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Transcript
Preconception counselling and lifestyle issues
Preconception counselling should begin with a thorough history, including family and social background.
Diseases that make a pregnancy high-risk should be discussed:




Diabetes: women with T1DM have a higher incidence of foetal abnormalities and complications, e.g.
foetal anomaly, foetal macrosomia, growth restriction and preterm labour. . Strict control of BSLs is
very important in order to avoid these.
Epilepsy: women with epilepsy have 3 times the risk of foetal structural anomalies. These women
should be reviewed before conception in order to find the least teratogenic anticonvulsant regimen
for them. Also, as many anticonvulsants are folate antagonists, these women are advised to take 5
mg/day of folic acid.
Other chronic disease, e.g. renal, thyroid, heart disease, hypertension, asthma.
Previous pregnancy problems, e.g. miscarriage, preterm labour, still birth.
Diet: a well balanced diet is very important in pregnancy. Multivitamins and supplements may reduce
abnormalities in pregnancy. Recommendations include:




Folic acid supplements to reduce the incidence of neural tube defects. Supplements should be
started before conception, 500 µg/day for a women who have never had an affected pregnancy,
and 5 mg/day for women with a previously affected offspring.
Soft cheese should be avoided due to the risk of Listeria infection from unpasteurised dairy
products.
Calcium intake should be maximised as pregnant women have a higher requirement for calcium.
Caffeine-containing drinks should be kept to a minimum as a high intake of caffeine has been linked
with reduced fertility and increased risk of miscarriage.
Lifestyle issues:








Birth and parenting education: cover information about pregnancy, labour, birth, breastfeeding and
early parenting.
Maternity leave: governmental leave, including unpaid leave, is usually 12 months and following
this leave the employee may resume employment at the same level of seniority. Private
organisations may have varying policies. Other entitlements may include maternity allowance,
family payments, the baby bonus and paternity leave (usually 1 week).
Seatbelts: should be worn with the lap band low on the abdomen and the shoulder harness
between the breasts but not across the anterior abdomen.
Air travel: in an uncomplicated pregnancy there is no reason to restrict travel, although airlines may
have their own policies.
Exercise: 30 minutes of moderate exercise per day is recommended in uncomplicated pregnancies.
Occupational work: physically demanding work, prolonged standing, shift and night work, as well as
exposure to toxic chemicals and radiation should be avoided.
Sexual activity: only contraindicated when the membranes have ruptured prematurely or when
antepartum haemorrhage has occurred, and advised against for a few days after threatened
miscarriage.
Weight: excessively low and high maternal weight should be avoided.
Pets:






Cats: there is a risk of catching toxoplasmosis, a parasite found in cat faeces, gardens cats frequent
and raw/undercooked meat. It can cause severe neurological defects in the foetus. To minimise the
risk, pregnant women should not change the kitty litter, should wear a mask and gloves while
gardening and avoid undercooked meat.
Dogs: the largest risk is dog bites once the baby is born.
Reptiles/Amphibians: contact with the faeces of these pets can result in the transmission of
salmonella. This is an important risk until the age of 5 years.
Birds: may carry campylobacter, salmonella, chlamydiosis, or some protozoal infections.
Farm animals: may carry listeria, campylobacter, salmonella or cryptosporidium.
All animals: women should avoid leaving their babies alone with pets and should make sure they
are flea and worm-free. Washing one’s hands after touching a pet is also important.
Social issues:


Support from partners, family and friends: lowers the risk of postnatal depression and anxiety. This
is important throughout the pregnancy, during labour and postnatally.
Women at particular risk (isolated women, single mothers, teenage mothers, those with a history of
mental illness, and those required to work late in pregnancy) may require extra professional
support.
Antenatal care: women should be advised at the beginning of their pregnancy about the possible models of
care they may access (e.g. midwifery care, obstetric care) and what would be most appropriate for them
according to the level of risk of their pregnancy.
References: Women’s Health: A Core Curriculum,
http://www.americanpregnancy.org/pregnancyhealth/pets.html
ANTENATAL SCREENING
Weeks
Visit
st
1 trimester
<7
1
(booking
visit)
Tests
 HCG (confirm pregnancy)
 Clinical assessment
 USS (> 5 weeks):
o Gestational age/pregnancy dating (EDD)
o Number of foetuses
o Heart beat
7-12
2
 FBE + Fe studies (Fe deficiency anaemia, Thalassemia)
 Blood group, Rh and antibodies
 Vitamin D
 Serology
o Rubella
o HIV
o Hep B/C (HbsAg)
o Syphilis (RPR/TPHA)
o Consider: toxoplasmosis, CMV, VZV, pap smear
 MSU (for asymptomatic bacteriuria)
 Tests to be offered at this visit:
o Maternal Serum Screening (MSS for Down Syndrome) – 10-12
weeks
o Nuchal Translucency Scan (NTS done via ultrasound) – 12 weeks
2nd trimester (every 4 weeks)
12-20
3
 Ultrasound Scan 18-20 week for fetal structural anomalies and placental
localization
 Maternal Serum Screening (quadraple test) – Down Syndrome, NTD,
Trisomy 18
 Measure BP (pre-eclampsia), check uterine size
18-22
4
 Measure BP, check uterine size
 Discuss blood sugar test for next visit
26-28
5
 Complete blood sugar test (GDM)
 Measure BP, check baby’s heartbeat, size and position
 If Rh –ve, FBE & Rh antibodies, Anti-D injection (28-30 weeks)
rd
3 trimester (every fortnight, then every week after 36 weeks
30-32
6
 Measure BP, check baby’s movements, heartbeat, size and position
33-36
7
 Measure BP, check baby’s movements, heartbeat, size and position
 FBE
 If Rh –ve, check Rh antibodies, Anti-D injection (34 weeks)
36-38
8
 Measure BP, check baby’s movements, heartbeat, size and position
 Group B Streptococcus Screen (either urine sample or vaginal swab)
 Fetus: lie, presentation, degree of engagement of presenting part
38-40
9&
 Measure BP, check baby’s movements, heartbeat, size and position
10
 Discuss signs of labour
40-42
10 &  Measure BP, check baby’s movements, heartbeat, size and position
11
 Discuss fetal monitoring, CTG and ultrasound if baby not delivered
 Discuss induction
 Possible vaginal examination
Tests for Down Syndrome:
1. MSS: 14-20 weeks (sensitivity 60-75%)
a. 10-14 weeks (FNT +/- PAPP-A, -HCG) – PAPPA is  and HCG  in DS
b. 15-22 weeks (-HCG, AFP , unconjugated oestriol)
c.
2. NTS: 11-13 weeks (sens 75-80%)
3. Diagnostic testing
a. Chorionic villus sampling (CVS) - ≥10 weeks (1% chance of miscarriage)
b. Amniocentesis  ≥15 weeks (0.5% chance of miscarriage)
c. Samples sent for cytogenetic analysis that allows rapid diagnosis of major
aneuploidies for chromosomes 13,18,21 and XY
Tests for Neural Tube Defect
1. MSS: 16-20 weeks (AFP)
2. US at 18-20 weeks
3. Amniocentesis after 15 weeks (to determine karyotype)
Group B Streptococcus
 Vaginal swab or urine sample 35-37 weeks
 Risk of infant sepsis, neonatal deafness, cerebral palsy and death
 Indication for intra-partum chemoprophylaxis
o Pre-term birth ≤37 weeks
o ROM ≥18 hours prior to delivery
o Maternal fever in labour >37.5 ˚C
o PHx of GBS colonization
o Previous infant with GBS
o GBS bacteriuria
 Rx:
o Chemoprophylaxis: penicillin ≥ 4 hours prior to delivery
 1.2 gm IV benzyl penicillin loading dose, then 600 mg 4 hourly till
delivery
o Clindamycin 600 mg IV 8 hourly in labour or
o Erythromycin 500 mg IV 6 hourly throughout labour
Useful links 
RANZCOG Antenatal Screening: www.ranzcog.edu.au/publications/statements/C-obs3.pdf
http://www.rcpamanual.edu.au/index.php?option=com_clinical&task=show_clinical&id=58&It
emid=27&msg=396
CAUSES OF INFERTILITY (DAN)
 Main causes:
o Reduced semen quality (40%)
o Ovulatory disorders (30%)
o Tubal problems (30%)
 Others:
o Male: impotence, retrograde ejaculation, anti-sperm antibodies
o Female: cervical factors, anti-sperm antibodies, severe endometriosis
o Unexplained infertility
COUNSELLING
 Detailed Hx & Ex of BOTH partners (including full social Hx)
o Ask about frequency of sexual intercourse, timing (in regards to ovulation),
technique, any problems, mood, feelings about infertility
 Male:
o Hx: STDs, mumps, previous surgery (inguinal hernia repair, orchidopexy), drugs
(antimitotic agents, β-blockers, excess alcohol)
o Ex: Genitalia (size & consistency of testicles, presence of vasa deferentia and/or
varicocoele
 Female:
o Hx: Past reproductive Hx, RFs for pelvic infection (STDs, IUD, previous pelvic
surgery), Sx of endometriosis (secondary dysmenorrhoea, dyspareunia)
o Ex: Secondary sexual development, PID, endometriosis
 Lifestyle changes
o Quit smoking, change drugs, reduce stress, weight loss (if BMI >29), exercise, folic
acid
INVESTIGATIONS
 Male:
o Semen analysis: obtain sample after 3 days abstinence from ejaculation. Masturbate
into wide-topped container. Must be brought to lab within 1 hr. Looks at sperm
count, motility & morphology
o Abnormal semen → serum FSH & testosterone
 Female:
o Establish that ovulation is occurring regularly: use basal body temperature chart
(0.3°C rise in temp between follicular and luteal phase). Serum progesterone 7 days
following expected ovulation also detects ovulation
o Tubal patency:
 Hysterosalpinography: introduction of radio-opaque material through the
cervix into the uterux & fallopian tubes
 Looks at intrauterine anatomy & tubal patency
 Can be done as outpatient procedure, but can be painful
 Laparoscopy with dye instillation ± hysteroscopy
 Performed under general anaesthesia
Infertility and subfertility Mx

Couples should try (properly) for 12 months
before further investigations
o Timing sexual intercourse
o
o


The most important factor when trying
to conceive is to have sexual
intercourse during the woman’s fertile
phase - that is, the five days leading up
to ovulation and the day of ovulation
itself.
Try Billing’s method of natural family
planning
Diet, exercise levels, weight,
cigarettes, alcohol are all modifiable
to increase fertility
Investigations
o Semen analysis
 3 days abstinence before sampling,
sent to lab within an hour
 If abnormal, do serum FSH and
testosterone levels
o Ultrasound
 To assess female reproductive
anatomy
o Mid-luteal progesterone level (7 days post
ovulation)
 >30nmol/L means ovulation happened
o Hysterosalpingography
 Done as outpatient procedure, does not reveal pelvic abnormalities unless it’s in
the fallopian tubes
o Laparoscopy with dye instillation
 Done under GA, scope is introduced through periumbilical incision
 Endometriosis, adhesions, ovarian diseases can be observed
 Dye is introduced through the cervix and patency of the reproductive organ is
observed – often hysteroscopy is done as well
Treatments for females
o Uterine Leiomyoma
 Depends on type
 Submucosal or polyp alters shape of the uterus and affects fertility and
placenta attachment (miscarriage)
 Removal of these 2 types of fibroids through surgery (hysteroscopic
myomectomy using diathermy)
o Inducing ovulation with clomiphene citrate (SERM) given at day 2 of menstrual cycle or
FSH injection
 For Polycystic Ovarian syndrome: FSH production is stimulated at the pituitary
level

 Reduce –ve feedback of estrogen
o Endometriosis
 Infertility is caused by adhesions and maybe interference on epithelium
mobility, ovarian functions
 Endometriosis may also cause subfertility by causing more sperm binding to the
ampullary epithelium thereby affecting sperm-endosalpingeal interactions
 Can try IUI (intrauterine insemination), IVF. Treating the disease will not affect
fertility unless endometriosis is mild to moderate in severity.
Treatments for males
o In vitro fertilization with/without Intra-cytoplasmic sperm injection
 2 injections
 FSH to stimulate follicles (growth is
monitored using serum oestrogen
blood test)
 Ovum is harvested using a needle and
Ultrasound guidance
 Egg is fertilized in the lab and
incubated for around 2 days until it
has developed 2-4 cells
 The zygote is then transferred back into the womb (embryo transfer)
using a small catheter
o Testicular biopsy
 Mainly for obstruction causes of infertility
 Eg. Tube scaring or vasectomy
o Intrauterine insemination for oligospermia
 Semen is washed to eliminate
immotile sperms
 Sometimes an intramuscular
injection (FSH) is given to stimulate
ovulation
 If not, the female’s
menstrual cycle is observed
and the procedure planned
to be done after ovulation
References
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Conceiving_a_baby_tips?open
http://www.bmj.com/content/321/7271/1259.full
http://doctor.ndtv.com/photodetail/ndtv/id/7723/10_Tips_to_help_a_woman_conceive.html
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Infertility_male?open
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Infertility_female?open
Women’s Health, A core curriculum, Finn et al.
http://www.fibroidsecondopinion.com/fibroids-and-pregnancy/
http://emedicine.medscape.com/article/271899-treatment
http://www.ecca.com.au/infertilityhttp://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/In_vitro_fertilisation
http://www.monashivf.com/Services/Male_Factor_Treatment.aspx
Amenorrhoea
Definition
Primary
Secondary
Condition in which girls fail to develop
Cessation of menstruation for more than 6
secondary sexual characteristics by age 14 or
months in a normal female reproductive age,
fail to menstruate by age 16
not due to pregnancy
Important

Familial (late puberty)

Hormonal dysfunction – very common
Causes

Turner’s syndrome

Hyperprolactinemia

Testicular feminisation syndrome

PCOS

Structural malformations

Premature menopause

Causes of secondary amenorrhoea (if

Pregnancy
established before menarche)

Intra-uterine adhesions

Developmental history

Developmental history

Family history

Menstrual, contraceptive, reproductive

As for secondary where relevant
History
Examination
Hx

Menopausal symptoms

↑Weight loss, exercise, stress

Psychological history

Family history

General appearance, height/weight

Virilising signs or galactorrhoea

External 2◦ sexual characteristics

Visual field disturbance, papilloedema

Abdominal exam, ?internal genitalia

Pelvic exam – outflow tract

As for secondary where relevant
abnormality, atrophic effects of hypooestrogenism
Investigations
Treatment
1

Karyotyping

B-HCG to exclude pregnancy

Pelvic ultrasound (structure)

Hormone tests

Hormone tests

Progestogen challenge

As for secondary where relevant

Pelvic ultrasound
Aim to where possible, help patient look
Depends on cause
normal, function sexually and reproduce if she

If low oestrogen – OCP or HRT1
wishes

Normal/high – treat as for PCOS
Given cyclically can restore normal menstrual rhythm; also important for progection against osteoporosis
Causes
Cause
Description
Hypothalamic/
Stress, ↑ weight loss or
Upsets control of the menstrual cycle  anovulatory
Pituitary
excessive exercise
cycles
Prolactinoma (or other
May present with galactorrhoea, mass effect
cause of ↑prolactin)
MRI to detect adenoma if high PRL levels (>1000pmol/L)
Treat with bromocriptine/cabergoline or surgery for
tumour
Some drugs can also cause raised PRL
Ovarian
Post-pill amenorrhoea
Persistence of negative feedback to pituitary
Sheehan’s syndrome
Post-partum pituitary necrosis (rare)
Kallman’s syndrome
Chronic GnRH deficiency (rare)
Premature menopause
Responsible for 1%
Stock of functional primary follicles is exhausted and
normal follicular development fails despite pituitary
producing increased amounts of FSH and LH
PCOS
Very common
Turner’s syndrome (XO)
Most common cause of gonadal dysgenesis - ovaries fail
to develop  failure of development of secondary sexual
characteristics
Testicular feminisation
Ovaries are absent but primitive testes are present
syndrome
Other
Autoimmune conditions, Swyer’s syndrome2, tumours
(e.g. adrenal or ovarian)
Uterine
Pregnancy
Must exclude!
Asherman’s syndrome
Uterine adhesions preventing endometrial proliferation
(e.g. after over-vigorous curettage, or with TB)
Structural malformations
Includes Mullerian agenesis, absent/rudimentary uterus,
imperforate hymen (apparent primary amenorrhoea)
2
XY gonadal dysgenesis
Hormone Tests

B-HCG
o





First priority – exclude pregnancy
TFTs
o
Hyper and hypothyroidism can cause period irregularities
o
Hypothyroidism may indicate pituitary failure  ↑TRH  ↑PRL
FSH and LH
o
Raised in ovarian failure (especially FSH)
o
Raised in PCOS (especially LH)
o
Low with stress, weight loss, excessive exercise (may be normal if mild)
Testosterone
o
Raised in PCOS
o
High with androgen secreting tumours (>5nmol/L)
Oestrodial
o
High in pituitary tumours
o
Low with ovarian failure or problem at hypothalamic or pituitary level
Prolactin
o
Increased by stress, prolactinoma, drugs
Progestogen Withdrawal Test

Give progestagen for 5 days then stop
o
Positive test (normal response) is menstruation on withdrawal
o
Normal hormone levels and negative test suggests outflow tract disorder or low
endogenous oestrogen
o

Normal hormone levels and positive test suggests anovulation
If withdrawal test negative, give oestrogen for 21 days followed by progesterone for 5 days
then stop
o
Negative test suggests outflow tract abnormality
o
Positive test suggests HPO axis issue
Polycystic Ovarian Syndrome
Generally speaking, it is a syndrome characterised by multiple small cysts in the ovaries, and an
overproduction of androgens by the ovaries. (The cysts are eggs that have failed to mature and be released)
Definition
Rotterdam criteria (2003)*:
After exclusion of related disorders, any 2 of:
1. Oligomenorrhoea or anovulation
2. Clinical or biochemical androgen excess
3. Polycyctic ovaries
“Hirsutism + menstrual disturbances, most likely have PCOS”
(Kumar and Clark 2005)
Hence patients may clinically present with:
1. Oligomenorrhoea (30-50%)
2. Amenorrhoea (19 – 51%)
3. Hirsutism (64 – 69%)
4. Obesity (35 – 41%)
5. Elevated serum LH (40 – 51%)
6. Elevated testosterone (29 – 50%)
7. Subfertility (up to 75%)
8. Also acne (30%), alopecia (5%), acanthosis nigricans (<1-3%)
Epidemiology
 Up to 20-25% of women have polycystic ovaries (on U/S)
 Polycystic ovarian syndrome affects around 5-10% of women of reproductive age**
 Commonest endocrine disturbance affecting women
 Women with PCOS increased risk of DM, dyslipidaemia, and possibly HT... hence higher
cardiovascular risk.
Patho-physiology
 Aetiology and pathogenesis poorly understood.
 Insulin resistance (due to complex genetic causes) is increasingly thought to be important.
 Resulting hyperinsulinaemia causes overproduction of ovarian androgens (insulin and LH
synergistically work to activate the ovarian production of androgens) and a decrease in
serum sex-hormone-binding globulin (SHBG) (insulin suppresses its hepatic production) –
leading to high serum-free testosterone.
 Excess androgen interferes with follicular growth and ovulation, causing menstrual problems
and infertility. Also leads to hirsutism, acne, alopecia, etc.
 Excess androgens may also cause increased LH levels***
 Insulin resistance increase chance of developing obesity.
Investigations
 Elevated serum testosterone levels
 Decreased SHBG
 Elevated LH levels
 Elevated LH:FSH ratio
 Increased fasting insulin levels
 Ultra-sound: polycystic ovaries (more than 8 (or 12) cysts depending on reference)
Treatment
Symptom orientated:
Obesity
NB: weight loss has shown to improve ovulation and the ability to conceive. Apparently it is
‘notoriously difficult’ to achieve in women with PCOS.
 Lifestyle changes
 Metformin: may be effective in some women.
Oligomenorrhoea/Amenorrhoea
NB: women tend to be anovulatory, but have normal or high levels of oestrogen. Hence theoretical
risk of unopposed oestrogenic stimulation of endometrium and increase in risk of endometrial
cancer.
NB: oligomenorrhoeic women tend to have infrequent but heavy bleeds as the endometrium that
develops under the influence of oestrogen eventually becomes unsustainable and sheds.
 Oral contraceptives: establishes normal menstruation, often will help hirsutism and acne
Hirstism
 Mechanical means – bleaching waxing, shaving, etc
 Metformin may help, according to a recent study.
 Spironolactone: anti-androgen drug that blocks androgen receptors. Can reduce sexual hair
by 40-80%, but may take 6 months to take effect.
Subfertility
 Clomiphene citrate (a SERM): can be used to induce ovulation in women with anovulatory
cycles. Clomiphene resistance is common in women with high LH concentrations – use IVF or
other means.
Long term management
 Increased risk of developing DM and CVD (promote good lifestyle)
 Screen for glucose intolerance and dyslipidaemias
NOTES
*: 1990 NIH criteria also exists. It doesn’t have polycystic ovaries as a criterion.
**: 2005 study showed that in Melbourne, the prevalence may be up to 12%
***: according to PCOS association of Australia
REFERENCES
1. PCOS association of Australia INC. <http://main.posaa.asn.au/>
2. Gynaecology by ten teachers
3. Womens health a core curriculum
The 2 main differentials for bleeding in early pregnancy:
1) Ectopic pregnancy
Clinical Features
 Abdominal/pelvic pain
 Delayed period (when the woman doesn’t know she’s pregnant)
 Vaginal bleeding
 Shock (if ruputured) – pallor, tachycardia and hypotension
 Peritonism
 Cervical excitation
Diagnosis
 Serial bHCG – >1500 IU/ml
 Transvaginal Ultrasound Scan
o showing no intrauterine gestation sac
o free fluid in the Pouch of Douglas and adnexal mass on TVS
 Progesterone over 25ng/mL suggests pregnancy
Management
 Methotrexate
o Only in asymptomatic patients, small tube ectopics, non-tubal ectopics and relatively
low bHCG
o It is an antimetabolite that interferes with DNA synthesis
 Laparoscopy – preferred if it is not an emergency
 Salpingectomy (more preferred) or salpingostomy
o Removing the whole fallopian tube or incising it to remove the POC
 If in shock – open laparotomy for greater vision and IV access for crossmatch and fluids
 Cervical pregnancy – embolization, Foley catheter tamponade and suction curettage
 Always give non-sensitised Rh- women with 250IU of anti-D IgG within 72h
2) Miscarriage
Definition and incidence



Is defined as expulsion of products of conception before 20w of gestation (Australia) or 24w
(outside Australia)
Spontaneous miscarriage happens in 20% of pregnancies and most common cause is sporadic
chromosomal abnormalities
Incidence of miscarriage for women aged 35-40 is 21% and 40% for over 40.
Types
Types
Clinical features
Threatened PV bleeding, contractions and
abnormal vaginal discharge
Inevitable
Similar with lower abdominal pain.
“Balooning of the LUS”
Complete
Incomplete
Inevitable features
Increasing cramping lower
abdominal pain with some POC
Missed
Usually none
Septic
Similar to inevitable with malaise
and fever
Explanation
Cervical dilatation is minimal and
membranes are intact. The baby is still alive
External os dilatation >3cm, internal os is
closed and membranes have ruptured. POC
has not been passed yet
Cervical os is closed but the uterus is empty
Internal os is open and POC is evident in the
canal. But some are still retained and
ERPOC is required
Diagnosed normally in first trimester, where
the US shows no foetal heartbeat. Cervix is
normally closed and SFH is less than
expected
“Blighted ovum” appearance (no foetal
pole)
Investigations
 Urine MSU – for infection
 Cervico-vaginal swab
 FBE (anaemia and leukocytosis)
 Blood group for rhesus negative
 Ultrasound: to confirm viability and AFI
Management
 Expectant management in the first trimester (but may need surgical evaluation)
 Anti-D IgG (250IU) within 72h
 Antibiotics if there is infection – erythromycin ± metronidazole or clindamycin for 7d
 For complete miscarriage, serial bHCG is needed for confirmation
 For threatened miscarriage, follow up bHCG is needed to confirm viability of pregnancy
 ERPOC – only for those who have heavy bleeding or prefer to remove it
 Examination of the POC – for trophoblastic disease or ectopic pregnancy
 For cervical incompetence, provide cervical cerclage
Other differentials:
3) Intrauterine fetal demise/ Fetal death syndrome / stillbirths
a. Is defined as death of a baby in the uterus, during pregnancy and before birth, after the
20th week of gestation.
b. Known causes of stillbrith:
i. bacterial infection
ii. birth defects, especially pulmonary hypoplasia
iii. chromosomal aberrations
iv. growth retardation
v. intrahepatic cholestasis of pregnancy
vi. maternal diabetes
vii. high blood pressure, including preeclampsia
viii. recreational drugs contraindicated in pregnancy
ix. postdate pregnancy
x. placental abruptions
xi. physical trauma
xii. radiation poisoning
xiii. Rh disease
xiv. umbilical cord accidents
4) Molar pregnancy (Gestational trophoblastic disease)
a. This is such a huge topic. We can discuss this on the next index case.
5) Postcoital bleeding (bleeding after sexual intercourse)
6) Trauma
Sources:
Women’s Health: Core Curriculum
Obstetrics By Ten Teachers
eMedicine
Thalassaemia

Hereditary (autosomal recessive) haemoglobinopathy
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Types
◦ thalassaemia minor – one allele of the gene is dysfunctional (carrier)
◦ beta thalassaemia major – severe anaemia (HbS)
◦ alpha thalassaemia major – Barts Hydrops (HbC)
▪ homozygous (major) may result in stillbirth, transfusion dependency, sickling
syndromes or adverse maternal outcomes
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Most common in people of:
◦ mediterranean
◦ middle east
◦ africa
◦ asia
◦ polynesia
◦ subcontinent
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Screening usually offered to couples during first antenatal care visit
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Investigations
◦ FBE
◦ serum ferritin
◦ haemoglobin electrophoresis
◦ DNA analysis in alpha thalassaemia major
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Treatment
◦ beta thalassaemia minor – high dose folic acid (5mg daily) throughout pregnancy
and lactation
◦ no iron supplement unless iron deficient (may have mild degree of iron overload)
◦ chronic blood transfusion therapy, iron chelation, splenectomy
Neural tube defects
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1-2/1000 live births (2nd most common fetal abnormality after cardiac)
Prevalence declining due to natural reasons and increase in antenatal screening
Failure of normal fusion of the neural plate to form the neural tube during the first 28 D
Most women may not be aware they are pregnant then
1-2/1000 live births (2nd most common fetal abnormality after cardiac abnormalities)
Having one affected foetus increased risk of 2nd affected foetus by 10-fold
Women are encouraged to have peri-conceptual folic acid supplementation – those who
have never had an affected pregnancy 500ug/day and those who have previously affected
offspring 5mg/day.
Failure to close at the cranial end:
Anencephaly
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Failure of development of most of the cranium and brain.
Affected infants are stillborn or die shortly after birth.
Encephalocele
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Extrusion of brain and meninges through a midline skull defect
Surgical correction but there are underlying cerebral malformations
Failure to close at the caudal end:
Spinal bifida occulta
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Failure of fusion of the vertebral arch.
May be associated with overlying skin lesion e.g. tuft of hair, lipoma, birth mark, small
dermal sinus, often in lumbar region
Meningocele
 Vertebrae develop normally but meninges are forced through the vertebral spaces.
Myelomeningocele
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An unfused section of the spinal column allows the spinal cord to protrude posteriorly in a
sac enclosed by the meninges. The protruded portion of the spinal cord and the nerves at
that level are not properly developed.
Complications
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Paralysis
Muscle imbalance which may cause dislocation of hips and talipes
Sensory loss
Bladder denervation
Bowel denervation
Scoliosis
Hydrocephalus from Arnold-Chiari malformation (where the cerebellar tonsils herniated
through the foramen magnum disrupting CSF flow)
Termination – Indications and Interventions
Indications:
Psychiatric
 Severe neuroses
 Psychoses
Medical
 Severe cardiac disease – heart failure
 Severe chronic renal disease – renal
failure
 Malignant disease (esp. breast/cervix)
Social
Foetal
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Ze
Viral infections
Haemolytic disease
Genetic defects
Congenital defects incompatible with
normal life (eg anencephaly, spina bifida)
Techniques:
Medical
 <9/40
 Mifepristone (RU486) or methotrexate
followed by misoprostol
 Misoprostol only
 Not available in Australia
 Induction of miscarriage
o Misoprostol 100-200ug bd pv (4
doses)
o Dinoprost pessaries
o RU468/misoprostol
Complications:
Abortion
Haemorrhage
Incomplete abortion
Uterine or pelvic infection
Ongoing intrauterine pregnancy, requiring a
surgical abortion for completion
Misdiagnosed/unrecognized ectopic pregnancy
Surgical
 D+C
 Suction curette
 STOP (D+E)
o Vacuum/manual
removal/curette
 Hysterotomy
o Similar to LUSCS
 Smaller incision
 IDX (Partial-birth abortion)
o Partial breech delivery
o Evacuation of foetal skull
Surgical specific
Hematometra (blood clots accumulating in the
uterus)
Uterine perforation
Cervical laceration
Termination
An estimated 80,000 - 90,000 surgical abortions are performed in Australia each year. This equates
to approximately 250 per day, or one abortion for every 2.8 live births. One in three Australian
women will have an abortion in their lifetime.
Legal factors
Abortion is legal in Victoria as determined in The Abortion Law Reform Act (2008). Abortion for any
reason is an option up to 24 weeks gestation. Late-term abortions are legal but usually only done for
severe foetal abnormalities. For a termination to occur after 24 weeks two doctors must agree and
make the decision while considering all factors including: medical, physical, psychological and social.
The act states the following obligation for health practitioners: if a woman requests a registered
health practitioner to advise on a proposed abortion, or to perform, direct, authorise or supervise an
abortion for that woman, and the practitioner has a conscientious objection to abortion, the
practitioner must— refer the woman to another registered health practitioner in the same regulated
health profession who the practitioner knows does not have a conscientious objection to abortion.
Ethical factors
Big question: When does life actually begin?
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Conception
Implantation
‘Quickening’ – when foetus moves into uterus (16-17 weeks)
o Historically, from this time onwards abortion was illegal
Tissue separation
Brain activity
Viability of the foetus
Birth
Arguments against abortion
Killing people is wrong
- Life begins at conception
- A foetus is a person/potential person
therefore are prematurely ending a
person’s life
Causing pain is wrong
Increasing tolerance of killing is wrong
- Not appreciating the sanctity of life
Abortion sidesteps the oppression of women
Megan Clancy
- For a woman who is raped, starving or in
a relationship who gets pregnant – the
problem is not that they got pregnant,
it’s the other thing
Arguments for abortion
Not necessarily wrong to end an innocent
person’s life:
- Conjoined twins – operation to separate
them may lead to death of one twin
- Mountaineering – one person can only
save their own life but cutting the rope
holding up a fallen colleague
Pregnant women has rights too
- Moral rights to ownership of her body
and to decide her own future
A foetus is not necessarily a person with rights,
just a collection of cells
Some cases where concern for maternal health
must override concern of survival of the foetus.
Religion
Most religions strongly discourage/forbid abortion unless for very serious reasons. Catholicism and
Sikhism believe life begins at conception. Some Buddhists are not opposed to abortion whereas
others believe it is murder. Overall, abortion on demand is not acceptable in most religions.
Support services
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GP/family doctor
Family Planning Victoria
The Action Centre (for under 25s)
Women’s health centre
Genetic Health Services Victoria
http://www.bbc.co.uk/ethics/abortion/
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Abortion_in_Australia
Breaking Bad News
1. Preparation:
a. Privacy and adequate time.
b. Patient comfort.
c. Be prepared, e.g. have results ready etc.
2. Set the scene:
a. Summarise what has happened to date.
b. Ask what patient is thinking/feeling.
c. Negotiate agenda of consultation.
3. Sharing information:
a. Assess patient’s understanding.
b. “Warning shot”.
c. Provide information simply and honestly (VERY important), avoid jargon and give
information in small chunks.
4. Be sensitive to the patient
a. Encourage patients to express their feelings and acknowledge and respond to this.
b. Look for non-verbal cues.
c. Pause for questions.
d. Allow time for patient to stop listening.
e. Check patient’s understanding.
5. Planning and support:
a. Give broad timeframe of what lies ahead.
b. Assist in prioritising patient concerns.
c. Plan what happens next.
d. Work together.
e. Discuss treatment options.
6. Follow up and closing:
a. Summarise consultation.
b. Arrange review.
c. Provide information on support services and provide written material.
d. Offer assistance to tell others.
7. Document consultation in patient record.