
l Septic abortion is an infected abortion. It is associated with high maternal morbidity and mortality when
treatment is delayed. It is often due to illegal abortion under unsterilized condition.
Recurrent abortion
l Also called habitual abortion, recurrent abortion is defined as three or more consecutive losses of pregnancy.
The incidence is 1% which is higher than when it occurs by chance. Therefore investigations for the underlying
cause are needed.
Management of abortion
Principles
l Rule out other causes of vaginal bleeding or pain complicating early pregnancy such as ectopic pregnancy
l Confirm fetal viability (see viable) with USG
l Counselling and evacuation of uterus when required
l The diagnosis and management is often easy nowadays with USG, but history and examination are still
essential, particularly when the USG finding is inconclusive
Counselling
l Explain the cause of abortion, the chance of abortion and successful pregnancy next time
l Investigate further in case of recurrent abortion, or second trimester abortion
Evacuation of uterus
l Owing to the advances in ultrasound and medicine, treatment of abortion has been changed in the recent
decades.

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l In the past, almost all women with abortion required surgical treatment to ascertain complete evacuation. With
the improved resolution with transvaginal scan, uterine cavity is much more accurately assessed. Women with
diagnosis of complete abortion by USG can then be managed conservatively.The USG film below shows an
incomplete abortion with products of gestation inside the uterus.
l Secondly, prostaglandin analogues, such as misoprostol, have effect of cervical softening and oxytocic effects.
When misoprostol is taken orally, it causes a complete evacuation of uterus in 70% of cases in 24 hours. It has
the advantages of minimizing operative complications such as perforation of uterus and introduction of
intrauterine infection. The side effects are mild and well tolerated, including diarrhea, vomiting and abdominal
pain. Occasionally, it may cause severe vaginal bleeding which requires an emergency surgical evacuation.
l Therefore, options of surgical and medical treatment should be offered to patients with abortion.
Discussion/Something to Consider
How would you counsel a patient who is diagnosed to have threatened abortion at 6 week of gestation? How would
you explain the treatment of uterine evacuation to a patient with incomplete abortion?

Recurrent abortion
Definition
Recurrent abortion or habitual abortion is defined as 3 or more consecutive abortion.
Incidence
The incidence is about 1% of all women and is greater than the rate expected by chance alone, suggesting that
there is a specific underlying cause in many cases.
Causes
In majority of cases, the causes are unknown. The following pathologies are identified causes:
Chromosomal abnormalities
l one of the couple may have some forms of chromosomal abnormalities that may be transmissable, resulting in
recurrent abortion. They themselves, however, may be phenotypically normal. A typical example is
translocation (reciprocal or robertsonian). The abortion usually present with absent fetal heart in-utero, in the
first or sometimes second trimester. Structural abnormalities may be present.
Uterine anomalies
l Congenital anomalies of uterus is associated with recurrent abortions. Implantation to the site of
underdeveloped uterine body, or hypoplastic and hypovascular area of the uterus may result in restriction of
fetal growth and abortion.
l Cervical incompetence typically presents with painless mid-trimester miscarriage
Endocrine disorders
l Poorly controlled diabetes is associated with early pregnancy failure. However, well-controlled DM,
asymptomatic or mild glucose intolerance are unlikely to cause pregnancy failure. OGTT to rule out occult
diabetes in case of recurrent abortion is therefore not necessary.
l Similarly clinical hypothyroidism is also a risk factor for recurrent abortion but subclinical disease is not.
Screening of thyroid disease is again not indicated.
l Hypersecretion of luteinizing hormone: It has been showed that polycystic ovarian disease (PCOD) with high
LH level is associated with recurrent pregnancy loss, usually in the first trimester.
Immunological disorders
l Autoimmune diseases such as antiphospholipid syndrome and systemic lupus erythematosus are associated
with fetal loss.
Other risk factors
l Environmental factors such as heavy alcohol consumption and heavy smoking may contribute to recurrent
pregnancy loss.
Congenital infections
l Congenital infections are unlikely to cause recurrent fetal loss, although they can result in sporadic loss.
Patients can develop immunity after primary infection such as in rubella, chickenpox.
Investigations for underlying causes of recurrent abortion
History
l History provides the most important information to look for the underlying aetiology, and guide the investigation.
Information such as when and how the abortions occurred, and whether there are abnormal fetal morphology,
presence of positive past medical history (DM, thyroid disease, PCOD) and social history (smoking and
alcoholism) are essential (see above).
Investigation tests
l Parental karyotyping
l Screening of autoimmune disorders: autoimmune disorders are suspected if there are positive symptoms and
signs, or thrombocytopenia and derangement of clotting profile.
l Investigation of uterine anomalies and cervical incompetence should only be performed on clinical suspicion.
l OGTT and thyroid function, screening of congenital infections are not necessary

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Management
Counselling
l Patients should be counselled that the underlying causes cannot be identified in majority of cases . There is
still a 60% chance that they will have a successful pregnancy in the future.
Treatment of underlying causes:
l Abnormal parental karyotyping
n Couples should be counselled the risk of transmission of chromosomal abnormalities in future pregnancy.
Prenatal diagnosis should be advised.
l Uterine abnormalities
n Various types of metroplasty may be indicated for congenital anomalies, and cervical cerclage is
indicated for cervical incompetence
l Control of medical disorders
n Medical treatment is indicated for autoimmune diseases and endocrine disorders. Patients should also be
advised to quit smoking and alcohol.

Septic abortion
Definition
l It is a condition in which the abortion is associated with an ascending intrauterine infection.
Causes
l It can be a result of surgical evacuation of uterus under inadequate aseptic technique. It commonly occurs in
the setting of illegal termination of pregnancy where sterilisation of instruments is poor. Septic abortion can
also follow incomplete abortion, or prolonged rupture of membranes before 24 weeks of gestation.
Clinical features
l Fever and tachycardia
l Pelvic pain and tenderness
l Vaginal bleeding or pusty discharge
l Cervical os may be opened
l There may be evidence of retained product of gestation (POG) under USG
Complications
l Septic shock
l Disseminated intravascular coagulopathy (DIC)
Management
l Antibiotics
l Evacuation of uterus if there is evidence of retained POG

Ectopic pregnancy
Definition
l A pregnancy with implantation outside the normal uterine cavity. The ectopic site can be:
l fallopian tubes: the most common site
l ovary: uncommon
l cornus of uterus: uncommon
l cervix of uterus: uncommon
l peritoneal or omental surface: very rare
Causes
l by chance
l previous tubal surgery or injury such as sterilisation, pelvic inflammatory disease
l after assisted reproductive procedures (see ART)
Presentation
Symptomatic
l The typical presentation is acute pelvic pain after missing the period (amenorrhea). Vaginal bleeding may
occur but is usually of small amount. There may be signs of internal bleeding such as abdominal distension,
tenderness and guarding, with hypotension, tachycardia and pallor. Pregnancy test is positive
Asymptomatic
l With the use of transvaginal ultrasound and HCG monitoring, ectopic pregnancy can now be diagnosed at an
earlier gestation when patients are asymptomatic or with only mild symptoms. Ectopic pregnancy is diagnosed
or suspected with USG which is done as a routine in early pregnancy, or for investigation of vaginal bleeding
complicating pregnancy
Ultrasound features of ectopic pregnancy
There are three major features:
l Gestational sac and fetal pole are seen outside the uterus

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 n these features can be seen in only 10% of cases, when the pregnancy is already big but not yet ruptured
n a definite diagnosis of ectopic pregnancy can be made in this situation
l Adnexal mass and free fluid in Pouch of Douglas
n It is the most common presentation
n the adnexal mass represents the tubal ectopic pregnancy surrounded by blood clots. The free fluid is the
bleeding from the ectopic pregnancy
n ectopic pregnancy is highly suspected in this situation. The differential diagnosis is a bleeding corpus
luteal cyst
l Absence of features of intra- or extra-uterine pregnancy
n Sometimes pregnancy test is positive, but there is no intrauterine gestational sac, neither is there any
positive ultrasonic feature of ectopic pregnancy as mentioned above
n The possibilities include:
u an early intrauterine pregnancy which is still not visualised by USG;
u an abortion of an intrauterine pregnancy has just occurred
u an early ectopic pregnancy that is still small and has not bled or ruptured yet
n In this situation, measuring serum HCG level will be helpful in making a diagnosis (see below).
n Sometimes an ectopic pregnancy may present with a pseudogestational sac that minmics a true
intrauterine sac.
n Serum HCG levels in ectopic pregnancy
u During the first trimester of a normal pregnancy, the serum HCG levels should be double in 2 days.
An intrauterine gestational sac is usually visible when the HCG level reaches 1500iu/L. Therefore,
l when there is a suboptimal rise in the HCG levels (which are taken 2 days apart), or when the
HCG levels have been above 1500iu/L but yet no intrauterine gestational sac is identified,
ectopic pregnancy should be suspected;
l when the HCG level is decreasing, abortion is more likely and it should be decided if the
abortion is complete or not;
l when the HCG level is rising normally, repeat USG to confirm a viable intrauterine pregnancy;
Diagnosis
l Diagnostic laparoscopy is the definite diagnostic tool for ectopic pregnancy and should be done if clinical
suspicion of ectopic, positive ultrasound features, or abnormal HCG result.
Treatment
Surgical Treatment
l It is the mainstay of treatment of ectopic pregnancy. In the radical surgical treatment, the whole ectopic
pregnancy including the products of gestation (POG) and the site (e.g. tubes) are excised together. In the
conservative approach, only the POG is removed. The surgery can be performed with laparotomy or
laparoscopy approach.
Radical surgery
l It ensures a complete removal of POG. The disadvantage is that part of the genital tract (e.g. tube) is excised.
Conservative surgery
l aims to preserve genital structure for fertility, e.g. in salpingotomy, the tube is cut open and POG is removed.
l Indications:
n Patients want to preserve the tube, particularly the other tube has already been damaged or excised
l Contra-indications:
n the ectopic pregnancy is too big that complete removal is unlikely
n the ectopic pregnancy has already ruptured
n there has been previous tubal damage
n patients have already required in vitro fertilisation
n patients have completed family
l Disadvantages:
n persistent ectopic pregnancy because of incomplete removal of POG: 5%
n risk of recurrence of ectopic at the same site in subsequent pregnancy: 5%
Medical Treatment
l Consists of systemic injection of methrotrexate which is a cytotoxic agent that kills the proliferating fetal and
trophoblastic tissue. Direct injection of methrotrexate or KCl into the site of ectopic pregnancy is not shown to
be effective.
l Success of treatment is confirmed by gradual reduction and disappearance of serum HCG.
l Medical treatment is rarely used in Hong Kong and is only indicated when:
n cervical ectopic pregnancy where surgical excision is difficult and associated with heavy bleeding.
n there is persistent ectopic pregnancy after conservative surgical treatment
n there is persistently detectable HCG but the site of ectopic is unknown
n patient refuses surgery
Chance of success is low when the initial HCG level is high, or the ectopic pregnancy is big
Complications of medical treatment are those of the side effects of cytotoxic: nausea, vomiting, liver function
derangement, etc.

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Discussion/Something to Consider
Which kinds of patients are contraindications for conservative surgery for tubal pregnancy?

Pseudo gestational sac

A pseudo gestational sac (or pseudosac) is an ultrasonic feature of ectopic pregnancy that may mimic a true
gestational sac. In case of ectopic pregnancy, the endometrium will still undergo a decidual reaction because of
hormonal effects. The secretion from the decidua is collected inside the uterine cavity, and appears as a cystic
structure under ultrasound. It may be mistaken as an intrauterine gestational sac, and the diagnosis of ectopic
pregnancy may therefore be missed. The pseudo gestational sac can be differentiated from a true gestational sac.
The former is centrally located, without an hyperechoic rim or fetal pole, while the latter is eccentrially located, with
hyperechoic rim (the trophobastic layer), and may have a fetal pole or a yolk sac.

Corpus luteal cyst

It is a common physiological ovarian cyst. Sometimes a corpus luteum becomes cystic, enlarged and persists,
particularly if the patient is pregnant. It usually regresses spontaneously after the first trimester, but may rupture or
bleed causing acute pelvic pain. When these occur during pregnancy, the clinical picture may be confused with
ectopic pregnancy. Ultrasound features are same as described in follicular cyst.

Hyperemesis gravidarum
Definition
Excessive vomiting during early pregnancy, to the extent of dehydration, weight loss, electrolyte imbalance and
acid-base disturbance.
Causes and pathophysiology
l Vomiting is one of the commonest early pregnancy complications, and is thought to be related to the
production of HCG which stimulates the chemoreceptor in the hypothalamus. The risk is higher in:
n multiple pregnancy
n gestational trophoblastic disease
n hyperthyroidism
n urinary tract infection
l The symptom is usually subside after the first trimester when the HCG level starts to decrease from the peak.
l Remark:
n Vomiting can be due to co-existing pathology of other systems, such as GI and CNS system. Careful
clerking and examination are very important not to miss the diagnosis.
Complications
l Hypokalemia
l Malnutrition
l Wernicke syndrome (due to deficiency of thiamine) rare
l Mallory-Weiss syndrome
Clinical features
Onset of symptoms:
l in the first trimester, around 6 to 8 weeks
Common features:
l nausea and vomiting
l loss of appetite
l weight loss
l signs of dehydrations
Investigation
To assess severity:
l Renal and liver function tests
l complete blood picture
To rule out underlying causes:
l USG to look for multiple pregnancy and gestational trophoblastic disease
l Thyroid function test
l Mid-stream urine for culture
Treatment
Regular monitoring
l Blood pressure and pulse
l fluid input and urine output
l urine ketone
l body weight
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Fluid electrolytes correction
l Rehydration with intravenous fluid
l Potassium supplement
Nutrition support
l dry food
l Vitamin supplement
Antiemetics
l Metroclopramide

Minor disorders of pregnancy

l Although they seldom cause any dangers to the mother and fetus, they are common and often cause
discomforts to the mother and sometimes annoying.
l The symptoms may also mimic those of severe disorders.
l Medical students are required to know how to explain, advise and manage these minor disorders for pregnant
women, and to differentiate them from major disorders.
Nausea and vomiting
l Most common symptom and is due to high HCG level
l Need to rule out multiple pregnancy and molar pregnancy when severe
l Usually improve after first trimester
l Avoid greasy or highly spiced foods; frequent small meals
l in severe form hyperemesis gravidarum, admit and rehydrate patients with intravenous fluid supplement and
give antiemetics
Heartburn
l Resulted form gastric reflux due to relaxation of the lower esophageal sphincter and pressure from the
enlarging uterus later in pregnancy
l Advise frequent, light bland meals; avoiding a late meal; raising the head of the bed; and use of antacid
Constipation
l Due to decreased bowel motility because of high levels of progesterone
l Increase dietary fibre and fluid intake
l Bulk laxative if necessary
Haemorrhoids
l Due to progesterone-induced venodilatation, obstruction of venous return from the lower body by the enlarged
uterus, and increased bearing down because of constipation or at delivery
Epistaxis
l Result of increased peripheral vascularity. Usually self-limiting
Varicose veins
l Occur mostly in the legs but also in the vulva.
l Cause aching and tiredness
l May be complicated with thrombophlebitis and deep vein thrombosis
l Treat with combination of elevation an use of full-length support tights
Backache
l A common symptom and results from increased joint laxity in the lumbar spine and the exaggerated lordosis
which occurs in pregnancy.
l Management is conservative, with rest, analgesia, and improvement in posture
Breast soreness
l Commonest in early pregnancy as the breasts increase in size.
l Reassurance and symptomatic relief with a brassiere that provides adequate support are all that is needed
Peripheral paraesthesiae
l Numbness and tingling occur due to compression of peripheral nerves because of fluid retention, most
commonly the median nerve (carpal tunnel syndrome)
l No treatment is usually required when the cause has been explained to the patient
Headache
l Usually a typical tension headache and is best treated by rest and mild analgesia
l Migraine often improves but may deteriorate, stay the same or occur de novo, in pregnancy
Postural hypotension
l More likely to occur in pregnancy because of venous pooling in the lower limbs
l It is best prevented by avoiding precipitating factors: standing up quickly, hot bath, standing in hot weather for
long time
Pruritus

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Generalized
l Generalized itching (pruritus gravidarum) usually begins in the third
l trimester and may be associated with cholestasis in pregnancy
l Treat with topical antipruritus
Pruritus vulva
l Usually due to candidiasis
l Treat with topical anti-fungal agent
Frequency of micturition
l Symptoms of early pregnancy when it may be due to increased renal filtration
l Also in late pregnancy when it is due to pressure from the enlarged uterus
l Urinary tract infection has to be excluded when there is also dysuria or urgency

4. Endometriosis

Endometriosis
Definition
l Presence of tissue outside the uterus that is histological similar to that of endometrium.
l Adenomyosis does not belong to the group of endometriosis by this definition
Incidence
l A very common gynaecological disease with incidence of 10 to 15%
l Presents in 20 to 40% of patients with infertility, and 17% of patients with chronic pelvic pain
Pathogenesis
l Retrograde menstruation and implantation (Sampson's theory)
l Lymphatic and haematogenous dissemination
l Transformation of coelomic epithelium
l Immunological and genetic factors
Remark:
l the above mechanisms are not mutually exclusive
l growth of endometriosis is estrogen dependent
l the ectopic endometriotic tissue induces inflammation, fibrosis and adhesions that cause complications
Pathology
Sites:
l most common in pelvic peritoneum and ovaries as there are high estrogen concentration
l rarely in vagina, bladder, rectum, umbilicus or lung
Forms:
l Peritoneal deposits:
n lesions of a few minimetres in size
n endometriotic tissue appears as red or bluish spots
n brownish spots represent haemosiderin
n whitish scarring resulted from inflammation and fibrosis
l Endometriomas (endometriotic cysts):
n also called chocolate cysts, as they are filled with chocolate-coloured liquid, representing debris from
cyclical menstruation within the cyst walls
n arise only from ovaries
l Adhesions:
n endometriosis induces pelvic inflammation and adhesion formation between ovaries, fallopian tubes,
posterior uterus, and sometimes bowel.
n adhesion is sometimes very dense and obliterates the pouch of Douglas, causeing bowel or ureteric
obstruction.
Histology:
l simulate endometrial tissue with glands, stroma, and evidence of menstrual cyclicity: ie: haemorrhage or
haemosiderin-laden macrophages. proliferative and secretary changes
Clinical features
Subclinical
l some women are asymptomatic and the diagnoses are made incidentally on routine examination or during
surgery for other reasons
Pelvic pain
l dysmenorrhea, dyspareunia, chronic pelvic pain that may be progressive, and not relieved by simple
analgesics
l Pain arises because of:
n prostaglandins production

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 n local inflammation
n adhesion and scarring
n stretching of nerves after scarring
l Remark: severity of endometriosis is not correlated to the degree of pain
Infertility
l Possible mechanisms of infertility in endometriosis include:
Problem area mechanism
ovarian function anovulation, luteolysis
coital function dyspareunia causing reduced penetration and coital frequency
tubal function altered tubal and cilial motility, impaired fimbrial oocytes pick-up
sperm function inactivation or destruction by inflammative changes
endometrium luteal phase deficiency, endometrial interference
early pregnancy failure increased abortion
Endometrioma
l presents with acute abdominal pain related to rupture or haemorrhage, or
l presents with pelvic mass under physical or ultrasonic examination
Others
l rarely presents with cyclic dysuria and haematuria (involving bladder) or cyclic rectal bleeding and tenesmus
(involving rectum)
Diagnosis
Diagnostic laparoscopy
l indications:
n patients with chronic pelvic pain, secondary dysmenorrhea or dyspareunia not responsive to simple
analgesic
n patients with infertility with above symptoms
l look for peritoneal deposits, endometrioma and pelvic adhesions (features as mentioned above)
Ultrasound
l while endometrioma can be picked up by USG, peritoneal deposits are not visible by USG
l USG features of endometrioma
n variable with homogenous or heterogeneous echogenic content
n usually around 3 to 7cm in diameter
n can be bilateral
n no papillary growth
Biopsy
l seldom required to diagnose peritoneal deposits as the gross features are obvious
l may be needed to confirm diagnosis when the endometriosis is found in atypical sites such as in bladder or
skin
Management
Principle
l endometriosis is a chronic disease that is difficult to be eradicated, without radical surgery
l the disease may present without causing significant symptoms
l high recurrent rate after medical or conservative surgical treatment
l Choice of treatment depends on the severity and type of symptoms, and desire of fertility, and can be
n expectant management
n hormonal treatment
n conservative surgery
n radical surgery
Expectant management
l Indications: asymptomatic or mildly symptomatic
l NSAID prn for pain relief
Hormonal treatment
l Indications:
n severe pain, want to preserve fertility
l Choices:
n Gonadotropin releasing hormone analogue (GnRHa)
n mechanism: suppresses ovarian function and hence endogenous estrogen production which supports
the growth of endometriosis
n advantages: effective pain relief (90%), no androgenic effects compared with danazol
n disadvantages: side effects of hypoestrogenism, delay fertility
l Danazol
n androgen that suppresses hypothalamic-pituitary-ovarian axis and therefore decreases endogenous
estrogen production
n advantages: effective pain relief (90%), no hypoestrogenic effects compared with GnRHa
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 n disadvantages: androgenic side effects; delay fertility
Conservative surgery
l Aims at pain relief and restoration of fertility
l Choices vary from cystectomy (for endometrioma), adhesiolysis, ablation of endometriotic spots
Radical surgery
l Consists of bilateral salpingo-oophorectomy and total hysterectomy
l Aims at pain relief and complete eradication of the disease
l Fertility is not preserved

5. Genital tract infection

Pelvic inflammatory disease

Definition
l The strict definition of pelvic inflammatory disease (PID) is the clinical syndrome attributed to the ascending
spread of microorganisms (unrelated to abdominal surgery or pregnancy) from the vagina and cervix to the
endometrium, fallopian tube and / or the contiguous structures.
l It implies sexual transmission as the main source of infection, or secondary to some procedures such as
uterine curetting. It is distinguished from pelvic infections resulted from other sources such as appendicitis,
diverticulitis, and pelvic tuberculosis from haematological spread.
l It is a clinical diagnosis and does not specified the exact location of infection. An anatomical terminology such
as endometritis, salpingitis, parametritis, or tub-ovarian abscess is more specific and preferred if the site of
infection can be identified via laparoscopy.
l It is subdivided into acute and chronic PID
Acute PID
Pathogenesis
l ascending infection: common organisms are gonorrhea and chlamydia
l secondary anaerobic invasion after the genital tract is infected and damaged
Clinical features
l acute or subacute pelvic pain, usually bilateral
l purulent vaginal discharge
l fever
l history of recent coitus
l cervical excitation pain
l raised white cell count
l pelvic ultrasound may reveal fluid in the pouch of Douglas (pus) or tubo-ovarian abscess formation
l acute appendicitis is the most common differential diagnosis
Complications of acute PID
l tubo-ovarian abscess
l septicemia
Long term
l tubal damage and infertility
l increase risk of ectopic pregnancy
l chronic PID and pelvic pain
Diagnosis
l clinical diagnosis of PID and empirical treatment with antibiotic is the mainstay of management
l in case of doubt, or if patient does not respond to antibiotics, diagnostic laparoscopy is performed to confirm
the diagnosis, and to rule out other pathology such appendicitis
l microbiological investigation: such as endocervical swabs for cultures
Treatment
l Antibiotic treatment
n penicillin group to cover gonorrhea
n tetracycline group or erythromycin to cover chlamydia
n metronidazole to cover anaerobes
l Surgical treatment
n indicated when patients do not respond to medical treatment, or tubo-ovarian abscesses are formed
n laparoscopic drainage of abscess and pus in pelvic cavity
l Counselling for screening of other sexually transmitted diseases and contact tracing
Chronic PID
l recurrent or chronic symptoms of pelvic pain resulted from chronic pelvic inflammatory changes, fibrosis and

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 adhesion which are consequences of previously partially treated acute PID
Clinical features
l chronic pelvic pain
l dysmenorrhea
l acute exacerbation may superimpose on a chronic PID
l there is usually but not always a history of acute PID because sometimes a diagnosis of acute PID may have
been missed in the past
l differential diagnosis is endometriosis
Diagnosis
l Diagnostic laparoscopy
Treatment
l no curative treatment as damage has already occurred
l aim to relief symptoms or treat infertility
Pain relief:
l medical: NSAID
l Hysterectomy in case of intractable pain and fertility is not required
Fertility
l tubal surgery or assisted reproductive procedure
Discussion/Something to Consider
How to differentiate acute PID and acute appendicitis when a young women presents to the A&E department
complaining of acute lower abdominal pain?
Are there any differences between the clinical presentations of acute PID caused by gonorrhea and that of
chlamydia?

Bartholin
Bartholin's gland is a pea-sized mucus-secreting gland situated in the lower part of each labium majus. It is
connected to the vaginal entrance by a duct. Its secretion contributes to vaginal lubrication. Obstruction of the duct
causes a Bartholin cyst. Inflammation may lead to abscess formation (Bartholin abscess). The treatment is
marsupialisation. It should be differentiated from other lesions of the perineum, such as sebaceous cysts, lipoma, as
the treatment is different.

Pyometra
It is a collection of pus inside endometrial cavity. It is usually due to outflow obstruction such as cervical stenosis
secondary to menopause, previous surgery, or cervical cancers. The obstruction results in stasis of endometrial
secretion and secondary infection. It may be asymptomatic, or presents with purulent vaginal discharge, or
symptoms of primary causes such as postmenopausal bleeding in case of cervical cancers. Pyometra should be
drained with Vabra aspiration and the collection should be sent for histological and microbiological examination.
Hysteroscopy is contraindicated as it may spread the infection.

6. Menstrual problems

Menstrual disorders
Type of menstrual disorders
l Abnormal volume
n Too much: Menorrhagia (Polymenorrhea)
n Too little: Hypomenorrhea
l Abnormal regularity
n Too infrequent: oligomenorrhea
n secondary amenorrhea
l Too frequent
n Abnormal onset and cessation
n menarche starts too early: precocious puberty
n menarche does not occur: primary amenorrhea
n menopause occurs too early: premature menopause
l Pain and discomfort
n Dysmenorrhea
n Premenstrual syndrome
l Remark:
n postcoital bleeding, postmenopausal bleeding are not 'menstrual' disorders.

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Menstrual cycle
l It is the rhythmicity of menstruation resulted from the changes in endometrium in response to sex hormones
which are under the regulation of the hypothalamic-pituitary-ovarian axis. The cyclic ovarian estrogens and
progesterone production under the stimulation of the higher centres, in turn stimulate the growth of
endometrium. During the first half of the cycle, estrogenic effect is dominant and causes proliferation of the
endometrial glands (proliferative phase). After ovulation, progestogenic effect becomes dominant and
stimulates the secretary function of the endometrial glands (secretary phase). When serum concentrations of
these hormones decline, endometrial shedding is initiated and the menstrual loss consists of endometrial
glands and secretions as well as blood.
l The first day of the onset of the menstruation of the preceding cycle is defined as the last menstrual period
(LMP).
l See also menstrual disorders.

Amenorrhea
Definition
Primary amenorrhea
l No menstruation by the age of 14 accompanied by failure to grow properly or develop secondary sexual
characteristics, or
l No menstruation by the age of 16 when growth and sexual development are normal
Secondary amenorrhea
l Absence of menses for six months (or greater than three times the previous cycle interval) in a woman who
has menstruation before
Causes
To have normal cyclic menstruation, one must have:
l an intact hypothalamus-pituitary-ovarian axis producing normal ovarian cycles
l a normal endometrium that respond to ovarian hormones
l a normal outflow tract: cervix, vagina and vulva
Therefore amenorrhea occurs when there are:
l Failure of hypothalamus-pituitary-ovarian axis:
n hypothalamus: anorexia nervosa, Kallman syndrome, etc
n pituitary:
n ovary: Turner syndrome, polycystic ovarian disease (PCOD), Testicular feminisation syndrome (patients
with testicular feminisation do not have ovaries and uterus), premature menopause, ovarian dysgenesis
n others: other endocrinopathologies such as hyperprolactinemia, and drug effects
l Absence of normal endometrium:
n uterine agenesis
n Asherman syndrome
l Obstruction of outflow tract:
n vulval: Imperforate hymen
n vaginal: transverse vaginal septum, vaginal agenesis or hypoplasia
Remarks:
l Endocrinopathologies usually cause secondary amenorrhea except primary ovarian failure such as Turner
syndrome and ovarian dysgenesis.
l Structural abnormalities of uterus and outflow tract often result in primary amenorrhea except in Asherman
syndrome.
l Pregnancy and natural menopause are two physiological causes of amenorrhea that should be considered in
women at reproductive age and perimenopausal age respectively.
Clinical evaluation
l General examination
l body weight
l body height
l growth
l secondary sexual characteristic
l breasts
l body hair
Investigations
Depends on the clinical suspicion, the following investigations are required:
l Karyotyping: Turner syndrome, testicular feminisation syndrome
l Hormonal profile: FSH for ovarian failure, LH/FSH ratio for PCOD, prolactin for hyperprolactinemia
l Radiological examination for structural abnormalities of genital tract such as uterine agenesis.
l Radiological examination of urinary tract may also be required in case of abnormal genital tract as both
systems are related in embryonic development

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Treatment
Principles:
l Treat underlying causes if possible
l Restore fertility:
n Endocrinopathologies are always associated with anovulation and infertility, and may require ovulation
induction or in vitro fertilisation.
n Patients with ovarian failure or absence of uterus or normal endometrium, are infertile. Oocyte donation
and surrogacy are the alternatives.
l Restore sexual function:
n Vaginal malformations (septum, hypoplasia, agenesis) require surgical correction
l Restore growth and development:
n Patients with Turner syndrome are short and with poor breasts development. Early hormonal
replacement therapy is required.
l Protect against any long-term complications
l Premature ovarian failure has the risk of hypoestrogenemia such as osteoporosis and cardiovascular disease
in long term. Hormonal replacement therapy reduces the risk.

Oligomenorrhea
It is defined as the occurrence of menses on the only five or fewer occasions per year, or a menstrual period of more
than 6 weeks in most of the cycles. It is common among teenagers as well as perimenopausal women, and is
usually associated with anovulation as a result of underlying endocrine disorders such as polycystic ovarian disease
(PCOD) and hyperprolactinemia.

Cryptomenorrhea
Cryptomenorrhea means hidden menstruation. This occurs when endometrial shedding takes place but the
menstrual loss cannot escape due to blockage of parts of the lower genital tract, usually as a result of congenital
malformations: e.g. in vaginal atresia, transverse vaginal septum, and imperforate hymen. The uterus or vagina is
distended with menstrual blood. Patients present with primary amenorrhea, cyclic lower abdominal pain, and
abdominal distension, and urinary retention (due to distended uterus).

Hyperprolactinemia
Causes of hyperprolactinemia
Physiological
l Prolactin levels are influenced by the time of day when blood is collected, and are also increased by stress
l Transient rises can occur at ovulation
l During pregnancy and lactation
Pathological
l Prolactinoma
l Other pituitary gland tumours that block the dopaminergic inhibitory tract from the hypothalamus
l Drug induced: anti-dopamingeric
l Other pituitary gland tumour
l Association with polycystic ovarian disease (PCOD)
Clinical presentation
l oligo-amenorrhea
l galactorrhea
Further investigation
l Mild hyperprolactinemia can be a transient physiological change (see above) and may require no further
investigation, or a repetition of the test.
l Significant hyperprolactinemia requires radiological investigation to rule out prolactinoma or other pituitary
gland tumours.
Principle of treatment
l Dopaminergic agent: bromocriptine
l Surgery for macro-prolactinoma or other pituitary gland tumours

Galactorrhea
It is the spontaneous milk secretion from breasts not associated with childbirth or the lactation. It is associated with
hyperprolactinemia.

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Polycystic Ovarian Disease (PCOD)
What is Polycystic ovarian disease
l A condition characterized by chronic anovulation with hyperandrogenemia, raised LH secretion with alternation
of the normal relationship between LH and FSH leading to raised LH to FSH ratio. No specific underlying
diseases of the adrenal or pituitary glands can be demonstrated.
Epidemiology
It affects:
l 2% of women in reproductive age
l 30% of women with amenorrhea
l 80% of women with oligomenorrhea
l 80% of women with anovulatory infertility
l 70% of women with hirsutism
Pathology of ovaries
Macroscopic:
l bilateral enlarged and lobular ovaries
Microscopic:
l multiple atretic follicles (represent the polycystic features), theca cell hyperplasia and generalised increase in
stroma
Pathogenesis
l There is evidence of autosomal dominant mode of inheritance, with variable expression
l The exact mechanism of endocrinopathology is unknown. It can be reside within the ovaries or secondary to
extra-ovarian disturbances (from adrenal glands or fatty tissue). However, once it is initiated, it is
self-perpetuating.
n Elevated estrogen level (resulted from conversion of androgens in fatty tissue and ovaries).
n High estrogen environment feedback on pituitary gland gonadotropin secretion leading to a relative
excess of LH secretion compared to that of FSH.
n Consequently, there is failure of ovulation as the developing Graafian follicle depends upon stimulation of
FSH.
n FSH stimulates the conversion of androgen to estrogen by inducing ovarian aromatase, is also impaired.
n Androgen production is also enhanced by LH.
n Increase in adrenal glands androgens (androstenedione DHEA and testosterone)
Clinical features
The four typical features are:
l oligo-amenorrhea
l infertility
l obesity
l hirsutism
l Remark: Not all patients have all the four features. Some features are more dominant while others may be less
obvious or absent.
Onset of symptoms:
l usually gradual
Complications
Reproductive disorders
l infertility
l recurrent abortion
l high risk of ovarian hyperstimulation syndrome (OHSS) when undergoing ovulation induction
Metabolic disorders
l risk of insulin resistance
Long term risk of cancer
l risk of endometrial hyperplasia and endometrial carcinoma
Biochemical features
l increased LH levels
l elevated (early follicular) LH/FSH ratio > 3
l increased sex-hormone-binding-protein
l increased androgen secretion
l associations with hyperprolactinemia and hyperinsulinemia
Ultrasound features
l bilateral enlarged ovaries, with
l multiple (>10 each side) small cysts of size 1-5mm arranged at the periphery of the ovaries (necklace
appearance)
l thickened stroma

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Diagnosis
Biochemical: more specific
l high LH to FSH ratio >3
Ultrasonic: less specific as it may occur in other endocrinopathologies that result in anovulation
l features as described above
Management
General measures
l Weight reduction
l Counsel for the risk of diabetes, endometrial carcinoma
l OGTT, endometrial sampling may be indicated
Treatment of menstrual problems
l Aim to regulate cycles as well as to protect against endometrial hyperplasia
l Can use combined oral contraceptives or progestogen if pregnancy is not wished
l Can use clomiphene citrate if pregnancy is wished
Treatment of infertility
l See ovulation induction
Treatment of hirsutism
l See hirsutism

Kallman syndrome
It is a rare congenital disease with two main features:
l failure of migration of GnRH producing neurons, resulting in absence of hypothalamic GnRH secretion, and
hence hypogonadotropic hypogonadism. Female patients therefore present with delayed puberty, absence of
breast development, primary amenorrhea and anovulation.
l absence of olfactory bulb resulting in anosmia (loss of sense of smell)
Treatment:
l Low doses of estradiol to encourage breast development, followed by
l Cyclic hormonal replacement therapy consisting of estrogen and progestogen
l Ovulation induction when patients want pregnancy. Pulsatile GnRH or gonadotropin is the treatment of choice.

Testicular feminisation syndrome

l End-organ resistance to androgens by absence of 5-alpha reductase or functional defect.
l Male genotype but female phenotype.
l Raised up as a girl.

Asherman syndrome
The partial or complete obliteration of the uterine cavity by adhesions (synechiae) caused by endometrial infection
(such as tuberculosis), or over-vigorous curettage after miscarriage or abortion. Depending on the severity of
adhesions, amenorrhea, hypomenorrhea, spontaneous abortion or infertility may occur. Endometrial ablation is a
surgical procedure aiming at reduction or complete cessation of menstrual flow by iatrogenically inducing Asherman
syndrome, through electrical cauterization of the endometrial cavity.

Anorexia nervosa
Introduction
Anorexia nervosa is one of the underlying causes of secondary amenorrhea in young women. Because of significant
weight reduction, the hypothalamus-pituitary-ovarian axis is suppressed, resulting in hypogonadotropic
hypogonadism. It is a potentially fatal disorder if not treated.
Epidemiology
l 1% of young females
l Predominant age group: 10-20+ years old
l Male to female ratio: at least 1:10
Subtypes
l Restrictive
l Bulimic
Clinical features
History
l Marked weight loss (of more than 15% of standard weight or BMI less than 16.5kg/m2), in the absence of any
primary medical disorder
l Food refusal attributed to fat-phobia, stomach bloating, no hunger, no appetite, fear of food.

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l Weight controlling behaviour: dieting, exercise, use of anorectics, laxatives or diuretics
l Self-induced or spontaneous vomiting, especially in fat-phobia
l Delusion of self body image
l Stunted growth (pre-pubertal)
l Amenorrhea
Physical signs
l Hypotension
l Bradycardia
l Lanugo
l Hypothermia
l Varying degrees of dysphoria, obsessionality, perfectionism or low self-esteem
l Biochemical disturbances
Aetiology
l Personal: personality
l Family: enmeshed or conflicting
l Environment: stress, peers, relationships, losses
l Socio-cultural: media publicity, gender role conflict, disempowerment
l Biological: genetics? neuroendocrine?
Management
Multi-disciplinary approach
Assessment:
l Physical condition, e.g., degree of weight loss
l Psychosocial factors:
n Suicidal risk
n Co-morbid psychiatric disorders
Treatment:
l Nutritional counselling, gradual weight gain, treat any physical condition if needed
l Psychological treatment
n Individual: motivation enhancement therapy
n Family therapy
l No medication is proven to be effective
Poor prognostic factors
l Significant weight loss
l Chronicity
l Presence of purging or bulimia

Menorrhagia
Definition
l Excessive cyclical menstrual bleeding
l The mean menstrual blood loss per menstruation in a healthy woman ranges between 37 to 43ml.
l Menstrual blood loss of more than 80ml is regarded as excessive, and this occurs in 9 to 14% of women. About
60% of these women would become anaemic. However, it is very difficult to document the volume of blood loss
clinically
l There is also a poor correlation between subjective and objective assessment of blood loss. Only about 50% of
women presenting with menorrhagia actually have a loss outside the normal range (>80ml).
Causes
Dysfunctional uterine bleeding (DUB)
l It is the most common cause of menorrhagia
l By the name implies, there is no underlying organic cause
l The diagnosis is made on clinical basis, after excluding other possible organic causes (see below)
Uterine fibroid
l common cause of menorrhagia
Adenomyosis
l also as common cause of menorrhagia with clinical picture similar to fibroids
Endometrial hyperplasia, endometrial carcinoma
l sometimes cause menorrhagia, although they usually cause irregular menstrual bleeding
Systemic causes:
l Hypothyroidism and bleeding tendency such as Von Willebrand's disease ( unknown incidence ), idiopathic
thrombocytopenia
l rare causes of menorrhagia
Assessment
Assess the severity

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l Volume of loss each period
n how many and how frequent does the patient change pad each day
n any flooding of blood clots
n how long does each period last
n how is the social life affected
l When does the menstrual problem start
l Are there any anaemia
n any anemic symptoms and sign
n check haemoglobin level and evidence of iron deficiency
n check if there is other cause for her anaemia
n What treatment has the patient tried the effectiveness
Diagnosis of underlying causes
l Enlarged uterus more suggestive to fibroid and adenomyosis
l need to rule out endometrial hyperplasia and carcinoma if there periods are short and irregular with
endometrial sampling
l look for clinical features of hypothyroidism and bleeding tendency, and check thyroid function, platelet count
when there is suspicion
Treatment
l Depends on the cause of menorrhagia, age of patients, wish of patients to preserve fertility, treatment can be
medical or surgical.
l Medical treatment includes:
n Tranexamic acid
n Mefenamic acid
n Combined oral contraceptives
n Danazol
n Progestogen
l Surgical treatment includes:
n endometrial ablation
n myomectomy
n hysterectomy
l In general, medical therapy should be attempted for DUB. Surgical treatment is considered if medical
treatment is failed, or in severe case of DUB.
l Medical treatment is less useful for fibroids and adenomyosis
l Myomectomy is only for treatment of fibroids if patients want to conserve uterus, otherwise fibroids and
adenomyosis are better dealt with hysterectomy.
l complex atypical endometrial hyperplasia and endometrial carcinoma should be treated with hysterectomy
Discussion/Something to Consider
Do you know any methods to estimate the menstrual blood loss clinically?

Metropathia haemorrhagia
A term to describe a very heavy menstruation after several weeks of amenorrhea which is associated with
anovulation cycles. Follicular development occurs and continues as ovulation fails to take place. This results in high
circulating oestrogen levels which continue to stimulate endometrial development in the absence of antagonism of
progesterone. The consequence is cystic glandular endometrial hyperplasia. Eventually, after several weeks the
endometrium breaks down and prolonged heavy bleeding occurs.

Dysfunctional uterine bleeding

What is dysfunctional uterine bleeding (DUB)?
It is a common disease diagnosed by exclusion. It is defined as heavy and / or irregular menses in the absence of
recognisable pelvic pathology, pregnancy or generalized bleeding disorder. It is the most common cause of
menorrhagia (60%) in reproductive women, especially at the extreme of reproductive age. The diagnosis should be
made after excluding any organic causes.
Pathophysiology of dysfunctional uterine bleeding (DUB)
The exact pathophysiology is not known but generally two patterns of DUB are recognised:
Anovulatory pattern:
l Anovulation is common among teenagers who have just started menarche, and perimenopausal women who
are approaching menopause. The endometrial glands continuously proliferate under unopposed stimulation of
estrogen (lack of progesterone), and result in irregular and heavy menstrual flow.
Ovulatory pattern:
l Some women ovulate with regular cycles but still have menorrhagia. The mechanism is unknown. It may be
related to the inadequate production of progesterone from corpus luteum, or a shift in endometrial conversion
of endoperoxide from the vasoconstrictor prostaglandin F2&alpha to vasodilator prostaglandin E2.
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Treatment of dysfunctional uterine bleeding (DUB)
Medical therapy
l Tranexamic acid from day 1 of mense to the end of the heaviest days
l Non-steroidal anti-inflammatory agents (NSAID) e.g. mefenamic acid from Day 1 to end of the heaviest days
l Combined oral contraceptives
l Progestogens - cyclical
l Levonorgestrel intra-uterine system (Mirena)
Surgical therapy
l Endometrial ablation
l Hysterectomy

Dysmenorrhea
Definition
Primary (idiopathic) dysmenorrhea
l Painful periods for which no organic or psychological cause can be found
Secondary dysmenorrhea
l Painful periods for which an organic or psychosexual cause can be demonstrated
Remark:
l the uses of the terms 'primary' and 'secondary' are different from that in infertility
Causes of primary dysmenorrhea
l The cause is unknown but there is a familial tendency, with a strong likelihood that the attitude of the mother
may influence the response of the daughter
l It occurs in ovulatory cycles during when prostaglandins production may cause vasoconstriction or myometrial
contraction, resulting in pain.
Causes of secondary dysmenorrhea
l Endometriosis
l chronic pelvic inflammatory disease
l Adenomyosis
l Submucosal fibroid
Clinical features of primary dysmenorrhea
l usually develops within the first 2 years of menarche
l cramping, sometimes intense, and can be crippling and disturb social activity
l site: over lower abdomen, radiates down the anterior aspects of thighs
l onset on the day of menses or a day before menstruation, and last for 2 to 3 days
l often associated with vomiting and diarrhea
l pain often disappears or improves after the birth of the first child
l no abnormal finding on physical examination
Clinical features of secondary dysmenorrhea
l usually develops later in reproductive age, can develop after childbirth
l dull, congestive pain
l site: over lower abdomen, radiate to back
l onset usually on the day of menstruation, but can be few days before that. Can last as long as the
menstruation, or even persist after menstruation
l organic pathology is identified on physical or ultrasound examination
Treatment of primary dysmenorrhea
l NSAID or combined oral contraceptives
Treatment of secondary dysmenorrhea
l Refer to individual pages for treatment of underlying causes

Mittelschmerz
It means pain in the middle. It is the lower abdominal pain in women which occurs at the mid-menstrual cycle and is
generally assumed to be related to ovulation. It is suggested that the pain is due to peritoneal irritation by follicular
fluid and blood following rupture of the follicle. However, the relation of the pain to the exact time of ovulation and to
the side on which ovulation has occurred is variable.

Premenstrual syndrome
Definition
Primary premenstrual syndrome (primary PMS)
l A disorder of non-specific somatic, psychological or behavioural symptoms that recur in the premenstrual

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 phase of the menstrual cycle, but resolve completely by the end of menstruation, leaving a symptom-free
period. The symptoms are of sufficient severity to produce social, familial, or occupational disruption.
Symptoms must have occurred in at least four of the six previous menstrual cycles.
Secondary premenstrual syndrome (secondary PMS)
l Similar to primary premenstrual syndrome except that the symptoms do not completely resolve when the
menstruation ceases (i.e. not symptom-free period), but does significantly improve for at least 1 week after
menstruation.
Remark:
l The implication of these definitions is that in secondary PMS there is an underlying psychological disorder
whose aetiology is similar to that of common psychiatric disorders such as depression or anxiety. Both primary
PMS and the cyclical component of secondary PMS are presumed to be related to the endocrine changes of
the ovarian cycle.
l Common somatic symptoms:
n breast pain, pelvic pain, abdominal bloatedness, lethargy and tiredness
l Common psychological symptoms:
n depressive mood, decreased libido, anorexia, insomnia
l Common behavioural symptoms:
n loss of self-control, loss of judgment, impulsive behaviour
Aetiology
l Unknown
Diagnosis
l Many women will have some forms of discomfort during or before menstruation. To make a diagnosis of PMS,
the symptoms must fulfill the definition of PMS: occur cyclically; be severe enough to cause disruption of
women daily living, and occur for at least 4 out of 6 cycles.
l Rule out underlying psychiatric disorder such as depression, anxiety and psychosexual problems, and
endocrine causes such as menopause, hyperthyroidism, and organic causes such as endometriosis, pelvic
inflammatory disease.
l There is no specific test to confirm PMS. In difficult case, GnRHa depot for 3 months may be indicated to
suppress menstruation. Total cessation of the symptoms after the menstruation has suppressed is a support of
the diagnosis of PMS.
Treatment
l There are various forms of medications proposed but none of them are well proven to be effective with
randomized controlled trials.
l Oral contraceptive pills, progestogens, vitamin B6 may be tried. Danazol and GnRHa can effectively suppress
menstruation but also have side-effects. In severe cases refractory to medical treatment, oophorectomy is the
last resort.

7. Menopause and HRT

Menopause
Definition
l In Greek meno means month and pauo means to stop.
l It is the permanent cessation of menstruation due to loss of ovarian follicular activity. Usually it is defined after
one year of amenorrhea.
l It is different from the term 'climacteric' which is an extended period of gradually declining ovarian function
often beginning years before and lasting years after menopause itself
l Premature menopause is defined as menopause occurred before 40 years old.
Epidemiology
l In Hong Kong the mean age of menopause is 50 years old.
Causes
l Natural menopause
l Iatrogenic: oophorectomy, post-chemotherapy, post-radiotherapy
l Inflammatory destruction of ovary: post-mump infection, tuberculosis, autoimmune diseases
Risk of menopause
l climacteric symptoms
l increase risk of osteoporosis and bone fractures
l increase risk of atherosclerotic cardiovascular diseases

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Climacteric
l In Greek 'klimakter' means the rung of a ladder. It is a 'critical' period of time around menopause when ovarian
function is gradually compromised.
l This is a time of decreasing fertility, decreasing oestrogen level and the appearance of the typical symptoms of
menopausal syndrome, although the menstrual periods will still be present.
l The menopausal symptoms include:
n Vasomotor symptoms: hot flushes, palpitation, 80% of patients
n Psychological symptoms; anxiety, depression, irritability, liability of mood, lack of concentration; in 30% of
patients
n Atrophic symptoms: vaginal dryness, urgency and frequency of micturition.
l The earliest endocrine change at the climacteric period is hypothalamic-pituitary hyperactivity due to lack of
negative feedback by follicular hormone. Therefore, elevated FSH is a early endocrine marker of climacteric
period.

Osteoporosis
Bone disease characterised by low bone mass, micro-architectural deterioration of bone tissue leading to
enhancement of bone fragility and a consequent increase in fracture risk. It is different from osteomalacia. Women
after menopause or with chronic hypoestrogenemia are at risk of development of osteoporosis. Bone fractures
secondary to osteoporosis causes significant morbidity and mortality in this group of patients, as well as medical
cost of the society. Hormonal replacement therapy effectively prevents bone loss in this high risk patients.

Premature menopause
Permanent cessation of menses (menopause) before age of 40 due to ovarian failure. It is more likely to be a
pathological rather than a natural menopause. See menopause for possible causes.

Hormonal replacement therapy

Definition
l Replacement of natural estrogen (with or without progestogen) to patients with deficiency of endogenous
estrogen due to ovarian failure in order to minimize the risk of lack of estrogen such as osteoporosis and
atherosclerotic heart diseases
Type of natural estrogen
l estradiol
l estradiol valerate
l equilin
Different preparation of estrogen
Oral estrogens
l first pass effect of liver leads to conversion of one-third of estrogen to weak estrone glucoronide which is
excreted quickly
l estrone to estradiol of 2:1 instead of natural ratio of 1:2
l also cause increase in sex hormone binding globulin, cortisol binding globulin, rennin substrate and HDL and a
depressant effect on anti-thrombin III, and therefore theoretically contraindicated in women with a history of
clotting disorders or hypertension
Vaginal estrogen cream
l for local treatment as well a systemic treatment
Percutaneous estrogen cream
l consists of 3mg estradiol in each daily 5g applicator of cream
l bypasses liver and achieves a 1:2 estrone to estradiol ratio
Transdermal patches
l consist of a thin multi-layered unit containing a drug reservoir, a rate-controlled ,membrane and an adhesive
layer
l patches have surface area of 5 to 20cm square and administer estradiol at a controlled rate of 25 to
100mcg/day in vivo
l need to change twice weekly
l troublesome skin reactions ranging from hyperaemia to blistering
Subcutaneous implants
l consist of 50mg estradiol pellet implanted subcutaneously
l estradiol level peaks at 2 to 3 months and declines to pretreatment level after 6 months
Progestogen
l is used with estrogen in case of intact uterus
l aims to oppose estrogen stimulation on endometrium and hence prevents endometrial cancer

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l on its own it is not a good HRT to control climacteric symptoms or prevent osteoporosis and atherosclerotic
heart disease
Different forms of combination of estrogen and progestogen
Unopposed (without progestogen)
l For those without uterus
Opposed (with progestogen)
l Cyclic: for those with uterus and want regular withdrawal bleeding
l Continuous: for those with uterus and want complete amenorrhea
Indications of HRT
l symptomatic relief of climacteric discomforts
l prophylaxis against osteoporosis
l prophylaxis against atherosclerotic cardiovascular diseases
Contra-indications of HRT
Absolute
l endometrial cancer
l breast cancer
l undiagnosed abnormal vaginal bleeding
Relative
l past history of thromboembolism
l active liver diseases
l hypertension and diabetes are not contraindications for hormonal replacement therapy provided that they are
under good control.
Side effects
Most are mild and well-tolerated:
l breast bloating and tenderness
l weight gain
l breakthrough bleeding: need to rule out underlying endometrial pathology when abnormal vaginal bleeding
occurs
Risk of breast cancer
l no firm evidence of increased risk
Discussion/Something to Consider
Should all menopausal women be given hormonal replacement therapy routinely?
A postmenopausal woman of age 55 who has been put on opposed HRT for 3 years, presents to you with persistent
vaginal bleeding for 2 week. What is your management and counselling?

8. Gynaecological surgery & investigations

Gynaecological surgery
Route of surgery
Conventional
l Via laparotomy
l Via vaginal route
Minimal invasive surgery
l Via laparoscopy
l Via Hysteroscopy
Aim of surgery
Excision of pathology
l hysterectomy, myomectomy, ovarian cystectomy, oophorectomy, salpingectomy
Destruction of pathology
l Endometrial ablation
Reconstruction of functioning organs
l Metroplasty: reconstruction of uterus for congenital uterine anomaly
l Salpingostomy: reconstruction of a fallopian opening for transfer of oocytes
l Pelvic floor repair: reconstruction of the pelvic floor to treat vaginal prolapse
l Vaginoplasty: reconstruction of vagina for sexual functioning
Special surgery
Oncological surgery
l Radical hysterectomy
l Exenteration
l Pelvic or para-aortic lymphadenectomy

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Urogynaecological surgery
l For treatment of genuine stress incontinence:
n Colposuspension
n Urethral sling
n Urethral injection of collagen
Fertility surgery
l tubal anastomosis, salpingostomy

Curettage
Definition
Uterine curettage is a minor gynaecological surgery in which part of the endometrial lining of the uterus is removed
by means of a hollow spoon-shaped instrument (curette). Dilatation of the cervix is required to admit all but the
smallest curette.
Indications
This operation is a diagnostic procedure to study hormonal or other changes (inflammatory, neoplastic) in the
endometerial cells, or a therapeutic procedure for the removal of retained products of conception (treatment of
incomplete abortion) or uterine polyps.
Complications
l Perforation of uterus, after which the bowel may also be injured by the curette
l Introduction of infection to the uterus
l Bleeding

Hysterotomy
It is a gynaecological surgery for termination of pregnancy in the early second trimester. The uterus is cut open
longitudinally and the products of gestation are removed. The procedure is essentially the same as that of a classical
caesarean section which is for delivery of babies after 24 weeks of gestation. Hysterotomy is rarely done nowadays
because of very effective and much safer medical methods of termination of pregnancy (with prostaglandins). The
risks of hysterotomy are haemorrhage, and uterine rupture in subsequent pregnancy.

Endometrial ablation
It is a relative minor gynaecological operation in which the endometrial lining down to the basal layer is destroyed, so
that no more or only minimal endometrial glands will be responsive to estrogen. It is used to treat dysfunctional
uterine bleeding (DUB).
Methods of ablation
There are various ways of ablating the endometrium including microwave, thermal balloon, and electrocautery via
hysteroscopy. The former two methods can be performed under local anaesthesia in an out -patient setting.

Ablation with diathermy using a rolling ball. The endometrium became pale after ablation
Efficacy
About 80% of patient will become amenorrhea after the treatment, 15% will still have menstruation but the flow is
much reduced, 5% have no improvement and require further treatment.
Advantages
Endometrial ablation has advantages over medical therapy of DUB:
l no hormonal side-effects
l no problem of drug compliance
Endometrial ablation also avoids the need of hysterectomy and subsequent morbidity and mortality.
Disadvantages

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l Contraception is not guarantied - patients have to continue practising contraception
High risk of miscarriage, intrauterine growth restriction, abnormal placental adherence (e.g. placenta accreta) if
pregnancy occurs.

Myomectomy
What is myomectomy
It is the excision of uterine fibroids. It is indicated when the fibroids become symptomatic or too large, and the patient
wants to preserve the uterus for fertility. Otherwise, hysterectomy is the preferred choice. Depends on the site of the
fibroids, it can be performed via laparotomy (for intramural fibroids), laparoscopy (for pedunculated fibroids), or
hysteroscopy (for submucosal fibroids).
Open myomectomy (via laparotomy)
The uterus is cut over the greatest diameter of the fibroid which is then enucleated. The uterine wound is finally
repaired with the dead space closed. The complications are excessive bleeding from the wound, and adhesion
formation. Pre-operative GnRHa or danazol may be used to decrease the size and vascularity of the fibroid.
Laparoscopic myomectomy
It is for pedunculated fibroids. The stalk of the fibroid is ligated or diathermized and cut. The fibroid is the morcelated
and removed in pieces via the small laparoscopic wound.
Hysteroscopic myomectomy
It is for small submucosal fibroid. A loop diathermy is used to cut the stalk, or the fibroid into pieces which are the
removed vaginally.
Outcome of myomectomy
l recurrence of fibroids (10%)
l recurrence of symptoms (10%)
l improvement of fertility in patient having fibroids as the sole cause of infertility (30%)
Discussion/Something to Consider
You are the houseofficer going to obtain the consent of a 26 years old patient with a 6cm intramural fibroid causing
menorrhagia. What would you explain to the patient about the operation?

Hysterectomy
What is hysterectomy
Excision of uterus. It can be divided into:
l Total (or simple) hysterectomy
n both the corpus and cervix of the uterus are excised
n it is the most common form of hysterectomy for benign uterine lesion
l Subtotal hysterectomy
n only the corpus uterus is removed
n cervix is sometimes preserved for the following reasons:
n patient's wish because of the belief of the role of cervix in sexual satisfaction
n surgical difficulty in case of dense adhesion around the cervix
n potential advantage in reducing ureteric and bladder injury
n potential advantage in maintaining pelvic floor support
l Extended hysterectomy
n the whole uterus together with the upper vagina are excised
n it is indicated when the pathology involves the vagina such as VAIN
l Radical hysterectomy
n choice for treatment of cervical cancer and uterine cancer with secondary involvement of the cervix
n the whole uterus, upper vagina, together with the parametrium are excised
n the procedure is extensive and operative morbidity and mortality is higher when compared to other form
of hysterectomy
Methods of hysterectomy
Laparotomy
l the traditional method of both benign and malignant lesions
l in general operative mortality is low but various morbidities are common
Vaginal hysterectomy
l method of choice for treatment of uterine prolapse
l operative morbidity and mortality are generally lower compared to laparotomy because:
n abdominal wound is avoided
n technically easier as patient selected for vaginal hysterectomy usually has a small, atrophic, prolapsed
uterus and less pelvic adhesion
n the drawback is that other pelvic pathology such as ovarian lesion may not be assessed in vaginal
hysterectomy
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Laparoscopic method
l aims to minimise the operative complications of laparotomy by converting it to a vaginal hysterectomy (LAVH),
or take the corpus uterus out via laparoscopic wound after morcelation (LASH)
l two common types:
n laparoscopic assisted vaginal hysterectomy (LAVH)
n laparoscopic assisted subtotal hysterectomy (LASH)
l case selection:
n benign uterine pathologies
n vaginal hysterectomy alone is not feasible
n uterine size less than 14 week
n no severe pelvic adhesion
Complications of hysterectomy
General complications
l Febrile morbidity
l Haemorrhage
l Infection
Visceral injury
l Ureteric and bladder injury
l Bowel injury

Hysteroscopy
What is hysteroscopy
It is a kind of minimal invasive gynaecological operation in which an instrument (hysteroscope) with lumination is
inserted through the cervix to allow have direct visualization of the uterine cavity, which should be distended with
CO2, normal saline or glycine. It allows visual diagnosis of any endometrial pathologies, guides biopsy, and other
surgical procedures.
Indications
Diagnostic: can be performed as a day-case under no anaesthesia or paracervical block
l Abnormal vaginal bleeding such as
l Intermenstrual bleeding and menorrhagia refractory to medical therapy which may be due to endometrial
polyps or submucosal fibroid)
l Postmenopausal bleeding (to rule out endometrial carcinoma)
l Suspected congenital uterine abnormality such as septated uterus
Therapeutic:
l Endometrial ablation
l Resection of submucosal fiborids or endometrial polyps
Contraindication
l Pyometra (risk of spreading infection to peritoneal cavity)
Complications
l Infection
l Haemorrhage
l Uterine perforation
l Cervical laceration

Normal endometrial cavity and left ostium fibroid polyp

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 endometrial cancer

Cryotherapy
Cryotherapy is also called cryocautery and cryosurgery, and is commonly used to treat CIN. It involves the use of a
metal probe cooled through isotropic expansion of a compressed gas released from a tank through a small orifice
under pressure. The gases mostly used are nitrous oxide and CO2. The destructive effect in the tissue depends on
the rapid lowering of the temperature, resulting in crystallization of cell water and disruption of cell membranes and
organelles. The success rate of the treatment is 80-90%.

Electrocautery
It is also called electrocoagulation, hot cautery or diathermy. It is commonly used to treat CIN, and for haemostasis
during operation. The device consisted of a heating instrument of high resistance similar to the soldering iron heated
to a dull red. The device delivers electric current from the generators. The procedure is very painful and usually
requires general anaesthesia.

Cold coagulation
It is commonly used method to treat CIN. The apparatus generates a probe temperature of 100 to 120 degree
Celsius which is 'cold' in comparison to electrocautery or electrocoagulation diathermy, hence the name "cold
coagulation". The heat is conveyed to the tissues via thermosounds, which are held against the lesion in several
overlapping applications, each lasting 20 to 30 seconds.

Marsupialisation
It is a surgical procedure in which a cyst is everted rather than excised. This is particularly used in the treatment of
Bartholin's cysts and makes the operation quicker and more bloodless than excision of the gland. It also reduces the
incidence of recurrence.

Endometrial sampling
Indications
It is the biopsy of the endometrial tissue for histological examination. It is mainly indicated for investigation of
abnormal uterine bleeding, in which case endometrial hyperplasia or endometrial carcinoma is suspected.
Occasionally it is indicated for investigation of infertility. It may help to diagnose ovulation and luteal phase
insufficiency by the presence of secretary phase changes. Endometrial tuberculosis can be diagnosed by the
presence of caseous granuloma or culture of the tissue.
Methods
Uterine curetting
l It is the traditional method that has to be performed under general anaesthesia, and is therefore much replaced
by the following methods nowadays.
l It is supposed that it provides the greatest yield of tissue
Aspiration technique, with endometrial sampler or Vabra aspirator
l It is a rapid and simple out-patient procedure, and provides a reasonable good yield of tissue for histological
examination.
Hysteroscopically directed biopsy
l The endometrial cavity is also examined at the same time via hysteroscopy. Localised suspicious lesions can
be targeted. The yield however is very limited due to because of the small-sized biopsy forceps.
In general, sampling by both uterine curetting and aspiration methods provide comparative good sensitivity for
histological diagnosis of endometrial pathologies. Hysteroscopic assessment allows visualisation of structural

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abnormalities such as submucosal fibroids or endometrial polyps that can be missed by the other two methods.
However, it has to be supplemented with endometrial sampling by other methods.
Complications
l Perforation of uterus
l Introduction of infection

Hysterosalpingogram
What is Hysterosalpingogram
Hysterosalpingogram (HSG) is an X-ray examination of the genital tract after contrast injection into the uterine cavity,
by which contour of the uterine cavity, fallopian tubes and endocervical canal are visualized. It is normally performed
within the first ten days of menstruation in order to avoid inadvertent exposure of the early embryo to irradiation
Indications
Investigations of the following:
l Patency of fallopian tubes (to investigate infertility)
n HSG is less invasive when compared with laparoscopy and chromotubation for the investigation of the
tubal patency. However, it has false positive result as the injected contrast may cause tubal spasm that
transiently blocks the tubes. In addition, laparoscopy allows assessment of any pelvic pathology such as
endometriosis, chronic pelvic inflammatory disease, and pelvic adhesion, that is not possible with HSG.
l Structural abnormalities of uterus: congenital uterine anomalies such as bicornuate uterus and septate
n sometimes submucosal fibroids and endometrial polyps can be identified incidentally with HSG but HSG
is not the primary diagnostic method of these lesions
l Cervical incompetence
n leaking of contrast from the internal os the cervix may be seen in case of cervical incompetence. However,
the diagnostic accuracy is still limited. See cervical incompetence for detail.
Contra-indications
l allergy reaction to contrast
l active pelvic inflammatory disease
l pregnancy

9. Miscellaneous topics in gynaecology

Postcoital bleeding
It is a vaginal bleeding after coitus. An acute onset can be due to trauma secondary to intercourse. Tear of hymen is
common after the first coitus, and tear of vagina sometimes occurs after a vigorous intercourse. Postcoital bleeding
is also a symptom of cervical lesions such as cervical cancer, cervical polyps, cervicitis, or occasionally endometrial
polyps.

Postmenopausal bleeding
It is any vaginal bleeding occurs after menopause. It is always abnormal and investigation should not be delayed.
There are many possible causes and genital malignancies should be ruled out in the menopausal age group of
patients.
Causes
Uterine pathology:
l Atrophic endometritis
n It is the most common cause and the diagnosis is made after excluding other pathologies
l Endometrial polyp
l endometrial carcinoma
l uterine sarcoma: rare
l endometrial glands activation following hormonal replacement therapy or stimulation by endogenous estrogen
from ovarian stromal tumours
Cervical pathology:
l cervical polyp
l cervical cancer
l cervicitis
Fallopian tube pathology:
l fallopian tube cancer: very rare but postmenopausal bleeding may be the sole symptom
Vaginal pathology:
l vaginal cancer
l vaginal infection ulcer: particularly decubitus ulcer following genital prolapse
l Vulval pathology:
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l vulval cancer
l vulval infection and ulcer
Assessment
l Any lower genital tract pathologies are usually picked up by speculum and digital examination.
l Diagnosis of endometrial pathologies requires a hysteroscopy or endometrial sampling.
Remark
l Sometimes per rectal bleeding or haematuria may be mistaken as vaginal bleeding. Clinical assessment
should be able to differentiate these conditions.

Dyspareunia
It means painful sexual intercourse. Pain on penetration may be superficial or deep. Deep dyspareunia often has a
underlying pathologies such as pelvic endometriosis and chronic pelvic inflammatory disease. Superficial
dyspareunia usually has a psychological element, and lack of lubrication during intercourse. Sometimes superficial
dyspareunia of acute onset is related to local pathologies such as vaginitis, vulval herpes and ulcer.

Retroversion of uterus
Uterus rotates backwards in relation to the vagina. A mobile retroversion is a variant of normal occurring in over 25%
of women. It is usually asymptomatic although many gynaecological symptoms including pelvic pain and infertility
have been attributed to it in the past. A fixed retroversion, however, results from adhesion formation secondary to
pelvic inflammatory disease or endometriosis. Both are common causes of pelvic pain, dyspareunia and infertility.
Very rarely, a gradually enlarging retroverted uterus may be eventually impacted inside the pelvic cavity, resulting in
incarceration. One more importance concerning retroversion is that when it is misdiagnosed as anteversion during
performing uterine curetting, the uterus would be perforated.

Follicular cyst
It is a common physiological ovarian cyst. Sometimes a developing follicle may not ovulate and become persistent.
It is associated with the use of progestogen contraceptive and ovulation induction agents. It has a thin wall and clear
content under ultrasound and often less than 5cm in diameter. Majority of them are asymptomatic but in few
occasions they present with acute lower abdominal pain as a result of haemorrhage or rupture.

Chronic pelvic pain

Introduction
l Chronic pelvic pain is one of the most common symptoms of women. Most of the time the symptom is
nonspecific, and no organic causes can be identified.
Possible causes
Gynaecological
l Endometriosis
l Chronic pelvic inflammatory disease

Imperforate hymen
It is a congenital disorder in which the hymen membrane remains intact. When patients start menarche, menstrual
blood flow is blocked and the blood accumulates and distends the vagina. Usually patients present at early teenage
with amenorrhea (cryptomenorrhea), cyclic abdominal pain, abdominal distension and urinary retention. On
examination, the hymen membrane is bulging out and appears blue because of the blood collection behind the
membrane. Ultrasound shows a distended vagina beneath the bladder. The treatment is excision and drainage.

A mild bulging intact hymen membrane.A foley catheter

is inserted because of urinary retention

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 The angle of the hymen membrane is lifted up before
incision

The hymen membrane is cut open. Chocolate material

(old blood) is drained

The hymen membrane is excised

The wound is repaired

Nabothian cyst
It is a small cyst beneath the epithelium of the uterine cervix of no clinical significance. It can be multiple and the size
is not more than 10mm. See transformation zone for the formation of Nabothian cyst.

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Adolescence
It encompasses physiological, social and cognitive changes leading to the development of an adult identity. It is
different from puberty.

Puberty
Definition
It encompasses physiological changes leading to the development of adult reproductive capacity.
It is different from adolescence.
Normal puberty
A normal puberty consists of following stages:
l Adrenache
n the beginning of pubic hair development
l Thearche
n the beginning of breast development
l Menarche
n the beginning of first menstrual period
Abnormal puberty
Precocious puberty

Precocious puberty
Definition
Features of puberty develop too early with:
l breast development before 8 years of age, or
l menarche before 10 years ( or more than 2 standard deviations before the mean ages of onset).
It is further classified according to the underlying pathophysiology:
l True or central
n due to gonadotrophin production driving the ovaries
l False or peripheral
n due to autonomous adrenal or ovary production of sex hormones

Tanner staging
Tanner staging of breast development at puberty:
Stage 1 Infantile stage
Stage 2 Bud stage: The breasts and papillae are elevated as a small
mound and there is an increase in the diameter of the areola
Stage 3 Small adult breast: The breasts and areola are further enlarged
with a continuous round contour
Stage 4 Secondary mound: The areola and papilla enlarge to form a
secondary mound projecting above the contour of the remainder
of the breast
Stage 5 Typical adult breast: The secondary mound disappear so that
the breasts have smooth rounded contour

Hirsutism
Definition
Excessive facial and body hair in otherwise femine women. It is different from virilism.
Causes
l Idiopathic: most common, there may be racial or familial element.
l Endogenous endocrine disorders: polycystic ovarian disease (PCOD), congenital adrenal hyperplasia,
Cushing syndrome
l Androgen secreting tumours of adrenal gland or ovary: very rare
l Drug induced: danazol, phenytoin, anabolic steroid, androgens
Investigations
Depend on clinical suspicion:
l Hormone profile
l Radiological investigation if tumour is suspected
Management
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Treat underlying causes accordingly
l e.g. surgical removal of adrenal tumour
Treatment of excessive body hair
Cosmetic treatment
l e.g. Waxing, shaving, electrolysis, depilatory creams, bleaching
l Takes 3-6 months for the effect to be apparent, and often needs a year for an acceptable improvement.
Therefore, it is important to forewarn patients of this so that cosmetic measures are continued during this time.
Medical treatment:
l Combined oral contraceptives
n With less androgenic progestogen (e.g. third generation progestagen), or with anti-androgen component
(e.g. cyproterone in Dianette)
l Anti-androgens
n cyproterone: first choice; either prescribed on its own (need additional contraceptive measures) or with
COC (e.g. Dianette)
n spironolactone: less effective
l Glucocorticoids
n Only useful for those with hirsutism due to an underlying adrenal cause, e.g. late onset congenital
adrenal hyperplasia. Dexamethasone to suppress excessive adrenal androgens

Virilism
It is the presence of one or more of the following: clitoral hypertrophy, breast atrophy, male-type baldness and
deepening of voice. It is different from hirsutism. It is invariably due to excessive endogenous androgen production,
such as congenital adrenal hyperplasia and androgen-secreting ovarian stromal cell tumour.

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Oncology

Gynae-oncology
Introduction
It is a subspecialty of gynaecology deals with malignant and pre-malignant lesion of the genital tract
Female genital cancer in Hong Kong
Hospital Authority 93/94 Report:
Cancer Incidence Death
Ca Cervix 459 144
Ca Ovary 230 126
Ca Corpus 215 43
Cervical cancers and ovarian cancers are the 4th and 10th most common cancers in female population in Hong
Kong
Topics
Premalignant lesion of genital tract
l cervical intraepithelial neoplasm (CIN)
l vaginal intraepithelial neoplasm (VAIN)
l vulval intraepithelial neoplasm (VIN)
l endometrial hyperplasia
Cervical cancers
l majority is squamous cell carcinoma
l rarely adenocarcinoma
Ovarian cancers
l majority is epithelial cancer
l the rest is non-epithelial cancer including: germ cell tumours and stromal cell tumours
Cancers of corpus uterus
l most are endometrial carcinoma
l rarely sarcoma arise from the smooth muscle tissue
Vaginal cancers
l Most are squamous cell cancer
l very rarely adenocarcinoma related to in utero exposure to DES
Vulval cancers
l Most are squamous cell cancer and rarely melanoma
Gestational trophoblastic diseases
l more common in Asian than in Caucasian
Modalities of treatment
Surgery
l mainstay of curative treatment for epithelial type of cancers: endometrial, ovarian, and cervical cancer
Chemotherapy
l mainstay of treatment for trophoblastic disease and germ cell ovarian tumours
Radiotherapy
l mainstay of treatment for cervical cancer
l adjuvant therapy for high-stage endometrial cancer
What should medical students know
Students should know cervical cancer, endometrial carcinoma, ovarian cancer, gestational trophoblastic disease and
premalignant lesions: CIN and endometrial hyperplasia as they are relatively common.
Sarcoma, vaginal and vulval premalignant lesions and cancers are very uncommon.

1. Malignant neoplasms of vagina and vulva

Staging of CA vagina
Staging CA vagina FIGO 1995
0 Intraepithelial neoplasia
I Invasive carcinoma confined to vagina mucosa
II Subvaginal infiltration not extending to the pelvic wall
III Extends to pelvic wall
IVa Involves mucosa of bladder or rectum
IVb Spread beyond the pelvis

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Staging of CA vulva
Staging CA vulva FIGO 1995
I Confined to vulva and / or perineum, less than 2cm in
maximum diameter. Groin nodes not palpable
Ia Stromal invasion no greater than 1mm
Ib Stromal invasion greater than 1mm
II Confined to vulva and / or perineum, more than 2cm in
maximum diameter. Groin nodes not palpable
III Extends beyond the vulva, vagina, lower urethra or
anus; or unilateral regional lymph nodes metastasis
IVa Involves the mucosa of rectum or bladder; upper
urethra, or pelvic bone; and / or bilateral regional lymph
nodes metastases
IVb Any distant metastasis, including pelvic lymph node

2. Malignant neoplasms of ovary

Ovarian cancer
Primary ovarian cancer
In general, primary ovarian cancer is divided into two types:
l Ovarian epithelial carcinoma which is subclassified into:
n Serous 40%
n Mucinous 10%
n Endometrioid 20%
n Clear cell 5%
n Brenner
n Mixed
l Non-epithelial cancer which include:
n germ cell tumours
n stromal cell tumours
l They are different not only in pathology, but also in epidemiology, clinical presentation and treatment. Please
refer to individual topics for detail.
Secondary ovarian cancer
l Metastasis from other sites such as bowel, stomach, and breast can occur. A characteristic secondary cancer
is called Krukenberg tumour.

Borderline malignancy of ovary

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

Germ cell tumour

Ovarian germ cell tumours, together with stromal cell tumours, are usually classified as non-epithelial carcinoma of
the ovary, as they are very different from ovarian epithelial carcinoma. Compared to epithelial type, germ cell
tumours are rare, and occur in younger age group of patients. They are in general more sensitive to chemotherapy.
They also have a specific and sensitive tumour marker. They are usually unilateral and solid. They arise from the
germ cell line of the ovary and are subclassified into:
l Teratoma
l Dysgerminoma
l Yolk sac tumour
l Choriocarcinoma
In general, the treatment consists of unilateral oophorectomy (lesion side) followed by chemotherapy. Radical
surgery is not required and fertility can be preserved. Bilateral oophorectomy and hysterectomy is advised for
patients who have completed family.

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Dysgerminoma
It is the most common malignant germ cell tumours of the ovary, and also account for 2 to 5% of all primary ovarian
cancers. It mainly affects the young women (< 30 year old). It is similar to seminoma of men.
It is solid, loculated, moderate in size, and usually has a long ovarian pedicle which is at risk of torsion. It is bilateral
in 10% of cases, and is spread through lymphatic channels to para-aortic, mediastinal and supraclavicular lymph
nodes. It does not produce hormones, but may contain elements of yolk sac tumour and choriocarcinoma, and their
presence may make the prognosis worse. Therefore, testing for serum level of alpha-feto protein and human
chorionic gonadotropin are important.
Dysgeminoma is very sensitive to both chemotherapy and radiotherapy. Treatment is usually oophorectomy
followed by chemotherapy. The contralateral ovary and uterus can be preserved for fertility.
Discussion/Something to Consider
As dysgeminoma is also radiosensitive, what is the reason that chemotherapy is preferably to radiotheray as a
post-surgical adjuvant treatment?

Yolk sac tumour

Also called endodermal sinus tumour, is the second most common malignant germ cell tumour of the ovary. It
usually affect children or young aged women. It is a rapid-growing solid tumour, and usually presents as an acute
abdomen due to rupture, necrosis and haemorrhage. The tumour secrets alpha-feto protein which acts as a
sensitive tumour marker, and is useful for monitoring of the disease. The tumour is very chemosensitive but not
radiosensitive. Treatment is oophorectomy followed by chemotherapy. As chemotherapy is very effective, the
contralateral ovary and the uterus can be preserved if they are not involved.

Krukenberg tumour
It is a secondary ovarian cancer with characteristic histological picture of mucin-ladin, signet-ring cells infiltrating a
hypoplastic ovarian stroma of spindle shaped cells, and is usually metastasized from stomach, colon, breast,
pancreas. It is usually bilateral, and most are lobulated, of moderate size, rapid growing, and retained the normal
shape of ovary.

3. Malignant neoplasms of uterine cervix

Cervical cancer
Introduction
l Squamous cell carcinoma is the most common type of cervical cancer. Only 5% belong to adenocarcinoma.
l Medical students are not required to know the detail of adenocarcinoma except the following:
n Adenocarcinoma is different from squamous cell type in the following aspects:
u it affects women of younger age
u it is difficult to be screened or diagnosed as it arises in the endocervical canal
n Adenocarcinoma is similar to squamous cell type in that there is a premalignant stage, and spread,
staging and treatment are the same.
l The rest of the content refers to squamous cell carcinoma.
Epidemiology
l most common gynaecological malignancy in HK
l median age of onset:
n CIN: 35-40
n cancer: 45-50
n trends toward younger age group
l Drastic reduction of mortality by pap smear screening
Aetiology and pathogenesis
l Abnormal squamous metaplasia of the cervical epithelium in the transformation zone associated with human
papillomavirus 16 and 18, resulting in cervical intraepithelial neoplasia (CIN) which progresses to carcinoma
Risk factors
l multiple sexual partners
l coitus at young age
l Sexually transmitted diseases esp HPV type 16 and 18
l multipara, age at first pregnancy
l lower social class
l prostitution
l cigarette smoking (more than 20 cigarettes/ day)
l compromised immune status
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l male partner with STD, penile CA
l History of cervical dysplasia (CIN)
Spread
l Mainly direct spread: upper and lower vagina, parametrium, pelvic side wall
l Lymphatic: obturator, hypogastric, external iliac, common iliac, para-aortic, rarely retrograde to inguinal
l rarely through blood to: liver, lung, bone, brain
Clinical features
Asymptomatic in some patients:
l screened by smear
Present with local symptoms:
l abnormal vaginal bleeding: Postcoital bleeding, Intermenstrual bleeding
l vaginal discharge: blood-stained, unpleasant smell
Rarely with symptoms associated with advanced disease
l bowel or urinary symptoms, bone pain, cachexia, weakness, SOB
Local signs:
l cervical tumour:
n hard, friable, irregular, enlarged, fixed, contact bleeding
n vaginal and parametrial involvement, pelvic side wall involvement
Systemic signs are uncommon:
l anaemia
l inguinal lymphadenopathy
l pulmonary involvement, hydronephosis, hepatomegaly, ascites
Staging
l Staging of CA cervix remains on clinical assessment (see staging of CA cervix)
Diagnosis
l Confirmed with cervical biopsy, which can be assisted with colposcopy. Pap smear is not a diagnostic tool.
Staging procedure
plan for option of treatment
provide information of prognosis
l Cystoscopy and examination under general anaesthesia
l USG, CT scan or MRI: assess liver, kidneys, lymph nodes involvement
l Proctoscopy, Barium enema: if rectal involvement is suspected
l IVU: look for urinary tract involvement, replaced with good USG
l Lymphangiography: limited role because of inaccuracy in assessing lymph node involvement
Treatment
Principle
l Radical surgery and radiotherapy are the mainstay of treatment
l Choice of treatment depends on staging, age, and medical fitness of patients
Stage Treatment
Ia1 simple hysterectomy
Ia2-IIa Radical hysterectomy and bilateral pelvic lymhadenectomy or RT
IIb-IV radiotherapy
Radiotherapy vs radical surgery for stage Ia2 to IIa
l Both achieve similar good cure rate but have advantages and disadvantages compared to each others:
Advantages of radical surgery :
l preservation of ovarian steroidogenesis
l better coital function
l avoid long term complications of RT
l accurate surgical staging & evaluation of aortic, pelvic LN
l psychological effect of extirpation of primary tumour
Disadvantages of radical surgery :
l immediate morbidity especially bladder and ureteric injury, excessive blood loss
l fistula formation
l bladder denervation
l lymphocyst
l obturator nerve damage
l DV T/ paralytic ileus/ sexual dysfunction
Disadvantages of RT :
l bowel irritation (nausea, vomiting, diarrhoea)
l bowel ulceration (ischaemic change)
l chronic haemorrhagic proctitis
l rectovaginal fistula
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l bowel obstruction
l haemorrhagic cystitis
Postoperative pelvic irradiation
Some patients would require adjuvant radiotherapy after a radical hysterectomy because of:
l surgical specimen margin involvement
l positive pelvic LN
Treatment of recurrent disease
Local recurrence:
l Radiation
l Pelvic exenteration
n extensive operation involves removal of bladder, rectum, uterus and vagina
n require colostomy and ileal conduit
Distant recurrence:
l Radiotherapy
l Chemotherapy
Prognosis
Stage 5yrs Survival
I 80%
II 50%
III 20%
IV 7%
Overall 57%
Prevention
l Routine pap smear effectively reduces the incidence and mortality. Patients with abnormal smear result should
be referred for colposcopy examination.
Discussion/Something to Consider
Why does the staging of cervical cancer still remain on clinical level?
Why is surgery not an effective treatment for stage IIB or beyond?
Which treatment, radical surgery or radiotherapy, would you advise to a young woman with stage Ia CA cervix but
otherwise healthy? and why?
In what way would the urinary tract get involved in CA cervix?

Staging of CA cervix
Staging CA Cervix FIGO
Stage Description
O preinvasive carcinoma (CIN or carcinoma-in-situ)
I Carcinoma confined to the cervix
Ia preclinical carcinoma diagnosed only by microscopy
Ia1 minimal microscopically evident stromal invasion
Ia2 depth of invasion from the base of epithelium from which it originates <=5mm, and horizontal spread
<=7mm
Ib dimension more than that of Ia2
II carcinoma extending beyond the cervix and involving the upper two-third of vagina, and /or infiltrating the
parametrium
IIa carcinoma has involved the upper two-third of vagina
IIb carcinoma has involved the parametrium
III carcinoma involving the lower third of vagina and / or extending to the pelvic side wall (there is no space
between the tumour and the pelvic side wall)
IIIa carcinoma involving the lower third of vagina
IIIb carcinoma extending to the pelvic side wall
IVa carcinoma involving the mucosa of the bladder or rectum and/ or extending beyond the true pelvis
IVb spread to distant organs

Exenteration
It is an ultra major gynaecological surgery in which the midline pelvic organs including the uterus, rectum, and
bladder are excised. Urinary diversion and colostomy are required after exenteration. It is subclassified into:
Anterior exenteration:radical hysterectomy together with total cystectomy
Posterior exenteration: radical hysterectomy plus excision of rectum and rectosigmoid
Total exenteration: anterior and posterior exenteration
It is indicated in and only in advanced primary or recurrent malignancy of the uterine cervix (or rarely uterine corpus)

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that has invaded the bladder and/or rectum, but still confined to the pelvis, so that excision of these major pelvic
organs may result in cure.
It is of high operative morbidity and mortality and patient selection for this surgery is very important.

4. Malignant neoplasms of uterine corpus

Endometrial carcinoma
Incidence
l Most common gynaecological malignancy in USA
l Lifetime risk: 2.2%
l Average age: 60
Risk factors
Mainly relat ed to chronic exposure of endogenous or exogenous estrogen:
l Early menarche and late menopause
l Nulliparity and infertility
l Exogenous estrogens
n estrogen used alone without progestogen: increases risk of CA endometrium by 4-9 time
l Polycystic ovary disease (PCOD)
n chronic anovulation develops CA endometrium at an earlier age, accounts for most of cases diagnosed
before age 40
l Obesity
n conversion of androstenedione to oestrone by fat cells, with subsequent conversion to oestradiol
l Hypertension
l DM
n 20% incidence of DM in patients with CA endometrium
Protective factors
l Pregnancy
l Oral contraceptive pills
Pathology
Histology type:
l Majority is endometrioid adenocarcinoma which is the least aggressive type
l Other types are papillary, clear cell adenocarcinoma, adenosquamous and squamous type which are in
general more aggressive
Grade:
l Good correlation between grade and prognosis
Grading Features
grade 1 (well-diff) glandular pattern with atypical cells
grade 2 (moderately diff) glandular pattern with some partly solid areas
grade 3 (poorly diff) absence of glandular pattern that is replaced by sheets of atypical cells
Spread
Local:
l Myometrium
l Cervix
l Adnexa
Lymphatic:
l Pelvic lymph nodes
l Para-aortic lymph nodes
Distant: rare
l Lung
Clinical features
Most cases present with abnormal vaginal bleeding:
l postmenopausal bleed, irregular short menstrual periods, menorrhagia
Rarely present with secondary symptoms:
l urinary or bowel symptoms
Physical examination:
l local signs are uncommon until it metastasis to cervix or beyond. Uterus may be enlarged
Diagnosis
Confirm with endometrial biopsy which can be obtained by:
l Endometrial sampler
l Vabra aspiration
l Dilatation and curettage
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Staging procedure
Surgical staging is used. Following preoperative assessments provide some ideas about the extent of the tumour:
l USG, CT scan, or MRI of abdomen for liver, pelvic and paraaortic LN enlargement
l hysteroscopy to assess any cervical involvement; it replaces the old fashion method: fractional curettage
l grading from histological examination
l cystoscopy, proctoscopy and examination under general anaesthesia if local spread is suspected
Surgical staging procedure:
l peritoneal cytology
l LN biopsy
l cut open the uterus after hysterectomy to look for the depth of myometrial invasion and the cervical invasion
see Staging of CA endometrium
Management
Stage I Grade 1
TAHBSO
l no need for lymhadenectomy (only 2 % involvement in stage I grade 1 disease)
l myometrial involvement >1/2, whole pelvic RT
Stage I Grade 2, 3
l TAHBSO + LN sampling
l 10% of LN involvement in grade 2; 25-30% LN involvement in grade 3
l if pelvic LN +ve, need whole pelvic irradiation
l if para-aortic LN +ve, need progestogen or chemotherapy
l If peritoneal cytology + ve
l at risk of peritoneal recurrence
l progestational agent
l chemotherapy
l intraperitoneal P32
Stage II
l radical hysterectomy or
l whole pelvic irradiation followed by intracavity Cesium, followed by TAHBSO
Stage III and IV
l TAHBSO +/- preop RT
Recurrence
l Progestational agents (effective in 1/3 recurrence) or chemotherapy
Prognostic factors
l histologic grading
l staging
l depth of myometrial invasion
l metastasis of LN
l peritoneal cytology
l cervical involvement
l adnexal involvement
l (uterine size is not a significant prognostic factor)
Prognosis
Stage 5 yr survival
I 75%
II 50%
III 25%
IV 5%
Discussion/Something to Consider
Why is the surgical treatment of early stage CA endometrium is different from that of CA cervix?

Staging of CA endometrium
Staging CA Endometrium FIGO
I Confined to corpus uterus
IaG123 Tumour limited to endometrium
IbG123 Invasion < half myometrium
IcG123 Invasion > half myometrium
II Spread to cervix but not outside uterus
IIaG123 Endocervical glandular involvement only
IIbG123 Cervical stromal invasion
III Spread outside uterus but not outside the true pelvis

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IIIaG123 Tumour invades serosa and / or adnexae and / or positive peritoneal cytology
IIIbG123 Vaginal metastasis
IIIcG123 Metastasis to pelvic and / or para-aortic lymph nodes
IV Spread outside the true pelvis or to the bladder or rectum
IVa Tumour invades bladder and / or bowel mucosa
IVb Distant metastases including intra-abdominal and / or inguinal lymph nodes

Remark:
G1: grade1 <5% solid pattern
G2: grade2 5-50% solid pattern
G3: grade3 >50% solid pattern
clear cell or papillary type of tumour upgrade the grade by 1

5. Premalignant lesions of genital tract

CIN
Definition
l Cervical intraepithelial neoplasm (CIN) describes the histopathological condition where part or whole of the
thickness of the cervical squamous epithelium is replaced by cells showing varying degrees of dysplasia.
l It is graded as CIN I, II, or III according to the differentiation of basal ,intermediate and superficial thirds of the
epithelium respectively, but the conditions are recognized as being part of a continuous process.
l When the whole thickness is involved (without invasion to underlying stroma) it is called carcinoma-in-situ
l It is a premalignant lesion that if left untreated, can progress to invasive cervical cancer
Cause
l associated with infection by human papillomavirus (type 16 and 18), which alters the normal squamous
metaplastic changes in the transformation zone of cervix
Progression
l CIN I: 46% regress and 26%progress to CIN III over 2 years
l CIN III: 18% progress to invasive cancer in years, and 36% in 20 years
Screening and diagnosis
l is screened regularly by pap smear
l is diagnosed with colposcopy and guided biopsy
l Features of CIN under colposcopic examination:
n usually has distinct acetowhite lesion with clear margins
n shows a mosaic vascular pattern
n punctatin (where a vessel rums perpendicular to the surface)
n In general, the high grade of CIN will be when:
u the more quickly and strongly the acetowhite changes develop,
u the clearer and more regular the margins of the lesion, and
u the more pronounced the mosaic or punctation
Treatment
The following options of surgical treatments are guided by colposcopy:
Ablative methods
l Cryotherapy
l Electrocautery
l Laser vaporization
l In general, ablative methods is quick, cheap and easy to peform. The main disadvantage is lack of histology for
review. About 1% of cases of CIN III may have invasive carcinoma that may be missed after ablative treatment.
Excisional methods
l Loop electrodiathermy excision procedure (LEEP)
l Cone excision using laser or knife
l knife excision requires general anaesthesia with high risk of primary and secondary haemorrhage. Laser
excision requires more technique
l Hysterectomy:
n for patients who have complete family. The advantage is no risk of recurrence

Cervical intraepithelial neoplasia

See CIN

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Dyskaryosis
A cytological term used to describe cells compatible with origin from epithelium with dysplasia.
In cervical intraepithelial neoplasia, dyskaryosis is classified as mild, moderate, or severe according to appearances
suggesting origin from CIN I, II, or III. The distinction between changes compatible with human papillomavirus (HPV)
infection or CIN I is particularly difficult to make.
Cytological grading correlates poorly with subsequent histological diagnosis. This correlation can be substantially
improved if the three cytological grades are merged to two.
Bethesda system divides abnormal smears into those showing high and low grade squamous intraepithelial lesions
(HGSIL and LGSIL)

Koilocyte
It represents the diagnostic cytopathic effect of human papillomavirus (HPV). Koilcytes are HPV-infected epithelial
cells with enlarged, wrinkled and sometimes hyperchromatic nuclei, which are surrounded by a clear space or halo.
Koilocytes are usually seen in the intermediate and superficial layers of the epithelium.

Acetowhite
It is a term used during colposcopy to describe any lesion that changes to white in colour after being treated with
acetic acid. Lesions that typically show acetowhite change include:
Cervical intraepithelial neoplasm (CIN)
Wart (human papillomavirus infection)
The intracellular protein content is high in these lesions and therefore the abnormal cells swell after being treated
with acetic acid. This results in change of refraction of light and hence the lesion appears white.
Other causes of acetowhite changes:
Sometimes normal columnar epithelium will also blanch briefly after exposure to acetic acid. It can be identified by
its villous or furrowed surface. Squamous metaplasia has a glassy white appearance but it is hard to distinguish from
CIN I. Subepithelial fibrosis secondary to previous cervical excision or destruction surgery may also appear white.
This can be recognised by the radial arrangement of lines of fine punctations.

Pap smear
Definition
l It is a cytological investigation of the cervical cells designed for screening of cervical intraepithelial neoplasia
(CIN), as a preventive measure against cervical cancer.
Who should be screened
l all women aged 20 to 64 who are or ever have been sexually active
When should be screening stopped
l at age 65
l however, women aged 65 or above should be encouraged to have a smear if they have not been screened
previously
How often should smears be taken
l every 3 to 5 years
l in HK, yearly in the first 3 years, then every 3 years
Frequency of screening Reduction in risk of developing invasive diseases
every 5 year 84%
every 3 year 93%
every year 95%
l As there is only 2% reduction of risk of invasive cancer by yearly screening when compared to 3-yearly
screening, the later is more cost-effective
How to take a pap smear
l Patient relaxes in the dorsal position.
l Perform speculum examination to visualise the whole cervix.
l Use a small amount of water-based lubricant so that it would not affect the smear.
l Swab away any blood or discharge.
l If the squamo-columar junction can be seen, take a smear from the transformation zone by 360 degree firm
surface sweep with a suitable spatula
l If the squamo-columar junction is sited within the endocervical canal then take a smear by rotating a cytobrush
in the canal.
l Spread the smear evenly over a labelled glass slide.
l Fix it rapidly with ethanol to avoid drying artifact.
How to examine a pap smear under microscope
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l The cytological features of individual cervical cells are examined. The degree of dyskaryosis depends on the
nuclear features and nuclear to cytoplasmic ratio, and is classified to mild, moderate and severe. Koilocytosis,
a feature of human papillomavirus infection may also be picked up.
l Because of the difficulties in differentiate the grading, an alternative classification system called Bethesda is
also commonly used. In the Bethesda system, CIN II and III are combined into high grade squamous
intraepithelial lesion (HGSIL), while CIN I and koilocyotosis are combined into low grade SIL. The Bethesda
system also includes 'atypical squamous cells of unknown origin' (ASCUS) of which cervical cells show mild
dyskaryosis but do not fit in low grade SIL. They are usually due to reactive changes toward inflammation.
l Besides, lower genital tract infection may sometimes be picked up from a smear: trichomonas vaginalis,
candidiasis, clue cells of bacterial vaginosis.
How good is a pap smear
l false negative rate of 15% in detection of histologically confirmed CIN.
Management of abnormal pap smear
For HGSIL (CIN II and III):
l Refer to colposcopy with early appointment
For LGSIL (CIN I and koilocyotosis):
l Refer to colposcopy
For ASCUS:
l Repeat smear after 6 months
Discussion/Something to Consider
What features of cervical cancer and pap smear fit the WHO criteria of screening?
Which factors account for the false negative of a pap smear?

Bethesda
What is Bethesda system
It is a reporting system for pap smear result as follows:
l Adequacy of the specimen
l Satisfactory for evaluation
l Satisfactory for evaluation but limited by... (specific reason)
l Unsatisfactory for evaluation (specific reason)
l General Categorization (optional)
l Within normal limits
l Benign cellular changes: See Descriptive Diagnosis
l Epithelial cell abnormality: See Descriptive Diagnosis
Descriptive Diagnoses
Benign cellular changes
l Infection
n Trichomonas vaginalis
n Fungal organisms morphologically consistent with Candida spp
n Predominance of coccobacilli consistent with shift in vaginal flora
n Bacteria morphologically consistent with Actinomyces spp
n Cellular changes associated with Herpes simplex virus
n Others
l Reactive changes
n Reactive cellular changes associated with:
n Inflammation (includes typical repair)
n Atrophy with inflammation ("atrophic vaginitis")
n Radiation
n Intrauterine contraceptive device
n Others
Epithelial cell abnormalities
l Squamous cell
n Atypical squamous cells of undetermined significance (ASCUS): Qualify*
n Low-grade squamous intraepithelial lesion encompassing:
n HPV** mild dysplasia/ CIN 1
n High-grade squamous intraepithelial lesion encompassing:
n Moderate and severe dysplasia. CIS/CIN 2&3
n Squamous cell carcinoma
l Glandular cell
n Endometrial cells, cytologically benign, in postmenopausal women
n Atypical glandular cells of undetermined significance (ASGUS): Qualify*
n Endocervical adenocarcinoma
n Endometrial adenocarcinoma
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 n Extrauterine adenocarcinoma
n Adenocarcinoma, NOS (not otherwise specify)
l Other malignant neoplasms: Specify
l Hormonal evaluation (applies to vaginal smears only)
l Hormonal pattern compatible with age and history
l Hormonal pattern incompatible with age and history: Specify
l Hormonal pattern not possible due to: Specify
Remark:
*Atypical squamous or glandular cells of undetermined significance should be further qualified as to whether a
reactive or a premalignant/malignant process is favoured.
**Cellular changes of human papillomavirus (HPV), previously termed koilocytosis, koilocytotic atypia, or
condylomatous atypia, are included in the category of low-grade squamous intraepithelial lesion.

Transformation zone
Formation of transformation zone
l Normally the endocervix is covered with columnar epithelium while the ectocervix with squamous epithelium.
The boundary is called squamo-columar junction (SCJ)
l During reproductive age when the cervix is under the influence of estrogen effects, it tends to evert leading to
the exposure of the columnar epithelium on the ectocervix. The thin columnar epithelium appears red and the
result is so often erroneously referred to as a cervical erosion or ectropian.
l The exposed part of columnar epithelium on the ectocervix is gradually replaced by a process of squamous
metaplasia spreading from the SCJ towards the cervical canal. The end result of this transformation is the
replacement of the ectopic columnar epithelium with mature squamous epithelium.
l If the squamous epithelium covers the entrance to a cervical crypt and the columnar cells continue to secrete
mucus in the crypt, a nabothian cyst results.
l The region of cervix in which the process of metaplasia take place
l In some women the transformation zone may extend on to the vaginal walls
Clinical significance of transformation zone
l cervical intraepithelial neoplasia (CIN) results from a disruption of the metaplastic process, with the possible
involvement of human papillomavirus (HPV)
l the transformation zone and the CIN lesion are visible under colposcopy

Colposcopy
What is colposcopy
l Colpo: vagina; scopy: view
l A detail examination of the female lower genital tract with the aids of low-power (magnification of 5 to 20 times )
illuminated binocular microscope.
Indications
Diagnostic:
l To examine and guide biopsy when there are abnormal pap smears or lesions of lower genital tract suspicious
of intraepithelial neoplasms (such as CIN, VIN and VAIN)
Therapeutic:
l To excise or destroy benign or premalignant lesions by means of loop electrosurgical excisional procedure
(LEEP), cryotherapy, electrocautery or laser therapy
How to perform colposcopy
l Bimanual examination and taking pap smear (if indicated):
n Essential to aid detection of frank invasive disease of cervix, an uterine or an ovarian mass
n Deferring the smear until after colposcopic inspection may provide a less satisfactory sample for
cytological examination
n After that, the cervix is examined under a microscope:
l Examination with saline:
n Remove any discharge with normal saline
n Look for any leukoplakia, viral condyloma and any evidence of invasive disease such as ulcerated or
irregular surface, and atypical vessels.
l Examination with acetic acid:
n Apply 5% acetic acid
n acetic acid causes tissue to swell, especially abnormal epithelium, which has a higher nuclear density,
high protein concentration. This results in change of refraction of light, and therefore the abnormal
epithelial tissue appears white (acetowhite lesion)
n Identify the squamo-columnar junction (SCJ) which is defined by the lower limit of normal columnar
epithelium. Failure to identify the SCJ correctly is one of the main pitfalls in colposcopy.
n Determine the nature of the lesion by assessing the colour, the margins and vascular markings of the
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 lesions:
u CIN lesions are acetowhite with distinct margin. They often show a mosaic vascular pattern with
patches of acetowhite separated by red vessels. Punctations are vessels running perpendicular to
the surface. In general, the more quickly and strongly the acetowhite changes develop, the clearer
and more regular the margins of the lesion, and the more pronounced the mosaic or punctation, the
more severe is the CIN lesion is.
u Flat warts usually present as acetowhite lesions of faint and very irregular margins. There are
usually isolated, satellite lesions.
u See acetowhite for other causes of acetowhite changes.
u Invasive lesions have very marked mosaic pattern or coarse punctation. There are atypical vessels
which run a bizarre course and are often corkscrew or comma-shaped, with large diameter, abruptly
appearing on and disappearing from the surface, and do not branch dichotomously like normal
vessels.
l Examination with Lugol solution (Schiller test):
n Normal squamous epithelium (which contains glycogen) stains dark brown by Lugol solution (iodine and
potassium iodine). whereas columnar or abnormal squamous epithelium do not.

LEEP
Loop electrosurgical excisional procedure, also called large loop excision of transformation zone (LLETZ), is
performed under guidance of colposcopy. It utilises electricity through a cutting loop to provide excision. It is
performed as a day-case without anaesthesia and requires simple equipment, and therefore has become the most
popular method to treat CIN lesions. The major disadvantage is that it is not easy to tailor the excision to the exact
area of the abnormality. In consequence, there is a risk of incomplete excision. Common complications are infection
and haemorrhage. Patients are advised to avoid coitus for two weeks after the procedure.

Endometrial hyperplasia
Classification
It is classified into four groups:
Simple (cystic) endometrial hyperplasia without atypia
l glands with single layer of glandular cells and dilated in a cystic pattern
l less than 1% chance of developing endometrial carcinoma
Simple endometrial hyperplasia with atypia
l glandular structure as above but individual cells nuclei are abnormal
l about 5% chance of developing endometrial carcinoma
Complex endometrial hyperplasia without atypia
l Glands are closely packed together with more than one layer. Cells nuclei are still normal
l about 5% chance of developing endometrial carcinoma
Complex endometrial hyperplasia with atypia
l Glands are closely packed together with more than one layer. dyskaryotic cells are present
l 10 to 15% chance of developing endometrial carcinoma
Causes
It is mainly secondary to chronic unopposed estrogenic stimulation. Following patients are particularly at risk:
l polycystic ovarian disease (PCOD)
l unopposed estrogen hormonal replacement therapy in patients with intact uterus
Presentation
l menorrhagia, irregular menstrual bleeding
Diagnosis
By endometrial sampling:
l endometrial sampler
l vabra aspiration
l uterine curettage
Treatment
Patients with complex atypical hyperplasia should be advised to have hysterectomy. High dose progestogen therapy
may be tried if patients are very keen to keep uterus for pregnancy. Other types of hyperplasia can be managed with
hormonal treatment.

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6. Trophoblastic diseases

Molar pregnancy
See gestational trophoblastic disease

Gestational trophoblastic disease

This is a group of disorders involving benign and malignant growth of trophoblastic tissue, and is classified into:
l Hydatiform mole which is subclassifed into complete and partial
l Invasive mole
l Choriocarcinoma: a rare but severe disease
l Placental site tumour: very rare
l Residual trophoblastic disease may follow a mole

Hydatiform mole
Also called molar pregnancy, is one form of gestational trophoblastic diseases and is further subclassified into
complete and partial mole.
Complete mole
l It is an abnormal conception without an embryo or fetus, but solely cytotrophoblastic and syncytotrophoblastic
hyperplasia, with loss of villous vascularity, causing gross hydropic swelling and central cistern formation.
l The karyotyping of the conception is usually 46XX
Incomplete mole
l It is an abnormal conception with presence of embryonic or fetal element, and a mixture of normal appearing
villi and focal villous swelling and trophoblastic hyperplasia.
l The karyotyping of the conception is usually 69XXY or 69XXX, as a result of fertilisation of an ovum by two
sperms or a sperm that has duplicated chromosomes
Epidemiology
l common in Asian: Asian to West ratio: 8:1
l 1 in 350 (HK); 1 in 82 (Taiwan); 1 in 1500 (USA)
l higher risk < 20 and > 40 years of age
Clinical presentation
l usually present between 8 and 24 weeks of gestation with peak at 14 weeks
l vaginal bleeding (occurs between 6-16 weeks, 95%)
l passed vesicular tissue vaginally
l uterus large for date (50%)
l hyperemesis gravidarum (30%)
l bilateral thecal-luteal cyst (15%)
Complications
l Anaemia (due to massive haemorrhage)
l Uterine perforation (due to invasion or surgical evacuation)
l Pelvic sepsis
l Clinical hyperthyroidism (10%, related to high HCG level)
l Residual trophoblastic disease
l Pre-eclampsia
l Disseminated intravascular coagulopathy (DIC)
l Trophoblastic pulmonary embolisation (rare)
Remark: clinical presentation is less severe and complications are less common in case of partial mole
Diagnosis
USG:
l A complete mole has a typical intrauterine vesicular features without fetal element. The differential diagnosis
would be cystic degeneration of a abortion. A partial mole may be difficult to detect under USG.
Biochemical:
l There is a very high serum level of HCG in complete mole. The elevation of HCG level in partial mole is less.
Management
l The mainstay of treatment is suction evacuation of uterus. The HCG level should be monitored
post-operatively until it returns to normal because of the risk of residual trophoblastic disease. Chemotherapy
may be required if there is a persistent elevation of HCG.
Prognosis
l complete mole (malignant : 15-20%)

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l partial mole (smaller risk)

Invasive mole
Invasive mole is one kind of gestational trophoblastic diseases and is always preceded by hydatiform mole. The
abnormal trophoblasts invade the myometrium and therefore it is much less readily removed by evacuation. It may
also metastasize to any part of the body such has lung, liver, brain and vagina. Invasive mole usually presents as
residual trophoblastic disease with persistent vaginal bleeding and a high serum human chorionic gonadotropin
(HCG) level after evacuation of uterus. Occasionally it presents with perforation of uterus as a result of invasion. The
diagnosis of invasive mole can only be confirmed by histological examination of the uterus after hysterectomy, which
is rarely required nowadays, unless there is uncontrolled bleeding or perforation. Therefore, invasive mole is usually
managed as residual trophoblastic disease with chemotherapy.

Choriocarcinoma
This is a rare but highly malignant tumour and can arise from;
l product of gestation: gestational choriocarcinoma, a kind of gestational trophoblastic disease)
l ovaries (a kind of germ cell tumour of ovary)
Gestational choriocarcinoma
Incidence
l 1 in 40,000 in the West and 1 in 13000 in the East
l 50% arise from complete mole; 25% from abortion/ tubal pregnancy; and 25% from term gestation
Pathology
l highly malignant with invasion and necrosis of uterine wall
l predominantly vascular spread with pulmonary metastasis in 70% of cases
l secret HCG which can be used as a tumour marker for monitoring of the disease as well as a prognostic factor.
Treatment
l Chemotherapy

Residual trophoblastic disease

It is a clinical diagnosis made when after evacuation of uterus for hydatiform mole, there is still evidence of
persistent molar tissue inside the body (e.g. persistent high HCG). Residual trophoblastic disease can be due to
invasive mole, or metastasis of the molar tissue.
Normally after the initial treatment of hydatiform mole, the HCG level will drop to pre-pregnant level gradually within
a few weeks. In some situation, however, the HCG level may stop to drop after reaching a plateau, or may even rise
again. Investigations including chest X-ray, lumbar puncture for HCG assay, and USG of liver should be performed
to look for any evidence of metastasis. Treatment is chemotherapy (choice according to Bagshawe score) which is
often effective. The serum HCG level should be checked to monitor the chemoresponse.

Bagshawe score
The Bagshawe score is designed to classify patients with gestational trophoblastic diseases into low risk, medium
and high risk according to the prognostic factors. Each prognostic factor is assumed to act as an independent
variable and the effects of the factors are additive. It helps to guide the clinical management:
l Low risk: methrotrexate
l Medium risk: etoposide or actinomyocin D
l High risk: EMA/CO regimen
Prognostic factors score 0 score 1 score 2 score 4
Age (years) <39 >39 / /
Antecedent pregnancy Mole Abortion Term /
Interval between end of antecedent 4 4-6 7-12 12
pregnancy and start of chemotherapy
(months)
3 3 4 4 5 5
HCG (iu/L) <10 10 -10 10 -10 >10
ABO group (female X male) / O X A or A X O B or AB /
Largest tumour / 3-5cm >5cm /
Site of metastases / Spleen, kidney GI tract, liver Brain
Number of metastases identified / 1-4 4-8 >8
Previous use of chemotherapy / / single drug 2 or more
The total score for a patient is obtained by adding the individual scores for each prognostic factor.
Total score: <4=low risk; 5-7= medium risk; >8= high risk

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Staging of GTD
FIGO staging of gestational trophoblastic diseases
Stage Disease development
0 Molar pregnancy
I Persistently elevated HCG titres (i.e. 6 months or more after
evacuation) and tumour confined to body of uterus
II Pelvic and / or vaginal metastasis
III Pulmonary metastasis
IV All other distance metastases
Remark: This staging system is not used by most major centres for trophoblastic diseases as it does not help in
treatment planning. The Bagshawe score which guides the use of chemotherapy is used more often.

7. Miscellaneous topics in oncology

Tumour marker
A tumour marker is a biochemical substance that can indicate the presence of some kinds of neoplasic disease. It
may be a product or a component of cancer cells from where the tumour marker is secreted into the circulation.
Measurement of the blood level of the marker may be used as (1) a diagnostic test, (2) a screening test, or (3) for
monitoring of the neoplastic disease and effectiveness of treatment.
An ideal tumour marker for a particular neoplasic disease should be:
l produced by and solely by that particular tumour (specific).
l always produced by that particular tumour (sensitive).
l that the blood level of the marker is proportional to the volume of the tumour.
Examples of tumour marker in gynae-oncology
l Alpha-feto protein for yolk sac tumour of ovary
l Human chorionic gonadotropin for gestational trophoblastic diseases and choriocarcinoma
l CA125 for ovarian epithelial carcinomas

CA125
CA125 is a kind of tumour-associated antigens, uses as a tumour marker for ovarian epithelial carcinoma. It has
several limitations:
l Although its level is elevated in 90% of advanced stage, it is only elevated in 50% of stage I disease and
therefore is not a good screening test for early disease.
l It is also found in many benign gynaecological conditions such as endometriosis, uterine fibroid, adenomyosis,
as well as other malignant lesions of endometrium, endocervix, fallopian tube, pancreas. Therefore it is not
specific.
l It is not sensitive for mucinous type and borderline ovarian epithelial cancer.
The clinical use of CA125 is therefore mainly as a monitoring of the disease and effectiveness of treatment. The
decline of the level after chemotherapy implies good chemo-response, while an increase in level suggests
recurrence of the disease.

Chemotherapy
Introduction
Chemotherapy plays a major role in treatment of various gynaecological malignancies especially gestational
trophoblastic disease, ovarian germ cell tumour and ovarian epithelial carcinoma. It may also used to treat some
cases of ectopic pregnancy (such as cervical pregnancy or residual ectopic pregnancy). The following discussion
will concentrate on the role of chemotherapy in gynae-oncology.
Role of Chemotherapy
Curative role
l Gestational trophoblastic diseases
n Chemotherapy is the primary treatment in residual gestational trophoblastic diseases. The rapidly
growing trophoblastic cells are very sensitive to chemotherapy.
n The advantages over surgical treatment are:
u Surgical morbidities are avoided. In particular, haemorrhage as the uterus would be very vascular.
u Distant spread of the disease can also be controlled with chemotherapy
u Uterus is preserved for future fertility.
n Usually a single cytotoxic agent, methrotrexate is used. It is very effective and has less side-effects.
Other cytotoxic drugs may be used depending on the Bagshawe score.
l Ovarian germ cell tumours
n Ovarian germ cell tumours, such as dysgerminoma, malignant teratoma, yolk sac tumour are very
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 aggressive. However, because of good responses to chemotherapy, these kinds of tumours can be
treated with unilateral oophorectomy followed by chemotherapy. The remaining ovary can be preserved if
not involved. Dysgeminoma are also sensitive to radiotherapy. However, chemotherapy is still the
preferred choice because of less side-effects.
l Other gynaecological tumours
n Cervical cancers, endometrial cancers, vulval and vaginal cancers are not chemosensitive.
Adjuvant role
l Ovarian epithelial cancers
l Ovarian epithelial cancers are less chemosensitive to the germ cells counterparts. Chemotherapy is used as
an adjuvant treatment to surgical excision.
Palliative role
l Chemotherapy is seldom use for palliative treatment in gynae-oncology. Tamoxifen or progestogens may be
used for advanced stage of endometrial cancers.
Commonly used cytotoxic agents are:
l Methrotrexate for gestational trophoblastic disease
l Platinum group for ovarian epithelial carcinoma

Radiotherapy
Radiotherapy plays critical therapeutic role in gynae-oncology, especially squamous cell carcinoma of cervi x.
It is applied in two major ways: internal (bradytherapy) and external (teletherapy).
l Bradytherapy
n Radioactive substances are inserted into vagina, targeting at the cervix, parametrium, and vagina. It is
used to treat carcinoma of the lower genital tract
n Complications are local skin effects, vaginal stenosis, cystitis and proctitis
l Teletherapy
n External beam of irradiation targeting at the pelvic and aortic lymph nodes where bradytherapy cannot
reach
n Complications are damages from small bowel and ovarian irradiation,
It is used as a primary curative treatment, adjuvant or palliative therapy, and can be either used alone or integrated
with surgery and cytotoxic chemotherapy:
l Curative:
n As a primary treatment for cancinomas of cervix, vagina and vulva.
l Adjuvant
n After radical surgical treatment for cervical cancers (when risk of distant metastasis is high) and
endometrial carcinoma (beyond stage I)
l Palliative
n For bone metastasis and pain control

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Reproductive medicine

Reproductive medicine and Endocrinology

Introduction
l It is a branch of gynaecology dealing with various kinds of hormonal disorders directly or indirectly involving the
hypothalamic-pituitary-ovarian axis, resulting in anovulation, infertility or ovarian failure (menopause), or
sometimes disorders of puberty.
l The management of these kinds of disorders is usually medical therapy, with ovulation induction, or hormonal
replacement therapy. It may also involve sophisticated bio-technicology when assisted reproductive
technology (ART) is used to treat infertility.
What medical students should know
Common disorders:
l Polycystic ovarian disease (PCOD)
l Hyperprolactinemia
l Various causes of infertility and the investigations
l Problems associated with menopause
Common treatments:
l Ovulation induction
l Hormonal replacement therapy
l Some ideas about ART

1. Anovulation and endocrinopathy

Infertility
Definition
Infertility is defined as failure of a heterosexual couple to conceive after one year of unprotected intercourse. This
definition is based on certain empiric statistical observation of conception rate as follow:
l After 3 months:30%
l After 6 months:50%-60%
l After 9 months:60%-70%
l After 12 months:80%-90%
l After 24 months:95%
Infertility is further defined as follow:
l Primary infertility
n Failure to conceive in a couple who have never achieved a pregnancy.
l Secondary infertility
n Failure to conceive after 1 or more pregnancies, regardless of the outcome of those pregnancies.
l Unexplained infertility
n Infertility with all standard clinical investigations (usually include: semen analysis, assessment of
ovulation, demonstration of tubal patency, some may include postcoital test) yield normal results
Incidence
As defined, it affects 10 to 20% of couples
Causes
Female infertility
l account for 40% of cases, due to:
l anovulation: 20%
l endometriosis: 6%
l tubal blockage: 14%
Male infertility:
l accounts for 30% of cases
l due to poor quality or quantity of sperms
Sexual dysfunction: 6%
Unexplained: 30%
Remark: there may be multiple causes of infertility
Evaluation
Principle:
l Interview both female and male partners
l Complete history of both partners including:
n general medical health especially sexually transmitted diseases, mump, pelvic surgery (female)
n occupational history: environmental and occupational exposure to heavy metals, toxins, etc
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 n social history: especially heavy smoking or alcoholism
n sexual history: coital frequency and difficulty
l Look for evidence of anovulation:
n irregular long menstrual cycles or amenorrhea
n features of polycystic ovarian disease (PCOD), hyperprolactinemia, hypogonaditropic hypogonadism
n confirm with hormonal studies
l Look for evidence of endometriosis:
n dysmenorrhea, dyspareunia, chronic pelvic pain
n endometriotic cyst from past history, physical examination or ultrasound
n confirm with laparoscopy
l Look for hints of tubal blockage which are often secondary to pelvic inflammatory disease:
n dysmenorrhea, dyspareunia, chronic pelvic pain
n history of pelvic inflammatory disease, pelvic surgery
n confirm with hysterosalpingogram or laparoscopy plus chromotubation
l screen for male infertility:
n by semen analysis
Treatment
Principle:
l Correct underlying causes if possible
l Try appropriate method with the least risk first
Treatment modalities include:
l ovulation induction
l in utero insemination with or without ovulation induction
l assisted reproductive procedure
n in vitro fertilisation (IVF)
n in vitro fertilisation with intracytoplasmic sperm injection (ICSI)
l Besides medical treatment, adoption should also be discussed
Treatment of anovulation
l treat with ovulation induction
n clomid is the first line
n HMG or FSH if clomid is failed or contraindicated
n ovarian drilling only for PCOD
Treatment of endometriosis
l Risk of infertility increases with severity of endometriosis
l Medical treatments relieve pelvic pain but not improve fertility
l Surgical treatments including cystectomy, ablation of endometriosis improve chance of fertility
l IVF should be considered if surgical treatment failed, or in case of severe endometriosis which is not easily
treated by surgery
Treatment of tubal blockage
l can be treated with tubal surgery or with in vitro fertilisation (IVF):
n tubal reanastomosis for previous sterilisation
n salpingostomy for simple and small hydrosalpinges
n severe tubal blockage is managed with IVF
Treatment of male infertility
l in utero insemination for mild impairment of semen quality
l in vitro fertilisation with ICSI for severe impairment
l sperm donation: insemination of donor sperm

Anovulation
It means absence of ovulation. Two different conditions occur in anovulation:
l Defective follicular phase and follicular development that result in hypoestrogenemia
l Apparently normal follicular phase but defective luteal phase, leading to normal or increased level of estrogens,
but deficient progesterone. It may result in endometrial hyperplasia
Causes of anovulation:
l Endocrine disorders involving the hypothalamo-pituitary-ovarian axis
n Ovary:
u Polycystic ovarian disease (PCOD), the most common cause
n Pituitary:
u Congenital absence of FSH or LH-secreting cells
u Sheehan syndrome
u Damage by surgery or radiotherapy
n Hypothalamus:

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 u Anorexia neurosa
u Weight and stress related causes of hypogonadotropism
u Kallman syndrome: rare
u Compression or destruction by intracranial tumour: uncommon
n Other endocrine disorders that indirectly affect the hypothalamo-pituitary-ovarian axis
u Hyperprolactinemia
u Hyper or hypothyroidism
u Hyperandrogenaemia
u Cushing disease, etc
n Permanent ovarian failure
u Such as Turner syndrome or menopause
Remark:
l Most of the causes (except PCOD) result in hypoestrogenic type of anovulation
Clinical features
Features of anovulation:
l Oligomenorrhea or amenorrhea
l Infertility
l Absence of biphasic changes of basal body temperature, etc
Features of underlying causes:
l Features of Turner syndrome, PCOD, menopause, thyroid disorders etc
Investigation
Confirm anovulation:
l Low progesterone at the middle of the supposed luteal phase (i.e. day 21 of 28-day menstrual cycle)
Look for underlying causes, such as:
l FSH, LH levels and LH: FSH ratio taken at the follicular phase
n LH: FSH ratio >3 or high LH level is diagnostic of PCOD
n High FSH suggests menopause
l Prolactin levels, etc
Management
Principles:
l Treat underlying causes
l Treat infertility with ovulation induction
l Prevent endometrial hyperplasia which is a complication of chronic anovulation associated with
hyperestrogenemia
l Prevent complications of hypoestrogenemia, usually with hormonal replacement therapy
Discussion/Something to Consider
How do different causes of anovulation affect the choice of ovulation induction?

Luteal phase
A phase of an ovarian cycle starting from ovulation to the next menstruation. It usually lasts 14 days. During this
period, the corpus luteum secrets progesterone which turns the endometrium into secretary state, becomes thicker,
more vascular and receptive to a blastocyst. The cervical mucus also becomes thicker and impenetrable to
spermatozoa. Luteal phase insufficiency may occur resulting in failure of a blastocyst to implant.

Luteal phase insufficiency

A condition proposed as a cause of infertility. There is ovulation but the luteal phase is short (< 10 days), with a low
luteal phase progesterone level. The endometrial glands do not show normal secretary phase changes. The
diagnostic criteria of this condition, however, is not well defined.

Follicular phase
The period of development in which the dominant follicle (with its oocyte and theca and granulosa cells) grow to
become a fully formed Graafian follicle, responsive to the pre-ovulatory LH surge.
The follicular phase usually last 14 days.

Sexual dysfunction
Sexual functioning involves a unique combination of physical, psychological and social expression. It allows a
couple to reproduce, bond and enjoy each other. Sexual dysfunction account for 5% of all cases of infertility. Both
male and female can be affected.
Female sexual dysfunction
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l Vaginismus
l Dyspareunia
Male sexual dysfunction
l Erectile or ejaculatory dysfunction

Postcoital test
What is a postcoital test (PCT)
It assesses the quality of the cervical mucus which may be one of the causes of infertility. Inflammation of cervix,
presence of antisperm antibodies in the cervical mucus may cause death or inactivation of sperm.
How to perform postcoital test
l Timing: 6 to 12 hours after a normal unprotected intercourse, performed just before the estimated date of
ovulation.
l Procedure: After passage of a speculum, a small amount of cervical mucus is aspirated and immediately
examined microscopically. The viability and mobility of sperms are assessed.
l Assessment: The test is considered adequate if 5 to 10 freely mobile sperms are seen per high power field.
Their motility is assessed: it may vary from highly active progressive movement to sluggish, or no, motility.
Clumping, shaking or agglutination (head to head or tail to tail) may suggest the presence of antisperm
antibodies.
How to interpret postcoital test result
l A good PCT indicates that intercourse is adequate, the male is likely to be fertile and the woman is normal up
to the level or the cervix. The prognosis for conception is good in the presence of good PCT.
l On the other hand, a single unsatisfactory test may not be of any significance as most commonly, the poor
cervical mucus is due to inappropriate timing of the test. When performed too early, it may not be fully
estrogenic; when performed too late, it may have become highly viscous under the influence of progesterone.
The test may need to be repeated.
l A gross deficiency of mucus (dry cervix) may result from amputation of the cervix and certain other operations
which destroy cervical glands. The presence of white blood cells may indicate inflammatory condition,
prejudicial to conception.
l If sperms are not present in repeated PCT despite a normal semen analysis, a coital problem should be
suspected.
Remark
l It is still controversial whether post-coital test should be a routine investigation in the management of infertile
couple. Due to the poor reproducibility and poor diagnostic and prognostic performance of postcoital test, it is
not routinely performed in our unit.

Basal body temperature

Ovulation leads to an increase in blood progesterone concentration which is associated with a small rise in body
temperature. A woman can therefore assess herself whether and when ovulation occurs simply by monitoring her
basal body temperature.
How to record and interpret a basal body temperature chart
l The temperature must be recorded daily under standard conditions, before rising in the morning, and before
eating or drinking.
l The woman also marks on the chart the days when intercourse has occurred.
l A lower temperature during menstruation and in the follicular phase of the cycle, followed by an increase of
approximately 0.5 degree Celsius throughout the second half of the cycle (biphasic changes) indicates that
ovulation has occurred.
l The temperature remains elevated if pregnancy has occurred.

2. Assisted reproductive procedures

ART
Assisted reproductive technology (ART) is a part of reproductive medicine which deals with means of conception
other than normal coitus. ART frequently involves the handling of gametes or embryos, and includes one or more of
the followings: ovarian stimulation; oocyte collection; sperm preparation; in vitro fertilisation; embryo transfer;
intra-uterine insemination; donor insemination; micro manipulation such as intracytoplasmic sperm injection (ICSI);
cryopreservation and other related procedures.

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Ovulation induction
What is ovulation induction
It is a procedure or treatment to induce ovulation artificially for patients suffering from infertility due to anovulation.
Methods of induction
Medical
l Anti-estrogen: Clomiphene citrate
l Gonadotropin therapy
l Pulsatile gonadotropin releasing hormone (GnRH)
l Dopamine agonists: bromocriptine (only for hyperprolactinemia)
Surgical (only for polycystic ovarian disease PCOD)
l Ovarian wedge resection
l Ovarian drilling
Two main complications of ovulation induction
l Multiple pregnancy
l Ovarian hyperstimulation syndrome (OHSS)

Clomiphene
Nature
l An oral non-steroidal anti-estrogen
l Racemic mixture of its 2 sterochemical isomers zuclomiphene (weak estrogen) and enclomiphene citrate
(potent antiestrogen)
Mechanism of action
l Its anti-estrogenic activities diminish the negative feedback and increase the release of endogenous
gonadotropin.
l An intact hypothalamic-pituitary axis and presence of endogenous oestrogen are essential for its effectiveness
Regime
l Start with a daily dose of 50mg, taken for 5 days from day 2 to day 6 of the menstrual cycle (some may start
from day 5)
l Confirm ovulation by basal body temperature chart or mid luteal progesterone
l Adjust the dosage according to the ovulation response. The maximum dose is 200mg daily
l The couple is advised to have intercourse on alternate days for 1 week around the time of ovulation
Efficacy
l ovulation rate: 40-60% per cycle
l conception rate: 15-20% per ovulatory cycle
l cumulative 6-month conception rate: 60-75%
l Remark: alternative method of ovulation induction should be consider if the patient is anovulatory even on
maximum dose of clomid or fail to conceive after 6 to 12 ovulatory cycles
Complications
l Usually safe with mild side effects
l Vasomotor flushes (10%), abdominal bloating (5%), breast discomfort (2%), headache (1%), visual symptoms
l Multiple pregnancy rate: 5% (mostly twin); higher multiple pregnancies rare
l Ovarian hyperstimulation is very rare
Advantages
l simple, safe and cheap
l orally active
l worth trying as the first line agent in those cases with intact hypothalamic-pituitary-ovarian axis

In vitro fertilisation
What is in vitro fertilisation
It is a 4-stage assisted reproductive procedure which includes:
l controlled ovarian hyperstimulation,
l oocyte retrieval under transvaginal ultrasound guidance,
l fertilization with sperm in vitro, and
l embryo replacement into the uterus.
Main indications
l tubal infertility
l moderate-to-severe endometriosis
l male infertility
l failure of other infertility treatments.

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Efficacy
l Conception rate: 10-30% per cycle (success rate decreases with increasing female age)
l Cumulative conception rate: 40-60% after five cycles (success rate decreases with increasing female age)
Complication
l Multiple pregnancy rate: 20-30%
l Ovarian hyperstimulation syndrome (1% risk of severe OHSS)
l Potential risks during oocyte retrieval. e.g. haemorrhage, infection, visceral injuries to vessels, bowels etc.
l Recent studies have suggested that it may be associated with a higher risk of carcinoma of ovary. This has not
be confirmed yet

Insemination
Intra-uterine insemination is an assisted reproduction technique (ART) in which a prepared specimen of semen is
injected by means of a cannula through the cervical canal, directly into the uterine cavity. The semen can be
prepared from husband, or from donor if it is a case of male infertility. The insemination is performed at the time of
ovulation as determined by ultrasound or hormone measurements, and is usually preceded by ovarian stimulation.
Complications of insemination itself is very low but ovarian hyperstimulation and multiple pregnancy may be resulted
from concurrent ovarian stimulation.
Intra-uterine insemination is particularly useful in women with a deficient cervical mucus. It is widely used for
unexplained infertility and mild endometriosis before resorting to in vitro fertilisation (IVF). Success in men with
impaired sperm concentration or motility and those with antisperm antibodies is doubtful. The technique is simpler
and cheaper than IVF and less objectionable in those who, on religious or personal grounds, may not wish to
undergo IVF.

ICSI
Intra-cytoplasmic sperm injection (ICSI) is one of the ART procedure to treat male infertility. A single spermatozoon
is injected into the cytoplasm of the oocyte using a microinjection pipette.
It overcomes the problem of severe oligospermia because only a few sperms are required, as compared to millions
in conventional in vitro fertilisation. It also helps in sperm dysfunction such as immotility and penetration failure,
since the sperm is injected directly into the oocyte. Provided that the injected sperm is viable, the chance of
fertilisation is good. The risk of the treatment is that as severe oligospermia or azospermia is associated with
chromosomal abnormalities, there is a higher chance of transmission of abnormal karyotype to the offsprings.

OHSS
What is Ovarian hyperstimulation syndrome
Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic condition arising from over-stimulation of the ovaries by
ovulation induction agents.
Pathophysiology
The basic pathophysiology is fluid shift from the int ravascular compartment to the third space (mainly the peritoneal
cavity). The exact mechanism is unclear but may be related to ovarian endocrine, paracrine and autocrine factors.
Hypovolaemia and haemoconcentration is resulted. In severe case there are ascites, pleural effusion, hypovolemic
shock, renal and liver dysfunction, and electrolyte disturbances. There is also an increased risk of thromboembolism
secondary to haemoconcentration.
Risk factors
OHSS is more likely to occur:
l ovulation induction with gonadotropin
l patients with PCOD
l development of high estrogen level and numerous small to medium sized follicles during the ovulation
induction procedure
l use of human chorionic gonadortropin (HCG)
Clinical features
Clinically, there are abdominal distension, nausea, vomiting, and diarrhea, dyspnea, oligouria.
Treatment
For mild cases, treatment is conservative:
l Monitoring of haemodynamic status, urine output, weight gain, electrolytes
l Fluid support which may consist of albumin or other kinds of colloid infusion
l support further luteal phase support with HCG
l prevent deep vein thrombosis with elastic stocking
For severe cases, surgical intervention may be required:
l pleural effusion: pleural drainage
l massive ascites: paracentesis

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l laparotomy or laparoscopy for ruptured or bleeding ovarian cysts

3. Male infertility

Spermatogenesis
l Formation of spermatozoa inside testes.
l Needs further maturation process through the epididymis.
l Impaired spermatogenesis occurs in chromosomal abnormality (e.g. Klinefelter's syndrome)

Male infertility
Male factor accounts of 30% of all cases of infertility. There are two major mechanisms for male infertility:
l Abnormalities in spermatogenesis
l Abnormalities in the delivery system of semen:
n blockage at vas deferens
n retrograde ejaculation
Abnormalities in spermatogenesis
Spermatogenesis can be affected by:
l General environmental factors:
n such as chronic smoking, alcoholism, toxin or heavy metal, hot environment
l Primary testicular failure resulted from:
n chromosomal abnormalities such as Klinefelter syndrome
n irradiation, chemotherapy, surgery, tuberculosis and mump infections
l Endocrine disorders such as:
n deficiency of hormones of pituitary gland and hypothalamus such as in Kallman syndrome
n Hyperprolactinemia
l Miscellaneous:
n Y-chromosome microdeletion is found in 10% of severe male infertility
n Varicoele which may result in a higher testicular temperature, is said to be associated with poor
spermatogenesis
Diagnosis of male infertility
Male infertility is screened with semen analysis. More sophisticated tests for sperm functions are not very useful
clinically.
Treatment of male infertility
General measures
l improvement of general health including stopping smoking and alcohol intake may improve semen quality in
patients with mild impairment of semen quality
Hormones
l Only for correction of endocrine disorders
Intrauterine insemination
l for mild impairment of semen analysis
In vitro fertilisation and ICSI
l for severe impairment of semen quality
Surgery
l for correction of blocking, retrograde ejaculation, and varicocele

Semen analysis
What is semen analysis (SA)
A laboratory test of seminal fluid carried out to investigate male fertility or the effectiveness of vasectomy. The
technique and range of normal values have been standardized by the World Health Organisation (WHO).
How to perform semen analysis
l Timing: the male have ejaculated at least once within the week prior to the test but not within the previous 2
days
l Collection: all semen samples should be obtained by masturbation into a clean, wide-mouthed nontoxic plastic
container and delivered to the laboratory as soon as possible, preferably within one hour
l Assessment: volume and liquefaction time of the semen, sperm count, motility and morphology
WHO criteria for normal semen characteristics:
Parameter Normal value
Volume 2ml or more
Concentration >=20 million/ml
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 Motility 50% or more sperms have progressive motility
Morphology 30% or more sperms have normal form
Liquefication complete in 30 min
How to interpret a SA report
l The most common reason for abnormal SA is the inaccurate collection of the specimen, or history of recent
illness (in 3 months) that may affect the production of sperm. Therefore, it is advisable to repeat the SA after a
3-month interval
l If the SA is grossly abnormal, further investigation should be taken to look for the underlying causes.

4. Sexual dysfunction

Libido
Sexual drive or desire. The intensity of libido varies from person to person, and may also vary in women in relation to
the menstrual cycle, pregnancy or menopause. Libido generally decreases in both sexes with advancing age. The
term must not be confused with orgasm.

Vaginismus
It is a kind of sexual dysfunction. It is involuntary painful spasm of the pubococcygeus muscle (see levator ani)
leading to closure of the vaginal introitus, preventing penetration. It is different from dyspareunia. The cause is
psychological rather than organic. Treatment is by gradual desensitization.

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Urogynaecology

Urogynaecology
Introduction
Urogynaecology is a subspecialty of gynaecology dealing with disorders of pelvic floor that result in two major
problems: genital prolapse and urinary incontinence. It also deals with other lower urinary tract problems such as
voiding disorder The diagnosis of urinary disorders usually requires urodynamic study.
What medical students should know
The physical examination and management of various types of genital prolapse which are usually vaginal
hysterectomy with pelvic floor repair (colporrhaphy), or conservatively with ring pessary
The two main causes of urinary incontinence in female: genuine stress incontinence and detrusor instability, and
how to differentiate them clinically and with urodynamic study.

1. Gential prolapse

Genital prolapse
Definition
It is a group of disorders caused by weakness of the pelvic floor resulting in abnormal descend of various pelvic
structures through the vagina. These include:
Cystocele
l Backward descend of the urinary bladder into the vagina and beyond. It appears as a protrusion of the anterior
vaginal wall
Urethrocele
l Backward descend of the urethra into the vagina and beyond. It appears as a small protrusion of the distal end
of anterior vaginal wall
Rectocele
l Forward descend of the rectum into the posterior vagina. It appears a protrusion of the posterior vaginal wall
into the vagina and beyond
Enterocele
l Herniation of the pouch of Douglas which often contains loops of small bowel, through the upper part of the
posterior vagina.
Uterine prolapse
l Downward displacement of the uterus towards or through the introitus
l Divided into three degrees:
n 1st degree: descend of the cervix within the vagina and not through the introitus
n 2nd degree: descend of the cervix, but not the whole uterus, through the introitus
n 3rd degree (or procidentia): descend of the cervix and the whole uterus through the introitus, usually
bringing with it the cystocoele, enterocele and rectocele
Vault prolapse
l Prolapse of the vaginal cuff in the hysterectomized patient.
Incidence
l Genital prolapse usually occurs after middle age, and affects 10% of multiparous women, and is very rare
among nulliparous.
Aetiology
l The above pelvic organs are normally supported by the pelvic floor, which consists of levator ani and pelvic
fascia. Its weakness results in genital prolapse. The main factors leading to the deficiency are trauma (often as
a result of childbirth), and ageing (collagen lack of estrogen support).
l Failure to support the vaginal vault by plicating it to the cardinal ligaments during hysterectomy may precipitate
vault prolapse subsequently, and colposuspension may also lead to enterocele or rectocele.
l Rarely, some genetic disorders associated with congenital weakness of collagen may contribute in a minority
of patients.
Clinical features
All kinds of genital prolapse may present with a mass protruding out of the vagina spontaneously, or after coughing
or straining. It is usually reducible. The protruded mass causes dragging pain, discomfort during walking or standing,
and may bleed secondary to rubbing or laceration.
Depends on the site and degree of prolapse, urinary, bowel or sexual problems may result:
l Cystocele and urethrole:
n stress incontinence, frequency of micturition, voiding difficulty
n Rarely in severe case of cystocele, there are kinking at the ureterovesical junction bilateral, leading to
bilateral hydronephrosis
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l Rectocele
n difficulty on defaecation
l Uterine prolapse, vault prolapse
n discomfort during coitus, dyspareunia
l Enterocele
n usually asymptomatic but rarely the enterocele may be performated leading to exposure of prolasped
small bowel and consequently bowel injury
Treatment
Principle:
Definite surgical correction is the mainstay of treatment which include:
l Vaginal hysterectomy (for uterine prolapse)
l Colporrhaphy (pelvic floor repair): anterior colporrhaphy for cystocele and urethrocele; posterior colporrhaphy
for rectocele
l Repair of enterocele
l Sacrocolpopexy for vault prolapse
Conservative management with vaginal ring pessary may be considered when:
l patients are physically unfit for surgery
l patients refuse surgery
l temporary relief while patients are waiting for surgery
l patients are pregnant or want to preserve uterus for fertility (rare)
Clinical approach to a case of genital prolapse
History
l Assess the degree of prolapse and severity of symptoms
l Look for any precipitating factors: childbirth history and birth injury; chronic cough, etc
l Ask for any medical illness and assess the physical fitness of patients
Physical examination
l General examination and examination after other systems: important as majority of patients are old and have
some form of medical illness. It help to assess whether patients are fit for surgery
l Examination of genital prolapse
Managment
l Investigate with urodynamic study when there are multiple urinary symptoms
l Investigate for fitness if patients also have medical disorders
l Decide the mode of treatment according to the type of prolapse, physical fitness and wish of patients
Discussion/Something to Consider
Besides genital prolapse, what other pathology may also present as a mass protruding out from the vagina?

Uterine prolapse
See genital prolapse for detail

Vault prolapse
See genital prolapse for detail

Cystocele
See genital prolapse for detail

Urethrocele
See genital prolapse for detail

Rectocele
See genital prolapse for detail

Enterocele
See genital prolapse for detail

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Examination of genital prolapse
Aim
To assess pelvic floor weakness, types and degree of genital prolapse and any urinary incontinence
Procedure
In lithotomy position:
l Inspect the external genitalia, look for any prolapse or protrusion
l Ask the patient to cough and look for any descend and stress incontinence
l If a there is already a huge prolapse, confirm if it is a third degree by palpating the fundus (get above the
prolapsed mass), and then examine the vaginal wall and cervix for any ulcer or laceration
l If there is no obvious prolapse or just a mild degree, proceed to the Sim speculum examination
In Sim position:
l Ask the patient to lie on her left, with the buttock at the right edge of the coach, and the right hip and knee
flexed. Ask the patient to hold up the right buttock with her right hand will provide a better exposure of the
genitalia
l Insert a sim speculum with adequate lubrication to the vagina, and retract the posterior vaginal wall. This would
facilitate the examination of the anterior wall. Cystocele and urethrocele appear to bulge backwards.
Sometimes a cystocele may obscure the view of the cervix
l Inert a pair of sponge-holding forceps to retract the anterior wall. This would help to expose the cervix.
l With the sponge-holding forceps retracting anteriorly, slowly withdraw the sim speculum. Enterocele will
appears as a bulge from the upper posterior vaginal wall, and the rectocele from the lower vaginal wall.
Digital examination
l Perform a bimanual pelvic examination
l assess the size and mobility of the uterus if vaginal removal is feasible
l look for any ovarian masses, presence of which may affect the choice of surgery
l assess the space of the pelvis is enough for vaginal surgery
l assess the distance between the posterior fornix and symphysis pubis in case a ring pessary is required
Finally a rectal examination may be necessary to differentiate rectocele from a enterocele, and to assess the anal
tone If the genital prolapse cannot be demonstrated at that moment, ask the patient to walk around for a while and
reexamine later.

Colporrhaphy
It is the vaginal surgical repair of the pelvic floor as the treatment of genital prolapse. It is often performed together
with vaginal hysterectomy.
Anterior colporrhaphy is the plication of the pubocervical fascia (a part of the pelvic fascia between the bladder and
the vagina) so that the descended bladder (cystocele) is elevated with the support of the fascia. It is however not a
effective treatment for genuine stress incontinence (50% success rate). The risk of the operation is perforation of the
bladder.
Posterior colporrhaphy is the plication of the part of levator ani muscle between the posterior vaginal wall and the
anterior rectal wall, so that the herniated rectum (rectocele) is reduced by the reinforced muscle. It is often
performed together with the repair of the perineum (perinorrhaphy). The risks of the procedure are perforation of
rectum, dyspareunia secondary to tight vaginal opening after repair.
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2. Urinary incontinence

Urgency
Sudden strong desire to void, if uncontrolled or unfulfilled, may result in urge incontinence. Motor urgency is
associated with uninhibited detrusor contractions. The most common cause is detrusor instability. Sensory urgency
is due to irritable lesions such as cystitis, calculus in which the detrusor is stable.

Incontinence
See urinary incontinence

Urinary incontinence
Introduction
Urinary incontinence is defined as an involuntary loss of urine which is objectively demonstrable and cause a social
or hygienic problem (definition of International Continence Society). It is reported to be very common in reproductive
aged women and postmenopausal women (20%). It is subdivided into various types (see below). Majority are belong
to stress incontinence and urge incontinence.
Types of urinary incontinence
Stress incontinence
l involuntary loss of urine when the intra-abdominal pressure is increased, such as during exercise, coughing,
and sneezing. It is most commonly due to genuine stress incontinence. Sometimes detrusor instability may
present as stress incontinence, and urodynamic study may be required to differentiate them.
Urge incontinence
l Inability to withhold the passage of urine with a sudden strong desire to micturate (urgency), due to
hyperexcitability of the bladder detrusor muscle. Hyperexcitability can be primary or secondary to infection or
irritation of the bladder wall.
Overflow incontinence
l involuntary loss of urine due to when the intravesical pressure exceeds maximum urethral pressure due to
bladder distension and in the absence of detrusor activity. It is secondary to bladder outflow obstruction.
True incontinence
l involuntary loss of urine due to a defect in the anatomical integrity of the urinary tract, such as vesicovaginal
fistula
What medical students should know
l definitions of various urinary symptoms
l Genuine stress incontinence and detrusor instability, and how to differentiate them clinically and with
urodynamic study.
l Principles of treatment of the above diseases

Stress incontinence
Involuntary loss of urine when the intra-abdominal pressure is increased, such as during exercise, coughing, and
sneezing. It is most commonly due to genuine stress incontinence or detrusor instability. See urinary incontinence
for detail.

Genuine stress incontinence

Genuine stress incontinence is the involuntary loss of urine resulted from an increase in intra-abdominal pressure,
which is transmitted to the bladder, and to an extent that exceeds the maximum urethral pressure. The detrusor
muscles remain quiescent (do not contract) and do not contribute to the increase of the intracystic pressure.

Urge incontinence
See urinary incontinence

Overflow incontinence
The involuntary loss of urine when the intravesical pressure exceeds maximum urethral pressure due to bladder
distension and in the absence of detrusor activity.

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True incontinence
See urinary incontinence

Reflex incontinence
The involuntary loss of urine due to abnormal spinal reflex activity in the absence of the sensation to micturate.

Colposuspension
Colpo means vagina. Each side of the vaginal vault are 'suspended' by stitching it to the ipsilateral iliopectineal
ligament. The bladder neck is therefore elevated. It is one of the most effective continence surgery (90%). The
surgical complications are de novo detrusor instability (5%), voiding disorder (5%), development of enterocele or
rectocele.

3. Other topics in urogynaecology

Frequency of micturition
It is voiding more than 7 times a day, or being woken twice or more for voiding at night whilst asleep (nocturia). It can
be due to:
Bladder irritation
l cystitis
l bladder stone
l detrusor instability
Decrease of functional volume of bladder
l cystocele
l bladder outflow obstruction and retention of urine
Increase of urine production
l Diabetes mellitus

Nocturia
Being woken twice or more for voiding at night whilst asleep. See also frequency of micturition for causes of nocturia
and frequency.

Dysuria
Pain during micturition. It is a symptom of urethritis or cystitis.

Interstitial cystitis
A chronic condition which presents with severe frequency of micturition, urgency, lower abdominal pain, dysuria and
haematuria in the absence of bacterial cystitis. At cystoscopy, ulcers with a granulomatous base and surrounding
hyperaemia are found. Biopsy of the lesion shows chronic non-specific ulceration.

Voiding disorder
Causes
l Urinary voiding disorder is less common in female than in male. It is either due to outflow obstruction, or
inadequate detrusor contractions. Sometimes it may be too painful to void in situations such as post-vaginal
surgery, or urethritis.
l The causes of obstruction in female include: large fibroids, or other pelvic masses, severe cystocele.
l Inadequate detrusor pressure can be due to various kinds of neurological disorders involving the central
nervous system, or the sacral plexus (neuropathic bladder). After regional anaesthesia, patients may also lose
the sensation of bladder filling as well as the motor function.
Clinical features
l Patient with chronic voiding difficulty usually complain of hesitancy, frequency of micturition, nocturia, poor
stream of urine, incomplete emptying, straining to void. Acute urinary retention may develop. On examination
during acute episode, a full bladder is demonstrated, and a large volume of residual urine is drained on
catheterization.
l There are also complications such as recurrent urinary tract infection.
Investigation

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l Uroflowmetry would show a low peak flow rate with a prolonged voiding time. There is also residual urine.

Detrusor instability
Definition
Abnormal contractions of the bladder muscle (detrusor) occur spontaneously or in response to a stimulus (e.g. filling
of bladder, coughing, sound of running water, etc), when the individual is attempting to inhibit micturition.
Aetiology
It can either be primary (idiopathic) or secondary to cystitis, urinary stones, atrophy, neuropathy, or post-surgery (de
novo DI).
Clinical features
Urinary symptoms including: urgency, frequency of micturition, urge incontinence, stress incontinence.
Diagnosis
Cystometry is diagnostic. It shows detrusor activities on provocation during the filling phase of the cystometry. Other
features are: gradually increased of baseline deterusor pressure during filling. early occurrence of the first sensation
of urgency. It is essential to differentiate detrusor instability from genuine stress incontinence because the
treatments are different from each other. Incorrect diagnosis and consequently wrong treatment will even make the
problem worse.
Treatment
Bladder retraining, biofeedback, hypnotherapy: successful in 60% of cases
Medicine
l Anti-cholinergices (oxybutynin)
l Amitriptylline (imipramine)
Surgery (Last resort)
Discussion/Something to Consider
As both detrusor instability and genuine stress incontinence can present with stress incontinence. Are there any
differences between the two in term of symptomatology?

Urodynamic study
The two most commonly performed urodynamic studies are:
l cystometry
l uroflowmetry
Occasionally video cystourethrography or urethral pressure profilometry may be indicated.

Cystometry
It is one of the most commonly performed urodynamic study in urogynaecology, in which the detrusor activity during
filling of the bladder and a series of provocation is assessed. The detrusor pressure (the pressure generated by the
detrusor contractions) cannot be measured directly but is calculated by subtracting intraabdominal pressure from
intracystic pressure.
It is mainly used to differentiate detrusor instability from genuine stress incontinence.
The indications are:
l Multiple urinary symptoms:
n urge incontinence, urgency, frequency of micturition, stress incontinence are suggestive of detrusor
instability and cystometry is indicated to confirm the diagnosis. Isolated stress incontinence is almost
always due to genuine stress incontinence and cystometry is not essential.
l Previous unsuccessful continence surgery
n to assess the severity of residual urinary problem and diagnosis of de novo detrusor instability
l Pre-continence surgery assessment
n Occasionally cystometry may be indicated before corrective surgery for genuine stress incontinence to
detect any subclinical pre-existing detrusor instability and voiding disorder which may get worse after
surgery
l Other conditions: voiding disorder, neuropathic bladder
How to perform cystometry
Setting
l Ask the patient to empty the bladder. Usually the patient voids on the flowmeter as uroflowmetry is usually
performed at the same setting.
l Catheter the bladder. The residual urine volume is recorded
l Insert a smaller fluid-filled catheter into the bladder via the urinary catheter. It is connected to an external
pressure transducer for measurement of the intracystic pressure
l Insert another catheter into the rectum for measurement of the intraadbominal pressure

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Filling phase
l The bladder is then filled up with normal saline at room temperature gradually at a rate of 10 to 100ml/min
l During filling, the following information are recorded over time:
l the changes in the volume, the intracystic pressure and intraabdominal pressure
l the time and volume at which the patient has the first and maximal desire to void
l Provocative tests are performed, with the following methods:
l coughing, change of position
l fast filling of bladder
l running water
Voiding phase
l After the maximal filling capacity of the bladder is reached, the patient is asked to stand up and cough. Any
leaking of urine is documented
l The patient is finally ask to void on the uroflowmeter again
Normal results and interpretation
l First desire to void: 150-200ml
l Maximal capacity: 400-600ml
l Detrusor pressure rise during filling phase: < 15cmH2O (abnormal high pressure indicates poor compliance of
the bladder)
l Absence of systolic detrusor contractions during filling and on provocation (Presence is diagnostic of detrusor
instability)
l No leakage on coughing (leaking in the absence of systolic detrusor contractions indicate genuine stress
incontinence)
l Voiding detrusor pressure rise: < 70cmH2O with a peak flow rate of > 15ml/s for a volume over 150ml
l Residual urine volume: < 50ml
Discussion/Something to Consider
Can your explain why the detrusor pressure is equal the the difference between the intracystic pressure and the
intraabdominal pressure?

Uroflowmetry
It is a simple non-invasive urodynamic study in urogynaecology, used to investigate voiding disorder. It is usually
performed together with cystometry.
The patient is asked to void to a toilet which is sensitive to the change of volume over time, from which the urine flow
rate is estimated.
The peak flow rate should be more than 15ml/s, and the normal flow curve is bell-shaped and duration of voiding
should not be prolonged. The urine volume should be at least 150ml as flow rates with a small volume are not
reliable.
Low peak flow rate, prolonged flow indicate a voiding disorder, which can be due to obstruction, or a neuropathic
bladder.

Cystoscopy
A endoscope is inserted via the urethra into the urinary bladder allowing examination of the interior wall. Biopsy and
excision surgery can be performed during cystocopy. It is indicated for:
l multiple irritable bladder symptoms such as urgency, dysuria, frequency of micturition, haematuria, in which
case chronic cystitis (e.g. interstitial cystitis), bladder stones are suspected
l investigation of urinary fistula
l staging of cervical cancer

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Miscellaneous

1. Basic clinical skills

History taking (Obs)

Past medical history
To identify any pre-existing diseases that may affect the pregnancy, or may get worse during pregnancy
l common diseases are hypertension, diabetes mellitus, thyroid disorders, epilepsy and psychiatric disorders
Past obstetric history
To look for any fetal or maternal complications in past pregnancies that may recur in current pregnancy
l such as preterm labour, pre-eclampsia, gestational diabetes
To review mode of deliveries of past pregnancies that may affect the management of current pregnancy
l such as caesarean section
Present obstetric history
To confirm the gestation
l Date of last menstrual period
l cycle length and regularity of menstrual period
l Date of pregnancy test, with both positive and negative results
l Result of any dating scan
l see dating of pregnancy
To look for any teratogenic agents
l any rash and fever during pregnancy
l any drug taken during pregnancy
To look for any symptoms related to the pregnancy
l such as nausea, vomiting (see minor disorders of pregnancy)
Family history
To look for any risk of having hereditary diseases
l such as thalassemia, haemophilia
To check consanguinity (particularly for Indian and Parkistian)
To look for any risk of having gestational maternal diseases
l such as gestational diabetes, pre-eclampsia or hypertension
Social history
l Drug abuses, smoking and alcohol intake
Family planning and childcare
l Plan of breast-feeding, childcare, and contraception.
Discussion/Something to Consider
In an antenatal clinic, you are seeing a patient who has an emergency caesarean section 4 years ago in China.
What question concerning that delivery would you want to ask your patient?

Symptomatology (Obs)
Vaginal bleeding
During pregnancy, any vaginal bleeding occurred after 24 weeks is defined as antepartum haemorrhage. Any
bleeding comes from the upper genital tract before that period is diagnosed as threatened abortion.
Abdominal pain
Uterine origin
l Uterine contractions pain
n It is usually related to the onset of labour.
n Sometimes it may just be a false labour or Braxton Hicks contractions
n Abruptio placentae, chorioamnionitis, uterine rupture give rise to constant severe pain
n Other causes: red degeneration of fibroids
Ovarian origin
l Co-existing ovarian pathologies such as tumour or cysts may bleed, rupture or undergo torsion resulting in
acute abdominal pain
Non-gynaecological origin
l Various kinds of surgical disorders such as appendicitis, cholecystitis, peptic ulcer diseases, pancreatitis, etc.

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Examination (Obs)
On every antenatal visit
The following examination should be performed:
l check for anaemia
l maternal weight
l blood pressure measurement
l urinalysis (urine protein and sugar)
l abdominal examination (see obstetric abdominal exam)
On first booking
In addition to above, the following examinations should be performed at the booking visit:
l measurement of maternal height
l examination of thyroid glands and signs of thyroid disorders
l examination of breasts
l examination of heart
l examination of perineum and lower genital tract (with speculum) for any pre-existing lesions. The cervix should
be examined for:
l warts, polyps and tumours
l length and dilatation (the cervix is dilated and shortened in case of cervical incompetence)
l pap smear to screen for cervical intra-epithelial neoplasia (CIN)
Digital vaginal examination
Digital examination is performed in the following conditions:
l Before induction of labour, assess the bishop score for the favourability (ripening) of cervix
l During labour, assess the cervical dilatation and effacement, station and position of the fetal presenting part
l Assess the size of the pelvis (see clinical pelvimetry).
Discussion/Something to Consider
You may notice in the antenatal clinic that the obstetricians often do a bimanual examination of the pelvis when
pregnant women come at the first trimester of pregnancy, but they seldom do so when the their patients come at a
later gestation. Do you know why?
You have found a 2cm cervical wart in a woman at her booking visit at 12 week of gestation. What are your
management and advice?

Obstetric abdominal exam

Positioning of patient
l Patient should lie as flat as possible
l Discrete exposure from just below the breasts to the symphysis pubis
Inspection
Inspect for signs of pregnancy:
l Linear nigra
n Pigmented linea alba
n May persist after the first pregnancy
l Striae gravidarum
n recent striae are purplish red while old striae from previous pregnancy are silvery white
n striae follow the lines of stress in the skin of the abdominal wall and may also occur on the lateral aspect
of the thighs and the breasts
l pigmented and flattened umbilicus
l Abdominal distension
Inspect for fetal movements
l Observable after 24 weeks
Inspect for any surgical scar
l Caesarean section is usually performed with Pfannenstiel incision
Palpation of uterus
Palpate the outline and contour of the uterus
l Irregular if there are fibroids or uterine anomalies
Palpate for any uterine tenderness
l Tender if abruptio placentae or intrauterine infection
Assess the size of the uterus
l 12 week: just palpable over the abdomen
l 14 week: a quarter-way from symphysis to umbilicus
l 16 week: midway between the symphysis and umbilicus
l 18 week: three-quarter-way from symphysis to umbilicus
l 20 week: uterus fundus at the umbilical level

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Measurement of symphysial-fundal height
l search for the fundus by palpating from above downward with the left hand
l locate the fundus with the ulnar border of the left hand
l put one end of the measure tape at the fundus
l locate the pubic symphysis with the right hand by sliding downward along the uterine body until the upper
border of the pubis bone is felt
l measure the distance between the fundus and the symphysis pubis
l After 20 week, the fundal height in centimetre correlates to gestation in week: e.g. the fundal height at 30 week
should be around 30 +/-2cm
Palpation of fetus
l Number of fetus:
n suspect multiple pregnancy if more than two fetal poles are identified
l Fetal lie:
n search for the fetal poles at the fundus and over the suprapubic region. If present, then it is longitudinal
lie;
n otherwise, search carefully at the frank region (transverse lie) or iliac fossa (oblique lie)
l Fetal presentation:
n Cephalic: hard round well-defined border
n Breech: soft, bulky
l Engagement:
n Some degree of engagement is common when gestation is near term. High floating presenting part
should lead to the suspicion of pelvic inlet obstruction or placenta praevia
l Fetal back:
n if it is longitudinal lie, push the fetus to the other size of the uterus and feel the fetus with the other hand,
and vise versa. The back is round and soft while the limbs are irregular, and moving
l Liquor volume:
n Fetal parts are difficult to define when there is significant polyhydramnios. The fundal height is large for
date. Fluid thrill may also be demonstrated.
n In oligohydramnios, the fetal parts are easily felt and prominent. The fundal height is also small for date.
Auscultation of fetal heart sound
Site:
l Best heard over the shoulder (back) of the fetus
l In cephalic presentation, it is at the level midway between the maternal umbilicus and the anterior superior
spine of the ilium
l In breech presentation, it is at or slightly above the level of the umbilicus
Instruments:
l Use a Pinard stethoscope or a doptone
Remark:
l Fetal parts are usually not palpable before 24 week
l Fetal heart sounds are usually not audiable with a Pinard stethoscope before 24 week
Discussion/Something to Consider
A patient comes at 30 week of gestation is found to have a fundal height of 35cm. Is it normal? What are the
possibilities account for the finding? How would you assess the case further?
A patient comes at 34 week of gestation is found to have a fundal height of 30cm. Is it normal? What are the
possibilities account for the finding? How would you assess the case further?
You has picked up a pulsative sound of rate 120bpm over the abdomen of a pregnant patient during an antenatal
clinic. Is it normal for fetal heart rate? Can it be maternal origin? How can you differentiate a maternal pulse from a
fetal pulse in this situation?

History taking (Gyn)

Gynaecological symptoms
l See symptomatology (Gyn) for various kinds of symptoms
l Ask for the development of the symptoms in chronological order
l Qualify and quantity the severity of symptoms
n e.g. number and type of pads for menorrhagia
l Note how the patient reacts to the symptoms:
n e.g. urinary incontinence may be so severe that makes the patient home-bound
l Ask for any relevant treatments or investigation results
n Many patients before coming to see a gynaecologist may have been managed by a general practitioners.
E.g. a patient may have been given various kinds of medication for dysfunctional uterine bleeding, and
Sexual history
Sexual practice
l number of sexual partners, frequency of coitus, sexual dysfunction, etc
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Contraceptive practice
l methods of contraception
Past obstetric history
l It is important in cases such as infertility, ectopic pregnancy and recurrent abortions
Past medical history
Concerns about:
l Risk factors to the development of present problem:
n e.g. past history of sexually transmitted diseases: related to pelvic inflammatory disease, ectopic
pregnancy, CIN and cervical cancer
l General health of the patient which may affect your management:
n History of diabetes, heart disease, hypertension may affect surgical and anaesthetic management
Social history
l Alcohol intake, smoking, drug abuse, occupation etc.

Symptomatology (Gyn)
Menstrual symptoms
l It is the most common group of symptoms in gynaecology.
l It may be abnormal in volume of flow, regularity, onset and cessation, or with associated pain and discomforts.
l See menstrual disorders for detail
Abnormal vaginal bleeding
l Related to menstruation (see menstrual disorders)
l In early pregnancy: various kinds of abortions and ectopic pregnancy
l Benign tumours or cancers of the genital tract, presented with:
n postcoital bleeding
n postmenopausal bleeding
Vaginal discharges
l Abnormal in colour and odour
l Usually due to infections, occasionally related to fistula formation between the urinary tract and genital tract
l See vaginal discharge for detail
Abdominal and pelvic pain
l Pain related to menstruation (see menstrual disorders)
l Pain related to coitus: dyspareunia
l Acute pelvic pain
l Chronic pelvic pain
Urinary symptoms
l Urinary incontinence
n stress incontinence, urge incontinence, overflow incontinence, etc
l Abnormal frequency
l Frequency of micturition, nocturia
l Discomfort
l dysuria, urgency

Examination (Gyn)
Attitude
l Be gentle
l Be considerate
l Be courteous
Pre-requisites
l Good light
l Chaperone
l Full exposure
l Empty bladder immediately prior to examination
l Gloves
Positioning of patient
l Lithotomy position
l Supine + knees drawn up & fall apart + heels together Sim position
l For examination of genital prolapse
Procedure
l Inspection of external genitalia
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l Speculum (bivalve) examination
l Bimanual palpation
l +/-Rectal examination
Examination of external genitalia
l Pubic hair: presence, distribution and hygiene
l Labia majora and labia minora: swelling, mass, ulcer
l Urethra
l Anus Remark: good exposure by separating the labia
Bivalve speculum examination
For inspection of
l Cervix
l Fornix
l Vaginal wall

Remark:
l Use lubrication
l Do not turn speculum
l Do not lock speculum
l Take pap smear if not been done recently
l Gently close speculum on withdrawal
Bimanual examination

To palpate pelvic organs between both hands

l Use lubrication
l Insert the right index and middle fingers into vagina, with the thumb upwards and away from the urethral orifice
l Place the Left hand over the suprapubic region and press downwards, while the right index and middle fingers
and press upwards
l Palpate the ut erus and bilateral adnexae between both hands
Assess:
l Cervix: size, consistency, tenderness (cervical excitation)
l Uterus: size, position (anteversion or retroversion of uterus), shape, mobility, consistency
l Adnexal region: mass: size, shape, consistency, mobility, tenderness
l Pouch of Douglas: mass, tenderness
Examination of genital prolapse
l See Examination of genital prolapse
Discussion/Something to Consider
How to differentiate the origin of a pelvic mass, whether it is from uterus or from ovary on examination?
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As we have high resolution ultrasound scanning which can visualise the pelvic organs clearly, what is the value of
clinical examination?
How to differentiate rectocoele from enterocoele, and what is the clinical importance of differentiation between these
two lesions?

Fundal height
Full name is symphysial-fundal height. It is the distance between the top of the uterus and the upper border of the
pubic symphysis at the midline. It is an objective method of monitoring uterine size which in term reflects fetal growth.
The fundal height in centimetre is correlated with gestation age in week, starting from 20 week of maturity. For
example, at 30 week, the fundal height is around 30cm+/-2cm. After 37 week, the fundal height may decrease, due
to the engagement of the fetus, as well as the reduction of amniotic fluid.

2. Drugs

Drugs
The following groups of drugs are commonly used in O&G:
Anti-hypertensives
Anti-convulsants
Antibiotics
Insulin
Tocolytics
Oxytocics
Contraceptives
l combined oral contraceptives
l progestogen-only pills (mini pills)
l progestogen injectable
Hormonal replacement therapy
Ovulation induction agents
l clomiphene citrate

Oxytocic
Definition
l From Greek: oxys: sharp, quick; tokos: childbirth (from tiktein: to bear); meaning hastening labour.
l It is a group of agents that are able to stimulate myometrial contractions.
l Common oxytocics include:
n oxytocin or syntocinon
n prostaglandins and their analogue
n ergometrine
Indication of oxytocics
In Obstetrics
l Induction of labour and augmentation of labour
l Prophylaxis and treatment of uterine atony
In Gynaecology
l Evacuation of uterus in abortion, and termination of pregnancy
Complications of oxytocics
l Uterine hyperstimulation, resulting in uterine rupture and severe bleeding
l Water intoxication with oxytocin
l Gastrointestinal and cardiorespiratory complications with prostaglandins
l Hypertension with ergometrine

Oxytocin
What is oxytocin
l It is a peptide hormone secreted from the hypothalamus and transported to the posterior lobe of the pituitary
where it is eventually released.
What are the effects of oxytocin
It has two major actions in human:
l Firstly, it stimulates smooth muscle contraction in uterus (oxytocic)
n It is essential for the initiation and progression of labour
n It binds to oxytocin receptors of myometrial cells and activate the contractile protein
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 n The number of oxytocin receptors increases gradually as pregnancy go on, and exponentially before
onset of labour. The production of receptors is stimulated by prostaglandins
n A positive feedback loop acts on the pituitary secretion of oxytocin. More oxytocin is secreted as uterine
contractions are stimulated and continued
l Secondly, it stimulates contractions of myoepithelial cells of mammary glands
n It facilitates lactation
l Besides, as its biochemical structure is similar to that of vasopressin (antidiuretic hormone also secreted from
the posterior pituitary gland), it also has weak antidiruetic effect.
How is oxytocin metabolised
The peptide is rapidly broken down into amnio acid by oxytocinase in blood. The half-life of oxytocin is therefore 3-4
minutes.
What are the clinical uses of oxytocin
See syntocinon for clinical uses

Syntocinon
Syntocinon is a synthetic oxytocin, and has the same biochemical structure, pharmacokinetic and
pharmacodynamic characteristics as oxytocin. It is given intravenously, as a bolus injection or infusion.
Clinical use of syntocinon
Intrapartum use:
l for induction of labour and augmentation of labour. Syntocinon is given as intravenous infusion. The rate of
infusion is titrated against the frequency of uterine contractions. The optimal frequency is 3 to 4 contractions in
10 minutes. Care must be taken to avoid uterine hyperstimulation.
l to overcome uterine inertia in the second stage delivery of twin pregnancy. Uterine contractions may diminish
after the first twin is delivered, and the second twin may not descend. Augmentation is required to hasten the
delivery of the second twin
Postpartum use:
l as an alternative of routine syntometrine in the third stage of labour against uterine atony. It is given as a bolus
injection.
l as a prevention or maintenance treatment against uterine atony in high risk cases such as placenta praevia,
abruptio placentae, twin pregnancy. It is given by continuous infusion
Other use:
l as an adjuvant agent for evacuation of uterus in treatment of abortions
l as an oxytocic in a stress test:
n syntocinon was used to stimulate uterine contractions in a stress test for fetal well-being. This test is
rarely required nowadays as less invasive tests for fetal well-being are now available.
Risks of syntocinon
The major risk is uterine hyperstimulation, which would result in fetal distress and uterine rupture. The other risks are
less common and mild, and include hypotension (related to direct peripheral vasodilatation), water intoxication
(related to anti-diuretic effect)

Syntometrine
It is a combined drug consisting of 5 units of syntocinon and 0.5mg of ergometrine. It is commonly given
intramuscularly during the third stage of labour routinely as a prophylaxis against uterine atony and postpartum
haemorrhage. The syntocinon component acts quickly in 2 minutes and produces clonic uterine contractions while
the ergometrine component stimulates sustained tonic contractions. It is contraindicated in hypertension and asthma
because of vasocontrictive effects of ergometrine.

Ergometrine
A compound oxytocic consisting of syntocinon and ergometrine used for prophylaxis or treatment of uterine atony in
the third stage of labour. It is given intramuscularly. It has the advantages of both syntocinon and ergometrine. It is
contraindicated in hypertension because of vasoconstrictive effect of ergometrine.

Prostaglandin
What are Prostaglandins
They are groups of compounds derived from unsaturated 20 carbon fatty acids, primarily arachidonic acid, via the
cyclooxygenase pathway. It was thought to be come from the prostate gland from which its name originated. It is
now well known that prostaglandins are found in many organs with diverse physiological effects in human. The most
important groups of prostaglandins in obstetrics and gynaecology are prostaglandin E (PGE) and prostaglandin F
(PGF). They are involved in the process of ovulation, initiation of labour, and pathogenesis of dysmenorrhea and

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menorrhagia. Synthetic PGE and PGF are also used in various obstetric situation including cervical ripening for
induction of labour, treatment of uterine atony, and in gynaecological conditions such as termination of pregnancy
and treatment of abortion

Misoprostol
Introduction
l A prostaglandin E1 analogue. Originally used for prevention and treatment of gastric ulcers associated wit h
the use of nonsteroidal anti-inflammatory drugs.
l Has become an important drug in obstetrics and gynaecology because of its uterotonic and cervical ripening
actions.
Pharmacology
Administration and absorption
l Can be given orally or vaginally.
l After oral administration, misoprostol is rapidly absorbed and converted to its pharmacologically active
metabolite, misoprostol acid. Plasma concentrations of misoprostol acid peak in 30 minutes and decline rapidly
thereafter.
l After vaginal administration, plasma concentrations peak in 1 to 2 hours and then decline slowly, resulting in
slower increases and lower peak plasma levels, but overall exposure to the drug is increased.
l Uterine contractility become plateaued 1 hour after oral administration. When given vaginally, uterine
contractility increases continuously for 4 hours and reaches a maximum level higher than that when given
orally.
Metabolism and excretion
l It is primarily metabolised in the liver and less than 1% of it is excreted in urine.
Side effects
Side effects are dose-dependent and less severe when the drug is administered vaginally.
l Gastrointestinal upset: Nausea, vomiting, diarrhea, abdominal pain.
l Fever, chills and shivering.
l Unlike prostaglandin E2 and F2, it would not cause bronchospasm or myocardial infarction.
l Teratogenicity: limbs defects, ring-shaped constrictions of the extremities, arthrogryposis, hydrocephalus,
holoprosencephaly, Mobius syndrome (congenital facial paralysis) are reported.
Obstetric and gynaecological Indications
l Medical termination of pregnancy
n Misoprostol when combined with mifepristone, can be used for termination of pregnancy at a gestation
less than 9 weeks. The regimens are:
u Oral mifepristone 600mg followed 48 hours by oral misoprostol 400mcg, or
u Oral mifepristone 200mg followed 48 hours by oral misoprostol 600mcg
n Efficacy:
u 95% complete abortion rate when used before 7 completed weeks
u 90% complete abortion rate when used between 8 to 9 completed weeks
l Treatment of miscarriage
l Cervical ripening before surgical abortion
l Induction of labour
l Postpartum haemorrhage

Tocolytic
Definition
In Greek toco means labour; lysis means dissolve; It is a group of agents that cause relaxation of uterine muscle and
hence dissolution of labour. It is opposite to oxytocic
Common tocolytic agents
Beta-sympathomimetic
l Ritodrine
n It is administered by continuous intravenous infusion, usually indicated for suppression of preterm labour.
The rate of infusion is titrated against the frequency of uterine contractions.
n Maternal side effects are:
u tachycardia and hypotension
u heart failure and pulmonary edema
u hypokalemia and hyerglycemia
n Fetal side effects are:
u fetal tachycardia
u fetal distress secondary to maternal hypotension
l Hexoprenaline

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 n It is usually given in bolus intravenous injection
n It is a short acting agent used mainly for uterine relaxation during external cephalic version (ECV) and
relief of uterine hyperstimulation
n types of side effects are similar to ritodrine but severity is much less because it is short-acting, and often
adminstered in a single bolus rather than by continuous infusion
Prostaglandin inhibitors
l Sulindac
n It is a kind of non-steroidal anti-inflammatory drugs (NSAID) that inhibit cyclooxygenase in the synthesis
of prostaglandin from arachidonic acid.
n It is administered orally
n Maternal side effects are not pronounced; fetal side effects not common but include oligohydramnios,
patent ductus arteriosus
Calcium channel blocker
l Nifedipine
n It is administered orally
n Maternal side effects are headache, flushing, hypotension and tachycardia
Indications of tocolytics
l Preterm labour
n The main aim of tocolytics is to allow more time for glucocortiocord to effect on lung maturation, in order
to prevent neonatal respiratory disease (RDS) and other complications of prematurity
n The first line treatment has been ritodrine until recently nifedipine has been proven to be as effective but
less side effects than ritodrine
l External cephalic version (ECV)
n Short-acting agents like hexoprenaline improve the chance of success by relaxing the uterus
l Uterine hyperstimulation
n Short-acting hexoprenaline may also help to relax the uterus rapidly and relieve fetal distress during
uterine hyperstimulation
Contraindications
l When continuation of pregnancy is of higher risk than inhibition of labour:
n Chorioamnionitis
n Abruptio placentae
l When the pregnancy has reached a maturity of low neonatal mortality or morbidity:
n >=34 weeks of gestation
l When there are co-existing maternal disorders that may be worsen with the tocolytics:
n Beta-sympathomimetic are contraindicated in thyrotoxicosis and major heart diseases
n Prostaglandin inhibitors are contraindicated in thrombocytopenia and peptic ulcer diseases
Discussion/Something to Consider
Can you explain why prenatal use of NSAID is associated with oligohydramnios and neonatal patent ductus
arteriosus?
Can you explain why ritodrine is associated with hypokalemia and hyperglycemia?

Anti-hypertensive
The role of anti-hypertensives in obstetrics is to prevent complications of hypertension such as stroke. It is indicated
in patients with pre-existing hypertension, or severe pre-eclampsia. However, it cannot alter the progress of
pre-eclampsia, which would only be resolved after delivery. The commonly used anti-hypertensives in obstetrics are:
Methyldopa
l A centrally acting agent that causes peripheral vasodilatation
l Given orally, requiring a high loading dose because of long half life, and is therefore not for acute control
l Very safe in pregnancy, and is therefore the first choice for long term treatment during antenatal period
l Side effects include depression, nightmares and postural hypotension
Hydralazine
l A potent direct smooth muscle relaxant leading to vasodilatation
l Usually given in bolus intravenously for acute control
l Also for maintenance therapy when given as infusion
l Side effects include headache, nausea and palpitation
Nifedipine
l A calcium channel blocker
l Acts quickly when given orally or sublingually, effective for acute control
l Slow releasing form is effective as a maintenance
l Side effects: headache
Labetolol

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l An alpha and beta-adrenergic blocker that causes peripheral vasodilatation
l is mainly used postnatally because of the risk of IUGR after long term use
l can be given orally for maintenance, or intravenously for acute control
l is contraindicated in heart failure

Diazepam
Diazepam is used as an anticonvulsant to stop acute seizure in eclampsic patients. It is given as an intravenous
bolus. It may also be used as a prophylactic agent but it would require continuous intravenous infusion. It is less
effective than MgSO4 as a prophylaxis, and sedation of mother and neonatal depression are the concerns.

MgSO4
Indication of Magnesium sulphate
It is an anticonvulsant for prophylaxis against development of eclampsia, or prevention of recurrent convulsions. It
has been shown to be more effective than diazepam in preventing recurrence of convulsions. It does not have side
effect of neonatal depression.
Administration of Magnesium sulphate
It is administered by bolus injection intramuscularly, followed by intravenous infusion for maintenance.
Side effects of Magnesium sulphate
Magnesium sulphate antagonizes calcium in the muscle contractility and nerve conduction. The side effects are
therefore muscle paralysis and cardiac arrest. The therapeutic range is narrow:
plasma level (mmol/l) Effect
2-4 therapeutic
>5 loss of patella reflex
>6 Prolonged AV conduction
>7.5 respiratory arrest
>12 cardiac arrest
Therefore, it is important to monitor the reflex, respiration, ECG for sign of toxicity during administration of MgSO4.
As magnesium is excreted via the renal system, the dosage have to be decreased when the urine output is
diminished.

Glucocorticoid
Glucocorticoid therapy for preterm pregnancy
Benefit of Glucocorticoid therapy
l Glucocorticoid therapy has been showed to reduce various neonatal complications of prematurity such as
respiratory distress, intraventricular haemorrhage, necrotizing enterocolitis.
Indications of Glucocorticoid therapy
l Patients undergoing preterm labour
l High risk of preterm delivery
n after an episode of antepartum haemorrhage due to placenta praevia or of unknown origin
n fetal complications that may require preterm delivery such as severe IUGR
n maternal complications such as pre-eclampsia that may require preterm delivery
Complications of Glucocorticoid therapy
l Side effects of steroid therapy are uncommon and mild. Repeated course of steroid however may result in fetal
complications such as adrenal suppression.

Tibolone
It is a synthetic steroid which exhibits all estrogenic, progestogenic and androgenic activity. It is used as a kind of
hormonal replacement therapy and is effective in suppressing climacteric symptoms as well as preventing bone loss.
The side effects are mainly androgenic, and is usually mild and well-tolerated.

Danazol
It is a synthetic androgen frequently prescribed in gynaecology. The pharmacodynamic effect is the suppression of
the hypothalamic-pituitary-ovarian axis, resulting in hypoestrogenemia. It is used to control symptoms of
endometriosis, menorrhagia due to dysfunctional uterine bleeding, and as a pre-myomectomy treatment to reduce
size and vascularity of fibroids. It is as effective as GnRHa, but the androgenic side effects (deepening of voice,
acnes, weight gain and cramping) may not be as acceptable as that of GnRHa to women. Some of these changes
may not be reversible. Prolonged use may also result in osteoporosis, so that the use of the drug is limited to 6
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months.

GnRHa
What is Gonadotropin releasing hormone analogue (GnRHa)
l GnRHa are synthetic substances in which one or more of the amino acids in GnRH are substituted by a
different amino acid, so that the activity and binding ability to receptors are altered. Their affinity to GnRH
receptors is usually higher than that of GnRH, and is more resistant to metabolism. Therefore, they produce a
down-regulatory effect on the pituitary glands. In long term use, it will result in hypogonadotropic
hypogonadism. This mechanism accounts for its therapeutic effects as well as its side effects
What are the clinical uses of GnRHa
Treatment of endometriosis
l Hypogonadotropic hypogonadism leads to the lack of endogenous estrogen stimulation on the growth of
endometriosis. The progress of the disease is arrested and symptoms are relieved.
Treatment of fibroids and menorrhagia
l The size of fibroids is decreased because of lack of estrogen stimulation. Menstrual flow is stopped or
diminished. It is however cannot be used as a definite treatment of fibroids or menorrhagia because the
problems often recur after stopping the treatment. It can be used before hysterectomy or myomectomy, as a
temporary relief of symptoms, or to shrink the size of the fibroids in order to facilitate surgery.
Use in assisted reproductive technology
l GnRHa is used as a pre-treatment before ovarian stimulation. The ovaries are first suppressed with GnRHa
before undergoing stimulation. This helps to synchronize the growth of oocytes. The endogenous premature
surge of LH is also suppressed.
Side effects of GnRHa
l The side effects are mainly related to hypoestrogenism and therefore patients will experience discomforts
similar to that of climacteric. Osteoporosis is the major long term complications that limit the use of GnRHa.
The duration of GnRHa should not be more than 6 months.

GnRH
Gonadotropin releasing hormone (GnRH) is a peptide hormone secreted from the hypothalamus in a pulsatile
manner. It stimulates pituitary gonadotropins secretion, and its secretion is inhibit by estrogen. They form the
hypothalamus-pituitary-ovarian axis for the control mechanism of ovulation.
The beginning of pulsatile GnRH secretion in teenage initiates the development of puberty. Psychological stress,
excessive exercise, significant weight reduction such as in anorexia neurosa result in suppression of GnRH
secretion.
Synthetic GnRH can be used as a ovulation induction when given in a pulsatile manner.
GnRH analogue (GnRHa), having a similar chemical structure, are used to treat various gynaecological disorders.

Gonadotropin
There are two kinds of pituitary gonadotropins: follicular stimulating hormone (FSH) and luteinizing hormone (LH).
They are glycoprotein hormones secreted from the anterior pituitary glands, under the stimulation of gonadotropin
releasing hormone (GnRH, which is secreted from the hypothalamus). They form the hypothalamus-pituitary-ovarian
system that control the mechanism of folliculogenesis and ovulation.
Absence of gonadotropins result in anovulation or failure to reach puberty such as in Kallman syndrome. On the
other hand, premature secretion results in precocious puberty.
Another gonadotropin is human chorionic gonadotropin secreted from the placenta.
Gonadotropins can be extracted from human (Human menopausal gonadotropin (HMG), highly-purified urinary
follicular stimulating hormone (hpFSH)) or synthesized by genetic engineering technology (Recombinant FSH) They
are powerful agents for ovulation induction. See gonadotropin therapy

Gonadotropin therapy
Nature
Gonadotropins are extracted from human or synthesized, and used as very effective ovulation induction agents:
l Human menopausal gonadotropin (HMG)
l Highly-purified urinary follicular stimulating hormone (FSH)
l Recombinant FSH
Mechanism of action
l Act directly on ovaries to stimulate folliculogenesis
Efficacy

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l ovulation rate: >95% per cycle
l conception rate: 20% per ovulatory cycle
l cumulative conception rate (6-month): 90%
Complications
l multiple pregnancy rate 10-30%, higher order pregnancy: 5%
l ovarian hyperstimulation syndrome (OHSS)
l Remark: Intensive monitoring in specialist clinic is necessary because of the higher risk of multiple
pregnancies and OHSS
Advantages
l most powerful
Disadvantages
l narrow therapeutic range, intensive monitoring necessary
l high risks of multiple pregnancy and ovarian hyperstimulation syndrome (OHSS)
l expensive

Augmentin
What is Augmentin
l Augmentin is one of the commonly used antibiotics, containing penicillin and clavulanic acid (a beta-lactamase
inhibitor)
Advantages
l Useful in those organisms resistant to penicillin
l E. coli is one of the most common organism causing urinary tract infection and now over half of them is
resistant to penicillin, but not Augmentin It also covers the anaerobes
Use in O&G
l Prophylactic antibiotics in emergency Caesarean section Prophylactic antibiotics in vaginal surgery (e.g.
vaginal hysterectomy)

Methrotrexate
Anti-metabolites used as a chemotherapuetic agent for residual trophoblastic disease or ectopic pregnancy
Can be used alone or in combination with other agents
Side effects
l Alopeccia
l Nausea and vomiting
l Myelosuppression

3. English usage

English usage
Parity O
l Nullipartiy is commonly said to be parity 'O'. It should be more correct to say parity 'zero'.
sure LMP
l It is common to say 'LMP is sure', or 'She has a sure LMP'. The correct way is 'She is sure of her LMP'.
rupture of membranes
l It should be in plural form as there are two membranous layers: amnion and chorion.
Large > date
l We use symbols '<' or '>' in the medical notes to denote whether the uterine size is normal for date for
convenience. However, we should not say 'uterus is larger than date' or 'smaller than date', as 'size' and 'date'
are two different parameters and are not comparable. It is correct to say 'uterus is large (small) for date', or
'uterus is larger (smaller) than expected (from date)'

Acronym
A word formed from the initial letters of a name, or by combining initial letters or parts of a series of words, such as:
l HELLP for Haemolysis, Elevated Liver enzymes, Low Platelets
l TORCH for Toxoplasmosis, Rubella, Cytomegalovirus, and Herpes
l OHSS for Ovarian Hyper-Stimulation Syndrome

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Eponym
Epi means on or upon, onyma means name. An eponym is one for whom or which something is named or supposed
named, for example:
l Down syndrome named after Down
l Apgar score named after Virginia Apgar (1909-1974), anaesthesiologist.

4. Infections

Fetal infection
Introduction
Fetus can acquire infection in the following ways:
l placental transmission
l ascending infection from lower genital tract
l majority is sexually transmitted diseases
l infection acquired during labour when the fetus passing through the birth canal
Micro-organisms
The followings are common or important micro-organisms:
Viral
l rubella, herpes-varicella (chickenpox), HIV. hepatitis B
Bacterial
l syphilis, group B streptococcus, gonorrhea, chlamydia
Protozal
l Toxoplasmosis
Fetal complications resulted from infection
Fetus can be damaged by infections in the following ways:
Congenital infection:
l Infection can be teratogenic and cause multiple malformations
l high risk when infection is acquired in the first trimester
l examples are Rubella and Syphilis infection
Neonatal infection:
n infection is acquired around the time of labour or delivery, often from the lower genital tract
n causes localised neonatal infections
n Examples are
u gonorrhea and chlamydia cause neonatal eye infection
u group B streptococcus causes neonatal pneumonia or meningitis
u chickenpox infection through placental transmission causes neonatal pneumonia
l Neonates become the carriers of the disease:
n fetus acquires the micro-organism and becomes a carrier
n the micro-organism does not cause any harm to the fetus or neonate immediately, but will cause
significant health problems in the later life
n Examples are
u hepatitis B: the child has high chance of developing CA liver in their later life
u Indirect fetal complications
u fetal health is also affected indirectly because of preterm labour and delivery secondary to
intrauterine infection or preterm rupture of membranes. Organisms such as group B streptococcus,
chlamydia are associated with preterm delivery
Common fetal infections that medical students should know
The following are chosen because they are relatively common, cause significant fetal morbidity and mortality, and
illustrate various ways how fetus or neonate are affected
l Rubella
l Herpes-zoster (chickenpox)
l syphilis
l gonorrhea and chlamydia
l group B streptococcus
l Listeriosis
l hepatitis B

Hepatitis
Viral hepatitis
l Hepatitis A

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l Hepatitis B
l Hepatitis C

Hepatitis B
Introduction
Hepatitis B infection is an important topic in Obstetrics because:
l acute hepatitis may mimic liver disorder specific to pregnancy, such as acute fatty liver and HELLP syndrome.
The differentiation of these diseases are important in the obstetric management.
l Vertical transmission is the main cause of endemicity in Hong Kong and perinatal infection is the major
predisposing factor of primary hepatocellular carcinoma. Neonatal prophylactic programme has been
implemented.
Epidemiology
l In Hong Kong, 10% adults are HBV carriers
l Vertical transmission results in >90% chronic carriage
Virology
l Double-stranded DNA virus (circular DNA with single stranded regions)
l Family: Hepadnaviridae; genus: Hepadnavirus
l Transmission via:
n Blood: transfusions, sharing of needles or razors, tattooing acupuncture, renal dialysis or organ donation
n Sexual intercourse
n close personal contact in horizontal transmission in children within families
n Vertical transmission: perinatal infection at delivery, or rarely transplacental
Complications
l Acute hepatitis
l Fulminant hepatitis (rare; 1%)
l Persistent infection (5%): chronic persistent hepatitis or chronic active hepatitis
l Risk of hepatocellular carcinoma in chronic carrier in future: in Hong Kong, 80% of hepatocellular carcinoma
cases are caused by HBV infection
Perinatal infection
l Vertical transmission usually occurs at delivery from maternal blood or body fluids, and transplacental
transmission is very rare
l Vertical transmission rate depends on the level of maternal viraemia. For HBsAg positive mothers, perinatal
infection occurs in 10-20%. For women who are positive for both HBsAg and HBeAg, the transmission rate is
90%.
l Acute maternal infection during the first or second trimesters rarely leads to vertical transmission, while
maternal infection during the third trimester or chronic carriers increase the risk of vertical transmission.
l Effect on neonates
l Neonates would become hepatitis B carriers. Over 90% of chronic carriers are a result of vertical transmission.
l Some of the infected neonates may develop hepatitis which is often mild. Rarely, fulminant hepatitis may occur.
l Teratogenic effects have not been reported.
Prevention of perinatal infection
l Every pregnant woman should be screened with HBsAg.
l Neonates of carriers should be given prophylactic Hepatitis B immunoglobulin immediately after delivery
(within 12 hours after birth) to prevent perinatal infection. The efficacy of treatment decreases if delayed.
l All neonates should receive Hepatitis B vaccination during postnatal period:
n the first dose must be administered within the first week, the second dose at 1 month of age, and the third
at 3-4 months.
n The efficacy is >90%. The child is tested after 1 year as 10% of neonates born to seropositive mothers
become chronic HBV carriers despite prophylaxis is given.
Management of acute hepatitis B infection during pregnancy
Principle
l It should be differentiated from other causes of hepatic dysfunction such as HELLP syndrome and acute fatty
liver, and other causes of hepatitis
Diagnosis
l Serology
Treatment
l Supportive care, control of symptoms like nausea and vomiting
l Dietary advice, e.g. hydration
l Monitoring of liver function
l Monitoring of fetal growth and health
l Monitoring of uterine activity
l Infection control measures
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l Contact tracing, testing and vaccination if necessary
l Follow-up for evidence of resolution or chronic carriage
l Counselling of family members of HBsAg-positive women and infants

Hepatitis C
Epidemiology
l In Hong Kong, <0.5% of the general population are HCV carriers.
l Vertical transmission rate depends on the level of viraemia and the overall risk appears to be 5-10% and
increased to 36% if the woman is co-infected with HIV.
l No effective way of preventing vertical transmission of HCV.
Virology
l Single-stranded (+ve) RNA virus
l Family: Flaviviridae; genus: Hepacavirus
l Enveloped

HIV
Virology
l Single-stranded(+ve) RNA virus: retroviridae
l Several types; type 1 is the most common and type 2 is similar to type 1, which is confined to West Africa and
less virulent
Epidemiology
l Worldwide distribution; Africa is the most prevalent area
l In the USA and Europe, AIDS is mainly caused by HIV-1; HIV-2 is responsible for a proportion of infections in
Africa
l Hong Kong (in July 1999): 1255 HIV positive cases have been reported, the male:female ratio of new cases is
around 6:1 with an increasing trend for females, 9 cases of vertical transmission were found.
l Parenteral transmission through blood and body fluids, sexual intercourse or from mother to the child
l Risk factors of infection:
n Multiple sexual partners
n Bisexual activity
n Sexually transmitted diseases (previous or current)
n IV drug addicts
n Transfusion of blood or blood products
n Originating from an endemic area.
Maternal infection
l Asymptomatic in early stage
l Some women may have early diseases like vulvovaginal candidiasis, pelvic inflammatory disease (PID) and
cervical dysplasia
l Anaemia, thrombocytopenia or neutropenia may occur
l Women with thrombocytopenia may have epistaxis, petechiae and menorrhagia
l Some may have non-specific symptoms like fever, arthralgias, myalgias and fatigue
l Advanced cases: at increased risk of opportunistic infections, such as Pneumocystis carinii pneumonia,
toxoplasmosis, lymphoma, cryptococcal meningitis
Perinatal infection
Transmission
l The transmission rate of HIV-1 to fetus was estimated to be 15-35%. Infections occur either in utero (13-33%)
or at delivery.
l The rate of transmission to infants by infected mothers increases with the clinical severity of maternal disease
and is inversely proportional to the maternal CD4+ T-lymphocyte count.
l The progress of the disease in these infants varies directly with the disease severity in the mother at the time of
delivery.
l Antenatal and intrapartum antiviral therapy decreases the transmission by 60-70%.
l Breast-feeding is associated with an additional 14% risk of transmission.
Clinical features
l No added risk of malformation
l Most infected infants develop symptoms within the first 2 years of life.
l Common clinical manifestations include bacterial infections, chronic parotitis, fever, lymphadenopathy,
hepatosplenomegaly, chronic or recurrent diarrhea, failure to thrive, and recurrent or persistent candidiasis.
Screening
l Serological screening of HIV status should be considered in high risk patients (see above). Consent is required
Diagnosis
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Maternal diagnosis
l PCR assays for HIV cDNA in serum
l Virus isolation (expensive and slow)
Neonatal diagnosis of perinatal infection
l Conventional serological assays are difficult to interpret as passively transferred maternal antibodies may take
up 18 months to disappear
l Other diagnostic tests include:
n PCR assays for HIV cDNA
n p24 antigen detection (ELISA)
n Virus isolation
n IgA class-specific antibody detection (EIA)
n Early diagnosis allows prophylaxis against opportunistic infections
Management of For HIV-positive carriers
Pre-conception counselling:
l Counselling of risks and prognosis of the child.
l Consider avoiding pregnancy.
Antenatal:
l Monitoring of CD4+ counts.
l Extensive and ongoing counselling.
l Zidovudine (azidothymidine, AZT) treatment is offered to the mother during pregnancy, labour and delivery,
and to the newborn. This reduces the risk of perinatal transmission.
l Looking for any development of opportunistic infections or AIDS.
Intrapartum:
l Elective caesarean section may reduce the risk of perinatal transmission.
Postnatal:
l The newborn's skin should be cleansed of all maternal secretions before being punctured by a needle.
l Breast-feeding is avoided if possible.
l Prevent the baby from contacting with maternal secretions.

Group B streptococcus
Organism
Group B streptococcus (GBS)
l gram positive aerobic coccus
Epidemiology
l In UK, 15-20% of women carry GBS in the vagina at delivery
l 40-70% of infants of mothers colonised antenatally with GBS are themselves colonised, but only 1% develop
evidence of infection affected by it
l nevertheless GBS infections are one of the commonest infective causes of neonatal morbidity and mortality in
the developed world with an incidence of 1-4/1000 birth
l the mortality rate for perinatal infection can be as high as 80% despite early recognition and prompt treatment
Fetal Risk
l neonatal pneumonia
l neonatal meningitis
l preterm rupture of membranes, preterm labour and delivery
Maternal Risk
l Patients are usually carriers and asymptomatic
l may cause vaginitis, and intrauterine infection after rupture of membranes
Screening and prevention
l routine screening for maternal colonisation and treatment
l Controversial
l GBS is only temporarily eradicated by short-term antibiotic therapy during pregnancy
l If treatment is based on a positive culture at 28 week up to 50% will be negative at delivery, and up to 15% of
culture-negative women at 28 weeks will be culture-positive by delivery. Thus some women would be
overtreated while others would be undertreated
Management
l Intrapartum antibiotic (ampicillin) prophylaxis to prevent perinatal infection

Toxoplasmosis
A systemic infection caused by the protozoon Toxoplasma gondii. It is either asymptomatic or confused with 'flu' or
other pregnancy symptoms

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Incidence
It is extremely uncommon in Hong Kong. The best estimate of the incidence in pregnant women in the UK is about
2/1000.
Congenital toxoplasmosis
Toxoplasma gondii can cause significant congenital abnormality of fetus:
During the first trimester, transmission to the fetus occurs in about 10% of maternal infection. Fetal death or severe
sequelae are likely.
During the second trimester, transmission is frequent with a high risk of congenital infection.
During the third trimester, transmission is very frequent but the risk of problems at birth is low. However, as many as
80% of children may develop chorioretinitis in later years.
Prevention
The best policy is prevention by avoiding undercooked meat, unpasterurised milk, and contact with cat litter;
washing all garden produce well and washing hands after gardening.

Rubella
Virology
l Family: Togaviridae; genus: Rubivirus
l Single-stranded RNA virus
l With haemagglutinin antigens
l Infects only humans
l spread by droplets infection
l Incubation period: 14 to 21 days
Clinical features
l 25% are subclinical
l usually present with mild febrile illness with macular rash and lymphadenopathy which lasts for 5 to 7 days
l Macular rash first appears on the face and behind the ears before spreading down the trunk and the limbs.
l The contagious period (i.e. viral shedding) extends from 8 days before to 8 days after the onset of the rash.
l Rubella antibodies are present by the time rash appears.
Fetal Risk
Congenital rubella syndrome
l Chance
Gestation at infection Chance of infection abnormalities
< 8 week up to 85% all infected fetuses will develop complications
< 12 week 50 - 80% 65 - 85% of infected fetuses have clinical defects
13 - 16 week 30% one third suffer sensorineural deafness
> 16 week 10% clinical manifestation rare
l Features of congenital rubella syndrome
n bilateral cataracts, microphthalmia
n sensorineural deafness
n mental retardation
n congenital heart disease especially patent ductus arteriosus
n intrauterine growth retardation
n abortion, intrauterine death
Diagnosis of maternal rubella
l As 25% are subclinical, diagnosis should not be based on clinical presentation alone
l Serologic confirmation is essential:
n Four-fold rise in IgG titres
n Rubella-specific IgM antibody (false positive occurs with rheumatic factor)
Diagnosis of congenital rubella after delivery
l virus isolated from infant's pharynx, urine and cerebrospinal fluid in the first three months of life
l IgM rubella-specific antibody present in cord blood
l Persistence of rubella antibodies after 6 months
Screening
l Immunity is screened with rubella antibody (IgG) at booking, or before pregnancy
l IgG ELISA test, latex agglutination test and radial immune haemolysis test can be used
Prevention
Vaccination before pregnancy
l live attenuated virus vaccine
l contraception are advised for 3 months post-vaccination although the chance of congenital rubella infection
caused by the live vaccine is very rare.

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Discussion/Something to Consider
During the booking visit at 9 weeks of gestation, a patient tell you that her child got a rubella rash 2 week ago. How
would you manage this case?
A subsequent test confirmed that the patient had recent rubella infection. How would you counsel and manage this
pregnancy?

Chickenpox
Virology
l Herpes varicella-zoster causes chickenpox in a primary infection, and shingles on reactivation.
l Incubation period: 10 - 21 days after initial contact (delayed up to 28 days if VZIg immunization is given)
l Infectious period: 2 days before onset of skin rash until cropping have ceased and crusted over (usually takes
about 5 days)
Chickenpox
l The name was meant to distinguish this weak form of the pox from smallpox (chicken being used, as in
chickenhearted, to mean weak or timid).
l It is a febrile disease with generalised skin rash, starts as an eruption of red papules (bumps) which become
vesicles (blisters) than pustules. Other symptoms include malaise, weakness, sore throat, cough and fever.
Maternal risk
l Complications including pneumonia and encephalitis are uncommon but can be severe in adults.
Fetal risk
l When infected during pregnancy, there is a risk of congenital varicella syndrome:
n 1% risk before 12 week of gestation
n 2% between 13 and 20 week
n minimal after 20 week
n syndrome consists of: mental retardation, microcephaly, neurological and visual deficit, IUGR and
deformity
l When infected during perinatal period, there is a risk of neonatal varicella
n risk is 20 to 30% when mothers develop chickenpox within 5 days before and 2 days after delivery
n neonatal mortality is 30%
Diagnosis
l Unlike rubella infection, chickenpox is always symptomatic, and diagnosis can often be made based on clinical
features. Serology is not required to confirm the diagnosis
Treatment of active chickenpox infection during pregnancy
l Give acyclovir to reduce severity and duration of disease.
l varicella-zoster immunoglobulin is not useful for established infection.
l Delay delivery, whenever practical, until at least 5 days after onset of skin rash, to allow passive placental
transfer of maternal antibodies.
Management of susceptible pregnant women who have contact with chickenpox
l Susceptible pregnant women (non-immune) should be given varicella-zoster immunoglobulin within 10 days of
significant contact with chickenpox
Varicella-zoster virus
l Epidemiology
n Primary infection (chicken pox) is common in childhood
n In Hong Kong, >90% of adults are seropositive, reactivation (herpes zoster) does not usually cause
problem in pregnancy as the fetus is protected by maternal antibodies
l Virology
n Double-stranded DNA virus
n Family: Herpesviridae; genera: alphaherpesvirinae; HHV-3
n Cubic, icosahedral symmetry
n Morphology: monomorphic, enveloped
l Clinical features
n Primary infection (chickenpox)
u Symptoms like fever, malaise and a vesicular rash develop 10-20 days after exposure
u The rash usually begins on the face and scalp which then spreads to the trunk
u Contagious period from 2 days before the appearance of rash to all ruptured vesicles become
crusted
u Highly infectious but mild in children
u More severe in adults and may associated with complications like encephalitis, myocarditis,
pericarditis, pneumonia, superinfection of skin lesions and adrenal insufficiency
u In pregnant women, the disease is more severe, pulmonary complications with initial symptoms
such as cough, tachypnoea, dyspnoea and chest pain. Gradually, the disease becomes
disseminated, oral lesions and higher fever develop, and finally respiratory insufficiency,

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 pneumothorax, pulmonary parenchymal fibrosis and bacterial superinfection may occur and lead to
death.
Gestation Abnormalities
l <20 weeks (the earlier the gestational age, the more severe the fetal damage)
l Fetal transmission in 25% and congenital defects in about 3% of cases
l Congenital varicella syndrome:
n Specific features: Cutaneous scarring, Hypoplasia of limbs, Muscular atrophy/limb paralysis,
Rudimentary digits
n Brain: Psychomotor retardation, Convulsions, Microcephaly, Cerebral cortical atrophy
n Eye: Chorioretinitis, Cataracts, Chorioretinal scarring Optic disc hypoplasia
n Others: Horner's syndrome
l Second and third trimester
n Subtle findings only
n A week before to a week after deliviery. Fatal disseminated disease in neonates due to acquisition of
virus with no transplacentally acquired maternal antibodies (30% of cases)Rash in mother beginning from
4 days before to 2 days after delivery has the highest risk.
n If systemic symptoms are severe, premature uterine activity may occur and lead to premature delivery
n Babies infected in utero may develop zoster in early infancy
Reactivation (herpes zoster; shingles)
l Dormant virus reactivates in times of stress
l Presents with patches of painful and pruritic vesicles with a erythematous base along the course of a
cutaneous nerve in a dermatomal pattern
l Rarely involves viscera except in immunosuppressed patients
l Has no effect on the fetus
Diagnosis
l Clinical presentation is reliable in most cases
l Laboratory confirmation:
n IgM detection
n Viral antigen detection
n Virus isolation from vesicle/scraping
Management Prenatal
l Counseling
l Monitoring of uterine activity Postnatal
l Infection control measures for congenitally infected infants
l Pediatric follow-up
Prophylaxis
Varicella-zoster immunoglobulin (VZIG) post-exposure prophylaxis is recommended for:
l VZ antibody negative pregnant women exposed at any stage of pregnancy
l Infants whose mother develops chicken pox in the period 7 days before to 28 days after delivery VZIG does not
prevent infection but can attenuate disease

Cytomegalovirus
Virology
l Double-stranded DNA virus belongs to Herpesviridae
Epidemiology of CMV infection
l Common; worldwide distribution
l Most infections occur subclinically in childhood
l In Hong Kong, about 95% of women at their childbearing age are seropositive
l In some European countries like the UK, 40% of adults are susceptible
l Seropositivity depends on age, socioeconomic class and country
l Congenital infection has a high incidence: 0.2-2.2% of live births
Pathogenesis
l Transmission via close contact with CMV-infected secretions (blood/marrow transfusion, sexual contact, close
contact in institutions)
l A replication in the nucleus of infected cells producing the characteristic nuclear inclusions
l Viraemia results in risk of transplacental transmission to the fetus
Clinical features
Primary CMV infection
l Usually asymptomatic except in immunosuppressed patients, but glandular fever-like illness may occur.
l During pregnancy, primary infection carries a fetal infection rate of 40%. The chance of fetal infection is not
affected by the gestational age, but the severity is higher in the first half of the pregnancy.
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Reactivation of latent CMV infection
l Common in pregnancy
l Almost always asymptomatic
l CMV may also be transmitted to the fetus, but the maternal antibodies can reduce the severity of fetal infection
when it occurs
Congenital CMV infection
l Resulted from transplacental transmission
l 5-10% of the infected infants are symptomatic at birth, of which 15% have classic cytomegalic inclusion
syndrome (CID)
l 15-20% of symptomatic infants die and 90% of survivors have sequelae like hearing loss and mental
retardation
l 5-15% of asymptomatic newborns also develop sequelae
l The prognosis of infants who are symptomatic at birth is poor
Cytomegalic inclusion syndrome (CID)
l Intrauterine growth retardation (IUGR)
l Central nervous system: microcephaly, intracerebral calcifications, encephalitis, chorioretinitis
l Hematological: anemia, thrombocytopenia, petechial hemorrhage
l Hepatic hepatosplenomegaly, elevated liver enzymes, jaundice
Perinatal infection
l Resulted from transmission via maternal secretions
l Common in infancy but does not harm the infant
Diagnosis
Screening of primary infection using serologic testing, e.g. ELISA
l CMV-specific IgM can only be detected in around 60% of primary infection
l CMV-specific IgM may reappear in about 20% of cases of reactivation
l Confirmatory results: seroconversion/IgG is negative and IgM is positive when first tested with a subsequent
seroconversion in IgG
Fetal
l Ultrasound examination
l Virus isolation from amniotic fluid
l Pathologic examination of the aborted tissue
Postnatal
l Congenitally infected infants may excrete virus for up to 5-7 years
l Congenital infection can be confirmed by virus isolation from urine and saliva taken within 3 weeks after birth
Management
Pre-pregnancy
l Discuss risks for women working in high-risk environment (e.g. nurseries, institutions)
Prenatal
l No treatment for acute maternal infection
l Counseling about fetal risks
l Monitoring of the fetus
l Termination of pregnancy is considered at early gestational age
At delivery
l Infection control
Postnatal
l Confirm the diagnosis
l Pediatric follow-up if infection is confirmed

Parvovirus
Virology
l Single-stranded DNA virus
l Family: Parvoviridae; genera: Parvovirus
l Infects only humans
l Transmission via respiratory route (aerosolized droplets)
l Viraemia develops 7-8 days after inoculation and ends when rash appears
l The contagious period lasts from inoculation to eruption of rash, and is increased during the 1-4 days of mild
fever and myalgias which precede the rash in up to 60% of patients.
Infection
Parvovirus causes erythema infectiosum or fifth disease which is a common viral infection among children. 25% of
adult infection are asymptomatic. Patients usually have rash or/and acute symmetrical peripheral polyarthralgia that
usually resolves within 2 weeks. Occasionally it may cause bone marrow suppression, anaemia and
thrombocytopenia. When a pregnant woman acquires the infection (B19 type), the fetus may be infected
transplacentally (33%), resulting in fetal anaemia and hydrops fetalis.
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Prenatal diagnosis and management
l Any pregnant woman who has been exposed to B19 infection or develops symptoms suggestive of B19
infection should be investigated serologically
n The presence of IgM confirms recent primary infection (appears >14 days after inoculation and is present
for 3-4 months)
n IgG appears in the third week and persists life-long, conferring immunity
l If the mother is found to be infected, the fetus should be monitored by ultrasonography. Hydropic changes may
manifest 4-12 weeks after maternal infection
l When signs of hydrops develop, fetal anaemia should be confirmed by cordocentesis. The presence of viral
infection can be confirmed with detection of B19 antigen or nucleic acid in fetal blood, or viral detection using
electron microscopy.
l Treatment is repeated intrauterine blood transfusion until the fetus is recovered from the viral infection. The
prognosis is good provided that prompt treatment is given.

Listeriosis
Epidemiology
l About 1 in 10000 birth in the UK
l About 25% of cases are pregnancy-related
Bacteriology
Listeria monocytogenes
l Gram-positive aerobic
l Non-spore forming bacilli
l Grows well at 4C (Can grow in refrigerated food)
l An animal pathogen which is widely distributed in nature: present in faeces of infected animals, soil, water or
sewage
l Pasteurisation may not eradicate the organism
l Human acquire the bacteria through:
l direct contact with infected animal
l handling raw meat
l outbreaks may occur by ingestion of diary products made from unpasturized milk or drinking infected milk
Clinical features
Maternal:
l Asymptomatic or flu-like illness and fever in healthy individuals
l Can result in preterm labour and meconium-stained amniotic fluid (MSL)
l Septicemia, pyrexia of unknown origin (PUO), pneumonia or meningitis in immunosuppressed patients
l Haematogenous spread of Listeria may result in intrauterine infection of fetus
Fetal:
l Infections in early in pregnancy: abortion
l Infections later in pregnancy: multi-organ morbidity, e.g., intraventricular hemorrhage, pneumonia, hepatitis,
neurological handicap and intrauterine death
l Fetal mortality may exceed 75%
Neonatal
l Early-onset manifestations due to transplacental transmission: premature, congenital granulomatous
pneumonia or respiratory distress
l Late-onset manifestations due to infection at delivery: meningitis
Maternal diagnosis
l Pregnant women who have flu-like illness, pyrexia, uterine irritability and bloody vaginal discharge should be
investigated
l Blood, vaginal and amniotic fluid cultures
l Demonstration of Listeria confirms the diagnosis
Management
l A combination of ampicillin and gentamicin (or tobramycin) for 3-6 weeks
l Gentamicin should be avoided in the absence of fetal infection since it has potential fetal ototoxicity

Sexually transmitted disease

Sexually transmitted diseases (STD) are a diverse group of infective diseases that are mainly transmitted via
sexually activity. Some of them confine to local cervical or vaginal infection (e.g. Trichomonas vaginalis, human
papillomavirus). Some may ascend to upper genital tract and spread to pelvic cavity (e.g. gonorrhea, chlamydia). a
few of them may cause systemic infection and complications such as syphilis and HIV. They are one of the major
areas in obstetrics and gynaecology.
STD in gynaecology

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l They are the major cause of pelvic inflammatory disease, which is associated with infertility and chronic pelvic
pain
l One of the organisms, human papillomavirus is associated with cervical cancer
STD in obstetrics
l They are associated with increased risk of preterm labour and preterm rupture of membranes
l Congenital infection causes fetal malformations: e.g. syphilis
l They can be acquired from birth canal during labour causing neonatal infection: e.g. gonorrhea and chlamydia
cause neonatal eye infection, herpes simplex causes neonatal encephalitis
Principles of management of STD
l Treat the primary organism
l Screen for other STD
l Contact tracing
l Advise on protection against further STD e.g. use of condom

Gonorrhea
Organism
l Neisseria gonorrheae, a gram-negative diplococci
Gonococcal infection in gynaecology
l Acute cervicitis
n usually asymmptomtic in women (80%)
l pelvic inflammatory disease
l Pharyngitis (oral sex)
l Disseminated gonococcal infection
n Consists of a bacteremic phase associated with malaise, fever, and a pustular haemorrhagic rash, and a
secondary septic arthritis stage with asymmetric involvement of the knees, wrists or ankles.
Gonococcal infection in Obstetrics
l It is associated with premature rupture of membranes, preterm labour, chorioamnionitis
l Neonates may acquire the bacteria during labour and result in eye infection (gonococcal ophthalmia
neonatorum).
Diagnosis
l microscopy (intracellular gram-negative diplococci) and culture from swab of the endocervix, oral pharynx or
pelvic cavity.
Treatment
l Penicillin group of antibiotics

Syphilis
Bacteriology
Treponema pallidium (a spirchaete)
l Slender, tightly coiled, helical cells, 6-14 fine spirals, often flexed in centre
l Cannot grow in vitro
l Requires special stains, silver, immunofluorescence or dark ground illumination to visualize it
l Transmission by:
n Sexual contact
n Intrauterine infection
n Transfusion of infected blood or blood products
n Direct inoculation
Incidence
l 0.05% of all pregnancies in PWH
Pathology and incubation period
enters body through skin abrasion
produces granulomas and necrotizing vasculitis
primary:
l 10-100 days
l painless ulcer (primary chancre) at the site of sexual contact
secondary:
l 4 -12 weeks after chancre
l Fever, malaise, lymphadenopathy, rash, patchy alopecia, condylomata lata, snail track ulcer on palate and lip
tertiary:
l follows period of 2 - 20 years (latent period) after secondary syphilis
l Gumma (noninfectious granulomatous lesion) in skin, bones, viscera, aorta, brain
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l General paralysis of insane (GPI)
n leading to dementia and psychiatric symptoms
n fatal if not treated
l Tabes doralis
n posterior column of spinal cord leading to ataxia, numbness, lightening limb pain, gastric crisis, absent
tendon reflexes, Charcot's joints
congenital
l Hutchinson's triad (developmental damage): notched teeth, nerve deafness, keratitis of sclera and cornea
l secondary syphilis after birth and tertiary syphilis in adolescence
Screening and diagnosis
VDRL test
l use as a screening test in antenatal care, sensitive
l false positive: due to pregnancy, autoimmune diseases, tuberculosis
l false negative:
FTA -ABS
l diagnostic test
l very specific
Treatment
l Procaine penicillin 2g/24 hours IM for 21 days
l Erythromycin 500mg/ 6 hours PO for 15 days
Discussion/Something to Consider
A patient is found to be VDRL positive on routine antenatal screening. How would you counsel the patient and what
further management would you do?

Trichomonas vaginalis
Trichomonas vaginalis is a motile protozoa with four unipolar flagellae. It is one of the common sexually transmitted
diseases.
Clinical features:
l Foul smelling mucopurulent vaginal discharge
l Dysuria
l Vulval soreness
l Physical examination often reveals severe vulvovaginitis, with perivulval intertrigo and petechial hemorrhage
on the vaginal wall and ectocervix ('strawberry cervix')
Diagnosis:
l A wet film will demonstrate the motile organisms, but the diagnosis may be confirmed by culture.
Treatment:
l Antibiotic - Metronidazole (Flagyl)
l STD screening
l Contact tracing

Chlamydia
It is a kind of atypical bacteria that replicate in cytoplasmic vacuoles within susceptible eukaryotic cells. Chlamydia
trachomatis is one of the commonest sexually transmitted diseases that causes many complications in Obstetrics
and Gynaecology.
Chlamydial infection in Gynaecology
l urethritis
l cervicitis
l pelvic inflammatory disease
Chlamydial infection in Obstetrics
l is associated with preterm labour and preterm rupture of membranes
l causes neonatal conjunctivitis acquired from the birth canal during vaginal delivery
Diagnosis
Immunofluorescence test for Chlamydial antigen
l uses smear from endocervix, urethra, conjunctivae, rectum and pus from pelvic cavity. etc
l fast and sensitive test
Tissue culture
l special transport medium and prompt delivery are required
Serology
l not useful clinically

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Treatment
A 2-week course of antibiotic
l tetracycline group: is the first line but is contraindicated in pregnancy because of tetratogenic effect
l erythromycin: second line when tetracycline is contraindicated

Bacterial vaginosis
l It is also known as non-specific vaginitis, Gardnerella vaginitis and anaerobic vaginosis as a mixture of these
kinds of bacteria is usually identified. Gardnerella vaginalis is an anaerobic gram-negative rod anaerobe
normally found in the vagina. During infection, the number of the bacteria increases enormously to produce the
characteristic grey vaginal discharge with a fishy odour. True itching does not occur but there may be vulval
soreness. It is one of the commonest causes of vaginal discharge in sexually active women. Diagnosis is
usually made clinically, with typical discharge, raised vaginal pH, and positive KOH amine ("sniff") test.
Examination of a stained vaginal smear shows the presence of 'clue cells' and culture on human blood agar
shows beta-haemolysis by Gardnerella vaginalis.
l The treatment is oral metronidazole or clindamycin vaginal cream.
Recent data suggests that the infection may be associated with preterm delivery.

Human papillomavirus
It belongs to the papovaviridae group (a small double-stranded DNA virus) that causes proliferation of the epithelium.
It is one kind of sexually transmitted disease and causes a soft wart-like growth on the genitalia. Today more than
100 different subtypes have been identified, approximately 40 occur predominantly or exclusively in the genital tract.
The subtype 16 and 18 are associated with the development of cervical epithelial neoplasia (CIN) and risk of
cervical cancer. They are present in approximately 70% of cervical cancer.

5. Instruments

Instruments
Instruments commonly used in obstetrics
l amnioscope
l amnihook
l amniostrix
l fetal scalp electrode
l intrauterine catheter
l ventouse in vacuum extraction
l forceps
l cardiotocogram
Instruments commonly used in gynaecology
l endometrial sampler
l hysteroscope
l laparoscope
l uterine curette
l intrauterine contraceptive device (IUCD)
l ring pessary
l spatula for taking pap smear

Pregnancy test
It is a simple bedside dipstick test for presence of human chorionic gonadotropin in urine. It is highly specific and
sensitive (detection limit of around 50iu/L), and produces a result in 1 to 2 minutes. The test can produce to positive
result as early as 14 days post-ovulation.

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Amnihook
It is a simple instrument with a small hook at the tip for amniotomy.

Amnioscope
This is a set of instruments for performing fetal scalp blood sampling. It includes:
l a hollow tube that is put into the vagina for the examiner to see through and perform the procedure
l a blade on a long handle to make a small incision on the fetal scalp
l a light source
l a capillary tube to aspirate blood from the fetal scalp

Amniostrix
Amniostrix is made of nitrazine paper which turns from orange to blue when contacting with alkaline fluid. As
amniotic fluid is alkaline, it can be used as a test of rupture of membranes. It is not specific as other fluid such as
blood, cervical mucus or urine may give a false positive result.

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Doptone
It is a hand-held electrical apparatus used for detection of fetal heart pulsation by doppler effect. It has several
advantages over the Pinard stethoscope:
l The fetal heart sounds are audible as early as 12 weeks of gestation
l It is more sensitive in picking up heart sounds, even though it is not placed exactly over the fetal back
l The mother can also hear the heart sounds at the same time
The disadvantages are:
l It requires battery to work
l Interference may occur when more than one doptone are used at the same time for multiple pregnancies
l Maternal pulse can be picked up easily and may be mistaken as the fetal pulse
Discussion/Something to Consider
l What are the advantages and disadvantages of using a doptone when compared to a Pinard stethoscope?

Intrauterine catheter
It is a long coil of catheter introduced into the uterine cavity transcervically during labour, as a mean of amnioinfusion.
It can also be connected to a pressure transducer to measure the actual intrauterine pressure during contractions
(the abdominal transducer used in ordinary cardiotocogram cannot measure the actual uterine pressure).

Fetal scalp electrode

It is an electrode anchored to the fetal scalp to monitor the fetal heart rate during intrapartum period. Unlike the
abdominal detector which uses doppler effect to detect the fetal heart rate, the scalp electrode can pick up the
electrocardiogram (ECG). The heart rate is computed by analyzing the PP interval. The ECG waveform analysis
may be a method of intrapartum fetal monitoring.

Pinard stethoscope
The pinard stethoscope is a simple instrument designed for auscultation of low-pitch fetal heart sounds
transabdominally. It is pressed firmly over the the site of the maternal abdomen where the back of the fetus is
supposed to be. The fetal heart sound is usually audible with the pinard stethoscope after 24 weeks of gestation.
Discussion/Something to Consider
What are the advantages and disadvantages of using a doptone when compared to a Pinard stethoscope?

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Endometrial sampler
A simple narrow plastic tube inserted into the uterine cavity for endometrial sampling. It provides reasonable good
yield of tissue for histological assessment.

Pad test
Pad test is a simple bedside assessment to verify and quantify urine loss. The patient wears a preweighed sanitary
towel, drinks 500ml of water and rests for 15 minutes. After a series of defined manoeuvers the pad is reweighed. A
urine loss of more than 1g is considered significant.

Ring pessary
A device made of silicon or plastic used as a conservative management for genital prolapse. It is put into the vagina
so that it rests in the posterior fornix and sits over the symphysis pubis. It is indicated when the patients are unfit or
refuse surgical treatment, want to preserve fertility, or as a temporary relief while waiting for surgery. However, it is
ineffective in severe degree of genital prolapse. There are various sizes of ring pessaries in reference the diameter
of the ring in minimetre. The size should fit the patient, as it would fall out when it is too small, or cause voiding
difficulty, laceration or pressure necrosis, and infection of vagina when it is too big. The appropriate size is the one
with a diameter equal to the distance between the posterior fornix and the symphysis pubis (can be assess by digital
vaginal examination). After it is inserted, the patient should be asked to walk around and void to see if any
discomfort. The patient should also be followed every 6 months for changing the pessaries, and look for any
complications.

Speculum
An instrument for dilating certain passages of the body, and throwing light within them, thus facilitating examination
or surgical operations. In Gynaecology, the bi-valve speculum and the sim speculum are commonly used for vaginal
examination and for carrying out gynaecological surgery. Using the bi-valve speculum, the anterior and posterior
walls of the vagina are retracted apart, providing a good exposure of the cervix and vaginal cavity.
The sim speculum is mainly used for examination of genital prolapse and vaginal surgery. One side of the vagina is
retracted by the speculum so that examination or procedure can be performed on the opposite side.

Sim speculum
See speculum

Spatula
An implement with a broad, flat, blunt blade, used especially for mixing or spreading. The Aryes spatula is designed
to take a pap smear from the cervical os. For postmenopausal women who usually have a tight stenotic cervical os,
it would be more appropriate to use a cytobrush.

Cytobrush
An instrument designed to take pap smear from a stenotic os which is more commonly encountered in
postmenopausal women.

6. Miscellaneous topics in O&G

Lithotomy
A term derived from one of the oldest known surgical operations, i.e. cutting for (bladder) stone (lith means stone,
tomy means cut). It is now used to refer to the position of the patient on the operating table used for many
gynaecological procedures. The patient is placed on the operating table on their back; the hips are flexed with the
thighs opened outwards and the legs supported by strrups attached to poles on the operating table, so that the
operator has easy access to the genital tract.

Rickets
A softening of the bone due to vitamin D deficiency. The weight of the upper torso then pushes the sacral
promontory towards the pubis, and the lumber spine develops an exaggerated lordosis. As a result the pelvic inlet
appears flattened, and this is called the platypoid pelvis. Women with rickets and platypoid pelvis develops inlet
disproportion.

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Rickets should be differentiated from osteoporosis.

Lordosis
An exaggerated anterior curving of the lumbar spine. Often occurs in rickets.

Alpha-feto protein
What is alpha-feto protein (AFP)
l It is an alpha-globulin which is similar in molecular weight to albumin. It is normally synthesized during
pregnancy in the yolk sac and fetal liver. Maternal serum AFP levels rise rapidly in pregnancy as a result of the
passage of fetal AFP into maternal circulation via the placenta. AFP is present in fetal serum and cerebrospinal
fluid at a concentration of about 30000 times greater than that in maternal serum and 150 times greater than
that in amniotic fluid
l It is also increased in non-pregnant patients with liver diseases such as primary hepatocellular carcinoma, and
malignant yolk sac tumour of ovary.
Alpha-feto protein in obstetrics
l Maternal serum AFP is increased in several fetal malformations including open neural tube defects,
gastroschisis and ophalmocele. It is used in some Caucasian countries as a screening test of neural tube
defects.
l Maternal serum AFP is decreased in pregnancy with Down syndrome. It is used in combination with human
chorionic gonadotropin or unconjugated estriol as a biochemical screening test for Down syndrome.
l Increased maternal serum AFP is also reported to be associated with poor fetal outcome such as IUGR.
Alpha-feto protein in gynaecology
l Serum AFP is secreted from ovarian tumours like yolk sac tumours, and other germ cell tumours. It is a very
sensitive and specific tumour marker for yolk sac tumours, and can be used for diagnosis, monitoring and
detection of recurrence.

Human chorionic gonadotropin

What is human chorionic gonadotropin
l Human chorionic gonadotropin (HCG) is a placental-derived glycoprotein, and is almost exclusively produced
by the placenta, with extremely small quantities are produced by the pituitary gland. Similar to other pituitary
glycoprotein hormones, it is composed of two subunits, alpha and beta. While the structure of alpha subunit is
the same as the other glycoproteins, HCG has a specific structure of the beta subunit. Some
radioimmunoassays for the measurement of the level of HCG are based on the detection of the beta subunit.
l The natural role of HCG is to maintain the corpus luteum for the first seven weeks of gestation, which secretes
progesterone essential for the continuation of the pregnancy.
l The half-life of HCG ranges from 6 to 24 hours. Serum HCG is measurable as early as 7 days post-ovulation
(detection limit around 0.1-0.3iu/L). During the first few weeks of pregnancy, the maternal serum level of HCG
doubles every 2 days, and rises to peak at 9 to 11 weeks. Subnormal rise or even a drop in the HCG level may
suggest ectopic pregnancy or abortion respectively.
Clinical use of HCG
l In pregnancy testing
l In assisting diagnosis of ectopic pregnancy and abortion
l As a tumour marker of gestational trophoblastic diseases and ovarian choriocarcinoma
l In ovulation induction program:
n to simulate LH surge. and
n as luteal phase support
l Association with hyperemesis gravidarum and transient hyperthyroidism during early pregnancy

Prolactin
A hormone secreted from the anterior pituitary gland, responsible for glandular proliferation of breasts and
establishment of lactation. It can also reduce gonadal activity by decreasing the pulsatile secretion of gonadotropin
releasing hormone from the hypothalamus, and blocks the action of luteinising hormone on the ovary. Normally the
secretion of prolactin is under the inhibition of dopamine secretion from the hypothalamus. Physiological
hyperprolactinemia occurs during pregnancy, after childbirth and continuation of lactation, and during stress.
Pathological hyperprolactinemia can be resulted from prolactinoma, other pituitary gland tumours that block the
dopaminergic tract from the hypothalamus, anti-dopaminergic agents such as anti-psychotic agents. Prolactin level
may also rise in case of polyscytic ovarian disease and hypothyroidism. Hyperprolactinemia results in amenorrhea,
anovulation, and galactorrhea.

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Ovulation
Definition
Ovulation is the process during which a Graafian follicle ruptures to release a mature oocyte with its surrounding
cumulus oophorus. This is initiated by a luteinizng hormone (LH) surge (a brief rise in LH started 36 to 38 hours
before ovulation), which precipitates the final changes in the follicular wall, follicular fluid volume and the oocytes
which are the necessary precursors to ovulation. The first meiotic division is completed at this stage and half of the
chromosome complement discarded as the first polar body.
How can we know the timing of ovulation
l It is sometimes necessary to know the time of ovulation for purpose of conception, treatment of fertility (such
as correct timing of artificial insemination or the transfer of previously frozen embryos.) and as well as
contraception (rhythmic method)
Clinical
l Ovulation usually occurs 14 days before the next expected menstruation (i.e. around day 14 in a 28 day cycle).
In longer cycles ovulation occurs later.
l Ovulation may be associated with temporary discomfort or pain (see Mittelschmerz).
l Soon after its occurrence there is a rise in the basal body temperature due to progesterone production.
l There are changes in cervical mucous before ovulation (spinnbarkeit sign and ferning)
USG monitoring
l serial ultrasound scans to monitor the growth of ovarian follicles and rupture
Measuring the LH
l The onset of the LH surge can be determined by measuring LH concentrations in blood and urine.
Measuring the progesterone
l Blood taken at the expected mid-luteal phase (i.e. day 21 in a normal 28-day cycle) shows a rise in
progesterone level.
Ovulation Induction
Some women fail to ovulate (see anovulation) and become infertile, because of various endocrinopathologies.
Ovulation induction is required
l In assisted reproductive technology (ART), the administration of hCG is used to trigger ovulation and time
oocyte collection (to simulate a LH Surge), particularly if spontaneous LH surges are suppressed by GnRHa.

Spinnbarkeit
The ability of cervical mucus to be drawn into threads. This is maximal a day or so before ovulation due to the
estrogen surge for the Graafian follicle. After ovulation this quality is lost and cervical mucus becomes thick (tacky)
due to the effect of progesterone. It is one of a bedside method to assess timing of ovulation.

Ferning
Ferning of cervical mucus
When cervical mucus obtained just before ovulation is dried and allowed to crystallize, a pattern resembling fern
leaves can be observed under microscope. This property of cervical mucus is resulted from the influence of
estrogens which makes the mucus more profuse and fluid just before ovulation. This is a favourable sign in the
assessment of quality of cervical mucus.
Ferning of amniotic fluid
A ferning pattern can also be observed under microscope after drying and crystallization of amniotic fluid. It can be
used as a test to confirm rupture of membranes when a specimen of fluid is obtained from the vagina (not from the
cervix). However, it is not very practical and is seldom applied clinically now.

Blood pressure measurement

Equipment
l Sphygmomanometer
l DINAMAP (stands for 'Device for Indirect Noninvasive Automatic Mean Arterial Pressure')
Method of blood pressure measurement in obstetric patients
l Use a correct size of cuff for each patient
l Hypertension in obese patients is over-diagnosed if the cuff is too small in relation to the arm circumference
2
Arm circumference (cm) Appropriate cuff size (cm )
<33 Regular cuff (12x23)
33-41 Larger cuff (15x33)
>41 Thigh cuff (18x36)
l Correct positioning of the patient during measurement
n Should be measured with the cuff at the level of the heart, with the patient either

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 n Sitting position, or lying on a bed or couch on the right side at 30 degrees of lateral tilt
l Use of the correct phase of the Korotkoff sounds in measuring diastolic pressure
n Either use Korotkoff sound IV (the sounds become muffled) or Korotkoff sound V (the sounds disappear)
to define the diastolic pressure

Asymptomatic bacteriuria
It is bacterial growth in a concentration of 10,000 or more per ml of urine without symptoms. This is present in about
8% of pregnant women, and about half of them will develop signs of urinary tract infection during pregnancy if
untreated.

Fertilisation
The process by which the male and female gametes unite to form a zygote. This begins when the spermatozoon first
contacts the oolemma (the oocyte surface membrane) and lasts until the genetic material of sperm and oocyte have
mixed and reduplicated as the zygote initiates its first division into two cells. In vivo, fertilisation occurs in the
fallopian tube, usually within one day of ovulation, and is completed in approximately 24 hours.

Conception
The process from fusion of the gametes through the early development of the conceptus, to implantation of the
blastocyst. The intervention of conception in order to prevent pregnancy to occur is called contraception.

Fecundity
A measure of the ability to produce offspring. This declines markedly with advancing maternal age, especially after
35 year old. The fecundability rate is the monthly probability of pregnancy when the opportunity for conception
exists.

Consanguinity
A relationship by descend from the same ancestor, or having a blood relationship. It is important for genetic
counselling when there is a positive family history of genetic disorder, and a couple has blood relationship.

Palliative
Palliative treatment in malignant diseases does not aim to cure but to improve a problem or condition such as
symptomatic relief. For example, radiotherapy or narcotic injection to relieve bone pain due to metastasis.

Doppler effect
Doppler Effect and use in medicine
l Doppler effect is a physical principle named after Doppler, Christian Johann, an Austrian physicist and
mathematician who first discovered in 1842. It is an 'apparent' change in the frequency of waves, as of light or
sound (including ultrasound), occurring when the source and observer are in motion relative to each other. The
frequency increases when the source and observer approach each other, and decreases when they move
apart.
l It can therefore, be used to estimate the velocity of the moving object by measuring the changes of frequency
of waves. In medicine, human blood flow can be examined by applying ultrasound waves which are then
reflected back by the moving red blood cells in the circulation, and analysed with electronic means.
l See Doppler studies for application in Obstetrics

Doppler studies
Doppler studies of blood flow in medicine
l Using the principle of Doppler effect, the blood flow in human circulation can be assessed with ultrasound. The
changes in frequency of reflected waves are analysed and displayed as a pattern of waveforms across time.
Various ratios using values at the systolic and the diastolic phase of blood flow are calculated to reflect the
degree of blood flow:
l A/B ratio (or S/D ratio)= systolic/diastolic
l pulsatity index
l resistance index
l Ratios rather than the actual velocity are calculated because the calculation of the later required the
knowledge of the angle between the path of the wave and the path of the moving object, which is not possible
in practice. This factor can be eliminated using the ratios.
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l The higher the indices, the higher is the resistance of flow, and therefore the lower the velocity of blood flow.
Application of Doppler effect in Obstetrics
Assessment of feto-placental blood flow
l Umbilical arterial blood flow is diminished in case of placental insufficiency, because of the increased placental
resistance flow. It is one of the methods of monitoring of fetal well-being. With the absence or reverse diastolic
flow, the chance of intrauterine death is high, and immediate delivery should be considered.

Screening
Definition
l Screening is a procedure designed to select a group of subjects which is thought to be at high risk of having a
disorder, from a general population. It is not itself diagnostic, but the selected group of subjects would be
offered a diagnostic test.
l A screening procedure can be a test, or history taking, or examination in Obstetrics
Criteria of a good screening test
To be a good screening test, the following criteria have to be fulfilled:
Disease characteristics
The disease to be screened should:
l cause significant morbidity and mortality of the society
l have a long latent period
l have a effective treatment
l early treatment is better than late treatment
l Test characteristics
The test itself should be:
l simple
l cheap
l sensitive
l specific
l safe
l acceptable by majority of population
Examples of screening tests in Obstetrics and Gynaecology
l Antenatal screening blood tests:
l Haemoglobin for anaemia
l ABO and rhesus blood group
l MCV for thalassemia carrier status
l Rubella antibody
l VDRL for syphilis
l Hepatitis B surface antigen
l Biochemical screening for Down syndrome
l Cervical pap smear for screening of CIN lesions and cervical cancer
Discussion/Something to Consider
Why is there screening of carcinoma of cervix but not for carcinoma of ovary?
Why is there an alpha feto-protein screening program for neural tube defects in Caucasian countries but not in Hong
Kong?

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Index
Abdominal circumference 51 CA125 150
Abortion 107 Caesarean section 92
Abruptio placentae 13 Calendar method 100
Acetowhite 144 Caput succedaneum 86
Acronym 178 Cardiotocogram 54
Acute fatty liver 72 Cephalopelvic disproportion 7
Adenomyosis 98 Cerebral palsy 29
Adolescence 134 Cervical cancer 138
Advanced maternal age 27 Cervical incompetence 19
Alpha-feto protein 194 Cervical intraepithelial neoplasia 143
Amenorrhea 117 Chemotherapy 150
Amnihook 191 Chickenpox 184
Amniocentesis 41 Chlamydia 189
Amnioinfusion 44 Chorioamnionicity 61
Amnioreduction 44 Chorioamnionitis 29
Amnioscope 191 Choriocarcinoma 149
Amniostrix 191 Chorionic villus sampling 41
Amniotic fluid 46 Chromosomal abnormalities 33
Amniotic fluid embolism 72 Chronic pelvic pain 132
Amniotic fluid index 47 CIN 143
Amniotomy 83 Climacteric 125
Anaemia 73 Clomiphene 156
Anatomy 4 Cold coagulation 130
Android 7 Colostrum 26
Anorexia nervosa 120 Colporrhaphy 162
Anovulation 153 Colposcopy 146
Antepartum care 8 Colposuspension 164
Antepartum haemorrhage 11 Combined oral contraceptives 101
Anthropoid 7 Conception 196
Anti-hypertensive 175 Condom 100
Antiphospholipid syndrome 73 Conjoint twin 61
Apgar score 88 Consanguinity 196
APH of unknown origin 14 Contraception 99
Appendicitis 74 Contracted pelvis 7
ART 155 Contraction stress test 56
Asherman syndrome 120 Controlled cord traction 94
Asymptomatic bacteriuria 196 Cord prolapse 16
Asynclitism 86 Cordocentesis 42
Augmentin 178 Corpus luteal cyst 111
Couvelaire uterus 14
Bacterial vaginosis 190 Crown-rump length 50
Bagshawe score 149 Cryotherapy 130
Bartholin 116 Cryptomenorrhea 118
Basal body temperature 155 CTG 54
Benign ovarian tumour 96 Curettage 127
Bethesda 145 Cystocele 161
Biochemical screening 34 Cystometry 165
Biophysical profile 54 Cystoscopy 166
Biparietal diameter 51 Cytobrush 193
Birth asphyxia 89 Cytomegalovirus 185
Birth trauma 32
Bishop score 82 Danazol 176
Blood pressure measurement 195 Dating of pregnancy 10
Borderline malignancy of ovary 137 Deep transverse arrest 86
Braxton Hicks contractions 29 Denominator 3
Breast milk 26 Dermoid cyst 98
Breast-feeding 26 Detrusor instability 115
Breech presentation 15 Dextrorotation of uterus 8
Brim 6 Diabetes mellitus 65
Diazepam 176
DIC 74
Doppler effect 196
Doppler studies 196
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Doptone 192 Genetic disorder 56
Down syndrome 35 Genital prolapse 160
Drugs 172 Genuine stress incontinence 163
Dysfunctional uterine bleeding 122 Germ cell tumour 137
Dysgerminoma 138 Gestational diabetes 66
Dyskaryosis 144 Gestational trophoblastic disease 148
Dysmenorrhea 123 Glucocorticoid 176
Dyspareunia 132 GnRH 177
Dystocia 84 GnRHa 177
Dysuria 164 Gonadotropin 177
Gonadotropin therapy 177
Early pregnancy complications 106 Gonorrhea 188
Eclampsia 70 Grand multipara 30
Ectopic pregnancy 109 Gravid 30
ECV 16 Group B streptococcus 182
Edward syndrome 37 Gynae-oncology 136
Electrocautery 130 Gynaecoid 7
Emergency contraception 104 Gynaecological surgery 126
Endometrial ablation 127 Gynaecology 96
Endometrial carcinoma 141
Endometrial hyperplasia 147 Haemophilia 57
Endometrial sampler 193 Heart disease 74
Endometrial sampling 130 HELLP syndrome 72
Endometriosis 113 Hepatitis 179
Engage 81 Hepatitis B 180
English usage 178 Hepatitis C 181
Engorgement of breasts 25 Hirsutism 134
Enterocele 161 History taking (Gyn) 169
Entonox 94 History taking (Obs) 167
Epidural anaesthesia 95 HIV 181
Epilepsy 71 Hormonal replacement therapy 125
Episiotomy 89 Human chorionic gonadotropin 194
Eponym 179 Human papillomavirus 190
Ergometrine 173 Hydatiform mole 148
Examination (Gyn) 170 Hydrops fetalis 39
Examination (Obs) 168 Hyperemesis gravidarum 111
Examination of genital prolapse 162 Hyperprolactinemia 118
Exenteration 140 Hypertension in pregnancy 67
Hysterectomy 128
Failure to progress 83 Hysterosalpingogram 131
Fecundity 196 Hysteroscopy 129
Femur length 52 Hysterotomy 127
Ferning 195
Fertilisation 196 ICSI 157
Fetal distress 54 Imperforate hymen 132
Fetal heart rate pattern 55 In vitro fertilization 156
Fetal infection 179 Incontinence 163
Fetal medicine 33 Incoordinate 86
Fetal movement 56 Induction of labour 83
Fetal scalp blood sampling 88 Infertility 152
Fetal scalp electrode 192 Inlet 6
Fetal skull 3 Insemination 157
Fetal well-being 53 Instrumental delivery 90
Fibroid 96 Instruments 190
Follicular cyst 132 Intermittent auscultation 88
Follicular phase 154 Interstitial cystitis 164
Fontanelle 4 Intertuberous diameter 6
Forceps 91 Intrapartum fetal monitoring 87
Frequency of micturition 164 Intrapartum management 78
Fundal height 172 Intrauterine catheter 192
Funnel pelvis 8 Invasive mole 149
Involution 25
Galactorrhea 118 Ischial spine 6
Gastroschisis 39 IUCD 103
Genetic counseling 42 IUGR 44

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Kallman syndrome 120 Oligohydramnios 48
Klinefelter syndrome 37 Oligohydramnios sequence 49
Koilocyte 144 Oligomenorrhea 118
Krukenberg tumour 138 Omphalocele 39
Operative delivery 90
Labour 78 Os 8
Labour pain relief 94 Osteoporosis 125
Lactation 25 Outlet 5
Lamda sign 62 Ovarian cancer 137
LEEP 147 Ovarian cystadenoma 96
Levator ani 4 Overflow incontinence 163
Levonorgestrel intra-uterine system 104 Ovulation 195
Libido 159 Ovulation induction 156
Lie 2 Oxytocic 172
Listeriosis 187 Oxytocin 172
Lithotomy 193
Lochia 25 Pad test 193
Lordosis 194 Palliative 196
Loveset maneuver 90 Pap smear 144
Lower segment 8 Partogram 82
Luteal phase 154 Parvovirus 186
Luteal phase insufficiency 154 Patau syndrome 36
PCOD 119
Macrosomia 46 Pearl index 100
Male infertility 158 Pelvic inflammatory disease 115
Malpresentation 14 Pelvimetry 5
Manual removal of placenta 94 Pelvis 5
Marsupialisation 130 Perinatal mortality 30
Maternal medicine 65 Perineal tear 89
Maternal mortality 30 Pharmacology in pregnancy 64
Menopause 124 Physiological changes in pregnancy 63
Menorrhagia 121 Pinard stethoscope 192
Menstrual cycle 117 Placenta 31
Menstrual disorders 116 Placenta praevia 11
Methrotrexate 178 Platypoid 7
Metropathia haemorrhagia 122 Polyhydramnios 49
MgSO4 176 Position 3
Minor disorders of pregnancy 112 Postcoital bleeding 131
Misoprostol 174 Postcoital contraception 105
Mitral stenosis 75 Postcoital test 155
Mittelschmerz 123 Postmenopausal bleeding 131
Molar pregnancy 148 Postpartum blue 27
Morbid adherence of placenta 93 Postpartum care 20
Moulding 86 Postpartum depression 26
MSL 50 Postpartum fever 21
Multiple pregnancy 59 Postpartum haemorrhage 22
Myomectomy 128 Postpartum psychosis 27
Postterm 28
Nabothian cyst 133 Potter syndrome 40
Narcotic analgesia 95 Pre-conception counseling 9
Neonatal death 31 Pre-eclampsia 68
Neural tube defect 38 Precocious puberty 134
Nocturia 164 Pregnancy test 190
Non-dysjunction 35 Premature menopause 125
Nuchal translucency 38 Premenstrual syndrome 123
Presentation 3
Obstetric abdominal exam 168 Preterm delivery 19
Obstetric anaesthesia 94 Preterm labour 18
Obstetric emergency 31 Progestogen injectable 102
Obstetric statistics 30 Progestogen-only pill 102
Obstetric surgery 31 Prolactin 194
Obstetrics 2 Prostaglandin 173
Obstructed labour 84 Pseudo gestational sac 111
Occipito-posterior 82 Puberty 134
OHSS 157 Pubic symphysis 7

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Puerperium 24 Tocolytic 174
Pulmonary embolism 76 Toxoplasmosis 182
Pyometra 116 Transformation zone 146
Trial of labour 86
Radiotherapy 151 Trichomonas vaginalis 189
Rectocele 161 Trimester 31
Recurrent abortion 108 Trisomy 34
Reflex incontinence 164 True incontinence 164
Renal agenesis 40 Tumour marker 150
Reproductive medicine and Endocrinology 152 Turner syndrome 37
Residual trophoblastic disease 149 Twin pregnancy 59
Retained placenta 93 Twin-twin transfusion 62
Retroversion of uterus 132
Rhesus 28 Urethrocele 161
Rhesus D iso-immunisation 28 Urge incontinence 163
Rickets 193 Urgency 163
Ring pessary 193 Urinary incontinence 163
Rubella 183 Urodynamic study 165
Rupture of membranes 20 Uroflowmetry 166
Urogenital diaphragm 5
Sagittal suture 4 Urogynaecology 160
Screening 197 USG (Obstetrics) 42
Second stage of labour 79 Uterine atony 22
Semen analysis 158 Uterine hyperstimulation 87
Septic abortion 109 Uterine inversion 24
Seven-day rule 102 Uterine prolapse 161
Sexual dysfunction 154 Uterine rupture 23
Sexually transmitted disease 187
Sheehan syndrome 24 Vacuum extraction 91
Shoulder dystocia 85 Vaginal breech delivery 81
Sim speculum 193 Vaginismus 159
Sinciput 4 Vasa praevia 14
Small-for-gestational-age 44 Vasectomy 105
Spatula 193 Vault prolapse 161
Speculum 193 Vertex 4
Spermatogenesis 158 Viable 106
Spinnbarkeit 195 Virilism 135
Staging of CA cervix 140 Voiding disorder 164
Staging of CA endometrium 142
Staging of CA vagina 136 Yolk sac tumour 128
Staging of CA vulva 137
Staging of GTD 150
Station 81
Sterilisation 105
Stillbirth 31
Stress incontinence 163
Subaponeurotic haematoma 32
Subpubic arch 6
Symptomatology (Gyn) 170
Symptomatology (Obs) 167
Syntocinon 173
Syntometrine 173
Syphilis 188

Tanner staging 134

Teratogen 41
Teratoma 99
Termination of pregnancy 106
Testicular feminisation syndrome 120
Thalassemia 58
Third stage of labour 80
Thrombocytopenia 76
Thromboembolism 76
Thyroid disorder 77
Tibolone 176 By Edward Chu, 1st January, 2004

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